Anesthaesia and Intensive Care

Short Answer Questions
Anaesthesia
& Intensive Care
For FCAI, FRCA & EDAIC
Part: 1 - Intensive Care Medicine
Modified by
AYMAN EDAROUS
Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]

‫ميحرلا نمحرلا هللا مسب‬
For Original Materials and Editors, Please refer to:
North Ireland School of Anaesthesia Website

http://www.nischoolofanaesthesia-finalfrca.org.uk/SAQs/intensivecare/
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 2
1- Ventilator Associated Pneumonia (VAP)
a) What is meant by the term Ventilator Associated Pneumonia (VAP)? (3 marks)
b) List the factors that increase the risk of the development of VAP. (10 marks)
c) What measures may reduce the risk of development of VAP? (7 marks)
 Ventilator Associated Pneumonia (VAP):

Pneumonia occurring 48-72 hours after ETT intubation,
characterised by (Diagnostic Criteria):
-Clinical Signs: Pyrexia, raised WCC, Purulent Bronchial Secretion.
-Microbiological Evidence: Positive Sputum Culture.
-Radiological Signs: New or Progressive Pulmonary Infiltrates.
The common pathogens associated with VAP:

Mainly caused by G-ve organisms, but G+ve bacteria such as MRSA are not uncommon.
Typically, bacteria causing early onset VAP include:
 Streptococcus pneumonia.
 Haemophilus influenzae.
 Methicillin-sensitive Staphylococcus aureus (MSSA).
 Gram-negative bacilli.
 Escherichia coli.
 Klebsiella pneumonia.
 Enterobacter and Proteus species.
 Serratia marcescens.
Culprits of late VAP are drug-resistant organisms such as MRSA, Acinetobacter, Pseudomonas
aeruginosa, and extended-spectrum beta-lactamase producing bacteria (ESBL).
Pathogenesis of VAP:
 It is thought to be caused by entry of infected secretions into distal bronchi.
 Patients are usually immunosuppressed, and their oropharynx becomes colonised with
organisms, especially G-ve bacteria.
 Oral and nasal tubes cause trauma, leading to infections such as sinusitis.
 The natural protections like cough reflex, tracheobronchial secretions, mucociliary linings,
saliva, and nasal mucosa are less effective in these patients.
 The pathogens enter the lower lung through mechanical routes such as around the
endotracheal tube cuff, suction catheter, and ventilation tubings.
 Factors that Increase the Risk of the Development of VAP:

1- Patient factors 2- Interventional factors:
Advanced age. Prolonged ventilation.
Low serum albumin. Level of sedation.
ARDS, COPD and other lung diseases Use of neuromuscular blocking agents.
Impaired consciousness. Use of Antacids,PPI and H2 blockers.
Trauma and Burns. Nasogastric tube.
Multiple Organ Failure. Supine position.
Large volume gastric aspirates. Frequent circuit changes.
Upper respiratory tract colonisation. Transfer outside ICU.

 Measures may reduce the Risk of development of VAP (VAP bundle):
General measures: Use of sterile equipment, regular hand washing, using barrier nursing such as
gloves and an apron, and minimal contact with patient usually reduce the incidence of any infection
in ICU.
Specific measures: This include reducing the load of pathogens and their entry into lower
respiratory tract.
Reducing Oral Colonisation

*Good Oral Cavity Care including Regular Brushing of Teeth.
*Use of Antiseptic Mouthwash (e.g. Chlorhexidine)
*Use of Silver coated ETT (prevents build up of Biofilms on ETT lumen)
*Selective decontamination of digestive tract (SDD) using non-absorbable
antimicrobials such as Polymyxin E and Amphotericin B has been tried with
variable success [NB: It encouraging Clostridium diffcilie, antimicrobial
resistance, and the emergence of multi-drug resistant pathogens].
• Reducing Aspiration
*Patients nursed in 30-45o degree head-up position
*Use of ETT with subglottic secretion drainage port with regular subglottic suction.
*Regular Monitoring /4 hr and maintainence of ETT Cuff Pressure (20-30 cmH2O).
• Minimising duration of Mechanical Ventilation:

*This is achieved by early tracheostomy, which has proven to lower the incidence of VAP.
*Periodic ‘sedative interruptions’ and daily assessment of readiness to extubate may reduce the
duration of mechanical ventilation.
• Stress Ulcer Prophylaxis:

*Reducing the acidity of stomach in stress ulcer prophylaxis
is claimed to increase the incidence of VAP by increasing
the proliferation of gram-negative bacteria. Use of H2
blockers or Sucralfate, instead of PPIs, are suggested to
reduce the risk.
*Enteral feeding can increase the risk of VAP by altering the
gastric acidity and risk of aspiration, but benefits of enteral
feeding usually outweigh this small risk.
•Deep Venous Thrombosis (DVT) Prophylaxis:

Clinical Pulmonary Infection Score (CPIS) for VAP
The CPIS takes into account:
 Clinical:Temperature, Presence of tracheal secretions.
 Physiological: Leucocytosis and worsening gas exchange.
 Microbiological: Positive culture of tracheal aspirate.
 Radiographic: evidence to assign a numerical value.
**Scores can range from 0 to 12 with a score of ≥ 6: good correlation with the presence of VAP.

2- Surviving Sepsis Campaign 2018
You are asked to assess a 45 year old woman in A&E resus who has a provisional
diagnosis of Gallbladder Sepsis.
a) Define (i) Sepsis (ii) Septic Shock (25%)
b) What diagnostic criteria for sepsis as suggested by the 2012 Surviving Sepsis Campaign would you
apply to this patient? (25%)
c) Outline the targets for management and categorise into accepted timeframes (25%)
d) What are the major changes in the 2012 recommendations compared to the original? (25%)
 Sepsis:
Life-threatening Organ Dysfunction caused by Dysregulated Host Response to Infection.
- Septic Shock:
Subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher
risk of mortality.

 Diagnostic criteria for sepsis as suggested by the 2016 Surviving Sepsis Campaign:

 The Targets for Management:
Hour-1 Surviving Sepsis Campaign Bundle of Care (2018)
Te most important change in the revision of the SSC bundles is that the 3-h and 6-h bundles have been
combined into a single “hour-1 bundle” with the explicit intention of beginning resuscitation and
management immediately. We believe this reflects the clinical reality at the bedside of these seriously
ill patients with sepsis and septic shock-that clinicians begin treatment immediately, especially in
patients with hypotension, rather than waiting or extending resuscitation measures over a longer
period.
More than 1 h may be required for resuscitation to be completed, but initiation of resuscitation and
treatment, such as obtaining blood for measuring lactate and blood cultures, administration of fluids
and antibiotics, and in the case of life-threatening hypotension, initiation of vasopressor therapy, are
all begun immediately.
 Measure Lactate Level

If initial lactate is elevated (> 2 mmol/L), it should be re-measured within 2–4 h to guide resuscitation
to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion.
 Obtain Blood Cultures (prior to Antibiotics)

Sterilization of cultures can occur within minutes of the first dose of an appropriate antimicrobial, so
cultures must be obtained before antibiotic administration to optimize the identification of pathogens
and improve outcomes. Appropriate blood cultures include at least two sets (aerobic and anaerobic).
Administration of appropriate antibiotic therapy should not be delayed in order to obtain blood
cultures.
 Administer Broad-Spectrum Antibiotics

Empiric broad-spectrum therapy with one or more intravenous antimicrobials to cover all likely
pathogens should be started immediately for patients presenting with sepsis or septic shock. Empiric
antimicrobial therapy should be narrowed once pathogen identification and sensitivities are
established, or discontinued if a decision is made that the patient does not have infection. The link
between early administration of antibiotics for suspected infection and antibiotic stewardship remains
an essential aspect of high-quality sepsis management. If infection is subsequently proven not to exist,
then antimicrobials should be discontinued.

 Administer Intravenous Fluid
Initial fluid resuscitation should begin immediately
upon recognizing a patient with sepsis and/or
hypotension and elevated lactate, and completed
within 3 h of recognition. The guidelines
recommend this should comprise a minimum of 30
ml/kg of intravenous crystalloid fluid.
Because some evidence indicates that a sustained

positive fluid balance during ICU stay is harmful,
fluid administration beyond initial resuscitation
requires careful assessment of the likelihood that
the patient remains fluid responsive.
 Apply Vasopressors
If blood pressure is not restored after initial
fluid resuscitation, then vasopressors should
be commenced within the first hour to
achieve mean arterial pressure (MAP) of ≥ 65
mmHg.

The major changes in the 2016 recommendations compared to 2012:

PATHOPHYSIOLOGY

3- Acute Respiratory Distress Syndrome (ARDS)
(a) What are the defining features of ARDS (according to the 2012 ARDS Definition Taskforce)?
(b) Why was a new definition felt to be necessary?
(c) Describe the pathophysiology of ARDS.
(d) Describe the management of ARDS in the ICU.
 Berlin Definition of ARDS:
 Why was a new definition felt to be necessary?

A number of issues regarding the old definition had emerged Including:
*No explicit criteria for defining Acute.
*High inter-observer variability in interpreting chest X-rays.
*Difficulties in ruling out cardiogenic causes of pulmonary oedema.
*PaO2/FiO2 ratio is sensitive to changes in ventilatory settings.
*Intensive care societies felt a definition that simplified the diagnosis and better prognosticated
outcomes was needed.
*The new definition predicted Mortality ever so slightly better than the existing definition however
the power of the new definition to predict mortality is still poor with an area under the curve of only
0.577 vs 0.536 for the old definition.

 The Pathophysiology of ARDS:
Regardless of the cause disease progression is the same.
Acute Phase:
*Lasts for up to 7 days from Onset.
*Hypoxemia, Infiltrates on the Chest Radiograph, and  in Pulmonary Compliance.
*Leakage of Protein-rich fluid into the Alveoli, Haemorrhage, and Diffuse Neutrophilic Alveolar
Infiltrate with resultant Endothelial and Epithelial Injury.
Proliferative Phase:
*Can occur from day 5 onwards.
*Characterised by persistent Hypoxaemia,  Dead Space, and  Lung Compliance.
*Accompanied by Interstitial Fibrosis, Proliferation of type 2 Alveolar Cells, and disruption of Capillary
function due to Microvascular Thrombus Formation.
*In some these changes resolve and clinical improvement follows; others progress into the Chronic or
Fibrotic Stage.
Chronic Phase (Fibrotic Stage):
*Not clearly defined.
*May starts as early as day 14 and can Last Weeks
*Widespread Pulmonary Fibrosis and Loss of the normal Lung Structure leads to worsening Lung
Compliance and an  in Dead Space.
*Clinically there is a  in CO2 excretion which may be accompanied by an improvement in
Oxygenation.
**All of the above happen in a heterogenous way throughout the Lungs with some parts worse
affected than others.
 Management of ARDS in the ICU:

 Respiratory Support:
Protective Lung Ventilation:
-Aim of mechanical ventilation is to maintain
adequate gas exchange until cellular damage
resolves without causing ventilator induced lung
injury.
*ARDSnet Tidal Volume study showed:

-High volume ventilation damages remaining healthy
lungs
-Low volume ventilation had significantly lower level of
circulatory cytokines, biotrauma and distant end organ
damage
-PEEP improved Oxygenation by maintaining patency
of injured alveoli, improvement in V/Q mismatch, 
in Shunt and preventing Atelectrauma.
Study couldn’t show superiority of high over low PEEP.
-Conclusion: Vt of 6ml/kg, Peak Pressures of less than 30cmH2O and PEEP.

Activated neutrophils adhere to endothelial cells and release inflammatory mediators, including oxygen-free radicals and proteases, to cause lung damage. Direct lung damage or endotoxins alone are
sufficient to damage endothelial cells with cytokine release and an inflammatory cascade. Endothelial damage results in increased capillary permeability and formation of protein-rich alveolar exudate
rich in neutrophils. Type I alveolar cell are damaged and type II cells proliferate. As the disease progresses, fibroblast infiltration and collagen proliferation cause microvascular obliteration
and widespread fibrosis. Areas of lung involvement are not fixed but shift to dependent areas. Within areas of reduced lung volume, some alveoli remain open and capable of gas exchange, whereas
others are filled with alveolar exudate. IPPV may cause damage more through excess volume (‘volutrauma’) than through pressure itself. The significance of oxygen toxicity is controversial.

 Circulatory support and Fluid Management:
FACTT trial showed conservative fluid management had a reduced number of days ventilated and
reduced ICU stay. Reductions in lung water with diuretics +/ albumin.
Treatment of the Cause: Antibiotic for Pneumonia.

 Glycaemic Control.
 DVT Prophylaxis.
 Gastric Ulcer Prophylaxis.
 Ventilator bundle.
 Central Catheter Care Bundle.
 Early Enteral Feeding.
 Other Interventions of improving Oxygenation:

-Nitric Oxide.
-Steroids:  edema.
-Activated protein C
-Intravenous B-agoinst therapy
-Prone Position enhances oxygenation and improves V/Q mismatching but at the minute hasn’t
been shown to improve survival overall
-Other trials are ongoing, eg. Statins for their ability to decrease inflammation.
-High frequency oscillatory ventilation (HFOV)
- ECMO: used to rescue some patients with severe ARDS who have primary single organ failure.

4- Severe Acute Pancreatitis
(a) Briefly describe the anatomy of the pancreas.
(b) What are the signs and symptoms of acute pancreatitis?
(c) How may it be further diagnosed?
(d) Describe a method of prognostication in the disease.
(e) What are the potential short and long term complications of pancreatitis?
 Anatomy of The Pancreas:

- Retroperitoneal organ, located at T12.
- Head lies centrally.
-Tail extends to overlap part of left kidney.
- Connects to duodenum via ampulla of vater.
- Arterial: branches of SMA, splenic A.
- Venous: SMA, splenic, portal
- Nervous: coeliac, superior mesenteric plexus
- Has functional Endocrine and Exocrine units
(Islets of Langerhans, Acini)
 Causes of Pancreatitis (I GET SMACHED):
Signs and Symptoms:

History:
- Risk Factors e.g. alcohol excess, gallstones, drugs,
previous incidents
- Severe upper abdominal pain radiating to back,
relieved by sitting forward.
- Nausea and vomiting.
Examination;
- Systemically unwell; SIRS response
- Abdominal distension, peritonism,
-Grey Turners (flanks).
-Cullens (peri umbilical) discoloration secondary to
retroperitoneal hge.
- Evidence of end organ dysfunction e.g. Respiratory Distress, Oligouria, Jaundice.
 Further Diagnosis:
- Serum Amylase (> 3X), Lipase (> 3X), Tryptase .
- CT scan early if diagnosis uncertain, at 48-72
hours for Prognostication and Management.
-MRCP, Endoscopic ultrasound (EUS) and USS
(diagnosis of gallstones).
 Complications of Pancreatitis:
Patients with severe pancreatitis can have systemic
and local complications, including:
Pleural effusion, ARDS, ileus, Gastric ulceration,
Renal failure and cardiovascular compromise.

Local complications include acute fluid collection leading to gastric outlet obstruction, pseudocyst,
Abscess, Necrosis, Pseudoaneurysm of the splenic artery and fistulation into an adjacent hollow
viscus.
Early Complications Late Complications

- Pancreatic Necrosis. - Diabetes
- Peripancreatic fluid collection; - Pancreatic Insufficiency
sterile and infected - Pseudoaneurysm
- Massive Haemorraghe. - Abscess
- Haemorragic Pancreatitis - Pseudocyst
- Portal Hypertension. - Death.
- Procoagulant state with VTE.
- Abdominal Compartmental Syndrome
- Death
 Prognostic Methods:
*APACHE II score: [Physiological Parameters and a Chronic Health Evaluation]
Score greater than 8 predicts a severe episode of pancreatitis,
maximum score 71.
*Modified Imrie/Glasgow score

-Described features in a population of patients with gallstone
pancreatitis.
-Score greater than or equal 3 predicts a severe episode of
pancreatitis.
*Ranson's Score:
Developed from an American of alcohol induced pancreatitis.
*Balthazar CT Severity Index.
*BISAP score.
 Management:
Early identification and management of
organ failure and aggressive resuscitation to
optimise tissue perfusion is important in
cases of severe pancreatitis.
Cholecystectomy in cases of mild gallstone-

induced pancreatitis should be performed
within 2 weeks of discharge. In cases of
severe pancreatitis, surgery should be
performed
once the patient has recovered.

5- Acute Kidney Injury (AKI) and Dialysis
(a) What is Acute Kidney Injury (AKI)? How might it be classified? (20%)
(b) What investigations should be performed in a patient in acute renal failure? (20%)
(c) What is your management of a patient admitted with ARF to ICU? (20%)
(d) Describe a RRT circuit - how does it work to remove fluid and solutes? (20%)
(e) What are the different methods of anticoagulation in patients on RRT? (20%)
 Acute Kidney Injury (AKI):
An abrupt (within 48 hours) Reduction in Kidney Function, defined as:
An absolute increase in serum Creatinine of at least 0.3mg/dl (26.4micromol/L),
OR
A percentage increase in serum creatinine of at least 50% (1.5x baseline)
OR
A reduction in urine output to 0.5ml/kg/hour or less for over 6 hours.
- Acute Kidney Injury Network (AKIN) 2007 Modified RIFLE Classification:
 The Investigations should be performed in a patient in Acute Renal Failure:
- Assessment of Circulation: MAP, UO, Pulse Oximetry, Acid-Base Status, CO and CVP.
- Specific Renal Investigations: Urea and Creatinine, Potassium, Liver Function Tests, Creatinine
Kinase(CK)/urinary Myoglobin, Urinary Sodium, Urine plasma:osmolality ratio, Urine Microscopy, U/S
renal tracts.
- Glomerular Filtration Rate (GFR) [Overall index of Renal Function].
-Rate at which Substances are Filtered from the Blood of the Glomeruli into the Bowman’s
Capsules of the Nephrons.
-Calculated by the clearance of specific substances which have a constant plasma concentration,
are freely filtered by the glomerulus, and are not subsequently secreted, reabsorbed or
metabolised. The clearance of substances from the plasma are used as an index of GFR.
-Creatinine clearance is the most common in clinical use.

