HANDBOOK

of
INTERNAL MEDICINE

COC (Medicine)
Hospital Authority

7th Edition
2015
 Disclaimer
DISCLAIMER

This handbook has been prepared by the COC (Medicine), Hospital

Authority and contains information and materials for reference only.
All information is compiled with every care that should have applied.
This handbook is intended as a general guide and reference only and not
as an authoritative statement of every conceivable step or circumstances
which may or could relate to the diagnosis and management of medical
diseases.

The information in this handbook provides on how certain problems

may be addressed is prepared generally without considering the specific
circumstances and background of each of the patient.

Users of this handbook should check the correct dosage and usage of
medications as appropriate to the context of individual patient,
including any allergic history.

The Hospital Authority and the compilers of this handbook shall not be
held responsible to users of this handbook on any consequential effects,
nor be liable for any loss or damage howsoever caused.
 PREFACE TO 7th EDITION
Internal medicine is a rapidly evolving specialty. Over the past 4 years,
there have been changes in some of the guidelines and recommendations

Preface
in the management of major medical diseases. This has prompted the
update of this pocket-sized Handbook of Internal Medicine. This
handbook is widely popular among our junior doctors. Many higher
physician trainees also find it useful in the preparation of the interim
assessment and exit examination of Advanced Internal Medicine. As in
the past, this handbook is intended to serve as a quick reference for
interns and clinicians working in the HA setting.

In this 7th edition, various parts have been revised and in particular, we
have added a section on palliative medicine. Updates of major
guidelines have also been included. I would like to express my heartfelt
thanks to every member of the Editorial Board and all the specialists
who have participated in the review and revision of this new edition.
Without their contributions, this handbook would not have been
materialized. Finally, I have to thank the Coordinating Committee in
Internal Medicine in the support of the publication of this handbook.

Dr LAO Wai Cheung

Chairman
Quality Assurance Subcommittee
Editorial Board Members

Dr. CHAN Ngai Yin

Editorial Board
Members
Dr. CHOI Cheung Hei

Dr. LAI Moon Sing

Dr. LAO Wai Cheung

Dr. LEUNG Moon Ho

Dr. TSANG Owen

Dr. WONG Wing Yin Winnie

Dr. YEUNG Hon Ming Jonas

Co-ordinating Committee in Internal Medicine

Hospital Authority
 CONTENTS
Cardiology
Cardiopulmonary Resuscitation (CPR) C 1-3
Arrhythmias C 4-12
Unstable Angina / Non –ST Elevation MI C 13-15
Acute ST Elevation Myocardial Infarction C 16-24
Acute Pulmonary Oedema C 25
Hypertensive Crisis C 26-28
Aortic Dissection C 29-30
Pulmonary Embolism C 31-32
Cardiac Tamponade C 33-34
Antibiotics Prophylaxis for Infective Endocarditis C 35
Perioperative Cardiovascular Evaluation for Noncardiac C 36-42

Contents
Surgery

Endocrinology
Diabetic Ketoacidosis (DKA) E 1-2
Diabetic Hyperosmolar Hyperglycaemic States E 3
Peri-operative Management of Diabetes Mellitus E 4-5
Insulin Therapy for DM Control E 6-7
Hypoglycaemia E 8
Thyroid Storm E 9
Myxoedema Coma E 10
Phaeochromocytoma E 10
Addisonian Crisis E 11-13
Acute Post-operative/Post-traumatic Diabetes Insipidus E 14
Pituitary Apoplexy E 15

Gastroenterology and Hepatology

Acute Liver Failure G 1-4
Hepatic Encephalopathy G 5-6
Ascites G 7
Orthotopic Liver Transplantation G 8-9
Variceal Haemorrhage G 10-11
Upper Gastrointestinal Bleeding G 12-13
Peptic Ulcers G 14-15
 Management of Gastro-oesophageal Reflux Disease G 16-17
Inflammatory Bowel Diseases G 18-20
Crohn’s Disease G 21-23
Ulcerative Colitis G 24-26
Acute Pancreatitis G 27-30

Haematology
Haematological Malignancies
Leukaemia H 1-2
Lymphoma H 2-3
Multiple Myeloma H 3-4
Extravasation of Cytotoxic Drugs H 4-5
Intrathecal Chemotherapy H 5-6
Contents

Performance Status H 6
Haematologital Toxicity H 6
Non-Malignant Haematological Emergencies/Conditions
Acute Haemolytic Disorders H 7-8
ImmuneThrombocytopenic Purpura (ITP) H 9-10
Thrombotic Thrombocytopenic Purpura (TTP) H 11
Pancytopenia H 11
Thrombophilia Screening H 12
Prophylaxis of Venous Thrombosis in Pregnancy H 12
Special Drug Formulary and Blood Products
Anti-emetic Therapy H 13
Haemopoietic Growth Factors H 13
Immunoglobulin Therapy H 13-14
Anti-thymocyte Globulin (ATG) H 14
rFVIIa (Novoseven) H 14-15
Novel Oral Anticoagulants (NOACs) H 15
Replacement for Hereditary Coagulation Disorders H 16-17
Transfusion
Acute Transfusion Reactions H 18-19
Transfusion Therapy H 20-21
Actions after Transfusion Incident & Adverse Reactions H 22
Nephrology
Renal Transplant – Donor Recruitment K 1-2
Electrolyte Disorders K 3-13
Systematic Approach to the Analysis of Acid-Base Disorders K 14-17
Peri-operative Management of Uraemic Patients K 18
Renal Failure K 19-20
Emergencies in Renal Transplant Patient K 21
Drug Dosage Adjustment in Renal Failure K 22-23
Protocol for Treatment of CAPD Peritonitis K 24-27
Protocol for Treatment of CAPD Exit Site Infection K 28-29

Neurology
Coma N 1-3
Delirium N 4-5

Contents
Acute Stroke N 6-9
Subarachnoid Haemorrhage N 10-11
Tonic-Clonic Status Epilepticus N 12-14
Guillain-Barre Syndrome N 15-16
Myasthenia Crisis N 17-18
Acute Spinal Cord Syndrome N 19
Delirium Tremens N 20
Wernicke’s Encephalopathy N 21-22
Peri-operative Management of Patients with Neurological N 23-24
Diseases

Respiratory Medicine
Massive Haemoptysis P 1-2
Spontaneous Pneumothorax P 3-4
Pleural Effusion P 5-6
Oxygen Therapy P 7-9
Adult Acute Asthma P 10-12
Long Term Management of Asthma P 13-16
Chronic Obstructive Pulmonary Disease (COPD) P 17-20
Obstructive Sleep Apnoea P 21
Pre-operative Evaluation of Pulmonary Functions P 22-23
Mechanical Ventilation P 24-26
Noninvasive Ventilation (NIV) P 27-28
 Rheumatology & Immunology
Approach to Inflammatory Arthritis R 1-2
Gouty Arthritis R 3-4
Septic Arthritis R 5-6
Rheumatoid Arthritis R 7-10
Ankylosing Spondylitis R 11-12
Psoriatic Arthritis R 13-14
Systemic Lupus Erythematosus R 15-21
Rheumatological Emergencies R 22-24
Non-steroidal Anti-inflammatory Drugs R 25-26

Infections
Community-Acquired Pneumonia In 1-2
Hospital Acquired Pneumonia In 3-4
Contents

Pulmonary Tuberculosis In 5-6

CNS Infection In 7-8
Urinary Tract Infections In 9
Enteric Infections In 10-12
Acute Cholangits In 13
Spontaneous Bacterial Peritonitis In 14
Necrotizing Fasciitis In 15
Skin & Soft Tissue Infection In 16
Septic Shock In 17
Antibiotics for Febrile Neutropenic Patients In 18-19
Malaria In 20-21
Chickenpox / Herpes Zoster In 22
HIV / AIDS In 23-30
Rickettsial Infection In 31
Influenza In 32-33
Infection Control In 34-36
Needlestick Injury/Mucosal Contact to HIV, HBV or HCV In 37-40
Middle East Respiratory Syndrome In 41-42
Viral Haemorrhagic Fever In 43-44
Palliative Medicine
Anorexia PM 1-2
Nausea and Vomiting PM 3
Cancer Pain Management PM 4
Guidelines on the Use of Morphine for Chronic Cancer Pain PM 5-6
Dyspnoea PM 7-8
Delirium PM 9-10
Malignant Bowel Obstruction PM 11-12
Palliative Care Emergencies: Massive Haemorrhage PM 13
Malignant Hypercalcaemia PM 14
Metastatic Spinal Cord Compression PM 15
Last Days of Life PM 16

General Internal Medicine

Contents
Anaphylaxis GM 1
Acute Poisoning GM 2
 General Measures GM 2-3
 Specific Drug Poisoning GM 4-9
 Non-pharmaceutical Poisoning GM 10-14
 Smoke Inhalation GM 15
 Snake Bite GM 16-17
Accidental Hypothermia GM 18
Heat Stroke / Exhaustion GM 19-20
Near Drowning / Electrical Injury GM 21
Rhabdomyolysis GM 22
Superior Vena Cava Syndrome GM 23
Malignancy-related SVCO GM 24-25
Neoplastic Spinal Cord / Cauda Equina Compression GM 26
Hypercalcaemia of Malignancy GM 27
Tumour Lysis Syndrome GM 28
Extravasation of Chemotherapeutic Agents GM 29
Brain Death GM 30-32

Procedures
Endotracheal Intubation Pr 1-2
Setting CVP Line Pr 3
Defibrillation Pr 4
Temporary Pacing Pr 5
Lumbar Puncture Pr 6-7
Bone Marrow Aspiration and Trephine Biopsy Pr 8-9
Care of Hickman Catheter Pr 10-11
Renal Biopsy Pr 12
Intermittent Peritoneal Dialysis Pr 13-14
Percutaneous Liver Biopsy Pr 15-16
Abdominal Paracentesis Pr 17
Pleural Aspiration Pr 18-19
Pleural Biopsy Pr 20-21
Chest Drain Insertion Pr 22-23

Geriatrics Medicine (Insert to electronic version only)

Altered Responsiveness or “Decreased GC” Gr 1-2
Assessment of Mental Competence Gr 3
Care of Dying Gr 4-6
Diabetes Mellitus in Old Age Gr 7-9
Falls Gr 10-12
Hypertension in Old Age Gr 13-14
Musculoskeletal Pain Gr 15-18
Neurocognitive Disorder Gr 19-24
Nursing Home-Acquired Pneumonia (NHAP) Gr 25-26
Orthostatic Hypotension Gr 27-29
Pharmacotherapy in Old Age Gr 30-31
Post-Operative Delirium Gr 32-33
Pressure Ulcers Gr 34-37
Spasticity Gr 38-40
Syncope Gr 41-43
Urinary Incontinence Gr 44-46
Urinary Retention Gr 47-50

Acknowledgement
Cardiology

Cardiology
 C 1

CARDIOPULMONARY RESUSCITATION (CPR)

1. Determine unresponsiveness
2. Call for Help, Call for Defibrillator
3. Wear PPE: N95/ surgical mask, gown, +/-(gloves, goggles, face
shield for high risk patients)
Primary CDAB Survey (Initiate chest compression before ventilation;
Ref: Field JM et al. Circulation 2010;122[Suppl 3]:S640-656)
C: Circulation Assessment
 Check carotid pulse for 5-10 s & assess other signs of
circulation (breathing, coughing, or movement)
 Chest compressions ≧100/min
 CPR 30 compressions (depth ≧2 inches) to 2 breaths
D: Defibrillate VF or VT as soon as identified

Cardiology
 Check pulse and leads
 Check all clear
 Deliver 360J for monophasic defibrillator, without lifting
paddles successively if no response; or equivalent 200J for
biphasic defibrillator, if defibrillation waveform is unknown
A: Assess the Airway
 Clear airway obstruction/secretions
 Head tilt-chin lift or jaw-thrust
 Insert oropharyngeal airway
B: Assess/Manage Breathing
 Ambubag + bacterial/viral filter + 100% O2 at 15L/min
 Plastic sheeting between mask and bag
 Seal face with mask tightly
 Give 2 rescue breaths, each lasting 2-4 s
C2
Secondary ABCD Survey
A: Place airway devices; intubation if skilled.
 If not experienced in intubation, continue Ambubag and call for
help
B: Confirm & secure airway; maintain ventilation.
 Primary confirmation: 5-point auscultation.
 Secondary confirmation: End-tidal CO2 detectors,
oesophageal detector devices.
C: Intravenous access; use monitor to identify rhythm.
D: Differential Diagnosis.
Common drugs used in resuscitation
Adrenaline 1 mg (10 ml of 1:10,000 solution) q3-5 min iv
Lignocaine 1 mg/kg iv bolus, then 1-4 mg/min infusion
Amiodarone In cardiac arrest due to pulseless VT or VF, 300 mg iv
bolus, further dose of 150 mg iv bolus if required
Atropine 1 mg iv push, repeat q3-5min to max dose of
0.04mg/kg
CaCl2 5-10 ml 10% solution iv slow push for hyperkalaemia
and calcium channel blocker overdose
NaHCO3 1 mEq/kg initially (e.g. 50 ml 8.4% solution) in
patients with hyperkalaemia
MgSO4 1-2g in 10ml D5 iv bolus in torsade de pointes
 C 3
Tracheal administration of Resuscitation Medications
(if iv line cannot be promptly established):
- Lignocaine, Epinephrine (adrenaline), Atropine, Narcan (L-E-A-N)
- Double dosage
- Dilute in 10 ml NS or water
- Put catheter beyond tip of ET tube
- Inject drug solution quickly down ET tube, followed by several
quick insufflations
- Withhold chest compression shortly during these insufflations
Post-resuscitation care:
- Correct hypoxia with 100% oxygen
- Prevent hypercapnia by mechanical ventilation
- Consider maintenance antiarrhythmic drugs
- Treat hypotension with volume expander or vasopressor
- Treat seizure with anticonvulsant (diazepam or phenytoin)
- Maintain blood glucose within normal range

Cardiology
- Routine administration of NaHCO3 not necessary
C4

ARRHYTHMIAS
(I)
Ventricular Fibrillation or
Pulseless Ventricular Tachycardia

Rapid Defibrillation
360 J monophasic shock or 200J biphasic shock
CPR for 2 minutes
then check rhythm

360 J monophasic shock or 200J biphasic shock

CPR for 2 minutes
Adrenaline 1 mg iv (10 ml of 1:10,000 solution)
Repeat every 3-5 min
Then check rhythm

360 J monophasic shock or 200J biphasic shock

CPR for 2 minutes

Consider antiarrhythmics

- Amiodarone 300 mg iv bolus, can consider a second dose of 150 mg

iv
- Lignocaine 1-1.5 mg/kg iv push, can repeat in 3-5 minutes
(maximum total dose 3 mg/kg)
- Procainamide 30 mg/min (maximum total dose 17 mg/kg)
 C 5
(II)
Pulseless Electrical Activity
(Electromechanical Dissociation)

Primary CDAB and Secondary ABCD

Consider causes (“6H’s and 6T’s”) and give specific treatment

Hypovolaemia Tablets (drug overdose, accidents)
Hypoxia Tamponade, cardiac
Hydrogen ion (acidosis) Tension pneumothorax
Hyper / hypokalemia Thrombosis, coronary (ACS)
Hypothermia Thrombosis, pulmonary (Embolism)
Hyper/hypoglycaemia Trauma

Cardiology
Adrenaline 1 mg iv (10 ml of 1:10,000 solution)
Repeat every 3-5 min

 Most common causes of PEA

 C6

(III) Asystole

Primary CDAB and Secondary ABCD

Consider causes*

Transcutaneous pacing
If considered, perform immediately
NOT for routine use

Adrenaline 1 mg iv (10 ml of 1:10,000 solution)

Repeat every 3-5 min

Consider to stop CPR for arrest victims who, despite successful

deployment of advanced interventions, continue in asystole for more
than 10 minutes with no potential reversible cause
Cardiology

* Consider causes: hypoxia, hyperkalemia, hypokalemia, acidosis,

drug overdose, hypothermia
 C 7
(IV)
Tachycardia

- Assess ABCs & vital signs - Review Hx and perform P/E

- Secure airway and iv line - Perform 12-lead ECG
- Administer oxygen - Portable CXR
- Attach BP, rhythm & O2 Monitors

Unstable?
(chest pain, SOB, decreased conscious state, low BP, shock,
pulmonary congestion, congestive heart failure, acute MI)

Yes

Immediate Synchronized No or

Cardiology
DC cardioversion 100J/200J/300J/360J Borderline
(except sinus tachycardia)

 Atrial fibrillation  Regular Narrow  Regular Wide

Atrial flutter Complex Tachycardia Complex Tachycardia

- For immediate cardioversion

 Consider sedation
 Note possible need to resynchronize after each
cardioversion
 If delays in synchronization, go immediately to
unsynchronized shocks
 C8

 Atrial fibrillation / Atrial flutter

1. Correct underlying causes

- hypoxia, electrolyte disorders, sepsis, thyrotoxicosis etc

2. Control of ventricular rate

 Diltiazem*0.25mg/kg iv bolus over 2 min, then 5-15mg/hr;

oral maintenance 120-360mg daily (ER)
 Verapamil* 0.075-0.15mg/kg iv bolus over 2 min, may give
additional 10mg after 30 min if no response, then
0.005mg/kg/min infusion
Risk of hypotension, check BP before 2nd dose
Oral maintenance 180-480mg daily (ER)
 Metoprolol* 2.5-5mg iv bolus over 2 min; up to 3 doses; oral
maintenance 25-100mg BD
Cardiology

 Amiodarone 300mg iv over 1 hr, then 10-50mg/hr over 24 hr;

oral maintenance 100-200mg daily
 Digoxin 0.25mg iv with repeat dosing to a maximum of
1.5mg over 24 hr; oral maintenance 0.125-0.25mg
daily

* Contraindicated in WPW Syndrome

- In AF complicating acute illness e.g. thyrotoxicosis, -blockers
and verapamil may be more effective than digoxin
- For impaired cardiac function (EF < 40%, CHF), use digoxin
or amiodarone

3. Anticoagulation
Prompt anticoagulation can be achieved with unfractionated heparin
with maintenance of aPTT 1.5-2 times control or low molecular
weight heparin. Long-term anticoagulation can be achieved with
warfarin with maintenance of PT 2-3 times control (depends on
general condition and compliance of patient and underlying heart disease)
 C 9

or “Novel oral anticoagulant” like Dabigatran, Rivaroxaban or

Apixaban.

