MRCS A Notes Reda v4 Unsecured

MRCS PART A NOTES - REDA
2. Physiology 1
Jugular Venous Pressure (JVP) 3
The Normal ECG 4
Acute Phase Proteins 5
Tumour Necrosis Factor (TNF) 5
Disorders of Acid - Base Balance 6
Arterial Blood Gas (ABG) Interpretation 7
Fluid Compartment Physiology 8
Cerebrospinal Fluid (CSF) 8
Coagulation Cascade 9
Interpretation Blood Clotting Test Results 10
Abnormal Coagulation 10
Hypercoagulability 10
Warfarin 11
Bleeding 11
Cardiac Physiology 12
Electrical Activity of the Heart 14
Inotropes and Cardiovascular Receptors 15
Anion Gap 15
Calcium Homeostasis 16
Hypocalcaemia: Causes and Management 16
Hypercalcaemia 17
Management Of Hypercalcaemia 17
Hyperkalaemia 18
Hypokalaemia 18
ECG Features in Hypokalemia 18
Hypomagnasaemia 19
Hyponatraemia 19
Hyperuricaemia 20
Potassium Secretion - GI Tract 20
Iron Metabolism 20
Pulmonary Artery Occlusion Pressure Monitoring 21
Respiratory Physiology: Lung Compliance 21
Transfer Factor 21
Control of Ventilation 22
Alveolar Ventilation 22
Oxygen Transport 23
Lung Volumes 24
Parathyroid Hormone 25
Glucagon 25
Gastrointestinal Secretions 25
Gastric Secretions 26
Peristalsis 28
Pancreas Endocrine Physiology 28
Pancreas Exocrine Physiology 28
Renal Physiology 29
Acute Renal Failure: Pre Renal Failure Vs. Acute Tubular Necrosis 30
Diuretic Agents 30
Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Causes 31
Renin 31
Renin-Angiotensin-Aldosterone System 32
Phases of Wound Healing 33
Response to Surgery 33
Stress Response: Endocrine and Metabolic Changes 34
Shock 36
Urinary Incontinence 38
Adrenal Physiology 39
Vitamin Deficiency 40
Vitamin B12 Deficiency 40
3. Pathology 41
Acute Inflammation 42
Chronic Inflammation 43
Gastritis 44
Lead Poisoning 44
Cell Death 45
Disseminated Intravascular Coagulation 46
Disseminated Intravascular Coagulation - Diagnosis 46
Cardiac Murmurs 47
Nerve Injury 47
Absence Of The Vas Deferens 48
Cleft Lip and Palate 48
Choanal Atresia 48
Achondroplasia 48
Genetics and Surgical Disease 49
Tumour Markers 49
Hodgkins Lymphoma 50
Acute Intermittent Porphyria 51
Aggressive Fibromatosis 51
Hereditary Spherocytosis 51
Hypersensitivity Reactions 51
Koebner Phenomenon 51
Adrenal Lesions - Incidental 52
Phaeochromocytoma and Adrenal Lesions 52
Glucagonoma 53
Glioma 53
Thymus 53
Sarcomas 54
Trypanosoma Cruzi 55
Actinomycosis 55
Burns 56
Collagen 57
4. Peri-operative care 59
American Society of Anesthesiologists Physical Status Scoring System
(ASA) 60
Preparation for Surgery 60
Pre-operative Fluid Management 61
Intra-operative Fluid Management 61
Intravenous Access 62
Atropine 62
Local Anaesthetic Agents 63
Anaesthetic Agents 64
Airway Management 64
Muscle Relaxants 65
Malignant Hyperthermia 65
Tourniquets 66
Blood Products - Cross Matching 67
Heparin 67
Thromboprophylaxis in Surgical Patients 68
Proactive Care of Older People Undergoing Surgery (POPS) 68
5. Post-op management and care 69
Acute Dystonic Reaction 70
Acute Renal Failure 70
Brain Death 70
Adult Respiratory Distress Syndrome 71
Circulatory Support of the Critically Ill 72
Cryoprecipitate 72
Massive Haemorrhage 73
Hypovolaemia and The Surgical Patient 73
Management of Pain 74
Neuropathic Pain 75
Nutrition Monitoring - NICE Guidelines 76
Nutrition Screening - NICE Guidelines 76
Refeeding Syndrome 76
Nutrition Prescriptions 77
Oral, Enteral and Parenteral Feeding - NICE Guidelines Summary 77
Post-Operative Fluid Management 78
Postoperative Cognitive Dysfunction (POCD) Management 78
Pulmonary Embolism: Investigation 79
Pulmonary Function Tests 79
Surgical Complications 80
Surgical Site Infection 82
6. Surgical technique and tech 83
Gases For Laparoscopic Surgery 84
Pneumoperitoneum - Therapeutic 84
Sterilisation 84
Suture Material 85
Suture Sizes 85
Methods of Wound Closure 86
Tissue Reconstruction 87
Biological Agents 88
Electrosurgery 88
Diathermy 89
Treatment of Suspicious Skin Lesions 89
7. Legal issues 91
Audit and Research 91
Audit Categories 92
Consent 92
Cluster Randomised Controlled Trials 93
Incidence and Prevalence 93
Forest Plots 93
Normal Distribution 94
Pre and Post Test Odds and Probability 94
Qualitative and Quantitative Data 95
Relative Risk 95
Absolute Risk Reduction 95
Positive Predictive Values 96
Screening Test Statistics 96
Significance Tests 97
Power Calculations and Statistical Error 97
Statistics 98
Study Design 99
Study Design: Evidence and Recommendations 99
8. Clinical microbiology 101
Surgical Microbiology 102
Antibiotics: Mechanism of Action 103
MRSA 103
Streptococci 104
Acute Tonsillitis 104
Salmonella 104
Bacterial Gastroenteritis 105
Gastro Intestinal Parasitic Infections 106
Hepatitis B 107
Hepatitis C 108
HIV Testing 108
Meleney's Gangrene and Necrotising Fasciitis 109
Osteomyelitis 110
Oncoviruses 110
9. Emergency medicine 111
Addisonian Crisis 112
Anaphylactic Shock 112
Compartment Syndrome 112
Fluid Resuscitation Burns 113
Hypothermia 114
Local Anaesthetic Toxicity 114
Chest Pain in Pregnancy 115
Imaging in the Pregnant Trauma Patient 115
Management of Acute Coronary Syndrome 116
Thrombolysis or Percutaneous Intervention in Myocardial Infarction 116
Ventricular Tachycardia 117
Ventricular Tachycardia: Management 117
Torsades De Pointes 118
Pulmonary Embolism: ECG Changes 118
Pulmonary Embolism: Management 118
Management of Hyperkalaemia 119
Thoracic Trauma 120
Tension Pneumothorax 121
Thoracic Aorta Rupture 122
Vascular Trauma 122
Stroke: Types 123
Head Injury Management - NICE Guidelines 124
Head Injury - Paediatrics 125
Craniomaxillofacial Injuries 126
Oculogyric Crisis 128
Opioid Misuse 128
Sickle Cell Anaemia 129
10. Surgical oncology 131
Extravasation Injury 132
Chemotherapy Agents 132
Chordoma 132
Notes and Mnemonics 132
Secondary Malignant Tumours of Bone 133
Lung Cancer: Non-Small Cell Management 133
Tissue Sampling 134
11. The abdomen 135
Abdominal Incisions 136
Abdominal Stomas 137
Right Iliac Fossa Pain 138
Abdominal Signs 138
Acute Abdominal Pain - Diagnoses 139
Gynaecological Causes of Abdominal Pain 140
Drain Types 141
Splenic Vein Thrombosis 141
Diarrhoea 142
Abdominal Wound Dehiscence 143
Hernia 144
Malabsorption 145
Mesenteric Vessel Disease 146
Abdominal Radiology 147
Irritable Bowel Syndrome (IBS) 147
Splenic Trauma 148
12. Upper gastrointestinal surgery 149
Upper Gastrointestinal Bleeding 150
Rockall Score 152
Dysphagia 152
Bariatric Surgery 153
Gastric Cancer 154
Gastric Emptying 156
Lower Gastrointestinal Bleeding 157
Oesophageal Disease 158
Oesophageal Cancer - Treatment 159
Nutrition Options in Surgical Patients 160
13. Hepatobiliary and pancreatic surgery 161
Benign Liver Lesions 162
Biliary Disease 163
Surgical Jaundice 164
Gallstones 166
Notes and Mnemonics 167
Pancreatic Cancer 168
Management of Acute Pancreatitis in The UK 169
Pancreatitis: Sequelae 170
14. Colorectal surgery 171
Ano Rectal Disease 172
Benign Proctology 173
Rectal Bleeding 174
Pilonidal Sinus 175
Colonic Polyps 176
Polyposis Syndromes 177
Laxatives 177
Genetics of Colorectal Cancer 178
Colorectal Cancer Screening and Diagnosis 179
Dukes Classification 179
Colorectal Cancer Treatment Summary of Procedures 180
Crohn’s Disease 182
Ulcerative Colitis 183
15. Breast and endocrine surgery 185
Mnemonics 186
Aberrations of Normal Development and Involution - Breast 186
Benign Breast Lesions & Non-Malignant Breast Disease 187
Breast Cancer 188
Pagets Disease of The Nipple 188
Breast Cancer Treatment 189
Breast Cancer - In Situ Disease 189
Nipple Discharge 190
Lymphoedema 191
Multiple Endocrine Neoplasia 192
Parathyroid Glands and Disorders of Calcium Metabolism 193
Thyroid Disease 194
Thyroid Function Tests 194
Thyroid Malignancy 195
Blood Testing in Thyroid Disease 195
Thyroiditis 196
16. Vascular surgery 197
Vasculitis 198
Vascular disorders of the upper limb 199
Axillary vein thrombosis 200
Ankle-Brachial pressure index 200
Acute limb ischaemia 201
Klippel-Trenaunay-Weber 201
Chronic venous insufficiency and varicose veins 202
Lower leg ulcers 204
Vascular disease 205
Peripheral vascular disease 206
Aortic dissection 207
Abdominal aorta aneurysm 208
Amputations 210
Vascular Investigations 211
17. Urology 213
Mnemonics 214
Scrotal swelling 214
Testicular cancer 215
Priapism 215
Prostate Cancer 216
Causes of Haematuria 217
Renal stones 218
Lower genitourinary tract trauma 219
Renal lesions 220
Hydronephrosis 221
Functional renal imaging 221
18. Organ transplantation 223
Transplant types 224
Organ transplantation: immunosuppressants 224
Complications following renal transplant 225
Renal transplant:HLA typing and graft failure 226
19. Head and neck surgery 227
Neck lumps 228
Neck Masses in Children 228
Submandibular glands disease 229
Parotid gland clinical 230
Diseases of nose and sinuses 232
Epistaxis 233
Voice production 233
Disorders affecting the ear 234
20. Skin disorders 235
Skin Diseases 236
Benign skin diseases 238
Sebaceous cysts 238
Malignancy and related lesions 239
Merkel cell tumours of the skin 240
21. Hand disorders 241
Hand diseases 241
22. Surgical disorders of the brain 243
Head injury 244
Third nerve palsy 245
Glasgow coma scale 245
Sub arachnoid haemorrhage 246
Head injury and hematoma 246
Von Hippel-Lindau syndrome 246
Notes & Mnemonics 246
23. Paediatric surgery 247
Congenital heart disease 248
Tetralogy of Fallot 248
Paediatric fluid management 249
Meckel's diverticulum 249
Paediatric Gastrointestinal disorders 250
Paediatric GI Bleeding 250
Bilious vomiting in neonates 251
Biliary atresia 251
Paediatric umbilical disorders 252
Paediatric inguinal hernia 252
Paediatric Urology - Foreskin disorders 253
Bronchogenic cysts 253
Urinary tract infection - Paediatric 254
Urethral valves 254
Vesicoureteric reflux 254
24. Orthopaedics 255
Avascular necrosis 256
Bone disease 257
Osteomalacia 257
Epiphyseal fractures 258
Scaphoid fractures 258
Eponymous fractures 259
Pathological fractures 260
Pseudogout 260
Knee injury 261
Knee collateral ligament 262
Paediatric orthopaedics 263
Perthes disease 263
Septic Arthritis - Paediatric 264
Talipes Equinovarus 264
Diseases affecting the vertebral column 265
Spinal disorders 266
Ankle injuries 269
Shoulder disorders 271
25. Reference Ranges 275
Reference ranges 275
1
2. Physiology – MRCS Notes - Reda

Jugular Venous Pressure (JVP) ....................................................................................................................... 3
The Normal ECG .............................................................................................................................................. 4
Acute Phase Proteins ...................................................................................................................................... 5
Tumour Necrosis Factor (TNF) ........................................................................................................................ 5
Disorders of Acid - Base Balance .................................................................................................................... 6
Arterial Blood Gas (ABG) Interpretation ........................................................................................................ 7
Fluid Compartment Physiology ...................................................................................................................... 8
Cerebrospinal Fluid (CSF) ................................................................................................................................ 8
Coagulation Cascade ....................................................................................................................................... 9
Interpretation Blood Clotting Test Results .................................................................................................. 10
Abnormal Coagulation .................................................................................................................................. 10
Hypercoagulability ........................................................................................................................................ 10
Warfarin ........................................................................................................................................................ 11
Bleeding......................................................................................................................................................... 11
Cardiac Physiology ........................................................................................................................................ 12
Electrical Activity of the Heart...................................................................................................................... 14
Inotropes and Cardiovascular Receptors ..................................................................................................... 15
Anion Gap...................................................................................................................................................... 15
Calcium Homeostasis .................................................................................................................................... 16
Hypocalcaemia: Causes and Management .................................................................................................. 16
Hypercalcaemia............................................................................................................................................. 17
Management Of Hypercalcaemia................................................................................................................. 17
Hyperkalaemia .............................................................................................................................................. 18
Hypokalaemia ............................................................................................................................................... 18
ECG Features in Hypokalemia ...................................................................................................................... 18
Hypomagnasaemia ....................................................................................................................................... 19
Hyponatraemia ............................................................................................................................................. 19
Hyperuricaemia............................................................................................................................................. 20
Potassium Secretion - GI Tract ..................................................................................................................... 20
Iron Metabolism ........................................................................................................................................... 20
Pulmonary Artery Occlusion Pressure Monitoring ...................................................................................... 21
Respiratory Physiology: Lung Compliance ................................................................................................... 21
Transfer Factor .............................................................................................................................................. 21
Control of Ventilation ................................................................................................................................... 22
Alveolar Ventilation ...................................................................................................................................... 22
Oxygen Transport ......................................................................................................................................... 23
Lung Volumes ................................................................................................................................................ 24
2. PHYSIOLOGY – MRCS NOTES - REDA 1

2
Parathyroid Hormone ................................................................................................................................... 25
Glucagon ....................................................................................................................................................... 25
Gastrointestinal Secretions .......................................................................................................................... 25
Gastric Secretions ......................................................................................................................................... 26
Peristalsis ...................................................................................................................................................... 28
Pancreas Endocrine Physiology .................................................................................................................... 28
Pancreas Exocrine Physiology ...................................................................................................................... 28
Renal Physiology ........................................................................................................................................... 29
Acute Renal Failure: Pre Renal Failure Vs. Acute Tubular Necrosis ............................................................ 30
Diuretic Agents.............................................................................................................................................. 30
Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Causes .......................................................... 31
Renin ............................................................................................................................................................. 31
Renin-Angiotensin-Aldosterone System ...................................................................................................... 32
Phases of Wound Healing ............................................................................................................................. 33
Response to Surgery ..................................................................................................................................... 33
Stress Response: Endocrine and Metabolic Changes .................................................................................. 34
Shock ............................................................................................................................................................. 36
Urinary Incontinence .................................................................................................................................... 38
Adrenal Physiology ....................................................................................................................................... 39
Vitamin Deficiency ........................................................................................................................................ 40
Vitamin B12 Deficiency ................................................................................................................................. 40

3
Jugular Venous Pressure (JVP)
As well as providing information on right atrial pressure, the jugular vein waveform may provide clues to underlying
valvular disease. A non-pulsatile JVP is seen in superior vena caval obstruction. Kussmaul's sign describes a paradoxical
rise in JVP during inspiration seen in constrictive pericarditis
'a' wave = atrial contraction

• large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
• absent if in atrial fibrillation
Cannon 'a' waves

• caused by atrial contractions against a closed tricuspid valve
• are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular
pacing
'c' wave
• closure of tricuspid valve
• not normally visible
'v' wave
• due to passive filling of blood into the atrium against a closed tricuspid valve
• giant v waves in tricuspid regurgitation
'x' descent = fall in atrial pressure during ventricular systole
'y' descent = opening of tricuspid valve
JVP
3 Upward deflections and 2
downward deflections
Upward deflections
a wave = atrial contraction
c wave = ventricular contraction
v wave = atrial venous filling
Downward deflections
x wave = atrium relaxes and
tricuspid valve moves down
y wave = ventricular filling
Absent a waves = Atrial fibrillation

Large a waves = Any cause of right ventricular hypertrophy, tricuspid stenosis
Cannon waves (extra large a waves) = Complete heart block
Prominent v waves = Tricuspid regurgitation
Slow y descent = Tricuspid stenosis, right atrial myxoma
Steep y descent = Right ventricular failure, constrictive pericarditis, tricuspid regurgitation

4
The Normal ECG
P wave
• Represents the wave of depolarization that spreads from the SA node throughout the atria
• Lasts 0.08 to 0.1 seconds (80-100 ms)
• The isoelectric period after the P wave represents the time in which the impulse is traveling within the AV node
P-R interval
• Time from the onset of the P wave to the beginning of the QRS complex
• Ranges from 0.12 to 0.20 seconds in duration
• Represents the time between the onset of atrial depolarization and the onset of ventricular depolarization
QRS complex
• Represents ventricular depolarization
• Duration of the QRS complex is normally 0.06 to 0.1 seconds
ST segment
• Isoelectric period following the QRS
• Represents period which the entire ventricle is depolarized and roughly corresponds to the plateau phase of the
ventricular action potential
T wave
• Represents ventricular repolarization and is longer in duration than depolarization
• A small positive U wave may follow the T wave which represents the last remnants of ventricular repolarization.
Q-T interval
• Represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly
estimates the duration of an average ventricular action potential.
• Interval ranges from 0.2 to 0.4 seconds depending upon heart rate.
• At high heart rates, ventricular action potentials shorten in duration, which decreases the Q-T interval.
Therefore, the Q-T interval is expressed as a "corrected Q-T (QTc)" by taking the Q-T interval and dividing it by
the square root of the R-R interval (interval between ventricular depolarizations). This allows an assessment of
the Q-T interval that is independent of heart rate.
• Normal corrected Q-Tc interval is less than 0.44 seconds.

5
Acute Phase Proteins
• CRP
• procalcitonin
• ferritin
• fibrinogen
• alpha-1 antitrypsin
• caeruloplasmin
• serum amyloid A
• haptoglobin
• complement
During the acute phase response the liver decreases the production of other proteins (sometimes referred to as negative
acute phase proteins). Examples include:
• albumin
• transthyretin (formerly known as prealbumin)
• transferrin
• retinol binding protein
• cortisol binding protein
Levels of CRP are commonly measured in acutely unwell patients. CRP is a protein synthesised in the liver and binds to
phosphocholine in bacterial cells and on those cells undergoing apoptosis. In binding to these cells it is then able to
activate the complement system. CRP levels are known to rise in patients following surgery. However, levels of greater
than 150 at 48 hours post operatively are suggestive of evolving complications.
Tumour Necrosis Factor (TNF)

Tumour necrosis factor (TNF) is a pro-inflammatory cytokine with multiple roles in the immune system
TNF is secreted mainly by macrophages and has a number of effects on the immune system, acting mainly in a paracrine
fashion:
• activates macrophages and neutrophils
• acts as costimulator for T cell activation
• key mediator of bodies response to Gram negative septicaemia
• similar properties to IL-1
• anti-tumour effect (e.g. phospholipase activation)
TNF-alpha binds to both the p55 and p75 receptor. These receptors can induce apoptosis. It also cause activation of NFkB
Endothelial effects include increase expression of selectins and increased production of platelet activating factor, IL-1
and prostaglandins
TNF promotes the proliferation of fibroblasts and their production of protease and collagenase. It is thought fragments
of receptors act as binding points in serum
Systemic effects include pyrexia, increased acute phase proteins and disordered metabolism leading to cachexia
TNF is important in the pathogenesis of rheumatoid arthritis - TNF blockers (e.g. infliximab, etanercept) are now licensed
for treatment of severe rheumatoid

6
Disorders of Acid - Base Balance
Disorders of acid- base balance are often covered in the MRCS part A, both in the SBA and EMQ sections.
1- Metabolic acidosis
• This is the most common surgical acid - base disorder.
• Reduction in plasma bicarbonate levels.
• Two mechanisms:
a. Gain of strong acid (e.g. diabetic ketoacidosis)
b. Loss of base (e.g. from bowel in diarrhoea)
- Classified according to the anion gap, this can be calculated by: (Na+ + K+) - (Cl- + HCO 3 -).
- If a question supplies the chloride level then this is often a clue that the anion gap should be calculated. The
normal range = 10-18 mmol/L
Normal anion gap ( = hyperchloraemic metabolic acidosis)
• Gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
• Renal tubular acidosis
• Drugs: e.g. acetazolamide
• Ammonium chloride injection
• Addison's disease
Raised anion gap
• Lactate: shock, hypoxia
• Ketones: diabetic ketoacidosis, alcohol
• Urate: renal failure
• Acid poisoning: salicylates, methanol
Metabolic acidosis secondary to high lactate levels may be subdivided into two types:
• Lactic acidosis type A: (Perfusion disorders e.g.shock, hypoxia, burns)
• Lactic acidosis type B: (Metabolic e.g. metformin toxicity)

7
2- Metabolic alkalosis
• Usually caused by a rise in plasma bicarbonate levels.
• Rise of bicarbonate above 24 mmol/L will typically result in renal excretion of excess bicarbonate.
• Caused by a loss of hydrogen ions or a gain of bicarbonate. It is due mainly to problems of the kidney or
gastrointestinal tract
Causes
• Vomiting / aspiration (e.g. Peptic ulcer leading to pyloric stenosis, nasogastric suction)
• Diuretics
• Liquorice, carbenoxolone
• Hypokalaemia
• Primary hyperaldosteronism
• Cushing's syndrome
• Bartter's syndrome
• Congenital adrenal hyperplasia
Mechanism of metabolic alkalosis
• Activation of renin-angiotensin II-aldosterone (RAA) system is a key factor
• Aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
• ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
• In hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality
3- Respiratory acidosis
• Rise in carbon dioxide levels usually as a result of alveolar hypoventilation
• Renal compensation may occur leading to Compensated respiratory acidosis
Causes
• COPD
• Decompensation in other respiratory conditions e.g. Life-threatening asthma / pulmonary oedema
• Sedative drugs: benzodiazepines, opiate overdose
4- Respiratory alkalosis
• Hyperventilation resulting in excess loss of carbon dioxide
• This will result in increasing pH
Causes
• Psychogenic: anxiety leading to hyperventilation
• Hypoxia causing a subsequent hyperventilation: pulmonary embolism, high altitude
• Early salicylate poisoning*
• CNS stimulation: stroke, subarachnoid haemorrhage, encephalitis
• Pregnancy
*Salicylate overdose leads to a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory
centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure)
may lead to an acidosis
Arterial Blood Gas (ABG) Interpretation

In advanced life support training, a 5 step approach to arterial blood gas interpretation is advocated.
1. How is the patient?
2. Is the patient hypoxaemic?
The Pa0 2 on air should be 10.0-13.0 kPa
3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)
4. What has happened to the PaCO 2 ?
If there is acidaemia, an elevated PaCO 2 will account for this
5. What is the bicarbonate level or base excess?
A metabolic acidosis will have a low bicarbonate level and a low base excess (< -2 mmol)
A metabolic alkalosis will have a high bicarbonate and a high base excess (> +2 mmol)

8
Fluid Compartment Physiology
Body fluid compartments comprise intracellular and extracellular compartments. The latter includes interstitial fluid,
plasma and transcellular fluid.
Typical figures are based on the 70 Kg male.
Body fluid volumes

Compartment Volume in litres Percentage of total volume
Intracellular 28 L 60-65%
Extracellular 14 L 35-40%
Plasma 3L 5%
Interstitial 10 L 24%
Transcellular 1L 3%
Figures are approximate
Cerebrospinal Fluid (CSF)

The CSF fills the space between the arachnoid mater and pia mater (covering surface of the brain). The total volume of
CSF in the brain is approximately 150ml. Approximately 500 ml is produced by the ependymal cells in the choroid plexus
(70%), or blood vessels (30%). It is reabsorbed via the arachnoid granulations which project into the venous sinuses.
Circulation
1. Lateral ventricles (via foramen of Munro)
2. 3rd ventricle
3. Cerebral aqueduct (aqueduct of Sylvius)
4. 4th ventricle (via foramina of Magendie and Luschka)
5. Subarachnoid space
6. Reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus
Composition
• Glucose: 50-80mg/dl
• Protein: 15-40 mg/dl
• Red blood cells: Nil
• White blood cells: 0-3 cells/ mm3

9
Coagulation Cascade
Two pathways lead to fibrin formation
Intrinsic pathway (components already present in the blood)
• Minor role in clotting
• Subendothelial damage e.g. collagen
• Formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and
Factor 12
• Prekallikrein is converted to kallikrein and Factor 12 becomes activated
• Factor 12 activates Factor 11
• Factor 11 activates 9, which with its co-factor Factor 8a form the tenase complex which activates Factor 10
Extrinsic pathway (needs tissue factor released by damaged tissue)
• Tissue damage
• Factor 7 binds to Tissue factor
• This complex activates Factor 9
• Activated Factor 9 works with Factor 8 to activate Factor 10
Common pathway
• Activated Factor 10 causes the conversion of prothrombin to thrombin
• Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to form links between
fibrin molecules
Fibrinolysis
Plasminogen is converted to plasmin to facilitate clot resorption
Intrinsic pathway Increased APTT Factors 8,9,11,12

Extrinsic pathway Increased PT Factor 7
Common pathway Increased APTT & PT Factors 2,5,10
Vitamin K dependent Factors 2,7,9,10

10
Interpretation Blood Clotting Test Results
Disorder PT / INR aPTT Thrombin Platelet Bleeding
time count time
Heparin ↔/↑ ↑↑ ↑↑ ↔ ↔
DIC ↑↑ ↑↑ ↑↑ ↓ ↑
Liver disease ↑ ↑ ↔/↑ ↔/↓ ↔/↑
Platelet defect ↔ ↔ ↔ ↔ ↑(↑)
Vitamin K deficiency / Warfarin ↑↑ ↑ ↔ ↔ ↔
Haemophilia ↔ ↑↑ ↔ ↔ ↔
von Willebrand's disease ↔ ↑↑ ↔ ↔ ↑(↑)
Aspirin ↔ ↔ ↔ ↔ ↑
Abnormal Coagulation
Cause Factors affected
Heparin Prevents activation factors 2,9,10,11
Warfarin Affects synthesis of factors 2,7,9,10
DIC Factors 1,2,5,8,11
Liver disease Factors 1,2,5,7,9,10,11
Hypercoagulability
Type of thrombophilia Features
Antithrombin deficiency Antithrombin inactivates thrombin and factor XII a, XIa, IXa and Xa
Rare defect, inherited in autosomal dominant fashion
10x increase in risk of thrombotic events
Heparin may be ineffective because it works via antithrombin
Protein C and S deficiency These are natural anticoagulants (vitamin K dependent synthesis)
Protein C produced by liver
Protein S produced by liver, megakaryocytes, Leydig cells and endothelial cells
Protein C and S bind to form activated complex which binds to factor V
Deficiency accounts for up to 5% of thrombotic episodes
Factor V Leiden Resistance to anticoagulant effect of activated protein C
May account for up to 20% or more of thrombotic episodes
Prevalence of 7% in Europe
Most common genetic defect accounting for DVT
Antiphospholipid syndrome Multi organ disease
Pregnancy involvement common
Arterial and venous thromboses
Either Lupus anticoagulant or Anti cardiolipin antibodies
APTT usually prolonged
Antibodies may be elevated following surgery, drugs or malignancy
Need anticoagulation with INR between 3 and 4

11
Warfarin
Warfarin is an oral anticoagulant which inhibits the reduction of vitamin K to its active hydroquinone form, which in turn
acts as a cofactor in the formation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C
Factors that may potentiate warfarin Aid to memoire: WEPT

• Liver disease Warfarin Extrinsic Prothrombin Time
• P450 enzyme inhibitors, e.g.: amiodarone, ciprofloxacin
• Cranberry juice
• Drugs which displace warfarin from plasma albumin, e.g. NSAIDs
• Inhibit platelet function: NSAIDs
Side-effects
• Haemorrhage
• Teratogenic
• Skin necrosis: when warfarin is first started biosynthesis of protein C is reduced. This results in a temporary
procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration.
Thrombosis may occur in venules leading to skin necrosis.
Bleeding
The initial response to bleeding, even if of relatively small volume is generalised splanchnic vasoconstriction mediated by
activation of the sympathetic nervous system. This process of vasoconstriction is usually sufficient to maintain renal
perfusion and cardiac output if the volume of blood lost is small. Over the following hours the circulating fluid volume is
restored and normal haemodynamics resume. Loss of greater volumes of blood will typically result in activation in the
renin angiotensin system (see diagram later).
Where the source of bleeding ceases these physiological measures will restore circulating volume. Ongoing bleeding will
result in haemorrhagic shock.
Blood loss is typically quantified by the degree of shock produced as outlined below:
Parameter Class I Class II Class III Class IV
Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml
Blood loss % <15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output >30ml 20-30ml 5-15ml <5ml
Symptoms Normal Anxious Confused Lethargic

12
Cardiac Physiology
• The heart has four chambers ejecting blood into both low pressure and high pressure systems.
• The pumps generate pressures of between 0-25mmHg on the right side and 0-120 mmHg on the left.
• At rest diastole comprises 2/3 of the cardiac cycle.
• The product of the frequency of heart rate and stroke volume combine to give the cardiac output which is typically
5-6L per minute.
Electrical properties
• Intrinsic myogenic rhythm within cardiac myocytes means that even the denervated heart is capable of
contraction.
• In the normal situation the cardiac impulse is generated in the sino atrial node in the right atrium and conveyed
to the ventricles via the atrioventricular node.
• The sino atrial node is also capable of spontaneous discharge and in the absence of background vagal tone will
typically discharge around 100x per minute. Hence the higher resting heart rate found in cardiac transplant
cases. In the SA and AV nodes the resting membrane potential is lower than in surrounding cardiac cells and will
slowly depolarise from -70mV to around -50mV at which point an action potential is generated.
• Differences in the depolarisation slopes between SA and AV nodes help to explain why the SA node will
depolarise first. The cells have a refractory period during which they cannot be re-stimulated and this period
allows for adequate ventricular filling. In pathological tachycardic states this time period is overridden and
inadequate ventricular filling may then occur, cardiac output falls and syncope may ensue.
Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. Sympathetic fibres release nor
adrenaline and circulating adrenaline comes from the adrenal medulla. Noradrenaline binds to β 1 receptors in the SA
node and increases the rate of pacemaker potential depolarisation.
Cardiac cycle
• Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic pressure is high.
• Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic volume 130-160ml.
• Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction. AV Valves bulge
into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected. Shortening of ventricles pulls
atria downwards and drops intra atrial pressure (x-descent).

13
• Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular pressure drops the
aortic pressure remains constant owing to peripheral vascular resistance and elastic property of the aorta. Brief
period of retrograde flow that occurs in aortic recoil shuts the aortic valve. Ventricles will contain 60ml end
systolic volume. The average stroke volume is 70ml (i.e. Volume ejected).
• Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave associated with
closure of the aortic valve increases aortic pressure. The pressure dip before this rise can be seen on arterial
waveforms and is called the incisura. During systole the atrial pressure increases such that it is now above zero
(v- wave). Eventually atrial pressure exceeds ventricular pressure and AV valves open - atria empty passively into
ventricles and atrial pressure falls (y -descent)
The negative atrial pressures are of clinical importance as they can allow air embolization to occur if the neck veins are
exposed to air. This patient positioning is important in head and neck surgery to avoid this occurrence if veins are
inadvertently cut, or during CVP line insertion.
Mechanical properties
• Preload = end diastolic volume
• Afterload = aortic pressure
It is important to understand the principles of Laplace's law in surgery.

• It states that for hollow organs with a circular cross section, the total circumferential wall tension depends upon
the circumference of the wall, multiplied by the thickness of the wall and on the wall tension.
• The total luminal pressure depends upon the cross sectional area of the lumen and the transmural pressure.
Transmural pressure is the internal pressure minus external pressure and at equilibrium the total pressure must
counterbalance each other.
• In terms of cardiac physiology, the law explains that the rise in ventricular pressure that occurs during the
ejection phase is due to physical change in heart size. It also explains why a dilated diseased heart will have
impaired systolic function.
Starlings law
• Increase in end diastolic volume will produce larger stroke volume.
• This occurs up to a point beyond which cardiac fibres are excessively stretched and stroke volume will fall once
more. It is important for the regulation of cardiac output in cardiac transplant patients who need to increase
their cardiac output.
Baroreceptor reflexes
• Baroreceptors located in aortic arch and carotid sinus.
• Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.
• They are stimulated by arterial stretch.
• Even at normal blood pressures they are tonically active.
• Increase in baroreceptor discharge causes:
o Increased parasympathetic discharge to the SA node.
o Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in
stroke volume.
o Decreased sympathetic discharge to venous system causing increased compliance.
o Decreased peripheral arterial vascular resistance
Atrial stretch receptors

• Located in atria at junction between pulmonary veins and vena cava.
• Stimulated by atrial stretch and are thus low pressure sensors.
• Increased blood volume will cause increased parasympathetic activity.
• Very rapid infusion of blood will result in increase in heart rate mediated via atrial receptors: the Bainbridge
reflex.
• Decreases in receptor stimulation results in increased sympathetic activity this will decrease renal blood flow-
decreases GFR-decreases urinary sodium excretion-renin secretion by juxtaglomerular apparatus-Increase in
angiotensin II.
• Increased atrial stretch will also result in increased release of atrial natriuretic peptide.

14
Electrical Activity of the Heart
Myocardial action potential
Phase Description Mechanism
0 Rapid depolarisation Rapid sodium influx
These channels automatically deactivate after a few ms
1 Early repolarisation Efflux of potassium
2 Plateau Slow influx of calcium
3 Final repolarisation Efflux of potassium
4 Restoration of ionic Resting potential is restored by Na+/K+ ATPase
concentrations There is slow entry of Na+ into the cell decreasing the potential difference until
the threshold potential is reached, triggering a new action potential
NB cardiac muscle remains contracted 10-15 times longer than skeletal muscle
Conduction velocity
Atrial conduction Spreads along ordinary atrial myocardial fibres at 1 m/sec
AV node 0.05 m/sec
conduction
Ventricular Purkinje fibres are of large diameter and achieve velocities of 2-4 m/sec (this allows a rapid and
conduction coordinated contraction of the ventricles

15
Inotropes and Cardiovascular Receptors
Inotropes are a class of drugs which work primarily by increasing cardiac output. They should be distinguished from
vasoconstrictor drugs which are used specifically when the primary problem is peripheral vasodilatation.
Catecholamine type agents are commonly used and work by increasing cAMP levels by adenylate cyclase stimulation.
This in turn intracellular calcium ion mobilisation and thus the force of contraction. Adrenaline works as a beta
adrenergic receptor agonist at lower doses and an alpha receptor agonist at higher doses. Dopamine causes dopamine
receptor mediated renal and mesenteric vascular dilatation and beta 1 receptor agonism at higher doses. This results in
increased cardiac output. Since both heart rate and blood pressure are raised, there is less overall myocardial ischaemia.
Dobutamine is a predominantly beta 1 receptor agonist with weak beta 2 and alpha receptor agonist properties.
Noradrenaline is a catecholamine type agent and predominantly acts as an alpha receptor agonist and serves as a
peripheral vasoconstrictor.
Phosphodiesterase inhibitors such as milrinone act specifically on the cardiac phosphodiesterase and increase cardiac
output.
Inotrope Cardiovascular receptor action

Adrenaline α-1, α-2, β-1, β-2
Noradrenaline α-1,( α-2), (β-1), (β-2)
Dobutamine β-1, (β 2)
Dopamine (α-1), (α-2), (β-1), D-1,D-2
Minor receptor effects in brackets
Effects of receptor binding

α-1, α-2 vasoconstriction
β-1 increased cardiac contractility and HR
β-2 vasodilatation
D-1 renal and spleen vasodilatation
D-2 inhibits release of noradrenaline
Anion Gap
The anion gap is calculated by:
(sodium + potassium) - (bicarbonate + chloride)
A normal anion gap is 8-14 mmol/L
It is useful to consider in patients with a metabolic acidosis:
Causes of a normal anion gap or hyperchloraemic metabolic acidosis

• gastrointestinal bicarbonate loss: diarrhoea, ureterosigmoidostomy, fistula
• renal tubular acidosis
• drugs: e.g. acetazolamide
• ammonium chloride injection
• Addison's disease
Causes of a raised anion gap metabolic acidosis

• lactate: shock, hypoxia
• ketones: diabetic ketoacidosis, alcohol
• urate: renal failure
• acid poisoning: salicylates, methanol

16
Calcium Homeostasis
Calcium ions are linked to a wide range of physiological processes. The largest store of bodily calcium is contained within
the skeleton. Calcium levels are primarily controlled by parathyroid hormone, vitamin D and calcitonin.
Hormonal regulation of calcium

Hormone Actions
Parathyroid hormone (PTH) • Increase calcium levels and decrease phosphate levels
• Increases bone resorption
• Immediate action on osteoblasts to increase ca2+ in extracellular fluid
• Osteoblasts produce a protein signaling molecule that activate osteoclasts which
cause bone resorption
• Increases renal tubular reabsorption of calcium
• Increases synthesis of 1,25(OH)2D (active form of vitamin D) in the kidney which
increases bowel absorption of Ca2+
• Decreases renal phosphate reabsorption
1,25-dihydroxycholecalciferol • Increases plasma calcium and plasma phosphate
(the active form of vitamin D) • Increases renal tubular reabsorption and gut absorption of calcium
• Increases osteoclastic activity
• Increases renal phosphate reabsorption
Calcitonin • Secreted by C cells of thyroid
• Inhibits intestinal calcium absorption
• Inhibits osteoclast activity
• Inhibits renal tubular absorption of calcium
Both growth hormone and thyroxine also play a small role in calcium metabolism.
Hypocalcaemia: Causes and Management

The clinical history combined with parathyroid hormone levels will reveal the cause of hypocalcaemia in the majority of
cases
Causes
• Vitamin D deficiency (osteomalacia)
• Acute pancreatitis
• Chronic renal failure
• Hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
• Pseudohypoparathyroidism (target cells insensitive to PTH)
• Rhabdomyolysis (initial stages)
• Magnesium deficiency (due to end organ PTH resistance)
Management
• Acute management of severe hypocalcaemia is with intravenous replacement. The preferred method is with
intravenous calcium chloride, 10ml of 10% solution over 10 minutes
• ECG monitoring is recommended
• Further management depends on the underlying cause
• Calcium and bicarbonate should not be administered via the same route

17
Hypercalcaemia
Main causes
• Malignancy (most common cause in hospital in-patients)
• Primary hyperparathyroidism (commonest cause in non hospitalised patients)
Less common
• Sarcoidosis (extrarenal synthesis of calcitriol )
• Thiazides, lithium
• Immobilisation
• Pagets disease
• Vitamin A/D toxicity
• Thyrotoxicosis
• MEN
• Milk alkali syndrome
Clinical features
Stones, bones, abdominal groans, and psychic moans
High serum calcium levels result in decreased neuronal excitability. Therefore sluggish reflexes, muscle weakness and
constipation may occur.
Management Of Hypercalcaemia
• Free Ca is affected by pH (increased in acidosis) and plasma albumin concentration
• ECG changes include: Shortening of QTc interval
• Urgent management is indicated if:
o Calcium > 3.5 mmol/l
o Reduced consciousness
o Severe abdominal pain
o Pre renal failure
Management:
• Airway Breathing Circulation
• Intravenous fluid resuscitation with 3-6L of 0.9% Normal saline in 24 hours
• Concurrent administration of calcitonin will also help lower calcium levels
• Medical therapy (usually if Corrected calcium >3.0mmol/l)
Bisphosphonates
• Analogues of pryrophosphate
• Prevent osteoclast attachment to bone matrix and interfere with osteoclast activity
• Inhibit bone resorption.
Agents
Drug Side effects Notes
IV Pamidronate pyrexia, leucopaenia Most potent agent
IV Zoledronate response lasts 30 days Used for malignancy associated hypercalcaemia
Calcitonin
• Quickest onset of action however short duration (tachyphylaxis) therefore only given with a second agent.
Prednisolone
• May be given in hypercalcaemia related to sarcoidosis, myeloma or vitamin D intoxication.

18
Hyperkalaemia
• Plasma potassium levels are regulated by a number of factors including aldosterone, acid-base balance and
insulin levels.
• Metabolic acidosis is associated with hyperkalaemia as hydrogen and potassium ions compete with each other
for exchange with sodium ions across cell membranes and in the distal tubule.
• ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a
sinusoidal pattern and asystole
Causes of hyperkalaemia
• Acute renal failure
• Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin,
heparin**
• Metabolic acidosis
• Addison's
• Tissue necrosis/rhabdomylosis: burns, trauma
• Massive blood transfusion
Foods that are high in potassium

• Salt substitutes (i.e. Contain potassium rather than sodium)
• Bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
*beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure
patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment
**both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by
inhibition of aldosterone secretion
Hypokalaemia
Potassium and hydrogen can be thought of as competitors. Hyperkalaemia tends to be associated with acidosis because
as potassium levels rise fewer hydrogen ions can enter the cells
Hypokalaemia with alkalosis

• Vomiting
• Diuretics
• Cushing's syndrome
• Conn's syndrome (primary hyperaldosteronism)
Hypokalaemia with acidosis

• Diarrhoea
• Renal tubular acidosis
• Acetazolamide
• Partially treated diabetic ketoacidosis
ECG Features in Hypokalemia

• U waves
• Small or absent T waves (occasionally inversion)
• Prolonged PR interval
• ST depression
• Long QT interval
In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT!

19
Hypomagnasaemia
Cause of low magnesium
• Diuretics
• Total parenteral nutrition
• Diarrhoea
• Alcohol
• Hypokalaemia, hypocalcaemia
Features
• Paraesthesia
• Tetany
• Seizures
• Arrhythmias
• Decreased PTH secretion → hypocalcaemia
• ECG features similar to those of hypokalaemia
• Exacerbates digoxin toxicity
Hyponatraemia
This is commonly tested in the MRCS (despite most surgeons automatically seeking medical advice if this occurs!). The
most common cause in surgery is the over administration of 5% dextrose.
Hyponatraemia may be caused by water excess or sodium depletion. Causes of pseudohyponatraemia include
hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm. Urinary sodium and osmolarity levels aid
making a diagnosis.
Classification
Urinary sodium > 20 mmol/l Sodium depletion, renal loss Mnemonic: Syndrome of
• Patient often hypovolaemic INAPPropriate Anti-Diuretic
• Diuretics (thiazides) Hormone:
• Addison's Increased
• Diuretic stage of renal failure Na (sodium)
• SIADH (serum osmolality low, urine PP (urine)
osmolality high, urine Na high)
• Patient often euvolaemic
Urinary sodium < 20 mmol/l Sodium depletion, extra-renal loss
• Diarrhoea, vomiting, sweating
• Burns, adenoma of rectum (if villous
lesion and large)
Water excess (patient often • Secondary hyperaldosteronism: CCF,
hypervolaemic and oedematous) cirrhosis
• Reduced GFR: renal failure
• IV dextrose, psychogenic polydipsia
Management
Symptomatic Hyponatremia:
Acute hyponatraemia with Na <120: immediate therapy. Central Pontine Myelinolisis, may occur from overly rapid
correction of serum sodium. Aim to correct until the Na is > 125 at a rate of 1 mEq/h. Normal saline with frusemide is an
alternative method.
The sodium requirement can be calculated as follows :

(125 - serum sodium) x 0.6 x body weight = required mEq of sodium

20
Hyperuricaemia
• Increased levels of uric acid may be seen secondary to either increased cell turnover or reduced renal excretion
of uric acid. Hyperuricaemia may be found in asymptomatic patients who have not experienced attacks of gout
• Hyperuricaemia may be associated with hyperlipidaemia and hypertension. It may also be seen in conjunction
with the metabolic syndrome
Increased synthesis
• Lesch-Nyhan disease
• Myeloproliferative disorders
• Diet rich in purines
• Exercise
• Psoriasis
• Cytotoxics
Decreased excretion
• Drugs: low-dose aspirin, diuretics, pyrazinamide
• Pre-eclampsia
• Alcohol
• Renal failure
• Lead
Potassium Secretion - GI Tract

Potassium secretions
Salivary glands Variable may be up to 60mmol/L
Stomach 10 mmol/L
Bile 5 mmol/L
Pancreas 4-5 mmol/L
Small bowel 10 mmol/L
Rectum 30 mmol/L
The above table provides average figures only and the exact composition varies depending upon the existence of disease,
serum aldosterone levels and serum pH.
A key point to remember for the exam is that gastric potassium secretions are low. Hypokalaemia may occur in vomiting,
usually as a result of renal wasting of potassium, not because of potassium loss in vomit.
Iron Metabolism
Absorption • Duodenum and upper jejunum
• About 10% of dietary iron absorbed
• Fe2+ (ferrous iron) much better absorbed than Fe3+ (ferric iron)
• Ferrous iron is oxidized to form ferric iron, which is combined with apoferritin to form ferritin
• Absorption is regulated according to body's need
• Increased by vitamin C, gastric acid
• Decreased by proton pump inhibitors, tetracycline, gastric achlorhydria, tannin (found in tea)
Transport In plasma as Fe3+ bound to transferrin
Storage Ferritin (or haemosiderin) in bone marrow
Excretion Lost via intestinal tract following desquamation
Distribution in body
Total body iron 4g
Haemoglobin 70%
Ferritin and haemosiderin 25%
Myoglobin 4%
Plasma iron 0.1%

21
Pulmonary Artery Occlusion Pressure Monitoring
The pulmonary artery occlusion pressure is an indirect measure of left atrial pressure, and thus filling pressure of the left
heart. The low resistance within the pulmonary venous system allows this useful measurement to be made. The most
accurate trace is made by inflating the balloon at the catheter tip and "floating" it so that it occludes the vessel. If it is not
possible to occlude the vessel in this way then the measurement gained will be the pulmonary artery end diastolic
pressure.
Interpretation of PAOP
PAOP mmHg Scenario
Normal 8-12
Low <5 Hypovolaemia
Low with pulmonary oedema <5 ARDS
High >18 Overload
When combined with measurements of systemic vascular resistance and cardiac output it is possible to accurately
classify patients.
Systemic vascular resistance

Derived from aortic pressure, right atrial pressure and cardiac output.
SVR=80(mean aortic pressure-mean right atrial pressure)/cardiac output
Respiratory Physiology: Lung Compliance

Lung compliance is defined as change in lung volume per unit change in airway pressure
Causes of increased compliance

• age
• emphysema - this is due to loss alveolar walls and associated elastic tissue
Causes of decreased compliance

• pulmonary oedema
• pulmonary fibrosis
• pneumonectomy
• kyphosis
Transfer Factor
The transfer factor describes the rate at which a gas will diffuse from alveoli into blood. Carbon monoxide is used to test
the rate of diffusion. Results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer
coefficient, KCO)
Causes of a raised TLCO Causes of a lower TLCO
• asthma • pulmonary fibrosis
• pulmonary haemorrhage (Wegener's, Goodpasture's) • pneumonia
• left-to-right cardiac shunts • pulmonary emboli
• polycythaemia • pulmonary oedema
• hyperkinetic states • emphysema
• male gender, exercise • anaemia
• low cardiac output
raised: asthma, haemorrhage, left-to-right shunts, polycythaemia. low: everything else.
KCO also tends to increase with age. Some conditions may cause an increased KCO with a normal or reduced TLCO
• pneumonectomy/lobectomy
• scoliosis/kyphosis
• neuromuscular weakness
• ankylosis of costovertebral joints e.g. ankylosing spondylitis

22
Control of Ventilation
• Control of ventilation is coordinated by the respiratory centres, chemoreceptors, lung receptors and muscles.
• Automatic, involuntary control of respiration occurs from the medulla.
• The respiratory centres control the respiratory rate and the depth of respiration.
Respiratory centres
Medullary respiratory Inspiratory and expiratory neurones. Has ventral group which controls forced voluntary
centre expiration and the dorsal group controls inspiration. Depressed by opiates.
Apneustic centre Lower pons
Stimulates inspiration - activates and prolongs inhalation
Overridden by pneumotaxic control to end inspiration
Pneumotaxic centre Upper pons, inhibits inspiration at a certain point. Fine tunes the respiratory rate.
Ventillatory variables
• Levels of pCO 2 most important in ventilation control
• Levels of O 2 are less important.
• Peripheral chemoreceptors: located in the bifurcation of carotid arteries and arch of the aorta. They respond to
changes in reduced pO 2 , increased H+ and increased pCO 2 in ARTERIAL BLOOD.
• Central chemoreceptors: located in the medulla. Respond to increased H+ in BRAIN INTERSTITIAL FLUID to
increase ventilation. NB the central receptors are NOT influenced by O 2 levels.
Lung receptors include:

• Stretch receptors: respond to lung stretching causing a reduced respiratory rate
• Irritant receptors: respond to smoke etc causing bronchospasm
• J (juxtacapillary) receptors
Alveolar Ventilation
Alveolar ventilation is the volume of fresh air entering the alveoli per minute.
Alveolar ventilation = Minute ventilation - Dead space volume
Minute ventilation
is the total volume of gas ventilated per minute.
MV (ml/min) = tidal volume x Respiratory rate (resps/min).
Dead space ventilation

describes the volume of gas not involved in exchange in the blood.
There are 2 types:
1. Anatomical dead space: 150mls
• Volume of gas in the respiratory tree not involved in gaseous exchange: mouth, pharynx, trachea, bronchi
up to terminal bronchioles
• Measured by Fowlers method
• Increased by: Standing, increased size of person, increased lung volume and drugs causing
bronchodilatation e.g. Adrenaline
2. Physiological dead space: normal 150 mls,

• Volume of gas in the alveoli and anatomical dead space not involved in gaseous exchange.
• Increases in: Ventilation/Perfusion mismatch e.g. PE, COPD, hypotension.

23
Oxygen Transport
Almost all oxygen is transported within erythrocytes. It has limited solubility and only 1% is carried as solution. Therefore
the amount of oxygen transported will depend upon haemoglobin concentration and its degree of saturation.
Haemoglobin
Globular protein composed of 4 subunits. Haem consists of a protoporphyrin ring surrounding an iron atom in its ferrous
state. The iron can form two additional bonds; one with oxygen and the other with a polypeptide chain. There are two
alpha and two beta subunits to this polypeptide chain in an adult and together these form globin. Globin cannot bind
oxygen but is able to bind to carbon dioxide and hydrogen ions, the beta chains are able to bind to 2,3
diphosphoglycerate. The oxygenation of haemoglobin is a reversible reaction. The molecular shape of haemoglobin is
such that binding of one oxygen molecule facilitates the binding of subsequent molecules.
Oxygen dissociation curve

• The oxygen dissociation curve describes the relationship between the percentage of saturated haemoglobin and
partial pressure of oxygen in the blood. It is not affected by haemoglobin concentration.
• Chronic anaemia causes 2, 3 DPG levels to increase, hence shifting the curve to the right
Haldane effect
• Shifts to left = for given oxygen tension there is increased saturation of Hb with oxygen i.e. Decreased oxygen
delivery to tissues
Bohr effect
• Shifts to right = for given oxygen tension there is reduced saturation of Hb with oxygen i.e. Enhanced oxygen
delivery to tissues
Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen delivery
• HbF, methaemoglobin, carboxyhaemoglobin • raised [H+] (acidic)
• low [H+] (alkali) • raised pCO 2
• low pCO 2 • raised 2,3-DPG (diphosphoglycerate)
• low 2,3-DPG • raised temperature
• low temperature

24
Lung Volumes
Tidal volume (TV) • Is the volume of air inspired and expired during each ventilatory cycle at rest.
• It is normally 500mls in males and 340mls in females.
Inspiratory reserve volume • Is the maximum volume of air that can be forcibly inhaled following a normal
(IRV) inspiration. 3000mls.
Expiratory reserve volume • Is the maximum volume of air that can be forcibly exhaled following a normal
(ERV) expiration. 1000mls.
Residual volume (RV) • Is that volume of air remaining in the lungs after a maximal expiration.
• RV = FRC - ERV. 1500mls.
Functional residual • Is the volume of air remaining in the lungs at the end of a normal expiration.
capacity (FRC) • FRC = RV + ERV. 2500mls.
Vital capacity (VC) • Is the maximal volume of air that can be forcibly exhaled after a maximal inspiration.
• VC = TV + IRV + ERV. 4500mls in males, 3500mls in females.
Total lung capacity (TLC) • Is the volume of air in the lungs at the end of a maximal inspiration.
• TLC = FRC + TV + IRV = VC + RV. 5500-6000mls.
Forced vital capacity (FVC) • The volume of air that can be maximally forcefully exhaled.

25
Parathyroid Hormone
Parathyroid hormone is secreted by the chief cells of the parathyroid glands. It acts to increase serum calcium
concentration by stimulation of the PTH receptors in the kidney and bone. PTH has a plasma half-life of 4 minutes.
Effects of PTH
Bone Binds to osteoblasts which signal to osteoclasts to cause resorption of bone and release calcium.
Kidney Active reabsorption of calcium and magnesium from the distal convoluted tubule. Decreases
reabsorption of phosphate.
Intestine via Increases intestinal calcium absorption by increasing activated vitamin D. Activated vitamin D
kidney increases calcium absorption.
Glucagon
Glucagon, the hormonal antagonist to insulin, is released from the alpha cells of the Islets of Langerhans in the pancreas.
It will result in an increased plasma glucose level.
Stimulation Inhibition
Decreased plasma glucose Somatostatin
Increased catecholamines Insulin
Increased plasma amino acids Increased free fatty acids and keto acids
Sympathetic nervous system Increased urea
Acetylcholine
Cholecystokinin
Gastrointestinal Secretions
Up to 7 litres of gastrointestinal secretions enter the lumen of the GI tract in a 24-hour period. The absorptive function of
the small bowel is such that by the time a formed stool is created, it will contain, on average 200ml water.
The common secretions together with their approximate volumes are demonstrated below:
Origin of secretion Volume in ml / 24 hour period Na +mmol/L K+mmol/L Cl-mmol/L HCO 3
Salivary glands 1500 10 26 10 30
Stomach 1500 60 10 130
Duodenum 100-2000 140 80 80
Pancreas 1000 140 5 70 115
Bile 50-800 145 5 100 35
Jejunum/ileum 3000 140 10 104 30
Colon 100 60 30 40
The regulation of these secretions is dependent upon location. In the salivary glands a complex interaction of flow rate
governed by the autonomic nervous system. The exact composition of sodium and potassium is regulated by
aldosterone. In the stomach hormones such as gastrin play a role and feedback is both endocrine and neurologically
mediated (vagus). In the duodenum CCK is released in response to duodenal distension and this causes contraction of
the gallbladder and release of bile.
Pancreatic secretions are affected by somatostatin. The secretions in the small bowel are affected by the osmolality of
the lumenal contents. This is in part due to the tightness of cellular junctions and in this regard the jejunum is more
permeable than the ileum. The practical implication of this is that if an individual has an extensive intestinal resection and
a high output, proximally sited stoma then administration of hypotonic rather than isotonic solutions will result in
worsening of electrolyte disturbances as electrolyte rich secretions will enter the jejunum.
In some individuals a colectomy or similar procedure results in formation of an end or loop ileostomy. Ileostomies
typically lose between 500 and 1000ml over a 24 hour period and patients with high output ileostomies can rapidly
become dehydrated. Ileostomy effluent typically contains 126mmol/L of sodium and 22mmol/L of potassium. Knowledge
of this fluid composition should guide fluid prescribing in replacing losses.

26
Gastric Secretions
Gastric acid
• Is produced by the parietal cells in the stomach
• pH of gastric acid is around 2 with acidity being maintained by the H+/K+ ATP ase pump. As part of the process
bicarbonate ions will be secreted into the surrounding vessels.
• Sodium and chloride ions are actively secreted from the parietal cell into the canaliculus. This sets up a negative
potential across the membrane and as a result sodium and potassium ions diffuse across into the canaliculus.
• Carbonic anhydrase forms carbonic acid which dissociates and the hydrogen ions formed by dissociation leave
the cell via the H+/K+ antiporter pump. At the same time sodium ions are actively absorbed. This leaves
hydrogen and chloride ions in the canaliculus these mix and are secreted into the lumen of the oxyntic gland.
Phases of gastric acid secretion

1. Cephalic phase (smell / taste of food)
• 30% acid produced
• Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells
2. Gastric phase (distension of stomach)
• Stomach distension/low H+/peptides causes Gastrin release
3. Intestinal phase (food in duodenum)
• High acidity/distension/hypertonic solutions in the duodenum inhibits gastric acid secretion via
enterogastrones (CCK, secretin) and neural reflexes.

27
Regulation of gastric acid production
Factors increasing production include:
• Vagal nerve stimulation
• Gastrin release
• Histamine release (indirectly following gastrin release) from enterochromaffin like cells
Factors decreasing production include:
• Somatostatin (inhibits histamine release)
• Cholecystokinin
• Secretin
Name Source Stimulus Actions

Gastrin G cells in Distension of stomach, Increase HCL, pepsinogen and IF secretion, increases gastric
antrum of the extrinsic nerves motility, trophic effect on gastric mucosa
stomach Inhibited by: low
antral pH,
somatostatin
CCK I cells in upper Partially digested Increases secretion of enzyme-rich fluid from pancreas,
small intestine proteins and contraction of gallbladder and relaxation of sphincter of
triglycerides Oddi, decreases gastric emptying, trophic effect on
pancreatic acinar cells, induces satiety
Secretin S cells in upper Acidic chyme, fatty Increases secretion of bicarbonate-rich fluid from pancreas
small intestine acids and hepatic duct cells, decreases gastric acid secretion,
trophic effect on pancreatic acinar cells
VIP Small intestine, Neural Stimulates secretion by pancreas and intestines, inhibits
pancreas acid and pepsinogen secretion
Somatostatin D cells in the Fat, bile salts and Decreases acid and pepsin secretion, decreases gastrin
pancreas and glucose in the secretion, decreases pancreatic enzyme secretion,
stomach intestinal lumen decreases insulin and glucagon secretion
inhibits trophic effects of gastrin, stimulates gastric mucous
production

28
Peristalsis
• Circular smooth muscle contracts behind the food bolus and longitudinal smooth muscle propels the food
through the oesophagus
• Primary peristalsis spontaneously moves the food from the oesophagus into the stomach (9 seconds)
• Secondary peristalsis occurs when food, which doesn't enter the stomach, stimulates stretch receptors to cause
peristalsis
• In the small intestine each peristalsis waves slows to a few seconds and causes mixture of chyme
• In the colon three main types of peristaltic activity are recognised (see below)
Colonic peristalsis
Segmentation contractions Localised contractions in which the bolus is subjected to local forces to maximise
mucosal absorption
Antiperistaltic contractions Localised reverse peristaltic waves to slow entry into colon and maximise
towards ileum absorption
Mass movements Waves migratory peristaltic waves along the entire colon to empty the organ prior
to the next ingestion of food bolus
Pancreas Endocrine Physiology

Hormones released from the islets of Langerhans
Beta cells Insulin (70% of total secretions)
Alpha cells Glucagon
Delta cells Somatostatin
F cells Pancreatic polypeptide
Pancreas Exocrine Physiology

Composition of pancreatic secretions
Pancreatic secretions are usually 1000-1500ml per 24 hours and have a pH of 8.
Secretion Source Substances secreted
Enzymic Acinar cells Trypsinogen
Procarboxylase
Amylase
Elastase
Aqueous Ductal and Centroacinar Sodium
cells Bicarbonate
Water
Potassium
Chloride
NB: Sodium and potassium reflect their plasma levels; chloride and
bicarbonate vary with flow rate
Regulation
The cephalic and gastric phases (neuronal and physical) are less important in regulating the pancreatic secretions. The
effect of digested material in the small bowel stimulates CCK release and ACh which stimulate acinar and ductal cells. Of
these CCK is the most potent stimulus. In the case of the ductal cells these are potently stimulated by secretin which is
released by the S cells of the duodenum. This results in an increase in bicarbonate.
Enzyme activation
Trypsinogen is converted via enterokinase to active trypsin in the duodenum. Trypsin then activates the other inactive
enzymes

29
Renal Physiology
Overview
• Each nephron is supplied with blood from an afferent arteriole that opens onto the glomerular capillary bed.
• Blood then flows to an efferent arteriole, supplying the peritubular capillaries and medullary vasa recta.
• The kidney receives up to 25% of resting cardiac output.
Control of blood flow
• The kidney is able to auto regulate its blood flow between systolic pressures of 80- 180mmHg so there is little
variation in renal blood flow.
• This is achieved by myogenic control of arteriolar tone, both sympathetic input and hormonal signals (e.g. renin)
are responsible.
Glomerular structure and function
• Blood inside the glomerulus has considerable hydrostatic pressure.
• The basement membrane has pores that will allow free diffusion of smaller solutes, larger negatively charged
molecules such as albumin are unable to cross.
• The glomerular filtration rate (GFR) is equal to the concentration of a solute in the urine, times the volume of
urine produced per minute, divided by the plasma concentration (assuming that the solute is freely diffused e.g.
inulin).
• In clinical practice creatinine is used because it is subjected to very little proximal tubular secretion.
• Although subject to variability, the typical GFR is 125ml per minute.
• Glomerular filtration rate = Total volume of plasma per unit time leaving the capillaries and entering the
bowman's capsule
• Renal clearance = volume plasma from which a substance is removed per minute by the kidneys
Substances used to measure GFR have the following features:
• Inert
• Free filtration from the plasma at the glomerulus (not protein bound)
• Not absorbed or secreted at the tubules
• Plasma concentration constant during urine collection
Examples: inulin, creatinine
urine concentration (mmol/l) x urine volume (ml/min)
𝐺𝐺𝐺𝐺𝐺𝐺 =
plasma concentration (mmol/l)
• The clearance of a substance is dependent not only on its diffusivity across the basement membrane but also
subsequent tubular secretion and / or reabsorption.
• So glucose which is freely filtered across the basement membrane is usually reabsorbed from tubules giving a
clearance of zero.
Tubular function
• Reabsorption and secretion of substances occurs in the tubules.
• In the proximal tubule substrates such as glucose, amino acids and phosphate are co-transported with sodium
across the semi permeable membrane.
• Up to two thirds of filtered water is reabsorbed in the proximal tubules.
• This will lead to increase in urea concentration in the distal tubule allowing for its increased diffusion.
• Substances to be secreted into the tubules are taken up from the peritubular blood by tubular cells.
• Solutes such as paraaminohippuric acid are cleared with a single passage through the kidneys and this is why it
is used to measure renal plasma flow. Ions such as calcium and phosphate will have a tubular reabsorption that
is influenced by plasma PTH levels.
• Potassium may be both secreted and re-absorbed and is co-exchanged with sodium.
Loop of Henle
• Approximately 60 litres of water containing 9000mmol sodium enters the descending limb of the loop of Henle
in 24 hours.
• Loops from the juxtamedullary nephrons run deep into the medulla.
• The osmolarity of fluid changes and is greatest at the tip of the papilla.
• The thin ascending limb is impermeable to water, but highly permeable to sodium and chloride ions.
• This loss means that at the beginning of the thick ascending limb the fluid is hypo osmotic compared with
adjacent interstitial fluid.
• In the thick ascending limb the reabsorption of sodium and chloride ions occurs by both facilitated and passive
diffusion pathways.
• The loops of Henle are co-located with vasa recta, these will have similar solute compositions to the
surrounding extracellular fluid so preventing the diffusion and subsequent removal of this hypertonic fluid.
• The energy dependent reabsorption of sodium and chloride in the thick ascending limb helps to maintain this
osmotic gradient.