- Serum and Urine Biochemistry: neither sensitive nor specific for renal dysfunction
- Urinalysis: lacks specificity, but can indicate severe renal dysfunction, and can be used to
differentiate between Prerenal and Intrarenal disease.
 Management of a patient admitted with ARF to ICU:

- ABC approach to correct any circulatory or respiratory impairment.
Avoid hypoxaemia, ventilate if necessary.
- Hypovolaemia is a recognised risk factor for AKI, so IV fluid loading is initially appropriate. Once
adequate fluid loading has been achieved, Inotropic and Vasopressor support can be used to achieve
an appropriate MAP.
- Treat Urinary Tract Obstruction. Consider urinary catheterisation, or percutaneous nephrostomies.
- Review Drug Chart. Modify doses of renally excreted drugs.
Hold Nephrotoxins (e.g. NSAIDs, ACE-Is, Contrast Media).
-Severe Metabolic Acidosis related to tubular dysfunction can be corrected with sodium bicarbonate
- Identify Underlying Cause, and initiate specific treatment.
*Rhabdomyolysis: Aggressive Fluid Replacement, Urinary Alkalinisation.
*Intra-abdominal hypertension/compartment syndrome:
-Supportive: diuretic therapy, renal replacement therapy.
-Definitive: surgical decompression.
*Allergic interstitial nephritis (rash, fever, urinary eosinophiluria):
Removal of offending agent (penicillin, cephalosporins).
- Renal Replacement Therapy (RRT); Indicated in:
*Hyperkalaemia: (s K+ > 6.5 mmol/L with ECG abnormalities)
*Uraemia: (>35mmol/L): Encephalopathy, Pericarditis, Bleeding.
*Acidaemia: (pH<7.1) ,
*Fluid Overload : resistant to diuretics.
 RRT circuit and how does it work to remove fluid and solutes:
Intermittent RRT: less expensive, simpler to run, requires less time, rapid fluid and solute removal is
possible. However, critically unwell patients may become haemodynamically unstable, and
hypotension may cause further renal injury.
Continuous RRT: slower and more expensive than Intermittent, and requires premixed fluids and
anticoagulation. Slower fluid and solute removal reduces risk of haemodynamic instability.
Peritoneal: inefficient at removing large amounts of fluid/solute. Increases intra-abdominal pressure,
which may splint diaphragm in unwell patients, so contraindicated in critical care.
-Veno-Venous circuit -pump driven, reliable high flow rates. Commonly used now.
-Arterio-Venous circuit –driven by patients own BP. Less reliable, associated with catheter related
complications, so rarely used now.
Mechanism of Fluid Removal (Ultrafiltration):
Produced by creating a positive pressure in the blood compartment of the dialyser and is facilitated
by creating a negative pressure in the dialysate compartment. The resulting trans-membrane
pressure is the driving force for ultrafiltration.

Mechanisms of Solute Removal (Haemodialysis)
Diffusion (Principle Process during Haemodialysis): The spontaneous migration of substances from
regions where their concentrations are high to regions where their concentrations are lower. During
haemodialysis, diffusive transport is driven by the solute concentration gradients that exist between
blood and dialysate. The dialysate runs countercurrent to blood flow, separated by a semipermeable
membrane.
Convection/ Hemofiltration (Solvent Drag): Occurs when a solute molecule is swept through a
membrane by a moving stream of ultrafiltrate. Convective transport is independent of any solute
concentration gradients that may be present across a membrane. The porosity of the membrane is a
major determinant of which molecules are removed but only the direction and force of trans-
membrane fluid flux determine the amount of convective transport.
 The Different Methods of Anticoagulation in Patients on RRT:

-Exposure of blood to a non-biological surface (the filter membrane) activates the clotting cascade.
-Aims of anticoagulation are to prolong filter life (prevent “clotting off”), whilst minimising systemic
anticoagulation.
Non-pharmacological measures:
-Ensure adequate CVP; optimise vascular access; predilution (adding a proportion of the replacement
fluid to the patient’s blood before it passes through the haemofilter).
-Anticoagulation is contraindicated when coagulopathy already exists; there is a high risk of bleeding;
activated protein C has been administered.
Pharmacological
Unfractionated Heparin:
-Typically a bolus followed by a prefilter infusion.
-Cost effective, can be fully reversed with protamine.
-Requires monitoring of APTT.
Low Molecular Weight Heparin:
-Lower incidence of heparin-induced thrombocytopenia.
-Longer half-life than UFH, only partially reversed by protamine.
Prostaglandins:
-Inhibit platelet function. Can be used alone, or with heparin (synergistic effect).
-Short half-life, so administered as infusion.
-Potent vasodilator, so can reduce MAP.
-May inhibit hypoxic pulmonary vasoconstriction, so may cause/worsen hypoxaemia.
-Expensive.
Sodium Citrate:
-Infused prefilter.
-Chelates calcium and inhibits clot formation.
-Calcium infusion required post filter.
-Cause metabolic derangements (hypoCa, hypoMg, hyperNa, metabolic alkalosis, or acidosis).

Fig. For the hemodialysis circuit, the green bag represents the dialysate and the yellow bag the used
dialysate. For the hemofiltration circuit, the yellow bag represents the ultrafiltrate and the purple
bag the postdilution replacement fluid.

6- Guillain Barre Syndrome (GBS)
(a) What is Guillain Barre Syndrome (GBS)? How is it sub classified?
(b) What are the symptoms and signs of GBS?
(c) How is it diagnosed?
(d) What is the differential diagnosis?
(e) Describe the airway management in GBS. What parameters are used to decide to intubate?
Guillain Barre Syndrome (GBS):

- An Acute Demyelinating Polyneuropathy.
- It is an Auto-immune phenomenon due to GI or Respiratory
Infection (Campylobacter jejuni, EBV, CMV, HIV …) or
Vaccination.
- Males are more affected.
Several different Clinical Pictures exist:
 Acute Inflammatory Demyelinating Poly-radiculopathy
(AIDP): Most common (90%).
 Acute Motor Axonal Neuropathy (AMAN): associated with Campylobacter jejuni.
 Acute Motor and Sensory Axonal Neuropathy (AMSAN): more severe and associated
with prolonged or only partial recovery.
 Millar-Fisher Syndrome (MFS) 5%: classic Triad of Ataxia, Areflexia and Ophthalmoplegia.
*It is unique in that this subtype begins with cranial nerve deficits (III – VII and IX – XII)
*Patients present with facial weakness mimicking Bell’s palsy, dysphagia, dysarthria,
ophthalmoplegia, and pupillary disturbances.
 Chronic Inflammatory Demyelinating Polyradiculoneuropathy: similar to AIDP but
has a chronic and relapsing course.

 Symptoms and Signs of GBS:
 It should be suspected in any patient with unexplainable weakness or sensory deficit affecting
the limbs. Signs and Symptoms vary according to subtype.
Motor Dysfunction:
- Progressive Motor Weakness, usually Symmetric, Ascending from the Legs.
- Reflexes: Areflexia (reflexes may be preserved in AMAN)
- Cranial Nerves: Facial Palsy and Bulbar Weakness.
- Eyes: Ophthalmoplegia, Ptosis and Diplopia.
- Respiratory Failure: secondary to Respiratory Muscle Weakness.
Sensory Dysfunction:
-Pain is most severe in the shoulder girdle, back, buttocks, and thighs.
-Paraesthesia and Numbness usually begins in the toes and fingertips and progresses upward but
generally does not extend beyond the wrists or ankles.
-Loss of vibration, proprioception, touch, and pain distally may be present
Autonomic Dysfunction:
-Tachycardia, Arrythmia, Labile Blood Pressure, Orthostatic Hypotension.
-Urinary Retention, Paralytic Ileus and Hyperhydriasis.
 Diagnosis:
- GBS should be suspected in all patients with unexplained motor weakness or a new sensory
deficit affecting the limbs
History: of recent Gastrointestinal or Respiratory infection should be sought.
Examination: Symptoms and Signs (SEE BEFORE).
Investigations:
- Daily measurement of Vital Capacity.
- Lumbar Puncture/ CSF analysis:  Protein and Normal WBC.
- Electrophysiological Studies: aid diagnosis and help to differentiate GBS from other
neuropathies. Each subtype has different electrophysiological features.
- Muscle biopsy: may help to distinguish GBS from a primary myopathy in unclear cases
- MRI: May show spinal nerve root enhancement with gadolinium
- Stool Cultures may show Campylobacter jejuni infection.
- Blood Tests: Anti-Ganglioside Antibody. Anti-GM1 antibodies are associated with a worse
prognosis and Anti-GQ1 antibody is associated with MFS.
 The Differential Diagnosis:

Neurological: Myasthenia gravis, Eaton-Lambert syndrome, MS and transverse myelitis
Metabolic: Hypokalaemia, Hyper-Mg4, Hypophosphataemia and Acute Intermittent Porphyria
Infective: Post Diptheria Neuropathy, Polio, Botulism and Tick Paralysis
Drugs/Toxins: Heavy Metal Poisoning (eg Lead), biological Toxins (eg Snake and Scorpion toxins)
and drugs (eg Nitrofurantion and Aminoglycosides)
Other: Acute Polymyositis and Intensive Care Unit Acquired Weakness.

 Management of GBS (ABCD protocol):
Airway
- 30% of patients require ventilatory support.
- Deterioration in respiratory function may be rapid and patients should have three times daily
measurement of Vital Capacity.
Clinical Indictors for Intubation:
 Vital Capacity < 20ml/kg.
 Max Inspiratory Pressure (MIP) < -30 cmH2O.
 Max Expiratory Pressure (MEP) < 40 cmH2O. (the 20/30/40 Rule).
 Bulbar involvement with Inability to Cough or Protect The Airway.
 Respiratory Failure on Blood Gas.
 Autonomic Instability.
Breathing
Patients with the following features are 85% likely to need Mechanically Ventilated
[Predictors of Respiratory Failure]:
 Time from onset to admission < 7 days.
 Inability to Cough.
 Inability to Stand.
 Inability to Lift Elbows.
 Inability to Lift Head.
  Liver Enzyme.
- Non-invasive ventilation is not useful as patients remain unable to clear secretions.
- Suxamethonium is Absolutely Contraindicated  Fatal Hyperkalemia.
- If prolonged ventilation seems likely then early Tracheostomy may improve patient comfort and aid
in clearance of secretions.
Circulation
 Adequate Circulating Volume.
 Β-Blockers, Atropine and Pacemakers have been used to manage Autonomic Disturbances.
Drugs and Disability (Specific Treatments):
IV Immunoglobulin (IgG):
 The initial treatment of choice
 IV 0.4mg/kg OD for 5 days.
 Much more convenient than plasma exchange, same efficacy and Less Side Effects.
 It should be commenced within 2 weeks of the onset of symptoms.
 Side Effects (Rare): nausea, fever, headache, a transient rise in liver enzymes, encephalopathy,
meningism and malaise. Serious SE; skin reactions (e.g. erythroderma) and hypercoagulability.
 Contraindications:
*IgA deficiency (increased incidence of Anaphylaxis) and Previous anaphylaxis to
immunoglobulin therapy. IgA levels must be checked in all patients prior to administration of
immunoglobulin.
* Renal impairment as renal function may deteriorate further with immunoglobulin therapy.
*Severe congestive cardiac failure is also a relative contraindication

Plasma Exchange:
 Involves the removal of about 200 ml/kg of plasma over 4–6 sessions and replacement with
4.5% human albumin solution.
 Thought to work by removal of a humoral demyelinating factor.
 This treatment does not influence mortality but reduce the duration of ventilator dependence
and hospital stay, and leads to earlier mobilisation if commenced within 2 weeks of the onset of
illness.
 It is associated with more significant side effects and contraindications compared with
immunoglobulin therapy. Administration is limited to specialist centres.
 Side effects: Hypotension, hypocalcaemia, coagulation abnormalities and septicaemia.
 Contraindications: Haemodynamic instability, Sepsis and severe haemostatic problems.
Physiotherapy: to prevent flexion contractures, Pressure sores and Nerve Palsies.
Thromoprophylaxis: LMWH and Compression Stocking due to high incidence of DVT.
Analgesia: for Neuropathic Pain (Carbamazepine, Pregabalin and Gabapentin)
Corticosteroids: There is insufficient evidence for the benefit of corticosteroids.
CSF filtration.
Psychotherapy.
Early enteral Feeding
What Other Problems Might They Encounter On ICU?

 Pneumonia.
 Line Infections.
 DVT.
 Nutritional Deficits.
 Psychological There Should Be Early And Active Psychological Support For the Patient And
Relatives.
 Autonomic Neuropathy: Ensure Adequate Circulating Volume And Sedation.
Β-Blockers, Atropine And Pacemakers Have Been Used To Manage Autonomic Disturbances.
 Pain Is Common (Especially In the Back and Lower Limbs) and Can Be a Major Problem.
Carbamazepine is Useful Adjuvant for Pain Control, Reducing Narcotic Requirements.
Intensive Physiotherapy Is Essential.
 GI Haemorrhage.
The Prognosis:
 Most patients (up to 85%) with GBS achieve a full and functional recovery within 6-12
months.
 Patients may have persistent weakness, areflexia, imbalance, or sensory loss.
 Some patients may have permanent neurologic sequelae including bilateral foot drop,
intrinsic hand muscle wasting, sensory ataxia, and dysaesthesia.
 The mortality rate is approximately 10%, usually from complications such as cardiac arrest
secondary to autonomic dysfunction, sepsis, pulmonary embolism and respiratory infection.
Poorer Prognosis Is Associated with:
 Older Patients
 Preceding Campylobacter Jejuni Infection
 Need For Mechanical Ventilation
 Rapid Progression of Symptoms
 Extensive disease.
7- Status Epilepticus
(a) What is the WHO definition of status epilepticus (SE)? How may it be classified?
(b) What are the systemic effects of SE?
(c) What are the causes of SE?
(d) Describe the pharmacological treatment options for SE.
(e) Describe the non-pharmacological options for treatment SE
The WHO definition of status epilepticus (SE):

A continuous, generalized, convulsive seizure lasting more than 5 minutes,
OR
Two or more seizures during which the patient does not return to baseline consciousness
Classification:
 The systemic effects of SE:
- CVS: early - hypertension, tachycardia; late - hypotension, bradycardia, dysrythmias

- Resp: Respiratory acidaemia, airway obstruction leading to Hypoxaemia, Hypercapnia and
Aspiration
- CNS: Increased CMR, hyperthermia, raised ICP and cerebral oedema
- Metabolic: Early: Lactic acidosis, hyperglycaemia; Late: Hypoglycaemia
- Endocrine: Increased circulating catecholamines.
- Renal: Rhabdomyolysis.
- Other: Trauma secondary to seizure: fractures, dental damage
 The causes of SE:

- Neurological: trauma, cerebral haemorrhage, infarction, tumours, infection (meningitis,
encephalitis)

- Drugs:
-Poor compliance with anti-epileptic medication in known epileptics,
-Toxicity including TCAs, flumazenil, Cocaine;
-Withdrawal e.g. from alcohol
- Electrolyte disorders e.g. hypoNa, hypoglycaemia, hypoCa, hypoMg
- Eclampsia
- Hepatic encephalopathy
- Uraemia
- Infection - pyrexia is common cause for seizures in paediatric population (called febrile seizures)
- Pseudoseizures
 Pharmacological treatment options for SE
- 1st line: Benzodiazepines

- 2nd line: - Anti-epileptic agents:
- 3rd line: - Anaesthetic agents as IV bolus +/- continuous infusion
- 1st line: Benzodiazepines

Lorazepam 0.1mg/kg IV, or Diazepam 0.1mg/kg.
-Diazepam can also be given rectally if IV access not
established, or Buccal midazolam.
-These work by increasing GABA-mediated cerebral
inhibition, decreasing seizure threshold.
- 2nd line: - Anti-epileptic agents:
Phenytoin 15mg/kg over at least 20minutes, with careful
cardiovascular monitoring (can cause
hypotension/bradycardia); Sodium Valproate as IV bolus
followed by infusion; Levetiracetam as IV bolus
- 3rd line: - Anaesthetic agents as IV bolus +/- continuous infusion
Propofol (causes myoclonic jerks but is not epileptogenic, can cease seizure activity), 2-4mg/kg bolus
+/- 5-10mg/kg/hr infusion; N.B. hypotension, bradycardia, be aware of propofol infusion syndrome
with prolonged infusion or paediatric population
Thiopentone which can be used to induce anaesthesia, cease seizure activity and also cause burst
suppression of neuronal activity, detected on EEG. IV bolus 3-7mg/kg, +/- 3-5mg/kg/hr continuous
infusion
**N.B. These are usually accompanied by a neuromuscular blocking agent in order to facilitate
tracheal intubation for the purpose of airway protection
-Neuromuscular blocking agents may stop overt seizure activity but patient may continue to have
NCSE
*N.B. In the case of the eclamptic fit, first line treatment is 4g MgSO4 IV over 15minutes, followed by
infusion as necessary. Benzodiazepines and other anti-epileptics are not used in this scenario.

The non-pharmacological options for treatment SE
- Use safe ABCDE approach
Supportive care includes airway maintenance and protection with opening manouvres, recovery
position to avoid aspiration, adjuncts or formal protection with intubation via a cuffed, ETT.
- Identify and correct any underlying cause e.g. hypoglycaemia or electrolyte disorders, antibiotics if
infection considered likely, if known cerebral tumour consider IV dexamethasone to reduce swelling
- Treat hypotension with IV fluid therapy initially taking care not to overload (N.B. be wary of
neurogenic pulmonary oedema or raising ICP);
Vasopressor agents can be used to prevent fluid overload
- Ensure patient is not at risk of injuring themselves or others whilst actively seizing
- Aim to achieve and maintain normothermia

8- ICU Acquired Weakness (ICUAW)
(a) What clinical features would make you suspect ICU acquired weakness?
(b) What are the differential diagnoses of ICUAW?
(c) What risk factors have been implicated in the development of ICUAW?
(d) What different categories of ICUAW exist? How they be distinguished from each other?
(e) What is the treatment for ICUAW?
 Clinical features would make you suspect ICU acquired weakness:
*ICU-acquired weakness (ICUAW) is: Clinically detected weakness in critically ill patients in whom
there is no plausible aetiology other than critical illness’.
*The criteria for diagnosing ICUAW are the presence of most of the following factors:
• Weakness developing after the onset of critical illness
• Weakness being generalised, symmetrical, flaccid, and generally sparing the cranial nerves (e.g.
facial grimace is intact)
• Muscle power assessed by the Medical Research Council (MRC) score of < 48 (or a mean score of <
4 in all testable muscle groups) noted on > 2 occasions separated by > 24 hours.
• Other causes of weakness having been excluded.
• Dependence on mechanical ventilation.
*Early Signs: facial grimacing without limb

movement in response to pain.
*Extraocular muscle involvement is rare
*Muscle wasting is variable and may be
disguised by oedema
*Sensory: unaffected in critical illness
myopathy, distal loss of pain, temperature,
vibration in critical illness polyneuropathy
*Autonomic: unaffected
 Differential Diagnoses of ICUAW:

- Brainstem Pathology: Pontine haemorrhage
or infarction (locked-in state)
- Spinal Cord Pathology: Transverse myelitis; Compressive lesions: tumour, abscess, oedema,
haemorrhage; Infiltrative lesions of the meninges: lymphoma, carcinoma
- Peripheral Nerve Pathology: Guillain-Barre Syndrome (acute inflammatory demyelinating
polyneuropathy); Phrenic nerve injury following thoracic/head and neck surgery or trauma; Toxic
neuropathy: arsenic, thallium and cyanide
- Neuromuscular Junction Pathology: Myasthenia Gravis; Lambert-Eaton Syndrome; Toxic:
botulism and pesticide poisoning
- Skeletal Muscle Pathology: Toxic myopathy: statins, amiodarone, propofol, bumetanide, alcohol-
related; Acute inflammatory primary myopathies: polymyosities, dermatomyosities; Severe
electrolyte disorders: hypokalaemia, hypophosphataemia, hypomagnesaemia

 Risk factors for CIP, CIM and CINM include:
• Female gender and increasing Age.
• Severe sepsis/septic shock with multi-organ failure
• Prolonged mechanical ventilation
• Prolonged bed rest
• Glucose and electrolyte abnormalities
• Use of parenteral nutrition, renal replacement therapy, Steroids, muscle relaxants, Vasopressors,
and Aminoglycosides.
 ICU Acquired Weakness Causes and Subgroups:

The causes are unknown, though they are thought to be a possible neurological manifestation of
systemic inflammatory response syndrome (SIRS).
1-Critical Illness Polyneuropathy (CIP).
2-Critical Illness Myopathy (CIM).
3-Critical Illness Neuro-myopathy (CINM).
What is the difference between CIP and CIM?