4. Termination of Arrhythmia
 For persistent AF (> 2 days), anticoagulate for 3 weeks before
conversion and
 continue for 4 weeks after (delayed cardioversion approach)
 Pharmacological conversion:
Amiodarone 150mg over 10min then 1mg/min for 6 hr then
0.5mg/min for 18 hr or orally 600-800mg daily in
divided doses up to 10g, then 200mg daily as
maintenance dose
Flecainide 200-300mg orally, preferably give betablocker or
nondihydropyridine calcium channel antagonist
30 minutes beforehand
Propafenone 450-600mg orally, preferably give betablocker or

Cardiology
nondihydropyridine calcium channel antagonist
30 minutes beforehand
Procainamide 15 mg/kg iv loading at 20 mg/min (max 1 g), then
2-6 mg/min iv maintenance,
or 250 mg po q4h

 Synchronized DC cardioversion
- Atrial fibrillation 100-200J and up
- Atrial flutter 50-100J and up

5. Prevention of Recurrence
 Class Ia, Ic, sotalol, amiodarone or dronedarone
 C 10

Stable Regular Narrow Complex Tachycardia

Vagal Manoeuvres *

#
ATP 10 mg rapid iv push
1-2 mins

ATP 20 mg rapid iv push

(may repeat once in 1-2 mins)

Blood pressure
Normal or
Elevated Low

Verapamil 2.5-5 mg iv
15-30 mins Synchronized DC
Cardiology

Verapamil 5-10 mg iv Cardioversion

- start with 50 J
- Increase by 50-100 J increments
Consider
- digoxin
- -blocker
- diltiazem
- amiodarone

* Carotid sinus pressure is C/I in patients with carotid bruits.

Avoid ice water immersion in patients with IHD.
# contraindicated in asthma & warn patient of transient flushing and
chest discomfort
 C 11

 Stable Wide Complex Tachycardia

Attempt to establish a specific diagnosis

Confirmed SVT Unknown type Confirmed VT

# Preserved EF < 40%,

ATP 10 mg rapid iv push
cardiac function CHF
1-2 mins
ATP 20 mg rapid iv push
Preserved EF < 40%,
cardiac function CHF Amiodarone Amiodarone
or lignocaine or
or lignocaine,

Cardiology
Sotalol or then
Procainamide cardioversion
Amiodarone Amiodarone
or then
Sotalol cardioversion
or
Procainamide

Dosing:
- Amiodarone 150 mg IV over 10 mins, repeat 150 mg IV over 10
mins if needed. Then infuse 600-1200 mg/d. (Max 2.2 g in 24 hours)
- Procainamide infusion 20-30 mg/min till max. total 17 mg/kg or
hypotension
- Lignocaine 0.5-0.75 mg/kg IV push and repeat every 5 to 10 mins,
then infuse 1 to 4 mg/min (Max. total dose 3 mg/kg)
# contraindicated in asthma & warn patient of transient flushing and
chest discomfort
 C 12

(V) Bradycardia

- Assess ABCs & vital signs - Review Hx and perform P/E

- Secure airway and iv line - Perform 12-lead ECG
- Administer oxygen - Portable CXR
- Attach BP, rhythm & O2 Monitors - Watch out for hyperkalaemia

Unstable?
(chest pain, SOB, decreased conscious state, low BP, shock,
pulmonary congestion, congestive heart failure, acute MI)

No Yes
Type II 2nd degree AV block? Intervention sequence:
Third degree AV block?  - Atropine 0.5-1 mg *
- Transcutaneous pacing (TCP) #
Cardiology

No Yes - Dopamine 5-20 micrograms/kg/min

- Adrenaline 2-10 micrograms/min
Observe Pacing
#
(bridge over with TCP)

* - Do not delay TCP while awaiting iv access to give atropine

- Atropine in repeat doses in 3-5 min (shorter in severe condition) up to a
max of 3 mg or 0.04 mg/kg. Caution in AV block at or below
His-Purkinje level (acute MI with third degree heart block and wide
complex QRS; and for Mobitz type II heart block)
 Never treat third degree heart block plus ventricular escape with
lignocaine
# Verify patient tolerance and mechanical capture. Analgesia and sedation
prn.
 C 13

UNSTABLE ANGINA / NON-ST ELEVATION

MYOCARDIAL INFARCTION
Aims of Treatment: Relieve symptoms, monitor for complications,
improve long-term prognosis
Mx
1. Admit CCU for high risk cases*.
2. Bed rest with continuous ECG monitoring
3. ECG stat and repeat at least daily for 3 days (more frequently in
severe cases to look for evolution to MI).
4. Cardiac enzymes daily for 3 days. Troponin stat (can repeat 6-12
hours later if 1st Troponin is normal)
5. CXR, CBP, R/LFT, lipid profile (within 24 hours), aPTT, INR as
baseline for heparin Rx.
6. Allay anxiety - Explain nature of disease to patient.
7. Morphine IV when symptoms are not immediately relieved by
nitrate e.g. Morphine 2-5 mg iv (monitor BP).

Cardiology
8. Correct any precipitating factors (anaemia, hypoxia,
tachyarrhythmia).
9. Stool softener & supplemental oxygen for respiratory distress.
10. Consult cardiologist to consider GP IIb/IIIa antagonist, IABP,
urgent coronary angiogram/revascularisation if refractory to
medical therapy
Specific drug treatment:
Antithrombotic Therapy
a. Aspirin 162-325mg loading, then 81-325mg daily
b. Clopidogrel 300-600mg stat, then 75mg daily OR
Ticagrelor 180mg stat, then 90mg BD OR
Prasugrel 60mg stat, then 10mg daily
c. Low-Molecular-Weight-Heparin e.g
Enoxaparin (Clexane) 1 mg/kg sc q12h.
Nadroparin (Fraxiparine) sc 0.4 ml bd if <50 kgf BW,
0.5 ml bd if 50-59 kgf BW, 0.6 ml bd if >60 kgf BW.
 C 14

Dalteparin (Fragmin) 120 international units /kg (max 10000

international units) sc q12h.

Anti-Ischemic Therapy
a. Nitrates
 reduces preload by venous or capacitance vessel dilatation.
 Contraindicated if sildenafil taken in preceding 24 hours.
Sublingual TNG 1 tab/puff Q5min for 3 doses for patients with
ongoing ischemic discomfort
IV TNG indicated in the first 48 h for persistent ischemia, heart
failure, or hypertension
NitroPhol 0.5-1mg/hr (max 8-10 mg/min)
Isosorbide dinitrate (Isoket) 2-10 mg/hr
- Begin with lowest dose, step up till pain is relieved
- Watch BP/P; keep SBP > 100 mmHg
 Isosorbide dinitrate - Isordil 10-30 mg tds
Cardiology

Isosorbide mononitrate - Elantan 20-40 mg bd or

Imdur 60-120 mg daily
b. ß-blockers (if not contraindicated)
 reduce HR and BP (titrate to HR<60)
 Metoprolol (Betaloc) 25-100 mg bd
 Atenolol (Tenormin) 50-100 mg daily
c. Calcium Antagonists (when -blocker is contraindicated in the
absence of clinically significant LV dysfunction)
 Diltiazem (Herbesser) 30-60 mg tds
 Verapamil 40-120 mg tds

Other Therapies
a. Hydroxymethyl glutaryl-coenzyme A reductase inhibitor (statin)
 Should be given regardless of baseline LDL-C level in the
absence of contraindications.
b. Angiotensin- converting enzyme inhibitor (ACEI)
 Should be administered within the first 24 hours in the absence of
hypotension or contraindications.
 C 15

 Angiotensin receptor blocker should be used if patient is

intolerant of ACEI

*High risk features (Consider Early PCI)

 Ongoing or recurrent rest pain
 Hypotension & APO
 Ventricular arrhythmia
 ST segment changes  0.1 mV; new bundle branch block
 Elevated Troponin > 0.1 mg/mL
 High Risk Score (TIMI, GRACE)

(Reference: O’Gara PT et al. 2013 ACCF/AHA guideline for the

management of ST-elevation myocardial infarction. JACC
2013;61(4):e78-140)

Cardiology
 C 16

ACUTE ST ELEVATION
MYOCARDIAL INFARCTION

Ix - Serial ECG for 3 days

 Repeat more frequently if only subtle change on 1st ECG; or
when patient complains of chest pain

Area of Infarct Leads with ECG changes

inferior II, III, aVF
lateral I, aVL, V6
anteroseptal V1, V2, V3
anterolateral V4, V5, V6
anterior V1 - V 6
right ventricular V3R, V4R

 Serial cardiac injury markers* for 3 days

Cardiology

 CXR, CBP, R/LFT, lipid profile (within 24 hours)

 aPTT, INR as baseline for thrombolytic Rx

General Mx
- Arrange CCU bed
- Close monitoring: BP/P, I/O q1h, cardiac monitor
- Complete bed rest (for 12-24 hours if uncomplicated)
- O2 by nasal prongs if hypoxic or in cardiac failure; routine O2 in
the first 6 hours
- Allay anxiety by explanation/sedation (e.g. diazepam 2-5 mg po
tds)
- Stool softener
- Adequate analegics prn e.g. morphine 2-5 mg iv (monitor BP &
RR)
* CK-MB; troponin; myoglobin (depending on availability)
 C 17

Specific Rx Protocol

Prolonged ischaemic-type chest discomfort

Aspirin 162-325mg loading, 81-325mg daily

ECG

ST elevation1 or new LBBB ST depression +/- T inversion

-blocker (if not contraindicated)2 Refer to NSTEMI

+ P2Y12 inhibitors**
+ Anticoagulation with LMWH*** or UFH

 12 Hr 12 Hr

Cardiology
Eligible for Not eligible for Not for4 Persistent
Fibrinolytic Fibrinolytic reperfusion Rx Symptoms

Fibrinolytic 3 Consider Cath then No Yes

(Consider direct PCI or CABG
PCI as alternative)

Other medical therapy Consider pharmacological

(ACE-I5 +statin  Nitrate6) or catheter-based reperfusion

Persistent / recurrent ischaemia or haemodynamic instability

or recurrent symptomatic arrhythmia
Yes No

- Consider IABP, angiography Continue medical Rx

+/- PCI
 C 18
1
At least 1mm in 2 or more contiguous leads
2
e.g. Metoprolol 25 mg bd orally.
Alternatively, metoprolol 5 mg iv slowly stat for 3 doses at 5 min
intervals (Observe BP/P after each bolus, discontinue if pulse <
60/min or systolic BP < 100 mmHg).
3
See “Fibrinolytic therapy”
4
Not for reperfusion Rx if e.g. too old, poor premorbid state
5
Starting within the first 24 hrs, esp. for anterior infarction or clinical
heart failure. Thereafter, prescribe for those with clinical heart failure
or EF < 40%, (starting doses of ACEI: e.g. acertil
1 mg daily; ramipril 1.25 mg daily; lisinopril 2.5 mg daily)
6
Prescribe if persistent chest pain / heart failure / hypertension
e.g. iv isosorbide dinitrate (Nitropohl/Isoket) 2-10 mg/h. (Titrate
dosage until pain is relieved; monitor BP/P, watch out for
hypotension, bradycardia or excessive tachycardia).
C/I if sildenafil taken in past 24 hours
** For primary PCI, give clopidogrel loading 600mg, 75mg daily
Cardiology

maintenance OR Prasugrel loading 60mg, 10mg daily maintenance

OR Ticagrelor loading 180mg, 90mg BD maintenance
For fibrinolytic therapy, give clopidogrel loading 300mg, 75mg
daily maintenance for age ≤75; and no loading dose for age>75
*** For age <75, Enoxaparin 30mg iv bolus, followed in 15 min by
1mg/kg sc Q12H; for age 75, no loading dose, 0.75mg/kg sc
Q12H; give up to 8 days or until revascularization
Detection and Treatment of Complications
a. Arrhythmia
 Symptomatic sinus bradycardia
- atropine 0.3-0.6 mg iv bolus
- pacing if unresponsive to atropine
 AV Block :
1st degree and Mobitz type I 2nd degree: Conservative
Mobitz Type II 2nd degree or 3rd degree: Pacing
(inferior MI, if narrow-QRS escape rhythm &
adequate rate, conservative Rx under careful monitoring
 C 19

is an alternative)
(Other indications for temporary pacing:
 Bifascicular block + 1st degree AV block
 Alternating BBB or RBBB + alternating LAFB/LPFB)
 Tachyarrhythmia
(Always consider cardioversion first if severe haemodynamic
compromise or intractable ischaemia)
PSVT
 ATP 10-20 mg iv bolus
 Verapamil 5-15 mg iv slowly (C/I if BP low or on
beta-blocker), beware of post-conversion angina
Atrial flutter/fibrillation
 Digoxin 0.25 mg iv/po stat, then 0.25 mg po q8H for 2 more
doses as loading, maintenance 0.0625-0.25 mg daily
 Diltiazem 10-15 mg iv over 5-10 mins, then 5-15 g/kg/min
 Amiodarone 5 mg/kg iv infusion over 60 mins as loading,

Cardiology
maintenance 600-900 mg infusion/24 h
Wide Complex Tachycardia (VT or aberrant conduction)
Treat as VT until proven otherwise
Stable sustained monomorphic VT :
 Amiodarone 150 mg infused over 10 minutes, repeat 150 mg iv
over 10 mins if needed, then 600-1200 mg infusion over 24h
 Lignocaine 50-100 mg iv bolus, then 1-4 mg/min infusion
 Procainamide 20-30 mg/min loading, then 1-4 mg/min infusion
up to 12-17 mg/kg
 Synchronized cardioversion starting with 100 J
Sustained polymorphic VT :
 Unsynchronized cardioversion starting with 200 J

b. Pump Failure
RV Dysfunction
 Set Swan-Ganz catheter to monitor PCWP. If low or normal,
volume expansion with colloids or crystalloids
 C 20

LV Dysfunction
 Vasodilators (esp. ACEI) if BP OK (+/- PCWP monitoring)
 Inotropic agents
- Preferably via a central vein
- Titrate dose against BP/P & clinical state every 15 mins
initially, then hourly if stable
- Start with dopamine 2.5 microgram/kg/min if SBP  90 mmHg,
increase by increments of 0.5 microgram/kg/min
- Consider dobutamine 5-15 microgram/kg/min when high dose
dopamine needed
 IABP, with a view for catheterization  revascularization
c. Mechanical Complications
- VSD, mitral regurgitation
- Mx depends on clinical and haemodynamic status
 Observe if stable (repair later)
Cardiology

 Emergency cardiac catheterization and repair if unstable

(IABP for interim support)
d. Pericarditis
 High dose aspirin
 NSAID e.g. indomethacin 25-50 mg tds for 1-2 days
Others: colchicines, acetaminophen

After Care (For uncomplicated MI)

- Advise on risk factor modification and treatment
(Smoking, HT, DM, hyperlipidaemia, exercise)
- Stress test (Pre-discharge or symptom limited stress 2-3 wks post MI)
- Angiogram if + ve stress test or post-infarct angina or other
high-risk clinical features
- Drugs for Secondary Prevention of MI
 -blocker : Metoprolol 25-100 mg bd
 Aspirin : 81-325 mg daily
 C 21

 ACEI (esp for large anterior MI, recurrent MI, impaired LV systolic
function or CHF) :
e.g. Lisinopril 5-20 mg daily; Ramipril 2.5-10 mg daily;
Acertil 2-8 mg daily
 Angiotensin receptor blocker should be used in patients intolerant
of ACEI and have heart failure or LVEF<40% or hypertension
 Aldosterone blocker should be used in patients without significant
renal dysfunction or hyperkalaemia and who are already on
therapeutic doses of ACEI and beta-blocker, with LVEF<40% +
diabetes or heart failure
 Statin should be used in all patients

Cardiology
 C 22

Fibrinolytic Therapy
Contraindications
Absolute: - Previous haemorrhagic stroke at any time, other
strokes or CVA within 3 months; except acute ischaemic
stroke within 4.5 hours
- Known malignant intracranial neoplasm (primary or
metastatic)
- Known structural cerebrovascular lesion (e.g. AV
malformation)
- Active bleeding or bleeding diathesis (does not include
menses)
- Suspected aortic dissection
- Significant closed head or facial trauma within 3 months
- Intracranial or intraspinal surgery within 2 months
- Severe uncontrolled hypertension (unresponsive to
emergency therapy)
Cardiology

- For Streptokinase, prior treatment within previous 6

months
Relative: - Severe uncontrolled hypertension on presentation (blood
pressure > 180/110 mm Hg)†
- History of chronic, severe, poorly controlled hypertension
- History of prior ischaemic stroke > 3 months or known
intracerebral pathology not covered in absolute
contraindications
- Traumatic or prolonged (>10min) CPR
- Oral anticoagulant therapy
- Major surgery < 3 weeks
- Noncompressible vascular punctures
- Recent (within 2-4 wks) internal bleeding
- Pregnancy
- Active peptic ulcer
†
Could be an absolute contraindication in low-risk patients with
myocardial infarction.
 C 23
Choice of fibrinolytic therapy

TNK-tPA iv bolus, 30mg (<60 kg), 35mg (60-69 kg), 40mg (70-79
kg), 45mg (80-89 kg), 50mg (90 kg)
 tPA15 mg iv bolus, then 0.75 mg/kg (max 50 mg) in 30 mins,
then 0.5 mg/kg (max 35 mg) over 1 hr
 Streptokinase 1.5 million units iv over 30-60 minutes

Cardiology
 C 24

Monitoring

- Use iv catheter with obturator in contralateral arm for blood taking

- Pre-Rx: Full-lead ECG, INR, aPTT, cardiac enzymes
- Repeat ECG 1. when new rhythm detected and
2. when pain subsided
- Monitor BP closely and watch out for bleeding
- Avoid percutaneous puncture and IMI
- If hypotension develops during infusion
 withhold infusion
 check for cause (treatment-related* vs cardiogenic)
* fluid replacement; resume infusion at ½ rate

Signs of Reperfusion

- chest pain subsides

Cardiology

- early CPK peak

- accelerated nodal or idioventricular rhythm
- resolution of ST elevation of at least 50% in the worst ECG lead at
60-90 minutes after fibrinolytic

(Reference: Amsterdam EA et al. 2014 AHA/ACC guideline for the

management of patients with non-ST-elevation acute coronary
syndromes. JACC 2014;64(24):e139-228)
 C 25

ACUTE PULMONARY OEDEMA

Acute Management :
General measures Identify and treat
1. Complete bed rest, prop up precipitating cause
2. Oxygen (may require high flow e.g. arrhythmia, IHD,
rate / concentration) uncontrolled HT, chest
3. Low salt diet + fluid restriction infection
(NPO if very ill)

BP Stable ?
Yes No

Medications (commonly considered) BP Medications (others)

1. Frusemide(Lasix) 40-120 mg iv stabilized Inotropic agents

Cardiology
2. IV nitrate e.g. nitropohl 1-8 mg/hr - Dopamine
3. Morphine 2-5 mg slow iv 2.5-10 g/kg/min
- Dobutamine
2.5-15 g/kg/min
Unsatisfactory
response
BP not stabilized
Monitor BP/P, I/O, SaO2, or APO refractory
CVP, RR clinical status to Rx
every 30-60 mins
Consider:
1. Intra-aortic balloon pump
Consider ventilatory support in case of (IABP)
desaturation, patient exhaustion, 2. PCI for ischaemic cause
cardiogenic shock of CHF
1. Intubation and mechanical ventilation 3. Intervention for significant
2. Non-invasive: BIPAP/CPAP valvular lesion
 C 26