30
Acute Renal Failure: Pre Renal Failure Vs. Acute Tubular Necrosis
Prerenal uraemia - kidneys retain sodium to preserve volume
Pre-renal uraemia Acute tubular necrosis
Urine sodium < 20 mmol/L > 30 mmol/L
Fractional sodium excretion* < 1% > 1%
Fractional urea excretion** < 35% >35%
Urine:plasma osmolality > 1.5 < 1.1
Urine:plasma urea > 10:1 < 8:1
Specific gravity > 1020 < 1010
Urine 'bland' sediment brown granular casts
Response to fluid challenge Yes No
*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100
**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100
Diuretic Agents
The diuretic drugs are divided into three major classes, which are distinguished according to the site at which they impair
sodium reabsorption: loop diuretics in the thick ascending loop of Henle, thiazide type diuretics in the distal tubule and
connecting segment; and potassium sparing diuretics in the aldosterone - sensitive principal cells in the cortical collecting
tubule.
In the kidney, sodium is reabsorbed through Na+/ K+ ATPase pumps located on the basolateral membrane. These pumps
return reabsorbed sodium to the circulation and maintain low intracellular sodium levels. This latter effect ensures a
constant concentration gradient.
Site of action Diuretic Carrier or channel inhibited % of filtered sodium excreted

Ascending limb of loop of Henle Frusemide Na+/K+ 2Cl -carrier Up to 25%
Distal tubule and connecting segment Thiazides Na+Cl- carrier Between 3 and 5%
Cortical collecting tubule Spironolactone Na+/K+ ATP ase pump Between 1 and 2%

31
Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Causes
Malignancy
• Especially small cell lung cancer
• Also: pancreas, prostate
Neurological
• Stroke
• Subarachnoid haemorrhage
• Subdural haemorrhage
• Meningitis/encephalitis/abscess
Infections
• Tuberculosis
• Pneumonia
Drugs
• Sulfonylureas
• SSRIs, tricyclics
• Carbamazepine
• Vincristine
• Cyclophosphamide
Other causes
• Positive end-expiratory pressure (PEEP)
• Porphyrias
Renin
Renin is secreted by juxtaglomerular cells and hydrolyses angiotensinogen to produce angiotensin I
Factors stimulating renin secretion
• Hypotension causing reduced renal perfusion
• Hyponatraemia
• Sympathetic nerve stimulation
• Catecholamines
• Erect posture
Factors reducing renin secretion
• Drugs: beta-blockers, NSAIDs

32
Renin-Angiotensin-Aldosterone System
Adrenal cortex (mnemonics GFR – ACD / “salt, sugar, sex”)
• Zona glomerulosa (on outside): mineralocorticoids, mainly aldosterone
• Zona fasciculata (middle): glucocorticoids, mainly cortisol
• Zona reticularis (on inside): androgens, mainly dehydroepiandrosterone (DHEA)
Renin
• Released by JGA cells in kidney in response to reduced renal perfusion, low sodium
• Hydrolyses angiotensinogen to form angiotensin I
Factors stimulating renin secretion
• Low BP
• Hyponatraemia
• Sympathetic nerve stimulation
• Catecholamines
• Erect posture
Angiotensin
• ACE in lung converts angiotensin I → angiotensin II
• Vasoconstriction leads to raised BP
• Stimulates thirst
• Stimulates aldosterone and ADH release
Aldosterone
• Released by the zona glomerulosa in response to raised angiotensin II, potassium, and ACTH levels
• Causes retention of Na+ in exchange for K+/H+ in distal tubule

33
Phases of Wound Healing
Phase Key features Cells Timeframe
Haemostasis • Vasospasm in adjacent vessels Erythrocytes Seconds /
• Platelet plug formation and generation of fibrin rich clot and platelets Minutes
Inflammation • Neutrophils migrate into wound (function impaired in diabetes). Neutrophils, Days
• Growth factors released, including basic fibroblast growth factor fibroblasts and
and vascular endothelial growth factor. macrophages
• Fibroblasts replicate within the adjacent matrix and migrate into
wound.
• Macrophages and fibroblasts couple matrix regeneration and clot
substitution.
Regeneration • Platelet derived growth factor and transformation growth factors Fibroblasts, Weeks
stimulate fibroblasts and epithelial cells. endothelial
• Fibroblasts produce a collagen network. cells,
• Angiogenesis occurs and wound resembles granulation tissue. macrophages
Remodelling • Longest phase of the healing process and may last up to one year Myofibroblasts 6 weeks to
(or longer). 1 year
• During this phase, fibroblasts become differentiated
(myofibroblasts) and these facilitate wound contraction.
• Collagen fibres are remodelled.
• Microvessels regress leaving a pale scar.
Response to Surgery
Sympathetic nervous system
• Noradrenaline from sympathetic nerves and adrenaline from adrenal medulla
• Blood diverted from skin and visceral organs; bronchodilatation, reduced intestinal motility, increased glucagon
and glycogenolysis, insulin reduced
• Heart rate and myocardial contractility are increased
Acute phase response

• TNF-α, IL-1, IL-2, IL-6, interferon and prostaglandins are released
• Excess cytokines may cause SIRS
• Cytokines increase the release of acute phase proteins
Endocrine response
• Hypothalamus, pituitary, adrenal axis
• Increases ACTH and cortisol production:
increases protein breakdown
increases blood glucose levels
• Aldosterone increases sodium re-absorption

• Vasopressin increases water re-absorption and causes vasoconstriction
Vascular endothelium
• Nitric oxide produces vasodilatation
• Platelet activating factor enhances the cytokine response
• Prostaglandins produce vasodilatation and induce platelet aggregation

34
Stress Response: Endocrine and Metabolic Changes
• Surgery precipitates hormonal and metabolic changes causing the stress response.
• Stress response is associated with: substrate mobilization, muscle protein loss, sodium and water retention,
suppression of anabolic hormone secretion, activation of the sympathetic nervous system, immunological and
haematological changes.
• The hypothalamic-pituitary axis and the sympathetic nervous systems are activated and there is a failure of the
normal feedback mechanisms of control of hormone secretion.
A summary of the hormonal changes associated with the stress response:

Increased Decreased No Change
Growth hormone Insulin Thyroid stimulating hormone
Cortisol Testosterone Luteinizing hormone
Renin Oestrogen Follicle stimulating hormone
Adrenocorticotrophic hormone (ACTH)
Aldosterone
Prolactin
Antidiuretic hormone
Glucagon
Sympathetic nervous system

• Stimulates catecholamine release
• Causes tachycardia and hypertension
Pituitary gland
• ACTH and growth hormone (GH) is stimulated by hypothalamic releasing factors, corticotrophin releasing factor
(CRF) and somatotrophin (or growth hormone releasing factor)
• Perioperative increased prolactin secretion occurs by release of inhibitory control
• Secretion of thyroid stimulating hormone (TSH), luteinizing hormone (LH) and follicle stimulating hormone (FSH)
does not change significantly
• ACTH stimulates cortisol production within a few minutes of the start of surgery. More ACTH is produced than
needed to produce a maximum adrenocortical response.
Cortisol
• Significant increases within 4-6 hours of surgery (>1000 nmol litre-1).
• The usual negative feedback mechanism fails and concentrations of ACTH and cortisol remain persistently
increased.
• The magnitude and duration of the increase correlate with the severity of stress and the response is not
abolished by the administration of corticosteroids.
• The metabolic effects of cortisol are enhanced:
o Skeletal muscle protein breakdown to provide gluconeogenic precursors and amino acids for protein
synthesis in the liver
o Stimulation of lipolysis
o 'Anti-insulin effect'
o Mineralocorticoid effects
o Anti-inflammatory effects
Growth hormone
• Increased secretion after surgery has a minor role
• Most important for preventing muscle protein breakdown and promote tissue repair by insulin growth factors
Alpha Endorphin
• Increased
Antidiuretic hormone
• An important vasopressor and enhances haemostasis
• Renin is released causing the conversion of angiotensinogen to angiotensin I
• Angiotensin II formed by ACE on angiotensin 1, which causes the secretion of aldosterone from the adrenal
cortex. This increases sodium reabsorption at the distal convoluted tubule

35
Insulin
• Release inhibited by stress
• Occurs via the inhibition of the beta cells in the pancreas by the α2-adrenergic inhibitory effects of
catecholamines
• Insulin resistance by target cells occurs later
• The perioperative period is characterized by a state of functional insulin deficiency
Thyroxine (T4) and tri-iodothyronine (T3)

• Circulating concentrations are inversely correlated with sympathetic activity and after surgery there is a
reduction in thyroid hormone production, which normalises over a few days.
Metabolic effect of endocrine response

Carbohydrate metabolism
• Hyperglycaemia is a main feature of the metabolic response to surgery
• Due to increase in glucose production and a reduction in glucose utilization
• Catecholamines and cortisol promote glycogenolysis and gluconeogenesis
• Initial failure of insulin secretion followed by insulin resistance affects the normal responses
• The proportion of the hyperglycaemic response reflects the severity of surgery
• Hyperglycaemia impairs wound healing and increase infection rates
Protein metabolism
• Initially there is inhibition of protein anabolism, followed later, if the stress response is severe, by enhanced
catabolism
• The amount of protein degradation is influenced by the type of surgery and also by the nutritional status of
the patient
• Mainly skeletal muscle protein is affected
• The amino acids released form acute phase proteins (fibrinogen, C reactive protein, complement proteins,
a2-macroglobulin, amyloid A and ceruloplasmin) and are used for gluconeogenesis
• Nutritional support has little effect on preventing catabolism
Lipid metabolism
• Increased catecholamine, cortisol and glucagon secretion, and insulin deficiency, promotes lipolysis and
ketone body production.
Salt and water metabolism
• ADH causes water retention, concentrated urine, and potassium loss and may continue for 3 to 5 days after
surgery
• Renin causes sodium and water retention
Cytokines
• Glycoproteins
• Interleukins (IL) 1 to 17, interferons, and tumour necrosis factor
• Synthesized by activated macrophages, fibroblasts, endothelial and glial cells in response to tissue injury
from surgery or trauma
• IL-6 main cytokine associated with surgery. Peak 12 to 24 h after surgery and increase by the degree of
tissue damage Other effects of cytokines include fever, granulocytosis, haemostasis, tissue damage
limitation and promotion of healing.
Modifying the response

• Opioids suppress hypothalamic and pituitary hormone secretion
• At high doses the hormonal response to pelvic and abdominal surgery is abolished. However, such doses
prolong recovery and increase the need for postoperative ventilatory support
• Spinal anaesthesia can reduce the glucose, ACTH, cortisol, GH and epinephrine changes, although cytokine
responses are unaltered
• Cytokine release is reduced in less invasive surgery
• Nutrition prevents the adverse effects of the stress response. Enteral feeding improves recovery
• Growth hormone and anabolic steroids may improve outcome
• Normothermia decreases the metabolic response

36
Shock
Shock occurs when there is insufficient tissue perfusion.
Septic shock
Septic shock is a major problem and those patients with severe sepsis have a mortality rate in excess of 40%. In those
who are admitted to intensive care mortality ranges from 6% with no organ failure to 65% in those with 4 organ failure.
Sepsis is defined as an infection that triggers a particular Systemic Inflammatory Response Syndrome (SIRS). This is
characterised by body temperature outside 36 oC - 38 o C, HR >90 beats/min, respiratory rate >20/min, WBC count
>12,000/mm3 or < 4,000/mm3, altered mental state or hyperglycaemia (in absence of diabetes).
Patients with infections and two or more elements of SIRS meet the diagnostic criteria for sepsis. Those with organ
failure have severe sepsis and those with refractory hypotension -septic shock.
During the septic process there is marked activation of the immune system with extensive cytokine release. This may be
coupled with or triggered by systemic circulation of bacterial toxins. These all cause endothelial cell damage and
neutrophil adhesion. The overall hallmarks are thus those of excessive inflammation, coagulation and fibrinolytic
suppression.
The surviving sepsis campaign (2012) highlights the following key areas for attention:
• Prompt administration of antibiotics to cover all likely pathogens coupled with a rigorous search for the source
of infection.
• Haemodynamic stabilisation. Many patients are hypovolaemic and require aggressive fluid administration. Aim
for CVP 8-12 cm H 2 O, MAP >65mmHg.
• Modulation of the septic response. This includes manoeuvres to counteract the changes and includes measures
such as tight glycaemic control. The routine use of steroids is not advised.
In surgical patients, the main groups with septic shock include those with anastomotic leaks, abscesses and extensive
superficial infections such as necrotising fasciitis. When performing surgery the aim should be to undertake the minimum
necessary to restore physiology. These patients do not fare well with prolonged surgery. Definitive surgery can be more
safely undertaken when physiology is restored and clotting in particular has been normalised.
Haemorrhagic shock
The average adult blood volume comprises 7% of body weight. Thus in the 70 Kg adult this will equate to 5 litres. This
changes in children (8-9% body weight) and is slightly lower in the elderly.
Parameter Class I Class II Class III Class IV

Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml
Blood loss % <15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output >30ml 20-30ml 5-15ml <5ml
Symptoms Normal Anxious Confused Lethargic
Decreasing blood pressure during haemorrhagic shock causes organ hypoperfusion and relative myocardial ischaemia.
The cardiac index gives a numerical value for tissue oxygen delivery and is given by the equation: Cardiac index= Cardiac
output/ body surface area. Where Hb is haemoglobin concentration in blood and SaO 2 the saturation and PaO 2 the
partial pressure of oxygen. Detailed knowledge of this equation is required for the MRCS Viva but not for part A, although
you should understand the principle.
In patients suffering from trauma the most likely cause of shock is haemorrhage. However, the following may also be the
cause or occur concomitantly:
• Tension pneumothorax
• Spinal cord injury
• Myocardial contusion
• Cardiac tamponade

37
When assessing trauma patients, it is worth remembering that in order to generate a palpable femoral pulse an arterial
pressure of >65mmHg is required.
Once bleeding is controlled and circulating volume normalised the levels of transfusion should be to maintain a Hb of 7-8
in those with no risk factors for tissue hypoxia and Hb 10 for those who have such risk factors.
Neurogenic shock
This occurs most often following a spinal cord transection, usually at a high level. There is resultant interruption of the
autonomic nervous system. The result is either decreased sympathetic tone or increased parasympathetic tone, the effect
of which is a decrease in peripheral vascular resistance mediated by marked vasodilation.
This results in decreased preload and thus decreased cardiac output (Starlings law). There is decreased peripheral tissue
perfusion and shock is thus produced. In contrast with many other types of shock peripheral vasoconstrictors are used to
return vascular tone to normal.
Cardiogenic shock
In medical patients the main cause is ischaemic heart disease. In the traumatic setting direct myocardial trauma or
contusion is more likely. Evidence of ECG changes and overlying sternal fractures or contusions should raise the suspicion
of injury. Treatment is largely supportive and transthoracic echocardiography should be used to determine evidence of
pericardial fluid or direct myocardial injury. The measurement of troponin levels in trauma patients may be undertaken
but they are less useful in delineating the extent of myocardial trauma than following MI.
When cardiac injury is of a blunt nature and is associated with cardiogenic shock the right side of the heart is the most
likely site of injury with chamber and or valve rupture. These patients require surgery to repair these defects and will
require cardiopulmonary bypass to achieve this. Some may require intra-aortic balloon pump as a bridge to surgery.
Anaphylactic shock
Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic
hypersensitivity reaction.
Anaphylaxis is one of the few times when you would not have time to look up the dose of a medication. The
Resuscitation Council guidelines on anaphylaxis have recently been updated. Adrenaline is by far the most important
drug in anaphylaxis and should be given as soon as possible. The recommended doses for adrenaline, hydrocortisone and
chlorpheniramine are as follows:
Adrenaline Hydrocortisone Chlorpheniramine

< 6 months 150 mcg (0.15ml 1 in 1,000) 25 mg 250 mcg/kg
6 months - 6 years 150 mcg (0.15ml 1 in 1,000) 50 mg 2.5 mg
6-12 years 300 mcg (0.3ml 1 in 1,000) 100 mg 5 mg
Adult and child 12 years 500 mcg (0.5ml 1 in 1,000) 200 mg 10 mg
Adrenaline can be repeated every 5 minutes if necessary. The best site for IM injection is the anterolateral aspect of the
middle third of the thigh.
Common identified causes of anaphylaxis

• food (e.g. Nuts) - the most common cause in children
• drugs
• venom (e.g. Wasp sting)

38
Urinary Incontinence
Involuntary passage of urine. Most cases are female (80%). It has a prevalence of 11% in those aged greater than 65
years. The commonest variants include:
• Stress urinary incontinence (50%)
• Urge incontinence (15%)
• Mixed (35%)
Males
Males may also suffer from incontinence although it is a much rarer condition in men. A number of anatomical factors
contribute to this. Males have 2 powerful sphincters; one at the bladder neck and the other in the urethra. Damage to
the bladder neck mechanism is a factor in causing retrograde ejaculation following prostatectomy. The short segment of
urethra passing through the urogenital diaphragm consists of striated muscle fibres (the external urethral sphincter) and
smooth muscle capable of more sustained contraction. It is the latter mechanism that maintains continence following
prostatectomy.
Females
The sphincter complex at the level of bladder neck is poorly developed in females. As a result the external sphincter
complex is functionally more important, its composition being similar to that of males. Innervation is via the pudendal
nerve and the neuropathy that may accompany obstetric events may compromise this and lead to stress urinary
incontinence.
Innervation
Somatic innervation to the bladder is via the pudendal, hypogastric and pelvic nerves. Autonomic nerves travel in these
nerve fibres too. Bladder filling leads to detrusor relaxation (sympathetic) coupled with sphincter contraction. The
parasympathetic system causes detrusor contraction and sphincter relaxation. Overall control of micturition is centrally
mediated via centres in the Pons.
Stress urinary incontinence

• 50% of cases, especially in females.
• Damage (often obstetric) to the supporting structures surrounding the bladder may lead to urethral
hypermobility.
• Other cases due to sphincter dysfunction, usually from neurological disorders (e.g. Pudendal neuropathy,
multiple sclerosis).
Urethral mobility:
Pressure not transmitted appropriately to the urethra resulting in involuntary passage of urine during episodes of raised
intra-abdominal pressure.
Sphincter dysfunction:
Sphincter fails to adapt to compress urethra resulting in involuntary passage of urine. When the sphincter completely
fails there is often to continuous passage of urine.
Urge incontinence
In these patients there is sense of urgency followed by incontinence. The detrusor muscle in these patients is unstable
and urodynamic investigation will demonstrate overactivity of the detrusor muscle at inappropriate times (e.g. Bladder
filling). Urgency may be seen in patients with overt neurological disorders and those without. The pathophysiology is not
well understood but poor central and peripheral co-ordination of the events surrounding bladder filling are the main
processes.
Assessment
Careful history and examination including vaginal examination for cystocele.
Bladder diary for at least 3 days
Consider flow cystometry if unclear symptomatology or surgery considered and diagnosis is unclear.
Exclusion of other organic disease (e.g. Stones, UTI, Cancer)

39
Management
Conservative measures should be tried first; Stress urinary incontinence or mixed symptoms should undergo 3 months of
pelvic floor exercise. Over active bladder should have 6 weeks of bladder retraining.
Drug therapy for women with overactive bladder should be offered oxybutynin (or solifenacin if elderly) if conservative
measures fail.
In women with detrusor instability who fail non operative therapy a trial of sacral neuromodulation may be considered,
with conversion to permanent implant if good response. Augmentation cystoplasty is an alternative but will involve long
term intermittent self catheterisation.
In women with stress urinary incontinence a urethral sling type procedure may be undertaken. Where cystocele is
present in association with incontinence it should be repaired particularly if it lies at the introitus.
NICE guidelines
• Initial assessment urinary incontinence should be classified as stress/urge/mixed.
• At least 3/7 bladder diary if unable to classify easily.
• Start conservative treatment before urodynamic studies if a diagnosis is obvious from the history
• Urodynamic studies if plans for surgery.
• Stress incontinence: Pelvic floor exercises 3/12, if fails consider surgery.
• Urge incontinence: Bladder training >6/52, if fails for oxybutynin (antimuscarinic drugs) then sacral nerve
stimulation.
• Pelvic floor exercises offered to all women in their 1st pregnancy.
Adrenal Physiology
Adrenal medulla
The chromaffin cells of the adrenal medulla secrete the catecholamines noradrenaline and adrenaline. The medulla is
innervated by the splanchnic nerves; the preganglionic sympathetic fibres secrete acetylcholine causing the chromaffin
cells to secrete their contents by exocytosis.
Phaeochromocytomas are derived from these cells and will secrete both adrenaline and nor adrenaline.
Adrenal cortex
Zone Location Hormone Secreted
Zona glomerulosa Outer zone Aldosterone
Zona fasciculata Middle zone Glucocorticoids
Zona reticularis Inner zone Androgens
The glucocorticoids and aldosterone are mostly bound to plasma proteins in the circulation. Glucocorticoids are
inactivated and excreted by the liver.

40
Vitamin Deficiency
Vitamin Effect of deficiency
A Night blindness
Epithelial atrophy
Infections
B1 Beriberi
B2 Dermatitis and photosensitivity
B3 Pellagra
B12 Pernicious anaemia
C Poor wound healing
Impaired collagen synthesis
D Rickets (Children)
Osteomalacia (Adults)
K Clotting disorders
Vitamin B12 Deficiency

Vitamin B12 is mainly used in the body for red blood cell development and also maintenance of the nervous system. It is
absorbed after binding to intrinsic factor (secreted from parietal cells in the stomach) and is actively absorbed in the
terminal ileum. A small amount of vitamin B12 is passively absorbed without being bound to intrinsic factor.
Causes of vitamin B12 deficiency

• Pernicious anaemia
• Post gastrectomy
• Poor diet
• Disorders of terminal ileum (site of absorption): Crohn’s, blind-loop, etc.
Features of vitamin B12 deficiency

• Macrocytic anaemia
• Sore tongue and mouth
• Neurological symptoms: e.g. Ataxia
• Neuropsychiatric symptoms: e.g. Mood disturbances
Management
• If no neurological involvement 1 mg of IM hydroxocobalamin 3 times each week for 2 weeks, then once every 3
months.
• If a patient is also deficient in folic acid, then it is important to treat the B12 deficiency first to avoid
precipitating subacute combined degeneration of the cord.

41
3. Pathology – MRCS Noes - Reda

Acute Inflammation ........................................................................................................................................ 2
Chronic Inflammation ..................................................................................................................................... 3
Gastritis ........................................................................................................................................................... 4
Lead Poisoning ................................................................................................................................................ 4
Cell Death ........................................................................................................................................................ 5
Disseminated Intravascular Coagulation ....................................................................................................... 6
Disseminated Intravascular Coagulation - Diagnosis .................................................................................... 6
Cardiac Murmurs ............................................................................................................................................ 7
Nerve Injury .................................................................................................................................................... 7
Absence Of The Vas Deferens ........................................................................................................................ 8
Cleft Lip and Palate ......................................................................................................................................... 8
Choanal Atresia ............................................................................................................................................... 8
Achondroplasia ............................................................................................................................................... 8
Genetics and Surgical Disease ........................................................................................................................ 9
Tumour Markers ............................................................................................................................................. 9
Hodgkins Lymphoma .................................................................................................................................... 10
Acute Intermittent Porphyria ....................................................................................................................... 11
Aggressive Fibromatosis ............................................................................................................................... 11
Hereditary Spherocytosis ............................................................................................................................. 11
Hypersensitivity Reactions ........................................................................................................................... 11
Koebner Phenomenon .................................................................................................................................. 11
Adrenal Lesions - Incidental ......................................................................................................................... 12
Phaeochromocytoma and Adrenal Lesions ................................................................................................. 12
Glucagonoma ................................................................................................................................................ 13
Glioma ........................................................................................................................................................... 13
Thymus .......................................................................................................................................................... 13
Sarcomas ....................................................................................................................................................... 14
Trypanosoma Cruzi ....................................................................................................................................... 15
Actinomycosis ............................................................................................................................................... 15
Burns ............................................................................................................................................................. 16
Collagen ......................................................................................................................................................... 17
3. PATHOLOGY – MRCS NOTES - REDA 1

42
Acute Inflammation
Inflammation is the reaction of the tissue elements to injury. Vascular changes occur, resulting in the generation of a
protein rich exudate. So long as the injury does not totally destroy the existing tissue architecture, the episode may
resolve with restoration of original tissue architecture.
Vascular changes
• Vasodilation occurs and persists throughout the inflammatory phase.
• Inflammatory cells exit the circulation at the site of injury.
• The equilibrium that balances Starlings forces within capillary beds is disrupted and a protein rich exudate will
form as the vessel walls also become more permeable to proteins.
• The high fibrinogen content of the fluid may form a fibrin clot. This has several important immunomodulatory
functions.
Sequelae
Resolution • Typically occurs with minimal initial injury
• Stimulus removed and normal tissue architecture results
Organisation • Delayed removal of exudate
• Tissues undergo organisation and usually fibrosis
Suppuration • Typically formation of an abscess or an empyema
• Sequestration of large quantities of dead neutrophils
Progression to chronic • Coupled inflammatory and reparative activities
inflammation • Usually occurs when initial infection or suppuration has been inadequately managed
Causes
• Infections e.g. Viruses, exotoxins or endotoxins released by bacteria
• Chemical agents
• Physical agents e.g. Trauma
• Hypersensitivity reactions
• Tissue necrosis
Presence of neutrophil polymorphs is a histological diagnostic feature of acute inflammation

43
Chronic Inflammation
Overview
Chronic inflammation may occur secondary to acute inflammation.In most cases chronic inflammation occurs as a
primary process. These may be broadly viewed as being one of three main processes:
• Persisting infection with certain organisms such as Mycobacterium tuberculosis which results in delayed type
hypersensitivity reactions and inflammation.
• Prolonged exposure to non-biodegradable substances such as silica or suture materials which may induce an
inflammatory response.
• Autoimmune conditions involving antibodies formed against host antigens.
Acute vs. Chronic inflammation

Acute inflammation Chronic inflammation
Changes to existing vascular structure and Angiogenesis predominates
increased permeability of endothelial cells
Infiltration of neutrophils Macrophages, plasma cells and lymphocytes predominate
Process may resolve with: Healing by fibrosis is the main result
• Suppuration
• Complete resolution
• Abscess formation
• Progression to chronic inflammation
• Healing by fibrosis
Granulomatous inflammation
A granuloma consists of a microscopic aggregation of macrophages (with epithelial type arrangement =epitheliod). Large
giant cells may be found at the periphery of granulomas.
Mediators
Growth factors released by activated macrophages include agents such as interferon and fibroblast growth factor (plus
many more). Some of these such as interferons may have systemic features resulting in systemic symptoms and signs,
which may be present in individuals with long standing chronic inflammation.
The finding of granulomas is pathognomonic of chronic inflammation, as

illustrated in this biopsy from a patient with colonic Crohn’s disease

44
Gastritis
Type of gastritis Features
Type A Autoimmune
Circulating antibodies to parietal cells, causes reduction in cell mass and hypochlorhydria
Loss of parietal cells = loss of intrinsic factor = B12 malabsorption
Absence of antral involvement
Hypochlorhydria causes elevated gastrin levels- stimulating enterochromaffin cells and
adenomas may form
Type B Antral gastritis
Associated with infection with helicobacter pylori infection
Intestinal metaplasia may occur in stomach and require surveillance endoscopy
Peptic ulceration may occur
Reflux gastritis Bile refluxes into stomach, either post surgical or due to failure of pyloric function
Histologically, evidence of chronic inflammation, and foveolar hyperplasia
May respond to therapy with prokinetics
Erosive gastritis Agents disrupt the gastric mucosal barrier
Most commonly due to NSAIDs and alcohol
With NSAIDs the effects occur secondary to COX 1 inhibition
Stress ulceration This occurs as a result of mucosal ischaemia during hypotension or hypovolaemia
The stomach is the most sensitive organ in the GI tract to ischaemia following hypovolaemia
Diffuse ulceration may occur
Prophylaxis with acid lowering therapy and sucralfate may minimise complications
Menetriers Gross hypertrophy of the gastric mucosal folds, excessive mucous production and
disease hypochlorhydria
Pre malignant condition
Lead Poisoning
Along with acute intermittent porphyria, lead poisoning should be considered in questions giving a combination of
abdominal pain and neurological signs
Features
• abdominal pain
• peripheral neuropathy (mainly motor)
• fatigue
• constipation
• blue lines on gum margin (only 20% of adult patients, very rare in children)
Investigations
• The blood lead level is usually used for diagnosis. Levels greater than 10 mcg/dl are considered significant
• Full blood count: microcytic anaemia. Blood film shows red cell abnormalities including basophilic stippling and
clover-leaf morphology
• Raised serum and urine levels of delta aminolaevulinic acid may be seen making it sometimes difficult to
differentiate from acute intermittent porphyria
• Urinary coproporphyrin is also increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly
increased)
Management - various chelating agents are currently used:

• Dimercaptosuccinic acid (DMSA)
• D-penicillamine
• EDTA
• Dimercaprol

45
Cell Death
Cells can die via two mechanisms; necrosis and apoptosis. These are outlined below:
Necrosis
Necrosis is characterised by bioenergetics failure. Loss of tissue perfusion results in hypoxia and an inability to generate
ATP. The integrity of the cellular membrane is lost and the loss of ATP results in loss of energy dependent cellular
transport mechanisms. There is an influx of water, ionic instability and cellular lysis. The release of intracellular contents
may stimulate an inflammatory response. Several types of necrosis are recognised; coagulative, colliquative, caseous,
gangrene, fibrinoid and fat necrosis. The type of tissue and the underlying cause determine the predominant necrosis
pattern.
Coagulative necrosis
• The commonest type, occurs in most organs
• Tissue is initially firm, later becomes soft as tissue is digested by macrophages
• In the early phases the histological appearances may demonstrate little change
• In later stages cellular outlines are seen with loss of intracellular detail
Colliquative necrosis
• Occurs in tissues with no supporting stroma
• Dominant necrosis pattern in the CNS
• Necrotic site may eventually become encysted
Caseous necrosis
• No definable structure seen in the necrotic tissue
• Amorphous eosinophilic tissue may be seen histologically
• Classically seen in tuberculosis
Gangrene
• Necrosis with putrefaction of tissue
• May complicate ischaemia
• Haemoglobin degenerates and results in the deposition of iron sulphide (which is why the tissue is black)
• Both wet and dry gangrene may occur, in wet gangrene there is often a liquefactive component and super-
added infection (which usually smells!)
Fibrinoid necrosis
• Classically seen in arterioles in patients with hypertension (malignant type)
• Necrosis of the smooth muscle wall occurs and plasma may extravasate into the media with fibrin deposition
Fat necrosis
• Direct trauma to fat can result in rupture of adipocytes
• Lipids incite a local inflammatory reaction
• Inflammatory cells phagocytose the lipid with eventual fibrosis
Apoptosis
• Also known as programmed cell death
• Energy dependent pathways are activated via a number of intracellular signalling mechanisms
• It is the result of the activation of caspases triggered by the bcl-2 family or the binding of the FAS ligand to its
receptor
• DNA fragments, mitochondrial function ceases, nuclear and cellular shrinkage occurs
• Phagocytosis of the cell does not occur, instead the cell degenerates into apoptotic bodies

46
Disseminated Intravascular Coagulation
Simultaneous coagulation and haemorrhage caused by initially formation of thrombi which consume clotting factors
(factors 5,8) and platelets, ultimately leading to bleeding
Causes include:
• Infection
• Malignancy
• Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm
• Liver disease
• Obstetric complications
Key points
• Clinically bleeding is usually a dominant feature, bruising, ischaemia and organ failure
• Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased fibrinogen
degradation products
• Treat the underlying cause and supportive management
Disseminated Intravascular Coagulation - Diagnosis

Under homeostatic conditions, coagulation and fibrinolysis are coupled. The activation of the coagulation cascade yields
thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis. The fibrinolytic
system breaks down fibrinogen and fibrin. Activation of the fibrinolytic system generates plasmin (in the presence of
thrombin), which is responsible for the lysis of fibrin clots. The breakdown of fibrinogen and fibrin results in polypeptides
(fibrin degradation products). In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic
enzyme of coagulation and is also necessary for fibrinolysis.
In DIC, the processes of coagulation and fibrinolysis are dysregulated, and the result is widespread clotting with resultant
bleeding. Regardless of the triggering event of DIC, once initiated, the pathophysiology of DIC is similar in all conditions.
One critical mediator of DIC is the release of a transmembrane glycoprotein (tissue factor =TF). TF is present on the
surface of many cell types (including endothelial cells, macrophages, and monocytes) and is not normally in contact with
the general circulation, but is exposed to the circulation after vascular damage. For example, TF is released in response
to exposure to cytokines (particularly interleukin 1), tumor necrosis factor, and endotoxin. This plays a major role in the
development of DIC in septic conditions. TF is also abundant in tissues of the lungs, brain, and placenta. This helps to
explain why DIC readily develops in patients with extensive trauma. Upon activation, TF binds with coagulation factors
that then triggers the extrinsic pathway (via Factor VII) which subsequently triggers the intrinsic pathway (XII to XI to IX)
of coagulation.
Diagnosis
Fibrin degradation products are often raised.
Disorder PT / INR aPTT Thrombin Platelet Bleeding

time count time
Heparin ↔/↑ ↑↑ ↑↑ ↔ ↔
DIC ↑↑ ↑↑ ↑↑ ↓ ↑
Liver disease ↑ ↑ ↔/↑ ↔/↓ ↔/↑
Platelet defect ↔ ↔ ↔ ↔ ↑(↑)
Vitamin K deficiency / Warfarin ↑↑ ↑ ↔ ↔ ↔
Haemophilia ↔ ↑↑ ↔ ↔ ↔
von Willebrand's disease ↔ ↑↑ ↔ ↔ ↑(↑)
Aspirin ↔ ↔ ↔ ↔ ↑

47
Cardiac Murmurs
Type of Murmur Conditions
Ejection systolic Aortic stenosis
Pulmonary stenosis, HOCM
ASD, Fallot's
Pan-systolic Mitral regurgitation
Tricuspid regurgitation
VSD
Late systolic Mitral valve prolapse
Coarctation of aorta
Early diastolic Aortic regurgitation
Graham-Steel murmur (pulmonary regurgitation)
Mid diastolic Mitral stenosis
Austin-Flint murmur (severe aortic regurgitation)
Nerve Injury
There are 3 types of nerve injury:

Neuropraxia • Nerve intact but electrical conduction is affected
• Full recovery
• Autonomic function preserved
• Wallerian degeneration does not occur
Axonotmesis • Axon is damaged and the myelin sheath is preserved. The connective tissue framework is not affected.
• Wallerian degeneration occurs.
Neurotmesis • Disruption of the axon, myelin sheath and surrounding connective tissue.
• Wallerian degeneration occurs.
Wallerian Degeneration
• Axonal degeneration distal to the site of injury.
• Typically begins 24-36 hours following injury.
• Axons are excitable prior to degeneration occurring.
• Myelin sheath degenerates and is phagocytosed by tissue macrophages.
Nerve repair
• Neuronal repair may only occur physiologically where nerves are in direct contact. Where a large defect is
present, the process of nerve regeneration is hampered. It may not occur at all or result in the formation of a
neuroma. Where nerve regrowth occurs it is typically at a rate of 1mm per day.

48
Absence Of The Vas Deferens
• Absence of the vas may be unilateral or bilateral
• Cystic fibrosis CFTR gene mutations are the cause in 40% of cases
• Some non CF cases are due to unilateral renal agenesis
• Sperm harvesting may allow for assisted conception
Cleft Lip and Palate

Cleft lip and palate are the most common congenital deformity affecting the orofacial structures. Whilst they may be an
isolated developmental malformation they are also a recognised component of more than 200 birth defects. The
incidence is as high as 1 in 600 live births. The commonest variants are:
• Isolated cleft lip (15%)
• Isolated cleft palate (40%)
• Combined cleft lip and palate (45%)
The aetiology of the disorder is multifactorial; both genetic (affected first degree relative increases risk) and
environmental factors play a role.
Cleft lip
Cleft lip occurs as a result of disruption of the muscles of the upper lip and nasolabial region. These muscles comprise a
chain of muscles viz; nasolabial, bilabial and labiomental. Defects may be unilateral or bilateral.
Cleft palate
The primary palate consists of all anatomical structures anterior to the incisive foramen. The secondary palate lies more
posteriorly and is sub divided into the hard and soft palate. Cleft palate occurs as a result of non-fusion of the two
palatine shelves. Both hard and soft palate may be involved. Complete cases are associated with complete separation of
the nasal septum and vomer from the palatine processes.
Treatment
Surgical reconstruction is the mainstay of management. The procedures are planned according to the extent of
malformation and child age. Simple defects are managed as a single procedure. Complex malformations are usually
corrected in stages. Affected individuals have a higher incidence of hearing and speech problems.
Choanal Atresia
• Congenital disorder with an incidence of 1 in 7000 births.
• Posterior nasal airway occluded by soft tissue or bone.
• Associated with other congenital malformations e.g. coloboma
• Babies with unilateral disease may go unnoticed.
• Babies with bilateral disease will present early in life as they can then only breathe through their mouth.
• Treatment is with fenestration procedures designed to restore patency.
Achondroplasia
Achondroplasia is a common cause of dwarfism and is caused by defects in the fibroblast growth factor receptor. In most
cases (approximately 70%) it occurs as a sporadic mutation. The main risk factor is advancing parental age at the time of
conception. Once present it is typically inherited in an autosomal dominant fashion.
Radiological features
• Large skull with narrow foramen magnum
• Short, flattened vertebral bodies
• Narrow spinal canal
• Horizontal acetabular roof
• Broad, short metacarpals
Treatment
There is no specific therapy. However, some individuals benefit from limb lengthening procedures. These usually involve
application of Ilizarov frames and targeted bone fractures. A clearly defined need and end point is the cornerstone of
achieving success with such procedures.

49
Genetics and Surgical Disease
Li-Fraumeni Syndrome
• Autosomal dominant
• Consists of germline mutations to p53 tumour suppressor gene
• High incidence of malignancies particularly sarcomas and leukaemias
• Diagnosed when:
*Individual develops sarcoma under 45 years
*First degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy
under 45 years or sarcoma at any age
BRCA 1 and 2
• Carried on chromosome 17 (BRCA 1) and Chromosome 13 (BRCA 2)
• Linked to developing breast cancer (60%) risk.
• Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2).
Lynch Syndrome
• Autosomal dominant
• Develop colonic cancer and endometrial cancer at young age
• 80% of affected individuals will get colonic and/ or endometrial cancer
• High risk individuals may be identified using the Amsterdam criteria
Amsterdam criteria
Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent,
child, sibling) relative of the other two.
Two successive affected generations.
One or more colon cancers diagnosed under age 50 years.
Familial adenomatous polyposis (FAP) has been excluded.
Gardners syndrome
• Autosomal dominant familial colorectal polyposis
• Multiple colonic polyps
• Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts
• Desmoid tumours are seen in 15%
• Mutation of APC gene located on chromosome 5
• Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal cancer
• Now considered a variant of familial adenomatous polyposis coli
Tumour Markers
Tumour markers may be divided into:
• monoclonal antibodies against carbohydrate or glycoprotein tumour antigens
• tumour antigens
• enzymes (alkaline phosphatase, neurone specific enolase)
• hormones (e.g. calcitonin, ADH)
It should be noted that tumour markers usually have a low specificity
Monoclonal antibodies
Tumour marker Association
CA 125 Ovarian cancer
CA 19-9 Pancreatic cancer
CA 15-3 Breast cancer
NB: The breast cancer tumour marker is not specific or sensitive enough to be used routinely.
Tumour antigens
Tumour marker Association
Prostate specific antigen (PSA) Prostatic carcinoma
Alpha-feto protein (AFP) Hepatocellular carcinoma, teratoma
Carcinoembryonic antigen (CEA) Colorectal cancer

50
Hodgkins Lymphoma
Presenting features
• Asymptomatic lympadenopathy
• Cough, Pel Ebstein fever, haemoptysis, dyspnoea
• B Symptoms - 10% weight loss, fever, night sweats
Staging
All patients are staged with CT scanning of the chest, abdomen and pelvis
The Ann Arbor staging system is commonly used
Stage Features
I Single lymph node region
II Two or more regions on the same side of the diaphragm
III Involvement of lymph node regions on both sides of the diaphragm
IV Involvement of extra nodal sites
Sub types
Classical Hodgkin lymphoma is classified into the following 4 types:
• Nodular sclerosing Hodgkin lymphoma (NSHL)
• Mixed-cellularity Hodgkin lymphoma (MCHL)
• Lymphocyte-depleted Hodgkin lymphoma (LDHL)
• Lymphocyte-rich classical Hodgkin lymphoma (LRHL)
A Reed Sternberg cell may be identified histologically.
A fifth sub type, Nodular lymphocyte-predominant Hodgkin lymphoma, is characterised by a different cell type Reed-
Sternberg cells are rarely seen.
Treatment
This may be multimodal and both chemo and radiotherapy are used.
Diagnosis
This is made by excision of a complete lymph node that is then submitted for detailed histological evaluation.
Pathogenesis
Infection with Ebstein Barr virus is linked to the condition (particularly mixed cellularity lymphoma).
Prognosis
Stage I disease is associated with survival figures of up to 85% at 5 years. The lymphocyte rich classical lymphoma has the
best prognosis. Lymphocyte depleted Hodgkins lymphoma, advancing age, male sex and stage IV disease are all
associated with a worsening of prognosis.

51
Acute Intermittent Porphyria
Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in porphobilinogen
deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxic accumulation of delta
aminolaevulinic acid and porphobilinogen. It characteristically presents with abdominal and neuropsychiatric symptoms
in 20-40 year olds. AIP is more common in females (5:1)
Features
• abdominal: abdominal pain, vomiting
• neurological: motor neuropathy
• psychiatric: e.g. depression
• hypertension and tachycardia common
Diagnosis
• classically urine turns deep red on standing
• raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)
• assay of red cells for porphobilinogen deaminase
• raised serum levels of delta aminolaevulinic acid and porphobilinogen
Aggressive Fibromatosis
Aggressive fibromatosis is a disorder consisting of desmoid tumours, which behave in a locally aggressive manner.
Desmoid tumours may be identified in both abdominal and extra-abdominal locations. Metastatic disease is rare. The
main risk factor (for abdominal desmoids) is having APC variant of familial adenomatous polyposis coli. Most cases are
sporadic.
Treatment is by surgical excision.
Hereditary Spherocytosis
Most common disorder of the red cell membrane, it has an incidence of 1 in 5000. The abnormally shaped erythrocytes
are prone to splenic sequestration and destruction. This can result in hyperbilirubinaemia, jaundice and splenomegaly. In
older patients an intercurrent illness may increase the rate of red cell destruction resulting in more acute symptoms.
Severe cases may benefit from splenectomy.
Hypersensitivity Reactions
The Gell and Coombs classification divides hypersensitivity reactions into 4 types
Type I Type II Type III Type IV
Description Anaphylactic Cytotoxic Immune complex Delayed type
Mediator IgE IgG, IgM IgG, Ig A, IgM T-cells
Antigen Exogenous Cell surface Soluble Tissues
Response time Minutes Hours Hours 2-3 days
Examples Asthma Autoimmune haemolytic anaemia Serum sickness Graft versus host disease
Hay fever Pemphigus SLE Contact dermatitis
Goodpasture's Aspergillosis
Koebner Phenomenon
The Koebner phenomenon describes skin lesions which appear at the site of injury. It is seen in:
• Psoriasis
• Vitiligo
• Warts
• Lichen planus
• Lichen sclerosus
• Molluscum contagiosum

52
Adrenal Lesions - Incidental
Incidentaloma of the adrenal glands have become increasingly common as CT scanning of the abdomen is widely
undertaken. Prevalences range from 1.5-9% in autopsy studies. Overall, 75% will be nonfunctioning adenomas. However,
a thorough diagnostic work up is required to exclude a more significant lesion.
Investigation
• Morning and midnight plasma cortisol measurements
• Dexamethasone suppression test
• 24-hour urinary cortisol excretion
• 24-hour urinary excretion of catecholamines
• Serum potassium, aldosterone and renin levels
Management
The risk of malignancy is related to the size of the lesion and 25% of all masses greater than 4cm will be malignant. Such
lesions should usually be excised. Where a lesion is a suspected metastatic deposit a biopsy may be considered. Smaller,
innocent lesions are usually followed up by serial CT scans at 6, 12 and 24 months.
Phaeochromocytoma and Adrenal Lesions

Neuroendocrine tumour of the chromaffin cells of the adrenal medulla. Hypertension and hyperglycaemia are often
found.
• 10% of cases are bilateral.
• 10% occur in children.
• 11% are malignant (higher when tumour is located outside the adrenal).
• 10% will not be hypertensive.
Familial cases are usually linked to the Multiple endocrine neoplasia syndromes (considered under its own heading).
Most tumours are unilateral (often right sided) and smaller than 10cm.
Diagnosis
• Urine analysis of vanillymandelic acid (VMA) is often used (false positives may occur e.g. in patients eating vanilla ice
cream!)
• Blood testing for plasma metanephrine levels.
• CT and MRI scanning are both used to localise the lesion.
Treatment
Patients require medical therapy first. An irreversible alpha adrenoreceptor blocker should be given, although minority
may prefer reversible blockade(1). Labetolol may be co-administered for cardiac chronotropic control. Isolated beta
blockade should not be considered as it will lead to unopposed alpha activity.
These patients are often volume depleted and will often require moderate volumes of intra venous normal saline
perioperatively.
Once medically optimised the phaeochromocytoma should be removed. Most adrenalectomies can now be performed
using a laparoscopic approach(2). The adrenals are highly vascular structures and removal can be complicated by
catastrophic haemorrhage in the hands of the inexperienced. This is particularly true of right sided resections where the
IVC is perilously close. Should the IVC be damaged a laparotomy will be necessary and the defect enclosed within a
Satinsky style vascular clamp and the defect closed with prolene sutures. Attempting to interfere with the IVC using any
instruments other than vascular clamps will result in vessel trauma and make a bad situation much worse.
Incidental adrenal lesions

Adrenal lesions may be identified on CT scanning performed for other reasons(3). Factors suggesting benign disease on
CT include (4):
• Size less than 3cm
• Homogeneous texture
• Lipid rich tissue
• Thin wall to lesion
All patients with incidental lesions should be managed jointly with an endocrinologist and full work up as described
above. Patients with functioning lesions or those with adverse radiological features (Particularly size >3cm) should
proceed to surgery.

53
Glucagonoma
• Rare pancreatic tumours arising from the alpha cells of the pancreas.
• Glucagon levels markedly elevated.
• Symptoms include diarrhoea, weight loss and necrolytic migratory erythema.
• A serum level of glucagon >1000pg/ml usually suggests the diagnosis, imaging with CT scanning is also required.
• Treatment is with surgical resection. However, careful staging is required for these tumours are usually malignant
and non resectable.
Glioma
Glioma is a tumour that is typically found in the CNS. These tumours arise from glial cells. They are sub categorised
according to the cell type they most closely resemble.
Glioma sub types

• Ependymomas- Ependymal cells
• Astocytomas- Astrocytes (including glioblastoma)
• Oligodendrogliomas- Oligodendrocytes
• Mixed- e.g. oligoastrocytomas
Gliomas are categorised as being either high or low grade lesions (the former has the worse prognosis). They may be
either supra or infra tentorial. Their symptoms will typically reflect their site of origin. Glioblastoma multiforme has the
worst prognosis and few patients will survive beyond 12 months.
Thymus
The thymus develops from the third and fourth pharyngeal pouches. It descends
to lie in the anterior superior mediastinum. It is encapsulated and is subdivided
into lobules, these consist of a cortex and a medulla. The cortex is composed of
tightly packed lymphocytes, the medulla consists largely of epithelial cells. The
medullary epithelial cells are concentrically arranged and may surround a
keratinised centre, known as Hassall's corpuscles.
The inferior parathyroid glands also develop from the third pharyngeal pouch and
may also be located with the thymus gland.
Its arterial supply is from the internal mammary artery or pericardiophrenic
arteries. Venous drainage is to the left brachiocephalic vein.
Hassall's corpuscles stained with H+E

54
Sarcomas
Malignant tumours of mesenchymal origin
Types (May be either bone or soft tissue in origin)
Bone sarcoma include:
• Osteosarcoma
• Ewing’s sarcoma (although non-bony sites recognised)
• Chondrosarcoma - originate from Chondrocytes
Soft tissue sarcomas are a far more heterogeneous group and include:
• Liposarcoma - adipocytes
• Rhabdomyosarcoma - striated muscle
• Leiomyosarcoma - smooth muscle
• Synovial sarcomas - close to joints (cell of origin not known but not synovium)
Malignant fibrous histiocytoma is a sarcoma that may arise in both soft tissue and bone.
Features
Certain features of a mass or swelling should raise suspicion for a sarcoma these include:
• Large > 5cm soft tissue mass
• Deep tissue location or intra muscular location
• Rapid growth
• Painful lump
Assessment
Imaging of suspicious masses should utilise a combination of MRI, CT and USS. Blind biopsy should not be performed
prior to imaging and where required should be done in such a way that the biopsy tract can be subsequently included in
any resection.
Ewing’s sarcoma
• Commoner in males
• Incidence of 0.3 / 1, 000, 000
• Onset typically between 10 and 20 years of age
• Location by femoral diaphysis is commonest site
• Histologically it is a small round tumour
• Blood borne metastasis is common and chemotherapy is often combined with surgery
Osteosarcoma
• Mesenchymal cells with osteoblastic differentiation
• 20% of all primary bone tumours
• Incidence of 5 per 1,000,000
• Peak age 15-30, commoner in males
• Limb preserving surgery may be possible and many patients will receive chemotherapy
Liposarcoma
• Malignancy of adipocytes
• Rare, approximately 2.5 per 1,000,000. They are the second most common soft tissue sarcoma
• Typically located in deep locations such as retroperitoneum
• Affect older age group usually >40 years of age
• May be well differentiated and thus slow growing although may undergo de-differentiation and disease
progression
• Many tumours will have a pseudocapsule that can misleadingly allow surgeons to feel that they can 'shell out'
these lesions. In reality, tumour may invade at the edge of the pseudocapsule and result in local recurrence if
this strategy is adopted
• Usually resistant to radiotherapy, although this is often used in a palliative setting
Malignant Fibrous Histiocytoma
• Tumour with large number of histiocytes
• Most common sarcoma in adults
• Also described as undifferentiated pleomorphic sarcoma NOS (i.e. Cell of origin is not known)
• Four major subtypes are recognised: storiform-pleomorphic (70% cases), myxoid (less aggressive), giant cell and
inflammatory
• ℞ is usually with surgical resection and adjuvant radiotherapy as this reduces the likelihood of local recurrence

55
Trypanosoma Cruzi
• Protozoan
• Causes Chagas disease
• Carried by bugs which infect the skin whilst feeding
• Penetrate through open wounds and mucous membranes
• Intracellular proliferation
• Major infective sites include CNS, intestinal myenteric plexus, spleen, lymph
nodes and cardiac muscle
• Chronic disease is irreversible, nifurtimox is used to treat acute infection
Actinomycosis
Chronic, progressive granulomatous disease caused by filamentous gram positive anaerobic bacteria from the
Actinomycetaceae family.
Actinomyces are commensal bacteria that become pathogenic when a mucosal barrier is breached.
The disease most commonly occurs in the head and neck, although it may also occur in the abdominal cavity and in the
thorax.
The mass will often enlarge across tissue planes with the formation of multiple sinus tracts.
Abdominopelvic actinomycosis occurs most frequently in individuals that have had appendicitis (65%) cases.
Pathology
• On histological examination gram positive organisms and evidence of sulphur granules.
• Sulphur granules are colonies of organisms that appear as round or oval basophilic masses.
• They are also seen in other conditions such as nocardiosis.
Treatment
• Long term antibiotic therapy usually with penicillin.
• Surgical resection is indicated for extensive necrotic tissue, non healing sinus tracts, abscesses or where biopsy
is needed to exclude malignancy.
The image shows an actinomycotic (sulfur) granule enveloped by an infiltrate

composed of neutrophils, foamy histiocytes, lymphocytes and plasma cells.

56
Burns
Burns may be thermal, chemical or electrical. In the former category are burns which occur as a result of heat. Chemical
burns occur when the skin is exposed to an extremely caustic or alkaline substance. Electrical burns occur following
exposure to electrical current. The immediate management includes removal of the burning source which usually
includes irrigation of the burned area. A detailed assessment then needs to be made of the extent of the burns and a
number of charts are available for recording this information. The degree of injury relates to the temperature and
duration of exposure. Most domestic burns are mainly scalds in young children.
Following the burn, there is a local response with progressive tissue loss and release of inflammatory cytokines.
Systemically, there are cardiovascular effects resulting from fluid loss and sequestration of fluid into the third space.
There is a marked catabolic response. Immunosupression is common with large burns and bacterial translocation from
the gut lumen is a recognised event. Sepsis is a common cause of death following major burns.
Type of burn Skin layers affected Skin appearance Blanching Management

Epidermal/Superficial Epidermis Red, moist Yes
Superficial partial Epidermis and part of papillary Pale, dry Yes Normally heals with no
thickness dermis affected intervention
Deep partial thickness Epidermis, whole papillary Mottled red No Needs surgical intervention
dermis affected colour (depending on site)
Full thickness Whole skin layer and Dry, leathery No Burns centre
subcutaneous tissue affected hard wound
Depth of burn assessment

• Bleeding on needle prick
• Sensation
• Appearance
• Blanching to pressure
Percentage burn estimation

• Lund Browder chart: most accurate even in children
• Wallace rule of nines
• Palmar surface: surface area palm = 0.8% burn
>15% body surface area burns in adults needs urgent burn fluid resuscitation
Transfer to burn centre if:

• Need burn shock resuscitation
• Face/hands/genitals affected
• Deep partial thickness or full thickness burns
• Significant electrical/chemical burns
Management
The initial aim is to stop the burning process and resuscitate the patient. Intravenous fluids will be required for children
with burns greater than 10% of total body surface area. Adults with burns greater than 15% of total body surface area
will also require IV fluids. The fluids are calculated using the Parkland formula which is; volume of fluid= total body
surface area of the burn % x weight (Kg) x4. Half of the fluid is administered in the first 8 hours. A urinary catheter should
be inserted. Analgesia should be given. Complex burns, burns involving the hand perineum and face and burns >10% in
adults and >5% in children should be transferred to a burns unit.
Circumferential burns affecting a limb or severe torso burns impeding respiration may require escharotomy to divide the
burnt tissue.
Conservative management is appropriate for superficial burns and mixed superficial burns that will heal in 2 weeks. More
complex burns may require excision and skin grafting. Excision and primary closure is not generally practised as there is a
high risk of infection.
There is no evidence to support the use of anti-microbial prophylaxis or topical antibiotics in burn patients.
Escharotomies
• Indicated in circumferential full thickness burns to the torso or limbs.
• Careful division of the encasing band of burn tissue will potentially improve ventilation (if the burn involves the
torso), or relieve compartment syndrome and oedema (where a limb is involved)

57
Collagen
Collagen is one of the most important structural proteins within the extracellular matrix, collagen together with
components such as elastin and glycosaminoglycans determine the properties of all tissues.
• Composed of 3 polypeptide strands that are woven into a helix, usually a combination of glycine with either
proline or hydroxyproline plus another amino acid
• Numerous hydrogen bonds exist within molecule to provide additional strength
• Many sub types but commonest sub type is I (90% of bodily collagen), tissues with increased levels of flexibility
have increased levels of type III collagen
• Vitamin c is important in establishing cross links
• Synthesised by fibroblasts
Collagen Diseases
Osteogenesis imperfecta:
• 8 Subtypes
• Defect of type I collagen
• Type I - The collagen is normal quality but insufficient quantity
• Type II - Poor quantity and quality
• Type III - Collagen poorly formed, normal quantity
• Type IV - Sufficient quantity but poor quality
Patients have bones which fracture easily, loose joint and multiple other defects depending upon which sub type they
suffer from.
Ehlers Danlos:
• Multiple sub types
• Abnormality of types 1 and 3 collagen
• Patients have features of hypermobility.
• Individuals are prone to joint dislocations and pelvic organ prolapse. In addition to many other diseases
related to connective tissue defects.

58

59
4. Peri-operative Care – MRCS Notes - Reda

American Society of Anesthesiologists Physical Status Scoring System (ASA)............................................. 2
Preparation for Surgery .................................................................................................................................. 2
Pre-operative Fluid Management .................................................................................................................. 3
Intra-operative Fluid Management ................................................................................................................ 3
Intravenous Access ......................................................................................................................................... 4
Atropine .......................................................................................................................................................... 4
Local Anaesthetic Agents................................................................................................................................ 5
Anaesthetic Agents ......................................................................................................................................... 6
Airway Management ...................................................................................................................................... 6
Muscle Relaxants ............................................................................................................................................ 7
Malignant Hyperthermia ................................................................................................................................ 7
Tourniquets ..................................................................................................................................................... 8
Blood Products - Cross Matching ................................................................................................................... 9
Heparin ............................................................................................................................................................ 9
Thromboprophylaxis in Surgical Patients .................................................................................................... 10
Proactive Care of Older People Undergoing Surgery (POPS) ...................................................................... 10
4. PERI-OPERATIVE CARE – MRCS NOTES - REDA 1

60
American Society of Anesthesiologists Physical Status Scoring System (ASA)
ASA grade Description
1 No organic physiological, biochemical or psychiatric disturbance. The surgical pathology is localised and
has not invoked systemic disturbance
2 Mild or moderate systemic disruption caused either by the surgical disease process or though underlying
pre-existing disease
3 Severe systemic disruption caused either by the surgical pathology or pre-existing disease
4 Patient has severe systemic disease that is a constant threat to life
5 A patient who is moribund and will not survive without surgery
Preparation for Surgery

Elective and emergency patients require different preparation.
Elective cases
• Consider pre admission clinic to address medical issues.
• Blood tests including FBC, U+E, LFT's, Clotting, Group and Save
• Urine analysis
• Pregnancy test
• Sickle cell test
• ECG/ Chest x-ray
Exact tests to be performed will depend upon the proposed procedure and patient fitness.
Risk factors for development of deep vein thrombosis should be assessed and a plan for thromboprophylaxis formulated.
Diabetes
Diabetic patients have greater risk of complications.
Poorly controlled diabetes carries high risk of wound infections.
Patients with diet or tablet controlled diabetes may be managed using a policy of omitting medication and checking
blood glucose levels regularly. Diabetics who are poorly controlled or who take insulin may require a intravenous sliding
scale. Potassium supplementation should also be given.
Diabetic cases should be operated on first.
Emergency cases
Stabilise and resuscitate where needed.
Consider whether antibiotics are needed and when and how they should be administered.
Inform blood bank if major procedures planned particularly where coagulopathies are present at the outset or
anticipated (e.g. Ruptured AAA repair)
Don't forget to consent and inform relatives.
Special preparation
Some procedures require special preparation:
• Thyroid surgery; vocal cord check.
• Parathyroid surgery; consider methylene blue to identify gland.
• Sentinel node biopsy; radioactive marker/ patent blue dye.
• Surgery involving the thoracic duct; consider administration of cream.
• Pheochromocytoma surgery; will need alpha and beta blockade.
• Surgery for carcinoid tumours; will need covering with octreotide.
• Colorectal cases; bowel preparation (especially left sided surgery)
• Thyrotoxicosis; lugols iodine/ medical therapy.

61
Pre-operative Fluid Management
Fluid management has been described in the British Consensus guidelines on IV fluid therapy for Adult Surgical patients
(GIFTASUP) and by NICE (CG174 December 2013)
The Recommendations include:

• Use Ringer's lactate or Hartmann's when a crystalloid is needed for resuscitation or replacement of fluids. Avoid
0.9% N. Saline (due to risk of hyperchloraemic acidosis) unless patient vomiting or has gastric drainage.
• Use 4%/0.18% dextrose saline or 5% dextrose in maintenance fluids. It should not be used in resuscitation or as
replacement fluids.
• Adult maintenance fluid requirements are: Na 50-100 mmol/day and K 40-80 mmol/day in 1.5-2.5L fluid per
day.
• Patients for elective surgery should NOT be nil by mouth for >2 hours (unless has disorder of gastric emptying).
• Patients for elective surgery should be given carbohydrate rich drinks 2-3h before. Ideally this should form part
of a normal pre op plan to facilitate recovery.
• Avoid mechanical bowel preparation.
• If bowel prep is used, simultaneous administration of Hartmann's or Ringer's lactate should be considered.
• Excessive fluid losses from vomiting should be treated with a crystalloid with potassium replacement. 0.9% N.
Saline should be given if there is hypochloraemia. Otherwise Hartmann's or Ringer lactate should be given for
diarrhoea/ileostomy/ileus/obstruction. Hartmann's should also be given in sodium losses secondary to diuretics.
• High risk patients should receive fluids and inotropes.
• An attempt should be made to detect pre or operative hypovolaemia using flow based measurements. If this is
not available, then clinical evaluation is needed i.e. JVP, pulse volume etc.
• In Blood loss or infection causing hypovolaemia should be treated with a balanced crystalloid or colloid (or until
blood available in blood loss). A critically ill patient is unable to excrete Na or H 2 0 leading to a 5% risk of
interstitial oedema. Therefore 5% dextrose as well as colloid should be given.
• If patients need IV fluid resuscitation, use crystalloids that contain sodium in the range 130-154 mmol/l, with a
bolus of 500 ml over less than 15 minutes (NICE Guidance CG 174).
Intra-operative Fluid Management

Composition of commonly used intravenous fluids mmol-1
Na K Cl Bicarbonate Lactate
Plasma 137-147 4-5.5 95-105 22-25 -
0.9% Saline 153 - 153 - -
Dextrose / saline 30.6 - 30.6 - -
Hartmans 130 4 110 - 28
Recommendations for intra operative fluid management

The latest set of NICE guidelines produced in 2013 relating to intravenous fluids did not specifically address the
requirements of intra operative fluid administration. The reason for this is that administration of fluids in this specific
situation does not lend itself to rigid algorithms.
With the introduction of enhanced recovery programmes 10 years ago there was an increasing emphasis of the concept
of fluid restriction. Historically, patients received very large volumes of saline rich solutions peri-operatively. Clearing the
sodium load of a single litre of saline may take up to 36 hours or more. This can have deleterious effects on the tissues
including the development of oedema. This results in poor perfusion, increased risk of ileus and wound breakdown. A
tailored approach to fluid administration is now practiced and far greater usage is made of cardiac output monitors in
providing goal directed fluid therapy.

62
Intravenous Access
Venous access
A number of routes for establishing venous access are available.
Peripheral venous cannula

Easy to insert with minimal morbidity. Wide lumen cannulae can provide rapid fluid infusions. When properly managed
infections may be promptly identified and the cannula easily re sited. Problems relate to their peripheral sites and they
are unsuitable for the administration of vaso active drugs, such as inotropes and irritant drugs such as TPN (except in the
very short term setting).
Central lines
Insertion is more difficult and most operators and NICE advocate the use of ultra sound. Coagulopathies may lead to
haemorrhage following iatrogenic arterial injury.
Central lines (and particularly subclavian lines) are risk factors for the development of pneumothorax.
Femoral lines are easier to insert and iatrogenic injuries easier to manage in this site however they are prone to high
infection rates. Internal jugular route is preferred. They have multiple lumens allowing for administration of multiple
infusions. The lumens are relatively narrow and thus they do not allow particularly rapid rates of infusion.
Intraosseous access
This is typically undertaken at the anteromedial aspect of the proximal tibia and provides access to the marrow cavity
and circulatory system. Although traditionally preferred in paediatric practice they may be used in adults and a wide
range of fluids can be infused using these devices.
Tunneled lines
Tunneled lines such as Groshong and Hickman lines are popular devices for patients with long term therapeutic
requirements. These devices are usually inserted using ultrasound guidance into the internal jugular vein and then
tunneled under the skin. A cuff of woven material is sited near the end and helps to anchor the device into the tissues.
These cuffs require formal dissection to allow the device to be removed. Tunneled lines can be linked to injection ports
that are located under the skin. These are especially popular in paediatric practice.
Peripherally inserted central cannula

Referred to as PICC lines, these are popular methods for establishing central venous access. Because they are inserted
peripherally they are less prone to major complications relating to device insertion than conventional central lines.
Atropine
Atropine is a muscarinic receptor antagonist (competitive antagonist for the muscarinic acetylcholine receptor). It
therefore inhibits parasympathetic activity.It was traditionally used as a premedication for anaesthesia because it
reduced bronchial secretions, salivary secretions and bradycardia from increased vagal tone on anaesthetic induction.
Modern anaesthetic techniques have reduced the need for routine use of this drug. Its other effects include urinary
retention and pupillary dilatation.

63
Local Anaesthetic Agents
All local anaesthetics have a chemical bond linking an amine to either an amide or an ester. Most local anaesthetics are
of the amino- amide types, these have a more favorable side effect profile and are more stable in solution. Procaine and
benzocaine have amino - ester groups, these are metabolized by pseudocholinesterases.
Lidocaine / Xylocaine / Lignocaine

• An amide
• Local anaesthetic and a less commonly used antiarrhythmic (affects Na channels in the axon)
• Hepatic metabolism, protein bound, renally excreted
• Toxicity: Due to IV or excess administration. Increased risk if liver dysfunction or low protein states. Note
acidosis causes lidocaine to detach from protein binding.
• Drug interactions: Beta blockers, ciprofloxacin, phenytoin
• Features of toxicity: Initial CNS over activity then depression as lidocaine initially blocks inhibitory pathways then
blocks both inhibitory and activating pathways. Cardiac arrhythmias.
• Increased doses may be used when combined with adrenaline to limit systemic absorption.
Cocaine
• Pure cocaine is a salt, usually cocaine hydrochloride. It is supplied for local anaesthetic purposes as a paste.
• It is supplied for clinical use in concentrations of 4 and 10%. It may be applied topically to the nasal mucosa. It
has a rapid onset of action and has the additional advantage of causing marked vasoconstriction.
• It is lipophilic and will readily cross the blood brain barrier. Its systemic effects also include cardiac arrhythmias
and tachycardia.
• Apart from its limited use in ENT surgery it is otherwise used rarely in mainstream surgical practice.
Bupivacaine
• Bupivacaine binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells,
which prevents depolarization.
• It has a much longer duration of action than lignocaine and this is of use in that it may be used for topical wound
infiltration at the conclusion of surgical procedures with long duration analgesic effect.
• It is cardiotoxic and is therefore contra indicated in regional blockage in case the tourniquet fails.
• Levobupivacaine (Chirocaine) is less cardiotoxic and causes less vasodilation.
Prilocaine
• Similar mechanism of action to other local anaesthetic agents. However, it is far less cardiotoxic and is therefore
the agent of choice for intravenous regional anaesthesia e.g. Biers Block.
All local anaesthetic agents dissociate in tissues and this contributes to their therapeutic effect. The dissociation constant
shifts in tissues that are acidic e.g. where an abscess is present, and this reduces the efficacy.
Doses of local anaesthetics

Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivacaine 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-morbidities.
Maximum total local anaesthetic doses

• Lignocaine 1% plain - 3mg/ Kg - 200mg (20ml)
• Lignocaine 1% with 1 in 200,000 adrenaline - 7mg/Kg - 500mg (50ml)
• Bupivacaine 0.5% - 2mg/kg- 150mg (30ml)
Maximum doses are based on ideal body weight
Effects of adrenaline
Adrenaline may be added to local anaesthetic drugs. It prolongs the duration of action at the site of injection and permits
usage of higher doses (see above). It is contra indicated in patients taking MAOI's or tricyclic antidepressants. The toxicity
of bupivacaine is related to protein binding and addition of adrenaline to this drug does not permit increases in the total
dose of bupivacaine, in contrast to the situation with lignocaine.

64
Anaesthetic Agents
The table below summarises some of the more commonly used IV induction agents
Agent Specific features
Propofol • Rapid onset of anaesthesia
• Pain on IV injection
• Rapidly metabolised with little accumulation of metabolites
• Proven anti emetic properties
• Moderate myocardial depression
• Widely used especially for maintaining sedation on ITU, total IV anaesthesia and for daycase surgery
Sodium • Extremely rapid onset of action making it the agent of choice for rapid sequence of induction
thiopentone • Marked myocardial depression may occur
• Metabolites build up quickly
• Unsuitable for maintenance infusion
• Little analgesic effects
Ketamine • May be used for induction of anaesthesia
• Has moderate to strong analgesic properties
• Produces little myocardial depression making it a suitable agent for anaesthesia in those who are
haemodynamically unstable
• May induce state of dissociative anaesthesia resulting in nightmares
Etomidate • Has favorable cardiac safety profile with very little haemodynamic instability
• No analgesic properties
• Unsuitable for maintaining sedation as prolonged (and even brief) use may result in adrenal
suppression
• Post-operative vomiting is common
Airway Management
Oropharyngeal • Easy to insert and use
airway • No paralysis required
• Ideal for very short procedures
• Most often used as bridge to more definitive airway
Laryngeal mask • Widely used
• Very easy to insert
• Device sits in pharynx and aligns to cover the airway
• Poor control against reflux of gastric contents
• Paralysis not usually required
• Commonly used for wide range of anaesthetic uses, especially in day surgery
• Not suitable for high pressure ventilation (small amount of PEEP often possible)
Endotracheal • Provides optimal control of the airway once cuff inflated
tube • May be used for long or short term ventilation
• Errors in insertion may result in oesophageal intubation (therefore end tidal CO 2 usually
measured)
• Paralysis often required
• Higher ventilation pressures can be used

65
Tracheostomy • Reduces the work of breathing (and dead space)
• May be useful in slow weaning
• Percutaneous tracheostomy widely used in ITU
• Dries secretions, humidified air usually required
Muscle Relaxants
Suxamethonium • Depolarising neuromuscular blocker
• Inhibits action of acetylcholine at the neuromuscular junction
• Degraded by plasma cholinesterase and acetylcholinesterase (affected by lack of
acetylcholinesterase)
• Fastest onset and shortest duration of action of all muscle relaxants
• Produces generalised muscular contraction prior to paralysis
• Adverse effects include hyperkalaemia, malignant hyperthermia, delayed recovery
Atracurium • Non depolarising neuromuscular blocking drug
• Duration of action usually 30-45 minutes
• Generalised histamine release on administration may produce facial flushing, tachycardia and
hypotension
• Not excreted by liver or kidney, broken down in tissues by hydrolysis
• Reversed by neostigmine
Vecuronium • Non depolarising neuromuscular blocking drug
• Duration of action approximately 30 - 40 minutes
• Degraded by liver and kidney and effects prolonged in organ dysfunction
• Effects may be reversed by neostigmine
Pancuronium • Non depolarising neuromuscular blocker
• Onset of action approximately 2-3 minutes
• Duration of action up to 2 hours
• Effects may be partially reversed with drugs such as neostigmine
Malignant Hyperthermia
Overview
• Condition seen following administration of anaesthetic agents ( rate of 1 in 15,000)
• Characterised by hyperpyrexia and muscle rigidity
• Cause by excessive release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle
• Associated with defects in a gene on chromosome 19 encoding the ryanodine receptor, which controls
Ca2+release from the sarcoplasmic reticulum
• Neuroleptic malignant syndrome may have a similar aetiology
Causative agents
• Halothane
• Suxamethonium
• Other drugs: antipsychotics (neuroleptic malignant syndrome)
Investigations
• CK raised
• Contracture tests with halothane and caffeine
Management
• Dantrolene - prevents Ca2+ release from the sarcoplasmic reticulum

66
Tourniquets
Tourniquets are used during surgery to minimise blood loss and ensure a clear operative field. They must be correctly
applied and monitored. They are applied to extremities and in most cases are inflated using a pressure monitoring
system.
There are a number of systemic effects that can accompany tourniquet use, these can be divided into those which occur
following inflation and those that occur once the tourniquet is deflated.
Post inflation
Increased systemic vascular resistance, increased CVP and increased BP
Slower gradual increase in BP over time
Induced hypercoagulable state
Slow increase in core temperature
Post deflation
Fall in CVP, BP and SVR
Increased end tidal carbon dioxide
Enhanced fibrinolysis
Fall in core temperature
Raised serum potassium and lactate levels
Contra indications
Absolute Relative
AV fistula Sickle cell disease
Severe peripheral vascular disease History of thromboembolic events
Previous vascular surgery Skin grafts
Bone fracture or thrombosis at the site of tourniquet application Localised infection
Lymphoedema
Local complications
• Damage to skin
• Damage to muscle (rarely compartment syndrome)
• Damage to vessels
• Neuropraxia

67
Blood Products - Cross Matching
Whole blood fractions
Fraction Key points
Packed red cells Used for transfusion in chronic anaemia and cases where infusion of large volumes of fluid
may result in cardiovascular compromise. Product obtained by centrifugation of whole blood.
Platelet rich plasma Usually administered to patients who are thrombocytopaenic and are bleeding or require
surgery. It is obtained by low speed centrifugation.
Platelet concentrate Prepared by high speed centrifugation and administered to patients with thrombocytopaenia.
Fresh frozen plasma • Prepared from single units of blood.
• Contains clotting factors, albumin and immunoglobulin.
• Unit is usually 200 to 250ml.
• Usually used in correcting clotting deficiencies in patients with hepatic synthetic
failure who are due to undergo surgery.
• Usual dose is 12-15ml/Kg-1.
• It should not be used as first line therapy for hypovolaemia.
Cryoprecipitate • Formed from supernatant of FFP.
• Rich source of Factor VIII and fibrinogen.
• Allows large concentration of factor VIII to be administered in small volume.
SAG-Mannitol Blood Removal of all plasma from a blood unit and substitution with:
• Sodium chloride
• Adenine
• Anhydrous glucose
• Mannitol
Up to 4 units of SAG M Blood may be administered. Thereafter whole blood is preferred. After
8 units, clotting factors and platelets should be considered.
Cross matching
Must be cross matched Can be ABO incompatible in adults
Packed red cells Platelets
Whole blood FFP
Cryoprecipitate
Heparin
Causes the formation of complexes between antithrombin and activated thrombin/factors 7,9,10,11 & 12
Advantages of low molecular weight heparin
• Better bioavailability
• Lower risk of bleeding
• Longer half life
• Little effect on APTT at prophylactic dosages
• Less risk of HIT
Complications
• Bleeding
• Osteoporosis
• Heparin induced thrombocytopenia (HIT): occurs 5-14 days after 1st exposure
• Anaphylaxis
In surgical patients that may need a rapid return to theatre, administration of unfractionated heparin is preferred; as low
molecular weight heparins have a longer duration of action and are harder to reverse.