• Similar symptoms and presentations
• Often distinguished largely on the basis of specialised electrophysiological testing or muscle and
nerve biopsy
(a) Critical Illness Polyneuropathy (CIP):

*Peripheral Nervous System Organ Failure due to Systemic Inflammation-induced Pathology
*Patient meets the criteria for ICUAW;
*Compound Motor Action Potential (CMAP) amplitudes are decreased to <80% of the
lower limit of normal in >2 nerves;
*Sensory Nerve Action Potential (SNAP) amplitudes are decreased to <80% of the
lower limit of normal in >2 nerves;
*Normal or near-normal nerve conduction velocities.
*The absence of a decremental response on repetitive nerve stimulation.
(b) Critical Illness Myopathy (CIM):

*Decline in Muscle Strength due to Functional and Structural Muscle Changes
Probable CIM: 1, 2, 3 or 4; or 1 and 5
Definite CIM: 1, 2, 5, 3 or 4
(1) Patient meets the criteria for ICUAW.
(2) SNAP amplitudes on Nerve Conduction Studies are >80% of the lower limit of normal in >2
nerves.
(3) EMG in >2 muscle groups demonstrating short-duration, low amplitude Motor Unit Potentials
(MUPs) with early or normal full recruitment with or without fibrillation potentials.
(4) Direct Muscle Stimulation:  excitability (Nerve:Muscle ratio >0.5 in >2 muscle group)
(5) Muscle (Biopsy): histology consistent with myopathy.
(c) Critical Illness Neuro-myopathy (CINM): All of Patient meets criteria for ICUAW; Patient meets
criteria for CIP; Patient meets criteria for probable or definite CIM

 Prevention of ICUAW:
*Minimise Risk Factors (see before).
*Avoid Prolonged Bed Rest and Inactivity.
Treatment:
*No Specific Treatment has shown benefit.
*Focus on supportive care to facilitate resolution of the underlying acute illness,
with daily screening for weakness as part of routine clinical assessment.
*Tight Glycaemic Control may reduce incidence of CIP, but is precluded by the NICE-
SUGAR study.
Rehabilitation: Should begin early during ICU admission, and continue throughout hospital stay and
after discharge; Phased physical and mobilisation therapy,
-Beginning with passive limb movement.
-Occupational therapy.
-Cycle Ergometry.
-Electrical Muscle Stimulation.

9- Diarrhoea in the Intensive Care Unit and Clostridium Difficile
(a) What are the causes of diarrhoea in the intensive care unit?
(b) What are the 5 moments when hand hygiene? Describe 7 steps of hand washing.
(c) What is Clostridium difficile? How is it diagnosed?
(d) Outline the principles of management of Clostridium difficile infection (CDI)
(e) Describe prevention of CDI.
 Causes of diarrhoea in the intensive care unit:

- Medications- antibiotics, antifungals, laxatives
- Enteral Feeding when more than 60% of energy target
- Clostridium Difficile
- Digestive malabsorption disorders
- Intestinal resection
 5 Moments of Hand Hygiene

1-Before touching patient,
2- After touching Patient
3- Before clean/aseptic procedure
4-After bodily fluid exposure
5-After touching patient environment
7 steps of hand hygiene

1-Palm to palm
2-Right hand over back of left hand and left hand over back of right hand
3-Palm to palm fingers interlocked
4- Back of fingers to palms with fingers interlocked
5- Each thumb rotational rubbing with palm of other hand
6-Palm of each hand with finger tips of opposite hand
7-Each wrist rotational rubbing with opposite palm
 What is Clostridium difficile? How is it diagnosed?

- Clostridium difficile is a Gram +ve anaerobic rod.
- Diagnosis is;
*Traditionally a stool assay of toxin B produced by bacteria.
*Newer Elisa tests are now available.
*Gold Standard is cell culture cytotoxicity assay.
CT is reserved for severe cases and those difficult to diagnose.
*Colonoscopy and biopsy may detect pseudomembranous involvement.
 Management of Clostridium difficile infection (CDI)

- Antibiotic treatment with antibiotics not enterally absorbed-
*First line Metronidazole- Can be given iv if not tolerated enterally
*Second line- oral Vancomycin- cannot be given iv but can be given PR
- Subtotal or total colectomy; for those with fulminant colitis. Peritonitis, ileus or toxic megacolon,

 Prevention of CDI (SIGHT)
- Suspect- in those with diarrhoea.
- Isolate- ideally in a single room with toilet and handwashing facilities.
- Gloves- and apron on staff and visitors to prevent horizontal spread.
- Handwashing –requires soap detergent, alcohol rubs are ineffective.
- Test.
- All equipment and bed spaces should be cleaned with Chlorine containing antisepsis daily and after
every toilet use.
- Good antibiotic stewardship- avoiding high risk antibiotics in high risk patients, stop unnecessary
antibiotics and have guidelines for narrow spectrum antibiotics.
- Careful use of proton pump inhibitors - Restoring enteral bacteria with live culture yoghurts
- Enteral infusion of emulsified faeces has been described
- Immunoglobulin is being trialed with positive results.

10- Nosocomial Infection and Antibiotic Resistance
(a) What is a nosocomial infection? What are the common pathogens causing nosocomial infections?
(b) What are the mechanisms whereby organisms may acquire resistance to antibiotics?
(c) What clinical factors should be considered in the choice of empirical antibiotic therapy?
(d) What are the principles of antibiotic use in ICU that may prevent acquisition of resistance?
(e) Explain the concept of minimum inhibitory concentration (MIC).
 Nosocomial infection (health-care Associated Infections /Hospital Acquired Infection):

-An infection acquired by a patient during hospital care which was not present or incubating at the
time of admission.
-This includes infections acquired in the hospital but appearing after discharge (after 48 hrs of
discharge)
–An infection acquired in hospital by a patient who was admitted for a reason other than that infection.
Common pathogens:
-MRSA – methicillin-resistant Staphylococcus aureus
-CNS – coagulase negative Staphylococcus
-Enterococcus spp.
-Pseudomonas aeruginosa
-Acinetobacter baumannii
-ESBL – extended spectrum beta-lactamases
 The mechanisms whereby organisms may acquire resistance to Antibiotics:

1. Drug inactivation or Enzyme Inhibition causing a change in structure of the antibiotic.
2. Alteration of binding proteins: prevents the antibiotics from binding onto the bacterial cell wall.
3. Alteration of bacterial cell wall permeability: it prevents antibiotics from penetrating the cell wall
4. Mechanisms to increase the action of efflux pumps to promote expulsion of the antibiotic.
5. Metabolic change to develop an alternative pathway or target to bypass the effect of antibiotic.
 If Prescribing Empirically, Consider:

-Where is the likely source.
-What are the possible causative organisms.
-Community/Hospital acquired.
-Ward/ICU acquired.
-Foreign travel and potential exposure to resistant organisms
-Has the patient been recently treated with antibiotics.
-What is the required penetration given likely source.
-Patient co-morbidities.
- Liver and renal function.
-Patient allergy status.
-Route of administration.
-Locally present organisms and associated resistance.
-Local antibiotic prescribing guidelines.

Principles of Good Antibiotic prescribing:
In order to help prevent the development of bacterial resistance, it is important to prescribe
antibiotics according to the principles of Antimicrobial Stewardship, which include:
> Prescribe antibiotics only when clinically indicated.

> Collect specimens for culture (e.g. Blood, sputum, urine, swabs) prior to starting therapy.
> Prescribe antibiotics according to local guidelines and seek microbiology advice if needed.
> Choose correct class of antibiotic that would be effective against suspected organism.
> Use targeted, narrow-spectrum agents where possible.
> If broad-spectrum therapy commenced, de-escalate as soon as possible based on microbiology-
sensitivity data.
> Ensure correct duration of treatment (start and stop dates).
> Ensure correct dose (adjust for weight, renal function, liver function and if on RRT).
> Do not change antibiotics until at least 24-48hrs to observe for a clinical improvement.
> Switch intravenous agents to oral preparation promptly.
> Source control where applicable (e.g. Drain collections).
> Pro-calcitonin level use in considering when to discontinue empirical antibiotics.
> Ensure surgical prophylaxis compliance to reduce surgical site infection: ideally antibiotics
should be administered 30 minutes prior to skin incision, they should be given before tourniquet
is inflated and re-dose if 1500 ml blood loss or duration of surgery >4 hours).
Antimicrobial Stewardship:
This refers to a coordinated programme that promotes the
appropriate prescribing and use of antimicrobials (including
antibiotics) in order to:
 Reduce microbial resistance.
 Decrease the spread of infection caused by multi-drug
resistant organisms.
 Improve patient outcomes.
 Minimum Inhibitory Concentration (MIC):

-The lowest concentration of antibiotic required to inhibit the visible growth of bacteria after
overnight incubation (in vitro).
-It can be used to confirm and monitor the development of antibiotic resistance.
> Minimum Bactericidal Concentration (MBC):

- Lowest concentration of antibiotic required to kill a particular bacterium in vitro.
> Concentration-dependent killing:

- Aminoglycosides – the ideal dosing regimen for these antibiotics maximise concentration, because
the higher the concentration, the more extensive and the faster is the degree of killing.
> Time-dependent killing:

-β-lactams: the ideal dosing regimen for these antibiotics maximise the duration of exposure.

11- Malnutrition and Calculation of Nutritional Requirements
(a) Why is feeding a critically ill patient a priority? (15%)
(b) What are the features of the Malnutrition Universal Screening Tool? (20%)
(c) What groups of patients are most at risk of malnourishment? (20%)
(d) What factors are taken into account in calculating nutritional requirements (15%)
(e) What are the normal daily nutritional requirements of water, energy, protein and electrolytes?
 Feeding of Critically Ill Patient is Priority as Malnutrition is associated with:
- Increased Morbidity And Mortality - A fall in Metabolic Rate

- Muscle Weakness - Depression and Lethargy
- Reduced Immunity - Fatty change in the Liver
- Hypothermia - Impaired Liver and Renal Function
- Impaired Gut integrity and Immunity - Protein Breakdown is marked.
- Reduced Cardiac Output
 The features of the Malnutrition Universal Screening Tool [MUST]:

- ‘MUST’ is a 5-steps screening tool to identify Adults, who are:
 Malnourished
 At Risk of Malnutrition (undernutrition)
 Obese.
It also includes Management Guidelines which can be used to develop a Care Plan.
Step 1: Measure Height and Weight to get a BMI score [using Chart provided].
Step 2: Note % of unplanned Weight Loss and score [using tables provided].
Step 3: Establish Acute Disease Effect and score.
Step 4: Add scores of steps 1 + 2 + 3 together to obtain overall Risk of Malnutrition.
Step 5: Use Management Guidelines and/or local policy to develop care plan.
Risk of Malnutrition
 Low Risk (0 score):

-Repeat screening Hospital – weekly Care Homes – monthly Community – annually for special groups
e.g. those >75 yrs.
 Medium Risk (1 score):

-Document dietary intake for 3 days.
-If adequate (little concern): Repeat Screening;
*Hospital - weekly.
*Care Home - at least monthly.
*Community - at least every 2-3 months .
-If inadequate (Clinical Concern):

Follow Local Policy, Set Goals.
Improve and Increase Overall Nutritional Intake.
Monitor and Review Care Plan Regularly.

 High Risk (>=2 score):
-Refer to dietician, Nutritional Support Team or implement Local Policy.
-Set goals, improve and increase overall nutritional intake.
-Monitor and review care plan Hospital – weekly Care Home – monthly Community – monthly.
 Groups of Patients are most at Risk of Malnourishment:

- Many patients who require HDU or ICU are already malnourished on admission.
- This may be due to Alcohol or Drug Dependency, Poor Social Circumstances.
- Malignancy, Chronic Cardiac, Respiratory or Gastrointestinal Disease.
- Acute illness can quickly render even healthy people malnourished.
- Nausea/vomiting, Pain, Anxiety, Depression, Malabsorption Syndromes.
 The Factors taken into account in Calculating Nutritional Requirements:

- Nutritional assessment can be difficult in the critically ill.
- Clinical observations are useful.
History Include:
*Weight Loss.
*Poor Diet
*Gastrointestinal Disturbance,
*Reduced Functional Capacity
* Medical Conditions which Interfere with Feeding.
Physical Signs
*Loss of Subcutaneous Fat
*Muscle Wasting,
*Peripheral Oedema and Ascites.
*Methods such as Triceps Skin-fold Thickness and Mid-arm circumference are
poor predictors because of the presence of Peripheral Oedema.
-Volitional Tests of Strength are often not possible in the sedated patient or in the presence of
critical illness poly-neuromyopathy.
-Laboratory indices, for example Serum Albumin or Urea Excretion, are occasionally utilized to
indicate nitrogen balance but are unreliable in the context of critical illness.
-Indirect Calorimetry is the Gold Standard in assessment of energy expenditure.
 Normal Daily Nutritional Requirements:
* Water 30ml/kg
* Energy 30 kcal/kg
* Nitrogen 0.2 g/kg
* Glucose 3 g/kg
* Lipid 2 g/kg
* Sodium 1 mmol/kg
* Potassium 1 mmol/kg
* Calcium 0.1–0.2 mmol/kg
* Magnesium 0.1–0.2 mmol/kg
* Phosphate 0.2–0.5 mmol/kg.

12- Refeeding Syndrome
(a) What are the metabolic changes in critical illness that make early feeding preferable?
(b) What guidelines exist favouring early nutrition?
(c) What are the advantages of the enteral feeding route?
(d) What are the potential complications of enteral feeding?
(e) What are the complications of parenteral feeding?
(f) What are the features of refeeding syndrome?
 The Metabolic Changes in Critical Illness that make Early Feeding preferable:
- Glycogen store utilization (Fasting hours)
- Insulin resistance Hyperglycaemia
- Cortisol Sodium and Water Retention (Stress Response)
- Catabolism:Protein Breakdown
- Increase Basal Metabolic Rate (BMR) by 40%
- Impaired Immune Function
- Poor wound healing
- Muscle Weakness
- Impaired Thermoregulation
- Increase Ventilator Dependent Days
 NICE guideline : Nutrition Support for Malnourished and at Risk of Malnourish

Malnourished
-BMI less than 18.5 kg/m2
-Unintentional Weight Loss > 10% in the past 3-6 months
-BMI of 20 kg/m2 and unintentional weight loss > 5% within the last 3-6 months
At Risk of Being Malnourished

-Have eaten little or nothing for the past 5 days and/or like to eat less/nothing for the next 5 days
-Have poor absorptive capacity and/or high nutrient losses and /or high nutritional needs from
causes such as catabolism.
ESPEN (European Society of Parenteral and Enteral Nurition) Guideline:

-All patients who are not expected to be on normal nutrition within 3 days should receive nutritional
support within 24 – 48 h of admission.
-Parenteral nutrition (PN) is commenced within 24 – 48 h if enteral nutrition (EN) is contraindicated
or cannot be tolerated
ASPEN (American Society of Parenteral and Enteral Nutrition):

- If early EN is not feasible or available in the first 7 days no nutrition support therapy should be
provided, that PN should be reserved for and initiated only after the first 7 days of hospitalization.
 Advantages of the enteral feeding route:
- Reduce risk of stress ulcer - More physiological
- Preserve gut integrity - Less hyperglycaemia
- Maintains gut flora - Maintains immune functions
- Reduce bacterial translocation

 Complications of Enteral Feeding:
- Complications from feeding tubes - Feeding route error
Nasogastric/Nasojejunal/PEG - Underfeeding
- Nasal skin necrosis from nasal feeding tube - Aspiration
- Post pyloric feeding diarrhoea - VAP
- Feeding tube blockage
 Complications of Parenteral Feeding

- Complications related to CV lines insertion: - Deranged liver function
Pneumothorax, Bleeding, Vessel Damage, Air - Overfeeding
Embolism, Endocarditis, Thrombosis, - Lactic Acidosis
- CRBSI - Raised triglycerides
- Refeeding Syndrome: deranged electrolytes - Cholestasis
- Hepatic steatosis - Gut Atrophy
 Features of Refeeding Syndrome:

Body’s metabolism shifts from the free fatty acid metabolism of starvation back to utilization of
Carbohydrate which   Insulin Production  Intracellular shift of Electrolytes 
Hypophosphataemia
- Intracellular shift of Electrolytes - Arrhythmias.

Hypoglycaemia - Pulmonary Oedema.
Hypokalaemia - Respiratory Muscle Weakness.
Hypomagnasaemia - Hypotension.
Hypophosphataemia - Immune Dysfunction.
- Thiamine Deficiency - Lactic Acidosis.
- Diarrhoea. - In extreme cases Coma and Seizures
- Sodium and Water Retention due to Cerebral Oedema.