HYPERTENSIVE CRISIS

 Malignant BP  220/120 mmHg + Grade III/IV fundal changes

 Emergency Malignant or severe HT + ICH, dissecting aneurysm,
APO, encephalopathy, phaeochromocytoma crisis,
eclampsia (end organ damage due to HT versus risk of
organ hypoperfusion due to rapid BP drop.
Need Immediate reduction of BP to target levels (initial
phase drop in BP by 20-25% of baseline).
 Urgency - Malignant HT without acute target organ damage
- HT associated with bleeding (post-surgery, severe
epistaxis, retinal haemorrhage, CVA etc.)
- Severe HT + pregnancy / AMI / unstable angina
- Catecholamine excess or sympathomimetic overdose
(rebound after withdrawal of clonidine / methyldopa;
LSD, cocaine overdose; interactions with MAOI)
Cardiology

BP reduction within 12-24 hours to target levels

Mx
1. Always recheck BP yourself at least twice
2. Look for target organ damage (neurological, cardiac)
3. Complete bed rest, low salt diet (NPO in HT emergency)
4. BP/P q1h or more frequently, monitor I/O (Close monitoring
in CCU/ICU with intra-arterial line in HT emergency)
5. Check CBP, R/LFT, cardiac enzymes, aPTT/PT, CXR, ECG,
urine x RBC and albumin
6. Aim: Controlled reduction (Rapid drop may ppt CVA / MI)
Target BP (mmHg)
Chronic HT, elderly, acute CVA 170-180 / 100
Previously normotensive, post
cardiac/vascular surgery 140 / 80
Acute aortic dissection 100-120 SBP
 C 27

7. Hypertensive urgency
- Use oral route, BP/P q15 mins for 60 mins
- Patients already on antiHT, reinstitute previous Rx
- No previous Px or failure of control despite reinstituting Rx for
4-6 hrs:
Metoprolol 50-200 mg bd / Labetalol 200 mg po stat, then 200 mg tds
Captopril 12.5-25 mg po stat, then tds po (if phaeo suspected)
Long acting Calcium antagonists (Isradipine 5mg/Felodipine 5mg)
If not volume depleted, lasix 20mg or higher in renal insufficiency
- Aim: Decrease BP to 160/110 over several hours
(Sublingual nifedipine may precipitate ischaemic insult due
to rapid drop of BP)

8. Malignant HT or Hypertensive emergency

- Labetalol 20 mg iv over 2 mins. Rept 40 mg iv bolus if
uncontrolled by 15 mins, then 0.5-2 mg/min infusion in D5 (max

Cardiology
300 mg/d), followed by 100-400 mg po bd
- Na Nitroprusside 0.25-10 microgram/kg/min iv infusion (50 mg
in 100 ml D5 = 500 microgram/ml, start with 10 ml/hr and titrate
to desired BP)
Check BP every 2 mins till stable, then every 30 mins
Protect from light by wrapping. Discard after every 12 hrs.
Esp good for acute LV failure, rapid onset of action.
Do not give in pregnancy or for > 48 hrs (risk of thiocyanide
intoxication
- Hydralazine 5-10 mg slow iv over 20 mins, repeat q 30 mins or iv
infusion at 200-300 microgram/min and titrate, then 10-100 mg
po qid (avoid in AMI, dissecting aneurysm)
- Phentolamine 5-10 mg iv bolus, repeat 10-20 mins prn (for
catecholamine crisis)
 C 28

9. Notes on specific clinical conditions

- APO -Nitroprusside/nitroglycerin + loop diuretic, avoid
diazoxide/hydralazine (increase cardiac work) or Labetalol &
Beta-blocker in LV dysfunction
- Angina pectoris or AMI - Nitroglycerin, nitroprusside, labetalol,
calcium blocker
(Diazoxide or hydralazine contraindicated)
- Increase in sympathetic activity (clonidine withdrawal,
phaeochromocytoma, autonomic dysfunction (GB Syndrome/post
spinal cord injury), sympathomimetic drugs
(phenylpropanolamine, cocaine, amphetamines, MAOI or
phencyclidine + tyramine containing foods)  Phentolamine,
labetalol or nitroprusside
Beta-blocker is contraindicated (further rise in BP due to
nopposed alpha-adrenergic vasoconstriction)
- Aortic dissection - aim: ↓systolic pressure to 100-120mmHg and
Cardiology

↓cardiac contractility, nitroprusside + labetalol / propanolol IV

- Pregnancy - IV hydralazine (pre-eclampsia or pre-existent HT),
Nicardipine / labetalol , no Nitroprusside (cyanide intoxication)
or ACEI

10. Look for causes of HT crisis, e.g. renal artery stenosis

 C 29

AORTIC DISSECTION

Suspect in patients with chest, back or abdominal pain and presence of

unequal pulses (may be absent) or acute AR

Dx - CXR, ECG, CK, TnI or TnT

- Transthoracic (not sensitive) +/- Transoesophageal echo
- Urgent Dynamic CT scan, MRA & rarely aortogram

Mx

1. NPO, complete bed rest, iv line

2. Oxygen 35-40% or 4-6 L/min
3. Analgesics, e.g. morphine iv 2-5 mg
4. Book CCU or ICU bed for intensive monitoring of BP/P

Cardiology
(Arterial line on the arm with higher BP), ECG & I/O
5. Look for life-threatening complication – severe HT, cardiac
tamponade, massive haemorrhage, severe AR, myocardial, CNS or
renal ischaemia
6. Medical Management
- To stabilize the dissection, prevent rupture, and minimize
complication from dissection propagation
- It should be initiated even before the results of confirmatory
imaging studies available
- Therapeutic goals: reduction of systolic blood pressure to
100-120mmHg (mean 60-75mmHg), and target heart rate of
60-70/min
 C 30

Intravenous Labetalol
10mg ivi over 2 mins, followed by additional doses of 20-80mg
every 10-15 mins (up to max total dose of 300mg)
Maintenance infusion: 2mg/min, and titrating up to
5-20mg/min.

Intravenous sodium nitroprusside

Starting dose 0.25 microgram/kg/min, increase every 2 mins by
10 g/min, max dose 8 microgram/kg/min
- Diltiazem and verapamil are acceptable alternatives when
beta-blockers are contraindicated (e.g. COAD)
(Avoid hydralazine or diazoxide as they produce reflex
stimulation of ventricle and increase rate of rise of aortic
pressure)

7. Start oral treatment unless surgery is considered

Cardiology

8. Contact cardiothoracic surgeon for all proximal dissection and

complicated distal dissection, e.g. shock, renal artery involvement,
haemoperitoneum, limbs or visceral ischaemia, periaortic or
mediastinal haematoma or haemoperitoneum (endovascular stent
graft is an evolving technique in complicated type B dissection with
high surgical risk).
Intramural hematoma should be managed as a classical case of
dissection.
 C 31

PULMONARY EMBOLISM

Investigations
Clotting time, INR, aPTT, ABG, D-dimer
CXR (usu. normal, pleural effusion, focal oligaemia, peripheral wedge)
ECG (sinus tachycardia, S1Q3T3, RBBB, RAD, P pulmonale)
TTE +/- TEE; lower limb Doppler (up to 50% -ve in PE)
CT pulmonary angiography (CTPA) or Spiral CT scan (sensitivity 91%,
specificity 78%)
Ventilation-Perfusion scan (if high probability: sensitivity 41%,
specificity 97%)

Treatment
1. Establish central venous access; oxygen 35-40% or 4-6 L/min.
2. Analgesics e.g. morphine iv 2-5 mg.
3. a) Haemodynamically insignificant

Cardiology
 Unfractionated heparin 5000 units iv bolus, then 500-1500
units/hr to keep aPTT 1.5-2.5X control or
Fraxiparine 0.4 ml sc q12h or enoxaparin 1 mg/kg q12h
 Start warfarin on Day 2 to 3: - 5 mg daily for 2 days, then 2 mg
daily on 3rd day, adjust dose to keep INR 1.5-2.5 x control.
Discontinue heparin on Day 7-10.
b) Haemodynamically significant or evidence of dilated RV or
dysfunction (no C/I to thrombolytic)
 Book ICU/CCU,
 Streptokinase 0.25 megaunit iv over 30 mins, then 0.1
megaunit/hr for 24 hrs; or r-tPA 100 mg iv over 2 hours
followed by heparin infusion 500-1500 units/hr to keep aPTT
1.5-2.5 x control
 Consider surgical embolectomy if condition continues to
deteriorate, or IVC filter if PE occurred while on warfarin, or
recurrent PE, mechanical ventilation in profound hypoxic
patient.
 C 32
Additional notes from Medical Oncology:
For PE in cancer patients, the duration of long term anticoagulation,
if not contraindicated, is at least 6 months AND preferably continued
beyond 6 months for those with active cancer or receiving
chemotherapy (ASCO guideline 2013 update). LMWH is preferred
over warfarin in malignancy-related thrombosis (if CrCl > 30
ml/min) for its lower rate of recurrent thromboembolism and less
drug interaction with systemic therapy. Both have similar bleeding
risks.
Cardiology
 C 33

CARDIAC TAMPONADE
Common causes:
- Neoplastic
- Pericarditis (infective or non-infective)
- Uraemia
- Cardiac instrumentation / trauma
- Acute pericarditis treated with anticoagulants
Diagnosis: - High index of suspicion (in acute case as little as 200ml of
effusion can result in tamponade)
Signs & symptoms:
- Tachypnoea, tachycardia, small pulse volume, pulsus paradoxus
- Raised JVP with prominent x descent, Kussmaul’s sign
- Absent apex impulse, faint heart sound, hypotension, clear chest
Investigation:
1. ECG: Low voltage, tachycardia, electrical alternans
2. CXR: enlarged heart silhouette (when >250ml), clear lung fields

Cardiology
3. Echo: RA, RV or LA collapse, distended IVC, tricuspid flow
increases & mitral flow decreases during inspiration
Management:
1. Expand intravascular volume - D5 or NS or plasma, full rate if in
shock
2. Pericardiocentesis with echo guidance – apical or subcostal
approach, risk of damaging epicardial coronary artery or cardiac
perforation
3. Open drainage under LA/GA
- permit pericardial biopsy
(Watch out for recurrent tamponade due to catheter blockage or
reaccumulation)

Treating tamponade as heart failure with diuretics, ACEI and

vasodilators can be lethal!
 C 34
Additional notes from Medical Oncology:
For patients with malignant pericardial effusion resulting in cardiac
tamponade stabilized by urgent pericardial drainage, please consult
oncologist to determine whether they could be benefited from surgical
pericardiectomy (pericardial window) and to plan the subsequent
oncological intervention for underlying disease control.
Cardiology
 C 35

ANTIBIOTIC PROPHYLAXIS FOR

INFECTIVE ENDOCARDITIS
1. Procedures to dental, oral, respiratory tract or infected skin/skin
structure, musculoskeletal tissue in patients at highest risk or adverse
outcome in case infective endocarditis developed
a) Amoxicillin 2 grams po 1 hr before or
b) Ampicillin 2 grams im/iv within 30 mins before or
c) # Clindamycin 600 mg or *Cephalexin 2 grams or
#Azithromycin/Clarithromycin 500 mg po 1 hr before or
d) # Clindamycin 600 mg im/iv or *Cefazolin 1 gram im/iv within 30
mins before procedure.
# History of allergy to ampicillin/amoxicillin.
*Avoid cephalosporin if allergic to penicillin group of antibiotics.

2. Genitourinary/Gastrointestinal Procedure

Cardiology
- Antibiotic prophylaxis solely to prevent infective endocarditis is not
recommended for GU or GI tract procedures.
- Antibiotic treatment to eradicate enterococcal infection or
colonization is indicated in high risk patients for infective
endocarditis undergoing GU or GI procedure.

High risk category:

- Prosthetic valves
- Previous infective endocarditis
- Cardiac transplant patients with valvulopathy
- Unrepaired cyanotic CHD, including palliative shunts and conduits
- Completely repaired CHD with prosthetic material or device,
whether placed by surgery or by catheter intervention, during the
first 6 months after the procedure†
- Repaired CHD with residual defects at the site or adjacent to the site
of a prosthetic patch or prosthetic device (which inhibit
endothelialization)
(Reference: Wilson W et al. Circulation 2007;116(15):1736-54)
 C 36

PERIOPERATIVE CARDIOVASCULAR
EVALUATION FOR NON-CARDIAC SURGERY

Basic evaluation by hx (assess functional capacity), P/E & review of ECG

Clinical predictors of increased perioperative CV risk (MI, CHF, death)
A) Active cardiac conditions mandate intensive Mx (may delay or
cancel OT unless emergent)
 Unstable coronary syndrome – recent (<30 days) or AMI with
evidence of important ischaemic risk by symptom or
non-invasive test, Canadian class III or IV angina
 Decompensated CHF.
 Significant arrhythmias – high grade AV block, symptomatic
ventricular arrhythmia in presence of underlying heart disease,
supraventricular arrhythmia with uncontrolled ventricular rate.
 Severe valvular disease e.g. severe AS or symptomatic MS.
B) Clinical risk factors (enhanced risk, need careful assessment of
Cardiology

current status)
 History of ischaemic heart disease
 History of compensated or prior CHF
 DM
 Renal impairment
C) Minor predictors (not proven to independently increase risk)
 Advanced age, abnormal ECG (LVH, LBBB, ST-T abn),
rhythm other than sinus
 Low functional capacity, hx of stroke, uncontrolled systemic HT
Cardiac risk stratification for noncardiac surgical procedures (If
the patient has risk factors for stable coronary artery disease,
estimate the perioperative risk for MACE [major adverse cardiac
events] by the combined clinical/surgical risk score
[http://www.surgicalriskcalculator.com])
A) Low risk (<1%)
B) Elevated risk (1%)
 C 37
Stepwise approach to preoperative cardiac assessment for patients with
known or risk factors for coronary artery disease

Yes
Need for emergency Clinical risk stratification
Step 1 non-cardiac OT
and proceed to surgery

- No

Acute coronary Yes Evaluate and treat

Step 2 according to
syndrome
guideline-directed medical
therapy

Cardiology
No
Estimate perioperative risk
Step 3 of MACE based on Elevated risk (1%)
combined clinical/surgical Step 5
risk socre

Step 4 Low risk (<1%) No further tests

Proceed to surgery
 C 38

Yes
Moderate or greater (4 No further tests
Step 5 METS) functional capacity
Proceed to surgery

No

Poor or unknown
Step 6
functional capacity (<4 Yes Pharmacologic stress
METS). testing
Will further testing impact
decision making OR
Cardiology

preoperative care?

normal abnormal
No

Proceed to surgery
Step 7 according to Coronary revascularization
guideline-directed medical according to existing
therapy OR alternative clinical practice guidelines
strategies (non-invasive
treatment, palliation)
 C 39

Algorithm for antiplatelet management in patients with coronary

stenting and non-cardiac surgery

Stent implantation Yes Yes Delay surgery until after

Elective surgery
≤4-6 weeks optimal period
(BMS: 30d; DES: 365d)
No

No Continue DAPT unless

risk of bleeding > risk of
stent thrombosis

DES 30d but ≤365d

Yes No

Cardiology
Risk of surgical delay > Does surgery demand
risk of DES thrombosis discontinuation of P2Y12
inhibitor?
Yes No

Yes
No
Proceed to surgery Delay surgery until after
after 180d optimal period
(BMS: 30d; DES: 365d)

Continue aspirin and restart

P2Y12 inhibitor ASAP Continue current DAPT
regimen
 C 40

Disease-specific approach
1) Hypertension
 Control of BP preoperatively reduces perioperative ischaemia
 Evaluate severity, chronicity of HT and exclude secondary HT
 Mild to mod. HT with no metabolic or CV abn. – no evidence that it is
beneficial to delay surgery
 Anti-HT drug continued during perioperative period
 Avoid withdrawal of beta-blocker
 Severe HT (DBP >110 or SBP >180)
elective surgery – for better control first
urgent surgery - use rapid-acting drug to control (esp. beta-blocker)

2) Cardiomyopathy & heart failure

 Pre-op assessment of LV function to quantify severity of systolic and
diastolic dysfunction (affect peri-op fluid Mx)
 HOCM avoid reduction of blood volume, decreasein systemic vascular
Cardiology

resistance or decrease in venous capacitance, avoid catecholamines

3) Valvular heart disease

 Antibiotic prophylaxis
 AS - postpone elective noncardiac surgery (mortality risk around 10%)
in severe & symptomatic AS. Need AVR or valvuloplasty
 AR - careful volume control and afterload reduction (vasodilators),
avoid bradycardia
 MS - mild or mod  ensure control of HR, severe  consider PTMC
or surgery before high risk surgery
 MR - afterload reduction & diuretic to stabilize haemodynamics before
high risk surgery

4) Prosthetic valve
 Minimal invasive procedures – reduce INR to subtherapeutic range (e.g.
INR <1.3), resume normal dose immediately following the procedure
 Assess risk & benefit of ↓anticoagulation Vs peri-op heparin (if both
risk of bleeding on anticoagulation & risk of thromboembolism off
anticoagulation are high)
 C 41

5) Arrhythmia
 Search for cardiopul. Ds., drug toxicity, metabolic derangement
 High grade AV block – pacing
 Intravent. conduction delays and no hx of advanced heart block or
symptoms – rarely progress to complete heart block
 AF - if on warfarin, may discontinue for few days; give FFP if rapid
reversal of drug effect is necessary
 Vent. arrhythmia
Simple or complex PVC or Nonsustained VT – usu require no Rx except
myocardial ischaemia or moderate to severe LV dysfunction is present
Sustained or symptomatic VT – suppressed preoperatively with lignocaine,
procainamide or amiodarone.

6) Permanent pacemaker
 Determine underlying rhythm, interrogate devices to determine its
threshold, settings and battery status
 If the pacemaker in rate-responsive mode  inactivated

Cardiology
 programmed to AOO, VOO or DOO mode prevents unwanted
inhibition of pacing
 electrocautery should be avoided if possible; keep as far as possible
from the pacemaker if used

7) ICD or antitachycardia devices

 programmed “OFF’ immediately before surgery & “ON’ again post-op
to prevent unwanted discharge
 for inappropriate therapy from ICD, suspend ICD function by placing a
ring magnet on the device (may not work for all ICD devices)
VF/unstable VT – if inappropriate therapy from ICD & external
cardioversion is required, paddles preferably >12cm from the device.
 C 42

Perioperative beta blocker therapy

1. Beta blockers should be continued in patients undergoing surgery who have

been on beta blockers chronically.

2. In patients with intermediate or high risk myocardial ischaemia noted in

preoperative risk stratification tests, it may be reasonable to begin preoperative
beta blockers.

3. In patients with 3 or more risk factors (e.g. DM, HF, coronary artery disease,
renal insufficiency, CVA), it may be reasonable to begin beta blockers before
surgery.