68
Thromboprophylaxis in Surgical Patients
Deep vein thrombosis may develop insidiously in many surgical patients. Untreated it may progress to result in
pulmonary embolism.
The following surgical patients are at increased risk of deep vein thrombosis:
• Surgery greater than 90 minutes at any site or greater than 60 minutes if the procedure involves the lower limbs
or pelvis
• Acute admissions with inflammatory process involving the abdominal cavity
• Expected significant reduction in mobility
• Age over 60 years
• Known malignancy
• Thrombophilia
• Previous thrombosis
• BMI >30
• Taking hormone replacement therapy or the contraceptive pill
• Varicose veins with phlebitis
Mechanical thromboprophylaxis
• Early ambulation after surgery is cheap and is effective
• Compression stockings (contra -indicated in peripheral arterial disease)
• Intermittent pneumatic compression devices
• Foot impulse devices
Therapeutic agents
Agent Mode of action Uses
Low molecular Binds antithrombin Thromboprophylaxis or treatment of thromboembolic events in those
weight heparin causing inhibition of with normal renal function. It is given as once daily subcutaneous
factor Xa injection
Unfractionated Binds antithrombin III Effective anticoagulation, administered intravenously it has a rapid
heparin affecting thrombin and onset and its therapeutic effects decline quickly on stopping and
factor Xa infusion. Its activity is measured using the APTT. If need be it can be
reversed using protamine sulphate
Dabigatran Orally administered Used prophylaxis in hip and knee surgery. It does not require
direct thrombin therapeutic monitoring. It should not be used in any patient in whom
inhibitor there is a risk of active bleeding or imminent likelihood of surgery. It is
reversed using Idarucizumab
Proactive Care of Older People Undergoing Surgery (POPS)

• Comprehensive geriatric assessment
• MDT assessment preoperatively
• Main predictors of complications are co-morbidities cardiac disease and reduced functional capacity -
preoperative assessment is the key to preventing adverse postoperative outcomes
• Patients screened for risk factors (albumin <30, co morbidities)
• Management plan made and disseminated to all involved
• Patients education: pain relief, post op exercises, nutrition
Outcomes:
• Fewer postoperative medical complications
• Reduced length of stay by 4.5 days

69
5. Post-op Management and Care – MRCS Notes - Reda

Acute Dystonic Reaction ................................................................................................................................. 2
Acute Renal Failure ......................................................................................................................................... 2
Brain Death ..................................................................................................................................................... 2
Adult Respiratory Distress Syndrome ............................................................................................................ 3
Circulatory Support of the Critically Ill ........................................................................................................... 4
Cryoprecipitate ............................................................................................................................................... 4
Massive Haemorrhage .................................................................................................................................... 5
Hypovolaemia and The Surgical Patient ........................................................................................................ 5
Management of Pain ...................................................................................................................................... 6
Neuropathic Pain ............................................................................................................................................ 7
Nutrition Monitoring - NICE Guidelines ......................................................................................................... 8
Nutrition Screening - NICE Guidelines............................................................................................................ 8
Refeeding Syndrome....................................................................................................................................... 8
Nutrition Prescriptions ................................................................................................................................... 9
Oral, Enteral and Parenteral Feeding - NICE Guidelines Summary ............................................................... 9
Post-Operative Fluid Management .............................................................................................................. 10
Postoperative Cognitive Dysfunction (POCD) Management ....................................................................... 10
Pulmonary Embolism: Investigation ............................................................................................................ 11
Pulmonary Function Tests ............................................................................................................................ 11
Surgical Complications .................................................................................................................................. 12
Surgical Site Infection ................................................................................................................................... 14
5. POST-OP MANAGEMENT AND CRITICAL CARE – MRCS NOTES - REDA 1

70
Acute Dystonic Reaction
The anti-dopaminergic drugs (such as antipsychotics) may result in extrapyramidal side effects. These may range from
mild parkinsonian symptoms such as resting tremor and bradykinesia. Through to acute dystonic reactions which are
characterised by abnormal and involuntary facial and bodily movements, such as spasmodic torticollis, oculogyric crisis
and oromandibular dystonia.
Chronic cases are generally only encountered in psychiatric units. In surgical practice the administration of the anti-
dopaminergic drug metoclopramide may be sufficient to precipitate an attack.
Treatment may be required if symptoms are sufficiently troublesome; benzhexol and procyclidine are two drugs which
may be used.
Acute Renal Failure

• Final pathway is tubular cell death.
• Renal medulla is a relatively hypoxic environment making it susceptible to renal tubular hypoxia.
• Renovascular autoregulation maintains renal blood flow across a range of arterial pressures.
• Estimates of GFR are best indices of level of renal function. Useful clinical estimates can be obtained by considering
serum creatinine, age, race, gender and body size. eGFR calculations such as the Cockcroft and Gault equation are
less reliable in populations with high GFR's.
• Nephrotoxic stimuli such as aminoglycosides and radiological contrast media induce apoptosis. Myoglobinuria and
haemolysis result in necrosis. Overlap exists and proinflammatory cytokines play and important role in potentiating
ongoing damage.
• Post-operative renal failure is more likely to occur in patients who are elderly, have peripheral vascular disease, high
BMI, have COPD, receive vasopressors, are on nephrotoxic medication or undergo emergency surgery.
• Avoiding hypotension will reduce risk of renal tubular damage.
• There is no evidence that administration of ACE inhibitors or dopamine reduces the incidence of post-operative
renal failure.
Brain Death
Criteria for brain stem death testing
• Deep coma of known aetiology.
• Reversible causes excluded
• No sedation
• Normal electrolytes
Testing for brain death

• Fixed pupils which do not respond to sharp changes in the intensity of incident light
• No corneal reflex
• Absent oculo-vestibular reflexes - no eye movements following the slow injection of at least 50ml of ice-cold
water into each ear in turn (the caloric test)
• No response to supraorbital pressure
• No cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation
• No observed respiratory effort in response to disconnection of the ventilator for long enough (typically 5
minutes) to ensure elevation of the arterial partial pressure of carbon dioxide to at least 6.0 kPa (6.5 kPa in
patients with chronic carbon dioxide retention). Adequate oxygenation is ensured by pre-oxygenation and
diffusion oxygenation during the disconnection (so the brain stem respiratory centre is not challenged by the
ultimate, anoxic, drive stimulus)
The test should be undertaken by two appropriately experienced doctors on two separate occasions. Both should be
experienced in performing brain stem death testing and have at least 5 years post graduate experience. One of them
must be a consultant. Neither can be a member of the transplant team (if organ donation contemplated).

71
Adult Respiratory Distress Syndrome
Defined as an acute condition characterized by bilateral pulmonary infiltrates and severe hypoxemia (PaO 2 /FiO 2 ratio <
200) in the absence of evidence for cardiogenic pulmonary oedema (clinically or pulmonary capillary wedge pressure of
less than 18 mm Hg).
It is subdivided into two stages. Early stages consist of an exudative phase of injury with associated oedema. The later
stage is one of repair and consists of fibroproliferative changes. Subsequent scarring may result in poor lung function.
Causes
• Sepsis
• Direct lung injury
• Trauma
• Long bone fracture or multiple fractures (through fat embolism)
• Head injury (causes sympathetic nervous stimulation which leads to acute pulmonary hypertension)
Clinical features
• Acute dyspnoea and hypoxaemia hours/days after event
• Multi organ failure
• Rising ventilatory pressures
Management
• Treat the underlying cause
• Antibiotics (if signs of sepsis)
• Negative fluid balance i.e. Diuretics
• Recruitment maneuvers such as prone ventilation, use of positive end expiratory pressure
• Mechanical ventilation strategy using low tidal volumes, as conventional tidal volumes may cause lung injury
(only treatment found to improve survival rates)

72
Circulatory Support of the Critically Ill
Circulatory support
Impaired tissue oxygenation may occur as a result of circulatory shock. Shock is considered further under its own topic
heading.
Patients requiring circulatory support require haemodynamic monitoring. At its simplest level this may simply be in the
form of regular urine output measurements and blood pressure monitoring. In addition, ECG monitoring will allow the
identification of cardiac arrhythmias. Pulse oximeter measurements will allow quick estimation haemoglobin oxygen
saturation in arterial blood.
Invasive arterial blood pressure monitoring is undertaken by the use of an indwelling arterial line. Most arterial sites can
be used although the radial artery is the commonest. It is important not to cannulate end arteries. The arterial trace can
be tracked to ventilation phases and those patients whose systolic pressure varies with changes in intrathoracic pressure
may benefit from further intravenous fluids.
Central venous pressure is measured using a CVP line that is usually sited in the superior vena cava via the internal
jugular route. The CVP will demonstrate right atrial filling pressure and volume status. When adequate intra vascular
volume is present a fluid challenge will typically cause a prolonged rise in CVP (usually greater than 6-8mmHg).
To monitor the cardiac output a Swan-Ganz catheter is traditionally inserted (other devices may be used and are less
invasive). Inflation of the distal balloon will provide the pulmonary artery occlusion pressure and the pressure distal to
the balloon will equate to the left atrial pressure. This gives a measure of left ventricular preload. Because the Swan-Ganz
catheter can measure several variables it can be used to calculate:
• Stroke volume
• Systemic vascular resistance
• Pulmonary artery resistance
• Oxygen delivery (and consumption)
Inotropes
In patients with an adequate circulating volume but on-going circulatory compromise a vasoactive drug may be
considered. These should usually be administered via the central venous route. Commonly used inotropes include:
Agent Mode of action Effect
Noradrenaline α agonist Vasopressor action, minimal effect on cardiac output
Adrenaline α and β receptor agonist Increases cardiac output and peripheral vascular resistance
Dopamine β1 agonist Increases contractility and rate
Dobutamine β1 and β2 agonist Increases cardiac output and decreases SVR
Milrinone Phosphodiesterase Elevation of cAMP levels improves muscular contractility, short half life
inhibitor and acts as vasodilator
Cryoprecipitate
• Blood product made from plasma
• Usually transfused as 6 unit pool
• Indications include massive haemorrhage and uncontrolled bleeding due to haemophilia
Composition
Agent Quantity
Factor VIII 100IU
Fibrinogen 250mg
von Willebrand factor Variable
Factor XIII Variable

73
Massive Haemorrhage
Definition
This is the loss of one blood volume in a 24 hour period or the loss of 50% of the circulating blood volume in 3 hours. A
blood loss of 150ml/ minute is also included. The normal adult blood volume is 7% of total adult body weight. The blood
volume equates to between 8 and 9% of a child's body weight.
Complications of massive transfusion

Complication Key points
Hypothermia Blood is refrigerated
Hypothermic blood impairs homeostasis
Shifts Bohr curve to the left
Hypocalcaemia Both FFP and platelets contain citrate anticoagulant, this may chelate calcium
Hyperkalaemia Plasma of red cells stored for 4-5 weeks contains 5-10 mmol K+
Delayed type transfusion Due to minor incompatibility issues especially if urgent or non cross matched blood
reactions used
Transfusion related lung injury Acute onset non cardiogenic pulmonary oedema
Leading cause of transfusion related deaths
Greatest risk posed with plasma components
Occurs as a result of leucocyte antibodies in transfused plasma
Aggregation and degranulation of leucocytes in lung tissue accounts for lung injury
Coagulopathy Anticipate once circulating blood volume transfused
1 blood volume usually drops platelet count to 100 or less
1 blood volume will both dilute and not replace clotting factors
Fibrinogen concentration halves per 0.75 blood volume transfused
Hypovolaemia and The Surgical Patient

Hypovolaemia often represents the end point of multiple pathological processes. It may be divided into the following
categories; overt compensated hypovolaemia, covert compensated hypovolaemia and decompensated hypovolaemia. Of
these three categories the covert compensated subtype of hypovolaemia remains the commonest and is accounted for
by the fact that class I shock will often produce no overtly discernible clinical signs. This is due, in most cases, to a degree
of splanchnic autotransfusion. The most useful diagnostic test for detection of covert compensated hypovolaemia
remains urinanalysis. This often shows increased urinary osmolality and decreased sodium concentration.
In overt compensated hypovolaemia the blood pressure is maintained although other haemodynamic parameters may
be affected. This correlates to class II shock. In most cases assessment can be determined clinically. Where underlying
cardiopulmonary disease may be present the placement of a CVP line may guide fluid resuscitation. Severe pulmonary
disease may produce discrepancies between right and left atrial filling pressures. This problem was traditionally
overcome through the use of Swann-Ganz catheters.
Untreated, hypovolaemia may ultimately become uncompensated with resultant end organ dysfunction. Microvascular
hypoperfusion may result in acidosis with a subsequent myocardial depressive effect, thereby producing a vicious circle.
The treatment of hypovolaemia is with intravenous fluids. In the first instance a fluid challenge such as the rapid infusion
of 250ml of crystalloid will often serve as both a diagnostic and resuscitative measure. In the event that this fails to
produce the desired response the patient will need to be re-evaluated clinically. More fluid may be needed. However, it
is important not to overlook mechanical ureteric obstruction in the anuric, normotensive patient.

74
Management of Pain
World Health Organisation Analgesic Ladder
• Initially peripherally acting drugs such as paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) are
given.
• If pain control is not achieved, the second part of the ladder is to introduce weak opioid drugs such as codeine
or dextropropoxyphene together with appropriate agents to control and minimise side effects.
• The final rung of the ladder is to introduce strong opioid drugs such as morphine. Analgesia from peripherally
acting drugs may be additive to that from centrally-acting opioids and thus, the two are given together.
The World Federation of Societies of Anaesthesiologists (WFSA) Analgesic Ladder

• For management of acute pain
• Initially, the pain can be expected to be severe and may need controlling with strong analgesics in combination
with local anaesthetic blocks and peripherally acting drugs.
• The second rung on the postoperative pain ladder is the restoration of the use of the oral route to deliver
analgesia. Strong opioids may no longer be required and adequate analgesia can be obtained by using
combinations of peripherally acting agents and weak opioids.
• The final step is when the pain can be controlled by peripherally acting agents alone.
Local anaesthetics
• Infiltration of a wound with a long-acting local anaesthetic such as Bupivacaine
• Analgesia for several hours
• Further pain relief can be obtained with repeat injections or by infusions via a thin catheter
• Blockade of plexuses or peripheral nerves will provide selective analgesia in those parts of the body supplied by
the plexus or nerves
• Can either be used to provide anaesthesia for the surgery or specifically for postoperative pain relief
• Especially useful where a sympathetic block is needed to improve postoperative blood supply or where central
blockade such as spinal or epidural blockade is contraindicated.
Spinal anaesthesia
Provides excellent analgesia for surgery in the lower half of the body and pain relief can last many hours after completion
of the operation if long-acting drugs containing vasoconstrictors are used.
Side effects of spinal anaesthesia include: hypotension, sensory and motor block, nausea and urinary retention.
Epidural anaesthesia
An indwelling epidural catheter inserted. This can then be used to provide a continuous infusion of analgesic agents. It
can provide excellent analgesia. They are still the preferred option following major open abdominal procedures and help
prevent post operative respiratory compromise resulting from pain.
Disadvantages of epidurals is that they usually confine patients to bed, especially if a motor block is present. In addition,
an indwelling urinary catheter is required. Which may not only impair mobility but also serve as a conduit for infection.
They are contraindicated in coagulopathies.
Transversus Abdominal Plane block (TAP)

In this technique an ultrasound is used to identify the correct muscle plane and local anaesthetic (usually bupivicaine) is
injected. The agent diffuses in the plane and blocks many of the spinal nerves. It is an attractive technique as it provides a
wide field of blockade but does not require the placement of any indwelling devices. There is no post-operative motor
impairment. For this reason, it is the preferred technique when extensive laparoscopic abdominal procedures are
performed. They will then provide analgesia immediately following surgery but as they do not confine the patient to bed,
the focus on enhanced recovery can begin sooner.
-The main disadvantage is that their duration of action is limited to the half-life of the local anaesthetic agent chosen. In
addition some anaesthetists do not have the USS skills required to site the injections.
Patient Controlled Analgesia (PCA)

Patients administer their own intravenous analgesia and titrate the dose to their own end-point of pain relief using a
small microprocessor - controlled pump. Morphine is the most popular drug used.

75
Strong Opioids
Severe pain arising from deep or visceral structures requires the use of strong opioids
Morphine
• Short half-life and poor bioavailability.
• Metabolised in the liver and clearance is reduced in patients with liver disease, in the elderly and the debilitated
• Side effects include nausea, vomiting, constipation and respiratory depression.
• Tolerance may occur with repeated dosage
Pethidine
• Synthetic opioid which is structurally different from morphine but which has similar actions. Has 10% potency of
morphine.
• Short half-life and similar bioavailability and clearance to morphine.
• Short duration of action and may need to be given hourly.
• Pethidine has a toxic metabolite (norpethidine) which is cleared by the kidney, but which accumulates in renal
failure or following frequent and prolonged doses and may lead to muscle twitching and convulsions. Extreme
caution is advised if pethidine is used over a prolonged period or in patients with renal failure.
Weak opioids
Codeine: markedly less active than morphine, has predictable effects when given orally and is effective against mild to
moderate pain.
Non opioid analgesics

Mild to moderate pain.
Paracetamol
• Inhibits prostaglandin synthesis.
• Analgesic and antipyretic properties but little anti-inflammatory effect
• It is well absorbed orally and is metabolised almost entirely in the liver
• Side effects in normal dosage and is widely used for the treatment of minor pain. It causes hepatotoxicity in
over dosage by overloading the normal metabolic pathways with the formation of a toxic metabolite.
NSAIDs
• Analgesic and anti-inflammatory actions
• Inhibition of prostaglandin synthesis by the enzyme Cyclooxygenase which catalyses the conversion of
arachidonic acid to the various prostaglandins that are the chief mediators of inflammation. All NSAIDs work in
the same way and thus there is no point in giving more than one at a time.
• NSAIDs are, in general, more useful for superficial pain arising from the skin, buccal mucosa, joint surfaces and
bone.
• Relative contraindications: history of peptic ulceration, gastrointestinal bleeding or bleeding diathesis;
operations associated with high blood loss, asthma, moderate to severe renal impairment, dehydration and any
history of hypersensitivity to NSAIDs or aspirin.
Neuropathic Pain
Neuropathic pain may be defined as pain which arises following damage or disruption of the nervous system. It is often
difficult to treat and responds poorly to standard analgesia. Examples include:
• diabetic neuropathy
• post-herpetic neuralgia
• trigeminal neuralgia
• prolapsed intervertebral disc
NICE issued guidance in 2010 on the management of neuropathic pain:

• First-line treatment*: oral amitriptyline or pregabalin
• If satisfactory pain reduction is obtained with amitriptyline but the person cannot tolerate the adverse effects,
consider oral imipramine or nortriptyline as an alternative
• Second-line treatment: if first-line treatment was with amitriptyline, switch to or combine with pregabalin. If
first-line treatment was with pregabalin, switch to or combine with amitriptyline
• Other options: pain management clinic, tramadol (not other strong opioids), topical lidocaine for localised pain if
patients unable to take oral medication
*Please note that for some specific conditions the guidance may vary. For example, carbamazepine is used first-line for
trigeminal neuralgia, duloxetine for diabetic neuropathy

76
Nutrition Monitoring - NICE Guidelines
• Weight: daily if fluid balance concerns, otherwise weekly reducing to monthly
• BMI: at start of feeding and then monthly
• If weight cannot be obtained: monthly mid arm circumference or triceps skin fold thickness
• Daily electrolytes until levels stable. Then once or twice a week.
• Weekly glucose, phosphate, magnesium, LFTs, Ca, albumin, FBC, MCV levels if stable, 2-4 weekly Zn, Folate, B12 and
Cu levels if stable
• 3-6 monthly iron and ferritin levels, manganese (if on home parenteral regime)
• 6 monthly vitamin D
• Bone densitometry initially on starting home parenteral nutrition then every 2 years
Nutrition Screening - NICE Guidelines

NICE Screening for malnutrition: A summary
• To be performed by an appropriate professional.
• All new hospital admissions, new GP patients, new care home patients and patients attending their first clinic
should be screened. Afterwards hospital in patients should be screened weekly.
• The favored screening tool in the UK is the Malnutrition Universal Screening Tool (MUST).
Nutritional support i.e. oral, enteral or parenteral 𝑘𝑘𝑘𝑘

𝐵𝐵𝐵𝐵𝐵𝐵 =
• Given to patients identified as being malnourished (see box…) 𝑚𝑚2
• Considered in people identified as being AT RISK of malnutrition (see box…)
NB if considering feed withdrawal refer to GMC guidance 'withholding and withdrawing life prolonging treatment'.
Patients identified as being malnourished AT RISK of malnutrition

• BMI < 18.5 kg/m2 • Eaten nothing or little > 5 days, who are
• Unintentional weight loss of > 10% over 3-6/12 likely to eat little for a further 5 days
• BMI < 20 kg/m2 and unintentional weight loss of > • Poor absorptive capacity
5% over 3-6/12 • High nutrient losses
• High metabolism
Refeeding Syndrome
Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of
starvation. The metabolic consequences include:
• Hypophosphataemia
• Hypokalaemia
• Hypomagnesaemia
• Abnormal fluid balance
These abnormalities can lead to organ failure.
Re-feeding problems
If patient not eaten for > 5 days, aim to re-feed at < 50% energy and protein levels
High risk for re-feeding problems

If one or more of the following: If two or more of the following:
• BMI < 16 kg/m2 • BMI < 18.5 kg/m2
• Unintentional weight loss >15% over 3-6 months • Unintentional weight loss > 10% over 3-6 months
• Little nutritional intake > 10 days • Little nutritional intake > 5 days
• Hypokalaemia, Hypophosphataemia or • History of: alcohol abuse, drug therapy including
hypomagnesaemia prior to feeding (unless high) insulin, chemotherapy, diuretics and antacids

77
Nutrition Prescriptions
National institute of clinical excellence (NICE) guidelines
For people not severely ill and not at risk of refeeding syndrome aim to give
• 25-35 kcal/kg/day (lower if BMI > 25)
• 0.8-1.5g protein /kg/day
• 30-35 ml fluid/kg/day
• Adequate electrolytes, minerals, vitamins
• Severely ill patients aim to give < 50% of the energy and protein levels over the first 24-48h.
For people at high risk of refeeding syndrome:

• Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
• Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and
supplements
• Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)
Oral, Enteral and Parenteral Feeding - NICE Guidelines Summary

Oral nutrition
• Identify patients who are or at risk of being malnourished (see box…)
• Check for dysphagia
• If safe swallow, provide food and fluid in adequate quantity and quality
• Give a balanced diet
• Offer multivitamins and minerals
Surgical patients: If malnourished and safe swallow and post-op caesarean/gynecological/abdominal surgery, aim for oral
intake within 24h
Identify unsafe / inadequate oral intake OR a non-functional GI tract / perforation / inaccessible

Consider parenteral nutrition:
• For feeding < 14 days consider feeding via a peripheral venous catheter
• For feeding > 30 days use a tunneled subclavian line
• Continuous administration in severely unwell patients
• If feed needed > 2 weeks consider changing from continuous to cyclical feeding
• Don't give > 50% of daily regime to unwell patients in first 24-48 hours
Surgical patients: if malnourished with unsafe swallow OR a non-functional GI tract/perforation/inaccessible then
consider peri-operative parenteral feeding.
Total parenteral nutrition (TPN)

• Commonly used in nutritionally compromised surgical patients.
• Bags contain combinations of glucose, lipids and essential electrolytes, the exact composition is determined by the
patient’s nutritional requirements.
• Although it may be infused peripherally, this may result in thrombophlebitis.
• Longer term infusions should be administered into a central vein (preferably via a PICC line).
• Complications are related to sepsis, re-feeding syndromes and hepatic dysfunction.
Enteral Feeding
• Identify patients as malnourished or at risk (see box…)
• Identify unsafe or inadequate oral intake with functional GI tract
• Consider for enteral feeding
• Gastric feeding unless upper GI dysfunction (then for duodenal or jejunal tube)
• Check NG placement using aspiration and pH (check post pyloric tubes with AXR)
• Gastric feeding > 4 weeks consider long-term gastrostomy
• Consider bolus or continuous feeding into the stomach
• ITU patients should have continuous feeding for 16-24h (24h if on insulin)
• Consider motility agent in ITU or acute patients for delayed gastric emptying. If this doesn't work then try post
pyloric feeding or parenteral feeding.
• PEG can be used 4 hours after insertion, but should not be removed until >2 weeks after insertion.
Surgical patients due to have major abdominal surgery: if malnourished, unsafe swallow/inadequate oral intake and
functional GI tract then consider pre-operative enteral feeding.

78
Post-Operative Fluid Management
Composition of commonly used intravenous fluids mmol-1
Na K Cl Bicarbonate Lactate
Plasma 137-147 4-5.5 95-105 22-25 -
0.9% Saline 153 - 153 - -
Dextrose / saline 30.6 - 30.6 - -
Hartmans 130 4 110 - 28
Post-operative fluid management

In the UK the GIFTASUP and NICE (CG174 2013) guidelines (see reference below) were devised to try and provide some
consensus guidance as to how intravenous fluids should be administered. A decade ago it was a commonly held belief
that little harm would occur as a result of excessive administration of normal saline and many oliguric post operative
patients received enormous quantities of IV fluids. As a result they developed hyperchloraemic acidosis. With greater
understanding of this potential complication, the use of electrolyte balanced solutions (Ringers lactate/ Hartmans) is now
favored over normal saline.
The other guidance includes:
• Fluids given should be documented clearly and easily available
• Assess the patient's fluid status when they leave theatre
• If a patient is haemodynamically stable and euvolaemic, aim to restart oral fluid intake as soon as possible
• Review patients whose urinary sodium is < 20
• If a patient is oedematous, hypovolaemia if present should be treated first. This should then be followed by a
negative balance of sodium and water, monitored using urine Na excretion levels
• Solutions such as Dextran 70 should be used in caution in patients with sepsis as there is a risk of developing
acute renal injury
Postoperative Cognitive Dysfunction (POCD) Management

Definition
• Deterioration in performance in a battery of neuropsychological tests that would be expected in < 3.5% of
controls
Or
• Long term, possibly permanent disabling deterioration in cognitive function following surgery
Early POCD
• Increasing age
• GA rather than regional
• Duration of anaesthesia
• Reoperation
• Postoperative infection
Late POCD
• Increasing age
• Emboli
• Biochemical disturbances
Anaesthetic technique and Post-operative cognitive impairment:

• Use of benzodiazepines preoperatively reduces long-term POCD (9.9% vs. 5%)
• Do not stop drugs for cognitive function
• Regional techniques reduce POCD in first week, but no difference at 3 months

79
Pulmonary Embolism: Investigation
The British Thoracic Society (BTS) published guidelines in 2003 on the management of patients with suspected
pulmonary embolism (PE)
Key points from the guidelines include:

• computed tomographic pulmonary angiography (CTPA) is now the recommended initial lung-imaging modality
for non-massive PE. Advantages compared to V/Q scans include speed, easier to perform out-of-hours, a
reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded
• if the CTPA is negative then patients do not need further investigations or treatment for PE
• ventilation-perfusion scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and
there is no significant symptomatic concurrent cardiopulmonary disease
Some other points

Clinical probability scores based on risk factors and history and now widely used to help decide on further
investigation/management
D-dimers
• sensitivity = 95-98%, but poor specificity
V/Q scan
• sensitivity = 98%; specificity = 40% - high negative predictive value, i.e. if normal virtually excludes PE
• other causes of mismatch in V/Q include old pulmonary embolisms, AV malformations, vasculitis, previous
radiotherapy
• COPD gives matched defects
CTPA
• peripheral emboli affecting subsegmental arteries may be missed
Pulmonary angiography
• the gold standard
• significant complication rate compared to other investigations
Pulmonary Function Tests

Pulmonary function tests can be used to determine whether a respiratory disease is obstructive or restrictive. The table
below summarises the main findings and gives some example conditions:
Obstructive lung disease Restrictive lung disease

FEV1 - significantly reduced FEV1 - reduced
FVC - reduced or normal FVC - significantly reduced
FEV1% (FEV1/FVC) - reduced (less than approx. 70%) FEV1% (FEV1/FVC) - normal or increased (over approx. 70%)
Asthma Pulmonary fibrosis
COPD Asbestosis
Bronchiectasis Sarcoidosis
Bronchiolitis obliterans Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis
Neuromuscular disorders

80
Surgical Complications
Anatomical principles
Understanding the anatomy of a surgical field will allow appreciation of local and systemic complications that may occur.
For example, nerve injuries may occur following surgery in specific regions. The table below lists some of the more
important nerves to consider and mechanisms of injury
Nerve Mechanism
Accessory Posterior triangle lymph node biopsy
Sciatic Posterior approach to hip
Common peroneal Legs in Lloyd Davies position
Long thoracic Axillary node clearance
Pelvic autonomic nerves Pelvic cancer surgery
Recurrent laryngeal nerves During thyroid surgery
Hypoglossal nerve During carotid endarterectomy
Ulnar and median nerves During upper limb fracture repairs
These are just a few. The detailed functional sequelae are particularly important and will often be tested.
In addition to nerve injuries certain procedures carry risks of visceral or structural injury. Again some particular favorites
are given below:
Structure Mechanism
Thoracic duct During thoracic surgery e.g. Pneumonectomy, oesphagectomy
Parathyroid glands During difficult thyroid surgery
Ureters During colonic resections/ gynaecological surgery
Bowel perforation Use of Verres Needle to establish pneumoperitoneum
Bile duct injury Failure to delineate Calots triangle carefully and careless use of diathermy
Facial nerve Always at risk during Parotidectomy
Tail of pancreas When ligating splenic hilum
Testicular vessels During re-do open hernia surgery
Hepatic veins During liver mobilization
Again many could be predicted from the anatomy of the procedure.
Physiological derangements
A very common complication is bleeding and this is covered under the section of haemorrhagic shock. Another variant is
infection either superficial or deep seated. The organisms are covered under microbiology and the features of sepsis
covered under shock. Do not forget that immunocompromised and elderly patients may present will atypical
physiological parameters.
Selected physiological and biochemical issues are given below:
Complication Physiological/ Biochemical Problem
Arrhythmias following cardiac Susceptibility to hypokalaemia (K+ <4.0 in cardiac patients)
surgery
Neurosurgical electrolyte SIADH following cranial surgery causing hyponatraemia
disturbance
Ileus following Fluid sequestration and loss of electrolytes
gastrointestinal surgery
Pulmonary oedema following Loss of lung volume makes these patients very sensitive to fluid overload
pneumonectomy
Anastamotic leak Generalised sepsis causing mediastinitis or peritonitis depending on site of leak
Myocardial infarct May follow any type of surgery and in addition to direct cardiac effects the decreased
cardiac output may well compromise grafts etc.

81
Diagnostic modalities: Depends largely on the suspected complication. In the acutely unwell surgical patient the following
baseline investigations are often helpful:
• Full blood count, urea and electrolytes, C- reactive protein (trend rather than absolute value), serum calcium,
liver function tests, clotting (don't forget to repeat if on-going bleeding)
• Arterial blood gases
• ECG (+cardiac enzymes if MI suspected)
• Chest x-ray to identify collapse/ consolidation
• Urine analysis for UTI
These will often identify the most common complications.
Special tests
• CT scanning for identification of intra-abdominal abscesses
• Doppler USS of leg veins- for identification of DVT
• CTPA for PE
• Sending peritoneal fluid for U+E (if ureteric injury suspected) or amylase (if pancreatic injury suspected)
• Echocardiogram if pericardial effusion suspected post cardiac surgery and no pleural window made.
Management of complications
The guiding principal should be safe and timely intervention. Patients should be stabilised and if an operation needs to
occur in tandem with resuscitation then generally this should be of a damage limitation type procedure rather than
definitive surgery (which can be more safely undertaken in a stable patient the following day).
Remember that recent surgery is a contra indication to thrombolysis and that in some patients IV heparin may be
preferable to a low molecular weight heparin (easier to reverse).
As a general rule laparotomies for bleeding should follow the core principle of quadrant packing and then subsequent
pack removal rather than plunging large clamps into pools of blood. The latter approach invariable worsens the situation
is often accompanied by significant visceral injury particularly when done by the inexperienced. If packing controls a
situation it is entirely acceptable practice to leave packs in situ and return the patient to ITU for pack removal the
subsequent day.

82
Surgical Site Infection
• Surgical site infections may occur following a breach in tissue surfaces and allow normal commensals and other
pathogens to initiate infection. They are a major cause of morbidity and mortality.
• Surgical site infections (SSI) comprise up to 20% of all healthcare associated infections and at least 5% of patients
undergoing surgery will develop an SSI as a result.
• In many cases the organisms are derived from the patient's own body.
• Measures that may increase the risk of SSI include:
o Shaving the wound using a razor (disposable clipper preferred)
o Using a non-iodine impregnated incise drape if one is deemed to be necessary
o Tissue hypoxia
o Delayed administration of prophylactic antibiotics in tourniquet surgery
Preoperatively
• Don't remove body hair routinely
• If hair needs removal, use electrical clippers with single use head (razors increase infection risk)
• Antibiotic prophylaxis if:
o Placement of prosthesis or valve
o Clean-contaminated surgery
o Contaminated surgery
• Use local formulary
• Aim to give single dose IV antibiotic on anaesthesia
• If a tourniquet is to be used, give prophylactic antibiotics earlier
Intraoperatively
• Prepare the skin with alcoholic chlorhexidine (Lowest incidence of SSI)
• Cover surgical site with dressing
• A recent meta-analysis has confirmed that administration of supplementary oxygen does not reduce the risk of
wound infection. In contrast to previous individual RCTs
• Wound edge protectors do not appear to confer benefit
Post operatively
Tissue viability advice for management of surgical wounds healing by secondary intention
Use of diathermy for skin incisions

In the NICE guidelines the use of diathermy for skin incisions is not advocated(3). Several randomised controlled trials
have been undertaken and demonstrated no increase in risk of SSI when diathermy is used.

83
6. Surgical Techniques and Technology – MRCS Notes - Reda

Gases For Laparoscopic Surgery ..................................................................................................................... 2
Pneumoperitoneum - Therapeutic ................................................................................................................. 2
Sterilisation ..................................................................................................................................................... 2
Suture Material ............................................................................................................................................... 3
Suture Sizes ..................................................................................................................................................... 3
Methods of Wound Closure ........................................................................................................................... 4
Tissue Reconstruction ..................................................................................................................................... 5
Biological Agents............................................................................................................................................. 6
Electrosurgery ................................................................................................................................................. 6
Diathermy ....................................................................................................................................................... 7
Treatment of Suspicious Skin Lesions ............................................................................................................ 7
6. SURGICAL TECHNIQUE AND TECHNOLOGY – MRCS NOTES - REDA 1

84
Gases For Laparoscopic Surgery
Laparoscopic surgery may be performed in a number of body cavities. In some areas irrigation solutions are preferred. In
the abdomen insufflation with carbon dioxide gas is commonly used. The amount of gas delivered is adjusted to maintain
a constant intra-abdominal pressure of between 12 and 15 mmHg. Excessive intra-abdominal pressure may reduce
venous return and lead to hypotension. Too little insufflation will risk obscuring the surgical view.
Pneumoperitoneum - Therapeutic
During a laparoscopic procedure a surgeon will need to create a pneumoperitoneum. This can be achieved by use of a
Verress needle (risk of visceral injury). An alternative is the open "Hassan" style technique. Once access to the abdominal
cavity is secured carbon dioxide gas is insufflated to induce a working space. Higher intra-abdominal pressures may
compromise venous return and reduce cardiac output. If the blood pressure is seen to drop in this way then release of
air, will often improve matters. Should this not be the case then a laparotomy may be necessary to exclude a more
significant internal injury.
Sterilisation
Surgical equipment has to be cleaned and sterilised prior to use. The extent to which these processes will be required
varies according to the type of equipment and the purpose for which it will be used. In general, the three processes are
relevant; cleaning, disinfection and sterilisation.
• Cleaning refers to removal of physical debris.
• Disinfection refers to reduction in numbers of viable organisms.
• Sterilisation is removal of all organisms and spores.
Methods
Method Details Indication
Autoclaving Air removed and high pressure Most reusable surgical equipment, must be physically
steam used (usually 134oc for 3min) cleaned prior to autoclaving, unsuitable for fragile items
Glutaraldehyde Colourless oily liquid, directly Specifically used for endoscopes and some laparoscopic
solution (2%) cytocidal and virucidal even at low items, staff can rapidly develop allergy to this substance
temperatures which has limited its more widespread use
Ethylene oxide 3% mixture of gas with carbon Used for packaged materials that cannot be heated, the
dioxide used gas is explosive and environmentally toxic, it is used
mainly in the industrial setting
Gamma irradiation Gamma rays emitted from Suitable for batch treatment of relatively thermostable
radioactive substance such as cobalt items, typically an industrial process
60 or caesium 137

85
Suture Material
Agent Classification Durability Uses Special points
Silk Braided Theoretically Anchoring devices, skin Knots easily, poor
Biological permanent closure cosmesis
although strength
not preserved
Catgut Braided 5-7 days Short term wound Poor cosmesis
Biological approximation Degrades rapidly
Not available in UK
Chromic catgut Braided Up to 12 weeks Apposition of deeply sited Unpredictable
Biological tissues degradation pattern
Not in use in UK
Polydioxanone Synthetic Up to 3 months Widespread surgical Used in most surgical
(PDS) Monofilament (longer with thicker applications including visceral specialties (avoid dyed
sutures) anastomoses, dermal closure, form in dermal closure)
mass closure of abdominal
wall*
Polyglycolic acid Braided Up to 6 weeks Most tissues can be apposed It has good handling
(Vicryl, Dexon) Synthetic using polyglycolic acid properties, the dyed form
of this suture should not
be used for skin closure
Polypropylene Synthetic Permanent Widely used, agent of choice Poor handling properties
(Prolene) Monofilament for vascular anastomoses
Polyester Synthetic Permanent Its combination of It is more expensive and
(Ethibond) Braided permanency and braiding has considerable tissue
makes it useful for drag
laparoscopic surgery
*PDS or polydioxanone is the ideal suture material. Non absorbable sutures have higher incidence of incisional herniae.
NB: Stainless steel clips for skin following thyroidectomy.
NB: For closure of sternum following CABG, a stainless steel wire is typically used.
Absorbable vs Non absorbable

• Time taken to degrade absorbable materials varies
• Usually by macrophages hydrolysing material
• Consider absorbable sutures in situations where long term tissue apposition is not required. In cardiac and
vascular surgery non-absorbable sutures are usually used.
Suture size
• The higher the index number the smaller the suture i.e.: 6/0 Prolene is finer than 2/0 Prolene.
• Finer sutures have less tensile strength. For example, 6/0 Prolene would not be a suture suitable for abdominal
mass closure but would be ideal for small Prolene distal arterial anastomoses.
Braided vs monofilament
Generally speaking braided sutures have better handling characteristics than non-braided. However, they are associated
with higher bacterial counts. Braided materials are unsuitable for use in vascular surgery as they are potentially
thrombogenic.
Suture Sizes
USP Suture size and corresponding suture diameter
USP Size Diameter in mm
11-0 0.01
10-0 0.02
6-0 0.07
3-0 0.2
0 0.35
1 0.4

86
Methods of Wound Closure
Method of closure Indication
Primary closure • Clean wound, usually surgically created or following minor trauma
• Standard suturing methods will usually suffice
• Wound heals by primary intention
Delayed primary closure • Similar methods of actual closure to primary closure
• May be used in situations where primary closure is either not achievable or not
advisable e.g. infection
Vacuum assisted closure • Uses negative pressure therapy to facilitate wound closure
• Sponge is inserted into wound cavity and then negative pressure applied
• Advantages include removal of exudate and versatility
• Disadvantages include cost and risk of fistulation if used incorrectly on sites such as
bowel
Split thickness skin grafts • Superficial dermis removed with Watson knife or dermatome (commonly from thigh)
• Remaining epithelium regenerates from dermal appendages
• Coverage may be increased by meshing
Full thickness skin grafts • Whole dermal thickness is removed
• Sub dermal fat is then removed and graft placed over donor site
• Better cosmesis and flexibility at recipient site
• Donor site "cost"
Flaps • Viable tissue with a blood supply
• May be pedicled or free
• Pedicled flaps are more reliable, but limited in range
• Free flaps have greater range but carry greater risk of breakdown as they require
vascular anastomosis

87
Tissue Reconstruction
Skin Grafts and Flaps
Skin flaps or grafts may be required where primary wound closure cannot be achieved or would entail either significant
cosmetic defect or considerable functional disturbance as a result of wound contraction.
Reconstructive ladder
Method Types
Direct closure The simplest option where possible
Grafting techniques • Split thickness
• Full thickness
• Skin Substitute
• Composite
Flap technique Local:
• Transposition
• Pivot
• Alphabetplasty (e.g. Z-Y)
Regional:
• Myocutaneous
• Fasciocutaneous
• Neurocutaneous
Distant:
• Free tissue transfer
Prelamination techniques Allows creation of specialised flaps e.g. buccal mucosa
Tissue expansion Involves placement of tissue expanders to increase amount of tissue at donor sites
Skin Grafts Vs. Flaps

Skin Grafts Flaps
No size limit (Split)/ Relative size limit (full thickness) Size limited by territory of blood supply
Rely on wound bed for blood supply Tissue has its own blood supply
Take better on clean well vascularised wound beds Will survive independent of the wound bed
Split skin graft donor site typically heals in 12 days Direct closure of donor site or secondary skin graft
Donor site may be reused Donor site cannot be reused
Split thickness skin grafts

• Available in range of thicknesses.
• Thigh is the commonest donor site
• Size may be increased by meshing the graft. However, this comes with compromise on cosmesis.
• Donor sites, especially if thin grafts are taken can be reused following re-epithelialisation
Full thickness grafts

• Most commonly used for facial reconstruction
• Include dermal appendages
• Provide superior cosmetic result
Composite grafts
These are grafts containing more than one tissue type, such as skin and fat. They are usually used to cover small defects
in cosmetically important areas.
Flaps
• Flaps have their own blood supply and may be pedicled or free.
• May have multiple components e.g. skin, skin + fat, skin + fat + muscle.
• They will have the ability to take regardless of the underlying tissue bed.
• The type of intrinsic blood supply is important. For example in breast surgery pedicled latissimus dorsi flaps will
be less prone to failure than microsvascular anastomosed free Diep flaps.
Also check methods of wound closure in ‘Emergency Medicine’ chapter…

88
Biological Agents
Agents Target Uses
Adalimumab TNF alpha inhibitor Crohn’s disease
Infliximab Rheumatoid disease
Etanercept
Bevacizumab Anti VEGF (anti angiogenic) Colorectal cancer
Renal
Glioblastoma
Trastuzumab HER receptor Breast cancer
Imatinib Tyrosine kinase inhibitor Gastrointestinal stromal tumours (GIST)
Chronic myeloid leukaemia
Basiliximab IL2 binding site Renal transplants
Cetuximab Epidermal growth factor inhibitor EGF positive colorectal cancers
Detailed understanding of the actions of biological agents is well beyond the scope of the MRCS syllabus. However, many
of these drugs are being frequently encountered in surgical patients.
Electrosurgery
Electrosurgery utilises the heat generated by the passage of high frequency alternating electrical current through living
tissues. The application of a voltage across human tissue results in the formation of an electrical circuit between the
voltage source and the tissue. The tissue acts as a resistor and the level of resistance is determined by the water content
of the tissue. It is this resistance that results in the formation of heat.
An alternating current constantly changes the direction in which the current flows, the speed with which this occurs is
measured in Hertz. Most diathermy units operate at a frequency of between 200,000 kHZ to 5MHz. This means that
tissue such as nerves and muscles will not depolarise (since this seldom occurs at frequencies above 10,000Hz). The
current waveform can be adjusted to deliver three main therapeutic modalities; cutting, coagulation and blend.
Types of current
Cutting • Sinusoidal and non-modulated waveform
• High average power and current density
• Precise cutting without thermal damage
Coagulation • Modulated current with intermittent dampened sine waves of high peak voltage
• Evaporation, rather than vaporisation of intracellular fluid occurs
• Results in formation of coagulum
Desication • Active electrode in direct contact with tissue
• Low current and high voltage system
• Results in loss of cellular water but no protein damage
Fulguration • Electrode probe is held away from tissue
• Produces spray effect with local, superficial tissue destruction
• Low amplitude and high voltage system
Blend • Alternating cutting and coagulation modes
• Total average power is less than with cutting

89
Diathermy
• Diathermy devices are used by surgeons in all branches of surgery.
• Use electric currents to produce local heat and thereby facilitate haemostasis or surgical dissection.
• Consist of a generator unit that is located outside the patient and can be set to the level of power required by the
surgeon.
• There are two major types of diathermy machine;
Monopolar
The current flows through the diathermy unit into a handheld device that is controlled by the surgeon. Electricity can
flow from the tip of the device into the patient. The earth electrode is located some distance away. The relatively narrow
tip of the diathermy device produces local heat and this can be used to vaporise and fulgurate tissues. The current can be
adjusted in terms of frequency so that different actions can be effected. In cutting mode sufficient power is applied to
the tissues to vaporise their water content. In coagulation mode the power level is reduced so that a coagulum is formed
instead. Some diathermy machines can utilise a setting known as blend that alternates cutting and coagulation functions,
these tend to be used during procedures such as colonoscopic polypectomy.
Bipolar
The electric current flows from one electrode to another however, both electrodes are usually contained within the
same device e.g. a pair of forceps. The result is that heating is localised to the area between the two electrodes and
surrounding tissue damage is minimised.
Ultrasound based devices

These include CUSA and Harmonic scalpel. They generate high frequency oscillations that seal and coagulate tissues.
They have different energy settings that allow them to dissect and simultaneously seal vessels if required. The CUSA
device leaves vessels intact that may then be divided.
Ligasure device
Delivers tailored energy levels to allow simultaneous haemostasis and dissection. The device senses the impedance of
the tissues and tailors energy levels accordingly.
Hazards of diathermy
• Inadvertent patient burn. This may result of careless handling of the device or in the case of monopolar devices
forgetting to apply a return electrode plate. In this situation patients may develop a contact burn when
electricity flows to earth
• Explosion or fire. This may occur when volatile anaesthetic gases or skin preparation fluid have been used
Treatment of Suspicious Skin Lesions

Skin lesions may be referred to surgeons for treatment or discovered incidentally. The table below outlines the various
therapeutic options:
Method Indication
Tru-cut Most often used for percutaneous sampling of deep seated lesions or used intra operatively for
biopsy visceral lesions
5mm punch Used for diagnostic confirmation of lesions that are suspected to be benign or where the definitive
biopsy management is unlikely to be surgical. Of limited usefulness in pigmented lesions where they do not
include sufficient tissue for accurate diagnosis. May be used in non-melanoma type skin disease to
establish diagnosis prior to more extensive resection.
Wide Where the complete excision of the lesion (with healthy margins) is the main objective. In cosmetically
excision sensitive sites, or where the defect is large, this may need to be complemented with plastic surgical
techniques
Incisional Used mainly for deep seated or extensive lesions where there is diagnostic doubt (usually following
biopsy core or tru-cut biopsy). Used rarely for skin lesions.
Diagnostic Primarily used for lesions that are suspicious for melanoma, the lesion is excised with a rim of normal
excision tissue. Excision of margins may be required subsequently.
Also check ‘Tissue Sampling’ in Surgical Oncology chapter.

90

91
7. Legal Issues and Statistics – MRCS Notes - Reda

Audit and Research ......................................................................................................................................... 1
Audit Categories.............................................................................................................................................. 2
Consent ........................................................................................................................................................... 2
Cluster Randomised Controlled Trials ............................................................................................................ 3
Incidence and Prevalence ............................................................................................................................... 3
Forest Plots ..................................................................................................................................................... 3
Normal Distribution ........................................................................................................................................ 4
Pre and Post Test Odds and Probability......................................................................................................... 4
Qualitative and Quantitative Data ................................................................................................................. 5
Relative Risk .................................................................................................................................................... 5
Absolute Risk Reduction ................................................................................................................................. 5
Positive Predictive Values .............................................................................................................................. 6
Screening Test Statistics ................................................................................................................................. 6
Significance Tests ............................................................................................................................................ 7
Power Calculations and Statistical Error ........................................................................................................ 7
Statistics .......................................................................................................................................................... 8
Study Design.................................................................................................................................................... 9
Study Design: Evidence and Recommendations ............................................................................................ 9
7. LEGAL ISSUES IN SURGERY – MRCS NOTES - REDA 1

92
Audit and Research
Clinical audit
Quality improvement process that seeks to improve patient care and outcomes 6 pillars of clinical governance:
through systematic review of care against explicit criteria and the implementation • Clinical effectiveness
of change. Aspects of the structure, processes, and outcomes of care are selected • Research and development
and systematically evaluated against explicit criteria. Where indicated, changes are
• Openness
implemented at an individual, team, or service level and further monitoring is used
• Risk management
to confirm improvement in healthcare delivery. (NICE).
• Education and training
• Clinical audit
Research
Aims to derive new knowledge which is potentially generalisable or transferable.
Audit Categories
Audits may be used in a variety of clinical settings. These range from standards based audits, which will be familiar to
most clinicians, through to systems based audits which focus more on the processes within an organisation.
Types of audit
Financial audit A historically oriented, independent evaluation performed for the purpose of attesting to the
fairness, accuracy, and reliability of financial data
Operational A future-oriented, systematic, and independent evaluation of organizational activities. Financial
audit data may be used, but the primary sources of evidence are the operational policies and
achievements related to organizational objectives. Internal controls and efficiencies may be
evaluated during this type of review.
Departmental A current period analysis of administrative functions, to evaluate the adequacy of controls,
review safeguarding of assets, efficient use of resources, compliance with related laws, regulations and
institutional policy and integrity of financial information.
Standards based Comparison of care or passage of care against set and widely agreed standards or outcomes.
audit
Systems based Evaluation of processes occurring within an institution.
audit
Systems based audits are an integral part of the process of clinical governance.
Consent
There are 3 types of consent: (Informed, Expressed, Implied)
Consent forms used in UK NHS
Consent Form 1 For competent adults who are able to consent for themselves where consciousness may be
impaired (e.g. GA)
Consent Form 2 For an adult consenting on behalf of a child where consciousness is impaired
Consent Form 3 For an adult or child where consciousness is not impaired
Consent Form 4 For adults who lack capacity to provide informed consent
Capacity
Key points include:
1. Understand and retain information
2. Patient believes the information to be true
3. Patient is able to weigh the information to make a decision
All patients must be assumed to have capacity
Consent in minors
Young children and older children who are not Gillick competent cannot consent for themselves. In British law the
patients biological mother can always provide consent. The child's father can consent if the parents are married (and the
father is the biological father), or if the father is named on the birth certificate (irrespective of marital status). If parents
are not married and the father is not named on the birth certificate then the father cannot consent.

93
Cluster Randomised Controlled Trials
• Groups are randomised rather than individuals
• Avoids cross contamination amongst participants
• Participants in any one cluster are more likely to respond in a similar fashion
• Higher risk of unit of analysis error as these studies should be analysed as clusters rather than on an individual basis.
This leads to a higher false positive rate.
• It is possible to adjust for clustering in statistical analyses
Incidence and Prevalence

These two terms are used to describe the frequency of a condition in a population.
The incidence is the number of new cases per population in a given time period.
For example, if condition X has caused 40 new cases over the past 12 months per 1,000 of the population the annual
incidence is 0.04 or 4%.
The prevalence is the total number of cases per population at a particular point in time.
For example, imagine a questionnaire is sent to 2,500 adults asking them how much they weigh. If from this sample
population, 500 of the adults were obese then the prevalence of obesity would be 0.2 or 20%.
Relationship
• Prevalence = incidence * duration of condition
• In chronic diseases the prevalence is much greater than the incidence
• In acute diseases the prevalence and incidence are similar. For conditions such as the common cold the
incidence may be greater than the prevalence
Forest Plots
A Forest plot is a graphical display designed to illustrate the relative strength of treatment effects in multiple quantitative
scientific studies, addressing the same question. It is often used to graphically display meta analyses of RCTs.
The graph may be plotted on a natural logarithmic

scale when using odds ratios or other ratio-based
effect measures, so that the confidence intervals
are symmetrical about the means from each study
and to ensure undue emphasis is not given to odds
ratios greater than 1 when compared to those less
than 1. The area of each square is proportional to
the study's weight in the meta-analysis. The
overall meta-analysed measure of effect is often
represented on the plot as a vertical line. This
meta-analysed measure of effect is commonly
plotted as a diamond, the lateral points of which
indicate confidence intervals for this estimate.
A vertical line representing no effect is also Generic Forest plot

plotted. If the confidence intervals for individual studies overlap with this line, it demonstrates that at the given level of
confidence their effect sizes do not differ from no effect for the individual study. The same applies for the meta-analysed
measure of effect: if the points of the diamond overlap the line of no effect the overall meta-analysed result cannot be
said to differ from no effect at the given level of confidence.

94
Normal Distribution
The normal distribution is also known as the Gaussian distribution or 'bell-shaped' distribution. It describes the spread of
many biological and clinical measurements
Properties of the Normal distribution

• symmetrical i.e. Mean = mode = median
• 68.3% of values lie within 1 SD of the mean
• This is often reversed, so that within 1.96 SD of the mean
lie 95% of the sample values
• The range of the mean - (1.96 *SD) to the mean + (1.96 *
SD) is called the 95% confidence interval, i.e. If a repeat
sample of 100 observations are taken from the same
group 95 of them would be expected to lie in that range
Standard deviation
• the standard deviation (SD) represents the average difference each observation in a sample lies from the
sample mean
• SD = square root (variance)
Pre and Post Test Odds and Probability

Pre-test probability
The proportion of people with the target disorder in the population at risk at a specific time (point prevalence) or time
interval (period prevalence)
For example, the prevalence of rheumatoid arthritis in the UK is 1%
Post-test probability
The proportion of patients with that particular test result who have the target disorder
Post-test probability = post test odds / (1 + post-test odds)
Pre-test odds
The odds that the patient has the target disorder before the test is carried out
Pre-test odds = pre-test probability / (1 - pre-test probability)
Post-test odds
The odds that the patient has the target disorder after the test is carried out
Post-test odds = pre-test odds x likelihood ratio
where the likelihood ratio for a positive test result = sensitivity / (1 - specificity)

95
Qualitative and Quantitative Data
Qualitative and quantitative data
Qualitative (categorical) data refers to different descriptions of a characteristic, although it may be possible to allocate a
number it has no scale.
Quantitative data is associated with numerical values on a numerical scale.
Since quantitative data is based on a numerical scale it can be organised to create a distribution curve. The central
tendency may be estimated using the mode, median and mean. The standard deviation gives an estimation of the spread
of data.
Relative Risk
Relative risk (RR) is the ratio of risk in the experimental group (experimental event rate, EER) to risk in the control group
(control event rate, CER)
𝐸𝐸𝐸𝐸𝐸𝐸
To recap 𝑅𝑅𝑅𝑅 =
𝐶𝐶𝐶𝐶𝐶𝐶
• EER = rate at which events occur in the experimental group
• CER = rate at which events occur in the control group
For example, if we look at a trial comparing the use of paracetamol for back pain compared to placebo we may get the
following results
Total number of patients Experienced significant pain relief

Paracetamol 100 60
Placebo 80 20
Experimental event rate, EER = 60 / 100 = 0.6

Control event rate, CER = 20 / 80 = 0.25
𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴𝐴 𝑅𝑅𝑅𝑅𝑅𝑅𝑅𝑅 𝐶𝐶ℎ𝑎𝑎𝑎𝑎𝑎𝑎𝑎𝑎 = 𝐸𝐸𝐸𝐸𝐸𝐸 − 𝐶𝐶𝐶𝐶𝐶𝐶
Therefore the relative risk = EER / CER = 0.6 / 0.25 = 2.4
If the risk ratio is > 1 then the rate of an event (in this case experiencing significant pain relief) is increased compared to
controls. It is therefore appropriate to calculate the relative risk increase if necessary (see below).
If the risk ratio is < 1 then the rate of an event is decreased compared to controls. The relative risk reduction should
therefore be calculated (see below).
Relative risk reduction (RRR) or relative risk increase (RRI)

𝐸𝐸𝐸𝐸𝐸𝐸 − 𝐶𝐶𝐶𝐶𝐶𝐶
Is calculated by dividing the absolute risk change by the control event rate 𝑅𝑅𝑅𝑅𝑅𝑅 =
𝐶𝐶𝐶𝐶𝐶𝐶
Using the above data, RRI = (EER - CER) / CER = (0.6 - 0.25) / 0.25 = 1.4 = 140%
Absolute Risk Reduction

The absolute risk reduction is the decrease in risk of a given activity or treatment in relation to a control activity or
treatment. It is the inverse of the number needed to treat.
The absolute risk reduction is usually calculated for two different treatments. For example, consider surgical resection (X)
versus watchful waiting (Y) for prostate cancer. A defined end point, such as 5-year survival is required. If the
probabilities pX and pY of this end point are known, then the absolute risk reduction is calculated (pX-pY).
The inverse / reciprocal of absolute risk reduction is the Number Needed to Treat. This is useful in determining the cost Vs
benefit of many treatments.
Number needed to treat

Definition: how many patients would need to receive a treatment to prevent one event. It is the absolute difference
between two treatments.

96
Positive Predictive Values
The positive predictive value (PPV) is the probability that an individual with a positive screening result has the disease. The
sensitivity is the probability that an individual with the disease is screened positive and the specificity is the probability
that an individual without the disease is screened negative.
Screening tests
• Sensitivity: proportion of true positives identified by a test
• Specificity: proportion of true negatives correctly identified by a test
• Positive predictive value: proportion of those who have a positive test who actually have the disease
• Negative predictive value: proportion of those who test negative who do not have the disease
Predictive values are dependent on the prevalence

• Likelihood ratio for a positive test result = sensitivity/(1-specificity)
• Likelihood ratio for a negative test result = (1-sensitivity)/specificity
Likelihood ratios are not prevalence dependent
Screening Test Statistics

It would be unusual for a medical exam not to feature a question based around screening test statistics. The available
data should be used to construct a contingency table as below:
TP = true positive; FP = false positive; TN = true negative; FN = false negative
Disease present Disease absent

Test positive TP FP
Test negative FN TN
The table below lists the main statistical terms used in relation to screening tests:
Sensitivity TP / (TP + FN ) Proportion of patients with the condition who have a positive
test result
Specificity TN / (TN + FP) Proportion of patients without the condition who have a
negative test result
Positive predictive value TP / (TP + FP) The chance that the patient has the condition if the diagnostic
test is positive
Negative predictive value TN / (TN + FN) The chance that the patient does not have the condition if the
diagnostic test is negative
Likelihood ratio for a positive sensitivity / (1 - How much the odds of the disease increase when a test is
test result specificity) positive
Likelihood ratio for a negative (1 - sensitivity) / How much the odds of the disease decrease when a test is
test result specificity negative
Positive and negative predictive values are prevalence dependent. Likelihood ratios are not prevalence dependent

97
Significance Tests
A null hypothesis (H 0 ) states that two treatments are equally effective (and is hence negatively phrased). A significance
test uses the sample data to assess how likely the null hypothesis is to be correct.
For example:
• 'there is no difference in the prevalence of colorectal cancer in patients taking low-dose aspirin compared to
those who are not'
The alternative hypothesis (H 1 ) is the opposite of the null hypothesis, i.e. There is a difference between the two
treatments
The p value is the probability of obtaining a result by chance at least as extreme as the one that was actually observed,
assuming that the null hypothesis is true. It is therefore equal to the chance of making a type I error (see below).
Two types of errors may occur when testing the null hypothesis
• Type I: The null hypothesis is rejected when it is true - i.e. Showing a difference between two groups when it
doesn't exist, a false positive. This is determined against a preset significance level (termed alpha). As the
significance level is determined in advance the chance of making a type I error is not affected by sample size. It
is however increased if the number of end-points are increased. For example, if a study has 20 end-points it is
likely one of these will be reached, just by chance.
• Type II: The null hypothesis is accepted when it is false - i.e. Failing to spot a difference when one really exists, a
false negative. The probability of making a type II error is termed beta. It is determined by both sample size and
alpha.
Study accepts H 0 Study rejects H 0

Reality H 0 Type 1 error (alpha)
Reality H 1 Type 2 error (beta) Power (1 - beta)
The power of a study is the probability of (correctly) rejecting the null hypothesis when it is false
• power = 1 - the probability of a type II error
• power can be increased by increasing the sample size
Power Calculations and Statistical Error

Statistical error
Type 1 Error • Test rejects true null hypothesis
• Rate of type 1 error is the given the value of α
• It usually equals the significance level of a test
Type 2 Error • Test fails to reject a false null hypothesis
• Rate of type 2 errors is given the value of β
• It is related to the power of the test
Statistical power
The power of a test is the probability that the test will reject the null hypothesis when it is false (thereby avoiding a type
2 error). Increasing the power of a test will reduce the probability of a type 2 error. Usually a value of 0.8 is selected.
Type I Error (alpha) Type II Error (beta)

98
Statistics
Statistics is a topic that generally strikes fear and dread into most surgeons’ hearts. The MRCS is not an examination
designed to test mathematical skill but the examiners do expect you to have working knowledge of commonly used tests
so that you can appraise the literature properly.
Data types
Before selecting a method of statistical analysis it is imperative that the type of data to be analysed is correctly
categorised. Commonly used terms include nominal, ordinal, interval and continuous.
Term Interpretation
Nominal Data can be allocated a numerical code that is arbitrary. For example allocating people as alive or dead
using codes of 0 or 1
Ordinal data Data using numbers that can be used on a scale. Severity of pain is often measured in this way
Interval Data is measured numerically. However, the zero point is arbitrary
scale
Continuous Data is measured numerically where the numerical value is a real number and may be any value.
Examples include height and weight
Analysing data
Having ascribed the data it is then possible to begin the process of analysis. Nominal data is often tabulated into
categories because of the nature of the underlying data sets. Continuous data may be displayed graphically often as
individual data points. When the sample size is large enough, continuous data can be analysed to determine the
distribution of the data points. Often, but not always these will be in the form of a gaussian distribution. Determining
whether data is normally distributed or not is key to making sense of the subsequent statistical tests. Parametric tests are
used to test normally distributed data, the T Test is one of the best examples. Data which is not normally distributed
cannot be analysed in this way and a non-parametric test must be used. Examples of such tests include Chi Squared and
Mann Whitney U tests. Chi squared tests often appear in the medical literature. There are some assumptions that are
made in relation to Chi squared tests; these include the need to use 2 degrees of freedom (usually) and the minimum
sample size. Where the sample size is small then a different test is appropriate and the Fishers exact test is often used.
In situations where data is normally distributed and paired samples are taken from the same individuals (such as
following an intervention) then the paired T Test may be used.
Multiple testing and post hoc analysis

In the ideal world statistical analysis is conducted on data that is collected prospectively according to pre set power
calculations and defined end points. Occasionally, data does not produce an expected outcome or a certain type of
patient appears to have a different result. Subsequent analysis of such groups is termed a post hoc analysis. This can be
perfectly legitimate, alternatively it can represent the last ditch attempt of a researcher to try and find any aspect of the
data that is worthwhile. This can lead to errors and false rejection of a null hypothesis. A statistically significant result is
more likely to occur if the same dataset is subjected to multiple analyses. To counteract this problem some researchers
will apply a Bonferroni correction, this adjusts the analysis to allow for multiple testing.