13- Nutrition post GI surgery
A 45-year-old man with a history of ulcerative colitis and alcohol abuse is admitted to the intensive
care unit for inotropic and ventilatory support following a laparotomy to excise atoxic megacolon.
His body mass index is 18kg/m2.
a) Why should this patient receive early nutritional support and what are the clinical benefits?
b) List the factors that increase the risk of the development of VAP. (10 marks)
c) What measures may reduce the risk of development of VAP? (7 marks).
 Early nutritional support and what are the clinical benefits:
• A screening tool should be used to assess nutritional state. The Nutritional Risk Score (NRS-2002) is
validated in ICU; a score >5 is indicative of a patient at high risk.
• This patient is highly likely to be nutritionally deplete

o Reduced BMI
o Intra-abdominal pathology
o Alcohol history
o Critically unwell
Increased BMR
Protein catabolism
o Likely vomiting prior to surgery
• Benefits
o Reduced length of ICU and hospital stay
o Reduced morbidity and mortality
o Reduced risk of muscle atrophy
♣ Improve weaning
o Improved immune function
♣ Reduced risk of infection
o Improved GIT blood flow (if enteral)
♣ Improved healing
 The specific composition of a nutritional regimen for this patient? (6marks)
• Weigh up risks vs. benefits of enteral nutrition (EN) vs. parenteral nutrition (PN)
• Multidisciplinary approach required. If end ileostomy formed and no issues with bowel continuity,
EN is preferable.
• Nutritional requirements
o Calories - 25-30 Kcal/Kg/Day
o Protein - 1.2-2 g/Kg/Day
• This patient is at high risk of re-feeding, therefore starting at 50% requirements for two days and
increasing by 300Kcal/day is appropriate
o 1.5 Kcal/ml feed running initially at 30ml/hr to increase after two days
o Close monitoring of electrolytes required
 The advantages and disadvantages of enteral nutrition:

• Advantages
o Increased caloric intake vs. oral food in this patient
♣ Reduced morbidity and mortality
♣ Reduced protein catabolism/ muscle atrophy
♣ Reduced ventilator and ICU days
♣ Attenuates disease severity
o Supports functional integrity of the GIT
♣ Induces the release of trophic endogenous agents
• Cholecystokinin, Gastrin, Bile salts
♣ Supports Gut-Associated Lymphoid Tissue (GALT)
• IG-A producing immunocytes
o B Cells and Plasma Cells
• Modulates stress and immune response
o Supports structural integrity of the GIT
♣ Maintains villous height
♣ Maintains tight junctions between intraepithelial cells
♣ Stimulates blood flow
o Cheaper than PN
o Avoids the need for central access
• Disadvantages
o More expensive than oral nutrition
o Increased aspiration risk
♣ Increased potential for Ventilator Associated Pneumonia (VAP)
o May unduly stress ischaemic bowel
o May precipitate/ potentiate anastomotic leak
o Nasogatric tube required with potential for
♣ Incorrect placement and aspiration
♣ Skin breakdown/ local trauma
♣ Perforation of oesophagus, pharynx, stomach or bowel
o Intolerance
♣ Vomiting, excessive aspirates, abdominal distension, diarrhoea
o Malabsorption possible – resulting in unrecognised low caloric intake

14- Care Bundles
(a) What is a care bundle? Summarise the key elements. (25%)
(b) What are the expected benefits of implementing a care bundle? (25%)
(c) What are the interventions in the ventilator care bundle? (25%)
(d) What are the interventions in the central line bundle? (25%)
 Care Bundle:
A set of evidence-based interventions that, when used together, significantly improve patient
outcomes than if implemented individually.
Key Elements
- Each intervention should be widely accepted as good practice and widely applicable
- Should be adhered to for every Patient 100% of the time
- Can be used to measure Evidence Based Practice
- Each step able to be audited - done/not done/ local exclusion
- Audit focused on organizational aspects of performing intervention rather than how well
intervention performed
- Only compliant with bundle when every intervention completed or a step is excluded for pre-
defined reason.
 Benefits of Implementing a Care Bundle:

- Direct benefit to patient; reduce Morbidity Mortality
- Reduce ICU stay
- Reduce Financial Cost
- Improve Resource Utilization & therefore benefit to other Patients outside the scope of Care
Bundle
 Ventilator Care Bundle:

- Hand Hygiene
- Close Tracheal Suction System
- Chlorhexidine Oral Decontamination
- Head of Bed Elevation 30 – 45O degrees
- Sedation Break and assessment of Readiness to Extubate.
- Peptic Ulcer disease Prophylaxis
- Venous Thromboembolism prophylaxis
 Central Line Bundle:

- Hand hygiene
- Maximal Barrier Precaution at insertion; Gown, Gloves, Mask, Hat.
- Chlorhexidine 2% skin Antisepsis left to Dry.
- Subclavian Central Line is the first choice & Avoid Femoral Line
- Indication for Central Line Daily Review and promp Removal of Unnecessary Line
Sepsis care Bundle

Three-hour bundle
• Measure lactate level

• Obtain blood cultures prior to administration of antibiotics
• Administer broad spectrum antibiotics
• Administer 30 mL/kg crystalloid for hypotension or lactate ≥ 4 mmol/L

15- ICU Delirium
(a) Define (i) Delirium (ii) Sedation. (20%)
(b) What are the risk factors for delirium on the ICU? (20%)
(c) List some methods of diagnosis and assessment of delirium. (20%)
(d) How may delirium be prevented on the ICU? (20%)
(e) What are the pharmacological and non-pharmacological methods of managing delirium?
 Delirium: Acute Confusional State, characterized by:
 Inattention.
 Disorganised thinking
 Altered level of consciousness.
- It is associated with increased duration of intensive care and hospital length of stay, increased
mortality and long-term cognitive impairment; Sub-types:
*Hyperactive Delirium: the person is agitated/Aggressive, may be a danger to themselves and staff.
*Hypoactive Delirium: appear apathetic, lethargic, drowsy and have Delay Response.
*Mixed Delirium: fluctuate between hypo-and hyperactive subtype.
-Sedation: reduction of Anxiety, Stress, Irritability, or Excitement by administration of a sedative drug
 Risk factors for Delirium on the ICU:

- Age: >70 years.
- Medical Hx: HTN, CCF, Stroke, Dementia, Renal/ Hepatic impairment, Visual or Hearing impairment
- Social Hx: Smoker, Alcohol Abuse, Malnutrition
- Environmental: Catheterisation (urinary or central venous), sleep deprivation and Physical Restrains.
- Medications: Benzodiazepines, Opiates and Anticholinergics.
- Acute presentation: Sepsis, Hypoxia, Pain and Metabolic (hypoglycaemia, electrolyte abnormalities).
 Methods of diagnosis and assessment of Delirium:

A- Confusion Assessment Method for the Intensive Care Unit (CAM-ICU)
*Performed once every 24hr
*Assesses patient performing tasks to command
*Can be used during mechanical ventilation

B- Intensive Care Delirium Screening Checklist (ICDSC):
 Prevention of Delirium:
ABCDEF bundle:
-Spnotaneous Awakening Trial
-Spnotaneous Breathing Trial.
-Choice of Sedatives.
-Delirium Monitoring
-Early Mobility and Exercise
-Family engagement.
Minimise Risk Factors: Medication

is often one of the most modifiable
factors eg; limit use of
Benzodiazepines, Opioids, GABA-
mimergic drugs (Zopiclone),
medicines with pro-serotonin
effects (Tramadol) or
Anticholinergic activity (Codeine)
……...etc).
Minimise Sleep Disruption
 Management of Delirium:
Pharmacological Non-Pharmacological
Haloperidol: Medical Hx
- Reduces Hallucinations and Delusions Correct Visual and Hearing Impairments.
- Side effects: Extra-pyramidal side effects, Correct Metabolic Derangement.
Prolonged QT interval, Neuroleptic Diagnose and Treat Infection.
Malignant Syndrome Adequate Tissue Oxygen Delivery.
Adequate Analgesia.
Atypical Anti-psychotics [Olanzipine]: Remove Lines and Catheters promptly.
- Dopamine Receptor Antagonist and Medications
Serotonin Receptor Antagonists (5-HT2A) Avoid Deliriogenic Drugs were possible.
- Enteral administation required. Environmental
Orientate Patient Regularly.
Dexmeditomedine Reduce Noise and Reduce Sleep Disturbance
Mobilise Where Possible.

16- Temperature Regulation in the ICU
(a) Define (i) Heat (ii) Temperature
(b) What are the physiological mechanisms of heat production bythe body?
(c) What are the mechanisms by which heat is lost?
(d) What are the systemic complications of hyperthermia?
(e) What are the systemic complications of hypothermia?
(f) Describe the methods by which a dangerously high temperature (>40oC) may be managed on the
intensive care unit.
Heat is a form of energy- the total kinetic and potential energy of particles within a substance and
can be transferred from a hotter substance to a colder substance.
Temperature is a measurement of the quantity of heat energy; the tendency of a substance to gain
or lose heat relative to its surroundings; it is proportional to the mean kinetic energy of the particles
in the substance. 3 major scales for measuring temperature are Kelvin (SI unit), Celsius and
Fahrenheit.
 Physiological Mechanisms of Heat Production by the Body:

*Heat is produced by basal metabolism and homeostatic mechanisms (Thyroxine for long-term
control, acutely- Adrenaline and Noradrenaline) to maintain core temperature
*Heat production can be increased by food consumption, exercise and an  in body temperature
*Muscle activity is the main method of heat generation- shivering (as a last resort, increases heat
production by 2-5 times), voluntary and behaviour
*In neonates- by non-shivering thermogenesis (brown adipose tissue)
 Mechanisms by which heat is lost:

*Radiation 40%. Transfer of energy by infrared rays from a hotter body to a cooler one
*Convection 30%. Transfer of heat by the motion of a gas or liquid across the surface of the skin
*Evaporation 15%. When water evaporates it requires energy to convert it from a liquid to a vapour-
latent heat of vaporization
*Respiration 10% (Pneumonic RCEA- Royal College Exam Room!) and
*Conduction 5%. Transfer of heat between molecules in direct contact
 Systemic complications of hyperthermia:

- Hyperthermia is a core temperature of over 38.0 oC.
- Fever is hyperthermia caused by an elevation in the thermoregulatory set point, for example by an
infectious process and is a core temperature above 38.3.
- Hyperpyrexia is a temperature above 40.0.
Systemic complications of hyperthermia are...
Cardiac- Hypotension, tachycardia
GI- Dehydration, nausea and vomiting
CNS- Confusion, seizures, coma
Renal- Failure, hyperkalaemia, metabolic acidosis, rhabdomyolysis
Death

Systemic complications of hypothermia:
Hypothermia is a mean core body temperature of below 35.0 oC.
It can be further classified into mild (32-35), moderate (28-32) or severe (<28)
Systemic complications of hypothermia are.....
*Cardiac:Bradycardia, -ve inotropy (and  oxygen delivery), heart block, Arrhythmias
*Metabolic/electrolyte- Hypoglycaemia, hypokalaemia, hypomagnesaemia
*CNS- Confusion, coma
*Haematology- Coagulopathy
*Immunology- Immunocompromise
* Shivering (increasing oxygen consumption and pain)
*Pressure sores
*Reduced drug clearance, hypovolaemia
*Death
◉ Management of Dangerously High Temperature (>40oC) in ICU :

The sequelae of worsening multiorgan failure that results when core temperature exceeds 40.5 oC
indicates that fever should be treated aggressively and promptly.
Management
Identify and remove potential trigger factors, e.g. volatile inhalational agents in MH
Physical Methods
*Uncovering the patient
*Using cold towels/ice packs in axilla, groin, across the chest (avoid direct skin contact) *Cooling
blanket
* Invasive: cooled IV fluids, cool fluids into the peritoneum, bladder, pleura & stomach
*Intravascular cooling catheters, haemodialysis, cardiopulmonary bypass.
Pharmacological Methods
*Non- specific to reduce heat production- Sedative agents, neuromuscular blocking drugs
*Specific antipyretics- Paracetamol, NSAIDs
*Dantrolene- only specific indication is for use in MH but has also been described for treatment of
*Neuroleptic Malignant Syndrome
*For serotonin syndrome 5-HT2A antagonists such as Cyproheptadine may be used
*May include dopamine agonists, e.g. Bromocriptine for NMS.

17 -Extra-Corporeal Membrane Oxygenation (ECMO)
(a) What is extracorporeal membrane oxygenation (ECMO)?
(b) What is the difference between ECMO and cardiopulmonary bypass?
(c) What are the indications for VA and VV-ECMO?
(d) What are the contraindications?
(e) What complications may result from the usage of ECMO in a patient?
 Extracorporeal Membrane Oxygenation (ECMO):
- ECMO is the use of a modified heart-lung machine to provide respiratory, circulatory

or both support at the bedside
- Can be used for days to weeks
- Can be used to manage severe but reversible causes of respiratory failure or
cardiogenic shock refractory to conventional treatment
- Provides peripheral oxygenation, ventilation and circulation
- ECMO circuit can be set up in three ways:
Veno-arterial (VA-ECMO): allows gas exchange and haemodynamic support while blood
is pumped from the venous to arterial side
Veno-venous (VV-ECMO): facilitates gas exchange but does not provide

haemodynamic support. Blood is removed from venous side and pumped back into it.
Arterio-venous (AV-ECMO): uses patient’s own arterial pressure to pump blood from
arterial to venous side, facilitating gas exchange.

Components of ECMO circuit: Pump
-Vascular access
-Tubing
-Pump
-Gas exchange mechanism
Gas exchange mechanism
 The difference between ECMO and cardiopulmonary bypass:
- Cardiopulmonary bypass provides short term support to patients undergoing cardiac

surgery.
- Incorporates other functions including suction and venting of field and cardiac
chambers and administration of cardioplegia.
Parameter ECMO Bypass

Oxygenation Yes Yes
Ventilation Yes Yes
Circulatory support Yes Yes
Venous reservoir No Yes
Ability to deliver cardioplegia No Yes
Ability to administer medications into the No Yes
circuit
Supplemental pumps e.g. Suction, vent No Yes
Heating and cooling Yes Yes
Ability to adjust oxygenation Yes Yes
Ability to add fluids directly to circuit No Yes
Ability to administer anaesthetics in line No Yes
 Indications for VA and VV-ECMO:
VA-ECMO:
- Refractory cardiogenic shock with underlying potentially reversible heart condition
- Weaning from cardiopulmonary bypass after cardiac surgery
- Bridge to cardiac transplantation or ventricular assist device
- Acute myocarditis
- Intractable arrhythmia

- Post-cardiac arrest as part of ALS (after 10 mins of adequate but unsuccessful ALS)
- Local anaesthetic toxicity
- Pulmonary hypertension
- Consider in patients with systolic BP < 85 mmHg, cardiac index < 1.2 l/min/m2 despite
adequate preload, > 2 inotropes in use, intra-aortic balloon counterpulsation and
systemic signs of low CO.
VV-ECMO:
- Aims to provide oxygenation and rest lungs, decreasing insult caused by mechanical
ventilation
- Any potentially reversible acute respiratory failure
- ARDS, associated with viral or bacterial pneumonia
- Graft dysfunction after lung transplantation
- Trauma (pulmonary contusion)
- Pulmonary embolism (if acceptable cardiac function)
 Contraindications:
- Irreversible organ damage
- Multi organ failure
- Patients who are not candidates for transplantation
- Patients who cannot be anticoagulated (relative)
- Severe aortic regurgitation (VA-ECMO)
- Aortic dissections (VA-ECMO)
- Patient / proxy refusal
- Patients with “do not resuscitate” orders
- Severe bleeding and PVD increases risk of complications
 Complications may result from the usage of ECMO:
- Haemorrhage
- Infection
- Lower limb ischaemia
- Abdominal compartment syndrome likely secondary to massive fluid resuscitation in
an effort to achieve adequate ECMO flows
- Clot formation
- Stroke
- Renal failure
- Nosocomial infection
- Mechanical mishaps e.g. Pump / oxygenator / circuit failure / breakage

18- Pulmonary Artery Catheters (PAC)
(a) What are the normal pressures within the heart that can be demonstrated with a PAC? Illustrate
with diagram. (20%)
(b) What are the uses of a pulmonary artery catheter? (20%)
(c) What are the values that can be measured with a PAC? What are the derived/calculated values?
(d) What are the complications associated with pulmonary arterial catheterisation?
(e) What are the pros and cons of pulmonary artery catheters on the ICU? (20%)
 Normal pressures within the heart that can be demonstrated with a PAC?
- As the PAC is floated through the right atrium a characteristic waveform is seen as
long as there is a competent tricuspid valve.
- This waveform represents venous return to the right atrium during ventricular
systole and right ventricular end-diastolic pressure.
- Normal right atrial pressure lies between 0-7/8 mmHg.
- As the PAC floats into the right ventricle the tracing changes.
- Ventricular systole is represented by the prominent upstroke and downstroke, while
ventricular diastole is represented by a more gradual upstroke that consists of an early
rapid filling phase, a slow filling phase and an atrial systolic phase.
- Two pressures are measured from the RV pressure waveform: the peak right
ventricular systolic pressure and the right ventricular end-diastolic pressure.
- Normal right ventricular systolic pressure varies from 15 to 25 mmHg and normal
right ventricular end-diastolic pressure varies from 3 to 12 mmHg.
- As the PAC passes through the pulmonary artery, the PAWP will be found when the
inflated balloon wedges in a distal branch of the pulmonary artery.
- This creates a static column of blood between the catheter tip and the left atrium.
- Pressure at both ends of the column equilibrates- therefore pressure at the distal
end of the catheter is equal to the pressure of the left atrium.
- Normal PAWP is between 6-15mmhg.
- The PAWP will represent the left ventricular end diastolic pressure as long as there is
no obstruction to flow between the left atrium and left ventricle.