4. In patients in whom beta blocker therapy is initiated, it may be reasonable to

begin the medication long enough in advance to assess safety and tolerability,
preferably > one day before surgery
Cardiology

(Reference : Fleisher LA et al. 2014 ACC/AHA guideline on

perioperative cardiovascular evaluation and management of patients
undergoing noncardiac surgery. JACC 2014;64(22):e77-137.)
Endocrinology

Endocrinology
 E 1

DIABETIC KETOACIDOSIS (DKA)

Diagnostic criteria: Plasma glucose > 14 mmol/L, arterial pH < 7.3, plasma
bicarbonate < 15 mmol/L, (high anion gap) and moderate ketonuria or
ketonemia (or high serum beta-hydroxybutyrate BHBA.)
Initial Hour Subsequent Hours
Ix Urine & Blood glucose Hourly urine and blood glucose
Urine + plasma ketones or
BAHA Na, K, urea, AG ( till blood glucose <14
mmol/L)
Na, K, PO4, Mg,
Anion gap (AG) Repeat ABG if indicated
Urea, Creatinine, Hb (intensive monitoring of electrolytes and
Arterial blood gas (ABG) acid/base is crucial in the first 24-48 hours)

If indicated: N.B. Urine ketone may not be very useful for

CXR, ECG monitoring as it fails to measure BAHA
Blood & urine culture and
sensitivity
Urine & serum osmolality
PT, APTT
(look for precipitating
causes)

Endocrinology
Parameters to Hourly BP/pulse, respiratory rate, conscious level, urine output, central
be monitored venous pressure (CVP)
2-hourly temperature

Ancillary Aspirate stomach if patient unconscious or vomiting

Measures (protect airway with cuffed endotracheal tube if necessary)
Catheterize bladder and set CVP as indicated
Give antibiotics if evidence of infection
Treat hypotension and circulatory failure
 E2

Rx Initial Hours Subsequent Hours

Hydration 1-2 litre 0.9% 1 litre/hour or 2 hours as appropriate
saline (NS) When serum Na > 150 mmol/L, use 0.45% NS
(modify in patients with impaired renal
function). Fluid in first 12 hrs should not
exceed 10% BW, watch for fluid overload in
elderly. When blood glucose  14 mmol/L,
change to D5
Insulin Regular human insulin Regular human insulin iv infusion 0.1
0.15 unit/kg as IV bolus, unit/kg/hr.
followed by infusion Aim at decreasing plasma glucose by 3-4
(preferably via insulin mmol/L per hour, double insulin dose to
pump) achieve this rate of decrease in blood glucose
if necessary.
When BG  14 mmol/L, change to D5 and
decrease dose of insulin to 0.05-0.1 unit/kg/hr
or give 5-10 units sc q4h, adjusting dose of
insulin to maintain blood glucose between
8-12 mmol/L.  monitoring to q2h-q4h
Change to maintenance insulin when AG
normal and normal diet is resumed
K 10 - 20 mmol/hr Continue 10-20 mmol/hr, change if
- K < 4 mmol/L,  to 30 mmol/hr
Endocrinology

- K < 3 mmol/L,  to 40 mmol/hr

- K > 5.5 mmol/L, stop K infusion
- K > 5 mmol/L,  to 8 mmol/hr
Aim at maintaining serum K between 4-5
mmol/L
NaHCO3 If pH between 6.9-7.0, give 50 mmol NaHCO3 in 1 hr.
If pH < 6.9, give 100 mmol NaHCO3 in 2 hrs.
Recheck ABG after infusion, repeat every 2 hrs until pH > 7.0.
Monitor serum K when giving NaHCO3.
 E 3

DIABETIC HYPEROSMOLAR
HYPERGLYCEMIC STATES

Diagnostic criteria: blood glucose > 33 mmol/L (arbitrary), arterial pH >

7.3, serum bicarbonate > 15 mmol/L, effective serum osmolality ((2x
measured Na) + glucose) > 320 mOsm/kg H2O, and mild ketonuria or
ketonemia, usually in association with change in mental state.

1. Management principles are similar to DKA

2. Fluid replacement is of paramount importance as patient is usually
very dehydrated
3. If plasma sodium is high, use hypotonic saline
4. Watch out for heart failure (CVP usually required for elderly)
5. Serum urea is the best prognostic factor
6. Insulin requirement is usually less than that for DKA, watch out for
too rapid fall in blood glucose and overshot hypoglycaemia

Endocrinology
 E4

PERIOPERATIVE MANAGEMENT
OF DIABETES MELLITUS
1. Pre-operative Preparation
a. Screen for DM complications, check standing/lying BP and
resting pulse
b. Glucose, HbA1c, electrolytes, RFT, HCO3, urinalysis, ECG
c. Admit 1-2 days before major OT for DM control
d. Aim at blood sugar of 5-11 mmol/L before operation
e. Well controlled patients: omit insulin / OHA on day of OT
f. Poorly controlled patients:
- Stabilise with insulin (+/-dextrose) drip for emergency OT:
Blood glucose (mmol/L) Actrapid HM Fluid
< 20 1-2 units/hr D5 q4-6h
> 20 4-10 units/hr NS q2-4h
(Crude guide only, monitor hstix q1h and adjust insulin dose, aim to
bring down glucose by 4-5 mmol/L/hr to within 5-10 mmol/L)
* May need to add K in insulin-dextrose drip
* Watch out for electrolyte disorders
* May use sc regular insulin for stabilisation if surgery elective
Endocrinology

2. Day of Operation
a. Schedule the case early in the morning
b. Check hstix and blood sugar pre-op, if blood glucose
> 11 mmol/L, postpone for a few hrs till better control if possible
c. For major Surgery
• For patients on insulin or high dose of OHA, start
dextrose-insulin-K (DKI) infusion at least 2 hrs
pre-operatively or after fasting:
- 6-8 units Actrapid HM + 10-20 mmoles K in 500 ml D5,
q4-6h (about 1 u insulin for 4 gm of glucose) (Flush iv line
with 40 ml DKI solution before connecting to patient)
- Monitor hstix q1h and adjust insulin, then q4h for 24 hrs
(usual requirement 1-3 units Actrapid/hour)
- Monitor K at 2-4 hours and adjust dose as required to
maintain serum K within normal range
 E 5
- Give any other fluid needed as dextrose-free solutions
• Patients with mild DM (diet alone or low dose of OHA)
- D5 500 ml q4h alone (usually do not require insulin)
- Monitor hstix and K as above, may need insulin and K
d. For Minor Surgery
• May continue usual OHA / diet on day of surgery
• Patients exposed to iodinated radiocontrast dyes, withhold
metformin for 48 hours post-op and restart only after
documentation of normal serum creatinine
• For well-controlled patients on insulin:
Either:
- Omit morning short-acting insulin
- Give 2/3 of usual dose of intermediate-acting insulin am,
and the remaining 1/3 when patient can eat
Or: (safer)
- Use DKI infusion till diet resumed. Then give 1/3 to 1/2
of usual intermediate-acting insulin
• For poorly-controlled patients on insulin:
- Control first, use insulin or DKI infusion for urgent OT

3. Post-operative Care

Endocrinology
a. ECG (serially for 3 days if patient is at high risk of IHD)
b. Monitor electrolytes and glucose q6h
c. Continue DKI infusion till patient is clinically stable, then
resume regular insulin (give first dose of sc insulin 30 minutes
before disconnecting iv insulin) / OHA when patient can eat
normally
d. In case of nasogastric tube feeding, give insulin (infusion or sc)
according to feeding schedule
 E6

INSULIN THERAPY FOR DM CONTROL

Common insulin regimes for DM control (Ensure dietary compliance
before dose adjustments):

1. For insulin-requiring type 2 DM

(May consider combination therapy (Insulin + OHA) for patients
with insulin reserve)
a. Fasting Glycaemia alone
- Give bed-time intermediate-acting insulin, start with 0.1- 0.2
unit/kg
- Continue metformin and other oral hypoglycemic agents if
appropriate
- Consider adding DPP4 inhibitor as adjunctive to insulin to
optimise control
b. Daytime Glycaemia
- Start with intermediate-acting or pre-mixed insulin 30 mins
before breakfast (AM insulin) and before dinner (PM insulin)
(Daily dose 0.2-0.5 unit/kg in ratio of 2:1 or 1:1)
- Adjust dosage according to fasting and post-meal h’stix
- If fasting glucose persistently high, check blood sugar at
Endocrinology

mid-night:
- If hypoglycaemic, reduce pre-dinner dose by 5-10%
(Somogyi phenomenon)
- If hyperglycaemic, may need to consider MDI (multiple dose
insulin regimes)

- Consult endocrinologist for insulin analogues in difficult cases with wide

glucose fluctuation. (N.B. Long-acting insulin analogues Glargine and Detemir
are indicated if patients have sub-optimal glycemic control on NPH with
frequent documented hypoglycaemia or sub-optimal glycemic control on NPH
with established CHD/PVD/Stroke or renal (eGFR<60ml/min) complications
with reasonable QoL. Short-acting insulin analogues Aspart, Gluisine and Lispro
are indicated if patients have brittle or poorly control DM despite multi-dose
conventional short acting insulin regimen and good compliance)
 E 7
2. For type 1 DM
- Start with twice daily or multiple daily dose regimes
- Consider use of Pens for convenience and ease of administration
- Start with 0.5 unit/kg/d. Adjust the following day according to
hstix (tds and nocte)

a. For twice daily regimes:

- Give 2/3 or half of total daily insulin dose pre-breakfast
and 1/3 or half pre-dinner in the evening (30 mins before
meals) in the form of pre-mixed insulin
- Advise on “multiple small meals” to avoid late afternoon
and nocturnal hypoglycaemia
b. For multiple daily dose regimes:
- Give 40-60% total daily dose as intermediate-acting
insulin before bed-time to satisfy basal needs. Adjust
dose according to fasting glucose.
- Give the remaining 40-60% as regular insulin, divided into
3 roughly equal doses pre-prandially (slightly higher AM
dose to cover for Dawn Phenomenon, and slightly higher
dose before main meal of the day)
c. For difficult cases, consult endocrinologist for considering

Endocrinology
insulin analogues or continuous subcutaneous insulin
delivered via a pump

Sliding scale, if employed at all, must be used judiciously:

1. Hstix must be performed as scheduled
2. Dose adjustment should take into consideration factors
that may affect patient’s insulin resistance
3. It should not be used for more than 1-2 days
 E8

HYPOGLYCAEMIA
1. Treatment
a. D50 40 cc iv stat, follow with D10 drip
b. Glucagon 1 mg IMI (avoid in suspected phaeochromocytoma)
or oral glucose (after airway protection) if cannot establish iv
line
c. Monitor blood glucose and h’stix every 1-2 hrs till stable
d. Duration of observation depends on R/LFT and type of
insulin/drug (in cases of overdose)

2. Tests for Hypoglycaemia

a. Prolonged OGTT
 To document reactive hypoglycaemia, limited use
 Overnight fast
 Give 75 g anhydrous glucose po
 Check plasma glucose and insulin at 60 min intervals for 5
hrs and when symptomatic
Endocrinology

b. Prolonged Fasting Test

 Hospitalise patient, place near nurse station
 Fast for maximum of 72 hrs
 At 72 hrs, vigorous exercise for 20 mins (if still no
hypoglycemia)
 H’stix q4h and when symptomatic
 Blood sugar, insulin, C-peptide at 0, 24, 48 and 72 hrs and
when symptomatic or h’stix < 3.0 mmol/L
 Terminate test if blood sugar confirmed to be < 3.0 mmol/L
 Consider to check urine hypoglycemic agents level in highly
suspected cases.
 E 9

THYROID STORM

Note: The following regimen is also applicable to patients with

uncontrolled thyrotoxicosis undergoing emergency operation.

1. Close monitoring: often need CVP, Swan-Ganz, cardiac monitor.

ICU care if possible
2. Hyperthermia : paracetamol (not salicylate), physical cooling
Dehydration : iv fluid (2-4 L/d)
iv Glucose, iv vitamin (esp. thiamine)
Supportive : O2 , digoxin / diuretics if CHF/AF  inotropes
Treat precipitating factors and/or co-existing illness
3. Propylthiouracil 150-200 mg q46h po / via NG tube.
Hydrocortisone 200 mg stat iv then 100 mg q6-8h
-blockers (exclude asthma / COAD or frank CHF): Propranolol
40-80 mg q4-6h po/NG or Propranolol/Betaloc 1-10 mg iv over 15
min every several hrs
If -blockers contraindicated, consider diltiazem 60-120 mg q8h as
alternative
4. 1 hour later, use iodide to block hormone release

Endocrinology
a. 6-8 drops Lugol’s solution / SSKI po q6-8h (0.2 g/d)
b. NaI continuous iv 0.5-1 g q12h or
c. Ipodate (Oragrafin) po 1-3 g/d
5. Consider LiCO3 250 mg q6h to achieve Li level 0.6-1.0 mmol/L if
ATD is contraindicated
6. Consider plasmapheresis and charcoal haemoperfusion for
desperate cases
 E 10

MYXOEDEMA COMA
1. Treatment of precipitating causes

2. Correct fluid and electrolytes, correct hypoglycaemia with D10

3. NS 200 - 300 cc/hr  vasopressors

4. Maintain body temperature

5. T4 200-500 micrograms po stat, then 100-200 micrograms po or

T3 20-40 micrograms stat, then 20 micrograms q8h po

6. Consider 5–20 micrograms iv T3 twice daily if oral route not

possible

7. Hydrocortisone 100 mg q6h iv

Endocrinology

PHAEOCHROMOCYTOMA (HT crisis)

1. Phentolamine 0.5-5 mg iv, then 2-20 micrograms/kg/hr infusion or
Nitroprusside infusion 0.3-8 micrograms/kg/min
2. Volume repletion
3. Propranolol if tachycardia (only after adequate -blockade)
4. Labetalol infusion at 1-2 mg/min (max 200 mg).
5. ICU monitoring
 E 11

ADDISONIAN CRISIS
1. Investigation:
a. RFT, electrolytes, glucose
b. Spot cortisol (during stress)  ACTH
c. Normal dose (250 micrograms) short synacthen test (not required
if already in stress)#
d. May consider low dose (1 microgram) short synacthen test if
secondary hypocortisolism is suspected@
e. Look out for the cause(s)

2. Treatment
Treat on clinical suspicion, do not wait for cortisol results
a. Hydrocortisone 100 mg iv stat, then q6h (may consider imi or
continuous iv infusion at 200 mg per day if no improvement)
b.  9-fludrocortisone 0.05-0.2 mg daily po, titrate to normalise K
and BP
c. Correct electrolytes
d. 4 litres of D5/NS at 500-1000 ml/hr, then 200-300 ml/hr, watch
out for fluid overload

Endocrinology
e. May use dexamethasone 4 mg iv/im q12h (will not interfere with
cortisol assays)

3. Relative Potencies of different Steroids*

Glucocorticoid Mineralocorticoid Equivalent
action action doses
Cortisone 0.8 0.8 25 mg
Hydrocortisone 1 1 20 mg
Prednisone 4 0.6 5 mg
Prednisolone 4 0.6 5 mg
Methylprednisolone 5 0.5 4 mg
Dexamethasone 25-30 0 0.75 mg
Betamethasone 25-30 0 0.75 mg
* Different in different tissues
 E 12
4. Steroid cover for surgery / trauma
- Indications:
 Any patient given supraphysiological doses of
glucocorticoids (>prednisolone 7.5 mg daily) for >2 wks in
the past year
 Patients currently on steroids, whatever the dose
 Suspected adrenal or pituitary insufficiency
a. Major Surgery
 Hydrocortisone 100 mg iv on call to OT room
 Hydrocortisone 50 mg iv in recovery room, then 50 mg iv
q6h + K supplement for 24 hrs or continuous iv infusion of
200 mg hydrocortisone per 24 hours
 Post-operative course smooth: Decrease Hydrocortisone to
25 mg iv q6h on D2, then taper to maintenance dose over
3-4 days
 Post-operative course complicated by sepsis, hypotension
etc: Maintain Hydrocortisone at 100 mg iv q6h (or 200
mg iv infusion per day) till stable
 Ensure adequate fluids and monitor electrolytes
b. Minor Surgery
 Hydrocortisone 100 mg iv one dose
 Do not interrupt maintenance therapy
Endocrinology

#
Normal dose short synacthen test
250 micrograms Synacthen iv/im as bolus
Blood for cortisol at 0, 30, 60 mins. Can perform at any
time of the day
Normal: Peak cortisol level > 550 nmol/L, Abnormal: <
400 nmol/L, Borderline: 400 – 550 nmol/L (depends on
type of cortisol assay)
@
Low dose short synacthen test
1 microgram Synacthen (mix 250 μg Synacthen into 1 pint
NS and withdraw 2 ml) IV as bolus
Blood for cortisol at 0, 30 mins.. Can perform at any time
of the day.
 E 13
Normal: Peak cortisol level > 550 nmol/L, Abnormal: <
400 nmol/L, Borderline: 400 – 550 nmol/L (depends on
type of cortisol assay)
May need to confirm by other tests (insulin tolerance test
or glucagon test) if borderline results

Endocrinology
 E 14

ACUTE POST-OPERATIVE /
POST-TRAUMATIC DIABETES INSIPIDUS

1. Remember possibility of a Triphasic pattern:

Phase I : Transient DI, duration hrs to days
Phase II : Antidiuresis, duration 2-14 days
Phase III : Return of DI (may be permanent)

2. Mx
a. Monitor I/O, BW, serum sodium and urine osmolarity closely
(q4h initially, then daily)
b. Able to drink, thirst sensation intact and fully conscious: Oral
hydration, allow patient to drink as thirst dictates
c. Impaired consciousness and thirst sensation:
 Fluid replacement as D5 or ½ : ½ solution (Calculate
volume needed by adding 12.5 ml/kg/d of insensible loss
to volume of urine)
 DDAVP 1-4 micrograms (0.5-1.0 ml) q12-24h sc/iv
Allow some polyuria to return before next dose
Give each successive dose only if urine volume > 200
Endocrinology

ml/hr in successive hours

3. Stable cases
Give oral DDAVP 100 - 200 micrograms bd to tds (tablet) or
60-120 micrograms bd to tds (lyophilisate) to maintain urine
output of 1 – 2 litres/day. Advice drug holiday if appropriate.
 E 15

PITUITARY APOPLEXY
1. Definite diagnosis depends on CT / MRI
2. Surgical decompression under steroid cover if
- signs of increased intracranial pressure
- change in conscious state
- evidence of compression on neighbouring structures

Endocrinology
 Gastroenterology
and Hepatology
Gastroenterology

Hepatology
&
 G 1

ACUTE LIVER FAILURE

Definition
 A severe liver injury (coagulopathy with INR ≥ 1.5)
 With onset of hepatic encephalopathy within 8 weeks of the first
symptoms (up to 26 weeks in some definitions)
 In the absence of pre-existing liver disease

Classification
Hyperacute Acute Subacute
Jaundice to 0 to 1 week >1 to 4 >4 to 26 weeks
encephalopathy weeks
interval
Prognosis (Survival) Moderate Poor Poor
Cerebral oedema Common Common Infrequent
PT Prolonged Prolonged Less Prolonged
Bilirubin Least raised Raised Raised

Search for aetiology and assess severity of acute liver failure (ALF)
 History – medications, herbal medicine, Amanita phylloides intake,
Ecstasy use
 CBP/ Clotting/ LRFT/ ABG/ Lactate
 Hepatitis (A, B, D, E) serology, HBV DNA
 Blood ammonia level (high levels are predictive of complications