99
Study Design
The following table highlights the main features of the main types of study:
Randomised Participants randomly allocated to intervention or control group (e.g. standard treatment or
controlled trial placebo)
Practical or ethical problems may limit use

Cohort study Observational and prospective. Two (or more) are selected according to their exposure to a
particular agent (e.g. medicine, toxin) and followed up to see how many develop a disease or
other outcome.
The usual outcome measure is the relative risk.
Examples include Framingham Heart Study

Case-control study Observational and retrospective. Patients with a particular condition (cases) are identified and
matched with controls. Data is then collected on past exposure to a possible causal agent for the
condition.
The usual outcome measure is the odds ratio.
Inexpensive, produce quick results

Useful for studying rare conditions
Prone to confounding
Cross-sectional Provide a 'snapshot', sometimes called prevalence studies
survey
Provide weak evidence of cause and effect
Study Design: Evidence and Recommendations

Levels of evidence
• I - Evidence from meta-analysis of randomised controlled trials
• II - Evidence derived from at least one properly designed randomised controlled trial
• III - Evidence from correlation and comparative studies or use of historical controls
• IV - Evidence from case series or case reports
• V - Expert opinion or founded on basic principles
Knowledge of the sub groups of the levels of evidence are not routinely tested in MRCS Part A.
Grading of recommendation
• Grade A - based on evidence from
at least one RCT (i.e. Ia or Ib)
• Grade B - based on evidence from
non-RCTs (i.e. IIa, IIb or III)
• Grade C - based on evidence
from a panel of experts (i.e. IV)

100

101
8. Clinical Microbiology – MRCS Notes - Reda

Surgical Microbiology ..................................................................................................................................... 2
Antibiotics: Mechanism of Action .................................................................................................................. 3
MRSA ............................................................................................................................................................... 3
Streptococci .................................................................................................................................................... 4
Acute Tonsillitis ............................................................................................................................................... 4
Salmonella....................................................................................................................................................... 4
Bacterial Gastroenteritis................................................................................................................................. 5
Gastro Intestinal Parasitic Infections ............................................................................................................. 6
Hepatitis B ....................................................................................................................................................... 7
Hepatitis C ....................................................................................................................................................... 8
HIV Testing ...................................................................................................................................................... 8
Meleney's Gangrene and Necrotising Fasciitis .............................................................................................. 9
Osteomyelitis ................................................................................................................................................ 10
Oncoviruses ................................................................................................................................................... 10
8. CLINICAL MICROBIOLOGY– MRCS NOTES - REDA 1

102
Surgical Microbiology
An extensive topic so an overview is given here. Organisms causing common surgical infections are reasonable topics in
the examination. However, microbiology is less rigorously tested than anatomy, for example.
Staphylococcus aureus Staphylococcus epidermidis

• Facultative anaerobe Tends to colonise plastic devices and forms a biofilm
which allows colonisation with other bacterial agents. It
• Gram positive coccus
is notoriously difficult to eradicate once established and
• Haemolysis on blood agar plates
the usual treatment is removal of the device.
• Catalase positive
• 20% population are long term carriers
• Exo and enterotoxin may result in toxic shock syndrome and gastroenteritis respectively (enterotoxin is pre-
formed → rapid onset of symptoms.)
• Ideally treated with penicillin although many strains now resistant through beta Lactamase production. In the
UK less than 5% of isolates are sensitive to penicillin.
• Resistance to methicillin (and other antibiotics) is mediated by the mec operon, essentially penicillin binding
protein is altered and resistance to this class of antibiotics ensues
• Common cause of cutaneous infections, abscesses, surgical site infections. Common cause of lactational mastitis
• Most common cause of septic arthritis.
Streptococcus pyogenes
• Gram positive, forms chain like colonies, Lancefield Group A Streptococcus
• Produces beta haemolysis on blood agar plates
• Rarely part of normal skin microflora
• Catalase negative
• Releases a number of proteins/ virulence factors into host including hyaluronidase, streptokinase which allow
rapid tissue destruction
• Releases superantigens such as pyogenic exotoxin A which results in scarlet fever
• Remains sensitive to penicillin, macrolides may be used as an alternative.
Escherichia coli Streptococcus viridans

(see later… ‘Bacterial Gastroenteritis’) • Affects heart valves
Campylobacter jejuni Streptococcus bovis

(see later… ‘Bacterial Gastroenteritis’) • Septicaemia is associated with
carcinoma of the colon.
Helicobacter pylori • Can also cause endocarditis.
• Gram negative, helix shaped rod, microaerophilic
• Produces hydrogenase that can derive energy from hydrogen released by intestinal bacteria
• Flagellated and mobile
• Those carrying the cag A gene may cause ulcers
• It secretes urease that breaks down gastric urea → CO 2 & NH 3 → Ammonium → Bicarbonate (simplified!).
The bicarbonate can neutralise the gastric acid.
• Usually colonises the gastric antrum and irritates resulting in increased gastrin release and higher levels of
gastric acid. These patients will develop duodenal ulcers. In those with more diffuse H-Pylori infection gastric
acid levels are lower and ulcers develop by local tissue damage from H-Pylori- these patients get gastric ulcers.
• Diagnosis may be made by serology (approx. 75% sensitive). Biopsy urease test during endoscopy probably the
most sensitive.
• In patients who are colonised 10-20% risk of peptic ulcer, 1-2% risk gastric cancer, <1% risk MALT lymphoma.
Actinomycosis spp
• Gram positive bacilli.
• Facultative anaerobes.
• May be difficult to culture. Direct visualisation of organisms and sulphur granules from lesions themselves is the
easiest way to make a diagnosis.
• It remains a differential of conditions such as hydradenitis suppurativa, particularly if it is occurring in odd
locations and with deeper abscesses than usual.

103
Antibiotics: Mechanism of Action
Inhibit cell wall formation
• Penicillins
• Cephalosporins
Inhibit protein synthesis

• Aminoglycosides
(cause misreading
of mrna)
• Chloramphenicol
• Macrolides
(e.g. Erythromycin)
• Tetracyclines
• Fusidic acid
Inhibit DNA synthesis

• Quinolones
(e.g. Ciprofloxacin)
• Metronidazole
• Sulphonamides
• Trimethoprim
Inhibit RNA synthesis

• Rifampicin
MRSA
Methicillin-resistant Staphylococcus aureus (MRSA) was one of the first organisms which highlighted the dangers of
hospital-acquired infections.
Who should be screened for MRSA?

• All patients awaiting elective admissions (exceptions include day patients having terminations of pregnancy and
ophthalmic surgery. Patients admitted to mental health trusts are also excluded)
• In the UK all emergency admissions are currently screened
How should a patient be screened for MRSA?

• Nasal swab and skin lesions or wounds
• The swab should be wiped around the inside rim of a patient's nose for 5 seconds
• The microbiology form must be labelled 'MRSA screen'
Suppression of MRSA from a carrier once identified

• Nose: mupirocin 2% in white soft paraffin, TDS for 5 days
• Skin: chlorhexidine gluconate, od for 5 days. Apply all over but particularly to the axilla, groin and perineum
The following antibiotics are commonly used in the treatment of MRSA infections:
• Vancomycin
• Teicoplanin
Some strains may be sensitive to the antibiotics listed below but they should not generally be used alone because
resistance may develop:
• Rifampicin
• Macrolides
• Tetracyclines
• Aminoglycosides
• Clindamycin
Relatively new antibiotics such as linezolid, quinupristin/dalfopristin combinations and tigecycline have activity against
MRSA but should be reserved for resistant cases

104
Streptococci
Streptococci may be divided into alpha and beta haemolytic types
Alpha haemolytic streptococci

The most important alpha haemolytic streptococcus is Streptococcus
pneumoniae (pneumococcus). Pneumococcus is a common cause of
pneumonia, meningitis and otitis media. Another clinical example is
Streptococcus viridans
Beta haemolytic streptococci

These can be subdivided into group A and B
Group A
• most important organism is Streptococcus pyogenes
• responsible for erysipelas, impetigo, cellulitis, type 2
necrotizing fasciitis and pharyngitis/tonsillitis
• immunological reactions can cause rheumatic fever or post-
streptococcal glomerulonephritis
• erythrogenic toxins cause scarlet fever
Group B
• Streptococcus agalactiae may lead to neonatal meningitis
and septicaemia Acute streptococcal tonsillitis
Acute Tonsillitis
• Characterised by pharyngitis, fever, malaise and lymphadenopathy.
• Over half of all cases are bacterial with Streptococcus pyogenes the most common organism
• The tonsils are typically oedematous and yellow or white pustules may be present
• Infectious mononucleosis may mimic the condition.
• Treatment with penicillin type antibiotics is indicated for bacterial tonsillitis.
• Bacterial tonsillitis may result in local abscess formation (quinsy)
Salmonella
The Salmonella group contains many members, most of which cause diarrhoeal diseases. They are facultative anaerobes,
Gram negative rods which are not normally present as commensals in the gut.
Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are
often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia
Features
• Initially systemic upset as above
• Relative bradycardia
• Abdominal pain, distension
• Constipation: although salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
• Rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
Possible complications include

• Osteomyelitis (especially in sickle cell disease where salmonella is one of the most common pathogens)
• GI bleed/perforation
• Meningitis
• Cholecystitis
• Chronic carriage (1%, more likely if adult females)

105
Bacterial Gastroenteritis
Causative organisms Features
Shigella spp. • Members of the enterobacteriaceae
• Gram negative bacilli
• Clinically causes dysentery
• Shigella soneii is the commonest infective organism (mild illness)
• Usually self-limiting, ciprofloxacin may be required if individual is in a high risk group
Salmonella spp. • Facultatively anaerobic, gram negative, enterobacteriaceae
• Infective dose varies according to subtype
• Salmonellosis: usually transmitted by infected meat (especially poultry) and eggs
Yersinia • Gram negative, coccobacilli
enterocolitica • Typically produces a protracted terminal ileitis that may mimic Crohn’s disease
• Δ Δ acute appendicitis
• May progress to septicaemia in susceptible individuals
• Usually sensitive to quinolone or tetracyclines
Vibrio cholera • Short, gram negative rods
• Transmitted by contaminated water, seafood
• Symptoms include sudden onset of effortless vomiting and profuse watery diarrhoea
• Correction of fluid and electrolyte losses are the mainstay of treatment
• Most cases will resolve, antibiotics are not generally indicated
E. coli • Gram negative rod
• Facultative anaerobe, non sporing
• Wide range of subtypes and some are normal gut commensals
o Enteropathogenic (EPEC): childhood diarrhea
o Enteroinvasive (EIEC): dysentery, large bowel necrosis/ulcers
o Enterotoxigenic (ETEC): small intestine, traveler’s diarrhoea
o Enterohaemorrhagic (EHEC): subtype 0157, cause haemolytic uraemic $,
haemorrhagic colitis, and thrombotic thrombocytopaenic purpura
• They are resistant to many antibiotics used to treat gram positive infections and acquire
resistance rapidly and are recognised as producing beta lactamases
• Most common organism implicated in cholangitis infections.
• Implicated in Fournier’s gangrene along with bacteroides
Campylobacter jejuni • Spiral / curved, gram negative rods, non sporulating bacteria
• Most common cause of acute infective diarrhoea
• Produces enteritis which is often diffuse and blood may be passed
• Usually infects caecum and terminal ileum. Local lymphadenopathy is common
• May mimic appendicitis as it has marked RIF pain (differential for RIF pain with diarrhoea)
• Reactive arthritis is seen in 1-2% of cases
• Self-limiting infection so antibiotics are not usually advised. However, the quinolones are
often rapidly effective.

106
Gastro Intestinal Parasitic Infections
Common infections
Enterobiasis • Due to organism Enterobius vermicularis
• Common cause of pruritus ani
• Diagnosis usually made by placing scotch tape at the anus, this will trap eggs that can then
be viewed microscopically
• Treatment is with mebendazole
Ancylostoma • Hookworms that anchor in proximal small bowel
duodenale • Most infections are asymptomatic although may cause iron deficiency anaemia
• Larvae may be found in stools left at ambient temperature, otherwise infection is difficult to
diagnose
• Infection occurs as a result of cutaneous penetration, migrates to lungs, coughed up and
then swallowed
Ascariasis • Due to infection with roundworm Ascaris lumbricoides
• Infections begin in gut following ingestion, then penetrate duodenal wall to migrate to lungs,
coughed up and swallowed, cycle begins again
• Diagnosis is made by identification of worm or eggs within faeces
Strongyloidiasis • Due to infection with Strongyloides stercoralis
• Rare in west
• Organism is a nematode living in duodenum of host
• Initial infection is via skin penetration. They then migrate to lungs and are coughed up and
swallowed. Then mature in small bowel are excreted and cycle begins again
• An auto infective cycle is also recognised where larvae will penetrate colonic wall
• Individuals may be asymptomatic, although they may also have respiratory disease and skin
lesions
• Diagnosis is usually made by stool microscopy
• In the UK mebendazole is used for treatment
Cryptosporidium • Protozoal infection
• Organisms produce cysts which are excreted and thereby cause new infections
• Symptoms consist of diarrhoea and cramping abdominal pains. Symptoms are worse in
immunosuppressed people
• Cysts may be identified in stools
• Treatment is with metronidazole
Giardiasis • Diarrhoeal infection caused by Giardia lamblia (protozoan)
• Infections occur as a result of ingestion of cysts
• Symptoms are usually gastrointestinal with abdominal pain, bloating and passage of soft or
loose stools
• Diagnosis is by serology or stool microscopy
• First line treatment is with metronidazole

107
Hepatitis B
Hepatitis B is a double-stranded DNA virus and is spread through exposure to infected blood or body fluids, including
vertical transmission from mother to child. The incubation period is 6-20 weeks.
Immunisation against hepatitis B

• Contains HBsAg absorbed onto aluminium hydroxide adjuvant and is prepared from yeast cells using
recombinant DNA technology
• Most schedules give 3 doses of the vaccine with a recommendation for a one-off booster 5 years following the
initial primary vaccination
• At risk groups who should be vaccinated include: healthcare workers, intravenous drug users, sex workers, close
family contacts of an individual with hepatitis B, individuals receiving blood transfusions regularly, chronic
kidney disease patients who may soon require renal replacement therapy, prisoners, chronic liver disease
patients
• Around 10-15% of adults fail to respond or respond poorly to 3 doses of the vaccine. Risk factors include age
over 40 years, obesity, smoking, alcohol excess and immunosuppression
• Testing for anti-HBs is only recommended for those at risk of occupational exposure (i.e. Healthcare workers)
and patients with chronic kidney disease. In these patients anti-HBs levels should be checked 1-4 months after
primary immunisation
• The table below shows how to interpret anti-HBs levels:
Anti-HBs level (mIU/ml) Response

> 100 Indicates adequate response, no further testing required. Should still receive booster at 5
years
10 - 100 Suboptimal response - one additional vaccine dose should be given. If immunocompetent
no further testing is required
< 10 Non-responder. Test for current or past infection. Give further vaccine course (i.e. 3 doses
again) with testing following. If still fails to respond then HBIG would be required for
protection if exposed to the virus
Complications of hepatitis B infection

• Chronic hepatitis (5-10%)
• Fulminant liver failure (1%)
• Hepatocellular carcinoma
• Glomerulonephritis
• Polyarteritis nodosa
• Cryoglobulinaemia
Management of hepatitis B
• Pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of
chronic carriers. A better response is predicted by being female, < 50 years old, low HBV DNA levels, non-Asian,
HIV negative, high degree of inflammation on liver biopsy
• However, due to the side-effects of pegylated interferon it is now used less commonly in clinical practice. Oral
antiviral medication is increasingly used with an aim to suppress viral replication (not in dissimilar way to
treating HIV patients)
• Examples include lamivudine, tenofovir and entecavir

108
Hepatitis C
Hepatitis C is likely to become a significant public health problem in the UK in the next decade. It is thought around
200,000 people are chronically infected with the virus. At risk groups include intravenous drug users and patients who
received a blood transfusion prior to 1991 (e.g. haemophiliacs).
Transmission
• The risk of transmission during a needle stick injury is about 2%
• The vertical transmission rate from mother to child is about 6%
• Breast feeding is not contraindicated in mothers with hepatitis C
• The risk of transmitting the virus during sexual intercourse is probably less than 5%
Features
• After exposure to the hepatitis C virus less than 20% of patients develop an acute hepatitis
Complications
• Chronic infection (80-85%) - only 15-20% of patients will clear the virus after an acute infection and hence the
majority will develop chronic hepatitis C
• Cirrhosis (20-30% of those with chronic disease)
• Hepatocellular cancer
• Cryoglobulinaemia
Management of chronic infection

• Currently a combination of pegylated interferon-alpha and ribavirin are used
• Up to 55% of patients successfully clear the virus, with success rates of around 80% for some strains
Complications of treatment
• Ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6 months of
stopping ribavirin as it is teratogenic
• Interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia
HIV Testing
HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever type illness.
Increased symptomatic severity is associated with poorer long term prognosis. It typically occurs 3-12 weeks after
infection
Features
• Sore throat
• Lymphadenopathy
• Malaise, myalgia, arthralgia
• Diarrhoea
• Maculopapular rash
• Mouth ulcers
• Rarely meningoencephalitis
Diagnosis
• Antibodies to HIV may not be present
• HIV PCR and p24 antigen tests can confirm diagnosis
HIV antibody test

• Most common and accurate test
• Usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory
Western Blot Assay
• Most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
p24 antigen test

• Usually positive from about 1 week to 3 - 4 weeks after infection with HIV
• Sometimes used as an additional screening test in blood banks

109
Meleney's Gangrene and Necrotising Fasciitis
Necrotising fasciitis
• Advancing soft tissue infection associated with fascial necrosis
• Uncommon, but can be fatal
• In many cases there is underlying background immunosuppression e.g. Diabetes
• Caused by polymicrobial flora (aerobic and anaerobic) and MRSA is seen increasingly in cases of necrotising
fasciitis
• Streptococcus is the commonest organism in isolated pathogen infection (15%)
Meleney’s gangrene
• Meleney’s is a similar principle but the infection is more superficially sited than necrotising fasciitis and often
confined to the trunk
Fournier’s gangrene
• Necrotising fasciitis affecting the perineum
• Polymicrobial with E-coli and Bacteroides acting in synergy
``
Clinical features
• Fever
• Pain
• Cellulitis
• Oedema
• Induration
• Numbness
Muscles are relatively spared
Late findings
• Purple/black skin discolouration
• Blistering
• Haemorrhagic bullae
• Crepitus (maybe present in 35%)
• Dirty Dishwater fluid discharge
• Septic shock
Diagnosis is mainly clinical
Management
• Radical surgical debridement forms the cornerstone of management
• Sterile dressing is used to dress the wound
• Reconstructive surgery is considered once the infection is completely treated (further surgery after 24-48h).

110
Osteomyelitis
Infection of the bone
Causes
• S aureus and occasionally Enterobacter or Streptococcusspecies
• In sickle cell: Salmonella species
Clinical features
• Erythema
• Pain
• Fever
Investigation
The Lautenbach procedure involves
• X-ray: lytic centre with a ring of sclerosis debridement, intramedullary reaming and
• Bone biopsy and culture the insertion of double-lumen tubes to
establish both a local antibiotic delivery
Treatment system and cavity analysis for volume and
• Prolonged antibiotics culture.
• Sequestra may need surgical removal
Oncoviruses
• Viruses which cause cancer
• These may be detected on blood test and prevented by vaccine
These are the main types of oncoviruses and their diseases:

Oncovirus Cancer
Epstein-Barr virus Burkitt's lymphoma
Hodgkin's lymphoma
Post transplant lymphoma
Nasopharyngeal carcinoma
Human papillomavirus 16/18 Cervical cancer
Anal cancer
Penile cancer
Vulval cancer
Oropharyneal cancer
Human herpes virus 8 Kaposi's sarcoma
Hepatitis B virus Hepatocellular carcinoma
Hepatitis C virus Hepatocellular carcinoma
Human T-lymphotropic virus 1 Tropical spastic paraparesis
Adult T cell leukaemia

111
9. Emergency Medicine and Trauma – MRCS Notes - Reda

Addisonian Crisis ............................................................................................................................................. 2
Anaphylactic Shock ......................................................................................................................................... 2
Compartment Syndrome ................................................................................................................................ 2
Fluid Resuscitation Burns ............................................................................................................................... 3
Hypothermia ................................................................................................................................................... 4
Local Anaesthetic Toxicity .............................................................................................................................. 4
Chest Pain in Pregnancy ................................................................................................................................. 5
Imaging in the Pregnant Trauma Patient ....................................................................................................... 5
Management of Acute Coronary Syndrome .................................................................................................. 6
Thrombolysis or Percutaneous Intervention in Myocardial Infarction ........................................................ 6
Ventricular Tachycardia .................................................................................................................................. 7
Ventricular Tachycardia: Management.......................................................................................................... 7
Torsades De Pointes ....................................................................................................................................... 8
Pulmonary Embolism: ECG Changes .............................................................................................................. 8
Pulmonary Embolism: Management.............................................................................................................. 8
Management of Hyperkalaemia..................................................................................................................... 9
Thoracic Trauma ........................................................................................................................................... 10
Tension Pneumothorax ................................................................................................................................ 11
Thoracic Aorta Rupture ................................................................................................................................ 12
Vascular Trauma ........................................................................................................................................... 12
Stroke: Types................................................................................................................................................. 13
Head Injury Management - NICE Guidelines ............................................................................................... 14
Head Injury - Paediatrics............................................................................................................................... 15
Craniomaxillofacial Injuries .......................................................................................................................... 16
Oculogyric Crisis ............................................................................................................................................ 18
Opioid Misuse ............................................................................................................................................... 18
Sickle Cell Anaemia ....................................................................................................................................... 19
9. EMERGENCY MEDICINE AND MANAGEMENT OF TRAUMA – MRCS NOTES - REDA 1

112
Addisonian Crisis
Causes
• Sepsis or surgery causing an acute exacerbation of chronic insufficiency (Addison's, Hypopituitarism)
• Adrenal haemorrhage e.g. Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
• Steroid withdrawal
Management
• Hydrocortisone 100mg IM or IV
• 1 litre normal saline infused over 30-60 min or with dextrose if hypoglycaemic
• Continue hydrocortisone 6 hourly until the patient is stable. No fludrocortisone is required because high cortisol
exerts weak mineralocorticoid action
• Oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
Anaphylactic Shock
Suspect if there has been exposure to an allergen
Management
• Remove allergen
• ABCD
• Drugs:
o Adrenaline 1:1000 0.5ml INTRAMUSCULARLY (not IV). Repeat after 5 min if no response.
o Then Chlorpheniramine 10mg IV
o Then Hydrocortisone 100-200mg IV
Compartment Syndrome
• This is a particular complication that may occur following fractures (or following ischaemia re-perfusion injury in
vascular patients). It is characterised by raised pressure within a closed anatomical space.
• The raised pressure within the compartment will eventually compromise tissue perfusion resulting in necrosis. The
two main fractures carrying this complication include supracondylar fractures and tibial shaft injuries.
Symptoms and signs

• Pain, especially on movement (even passive)
• Parasthesiae
• Pallor may be present
• Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
• Paralysis of the muscle group may occur
Diagnosis
• Is made by measurement of intracompartmental pressure measurements. Pressures in excess of 20mmHg are
abnormal and >40mmHg is diagnostic.
Treatment
• This is essentially prompt and extensive fasciotomies
• In the lower limb the deep muscles may be inadequately decompressed by the inexperienced operator when
smaller incisions are performed
• Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients
require aggressive IV fluids
• Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to
be considered
• Death of muscle groups may occur within 4-6 hours

113
Fluid Resuscitation Burns
Indication: >15% total body area burns in adults (>10% children)
• The main aim of resuscitation is to prevent the burn deepening
• Most fluid is lost 24 hours after injury
• First 8-12 hours, fluid shifts are from intravascular to interstitial fluid compartments
• Therefore, circulatory volume can be compromised. However fluid resuscitation causes more fluid into the
interstitial compartment especially colloid (therefore avoided in first 8-24 hours)
• Protein loss occurs
Fluid resuscitation formula

Parkland formula
(Crystalloid only e.g. Hartman's solution / Ringers' lactate)
Total fluid requirement in 24 hours =

4ml x total burn surface area (%) x body weight (kg)
• 50% given in first 8 hours
• 50% given in next 16 hours
Resuscitation endpoint: Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this)
Points to note:
• Starting point of resuscitation is time of injury
• Deduct fluids already given
After 24 hours
• Maintenance crystalloid (usually dextrose-saline) is continued at a rate of 1.5 ml x (burn area) x (body weight)
• Colloids are rarely used (e.g. albumin)
• Antioxidants, such as vitamin C, can be used to minimize oxidant-mediated contributions to the inflammatory
cascade in burns
• High tension electrical injuries and inhalation injuries require more fluid
• Monitor: packed cell volume, plasma sodium, base excess, and lactate

114
Hypothermia
Core body temperature below 35oC. Severe hypothermia is present when the core temperature is below 30oC.
Hypothermia is associated with a reduction in both respiratory and cardiac activity.
Management
An organised cardiac rhythm may be converted to fibrillation if CPR is attempted inappropriately so ECG should be
analysed with care. The rewarming technique used depends upon the degree of hypothermia and the physiological state
of the patient. Mild hypothermia may respond to external rewarming devices. Severe hypothermia may require active
core rewarming techniques such as peritoneal lavage, haemodialysis or cardiac bypass. Patients who develop cardiac
arrhythmias who are severely hypothermic may respond to bretylium tosylate (sadly no longer available in most centres),
but do not generally respond to standard therapies or DC cardioversion.
Local Anaesthetic Toxicity

Toxicity results from either accidental intravascular injection (rapid onset of symptoms-usually correct dose), or from
excessive dosage (slower onset). Local anaesthetic agents not only exert a membrane stabilising effect on peripheral
nerves but will also act on excitable membranes within the CNS and Heart. The sensory neurones in the CNS are
suppressed before the motor ones. As a result, the early symptoms will typically be those of circumoral paraesthesia and
tinnitus, followed by falling GCS and eventually coma.
Management of toxicity
• Stop injecting the anaesthetic agent
• High flow 100% oxygen via face mask
• Cardiovascular monitoring
• Administer lipid emulsion (Intralipid 20%) at 1.5ml/Kg over 1 minute as a bolus
• Consider lipid emulsion infusion, at 0.25ml/ Kg/ minute
• If toxicity due to prilocaine then administer methylene blue
Safe doses
10ml of lignocaine 1% contains 100mg of drug, this would constitute 70% of the maximum safe dose in a 50 kg patient.
Up to 7mg / kg can be administered if adrenaline is added to the solution.
Doses of local anaesthetics

Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivicane 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-morbidities.

115
Chest Pain in Pregnancy
Aortic dissection
• Predisposing factors in pregnancy are hypertension, congenital heart disease and Marfan's syndrome
• Mainly Stanford type A dissection
• Sudden tearing chest pain, transient syncope
• Patient may be cold and clammy, hypertensive and have an aortic regurgitation murmur
• Involvement of the right coronary artery may cause inferior myocardial infarction
Surgical management
Gestational timeframe Management
< 28/40 Aortic repair with the fetus kept in utero
28-32/40 Dependent on fetal condition
> 32/40 Primary Cesarean section followed by aortic repair at the same operation
Mitral stenosis
• Most cases associated with rheumatic heart disease
• Becoming less common in British women; suspect in Immigrant women
• Commonest cardiac condition in pregnancy
• Commonly associated with mortality
• Valve surgery; balloon valvuloplasty preferable
Pulmonary embolism
• Leading cause of mortality in pregnancy
• Half dose scintigraphy; CT chest if underlying lung disease, should aid diagnosis
• Treatment with low molecular weight heparin throughout pregnancy and 4-6 weeks after childbirth
• Warfarin is contra indicated in pregnancy (though may be continued in women with mechanical heart valves
due to the significant risk of thromboembolism)
Imaging in the Pregnant Trauma Patient

Sonography and FAST scanning are established in pregnancy and have the advantage of avoiding ionising radiation.
However, the sensitivity of the FAST scan is reduced in pregnancy especially with advanced gestational age. Sensitivity of
FAST scanning is 60-80% across all trimesters and 90% in the first. CT scanning remains the first line investigation in
major trauma where significant visceral injury is suspected. The maximum permitted safe dose of radiation in pregnancy
is 5mSv. A pelvic CT scan would fall below this level. That said, early exposure to radiation will increase the risk of
developmental anomalies and foetal loss. Late exposure increases the risk of childhood cancer twofold. CT scanning
remains the most sensitive test for identifying complications such as placental abruption in this group.

116
Management of Acute Coronary Syndrome
NICE produced guidelines in 2010 on the management of unstable angina and non-ST elevation myocardial infarction
(NSTEMI). They advocate managing patients based on the early risk assessment using a recognised scoring system such
as GRACE (Global Registry of Acute Cardiac Events) to calculate a predicted 6 month mortality.
All patients should receive

• Aspirin 300mg
• Nitrates or morphine to relieve chest pain if required
Whilst it is common that non-hypoxic patients receive oxygen therapy there is little evidence to support this approach.
The 2008 British Thoracic Society oxygen therapy guidelines advise not giving oxygen unless the patient is hypoxic.
Antithrombin treatment. Low molecular weight heparin should be offered to patients who are not at a high risk of
bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a
patients creatinine is > 265 umol/l unfractionated heparin should be given.
Clopidogrel 300mg should be given to patients with a predicted 6 month mortality of more than 1.5% or patients who
may undergo percutaneous coronary intervention within 24 hours of admission to hospital. Clopidogrel should be
continued for 12 months.
Intravenous glycoprotein IIb/IIIa receptor antagonists(eptifibatide or tirofiban) should be given to patients who have an
intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are
scheduled to undergo angiography within 96 hours of hospital admission.
Coronary angiography should be considered within 96 hours of first admission

to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as
possible in patients who are clinically unstable.
Thrombolysis or Percutaneous Intervention in Myocardial Infarction

Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. They
in primarily used in patients who present with a ST elevation myocardial infarction. Other indications include acute
ischaemic stroke and pulmonary embolism, although strict inclusion criteria apply.
Examples Indications for thrombolysis or PCI: (Any of the following ECG changes):
• Alteplase • ST elevation of > 2mm (2 small squares) in 2 or more
• Tenecteplase consecutive anterior leads (V1-V6)
• Streptokinase • ST elevation of > 1mm (1 small square) in greater than 2
consecutive inferior leads (II, III, avF, avL)
Contraindications to thrombolysis • New Left Bundle Branch Block
• Active internal bleeding
• Recent haemorrhage, trauma or surgery (including dental extraction)
• Coagulation and bleeding disorders
• Intracranial neoplasm
• Stroke < 3 months
• Aortic dissection
• Recent head injury
• Pregnancy
• Severe hypertension
Side-effects
• Haemorrhage
• Hypotension - more common with streptokinase
• Allergic reactions may occur with streptokinase

117
Ventricular Tachycardia
Ventricular tachycardia (VT)is broad-complex tachycardia originating from a ventricular ectopic focus. It has the potential
to precipitate ventricular fibrillation and hence requires urgent treatment.
There are two main types of VT:

• monomorphic VT: most commonly caused by myocardial infarction
• polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the
QT interval. The causes of a long QT interval are listed below
Causes of a prolonged QT interval

Congenital Drugs Other
• Jervell-Lange-Nielsen syndrome • Amiodarone, sotalol, class 1a • Electrolyte: hypocalcaemia,
(includes deafness and is due to antiarrhythmic drugs hypokalaemia, hypomagnesaemia
an abnormal potassium channel) • Tricyclic antidepressants, • Acute myocardial infarction
• Romano-Ward syndrome (no fluoxetine • Myocarditis
deafness) • Chloroquine • Hypothermia
• Terfenadine • Subarachnoid haemorrhage
• Erythromycin
Ventricular Tachycardia: Management

Whilst a broad complex tachycardia may result from a supraventricular rhythm with aberrant conduction, the European
Resuscitation Council advise that in a peri-arrest situation it is assumed to be ventricular in origin
If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure or rate > 150 beats/min) then immediate
cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical
cardioversion may be needed with synchronised DC shocks
Drug therapy
• Amiodarone: ideally administered through a central line
• Lidocaine: use with caution in severe left ventricular impairment
• Procainamide
Verapamil should NOT be used in VT
If drug therapy fails

• Electrophysiological study (EPS)
• Implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired
LV function

118
Torsades De Pointes
Torsades de pointes ('twisting of the points') is a rare arrhythmia associated with a long QT interval. It may deteriorate
into ventricular fibrillation and hence lead to sudden death
Causes of long QT interval

• Congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome
• Antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
• Tricyclic antidepressants
• Antipsychotics
• Chloroquine
• Terfenadine
• Erythromycin
• Electrolyte: hypocalcaemia, hypokalaemia,
hypomagnesaemia
• Myocarditis
• Hypothermia
• Subarachnoid haemorrhage
Management
• IV magnesium sulphate
Pulmonary Embolism: ECG Changes

• No changes
• S1, Q3, T3
• Tall R waves: V1
• P pulmonale (peaked P waves): inferior leads
• Right axis deviation, Right bundle branch block
• Atrial arrhythmias
• T wave inversion: V1, V2, V3
• Right ventricular strain: if identified is associated
with adverse short-term outcome and adds
prognostic value to echocardiographic evidence of
right ventricular dysfunction in patients with acute
pulmonary embolism and normal blood pressure.
Pulmonary Embolism: Management

A summary of the British Thoracic Society guidelines
• Heparin should be given if intermediate or high clinical probability before imaging.
• Unfractionated heparin (UFH) should be considered (a) as a first dose bolus, (b) in massive PE, or (c) where rapid
reversal of effect may be needed.
• Otherwise, low molecular weight heparin (LMWH) should be considered as preferable to UFH, having equal
efficacy and safety and being easier to use.
• Oral anticoagulation should only be commenced once VTE has been reliably confirmed.
• The target INR should be 2.0-3.0; when this is achieved, heparin can be discontinued.
• The standard duration of oral anticoagulation is: 4 to 6 weeks for temporary risk factors, 3 months for first
idiopathic, and at least 6 months for other; the risk of bleeding should be balanced with that of further VTE.
Massive PE
• CTPA or echocardiography will reliably diagnose clinically massive PE.
• Thrombolysis is 1st line for massive PE (ie circulatory failure) and may be instituted on clinical grounds alone if
cardiac arrest is imminent; a 50 mg bolus of alteplase is recommended.
• Invasive approaches (thrombus fragmentation and IVC filter insertion) should be considered where facilities and
expertise are readily available.

119
Management of Hyperkalaemia
Untreated hyperkalaemia may cause life-threatening arrhythmias. Precipitating factors should be addressed (e.g. acute
renal failure) and aggravating drugs stopped (e.g. ACE inhibitors). Management may be categorised by the aims of
treatment
Stabilisation of the cardiac membrane

• Intravenous calcium gluconate
Short-term shift in potassium from extracellular to intracellular fluid compartment

• Combined insulin/dextrose infusion
• Nebulised salbutamol
Removal of potassium from the body

• Calcium resonium (orally or enema)
• Loop diuretics
• Dialysis

120
Thoracic Trauma
Types of thoracic trauma
Tension • Often laceration to lung parenchyma with flap
pneumothorax • Pressure develops in thorax
• Most common cause is mechanical ventilation in patient with pleural injury
• Symptoms overlap with cardiac tamponade, hyper-resonant percussion note is more likely in
tension pnemothorax
Flail chest • Chest wall disconnects from thoracic cage
• Multiple rib fractures (at least two fractures per rib in at least two ribs)
• Associated with pulmonary contusion
• Abnormal chest motion
• Avoid over hydration and fluid overload
Pneumothorax • Most common cause is lung laceration with air leakage
• Most traumatic pneumothoraces should have a chest drain
• Patients with traumatic pneumothorax should never be mechanically ventilated until a chest
drain is inserted
Haemothorax • Most commonly due to laceration of lung, intercostal vessel or internal mammary artery
• Haemothoraces large enough to appear on CXR are treated with large bore chest drain
• Surgical exploration is warranted if >1500ml blood drained immediately
Cardiac • Beck's triad: elevated venous pressure, reduced arterial pressure, reduced heart sounds
tamponade • Pulsus paradoxus
• May occur with as little as 100ml blood
Pulmonary • Most common potentially lethal chest injury
contusion • Arterial blood gases and pulse oximetry important
• Early intubation within an hour if significant hypoxia
Blunt cardiac • Usually occurs secondary to chest wall injury
injury • ECG may show features of myocardial infarction
• Sequelae: hypotension, arrhythmias, cardiac wall motion abnormalities
Aorta disruption • Deceleration injuries
• Contained haematoma
• Widened mediastinum
Diaphragm • Most due to motor vehicle accidents and blunt trauma causing large radial tears (laceration
disruption injuries result in small tears)
• More common on left side
• Insert gastric tube, may pass into intrathoracic stomach
Mediastinal • Entrance wound in one hemithorax and exit wound/foreign body in opposite hemithorax
traversing • Mediastinal haematoma or pleural cap suggests great vessel injury
wounds • Mortality is 20%

121
Tension Pneumothorax
Tension pneumothorax is a state of positive pressure
within a pneumothorax throughout the respiratory
cycle. A breach in the pleura allows air into the intra
pleural space via a one way valve. The initial pressure
pneumothorax expands until positive pressure is
present throughout the respiratory cycle. The risk is
greatest in the ventilated trauma patient as positive
pressure is used. Undiagnosed tension pneumothorax
accounts for 3.8% of trauma deaths.
Clinically, the classic features include chest pain,

dyspnoea, hypoxia, hypotension, tracheal deviation,
ipsilateral hyperpercussion note, decreased air entry.
In ventilated patients, cardiovascular disturbance and
sub cutaneous emphysema are relatively common and
more so than in a case where the patient is breathing
spontaneously.
Chest x-ray features

• Lung collapse towards the hilum
• Diaphragmatic depression Increased rib
separation
• Increased thoracic volume Image showing mediastinal shift with a tension pneumothorax
• Ipsilateral flattening of the heart border
• Contra lateral mediastinal deviation
Management
Immediate needle decompression followed by definitive wide bore chest drain insertion

122
Thoracic Aorta Rupture
• Mechanism of injury: Decelerating force i.e. RTA, fall from a great height
• Most people die at scene
• Survivors may have an incomplete laceration at the ligamentum arteriosum of the aorta.
Clinical features
• Contained haematoma: persistent hypotension
• Detected mainly by history, CXR changes
CXR changes
• Widened mediastinum
• Trachea/Oesophagus to right
• Depression of left main stem bronchus
• Widened paratracheal stripe/paraspinal interfaces
• Space between aorta and pulmonary artery obliterated
• Rib fracture/left haemothorax
Diagnosis
Angiography, usually CT aortogram.
Treatment
Repair or replacement. Ideally they should undergo endovascular repair.
Vascular Trauma
Assessment
• Check for signs of distal perfusion
• Doppler signal distally (monophasic/ biphasic or triphasic)
• Anatomical location (which vessel is likely to be involved)
• Duplex scanning and angiography are "gold standard" tests but may not be immediately available in the trauma
setting
Management
• Almost always operative.
• Obtaining proximal and distal control of affected vessels is crucial.
• Simple lacerations of arteries may be directly closed, or a vein patch applied if there is a risk of subsequent
stenosis.
• Transection of the vessel should be treated by either end to end anastomosis (often not possible) or an
interposition vein graft.
• Use of PTFE in traumatic open injuries will invariably result in infection.

123
Stroke: Types
Primary intracerebral • Presents with headache, vomiting, loss of consciousness
haemorrhage (PICH, c. 10%)
Total anterior circulation • Involves middle and anterior cerebral arteries
infarcts (TACI, c. 15%) • Hemiparesis/hemisensory loss
• Homonymous hemianopia
• Higher cognitive dysfunction e.g. Dysphasia
Partial anterior circulation • Involves smaller arteries of anterior circulation e.g. upper or lower division of
infarcts (PACI, c. 25%) middle cerebral artery
• Higher cognitive dysfunction or two of the three TACI features
Lacunar infarcts (LACI, c. 25%) • Involves perforating arteries around the internal capsule, thalamus and basal
ganglia
• Present with either isolated hemiparesis, hemisensory loss or hemiparesis with
limb ataxia
Posterior circulation infarcts • Vertebrobasilar arteries
(POCI, c. 25%) • Presents with features of brainstem damage
• Ataxia, disorders of gaze and vision, cranial nerve lesions
Lateral medullary syndrome • Wallenberg's syndrome
(posterior inferior cerebellar • Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy
artery) • Contralateral: limb sensory loss
Weber's syndrome • Ipsilateral III palsy
• Contralateral weakness
Anterior cerebral artery (branch of ICA)

• Contralateral hemiparesis and sensory loss, lower extremity > upper
• Disconnection syndrome
Middle cerebral artery (branch of ICA)

• Contralateral hemiparesis and sensory loss, upper extremity > lower
• Contralateral hemianopia
• Aphasia (Wernicke's) Indications for hemicranieotomy include:
• Gaze abnormalities • Age under 60 years
• Clinical deficit in middle cerebral artery territory
Posterior cerebral artery (terminal branch of Basilar artery) • Decreased consciousness
• Contralateral hemianopia with macular sparing • > 50% territory infarct
• Disconnection syndrome
Lacunar
• Present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
Lateral medulla (posterior inferior cerebellar artery)

• Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g.
Horner's If patient is within 3h of symptom onset of a stroke.

• Contralateral: limb sensory loss Therefore, he should be urgently referred to the
medical team for thrombolysis, BEFORE Aspirin is
Pontine given. There are concerns that high dose aspirin
• VI nerve: horizontal gaze palsy would increase the risk of intracerebral
• VII nerve
haemorrhage if thrombolysis is undertaken.
• Contralateral hemiparesis

124
Head Injury Management - NICE Guidelines
Summary of guidelines
• All patients should be assessed within 15 minutes on arrival to A&E
• Document all 3 components of the GCS
• If GCS <8 or = to 8, consider stabilising the airway
• Treat pain with low dose IV opiates (if safe)
• Full spine immobilisation until assessment if:
o GCS < 15
o neck pain/tenderness
o paraesthesia extremities
o focal neurological deficit
o suspected c-spine injury
If a c-spine injury is suspected a 3 view c-spine x-ray is indicated. CT c-spine is preferred if:
• Intubated
• GCS <13
• Normal x-ray but continued concerns regarding c-spine injury
• Any focal neurology
• A CT head scan is being performed
• Initial plain films are abnormal
Immediate CT head (within 1 hour) if:

• GCS < 13 on admission
• GCS < 15 2 hours after admission
• Suspected open or depressed skull fracture
• Suspected skull base fracture (panda eyes, Battle's sign, CSF from nose/ear, bleeding ear)
• Focal neurology
• Vomiting > 1 episode
• Post traumatic seizure
• Coagulopathy
Contact neurosurgeon if:

• Persistent GCS < 8 or = 8
• Unexplained confusion > 4h
• Reduced GCS after admission
• Progressive neurological signs
• Incomplete recovery post seizure
• Penetrating injury
• Cerebrospinal fluid leak
Observations
• 1/2 hourly GCS until 15

125
Head Injury - Paediatrics
Criteria for immediate request for CT scan of the head (children)
• Loss of consciousness lasting more than 5 minutes (witnessed)
• Amnesia (antegrade or retrograde) lasting more than 5 minutes
• Abnormal drowsiness
• Three or more discrete episodes of vomiting
• Clinical suspicion of non-accidental injury
• Post-traumatic seizure but no history of epilepsy
• GCS less than 14, or for a baby under 1 year GCS (paediatric) less than 15, on assessment in the emergency
department
• Suspicion of open or depressed skull injury or tense fontanelle
• Any sign of basal skull fracture (haemotympanum, panda' eyes, cerebrospinal fluid leakage from the ear or nose,
Battle's sign)
• Focal neurological deficit
• If under 1 year, presence of bruise, swelling or laceration of more than 5 cm on the head
• Dangerous mechanism of injury (high-speed road traffic accident either as pedestrian, cyclist or vehicle
occupant, fall from a height of greater than 3 m, high-speed injury from a projectile or an object)

126
Craniomaxillofacial Injuries
In the UK are due to: Interpersonal violence (52%), Motor vehicle accidents (16%), Sporting injuries (19%), Falls (11%)
Le Fort Fractures
Grade Feature
Le Fort 1 The fracture extends from the nasal septum to the lateral pyriform rims, travels horizontally above the teeth
apices, crosses below the zygomaticomaxillary junction, and traverses the pterygomaxillary junction to interrupt
the pterygoid plates.
Le Fort 2 These fractures have a pyramidal shape and extend from the nasal bridge at or below the nasofrontal suture
through the frontal process of the maxilla, inferolaterally through the lacrimal bones and inferior orbital floor and
rim through or near the inferior orbital foramen, and inferiorly through the anterior wall of the maxillary sinus; it
then travels under the zygoma, across the pterygomaxillary fissure, and through the pterygoid plates.
Le Fort 3 These fractures start at the nasofrontal and frontomaxillary sutures and extend posteriorly along the medial wall
of the orbit through the nasolacrimal groove and ethmoid bones. The thicker sphenoid bone posteriorly usually
prevents continuation of the fracture into the optic canal. Instead, the fracture continues along the floor of the
orbit along the inferior orbital fissure and continues superolaterally through the lateral orbital wall, through the
zygomaticofrontal junction and the zygomatic arch. Intranasally, a branch of the fracture extends through the
base of the perpendicular plate of the ethmoid, through the vomer, and through the interface of the pterygoid
plates to the base of the sphenoid. This type of fracture predisposes the patient to CSF rhinorrhea more
commonly than the other types.

127
Ocular injuries
Superior orbital fissure syndrome
Severe force to the lateral wall of the orbit resulting in compression of neurovascular structures. Results in:
• Complete opthalmoplegia and ptosis (Cranial nerves 3, 4, 6 and nerve to levator palpebrae superioris)
• Relative afferent pupillary defect
• Dilatation of the pupil and loss of accommodation and corneal reflexes
• Altered sensation from forehead to vertex (frontal branch of trigeminal nerve)
Orbital apex syndrome

This is an extension of superior orbital fissure syndrome and includes compression of the optic
nerve passing through the optic foramen. It is indicated by features of superior orbital fissure
syndrome and ipsilateral afferent pupillary defect.
Orbital blow out fracture

Typically occurs when an object of slightly larger diameter than the orbital rim strikes the incompressible eyeball. The bone
fragment is displaced downwards into the antral cavity, remaining attached to the orbital periosteum. Periorbital fat may
be herniated through the defect, interfering with the inferior rectus and inferior oblique muscles which are contained
within the same fascial sheath. This prevents upward movement and outward rotation of the eye and the patient
experiences diplopia on upward gaze. The initial bruising and swelling may make assessment difficult and patients should
usually be reviewed 5 days later. Residual defects may require orbital floor reconstruction.
Nasal Fractures
• Common injury
• Ensure new and not old deformity
• Control epistaxis
• CSF rhinorrhoea implies that the cribriform plate has been breached and antibiotics will be required.
• Usually best to allow bruising and swelling to settle and then review patient clinically. Major persistent deformity
requires fracture manipulation, best performed within 10 days of injury.
Retrobulbar haemorrhage
Rare but important ocular emergency.
Presents with:
• Pain (usually sharp and within
the globe)
• Proptosis
• Pupil reactions are lost
• Paralysis (eye movements lost)
• Visual acuity is lost (colour vision
is lost first)
May be the result of Le Fort type facial
fractures.
Management:
• Mannitol 1g/Kg as 20% infusion, Osmotic diuretic, Contra-indicated in congestive heart failure and pulmonary oedema
• Acetazolamide 500mg IV, (Monitor FBC/U+E) Reduces aqueous pressure by inhibition of carbonic anhydrase (used in
glaucoma)
• Dexamethasone 8mg orally or intravenously
• In a traumatic setting an urgent cantholysis may be needed prior to definitive surgery.

128
Oculogyric Crisis
An oculogyric crisis is a dystonic reaction to certain drugs or medical conditions
Features
• Restlessness, agitation
• Involuntary upward deviation of the eyes
Causes
• Phenothiazines
• Haloperidol
• Metoclopramide
• Postencephalitic Parkinson's disease
Management
• Procyclidine
Opioid Misuse
Opioids are substances which bind to opioid receptors. This includes both naturally occurring opiates such as morphine
and synthetic opioids such as buprenorphine and methadone.
Features of opioid misuse

• Rhinorrhoea
• Needle track marks
• Pinpoint pupils
• Drowsiness
Complications of intravenous opioid misuse

• Viral infection secondary to sharing needles: HIV, hepatitis B & C
• Bacterial infection secondary to injection: infective endocarditis, septic arthritis, septicaemia, necrotising
fasciitis, groin abscess
• Pseudoaneurysm
• Venous thromboembolism
• Osteomyelitis
• Overdose may lead to respiratory depression and death
Emergency management of opioid overdose

• IV or IM naloxone: has a rapid onset and relatively short duration of action

129
Sickle Cell Anaemia
• Autosomal recessive
• Single base mutation
• Deoxygenated cells become sickle in shape
• Causes: short red cell survival, obstruction of microvessels and infarction
• Sickling is precipitated by: dehydration, infection, hypoxia
• Manifest at 6 months of age A combination of a high reticulocyte count and severe
• Africans, Middle East, Indian anaemia indicates sickle cell anaemia, however another
• Diagnosis: Hb electrophoresis differential can be of a transient aplastic crisis due to
parvovirus. This is less likely as this causes a
Sickle crises reticulocytopenia rather than a reticulocytosis.
• Bone pain
• Pleuritic chest pain: acute sickle chest syndrome commonest cause of death
• CVA, seizures
• Papillary necrosis
• Splenic infarcts
• Priapism
• Hepatic pain
Hb does not fall during a crisis, unless there is Parvovirus B19 infects erythroid progenitor cells in the
• Aplasia: Parvovirus bone marrow and causes temporary cessation of red
• Acute sequestration blood cell production, patients who have underlying
• Haemolysis hematologic abnormalities are at risk of cessation of
red blood cell production if they become infected. This
Long-term complications can result in a transient aplastic crisis. Thus, patients
with sickle cell anaemia are at risk. Typically, these
• Infections: Streptococcus pnemoniae
patients have a viral prodrome followed by anaemia,
• Chronic leg ulcers often with haemoglobin concentrations falling below
• Gallstones: haemolysis 5.0 g/dL and reticulocytosis.
• Aseptic necrosis of bone
• Chronic renal disease
• Retinal detachment, proliferative retinopathy
Surgical complications
• Bowel ischaemia
• Cholecystitis
• Avascular necrosis
Management
• Supportive
• Hydroxyurea
• Repeated transfusions pre operatively
• Exchange transfusion in emergencies
Sickle cell trait

• Heterozygous state
• Asymptomatic
• Symptoms associated with extreme situations ie anaesthesia complications
• Protective against Plasmodium falciparum

130

131
10. Surgical Oncology – MRCS Notes - Reda

Extravasation Injury ........................................................................................................................................ 2
Chemotherapy Agents .................................................................................................................................... 2
Chordoma........................................................................................................................................................ 2
Notes and Mnemonics .................................................................................................................................... 2
Secondary Malignant Tumours of Bone......................................................................................................... 3
Lung Cancer: Non-Small Cell Management.................................................................................................... 3
Tissue Sampling............................................................................................................................................... 4
10. PRNCIPLES OF SURGICAL ONCOLOGY – MRCS NOTES - REDA 1

132
Extravasation Injury
Chemotherapy may be complicated by extravasation reactions in up to 6% of cases. The following chemotherapy agents
are recognised causes of extravasation reactions; doxorubicin, vincristine, vinblastine, adriamycin, cisplatin, mitomycin
and mithramycin.
Up to 30% of extravasation reactions may be complicated by the development of ulceration.
When an extravasation reaction is suspected, the infusion should be stopped and the infusing device aspirated. The
extremity should be elevated. As a general rule cold compresses have been shown to reduce the incidence of subsequent
ulceration with doxorubicin. Warm compresses have been found to be beneficial in extravasation of vinca alkaloids.
Dimethylsulfoxide may be infused in some cases, ideally within 5 hours of the event occurring. No conclusive evidence
exists to support the use of corticosteroids or sodium bicarbonate for extravasation injuries.
Extravasation of total parenteral nutrition (TPN) solutions is usually managed by the local administration of hyaluronidase
to the infusion site.
Chemotherapy Agents
Class Example Mode of action
Antimetabolites 5 FU S Phase specific drug, mimics uracil and is incorporated into RNA
Anthracyclines* Doxorubicin Inhibits DNA and RNA synthesis by intercalating base pairs
Topoisomerase inhibitors** Etoposide Inhibits topoisomerase II, prevents efficient DNA coiling
Platinum Cisplatin Crosslinks DNA, this then distorts molecule and induces apoptosis
(similar to alkylating agents)
Alkylating agent Cyclophosphamide Phosphoramide mustard forms DNA crosslinks and then cell death
Taxanes Docetaxal Disrupts microtubule formation
*=Main adverse effect cardiotoxicity
**=Irinotecan is a similar drug which works by inhibition of topoisomerase I
Chordoma
Chordoma is a rare slow-growing bone tumour. Their favored origin is remnants of the notochord.
Chordomas can arise anywhere from the skull base to the sacrum. The two most common locations are the skull base
and sacrum.
There are three histological variants of chordoma: classical (or "conventional"), chondroid and de-differentiated.
• The histological appearance of classical chordoma is of a lobulated tumor composed of groups of cells separated
by fibrous septa. The cells have small round nuclei and abundant vacuolated cytoplasm.
• Chondroid chordomas histologically show features of both chordoma and chondrosarcoma.
The 10-year tumor free survival rate for sacral chordoma was 46%. Chondroid chordomas appear to have a more
indolent clinical course.
In most cases, complete surgical resection followed by radiation therapy offers the best chance of long-term control.
Unfortunately, the lesion has a close proximity to the spine itself and this can compromise resection margins.
Chordomas are relatively radioresistant, requiring high doses of radiation to be controlled. The proximity of chordomas
to vital neurological structures such as the brain stem and nerves limits the dose of radiation that can safely be delivered.
Therefore, highly focused radiation such as proton therapy and carbon ion therapy are more effective than conventional
x-ray radiation.
Notes and Mnemonics

Contraindications to lung cancer surgery include:
• SVC obstruction
• FEV < 1.5
• Malignant pleural effusion
• Vocal cord paralysis (implies extracapsular spread to mediastinal nodes and is an indication of inoperability).

133
Secondary Malignant Tumours of Bone
Metastatic lesions affecting bone are more common than primary bone tumours.
75% cases will affect those over the age of 50.
The typical tumours that spread to bone include: The commonest bone sites affected are:
• Breast • Vertebrae (usually thoracic)
• Bronchus • Proximal femur
• Renal • Ribs
• Thyroid • Sternum
• Prostate • Pelvis
• Skull
Pathological fracture
Osteolytic lesions are the greatest risk for pathological fracture
The risk and load required to produce fracture varies according to bone site. Bones with lesions that occupy 50% or less
will be prone to fracture under loading (Harrington). When 75% of the bone is affected the process of torsion about a
bony fulcrum may produce a fracture.
Mirel’s Scoring system used to help determine the risk of fracture

Score points Site Radiographic appearance Width of bone involved Pain
1 Upper extremity Blastic Less than 1/3 Mild
2 Lower extremity Mixed 1/3 to 2/3 Moderate
3 Peritrochanteric Lytic More than 2/3 Aggravated by function
Depending upon the score the treatment should be as follows:

Score Risk of fracture Treatment
9 or greater Impending (33%) Prophylactic fixation
8 Borderline Consider fixation
7 or less Not impending (4%) Non operative management
Where the lesion is an isolated metastatic deposit consideration should be given to excision and reconstruction as the
outcome is better.
Non operative treatments

Hypercalcaemia: Treat with re hydration and bisphosphonates.
Pain: Opiate analgesics and radiotherapy.
Some tumours such as breast and prostate will benefit from chemotherapy and or hormonal agents.
Lung Cancer: Non-Small Cell Management

Management
• Only 20% suitable for surgery
• Mediastinoscopy performed prior to surgery as CT does not always show mediastinal lymph node involvement
• Curative or palliative radiotherapy
• Poor response to chemotherapy
Surgery contraindications
• Assess general health
• Stage IIIb or IV (i.e. metastases present)
• FEV1 < 1.5 litres is considered a general cut-off point*
• Malignant pleural effusion
• Tumour near hilum
• Vocal cord paralysis
• SVC obstruction
* However if FEV1 < 1.5 for lobectomy or < 2.0 for pneumonectomy then some authorities advocate further lung function
tests as operations may still go ahead based on the results

134
Tissue Sampling
Tissue sampling is an important surgical process. Biopsy modalities vary according to the site, experience and subsequent
planned therapeutic outcome
The modalities comprise:

• Fine needle aspiration cytology
• Core biopsy
• Excision biopsy
• Tru cut biopsy
• Punch biopsy
• Cytological smears
• Endoscopic or laparoscopic biopsy
When the lesion is superficial the decision needs to be taken as to whether complete excision is desirable or whether
excision biopsy is acceptable. In malignant melanoma for example the need for safe margins will mean that a more
radical surgical approach needs to be adopted after diagnostic confirmation from excision biopsy than would be the case
in basal cell carcinoma. Punch biopsies are useful in gaining histological diagnosis of unclear skin lesions where excision
biopsy is undesirable such as in establishing whether a skin lesion is vasculitic or not.
Fine needle aspiration cytology (FNAC) is an operator dependent procedure that may or may not be image guided and
essentially involves passing a needle through a lesion whilst suction is applied to a syringe. The material thus obtained is
expressed onto a slide and sent for cytological assessment. This test can be limited by operator inexperience and also by
the lack of histological architectural information (e.g. Follicular carcinoma of the thyroid). Where a discharge is present a
sample may be sent for cytology although in some sites (e.g. Nipple discharge ) the information gleaned may be
meaningless.
Tissue samples may be obtained by both core and tru cut biopsy. A core biopsy is obtained by use of a spring loaded gun
with a needle passing quickly through the lesion of interest. A tru cut biopsy achieves the same objective but the needle
moved by hand. When performing these techniques image guidance may be desirable (e.g. In breast lesions).
Consideration needs to be given to any planned surgical resection as it may be necessary to resect the biopsy tract along
with the specimen (e.g. In sarcoma surgery).
Visceral lesions may be accessed percutaneously under image guidance such as ultrasound guided biopsy of liver
metastases. Or under direct vision such as a colonoscopic biopsy.
Core biopsy
Punch biopsy

135
11. The Abdomen – MRCS Notes - Reda

Abdominal Incisions........................................................................................................................................ 2
Abdominal Stomas .......................................................................................................................................... 3
Right Iliac Fossa Pain....................................................................................................................................... 4
Abdominal Signs ............................................................................................................................................. 4
Acute Abdominal Pain - Diagnoses ................................................................................................................ 5
Gynaecological Causes of Abdominal Pain .................................................................................................... 6
Drain Types ..................................................................................................................................................... 7
Splenic Vein Thrombosis................................................................................................................................. 7
Diarrhoea ........................................................................................................................................................ 8
Abdominal Wound Dehiscence ...................................................................................................................... 9
Hernia ............................................................................................................................................................ 10
Malabsorption .............................................................................................................................................. 11
Mesenteric Vessel Disease ........................................................................................................................... 12
Abdominal Radiology.................................................................................................................................... 13
Irritable Bowel Syndrome (IBS) .................................................................................................................... 13
Splenic Trauma.............................................................................................................................................. 14
11. THE ABDOMEN – MRCS NOTES - REDA 1

136
Abdominal Incisions
Midline incision • Commonest approach to the abdomen
• Structures divided: linea alba, transversalis fascia, extraperitoneal fat, peritoneum (avoid
falciform ligament above the umbilicus)
• Bladder can be accessed via an extraperitoneal approach through the space of Retzius
Paramedian • Parallel to the midline (about 3-4cm)
incision • Structures divided/retracted: anterior rectus sheath, rectus (retracted), posterior rectus sheath,
transversalis fascia, extraperitoneal fat, peritoneum
• Incision is closed in layers
Battle • Similar location to paramedian but rectus displaced medially (and thus denervated)
• Now seldom used
Kocher's Incision under right subcostal margin e.g. Cholecystectomy (open)
Lanz Incision in right iliac fossa e.g. Appendicectomy
Gridiron Oblique incision centered over McBurney’s point- usually appendicectomy (less cosmetically
acceptable than Lanz
Gable Rooftop incision e.g. Pancreatectomy
Pfannenstiel's Transverse supra pubic, primarily used to access pelvic organs, C-section
McEvedy’s Groin incision e.g. Emergency repair strangulated femoral hernia
Rutherford Extraperitoneal approach to left or right lower quadrants. Gives excellent access to iliac vessels and is
Morrison the approach of choice for first time renal transplantation.

137
Abdominal Stomas
Stomas may be sited during a range of abdominal procedures and involve bringing the lumen or visceral contents onto
the skin. In most cases this applies to the bowel. However, other organs or their contents may be diverted in case of
need.
With bowel stomas the type method of construction and to a lesser extent the site will be determined by the contents of
the bowel. In practice, small bowel stomas should be spouted so that their irritant contents are not in contact with the
skin. Colonic stomas do not need to be spouted as their contents are less irritant.
In the ideal situation the site of the stoma should be marked with the patient prior to surgery. Stoma siting is important
as it will ultimately influence the ability of the patient to manage their stoma and also reduce the risk of leakage. Leakage
of stoma contents and subsequent maceration of the surrounding skin can rapidly progress into a spiraling loss of control
of stoma contents.
Types of stomas
Name of stoma Use Common sites
Gastrostomy • Gastric decompression or fixation Epigastrium
• Feeding
Loop • Seldom used as very high output Any location according to
jejunostomy • May be used following emergency laparotomy with planned early need
closure
Percutaneous • Usually performed for feeding purposes and site in the proximal Usually left upper quadrant
jejunostomy bowel
Loop ileostomy • Defunctioning of colon e.g. following rectal cancer surgery Usually right iliac fossa
• Does not decompress colon (if ileocaecal valve competent)
End ilestomy • Usually following complete excision of colon or where ileo-colic Usually right iliac fossa
anastomosis is not planned
• May be used to defunction colon, but reversal is more difficult
End colostomy Where a colon is diverted or resected and anastomosis is not primarily Either left or right iliac fossa
achievable or desirable
Loop colostomy • To defunction a distal segment of colon May be located in any region
• Since both lumens are present the distal lumen acts as a vent of the abdomen, depending
upon colonic segment used
Caecostomy Stoma of last resort where loop colostomy is not possible Right iliac fossa
Mucous fistula • To decompress a distal segment of bowel following colonic May be located in any region
division or resection of the abdomen according to
• Where closure of a distal resection margin is not safe or clinical need
achievable
Hartmann's procedure with reversal

138
Right Iliac Fossa Pain
Appendicitis • Pain radiating to right iliac fossa
• Anorexia (very common)
• Short history
• Diarrhoea and profuse vomiting rare
Crohn's disease • Often long history
• Signs of malnutrition
• Change in bowel habit, especially diarrhoea
Mesenteric • Mainly affects children
adenitis • Causes include Adenoviruses, Epstein Barr Virus, Beta-haemolytic Streptococcus, Staphylococcus
spp., Escherichia coli, Streptococcus viridans and Yersinia spp.
• Patients have a higher temperature than those with appendicitis
• If laparotomy is performed, enlarged mesenteric lymph nodes will be present
Diverticulitis • Both left and right sided disease may present with right iliac fossa pain
• Clinical history may be similar, although some change in bowel habit is usual
• When suspected, a CT scan may help in refining the diagnosis
Meckel's • A Meckel's diverticulum is a congenital abnormality that is present in about 2% of the population
diverticulitis • Typically 2 feet proximal to the ileocaecal valve
• May be lined by ectopic gastric mucosal tissue and produce bleeding
• May be asymptomatic if lined by ileal mucosa
Perforated peptic • This usually produces upper quadrant pain but pain may be lower
ulcer • Perforations typically have a sharp sudden onset of pain in the history
Incarcerated right • Usually only right iliac fossa pain if right sided or bowel obstruction.
inguinal / femoral
hernia
Bowel perforation • Seldom localised to right iliac fossa, although complete large bowel obstruction with caecal
2ry to caecal or distension may cause pain prior to perforation.
colon carcinoma
Gynaecological • Pelvic inflammatory disease / Salpingitis / Pelvic abscess / Ectopic pregnancy / Ovarian torsion /
causes Threatened or complete abortion / Mittelschmerz
Urological causes • Ureteric colic / UTI / Testicular torsion
Other causes • TB / Typhoid / Herpes Zoster / AAA / Situs inversus
Abdominal Signs
A number of eponymous abdominal signs are noted. These include:
• Rovsing’s sign - appendicitis
• Boas sign - cholecystitis
• Murphy’s sign - cholecystitis
• Cullen’s sign - pancreatitis (other intraabdominal haemorrhage)
• Grey-Turners sign - pancreatitis (or other retroperitoneal haemorrhage)
In clinical practice haemorrhagic pancreatitis is thankfully rare. The signs are important and thus shown below:
Grey Turner's sign

Cullen’s sign

139
Acute Abdominal Pain - Diagnoses
Conditions presenting with acute abdominal pain
Condition Features Investigations Management
Appendicitis History of migratory pain. Differential white cell count Appendicectomy
Fever. Pregnancy test
Anorexia. C-Reactive protein
Evidence of right iliac fossa tenderness. Amylase
Mild pyrexia. Urine dipstick testing
Mesenteric Usually recent upper respiratory tract FBC - may show slightly Conservative management-
adenitis infection. raised white cell count appendicectomy if diagnostic
High fever. Urine dipstick often normal doubt
Generalised abdominal discomfort- true Abdominal USS - usually no
localised pain and signs are rare. free fluid
Mittelschmerz Only seen in females Full blood count- normal Manage conservatively if
Mid cycle pain Urine dipstick- normal doubt or symptoms fail to
Usually occurs two weeks after last Abdominal and pelvic settle then laparoscopy
menstrual period ultrasound- may show a
Pain usually has a supra-pubic location trace of pelvic free fluid
Usually subsides over a 24-48h period.
Fitz-Hugh Disseminated infection with Chlamydia. Abdominal USS - may show Usually medically managed-
Curtis Usually seen in females. free fluid doxycycline or azithromycin
syndrome Consists of evidence of PID together High vaginal swabs - may
with peri-hepatic inflammation and show evidence of sexually
subsequent adhesion formation. transmitted infections
Abdominal Sudden onset of abdominal pain Patients who are Unstable patients should
aortic radiating to the back in older adults (look haemodynamically stable undergo immediate surgery
aneurysm for risk factors). should have a CT scan (unless it is not in their best
(ruptured) Collapse. interests).
May be moribund on arrival in casualty, Those with evidence of
more stable if contained haematoma. contained leak on CT should
Careful clinical assessment may reveal undergo immediate surgery
pulsatile mass. Increasing unruptured
aneurysmal size is an
indication for urgent surgical
intervention (that can wait
until the next working day)
Perforated Sudden onset of pain (usually epigastric). Erect CXR may show free Laparotomy (laparoscopic
peptic ulcer Often preceding history of upper air. A CT scan may be surgery for perforated peptic
abdominal pain. indicated where there is ulcers is both safe and feasible
Soon develop generalised abdominal diagnostic doubt in experienced hands)
pain.
On examination may have clinical
evidence of peritonitis.
Intestinal Colicky abdominal pain and vomiting A plain abdominal film may In those with a virgin abdomen
obstruction (the nature of which depends on the help with making the a lower and earlier threshold
level of the obstruction). diagnosis. A CT scan may for laparotomy should exist
Abdominal distension and constipation be useful where diagnostic than in those who may have
(again depending upon site of uncertainty exists adhesional obstruction
obstruction).
Features of peritonism may occur where
local necrosis of bowel loops is
occurring.
Mesenteric Embolic events present with sudden Arterial pH and lactate Immediate laparotomy and
infarction pain and forceful evacuation. Arterial phase CT scanning resection of affected
Acute on chronic events usually have a is the most sensitive test segments, in acute embolic
longer history and previous weight loss. events SMA embolectomy may
On examination the pain is typically be needed.
greater than the physical signs would
suggest.