 Uses of a pulmonary artery catheter:
- Use of PAC is controversial as no study has convincingly shown improvement in
patient outcome with the use of PAC.
- In general the decision to place a pulmonary artery catheter should be based upon a
specific question regarding a patient's hemodynamic status that cannot be
satisfactorily answered by clinical or non-invasive assessment.
- If the answer could change management, then placement of the catheter is
indicated.
- Uses can be divided into diagnostic and therapeutic:
Diagnosis:
Differentiation among causes of shock:
Cardiogenic/Hypovolemic/Distributive/Obstructive
Differentiation between mechanisms of pulmonary oedema: Cardiogenic/Non-
cardiogenic
Evaluation of pulmonary hypertension
Diagnosis of pericardial tamponade
Diagnosis of left-to-right intracardiac shunt
Diagnosis of lymphangitic spread of tumour and fat embolism
Therapeutic:
Management of perioperative patient with unstable cardiac status/complicated
MI/following cardiac surgery
Management of severe preeclampsia
Guide to pharmacologic therapy: Vasopressors/Inotropes/Vasodilators
Guide to non-pharmacologic therapy
Fluid management
Gastrointestinal bleed
Traumatic exsanguination
Burns
Renal failure
Sepsis
Heart failure
The values and derived/calculated values that can be measured with a PAC:
Values that can be obtained from a PAC include pressures and waveforms for:
- Central venous pressures
- Right atrial pressure
- Right ventricular systolic and diastolic pressures
- Pulmonary artery systolic and diastolic pressures
- Pulmonary artery wedge pressure
Measurements may be derived or calculated:
- Left ventricular end diastolic volume
- Left ventricular end diastolic pressure
- Stroke volume
- Cardiac output via thermodilution
- Pulmonary vascular resistance
- Systemic vascular resistance
 Complications associated with pulmonary arterial catheterisation? (20%)

Those related to insertion of central venous access
Early:
Bleeding
Arterial puncture
Arrhythmia
Air embolism
Thoracic duct injury (with left SC or left IJ approach)
Catheter malposition
Pneumothorax or hemothorax
Late:
Infection
Venous thrombosis, pulmonary emboli
Catheter migration
Catheter embolization
Myocardial perforation
Nerve injury
Those related to insertion of the PAC itself:

Atrial and ventricular arrhythmias
Knotting of the catheter in a heart chamber
Valvular damage
Heart rupture
Those related to maintenance and use of the catheter

Pulmonary artery rupture
Pulmonary infarction
Thromboembolic events
Pulmonary artery psuedoaneurysm
Mural thrombi
Endocarditis
Sterile valve vegetations
Venous air embolism
Those related to the interpretation of hemodynamic data

Sources of error:
Improperly calibrated pressure monitors
Transduction of airway pressures under non-zone 3 conditions
Overestimation of PCWP because of incomplete pulmonary artery branch occlusion
Inter-observer variability in the interpretation of hemodynamic data
 The pros and cons of pulmonary artery catheters on the intensive care unitPros of
PAC in ICU:
As for the indications for PAC use
- For the use in diagnosis of complex conditions
- To measure the responses to therapy
- Can be used to answer a question that is not answered by standard monitoring and
whose answer could affect treatment choice
Cons of PAC in ICU:

- In one study patients who underwent right heart catheterization had an increased
30-day mortality compared to those who did not undergo the procedure
- Studies have not shown any improvement in overall outcome
- Studies haven’t shown any improvement in mortality rate, days in hospital
- Overall trend away from using PAC in ICU means when they are indicated staff are
not confident in their use or in interpretation of results

19- Pulse Contour Analysis
(a) Define (i) Shock (ii) Cardiac Output (iii) Preload (iv) Afterload, (v) Contractility (vi) SVR
(b) What are the clinical indicators of cardiac output?
(c) What parameters may be derived from arterial pulse contour analysis?
(d) What are the factors affecting the accuracy of pulse contour analysis?
(e) What are the advantages and disadvantages of PICCO?
 Shock is failure to deliver adequate oxygen to the tissues
Cardiac output is the volume of blood ejected by the left ventricle per minute (equals Stroke volume
x heart rate). Influenced by preload, contractility and afterload
Preload is the end diastolic ventricular wall tension (tension at the point of maximal filling) – mainly
determined by venous return
Afterload is tension developed in ventricular wall during systole – largely determined by SVR
Systemic vascular resistance is all the forces that oppose blood flow through the systemic vasculature
– mainly determined by vasoconstriction in the arteriolar bed
 Clinical indicators of cardiac output:

Include skin colour, skin temperature, core peripheral temperature difference, cap refill time, heart
rate, urine output, mental state. Bp can be used but often unhelpful as vasoconstriction occurs in
response to poor CO. Raised lactate may be helpful
 What parameters may be derived from arterial pulse contour analysis?

Cardiac output, cardiac index (cardiac output adjusted for body size), heart rate, stroke volume
variation (indicator of fluid responsiveness)
 Factors affecting the accuracy of pulse contour analysis?

Rely on optimal arterial signal – over/under damping leads to inaccuracies
Arrhythmias, aortic regurg and intra-aortic balloon pumps affect accuracy
 Advantages and disadvantages of PICCO:

PiCCO uses transpulmonary thermodilution to calibrate. Cold injectate introduced into SVC via
central line. Art line with thermistor placed in major artery and change in temp of blood measured
after injection. Thermodilution equation used to calculate CO.
Advantages
less invasive than PAC, less skill required as PAC not needed to be accurately positioned.
In general good agreement with CO measurements from PAC
Dynamic continuous measurement
Measures extra-vascular lung water – shown to correlate in severity of ARDS, no of ventilator days,
ICU duration and mortality
Can stay in patient for up to 10 days (unlike PAC – 72 hours)
No CXR required
Claimed to be cheaper
Patients usually already require a CVL and arterial line

Disadvantages
*Requires intermittent calibration
*Thermodilution via pulmonary art catheter measures right heart CO but PiCCO measures left heart
CO – in pts with intra-cardiac or intra-pulmonary shunt CO measurements will differ from “gold
standard”
*Indicator loss into the lungs
*Inaccurate with aortic regurg, intra-aortic balloon pump
*Should be recalibrated with changes in position, therapy or condition to account for compliance of
vascular bed.

20- Intra Aortic Balloon Counterpulsation Pump (IABP)
(a) Mechanism of action.
(b) Indications for IABP use
(c) Contraindications for IABP use
(d) Complications of IABP use
(e) IABP troubleshooting
 Mechanism of Action:
The Intra-aortic balloon pump (IABP) is a mechanical device
that increases myocardial oxygen perfusion while at the same
time increasing cardiac output   Coronary Blood Flow and
therefore Increasing Myocardial Oxygen Delivery.
It consists of a cylindrical polyethylene balloon that sits in the
aorta, approximately 2 centimeters from the left subclavian
artery and Counterpulsates:
 That is, it actively deflates in systole, increasing forward
blood flow by reducing afterload through a vacuum effect.
 It actively inflates in diastole, increasing blood flow to the
coronary arteries via retrograde flow. These actions combine
to Decrease Myocardial Oxygen Demand and Increase
Myocardial Oxygen Supply.
A computer-controlled mechanism inflates the balloon with
helium from a cylinder during diastole, usually linked to either
an electrocardiogram (ECG) or a pressure transducer at the distal tip of the catheter; some IABPs,
such as the Datascope System 98XT, allow asynchronous counterpulsation at a set rate, though this
setting is rarely used.
Helium is used because its low viscosity allows it to travel quickly through the long connecting tubes,
and has a lower risk than air of causing an embolism should the balloon rupture.

The haemodynamic effects of IABP therapy:
Aorta ↓systolic pressure, ↑diastolic pressure

Left ventricle ↓systolic pressure, ↓end-diastolic pressure, ↓volume, ↓wall tension
Heart ↓afterload, ↓preload, ↑cardiac output
Blood flow ↑→ coronary blood flow
 Indications for IABP use:

Acute myocardial infarction Refractory LV failure
Cardiogenic shock Refractory ventricular arrhythmias
Acute MR and VSD Cardiomyopathies
Catheterization and angioplasty Sepsis9
Refractory unstable angina Infants and children with complex cardiac anomalies10
Contraindications for IABP use:

Absolute Relative
 Aortic regurgitation  Uncontrolled sepsis
 Aortic dissection  Abdominal aortic aneurysm
 Chronic end-stage heart disease  Tachyarrhythmias
with no anticipation of recovery  Major arterial reconstruction surgery
 Aortic stents  Severe peripheral vascular disease
 Uncontrolled coagulopathy  Contraindications to anticoagulation.
 Complications of IABP use:

Transient loss of peripheral pulse
Limb ischaemia
Thromboembolism
Compartment syndrome11
Aortic dissection
Local vascular injury:false aneurysm, haematoma, bleeding from the wound
Infection
Balloon rupture (can cause Helium gas embolus)
Balloon entrapment
Haematological changes, for example thrombocytopenia, haemolysis
Malpositioning causing cerebral or renal compromise
Cardiac tamponade

One complete cardiac cycle and the corresponding waveform of the IABP during inflation and deflation

 IABP troubleshooting

21- Tracheostomies on the Critical Care Unit
The 4th NAP on airway complications identified a high incident of airway events in the ICU, especially
involving tracheostomies.
(a) Describe the technique of percutaneous tracheostomy (20%)
(b) What are the potential complications of tracheostomy insertion? (20%)
(c) What basic principles were agreed by the National Tracheostomy Safety Project that would underpin
guideline development for patients with surgical airways? (20%)
(d) Describe the 'green' algorithm for emergencies involving a patent upper airway. Contrast this with the 'red'
algorithm. (20%)
(e) What are the recommended bedside pieces of equipment for patients with tracheostomy or laryngectomy?
(20%)
 Technique of percutaneous tracheostomy, including anatomy:

Pre-Procedure
*Cervical and tracheal anatomy should be assessed by clinical examination and ultrasound scanning
of the neck.
*Any lesions,scars and masses in the central thyroid and tracheal area should be noted.
*Any aberrant blood vessels should be identified with the help of ultrasound to prevent massive
haemorrhage.
*The operator should feel the landmarks, including suprasternal notch, cricoid cartilage, and tracheal
rings.
*Any anticoagulants, including heparin infusion, infusion of activated protein C or any other
antiplatelet agents should be discontinued.
*The coagulation profile and platelet count should be routinely checked, and there may be a need
for FFP/Platelets if the INR greater than 1.5 or platelet count is less than 50,000.
*Patients requiring high inspired oxygen (FiO2 > 0.5) and PEEP >10 cm H2O should be deferred until
oxygenation and gas exchange have improved.
*Due consideration should be given to determine the size of tracheostomy tube required for an
individual patient.
Procedure
*Percutaneous tracheostomy can be performed under local
anaesthesia but in the ICU it is usually performed under general
anaesthesia.
*Patient supine and the neck extended.
*Requires 2 people for the procedure: 1 to maintain the airway at
the top end , and 1 to perform the tracheostomy
*Ultrasound scanning of the neck reveals any abnormal vessels
near the surgical site.
* Landmarks are marked, including the suprasternal notch, cricoid
cartilage and tracheal rings when palpable.
*The components of the tracheostomy set and other equipment
are checked
*Lidocaine with Adrenaline 1:200,000 up to 10 ml is infiltrated into the
surgical site.

*The patient is paralysed and ventilated with 100% oxygen.
*Continuous monitoring of ECG, blood pressure, saturation of oxygen in arterial blood flow (SpO2)
and capnography is essential.
Steps
*Small transverse incision is made at the level of the 2nd tracheal ring (the midpoint between cricoid
cartilage and suprasternal notch in patients with normal anatomy).
*Blunt dissection is carried out until the trachea is felt with a finger.
*The existing endotracheal tube is withdrawn over the endoscope until the cuff is near the vocal
cords. The procedure can also be done with an LMA
*A Bonfils semi-rigid scope (or similar) or a flexible fibreoptic scope is used to visualise the airway
with display of images on a monitor
*The introducer needle and cannula is inserted into the trachea preferably below the second
tracheal ring in the midline under endoscopic visualization
*Following removal of the needle, a J-tipped guide-wire is inserted.
*A small starter dilator is inserted into the trachea to open a tract and is then removed.
A guiding catheter is then inserted over the guide-wire and followed
by an appropriate dilator (e.g. single-tapered dilator;
A tracheostomy tube of appropriate size is then inserted over the
loading dilator via the stoma
The entire procedure is performed under continuous endoscopic guidance to help reduce the risk of
malposition and false passage.persistent stoma and tracheal stenosis.

Potential complications of tracheostomy insertion:
Immediate Delayed Late

(perioperative period) (postoperative period < 7 (late postoperative period >7
days) days)
*Haemorrhage *Tube blockage with secretions *Tracheal stenosis
*Misplacement of tube - within or blood. *Tracheomalacia
tissues around trachea or to *Partial or complete tube *Swallowing problems
main bronchus displacement * Granulomata of the trachea
*Pneumothorax *Infection of the stoma site may cause respiratory difficulty
*Tube occlusion Infection of the bronchial tree when the tracheostomy tube is
*Surgical emphysema (pneumonia) removed
*Loss of the upper airway *Ulceration, and/or necrosis of *Tracheo-oesophageal fistula
trachea or mucosal ulceration *Tracheo-innominate artery
by tube migration fistula (Haemorrhage)
*Risk of occlusion of the
tracheostomy tube in obese or
fatigued patients who have
difficulty extending their neck
*Haemorrhage (local tissue
trauma or erosion through
blood vessels)
 Basic principles were agreed by the National Tracheostomy Safety Project that would underpin
guideline development for patients with surgical airways:
Patients with tracheostomies or laryngectomies may be considered to have airways that are difficult
to manage, either leading to the formation of the airway stoma itself or as a result
Distinct bedside information and algorithms were required for patients with a potentially patent
upper airway and those with a laryngectomy. Bedside Information cards displaying whether the
patient had a tracheostomy or laryngectomy, type of tracheostomy, size or tube and date insertion.
This allows first responders to rapidly assess management options
It was recognised that separate algorithms were needed for patients with a potentially patent
upper airway and those with a laryngectomy
Overall style of the algorithms was to be based on the highly successful flow charts produced by DAS
to build on the success of previous guidance, highlighting how effective emergency management
requires careful advanced planning and a multi-disciplinary team approach
Oxygenation of the patient takes priority (not necessarily securing the airway immediately and
definitively, unless required for oxygenation)
Best assistance should be sought early
Generic algorithm developed that would cover the vast majority of common and easil reversible
clinical situations that arise whilst accepting that a number of special circumstances do exist
Competencies and training are likely to be divided between those of the primary and secondary
responder. The primary responder (typically a nurse, junior doctor or allied health professional)
needs to be guided to detect airway problems, to assess tracheostomy and airway patency and to
provide basic emergency oxygenation. The secondary responder (typically an anaesthetist,
intensivist, head and neck surgeon or specialist practitioner) will have skills in conventional airway
management and will also be guided to use skills in managing the tracheostomy or stoma
Maximum benefits of the guidelines would be achieved through education.
The 'GREEN' algorithm for emergencies involving a patent upper airway. Contrast this with the
'RED' algorithm.
Green Algorithm: National Tracheostomy Safety Project 2012
Paired with green sign placed over bedspace of tracheostomy patient
For Tracheostomy patients (who have an anatomically connected and potentially patent upper
airway)
Date of insertion / Type / Size of tube documented
Step 1: Call for help
Step 2: Look listen feel at site of tracheostomy – Is the patient Breathing?
Step 3: If no start CPR, If yes apply high flow oxygen to face and tracheostomy site
Step 4: Assess tracheostomy patency;
Remove speaking valve
Remove inner tube
Suction catheter down inner tube
Step 5: If tracheostomy patent suction airway and continue ABCDE assessment. If tracheostomy not
patent:
Step 6: Deflate cuff and look, listen,feel
Step 7: Remove tracheostomy
Step 8: Primary Oxygenation: Bag mask ventilation (BMV) via face. If fails: BMV via tracheostomy
Step 9: Secondary Oxygenation: Oral Intubation (may be difficult). If fails: attempt intubation of
stoma (Size 6.0 ETT + Bougie)
Red Algorithm: National Tracheostomy Safety Project 2012

Paired with red sign over bedspace of laryngectomy patient
For laryngectomy patients who do not have an upper airway in continuity with the lungs
Same principles of assessing stoma patency apply e.g remove tube (if present) and pass suction
catheter
Patients cannot be oxygenated via the mouth/nose as there is no anatomical connection
Primary Oxygenation: Bag Mask Ventilation through stoma ONLY (not face)
Secondary Oxygenation: Intubation of Stoma ONLY (not oral)
Do not remove Transesophagel Puncture (TEP) valves
For both Green and Red Algorithms, capnography or Mapleson C circuit should be used

Recommended bedside pieces of equipment for patients with tracheostomy or laryngectomy:
National Tracheostomy Safety Project Guidelines 2012
Bedside equipment
• Humidification equipment
• Suction with selection of appropriate suction catheters
• Spare tracheostomy tubes
One the same size
One tube one size smaller
• Clean pot for spare inner cannula
• Sterile water for cleaning the suction tube
• Scissors (and stitch cutter if tracheostomy tube is sutured)
• Water soluble lubricating jelly
• Sterile dressing pack
• Tracheostomy dressings
• Tracheostomy tapes
• Personal protective equipment (gloves, aprons, eye protection)
• Sterile gloves for performing deep suction
• Nurse call bell: the patient may be unable to call for help verbally
• Communication aids: the patient may not be able to verbalise
• Bedside equipment checklist
Emergency equipment
• Basic airway equipment – oxygen masks, self inflatingbags, oral and nasal airways
• Advanced airway equipment – laryngeal mask airways and laryngoscopes with appropriate tubes
(arrest trolley or similar)
• Capnography (should be available immediately in critical care)
• A fibreoptic ‘scope (should be available immediately in critical care)
• Tracheal dilators
• Bougies

22- Oral Poisoning and Tricyclic Antidepressant Drugs (TCA)
(a) What are the key items to elicit in the history in the patient presenting with an oral poisoning
syndrome? (3 marks)
(b) Describe the methods by which a drug can be removed from the body in the case of poisoning.
(c) Describe the mechanism of action of tricyclic antidepressant (TCA) drugs? (3 marks)
(d) What are the peripheral and central manifestations of TCA poisoning? (4 marks)
(e) What features in the ECG suggest cardiotoxicity? (3 marks)
(f) What is the role of sodium bicarbonate in the management of TCA overdoses? (3 marks
 The Key items to elicit in the history in the patient presenting with an oral poisoning syndrome:
- Risk assessment: Obtain specific history from patient / ambulance crew / relatives / collateral
history – including last time seen prior to ingestion and time found
- Timing of ingestion / amount taken / other ingested substances including alcohol
- Check clothing / look for empty packets of medication or any written notes
- History of previous episodes or underlying medical conditions including psychiatric disorders
- Aim to identify substance or substances
- Any suggestion / evidence of seizure activity / other injuries sustained
 Describe the methods by which a drug can be removed from the body in the case of poisoning
Gastric Decontamination: aim to limit absorption and promote elimination

- Activated Charcoal: absorbs most drugs and chemicals by generating weak van der waals forces
that bind the substance within the GIT. Ideally given within 1 hour of ingestion. Given orally or via
NGT with the usual dose being 25-50g /kg. Repeat dose 4-6 hourly with slow release preparations as
this can interrupt the enteropathic circulation of the drug.
Gastric Lavage: significant morbidity and mortality with no data of improved outcome against or
with activated charcoal.
- Induced emesis: Not recommended
- Whole bowel irrigation: only consider in poisoning with sustained release or enteric coated
preparations
Increased Elimination
Alkaline diuresis enhances elimination of weak
acids. Sodium bicarbonate is administered to
keep urinary pH between 7.5 – 8.5
Haemodialysis
Usefulness dependent on properties of ingested
drug. Substance needs to have a low molecular
weight < 5000 Da / low protein binding / low
water solubility and a low volume of distribution
Useful for ethylene glycol / methanol / lithium /
theophylines and salicylates

Describe the mechanism of action of tricyclic antidepressant (TCA) drugs? (3 marks)
- Primary mechanism for the therapeutic effect of TCA is via the pre-synaptic inhibition of nor-
adrenaline and serotonin reuptake.
- Other effects, particularly in overdose, include the blockade of several other receptors including
cardiac rapid sodium channels, peripheral alpha 1 receptors, histamine 1 receptors, GABA A
receptors and muscarinic Ach receptors.
 What are the peripheral and central manifestations of TCA poisoning? (4 marks)
Peripheral effects:
Sinus tachycardia and cardiac arrhythmias
Hot dry skin
Dry mouth
Dilated pupils
Urinary retention
Central
Ataxia / Nystagmus / Divergent squint
Drowsiness
Increase tone / Hypereflexia / Extensor plantars
Seizures
Agitation / confusion / hallucinations
 What features in the ECG suggest cardiotoxicity? (3 marks)