Gastroenterology
and Hepatology
and increased mortality)
 Autoimmune markers (ANA, ASMA, anti-LKM1)
 Metabolic markers (Caeruloplasmin for patients < 50 yrs old)
 Toxicology screening especially paracetamol level
 Anti-HIV (informed consent) if liver transplant considered
 Review herbal formula by Poison Information Centre (Tel:
27722211, Fax: 22051890) or identification of herbal medicine by
Toxic Reference Laboratory (Tel: 29901941, Fax: 29901942)
 Transjugular liver biopsy in selected cases
 G2
Management
 Close monitoring, preferably in ICU
 Nutritional support: 1 to 1.5g enteral protein/kg/day (lower level for
patients with worsening hyperammonaemia or at high risk for
intracranial hypertension)
 Avoid use of paracetamol
 Consider N-acetylcysteine (NAC) for both paracetamol- and
non-paracetamol-related ALF.
Alternative NAC regime for non-paracetamol ALF:
Loading dose: NAC 150mg/kg/hr in D5 over 1 hour,
Then 12.5mg/kg/hr in D5 over 4 hours,
Then 6.25mg/kg/hr in D5 infusion for 67 hours (i.e. 72 hrs in total)
 Start nucleos(t)ide analogues for HBV-related ALF, particularly for
transplant candidates
 Liaise with QMH Liver Transplantation Centre if indicated

Hepatic encephalopathy
Grade I/II
 Consider liver transplantation
 CT brain to exclude other causes of altered consciousness
 Avoid stimulation/ sedation
 Lactulose

Grade III/IV
Gastroenterology
and Hepatology

 Early endotracheal intubation and mechanical ventilation

 Choice of sedation: Propofol (small dose adequate; long T½ in
patient with hepatic failure). Avoid neuromuscular blockade as it
may mask clinical evidence of seizure activity
 Elevate head of patient ~ 30, limit neck rotation or flexion
 Prophylactic anti-convulsant not recommended. Immediate control
of seizure with minimal doses of benzodiazepine. Control seizure
activity with phenytoin
 Consider ICP monitoring especially if patient listed for liver
transplant with high risk of cerebral oedema
 G 3
Intracranial hypertension
1. Mannitol
 Dose: 0.5-1g/kg IV bolus, can repeat once / twice Q4H if needed
 Stop if serum osmolality > 320 mosm/L
 Risk of volume overload in renal impairment and hypernatraemia
 Prophylactic use not recommended
 Use in conjunction with RRT in renal failure

2. Hyperventilation
 Indicated when increased ICP not controlled with mannitol
 Keep PaCO2 at 4 to 6 kPa
 Sustained hyperventilation should be avoided

3. Others (ICU setting preferred if available)

 Hypertonic saline solution and barbiturate for refractory intracranial
hypertension
 Therapeutic hypothermia (cooling to a core temperature of 32 to
34C)

Infection
 Screening for sepsis to detect bacterial and fungal infection
 Low threshold to start appropriate wide-spectrum anti-bacterial/
antifungal therapy as usual clinical signs of infection may be absent

Gastroenterology
and Hepatology
Coagulopathy and bleeding
 Spontaneous and clinically overt bleeding uncommon in ALF
 Variceal bleeding in the setting of ALF should raise suspicion of
Budd-Chiari syndrome
 Give prophylactic Pepcidine or PPI to reduced stress-related GIB
 Give Vitamin K1 10mg IV Q24H
 Replacement therapy for thrombocytopenia (< 50,000 – 700,000/
mm3) and/ or prolonged prothrombin time (INR ≥ 1.5) only in the
setting of haemorrhage or before invasive procedures
 G4
Haemodynamic/ Renal failure
 Fluid replacement for intravascular volume deficits (colloids
preferred)
 All solutions should contain dextrose to maintain euglycaemia
 Maintain mean arterial pressure (MAP) > 75 mmHg
 Use vasopressor (adrenaline/noradrenaline/dopamine) when fluid
replacement fails to maintain adequate MAP
 Assess adrenal function in patient requiring vasopressors
 Consider pulmonary artery catheterization in haemodynamically
unstable patient to ensure adequate volume replacement
 CVVH preferred for acute renal failure requiring dialysis

Considerations for liver transplantation

King’s College Hospital prognostic criteria
Paracetamol Non-paracetamol
pH < 7.3, or PT > 100 (INR > 6.5), or
All 3 criteria: Three out of 5 criteria:
1. PT > 100s 1. Age < 10 or > 40
(INR > 6.5) 2. Aetiology: Drug-induced,
2. Cr > 300 mol/L indeterminate
3. Grade III/ IV hepatic 3. Bilirubin > 300 mol/L
encephalopathy 4. Jaundice to coma interval > 7 days
5. PT > 50 (INR 3.5)
Gastroenterology
and Hepatology

Calculate MELD score for reference

Contraindications for liver transplantation

 HIV infection
 Active alcohol or substance abuse
 Systemic infections
 Life-limiting co-existing medical conditions: advanced heart, lung
or neurologic conditions.
 Uncontrolled psychiatric disorder
 Inability to comply with pre- and post-transplant regimens
 G 5

HEPATIC ENCEPHALOPATHY

Child-Pugh Grading of Severity of Chronic Liver Disease

Points: 1 2 3
Parameters:
Encephalopathy None I and II III and IV
Ascites Absent Mild Moderate
Bilirubin (umol/l) <35 35 – 50 >50
for PBC (umol/l) <70 70 – 170 >170
Albumin (g/l) >35 28 – 35 <28
Prothrombin time 1-3 4-6 >6
(sec prolonged)
Grades: A: 5-6 points, B: 7-9 points, C: 10-15 points

Grading (Grade 0-I: Covert HE; Grade II-IV: Overt HE)

0 Psychometric or neuropsychological alteration of tests
(psychometric, psychomotor or neurophysiological) without
clinical evidence of mental change
I Euphoria, mild confusion, mental slowness, shortened attention
span, slurred speech, disordered sleep
II Lethargy or apathy, disorientation, moderate confusion,
inappropriate behaviour, drowsiness
III Marked confusion, incoherent speech, somnolence or
semi-stupor, response to stimuli, bizarre behaviour

Gastroenterology
and Hepatology
IV Coma, initially responsive to noxious stimuli, later unresponsive

Management of hepatic encephalopathy in cirrhotic patients

- Initiate care for patients with altered consciousness
- Look for other causes of altered mental state

A. Identify and correct precipitating factors

 Watch out for infection, constipation, gastrointestinal bleeding,
diuretic overdose, electrolyte disorder. (other possible
precipitating factors: excess dietary intake of protein, vomiting,
 G6
large volume paracentesis, recent alcohol binge, vascular
occlusion and primary HCC)
 Avoid sedatives, alcohol, diuretic, hepatotoxic and nephrotoxic
drugs
 Correct electrolyte imbalance (azotaemia, hyponatraemia,
hypokalaemia, metabolic alkalosis/acidosis)

B. Treatment
 Tracheal intubation should be considered in patient with deep
encephalopathy
 Nutrition: In case of deep encephalopathy, oral intake should be
withheld 24-48hr and i.v. glucose should be provided until
improvement. Enteral nutrition by gastric tube can be started if
patients are unable to eat after this period. Protein intake begins
at a dose of 0.5g/kg/day, with progressive increase to
1.2-1.5g/kg/day. Vegetable and dairy sources are preferable to
animal protein. Liaise with dietitian if necessary.
 Oral formulation of branched chain amino acids (BCAA) may
provide better tolerated source of protein in patients with chronic
encephalopathy and dietary protein intolerance
 Lactulose ( oral / via nasogastric tube) 30-40 ml q8h and titrate
until 2-3 soft stools/day
 Antibiotics in suspected sepsis
 Consider referral for liver transplantation in selected cases –
Gastroenterology

recurrent intractable overt HE

and Hepatology
 G 7

ASCITES
A. Investigations
- Diagnostic paracentesis, USG abdomen, alpha-fetoprotein
B. Conservative Treatment (aim to reduce BW by 0.5 kg/day)
1. Low salt diet (2g/day)
2. Fluid restriction (1-1.5L/day) if dilutional hyponatremia Na
<120-125 mmol/L
3. Monitor input/output, body weight, urine sodium
4. Spironolactone starting at 50 mg daily (single morning dose)
alone or with Lasix 20 mg daily as combination therapy.
5. Increase the dose stepwise (maintaining the 100mg:40mg
ratio) every 5-7days to the maximum spironolactone
400mg/day and Lasix 160mg/day if no response (if weight
loss and natriuresis are inadequate)
6. Amiloride (10-40mg/day) can be substituted for
spironolactone in patients with tender gynaecomastia
7. Once ascites has largely resolved, dose of diuretics should be
reduced and discontinued later whatever possible.
8. All diuretics should be discontinued if there is severe
hyponatraemia <120 mmol/L, progressive renal failure,
worsening hepatic encephalopathy, or incapacitating muscle
cramps
- Lasix should be stopped if there is severe hypokalemia
(<3 mmol/L)

Gastroenterology
and Hepatology
- Spironolactone should be stopped if there is severe
hyperkalaemia (>6 mmol/L)
C. Therapeutic paracentesis can be used in refractory ascites
- Exclude spontaneous bacterial peritonitis before paracentesis
- Caution in patients with hypotension and raised serum
creatinine, monitor vital signs during paracentesis
- If >5L fluid removed, give IV albumin 6-8g per litre tapped
D. Consider TIPS in refractory ascites
E. Referral to liver transplant centre for potential candidate
 G8

GENERAL GUIDELINES FOR

CONSIDERATION OF ORTHOTOPIC LIVER
TRANSPLANTATION (OLT) IN CHRONIC
LIVER DISEASE OR HEPATOCELLULAR
CARCINOMA
Chronic liver disease and hepatocellular carcinoma
Patients who have an estimated survival of less than 80% chance after 1
year as a result of liver cirrhosis should be referred for consideration of
liver transplantation. If any of the following are present, it may be
appropriate to refer the patient:
A. Child-Pugh score 8 or above
B. Complications of cirrhosis
a. Refractory ascites or hydrothorax
b. Spontaneous bacterial peritonitis
c. Encephalopathy
d. Very poor cirrhosis related quality of life
e. Hepatorenal syndrome, hepatopulmonary syndrome, or
portopulmonary hypertension
f. Portal hypertensive bleeding not controlled by endoscopic
therapy or transjugular intra-hepatic porto-systemic shunt
C. For patients with unresectable hepatocellular carcinoma and those
with hepatocellular carcinoma and underlying cirrhosis
a. Solitary tumour of less than 5cm in diameter or those with
Gastroenterology
and Hepatology

up to 3 tumours (each of which should be < 3 cm)

b. For tumours beyond the above criteria, patients may still be
eligible for liver transplantation if
i. There is a potential living-related donor and
 G 9
ii. Single tumour not exceeding 6.5cm, or 2-3 lesions none
exceeding 4.5cm, with the total tumour diameter less
than 8cm

Acute liver failure/acute on chronic liver failure

These patients should be referred early to avoid delay in work-up
for potential liver transplantation if they have any of the
following criteria
 Those with rising INR (>2.0)
 Evidence of early hepatic encephalopathy

Relative contra-indications to liver transplantation

 Alcoholic patients with less than 6 months abstinence
 Extra-hepatic malignancy
 Severe/uncontrolled extra-hepatic infection
 Multi-system organ failure
 Significant cardiovascular, cerebrovascular, or pulmonary
disease
 Advanced age

If in doubt, discuss with the liver transplant team

Gastroenterology
and Hepatology
 G 10

VARICEAL HAEMORRHAGE

A. Initial Management (as in upper GI bleeding)

 maintain systolic BP at 90-100mmHg but avoid excessive volume
restitution (increase portal pressure  early rebleeding)
 restrictive blood transfusion, aim at Hb 7-8g/dl, haematocrit 21-24%
 correction of significant coagulopathy and thrombocytopenia may be
considered
 Routine use of NG tube is not recommended but it may be used in
cases of hepatic encephalopathy

B. Vasoactive agents should be initiated before endoscopy to patient with

suspected variceal bleeding and maintained for 2-5 days after
endoscopic treatment.
 Terlipressin* 2 mg IV bolus Q4H
 Octreotide 50 micrograms iv bolus, then 50 micrograms/hour IV
infusion
 Somatostatin 250 micrograms iv bolus, then 250 microgram/hour IV
infusion
* Beware of side-effects related to vasoconstriction such as bowel
ischaemia, hypertension, myocardial ischemia, peripheral
vascular ischaemia

C. IV thiamine for those with alcohol excess

D. Anti-encephalopathy regimen
 Correct fluid and electrolyte imbalances
Gastroenterology
and Hepatology

 Lactulose 10-20 ml q4-8H PO or via NG tube aims at 2-3 bowel

motions per day. It can be given as enema (300ml in 1L water)
retained for 1 hr with patient in Trendelenburg position

E. Prevention of sepsis
 Short-term (7d) prophylactic antibiotic: IV ciprofloxacin 400-500mg
bd (patients with preserved liver function), or IV ceftriaxone 1g/day
(patients with advanced cirrhosis or known quinolone-resistance), or
IV ertapenem 1g/day (patients with recent ESBL-Enterobacteriaceae
infection)
 G 11
F. Endoscopic treatment
 Upper endoscopy should be arranged as soon as possible after
admission once haemodynamic condition is stabilised (sBP
>70mmHg)
 Patients with altered mental state or massive bleeding should
undergo endotracheal intubation and mechanical ventilation prior to
endoscopy
 Esophageal variceal ligation (EVL) / sclerotherapy for oesophageal
varices; Tissue glue like N-butyl-cyanoacrylate injection for gastric
varices
 Vasoactive agents should be initated within 30 min after
confirmation of variceal bleeding if not given prior to endoscopy
 Proton-pump inhibitor (PPI) or sucralfate should be given for 2
weeks

G. Uncontrolled/recurrent variceal bleeding

 Recurrent bleeding should be managed by repeated endoscopy
 Refer to emergency surgery (port-systemic shunting,
devascularisation) or TIPS as salvage therapies for uncontrolled
bleeding
 Balloon tamponade should only be used as temporary measure (max
12-24 hr) until definite therapy is planned. If haemostasis is not
achieved, other therapeutic options should be considered

H. Prevention of rebleeding
 EVL combined with a non-selective beta-blocker* (NSBB) is
recommended as secondary prevention

Gastroenterology
and Hepatology
 Combined NSBB and isosorbide 5-mononitrate# are recommended if
patient is unsuitable for EVL

* NSBB (non-selective beta-blocker): propranolol, nadolol or carvedilol should start at

low dose and titrate up till 25% reduction in resting heart rate but not lower that 55
beats/min.
# Nitrate may have adverse effect on kidney function especially in patients aged over 50.
 G 12

UPPER GASTROINTESTINAL BLEEDING

A. Initial Management (Consider ICU if severe bleeding)
 Nil by mouth
 Insert large bore IV cannula
 Closely monitor BP, Pulse, I/O
 Risk stratification applying Blatchford score or Rockall score
 Blood transfusion when Hb<7g/dL (except for massive bleeding) and
fluid replacement as required
 Withhold anticoagulants and antiplatelet if possible. Weight against
the thrombotic risk of an individual patient before REVERSAL of
anticoagulation
 Cuffed ET tube to prevent aspiration if massive haematemesis or
suspected compromised respiratory or airway condition
 Nasogastric tube if massive haematemesis or signs suggestive of GI
obstruction
 Tranexamic acid is not recommended as insufficient evidence
 Pre-endoscopy IV proton-pump inhibitor (PPI) treatment is
recommended if early endoscopy (within 24 hours) cannot be arranged
 IV antibiotics in all cirrhotic patients with GI bleeding: IV Augmentin
1.2g Q8H/ IV levofloxacin 500mg Q24H (max 7d)
 Arrange early (within 24 hours) upper endoscopy after initial
stabilization
B. Indications for Emergency Endoscopy
 Haemodynamic shock
 Massive haematemesis/bloody NG aspirate
Gastroenterology

 Suspected gastroesophageal variceal bleeding

and Hepatology

C. Contraindications for Endoscopy

 Suspected intestinal perforation
 Unstable cardiac or pulmonary status
D. Post-endoscopy Management
 After endoscopic treatment of patients with actively bleeding ulcer,
ulcer with visible vessel or ulcers with adherent clot resistant to
vigorous irrigation, IV PPI infusion should be given for 72 hours
 IV PPI Infusion: pantoprazole/esomeprazole 80mg IV bolus stat
followed by 8mg/hr infusion
E. Recurrent bleeding
 Repeated endoscopy should be attempted
 G 13
 If bleeding cannot be controlled or recurs, surgical intervention
becomes necessary
 Interventional radiology may be considered as an alternative if
expertise is available

Rockall Score (ABCDE)

Variables 0 1 2 3
Age <60 60-79 >80
No shock Tachycardia
Hypotension
Pre-endoscopic

Blood pressure sBP >100 sBP>100

sBP<100
P <100 P>100
Renal failure,
CHF, IHD, major
Co-morbidity No liver failure,
diseases
metastatic ca
All other Dx
Dx at time of Mallory-Weiss,
Endoscopic

except GI malignancy
OGD no SRH
malignancy
Evidence of No, or dark spot Blood, adherent
bleeding only clot, spurter
Pre-endoscopy score Full score (Pre-endoscopic + endoscopic)
0: Early discharge or non-admission 0-3: excellent, consider early discharge
0-1: Low risk >8: high risk of death and rebleeding
2-3: Moderate risk
>4: High risk of death

Glasgow-Blatchford Score (GBS)

Score
6.5-<8 2
8-<10 3
Blood Urea
10-<25 4
>25 6  0: can be safely managed as

Gastroenterology
and Hepatology
Male Female outpatient without early
12-<13 10-<12 1 endoscopy
Hb
10-<12 3  >0: increased risk for
<10 <10 6 intervention and inpatient
100-109 1 management is
Systolic BP 90-99 2 recommended
<90 3  >6: > 50% risk of needing an
Pulse >100 1 intervention
Melena Yes 1
Syncope Yes 2
Hepatic disease Yes 2
Cardiac failure Yes 2
 G 14

PEPTIC ULCERS
A. Ulcer-healing drugs
 H2-antagonists for 8 weeks
Famotidine 20 mg bd or 40 mg nocte
 Proton-pump inhibitors (PPI)* for 4 - 6 weeks
Omeprazole/ Esomeprazole 20 mg om
Rabeprazole 20mg om
Lansoprazole 30 mg om
Pantoprazole 40 mg om
*PPI should be taken 30-60 min before meals
B. Anti-Helicobacter pylori therapy
1. First line therapy
Standard triple PPI (bd) + clarithromycin (500mg bd) +
therapy amoxicillin (1g bd) for 7 days
(substitute amoxicillin with metronidazole 500mg
bd in case of penicillin allergy)
2. Salvage therapy
Levofloxacin-based PPI (bd) + levofloxacin (500mg daily) +
triple therapy amoxicillin (1g BD) for 10 days
Bismuth-containing PPI (bd) + bismuth subsalicylate (524mg qid) +
quadruple therapy tetracycline (500mg qid) + metronidazole (500mg
qid) for 10-14 days
Rifabutin-based PPI (bd) + rifabutin (150mg bd) + amoxicillin (1g
triple therapy bd) for 14 days
C. NSAID/ aspirin user with active peptic ulcer
 NSAID user: discontinue NSAID during PPI treatment
Gastroenterology
and Hepatology

 Aspirin user with non-bleeding peptic ulcer: continue aspirin with PPI
treatment
 Aspirin user with bleeding peptic ulcer: resume aspirin with PPI
treatment once hemostasis is secured in order to minimize
cardiovascular risk
D. Ulcer prevention
 H pylori ulcer:
- maintenance acid suppression therapy not neccessary after H pylori
eradication
 G 15
 NSAID ulcer:
- avoid NSAID if high GI risk^ or prior complicated peptic ulcer
- add PPI or misoprostol (200 micrograms bd) as prophylaxis with
NSAID or COX-2 inhibitor use
 Aspirin ulcer:
- review the need for aspirin
- add PPI as prophylaxis when resume aspirin
 Idiopathic ulcer:
- consider long-term maintenance PPI
^High GI risk = more than 2 of the followings: age>65, high dose NSAID,
previous history of peptic ulcer, concomitant use of aspirin, corticosteroids
or anti-coagulants
E. Follow-up Endoscopy
 Uncomplicated DU => Unnecessary if asymptomatic
 GU or complicated (bleeding/ obstruction) or giant DU (>2cm) =>
Necessary till complete healing confirmed

Gastroenterology
and Hepatology
 G 16

MANAGEMENT OF GASTRO-OESOPHAGEAL
REFLUX DISEASE (GERD)

A. Empirical PPI (Proton-pump inhibitor) trial [bd dose PPI for 4 weeks]:
 For patients with typical GERD symptoms (heartburn and
regurgitation), an initial trial of empirical PPI is appropriate
 Patients with chest pain suspected due to GERD should have IHD
excluded before empirical PPI trial.