140
Gynaecological Causes of Abdominal Pain
In addition to routine diagnostic work up of abdominal pain, all female patients should also undergo a bimanual vaginal
examination, urine pregnancy test and consideration given to abdominal and pelvic USS. When diagnostic doubt persists
a laparoscopy provides a reliable method of assessing suspected tubulo-ovarian pathology.
Diagnosis Features Investigation Treatment
Mittelschmerz Usually mid cycle pain. FBC - usually normal Conservative
Often sharp onset. USS - may show small
Little systemic disturbance. quantity of free fluid
May have recurrent episodes.
Usually settles over 24-48 hours.
Endometriosis 25% asymptomatic, in a further 25% associated with USS - may show free Usually managed
other pelvic organ pathology. fluid medically, complex
Remaining 50% may have menstrual irregularity, Laparoscopy will usually disease will often
infertility, pain and deep dyspareunia. show lesions require surgery and
Complex disease may result in pelvic adhesional some patients will
formation with episodes of intermittent small bowel even require
obstruction. formal colonic and
Intra-abdominal bleeding may produce localised rectal resections if
peritoneal inflammation. these areas are
Recurrent episodes are common. involved
Ovarian Usually sudden onset of deep seated colicky USS may show free fluid Laparoscopy
torsion abdominal pain. Laparoscopy is usually
Associated with vomiting and distress. both diagnostic and
Vaginal examination may reveal adnexal tenderness. therapeutic
Ectopic Symptoms of pregnancy without evidence of intra Ultrasound showing no Laparoscopy or
gestation uterine gestation. intra uterine pregnancy laparotomy is
Present as an emergency with evidence of rupture or and beta HCG that is haemodynamically
impending rupture. elevated unstable. A
Open tubular ruptures may have sudden onset of May show intra- salphingectomy is
abdominal pain and circulatory collapse, in other the abdominal free fluid usually performed.
symptoms may be more prolonged and less marked.
Small amount of vaginal discharge is common.
There is usually adnexal tenderness.
Pelvic Bilateral lower abdominal pain associated with FBC - Leucocytosis Usually medical
inflammatory vaginal discharge. Pregnancy test negative management
disease Dysuria may also be present. (Although infection and
(PID) Peri-hepatic inflammation secondary to Chlamydia pregnancy may co-exist)
(Fitz Hugh Curtis Syndrome) may produce right upper Amylase - usually
quadrant discomfort. normal or slightly raised
Fever >38o High vaginal and
urethral swabs

141
Drain Types
Type of drain Features
Redivac • Suction type of drain
• Closed drainage system
• High pressure vacuum system
Low pressure • Consist of small systems such as the lantern style drain that may be used for short term drainage
drainage systems of small wounds and cavities
• Larger systems are sometimes used following abdominal surgery, they have a lower pressure than
the redivac system, which decreases the risks of fistulation
• May be emptied and re-pressurised
Latex tube drains • May be shaped (e.g. T Tube) or straight
• Usually used in non pressurised systems and act as sump drains
• Most often used when it is desirable to generate fibrosis along the drain track (e.g. following
exploration of the CBD)
Chest drains • May be large or small diameter (depending on the indication)
• Connected to underwater seal system to ensure one way flow of air
Corrugated drain • Thin, wide sheet of plastic, usually soft
• Contains corrugations, along which fluids can track
Abdominal compartment syndrome

Background
Intra-abdominal pressure is the steady state pressure concealed within the abdominal cavity.
• In critically ill adults the normal intra-abdominal pressure = 5-7mmHg
• Intra-abdominal hypertension has pressures of 12-25mmHg
• Changes >15mmHg are associated with microvascular hypoperfusion
• Abdominal compartment syndrome is defined as sustained intra-abdominal pressure >20mmHg coupled with
new organ dysfunction / failure
• It may occur either primarily without previous surgical intervention e.g. Following intestinal ischaemia or
secondarily following a surgical procedure
• Diagnosis is typically made by transvesical pressure measurements coupled with an index of clinical suspicion.
Management
Once the diagnosis is made non operative measures should be instituted including:
• Gastric decompression
• Improve abdominal wall compliance e.g. muscle relaxants/ sedation
• Drain abdominal fluid collections.
• Consider fluid restriction/ diuretics if clinically indicated.
In those whom non operative treatment is failing; the correct treatment is laparotomy and laparostomy. Options for
laparostomy are many although the Bogota bag or VAC techniques are the most widely practised. Re-look laparotomy
and attempts at delayed closure will follow in due course.
Splenic Vein Thrombosis

Thrombosis of the splenic vein may complicate pancreatitis, pancreatic carcinoma, iatrogenic trauma and
hypercoagulable diseases. The condition may predispose to the development of gastric varices, oesophageal varices are
uncommon in splenic vein thrombosis alone.
Diagnosis is made by CT angiography.
Treatment is with splenectomy.

142
Diarrhoea
World Health Organisation definitions
Diarrhoea: > 3 loose or watery stool per day
Acute diarrhoea < 14 days
Chronic diarrhoea > 14 days
Acute Diarrhoea
Gastroenteritis May be accompanied by abdominal pain or nausea/vomiting
Diverticulitis Classically causes left lower quadrant pain, diarrhoea and fever
Antibiotic therapy More common with broad spectrum antibiotics
Clostridium difficile is also seen with antibiotic use
Constipation causing overflow A history of alternating diarrhoea and constipation may be given
May lead to faecal incontinence in the elderly
Chronic Diarrhoea
Irritable bowel Extremely common. The most consistent features are abdominal pain, bloating and change in bowel
syndrome habit. Patients may be divided into those with diarrhoea predominant IBS and those with constipation
predominant IBS.
Features such as lethargy, nausea, backache and bladder symptoms may also be present
Ulcerative Bloody diarrhoea may be seen. Crampy abdominal pain and weight loss are also common. Faecal urgency
colitis and tenesmus may occur
Crohn's Crampy abdominal pains and diarrhoea. Bloody diarrhoea less common than in ulcerative colitis. Other
disease features include malabsorption, mouth ulcers perianal disease and intestinal obstruction
Colorectal Symptoms depend on the site of the lesion but include diarrhoea, rectal bleeding, anaemia and
cancer constitutional symptoms e.g. Weight loss and anorexia
Coeliac • In children: may present with failure to thrive, diarrhoea and abdominal distension
disease • In adults: lethargy, anaemia, diarrhoea and weight loss are seen. Other autoimmune conditions may
coexist
Other conditions associated with diarrhoea include:

• Thyrotoxicosis
• Laxative abuse
• Appendicitis with pelvic abscess or pelvic appendix
• Radiation enteritis
Diagnosis
• Stool culture
• Abdominal and digital rectal examination
• Consider colonoscopy (radiological studies unhelpful)
• Thyroid function tests, serum calcium, anti endomysial antibodies, glucose

143
Abdominal Wound Dehiscence
• This is a significant problem facing all surgeons who undertake abdominal surgery on a regular basis. Traditionally, it
is said to occur when all layers of an abdominal mass closure fail and the viscera protrude externally (associated with
30% mortality).
• It can be subdivided into superficial, in which the skin wound alone fails and complete, implying failure of all layers.
Factors which increase the risk are:

• Malnutrition
• Vitamin deficiencies
• Jaundice
• Steroid use
• Major wound contamination (e.g. faecal peritonitis)
• Poor surgical technique (Mass closure technique is the preferred method-Jenkins Rule)
When sudden full dehiscence occurs the management is as follows:

• Analgesia
• Intravenous fluids
• Intravenous broad spectrum antibiotics
• Coverage of the wound with saline impregnated gauze (on the ward)
• Arrangements made for a return to theatre
Surgical strategy
• Correct the underlying cause (e.g. TPN or NG feed if malnourished)
• Determine the most appropriate strategy for managing the wound
Options
Resuturing of This may be an option if the wound edges are healthy and there is enough tissue for sufficient
the wound coverage. Deep tension sutures are traditionally used for this purpose.
Application of a This is a clear dressing with removable front. Particularly suitable when some granulation tissue is
wound manager present over the viscera or where there is a high output bowel fistula present in the dehisced wound.
Application of a This is a clear plastic bag that is cut and sutured to the wound edges and is only a temporary measure
'Bogota bag' to be adopted when the wound cannot be closed and will necessitate a return to theatre for definitive
management.
Application of a These can be safely used BUT ONLY if the correct layer is interposed between the suction device and
VAC dressing the bowel. Failure to adhere to this absolute rule will almost invariably result in the development of
system multiple bowel fistulae and create an extremely difficult management problem.

144
Hernia
Hernias occur when a viscus or part of it protrudes from within its normal anatomical cavity. Specific hernias are covered
under their designated titles the remainder are addressed here.
Spigelian hernia
• Interparietal hernia occurring at the level of the arcuate line
• Rare
• May lie beneath internal oblique muscle. Usually between internal and external oblique
• Equal sex distribution
• Position is lateral to rectus abdominis
• Both open and laparoscopic repair are possible, the former in cases of strangulation
Lumbar hernia
The lumbar triangle (through which these may occur) is bounded by:
Crest of ilium (inferiorly), External oblique (laterally), Latissimus dorsi (medially)
Primary lumbar herniae are rare, most are incisional hernias following renal surgery
Direct anatomical repair with or without mesh re-enforcement is the procedure of choice
Obturator hernia
• Herniation through the obturator canal
• Commoner in females
• Usually lies behind pectineus muscle
• Elective diagnosis is unusual most will present acutely with obstruction
• When presenting acutely most cases with require laparotomy or laparoscopy (and small bowel resection if
indicated)
Richters hernia
• Condition in which part of the wall of the small bowel (usually the anti mesenteric border) is strangulated within
a hernia (of any type)
• They do not present with typical features of intestinal obstruction as lumenal patency is preserved
• Where vomiting is prominent it usually occurs as a result of paralytic ileus from peritonitis (as these hernias may
perforate)
Incisional hernia
• Occur through sites of surgical access into the abdominal cavity
• Most common following surgical wound infection
• To minimise following midline laparotomy Jenkins Rule should be followed and this necessitates a suture length
4x length of incision with bites taken at 1cm intervals, 1 cm from the wound edge
• Repair may be performed either at open surgery or laparoscopically and a wide variety of techniques are
described
Bochdalek hernia
• Typically congenital diaphragmatic hernia
• 85% cases are located in the left hemi diaphragm
• Associated with lung hypoplasia on the affected side
• More common in males
• Associated with other birth defects
• May contain stomach
• May be treated by direct anatomical apposition or placement of mesh. In infants that have severe respiratory
compromise mechanical ventilation may be needed and mortality rate is high

145
Morgagni Hernia
• Rare type of diaphragmatic hernia (approx 2% cases)
• Herniation through foramen of Morgagni
• Usually located on the right and tend to be less symptomatic
• More advanced cases may contain transverse colon
• As defects are small pulmonary hypoplasia is less common
• Direct anatomical repair is performed
Umbilical hernia
• Hernia through weak umbilicus
• Usually presents in childhood
• Often symptomatic
• Equal sex incidence
• 95% will resolve by the age of 2 years
• Surgery performed after the third birthday
Paraumbilical hernia
• Usually a condition of adulthood
• Defect is in the linea alba
• More common in females
• Multiparity and obesity are risk factors
• Traditionally repaired using Mayos technique - overlapping repair, mesh may be used though not if small bowel
resection is required owing to acute strangulation
Littres hernia
• Hernia containing Meckels diverticulum
• Resection of the diverticulum is usually required and this will preclude a mesh repair
Malabsorption
Malabsorption is characterised by diarrhoea, steatorrhoea and weight loss. Causes may be broadly divided into intestinal
(e.g. villous atrophy), pancreatic (deficiency of pancreatic enzyme production or secretion) and biliary (deficiency of bile-
salts needed for emulsification of fats)
Intestinal causes of malabsorption

• Coeliac disease
• Crohn's disease
• Tropical sprue
• Whipple's disease
• Giardiasis
• Brush border enzyme deficiencies (e.g. Lactase insufficiency)
Pancreatic causes of malabsorption

• Chronic pancreatitis
• Cystic fibrosis
• Pancreatic cancer
Biliary causes of malabsorption

• Biliary obstruction
• Primary biliary cirrhosis
Other causes
• Bacterial overgrowth (e.g. Systemic sclerosis, diverticulae, blind loop)
• Short bowel syndrome
• Lymphoma

146
Mesenteric Vessel Disease
Mesenteric ischaemia accounts for 1 in 1000 acute surgical admissions. It is primarily caused by arterial embolism
resulting in infarction of the colon. It is more likely to occur in areas such as the splenic flexure that are located at the
borders of the territory supplied by the superior and inferior mesenteric arteries.
Types
Acute mesenteric • Sudden onset abdominal pain followed by profuse diarrhoea.
embolus • May be associated with vomiting.
(commonest 50%) • Rapid clinical deterioration.
• Serological tests: WCC, lactate, amylase may all be abnormal particularly in established disease.
These can be normal in the early phases.
Acute on chronic • Usually longer prodromal history.
mesenteric • Post prandial abdominal discomfort and weight loss are dominant features. Patients will usually
ischaemia present with an acute on chronic event, but otherwise will tend not to present until mesenteric
flow is reduced by greater than 80%.
• When acute thrombosis occurs presentation may be as above. In the chronic setting the
symptoms will often be those of ischaemic colitis (mucosa is the most sensitive area to this
insult).
Mesenteric vein • Usually a history over weeks.
thrombosis • Mesenteric vein thrombosis may complicate severe intra-abdominal sepsis and when it
progresses may impair bowel perfusion.
• Overt abdominal signs and symptoms will not occur until venous thrombosis has reached a
stage to compromise arterial inflow.
• Thrombophilia accounts for 60% of cases.
Low flow • This occurs in patients with multiple co morbidities in whom mesenteric perfusion is
mesenteric significantly compromised by overuse of inotropes or background cardiovascular compromise.
infarction • The end result is that the bowel is not adequately perfused and infarcts occur from the mucosa
outwards.
Diagnosis
• Serological tests: WCC, lactate, CRP, amylase (can be normal in early disease).
• Cornerstone for diagnosis of arterial AND venous mesenteric disease is CT angiography scanning in the arterial
phase with thin slices (<5mm). Venous phase contrast is not helpful.
• SMA duplex USS is useful in the evaluation of proximal SMA disease in patients with chronic mesenteric
ischaemia.
• MRI is of limited use due to gut peristalsis and movement artefact.
Management
• Overt signs of peritonism: Laparotomy
• Mesenteric vein thrombosis: If no peritonism: Medical management with IV heparin
• At operation limited resection of frankly necrotic bowel with view to relook laparotomy at 24-48h. In the interim
urgent bowel revascularisation via endovascular (preferred) or surgery.
Prognosis
Overall poor. Best outlook is from an acute ischaemia from an embolic event where surgery occurs within 12h. Survival
may be 50%. This falls to 30% with treatment delay. The other conditions carry worse survival figures.

147
Abdominal Radiology
Plain abdominal x-rays are often used as a first line investigation in patients with acute abdominal pain. A plain
abdominal film may demonstrate free air, evidence of bowel obstruction and possibly other causes of pain (e.g. renal or
gallbladder stones).
Investigation of potential visceral perforation is usually best performed by obtaining an erect chest x-ray, as this is a more
sensitive investigation for suspected visceral perforation than recumbent films.
Features which are usually abnormal

• Large amounts of free air (colonic perforation), smaller volumes seen with more proximal perforations.
• A positive Rigler sign (gas on both sides of the bowel wall).
• Caecal diameter of >8cm
• Fluid levels in the colon
• Ground glass appearance to film (usually due to large amounts of free fluid).
• Sentinel loop in patients with inflammation of other organs (e.g. pancreatitis).
Features which should be expected/ or occur without pathology

• In Chilaiditi’s sign, a loop of bowel may be interposed between the liver and diaphragm, giving the mistaken
impression that free air is present.
• Following ERCP (and sphincterotomy) air may be identified in the biliary tree.
• Free intra-abdominal air following laparoscopy / laparotomy, although usually dissipates after 48-72 hours.
Irritable Bowel Syndrome (IBS)

The diagnosis of irritable bowel syndrome is made according to the ROME III diagnostic criteria which state:
Recurrent abdominal pain or discomfort at 3 days per month for the past 3 months associated with two or more of the
following:
• Improvement with defecation.
• Onset associated with a change in the frequency of stool.
• Onset associated with a change in the form of the stool.
Features such as lethargy, nausea, backache and bladder symptoms may also support the diagnosis
Red flag features should be inquired about:

• Rectal bleeding
• Unexplained/unintentional weight loss
• Family history of bowel or ovarian cancer
• Onset after 60 years of age
Suggested investigations are:

• Full blood count
• ESR/CRP
• Coeliac disease screen (tissue transglutaminase antibodies)
• Colonoscopy (if worrying symptoms, positive family history)
• Thyroid function tests
• Glucose (ensure not diabetic)
The NICE criteria state that blood tests alone will suffice in people fulfilling the diagnostic criteria. We would point out that
luminal colonic studies should be considered early in patients with altered bowel habit referred to hospital and a diagnosis
of IBS should still be largely one of exclusion.
Treatment
• Usually reduce fibre intake.
• Tailored prescriptions of laxatives or loperamide according to clinical picture.
• Dietary modification (caffeine avoidance, less carbonated drinks).
• Consider low dose tricyclic antidepressants if pain is a dominant symptom.
• Biofeedback may help.

148
Splenic Trauma
• The spleen is one of the more commonly injured intra-abdominal organs
• In most cases the spleen can be conserved. The management is dictated by the associated injuries, haemodynamic
status and extent of direct splenic injury.
Management of splenic trauma

Conservative Small subcapsular haematoma
Minimal intra-abdominal blood
No hilar disruption
Laparotomy with conservation Increased amounts of intraabdominal blood
Moderate haemodynamic compromise
Tears or lacerations affecting <50%
Resection Hilar injuries
Major haemorrhage
Major associated injuries
Splenectomy Technique
Trauma
• GA
• Long midline incision
• If time permits insert a self-retaining retractor (e.g. Balfour/ omnitract)
• Large amount of free blood is usually present. Pack all 4 quadrants of the abdomen. Allow the anaesthetist to
'catch up'
• Remove the packs and assess the viability of the spleen. Hilar injuries and extensive parenchymal lacerations will
usually require splenectomy.
• Divide the short gastric vessels and ligate them.
• Clamp the splenic artery and vein. Two clamps on the patient side are better and allow for double ligation and
serve as a safety net if your assistant does not release the clamp smoothly.
• Be careful not to damage the tail of the pancreas, if you do then this will need to be formally removed and the
pancreatic duct closed.
• Wash out the abdomen and place a tube drain to the splenic bed.
• Some surgeons implant a portion of spleen into the omentum, whether you decide to do this is a matter of
personal choice.
• Post operatively the patient will require prophylactic penicillin V and pneumococcal vaccine.
Elective
Elective splenectomy is a very different operation from that performed in the emergency setting. The spleen is often
large (sometimes massive). Most cases can be performed laparoscopically. The spleen will often be macerated inside a
specimen bag to facilitate extraction.
Complications
• Haemorrhage (may be early and either from short gastrics or splenic hilar vessels
• Pancreatic fistula (from iatrogenic damage to pancreatic tail)
• Thrombocytosis: prophylactic aspirin
• Encapsulated bacteria infection e.g. Strep. pneumoniae, Haemophilus influenzae and Neisseria meningitidis

149
12. Upper GI Surgery – MRCS Notes - Reda

Upper Gastrointestinal Bleeding .................................................................................................................... 2
Rockall Score ................................................................................................................................................... 4
Dysphagia ........................................................................................................................................................ 4
Bariatric Surgery ............................................................................................................................................. 5
Gastric Cancer ................................................................................................................................................. 6
Gastric Emptying ............................................................................................................................................. 8
Lower Gastrointestinal Bleeding .................................................................................................................... 9
Oesophageal Disease .................................................................................................................................... 10
Oesophageal Cancer - Treatment ................................................................................................................. 11
Nutrition Options in Surgical Patients ......................................................................................................... 12
12. UPPER GASTROINTESTINAL SURGERY – MRCS NOTES - REDA 1

150
Upper Gastrointestinal Bleeding
Patients may present with the following:
• Haematemesis and/ or malaena
• Epigastric discomfort
• Sudden collapse
The extent to which these will occur will depend upon the source. Mortality is higher in patients presenting with
haematemesis than malaena alone.
Oesophageal bleeding
Cause Presenting features
Oesophagitis Small volume of fresh blood, often streaking vomit. Malaena rare. Often ceases spontaneously. Usually
history of antecedent GORD type symptoms.
Cancer Usually small volume of blood, except as pre terminal event with erosion of major vessels. Often
associated symptoms of dysphagia and constitutional symptoms such as weight loss. May be recurrent
until malignancy managed.
Mallory Weiss Typically brisk small to moderate volume of bright red blood following bout of repeated vomiting.
Tear Malaena rare. Usually ceases spontaneously.
Varices Usually large volume of fresh blood. Swallowed blood may cause malaena. Often associated with
haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately
managed.
Gastric Bleeding
Gastric cancer May be frank haematemesis or altered blood mixed with vomit. Usually prodromal features of dyspepsia
and may have constitutional symptoms. Amount of bleeding variable but erosion of major vessel may
produce considerable haemorrhage.
Dieulafoy Often no prodromal features prior to haematemesis and malaena, but this arteriovenous malformation
Lesion may produce quite considerable haemorrhage and may be difficult to detect endoscopically.
Diffuse erosive Usually haematemesis and epigastric discomfort. Usually there is an underlying cause such as recent
gastritis NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise.
Gastric ulcer Small low volume bleeds more common so would tend to present as iron deficiency anaemia. Erosion into
a significant vessel may produce considerable haemorrhage and haematemesis.
Duodenum
Most common cause of major haemorrhage is a posteriorly sited duodenal ulcer. However, ulcers at any site in the
duodenum may present with haematemesis, malaena and epigastric discomfort. The pain of duodenal ulcer is slightly
different to that of gastric ulcers and often occurs several hours after eating. Peri ampullary tumours may bleed but
these are rare. In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but
important cause of major haemorrhage associated with high mortality.

151
Management
• Admission to hospital careful monitoring, cross match blood, check FBC, LFTs, U+E and Clotting (as a minimum)
• Patients with on-going bleeding and haemodynamic instability are likely to require O negative blood pending
cross matched blood
• Early control of airway is vital (e.g. Drowsy patient with liver failure)
• Patients with suspected varices should receive terlipressin prior to endoscopy
• Ideally all patients admitted with upper gastrointestinal haemorrhage should undergo Upper GI endoscopy
within 24 hours of admission. In those who are unstable this should occur immediately after resuscitation or in
tandem with it. The endoscopy department is a potentially dangerous place for unstable patients and it may be
safer to perform the endoscopy in theatre with an anaesthetist present.
• Varices should be banded or subjected to sclerotherapy. If this is not possible owing to active bleeding, then a
Sengaksten- Blakemore tube (or Minnesota tube) should be inserted. This should be done with care; gastric
balloon should be inflated first and oesophageal balloon second. Remember the balloon will need deflating after
12 hours (ideally sooner) to prevent necrosis. Portal pressure should be lowered by combination of medical
therapy +/- TIPSS.
• Patients with erosive oesophagitis / gastritis should receive a proton pump inhibitor.
• Mallory Weiss tears will typically resolve spontaneously
• Identifiable bleeding points should receive combination therapy of injection of adrenaline and either a thermal
or mechanical treatment. All who have received intervention should receive a continuous infusion of a proton
pump inhibitor (IV omeprazole for 72 hours) to reduce the re-bleeding rate.
• Patients with diffuse erosive gastritis who cannot be managed endoscopically and continue to bleed may
require gastrectomy
• Bleeding ulcers that cannot be controlled endoscopically may require laparotomy and ulcer underruning
Indications for surgery

• Patients > 60 years
• Continued bleeding despite endoscopic intervention
• Recurrent bleeding
• Known cardiovascular disease with poor response to hypotension
Surgery
Duodenal ulcer
Laparotomy, duodenotomy and under running of the ulcer. If bleeding is brisk then the ulcer is almost always posteriorly
sited and will have invaded the gastroduodenal artery. Large bites using 0 Vicryl are taken above and below the ulcer
base to occlude the vessel. The duodenotomy should be longitudinal but closed transversely to avoid stenosis.
For gastric ulcer

Under-running of the bleeding site
Partial gastrectomy-antral ulcer
Partial gastrectomy or under running the ulcer- lesser curve ulcer (involving left gastric artery)
Total gastrectomy if bleeding persists
Summary of Acute Upper GI bleeding recommendations:

The need for admission and timing of endoscopic intervention may be predicted by using the Blatchford score. This
considers a patients Hb, serum urea, pulse rate and blood pressure. Those patients with a score of 0 are low risk, all
others are considered high risk and require admission and endoscopy.
The requirement for pre endoscopic proton pump inhibition is contentious. In the UK the National Institute of Clinical
Excellence guidelines suggest the pre endoscopic PPI therapy is unnecessary. Whilst it is accepted that such treatment
has no impact on mortality or morbidity a Cochrane review of this practice in 2007 did suggest that it reduced the
stigmata of recent haemorrhage at endoscopy. As a result, many will still administer PPI to patients prior to endoscopic
intervention.
Following endoscopy, it is important to calculate the Rockall score for patients to determine their risk of rebleeding and
mortality. A score of 3 or less is associated with a rebleeding rate of 4% and a very low risk of mortality and identifies a
group of patients suitable for early discharge.

152
Rockall Score
A patients should have their Rockall score calculated following endoscopy for upper GI haemorrhage
Mnemonic for Rockall score

ABCDE
A: Age
B: Blood pressure drop (Shock)
C: Co-morbidity
D: Diagnosis
E: Evidence of bleeding
Applies to upper gastrointestinal bleeding

Variable Score 0 Score 1 Score 2 Score 3
Age <60 60-79 >80
Shock None Pulse >100 Hypotension (systolic <100mmHg)
Co-Morbidity Nil or minimal Major organ disease e.g. IHD, CCF Renal or liver failure,
metastatic cancer
Diagnosis Mallory-Weiss All GI Cancer
Evidence of Bleeding None Clot, Blood, spurting vessel
Score <3 = Good prognosis (mortality approx. 2%)

Score >8= High mortality (Mortality approx. 40%)
Dysphagia
Extrinsic • Mediastinal masses
• Cervical spondylosis
Oesophageal wall • Achalasia
• Diffuse oesophageal spasm
• Hypertensive lower oesophageal sphincter
Intrinsic • Tumours
• Strictures
• Oesophageal web
• Schatzki rings
Neurological • CVA
• Parkinson's disease
• Multiple Sclerosis
• Brainstem pathology
• Myasthenia Gravis
Investigations
• All patients require an upper GI endoscopy unless there are compelling reasons for this not to be performed.
Motility disorders may be best appreciated by undertaking fluoroscopic swallowing studies.
• A full blood count should be performed.
• Ambulatory oesophageal pH and manometry studies will be required to evaluate conditions such as achalasia
and patients with GORD being considered for fundoplication surgery.

153
Bariatric Surgery
Obesity is a major health problem in the Western world. Surgical solutions to the problem have evolved dramatically over
the past few years. Randomised controlled trials have shown that dramatic weight loss can be achieved following surgical
interventions compared with standard medical therapy. The weight loss process is also more durable following surgery
than with non-surgical interventions.
Case selection
BMI >/= 40 kg/m2 or between 35-40 kg/m2 and other significant disease (for example, type 2 diabetes, hypertension) that
could be improved with weight loss.
Pre-requisites to surgery (NICE UK Guidelines)

• All non-surgical measures have failed to achieve or maintain adequate clinically beneficial weight loss for at least
6 months.
• Will receive intensive specialist management
• They are generally fit for anaesthesia and surgery
• They commit to the need for long-term follow-up
• First-line option for adults with a BMI > 40 kg/m2 in whom surgical intervention is considered appropriate;
consider orlistat if there is a long waiting list.
Surgical options
Adjustable gastric • Laparoscopic placement of adjustable band around proximal stomach.
band • Contains an adjustable filling port
• Effective method for lifestyle control
• Reversible
• Takes longer to achieve target weight
• Complications such as band erosion (rare), slippage or loss of efficacy may require re-
intervention
Gastric bypass • Combines changes to reservoir size with malabsorptive procedure for more enduring weight
loss.
• Technically more challenging
• Risks related to anastomoses (2% leak rate)
• Irreversible
• Up to 50% may become B12 deficient
Sleeve gastrectomy • Resection of stomach using stapling devices
• Less popular now as initial promising results not sustained

154
Gastric Cancer
Overview
There are 700,000 new cases of gastric cancer worldwide each year. It is most common in Japan and less common in
western countries. It is more common in men and incidence rises with increasing age. The exact cause of many sporadic
cancer is not known, however, familial cases do occur in HNPCC families. In addition, smoking and smoked or preserved
foods increase the risk. Japanese migrants retain their increased risk (decreased in subsequent generations). The
distribution of the disease in western countries is changing towards a more proximal location (perhaps due to rising
obesity).
Pathology
There is some evidence of support a stepwise progression of the disease through intestinal metaplasia progressing to
atrophic gastritis and subsequent dysplasia, through to cancer. The favoured staging system is TNM. The risk of lymph
node involvement is related to size and depth of invasion; early cancers confined to submucosa have a 20% incidence of
lymph node metastasis. Tumours of the gastro-oesophageal junction are classified as below:
Type 1 True oesophageal cancers and may be associated with Barrett's oesophagus.
Type 2 Carcinoma of the cardia, arising from cardiac type epithelium
or short segments with intestinal metaplasia at the oesophagogastric junction.
Type 3 Sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric cancer.
Groups for close endoscopic monitoring

• Intestinal metaplasia of columnar type
• Atrophic gastritis
• Low to medium grade dysplasia
• Patients who have previously undergone resections for benign peptic ulcer disease (except highly selective
vagotomy).
Referral to endoscopy
Patients of any age with dyspepsia and Patients without dyspepsia Worsening dyspepsia
any of the following
Chronic gastrointestinal bleeding Dysphagia Barretts oesophagus
Dysphagia Unexplained abdominal pain Intestinal metaplasia
or weight loss
Weight loss Vomiting Dysplasia
Iron deficiency anaemia Upper abdominal mass Atrophic gastritis
Upper abdominal mass Jaundice Patient aged over 55 years with unexplained
or persistent dyspepsia
Upper GI endoscopy performed for dyspepsia. The addition of dye spraying (as shown in the bottom right) may facilitate
identification of smaller tumours

155
Staging
• CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in most centres.
• Laparoscopy to identify occult peritoneal disease
• PET CT (particularly for junctional tumours)
Treatment
• Proximally sited disease greater than 5-10cm from the OG junction may be treated by subtotal gastrectomy
• Total gastrectomy if tumour is <5cm from OG junction
• For type 2 junctional tumours (extending into oesophagus) oesophagogastrectomy is usual
• Endoscopic sub mucosal resection may play a role in early gastric cancer confined to the mucosa and perhaps
the sub mucosa (this is debated)
• Lymphadenectomy should be performed. A D2 lymphadenectomy is widely advocated by the Japanese, the
survival advantages of extended lymphadenectomy have been debated. However, the overall recommendation
is that a D2 nodal dissection be undertaken.
• Most patients will receive chemotherapy either pre or post operatively.
Prognosis UK Data
Disease extent Percentage 5 year survival
All RO resections 54%
Early gastric cancer 91%
Stage 1 87%
Stage 2 65%
Stage 3 18%
Operative procedure
Total Gastrectomy , lymphadenectomy and Roux en Y anastomosis
General anaesthesia
Prophylactic intravenous antibiotics
Incision: Rooftop.
Perform a thorough laparotomy to identify any occult disease.
Mobilise the left lobe of the liver off the diaphragm and place a large pack over it. Insert a large self-retaining retractor
e.g. omnitract or Balfour (take time with this, the set up should be perfect). Pack the small bowel away.
Begin by mobilising the omentum off the transverse colon.
Proceed to detach the short gastric vessels.
Mobilise the pylorus and divide it at least 2cm distally using a linear cutter stapling device.
Continue the dissection into the lesser sac taking the lesser omentum and left gastric artery flush at its origin.
The lymph nodes should be removed en bloc with the specimen where possible.
Place 2 stay sutures either side of the distal oesophagus. Ask the anaesthetist to pull back on the nasogastric tube. Divide
the distal oesophagus and remove the stomach.
The oesphago jejunal anastomosis should be constructed. Identify the DJ flexure and bring a loop of jejunum up to the
oesophagus (to check it will reach). Divide the jejunum at this point. Bring the divided jejunum either retrocolic or
antecolic to the oesophagus. Anastamose the oesophagus to the jejunum, using either interrupted 3/0 vicryl or a stapling
device. Then create the remainder of the Roux en Y reconstruction distally.
Place a jejunostomy feeding tube.
Wash out the abdomen and insert drains (usually the anastomosis and duodenal stump). Help the anaesthetist insert the
nasogastric tube (carefully!)
Close the abdomen and skin.
Enteral feeding may commence on the first post-operative day. However, most surgeons will leave patients on free NG
drainage for several days and keep them nil by mouth.

156
Gastric Emptying
• The stomach serves both a mechanical and immunological function. Solid and liquid are retained in the stomach
during which time repeated peristaltic activity against a closed pyloric sphincter will cause fragmentation of food
bolus material. Contact with gastric acid will help to neutralise any pathogens present.
• The amount of time material spends in the stomach is related to its composition and volume. For example, a glass of
water will empty more quickly than a large meal. The presence of amino acids and fat will all serve to delay gastric
emptying.
Controlling factors
Neuronal stimulation of the stomach is mediated via the vagus and the parasympathetic nervous system will tend to
favor an increase in gastric motility. It is for this reason that individuals who have undergone truncal vagotomy will tend
to routinely require either a pyloroplasty or gastro-enterostomy as they would otherwise have delayed gastric emptying.
The following hormonal factors are all involved:

Delay emptying Increase emptying
Gastric inhibitory peptide Gastrin
Cholecystokinin
Enteroglucagon
Diseases affecting gastric emptying

All diseases that affect gastric emptying may result in bacterial overgrowth, retained food and eventually the formation
of bezoars that may occlude the pylorus and make gastric emptying even worse. Fermentation of food may cause
dyspepsia, reflux and foul smelling belches of gas.
Iatrogenic
Gastric surgery can have profound effects on gastric emptying. As stated above any procedure that disrupts the vagus
can cause delayed emptying. Whilst this is particularly true of vagotomy, this operation is now rarely performed.
Surgeons are divided on the importance of vagal disruption that occurs during an oesophagectomy, some will routinely
perform a pyloroplasty and others will not.
When a distal gastrectomy is performed, the type of anastomosis performed will impact on emptying. When a gastro-
enterostomy is constructed, a posterior, retrocolic gastroenterostomy will empty better than an anterior one.
Diabetic gastroparesis
This is predominantly due to neuropathy affecting the vagus nerve. The stomach empties poorly and patients may have
episodes of repeated and protracted vomiting. Diagnosis is made by upper GI endoscopy and contrast studies, in some
cases a radio nucleotide scan is needed to demonstrate the abnormality more clearly. In treating these conditions, drugs
such as metoclopramide will be less effective as they exert their effect via the vagus nerve. One of the few prokinetic
drugs that do not work in this way is the antibiotic erythromycin.
Malignancies
Obviously a distal gastric cancer may obstruct the pylorus and delay emptying. In addition, malignancies of the pancreas
may cause extrinsic compression of the duodenum and delay emptying. Treatment in these cases is by gastric
decompression using a wide bore nasogastric tube and insertion of a stent or, if that is not possible, by a surgical
gastroenterostomy. As a general rule gastroenterostomies constructed for bypass of malignancy are usually placed on
the anterior wall of the stomach (in spite of the fact that they empty less well). A Roux en Y bypass may also be
undertaken, but the increased number of anastomoses for this, in malignant disease that is being palliated, is probably
not justified.
Congenital Hypertrophic Pyloric Stenosis

This is typically a disease of infancy. Most babies will present around 6 weeks of age with projectile non bile stained
vomiting. It has an incidence of 2.4 per 1000 live births and is more common in males. Diagnosis is usually made by
careful history and examination and a mass may be palpable in the epigastrium (often cited seldom felt!). The most
important diagnostic test is an ultrasound that usually demonstrates the hypertrophied pylorus. Blood tests may reveal a
hypochloraemic metabolic alkalosis if the vomiting is long standing. Once the diagnosis is made the infant is resuscitated
and a pyloromyotomy is performed (either open or laparoscopically). Once treated there are no long term sequelae.

157
Lower Gastrointestinal Bleeding
Colonic bleeding
This typically presents as bright red or dark red blood per rectum. Colonic bleeding rarely presents as malaena type stool,
this is because blood in the colon has a powerful laxative effect and is rarely retained long enough for transformation to
occur and because the digestive enzymes present in the small bowel are not present in the colon. Up to 15% of patients
presenting with haemochezia will have an upper gastrointestinal source of haemorrhage.
As a general rule right sided bleeds tend to present with darker coloured blood than left sided bleeds. Haemorrhoidal
bleeding typically presents as bright red rectal bleeding that occurs post defecation either onto toilet paper or into the
toilet pan. It is very unusual for haemorrhoids alone to cause any degree of haemodynamic compromise.
Causes
Colitis Bleeding may be brisk in advanced cases, diarrhoea is commonly present. Abdominal x-ray may
show featureless colon.
Diverticular disease Acute diverticulitis often is not complicated by major bleeding and diverticular bleeds often occur
sporadically. 75% all will cease spontaneously within 24-48 hours. Bleeding is often dark and of large
volume.
Cancer Colonic cancers often bleed and for many patients this may be the first sign of the disease. Major
bleeding from early lesions is uncommon
Haemorrhoidal Typically bright red bleeding occurring post defecation. Although patients may give graphic
bleeding descriptions bleeding of sufficient volume to cause haemodynamic compromise is rare.
Angiodysplasia Apart from bleeding, which may be massive, these arteriovenous lesions cause little in the way of
symptoms. The right side of the colon is more commonly affected.
Management
• Prompt correction of any haemodynamic compromise is required. Unlike upper gastrointestinal bleeding the
first line management is usually supportive. This is because in the acute setting endoscopy is rarely helpful.
• When haemorrhoidal bleeding is suspected a proctosigmoidoscopy is reasonable as attempts at full
colonoscopy are usually time consuming and often futile.
• In the unstable patient the usual procedure would be an angiogram (either CT or percutaneous), when these
are performed during a period of haemodynamic instability they may show a bleeding point and may be the
only way of identifying a patch of angiodysplasia.
• In others who are more stable the standard procedure would be a colonoscopy in the elective setting. In
patients undergoing angiography attempts can be made to address the lesion in question such as coiling.
Otherwise surgery will be necessary.
• In patients with ulcerative colitis who have significant haemorrhage the standard approach would be a sub total
colectomy, particularly if medical management has already been tried and is not effective.

Patients > 60 years
Continued bleeding despite endoscopic intervention
Recurrent bleeding
Known cardiovascular disease with poor response to hypotension
Surgery
Selective mesenteric embolisation if life threatening bleeding. This is most helpful if conducted during a period of relative
haemodynamic instability. If all haemodynamic parameters are normal then the bleeding is most likely to have stopped
and any angiography normal in appearance. In many units a CT angiogram will replace selective angiography but the
same caveats will apply.
If the source of colonic bleeding is unclear; perform a laparotomy, on table colonic lavage and following this attempt a
resection. A blind sub total colectomy is most unwise, for example bleeding from an small bowel arterio-venous
malformation will not be treated by this manoeuvre.

158
Summary of Acute Lower GI bleeding recommendations
Consider admission if:
* Over 60 years
* Haemodynamically unstable/profuse PR bleeding
* On aspirin or NSAID
* Significant co morbidity
Management
• All patients should have a history and examination, PR and proctoscopy
• Colonoscopic haemostasis aimed for in post polypectomy or diverticular bleeding
Oesophageal Disease
Disorder Features
Mallory-Weiss Tear Usually history of antecedent vomiting. This is then followed by the vomiting of a small
amount of blood. There is usually little in the way of systemic disturbance or prior symptoms.
Hiatus hernia of gastric Often longstanding history of dyspepsia, patients are often overweight. Uncomplicated hiatus
cardia hernias should not be associated with dysphagia or haematemesis.
Oesophageal rupture Complete disruption of the oesophageal wall in absence of pre-existing pathology. Left
postero-lateral oesophageal is commonest site (2-3cm from OG junction). Suspect in patients
with severe chest pain without cardiac diagnosis and signs suggestive of pneumonia without
convincing history, where there is history of vomiting. Erect CXR shows infiltrate or effusion in
90% of cases.
Squamous cell carcinoma History of progressive dysphagia. Often signs of weight loss. Usually little or no history of
of the oesophagus previous GORD type symptoms. (↑ risk é achalasia)
Adenocarcinoma of the Progressive dysphagia, may have previous symptoms of GORD or Barrett’s oesophagus.
oesophagus
Peptic stricture Longer history of dysphagia, often not progressive. Usually symptoms of GORD. Often lack
systemic features seen with malignancy
Dysmotility disorder May have dysphagia that is episodic and non-progressive. Retrosternal pain may accompany
the episodes.
Diagnosis
Most of the differential diagnoses listed above can be accurately categorised by upper GI endoscopy (usually most
patients). Where this fails to demonstrate a mechanical stricture the use of pH and manometry studies together with
radiological contrast swallows will facilitate the diagnosis.

159
Oesophageal Cancer - Treatment
Treatments for SCC's and adenocarcinomas of the oesophagus differ. This is primarily due to the positive outcomes that
are observed when localised SCC's (particularly of the proximal oesophagus are treated with radical Chemoradiotherapy,
obviating the need for surgery).
Only those patients whose staging investigations are negative for metastatic disease should be considered for surgery.
Surgical options
Endoscopic mucosal Treatment for early localised adenocarcinoma of the distal oesophagus. Survival mirrors that of
resection surgical resection for Tis and T1 disease
Transhiatal Most commonly used for junctional (type II) tumours where limited thoracic oesophageal
oeosphagectomy resection is required. Less morbidity than two field oesophagectomy
Ivor Lewis Two stage approach for middle and distal tumours. Very commonly performed, intrathoracic
oesophagectomy anastomosis will result in mediastinitis in event of anastomotic leak. Lower incidence of recurrent
laryngeal nerve injury
McKeown Three field approach, may be useful for proximal tumours. Anastomotic leakage is less serious.
oesophagectomy Higher incidence of recurrent laryngeal nerve injury
Neoadjuvant and adjuvant treatment

• Neoadjuvant radiotherapy alone prior to resection confers little benefit and is not routinely performed
• Preoperative chemotherapy is associated with a survival advantage (OE02 trial)
• Peri operative (pre and post-operative) chemotherapy confers a survival advantage in junctional tumours
• Post-operative chemotherapy is not generally recommended following oesophageal resections outside clinical
trials
Palliation strategies
• Combination chemotherapy improves quality of life and survival in non-operable disease
• Trastuzumab may improve survival in patients with HER 2 positive tumours
• Oesophageal intubation with self-expanding metal stents is the treatment of choice in patients with occluding
tumours >2cm from the cricopharyngeus
• Covered metal stents are useful in cases of malignant fistulas
• Laser therapy and argon plasma coagulation may be useful as therapies for tumour overgrowth and bleeding
• Photodynamic therapy and ethanol injections confer little benefit and should not be routinely used

160
Nutrition Options in Surgical Patients
Oral intake • Easiest option
• May be supplemented by calorie rich dietary supplements
• May contra indicated following certain procedures
Naso gastric feeding • Usually administered via fine bore naso gastric feeding tube
(NGT) • Complications relate to aspiration of feed or misplaced tube
• May be safe to use in patients with impaired swallow
• Often contra indicated following head injury due to risks associated with tube insertion
Naso jejunal feeding • Avoids problems of feed pooling in stomach (and risk of aspiration)
• Insertion of feeding tube more technically complicated (easiest if done intra operatively)
• Safe to use following oesophagogastric surgery
Feeding jejunostomy • Surgically sited feeding tube
• May be used for long term feeding
• Low risk of aspiration and thus safe for long term feeding following upper GI surgery
• Main risks are those of tube displacement and peritubal leakage immediately following
insertion, which carries a risk of peritonitis
Percutaneous endoscopic • Combined endoscopic and percutaneous tube insertion
gastrostomy • May not be technically possible in those patients who cannot undergo successful
(PEG) endoscopy
• Risks include aspiration and leakage at the insertion site
Total parenteral nutrition • The definitive option in those patients in whom enteral feeding is contra indicated
(TPN) • Individualised prescribing and monitoring needed
• Should be administered via a central vein as it is strongly phlebitic
• Long term use is associated with fatty liver and deranged LFT's

161
13. Hepatobiliary and pancreatic surgery – MRCS Notes - Reda

Benign Liver Lesions........................................................................................................................................ 2
Biliary Disease ................................................................................................................................................. 3
Surgical Jaundice ............................................................................................................................................. 4
Gallstones........................................................................................................................................................ 6
Notes and Mnemonics .................................................................................................................................... 7
Pancreatic Cancer ........................................................................................................................................... 8
Management of Acute Pancreatitis in The UK............................................................................................... 9
Pancreatitis: Sequelae .................................................................................................................................. 10
13. HEPATOBILIARY AND PANCREATIC SURGERY – MRCS NOTES - REDA 1

162
Benign Liver Lesions
Haemangioma • Most common benign tumours of mesenchymal origin
• Incidence in autopsy series is 8%
• Cavernous haemangiomas may be enormous
• Clinically they are reddish purple hypervascular lesions
• Lesions are normally separated from normal liver by ring of fibrous tissue
• On ultrasound they are typically hyperechoic. Serum AFP normal.
Liver cell • 90% develop in women in their third to fifth decade
adenoma • Linked to use of oral contraceptive pill
• Lesions are usually solitary
• They are usually sharply demarcated from normal liver although they usually lack a fibrous capsule
• On ultrasound the appearances are of mixed echoity and heterogeneous texture. On CT most
lesions are hypodense when imaged prior to administration of IV contrast agents
• In patients with haemorrhage or symptoms removal of the adenoma may be required
Mesenchymal Congential and benign, usually present in infants. May compress normal liver
hamartomas
Liver abscess • Biliary sepsis is a major predisposing factor
• Structures drained by the portal venous system form the second largest source
• Common symptoms include fever, right upper quadrant pain. Jaundice may be seen in 50%
• Ultrasound will usually show a fluid filled cavity, hyperechoic walls may be seen in chronic
abscesses
Amoebic • Liver abscess is the most common extra intestinal manifestation of amoebiasis
abscess • Between 75 and 90% lesions occur in the right lobe
• Presenting complaints typically include fever and right upper quadrant pain
• Ultrasonography will usually show a fluid filled structure with poorly defined boundaries
• Aspiration yield sterile odourless fluid which has an anchovy paste consistency
• Treatment is with metronidazole
Hydatid cysts • Seen in cases of tapeworm parasite Echinococcus granulosus infection
• Typically, an intense fibrotic reaction occurs around sites of infection
• The cyst has no epithelial lining
• Cysts are commonly unilocular and may grow to 20cm in size. The cyst wall is thick and has an
external laminated hilar membrane and an internal enucleated germinal layer
• These cysts are allergens which precipitate a type 1 hypersensitivity
• In biliary ruputure there may be the classical triad of: Biliary colic, Jaundice, and Urticaria
• Typically presents with malaise and right upper quadrant pain. Secondary bacterial infection occurs
in 10%.
• Liver function tests are usually abnormal and eosinophilia is present in 33% cases
• Ultrasound may show septa and hydatid sand or daughter cysts.
• CT is the best investigation to differentiate hydatid cysts from amoebic and pyogenic cysts.
• Percutaneous aspiration is contra indicated
• Treatment is by sterilisation of the cyst with mebendazole and may be followed by surgical
resection. Hypertonic swabs are packed around the cysts during surgery
Polycystic liver • Usually occurs in association with polycystic kidney disease
disease • Autosomal dominant disorder
• Symptoms may occur as a result of capsular stretch
Cystadenoma • Rare lesions with malignant potential
• Usually solitary multiloculated lesions
• Liver function tests usually normal
• Ultrasonography typically shows a large anechoic, fluid filled area with irregular margins. Internal
echos may result from septa
• Surgical resection is indicated in all cases

163
Biliary Disease
Diagnosis Typical features Pathogenesis
Gallstones Typically history of biliary Usually small calibre gallstones which can pass through the
colic or episodes of cystic duct. In Mirizzi syndrome the stone may compress the
chlolecystitis. Obstructive bile duct directly- one of the rare times that cholecystitis may
type history and test results. present with jaundice
Cholangitis Usually obstructive and will Ascending infection of the bile ducts usually by E. coliand by
have Charcot's triad of definition occurring in a pool of stagnant bile.
symptoms (pain, fever,
jaundice)
Pancreatic cancer Typically painless jaundice Direct occlusion of distal bile duct or pancreatic duct by
with palpable gallbladder tumour. Sometimes nodal disease at the portal hepatis may be
(Courvoisier's Law) the culprit in which case the bile duct may be of normal
calibre.
TPN (total parenteral Usually follows long term Often due to hepatic dysfunction and fatty liver which may
nutrition) associated use and is usually painless occur with long term TPN usage.
jaundice with non-obstructive
features
Bile duct injury Depending upon the type of Often due to a difficult laparoscopic cholecystectomy when
injury may be of sudden or anatomy in Calot’s triangle is not appreciated. In the worst
gradual onset and is usually scenario the bile duct is excised and jaundice develops rapidly
of obstructive type post operatively. More insidious is that of bile duct stenosis
which may be caused by clips or diathermy injury.
Cholangiocarcinoma Gradual onset obstructive Direct occlusion by disease and also extrinsic compression by
pattern nodal disease at the porta hepatis.
Septic surgical patient Usually hepatic features Combination of impaired biliary excretion and drugs such as
ciprofloxacin which may cause cholestasis.
Metastatic disease Mixed hepatic and post Combination of liver synthetic failure (late) and extrinsic
hepatic compression by nodal disease and anatomical compression of
intra hepatic structures (earlier)

164
Surgical Jaundice
Jaundice can present in a manner of different surgical situations. As with all types of jaundice a careful history and
examination will often give clues as to the most likely underlying cause. Liver function tests whilst conveying little in the
way of information about liver synthetic function, will often facilitate classification as to whether the jaundice is pre
hepatic, hepatic or post hepatic. The typical LFT patterns are given below:
Location Bilirubin ALT/ AST Alkaline phosphatase
Pre hepatic Normal or high Normal Normal
Hepatic High Elevated (often very high) Elevated but seldom to very high levels
Post hepatic High-very high Moderate elevation High- very high
In post hepatic jaundice the stools are often of pale colour and this feature should be specifically addressed in the
history.
Modes of presentation
These are addressed in the table (see previous page)
Diagnosis
An ultrasound of the liver and biliary tree is the most commonly used first line test. This will establish bile duct calibre,
often ascertain the presence of gallstones, may visualise pancreatic masses and other lesions. The most important
clinical question is essentially the extent of biliary dilatation and its distribution.
Where pancreatic neoplasia is suspected, the next test should be a pancreatic protocol CT scan. With liver tumours and
cholangiocarcinoma an MRI/ MRCP is often the preferred option. PET scans may be used to stage a number of
malignancies but do not routinely form part of first line testing.
Where MRCP fails to give adequate information an ERCP may be necessary. In many cases this may form part of patient
management. It is however, invasive and certainly not without risk and highly operator dependent.

165
Management
Clearly this will depend to an extent upon the underlying cause but relief of jaundice is important, even if surgery forms
part of the planned treatment. Patients with unrelieved jaundice have a much higher incidence of septic complications,
bleeding and death.
Screen for and address any clotting irregularities
In patients with malignancy a stent will need to be inserted. These come in two main types; metal and plastic. Plastic
stents are cheap and easy to replace and should be used if any surgical intervention (e.g. Whipples) is planned. However,
they are prone to displacement and blockage. Metal stents are much more expensive and may compromise a surgical
resection. However, they are far less prone to displacement and to a lesser extent blockage than their plastic
counterparts.
If malignancy is in bile duct/ pancreatic head and stenting has been attempted and has failed, then an alternative
strategy is to drain the biliary system percutaneously via a transhepatic route. It may also be possible to insert a stent in
this way. One of the main problems with temporary PTC's is their propensity to displacement, which may result in a bile
leak.
In patients who have a bile duct injury surgery will be required to repair the defect. If the bile duct has been
inadvertently excised then a hepatico-jejunostomy will need to be created (difficult!)
If gallstones are the culprit, then these may be removed by ERCP and a cholecystectomy performed. Where there is
doubt about the efficacy of the ERCP an operative cholangiogram should be performed and bile duct exploration
undertaken where stones remain. When the bile duct has been formally opened the options are between closure over a
T tube, a choledochoduodenostomy or choledochojejunostomy.
Patients with cholangitis should receive high dose broad spectrum antibiotics via the intravenous route. Biliary
decompression should follow soon afterwards, instrumenting the bile duct of these patients will often provoke a septic
episode (but should be done anyway).

166
Gallstones
Up to 24% of women and 12% of men may have gallstones. Of these up to 30% may develop local infection and
cholecystitis. In patients subjected to surgery 12% will have stones contained within the common bile duct. The majority
of gallstones are of a mixed composition (50%) with pure cholesterol stones accounting for 20% of cases.
The aetiology of CBD stones differs in the world, in the West most CBD stones are the result of migration. In the East a far
higher proportion arise in the CBD de novo.
The classical symptoms are of colicky right upper quadrant pain that occurs post prandially. The symptoms are usually
worst following a fatty meal when cholecystokinin levels are highest and gallbladder contraction is maximal.
Investigation
In almost all suspected cases the standard diagnostic work up consists of abdominal ultrasound and liver function tests.
Of patients who have stones within the bile duct, 60% will have at least one abnormal result on LFT's. Ultrasound is an
important test, but is operator dependent and therefore may occasionally need to be repeated if a negative result is at
odds with the clinical picture. Where stones are suspected in the bile duct, the options lie between magnetic resonance
cholangiography and intraoperative imaging. The choice between these two options is determined by the skills and
experience of the surgeon. The advantages of intra operative imaging are less useful in making therapeutic decisions if
the operator is unhappy about proceeding the bile duct exploration, and in such circumstances pre operative MRCP is
probably a better option.
Specific gallstone and gallbladder related disease

Disease Features Management
Biliary colic Colicky abdominal pain, worse post prandially, If imaging shows gallstones and history compatible
worse after fatty foods then laparoscopic cholecystectomy
Acute • Right upper quadrant pain Imaging (USS) and cholecystectomy (ideally within
cholecystitis • Fever 48 hours of presentation) (2)
• Murphys sign on examination
• Occasionally mildly deranged LFT's (especially
if Mirizzi syndrome)
Gallbladder • Usually prodromal illness and right upper Imaging with USS +/- CT Scanning
abscess quadrant pain Ideally surgery, subtotal cholecystectomy may be
• Swinging pyrexia needed if Calots triangle is hostile
• Patient may be systemically unwell In unfit patients percutaneous drainage may be
• Generalised peritonism not present considered
Cholangitis • Patient severely septic and unwell • Fluid resuscitation
• Jaundice • Broad spectrum intravenous antibiotics
• Right upper quadrant pain • Correct any coagulopathy
• Early ERCP
Gallstone • Patients may have a history of previous Laparotomy and removal of gallstone from small
ileus cholecystitis and known gallstones bowel, the enterotomy must be made proximal to
• Small bowel obstruction (may be intermittent) the site of obstruction and not at the site of
obstruction. The fistula between the gallbladder
and duodenum should not be interfered with.
Acalculous • Patients with inter current illness (e.g. If patient fit then cholecystectomy, if unfit then
cholecystitis diabetes, organ failure) percutaneous cholecystostomy
• Patient of systemically unwell
• Gallbladder inflammation in absence of
stones
• High fever

167
Treatment
Patients with asymptomatic gallstones rarely develop symptoms related to them (less than 2% per year) and may
therefore be managed expectantly. In almost all cases of symptomatic gallstones the treatment of choice is
cholecystectomy performed via the laparoscopic route. In the very frail patient there is sometimes a role for selective use
of ultrasound guided cholecystostomy.
During the course of the procedure some surgeons will routinely perform either intra operative cholangiography or
laparoscopic USS to either confirm anatomy or to exclude CBD stones. The latter may be more easily achieved by use of
laparoscopic ultrasound. If stones are found then the options lie between early ERCP in the day or so following surgery or
immediate surgical exploration of the bile duct. When performed via the trans cystic route this adds little in the way of
morbidity and certainly results in faster recovery. Where transcystic exploration fails the alternative strategy is that of
formal choledochotomy. The exploration of a small duct is challenging and ducts of less than 8mm should not be
explored. Small stones that measure less than 5mm may be safely left and most will pass spontaneously.
Risks of ERCP
• Bleeding 0.9% (rises to 1.5% if sphincterotomy performed)
• Duodenal perforation 0.4%
• Cholangitis 1.1%
• Pancreatitis 1.5%
Notes and Mnemonics

Courvoisiers Law:
Obstructive jaundice in the presence of a palpable gallbladder is unlikely to be due to stones.
This is due to the fibrotic effect that stones have on the gallbladder. Like all these laws there are numerous exceptions
and many cases will not present in the typical manner.
The development of jaundice in association with a smooth right upper quadrant mass is typical of distal biliary
obstruction secondary to pancreatic malignancy
Mnemonic for the assessment of the severity of pancreatitis: PANCREAS

P a02 < 60 mmHg
A ge > 55 years
N eutrophils > 15 x 10/l
C alcium < 2 mmol/l
R aised urea > 16 mmol/l
E nzyme (lactate dehydrogenase) > 600 units/l
A lbumin < 32 g/l
S ugar (glucose) > 10 mmol/l
> 3 positive criteria indicates severe pancreatitis.
Acute early fluid collections are seen in 25% of patients with pancreatitis and require no specific treatment. Attempts at
drainage may introduce infection and result in pancreatic abscess formation.
In Mirizzi syndrome the gallstone becomes impacted in Hartmans pouch. Episodes of recurrent inflammation occur and
this causes compression of the bile duct. In severe cases this then progresses to fistulation. Surgery is extremely difficult
as Calots triangle is often completely obliterated and the risks of causing injury to the CBD are high.

168
Pancreatic Cancer
• Adenocarcinoma (ductal epithelial origin)
• Risk factors: Smoking, diabetes, adenoma, familial adenomatous polyposis
• Mainly occur in the head of the pancreas (70%)
• Spread locally and metastasizes to the liver
• Carcinoma of the pancreas should be differentiated from other periampullary tumours with better prognosis
Clinical features
• Weight loss
• Painless jaundice
• Epigastric discomfort (pain usually due to invasion of the coeliac plexus is a late feature)
• Pancreatitis
• Trousseau's sign: migratory superficial thrombophlebitis
Investigations
• USS: May miss small lesions
• CT Scanning (pancreatic protocol). If unresectable on CT then no further staging needed
• PET/CT for those with operable disease on CT alone
• ERCP/ MRI for bile duct assessment
• Staging laparoscopy to exclude peritoneal disease
Management
• Head of pancreas: Whipple's resection (SE dumping and ulcers). Newer techniques include pylorus preservation
and SMA/ SMV resection
• Carcinoma body and tail: poor prognosis, distal pancreatectomy, if operable
• Usually adjuvent chemotherapy for resectable disease
• ERCP and stent for jaundice and palliation
• Surgical bypass may be needed for duodenal obstruction
Whipple's Procedure

169
Management of Acute Pancreatitis in The UK
Diagnosis
• Traditionally hyperamylasaemia has been utilised with amylase being elevated three times the normal range.
• However, amylase may give both false positive and negative results.
• Serum lipase is both more sensitive and specific than serum amylase. It also has a longer half-life.
• Serum amylase levels do not correlate with disease severity.
Differential causes of hyperamylasaemia

• Pancreatic pseudocyst
• Mesenteric infarct
• Perforated viscus
• Acute cholecystitis
• Diabetic ketoacidosis
Assessment of severity
• Glasgow, Ranson scoring systems and APACHE II
• Biochemical scoring e.g. using CRP
Features that may predict a severe attack within 48 hours of admission to hospital
Initial assessment • Clinical impression of severity
• Body mass index >30
• Pleural effusion
• APACHE score >8
24 hours after admission • Clinical impression of severity
• APACHE II >8
• Glasgow score of 3 or more
• Persisting multiple organ failure
• CRP>150
48 hours after admission • Glasgow Score of >3
• CRP >150
• Persisting or progressive organ failure
Management
Nutrition
• There is reasonable evidence to suggest that the use of enteral nutrition does not worsen the outcome in
pancreatitis
• Most trials to date were underpowered to demonstrate a conclusive benefit.
• The rationale behind feeding is that it helps to prevent bacterial translocation from the gut, thereby
contributing to the development of infected pancreatic necrosis.
Use of antibiotic therapy

• Many UK surgeons administer antibiotics to patients with acute pancreatitis. However, there is very little
evidence to support this practice.
• A recent Cochrane review highlights the potential benefits of administering Imipenem to patients with
established pancreatic necrosis in the hope of averting the progression to infection.
• There are concerns that the administration of antibiotics in mild attacks of pancreatitis will not affect outcome
and may contribute to antibiotic resistance and increase the risks of antibiotic associated diarrhoea.
Surgery
• Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy.
• Patients with obstructed biliary system due to stones should undergo early ERCP.
• Patients with extensive necrosis where infection is suspected should usually undergo FNA for culture.
• Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy. The choice
of procedure depends upon local expertise.

170
Pancreatitis: Sequelae
Peripancreatic • Occur in 25% cases
fluid collections • Located in or near the pancreas and lack a wall of granulation or fibrous tissue
• May resolve or develop into pseudocysts or abscesses
• Since most resolve aspiration and drainage is best avoided as it may precipitate infection
Pseudocysts • In acute pancreatitis result from organisation of peripancreatic fluid collection. They may or may
not communicate with the ductal system.
• The collection is walled by fibrous or granulation tissue and typically occurs 4 weeks or more
after an attack of acute pancreatitis
• Most are retrogastric
• 75% are associated with persistent mild elevation of amylase
• Investigation is with CT, ERCP and MRI or Endoscopic USS
• Symptomatic cases may be observed for 12 weeks as up to 50% resolve
• Treatment is either with endoscopic or surgical cystogastrostomy or aspiration
Pancreatic • Pancreatic necrosis may involve both the pancreatic parenchyma and surrounding fat
necrosis • Complications are directly linked to extent of parenchymal necrosis and extent of necrosis
overall
• Early necrosectomy is associated with a high mortality rate (and should be avoided unless
compelling indications for surgery exist)
• Sterile necrosis should be managed conservatively (at least initially)
• Some centres will perform fine needle aspiration sampling of necrotic tissue if infection is
suspected. False negatives may occur. The extent of sepsis and organ dysfunction may be a
better guide to surgery
Pancreatic • Intra-abdominal collection of pus associated with pancreas but in the absence of necrosis
abscess • Typically occur as a result of infected pseudocyst
• They are usually managed by placement of percutaneous drains
Haemorrhage • Infected necrosis may involve vascular structures with resultant haemorrhage that may occur de
novo or as a result of surgical necrosectomy.
• When retroperitoneal haemorrhage occurs Grey Turners sign may be identified
Acute pancreatitis is known to precipitate ARDS. ARDS is characterised by bilateral pulmonary infiltrates and hypoxaemia.
Note that pulmonary oedema is excluded by the CVP reading < 18mmHg.

171
14. Colorectal Surgery – MRCS Notes - Reda

Ano Rectal Disease.......................................................................................................................................... 2
Benign Proctology ........................................................................................................................................... 3
Rectal Bleeding ............................................................................................................................................... 4
Pilonidal Sinus ................................................................................................................................................. 5
Colonic Polyps ................................................................................................................................................. 6
Polyposis Syndromes ...................................................................................................................................... 7
Laxatives.......................................................................................................................................................... 7
Genetics of Colorectal Cancer ........................................................................................................................ 8
Colorectal Cancer Screening and Diagnosis ................................................................................................... 9
Dukes Classification ........................................................................................................................................ 9
Colorectal Cancer Treatment Summary of Procedures ............................................................................... 10
Crohn’s Disease ............................................................................................................................................. 12
Ulcerative Colitis ........................................................................................................................................... 13
14. COLORECTAL SURGERY – MRCS NOTES - REDA 1

172
Ano Rectal Disease
Location: 3, 7, 11 o'clock position
Haemorrhoids Internal or external
Treatment: Conservative, Rubber band ligation, Haemorrhoidectomy
Fissure in ano Location: midline 6 (posterior midline 90%) and 12 o'clock position. Distal to the dentate line
Chronic fissure > 6/52: triad: Ulcer, sentinel pile, enlarged anal papillae
Proctitis Causes: Crohn's, ulcerative colitis, Clostridium difficile
Ano rectal E.coli, staph aureus
abscess Positions: Perianal, Ischiorectal, Pelvirectal, Intersphincteric
Anal fistula Usually due to previous ano-rectal abscess
Intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric. Goodsalls rule determines
location
Rectal prolapse Associated with childbirth and rectal intussceception. May be internal or external
Pruritus ani Systemic and local causes
Anal neoplasm Squamous cell carcinoma commonest unlike adenocarcinoma in rectum
Solitary rectal Associated with chronic straining and constipation. Histology shows mucosal thickening, lamina propria
ulcer replaced with collagen and smooth muscle (fibromuscular obliteration)
Rectal prolapse
• Common especially in multiparous women.
• May be internal or external.
• Internal rectal prolapse can present insidiously.
• External prolapse can ulcerate and in long term impair continence.
• Diagnostic work up includes colonoscopy, defecating proctogram, ano rectal manometry studies and if doubt
exists an examination under anaesthesia.
• Treatments for prolapse
• In the acute setting reduce it (covering it with sugar may reduce swelling.
• Delormes procedure which excises mucosa and plicates the rectum (high recurrence rates) may be used for
external prolapse.
• Altmeirs procedure which resects the colon via the perineal route has lower recurrence rates but carries
the risk of anastamotic leak.
• Rectopexy is an abdominal procedure in which the rectum is elevated and usually supported at the level of
the sacral promontory. Post-operative constipation may be reduced by limiting the dissection to the
anterior plane (laparoscopic ventral mesh
rectopexy).
Pruritus ani
• Extremely common.
• Check not secondary to altered bowel habits (e.g.
Diarrhoea)
• Associated with underlying diseases such as
haemorrhoids.
• Examine to look for causes such as worms.
• Proctosigmoidoscopy to identify associated
haemorrhoids and exclude cancer.
• Treatment is largely supportive and patients should
avoid using perfumed products around the area.
Fissure in ano
• Typically painful PR bleeding (bright red).
• Nearly always in the posterior midline.
• Usually solitary.
• Treatment Goodsall's rule for anal fistula
• Stool softeners.
• Topical diltiazem (or GTN).
• If topical treatments fail, then botulinum toxin should be injected.
• If botulinum toxin fails, then males should probably undergo lateral internal sphincterotomy.
• Females who do not respond to botulinum toxin should undergo ano rectal manometry studies and endo
anal USS prior to being offered surgery such as sphincterotomy.