- Sinus tachycardia very common due to anticholinergic effects and haemodynamic compensation
- Arrhythmias can develop quickly with conduction abnormalities that can degenerate into VT or VF
- Cardiotoxicity suggested by the presence of either of the following:
- Prolonged QRS > 100 msecs
- Abnormal QRS morphology – deep slurred s wave in lead 1, AVL
- Abnormal size and ratio of the R and S waves in AVR
- Important to remember that toxicity can occur despite normal ECG indices
- QRS widening is the most prominent ECG manifestation of toxicity
- A prospective series demonstrated that those with a QRS duration < 100msecs had no seizure
activity whereas those >100msecs had a 25% incidence of seizure / > 160msec a 50% incidence of
VT.
- Other possible signs include a prolonged PR interval, prolonged QT interval and evidence of
conduction system block particularly a right bundle branch block which is especially sensitive to TCA
- Prolonged QT common in OD although the polymorphic VT normally associated with prolonged QT
is not common.
 What is the role of sodium bicarbonate in the management of TCA overdoses? (3 marks)
- Most efficacy of use comes from clinical experience.
- Animal studies demonstrate it narrows the QRS complex, improves systolic BP and controls
ventricular arrhythmias
- Indicated if QRS duration > 100msecs or Ventricular arrhythmia
- Initial loading dose of 1-2ml/kg 8.4% sodium bicarbonate as a bolus which can be repeated after 5
minutes if no improvement in ECG changes followed by an infusion

- Therapeutic benefit via 2 effects:
- Increase serum pH: favours non ionised form drug resulting in less free drug available to bind
sodium channels. Aiming for pH 7.5-7.55
- Increase in extracellular sodium concentrations increases electrochemical gradient across cardiac
cell membranes attenuating TCA induced blockade

23- Ecstasy Toxicity
A 21 year old man is brought into the A&E department as he has become confused and agitated
during a night out. His friends say he purchased several tablets of ‘ecstasy’. His heart rate is 170
beats/min,his BP is 200/110 and he is becoming increasingly aggressive.
(a) Describe your general management of this patient
(b) What specific therapies may be employed in toxicity related to Amphetamines
(c) Briefly describe the pharmacology of ‘ecstasy’.
(d) What are the causes of the morbidity and mortality when seen in amphetamine OD?
(e) What are the features of serotonin syndrome?
 General management of this patient

ABC approach – O2, monitoring, venous access, blds (FBC, U and E, LFT, CK, coag,
paracetamol/salicylates), 12 lead ECG, ABG, check temp and blood glucose levels
If unable to maintain own airway this will need secured
If within 1hr of ingestion and airway protected consider activated charcoal
If diagnosis unclear may require imaging e.g. CT brain once stabilised
 What specific therapies may be employed in toxicity related to amphetamines

Anxiety – Diazepam 0.1-0.3mg/kg PO/IV
Seizures – Diazepam 0.1-0.3mg/kg IV
Hyponatremia – Fluid restrict – consider hypertonic saline if severe
Metabolic acidosis – correct (esp if QT interval prolonged) using sodium bicarb
Severe hypertension – consider labetalol infusion
Hypotension – volume expansion, consider central line
Hyperthermia – simple cooling methods. If temp >39 after initial measures give dantrolene and will
likely need intubation and ventilation (paralysing will reduce temp)
Organ failure – conventional support – promote diuresis 1-2ml/kg/hr with mannitol or furosemide
 Briefly describe the pharmacology of ‘ecstasy’.

MDMA causes release of serotonin, dopamine and noradrenaline in CNS. Also inhibits re-uptake
especially of 5-HT. Therefore increase in synaptic concentration of these transmitters. Also has slight
MAO inhibiting activity. Plasma half life 7.6hr. Oral ingestion effects within 1hr and last 4-6hrs.
Metabolised by COMT catalysed methylation.
 What are the causes of the morbidity and mortality when seen in amphetamine OD?
Sudden death – sympathomimetic effects precipitate dysrhymias – likely in pts with undiagnosed
cardiomyopathy, viral myocarditis or congential cardiac conditions eg WPW or Brugada
Hyperpyrexia, rhabdomyolysis and multi-organ failure - 5HT/dopamine involved in central control of

thermoregulation. Also ?direct effect of MDMA on muscle contraction. Assoc with exertion and
inadequate fluid replacement. Multi-organ failure can rapidly follow the hyperpyrexia, muscle
rigidity, hyper-reflexia and rhabdomyolysis.
Hyponatremia and cerebral oedema – dilutional hyponatremia from drinking large amts water
Presents with confusion, convulsions and can progress to coma and death from coning –

cause? secondary to ”harm reduction” message to drink fluids ?excess ADH production
Liver failure – centrilobular necrosis and steatosis – can lead to fulminant hepatic failure and
encephalopathy
 Features of Serotonin Syndrome:

Rapid onset with confusion, diaphoresis, diarrhoea and cardiovascular instability. Increased muscle
tone and rigidity accompanied by shivering, tremor, increased tendon reflexes and myoclonus.
Excessive muscle contraction may cause hyperthermia and death. Mortality 10-15%
Associated with MDMA toxicity as well as cocaine, MAOI and SSRI as well as pethidine, tramadol,
methadone and linezolid

24- Paracetamol Toxicity
An 18 year old woman is admitted to the ICU in acute liver failure thought to be the result of an
undiagnosed late presentation of paracetamol OD.
(a) What is the theoretical mechanism of action of paracetamol as a therapeutic agent?
(b) What is the mechanism of paracetamol toxicity? (15%)
(c) What are the systemic effects of paracetamol OD? (20%)
(d) Outline the ICU management of a patient presenting in ALF secondary to paracetamol OD
(e) What are the features of the King’s College criteria for liver transplantation in acute liver failure?
 The Mechanism of action of Paracetamol as a therapeutic agent:

- Exact mechanism largely still unknown; it is analgesic and antipyretic, but it is NOT thought to be
anti-inflammatory.
- Multimodal mechanism of action:
Prostaglandin Inhibition
Arachadonic acid prostanoids requires prostaglandin H2 synthetase (PGHS, usually referred to as
cyclo-oxygenase) and is a two stage process
PGHS has two sites: COX and POX (cyclo-oxygenase and peroxidase)
Paracetamol acts via POX, reducing prostaglandin synthesis (mainly in intact cells, and therefore does
not act when cell membranes are disrupted in inflammatory processes)
Endocannabinoid reuptake inhibition
Paracetamol p-aminophenol (in liver) plus arachadonic acid AM404 (N-arachidonoylphenolamine)
which increases amandamide levels (a natural cannabinoid)
Seretonergic descending pathway modulation
This can be partially antagonised by e.g. 5HT3 inhibitors such as Ondansetron, thus reducing
paracetamol’s efficacy
Others:
Nitric oxide modulation
TNF-alpha modulation
 Mechanism of Paracetamol Toxicity:

- Mainly via inadequate clearance of the destructive breakdown product NAPQI (see below), which
can disrupt cell membranes leading to hepatic, renal and brain damage.
This is accentuated in glutathione deplete states.
- Normal metabolism, once absorbed from SB:
Majority: Glucuronidation and sulphation to inactive metabolites; renal excretion
Small amount: oxidation via CYP450 to NAPQI (N-acetyl-p-benzo-quinone imine), which is highly toxic
NAPQI detoxification via conjugation with glutathione cysteine & mercapturatic acid conjugates renal
excretion
In glutathione deficiency, or once it becomes depleted (with paracetamol excess), NAPQI builds up
and causes local and systemic toxic effects.
Genetics: variant polymorphisms of the iso-enzyme CYP-2D6 exist, resulting in ultra-rapid extensive
metabolisers, and slow metabolisers; ultra-rapid metabolisers produce the toxic NAPQI more
effectively and are therefore more at risk of toxicity.

 The systemic effects of Toxicity resulting from Paracetamol:
Hepatic:
Acute fulminant liver failure
Renal:
Usually minor renal impairment
More rarely: ATN, ARF, interstitial nephritis
Depletion of glutathione renders cells more prone to oxidative damage
Respiratory:
Linked with asthma development (incl. in childhood)
Wheezing and rhinitis in children (dose and frequency dependent)
Rarely: bronchospasm
Glutathione is a pulmonary antioxidant
GIT:
Abdominal pain
N&V, bloating
Rarely: acute pancreatitis, cholestasis
Haematological
Those from Acute liver failure
Thrombocytopaenia, neutropaenia, leucopaenia (all rare)
Methaemaglobinaemia
2xfold increased risk of haematological malignancies with chronic use
CVS: Hypotension
Dermatological: Pain on injection
Very rare: Stevens-Johnson syndrome, TEN, bullous erythema
 The ICU management of a patient presenting in ALF 2ry to Paracetamol OD:

*Goals are: decision to refer for transplantation; clarification of single or staggered overdose;
supportive management for all systems above; grading encephalopathy; paracetamol levels with
respect to drug ingestion time and N-acetylcysteine (NAC)infusion commencement; should GI
decontamination be administered?
*General management for any patient includes: full careful history, resuscitation of the
patient in a systematic ABCDE manner as appropriate, full clinical examination, targeted
investigations (laboratory, radiological, physiological), formulating a prognosis, and treating the
underlying illness(es) as appropriate.
*Specific to ALF secondary to Paracetamol OD:
History:
*Timing, preparation, quantity of ingestion
*Other toxins ingested
*Intent of OD / psychiatry history / risk management
*Risk factors for toxicity (check medications, SHx, diet, PMHx)
Examination:
*Looking for ALF features – jaundice etc
*GCS
*Nutritional state
?Any other drug toxic signs
Investigations:
*Paracetamol levels (with respect to drug ingestion timings)
*LFTs / Tox screen / Coag / glucose / lactate / U&E / Ammonia
*ECG, Pregnancy test
Resuscitation:
?Intubation
*Lung protective ventilation
*Volume resuscitation and CVS support
*Sugar / nutrition / GCS support
*Temperature control
Treatment:
*WEIGH THE PATIENT
*Specific to the Paracetamol OD
*Decontamination with activated charcoal (if
<4 hours)
*Toxbase for other substances
*NEW MRHA guidance (single treatment line, LD over 1 hour, now NO contraindications to NAC)
*N-acetylcysteine mainstay of treatment (150mg/kg LD over 60 mins, the 50mg/kg over 4 hours,
100mg /kg over 16 hours)
*Start NAC if staggered OD is suspected, regardless of paracetamol level
*If single OD, treat if 4 hr level > 100mg/l, or 15 hour level > 15mg/L
*Check NEW treatment nomogram (no longer high and low risk lines)
Liver Failure Management

?needs referral to Kings
*Damage limitation with NAC
*Aim normothermia / normal electrolytes (Na / K) / normocapnia (ventilate if necessary – for
Cerebral protection)
*Glucose and ammonia monitoring
*Observe for coagulopathy complications
?Thiopentone infusion
?MARS
General
*Nutrition / VTE prophylaxis / ventilator care bundles
*GI prophylaxis
*Good nursing care
*Prognosis and Disposal
*Various scoring systems (Kings / MELD / APACHE etc)

*Prognosticate if possible
*Early liaison with Kings / local liver unit
*Transfer if appropriate
*MRHA discharge letter
 Features of the King’s College Criteria for liver transplantation in acute liver
failure:
2 Main criteria for referral depending on underlying mechanism of damage:
Paracetamol vs Non-paracetamol related.

25- Burns and Inhalational Injury
You are asked to assess a 24-year-old male who has been admitted to the Emergency Department
with 30% burns from a house fire.
a) What clinical features would lead you to suspect significant inhalational injury? (10 marks)
b) List the indications for early tracheal intubation to secure the airway. (4 marks)
c) Which investigations would you use to assess the severity of the inhalational injury:
 Clinical Features of Inhalational Injury:
● Orofacial Burns
● Singed Eyebrows / Hair
● Soot in Nasal Passages
● Swollen Uvula
● Voice Changes/Hoarseness
● Stridor
● Cough with copious Carbonaceous Secretions
● Respiratory Distress
● Hypoxaemia/Hypercarbia
● Confusion/Agitation/decreased GCS
● Increased Carboxyhaemoglobin Levels
 Indications for Early Tracheal Intubation

● Impending or Actual Airway Obstruction (low GCS/stridor/oropharyngeal swelling)
● Respiratory Distress/Hypoxaemia/Hypercapnia
● Deep facial or Full Thickness/Circumferential Neck Burns
● To facilitate Transfer to Theatre or Tertiary Centre
 Investigations:
Arterial Blood Gases:
likely to show Hypoxaemia, high serum Lactate and reduced AV difference due to impaired Oxygen
Delivery and reduced tissue Oxygen utilisation in CO poisoning
Nasendoscopy:
Nasopharyngeal Oedema and Swelling of Cords;
Bronchoscopy will show evidence of particulate matter and exudate, Carbonaceous Debris, Mucosal
Pallor, Ulceration and Erythema. There may also be evidence of Haemorrhage
Chest X-ray:
Early X-raymay be normal but later may show diffuse Atelectasis, Pulmonary Oedema and
Bronchopneumonia
10
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE
0
26- Burns and Fluid Calculation
A 23 year old woman is brought into A&E with severe dermal burns limited to her chest, face and
hands. She is 60kg. Her GCS is 14.
(a) List the reasons a burns patient may require intubation and ventilation (20%)
(b) What difficulties may you encounter with routine monitoring in these patients? (10%)
(c) What are the referral criteria for a burns patient to a specialist centre? (15%)
(d) Describe the ‘Rule of 9 & Parkland formula. Estimate the fluid resuscitation required by the patient
(e) List the complications that can result from severe burn injury. (15%)
(f) What are the key principles of ICU management in a patient with severe burns? (20%)
 Reasons a burns patient may require intubation and ventilation:

For airway protection if GCS < 8- may be the reason which may have lead to the burns (for example
alcohol intoxication) or occurred as a result of burns (carbon monoxide poisoning, head injury)
If patient delirious/confused or unco-operative. May again be due to cause of burn or as a result of it
Hypoxia, hypercarbia or stridor
Signs of airway obstruction or imminent airway obstruction (oropharyngeal oedema/deep facial
burns/full-thickness neck burns- may be determined by nasal soot or soot in oropharynx)
To facilitate transfer to a tertiary burns specialist centre
For changing dressings (often extremely painful)
If patient requiring surgery for debridement, escharotomy, plastic surgery for grafting, trauma
surgery for fractures etc.
If intubating a burns patient remember NOT to cut the tube (as airway swelling usually occurs after
intubation and allows bronchoscopy. Suxamethonium is SAFE in the first 24 hours after a burn.
 Difficulties may you encounter with routine monitoring in these patients? (10%)
Difficulty applying monitors, for example, ECG electrodes unlikely to stick on burns, Oxygen
saturation probes likely to be sore on burnt skin
Use alternative sites, for example nose, ear, lips
Use skin staples or subcutaneous needles attached to crocodile clips for ECG monitoring
End tidal C02 may not reflect PaCO2 as increased dead space in inhalational injury
Blood pressure- invasive access versus non-invasive BP cuff application
IV access, peripheral or central for medication, fluids or CVP monitoring may be difficult and might
require sutures to keep in place.
The referral criteria for a burns patient to a specialist centre:

British Burns Referral Criteria
Extremes of age (<5 or >60)
Site of burns (dermal or full-thickness)- face, hands, perineum or feet; or any flexure particularly the
neck or axilla; any circumferential dermal or full-thickness burns of the limbs, torso or neck
Any significant inhalational injury, excluding pure carbon monoxide poisoning
Mechanism of injury (chemical >5% TBSA), exposure to ionizing radiation, high pressure steam injury,
high tension electrical injury, hydrofluoric acid injury, suspicion of non-accidental injury
Size of injury- <16 with >5% TBSA; >16 with >10% TBSA
Pre-existing co-morbidities- Significant cardiorespiratory disease, diabetes, pregnancy,
immunosuppression, hepatic impairment, cirrhosis
10
1
Associated injuries- crush injuries; fractures; head injury; penetrating injury
The ‘Rule of Nines’ and Parkland formula.

The Wallace ‘Rule of Nines’ is a method of calculating the % burns, in adults the calculation differs
from children due to surface area differences.
In adults each upper limb is 9%, each lower limb 18%, chest 18%, back 18%, head 9% (total) and
perineum 1%.
In kids each upper limb 9%, each lower limb 13.5%, chest 18%, back 18%, head 18% (total)
Parkland formula is a guide and resuscitation should be titrated to clinical response. Crystalloid
resuscitation fluid=4mls/kg/% burn. 50% of fluid resus should be given in the first 8 hours since burn
occurred (not since arrival in hospital), the second 50% over the remaining 16 hours
= 4 x 60 x 24.5 (18 +4.5 +2)= 5880mls
The Complications that can result from severe burn injury.