B. Indications for endoscopy in GERD

 Not for diagnosis of GERD with typical symptom.
 presence of alarm features (dysphagia, odynophagia, unintentional weight
loss, anaemia, haematemesis and/or melaena, recurrent vomiting, family
history of gastric and/or esophageal cancer, chronic non-steroidal
anti-inflammatory drug use, age >40 years in areas of a high prevalence of
gastric cancer).
 persistent symptom after empirical PPI trial (need to stop PPI for at
least 1 week prior to endoscopy).
 diagnosis of complications of GERD including oesophagitis,
Barrett’s esophagus.
 severe esophagitis (LA Grade C-D*) after 8-week PPI treatment to
assess healing and exclude Barrett’s esophagus.
 history of oesophageal stricture who have recurrent dysphagia.
 evaluation before anti-reflux surgery.

C. Indications for oesophageal pH monitoring

Gastroenterology

 when diagnosis of GERD is in doubt (off PPI before test).

and Hepatology

 when treatment is ineffective (keep PPI before test) to define those

with or without continued abnormal acid exposure times.
 evaluation before endoscopic or surgical therapy (off PPI before test).
 persistent/recurrent symptoms after reflux surgery.

D. Indications for esophageal manometry

 Not indicated for uncomplicated GERD.
 Pre-operative assessment to exclude severe oesophageal motility
disorders before antireflux surgery.
 G 17

E. Indications for oesophageal impedance testing

 To detect non-acid reflux when oral PPI therapy is ineffective

F. Management
 Lifestyle modification: body position, food, weight reduction,
behaviour.
 Severe oesophagitis (LA Grade C-D): standard PPI dose# for 8
weeks. Doubling the dose to bd daily may be necessary in some
patients when symptoms or oesophagitis are not well controlled.
Maintenance therapy is required in severe oesophagitis/Barrett’s
esophagus and lowest PPI dose should be used to minimize long
term adverse effects.
 Non-erosive GERD (NERD)/ mild oesophagitis (LA Grade A-B):
standard dose H2 antagonists (H2RA) or PPI# for 8 weeks.
On-demand/intermittent H2RA can be used as maintanence
treatment.

G.Indications for anti-reflux surgery

 Unresponsive or intolerant to medical treatment
 Complications of GERD unresponsive to medical therapy

*Los Angeles classification of reflux oesophagitis

A mucosal break(s) <5mm, no extension between tops of mucosal folds
B mucosal break >5mm, no extension between tops of mucosal folds
C mucosal breaks continuous between tops of mucosal folds, but not
circumferential

Gastroenterology
and Hepatology
D mucosal break(s) involving >75% of circumference
#
Standard dose acid suppressants for GERD:
omeprazole 20mg, lansoprazole 30mg, pantoprazole 40mg, rabeprazole 20mg,
esomeprazole 40mg, dexlansoprazole 30mg, famotidine 20mg bd.
All PPIs except dexlansoprazole should be administered 30-60min before meals to
assure maximal efficacy.
 G 18

INFLAMMATORY BOWEL DISEASES: OVERVIEW

DIAGNOSIS = clinical + haematologic + endoscopic
+ histologic + imaging evaluation
A. History:
‐ recent travel, medication (antibiotics, NSAID), sexual and vaccination
‐ smoking, prior appendicectomy, family history, recent episodes of infectious
GE
‐ bowel habit: stool frequency and consistency (nocturnal, usually >6wk
duration), urgency, tenesmus, per rectal passage of blood and mucus
‐ abdominal pain, malaise, fever, wt loss
‐ perianal abscess / fistulae: current or in the past
‐ EIM: joint, eye, skin, oral ulcer

B. Physical Examination:
‐ G/C, hydration, Temp, wt, BMI, nutritional assessment, BP/P, pallor, oral
ulcer
‐ abdominal distension or tenderness, palpable masses, perianal inspection and
PR

C. Endoscopy and Bx for histological evaluation

1. Sigmoidoscopy: in acute severe colitis, take 2 Bx samples
2. Ileocolonoscopy:
a. Crohn’s disease
Gastroenterology
and Hepatology

‐ patchy distribution of inflammation with skip lesions, rectal sparing is often

‐ deep, stellate, linear ulcers, multiple aphthous ulcers, cobblestoning mucosa
‐ a minimum of 2 Bx from each of the 6 segments (TI, asc, trans, desc,
sigmoid and rectum) including macroscopically normal segments
‐ ulcer: Bx taken from the edges (increase yield of granuloma)
b. Ulcerative colitis
‐ rectal involvement, extend proximally in a continuous, confluent and
concentric fashion; clear and abrupt demarcation between inflamed and
normal mucosa;
‐ caecal patch: patchy inflammation in caecum, observed in L-sided colitis
 G 19
‐ backwash ileitis: continuous extension of macroscopic or microscopic
inflammation from caecum to distal ileum, observed in up to 20% of patients
with pancolitis; associated with a more refractory course
‐ severity:
mild: mucosal erythema, decreased vascular pattern, mild friability
moderate: marked erythema, absent vascular pattern, friability, erosions
severe: spontaneous bleeding, ulceration
3. Anorectal ultrasound: for assessment of perianal CD
4. Small bowel capsule endoscopy: high clinical suspicion of CD but -ve
endoscopic/radiologic findings

D. Radiology
1. AXR: small bowel or colonic dilatation (toxic megacolon: transverse colon
diameter >5cm), assess disease extent (ulcerated colon contains no solid
faeces), mass in right iliac fossa, calcified calculi, sacroiliitis
2. CT/MR abd/pelvis /small bowel: dis extent and activity, inflammatory vs
fibrotic stricture, extraluminal Cx, internal fistulization, perianal disease
3. Barium fluoroscopy: superior sensitivity for subtle early mucosal disease

E. Laboratory Ix:
1. CBP and ESR: anaemia, thrombocytosis
‐ LFT, electrolytes, RFT, Mg, CRP: active disease, infective Cx, ~ risk of
relapse
‐ Iron studies, vit B12 and folate level

Gastroenterology
‐ Antibodies: adjunct to diagnosis
and Hepatology
Anti-Saccharomyces cerevisiae antibody (ASCA): Crohn’s disease
p-Anti-neutrophil cytoplasmic antibody (p-ANCA): Ulcerative colitis
2. Stool
‐ R/M: presence of WBC indicates mucosal inflammation
‐ Culture to rule out infective cause e.g. Clostridium difficile (high
prevalence in IBD), Campylobacter spp., E.coli 0157:H7, amoebae and
other parasites
3. Cytomegalovirus: in severe or refractory colitis
 G 20
4. Faecal markers: calprotectin
‐ marker of colonic inflammation
‐ useful to differentiate IBD from functional diarrhoea, assessing disease
activity
‐ not available in HK

MANAGEMENT
1. Nutrition:
‐ an adjunct to treatment
‐ dairy free diet in case of active colitis
‐ calcium, vitamin D, fat soluble vitamin, zinc, iron, vit B12 status
2. Fluid and electrolyte correction: hypoK and hypoMg can exacerbate toxic
dilatation
3. Smoking cessation:
‐ a risk factor of CD: higher operative risk and anastomosis recurrence
4. An alternative explanation for symptom should be considered e.g.
infection, bacterial overgrowth, bile salt malabsorption, dysmotility,
gallstones
5. Objective evidence of disease activity should be obtained before starting
or changing medical therapy
6. Avoid NSAID, anticholinergic, antidiarrhoeal, opioids (ppt colonic
dilatation)
Gastroenterology
and Hepatology
 G 21

CROHN’S DISEASE
Risk factors: smoking, prior appendicectomy, family history of IBD, hx of
infectious GE in the prior one year
Montréal phenotypic classification
A. Age of onset: A1 <16 yrs
A2 17 – 40 yrs
A3 >40 yrs
B. Disease location: L1 Ileal
L2 Colonic
L3 Ileocolonic
L4 Isolated upper GI (a modifier that can be added
to L1-L3 when concomitant UGI disease is
present)
C. Disease behavior: B1 Non-stricturing, non-penetrating
B2 Stricturing
B3 Penetrating
p Perianal fistulae / abscess (added to B1-B3
when concomitant perianal disease is present)
Medical Management: to induce and maintenance remission, taking into
account on activity, site, disease behaviour and patient preference
Disease activity
Mild Moderate Severe
CDAI 150 – 220 220 – 450 >450
General Ambulatory Intermittent vomiting
Eating and drinking
Weight loss <10% loss >10% Cachexia, BMI <18
Examination Tenderness mass Abscess

Gastroenterology
and Hepatology
No overt obstruction Obstruction
Treatment Ineffective for mild disease Persistent symptom despite
intensive treatment
CRP Usually > ULN >ULN Increased
‐ a trend towards early introduction of immunomodulator and biologics in
patients with adverse prognostic factors:
1. young age <40
2. extensive small bowel disease
3. requiring steroid in initial treatment
4. perianal disease
5. stricturing disease
6. deep colonic ulcers
 G 22
A. Aminosalicylates:
‐ no consistent evidence that it is effective in maintenance of remission
‐ monitor CBP and RFT
‐ Sulphalazine: 3-6g/day is modestly effective in colonic disease
‐ Mesalazine: limited efficacy for ileal or colonic disease
B. Antibiotics:
‐ septic Cx, symptom attributed to bacterial overgrowth, perianal disease
C. Corticosteroid:
‐ effective to induce remission, ineffective in maintenance of remission
‐ Ca and vit D supplements, +/- osteoprotective therapy if given >12 wks
Systemic steroid: no evidence to support use of a particular regimen but a
standard tapering strategy is recommended
e.g. prednisolone 40mg/day, reducing by 5mg/day at weekly intervals
20mg/day x 4 wks, then reduce by 5mg/day at weekly
intervals
Budesonide: 9mg daily, for TI or ileocaecal disease, less effective
D. Immunomodulator
‐ Thiopurines: to maintain remission, steroid-sparing effect
check thiopurine methyl-transferase (TPMT) level if available
Azathioprine 1.5-2.5mg/kg/day or Mercaptopurine 0.75-1.5mg/kg/day
delay onset of action, takes 8-12 wks, monitor CBP and LFT
‐ Methrotrexate: active or relapsing CD refractory to/intolerant of
thiopurines or anti-TNF, monitor CBP and LFT
Induction: 25mg/wk x 16 wks, maintenance: 15mg/wk, IM or SC
folic acid 5mg weekly, given po 3 days after methotrexate
Gastroenterology

E. Biologics (anti-TNF):
and Hepatology

‐ contraindications: latent untreated or active TB, NYHA Class III- IV heart

failure, hx of demyelinating disease, optic neuritis, history of lymphoma.
‐ Infliximab: chimeric anti-TNF antibody, 75% human IgG and 25% murine
loading with 5mg/kg at 0, 2 and 6 wk, then at 8-weekly intervals IV
infusion
‐ Adalimumab: humanised anti-TNF
loading with 80mg/40mg or 160mg/80mg at 0 and 2 wk, then 40mg
every other week, sc
‐ similar efficacy, choice depends on patient’s preference, cost, route of
delivery
 G 23
‐ covered by Samaritan fund for 1) fistulizing CD, 2) CDAI ≥ 300, check
HA intranet for updates (ha.home > Guidelines > Non-clinical Manual /
Guidelines > Samaritan Fund)
F. Proton pump inhibitors: for upper GI involvement
Surgical Management: aim at bowel conservation
‐ an option in localized dis, septic Cx, non-inflammatory obstructive
symptom (stricturoplasty for small bowel, endoscopic dilatation for large
bowel)
‐ perianal disease: examination under anaesthesia (EUA) to assess extent of
disease, drain collections, seton drainage, advancement flaps, fistula plugs

Gastroenterology
and Hepatology
 G 24

ULCERATIVE COLITIS
A chronic relapsing and remitting inflammatory condition leading to continuous
colonic mucosal inflammation, affecting the rectum and to a variable extent of
the colon.
Protective factors: appendicectomy (for genuine appendicitis), smoking
Risk factors: family history of IBD, non-selective NSAID in exacerbation of UC

Montréal phenotypic classification: according to the maximal extent of

inflammation observed at colonoscopy
‐ influences treatment modality, oral and / or topical
‐ influences timing of starting surveillance and its frequency
E1 Proctitis involvement limited to the rectum
E2 Left-sided (distal UC) involvement extending up to splenic flexure
E3 Extensive (pancolitis) involvement extends proximal to the splenic
flexure

Medical Management
‐ depends on disease activity, extent and pattern of disease, taking patient
preference into account

Disease activity Modified Truelove and Witt’s criteria for clinical practice
Mild Moderate Severe
Bloody stools / day <4 ≥4 ≥6
Pulse < 90 bpm ≤ 90 bpm >90 bpm
Temperature <37.5 oC ≤37.8 oC >37.8 oC
Haemoglobin >11.5g/dL ≥10.5g/dL <10.5g/dL
Gastroenterology
and Hepatology

ESR <20 mm/h ≤30 mm/h >30 mm/h

or CRP Normal ≤30mg/L >30mg/L
‐ immediate admission warranted in severe disease
‐ toxic megacolon: total or segmental non-obstructive dilatation of colon
>5.5cm or caecum >9cm, associated with systemic toxicity

Prognostic indicators:
1. patients diagnosed before the age of 16 have a more aggressive initial
course
2. older age of diagnosis is associated with a lower risk of colectomy
 G 25
3. CRP >45mg/dL on D3 of hospital admission and 3 – 8 stools/day as
predictor of colectomy
4. CRP >10mg/dL after a year of extensive colitis predicts an increased rate
of surgery
5. Presence of sclerosing cholangitis increases risk for colorectal cancer
Dose/day Induction Maintenance
Mesalazine
Suppository: distal 500mg bd / 1gm 0.5 – 1 gm
Mild to Moderate Disease

10cm 1-4 gm 1 – 4 gm
Enema: to splenic
Topical
flexure 20mg
Steroid enema 2gm
Prednisolone
Budesonide
Aminosalicylate
Sulphasalazine 4 – 6 gm 2 – 4 gm
Mesalazine tab 2 – 4 gm ≥2gm
Mesalazine granules 1.5 – 4 gm 1.5 – 2 gm
Steroid
Oral
Prednisolone 20 – 40 mg
Budesonide 9mg
Thiopurine
Azathioprine 1.5 – 2.5mg / kg
Mercaptopurine 0.75 – 1.5 mg / kg
Steroid
Severe Disease

IV
Hydrocortisone 100mg Q 6 – 8H
Anti-TNF
Infliximab (IV) 5mg / kg at wk 0, 2, 6 5mg / kg every 8 wks

Gastroenterology
and Hepatology
Adalimumab (sc) 160mg / 40mg at wk 0 and 2 40mg every other
Rescue Calcineurin inhibitor week, from wk 4
Cyclosporin (IV) 2mg / kg
Tacrolimus (po) 0.05mg / kg to keep trough
conc of 10-15ng/mL
Surgery: no response to rescue therapy in 4 – 7 days
Mild L sided disease: start with topical treatment
Extensive disease: oral therapy
Combination therapy (oral and topical) is more effective in inducing remission
than either modality alone
 G 26
Severe disease: consider rescue therapy early in steroid-refractory disease (~D3)
‐ early surgical input, consider colectomy if no improvement within 4-7
days of salvage therapy
‐ predictors of colectomy: Colectomy
rate
1. BO >12/day on D2 of IV steroid 55%
2. BO >8/day or BO 3-8/day + CRP >45 on D3 IV steroid 85%
3. Stool frequency x 0.14 CRP on D3 IV steroid ≥8 75%
4. High CRP, low albumin and pH, ESR >75, temp >38o on admission 5–9x
5. Colonic dilatation >5.5cm 75%
6. Ileus with ≥3 small bowel loops of gas 73%
Gastroenterology
and Hepatology
 G 27

ACUTE PANCREATITIS

High index of suspicion is needed. Suspect acute pancreatitis in

any patient with upper abdominal pain (esp. with vomiting),
unexplained shock or elevated serum amylase (at least 3 x ULN,
excluding other causes of acute abdomen is of paramount
importance).