173
Benign Proctology
Condition Features Treatment
Fissure in ano Painful, bright red rectal bleeding Stool softeners, topical diltiazem or GTN, botulinum
toxin, Sphincterotomy
Haemorroids Painless, bright red rectal bleeding occurs Stool softeners, avoid straining, surgery (see below)
following defecation and bleeds onto the (Stapled haemorroidopexy, Milligan Morgan
toilet paper and into the toilet pan haemorroidectomy)
Fistula in ano May initially present with an abscess and then • Lay open if low, no sphincter involvement nor IBD.
persisting discharge onto the perineum, • Insert seton if complex, high or IBD, and consider
separate from the anus other options (see below).
• Don’t probe during acute sepsis.
Peri anal Peri anal swelling and surrounding erythema Incision and drainage, leave the cavity open to heal
abscess by secondary intention
Pruritus ani Peri anal itching, occasional mild bleeding (if Avoid scented products, use wet wipes rather than
severe skin damage) tissue, avoidance of scratching, ensure no underlying
faecal incontinence
Overview of surgical therapies

Haemorroidal disease
The treatment of haemorroids is usually conservative. Acutely thrombosed haemorroids may be extremely painful.
Treatment of this acute condition is usually conservative and consists of stool softeners, ice compressions and topical
GTN or diltiazem to reduce sphincter spasm. Most cases managed with this approach will settle over the next 5-7 days.
After this period there may be residual skin tags that merit surgical excision or indeed residual haemorroidal disease that
may necessitate haemorroidectomy.
Patients with more chronic symptoms are managed according to the stage of their disease, small mild internal
haemorroids causing little symptoms are best managed conservatively. More marked symptoms of bleeding and
occasional prolapse, where the haemorroidal complex is largely internal may benefit from stapled haemorroidopexy. This
procedure excises rectal tissue above the dentate line and disrupts the haemorroidal blood supply. At the same time the
excisional component of the procedure means that the haemorroids are less prone to prolapse. Adverse effects of this
procedure include urgency, which can affect up to 40% of patients (but settles over 6-12 months) and recurrence. The
procedure does not address skin tags and therefore this procedure is unsuitable if this is the dominant symptom.
Large haemorroids with a substantial external component may be best managed with a Milligan Morgan style
conventional haemorroidectomy. In this procedure three haemorroidal cushions are excised, together with their vascular
pedicle. Excision of excessive volumes of tissue may result in anal stenosis. The procedure is quite painful and most
surgeons prescribe metronidazole post operatively as it decreases post-operative pain.
Fissure in ano
Probably the most efficient and definitive treatment for fissure in ano is lateral internal sphincterotomy. The treatment is
permanent and nearly all patients will recover. Up to 30% will develop incontinence to flatus. There are justifiable
concerns about using this procedure in females as pregnancy and pelvic floor damage together with a sphincterotomy
may result in faecal incontinence. The usual first line therapy is relaxation of the internal sphincter with either GTN or
diltiazem (the latter being better tolerated) applied topically for 6 weeks. Treatment failures with topical therapy will
usually go on to have treatment with botulinum toxin. This leads to more permanent changes in the sphincter and this
may facilitate healing.
Typical fissures usually present in the posterior midline, multiple or unusually located fissures should prompt a search for
an underlying cause such as inflammatory bowel disease or internal prolapse.
Refractory cases where the above treatments have failed may be considered for advancement flaps.
Fistula in ano
The most effective treatment for fistula is laying it open (fistulotomy). When the fistula is below the sphincter and
uncomplicated, this is a reasonable option. Sphincter involvement and complex underlying disease should be assessed
both surgically and ideally with imaging (either MRI or endoanal USS). Surgery is then usually staged, in the first instance
a draining seton suture may be inserted. This avoids the development of recurrent sepsis and may allow resolution. In
patients with Crohns disease the seton should be left in situ long term and the patient managed medically, as in these
cases attempts at complex surgical repair nearly always fail. Fistulas not associated with IBD may be managed by
advancement flaps, instillation of plugs and glue is generally unsuccessful. A newer technique of ligation of
intersphincteric tract (LIFT procedure) is reported to have good results in selected centres.

174
Rectal Bleeding
Rectal bleeding is a common cause for patients to be referred to the surgical clinic. In the clinical history it is useful to try
and localise the anatomical source of the blood. Bright red blood is usually of rectal anal canal origin, whilst dark red
blood is more suggestive of a proximally sited bleeding source. Blood which has entered the GI tract from a gastro-
duodenal source will typically resemble malaena due to the effects of the digestive enzymes on the blood itself.
Cause Type of bleeding Features in history Examination findings

Fissure in ano Bright red rectal Painful bleeding that occurs post Muco-epithelial defect usually in the
bleeding defecation in small volumes. Usually midline posteriorly (anterior fissures more
antecedent features of constipation likely to be due to underlying disease)
Haemorroids Bright red rectal Post defecation bleeding noted both on Normal colon and rectum. Proctoscopy may
bleeding toilet paper and drips into pan. May be show internal haemorrhoids. Internal
alteration of bowel habit and history of haemorrhoids are usually impalpable.
straining. No blood mixed with stool. No
local pain.
Crohns Bright red or Bleeding that is accompanied by other Perineal inspection may show fissures or
disease mixed blood symptoms such as altered bowel habit, fistulae. Proctoscopy may demonstrate
malaise, history of fissures (especially indurated mucosa and possibly strictures.
anterior) and abscesses. Skip lesions may be noted at colonoscopy.
Ulcerative Bright red Diarrhoea, weight loss, nocturnal Proctitis is the most marked finding. Peri
colitis bleeding often incontinence, passage of mucous PR. anal disease is usually absent. Colonoscopy
mixed with stool will show continuous mucosal lesion.
Rectal cancer Bright red blood Alteration of bowel habit. Tenesmus may Usually obvious mucosal abnormality.
mixed volumes be present. Symptoms of metastatic Lesion may be fixed or mobile depending
disease. upon disease extent. Surrounding mucosa
often normal, although polyps may be
present.
Image showing a fissure in ano. Typically, these are located Colonoscopic image of internal haemorroids. Note these may
posteriorly and in the midline. Fissures at other sites may be often be impalpable
associated with underlying disease.
Investigation
• All patients presenting with rectal bleeding require digital rectal examination and procto-sigmoidoscopy as a
minimal baseline.
• Remember that haemorrhoids are typically impalpable and to attribute bleeding to these in the absence of
accurate internal inspection is unsatisfactory.
• In young patients with no other concerning features in the history a carefully performed sigmoidoscopy that
demonstrates clear haemorrhoidal disease may be sufficient. If clear views cannot be obtained then patients
require bowel preparation with an enema and a flexible sigmoidscopy performed.
• In those presenting with features of altered bowel habit or suspicion of inflammatory bowel disease a
colonoscopy is the best test.
• Patients with excessive pain who are suspected of having a fissure may require an examination under general or
local anaesthesia.
• In young patients with external stigmata of fissure and a compatible history it is acceptable to treat medically
and defer internal examination until the fissure is healed. If the fissure fails to heal then internal examination
becomes necessary along the lines suggested above to exclude internal disease.

175
Special tests
• In patients with a malignancy of the rectum the staging investigations comprise an MRI of the rectum to identify
circumferential resection margin compromise and to identify mesorectal nodal disease. In addition to this CT
scanning of the chest abdomen and pelvis is necessary to stage for more distant disease. Some centres will still
stage the mesorectum with endo rectal ultrasound but this is becoming far less common.
• Patients with fissure in ano who are being considered for surgical sphincterotomy and are females who have an
obstetric history should probably have ano rectal manometry testing performed together with endo anal
ultrasound. As this service is not universally available it is not mandatory but in the absence of such information
there are continence issues that may arise following sphincterotomy.
Management
Disease Management
Fissure in ano GTN ointment 0.2% or diltiazem cream applied topically is the usual first line treatment. Botulinum
toxin for those who fail to respond. Internal sphincterotomy for those who fail with botox, can be
considered earlier in males.
Haemorroids Lifestyle advice, for small internal haemorrhoids can consider injection sclerotherapy or rubber
band ligation. For external haemorrhoids consider haemorrhoidectomy. Modern options include
HALO procedure and stapled haemorrhoidectomy.
Inflammatory Medical management- although surgery may be needed for fistulating Crohns (setons).
bowel disease
Rectal cancer Anterior resection or abdomino-perineal excision of the colon and rectum. Total mesorectal
excision is now standard of care. Most resections below the peritoneal reflection will require
defunctioning ileostomy. Most patients will require preoperative radiotherapy.
Pilonidal Sinus
• Occur as a result of hair debris creating sinuses in the skin (Bascom theory).
• Usually in the natal cleft of male patients after puberty.
• It is more common in Caucasians related to their hair type and growth patterns.
• The opening of the sinus is lined by squamous epithelium, but most of its wall consists of granulation tissue. Up
to 50 cases of squamous cell carcinoma have been described in patients with chronic pilonidal sinus disease.
• Hairs become trapped within the sinus.
• Clinically the sinus presents when acute inflammation occurs, leading to an abscess. Patients may describe
cycles of being asymptomatic and periods of pain and discharge from the sinus.
• Treatment is difficult and opinions differ. Definitive treatment should never be undertaken when acute infection
or abscess is present as this will result in failure.
• Definitive treatments include the Bascom procedure with excision of the pits and obliteration of the underlying
cavity. The Karydakis procedure involves wide excision of the natal cleft such that the surface is recontoured
once the wound is closed. This avoids the shearing forces that break off the hairs and has reasonable results.
Pilonidal sinuses are most commonly located in the

midline of the natal cleft.

176
Colonic Polyps
May occur in isolation, or greater numbers as part of the polyposis syndromes. In FAP greater than 100 polyps are
typically present. The risk of malignancy in association with adenomas is related to size, and is the order of 10% in a 1cm
adenoma. Isolated adenomas seldom give risk of symptoms (unless large and distal). Distally sited villous lesions may
produce mucous and if very large, electrolyte disturbances may occur.
Follow up of colonic polyps

Group Features Action
Low risk 1 or 2 adenomas less than 1cm No follow up or re-colonoscopy at 5
years
Moderate risk 3 or 4 small adenomas or 1 adenoma greater than 1cm Re-scope at 3 years
High risk More than 5 small adenomas or more than 3 with 1 of them Re scope at 1 year
greater than 1cm
From Atkins and Saunders Gut 2002 51 (suppl V:V6-V9). It is important to stratify patients appropriately and ensure that
a complete colonoscopy with good views was performed.
Segmental resection or complete colectomy should be considered when:

1. Incomplete excision of malignant polyp
2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy
-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.
Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.

177
Polyposis Syndromes
Syndrome Genetic defect Features Screening and Mx Associated disorders
Familial Mutation of APC Typically over 100 colonic If known to be at risk then Gastric fundal polyps
adenomatous gene (80%) adenomas predictive genetic testing as (50%).
polyposis cases, dominant Cancer risk of 100% teenager Duodenal polyps
20% are new mutations Annual flexible 90%.
sigmoidoscopy from 15 years If severe duodenal
If no polyps found then 5 polyposis cancer risk
yearly colonoscopy started at of 30% at 10 years.
age 20 Abdominal desmoid
Polyps found = resectional tumours.
surgery (resection and pouch
Vs sub total colectomy and
IRA)
MYH Biallelic Multiple colonic polyps Once identified resection and Duodenal polyposis in
associated mutation of mut Later onset right sided ileoanal pouch 30%
polyposis Y human cancers more common than reconstruction is Associated with
homologue in FAP recommended increased risk of
(MYH) on 100% cancer risk by age 60 Attenuated phenotype - breast cancer (self
chromosome 1p, regular colonoscopy examination)
recessive
Peutz - STK11 (LKB1) Multiple benign intestinal Annual examination Malignancies at other
Jeghers mutation on hamartomas Pan intestinal endoscopy sites
syndrome chromosome 19 Episodic obstruction and every 2-3 years Classical
in some (but not intussceception pigmentation pattern
all) cases, Increased risk of GI cancers
dominant (colorectal cancer 20%,
gastric 5%)
Increased risk of breast,
ovarian, cervical pancreatic
and testicular cancers
Cowden Mutation of Macrocephaly Targeted individualised Breast cancer (81%
disease PTEN gene on Multiple intestinal screening risk)
chromosome hamartomas Thyroid cancer and
10q22, Multiple trichilemmomas non toxic goitre
dominant 89% risk of cancer at any site Uterine cancer
16% risk of colorectal cancer
HNPCC Germline Colo rectal cancer 30-70% Colonoscopy every 1-2 years Extra colonic cancers
(Lynch mutations of Endometrial cancer 30-70% from age 25
syndrome) DNA mismatch Gastric cancer 5-10% Consideration of prophylactic
repair genes Scanty colonic polyps may be surgery
present Extra colonic surveillance
Colonic tumours likely to be recommended
right sided and mucinous
Laxatives
Bulk forming laxatives: Osmotic laxatives: Stimulant laxatives:
Bran Magnesium sulphate Docusates
Psyllium Magnesium citrate Bisacodyl
Methylcellulose Sodium phosphate Sodium picosulphate
Sodium sulphate Senna
Potassium sodium tatrate Ricinoleic acid
Polyethylene glycol

178
Genetics of Colorectal Cancer
Genetics of inherited colorectal cancer syndromes
Syndrome Features Genes implicated
FAP More than 100 adenomatous polyps affecting the colon and rectum. APC (over 90%)
Duodenal and fundic glandular polyps
Gardner syndrome As FAP but with desmoid tumours and mandibular osteomas APC
Turcots syndrome Polyposis and colonic tumours and CNS tumours APC +MLH1 and PMS2
HNPCC Colorectal cancer without extensive polyposis. Endometrial cancer, MSH2, MLH1, PMS2 and
(Lynch $) renal and CNS GTBP
Peutz-Jeghers Hamartomatous polyps in GI tract and increased risk of GI malignancy LKB1 andSTK11 (in up to
syndrome 70%)
Cowden disease Multiple hamartomas (see below) PTEN (85%)
MYH associated Autosomal recessive, multiple adenomatous polyps in GI tract, those MYH
polyposis in colon having somatic KRAS mutations
FAP
Autosomal dominant condition, affects 1 in 12,000. Accounts for 0.5% of all CRCs. Lifetime incidence of colorectal cancer
in untreated FAP =100%. Up to 25% cases are caused by de-novo germ line mutations and show no prior family history.
The APC tumour suppressor gene is affected in most cases.
APC in non-inherited colorectal cancer

Up to 80% of sporadic colorectal cancers will have somatic mutations that inactivate APC. Both alleles are usually
affected. Although the APC protein more than likely has multiple critical cellular functions, the best-established role for
APC in the cancer process is as a major binding partner and regulator of the β- catenin protein in the so-called canonical
or β- catenin dependent Wnt signaling pathway.
HNPCC (Lynch syndrome)

HNPCC cancers differ from conventional tumours in a number of respects. In the colon the tumours are more likely to be
right sided, histologically they are more likely to be mucinous and have dense lymphocytic infiltrates. To be diagnosed as
having HNPCC individuals must show typically HNPCC tumours in at least three individuals, (one of whom must be a first
degree relative to the other two). In at least two successive generations. At least one cancer must be diagnosed under
the age of 50. FAP must be excluded and tumours should be verified by pathological identification (Amsterdam criteria).
The genetic changes in HNPCC stem primarily from microsatellite instability affecting DNA mismatch repair genes. In
HNPCC the mismatch repair genes most commonly implicated include; MSH2 and MLH1 and these occur in up to 70% of
people with HNPCC. The finding of microsatellite instability is unusual in sporadic colorectal cancers. Approximately 60%
of individuals who fulfill the Amsterdam criteria will not be found to have evidence of mismatch repair gene defects on
genetic testing. The risk of developing colorectal cancer in those who have not demonstrated mutation of the mis match
repair genes is increased if they fulfill the Amsterdam criteria, but not
the extent that it is increased in those who fulfill the criteria AND have evidence of mis match repair gene defects.
KRAS Mutations
The RAS family of small G proteins act as molecular switches downstream of growth factor receptors. KRAS and the other
two members of the family; HRAS and NRAS, are the site of mutation in approximately 40% of colorectal cancers. When
adenomas are examined the proportion of adenomas less than 1cm showing KRAS mutations was only 10% which
contrasts with 50% in those lesions greater than 1cm.
p53 mutations
The p53 protein functions as a key transcriptional regulator of genes that encode proteins with functions in cell-cycle
checkpoints at the G1/S and G2/M boundaries, in promoting apoptosis, and in restricting angiogenesis . As such,
selection for p53 defects at the adenoma-carcinoma transition may reflect the fact that stresses on tumor cells activate
cell-cycle arrest, apoptotic, and antiangiogenic pathways in cells with wild-type p53 function. Many colonic tumours will
demonstrate changes in the p53 gene that may facilitate tumour progression through from adenoma to carcinoma.

179
Cowden syndrome
Also known as multiple hamartoma syndrome. Rare autosomal dominant condition with incidence of 1 in 200,000. It is
characterised by multiple mucocutaneous lesions, trichilemmomas, oral papillomas and acral keratosis. Most often
diagnosed in third decade of life. Breast carcinoma may occur in up to 50% of patients and conditions such as fibrocystic
disease of the breast may occur in 75% of women. Thyroid disease occurs in 75% and may include malignancy.
Endoscopic screening will identify disease in up to 85% although the small bowel is rarely involved. There is a 15-20% risk
of developing colorectal cancer and regular colonoscopic screening from age 45 is recommended.
Terminology
Oncogene Oncogenes are genes which have the potential to induce cellular proliferation and avoid apoptosis.
Oncogene mutations are general gain of function and are therefore dominant. Increased expression
of oncogenes are found in most tumours
Tumour These genes generally inhibit cellular proliferation or induce apoptosis. Mutations in tumour
suppressor suppressor genes are generally loss of function mutations, and are therefore recessive. Mutations in
gene both tumour suppressor gene alleles allow cells to proliferate without restraint
Colorectal Cancer Screening and Diagnosis

Overview
• Most cancers develop from adenomatous polyps. Screening for colorectal cancer has been shown to reduce
mortality by 16%
• The NHS now has a national screening programme offering screening every 2 years to all men and women aged
60 to 69 years. Patients aged over 70 years may request screening
• Eligible patients are sent faecal occult blood (FOB) tests through the post
• Patients with abnormal results are offered a colonoscopy
At colonoscopy, approximately:
• 5 out of 10 patients will have a normal exam
• 4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
• 1 out of 10 patients will be found to have cancer
Diagnosis
Essentially the following patients need referral:
• Altered bowel habit for more than six weeks
• New onset of rectal bleeding
• Symptoms of tenesmus
Colonoscopy is the gold standard, provided it is complete and good mucosal visualisation is achieved. Other options
include double contrast barium enema and CT colonography.
Staging
Once a malignant diagnosis is made patients with colonic cancer will be staged using chest / abdomen and pelvic CT.
Patients with rectal cancer will also undergo evaluation of the mesorectum with pelvic MRI scanning.
For examination purposes the Dukes and TNM systems are preferred.
Tumour markers
Carcinoembryonic antigen (CEA) is the main tumour marker in colorectal cancer. Not all tumours secrete this, and it may
be raised in conditions such as IBD. However, absolute levels do correlate (roughly) with disease burden and it is once
again being used routinely in follow up.
Dukes Classification
Gives the extent of spread of colorectal cancer
Dukes A Tumour confined to the bowel but not extending beyond it, without nodal metastasis (95%)
Dukes B Tumour invading bowel wall, but without nodal metastasis (75%)
Dukes C Lymph node metastases (50%)
Dukes D Distant metastases (6%) (25% if resectable)
5-year survival in brackets

180
Colorectal Cancer Treatment Summary of Procedures
Patients diagnosed as having colorectal cancer should be completely staged using CT of the chest/ abdomen and pelvis.
Their entire colon should have been evaluated with colonoscopy or CT colonography. Patients whose tumours lie below
the peritoneal reflection should have their mesorectum evaluated with MRI.
Once their staging is complete patients should be discussed within a dedicated colorectal MDT meeting and a treatment
plan formulated.
Treatment of colonic cancer

Cancer of the colon is nearly always treated with surgery.
Stents, surgical bypass and diversion stomas may all be used as
palliative adjuncts. Resectional surgery is the only option for
cure in patients with colon cancer. The procedure is tailored to
the patient and the tumour location. Some patients may have
confounding factors that will govern the choice of procedure,
for example a tumour in a patient from a HNPCC family may be
better served with a panproctocolectomy rather than
segmental resection. Following resection the decision has to be
made regarding restoration of continuity. For an anastomosis to
heal the key technical factors include; adequate blood supply,
mucosal apposition and no tissue tension. Surrounding sepsis,
unstable patients and inexperienced surgeons may compromise
these key principles and in such circumstances it may be safer
to construct an end stoma rather than attempting an anastomosis. When a colonic cancer presents with an obstructing
lesion; the options are to either stent it or resect. In modern practice it is unusual to simply defunction a colonic tumour
with a proximal loop stoma. This differs from the situation in the rectum (see below). Following resection patients with
risk factors for disease recurrence are usually offered chemotherapy, a combination of 5FU and oxaliplatin is common.
Rectal cancer
The management of rectal cancer is slightly different to that of colonic cancer. This reflects the rectum's anatomical
location and the challenges posed as a result. Tumours located in the rectum can be surgically resected with either an
anterior resection or an abdomino-perineal resection. The technical aspects governing the choice between these two
procedures can be complex to appreciate and the main point to appreciate for the MRCS is that involvement of the
sphincter complex or very low tumours require APER. In the rectum a 2cm distal clearance margin is required and this
may also impact on the procedure chosen. Because the rectum is an extraperitoneal structure (until you remove it that
is!) it is possible to irradiate it, something which cannot be offered for colonic tumours. This has a major impact in rectal
cancer treatment and many patients will be offered neoadjuvent radiotherapy (both long and short course) prior to
resectional surgery. Patients with T1, 2 and 3 /N0 disease on imaging do not require irradiation and should proceed
straight to surgery. Patients with T4 disease will typically have long course chemo-radiotherapy. Patients presenting with
large bowel obstruction from rectal cancer should not undergo resectional surgery without staging as primary treatment
(very different from colonic cancer). This is because rectal surgery is more technically demanding, the anastomotic leak
rate is higher and the danger of a positive resection margin in an unstaged patient is high. Therefore, patients with
obstructing rectal cancer should have a defunctioning loop colostomy.
These commonly performed procedures are core knowledge for the MRCS and should be understood.
Site of cancer Type of resection Anastomosis Risk of leak
See Before… (Abdominal Stomas)
Right colon Right hemicolectomy Ileo-colic Low <5%

Transverse Extended right hemicolectomy Ileo-colic Low <5%
Splenic flexure Extended right hemicolectomy Ileo-colic Low <5%
Splenic flexure Left hemicolectomy Colo-colon 2-5%
Left colon Left hemicolectomy Colo-colon 2-5%
Sigmoid colon High anterior resection Colo-rectal 5%
Upper rectum Anterior resection (TME) Colo-rectal 5%
Low rectum Anterior resection (Low TME) Colo-rectal 10%
(+/- Defunctioning stoma)
Anal verge Abdomino-perineal excision of colon and rectum None n/a
In the emergency setting, where the bowel has perforated, the risk of an anastomosis is much greater, particularly when
the anastomosis is colon-colon. In this situation, an end colostomy is often safer and can be reversed later. When
resection of the sigmoid colon is performed and an end colostomy is fashioned the operation is referred to as a
Hartmann’s procedure. Whilst left sided resections are riskier, ileo-colic anastomoses are relatively safe even in the
emergency setting and do not need to be defunctioned.

181
Remember that…
• Right sided colonic cancers should proceed straight to surgery. Radiotherapy to this area is poorly tolerated
and almost never offered as first line treatment. The decision as to whether or not chemotherapy is given
is dependent upon the final histology.
• Chemotherapy for colonic cancer is usually with oxaliplatin.
• T4 rectal cancers are managed with long course chemoradiotherapy. A dramatic response is not
uncommon. To embark on attempted resection at this stage is to court failure.
Common scenarios you might face in the exam:

Scenario Procedure Stoma
Small (<2cm) appendiceal carcinoid tumour. Discharge
Right hemicolectomy and
Large (>5cm) appendiceal carcinoid tumour.
ileocolic anastomosis
Obstructing carcinoma of the colonic hepatic flexure Right hemicolectomy
Extended right hemicolectomy
Obstructing carcinoma of the splenic flexure + ileocolic anastomosis
OR Left hemicolectomy 1
Obstruction, carcinoma of the sigmoid colon and End ileostomy
Subtotal colectomy
perforation of the caecum. OR ileorectal anastomosis 2
Obstruction, sigmoid lesion with liver metastasis. Loop colostomy
Stent (ideal)
± caecum measures 11cm. (if stent not available)
Perforated sigmoid tumour. Hartmann’s procedure End colostomy
Carcinoma of the upper rectum. Anterior resection and
Staging done colorectal anastomosis
Obstruction from a proximal / low rectal cancer. Definitive surgery should wait
Loop colostomy 4
First presentation / Staging NOT done until staging is completed 3
Obstructing low rectal cancer / 10cm from anal verge.
Ant resection 5 Loop ileostomy 6
Staging done ± Chemoradiotherapy
Carcinoma of the low rectum. Abdominoperineal excision of
Within 1cm / invades the dentate line colon and rectum (APER)
UC with megacolon, failure of medical therapy Subtotal colectomy End ileostomy
CD with rectal disease, previous subtotal colectomy Proctectomy
1
Ileocolic anastomosis has a lower leak rate, particularly when the bowel is obstructed
2
Ileorectal anastomosis (not in emergency setting)
3
Rectal cancers are staged with MRI rectum (and sometimes Endoluminal USS for low T1 lesions) together with CT
scanning of the chest, abdomen and pelvis.
4
This patient should be defunctioned, definitive surgery should wait until staging is completed. A loop ileostomy will not
satisfactorily decompress an acutely obstructed colon. Low rectal cancers that are obstructed should not usually be
primarily resected. The obstructed colon that would be used for anastomosis would carry a high risk of anastomotic
dehisence. In addition, as this is an emergency presentation, staging may not be completed, an attempted resection may
therefore compromise the circumferential resection margin, with an associated risk of local recurrence.
5
Low rectal cancers are usually treated with a low anterior resection. Contraindications to this include involvement of the
sphincters and poor sphincter function that would lead to unsatisfactory function post resection. Most colorectal surgeons
defunction resections below the peritoneal reflection as they have an intrinsically high risk of anastomotic leak. A loop
ileostomy provides a safe and satisfactory method of defunctioning these patients. A contrast enema should be performed
prior to stoma reversal.
6
A covering loop ileostomy should be constructed to mitigate the effects of any anastomotic leakage.

182
Crohn’s Disease
Crohn’s disease is a chronic transmural inflammation of a segment(s) of the gastrointestinal tract and may be associated
with extra intestinal manifestations. Frequent disease patterns observed include ileal, ileocolic and colonic disease. Peri-
anal disease may occur in association with any of these. The disease is often discontinuous in its distribution.
Inflammation may cause ulceration, fissures, fistulas and fibrosis with stricturing. Histology reveals a chronic
inflammatory infiltrate that is usually patchy and transmural.
Ulcerative colitis Vs Crohn’s

Crohn's disease Ulcerative colitis
Distribution Mouth to anus Rectum and colon
Macroscopic changes Cobblestone appearance, aphthoid ulceration Contact bleeding
Depth of disease Transmural inflammation Superficial inflammation
Distribution pattern Patchy Continuous
Histological features Granulomas (non caseating epithelioid cell aggregates Crypt abscesses, Inflammatory cells in the
with Langhans' giant cells) lamina propria
Extraintestinal manifestations of Crohns

Related to disease extent Unrelated to disease extent
Aphthous ulcers (10%) Sacroiliitis (10-15%)
Erythema nodosum (5-10%) Ankylosing spondylitis (1-2%)
Pyoderma gangrenosum (0.5%) Primary sclerosing cholangitis (Rare)
Acute arthropathy (6-12%) Gallstones (up to 30%)
Ocular complications (up to 10%) Renal calculi (up to 10%)
Diarrhoea in Crohn’s
Diarrhoea in Crohn’s may be multifactorial since actual inflammation of the colon is not common. Causes therefore
include the following:
• Bile salt diarrhoea secondary to terminal ileal disease
• Entero-colic fistula
• Short bowel due to multiple resections
• Bacterial overgrowth
Surgical interventions in Crohn’s disease

The commonest disease pattern in Crohn’s is stricturing terminal ileal disease and this often culminates in an ileocaecal
resection. Other procedures performed include segmental small bowel resections and stricturoplasty. Colonic
involvement in patients with Crohn’s is not common and, where found, distribution is often segmental. However, despite
this distribution segmental resections of the colon in patients with Crohn’s disease are generally not advocated because
the recurrence rate in the remaining colon is extremely high. As a result, the standard options of colonic surgery in
Crohn’s patients are generally; subtotal colectomy, panproctocolectomy and staged subtotal colectomy and
proctectomy. Restorative procedures such as ileoanal pouch have no role in therapy.
Crohn’s disease is notorious for the developmental of intestinal fistulae; these may form between the rectum and skin
(peri anal) or the small bowel and skin. Fistulation between loops of bowel may also occur and result in bacterial
overgrowth and malabsorption. Management of enterocutaneous fistulae involves controlling sepsis, optimising
nutrition, imaging the disease and planning definitive surgical management.

183
Ulcerative Colitis
Ulcerative colitis is a form of inflammatory bowel disease. Inflammation always starts at rectum, does not spread beyond
ileocaecal valve (although backwash ileitis may occur) and is continuous. The peak incidence of ulcerative colitis is in
people aged 15-25 years and in those aged 55-65 years. It is less common in smokers.
The initial presentation is usually following insidious and intermittent symptoms. Features include:
• bloody diarrhoea
• urgency
• tenesmus
• abdominal pain, particularly in the left lower quadrant
• extra-intestinal features (see below)
Questions regarding the 'extra-intestinal' features of inflammatory bowel disease are common. Extra-intestinal features
include sclerosing cholangitis, iritis and ankylosing spondylitis.
Common to both Crohn's disease and UC Notes

Related to disease Arthritis: pauciarticular, asymmetric Arthritis is the most common extra-intestinal
activity Erythema nodosum feature in both CD and UC
Episcleritis Episcleritis is more common in Crohn’s
Osteoporosis disease
Unrelated to disease Arthritis: polyarticular, symmetric Primary sclerosing cholangitis is much more
activity Uveitis common in UC
Pyoderma gangrenosum Uveitis is more common in UC
Clubbing
Primary sclerosing cholangitis
Pathology
• Red, raw mucosa, bleeds easily
• No inflammation beyond submucosa (unless fulminant disease)
• Widespread superficial ulceration with preservation of adjacent mucosa which has the appearance of polyps
('pseudopolyps')
• Inflammatory cell infiltrate in lamina propria
• Neutrophils migrate through the walls of glands to form crypt abscesses
• Depletion of goblet cells and mucin from gland epithelium
• Granulomas are infrequent
Barium enema
• Loss of haustrations
• Superficial ulceration, 'pseudopolyps'
• Long standing disease: colon is narrow and short -'drainpipe colon'
Endoscopy
• Superficial inflammation of the colonic and rectal mucosa
• Continuous disease from rectum proximally
• Superficial ulceration, mucosal islands, loss of vascular definition and continuous ulceration pattern.
Management
• Patients with long term disease are at increased risk of development of malignancy
• Acute exacerbations are generally managed with steroids. In chronic patients, agents such as azathioprine and
infliximab may be used.
• Individuals with medically unresponsive disease usually require surgery- in the acute phase a sub total
colectomy and end ileostomy. In the longer term a proctectomy will be required. An ileoanal pouch is an option
for selected patients

184

185
15. Breast and Endocrine Surgery – MRCS Notes - Reda

Mnemonics...................................................................................................................................................... 2
Aberrations of Normal Development and Involution - Breast ...................................................................... 2
Benign Breast Lesions & Non-Malignant Breast Disease .............................................................................. 3
Breast Cancer .................................................................................................................................................. 4
Pagets Disease of The Nipple ......................................................................................................................... 4
Breast Cancer Treatment ................................................................................................................................ 5
Breast Cancer - In Situ Disease ....................................................................................................................... 5
Nipple Discharge ............................................................................................................................................. 6
Lymphoedema ................................................................................................................................................ 7
Multiple Endocrine Neoplasia ........................................................................................................................ 8
Parathyroid Glands and Disorders of Calcium Metabolism .......................................................................... 9
Thyroid Disease ............................................................................................................................................. 10
Thyroid Function Tests.................................................................................................................................. 10
Thyroid Malignancy ...................................................................................................................................... 11
Blood Testing in Thyroid Disease ................................................................................................................. 11
Thyroiditis ..................................................................................................................................................... 12
15. BREAST AND ENDOCRINE SURGERY – MRCS NOTES - REDA 1

186
Mnemonics
Causes of gynaecomastia: METOCLOPRAMIDE Drugs causing gynaecomastia: DISCO

M etoclopramide D igitalis
E ctopic oestrogen I soniazid
T rauma skull/tumour breast, testes S pironolactone
O rchitis C imetidine
C imetidine, Cushings O estrogen
L iver cirrhosis
O besity
P araplegia
RA
A cromegaly
M ethyldopa
I soniazid
D igoxin
E thionamide
Aberrations of Normal Development and Involution - Breast

Fibroadenoma
Under the age of 25 years the breast is usually classified as undergoing development. Lobular units are being formed and
a dense stroma is formed within the breast tissue. This may result in the development of fibroadenomas.
As a group, fibroadenomas account for 13% of all palpable breast lesions. However, in women aged 18-25 they
constitute up to 60% of all palpable breast lesions. They are classified as juvenile, common and giant. The former occur in
early adolescence and the latter are characterised by a size greater than 4cm. In young females with small
fibroadenomas (less than 3cm on imaging) a policy of watchful waiting without biopsy may be adopted. A size of greater
than 4cm attracts a recommendation for core biopsy to exclude a phyllodes tumour. The natural history of
fibroadenomas is that 10% will increase in size, 30% regress and the remainder stay the same. This does not apply during
pregnancy and lactation when they may increase in size substantially and subsequently sequester milk.
Some women may wish to have their fibroadenomas excised, they can usually be shelled out through a circumareolar
incision. Smaller lesions may be removed using a mammotome.
Breast cysts
Palpable cysts constitute 15% of all breast lumps. They occur most frequently in perimenopausal females and are caused
by distended and involuted lobules.
They may be readily apparent on clinical examination as soft, fluctuant swellings. It is important to exclude the presence
of an underlying mass lesion. On imaging they will usually show a "halo appearance" on mammography. Ultrasound will
confirm the fluid filled nature of the cyst. Symptomatic cysts may be aspirated and following aspiration the breast re-
examined to ensure that the lump has gone.
Duct ectasia
As women progress through the menopause the breast ducts shorten and dilate. In some women this may cause a
cheese like nipple discharge and slit like retraction of the nipple. No specific treatment is required.

187
Benign Breast Lesions & Non-Malignant Breast Disease
Lesion Features Treatment
Fibroadenoma • Develop from a whole lobule If >3cm surgical excision
• Mobile, firm breast lumps is usual, Phyllodes
• 12% of all breast masses tumours should be widely
• Over a 2-year period up to 30% will get smaller excised (mastectomy if
• No increase in risk of malignancy the lesion is large)
Breast cyst • 7% of all Western females will present with a breast cyst Cysts should be aspirated,
• Usually presents as a smooth discrete lump (may be fluctuant) those which are blood
• They will usually show a "halo appearance" on mammography. stained or persistently
• Small increased risk of breast cancer (especially if younger) refill should be biopsied
or excised
Sclerosing adenosis • Usually presents as a breast lump or breast pain Lesions should be
(radial scars and • Causes mammographic changes which may mimic carcinoma biopsied, excision is not
complex sclerosing • Cause distortion of the distal lobular unit, without hyperplasia mandatory
lesions) (complex lesions will show hyperplasia)
• Considered a disorder of involution, no increase in malignancy
risk
Epithelial • Variable clinical presentation ranging from generalised If no atypical features
hyperplasia lumpiness through to discrete lump then conservative, those
• Disorder consists of increased cellularity of terminal lobular with atypical features
unit, atypical features may be present require either close
• Atypical features and family history of breast cancer confers monitoring or surgical
greatly increased risk of malignancy resection
Fat necrosis • Up to 40% cases usually have a traumatic aetiology Imaging and core biopsy
• Physical features usually mimic carcinoma
• Mass may increase in size initially
Duct ectasia • Mammary duct ectasia may be seen in up to 25% of normal If U1 → reassurance.
female breasts If troublesome →
• Patients usually present with nipple discharge, which may be microdochectomy (if
from single or multiple ducts (usually present age >50 years) young) or total duct
• The discharge is often thick and green excision (if older).
• Duct ectasia is a normal variant of breast involution and is not
the same condition as periductal mastitis
Periductal mastitis • Present at younger age than duct ectasia
• May present with features of inflammation, abscess or
mammary duct fistula
• Strongly associated with smoking
• Usually treated with antibiotics, abscess will require drainage
Duct papilloma • Usually present with nipple discharge Microdochectomy
• Large papillomas may present with a mass
• The discharge usually originates from a single duct
• No increased risk of malignancy
Breast abscess • Lactational mastitis is common Antibiotics and
• Infection is usually with Staphylococcus aureus ultrasound guided
• On examination there is usually a tender fluctuant mass aspiration.
• Overlying skin necrosis is an indication for surgical
debridement, which may be complicated by the development
of a subsequent mammary duct fistula.
Tuberculosis • Rare in western countries, usually secondary TB
• Affects women later in child bearing period
• Chronic breast or axillary sinus is present in up to 50% cases
• Diagnosis is by biopsy culture and histology

188
Breast Cancer
• Commoner in the older age group
• Invasive ductal carcinomas are the most common type. Some may arise as a result of ductal carcinoma in situ (DCIS).
There are associated carcinomas of special type e.g. Tubular that may carry better prognosis.
• The pathological assessment involves assessment of the tumour and lymph nodes, sentinel lymph node biopsy is
often used to minimise the morbidity of an axillary dissection.
• Treatment, typically this is either wide local excision or mastectomy. There are many sub types of both of these that
fall outside of the MRCS. Some key rules to bear in mind.
• Whatever operation is contemplated the final cosmetic outcome does have a bearing. A woman with small breasts
and a large tumour will tend to fare better with mastectomy, even if clear pathological and clinical margins can be
obtained. Conversely a women with larger breasts may be able to undergo breast conserving surgery even with a
relatively large primary lesion (NB tumours >4cm used to attract recommendation for mastectomy). For screen
detected and impalpable tumour image guidance will be necessary.
• Reconstruction is always an option following any resectional procedure. However, its exact type must be tailored to
age and co-morbidities of the patient. The main operations in common use include latissimus dorsi myocutaneous
flap and sub pectoral implants. Women wishing to avoid a prosthesis may be offered TRAM or DIEP flaps.
Surgical options: Mastectomy vs Wide local excision

Mastectomy Wide Local Excision
Multifocal tumour Solitary lesion
Central tumour Peripheral tumour
Large lesion in small breast Small lesion in large breast
DCIS >4cm DCIS <4cm
Patient Choice Patient choice
Central lesions may be managed using breast conserving surgery where an acceptable cosmetic result may be obtained,
this is rarely the case in small breasts
A compelling indication for mastectomy, a larger tumour that would be unsuitable for breast conserving surgery
Nottingham Prognostic Index

The Nottingham Prognostic Index can be used to give an indication of survival. In this system the tumour size is weighted
less heavily than other major prognostic parameters.
Calculation of NPI: Tumour Size x 0.2 + Lymph node score (From table below) + Grade score (From table below).
Score Lymph nodes involved Grade
1 0 1
2 1-3 2
3 >3 3
Prognosis
Score Percentage 5 year survival
2.0 to 2.4 93%
2.5 to 3.4 85%
3.5 to 5.4 70%
>5.4 50%
This data was originally published in 1992. It should be emphasised that other factors such as vascular invasion and
receptor status also impact on survival and are not included in this data and account for varying prognoses often cited in
the literature.
Pagets Disease of The Nipple

Is an eczematoid change of the nipple associated with an underlying breast malignancy and it is present in 1-2% of
patients with breast cancer. In half of these patients, it is associated with an underlying mass lesion and 90% of such
patients will have an invasive carcinoma. 30% of patients without a mass lesion will still be found to have an underlying
carcinoma. The remainder will have carcinoma in situ. Pagets disease differs from eczema of the nipple in that it involves
the nipple primarily and only latterly spreads to the areolar (the opposite occurs in eczema).
Diagnosis: is made by punch biopsy, mammography and ultrasound of the breast. ℞: depends on the underlying lesion.

189
Breast Cancer Treatment
Treatment Indication
Endocrine therapy • Oestrogen receptor positive tumours
• Downstaging primary lesions
• Definitive treatment in old, infirm patients
Irradiation • Wide local excision
• Large lesion, high grade or marked vascular invasion following mastectomy
Chemotherapy • Downstaging advanced lesions to facilitate breast conserving surgery
• Patients with grade 3 lesions or axillary nodal disease
Endocrine agents
Tamoxifen is used and works as a partial oestrogen
receptor agonist. It will typically block activity at the
breast. It does, however, stimulate the receptors at
other sites and it is this that accounts for its
association with endometrial cancer. In post
menopausal women the process of aromatisation
accounts for most oestrogen production. Therefore
in this group aromatase inhibitors are the preferred
agents. Women who are perimenopausal start on
tamoxifen and switch at 3 years.
More recent studies (aTTom and ATLAS) have
demonstrated benefits for continuing the drug for
10 years. In pre-menopausal women, there is
increasing preference for the use of Exemestane
over tamoxifen.
Chemotherapy
The FEC regime is most commonly used (Fluorouracil, epirubicin and cyclophosphamide). This was found to be superior
to the older CMF regime. The Taxanes are commonly used in high risk patients and in this setting a regime of docetaxal,
doxorubicin and cyclophosphamide may be used. The anthracycline class drugs have marked cardiotoxicity (a property
that they share with trastuzumab) and this can limit their use.
Whatever surgical option is chosen the aim should be to have a local recurrence rate of 5% or less at 5 years.
Breast Cancer - In Situ Disease

Breast cancer that has yet to invade the basement membrane is referred to as in situ disease. Both ductal and lobular in
situ variants are recognised.
Ductal carcinoma in situ

• Sub types include; comedo, cribriform, micropapillary and solid
• Comdeo DCIS is most likely to form microcalcifications
• Cribriform and micropapillary are most likely to be multifocal
• Most lesions are mixed (composed of multiple subtypes)
• High nuclear grade DCIS is associated with more malignant characteristics (loss of p53, increased erbB2
expression)
• Local excision of low nuclear grade DCIS will usually produce satisfactory outcomes.
• Multifocal lesions, large and high nuclear grade lesions will usually require mastectomy
• Whole breast irradiation improves locoregional control when breast conserving surgery is performed
Lobular carcinoma in situ
• Much rarer than DCIS
• Does not form microcalcifications
• Usually single growth pattern
• When an invasive component is found it is less likely to be associated with axillary nodal metastasis than with
DCIS
• Low grade LCIS is usually treated by monitoring rather than excision

190
Nipple Discharge
Causes of nipple discharge
Physiological During breast feeding
Galactorrhoea Commonest cause may be response to emotional events, drugs such as histamine receptor
antagonists are also implicated
Hyperprolactinaemia • Commonest type of pituitary tumour
• Microadenomas <1cm in diameter
• Macroadenomas >1cm in diameter
• Pressure on optic chiasm may cause bitemporal hemianopia
Mammary duct ectasia • Dilatation breast ducts.
• Most common in menopausal women
• Discharge typically thick and green in colour
• Most common in smokers
Carcinoma • Often blood stained
• May be underlying mass or axillary lymphadenopathy
Intraductal papilloma • Commoner in younger patients
• May cause blood stained discharge
• There is usually no palpable lump
Assessment of patients
• Examine breast and determine whether there is mass lesion present
• All mass lesions should undergo Triple assessment.
Reporting of investigations
Where a mass lesion is suspected or investigations are requested these are prefixed using a system that denotes the
investigation type e.g. M for mammography, followed by a numerical code as shown below:
1 No abnormality
2 Abnormality with benign features
3 Indeterminate probably benign
4 Indeterminate probably malignant
5 Malignant
Management of non-malignant nipple discharge

• Exclude endocrine disease
• Nipple cytology unhelpful
• Smoking cessation advice for duct ectasia
• For duct ectasia with severe symptoms, total duct excision may be warranted. (If no symptoms / U1 → reassure)

191
Lymphoedema
• Due to impaired lymphatic drainage in the presence of normal capillary function.
• Lymphoedema causes the accumulation of protein rich fluid, subdermal fibrosis and dermal thickening.
• Characteristically fluid is confined to the epifascial space (skin and subcutaneous tissues); muscle compartments are
free of oedema. It involves the foot, unlike other forms of oedema. There may be a 'buffalo hump' on the dorsum of
the foot and the skin cannot be pinched due to subcutaneous fibrosis.
Causes of lymphoedema
Primary • Congenital < 1 year: sporadic, Milroy's disease
• Onset 1-35 years: sporadic, Meige's disease
• > 35 years: Tarda
Secondary • Bacterial/fungal/parasitic infection (filariasis)
• Lymphatic malignancy
• Radiotherapy to lymph nodes
• Surgical resection of lymph nodes
• DVT
• Thrombophlebitis

• Marked disability or deformity from limb swelling
• Lymphoedema caused by proximal lymphatic obstruction with patent distal lymphatics suitable for a lymphatic
drainage procedure
• Lymphocutaneous fistulae and megalymphatics
`
Procedures
Homans operation Reduction procedure with preservation of overlying skin (which must be in good condition). Skin
flaps are raised and the underlying tissue excised. Limb circumference typically reduced by a
third.
Charles operation All skin and subcutaneous tissue around the calf are excised down to the deep fascia. Split skin
grafts are placed over the site. May be performed if overlying skin is not in good condition.
Larger reduction in size than with Homans procedure.
Lymphovenous Identifiable lymphatics are anastomosed to sub dermal venules. Usually indicated in 2% of
anastomosis patients with proximal lymphatic obstruction and normal distal lymphatics.

192
Multiple Endocrine Neoplasia
Multiple endocrine neoplasia (MEN) is inherited as an autosomal dominant disorder.
The table below summarises the three main types of MEN:

MEN type I MEN type IIa MEN type IIb
Mnemonic 'three P's': • Phaeochromocytoma Same as MEN IIa with addition of:
• Medullary thyroid cancer (70%) • Marfanoid body habitus
• Parathyroid (95%): Parathyroid adenoma • Hyperparathyroidism (60%) • Mucosal neuromas
• Pituitary (70%): Prolactinoma/ACTH/Growth (usually hyperplasia)
Hormone secreting adenoma
• Pancreas (50%): Islet cell tumours/Zollinger
Ellison syndrome
also: Adrenal (adenoma) and thyroid

(adenoma)
MENIN gene (chromosome 11) RET oncogene (chromosome 10) RET oncogene (chromosome 10)
Most common presentation = hypercalcemia

193
Parathyroid Glands and Disorders of Calcium Metabolism
Hyperparathyroidism
Disease type Hormone profile Clinical features Cause
Primary • PTH (Elevated) • May be asymptomatic if mild Most cases due to solitary
hyperparathyroidism • Ca2+(Elevated) • Recurrent abdominal pain adenoma (80%), multifocal
• Phosphate (Low) (pancreatitis, renal colic) disease occurs in 10-15% and
• Urine calcium : creatinine • Changes to emotional or parathyroid carcinoma in 1%
clearance ratio > 0.01 cognitive state or less
Secondary • PTH (Elevated) • May have few symptoms Parathyroid gland
hyperparathyroidism • Ca2+ (Low or normal) • Eventually may develop bone hyperplasia occurs as a result
• Phosphate (Elevated) disease, osteitis fibrosa cystica of low calcium, almost
• Vitamin D levels (Low) and soft tissue calcifications always in a setting of chronic
renal failure
Tertiary • PTH (Elevated) • Metastatic calcification Occurs as a result of ongoing
hyperparathyroidism • Ca2+(Normal or high) • Bone pain and / or fracture hyperplasia of the
• Phosphate levels • Nephrolithiasis parathyroid glands after
(Decreased or Normal) • Pancreatitis correction of underlying
• Vitamin D (Normal or renal disorder, hyperplasia of
decreased) all 4 glands is usually the
• Alkaline phosphatase cause
(Elevated)
Differential diagnoses
It is important to consider the rare but relatively benign condition of benign familial hypocalciuric hypercalcaemia,
caused by an autosomal dominant genetic disorder. Diagnosis is usually made by genetic testing and concordant
biochemistry (urine calcium : creatinine clearance ratio <0.01-distinguished from primary hyperparathyroidism).
Treatment
Primary hyperparathyroidism
Indications for surgery:
• Elevated serum Calcium > 1mg/dL above normal
• Hypercalciuria > 400mg/day
• Creatinine clearance < 30% compared with normal
• Episode of life threatening hypercalcaemia
• Nephrolithiasis
• Age < 50 years
• Neuromuscular symptoms
• Reduction in bone mineral density of the femoral neck, lumbar spine, or distal radius of more than 2.5
standard deviations below peak bone mass (T score lower than -2.5)
Secondary hyperparathyroidism
Usually managed with medical therapy.
Indications for surgery in secondary (renal) hyperparathyroidism:
• Bone pain
• Persistent pruritus
• Soft tissue calcifications
Tertiary hyperparathyroidism
Allow 12 months to elapse following transplant as many cases will resolve
The presence of an autonomously functioning parathyroid gland may require surgery. If the culprit gland can be
identified then it should be excised. Otherwise total parathyroidectomy and re-implantation of part of the gland may
be required.

194
Thyroid Disease
Patients may present with a number of different manifestations of thyroid disease. They can be broadly sub classified
according to whether they are euthyroid or have clinical signs of thyroid dysfunction. In addition it needs to be
established whether they have a mass or not.
Assessment
• History
• Examination including USS
• If a nodule is identified, then it should be sampled ideally via an image guided fine needle aspiration
• Radionucleotide scanning is of limited use
Thyroid Tumours
• Papillary carcinoma
• Follicular carcinoma
• Anaplastic carcinoma
• Medullary carcinoma
• Lymphoma's
Multinodular goitre
• One of the most common reasons for presentation
• Provided the patient is euthyroid and asymptomatic and no discrete nodules are seen, they can be reassured.
• In those with compressive symptoms surgery is required and the best operation is a total thyroidectomy.
• Sub total resections were practised in the past and simply result in recurrent disease that requires a difficult
revisional resection.
Endocrine dysfunction
• In general these patients are managed by physicians initially.
• Surgery may be offered alongside radio iodine for patients with Graves disease that fails with medical
management or in patients who would prefer not to be irradiated (e.g. pregnant women).
• Patients with hypothyroidism do not generally get offered a thyroidectomy. Sometimes people inadvertently get
offered resections during the early phase of Hashimotos thyroiditis, however, with time the toxic phase passes
and patients can simply be managed with thyroxine.
Complications following surgery

• Anatomical such as recurrent laryngeal nerve damage.
• Bleeding. Owing to the confined space haematoma's may rapidly lead to respiratory compromise owing to
laryngeal oedema.
• Damage to the parathyroid glands resulting in hypocalcaemia.
Thyroid Function Tests

The interpretation of thyroid function tests is usually straightforward:
Disorder TSH Free T4
Thyrotoxicosis (e.g. Graves' disease) Low High In T3 thyrotoxicosis the free T4 will be
normal
Primary hypothyroidism (primary atrophic High Low
hypothyroidism)
Secondary hypothyroidism Low Low Replacement steroid therapy is
required prior to thyroxine
Sick euthyroid syndrome* Low** Low Common in hospital inpatients
Poor compliance with thyroxine High Normal / high
Steroid therapy Low Normal
*now referred to as non-thyroidal illness
**TSH may be normal in some cases

195
Thyroid Malignancy
Papillary • Commonest sub-type
carcinoma • Accurately diagnosed on fine needle aspiration cytology
(60%) • Histologically, they may demonstrate psammoma bodies (areas of calcification) and so called
'orphan Annie' nuclei (non-capsulated with pale empty nuclei)
• They typically metastasise via the lymphatics and thus laterally located apparently ectopic thyroid
tissue is usually a metastasis from a well differentiated papillary carcinoma
• Prognosis for localized Papillary Ca is excellent.
Follicular • Are less common than papillary lesions
carcinoma • Like papillary tumours, they may present as a discrete nodule. Although they appear to be well
(20%) encapsulated macroscopically there is invasion on microscopic evaluation (Oxyphil cells + scanty
colloid)
• Lymph node metastases are uncommon and these tumours tend to spread haematogenously. This
translates into a higher mortality rate
• Follicular lesions cannot be accurately diagnosed on fine needle aspiration cytology and thus all
follicular FNA's (THY 3f) will require at least a hemi thyroidectomy
• Hurthle cell subtype carry the worst prognosis
• Check recurrence by serum thyroglobulin
Anaplastic • Less common and tend to occur in elderly females
carcinoma • Local invasion is a common feature.
(10%) • Disease is usually advanced at presentation and often only palliative decompression and
radiotherapy can be offered.
Medullary • These are tumours of the parafollicular cells (C Cells) and are of neural crest origin.
carcinoma • They may be familial and occur as part of the MEN -2A disease spectrum.
• Pheochromocytoma may be present, young adults.
• Spread may be either lymphatic or haematogenous and as these tumours are not derived primarily
from thyroid cells they are not responsive to radioiodine.
• The serum calcitonin may be elevated which is of use when monitoring for recurrence.
Lymphoma • These respond well to radiotherapy
• Radical surgery is unnecessary once the disease has been diagnosed on biopsy material. Such
biopsy material is not generated by an FNA and thus a core biopsy has to be obtained (with care!).
Thyroid - Radioiodine vs. Surgery

Surgery Radioiodine
Symptomatic improvement within 10 days Symptomatic improvement takes up to 2 months
No effect on ophthalmopathy Eye signs may worsen
Risk of damage to adjacent anatomical structures No risk of anatomical damage
No restrictions on contact No contact with children for 4 weeks
Blood Testing in Thyroid Disease

Assay Usage
Thyroid peroxidase • Found in autoimmune disease affecting the thyroid (Hashimotos 100%) and
(microsomal) antibodies Graves (70%)
Antibodies to TSH receptor • Individuals with Graves disease (95%)
Thyroglobulin antibodies • Not useful for clinically distinguishing between different types of thyroid
disease, may be used as part of thyroid cancer follow up
Calcitonin • Released from the parafollicular cells
• Usually found in patients with medullary carcinoma of the thyroid

196
Thyroiditis
Sub-acute thyroiditis
Subacute thyroiditis (also known as De Quervain's thyroiditis) is thought to occur following viral infection and typically
presents with hyperthyroidism
Features
• Hyperthyroidism
• Painful goitre
• Raised ESR
• Globally reduced uptake on iodine-131 scan
Management
• Usually self-limiting - most patients do not require treatment
• Thyroid pain may respond to aspirin or other NSAIDs
• In more severe cases steroids are used, particularly if hypothyroidism develops
Hashimoto’s thyroiditis
Hashimoto’s thyroiditis is an immunological disorder in which lymphocytes become sensitised to thyroidal antigens. The
three most important antibodies include; thyroglobulin, TPO and TSH-R. During the early phase of Hashimoto’s, the
thyroglobulin antibody is markedly elevated and then declines.
Features
• Goitre and either euthyroid or mild hypothyroidism
• Progressive hypothyroidism (and associated symptoms)
Management
• During the hyperthyroid phase of illness beta blockers may manage symptoms
• As hypothyroidism develops patients may require thyroxine

197
16. Vascular Surgery – MRCS Notes - Reda

Vasculitis ......................................................................................................................................................... 2
Vascular disorders of the upper limb ............................................................................................................. 3
Axillary vein thrombosis ................................................................................................................................. 4
Ankle-Brachial pressure index ........................................................................................................................ 4
Acute limb ischaemia...................................................................................................................................... 5
Klippel-Trenaunay-Weber .............................................................................................................................. 5
Chronic venous insufficiency and varicose veins ........................................................................................... 6
Lower leg ulcers .............................................................................................................................................. 8
Vascular disease.............................................................................................................................................. 9
Peripheral vascular disease .......................................................................................................................... 10
Aortic dissection ........................................................................................................................................... 11
Abdominal aorta aneurysm .......................................................................................................................... 12
Amputations ................................................................................................................................................. 14
Vascular Investigations ................................................................................................................................. 15
16. VASCULAR SURGERY – MRCS NOTES - REDA 1

198
Vasculitis
Vessel diameter and vasculitis classification
Aorta and branches • Takayasu's arteritis
• Buergers disease
• Giant cell arteritis
Large and medium sized arteries • Buergers disease
• Giant cell arteritis
• Polyarteritis nodosa
Medium sized muscular arteries • Polyarteritis nodosa
• Wegeners granulomatosis
Small muscular arteries • Wegeners granulomatosis
• Rheumatoid vasculitis
Specific conditions
Takyasu's arteritis • Inflammatory, obliterative arteritis affecting aorta and branches
• Females> Males
• Symptoms may include upper limb claudication
• Clinical findings include diminished or absent pulses
• ESR often affected during the acute phase
Buergers disease • Segmental thrombotic occlusions of the small and medium sized lower limb vessels
• Commonest in young male smokers
• Proximal pulses usually present, but pedal pulses are lost
• An acuter hypercellular occlusive thrombus is often present
• Tortuous corkscrew shaped collateral vessels may be seen on angiography
Giant cell arteritis • Systemic granulomatous arteritis that usually affects large and medium sized vessels
• Females > Males
• Temporal arteritis is commonest type
• Granulomatous lesions may be seen on biopsy (although up to 50% are normal)
Polyarteritis nodosa • Systemic necrotising vasculitis affecting small and medium sized muscular arteries
• Most common in populations with high prevalence of hepatitis B
• Renal disease is seen in 70% cases
• Angiography may show saccular or fusiform aneurysms and arterial stenoses
Wegeners • Predominantly affects small and medium sized arteries
granulomatosis • Systemic necrotising granulomatous vasculitis
• Cutaneous vascular lesions may be seen (ulceration, nodules and purpura)
• Sinus imaging may show mucosal thickening and air fluid levels

199
Vascular disorders of the upper limb
Upper limb arterial disease is less common than lesions causing symptoms in the lower limb. The upper limb circulation
may be affected by embolic events, stenotic lesions (both internal and extrinsic), inflammatory disorders and venous
diseases.
The anatomy of the collateral circulation of the arterial inflow may impact on the history and nature of disease
presentation. In the region of the subclavian and axillary arteries the collateral vessels passing around the shoulder joint
may provide pathways for flow if the main vessels are stenotic or occluded. During periods of increased metabolic
demand the collateral flow is not sufficient and the vertebral arteries may have diminished flow. This may result in
diminished flow to the brain with neurological sequelae such as syncope.
Vascular disease of the upper limb

Condition Features
Axillary/Brachial • 50% of upper limb emboli will lodge in the brachial artery
embolus • 30% of upper limb emboli will lodge in the axillary artery
• Sudden onset of symptoms; pain, pallor, paresis, pulselessness, paraesthesia
• Sources are left atrium with cardiac arrhythmia (mainly AF), mural thrombus
• Cardiac arrhythmias may result in impaired consciousness in addition to the embolus
Arterial • Those resulting from atheroma are the most common, trauma may result in vascular changes
occlusions and long term occlusion but this is rare
• Features may include claudication, ulceration and gangrene. Proximally sited lesions may
result in subclavian steal syndrome
• The progressive nature of the disease allows development of collaterals, acute ischaemia may
occur as a result of acute thrombosis
Raynaud's • Idiopathic condition affecting young females
disease • Usually affects hands > feet
• Digits become: white → blue → red
• Treatment is with calcium antagonists
Upper limb • Gradual onset of upper limb swelling and discomfort.
venous • Sensation and motor function are normal
thrombosis • Condition may complicate pre-existing malignancy (especially breast cancer) or arise as a
result of repetitive use of the limb in a task such as painting a ceiling
• The condition is diagnosed with duplex ultrasound and treatment is with anticoagulation
Cervical rib • 0.2-0.4% incidence
• Consist of an anomalous fibrous band that often originates from C7 and may arc towards, but
rarely reaches the sternum
• Congenital cases may present around the third decade. Some cases are reported to occur
following trauma.
• Bilateral in up to 70%
• Compression of the subclavian artery may produce absent radial pulse on clinical examination
and in particular may result in a positive Adson’s test (lateral flexion of the neck away from
symptomatic side and traction of the symptomatic arm- leads to obliteration of radial pulse)
• Treatment is most commonly undertaken when there is evidence of neurovascular
compromise. A trans-axillary approach is the traditional operative method for excision

200
Axillary vein thrombosis
• 1-2% of all deep venous thrombosis
• Primary cause is associated with trauma, thoracic outlet obstruction or repeated effort in a dominant arm (young
active individuals)
• Secondary causes include central line insertion, malignancy, pacemakers
Clinical features
• Pain and swelling (non-pitting)
• Numbness
• Discolouration: mottling, dusky
• Pulses present
• Congested veins
Investigations
• FBC: viscosity, platelet function
• Clotting
• Liver function tests
• D-dimer
• Duplex scan: investigation of choice
• CT scan: thoracic outlet obstruction
Treatment
• Local catheter directed TPA
• Heparin
• Warfarin
Ankle-Brachial pressure index

• Measurement of ankle- brachial pressure index (ABPI) is a commonly performed vascular investigation.
• Calculated by dividing lower limb pressure by the highest upper limb pressure.
Results of ABPI
1.2 or greater Usually due to vessel calcification
1.0- 1.2 Normal
0.8-1.0 Minor stenotic lesion
Initiate risk factor management
0.50-0.8 Moderate stenotic lesion
Consider duplex
Risk factor management
If mixed ulcers present then avoid tight compression bandages
0.5- 0.3 Likely significant stenosis
Duplex scanning to delineate lesions needed
Compression bandaging contra indicated
Less than 0.3 Indicative of critical ischaemia
Urgent detailed imaging required

201
Acute limb ischaemia
• Thrombosis of a pre-existing site of atherosclerosis if the commonest cause of acute limb ischaemia
• Acute thrombosis of popliteal aneurysms poses the greatest threat to the limb
• Sudden occlusion of a large proximal vessel results in the typical appearances of acute limb ischaemia
Clinical appearances
• Less than 6 hours = White leg
• At 6 -12 hours = Mottled limb with blanching on pressure
• More than 12-24 hours = Fixed mottling
Management of acutely ischaemic leg

Clinical picture Treatment
White leg with sensorimotor deficit Surgery and embolectomy
Dusky leg, mild anaesthesia Angiography
Fixed mottling Primary amputation
Role of thrombolysis
• Intra-arterial thrombolysis is better than peripheral thrombolysis
• Mainly indicated in acute on chronic thrombosis
• Avoid if within 2 months of CVA or 2 weeks of surgery
• Aspiration of clot may improve success rate if the thrombosis is large
Surgery
• Both groins should be prepared
• Transverse arteriotomy is easier to close
• Poor inflow should be managed with iliac trawl- if this fails to improve then consider a femoro-femoral cross
over or axillo-femoral cross over.
• A check angiogram should be performed on table and prior to closure
• Systemic heparinisation should follow surgery
• Fasciotomy should be considered if the time between onset and surgery exceeds 6 hours
Klippel-Trenaunay-Weber
Klippel-Trenaunay-Weber syndrome generally affects a single extremity, although cases of multiple affected limbs have
been reported. The leg is the most common site followed by the arms, the trunk, and rarely the head and the neck
Signs and symptoms

The birth defect is diagnosed by the presence of a combination of these symptoms:
• One or more distinctive port-wine stains with sharp borders
• Varicose veins
• Hypertrophy of bony and soft tissues, that may lead to local gigantism or shrinking.
• An improperly developed lymphatic system
In some cases, port-wine stains (capillary port wine type) may be absent. Such cases are very rare and may be classified
as "atypical Klippel-Trenaunay syndrome".
KTS can either affect blood vessels, lymph vessels, or both. The condition most commonly presents with a mixture of the
two. Those with venous involvement experience increased pain and complications.