Early
*Hypothermia
*DVT
* Stress ulcers
*ARDS
*Renal Failure (from inadequate fluid resus, sepsis or
haemolysis)
Late
*Infection, especially skin, significant cause of mortality
from burns
*Pulmonary fibrosis
*Chronic pain
*PTSD, depression, sleep disorders
 ICU management in a patient with severe burns:

*Multidisciplinary approach including physio, OT,
dieticians
*Infection control paramount as sepsis is (along with
multi-organ failure) the most frequently reported cause of death
*Good analgesia/pain management- multimodal approach- involve acute pain service and likely to
also require chronic pain management
*Lung protection strategies to prevent ARDS
*Early enteral nutrition to maintain gut integrity
*PPI for stress ulcer prophylaxis
*Maintain normal electrolyte and normoglycaemia
*Maintain normothermia (prone to hypothermia as skin large barrier contributing to heat
conservation)
*Ensuring before extubation that the endotracheal cuff is deflated and that a leak is present (i.e
airway still not significantly oedematous and swollen)
*Early tracheostomy as likely to be slow wean
10
2
*Maintain and optimise oxygen delivery (burns is a catabolic state and potential massive blood loss
may contribute to compromise in oxygen delivery).
10
3
27- Coma and altered Consciousness
(a) Define the state of coma. How may coma states be classified? (3 marks)
(b) What are the different causes of coma? (4 marks)
(c) How can coma be differentiated from persistent vegetative state (PVS), minimally conscious state (MCS), or
locked-in syndrome? (3 marks)
(d) Describe the spectrum of states of altered consciousness (3 marks)
(e) What disorders may mimic coma? (3 marks)
(f) What investigations may be helpful in identifying the cause of the coma? (4 marks)
 Define the state of coma. How many coma states can be classified? (3 marks)
- Coma can be defined as unarousable unresponsiveness or the absence of any psychologically
understandable response to external stimulus or inner need.
- Coma can be classified into 4 groups:
Coma with intact brainstem function, no meningism and no lateralising signs
Coma with intact brainstem function and lateralising signs
Coma with meningism (with or without intact brainstem function and lateralising signs)
Coma with signs of focal brainstem dysfunction
 What are the different causes of coma?
10
4
 How can coma be differentiated from persistent vegetative state (PVS), minimally conscious state
(MCS) or locked-in syndrome? (3 marks)
Coma is a state of unarousable unresponsiveness. The patient is unaware of self and environment
and does not respond to vigorous stimulation.
Patients with PVS are in a state of partial arousal and may briefly respond to sound or visual stimuli.
They withdraw to noxious stimuli but are unable to interact or respond voluntarily or purposefully
when stimulated. It is a chronic condition, diagnosed after 30 days of persistent altered
consciousness.
Patients in MCS display deliberate or cognitively mediated behaviour. They may intermittently follow
commands or have intelligible but inconsistent verbal output. Patients can evolve from coma or PVS
to MCS.
Patients with locked-in syndrome have intact cognition but complete paralysis of voluntary muscles
in all parts of the body. Can communicate using blinking / up-and-down eye movements.
 Describe the spectrum of states of altered consciousness (3 marks)
There is considerable overlap between intermediate states on the spectrum of altered consciousness
Clouding of consciousness: a state of reduced wakefulness or awareness, characterised by impaired
attention and memory. Patient is easily distracted and sometimes hyperexcitable, startled by stimuli.
Acute confusional state: impairment of consciousness in which stimuli are intermittently
misinterpreted. Patients are drowsy, disorientated in time and occasionally place and person and
have poor short-term memory.
Delirium: acutely developing impairment of consciousness, attention, disordered thinking – fear,
disorientation, visual hallucinations, delusions and misperceptions of sensory stimuli. Can be
interspersed with lucid intervals. Commonly due to metabolic, toxic, or endocrine derangements.
Very common in hospitalised patients. Follows a fluctuating course and rarely lasts more than a
week.
Obtundation: mental blunting with apathy and inactivity. Patient is drowsy with reduced alertness,
has a decreased interest in the environment and responds slowly to stimulation.
Stupor: similar to deep sleep or unresponsiveness. Patient can be aroused by episodes of repeated,
vigorous stimuli. As stimulation decreases, patient lapses back into a state of decreased
responsiveness. Even when aroused, communication is by monosyllabic sounds and simple
behaviour.
 What disorders may mimic coma? (3 marks)

Guillain-Barre syndrome
Locked-in syndrome
Botulism
Psychogenic unresponsiveness
 What investigations may be helpful in identifying the cause of the coma? (4 marks)
Glucose
Urea and electrolytes
Full blood count
Arterial blood gas
Blood cultures if pyrexial / hypothermic / suspect infection
Urine screen for drugs and toxins
CT brain – detects intracranial haemorrhage, hydrocephalus and structural abnormalities
MRI brain superior in early detection of ischaemic strokes
CT venogram and angiogram may be required to exclude basilar artery thrombus or sinus venous
10
5
thrombosis
EEG to rule out non-convulsive status epilepticus
Lumbar puncture if infection or inflammation suspected.
10
6
28- Necrotising Fasciitis
(a) What is necrotising fasciitis (NF)?
(b) What pathogens may potentially be responsible for causing necrotising fasciitis?
(c) What are the risk factors for developing NF?
(d) How may it be diagnosed?
(e) Describe the management of NF
 Necrotizing fasciitis (NF) is a progressive, fulminant bacterial infection of subcutaneous tissue that
spreads rapidly through the fascial planes causing extensive tissue destruction.
NF can affect any part of the body and is the most serious
presentation of necrotizing soft tissue infection (NSTI); it is a
rare but potentially fatal condition.
Prompt recognition and intervention is essential, as mortality is

directly proportional to time to intervention
 What pathogens may potentially be responsible for causing

necrotising fasciitis?
- Type I infections are the most common form o the disease.
They are polymicrobial and woun tissue isolates identify on
average four differen organisms. Causative microbes include a
combination of Gram-positive cocci, Gram-negative rods, and
anaerobes.
- Type 2 infection is caused by the group A streptococcus

(Streptococcus pyogenes) either alone or in association with Staphylococcus aureus
- Type III is a Gram-negative monomicrobial NF. The most common Gram-negative responsible are
Vibrio spp., such as V. damselae and V. vulnificus
- Type IV describes fungal cases of Candida NF.
 What are the risk factors for developing NF?

Immunosuppression
Diabetes
Chronic disease
Drugs, for example, steroids
Malnutrition
Age >60
I.V. drug misuse
Peripheral vascular disease
Renal failure
Underlying malignancy
Obesity
Blunt or penetrating trauma
Soft tissue infections
10
7
Surgery
I.V. drug use
Childbirth
Burns
Muscle injuries
 How may it be diagnosed?

- Diagnosis is essentially clinical. There are similarities of this illness to cellulitis, however NF displays
disproportionate pain. Severe skin changes may be late. Changes include erythema, tenderness
beyond the erythema, swelling, hot skin, formation of skin bullae, blister, skin fluctuation,
haemorrhagic bullae, crepitus, skin necrosis, and gangrene.
Bloods may show high/low WCC, low plts, coagulopathy, DIC, increased CK, low Ca, raised CRP,
raised creatinine, urea, lactate, metabolic acidosis, low albumin, low sodium.
- Blood cultures may be positive in 60% of cases and histology will show underlying thrombi,
necrosis, polymorphonuclear infiltrates, microorganisms, and vasculitis.
CT, US and MRI can be used to aid diagnosis
 Management of NF:
- Early diagnosis, aggressive resuscitation, surgical debridement, antibiotic therapy, and supportive
intensive care are necessary for managing patients with NF. Effective communication between the
intensivist, surgeon, anaesthetist, and microbiologist is essential.
- The aim of resuscitation is to establish an adequate tissue perfusion and oxygen delivery. Invasive
arterial pressure monitoring and central venous access may be required; goal-directed therapy
targets for haemodynamic resuscitation in patients with sepsis secondary to NF are as suggested by
the Surviving Sepsis Campaign.
- Several studies have shown that the most important factor affecting mortality is timing and
adequacy of initial surgical debridement. Debridement removes the source of infection and toxins,
and furthermore, removal of infarcted tissue improves the subsequent penetration of antibiotics.
Multiple debridement’s may be required.
Empiric therapy requires an antibiotic combination that covers the variety of organisms that may
cause NF. A broad-spectrum agent such as Tazocin or a Carbapenem, can be combined with
Clindamycin. If Group A streptococcus alone is responsible, antibiotics may be rationalized to a
combination of Penicillin and Clindamycin. When MRSA is suspected, Linezolid is preferred to
Vancomycin as it inhibits exotoxin production.
- The use of i.v. immunoglobulin is based on the theoretical mechanism that it can bind
staphylococcal- and streptococcal derived exotoxin, so limiting the systemic cytokine release
associated with systemic inflammatory response syndrome. There is very limited evidence which
suggests a decreased mortality from using IVIG in group A streptococcal NF.
For synergistic infections, particularly involving Clostridium spp., hyperbaric oxygen switches off toxin
production.
- These patients need managed in a critical care setting, with facilities for organ support.
10
8
29- Heparin Induced Thrombocytopaenia (HIT)
(a) What is the mechanism of action of (i) unfractionated heparin? (ii) LMWH? (20%)
(b) List the potential causes of thrombocytopaenia in an intensive care patient. (20%)
(c) What is heparin induced thrombocytopaenia? (20%)
(d) How may it be diagnosed? (20%)
(e) What are the alternatives (their modes of action) to heparin for short-term anticoagulation
 Mechanism of action of (i) unfractionated heparin? (ii) low molecular weight heparin:
- Heparin inhibits antithrombin-III
A pentasaccharide on the heparin molecule binds to AT-III producing a conformational changein its
reactive site.
This enhances AT-III’s neutralizing of factors VIIa, IXa, Xia, XIIa and thrombin and prevents them
forming complexes.
Inactivation of thrombin inhibits fibrin formation and activation of factors V, VII.
- Heparin molecule dissociates then and can be reused.
- Heparin induces a vascular endothelial tissue factor pathway inhibitor (TFPI) which antagonises TF-
VII complex.
- Heparin may inhibit VW dependent platelet function.
- Heparin inhibits platelet aggregation in high doses.
ii) LMWHs bind and neutralize factor Xa. They are too small to bind well to AT-III and thrombin
simultaneously. Different preparations have different AntiXa/Antithrombin activity ratios.
 List the potential causes of thrombocytopaenia in an intensive care patient. (20%)

(Most common in ICU particularly in bold)
- Decreased Production
BM suppression
Postviral (rubella, mumps, varicella, parvovirus, hepatitis C, and Epstein-Barr virus)
Viral (HIV)
Chemo or radiotherapy (eg. Nodal)
Congenital or acquired bone marrow aplasia/hypoplasia eg. Fanconi’s
Alcohol toxicity
B12, folate deficiency
- Increased Destruction
ITP, SLE- autoimmune antiplatelet antibodies
Drugs- Heparin, quinine, valproate, linezolid, rifampicin, ranitidine
Alloimmune- transfusion, transplantation
DIC
TTP-HUS- idiopathic, Shigella
Antiphospholipid
HELLP
Physical destruction eg. CPB
10
9
Dilutional
Distributional- congestive splenomegaly
Spurious-
Insufficient anticoagulation- clumps counted as leukocytes by machine
G2a/3b inhibitors
Satellitism (clumping around leukocytes)
 What is heparin induced thrombocytopaenia? (20%)

There are two types of HIT
Type 1- Non-immune- may be a direct effect of heparin- and inconsequential. Results in a slight fall in
platelet count, within the first 2 days after heparin initiation. It often returns to normal with
continued heparin administration
Type 2- Immune- antibodies against the heparin-platelet factor 4 complex- and serious. Incidence
2.6%. RFs- UFH, female, long duration, surgical patient. Occurs 5-10 days after starting. Major clinical
manifestation in thrombosis.
 How may it be diagnosed? (20%)

Diagnosis-
Clinical suspicion:
4T pretest clinical score
Thrombocytopaenia >50%, nadir >20
Timing- 5-10 days
new Thrombosis
no other cause for Thrombocytopaenia present
Serotonin release assay- gold standard

Platelet aggregation assay
Solid phase immunoassay
 What are the alternatives (and their modes of action) to heparin for short-term
anticoagulation? (20%)
Direct thrombin inhibitors- Bivalirudin, Argatroban, Lepirudin
Factor Xa inhibitors- Fondaparinux
Heparinoid- Danaparoid
11
0
11
1
11
2
30- Management of Ischaemic Stroke (CVA)
(a) How may the clinical presentation of stroke may used to distinguish between an infarct of: (i) Anterior
Circulation (ii) Partial Anterior Circulation (iii) Lacunar Area (iv) Posterior Circ.
(b) What risk factors do you know for ischaemic stroke?
(c) What are the exclusion criteria for lysis of a cerebral infarction?
(d) Describe the non pharmacological management of a cerebral infarction
(e) What are the aims of critical care in management of ischaemic stroke?
Total Anterior circulation (TACS) – all of:

Unilateral motor, sensory deficit, or both affecting at least 2 of face, arm and leg
Higher cerebral dysfunction e.g. dysphasia, dyspraxia, neglect, dyscalculia
Homonymous hemianopia
Partial anterior circulation (PACS) – 2 out of 3 components of TACS or pure higher cortical
dysfunction or pure motor or sensory deficit not as extensive as for lacunar syndromes
Lacunar syndrome (LACS): Pure motor or sensory deficit affecting at least 2 of face, arm or leg
Sensorimotor deficit
Ataxic hemiparesis
Dysarthria, clumsy hand syndrome
Acute onset movement disorder
Posterior circulation (POCS): Isolated hemianopia

Brainstem signs
Cerebellar ataxia
 What risk factors do you know for ischaemic stroke?

Age, Hypertension, Smoking, Diabetes, AF, Heart disease, Dyslipidaemia, Alcohol, Obesity, Carotid
stenosis
 What are the exclusion criteria for lysis of a cerebral infarction?

Haemorrhage seen on CT
History suggestive of subarachnoid haemorrhage
Seizure at stroke onset
BP > 185 mmHg systolic (or diastolic > 110 mmHg)
BM < 2.8 or > 22 mmol/l
Platelet count < 100
If on Warfarin, INR >1.3
Bacterial Endocarditis / Pericarditis
Treated with LMW Heparin within last 48 hours & APTT is still raised
NIH Stroke Scale <5 [ very minor neurological deficit ] or > 25
Neurological symptoms very rapidly improving
or History of:
⇒ Another stroke or head injury in last 3 months
⇒ GI, urinary or menstrual bleeding in last 21 days
⇒ Surgery or significant trauma in last 14 days
⇒ Arterial puncture at non-compressible site in last 10 days
⇒ Severe liver disease (hepatic failure, cirrhosis, varices etc)
11
3
⇒ Possibility of pregnancy
 Describe the non pharmacological management of a cerebral infarction

Optimal positioning, passive movements and preventing contractures
Avoidance of aspiration pneumonia (SALT assessment)
Supplemental hydration/nutrition including NG feed in those unable to take oral nutrition within
24hrs
Avoid hypotonic fluids
Avoid hyperthermia
Avoid hyperglycaemia
Only give oxygen if sats <95%
All pts should be discharged to dedicated stroke unit
 What are the aims of critical care in management of ischaemic stroke?

Avoiding secondary brain injury by optimising cerebral blood flow, cerebral perfusion pressure and
preventing rises in ICP
Airway management as required
Keeping PaO2 >9.3kPa and PaCO2 in normal range
Monitoring and treating for dysrhythmias e.g. AF
Maintenance of adequate BP/ cerebral perfusion pressure
Treating hypertension if SBP>220 or DBP>120 or MAP >130
Maintaining blood sugars between 4 and 11
Actively treating hyperthermia
Preventing DVT – with intermittent pneumatic compression devices
Physiotherapy
Instituting enteral nutrition
Medical treatment of complications e.g. sepsis
11
4
31- Brainstem Death (BSD) and Testing
A 35 year old woman is apnoeic on the ventilator following a large SAH and the decision is taken to
perform brainstem death testing after speaking to the family.
(a) What are the preconditions for brainstem death testing (BSD)? (20%)
(b) Describe the principles of the apnoea test component of BSD testing - describe the physiology for
maintenance of oxygenation. (20%)
(c) List the other components of the BSD tests. (20%)
(d) What additional investigations apart from brainstem death tests may confirm brainstem death?
(e) What are the physiological consequences of brainstem death?(20%)
 There are a number of pre-conditions for BSD.

There must be an identified cause of the irreversible brain damage
The patients low GCs and apnoea cannot be due to other causes of a low GCS. Hypothermia must be
ruled out and the patient’s core temperature must be greater than 34oC. Depressive drugs for
example opioids, benzodiazepines must be ruled out as a cause for low GCS. The time taken for
these drugs to be cleared from the body depends on the pharmacokinetics of the drug, any co-
existing renal or liver failure that would affect metabolism and excretion and duration of the
infusions. Specific blood levels can be tested for. Muscle relaxants can be ruled out as a cause of
apnoea by demonstrating TOF.
Significant circulatory, metabolic or endocrine disturbance must be ruled out as a cause. For example
hyponatraemia. Electrolyte abnormalities should be corrected cautiously to within realistic ranges
and though rare, any suspicion of myxoedema coma or addisions crisis should be investigated.
The patient must be apnoeic needing ventilator support with no reversible cause for this possible.
- The apnoea test is only performed when all other test for BSD have shown absent response.
- Inspired oxygen is increased to 100% for at least 5 minutes before hand. - An arterial blood sample
if then taken to assess pH, paO2, and paCO2. Minute ventilation is then decreased to allow the
paCO2 to rise to more than 6kPa and the pH to fall below 7.4. Higher levels of paCO2 may be needed
in patients with chronic retention of CO2.
- The patient is then disconnected from the ventilator for 5 minutes and observed for respiratory
effort.
- A repeat blood gas is then taken- a PaCO2 gain of 0.5kPa or more demonstrates adequate
respiratory stimulus. The patient is reconnected to the ventilator at the end of the test.
Oxygenation is maintained throughout this period by insufflating 5L/min of oxygen via a tracheal
catheter to avoid hypoxia. This means that the test will only assess the stimulation of respiration to
arterial carbon dioxide tension alone. If saturations fall, CPAP or recruitment manoeuvres can be
carried out.
BSD testing should be carried out by two doctors with at least 5 years registration with one of the
two of consultant grade.
Pupillary response to light: the pupils don’t respond to direct or consensually to sharp changes in the
intensity of light. This tests CN 2 afferent and 3 efferent
Corneal reflex: there is no response following direct stimulation of the cornea with a cotton bud.
Test cranial nerve 5 afferent and 7 efferent
Vestibulo-ocular reflex: no eye movements are seen following slow injection of at least 50mls of ice
cold water to the external auditory meatus. Normal response would be eye movement away from
11
5
the ear injected. This tests CN 8 afferent and 3, 4, 6 efferent.
Motor response: no motor response with supraorbital pressure. Tests CN 5 afferent and CN 7
efferent
Gag Reflex: No contraction of the soft palate following direst stimulation of the uvula. Tests CN 9 and
10.
Cough Reflex: no response to bronchial stimulation at the level of the carina by suction catheter.
Tests CN 9 and 10
Apnoea Test: As above
Occasionally it may be difficult to perform BSD testing, for example with facial trauma. In these
situations ancillary testing may be needed to confirm the diagnosis.
Tests are divided in three groupings;
Blood flow in the larger cerebral arteries: Four vessel angiography
Transcranial Doppler
Magnetic resonance angiography
CT angiography
Brain tissue perfusion: Cerebral scintigraphy
Xenom CT
Position emission tomography
Neurophysiology: EEG
Evoked potentials
A number of changes occur as brain damage progresses, the subsequent organ damage
associated with cardiovascular derangement is well recognised.
Sympathetic storm: Hypertension and bradycardia are initially seen as ICP rises and the brainstem
becomes ischaemic. Critical ischaemia and infarction of the brainstem causes intense autonomic
activity and a surge of catecholamine release- causing increases in heart rate, BP, CO and PVR.
Myocardial ischaemia, conduction abnormalities and arrhythmias can also occur at this point. As
brain stem infarction causes death of the vasomotor centres, sympathetic activity is lost and
hypotension develops which will lead to asystole if untreated.
Lungs: Neurogenic pulmonary oedema is common and is related to a combination of elevated

pulmonary capillary hydrostatic pressure caused by acute LV dysfunction and increased capillary
permeability. This is part of an overall inflammatory response.
Endocrine system: Failure of the hypothalamic-pituitary axis leads to a decline in plasma hormone
concentrations. ADH, thyroid hormone, cortisol and insulin levels all fall. Lack of ADH leads to
diabetes insipidus which untreated leads to electrolyte abnormalities and hypovolaemia. Lack of T3
is associated with loss of cardiac contractility and accumulation of lactate. Low cortisol levels impair
the donor stress response and contributes to cardiovascular collapse. Lack of insulin leads to
hyperglycaemia.
Temperature Regulation: Hypothalamic temperature regulation is lost and hypothermia is common.
Haematology: Thromboplastin release by the ischaemic brain tissue causes coagulopathy.
11
6
Immunological effects: There is increasing evidence that part of brainstem death causes
immunogenicity of solid organs by a variety of mechanisms which may contribute to rejection of the
donor organ in the recipient.
11
7
11
8
32- Brainstem Death and Physiological Changes
a) List the main adverse cardiovascular changes associated with brainstem death.
b) What are the physiological goals (with values) required to ensure optimisation of this donor?
c) Outline the measures and drugs that may be used to achieve these goals. (8 marks)
 Cardiovascular changes associated with brainstem death:
Following brainstem death, cardiovascular changes occur secondary to increasing ICP and cerebral
herniation.
Initial changes include:

1) Increased Arterial Blood Pressure (to maintain CPP & compensate for increasing ICP) Ensuring
brain herniation with associated Pontine Ischaemia and hyper-adrenergic state causes:
2) Pulmonary Hypertension.
3) Increased Right & Left Ventricular Afterload causing Myocardial Ischaemic
4) Cushing reflex (1/3 patients): HTN and Bradycardia
After Foramen Magnum Herniation:

5) Loss of vasomotor tone (vasodilatation) and impaired Cardiac Output (due to loss of sympathetic
tone)
6) Reduced preload and afterload reduces aortic diastolic pressure – decreasing myocardial
perfusion
In summary:
• Catecholamine damage – secondary to coning.
• Arrhythmias – secondary to catecholamines, altered autonomic tone, acidosis, electrolyte
disturbance.
 The physiological goals (with values) required to ensure optimisation of this donor:
1) Heart rate 60-120/min

2) SBP > 100mmHg.
3) MAP > 70mmHg but < 95mmHg.
4) CVP: 6-10 mmHg
5) Stroke volume variation: < 10%
6) Cardiac index > 2.1 l/min/m2
7) Mixed venous saturations (SvO2): > 60%
8) cFt (oesophageal Doppler): 330-360 ms
9) Pulm Artery occlusion pressure: 10-15mmHg
10) Serum Glucose: 4-8mmol/L.
11) SpO2: > 95% (PaO2 > 10kPa)
12) pH 7.35-7.45
13) PaCO2: 4.5-6.0 kPa
14) Peak inspiratory pressure < 25cm H2O
15) PEEP > 5cm H2O
16) Tidal Volume (Vt): 6-8 mls/kg
11
9
 The measures and drugs that may be used to achieve the physiological goals:
1) Blood pressure management: vasoactive solutions can be stopped/weaned and short acting drugs
used to control hypertension (e.g. Esmolol, GTN, Sod. nitroprusside)
2) Hypotension resistant to fluid therapy: Vasopressin is the 1st line agent.
3) Thyroxine (T3) administration can improve cardiac function in the haemodynamically unstable
donor
4) Arrhythmias: Tachycardia’s can be treated with Amiodarone.
5) TTE and oesophageal Doppler: guide fluid, inotrope and vasopressor therapy
6) Lung protective ventilation strategy: as post brain stem death there is an active inflammatory
process that render lungs vulnerable to damage. Uses minimal FiO2 to achieve
7) Extravascular Lung water can be minimised used IV Methylprednisolone (15mg/kg).
8) Diabetes Inspidus: meticulous fluid status/electrolyte monitoring, early use of

Vasopressin/Desmopressin.
9) Titration of Insulin to maintain BM 4-8mmol/L.
12
0
33- Donation after Brainstem Death (DBD)
You have confirmed brainstem death in a patient in the ICU with a catastrophic brain injury. The
organ transplant coordinator has been informed.
(a) Distinguish between the terms DCD and DBD (10%)

(b) What are the challenges in management of the DBD donor in the ICU? (20%)
(c) What is the role of the anaesthetist during organ harvest? (20%)
(d) Distinguish between the terms ‘opt in’ and ‘opt out’, indicating the current situation in the UK.
(e) What is the role of (i) the patient (ii) family members in supplying consent for organ retrieval (DCD
or DBD)? (30%)
Distinguish between the terms DCD and DBD in reference to organ donation
DCD: Donation after Cardiac Death
Classified by the Maastricht Classification
Either controlled or uncontrolled cardiac arrest
Viability of organs depends on the warm ischemic time
DBD: Donation after Brainstem Death

Confirmed brain stem death
Mechanically ventilated
Cardiopulmonary function remains intact
The challenges in management of the DBD donor in ICU:

-Initial period of hypertension and bradycardia (the ‘Cushing’ reflex), followed by unopposed
adrenergic activity, marked haemodynamic lability and profound vasoconstriction can cause
myocardial ischaemia and ventricular dysfunction
-Sustained phase of profound vasodilation, hypothermia and hypotension requiring careful fluid
resuscitation, warming blankets and vasopressor/catecholamines
-Renal function benefits from generous fluid administration-may adversely affect lung retrieval
-Brainstem death is associated with variety of neuroendocrine complications due to a decrease in

ADH, T3, ACTH and insulin. This results in hypotension, Diabetes Insipidus, hypoglycaemia and
metabolic acidosis.
-Current evidence suggests hormone therapy may be beneficial

-Continue feeding patient
-Release of inflammatory cytokines and thromboplastin causing end organ dysfunction and DIC
Role of the anaesthetist in theatre during organ retrieval

-Maintain haemodynamic stability
-Continue vasoactive drugs
-Transfuse blood and blood products if required
-Provide muscle relaxation to eliminate spinal reflex movements
-Steroid supplementation and antibiotic cover
-Obtain blood samples for retrieval team
12
1
-Systemic heparinization prior to aortic cross clamping
-If lungs to be retrieved: withdrawing of the ETT and a maximum tidal volume to be given prior to
stapling of trachea
Distinguish between the terms ‘opt in’ and ‘opt out’, indication the current situation in the UK
Opt in: informed consent presumes the patient is not willing to donate unless either; individual has
made clear statement of intention before death by registering with the national organ registry or
indicating a clear willingness to donate to relatives or friends or consent is obtained from relative or
nominated individual after death
Opt out: Presumed consent presumes consent is given unless the individual has made a clear
statement of refusal to donation, normally in writing. This varies in the different countries that have
this method
‘soft’ approach: relatives can refuse donation on behalf of the deceased
‘hard’ approach: relatives cannot refuse donation if the individual has not previously registered
refusal
The UK’s current model is ‘opt in’ however in recent years due to the shortfall of donated organs and
concerns that not all potential donors are being considered an ‘opt out’ model is being considered.
Role of (i) the patient (ii) family members in supplying consent for organ retrieval (DCD or DBD)
The patient
-Human Tissue Act 2004 gives primacy to the individuals wishes
-This wish to donate may be recorded or stated in a number of ways
-Verbally
-By having a Donor Card
-In writing
-Via accessing the NHS Organ Donor Register
Family members
-To define the known or likely wishes of an individual. If the wishes of individual are unknown-
authority for decision making passes to a nominated representative
-No authority at law to overturn the known wishes of an individual
-In Scotland families who object required to sign a disclaimer if they wish to over-ride patient’s
wishes
12
2
Critica pathways for organ donaf1on*
POSSIBLE DECEASEDORGAN DONOR
A patient with a devastating brain injury or lesion OR a patient with circulatory failure
AND apparently medically suitable for organ donation
Tr eat ing ph y s ician
Donation after Circulatory Death (DCD)/ ,, to 1dentifyfrefer a potential donor Donat.ion after BrainDeath (DBD)
POTENTIAL DCD DONOR POTENTIAL DBD DONOR
A. A person whose circulatory and respiratory Reasons why a potential donor A person whose clinical condttion is suspected to
functions have ceased and resuscitative does not become a utilized donor fulfill brain death criteria.
measures are not to be attempted or continued.
System
or
• Failure to identify/refer a potential or eligible donor
B. A person in whom the cessation of circulatory
• Brain death diagnosis not confirmed (e.g.
and respiratory functions is anticipated to occur
within a time frame that will enable organ does not fulfill criteria) or completed
recovery. (e.g. lack of technical resources or clinician
to make diagnosis or perform confirmatory tests)
J,
! • Circulatory death not declared within the appropriate
time frame. ELIGIBLE DBDDONOR
ELIGIBLE DCD DONOR
• Logistical problems (e.g. no recovery team)
A medically suitable person who has been A medically suitable person who has been
• Lack of appropriate recipient (e.g. child, blood type,
declared dead based on the irreversible absence declared dead based on neuroloigc criteria as
serology positive)
of circulatory and respiratory funcitons as stipulated by the law of the relevant jurisdiction.
stipulated by the law of the relevant jurisdiction, Donor/Organ
within a time frame that enables organ recovery. • Medical unsuitability (e.g. serology positi,ve neoplasia)
• Haemodynamic inslabilily Iunanticipated cardiac '¥
y
arrest ACTUAL DBD DONOR
ACTUAL DCD DONOR
• Anatomic al, histological and/or functional A consented eligible donor:
A consented eligible donor. abnonnalities of organs A. In whom an operative incision was made
A In whom an operative incision was made • Organs damaged during recovery with the intent of organ recovery for the
with the intent of organ recovery for the
• Inadequate perfusion of organs or thrombosis purpose of transplantation.
purpose of transplantation. or
or Permission
B. From whom at least one organ was
B. From whom at least one organ was • Expressed intent of deceased not to be donor
recovered forthe purpose of transplantation. recovered for the p urpose of transplantaiton.
y
• Relative's refusal of permission for organ donation
• Refusal by coroner or other judicial officer to allow
..,
donation for forensic reasons UTILIZED DBD DONOR
UTILIZED DCD DONOR
An actual donor from whom at least one organ
An actual donor from whom at least one organ
was transplanted.
was transplante d.
34- Donation after Circulatory Death (DCD)
In terms of organ donation, the rates of donation after circulatory death are expected
to rise markedly over the next decade.
(a) Define and classify the term “donation after circulatory death”.
(b) Distinguish between the terms warm and cold ischaemia.
(c) Define ‘stand down time’ for various organ retrieval
(d) What are the contraindications to donation after circulatory death?
(e) Outline the donation process, including the staff groups involved.
 Define and classify the term “donation after circulatory death”.

Circulatory death is irreversible cessation of circulatory function
DCD previously known as non-beating heart donation, or donation after cardiac death
Two classes:
Controlled: death following withdrawal of life sustaining treatment
Uncontrolled: unexpected sudden death
Other classification: Maastrict Classification (depending on circumstances of death)
Distinguish between the terms Warm and Cold Ischaemia.

Warm ischaemia: (two types)
Donor warm ischaemia: time from asystole cold perfusion
Recipient warm ischaemia: time from removal from cold perfusion reperfusion
Cold Ischaemia: period between donor and recipient warm ischaemia times
[Functional warm ischaemia: Donor’s SBP < 50 mmHg or SaO2 < 70%]
12
MODIFIED BY AYMAN EDAROUS INTENSIVE CARE ME DICINE
4
‘Stand Down Time’ for Various Organ Retrieval
Each organ is susceptible to warm ischaemia by various amounts, which has

implications for graft function and complications following transplantation
Stand down time = allowed period of functional warm ischaemia (FWI), or from time of
withdrawal of life sustaining treatment (WLST) until asystole; this is specific for each
organ. Stand down times are also specific for each centre
Examples of typical stand down times:
Kidney: 120 mins of FWI or from WLST
Liver: 30 mins FWI, 60 mins from WLST
Pancreas: 30 mins FWI or from WLST
Contraindications to donation after circulatory death

Untreated systemic infection
HIV disease (but HIV positive status not an absolute CI)
Active invasive cancer in the last three years (excl. primary brain and non-
melanomatous skin cancer)
Haematological malignancy
nvCJD
(age > 90 years occasionally mentioned)
Outline the donation process, including the staff groups involved.
For controlled DCD:

Decision WLST (independent of any consideration for transplant)
12
5
Medical staff
Assessment for donation potential
Medical staff
SN-OD
Organ donor register
Family (assent)
Lab staff (tissue typing etc)
Consent and authorisation
Involvement of recipient centres
Medical staff
SN-OD
Maintenance of donation potential / donor optimisation
Mobilisation of retrieval teams
Notification of donor recipients & their respective teams
Medical staff – optimisation of donor
SN-OD and paramedical staff
WLST, diagnosis of death, transfer to theatre for retrieval (within constraints of stand
down times)
Critical care and theatre staff
Retrieval team(s) with transport staff
Cold perfusion, packaging, departure of retrieval teams
Last offices / clerical input
Mortuary staff
Portering staff
Post donation debrief
Contact with family
Medical, nursing, paramedical staff
12
6
12
7
35- Post Cardiac Arrest Care and Cooling
You have been asked to admit a 75 year old man to ICU who has had an OOH VF arrest
for ventilation and therapeutic hypothermia.
(a) What were the major changes in the ILCOR 2010 resuscitation guidelines for adult cardiac arrest?
(b) What is induced hypothermia and what is the proposed mechanism by which it exerts its effects?
(c) What are the adverse systemic consequences of hypothermia? (15%)
(d) Outline the principles of management of therapeutic hypothermia (30%)
(e) Describe a scoring system by which neurological outcome may be predicted post critical care
admission (15%)
 The Major Changes in the ILCOR 2010 Resus. Guidelines for Cardiac Arrest in Adults
removal of rescue breaths
early CPR
minimally interrupted CPR; less than 5 seconds
CPR during charging of defibrillator
use of cpr feedback devices
role of praecordial thump de emphasised
drugs no longer recommended via trachael route
drugs recommended via IO route if IV cannot be established
less focus on early intubation unless expert assistance available
capnography recommended for intubated patient
atropine removed from PEA algorithm
amiodarone and adrenaline recommended at 3rd shock/cycle in shockable algorithm
recognition of potential of USS in cardiac arrest e.g. FEEL algorithm
focus on post arrest syndrome care

unconscious adult patients with spontaneous circulation after out-of-hospital cardiac
arrest should be cooled to 32-34°C for 12 to 24 hours when the initial arrest rhythm
was ventricular fibrillation (VF).
therapeutic hypothermia may also be useful in cases where the initial rhythm was non-
shockable or after in-hospital arrest
 What is induced hypothermia and what is the proposed mechanism by which it

exerts its effects?(20%)
induced hypothermia - intentional reduction of patient's core temperature to below 36
degrees
therapeutic hypothermia - induced hypothermia between 32-34 degrees
mechanism not fully known
12
8
reduces ICP
reduces CMRO2; 7% for every degree of cooling
reduces reperfusion injury;
free radical release, excitatory amino acid production, calcium shifts
What are the adverse systemic consequences of hypothermia? (15%)

cardiac - pro arrythmic, reduced contractility, diastolic dysfunction, hypertension.
renal - diuresis, electrolyte disturbances, hypokalaemia, phosphataemia, magnesaemia
endocrine - hyperglycaemia
respiratory - alteration in solubility of gases in blood
haematology - coagulopathy, platelet dysfunction
biochemical - use alpha stat analysis for blood gases, caution with drug administration
(reduced metabolism)
skin - burns, pressure sores
shivering
immunosuppression
 Outline the principles of management of therapeutic hypothermia (30%)
decision to cool - meets criteria for cooling, feasible in centre, intubated and ventilated
aim to cool within 2-4 hours for 12-24 hours
induction - cool core temperature to 32-34 degrees as rapidly as possible

maintenance - maintain with 0.2-0.5 degree fluctuations
re warming - aim to passively reward 0.2-.3 degrees per hour, max 0.5
paralyse to avoid shivering (40-100% increase in o2 consumption) above 34 degrees

avoid long term paralysis
sedate adequately
adjust ventilator settings appropriately
acknowledge normal physiology of hypothermia e.g. deranged lfts
monitor for sepsis
reduce feeding rate
consider platelets before invasive procedure
 Describe a scoring system by which neurological outcome may be predicted post

critical care admission (15%)
Prognosis after resuscitation score (PAR)
validated against inpatient cardiac arrest population
point based system with score >5 predicting non survival (this has since been shown not
12
9
to be the case)
metastatic malignancy 10
non metastatic malignancy 3
sepsis 5
dependent functional status 5
pneumonia 3
creatinine >130 3
age > 70 2
acute MI -2
other predictors include;

Day 1 myoclonus status
Day 3 absent pupil reflexes, absent or extensor reflexes
Day 4 GCS persistently <4
13
0
13
1
13
2
36- Management of MI
13
3
13
4
13
5
13
6
13
7
13
8
GOOD LUCK FOR ALL
Ayman Edarous, 2018

Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]
https://t.me/joinchat/DRLToA7sXfLoguTCkCxi9w
13
9

Anesthaesia and Intensive Care

Enviado por

Dados do documento

Descrição 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

Anesthaesia and Intensive Care

Enviado por

Direitos autorais:

Formatos disponíveis

Short Answer Questions

Anaesthesia, Pain & Intensive Care Secrets Academy [APICSA]

For Original Materials and Editors, Please refer to:

North Ireland School of Anaesthesia Website

 Ventilator Associated Pneumonia (VAP):

The common pathogens associated with VAP:

 Factors that Increase the Risk of the Development of VAP:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 3

Reducing Oral Colonisation

• Minimising duration of Mechanical Ventilation:

• Stress Ulcer Prophylaxis:

•Deep Venous Thrombosis (DVT) Prophylaxis:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 4

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 5

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 7

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 8

 Measure Lactate Level

 Obtain Blood Cultures (prior to Antibiotics)

 Administer Broad-Spectrum Antibiotics

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 9

Because some evidence indicates that a sustained

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 10

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 11

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 14

 Berlin Definition of ARDS:

 Why was a new definition felt to be necessary?

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 16

 Management of ARDS in the ICU:

*ARDSnet Tidal Volume study showed:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 17

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 18

Treatment of the Cause: Antibiotic for Pneumonia.

 Other Interventions of improving Oxygenation:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 21

 Anatomy of The Pancreas:

 Causes of Pancreatitis (I GET SMACHED):

Signs and Symptoms:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 24

Early Complications Late Complications

*Modified Imrie/Glasgow score

Cholecystectomy in cases of mild gallstone-

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 25

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 27

 Management of a patient admitted with ARF to ICU:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 28

 The Different Methods of Anticoagulation in Patients on RRT:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 29

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 30

Guillain Barre Syndrome (GBS):

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 31

 The Differential Diagnosis:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 32

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 34

What Other Problems Might They Encounter On ICU?

The WHO definition of status epilepticus (SE):

 The systemic effects of SE:

- CVS: early - hypertension, tachycardia; late - hypotension, bradycardia, dysrythmias

 The causes of SE:

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 36

 Pharmacological treatment options for SE

- 1st line: Benzodiazepines

- 1st line: Benzodiazepines

MODIFIED BY AYMAN EDAROUS INTENSIVE CARE MEDICINE 37