A. Assessment of severity and prognosis

 Risk factors of severity at admission include age >55, obesity
(BMI >30), altered mental state, and co-morbid disease
 Clinical Parameters
Variable Ranson Glasgow APACHE II
At At within first admission,
0 hrs 48 hrs 48 hrs then daily
Age (years) >55 >55 +
WBC count (x109/l) >16 >15 +
Blood glucose >11.1 >10 -
(mmol/l)
AST (U/l) >250 - -
LDH (U/l) >350 >600 -
Serum urea (mmol/l)  >1.8 >16 creatinine
Serum Ca (mmol/l) <2 <2 -

Gastroenterology
and Hepatology
Serum Alb (g/l) - <32 -
PaO2 (kPa) <8 <8 +
Base deficit >4 - Arterial pH
Fluid sequestration >6 L - -
Haematocrit (%)  ≥10% - +
Serum Na - - - +
Serum K - - - +
Temperature - - - +
Mean arterial BP - - - +
 G 28

Heart rate - - - +
Respiratory rate - - - +
Glasgow coma scale - - - (15 - actual
score)
Chronic health score - - - +
Suggested cut off 11 criteria: <3 8 criteria: ≥ 14 criteria: ≥8
number criteria indicate mild 3 criteria points*
AP indicate indicate severe
severe AP AP
* Points system per variable: from 0 (normal) to +4 (very abnormal).
Minimal score: 0, maximum score: 71.
 C-reactive Protein: 150mg/l at 48hrs predicts a severe attack
 Contrast-enhanced CT pancreas: to diagnose severity of AP and to
identify complications, especially pancreatic necrosis, full extent
of which cannot be appreciated until at least 3 days after symptom
onset. Best done on D6-D10 after admission.
Balthazar CT severity index = grade of AP (0-4) + percentage of
necrosis (0-6). Score of 7-10 associated with morbidity of 92%,
mortality 17%.
Grade of Pancreatitis Points Percentage of Points
Necrosis
Normal pancreas 0 0% 0
Focal or diffuse enlargement 1 <30% 2
Gastroenterology
and Hepatology

Pancreatic or peripancreatic 2 30-50% 4

inflammation
Single peripancreatic fluid 3 >50% 6
collection
Multiple fluid collection and/or 4
retroperitoneal air
 G 29
B. Watch out for biliary pancreatitis
 ALT > 3 ULN in a non-alcoholic patient would highly
suggestive of gallstone aetiology
 USG hepatobiliary system for detection of gallstone and
dilated bile ducts; pancreas can only be visualized in 50% of
cases
 EUS is the most accurate test for diagnosing or ruling out
biliary etiology
 Arrange early ERCP and sphincterotomy within 24 to 72
hours after admission, if there is acute cholangitis or
evidence of persistent CBD stones

C. Management (ICU care for severe cases)

 Laboratory Ix for assessment of severity (see above)
 CXR, AXR (erect and supine films for excluding other
causes of acute abdomen, serially for monitoring), ECG
 Closely monitor vital signs, I/O, RFT, Ca, glucose  ABG
 Adequate intravenous hydration is crucial (to produce urine
output of 0.5ml/kg/hr in the absence of renal failure) and
supplemental oxygen
 Correct electrolyte and glucose abnormalities
 Cardiovascular, respiratory and renal support as required
 Analgesics - Pethidine for pain control
 Nil by mouth till nausea and vomiting settle. Nasogastric
suction if ileus or protracted vomiting

Gastroenterology
and Hepatology
 Early oral feeding is encouraged in mild acute pancreatitis
 Nutritional support via enteral route is preferred to parenteral
route. Nasogastric or nasojejunal feeding appear comparable
in efficacy and safety.
 Parenteral nutrition should be considered if the enteral route
is not available, not tolerated, or not meeting caloric
requirements.
 G 30
Recommended nutrient requirements in acute severe pancreatitis
Energy 25-35
kcal/kg/day
Protein 1.2-1.5
g/kg/day
Carbohydrates 3-6 g/kg/day
Lipids 2 g/kg/day
Fat administration is safe provided hypertriglyceridaemia (>12
mmol/l) is avoided
 Antibiotics
- Given on demand: biliary sepsis, newly developed sepsis or
systemic inflammatory response syndrome, infected pancreatic
necrosis, an increase in CRP in combination with other
evidence supporting the possibility of infection.
- Prophylactic antibiotic treatment generally not recommended
but may be considered in patients with pancreatic necrosis of
>30% involvement by CT. It should be active against enteric
organisms (e.g. imipenem) and be given for one to two weeks.
 Look out for complications e.g. pseudocyst or pancreatic sepsis.
CT-guided FNA of pancreas for Gram stain and culture if
suspected infection of pancreatic necrosis with ongoing fever,
leucocytosis and worsening abdominal pain
 Consult surgeon in severe cases or when complication arise.
Gastroenterology
and Hepatology
Haematology

Haematology
 H 1

HAEMATOLOGICAL MALIGNANCIES

(1) LEUKAEMIA
1. Investigations at diagnosis
a. Blood tests
CBP, PT/APTT
D-dimer, fibrinogen (if suspicious of APL or DIC)
G6PD, HBsAg, antiHBc, antiHBs
RFT, LFT, Ca/P, Urate, Glucose, LDH, Type&Screen
HCV Ab, HIV Ab, HBV DNA for HBV carrier
Serum lysozyme for AML M4/M5/CMML
Flow cytometry, Coombs’ test and serum protein IEP,
Fluorescence in situ hybridization (FISH) for CLL
Tartrate resistant acid phosphatase (TRAP) for HCL
b. Bone marrow aspiration and trephine
Contact haematologist for cytogenetic and molecular studies
before BM biopsy
2. Initial management
a. Start allopurinol or febuxostat
b. Ensure adequate hydration
c. Blood product support:
RBC/blood transfusion if symptoms of anaemia are present
Platelet transfusion if platelet count ≤10 x 109/L or ≤20x109/L if
fever or bleeding
Give FFP if there is evidence of bleeding due to DIC
d. Do sepsis workup if patient has fever
e. Antibiotic therapy:
Give appropriate antibiotic if there is evidence of infection
PCP prophylaxis for patients with acute lymphoblastic leukaemia:
Haematology

i. Septrin tab 2 daily three days per week, or

ii. Pentamidine inhalation 300mg/dose (or 5mg/kg) once every
4 weeks.
f. Record patient’s performance status (PS)
 H2
3. Inform haematologist the following medical emergencies
a. Hyperleucocytosis (e.g. WBC 100x109/L) for chemotherapy
 leucopheresis. Avoid blood transfusion till WBC is lowered
b. APL (acute promyelocytic leukaemia) for early use of
all-trans-retinoic acid (ATRA)
4. Subsequent management
a. Consult haematologist for long-term treatment plan
b. Arrange Hickman line insertion if indicated
c. Arrange HLA typing for patient’s siblings if HSCT is
anticipated
d. CMV negative blood product for potential HSCT recipient if
patient is CMV seronegative.

(2) LYMPHOMA
1. Investigations at diagnosis
a. Blood tests
CBP, ESR, PT/APTT, G6PD
RFT, LFT, Ca/P, LDH, Urate, Glucose, Direct Coombs’ test
Serum IgG/IgA/IgM levels, serum IEP
HBsAg, anti-HBc, anti-HBs, HBV DNA (optional)
b. Biopsy
Excisional biopsy of lymph node or other tissue (send fresh
specimen, no formalin)
Send fresh specimen for study (immune markers, EM, DNA)
c. Bilateral iliac crest aspiration and trephine
d. Radiology
PET/CT scan (preferred, especially in diffuse large B cell
lymphoma, Hodgkin’s lymphoma) or CT scan of thorax,
abdomen and pelvis or other sites of involvement
Haematology

e. Other investigations
Endoscopic and Waldeyer’s ring exam for GI lymphoma
LP with cytospin for patients with high risk of CNS lymphoma
(high grade lymphoma, nasal/ testicular/ marrow lymphoma)
Cardiopulmonary assessment – optional
 H 3

2. Initial management
a. Start allopurinol or febuxostat and ensure adequate hydration
b. Record patient’s performance status (PS)

3. Note the following medical emergencies

a. SVC obstruction due to huge mediastinal lymphoma
b. Hypercalcaemia
c. Tumour lysis syndrome
d. Spinal cord compression

4. Subsequent management
- Consult haematologist for long-term treatment plan

(3) MULTIPLE MYELOMA

1. Investigations at diagnosis
a. Blood tests
CBP, ESR, RFT, LFT, Ca/P, LDH, Urate, Glucose
Serum Immunoelectropheresis (IEP) and paraprotein level
Serum IgG/IgA/IgM level, Serum free light chain level
2 M, CRP, HBsAg, anti-HBc, anti-HBs, G6PD
b. Urinalysis - Bence Jones Protein (BJP) and free light chains
c. Radiology – skeletal survey or Total Body MRI or PET/CT
d. Bone marrow aspiration and trephine (+/- FISH)

2. Staging
a. International Staging System (ISS) (JCO 23:3412, 2005)
Stage Serum Albumin (g/l) Serum Median survival
2-microglobulin ( months )
(mg/l)
I > 35 <3.5 62
Haematology

II Neither stage I or III 45

III -- >5.5 29
 H4

b. Symptomatic Vs asymptomatic myeloma

Symptomatic: presence of end-organ damage: CRAB:

Calcium elevation: (>2.9 mmol/L)

Renal insufficiency: (creatinine >176.8mol/L)
Anaemia (Hb <10 or 2g < normal)
Bone disease (lytic or osteopenic)

3. Initial management
a. Ensure adequate hydration and start allopurinol 300 mg daily or
febuxostat
Correct hypercalcaemia – pamidronate or Zometa.
c. Renal dialysis  plasmapheresis for patients with renal failure
d. Record patient’s performance status (PS)
e. Consult Radiotherapy or Orthopaedic Team for patients
presenting with skeletal complications (pathologic fracture or
spinal cord compression)

4. Subsequent management
Consult haematologist for long-term treatment plan

(4) EXTRAVASATION OF CYTOTOXICS (also see page GM 29

Oncological Emergency)
1. Prevention
a. Extreme care and never give it in a hurry
b. Choose appropriate veins
c. Confirm patency of iv site with NS before injection of cytotoxics
d. Flush with NS on completion of infusion/injection of cytotoxic
drugs
Haematology

e. Stop when patient complains of discomfort, swelling, redness

f. Use central line if indicated e.g. Hickman line
 H 5
2. Extravasation suspected
a. Leave iv needle in place and suck out any residual drug
b. If there is a bleb, aspirate it with a 25-gauge needle
Anthracycline – apply ice pack
Vinca alkaloid – apply heat
c. Potential antidotes
Anthracycline- DMSO or hydrocortisone or NaHCO3 locally
Vinca alkaloid- apply hydrocortisone locally
Cisplatinum- sodium thiosulphate
d. Record the event in clinical notes and inform seniors
(5) INTRATHECAL CHEMOTHERAPY
1. Prescription
a. All intrathecal chemotherapy should be prescribed in a separate
prescription form.
b. Methotrexate, cytarabine and hydrocortisone are the only THREE
drugs that can be prescribed for intrathecal chemotherapy
administration.
c. The route of administration “Intrathecal” must be written in full in
the prescription.
d. Platelet count and clothing profile should be checked beforehand.
2. Dispensing
a. All dispensed intrathecal drugs must be labeled with a warning
message “ For Intrathecal Use Only”.
b. All dispensed intrathecal chemotherapy must be dispatched
separately in a designated container or in a sealed envelope/bag
(marked “Intrathecal drug”).
3. Consent
a. Prior to intrathecal chemotherapy administration, the medical staff
who is responsible for the procedure, must obtain an informed
Haematology

written consent from the patient.

4. Administration
a. Parenteral drug(s) and intrathecal drug must be administered as
separate procedures, i.e. separated in time in setting up and
initiating the administration.
 H6
b. The staff responsible for the drug administration must verify the 5
“Rights” (Right patient, right time, right drug, right dose and right
route) against the prescription. A second trained staff is required to
independently verify the patient identification and drug checking
process.
c. Both staff must sign the medication administration (MAR) record.
(6) PERFORMANCE STATUS
WHO/ECOG Performance Status
Score Activities

0 Fully active; able to carry on all pre-disease performance without restriction.

Restricted in physically strenous activity, but ambulatory and able to carry out
1
work of a light or sedentary nature, e.g. light housework, office work.
Ambulatory and capable of all self-care but unable to carry out any work
2
activities; up and about more than 50% of waking hours.
Capable of only limited self-care, confined to bed or chair more than 50% of
3
waking hours.
Completely disabled; cannot carry on any self-care; totally confined to bed or
4
chair.

(7) HAEMATOLOGICAL TOXICITY

WHO Haematological Toxicity Scale
Parameter Grade 0 Grade 1 Grade 2 Grade 3 Grade 4
Haemoglobin
≥11 9.5-10.9 8-9.4 6.5-7.9 <6.5
(g/dL)
Leucocytes
≥4 3-3.9 2-2.9 1-1.9 <1
(x109/L)
Haematology

Neutrophils
≥2 1.5-1.9 1-1.4 0.5-0.9 <0.5
(x109/L)
Platelets
≥100 75-99 50-74 25-49 <25
(x109/L)
Mild blood Gross blood Debilitating
Haemorrhage None Petechiae
loss loss blood loss
 H 7

NON-MALIGNANT HAEMATOLOGICAL
EMERGENCIES/CONDITIONS
(1) ACUTE HAEMOLYTIC DISORDERS
1. Approaches
a. Collect evidence of haemolysis
- evidence of increased Hb break down
 indirect bilirubin,  haptoglobin,  LDH
Methaemalbuminaemia*, Haemoglobinaemia*,
urinary and faecal urobilinogen, Haemoglobinuria*
Haemosiderinuria*
(* :evidence of intravascular haemolysis)
- evidence of compensatory erythroid hyperplasia
Reticulocytosis, erythroid hyperplasia of bone marrow
- evidence of damage to red cells
Spherocytosis, RBC fragility, Fragmented RBC, Heinz bodies
- evidence of shortened red cell life span
Chromium51 labelled red cell study
b. Document the cause and nature of haemolysis
- Intracorpuscular/Extracorpuscular defect - Congenital/Acquired
- Intravascular/Extravascular haemolysis - Acute/Chronic
2. Investigations
a. Blood tests
CBP, Reticulocyte count, Peripheral smear, Hb pattern
RFT, LFT, Bilirubin(direct/indirect), LDH, Haptoglobin
Direct Coombs’ test, ANF, Viral study, Screening for malaria
Cold agglutinins (arrange with laboratory)
Sucrose lysis test / PNH screening test(arrange with laboratory)
G6PD assay (may be normal during acute haemolysis, consider
Haematology

repeating test a few weeks after recovery)

b. Urine test
Urobilinogen, Haemoglobin, Haemosiderin
3. Management
a. Must identify cause of haemolysis, then treat accordingly
 H8
b. Consult haematologist

4. Common agents reported to induce haemolytic anaemia in

subjects with G6PD deficiency
Unsafe for class I, II, & III variants Safe for class II & III variants*
Acetanilid Acetaminophen (paracetamol)
Dapsone Aminopyrine
Furazolidone Ascorbic acid except very high dose
Methylene blue Aspirin
Nalidixic acid Chloramphenicol
Naphthalene (mothballs, henna) Chloroquine
Niridazole Colchicine
Nitrofurantoin Diphenhydramine
Phenazopyridine Isoniazid
Phenylhydrazine L-DOPA
Primaquine Menadione
Sulfacetamide Para-aminobenzoic acid
Sulfamethoxazole Phenacetin
Sulfanilamide Phenytoin
Sulfapyridine Probenecid
Thiazosulfone Procainamide
Toluidine blue Pyrimethamine
Trinitrotoluene Quinidine
Chinese Herbs: Quinine
plum flower (腊梅花) Streptomycin
chuan lianzi (川蓮) Sulfamethoxpyridazine
zhen zhu (珍珠末) Sulfisoxazole
jin yin hua (金銀花) Trimethoprim
niu huang (牛黃) Tripelennamine
Vitamin K
Haematology

5. Safety for class I variants is usually not known.

Data from Beutler, E, Blood 1994; 84:3613.
Class 1 (severe deficiency with nonspherocytic hemolytic anaemia),
Class II (severe deficiency with intermittent hemolysis), and
Class III (moderate to mild deficiency). Beutler, E, Blood 1994; 84:3613
 H 9

(2) IMMUNE THROMBOCYTOPENIC

PURPURA (ITP)
1. Definition
Isolated thrombocytopenia due to peripheral destruction with no
clinically apparent causes but of presumed autoimmune aetiology
Secondary causes:
- SLE - MDS - TTP - HIV infection
- Gestational thrombocytopenia - Alloimmune thrombocytopenia
- Lymphoproliferative disorders - 1oanti-phospholipid syndrome
- Infection (eg. viral, malaria)
- Drugs e.g. heparin induced thrombocytopenia (HIT)

The 4Ts: A clinical probability scoring system for diagnosis of HIT

4Ts 2 Points 1 Point 0 Point
Thrombocytopenia Platelet count fall Platelet count fall Platelet count fall
>50% and platelet 30-50% or platelet <30% or platelet
nadir ≥20 x109/L nadir 10-19 x109/L nadir <10 x109/L
Timing of platelet Clear onset Consistent with Platelet count fall
count fall between days 5-14 days 5-14 fall, but 4 day without
or platelet fall 1 not clear (e.g. recent exposure
day (prior heparin missing platelet
exposure within 30 counts) or onset
days) after day 14 or fall
1 day (prior
heparin exposure
30-100 days)
Thrombosis or New thrombosis Progressive or None
other sequelae (confirmed); skin recurrent
necrosis at heparin thrombosis;
injection sites; Non-necrotizing
anaphylactoid (erythematous)
reacton after IV skin lesion;
Haematology

heparin bolous Supected

thrombosis (not
confirmed)
OTher causes of None apparent Possibile Definite
thrombocytopenia
High probability (6-8 points), intermedicate probability (4-5 points), low probability (3 points).
Adapted from Lo et al., J Thromb Haemost 2006;4:759
 H 10
2. Investigations
a. CBP and blood film (to ensure no red cell fragments, leukaemia)
b. Bone marrow examination not mandatory, indicated if
i. the diagnosis of ITP is not certain
ii. in patients age over 60 years to rule out myelodysplasia
iii. prior to splenectomy
iv. if response to treatment is poor
c. Autoimmune profile and APTT
d. anti-HIV serology in patients at risk
3. Management
a. Consult haematologist
b. Initial treatment: Prednisolone 1 mg/kg/day, or
Pulse dexamethasone 20- 40mg/day for 4 days
c. For acute life-threatening bleeding
- IVIg 0.4 g/kg/day for 5 days or 1.0 g/kg/day for 2 days
(80% effective, lasts 2-3 weeks)
- or Methylprednisolone 1 g iv in 1 hour daily for 3 days
- or Pulse dexamethasone 40 mg po daily for 4 days
- or Intravenous anti-Rh0 (D)
d. Second line therapy: thrombopoietin mimetics (Eltrombopag,
Romiplostim), splenectomy, Rituximab, other immunomodulatory
agents
e. Avoid aspirin and other antiplatelet agents and im injection
f. Platelet transfusion only for life-threatening bleeding
4. Management of ITP in Pregnant Women
a. Consult haematologist
b. During pregnancy
Platelet count > 50 x109/L and no bleeding – no treatment
Platelet count <50 x109/L- consider steroid or IVIg
Be cautious with use of steroid in first trimester
Haematology

c. At delivery
- Mode of delivery according to obstetrical indication. Maternal
platelet count  50 x 109 /L is sufficient to prevent complications
due to vaginal delivery or cesarean section.
- Avoid epidural or spinal anaesthesia if platelet count < 80 x 109 /L.
- Check infant’s platelet count at delivery
 H 11

(3) THROMBOTIC THROMBOCYTOPENIC

PURPURA (TTP)
1. Diagnosis
a. Classical pentad – microangiopathic anaemia, thrombocytopenia,
fever,
renal impairment, neurologic symptoms and signs
b. Redefined as a syndrome of Coombs’-negative haemolytic
anaemia and thrombocytopenia in the absence of other
possible causes of these manifestations
c. Important to examine blood film for micro-angiopathic features
2. Investigations
CBP, Peripheral smear (for features of micro-angiopathic
haemolytic anaemia), retic, RFT, LFT, LDH, Haptoglobin,
Direct Coombs’ test, Coagulation profile (relatively normal)
3. Treatment
a. Consult haematologist
b. Daily plasma exchange should be commenced immediately with
exchange for FFP or cryosupernatant
c. Platelet transfusion is contraindicated