202
Chronic venous insufficiency and varicose veins
Wide spectrum of disease ranging from minor cosmetic problem through to ulceration and disability. It is commoner in
women than men and is worse during pregnancy. Varicose veins are best considered as being a saccular dilation of veins
(WHO). Chronic venous insufficiency is a series of tissue changes which occur in relation to pooling of blood in the
extremities with associated venous hypertension occurring as a result of incompetent deep vein valves.
The veins of the lower limb consist of an interconnected network of superficial and deep venous systems. Varices occur
because of localised weakness in the vein wall resulting in dilatation and reflux of blood due to non union of valve cusps.
Histologically the typical changes include fibrous scar tissue dividing smooth muscle within media in the vessel wall.
Tissue damage in chronic venous insufficiency occurs because of perivascular cytokine leakage resulting in localised
tissue damage coupled with impaired lymphatic flow.
Diagnosis
Typical symptoms of varicose veins include:
• Cosmetic appearance
• Aching
• Ankle swelling that worsens as the day progresses
• Episodic thrombophlebitis
• Bleeding
• Itching
Symptoms of chronic venous insufficiency include:

• Dependant leg pain
• Prominent leg swelling
• Oedema extending beyond the ankle
• Venous stasis ulcers
The typical venous stasis ulcer is:

• Located above the medial malleolus
• Indolent appearance with basal granulation tissue
• Variable degree of scarring
• Non ischaemic edges
• Haemosiderin deposition in the gaiter area (and also lipodermatosclerosis).
Differential diagnosis
• Lower limb arterial disease
• Marjolins ulcer
• Claudication
• Spinal stenosis
• Swelling due to medical causes e.g. CCF.
Exclusion of these differentials is by means of physical examination and ankle brachial pressure index measurement.
Examination
• Assess for dilated short saphenous vein (popliteal fossa) and palpate for saphena varix medial to the femoral
artery
• Brodie-Trendelenburg test: to assess level of incompetence
• Perthes' walking test: assess if deep venous system competent
Investigation
• Doppler exam: if incompetent a biphasic signal due to retrograde flow is detected
• Duplex scanning: to ensure patent deep venous system (do if DVT or trauma)

203
All patients should have a Doppler assessment to assess for venous reflux and should be classified as having
uncomplicated varicose veins or varicose veins with associated chronic venous insufficiency. In the history establishing a
previous thrombotic event (DVT/ lower limb fracture) is important and patients with such a history and all who have
evidence of chronic venous insufficiency should have a duplex scan performed.
Owing to litigation patients with saphenopopliteal incompetence should have a duplex scan performed and the site
marked by scan on the day of surgery.
Treatment
Indications for surgery:
• Cosmetic: majority
• Lipodermatosclerosis causing venous ulceration
• Recurrent superficial thrombophlebitis
• Bleeding from ruptured varix
Condition Therapy
Minor varicose veins - no Reassure/ cosmetic therapy
complications
Symptomatic In those without deep venous insufficiency options include; endothermal ablation, foam
uncomplicated varicose sclerotherapy, saphenofemoral / popliteal disconnection, stripping and avulsions,
veins compression stockings
Varicose veins with skin Therapy as above (if compression minimum is formal class I stockings)
changes
Chronic venous Class 2-3 compression stockings (ensure no arterial disease).
insufficiency or ulcers
• Application of formal compression stockings (usually class II/III). In patients who have suffered ulceration,
compression stockings should be worn long term. Where ulceration is present and established saphenofemoral
reflux exists this should be addressed surgically for durable relief of symptoms, either at the outset or following
ulcer healing.
• Injection sclerotherapy (5% Ethanolamine oleate), foam is increasingly popular, though transient blindness has
been reported. Endo venous laser therapy is another minimally invasive option
• Sapheno-femoral or sapheno-popliteal ligation, in the case of the LSV; stripping and multiple phlebectomies
Current best practice guidance

In the United Kingdom the National Institute of Clinical Excellence guidance on varicose veins suggests that for patients
with symptomatic varicose veins the first line procedure of choice should be endothermal ablation (see reference for
more information). Where this is unavailable or unsuitable then foam sclerotherapy should be the second line option.
Surgery is currently the third line treatment option.
Trendelenburg procedure (sapheno-femoral junction ligation)

• Head tilt 15 degrees and legs abducted
• Oblique incision 1cm medial from artery
• Tributaries ligated (Superficial circumflex iliac vein, Superficial inferior epigastric vein, Superficial and deep
external pudendal vein)
• SF junction double ligated
• Saphenous vein stripped to level of knee/upper calf. NB increased risk of saphenous neuralgia if stripped more
distally

204
Lower leg ulcers
Venous leg ulcers
• Most due to venous hypertension, secondary to chronic venous insufficiency (other causes include calf pump
dysfunction or neuromuscular disorders)
• Ulcers form due to capillary fibrin cuff or leucocyte sequestration
• Features of venous insufficiency include oedema, brown
pigmentation, lipodermatosclerosis, eczema
• Location above the ankle, painless
• Deep venous insufficiency is related to previous DVT and
superficial venous insufficiency is associated with varicose veins
• Doppler ultrasound looks for presence of reflux and duplex
ultrasound looks at the anatomy/ flow of the vein
• Management: 4-layer compression banding after exclusion of
arterial disease or surgery
• If fail to heal after 12 weeks or >10cm2 skin grafting may be
needed
Marjolin's ulcer
• Squamous cell carcinoma
• Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
• Mainly occur on the lower limb
If after many years an ulcer becomes heaped up and irregular, with rolled edges then suspect a SCC.
Arterial ulcers
• Occur on the toes and heel
• Painful
• There may be areas of gangrene
• Cold with no palpable pulses
• Low ABPI measurements
Neuropathic ulcers
• Commonly over plantar surface of metatarsal head and plantar surface of hallux
• The plantar neuropathic ulcer is the condition that most commonly leads to amputation in diabetic patients
• Due to pressure
• Management includes cushioned shoes to reduce callus formation
Pyoderma gangrenosum
• Associated with inflammatory bowel disease/RA
• Can occur at stoma sites
• Erythematous nodules or pustules which ulcerate
Marjolin's ulcer Pyoderma gangrenosum

205
Vascular disease
Patent • Ductus arteriosus is a normal
ductus foetal vessel that closes
arteriosus spontaneously after birth
• Results in high pressure,
oxygenated blood entering
the pulmonary circuit
• Untreated patients develop
symptoms of congestive
cardiac failure
Cervical rib • Supernumery fibrous band arising from seventh cervical vertebra
• Incidence of 1 in 500
• May cause thoracic outlet syndrome
• Treatment involves surgical division of rib
Coarctation • Aortic stenosis at the site of the ductus arteriosus insertion
of the aorta • More prevalent in boys or females with Turners syndrome
• Patients may present with symptoms of arterial insufficiency, such as
syncope and claudication
• Blood pressure mismatch may be seen, as may mismatch of pulse pressure in
the upper and lower limbs
• Treatment is either with angioplasty or surgical resection (the former is the
most common)
Takayasu's • Large vessel granulomatous vasculitis

arteritis • Results in intimal narrowing
• Most commonly affects young asian females
• Patients present with features of mild systemic illness, followed by pulseless phase with symptoms of
vascular insufficiency
• Treatment is with systemic steroids
Subclavian • Due to proximal stenotic lesion of the subclavian artery
steal • Results in retrograte flow through vertebral or internal
syndrome thoracic arteries
• The result is that decrease in cerebral blood flow may
occur and produce syncopal symptoms
• A duplex scan and/ or angiogram will delineate the
lesion and allow treatment to be planned
Aortic • Chest pain (anterior chest pain- ascending aorta, back pain - descending aorta)
dissection • Widening of aorta on chest x-ray
• Diagnosis made by CT scanning
• Treatment is either medical (Type B disease) or surgical (Type A disease)

206
Peripheral vascular disease
Indications for surgery to revascularise the lower limb
• Intermittent claudication
• Critical ischaemia
• Ulceration
• Gangrene
Intermittent claudication that is not disabling may provide a relative indication, whilst the other complaints are often
absolute indications depending upon the frailty of the patient.
Assessment
• Clinical examination
• Ankle brachial pressure index measurement
• Duplex arterial ultrasound
• Angiography (standard, CT or MRI): usually performed only if intervention being considered.
Angioplasty
In order for angioplasty to be undertaken successfully the artery has to be accessible. The lesion relatively short and
reasonable distal vessel runoff. Longer lesions may be amenable to sub-intimal angioplasty.
Surgery
Surgery will be undertaken where attempts at angioplasty have either failed or are unsuitable. Bypass essentially involves
bypassing the affected arterial segment by utilizing a graft to run from above the disease to below the disease. As with
angioplasty good runoff improves the outcome.
• In patients with major cardiac co-morbidities the safest option is to choose an axillo-bifemoral bypass graft. The long
term patency rates are less good than with aorto-bifemoral bypass grafts, however, the operation is less major.
• Femoro-femoral cross over grafts are an option for treatment of iliac occlusions in patients with significant co-
morbidities and healthy contralateral vessels.
Some key concepts with bypass surgery:

Superficial femoral artery occlusion to the above knee popliteal
In the ideal scenario, vein (either in situ or reversed LSV) would the used as a conduit. However, prosthetic material has
reasonable 5-year patency rates and some would advocate using this in preference to vein so that vein can be used for
other procedures in the future. In general terms either technique is usually associated with an excellent outcome (if run
off satisfactory).
Procedure
• Artery dissected out, IV heparin 3,000 units given and then the vessels are cross clamped
• Longitudinal arteriotomy
• Graft cut to size and tunneled to arteriotomy sites
• Anastomosis to femoral artery usually with 5/0 'double ended' Prolene suture
• Distal anastomosis usually using 6/0 'double ended' Prolene
Distal disease
• Femoro-distal bypass surgery takes longer to perform, is more technically challenging and has higher failure
rates.
• In elderly diabetic patients with poor runoff, a primary amputation may well be a safer and more effective
option. There is no point in embarking on this type of surgery in patients who are wheelchair bound.
• In femorodistal bypasses vein gives superior outcomes to PTFE.
Rules
• Vein mapping 1st to see whether there is suitable vein (the preferred conduit). Sub intimal hyperplasia occurs
early when PTFE is used for the distal anastomosis and will lead to early graft occlusion and failure.
• Essential operative procedure as for above knee fem-pop.
• If there is insufficient vein for the entire conduit, then vein can be attached to the end of the PTFE graft and
then used for the distal anastomosis. This type of 'vein boot' is technically referred to as a Miller Cuff and is
associated with better patency rates than PTFE alone.
• Remember the more distal the arterial anastomosis the lower the success rate.

207
Aortic dissection
• More common than rupture of the abdominal aorta
• 33% of patients die within the first 24 hours, and 50% die within 48 hours if no treatment received
• Associated with hypertension
• Features of aortic dissection: tear in the intimal layer, followed by formation and propagation of a subintimal
hematoma. Cystic medial necrosis (Marfan's)
• Most common site of dissection: 90% occurring within 10 centimetres of the aortic valve
Stanford Classification
Type Location Treatment
A Ascending aorta/ aortic root Surgery- aortic root replacement
B Descending aorta Medical therapy with antihypertensives
DeBakey classification
Type Site affected
I Ascending aorta, aortic arch, descending aorta
II Ascending aorta only
III Descending aorta distal to left subclavian artery
Clinical features
• Tearing, sudden onset chest pain (painless 10%)
• Hypertension or Hypotension
• A blood pressure difference (in each arm) greater than
20 mm Hg
• Neurologic deficits (20%)
Investigations
• CXR: widened mediastinum, abnormal aortic knob, ring
sign, deviation of the trachea/oesophagus
• CT angiography of the thoracic aorta
• MRI angiography
• Conventional angiography (now rarely used
diagnostically)
Management
• Beta-blockers: aim HR 60-80 bpm and systolic BP 100-120 mm Hg
• For type A dissections the standard of care is aortic root replacement

208
Abdominal aorta aneurysm
• Abdominal aortic aneurysms are a common problem in vascular surgery.
• They may occur as either true or false aneurysm. With the former all 3 layers of the arterial wall are involved, in the
latter only a single layer of fibrous tissue forms the aneurysm wall.
• True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people. They are commonest in
elderly men and for this reason the UK is now introducing the aneurysm screening program with the aim of
performing an abdominal aortic ultrasound measurement in all men aged 65 years.
Pathology
Abdominal aortic aneurysms occur primarily as a result of the failure of elastic proteins within the extracellular matrix.
Aneurysms typically represent dilation of all layers of the arterial wall. Most aneurysms are caused by degenerative
disease. After the age of 50 years the normal diameter of the infrarenal aorta is 1.5cm in females and 1.7cm in males.
Diameters of 3cm and greater, are considered aneurysmal. The pathophysiology involved in the development of
aneurysms is complex and the primary event is loss of the intima with loss of elastic fibres from the media. This process is
associated with, and potentiated by, increased proteolytic activity and lymphocytic infiltration.
Major risk factors for the development of aneurysms include smoking and hypertension. Rare but important causes
include syphilis and connective tissues diseases such as Ehlers Danlos type 1 and Marfans syndrome.
Causes
• Several different groups of patients suffer from
aneurysmal disease.
• The commonest group is those who suffer from standard
arterial disease, i.e. Those who are hypertensive and have
been or are smokers.
• Other patients such as those suffering from connective
tissue diseases such as Marfan's may also develop
aneurysms. In patients with abdominal aortic aneurysms
the extracellular matrix becomes disrupted with a change
in the balance of collagen and elastic fibres.
Management
• Most abdominal aortic aneurysms are an incidental
finding.
• Symptoms most often relate to rupture or impending
rupture.
• 20% rupture anteriorly into the peritoneal cavity. Very
poor prognosis.
• 80% rupture posteriorly into the retroperitoneal space
• The risk of rupture is related to aneurysm size, only 2% of
aneurysms measuring less than 4cm in diameter will
rupture over a 5-year period. This contrasts with 75% of
aneurysms measuring over 7cm in diameter.
• This is well explained by Laplace’s' law which relates size to
transmural pressure.
• For this reason, most vascular surgeons will subject
patients with an aneurysm size of 5cm or greater to CT
scanning of the chest, abdomen and pelvis with the aim of
delineating anatomy and planning treatment. Depending
upon co-morbidities, surgery is generally offered once the
A CT reconstruction showing an infrarenal abdominal
aneurysm is between 5.5cm and 6cm.
aortic aneurysm. The walls of the sac are calcified which
may facilitate identification on plain x-rays
• Symptomatic aneurysms (80% annual mortality if untreated)
• Increasing size above 5.5cm if asymptomatic
• Rupture (100% mortality without surgery)

209
Special groups
Ruptured AAA
Pre-operatively the management depends upon haemodynamic instability. In patients with symptoms of rupture
(typical pain, haemodynamic compromise and risk factors) then ideally prompt laparotomy. In those with vague
symptoms and haemodynamic stability the ideal test is CT scan to determine whether rupture has occurred or not.
Most common rupture site is retroperitoneal 80%. These patients will tend to develop retroperitoneal haematoma.
This can be disrupted if BP is allowed to rise too high so aim for BP 100mmHg.
Operative details are similar to elective repair although surgery should be swift, blind rushing often makes the
situation worse. Plunging vascular clamps blindly into a pool of blood at the aneurysm neck carries the risk of injury
the vena cava that these patients do not withstand. Occasionally a supracoeliac clamp is needed to effect temporary
control, although leaving this applied for more than 20 minutes tends to carry a dismal outcome.
Supra renal AAA

These patients will require a supra renal clamp and this carries a far higher risk of complications and risk of renal
failure.
EVAR
Increasingly patients are now being offered endovascular aortic aneurysm repair. This is undertaken by surgeons and
radiologists working jointly. The morphology of the aneurysm is important and not all are suitable. Here is a typical
list of those features favoring a suitable aneurysm:
• Long neck
• Straight iliac vessels
• Healthy groin vessels
Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated grafts can allow
supra renal AAA to be treated.
Types of Aneurysms

210
Amputations
Amputations are indicated when the affected limb is one of the following:
• Dead non-viable
• Deadly where it is posing a major threat to life
• Dead useless where it is viable but a prosthesis would be preferable
Orthopaedic surgery
• Amputation is often undertaken as an option of last resort e.g. Limb salvage has failed and the limb is so
nonfunctional that mobility needs would be best met with prosthesis.
• Chronic fracture nonunion or significant limb shortening following trauma would fit into this category.
Occasionally following major trauma, a primary amputation is preferable. This would be the case in an open
fracture with major distal neurovascular compromise and other more life threatening injuries are present.
Vascular surgery
• The first two categories are the most prevalent.
• Diabetic foot sepsis is often a major cause of sepsis which can spread rapidly in the presence of established
peripheral vascular disease.
• As a general rule the main issue in vascular surgery is to optimise vascular inflow prior to surgery. The more
distal the planned amputation is to be, the more important this rule becomes.
• In other situations there has been something such as an embolic event that has not been revascularised in time.
In this case the limb shows fixed mottling and an amputation will be needed.
Types of amputations
As the vast majority of commonly performed amputations affect the lower limbs these will be covered here.
The main categories of amputations are:

• Pelvic disarticulation (hindquarter)
• Above knee amputation
• Gritti Stokes (through knee amputation)
• Below knee amputation (using either Skew or Burgess flaps)
• Syme's amputation (through ankle)
• Amputations of mid foot and digits
Choosing a level of amputation depends on:

• The disease process being treated
• Desired functional outcome
• Co-morbidities of the patient
Above knee amputations

• Quick to perform
• Heal reliably
• Patients regain their general health quickly
• For this benefit, a functional price has to be paid and many patients over the age of 70 will never walk on an
above knee prosthesis.
• Above knee amputations use equal anterior-posterior flaps
Below knee amputations

• Technically more challenging to perform
• Heal less reliably than their above knee counterparts.
• However, many more patients are able to walk using a below knee prosthesis.
• In below knee amputations the two main flaps are Skew flaps or the Burgess long posterior flap. Skew flaps
result in a less bulky limb that is easier to attach a prosthesis to.
It is worth remembering that whilst it may be technically feasible to offer a below knee amputation there may be
circumstances where an above knee option is preferable. For example, in fixed flexion deformities of the lower limb, little
functional benefit would be gained from below knee amputation surgery.

211
Vascular Investigations
Venous disease
Venous Doppler
The simplest investigation for assessment of venous junctional incompetence is a Doppler assessment. This involves the
patient standing and manual compression of the limb distal to the junction of interest. Flow should normally occur in one
direction only. Where junctional incompetence is present reverse flow will occur and is relatively easy to identify.
Venograms and duplex scans

Structural venous information is historically obtained using a venogram. This is an invasive test and rarely required in
modern clinical practice. The most helpful test is a venous duplex scan which will provide information relating to flow and
vessel characteristics. Duplex is also useful in providing vein maps for bypass surgery.
Arterial disease
Ankle-brachial pressure
The ankle brachial pressure index measurement is an important investigation as it will allow classification of the severity
of the flow compromise present. False readings may occur in those with calcified vessels such as diabetics and results in
such settings should be interpreted with caution. When auscultating the vessel note should be made of the character of
the signal. Monophasic signals are associated with a proximal stenosis and reduction in flow. Triphasic signals provide
reassurance of a healthy vessel.
Arterial Duplex
As with the vein the duplex scan can provide a substantial amount of information about arterial patency and flow
patterns. In skilled hands they can provide insight as to the state of proximal vessels that are anatomically inaccessible to
duplex (e.g. Iliacs). Through assessment of distal flow patterns. It is an operator dependent test.
An arterial duplex should be performed first, before progression to an angiography.
Conventional angiogram
Vessel puncture and catheter angiography is the gold standard method of assessing arteries. High quality information can
usually be obtained. Limitations of the technique include the risk of contrast toxicity and risks of vessel damage. Severely
calcified vessels may be difficult to puncture and in this situation a remote access site (e.g. brachial) may be used. This
technique is particularly useful in providing a distal arterial roadmap prior to femoro-distal bypass.
CT angiography
These tests provide a considerable amount of structural and flow information. They require contrast and thus carry the
risks associated with this. They are particularly useful in the setting of GI bleeding as they are rapidly available and can be
performed by a non-vascular radiologist. However, they lack the facility for endovascular intervention. In general they do
not provide high enough resolution for distal arterial surgery.
Magnetic resonance angiography

This has the advantage of being non-invasive and not using nephrotoxic contrast. Movement artifact remains a problem
in some sites and distal arterial resolution is imperfect.

212

213
17. Urology – MRCS Notes - Reda

Mnemonics...................................................................................................................................................... 2
Scrotal swelling ............................................................................................................................................... 2
Testicular cancer ............................................................................................................................................. 3
Priapism........................................................................................................................................................... 3
Prostate Cancer ............................................................................................................................................... 4
Causes of Haematuria ..................................................................................................................................... 5
Renal stones .................................................................................................................................................... 6
Lower genitourinary tract trauma.................................................................................................................. 7
Renal lesions ................................................................................................................................................... 8
Hydronephrosis ............................................................................................................................................... 9
Functional renal imaging ................................................................................................................................ 9
`
17. UROLOGY – MRCS NOTES - REDA 1

214
Mnemonics
Schistosoma haematobium causes haematuria
Scrotal swelling
Differential diagnosis
Inguinal hernia If inguinoscrotal swelling; cannot "get above it" on examination
Cough impulse may be present
May be reducible
Testicular tumours Often discrete testicular nodule (may have associated hydrocele)
Symptoms of metastatic disease may be present
USS scrotum and serum AFP and β HCG required
Acute epididymo- Often history of dysuria and urethral discharge
orchitis Swelling may be tender and eased by elevating testis
Most cases due to Chlamydia
Infections with other gram negative organisms may be associated with underlying structural
abnormality
Epididymal cysts Painless
Single or multiple cysts
May contain clear or opalescent fluid (spermatoceles)
Usually occur over 40 years of age
Lie above and behind testis
Testis can be felt separately i.e palpated unlike hydrocele
It is usually possible to "get above the lump" on examination
Hydrocele Non painful, soft fluctuant swelling
Usually contain clear fluid
Will often transilluminate
May be presenting feature of testicular cancer in young men
Testis is NOT palpated
Often possible to "get above it" on examination
Can be secondary (causes include trauma, infection and tumour)
Testicular torsion Severe, sudden onset testicular pain
Risk factors include abnormal testicular lie
Typically affects adolescents and young males
On examination testis is tender and pain not eased by elevation
Urgent surgery is indicated, the contra lateral testis should also be fixed
Varicocele Varicosities of the pampiniform plexus
Typically occur on left (because testicular vein drains into renal vein)
May be presenting feature of renal cell carcinoma
Affected testis may be smaller and bilateral varicoceles may affect fertility
Management
• Testicular malignancy is always treated with orchidectomy via an inguinal approach. This allows high ligation of
the testicular vessels and avoids exposure of another lymphatic field to the tumour.
• Torsion is commonest in young teenagers and the history in older children can be difficult to elicit. Intermittent
torsion is a recognised problem. The treatment is prompt surgical exploration and testicular fixation. This can be
achieved using sutures or by placement of the testis in a Dartos pouch.
• Varicoceles are usually managed conservatively. If there are concerns about testicular function or infertility, then
surgery or radiological management can be considered.
• Epididymal cysts can be excised using a scrotal approach
• Hydroceles are managed differently in children where the underlying pathology is a patent processus vaginalis
and therefore an inguinal approach is used in children so that the processus can be ligated. In adults a scrotal
approach is preferred and the hydrocele sac excised or plicated (Jaboulay’s procedure).

215
Testicular cancer
Testicular cancer is the most common malignancy in men aged 20-30 years. Around 95% of cases of testicular cancer are
germ-cell tumours. Germ cell tumours may essentially be divided into:
Tumour type Key features Tumour markers Pathology

Seminoma • Commonest subtype (50%) • AFP usually normal Sheet like lobular
• Average age at diagnosis = 40 • HCG elevated in patterns of cells with
• Even advanced disease 10% seminomas substantial fibrous
associated with 5 year survival • Lactate component. Fibrous
of 73% dehydrogenase; septa contain
elevated in 10-20% lymphocytic inclusions
seminomas (but also and granulomas may be
in many other seen.
conditions)
Non seminomatous germ • Younger age at presentation: 20- • AFP elevated in up Heterogenous texture
cell tumours (42%) 30 years to 70% of cases with occasional ectopic
• Teratoma • Advanced disease carries worse • HCG elevated in up tissue such as hair
• Yolk sac tumour prognosis (48% at 5 years) to 40% of cases
• Choriocarcinoma • Retroperitoneal lymph node • Other markers
• Mixed germ cell dissection may be needed for rarely helpful
tumours (10%) residual disease after chemotherapy
Priapism
Prolonged unwanted erection, in the absence of sexual desire, lasting more than 4 hours.
Classification of priapism
Low flow priapism Due to veno-occlusion (high intracavernosal pressures).
• Most common type
• Often painful
• Often low cavernosal flow
• If present for > 4 hours requires emergency treatment
High flow priapism Due to unregulated arterial blood flow.
• Usually presents as semi rigid painless erection
Recurrent priapism Typically seen in sickle cell disease, most commonly of high flow type.
Causes
• Intracavernosal drug therapies (e.g. for erectile dysfunction>
• Blood disorders such as leukaemia and sickle cell disease
• Neurogenic disorders such as spinal cord transection
• Trauma to penis resulting in arterio-venous malformations
Tests
• Exclude sickle cell/ leukaemia
• Consider blood sampling from cavernosa to determine whether high or low flow (low flow is often hypoxic)
Management
• Ice packs/ cold showers
• If due to low flow then blood may be aspirated from copora or try intracavernosal alpha adrenergic agonists.
• Delayed therapy of low flow priapism may result in erectile dysfunction.

216
Prostate Cancer
Diagnosis
• Early prostate cancers have few symptoms.
• Metastatic disease may present as bone pain.
• Locally advanced disease may present as pelvic
pain or with urinary symptoms.
• Prostate specific antigen measurement
• Digital rectal examination
• Trans rectal USS (+/- biopsy)
• MRI/ CT and bone scan for staging.
PSA Test
The normal upper limit for PSA is 4ng/ml. However,
in this group will lie patients with benign disease
and some with localised prostate cancer. False
positives may be due to prostatitis, UTI, BPH,
vigorous DRE.
The percentage of free: total PSA may help to
distinguish benign disease from cancer. Values of
<20% are suggestive of cancer and biopsy is
advised.
Pathology Gleason grading system

• 95% adenocarcinoma
• In situ malignancy is sometimes found in areas adjacent to cancer. Multiple biopsies needed to call true in situ
disease.
• Often multifocal, 70% lie in the peripheral zone.
• Graded using the Gleason grading system, two grades awarded 1 for most dominant grade (on scale of 1-5) and
2 for second most dominant grade (scale 1-5). The two added together give the Gleason score. Where 2 is best
prognosis and 10 the worst.
• Lymphatic spread occurs first to the obturator nodes and local extra prostatic spread to the seminal vesicles is
associated with distant disease.
Treatment
• Watch and wait: Elderly, multiple co-morbidities, low Gleason score
• Radiotherapy (External): Both potentially curative and palliative therapy possible. However, radiation proctitis
and rectal malignancy are late problems. Brachytherapy is a modification allowing internal radiotherapy.
• Surgery: Radical prostatectomy. Surgical removal of the prostate is the standard treatment for localised disease.
The robot is being used increasingly for this procedure. As well as the prostate the obturator nodes are also
removed to complement the staging process. Erectile dysfunction is a common side effect. Survival may be
better than with radiotherapy (see references).
• Hormonal therapy: Testosterone stimulates prostate tissue and prostatic cancers usually show some degree of
testosterone dependence. 95% of testosterone is derived from the testis and bilateral orchidectomy may be
used for this reason. Pharmacological alternatives include LHRH analogues and anti-androgens (which may be
given in combination).
• In the UK the National Institute for Clinical Excellence (NICE) suggests that active surveillance is the preferred
option for low risk men. It is particularly suitable for men with clinical stage T1c, Gleason score 3+3 and PSA
density < 0.15 ng/ml/ml who have cancer in less than 50% of their biopsy cores, with < 10 mm of any core
involved.
Candidates for active surveillance should:
• have had at least 10 biopsy cores taken
• have at least one re-biopsy.
If men on active surveillance show evidence of disease progression, offer radical treatment. Treatment decisions
should be made with the man, taking into account co-morbidities and life expectancy.

217
Causes of Haematuria
Trauma • Injury to renal tract
• Renal trauma commonly due to blunt injury (others penetrating injuries)
• Ureter trauma rare: iatrogenic
• Bladder trauma: due to RTA or pelvic fractures
Infection • Remember TB
Malignancy • Renal cell carcinoma (remember paraneoplastic syndromes): painful or painless
• Urothelial malignancies: 90% are transitional cell carcinoma, can occur anywhere along the
urinary tract. Painless haematuria.
• Rare bladder tumours (Squamous cell carcinoma and Adenocarcinoma)
• Prostate cancer
• Penile cancers: SCC
TCC of the renal pelvis may seed down the ureter.
SCC of the kidney usually arises in an area of chronic inflammation such as a staghorn calculus.
Renal adenocarcinoma on the left side may invade the gonadal vein and produce varicocele.
They also have paraneoplastic phenomena such as hypercalcaemia.
Renal disease • Glomerulonephritis
Stones • Microscopic haematuria common
Structural • Benign prostatic hyperplasia (BPH) causes haematuria due to hypervascularity of the
abnormalities prostate gland
• Cystic renal lesions e.g. polycystic kidney disease
• Vascular malformations
• Renal vein thrombosis due to renal cell carcinoma
Coagulopathy • Causes bleeding of underlying lesions
Drugs • Cause tubular necrosis or interstitial nephritis: aminoglycosides, chemotherapy
• Interstitial nephritis: penicillin, sulphonamides, and NSAIDs
• Anticoagulants
Benign • Exercise
Gynaecological • Endometriosis: flank pain, dysuria, and haematuria that is cyclical
Iatrogenic • Catheterisation
• Radiotherapy; cystitis, severe haemorrhage, bladder necrosis
Pseudohaematuria For example following consumption of beetroot, rhubarb, blackberries, Rifampicin

218
Renal stones
Type of stones Features Percentage of all calculi
Calcium Hypercalciuria is a major risk factor (various causes) 85%
oxalate Hyperoxaluria may also increase risk
Hypocitraturia increases risk because citrate forms complexes with calcium
making it more soluble
Hyperuricosuria may cause uric acid stones to which calcium oxalate binds
Stones are radio-opaque (though less than calcium phosphate stones)
Cystine Inherited recessive disorder of transmembrane cystine transport leading to 1%
decreased absorption of cystine from intestine and renal tubule
Multiple stones may form
Relatively radiodense bec they contain sulphur (Semi-opaque, ‘ground-glass’)
Uric acid Uric acid is a product of purine metabolism 5-10%
May precipitate when urinary pH low
May be caused by diseases with extensive tissue breakdown e.g. malignancy
More common in children with inborn errors of metabolism
Radiolucent
Calcium May occur in renal tubular acidosis, high urinary pH increases supersaturation 10%
phosphate of urine with calcium and phosphate
Renal tubular acidosis types 1 and 3 increase risk of stone formation (types 2
and 4 do not)
Radio-opaque stones (composition similar to bone)
Struvite Stones formed from magnesium, ammonium and phosphate. 2-20%
Occur as a result of urease producing bacteria (and are thus associated with
chronic infections, for example Infection with Proteus mirabilis).
Under the alkaline conditions produced, the crystals can precipitate.
Slightly radio-opaque.
Effect of urinary pH on stone formation

Urine pH will show individual variation (from pH 5-7). Post prandially the pH falls as purine metabolism will produce uric
acid. Then the urine becomes more alkaline (alkaline tide). When the stone is not available for analysis the pH of urine
may help to determine which stone was present.
Stone type Urine acidity Mean urine pH
Calcium phosphate Normal- alkaline >5.5
Calcium oxalate Variable 6
Uric acid Acid 5.5
Struvate Alkaline >7.2
Cystine Normal 6.5
Therapeutic selection
Disease Option
Ureteric calculi less than 5mm Manage expectantly
Stone burden of less than 2cm Lithotripsy (or Ureteroscopy if pregnant female or impacted)
Complex renal calculi and staghorn calculi Percutaneous nephrolithotomy
Stone any size + obstructed, infected system Urgent decompression (ureteroscopy, nephrostomy)

219
Lower genitourinary tract trauma
• Most bladder injuries occur due to blunt trauma
• 85% associated with pelvic fractures
• Easily overlooked during assessment in trauma
• Up to 10% of male pelvic fractures are associated with urethral or bladder injuries
Types of injury
Urethral injury • Mainly in males
• Blood at the meatus (50% cases)
• There are 2 types:
1- Bulbar rupture
- Most common
- Straddle type injury e.g. bicycles
- Triad signs: urinary retention, perineal haematoma, blood at the meatus
2- Membranous rupture
- Can be extra or intraperitoneal
- Commonly due to pelvic fracture
- Penile or perineal oedema/haematoma
- PR: Prostate displaced upwards (beware co-existing retroperitoneal
haematomas as they may make examination difficult)
• Investigation: Ascending urethrogram
• Management: Suprapubic catheter (surgical placement, not percutaneously)
External genitalia injuries • Secondary to injuries caused by penetration, blunt trauma, continence- or
(i.e., the penis and the scrotum) sexual pleasure-enhancing devices, and mutilation
Bladder injury • Rupture is intra or extraperitoneal
• Presents with haematuria or suprapubic pain
• History of pelvic fracture and inability to void: always suspect bladder or
urethral injury
• Inability to retrieve all fluid used to irrigate the bladder through a Foley catheter
indicates bladder injury
• Investigation: IVU or cystogram
• Management: laparotomy if intraperitoneal, conservative if extraperitoneal

220
Renal lesions
Lesion Disease specific features Treatment

Renal cell • Most present with haematuria (50%) Usually radical or partial
carcinoma • Common renal tumour (85% cases) nephrectomy
(adenocarcinoma) • Paraneoplastic features include hypertension and polycythaemia
• Features include: Renal vein thrombosis, PUO, left varicocele
• Ix: CT (Biopsy not done if nephrectomy is planned)
• Most commonly has haematogenous metastasis
Nephroblastoma • Rare childhood tumour Surgical resection
• It accounts for 80% of all genitourinary malignancies in those combined with
under the age of 15 years chemotherapy (usually
• Up to 90% will have a mass vincristine, actinomycin D
• 50% will be hypertensive and doxorubicin)
• Diagnostic work up includes ultrasound and CT scanning
Neuroblastoma • Most common extracranial tumour of childhood Surgical resection,
• 80% occur in those under 4 years of age radiotherapy and
• Tumour of neural crest origin (up to 50% occur in the adrenal chemotherapy
gland)
• The tumour is usually calcified and may be diagnosed using
MIBG scanning
• Staging is with CT
Transitional cell • Accounts for 90% of lower urinary tract tumours, but only 10% Radical
carcinoma of renal tumours nephroureterectomy
• Males affected 3x more than females
• Occupational exposure to industrial dyes and rubber chemicals
may increase risk
• Up to 80% present with painless haematuria
• Diagnosis and staging is with CT IVU
Angiomyolipoma • 80% of these hamartoma type lesions occur sporadically, the 50% of patients with
remainder are seen in those with tuberous sclerosis lesions >4cm will have
• Tumour is composed of blood vessels, smooth muscle and fat symptoms and will
• Massive bleeding may occur in 10% of cases require surgical resection
Adult Polycystic • APKD is associated with liver cysts (70%), berry aneurysms (25%) Supportive / Symptomatic
Kidney Disease and pancreatic cysts (10%). Patients may have a renal mass,
(ADPKD/APKD) hypertension, renal calculi and macroscopic haematuria.
SCC of the kidney usually arises in an area of chronic inflammation such as staghorn calculus.
Renal Cell Carcinoma Staging

221
Hydronephrosis
Causes of hydronephrosis: SUPER PACT
Bilateral: SUPER Unilateral: PACT
• Stenosis of the urethra • Pelvic-ureteric obstruction (congenital or acquired)
• Urethral valve • Aberrant renal vessels
• Prostatic enlargement • Calculi
• Extensive bladder tumour • Tumours of renal pelvis
• Retro-peritoneal fibrosis
Investigation
• USS- identifies presence of hydronephrosis and can assess the kidneys
• IVU- assess the position of the obstruction
• Antegrade or retrograde pyelography- allows treatment
• If renal colic suspected: non contrast CT scan (majority of stones are detected this way)
Management
• Remove the obstruction and drainage of urine
• Acute upper urinary tract obstruction: Nephrostomy tube
• Chronic upper urinary tract obstruction: Ureteric stent or a pyeloplasty
Functional renal imaging

DMSA scan
Dimercaptosuccinic acid (DMSA) scintigraphy
DMSA localises to the renal cortex with little accumulation in the renal papilla and medulla. It is useful for the
identification of cortical defects and ectopic or aberrant kidneys. It does not provide useful information on the ureter of
collecting system.
Diethylene-triamine-penta-acetic acid (DTPA)

This is primarily a glomerular filtration agent. It is most useful for the assessment of renal function. Because it is filtered
at the level of the glomerulus it provides useful information about the GFR. Image quality may be degraded in patients
with chronic renal impairment and derangement of GFR.
MAG 3 renogram
Mercaptoacetyle triglycine is an is extensively protein bound and is primarily secreted by tubular cells rather than filtered
at the glomerulus. This makes it the agent of choice for imaging the kidneys of patients with existing renal impairment
(where GFR is impaired).
Micturating cystourethrogram (MCUG scan)

This scan provides information relating to bladder reflux and is obtained by filling the bladder with contrast media (via a
catheter) and asking the child to void. Images are taken during this phase and the degree of reflux can be calculated
Intra venous urography

This examination is conducted by the administration of intravenous iodinated contrast media. The agent is filtered by the
kidneys and excreted and may provide evidence of renal stones or other structural lesions. A rough approximation of
renal function may be obtained using the technique. But it is not primarily a technique to be used for this purpose. With
the advent of widespread non contrast CT scan protocols for the detection of urinary tract calculi it is now rarely used.
PET/CT
This may be used to evaluate structurally indeterminate lesions in the staging of malignancy.

222

223
18. Organ Transplantation – MRCS Notes - Reda

Transplant types ............................................................................................................................................. 2
Organ transplantation: immunosuppressants............................................................................................... 2
Complications following renal transplant ...................................................................................................... 3
Renal transplant:HLA typing and graft failure ............................................................................................... 4
18. ORGAN TRANSPLANTATION – MRCS NOTES - REDA 1

224
Transplant types
Graft Features Uses
Allograft Transplant of tissue from genetically non identical donor Solid organ transplant from non-related
from the same species donor
Isograft Graft of tissue between two individuals who are Solid organ transplant in identical twins
genetically identical
Autograft Transplantation of organs or tissues from one part of the Skin graft
body to another in the same individual
Xenograft Tissue transplanted from another species Porcine heart valve
Organ transplantation: immunosuppressants

A number of drugs are available which help to mitigate the processes resulting in acute rejection. Cyclosporin and
tacrolimus are commonly used drugs.
Example regime
• Initial: ciclosporin/tacrolimus with a monoclonal antibody
• Maintenance: ciclosporin/tacrolimus with MMF or sirolimus
• Add steroids if more than one steroid responsive acute rejection episode
Ciclosporin
• Inhibits calcineurin, a phosphatase involved in T cell activation
• Nephrotoxic
• Monitor levels
Azathioprine
• Metabolised to form 6 mercaptopurine which inhibits DNA synthesis and cell division
• Side effects include myelosupression, alopecia and nausea
Tacrolimus
• Lower incidence of acute rejection compared to ciclosporin
• Also less hypertension and hyperlipidaemia
• However, high incidence of impaired glucose tolerance and diabetes
• Tacrolimus is metabolised by the P450 enzyme system. This is inhibited by a number of naturally occurring
substances, these include grapefruit, watercress and St. John’s Wort. These should all be avoided in
immunosupressed patients taking tacrolimus.
Mycophenolate mofetil (MMF)

• Blocks purine synthesis by inhibition of IMPDH
• Therefore inhibits proliferation of B and T cells
• Side-effects: GI and marrow suppression
Sirolimus (rapamycin)
• Blocks T cell proliferation by blocking the IL-2 receptor
• Can cause hyperlipidaemia
Monoclonal antibodies
• Selective inhibitors of IL-2 receptor
• Daclizumab
• Basilximab

225
Complications following renal transplant
Renal transplantation is widely practised. The commonest technical related complications are related to the ureteric
anastomosis. The warm ischaemic time is also of considerable importance and graft survival is directly related to this.
Long warm ischaemic times increase the risk of acute tubular necrosis which may occur in all types of renal
transplanation and provided other insults are minimised, will usually recover. Organ rejection may occur at any phase
following the transplantation process.
Immunological complications
Types of organ rejection
• Hyperacute. This occurs immediately through presence of pre formed antibody (such as ABO incompatibility).
• Acute. Occurs during the first 6 months and is usually T cell mediated. Usually tissue infiltrates and vascular
lesions.
• Chronic. Occurs after the first 6 months. Vascular changes predominate.
Type of rejection Key features

Hyperacute Occurs within minutes of clamp release
Due to pre formed antibodies*
Immediate loss of graft occurs
Accelerated acute Occurs in first few days following surgery
Involved both cellular and antibody mediated injury
Pre-sensitisation of the donor is a common cause
Acute Traditionally the most common type of rejection
Seen days to weeks after surgery
Predominantly a cell mediated process mediated by lymphocytes
Organ biopsy demonstrates cellular infiltrates and graft cell apoptosis
Chronic Increasingly common problem
Typically; graft atrophy and atherosclerosis are seen. Fibrosis often occurs as a late event
* Episodes of hyperacute rejection are typically due to preformed antibodies. ABO mismatch is the best example. However,
IgG anti HLA Class I antibodies are another potential cause. These events are now seen less commonly because the cross
matching process generally takes this possibility into account
Technical complications
Complication Presenting features Treatment
Renal artery Sudden complete loss of urine output Immediate surgery may salvage the graft, delays beyond
thrombosis 30 minutes are associated with a high rate of graft loss
Renal artery Uncontrolled hypertension, allograft Angioplasty is the treatment of choice
stenosis dysfunction and oedema
Renal vein Pain and swelling over the graft site, The graft is usually lost
thrombosis haematuria and oliguria
Urine leaks Diminished urine output, rising USS shows perigraft collection, necrosis of ureter tip is
creatinine, fever and abdominal pain the commonest cause and the anastomosis may need
revision
Lymphocele Common complication (occurs in May be drained with percutaneous technique and
15%), may present as a mass, if large sclerotherapy, or intraperitoneal drainage
may compress ureter

226
Renal transplant:HLA typing and graft failure
The human leucocyte antigen (HLA) system is the name given to the major histocompatibility complex (MHC) in humans.
It is coded for on chromosome 6.
Some basic points on the HLA system

• Class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR
• When HLA matching for a renal transplant the relative importance of the HLA antigens are as follows DR > B > A
Graft survival
• 1 year = 90%, 10 years = 60% for cadaveric transplants
• 1 year = 95%, 10 years = 70% for living-donor transplants
Post-op problems
• ATN of graft
• Vascular thrombosis
• Urine leakage
• UTI
Hyperacute acute rejection

• Due to antibodies against donor HLA type 1 antigens
• Rarely seen due to HLA matching
Acute graft failure (< 6 months)

• Usually due to mismatched HLA
• Other causes include cytomegalovirus (CMV) infection
• Management: give steroids, if resistant use monoclonal antibodies
Causes of chronic graft failure (> 6 months)

• Chronic allograft nephropathy
• Ureteric obstruction
• Recurrence of original renal disease (MCGN > IgA > FSGS)

227
19. Head and Neck Surgery – MRCS Notes - Reda

Neck lumps ...................................................................................................................................................... 2
Neck Masses in Children ................................................................................................................................. 2
Submandibular glands disease ....................................................................................................................... 3
Parotid gland clinical....................................................................................................................................... 4
Diseases of nose and sinuses.......................................................................................................................... 6
Epistaxis........................................................................................................................................................... 7
Voice production............................................................................................................................................. 7
Disorders affecting the ear ............................................................................................................................. 8
19. HEAD AND NECK SURGERY – MRCS NOTES - REDA 1

228
Neck lumps
Reactive By far the most common cause of neck swellings. There may be a history of local infection or a
lymphadenopathy generalised viral illness
Lymphoma Rubbery, painless lymphadenopathy
The phenomenon of pain whilst drinking alcohol is very uncommon
There may be associated night sweats and splenomegaly
Thyroid swelling May be hypo-, eu- or hyperthyroid symptomatically
(midline) Moves upwards on swallowing
Thyroglossal cyst More common in patients < 20 years old
(midline) Usually midline, between the isthmus of the thyroid and the hyoid bone
Moves upwards with protrusion of the tongue. May be painful if infected.
℞ Sistrunk procedure (excision of cyst + associated track).
Pharyngeal pouch More common in older men
(Ant|Post ∆) Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen, but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough
Cystic hygroma A congenital lymphatic lesion (lymphangioma) typically found in the neck, classically on the left side
(Post ∆) Most are evident at birth, around 90% present before 2 years of age
Branchial cyst An oval, mobile cystic mass that develops between the sternocleidomastoid muscle and the pharynx
(Ant ∆) Develop due to failure of obliteration of the second branchial cleft in embryonic development
Usually present in early adulthood, rare above the age of 40
At risk excision: Mandibular branch of facial nerve, greater auricular nerve and accessory nerve.
Cervical rib More common in adult females
(Post ∆) Around 10% develop thoracic outlet syndrome
Carotid aneurysm Pulsatile lateral neck mass which doesn't move on swallowing
Carotid body Typically present as painless masses. They may compress the vagus or hypoglossal nerves with
tumour symptoms attributable to these structures. Over 90% occur spontaneously and are more common in
(Ant ∆) people living at high altitude. In familial cases up to 30% may be bilateral. ℞ is with excision.
Neck Masses in Children

Thyroglossal cyst • Located in the anterior triangle, usually in the midline and below the hyoid (65% cases)
(midline) • Derived from remnants of the thyroglossal duct
• Thin walled and anechoic on USS (echogenicity suggests infection of cyst)
Branchial cyst • Six branchial arches separated by branchial clefts
(Ant ∆) • Incomplete obliteration of the branchial apparatus may result in cysts, sinuses or fistulae
• 75% of branchial cysts originate from the second branchial cleft
• Usually located anterior to the sternocleidomastoid near the angle of the mandible
• Unless infected the fluid of the cyst has a similar consistency to water and is anechoic on USS
Dermoids • Derived from pleuripotent stem cells and are located in the midline
(midline) • Most commonly in a suprahyoid location
(superficial) • They have heterogeneous appearances on imaging and contain variable amounts of calcium
and fat
Thyroid gland • True thyroid lesions are rare in children and usually represent thyroglossal cysts or tumours like
lymphoma
Lymphatic • Usually located posterior to the sternocleidomastoid
malformations • Cystic hygroma result from occlusion of lymphatic channels
• The painless, fluid filled, lesions usually present prior to the age of 2
• They are often closely linked to surrounding structures and surgical removal is difficult
• They are typically hypoechoic on USS
Infantile • May present in either triangle of the neck
haemangioma • Grow rapidly initially and then will often spontaneously regress
(Ant|Post ∆) • Plain x-rays will show a mass lesion, usually containing calcified phleboliths
• As involution occurs the fat content of the lesions increases
Lymphadenopathy • Located in either triangle of the neck
(Ant|Post ∆) • May be reactive or neoplastic
• Generalised lymphadenopathy usually secondary to infection in children (very common)

229
Superficial Lateral Structures
Midline structures
Structures Anterior triangle Posterior triangle
Sebaceous cyst Thyroglossal cysts Branchial cyst Cystic Hygroma
Lipoma Thyroid swelling Thyroid lobe swellings
Abscess Chondroma of thyroid cartilage Submandibular lymph gland pathology Cervical rib
Submental lymph nodes Lymphadenopathy
Dermoid cyst Dermoid cyst Parotid gland swelling
Laryngeal swelling Laryngocoele Torticollis
Carotid body tumour
Carotid artery aneurysm Subclavian aneurysm
Infantile Hemangioma
Pharyngeal Pouch
Submandibular glands disease

The submandibular glands secrete approximately 800- 1000ml saliva per day. They typically produce mixed seromucinous
secretions. When parasympathetic activity is dominant; the secretions will be more serous.
The parasympathetic fibres are derived from the chorda tympani nerves and the submandibular ganglion.
Sensory fibres are conveyed by the lingual branch of the mandibular nerve (V 3 ).
Salivary Glands
Sialolithiasis • Parotid
• 80% of all salivary gland calculi occur in the submandibular gland • Sublingual
• 70% of the calculi are radio-opaque • Submandibular
• Stones are usually composed of calcium phosphate or calcium carbonate
• Patients typically develop colicky pain and post prandial swelling of the gland
• Investigation involves sialography to demonstrate the site of obstruction and associated other stones
• Stones impacted in the distal aspect of Wharton’s duct may be removed orally, other stones and chronic inflammation
will usually require gland excision
Sialadenitis (inflammation of a salivary gland)
• Usually occurs as a result of Staphylococcus aureus infection
• Pus may be seen leaking from the duct, erythema may also be noted
• Development of a sub mandibular abscess is a serious complication as it may spread through the other deep fascial
spaces and occlude the airway
Submandibular tumours
• Only 8% of salivary gland tumours affect the sub mandibular gland
• Of these 50% are malignant (usually adenoid cystic carcinoma)
• Diagnosis usually involves fine needle aspiration cytology
• Imaging is with CT and MRI
• In view of the high prevalence of malignancy, all masses of the submandibular glands should generally be excised.

230
Parotid gland clinical
Benign neoplasms
Up to 80% of all salivary gland tumours occur in the parotid gland and up to 80% of these are benign. There is no
consistent correlation between the rate of growth and the malignant potential of the lesion. However, benign tumours
should not invade structures such as the facial nerve.
With the exception of Warthins tumours, they are commoner in women than men. The median age of developing a
lesion is in the 5th decade of life.
Benign tumour types

Tumour type Features
Benign pleomorphic Most common parotid neoplasm (80%)
adenoma Proliferation of epithelial and myoepithelial cells of the ducts and an increase in stromal
(Benign mixed tumor) components (classic biphasic histological appearance)
Slow growing, lobular, and not well encapsulated
Recurrence rate of 1-5% with appropriate excision (parotidectomy)
Recurrence possibly secondary to capsular disruption during surgery
Malignant degeneration occurring in 2-10% of adenomas observed for long periods, with
carcinoma ex-pleomorphic adenoma occurring most frequently as adenocarcinoma
Warthin tumor Second most common benign parotid tumor (5%)
(Papillary cystadenoma Most common bilateral benign neoplasm of the parotid
lymphoma) Marked male as compared to female predominance
(Adenolymphoma) Occurs later in life (sixth and seventh decades), smokers.
Presents as a lymphocytic infiltrate and cystic epithelial proliferation
May represent heterotopic salivary gland epithelial tissue trapped within intraparotid
lymph nodes
Incidence of bilaterality and multicentricity of 10%
Malignant transformation rare (almost unheard of)
Monomorphic adenoma Account for less than 5% of tumours
Slow growing
Consist of only one morphological cell type (hence term mono)
Include; basal cell adenoma, canalicular adenoma, oncocytoma, myoepitheliomas
Haemangioma Should be considered in the differential of a parotid mass in a child
Accounts for 90% of parotid tumours in children less than 1 year of age
Hypervascular on imaging
Spontaneous regression may occur and malignant transformation is almost unheard of
Malignant salivary gland tumours

Types of malignancy
Mucoepidermoid 30% of all parotid malignancies
carcinoma Usually low potential for local invasiveness and metastasis (depends mainly on grade)
Adenoid cystic carcinoma Unpredictable growth pattern
Tendency for perineural spread
Nerve growth may display skip lesions resulting in incomplete excision
Distant metastasis more common (visceral rather than nodal spread)
5 year survival 35%
Mixed tumours Often a malignancy occurring in a previously benign parotid lesion
Acinic cell carcinoma Intermediate grade malignancy
May show perineural invasion
Low potential for distant metastasis
5 year survival 80%
Adenocarcinoma Develops from secretory portion of gland
Risk of regional nodal and distant metastasis
5 year survival depends upon stage at presentation, may be up to 75% with small lesions
with no nodal involvement
Lymphoma Large rubbery lesion, may occur in association with Warthins tumours
Diagnosis should be based on regional nodal biopsy rather than parotid resection
Treatment is with chemotherapy (and radiotherapy)

231
Diagnostic evaluation
• Plain x-rays may be used to exclude calculi
• Sialography may be used to delineate ductal anatomy
• FNAC is used in most cases
• Superficial parotidectomy may be either diagnostic of therapeutic depending upon the nature of the lesion
• Where malignancy is suspected the primary approach should be definitive resection rather than excisional
biopsy
• CT/ MRI may be used in cases of malignancy for staging primary disease
Treatment
For nearly all lesions this consists of surgical resection, for benign disease this will usually consist of a superficial
parotidectomy. For malignant disease a radical or extended radical parotidectomy is performed. The facial nerve is
included in the resection if involved. The need for neck dissection is determined by the potential for nodal involvement.
Other parotid disorders

HIV infection
• Lymphoepithelial cysts associated with HIV occur almost exclusively in the parotid
• Typically presents as bilateral, multicystic, symmetrical swelling
• Risk of malignant transformation is low and management usually conservative
Sjogren syndrome
• Autoimmune disorder characterised by parotid enlargement, xerostomia and keratoconjunctivitis sicca
• 90% of cases occur in females
• Second most common connective tissue disorder
• Bilateral, non-tender enlargement of the gland is usual
• Maybe secondary (for e.g. RA)
• Histologically, the usual findings are of a lymphocytic infiltrate in acinar units and epimyoepithelial islands
surrounded by lymphoid stroma
• Treatment is supportive
• There is an increased risk of subsequent lymphoma
Sarcoid
• Parotid involvement occurs in 6% of patients with sarcoid
• Bilateral in most cases
• Gland is not tender
• Xerostomia may occur
• Facial nerve palsy
• Management of isolated parotid disease is usually conservative, improvement with steroid.
`

232
Diseases of nose and sinuses
Benign Tumours
• Simple papillomas may be an incidental finding or present with obstructive symptoms. Excision under general
anaesthesia is sufficient management.
• Transitional cell papillomas may be more extensive and produce obstructive symptoms. Erosion of local
structures is a recognised complication. These lesions may rarely undergo malignant transformation and
therefore careful and complete excision is required, some cases may require partial or total maxillectomy.
• Pleomorphic adenomas of the maxillary sinuses are reported but are extremely rare, their symptoms typically
include nasal obstruction and pain if the sinus is obstructed. Treatment is by complete surgical excision, the
diagnosis is not infrequently made post operatively.
• Benign osteomas may develop in the paranasal sinuses, the frontal sinus is the most frequent location of such
lesions. Symptoms include; pain, rhinorrhoea and anosmia. Most osteomas may be observed if asymptomatic,
sphenoid osteomas should be resected soon after diagnosis as enlargement may compromise visual fields.
Many sinus osteomas can now be resected endoscopically, complete surgical resection is required.
• Nasal polyps are benign lesions of the ethmoid sinus mucosa. Many patients may also have asthma, cystic
fibrosis and a sensitivity to aspirin. Symptoms include watery rhinorrhoea, infection and anosmia. The polyps are
usually a semitransparent grey mass. They are rare in childhood. Treatment is either with systemic steroids or
surgical resection. The latter should be combined with antral washout. Low dose, nasal, steroid drops may
reduce the risk of recurrence.
Malignant disease
• Malignancies encountered in the nose and paranasal sinuses include; adenoid cystic carcinoma, squamous cell
carcinoma and adenocarcinoma.
• Adenocarcinoma of the paranasal sinuses and nasopharynx is strongly linked to exposure to hard wood dust
(after >10 years exposure).
• Adenoid cystic carcinoma usually originate in the smaller salivary glands.
• The majority of cancers (50%) arise from the lateral nasal wall, a smaller number (33%) arise from the maxillary
antrum, ethmoid and sphenoid cancers comprise only 7%.
• Signs of malignancy on clinical examination include loose teeth, cranial nerve palsies and lymphadenopathy.
• Nasopharyngeal cancers are most common in individuals presenting from China and Asia and are linked to viral
infection with Epstein Barr Virus. Radiotherapy and chemotherapy are the most commonly used modalities.
Maxillary sinusitis
• Common symptoms include post nasal discharge, pain, headache and toothache.
• Imaging may show a fluid level in the antrum.
• Common organisms include Haemophilus influenzae or Streptococcus pneumoniae.
• Treatment with antral lavage may facilitate diagnosis and relieve symptoms. Antimicrobial therapy has to be
continued for long periods. Antrostomy may be needed.
Frontoethmoidal sinusitis
• Usually presents with frontal headache, nasal obstruction and altered sense of smell.
• Inflammation may progress to involve periorbital tissues. Ocular symptoms may occur and secondary CNS
involvement brought about by infection entering via emissary veins.
• CT scanning is the imaging modality of choice. Early cases may be managed with antibiotics. More severe cases
usually require surgical drainage.

233
Epistaxis
Usually trivial and insignificant but severe haemorrhage may compromise airway and pose a risk to life.
Arterial supply
• From internal and external carotid
• An arterial plexus exists at Little's area and is the source of bleeding in 90% cases
• Major arterial supply is from the sphenopalatine and greater palatine arteries (branches of the maxillary artery)
• The facial artery supplies the more anterior aspect of the nose
• Ethmoidal arteries are branches of the ophthalmic artery. They supply the posterosuperior nasal cavity
Venous drainage follows the arterial pattern
Classification
• Primary idiopathic epistaxis accounts for 75% of all cases
• Secondary cases arise as a result of events such as anticoagulants, trauma and coagulopathy
• Classification into anterior and posterior epistaxis may help to locate the source and becomes more important
when invasive treatment is required
Management
• Resuscitate if required
• Subject should sit upright and pinch nose firmly
• Nasal cavity should be examined using a headlight
• Simple anterior epistaxis may be managed using silver nitrate cautery. If difficult to manage then custom
manufactured packs may be inserted
• Posterior packing or tamponade may be achieved by passing a balloon tamponade device and inflating it. This is
indicated where anterior packing alone has failed to achieve haemostasis.
• Post nasal pack patients should receive antibiotics
• Failure of these methods will require more invasive therapy. Where a vascular radiology suite is available,
consideration may be given to angiographic techniques. Direct ligation of the nasal arterial supply may also be
undertaken. Of the arterial ligation techniques available, the endo nasal sphenopalatine arterial ligation
procedure is most popular.
Voice production
There are 2 main nerves involved:
Superior laryngeal nerve (SLN) (External laryngeal nerve “motor” and Internal laryngeal nerve “sensory”)
Innervates the cricothyroid muscle
Since the cricothyroid muscle is involved in adjusting the tension of the vocal fold for high notes during singing, SLN
paresis and paralysis result in:
• Abnormalities in pitch
• Inability to sing with smooth change to each higher note (glissando or pitch glide)
Recurrent laryngeal nerve (RLN) (Inferior laryngeal nerve)

Innervates intrinsic larynx muscles
• Opening vocal folds (as in breathing, coughing)
• Closing vocal folds for vocal fold vibration during voice use
• Closing vocal folds during swallowing
Injury of RLN
• Unilateral: diplophonia, dysphagia
• Bilateral: aphonia

234
Disorders affecting the ear
Variant Cause Features Treatment
Acute Boil in external auditory meatus Acute pain on moving the pinna Ear packs may be used
otitis Conductive hearing loss if lesion is large Topical antibiotics
externa When rupture occurs pus will flow from Operative debridement may
ear be needed in severe cases
Chronic Chronic combined infection in Chronic discharge from affected ear, Cleansing of the external ear
otitis the external auditory meatus hearing loss and severe pain rare and treatment with
externa usually combined staphylococcal antifungal and antibacterial
and fungal infection ear drops
Malignant otitis externa

• Uncommon type of otitis externa that is found in immunocompromised individuals (90% in diabetics)
• Infective organism is usually Pseudomonas aeruginosa
• Infection commences in the soft tissues of the external auditory meatus, then progresses to involve the soft
tissues and into the bony ear canal
• Progresses to temporal bone osteomyelitis
Treatment Key features in history
• Anti pseudomonal antimicrobial agents • DM (90%) or immunosuppression (illness or
• Topical agents treatment related)
• Hyperbaric oxygen is sometimes used in • Severe, unrelenting, deep-seated otalgia
refractory cases • Temporal headaches
• Purulent otorrhea
Possibly dysphagia, hoarseness, and/or facial nerve
dysfunction
Otitis media
Variant Cause Features Treatment
Acute Viral induced middle ear • Most common in children and Antibiotics (usually amoxicillin)
suppurative effusions secondary to rare in adults
otitis media eustachian tube dysfunction • May present with symptoms
elsewhere (e.g. vomiting) in children
• Severe pain and sometimes fever
• May present with discharge is
tympanic rupture occurs
Chronic • May occur with or without • Those without cholesteatoma may • Simple pars tensa
suppurative cholesteatoma complain of intermittent discharge perforations may be managed
otitis media • Those without cholesteatoma (non-offensive) non operatively or a
have a perforation of the pars • Those with cholesteatoma have myringoplasty considered if
tensa impaired hearing and foul smelling symptoms troublesome.
• Those with cholesteatoma discharge • Pars flaccida perforations
have a perforation of the pars will usually require a radical
flaccida mastoidectomy
Otosclerosis
• Progressive conductive deafness
• Secondary to fixation of the stapes in the oval window
• Treatment is with stapedectomy and insertion of a prosthesis
Acoustic neuroma
• Symptoms of gradually progressive unilateral perceptive deafness and tinnitus
• Involvement of the vestibular nerve may cause vertigo
• Extension to involve the facial nerve may cause weakness and then paralysis.
Pre auricular sinus

• Common congenital condition in which an epithelial defect forms around the external ear
• Small sinuses require no treatment
• Deeper sinuses may become blocked and develop episodes of infection, they may be closely related to the facial
nerve and are challenging to excise

235
20. Skin Disorders – MRCS Notes - Reda

Skin Diseases ................................................................................................................................................... 2
Benign skin diseases ....................................................................................................................................... 4
Sebaceous cysts .............................................................................................................................................. 4
Malignancy and related lesions...................................................................................................................... 5
Merkel cell tumours of the skin ..................................................................................................................... 6
20. SKIN DISORDERS – MRCS NOTES - REDA 1

236
Skin Diseases
Skin lesions may be referred for surgical assessment, but more commonly will come via a dermatologist for definitive
surgical management. Skin malignancies include basal cell carcinoma, squamous cell carcinoma and malignant
melanoma.
Basal Cell Carcinoma

• Most common form of skin cancer.
• Commonly occur on sun exposed sites apart from the ear.
• Sub types include nodular, morphoeic, superficial and pigmented.
• Typically slow-growing with low metastatic potential.
• Standard surgical excision, topical chemotherapy and radiotherapy are all successful.
• As a minimum a diagnostic punch biopsy should be taken if treatment other than standard surgical excision is
planned.
Squamous Cell Carcinoma

• Again related to sun exposure.
• May arise in pre - existing solar
keratoses.
• May metastasize if left.
• Immunosupression (e.g. following
transplant), increases risk.
• Wide local excision is the treatment
of choice and where a diagnostic
excision biopsy has demonstrated
SCC, repeat surgery to gain adequate
margins may be required.
Malignant Melanoma
The main diagnostic features (major criteria): Secondary features (minor criteria)
• Change in size • Diameter >6mm
• Change in shape • Inflammation
• Change in colour • Oozing or bleeding
• Altered sensation
Treatment
• Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision
biopsy can make subsequent histopathological assessment difficult.
• Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-
excision of margins is required (Margins of excision - Related to Breslow thickness):
Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional
lymph node groups should be selectively applied.
Kaposi Sarcoma
• Tumour of vascular and lymphatic endothelium.
• Purple cutaneous nodules.
• Associated with immuno suppression.
• Classical form affects elderly males and is slow growing.
• Immunosuppression form is much more aggressive and tends
to affect those with HIV related disease.
Kaposi’s Sarcoma

237
Non-malignant skin disease
Dermatitis Herpetiformis
• Chronic itchy clusters of blisters.
• Linked to underlying gluten enteropathy (coeliac disease).
Dermatofibroma (see later)

• Benign lesion.
• Firm elevated nodules.
• Usually history of trauma.
• Lesion consists of histiocytes, blood vessels and fibrotic changes.
Pyogenic granuloma
Present as friable overgrowths of granulation at sites of minor trauma. They may be ulcerated and bleeding on contact is
common. They may be treated with curettage and cautery. Formal excision may be used if there is diagnostic doubt.
• Overgrowth of blood vessels.
• Red nodules.
• May mimic amelanotic melanoma.
Acanthosis nigricans
• Brown to black, poorly defined, velvety hyperpigmentation of the skin.
• Usually found in body folds such as the posterior and lateral folds of the neck, the axilla, groin, umbilicus,
forehead, and other areas.
• The most common cause of acanthosis nigricans is insulin resistance, which leads to increased circulating insulin
levels. Insulin spillover into the skin results in its abnormal increase in growth (hyperplasia of the skin).
• In the context of a malignant disease, acanthosis nigricans is a paraneoplastic syndrome and is then commonly
referred to as acanthosis nigricans maligna. Involvement of mucous membranes is rare and suggests a
coexisting malignant condition.

238
Benign skin diseases
Seborrhoeic keratosis
• Most commonly arise in patients over the age of 50 years, often idiopathic
• Equal sex incidence and prevalence
• Usually multiple lesions over face and trunk
• Flat, raised, filiform and pedunculated subtypes are recognised
• Variable colours and surface may have greasy scale overlying it
• Treatment options consist of leaving alone or simple shave excision
Melanocytic naevi
Congenital • Typically appear at, or soon after, birth
melanocytic naevi • Usually greater than 1cm diameter
• Increased risk of malignant transformation (increased risk greatest for large lesions)
Junctional • Circular macules
melanocytic naevi • May have heterogeneous colour even within same lesion
• Most naevi of the palms, soles and mucous membranes are of this type
Compound naevi • Domed pigmented nodules up to 1cm in diameter
• Arise from junctional naevi, usually have uniform colour and are smooth
Spitz naevus • Usually develop over a few months in children
• May be pink or red in colour, most common on face and legs
• May grow up to 1cm and growth can be rapid, this usually results in excision
Atypical naevus • Atypical melanocytic naevi that may be autosomally dominantly inherited
syndrome • Some individuals are at increased risk of melanoma (usually have mutations of CDKN2A
gene)
• Many people with atypical naevus syndrome AND a parent sibling with melanoma will
develop melanoma
Epidermoid cysts
• Common and affect face and trunk
• They have a central punctum, they may contain small quantities of sebum
• The cyst lining is either normal epidermis (epidermoid cyst) or outer root sheath of hair follicle (pilar cyst)
Dermatofibroma
• Solitary dermal nodules
• Usually affect extremities of young adults
• Lesions feel larger than they appear visually
• Histologically they consist of proliferating fibroblasts merging with sparsely cellular dermal tissues
Painful skin lesions

• Eccrine spiradenoma
• Neuroma
• Glomus tumour
• Leimyoma
• Angiolipoma
• Neurofibroma (rarely painful) and dermatofibroma (rarely painful)
Sebaceous cysts
• Originate from sebaceous glands and contain sebum.
• Location: anywhere but most common scalp, ears, back, face, and upper arm (not palms of the hands and soles
of the feet).
• They will typically contain a punctum.
• Excision of the cyst wall needs to be complete to prevent recurrence.
• A Cock's 'Peculiar' Tumour is a suppurating and ulcerated sebaceous cyst. It may resemble a squamous cell
carcinoma- hence its name.

239
Malignancy and related lesions
Non melanoma skin cancer (BCC and SCC) are some of the commonest types of human malignancy. Up to 80% of these
are BCC's with approximately 20% comprising SCC's. The incidence of NMSC's increases with age and whilst there is a
female preponderance in those under 40 years of age, in later life the sex incidence is roughly equal.
The vast majority of NMSC's are related to UV light exposure. For SCC's the major pattern is chronic long term exposure.
For BCC's, the pattern of sporadic exposure with episodes of burning is more important. Organ transplant recipients have
a markedly increased incidence of SCC, risk factors include length of immunosuppression, ethnic origin and associated
sunlight exposure. Human papilloma virus DNA is found in the majority of transplant recipient SCC's. In addition to this
increased risk, transplant recipients are also more likely to develop locoregional recurrences following treatment.
Actinic keratosis and SCC

Actinic keratosis is viewed as a premalignant lesion because there are atypical keratinocytes present in the epidermis. In
a person with 7 actinic keratosis the risks of subsequent SCC is of the order of 10% at 10 years. The primary lesion is a
rough erythematous papule with a white to yellow scale. Lesions are typically clustered at sites of chronic sun exposure.
Squamous cell carcinoma in situ

Also known as Bowens disease the commonest presentation of in situ SCC is with an erythematous scaling patch or
elevated plaque arising on sun exposed skin in an elderly patient. Lesions may arise de novo or from pre-existing actinic
keratosis.
Pathologically there is full thickness atypia of dermal keratinocytes over a broad zone. Nuclear pleomorphism, apoptosis
and abnormal mitoses are all seen.
Invasive SCC
The commonest clinical presentation of SCC is with an erythematous keratotic papule or nodule on a background of sun
exposure. Ulceration may occur and both exophytic and endophytic areas may be seen. Regional lymphadenopathy may
be present.
Pathologically there is downward proliferation of malignant cells and invasion of the basement membrane. Poorly
differentiated lesions may show perineural invasion and require immunohistochemistry with S100 to distinguish them
from melanomas (which stain strongly positive with this marker).
Basal cell carcinoma

Nodular BCC • Commonest variant (60%)
• Raised translucent papule
• Usually affect the face
• Large nodular BCC's are locally destructive
Superficial BCC • Usually appears as superficial erythematous macule affecting the trunk
• Younger age at presentation (mean 57)
• May show areas of spontaneous regression
• Horizontal growth pattern predominates
• High recurrence rate (due to sub clinical lateral spread)
Morpheaform BCC • Macroscopically resembles flat, slightly atrophic lesion or plaque without well-defined borders
• Tumour has sub clinical lateral spread which increases recurrence rates
Cystic BCC • Often have clear or blue - grey appearance
• Cystic degeneration may not be clinically obvious and tumour may resemble nodular BCC
Basosquamous • Atypical BCC
carcinoma • Basaloid histological BCC features with eosinophillic squamoid features of SCC
• Biologically more aggressive and are more locally destructive
• Rare lesion accounts for 1% of all non melanoma skin cancers
• Metastatic disease may occur in 9-10% of cases and resemble an SCC
Keratoacanthoma
Dome shaped erythematous lesions that develop over a period of days and grow rapidly. They often contain a central pit
of keratin. They then begin to necrose and slough off. They are generally benign lesions although some do view them as
precursors of malignancy. They may be treated by curettage and cautery. If there is diagnostic doubt (they can mimic
malignancy) then formal excision biopsy is warranted.

240
Merkel cell tumours of the skin

• Rare but aggressive tumour.
• Develops from intra epidermal Merkel cells.
• Usually presents on elderly, sun damaged skin. The periorbital area is the
commonest site.
• Histologically these tumours appear within the dermis and subcutis. The
lesions consist of sheets and nodules of small hyperchromatic epithelial
cells with high rates of mitosis and apoptosis. Lymphovascular invasion is
commonly seen.
• Pre-existing infection with Merkel Cell Polyomavirus is seen in 80% cases.
Treatment
Surgical excision is first line. Margins of 1cm are required. Lesions >10mm in
diameter should undergo sentinel lymph node biopsy. Adjuvant radiotherapy
is often given to reduce the risk of local recurrence.
Prognosis
• With lymph node metastasis 5-year survival is 50% or less.
• Small lesions without nodal spread are usually associated with
a 5-year survival of 80%.

241
21. Hand Disorders – MRCS Notes – Reda

Hand diseases
Dupuytrens contracture
• Fixed flexion contracture of the hand where the fingers bend towards the palm and cannot be fully extended.
• Caused by underlying contractures of the palmar aponeurosis. The ring finger and little finger are the fingers
most commonly affected. The middle finger may be affected in advanced cases, but the index finger and the
thumb are nearly always spared.
• Progresses slowly and is usually painless. In patients with this condition, the tissues under the skin on the palm
of the hand thicken and shorten so that the tendons connected to the fingers cannot move freely. The palmar
aponeurosis becomes hyperplastic and undergoes contracture.
• Association with liver cirrhosis and alcoholism. However, many cases
are idiopathic.
• Commonest in males over 40 years of age.
• Treatment is surgical and involves fasciectomy. However, the
condition may recur and many surgical therapies are associated with
risk of neurovascular damage to the digital nerves and arteries.
Carpel tunnel syndrome

• Idiopathic median neuropathy at the carpal tunnel.
• Characterised by altered sensation of the lateral 3 fingers.
• The condition is commoner in females and is associated with other connective tissue disorders such as
rheumatoid disease. It may also occur following trauma to the distal radius.
• Symptoms occur mainly at night in early stages of the condition.
• Examination may demonstrate wasting of the muscles of the thenar eminence and symptoms may be
reproduced by Tinel’s test (compression of the contents of the carpal tunnel).
• Formal diagnosis is usually made by electrophysiological studies.
• Treatment is by surgical decompression of the carpal tunnel, a procedure achieved by division of the flexor
retinaculum. Non - surgical options include splinting and bracing.
Miscellaneous hand lumps

Osler's Osler's nodes are painful, red, raised lesions found on the hands and feet. They are the result of the
nodes deposition of immune complexes.
Bouchards Hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints (the middle joints of
nodes fingers or toes.) They are a sign of osteoarthritis, and are caused by formation of calcific spurs of the
articular cartilage.
Heberdens Typically develop in middle age, beginning either with a chronic swelling of the affected joints or the
nodes sudden painful onset of redness, numbness, and loss of manual dexterity. This initial inflammation and
pain eventually subsides, and the patient is left with a permanent bony outgrowth that often skews the
fingertip sideways. It typically affects the DIP joint.
Ganglion Swelling in association with a tendon sheath commonly near a joint. They are common lesions in the
wrist and hand. Usually they are asymptomatic and cause little in the way of functional compromise.
They are fluid filled although the fluid is similar to synovial fluid it is slightly more viscous. When the
cysts are troublesome they may be excised.
Osler's nodes
21. HAND DISORDERS – MRCS NOTES - REDA 1

242
21. HAND DISORDERS – MRCS NOTES - REDA 2

243
22. Surgical Disorders of the Brain – MRCS Notes - Reda

Head injury ...................................................................................................................................................... 2
Third nerve palsy ............................................................................................................................................ 3
Glasgow coma scale ........................................................................................................................................ 3
Sub arachnoid haemorrhage .......................................................................................................................... 4
Head injury and hematoma ............................................................................................................................ 4
Von Hippel-Lindau syndrome ......................................................................................................................... 4
Notes & Mnemonics ....................................................................................................................................... 4
22. SURGICAL DISORDERS OF THE BRAIN– MRCS NOTES - REDA 1

244
Head injury
Patients who suffer head injuries should be managed according to ATLS principles and extra cranial injuries should be
managed alongside cranial trauma. Inadequate cardiac output will compromise CNS perfusion irrespective of the nature
of the cranial injury.
Intracranial Hemorrhage & Types of traumatic brain injury

Extradural Bleeding into the space between the dura mater and the skull. Often results from
haematoma acceleration-deceleration trauma or a blow to the side of the head. The majority of
extradural haematomas occur in the temporal region where skull fractures cause a rupture
of the middle meningeal artery.
Features
• Raised intracranial pressure
• Some patients may exhibit a lucid interval
Subdural • Bleeding into the outermost meningeal layer. Most commonly occur around the frontal
haematoma and parietal lobes. May be either acute or chronic.
• Risk factors include old age and alcoholism.
• Slower onset of symptoms than a extradural haematoma.
Intracerebral Usually hyperdense lesions on CT scanning. Arise in areas of traumatic contusion with fuse to
haematoma become a haematoma. Areas of clot and fresh blood may co-exist on the same CT scan (Swirl
sign). Large haematomas and those associated with mass effect should be evacuated.
Subarachnoid Usually occurs spontaneously in the context of a ruptured cerebral aneurysm but may be
haemorrhage seen in association with other injuries when a patient has sustained a traumatic brain injury
Intraventricular Haemorrhage that occurs into the ventricular system of the brain. It is relatively rare in adult
haemorrhage surgical practice and when it does occur, it is typically associated with severe head injuries.
In premature neonates it may occur spontaneously. The blood may clot and occlude CSF
flow, hydrocephalus may result.
In neonatal practice the vast majority of IVH occur in the first 72 hours after birth, the
aetiology is not well understood and it is suggested to occur as a result of birth trauma
combined with cellular hypoxia, together with the delicate neonatal CNS.
Pathophysiology
• Primary brain injury may be focal (contusion/ haematoma) or diffuse (diffuse axonal injury)
• Diffuse axonal injury occurs as a result of mechanical shearing following deceleration, causing disruption and
tearing of axons
• Intra-cranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to
(coup) or contralateral (contre-coup) to the side of impact
• Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation
exacerbates the original injury. The normal cerebral auto regulatory processes are disrupted following trauma
rendering the brain more susceptible to blood flow changes and hypoxia
• The Cushings reflex (hypertension and bradycardia) often occurs late and is usually a pre terminal event
Management
• Where there is life threatening rising ICP such as in extra dural haematoma and whilst theatre is prepared or
transfer arranged use of IV mannitol/ frusemide may be required.
• Diffuse cerebral oedema may require decompressive craniotomy
• Exploratory Burr Holes have little management in modern practice except where scanning may be unavailable
and to thus facilitate creation of formal craniotomy flap
• Depressed skull fractures that are open require formal surgical reduction and debridement, closed injuries may
be managed non operatively if there is minimal displacement.
• ICP monitoring is appropriate in those who have GCS 3-8 and normal CT scan.
• ICP monitoring is mandatory in those who have GCS 3-8 and abnormal CT scan.
• Hyponatraemia is most likely to be due to syndrome of inappropriate ADH secretion.
• Minimum of cerebral perfusion pressure of 70mmHg in adults.
• Minimum cerebral perfusion pressure of between 40 and 70 mmHg in children.

245
Interpretation of pupillary findings in head injuries
Pupil size Light response Interpretation
Unilaterally dilated Sluggish or fixed 3rd nerve compression secondary to tentorial
herniation
Unilaterally dilated or equal Cross reactive (Marcus - Gunn) Optic nerve injury
Bilaterally dilated Sluggish or fixed • Poor CNS perfusion
• Bilateral 3rd nerve palsy
Bilaterally constricted May be difficult to assess • Opiates
• Pontine lesions
• Metabolic encephalopathy
Unilaterally constricted Preserved Sympathetic pathway disruption
Third nerve palsy

Features
• Eye is deviated 'down and out'
• Ptosis
• Pupil may be dilated (sometimes called a 'surgical' third nerve palsy)
Causes
• Diabetes mellitus
• Vasculitis e.g. temporal arteritis, SLE
• False localizing sign* due to uncal herniation through tentorium if raised ICP
• Posterior communicating artery aneurysm (pupil dilated, painful)
• Cavernous sinus thrombosis
• Weber's syndrome: ipsilateral third nerve palsy with contralateral hemiplegia - caused by midbrain strokes
• Other possible causes: amyloid, multiple sclerosis
*This term is usually associated with sixth nerve palsies but it may be used for a variety of neurological presentations
Glasgow coma scale

Modality Options
Eye opening • Spontaneous
• To speech
• To pain
• None
Verbal response • Orientated
• Confused
• Words
• Sounds
• None
Motor response • Obeys commands
• Localises to pain
• Withdraws from pain
• Abnormal flexion to pain (decorticate posture)
• Extending to pain
• None

246
Sub arachnoid haemorrhage
Spontaneous intracranial haemorrhage
Most commonly sub arachnoid haemorrhage. It is due to intra cranial aneurysm in 85% cases. Approximately 10% of
cases will have normal angiography and the cause will remain unclear. Patients with inherited connective tissue disorders
are at higher risk although most cases are sporadic.
>95% cases will have headache (often thunderclap)
>15% will have coma
Investigation
CT scan for all (although as CSF blood clears the sensitivity declines)
Lumbar puncture if CT normal (very unlikely if normal)
CT angiogram to look for aneurysms.
Management
Supportive treatment, optimising BP (not too high if untreated aneurysm) and ventilation if needed.
Nimodipine reduces cerebral vasospasm and reduces poor outcomes.
Untreated patients most likely to rebleed in first 2 weeks.
Patients developing hydrocephalus will need a V-P shunt (external ventricular drain acutely).
Electrolytes require careful monitoring and hyponatraemia is common.
Treatment of aneurysm
>80% aneuryms arise from the anterior circulation
Craniotomy and clipping of aneurysm is standard treatment, alternatively suitable lesions may be coiled using an
endovascular approach. Where both options are suitable data suggests that outcomes are better with coiling than
surgery.
Head injury and hematoma

Risk of haematoma (requiring removal) in adults attending accident and emergency units following head injury.
Injury Conscious level Risk of haematoma requiring removal
Concussion, no skull fracture Orientated 1 in 6000
Concussion, no skull fracture Not orientated 1 in 120
Skull fracture Orientated 1 in 32
Skull fracture Not orientated 1 in 4
Von Hippel-Lindau syndrome

Von Hippel-Lindau (VHL) syndrome is an autosomal dominant condition predisposing to neoplasia. It is due to an
abnormality in the VHL gene located on short arm of chromosome 3
Features
• Cerebellar haemangiomas
• Retinal haemangiomas: vitreous haemorrhage
• Renal cysts (premalignant)
• Phaeochromocytoma
• Extra-renal cysts: epididymal, pancreatic, hepatic
• Endolymphatic sac tumours
Notes & Mnemonics

PITS (Parietal-Inferior, Temporal-Superior)
Superior quadranopia = temporal lobe lesion
Inferior quadranopia = parietal lobe lesion
Painful third nerve palsy = posterior communicating artery aneurysm

247
23. Pediatric Surgery – MRCS Notes - Reda

Congenital heart disease ................................................................................................................................ 2
Tetralogy of Fallot ........................................................................................................................................... 2
Paediatric fluid management ......................................................................................................................... 3
Meckel's diverticulum..................................................................................................................................... 3
Paediatric Gastrointestinal disorders............................................................................................................. 4
Paediatric GI Bleeding..................................................................................................................................... 4
Bilious vomiting in neonates .......................................................................................................................... 5
Biliary atresia .................................................................................................................................................. 5
Paediatric umbilical disorders ........................................................................................................................ 6
Paediatric inguinal hernia............................................................................................................................... 6
Paediatric Urology - Foreskin disorders ......................................................................................................... 7
Bronchogenic cysts ......................................................................................................................................... 7
Urinary tract infection - Paediatric................................................................................................................. 8
Urethral valves ................................................................................................................................................ 8
Vesicoureteric reflux ....................................................................................................................................... 8
23. PAEDIATRIC SURGERY – MRCS NOTES - REDA 1

248
Congenital heart disease
Acyanotic - most common causes
• Ventricular septal defects (VSD) - most common, accounts for 30%
• Atrial septal defect (ASD)
• Patent ductus arteriosus (PDA)
• Coarctation of the aorta
• Aortic valve stenosis
VSDs are more common than ASDs. However, in adult patients ASDs are the more common new diagnosis as they
generally present later.
Cyanotic - most common causes

• Tetralogy of Fallot
• Transposition of the great arteries (TGA)
• Tricuspid atresia
• Pulmonary valve stenosis
Tetralogy of Fallot
Tetralogy of Fallot (TOF) is the most common cause of cyanotic congenital heart disease*. It typically presents at around
1-2 months, although may not be picked up until the baby is 6 months old
The four characteristic features are:

• ventricular septal defect (VSD)
• right ventricular hypertrophy
• right ventricular outflow tract obstruction, pulmonary stenosis
• overriding aorta
The severity of the right ventricular outflow tract obstruction determines the
degree of cyanosis and clinical severity
Other features
• Cyanosis
• Right-to-left shunt
• Ejection systolic murmur due to pulmonary stenosis (the VSD
doesn't usually cause a murmur)
• A right-sided aortic arch is seen in 25% of patients
• Chest x-ray shows a 'boot-shaped' heart, ECG shows right
ventricular hypertrophy
Management
• Surgical repair is often undertaken in two parts
• Cyanotic episodes may be helped by beta-blockers to reduce
infundibular spasm
*However, at birth transposition of the great arteries is the more common

lesion as patients with TOF generally present at around 1-2 months

249
Paediatric fluid management
Since 2000 there have been at least 4 reported deaths from fluid induced hyponatraemia in children. This led to the
National Patient Safety Agency introducing revised guidelines in 2007.
Indications for IV fluids include:
• Resuscitation and circulatory support
• Replacing on-going fluid losses
• Maintenance fluids for children for whom oral fluids are not appropriate
• Correction of electrolyte disturbances
Fluids to be avoided
Outside the neonatal period saline / glucose solutions should not be given. The greatest risk is with saline 0.18 / glucose
4% solutions. The report states that 0.45% saline / 5% glucose may be used. But preference should be given to isotonic
solutions and few indications exist for this solution either.
Fluids to be used
• 0.9% saline
• 5% glucose (though only with saline for maintenance and not to replace losses)
• Hartmann's solution
Potassium should be added to maintenance fluids according patients plasma potassium levels (which should be
monitored).
Intraoperative fluid management

Neonates should receive glucose 10% during surgery.
Other children should receive isotonic crystalloid.
Maintenance fluids
Weight Water requirement/kg/day Na mmol/kg/day K mmol/kg/day
First 10Kg body weight 100ml 2-4 1.5-2.5
Second 10Kg body weight 50ml 1-2 0.5-1.5
Subsequent Kg 20ml 0.5-1.0 0.2-0.7
Glucose will need to be given to neonates- usually 10% at a rate of 60ml/Kg/day.
Meckel's diverticulum
• Congenital abnormality resulting in incomplete obliteration of the vitello-intestinal duct
• Normally, in the foetus, there is an attachment between the vitello-intestinal duct and the yolk sac.This disappears
at 6 weeks gestation.
• The tip is free in majority of cases.
• Associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas.
• Arterial supply: omphalomesenteric artery.
• 2% of population, 2 inches long, 2 feet from the ileocaecal valve.
• Typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic ulceration. Pancreatic
and jejunal mucosa can also occur.
Clinical
• Normally asymptomatic and an incidental finding.
• Complications are the result of obstruction, ectopic tissue, or inflammation.
• Removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection
and anastomosis.

250
Paediatric Gastrointestinal disorders
Pyloric stenosis • M>F
• 5-10% Family history in parents
• Projectile non bile stained vomiting at 4-6 weeks of life
• Diagnosis is made by test feed or USS
• Treatment: Ramstedt pyloromyotomy (open or laparoscopic)
Acute • Uncommon under 3 years
appendicitis • When occurs may present atypically
Mesenteric • Central abdominal pain and URTI
adenitis • Conservative management
Intussusception • Telescoping bowel
• Proximal to or at the level of, ileocaecal valve
• 6-9 months of age
• Colicky pain, diarrhoea and vomiting, sausage shaped mass, red jelly stool.
• Treatment: reduction with air insufflation
Malrotation • High caecum at the midline
• Feature in exomphalos, congenital diaphragmatic hernia, intrinsic duodenal atresia
• May be complicated by development of volvulus, infant with volvulus may have bile stained
vomiting
• Diagnosis is made by upper GI contrast study and USS
• Treatment is by laparotomy, if volvulus is present (or at high risk of occurring then a Ladd’s
procedure is performed
Hirschsprung's • Absence of ganglion cells from myenteric and submucosal plexuses
disease • Occurs in 1/5000 births
• Full thickness rectal biopsy for diagnosis
• Delayed passage of meconium and abdominal distension
• Treatment is with rectal washouts initially, thereafter an anorectal pull through procedure
Oesophageal • Associated with tracheo-oesophageal fistula and polyhydramnios
atresia • May present with choking and cyanotic spells following aspiration
• VACTERL associations
Meconium ileus • Usually delayed passage of meconium and abdominal distension
• Majority have cystic fibrosis
• X-Rays may not show a fluid level as the meconium is viscid (depends upon feeding), PR
contrast studies may dislodge meconium plugs and be therapeutic
• Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to
remove the plugs
Biliary atresia • Jaundice > 14 days
• Increased conjugated bilirubin
• Urgent Kasai procedure
Necrotising • Prematurity is the main risk factor
enterocolitis • Early features include abdominal distension and passage of bloody stools
• X-Rays may show pneumatosis intestinalis and evidence of free air
• Increased risk when empirical antibiotics are given to infants beyond 5 days
• Treatment is with total gut rest and TPN, babies with perforations will require laparotomy
• Gastroschisis: Isolated abnormality, bowel lies outside abdominal wall through defect located to right of umbilicus.
• Exomphalos (Omphalocele): Liver and gut remain covered with membranous sac connected to umbilical cord. It is
associated with other developmental defects.
Paediatric GI Bleeding
Site Newborn 1 month to 1 year 1 to 2 years Older than 2 years
Upper • Haemorrhagic disease • Oesophagitis • Peptic ulcer disease • Varices
GI tract • Swallowed maternal blood • Gastritis
Lower • Anal fissure • Anal fissure • Polyps • IBD
GI tract • NEC • Intussusception • Meckel’s diverticulum • Polyps
• Intussusception

251
Bilious vomiting in neonates
Causes of intestinal obstruction with bilious vomiting in neonates
Disorder Incidence & causation Age at presentation Diagnosis Treatment
Duodenal 1 in 5000 (higher in Few hours after birth AXR shows "double Duodenoduodenostomy
atresia Downs syndrome) bubble sign, contrast
study may confirm
Malrotation Usually cause by Usually 3-7 days after Upper GI contrast Ladd's procedure
with volvulus incomplete rotation birth, volvulus with study may show DJ
during embryogenesis compromised flexure is more
circulation may result medially placed, USS
in peritoneal signs and may show abnormal
haemodynamic orientation of SMA
instability and SMV
Jejunal/ ileal Usually caused by Usually within 24 AXR will show air- Laparotomy with
atresia vascular insufficiency in hours of birth fluid levels primary resection and
utero, usually 1 in 3000 anastomosis
Meconium Occurs in between 15 Typically in first 24-48 Air - fluid levels on Surgical decompression,
ileus and20% of those babies hours of life with AXR, sweat test to serosal damage may
with cystic fibrosis, abdominal distension confirm cystic fibrosis require segmental
otherwise 1 in 5000 and bilious vomiting resection
Necrotising Up to 2.4 per 1000 Usually second week Dilated bowel loops Conservative and
enterocolitis births, risks increased in of life on AXR, pneumatosis supportive for non
prematurity and inter- and portal venous air perforated cases,
current illness laparotomy and
resection in cases of
perforation of ongoing
clinical deterioration
Biliary atresia
• 1 in 17000 affected
• Biliary tree lumen is obliterated by an inflammatory cholangiopathy causing progressive liver damage
Clinical features
• Infant well in 1st few weeks of life
• No family history of liver disease
• Jaundice in infants > 14 days in term infants (>21 days in pre term infants)
• Pale stool, yellow urine (colourless in babies)
• Associated with cardiac malformations, polysplenia, situs inversus
Investigation
• Conjugated bilirubin (prolonged physiological jaundice or breast milk jaundice will cause a rise in unconjugated
bilirubin, whereas those with obstructive liver disease will have a rise in conjugated bilirubin)
• Ultrasound of the liver (excludes extrahepatic causes, in biliary atresia infant may have tiny or invisible
gallbladder)
• Hepato-iminodiacetic acid radionuclide scan (good uptake but no excretion usually seen)
Management
• Early recognition is important to prevent liver transplantation.
• Nutritional support.
• Roux-en-Y portojejunostomy (Kasai procedure).
• If Kasai procedure fails or late recognition, a liver transplant becomes the only option.

252
Paediatric umbilical disorders
Embryology
During development the umbilicus has two umbilical arteries and one umbilical vein. The arteries are continuous with the
internal iliac arteries and the vein is continuous with the falciform ligament (ductus venosus). After birth the cord
dessicates and separates and the umbilical ring closes.
Umbilical hernia
Up to 20% of neonates may have an umbilical hernia, it is more common in premature infants. The majority of these
hernias will close spontaneously (may take between 12 months and three years). Strangulation is rare.
Paraumbilical hernia
These are due to defects in the linea alba that are in close proximity to the umbilicus. The edges of a paraumbilical hernia
are more clearly defined than those of an umbilical hernia. They are less likely to resolve spontaneously than an umbilical
hernia.
Omphalitis
This condition consists of infection of the umbilicus. Infection with Staphylococcus aureus is the commonest cause. The
condition is potentially serious as infection may spread rapidly through the umbilical vessels in neonates with a risk of
portal pyaemia, and portal vein thrombosis. Treatment is usually with a combination of topical and systemic antibiotics.
Umbilical granuloma
These consist of cherry red lesions surrounding the umbilicus, they may bleed on contact and be a site of seropurulent
discharge. Infection is unusual and they will often respond favorably to chemical cautery with topically applied silver
nitrate.
Persistent urachus
This is characterised by urinary discharge from the umbilicus. It is caused by persistence of the urachus which attaches to
the bladder. They are associated with other urogenital abnormalities.
Persistent vitello-intestinal duct

This will typically present as an umbilical discharge that discharges small bowel content. Complete persistence of the
duct is a rare condition. Much more common is the persistence of part of the duct (Meckels diverticulum). Persistent
vitello-intestinal ducts are best imaged using a contrast study to delineate the anatomy and are managed by laparotomy
and surgical closure.
Paediatric inguinal hernia

Inguinal hernias are a common disorder in children. They are commoner in males as the testis migrates from its location
on the posterior abdominal wall, down through the inguinal canal. A patent processus vaginalis may persist and be the
site of subsequent hernia development.
Children presenting in the first few months of life are at the highest risk of strangulation and the hernia should be
repaired urgently. Children over 1 year of age are at lower risk and surgery may be performed electively. For paediatric
hernias a herniotomy without implantation of mesh is sufficient. Most cases are performed as day cases, neonates and
premature infants are kept in hospital overnight as there is a recognised increased risk of post operative apnoea.

253
Paediatric Urology - Foreskin disorders

Disorders of the foreskin
At birth and in the neonatal period the normal foreskin is non retractile due to the presence of adhesions between the
foreskin and glans. In most cases these will separate spontaneously. By the end of puberty 95% of foreskins can be
retracted. In some children the non-retractile foreskin may balloon during micturition. This is a normal variant and
requires no specific treatment.
Balanitis This is inflammation of the glans penis. It may occur in both circumcised and non-circumcised
individuals.
Posthitis This is inflammation of the foreskin. It may occur as a result of infections such as gonorrhoea and
other STD's. It may also complicate diabetes. Posthitis may progress to phimosis and as this may
make cleaning of the glans difficult and allow progression to balanoposthitis.
Paraphimosis Prolonged retraction of the foreskin proximal to the glans may allow oedema to occur. This may
then make foreskin manipulation difficult. It can usually be managed by compression to reduce the
oedema and replacement of the foreskin. Where this fails a dorsal slit may be required and this
followed by delayed circumcision.
Phimosis This is inability to retract the foreskin and may be partial or complete. It may occur secondary to
balanoposthitis or balanitis xerotica obliterans. Depending upon the severity and symptoms
treatment with circumcision may be required.
Balanitis xerotica This is a dermatological condition in which scarring of the foreskin occurs leading to phimosis. It is
obliterans rare below the age of 5 years. Treatment is usually with circumcision.
Bronchogenic cysts
Overview
Bronchogenic cysts most commonly arise as a result of anomalous development of the ventral foregut. They are most
commonly single, although multiple cysts are described.
They often lie near the midline and most frequently occur in the region of the carina. They may be attached to the
tracheobronchial tree, although they are seldom in direct connection with it.
Cases may be asymptomatic or present with respiratory symptoms early in the neonatal period.
They are the second most common type of foregut cysts (after enterogenous cysts) in the middle mediastinum. Up to
50% of cases are diagnosed prior to 15 years of age.
Investigation
Many cases are diagnosed on antenatal ultrasound. Others may be detected on conventional chest radiography as a
midline spherical mass or cystic structure. Once the diagnosis is suspected a CT scan should be performed.
Treatment
Thorascopic resection is the ideal treatment. Very young babies can be operated on once they reach six weeks of age.

254
Urinary tract infection - Paediatric

• UTI's may occur in 5% of young girls and 1-2% males. The incidence is higher in premature infants.
• E-Coli accounts for 80% cases.
• In children with UTI it is important to establish whether there is underlying urinary stasis or vesico-ureteric
reflux (or both).
• Pyelonephritis in children carries the risk of renal scarring 10% and this translates into a 10% risk of developing
end stage renal disease.
Diagnosis
• Pyrexia lasting for more than 3 days mandates urine testing.
• Samples may be taken from mid-stream urine samples or supra pubic aspiration. Urine collected from nappies
usually have faecal contaminants. In samples showing mixed growth contamination of the sample has usually
occurred.
• As in adults >105 colony forming units of a single organism are usually indicative of a UTI.
Management
• A single isolated UTI (in girls) may be managed expectantly.
• > 2 UTI's (or 1 in males) in a 6 month period should prompt further testing.
• Voiding cystourethrograms show the greatest anatomical detail and is the ideal first line test in males; isotope
cystography has a lower radiation dose and is the first line test in girls.
• USS should also be performed. Renal cortical scintigraphy should be performed when renal scarring is
suspected.
Urethral valves
Posterior urethral valves are the commonest cause of infravesical outflow obstruction in males. They may be diagnosed
on ante natal ultrasonography. Because the bladder has to develop high emptying pressures in utero, the child may
develop renal parenchymal damage. This translates to renal impairment noted in 70% of boys at presentation. Treatment
is with bladder catheterisation. Endoscopic valvotomy is the definitive treatment of choice with cystoscopic and renal
follow up.
Vesicoureteric reflux
Vesicoureteric reflux (VUR) is the abnormal backflow of urine from the bladder into the ureter and kidney. It is relatively
common abnormality of the urinary tract in children and predisposes to urinary tract infection (UTI), being found in
around 30% of children who present with a UTI. As around 35% of children develop renal scarring it is important to
investigate for VUR in children following a UTI
Pathophysiology of VUR
• ureters are displaced laterally, entering the bladder in a more perpendicular fashion than at an angle
• therefore shortened intramural course of ureter
• vesicoureteric junction cannot therefore function adequately
The table below summarises the grading of VUR
{Grade}
I Reflux into the ureter only, no dilatation
II Reflux into the renal pelvis on micturition, no dilatation
III Mild/moderate dilatation of the ureter, renal pelvis and calyces
IV Dilation of the renal pelvis and calyces with moderate ureteral tortuosity
V Gross dilatation of the ureter, pelvis and calyces with ureteral tortuosity
Investigation
• VUR is normally diagnosed following a micturating cystourethrogram
• a DMSA scan may also be performed to look for renal scarring

255
24. Orthopaedics – MRCS Notes – Reda

Avascular necrosis .......................................................................................................................................... 2
Bone disease ................................................................................................................................................... 3
Osteomalacia .................................................................................................................................................. 3
Epiphyseal fractures ....................................................................................................................................... 4
Scaphoid fractures .......................................................................................................................................... 4
Eponymous fractures ...................................................................................................................................... 5
Pathological fractures ..................................................................................................................................... 6
Pseudogout ..................................................................................................................................................... 6
Knee injury ...................................................................................................................................................... 7
Knee collateral ligament ................................................................................................................................. 8
Paediatric orthopaedics .................................................................................................................................. 9
Perthes disease ............................................................................................................................................... 9
Septic Arthritis - Paediatric........................................................................................................................... 10
Talipes Equinovarus ...................................................................................................................................... 10
Diseases affecting the vertebral column ..................................................................................................... 11
Spinal disorders............................................................................................................................................. 12
Ankle injuries ................................................................................................................................................ 15
Shoulder disorders ........................................................................................................................................ 17
24. ORTHOPAEDICS– MRCS NOTES - REDA 1

256
Avascular necrosis
• Cellular death of bone components due to interruption of the blood supply, causing bone destruction
• Main joints affected are hip, scaphoid, lunate and the talus.
• It is not the same as non-union. The fracture has usually united.
• Radiological evidence is slow to appear.
• Vascular ingrowth into the affected bone may occur. However, many joints will develop secondary osteoarthritis.
Presentation Causes “PLASTIC RAGS”

Usually pain. Often despite apparent fracture union. Pancreatitis
Lupus
Investigation Alcohol
MRI scanning will show changes earlier than plain films. Steroids
Trauma
Treatment Idiopathic, Infection
• In fractures at high risk sites anticipation is key. Early prompt and Caisson disease, Collagen vascular disease
accurate reduction is essential.
Radiation, rheumatoid arthritis
• Non weight bearing may help to facilitate vascular regeneration.
Amyloid
• Joint replacement may be necessary, or even the preferred option (e.g.
Hip in the elderly). Gaucher disease
Sickle cell disease

257
Bone disease
Disease Features Treatment
Pagets • Focal bone resorption followed by excessive and chaotic bone deposition Bisphosphonates
• Affects (in order): spine, skull, pelvis and femur
• Serum alkaline phosphatase raised (other parameters normal)
• Abnormal thickened, sclerotic bone on x-rays
• Risk of cardiac failure with >15% bony involvement
• Small risk of sarcomatous change
Osteoporosis • Excessive bone resorption resulting in demineralised bone Bisphosphonates,
• Commoner in old age calcium and
• Increased risk of pathological fracture, otherwise asymptomatic vitamin D
• Alkaline phosphatase normal, calcium normal
Secondary bone • Bone destruction and tumour infiltration Radiotherapy,
tumours • Mirel scoring used to predict risk of fracture prophylactic
• Appearances depend on primary (e.g.sclerotic - prostate, lytic - breast) fixation and
• Elevated serum calcium and alkaline phosphatase may be seen analgesia
Osteomalacia
Basics
• Normal bony tissue but decreased mineral content
• Rickets if when growing
• Osteomalacia if after epiphysis fusion
Types
• Vitamin D deficiency e.g. malabsorption, lack of sunlight, diet
• Renal failure
• Drug induced e.g. anticonvulsants
• Vitamin D resistant; inherited
• Liver disease, e.g. cirrhosis
Features
• Rickets: knock-knee, bow leg, features of hypocalcaemia
• Osteomalacia: bone pain, fractures, muscle tenderness, proximal myopathy
Investigation
• Low calcium, phosphate, 25(OH) vitamin D
• Raised alkaline phosphatase
• X-ray: children - cupped, ragged metaphyseal surfaces; adults - translucent bands (Looser's zones or
pseudofractures)
Treatment
• Calcium with vitamin D tablets

258
Epiphyseal fractures
Fractures involving the growth plate in children are classified using the Salter - Harris system.
There are 5 main types.
Salter Harris Classification – SALTER Mnemonic

Type Description
Type 1 – S Slip - Transverse fracture through the growth plate
Type 2 – A Above - Fracture through the growth plate to the metaphysis (commonest type)
Type 3 – L Lower - Fracture through the growth plate and the epiphysis with metaphysis spared
Type 4 – TE Though Everything - Fracture involving the growth plate, metaphysis and epiphysis
Type 5 - R Rammed (Crushed) - Compression fracture of the growth plate (worst outcome)
Management
Non displaced type 1 injuries can generally be managed conservatively. Unstable or more extensive injuries will usually
require surgical reduction and/ or fixation, as proper alignment is crucial.
Scaphoid fractures
• Scaphoid fractures are the commonest carpal fractures.
• Surface of scaphoid is covered by articular cartilage with small area available for blood vessels (fracture risks
blood supply)
• Forms floor of anatomical snuffbox
• Risk of fracture associated with fall onto outstretched hand (tubercle, waist, or proximal third)
• Ulnar deviation AP needed for visualization of scaphoid
• Immobilization of scaphoid fractures difficult
Management
Non-displaced fractures • Casts or splints
• Percutaneous scaphoid fixation
Displaced fracture Surgical fixation, usually with a screw
Complications
• Non union of scaphoid
• Avascular necrosis of the scaphoid
• Scapholunate disruption and wrist collapse
• Degenerative changes of the adjacent joint

259
Eponymous fractures
Colles' fracture (dinner fork deformity)
• Fall onto extended outstretched hand
• Classical Colles' fractures have the following 3 features:
1. Transverse fracture of the radius
2. 1 inch proximal to the radio-carpal joint
3. Dorsal displacement and angulation
Smith's fracture (reverse Colles' fracture)

• Volar angulation of distal radius fragment (Garden spade deformity)
• Caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed
Bennett's fracture
• Intra-articular fracture of the first carpometacarpal joint
• Impact on flexed metacarpal, caused by fist fights
• X-ray: triangular fragment at ulnar base of metacarpal
Monteggia's fracture
• Dislocation of the proximal radioulnar joint in association with an ulna fracture
• Fall on outstretched hand with forced pronation
• Needs prompt diagnosis to avoid disability
Galeazzi fracture
• Radial shaft fracture with associated dislocation of the distal radioulnar joint
• Direct blow
Pott's fracture
• Bimalleolar ankle fracture
• Forced foot eversion
Barton's fracture
• Distal radius fracture (Colles'/Smith's) with associated radiocarpal dislocation
• Fall onto extended and pronated wrist
• Involvement of the joint is a defining feature
Bennett's fracture Monteggia’s fracture Rolando fracture

260
Pathological fractures
• A pathological fracture occurs in abnormal bone due to insignificant injury
Causes
Metastatic tumours • Breast
• Lung
• Thyroid
• Renal
• Prostate
Bone disease • Osteogenesis imperfecta
• Osteoporosis
• Metabolic bone disease
• Paget's disease
Local benign conditions • Chronic osteomyelitis
• Solitary bone cyst
Primary malignant tumours • Chondrosarcoma
• Osteosarcoma
• Ewing's tumour
Pseudogout
Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate in the
synovium
Risk factors
• Hyperparathyroidism
• Hypothyroidism
• Haemochromatosis
• Acromegaly
• Low magnesium, low phosphate
• Wilson's disease
Features
• Knee, wrist and shoulders most commonly affected
• Joint aspiration: weakly-positively birefringent rhomboid shaped crystals
• X-ray: chondrocalcinosis
Management
• Aspiration of joint fluid, to exclude septic arthritis
• NSAIDs or intra-articular, intra-muscular or oral steroids as for gout

261
Knee injury
Types of injury
Ruptured anterior • Sport injury
cruciate ligament • Mechanism: high twisting force applied to a bent knee
• Typically presents with: loud crack, pain and RAPID joint swelling (haemoarthrosis)
• Poor healing
• Management: intense physiotherapy or surgery
Ruptured posterior • Mechanism: hyperextension injuries
cruciate ligament • Tibia lies back on the femur
• Paradoxical anterior draw test
Rupture of medial • Mechanism: leg forced into valgus via force outside the leg
collateral ligament • Knee unstable when put into valgus position
Menisceal tear • Rotational sporting injuries
• Delayed knee swelling
• Joint locking (Patient may develop skills to "unlock" the knee
• Recurrent episodes of pain and effusions are common, often following minor trauma
Chondromalacia • Teenage girls, following an injury to knee e.g. Dislocation patella
patellae • Typical history of pain on going downstairs or at rest
• Tenderness, quadriceps wasting
Dislocation of the • Most commonly occurs as a traumatic primary event, either through direct trauma or
patella through severe contraction of quadriceps with knee stretched in valgus and external
rotation
• Genu valgum, tibial torsion and high riding patella are risk factors
• Skyline x-ray views of patella are required, although displaced patella may be clinically
obvious
• An osteochondral fracture is present in 5%
• The condition has a 20% recurrence rate
Fractured patella • 2 types:
• Direct blow to patella causing undisplaced fragments
• Avulsion fracture
Tibial plateau • Occur in the elderly (or following significant trauma in young)
fracture • Mechanism: knee forced into valgus or varus, but the knee fractures before the ligaments
rupture
• Varus injury affects medial plateau and if valgus injury, lateral plateau depressed fracture
occurs
• Classified using the Schatzker system (see below)
Schatzker Classification system for tibial plateau fractures

262
Knee collateral ligament
Anatomy
The tibial collateral ligament is a broad, flat band. Its upper end has an extensive attachment to the medial epicondyle of
the femur with some fibres projecting onto the adductor magnus tendon. The ligament passes downwards and forwards
to the medial side of the tibia. The deepest fibres are fused with the medial meniscus.
The fibular collateral ligament is round and cord like and stands clear of the thin, lateral part of the fibrous capsule. It is
enclosed within the fascia lata. It passes from the lateral epicondyle of the femur to the head of the fibula in front of its
highest point and splits the tendon of biceps femoris. On the lateral side of the joint the fibres are short and weak and
bridge the interval between the femoral and tibial condyles. The popliteus tendon intervenes between the lateral
meniscus and the capsule.
The tibial and fibular collateral ligaments prevent disruption of the joint at the sides. They are most tightly stretched in
extension, and then their direction- the fibular ligament downwards and backwards, the tibial downwards and forwards-
prevents rotation of the tibia laterally or the femur medially. Rotation may be demonstrated in the flexed knee.
Injury
The collateral ligaments are commonly injured, the medial is most often affected. It requires a significant force such as
sporting tackle or motor vehicle to strike the side of the leg. Associated injuries to both the tibial plateau or menisci are
not uncommon.
Grading and treatment

Grade of injury Features Treatment
1 Minor tearing of ligament fibres Conservative (analgesia and physiotherapy)
Negative instability tests
2 Ligament laxity (seen with knee in 30o flexion) Usually splinting or casting for 4-6 weeks
Knee stable when joint extended
3 Ligament completely torn Surgical ligament reconstruction
Joint instability

263
Paediatric orthopaedics
Diagnosis Mode of presentation Treatment Radiology
Developmental Usually diagnosed in infancy by Splints and harnesses or Initially no obvious change
dysplasia of the screening tests. May be bilateral, traction. In later years on plain films and USS gives
hip when disease is unilateral there osteotomy and hip realignment best resolution until 3
may be leg length inequality. As procedures may be needed. In months of age. On plain
disease progresses child may limp arthritis a joint replacement may films Shentons line should
and then early onset arthritis. be needed. However, this is best form a smooth arc
More common in extended deferred if possible as it will
breech babies. almost certainly require revision
Perthes Disease Hip pain (may be referred to the Remove pressure from joint to X-rays will show flattened
knee) usually occurring between allow normal development. femoral head. Eventually in
5 and 12 years of age. Bilateral Physiotherapy. Usually self- untreated cases the
disease in 20%. limiting if diagnosed and treated femoral head will fragment.
promptly.
Slipped upper Typically seen in obese male Bed rest and non-weight X-rays will show the femoral
femoral adolescents. Pain is often bearing. Aim to avoid avascular head displaced and falling
epiphysis referred to the knee. Limitation necrosis. If severe slippage or inferolaterally (like a
to internal rotation is usually risk of it occurring then melting ice cream cone)
seen. Knee pain is usually present percutaneous pinning of the hip The Southwick angle gives
2 months prior to hip slipping. may be required. indication of disease
Bilateral in 20%. severity
Perthes disease
Perthes disease
• Idiopathic avascular necrosis of the femoral epiphysis of the femoral head
• Impaired blood supply to femoral head, causing bone infarction. New vessels develop and ossification occurs.
The bone either heals or a subchondral fracture occurs.
Clinical features
• Males 4x's greater than females
• Age between 2-12 years (the younger the age of onset, the better the prognosis)
• Limp
• Hip pain
• Bilateral in 20%
Diagnosis
Plain x-ray, Technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist.
Catterall staging
Stage Features
Stage 1 Clinical and histological features only
Stage 2 Sclerosis with or without cystic changes and preservation of the articular surface
Stage 3 Loss of structural integrity of the femoral head
Stage 4 Loss of acetabular integrity
Management
• To keep the femoral head within the acetabulum: cast, braces
• If less than 6 years: observation
• Older: surgical management with moderate results
• Operate on severe deformities
Indication for treatment (aide memoire): Half a dozen, half a head
Those aged greater than 6 years with >50% involvement of the femoral head should almost always be treated.
Prognosis
Most cases will resolve with conservative management. Early diagnosis improves outcomes.

264
Septic Arthritis - Paediatric
Septic arthritis
• Staph aureus commonest organism
• Urgent washout and antibiotics otherwise high risk of joint destruction
Diagnosis
• Plain x-rays
• Consider aspiration
• Utilise the Kocher criteria (see below)
Kocher criteria:
1. Non weight bearing on affected side
2. ESR > 40 mm/hr
3. Fever
4. WBC count of >12,000 mm3
When 4/4 criteria are met, there is a 99% chance that the child has septic arthritis
Treatment
Surgical drainage of the affected joint is required, this should be done as soon as possible since permanent damage to
the joint may occur. In some cases repeated procedures are necessary. Appropriate intravenous antibiotics should be
administered.
Talipes Equinovarus
Congenital talipes equinovarus.
Features:
• Equinus of the hindfoot.
• Adduction and varus of the midfoot.
• High arch.
Most cases in developing countries. Incidence in UK is 1 per 1000 live

births. It is more common in males and is bilateral in 50% cases.
There is a strong familial link. It may also be associated with other
developmental disorders such as Down's syndrome.
Key anatomical deformities:

• Adducted and inverted calcaneus
• Wedge shaped distal calcaneal articular surface
• Severe Tibio-talar plantar flexion.
• Medial Talar neck inclination
• Displacement of the navicular bone (medially)
• Wedge shaped head of talus
• Displacement of the cuboid (medially)
Management
Conservative first, the Ponseti method is best described and gives comparable
results to surgery. It consists of serial casting to mold the foot into correct shape.
Following casting around 90% will require a Achilles tenotomy. This is then followed
by a phase of walking braces to maintain the correction.
Surgical correction is reserved for those cases that fail to respond to conservative
measures. The procedures involve multiple tenotomies and lengthening procedures.
In patients who fail to respond surgically an Ilizarov frame reconstruction may be
attempted and gives good results.

265
Diseases affecting the vertebral column
Ankylosing • Chronic inflammatory disorder affecting the axial skeleton
spondylitis • Sacro-ilitis is a usually visible in plain films
• Up to 20% of those who are HLA B27 positive will develop the condition
• Affected articulations develop bony or fibrous changes
• Typical spinal features include loss of the lumbar lordosis and progressive kyphosis of the
cervico-thoracic spine
Scheuermann's • Epiphysitis of the vertebral joints is the main pathological process
disease • Predominantly affects adolescents
• Symptoms include back pain and stiffness
• X-ray changes include epiphyseal plate disturbance and anterior wedging
• Clinical features include progressive kyphosis (at least 3 vertebrae must be involved)
• Minor cases may be managed with physiotherapy and analgesia, more severe cases may
require bracing or surgical stabilisation
Scoliosis • Consists of curvature of the spine in the coronal plane
• Divisible into structural and non structural, the latter being commonest in adolescent females
who develop minor postural changes only. Postural scoliosis will typically disappear on
manoeuvres such as bending forwards
• Structural scoliosis affects > 1 vertebral body and is divisible into idiopathic, congential and
neuromuscular in origin. It is not correctable by alterations in posture
• Within structural scoliosis, idiopathic is the most common type
• Severe, or progressive structural disease is often managed surgically with bilateral rod
stabilisation of the spine
Spina bifida • Non fusion of the vertebral arches during embryonic development
• Three categories; myelomeningocele, spina bifida occulta and meningocele
• Myelomeningocele is the most severe type with associated neurological defects that may
persist in spite of anatomical closure of the defect
• Up to 10% of the population may have spina bifida occulta, in this condition the skin and
tissues (but not not bones) may develop over the distal cord. The site may be identifiable by a
birth mark or hair patch
• The incidence of the condition is reduced by use of folic acid supplements during pregnancy
Spondylolysis • Congenital or acquired deficiency of the pars interarticularis of the neural arch of a particular
vertebral body, usually affects L4/ L5
• May be asymptomatic and affects up to 5% of the population
• Spondylolysis is the commonest cause of spondylolisthesis in children
• Asymptomatic cases do not require treatment
Spondylolisthesis • This occurs when one vertebra is displaced relative to its immediate inferior vertebral body
• May occur as a result of stress fracture or spondylolysis
• Traumatic cases may show the classic "Scotty Dog" appearance on plain films
• Treatment depends upon the extent of deformity and associated neurological symptoms,
minor cases may be actively monitored. Individuals with radicular symptoms or signs will
usually require spinal decompression and stabilisation

266
Spinal disorders
Dorsal column lesion • Loss vibration and proprioception
• Tabes dorsalis, SACD
Spinothalamic tract lesion • Loss of pain, sensation and temperature
Central cord lesion • Flaccid paralysis of the upper limbs
Osteomyelitis • Normally progressive
• Staph aureus in IVDU, normally cervical region affected
• Fungal infections in immunocompromised
• Thoracic region affected in TB
Infarction spinal cord • Dorsal column signs (loss of proprioception and fine discrimination)
Cord compression • UMN signs • Haematoma
• Malignancy • Fracture
Brown-sequard syndrome • Hemisection of the spinal cord
• Ipsilateral paralysis
• Ipsilateral loss of proprioception and fine discrimination
• Contralateral loss of pain and temperature
Dermatomes
• C2 to C4 The C2 dermatome covers the occiput and the top part of the neck. C3 covers the lower part of the
neck to the clavicle. C4 covers the area just below the clavicle.
• C5 to T1 Situated in the arms. C5 covers the lateral arm at and above the elbow. C6 covers the forearm and the
radial (thumb) side of the hand. C7 is the middle finger, C8 is the medial aspect of the hand, and T1 covers the
medial side of the forearm.
• T2 to T12 The thoracic covers the axillary and chest region. T3 to T12 covers the chest and back to the hip girdle.
The nipples are situated in the middle of T4. T10 is situated at the umbilicus. T12 ends just above the hip girdle.
• L1 to L5 The cutaneous dermatome representing the hip girdle and groin area is innervated by L1 spinal cord. L2
and 3 cover the front part of the thighs. L4 and L5 cover medial and lateral aspects of the lower leg.
• S1 to S5 S1 covers the heel and the middle back of the leg. S2 covers the back of the thighs. S3 cover the medial
side of the buttocks and S4-5 covers the perineal region. S5 is of course the lowest dermatome and represents
the skin immediately at and adjacent to the anus.
Myotomes
Upper limb Lower limb
Elbow flexors/Biceps C5 Hip flexors (psoas) L1 and L2
Wrist extensors C6 Knee extensors (quadriceps) L3
Elbow extensors/Triceps C7 Ankle dorsiflexors (tibialis anterior) L4 and L5
Long finger flexors C8 Toe extensors (hallucis longus) L5
Small finger abductors T1 Ankle plantar flexors (gastrocnemius) S1
S2,3,4 keeps the 3 P's off the floor (Penis, Poo, and Pee). S2,3,4 innervates the anal sphincter, urethral sphincter, and causes erection.
1, 2 Buckle my shoe (Ankle). 3, 4 Kick the door (Knee).
5, 6 Pick up sticks (Biceps & Brachioradialis). 7, 8 Shut the gate (Triceps).
C5, 6, 7 Raise your arms up to heaven (Serratus anterior) Nerve root for Long Thoracic Nerve.

267

268

269
Ankle injuries
An ankle fracture relates to a fracture around the tibio-talar joint. It generally refers to a fracture involving the lateral,
and/or medial and/or posterior malleolus. Pilon and Tillaux fractures are also considered to be ankle fractures, but are
not covered here.
Ankle fractures are common. They effect men and women in equal numbers, but men have a higher rate as young adults
(sports and contact injuries), and women a higher rate post-menopausal (fragility type fracture).
Osseous anatomy
The ankle (or mortise) joint consists of the distal tibia (tibial plafond and posterior malleolus), the distal fibula (lateral
malleolus), and the talus. The main movement at the ankle joint is plantar and dorsiflexion.
Ligamentous anatomy
Medial side: Deltoid ligament. This is divided into superficial and deep portions. It is the primary restraint to valgus tilting
of the talus.
Lateral side: Lateral ligament complex consisting from anterior to posterior of the anterior talofibular ligament (ATFL),
calcaneofibular ligament (CFL), and the posterior talofibular ligament (PTFL). Together they resist valgus stress to the
ankle, and are a restraint to anterior translation of the talus within the mortise joint.
Syndesmosis: The syndesmosis is a ligament complex between the distal tibia and fibula, holding the two bones together.
It is fundamental to the integrity of the ankle joint, and its disruption leads to instability. It consists of (from anterior to
posterior) the anterior-inferior tibiofibular ligament (AITFL), the transverse tibiofibular ligament (TTFL), the interosseous
membrane, and the posterior-inferior tibiofibular ligament (PITFL).
Presentation and initial management

Patients will present following a traumatic event with a painful, swollen ankle, and reluctance/inability to weight bear.
The Ottawa rules can be applied to differentiate between an ankle fracture and sprain, but can be unreliable.
In high energy injuries, management should follow ATLS principles to identify more significant injuries first.
Neurovascular status of the foot should be documented, and open injuries should be excluded. If an open injury is
identified, it should be managed in line with BOAST 4 principles 1 . If an obvious deformity exists, it should be reduced as
soon as possible with appropriate analgesia or conscious sedation. Radiographs of clearly deformed or dislocated joints
are not necessary, and removing the pressure on the surrounding soft tissues from the underlying bony deformity is the
priority. If the fracture pattern is not clinically obvious then plain radiographs are appropriate and will guide the
subsequent manipulation during plaster-of-paris below knee backslab application.
Imaging
AP, lateral and mortise views (20o internal rotation) are essential to evaluate fracture displacement and syndesmotic
injury. Decreased tibiofibular overlap, medial joint clear space and lateral talar shift all indicate a syndesmotic injury. (In
subtle cases of shift, imaging the uninjured ankle can be helpful as a proportion of the population have little or no
tibiotalar overlap 2 .)
Where there is suspicion of syndesmosis involvement in the absence of radiographic evidence, stress radiographs can be
diagnostic.
Complex fracture patterns (and increasingly posterior malleolar fractures) are best defined using CT.
Classification: The most commonly used classifications are Lauge-Hansen and Danis-Weber.
Lauge-Hansen
Comprises two parts: first part is the foot position, and the second part is the force applied. Useful for understanding the
forces involved and therefore predict the ligamentous or bony injury. Results in four injury patterns:
Supination - Adduction (SA) - 10-20%
Supination - External rotation (SER) - 40-75%
Pronation - Abduction (PA) - 5-20%
Pronation - External rotation (PER) - 5-20%
Not often used in clinical practice but good for understanding the principles of ankle fracture.

270
Danis-Weber
Commonly used. Based on the level of
the fibula fracture in relation to the
syndesmosis. The more proximal, the
greater the risk of syndesmotic injury
and therefore fracture instability.
A - fracture below the level of the
syndesmosis
B - fracture at the level of the
syndesmosis / level of the tibial plafond
C - fracture above the level of the
syndesmosis. This includes Maisonneuve
fractures (proximal fibula fracture),
which can be associated with ankle
instability. Beware the high fibula
fracture - it may be an ankle fracture!
The Weber classification is based purely on

the the lateral side. All injuries can include a
medial or posterior bony or ligamentous
injury which also dictates fracture stability
(bimalleolar and trimalleolar fractures are
more unstable).
Treatment
When deciding upon treatment for an ankle fracture, one must consider both the fracture and the patient. Diabetic patients and
smokers are at greater risk of post-operative complication, especially wound problems and infection. Likewise, the long term outcome
of post-traumatic arthritis from a malunited ankle fracture is extremely important for a young patient, but not as relevant in the elderly.
Therefore, normal surgical decision processes apply as with all fractures.
Defining stability of an ankle fracture underpins the treatment decision.

Weber A - Unimalleolar Weber A Weber fractures by definition are stable and therefore can be mobilised fully weight
bearing in an ankle boot.
Weber C - Fractures tend to include syndesmotic disruption and are usually bimalleolar (either bony or ligamentous).
They are therefore unstable and usually require operative fixation. In addition to the fracture fixation, the syndesmosis
usually requires reconstruction/augmentation with screws to restore the joint integrity and function.
Weber B - B fractures vary greatly. They can be part of a trimalleolar injury and therefore extremely unstable, requiring
fixation. Alternatively, a uni-malleolar Weber B fracture can be a stable injury, and therefore mobilised immediately in an
ankle boot. Defining the stability can be challenging, and often involves stress radiographs, or a trial of mobilisation and
repeat radiographs. Defining stability is the subject of much ongoing research. However, treating undisplaced ankle
fractures in a below knee plaster, non-weight bearing for six weeks is still widely practised, and a safe approach.
When operative fixation is appropriate, it is usually via open reduction and internal fixation using plates and screws. It
must be carried out when soft tissue swelling has settled in order to minimise the risk of wound problems. This can often
take a week to settle.
The use of fibula nails is expanding, but is not yet mainstream. Ankle fractures can also be treated with external fixation,
or with a hind foot nail in patients who need fixation but where soft tissue or bone quality is poor.
Post-operative management
Ankle fractures generally take 6 weeks to unite enough to prevent secondary displacement. This is therefore an
appropriate time period to keep a cast on in a conservatively managed patient. Weight bearing post-operatively depends
on the quality of the fixation and bone quality, and preference varies between surgeons, ranging from aggressive early
mobilisation to a period of non-weight bearing. Return to activities takes approximately three months, and often requires
assistance of a physiotherapist to improve range-of-movement and muscle strengthening.

271
Shoulder disorders
Fractures
See Ortho Reference
Dislocations
Types
Dislocations around the shoulder joint include glenohumeral dislocation, acromioclavicular joint disruption and
sternoclavicular dislocation. Only glenohumeral dislocation will be covered here.
Glenohumeral dislocation
Diagnosis, classification and management are covered here.
Background
Shoulder dislocation is commonly seen in A&E. It has a high recurrence rate that is as high as 80% in teenagers. Initial
management requires emergent reduction to prevent lasting chondral damage.
Early assessment and management

Usually a traumatic cause (multi-directional instability in frequent dislocations requires discussion with orthopaedics and
is not covered here). Careful history, examination and documentation of neurovascular status of the limb, in particular
the axillary nerve (regimental badge sensation). This should be re-assessed post manipulation. Early radiographs to
confirm direction of dislocation.
Initial management consists of emergent closed reduction under under entanox and analgesia, but often requires
conscious sedation. Arm should then be immobilised in a polysling, and XR to confirm relocation.
Imaging - True anteroposterior (AP), axillary lateral and/or scapula Y view. Reduced humeral head should lie between
acromion and coracoid on lateral/scapula view.
Types
Direction Features Cause Examination Reduction techniques
Anterior Most Usually traumatic - anterior force Loss of shoulder contour - Hippocratic.
Common on arm when shoulder is sulcus sign. Humeral head Milch.
>90% abducted, eternally rotated can be felt anteriorly. Stimson.
Kocher not advised due to

complication of fracture
Posterior 50% 50% traumatic, but classically Shoulder locked in internal Gentle lateral traction to
missed in post seizure or electrocution rotation. XR may show adducted arm.
A&E lightbulb appearance.
Inferior Rare Associated with pectorals and As for primary injury Management of primary
rotator cuff tears, and glenoid injury
fracture
Superior Rare Associated with As for primary injury Management of primary
acrominon/clavicle fracture injury
Associated injuries
• Bankart lesion - avulsion of the anterior glenoid labrum with an anterior shoulder dislocation (reverse Bankart if
poster labrum in posterior dislocation).
• Hill Sachs defect - chondral impaction on posteriosuperior humeral head from contact with gleonoid rim. Can be
large enough to lock shoulder, requiring open reduction. (Reverse Hill Sachs in posterior dislocation).
• Rotator cuff tear - increases with age.
• Greater or lesser tuberosity fracture - increases with age.
• Humeral neck fracture - shoulder fracture dislocation. More common in high energy trauma and elderly. Should
be discussed with orthopaedics prior to any attempted reduction.

272
Rotator Cuff Disease
Rotator cuff disease is a spectrum of conditions that ranges from subacromial impingement to rotator cuff tears and
eventually to rotator cuff arthropathy (arthritis).
Anatomy
The rotator cuff is a group of four muscles that are important in shoulder movements, and maintenance of glenohumeral
stability.
Muscle Scapular attachment Humeral attachment Action Innervation
Supraspinatus Supraspinatus fossa Superior facet of Initiation of abduction Suprascapular nerve
greater tuberosity of humerus
Infraspinatus Infraspinatus fossa Posterior facet of External rotation of Suprascapular nerve
greater tuberosity humerus
Teres Minor Lateral border Inferior facet of External rotation of Axillary Nerve
greater tuberosity humerus
Subscapularis Subscapular fossa Lesser tuberosity Internal rotation of Upper and lower
humerus subscapular nerve
• The inferior rotator cuff muscles (infraspinatus, teres minor, and subscapularis) balance the superior pull of the
deltoid. Injury/tear results in upward migration of the humeral head on the glenoid (can be seen on AP
radiograph).
• Likewise, the anterior muscles (subscapularis) are balanced with the posterior muscles (infraspinatus, teres
minor).
Subacromial Impingement
• The most common cause of shoulder pain, which results from impingement of the superior cuff on the
undersurface of the acromion, and an inflammatory bursitis.
• Associated with certain types of acromial morphology (Bigliani classification).
• Presents as insidious pain which is exacerbated by overhead activities.
Rotator Cuff Tear

• Often presents as an acute event on the background of chronic subacromial impingement in the older patient,
but can present as an avulsion injury in younger patients.
• Majority of tears are to the superior cuff (supraspinatus, infraspinatus, teres minor), though a tear to
subscapularis is associated with subcoracoid impingement.
• Tears present as pain and weakness when using the muscles in question.
Rotator Cuff Arthropathy

• Defined as shoulder arthritis in the setting of rotator cuff dysfunction. Results from superior migration due to
the loss of rotator cuff function and integrity. Unopposed deltoid pulls the humeral head superiorly.
• Associated with massive chronic cuff tears.
Imaging
Plain radiographs
• AP of the shoulder may show superior migration of the humerus with a cuff tear, and features of arthritis with
arthropathy. Other causes of pain may also be identified (e.g. calcific tendonitis/fracture)
• Outlet view is useful for defining the acromial morphology
USS
• Allows dynamic imaging of the cuff, and is inexpensive. However, it is very user dependent.
MRI
• Best imaging modality for cuff pathology.
• Also allows imaging of the rest of the shoulder. When intra-articular pathology is suspected, can be combined
with an arthrogram for improved sensitivity and specificity.

273
Treatment
Subacromial impingement
• Physiotherapy, oral anti-inflammatory medication
• Subacromial steroid injection can settle inflammation
• Arthroscopic subacromial decompression by shaving away the undersurface of the acromion,
more space is created for the rotator cuff. Cuff integrity is assessed also at time of surgery, and
can be repaired if necessary.
Rotator cuff tear

• When considering repair of a cuff tear, the age and activity of the patient, the nature of the tear
(degenerative vs. acute traumatic), and the size and retraction of the tear should be considered
when making a surgical plan.
• Mild tears or tears in the elderly can be managed conservatively, as outlined above.
• Moderate tears can be repaired arthroscopically. Massive or retracted tears will often require an
open repair (occasionally with a tendon transfer). Subacromial decompression is performed at the
same time to reduce impingement, symptoms and recurrence.
Calcific tendonitis
Calcific tendonitis involves calcific deposits within tendons anywhere in the body, but most commonly in the rotator cuff
(specifically the supraspinatus tendon). When present in the shoulder, it is associated with subacromial impingement and
pain.
Pathology
• More common in women aged 30-60 years.
• Association with diabetes and hypothyroidism
There are three stages of calcification

• Formative phase characterized by calcific deposits
• Resting phase deposit is stable, but presents with impingement problems
• Resorptive phase phagocytic resorption. Most painful stage.
Presentation
• Similar in presentation to subacromial impingement, with pain especially with over head activities. Atraumatic in
nature.
Imaging
• Plain radiographs show calcification of the rotator cuff, usually within 1.5cm of its insertion on the humerus.
Supraspinatus outlet views can show level of impingment. Further imaging is rarely needed.
Treatment
• Non-operative NSAIDS, steroid injection (controversial, but practiced) and physiotherapy. Approximately 75%
will resolve by 6 months with conservative management.
• Ultrasound guided or surgical needle barbotage can break down deposits and resolve symptoms. Occasionally
surgical excision is required.

274
Adhesive capsulitis (Frozen Shoulder)
• Pain and loss of movement of shoulder joint, which involves fibroplastic proliferation of capsular tissue, causing soft
tissue scarring and contracture. Patients present with a painful and decreased arc of motion.
• Associated with prolonged immobilization, previous surgery, thyroid disorders (AI) and diabetes
• Classically three stages which can take up to two years to resolve:
o Stage one the freezing and painful stage
o Stage two the frozen and stiff stage
o Stage three the thawing stage, where shoulder movement slowly improves
Imaging
• Plain radiographs to exclude other causes of a painful shoulder
• MRI arthrogram may show capsular contracture, and again may be used to exclude cuff pathology. However,
often not performed as diagnosis is largely clinical.
Treatment
• Non-operative NSAIDS, steroid injection and physiotherapy. Patience is required as condition can take up to 2
years to improve.
• Operative MUA or arthroscopic adhesiolysis (release of adhesions) can expedite recovery, followed by intensive
physiotherapy.
Glenohumeral Arthritis
Background
• May be osteoarthritis (primary or secondary to cuff tear or trauma), rheumatoid arthritis, or as part of a
spondyloarthropathy. Majority of those with RA will develop symptoms.
• More common in the elderly
• Presents like any other arthritis - pain at night and with movement
Imaging
• AP and axillary radiographs will show features of arthritis.
• CT/MRI is often useful to classify the shape of the glenoid and extent of bone loss when considering
arthroplasty. MRI also essential to asses integrity of rotator cuff if considering shoulder replacement.
Treatment
Like all orthopaedics, start with simple measures:
• NSAIDS, management of RA, physiotherapy, steroid injection.
• Hemiarthroplasty can sometimes be considered if glenoid is in excellent condition or if patient has large
comorbidity.
• Arthroscopic debridement is useful if patient has isolated ACJ arthritis, but is rarely used for glenohumeral
arthritis.
• Total shoulder replacement is shown to produce superior outcome when compared to hemiarthroplasty in
terms of pain relief, function and implant survival.
• Total shoulder replacement can be anatomical (ball on humerus, with cup on glenoid), or reverse geometry (ball
on glenoid, with cup on humerus). Anatomical TSR requires an in tact rotator cuff, so often reverse is preferable
when the cuff if questionable in integrity.

275
Reference ranges
Reference ranges vary according to individual labs. All values are for adults unless otherwise stated
Full blood count

Haemoglobin Men: 13.5-18 g/dl Women: 11.5-16 g/dl
Mean cell volume 82-100 fl
Platelets 150-400 * 109/l
White blood cells 4-11 * 109/l|
Urea and electrolytes

Sodium 135-145 mmol/l
Potassium 3.5 - 5.0 mmol/l
Urea 2.0-7 mmol/l
Creatinine 55-120 umol/l
Bicarbonate 22-28 mmol/l
Chloride 95-105 mmol/l
Liver function tests

Bilirubin 3-17 umol/l
Alanine transferase (ALT) 3-40 iu/l
Aspartate transaminase (AST) 3-30 iu/l
Alkaline phosphatase (ALP) 30-100 umol/l
Gamma glutamyl transferase (yGT) 8-60 u/l
Albumin 35-50 g/l
Total protein 60-80 g/l
Other haematology
Erythrocyte sedimentation rate (ESR) Men: < (age / 2) mm/hr Women: < ((age + 10) / 2) mm/hr
Prothrombin time (PT) 10-14 secs
Activated partial thromboplastin time (APTT) 25-35 secs
Ferritin 20-230 ng/ml
Vitamin B12 200-900 ng/l
Folate 3.0 nmol/l
Reticulocytes 0.5-1.5%
D-Dimer < 400 ng/ml
Other biochemistry
Calcium 2.1-2.6 mmol/l
Phosphate 0.8-1.4 mmol/l
CRP < 10 mg/l
Thyroid stimulating hormone (TSH) 0.5-5.5 mu/l
Free thyroxine (T4) 9-18 pmol/l
Total thyroxine (T4) 70-140 nmol/l
Amylase 70-300 u/l
Uric acid 0.18-0.48 mmol/l
Arterial blood gases

pH 7.35 - 7.45
pCO2 4.5 - 6.0 kPa
pO2 10 - 14 kPa
Lipids (Desirable lipid values depend on other risk factors for cardiovascular disease, below is just a guide.)
Total cholesterol < 5 mmol/l
Triglycerides < 2 mmol/l
HDL cholesterol > 1 mmol/l
LDL cholesterol < 3 mmol/l
REFERENCE RANGES – MRCS NOTES - REDA 1

MRCS A Notes Reda v4 Unsecured

Enviado por

Dados do documento

Título original

Direitos autorais

Formatos disponíveis

Compartilhar este documento

Compartilhar ou incorporar documento

Opções de compartilhamento

Você considera este documento útil?

Este conteúdo é inapropriado?

Direitos autorais:

Formatos disponíveis

MRCS A Notes Reda v4 Unsecured

Enviado por

Direitos autorais:

Formatos disponíveis

MRCS PART A NOTES - REDA

2. Physiology – MRCS Notes - Reda

2. PHYSIOLOGY – MRCS NOTES - REDA 1

2. PHYSIOLOGY – MRCS NOTES - REDA 2

'a' wave = atrial contraction

Cannon 'a' waves

'x' descent = fall in atrial pressure during ventricular systole

'y' descent = opening of tricuspid valve

Absent a waves = Atrial fibrillation

2. PHYSIOLOGY – MRCS NOTES - REDA 3

2. PHYSIOLOGY – MRCS NOTES - REDA 4

Tumour Necrosis Factor (TNF)

2. PHYSIOLOGY – MRCS NOTES - REDA 5

2. PHYSIOLOGY – MRCS NOTES - REDA 6

Arterial Blood Gas (ABG) Interpretation

2. PHYSIOLOGY – MRCS NOTES - REDA 7

Body fluid volumes

Cerebrospinal Fluid (CSF)

2. PHYSIOLOGY – MRCS NOTES - REDA 8

Intrinsic pathway Increased APTT Factors 8,9,11,12

2. PHYSIOLOGY – MRCS NOTES - REDA 9

2. PHYSIOLOGY – MRCS NOTES - REDA 10

Factors that may potentiate warfarin Aid to memoire: WEPT

2. PHYSIOLOGY – MRCS NOTES - REDA 11

2. PHYSIOLOGY – MRCS NOTES - REDA 12

It is important to understand the principles of Laplace's law in surgery.

Atrial stretch receptors

2. PHYSIOLOGY – MRCS NOTES - REDA 13

2. PHYSIOLOGY – MRCS NOTES - REDA 14

Inotrope Cardiovascular receptor action

Effects of receptor binding

A normal anion gap is 8-14 mmol/L

It is useful to consider in patients with a metabolic acidosis:

Causes of a normal anion gap or hyperchloraemic metabolic acidosis

Causes of a raised anion gap metabolic acidosis

2. PHYSIOLOGY – MRCS NOTES - REDA 15

Hormonal regulation of calcium

Hypocalcaemia: Causes and Management

2. PHYSIOLOGY – MRCS NOTES - REDA 16

2. PHYSIOLOGY – MRCS NOTES - REDA 17

Foods that are high in potassium

Hypokalaemia with alkalosis

Hypokalaemia with acidosis

ECG Features in Hypokalemia

2. PHYSIOLOGY – MRCS NOTES - REDA 18

The sodium requirement can be calculated as follows :

2. PHYSIOLOGY – MRCS NOTES - REDA 19

Potassium Secretion - GI Tract

2. PHYSIOLOGY – MRCS NOTES - REDA 20

Systemic vascular resistance

Respiratory Physiology: Lung Compliance

Causes of increased compliance

Causes of decreased compliance

2. PHYSIOLOGY – MRCS NOTES - REDA 21

Lung receptors include:

Dead space ventilation

2. Physiological dead space: normal 150 mls,

2. PHYSIOLOGY – MRCS NOTES - REDA 22

Oxygen dissociation curve

2. PHYSIOLOGY – MRCS NOTES - REDA 23

2. PHYSIOLOGY – MRCS NOTES - REDA 24

2. PHYSIOLOGY – MRCS NOTES - REDA 25

Phases of gastric acid secretion