(4) PANCYTOPENIA
1. Approaches to determine the cause of pancytopenia
a. Bone Marrow disorder (defective synthesis)
- Aplastic anaemia - Reactive haemophagocytosis
- Subleukaemic leukaemia - Megaloblastic anaemia
- MDS - Disseminated tuberculosis
- Marrow infiltration: lymphoma, myeloma, marrow fibrosis,
Haematology

carcinoma
b. Peripheral destruction
- SLE - DIC - Hypersplenism
- Paroxysmal nocturnal haemoglobinuria (PNH)
2. Investigations
CBP, Peripheral smear, Bone marrow aspiration and trephine
 H 12

(5) THROMBOPHILIA SCREENING

1. Screening Tests
a. Lupus anticoagulant(LA) Anti-cardiolipin Ab ANF
b. Protein C (PC), Protein S (PS), Antithrombin (AT),
Activated Protein C Resistance (APCR), Factor V Leiden
2. Indications
a. Young patients with idiopathic venous thrombosis
b. Recurrent venous thrombosis or superficial thrombophlebitis
c. Unusual sites of thrombosis (mesenteric, renal, portal veins,
cerebral venous sinus)
d. Warfarin induced skin necrosis
e. Arterial thrombosis with age < 40
f. Recurrent miscarriage

(6) PROPHYLAXIS OF VENOUS THROMBOSIS IN

PREGNANCY

1. Pre-delivery and delivery

a. Consult haematologist for dosage of LMWH and monitoring
b. Monitoring of plasma anti-Xa activity may be required
c. If need epidural/spinal anesthesia, withhold LMWH 12-24h before
the procedure.
2. Post-delivery
a. Same dose of LMWH is continued until INR on warfarin is
2.0 to 3.0
b. Warfarin is continued for 6-8 weeks
Haematology
 H 13

DRUGS AND
BLOOD PRODUCTS

(1) ANTI-EMETIC THERAPY

1. 5-HT3 antagonists (for patients on cytotoxic chemotherapy)
a. Zofran (ondansetron) 8 mg iv Q8H/Q12H or 8 mg po tds
b. Kytril (granisetron) 3-6 mg iv once daily or transdermal patch
c. Navoban (tropisetron) 5 mg iv/po once daily
2. Maxolon 10 mg iv Q6H prn
3. Emend ( Aprepitant )
use in combination with corticosteroid or other 5-HT3 antagonist :
125mg po on day 1, 80mg po daily on day 2-3

(2) HAEMOPOIETIC GROWTH FACTORS

Granulocyte Colony Stimulating Factor (G-CSF)
1. Indications
- Mobilization of haemopoietic stem cells for transplantation
- Shortening of neutropenia after chemotherapy given when
absolute neutrophil 1x109/L
- Drug-induced agranulocytosis
- Other conditions of severe neutropenia associated with
infection e.g. cyclical neutropenia
2. Dosage (usage endorsed by haematologist)
G-CSF: 5 micrograms/kg/day sc/iv (1 vial contains 300 micrograms)

(3) IMMUNOGLOBULIN THERAPY

1. Indications
a. As replacement
Primary immunodeficiencies with significant past infections
Haematology

Secondary Ab deficiencies: CLL, multiple myeloma, post HSCT

patients with chronic GvHD and significant past infections
b. As an immunomodulator (haematology)
Proven benefit-ITP with life threatening bleeding or pregnancy
 H 14
Probable benefit – autoimmune haemolytic anaemia
post infectious thrombocytopenia
Possible benefit – coagulopathy with factor VIII inhibitor
2. Dosage
a. Replacement – 0.2 g/kg Q3weeks
b. Immunomodulator e.g. ITP – 0.4 g/kg/day for 5 days or 1g/kg/day
for 2 days
3. Contraindications
a. Previous history of allergy to IVIg
b. IgA deficiency

(4) ANTITHYMOCYTE GLOBULIN (ATG)

1. Indication
Very severe AA
 Bone marrow cellularity <25% and
 Neutrophils <0.2 x109/L and
 Platelets <20 x109/L or reticulocytes <20 x109/L
Severe AA
 Bone marrow cellularity <25% and two of the following three
 Neutrophils 0.2- <0.5 x109/L
 Platelets <20 x109/L
 Reticulocytes <20 x109/L
2. Premedication (1 hour before ATG)
a. Paracetamol 1gm and chlorpheniramine (piriton) 4mg po
Methylprednisolone 2-3 mg/kg in 100ml normal saline iv in 1 hour
3. Test dose: 10mg ATG in 100ml normal saline iv in 1 hour
Physician in attendance, anaphylaxis 1 in 50
4. Daily dose: ATG 40mg/kg iv in 4 hours for 4 days
Haematology

(5) rFVIIa (NOVOSEVEN)

Dosage:
90-120 micrograms/kg/dose
may be repeated every 2-4 hours
Indications: (Please refer to latest HA drug formulary)
- haemophilc patients with inhibitor activity and active bleeding
 H 15
- factor VII deficiency
- patients with acquired inhibitors and active bleeding

(6) NOVEL ORAL ANTICOAGULANTS (NOACs)

Clinical setting
Prevention of venous
thromboembolism post total
hip/knee replacement
Dabigatran Rivaroxaban Apixaban
Knee: 110mg once Knee:10mg daily for 12 Knee: 2.5mg BD
within 1-4 hours of days with or without food for 12 days
completed surgery, then
220mg daily for 10 days

Hip: 110mg once within Hip: 10mg daily for 35 Hip: 2.5mg BD for
1-4 hours of completed days with or without food 35 days
surgery, then 220mg
daily for 28-35 days
Non-valvular Atrial CrCl>30mL/min: 150mg CrCl>50mL/min:20mg 5mg BD (2.5mg
fibrillation BD; CrCl 15-30mL/min: daily with evening meal; BD with any 2 of
75mg BD CrCl 15-50mL/min: 15mg the followings:
daily with evening meal ≥80 years old;
BW≤60kg, serum
Cr ≥132.6mol/L
DVT treatment CrCl>30mL/min: 150mg 15mg BD for 21days with 10mg BD for 7
PE treatment BD; CrCl≤30mL/min or food, then 20mg QD for 6 days, then 5mg BD
on dialysis: Dosing months, for remaining
recommendation cannot treatment
be provided
Prevention of recurrent VTE CrCl>30mL/min: 150mg 20mg daily with food 2.5mg BD after at
BD; CrCl≤30mL/min or least 6 months of
on dialysis: Dosing treatment of
recommendation cannot DVT/PE
be provided
The table shows the doses of each OAC in different clinical settings. However, the dose has to
be adjustecd if the patient has underlying renal impairment.

Reversal of NOACs:
At the time of writing, there is no specific antidote (only available in
clinical trial). Management of bleeding should be through cessation
of treatment and general haemostatic measures.
Dabigatran: oral activated charcoal may decrease further
absorption if intake is less than 2 hours. Haemodialysis offers the
Haematology

possibility of enhanced clearance of the active drug.

Rivaroxaban/Apixaban: Oral activated charcoal may decrease further
absorption while haemodysis does not help.
In life-threatening bleeding condition, prothrombin complex
concentrates (PCC) 25-50 unit/kg can be given while the effect of
rFVIIa is unpredictable
 H 16

(7) REPLACEMENT FOR HEREDITARY

COAGULATION DISORDERS
General information for therapy in hereditary coagulation disorders
Factors half life replacement material
VIII 10 hrs VIII conc1 DDAVP3 cryoprecipitate*
IX 25 hrs IX conc FFP*
2

VWF - DDAVP FVIII/VWF containing conc

Cryoprecipitate FFP
Fibrinogen 90 hrs Cryoprecipitate FFP
V 36-80 hrs FFP
VII 5 hrs FVIIa FFP
X 40 hrs prothrombin complex concentrates FFP
XI 45 hrs FFP
*
For Factor VIII and Factor IX deficiencies, use cryoprecipitate / FFP
only when specific factor concentrate is not available
1
1 unit/kg BW of infused Factor VIII raises plasma level by 2%
2
1 unit/kg BW of infused Factor IX raises plasma level by 1%
3
DDAVP is useful for mild haemophilia A if a 3x increase in Factor
VIII suffices. Each patient’s response should be tested prior to
therapeutic use as there are individual variations. 0.3 microgram/kg in
50 ml normal saline iv in 20 minutes causes a peak in Factor VIII level
at 30 minutes. Intranasal DDAVP may be used. As DDAVP stimulates
fibrinolysis, tranexamic acid 500 mg Q8H is used concomitantly for
dental procedures. Prolonged use of DDAVP causes tachyphylaxis

Suggested Plasma Factor Peak Level and Duration of

Administration for Haemophilia A and B
(WFH Guidelines for the Management of Hemophilia 2012.
www.wfh.org)
Haematology
 Haematology
H 17
 H 18

TRANSFUSION
Please refer to latest version of HAHO Transfusion Guidelines at
HA webpage (version 2.0, effective date: 13 Dec 2013)
Acute Transfusion Cause Signs & Symptoms Management
Reaction
(Estimated risk)

Allergic reaction Sensitivity to plasma 1.Flushing 1. Stop transfusion immediately and

(1:100 to 1:300) protein or donor antibody 2.Itching, rash keep vein open
3.Urticaria, hives 2. Give antihistamine as directed
4.Shortness of breath, 3. Observe for anaphylaxis
wheezing 4. If hives are the only sign, the
5.Laryngeal oedema transfusion may sometimes continue
6.Anaphyxis at a slower rate
5. For anaphylaxis, adrenaline
injection may be required.

Febrile, Immunological reactions 1. Flushing 1. Stop transfusion immediately, keep

non-haemolytic between recipient HLA or 2. Fever vein open and inform clinician for
transfusion granulocyte specific 3. Tachycardia assessment
reaction(FNHTR) antibodies with donor 4. Sometimes rigors 2. Clerical check for compatibility
(1:100 with leukocytes or reaction to between recipient and blood unit(s)
non-leukoreduced the pyrogenic cytokines Symptoms usually occur given
blood components) released from donor about 30 mins.to 2 3. Antipyretic e.g. paracetamol can be
leukocytes during storage hrs.after starting a red given
cell transfusion. Even 4. For mild febrile reaction and rapidly
earlier after a platelet resolving symptoms, transfusion
transfusion may be resumed slowly.
5. For severe febrile reaction (e.g. rise
in temperature > 1.5 °C), the same
unit should not be restarted.
6. Haemolytic transfusion reaction
and septic reaction should always
be suspected,investigated and
managed

Septic reaction Transfusion of bacterial 1. Rapid onset of chills 1. Stop transfusion immediately, keep
(Red cell 1 : contaminated whole blood and rigors vein open and inform clinician for
500,000 / blood components 2. High fever usually > 2 assessment
Platelet 1 : 10,000) °C 2. Monitor patient closely for
3. Nausea, vomiting, septicaemic shock
diarrhoea 3. Clerical check for compatibility
4. Hypotension between recipient and blood unit(s)
5. DIC given and exclude haemolytic
6. Intravascular transfusion reaction accordingly
haemolysis 4. Obtain patient’s blood for septic
7. Renal failure workup and send blood bags and
Haematology

administration set for culture

5. Treat septicaemia with intravenous
broad spectrum antibiotics with
adequate anti-pseudomonas
coverage
6. Report through hospital blood bank
to HKRCBTS forfurther
investigation

Circulatory Whole blood / blood
overload component(s) was
(1 : 10,000) administered at a rate or
volume more than the
recipient circulatory
system can accommodate.
Haemolytic Infusion of incompatible
transfusion reaction whole blood / blood
(1 in 250,000 – components
1,000,000)
Transfusion related ? due to the presence of
acute lung injury antibodies
(TRALI) (anti-granulocyte-specific,
(1 in 50,000 – anti-HLA class I,
200,000 reported anti-HLA class II,
in the literature) anti-IgA, other ?) from
donors to cause immune
reaction in the recipient
resulting in the clinical
manifestation in the lung.
1. Rise in jugular venous
pressure with
distended neck veins
2. Dyspnoea
3. Cough
4. Crackles in bases of
lung
1. Fever, chills and
rigors or both
2. Pain at the infusion
site or localized to the
loins, abdomen, chest
or head
3. Hypotension,
tachycardia or both
4. Agitation, distress and
confusion; particularly
in the elderly
5. Nausea or vomiting
6. Dyspnoea
7. Flushing
8. Haemoglobinuria
1. Acute respiratory
distress occurring
within 6 hour of
starting a transfusion
2. Severe bilateral
pulmonary edema
3. Severe hypoxia
4. Fever
5. Chest X ray shows
peri-hilar and nodular
shadowing in themid
and lower zone
H 19
1. Withhold transfusion immediately
and exclude other causes
2. Support treatment e.g. place patient
upright with feet in dependent
position; give diuretics, oxygen
supplement, etc.
3. May require intubation if severe
dyspnoea
1. Stop transfusion immediately and
spigot off the unit. (save the blood
units and blood giving set for
investigation)
2. Use a new giving set and keep vein
open with normal saline
3. Inform clinician for urgent
assessment
4. Clerical check for compatibility
between recipient and blood unit(s)
given
5. Inform blood bank to return blood
units for investigations and collect
additional blood samples
6. Treat shock if present
7. Collect urine samples
8. Maintain BP with IV colloid
solutions. Give diuretics as
prescribed to maintain adequate
urine output
9. Insert indwelling catheter to monitor
hourly urine output. Patient may
require dialysis if renal failure
occurs
1. Withhold transfusion immediately
and exclude other causes of
shortness of breath e.g. circulatory
overload
2. Prompt and full respiratory support
3. If properly treated, reversible and
recovered without sequelae
(pulmonary edema can clear usually
in72 hr)
4. Report through hospital blood bank
to HKRCBTS for further
investigation
Haematology
 H 20
Whole blood / Blood Dosage
components
Fresh whole blood (≤ 1 -2 units
5 days from donation)
Whole blood / Red Dosage depends on clinical
cells situations
One standard unit (derived
from 450 ml whole blood
donation) should raise Hb level
by up to 1.2 g/dL in a 70 kg
adult.
One small unit (derived from
350 ml whole blood donation)
should raise Hb level by about
0.85 g/dL in a 70 kg adult.
For children, 4 ml/kg should
raise Hb
level by 1 g/dL
Platelet concentrates 4 random donor units (each
(either prophylactic or derived from 350 ml or 450 ml
therapeutic) whole blood donation) for
adults up to 70 kg;
each unit should raise platelet
count by 7-10 x109/L
5 units/M2 for paediatric
patients
1 unit of apheresis platelet
concentrate is equivalent to one
standard adult dose (for adults
up to 70 kg)
Buffy coat/ 10 units/day for 4 days or until
granulocytes (must be fever subsides
irradiated)
(Require special
arrangement with the
HKRCBTS)
Fresh frozen plasma Typical dosage:
Haematology
(FFP) 2 -4 units for adults
12 -15 ml/kg for paediatric
patients
** always reassess for clinical
and laboratory responses
Indications
Exchange transfusion or massive blood loss in neonates
There is no single haemoglobin value that must be taken as
the transfusion trigger. However, a trend towards cautious
blood transfusion trigger has been observed but patients’
condition may affect clinical decision. The initiation of
transfusion is a clinical decision by the attending clinician.
Ingeneral, the following principles are considered:
1. Haemoglobin concentration <7g/dL and assessment on
the rate of ongoing red cell loss.
2. For haemoglobin concentration between 7 and 10 g/dL,
transfusion strategy is less clear but general view is that
transfusion is often not justified purely based on
haemoglobin concentration.
3. A higher haemoglobin concentration may be required in
patients who may tolerate anaemia poorly, e.g. patients
over the age of 65 years and patients with cardiovascular
or respiratory disease.
1. Platelet <10 x109/L in stable patients (usually NOT
indicated in idiopathic thrombocytopenia, systemic lupus
erythromatosis, thrombotic thrombocytopenia and
hemolytic-uraemic syndrome).
2. Platelet <20 x109/L in patients with fever or sepsis.
3. Platelet <50 x109/L with diffuse microvascular/mucosal
bleeding, major bleeding or before invasive procedures.
4. Platelet <100 x109/L with retinal or central nervous
system bleeding/ surgery, or with active bleeding in
postcardiopulmonary bypass.
5. Platelet <50 x109/L in stable premature neonates or
platelet <100. x109/L in sick premature neonates
6. Suspected platelet dysfunction with active bleeding or
before invasive procedures.
7. Suspected platelet deficiency with severe active
bleeding or following massive transfusion.
Neutropenia (<0.5 x109/L) with documented infection
unresponsive to broad spectrum antibiotics including
antifungal agents for at least 48 hours.
1. Thrombotic thrombocytopenic purpura.
2. When clotting factors deficiency is suspected or
anticipated with active bleeding during operation or
following massive transfusion,
3. Immediate reversal of warfarin overdose (bleeding or
impending surgery).
4. Prothrombin time/ activated partial thromboplastin time
(PT/APTT) >1.5x control values with active bleeding or
before invasive procedure in the following situations:
 Single or multiple clotting factor deficiency (other than
haemophilia A/B).
 H 21
 Disseminated intravascular coagulopathy).
 Hepatic failure.

Methylene Blue Supply for pediatric patients As for fresh frozen plasma, with lower residual infectious
treated FFP only. risk

Cryoprecipitate Depends on the target factor
levels in particular diseases and
clinical situations, ranging from
6 -30 units/dose; 10 units per
dose for adults up to 70 kg
1. von Willebrand disease (if desmopressin or factor
concentrate is inappropriate).
2. Documented fibrinogen deficiency (<100 mg/dL) or
dysfunction.
3. Documented factor XIII deficiency.

Leucodepleted Same as other red cell As indicated for whole blood/red cells, but especially
(filtered) red cells preparations indicated for:
1. All thalassaemia patients on regular transfusion
regimens;
2. Haematological diseases;
3. Documented severe febrile non-haemolytic transfusion
reaction (≥ 2 episodes);
4. Paediatric oncology patients.

Irradiated cellular Same as non-irradiated For prevention of transfusion-related graft versus host
blood components counterparts disease in circumstances such as:
1. Foetuses requiring intrauterine transfusion.
2. Patients with severe congenital cellular
immunodeficiency.
3. Haemopoeitic stem cell transplantation patients.
4. Patients receiving transfusion from close relatives.

Cytomegalovirus Dosage according to individual 1. CMV-antibody-negative pregnant women

(CMV) negative cellular blood components 2. CMV-antibody-negative recipients of allogeneic stem
cellular blood cell grafts
components 3. Intrauterine transfusions
4. Patients with human immunodeficiency virus (HIV)
disease

Rhesus D (Rh(D)) Same as Rh(D) positive red In this order of priority:

negative red cells cells 1. Haemolytic disease of newborn due to anti-D.
2. Rh(D) negative individuals with anti-D.
3. Rh(D) negative females prior to menopause.
4. Emergency resuscitation of Caucasian females in
reproductive age with unknown Rh(D) status.
5. Other Rh(D) negative individuals

Haematology
Haematology
H 22
Nephrology

Nephrology
 K 1

RENAL TRANSPLANT–
DONOR RECRUITMENT
Protocol for preparation and management of potential organ donor:
Identification of potential organ donor:
a. definite diagnosis, irreversible CNS damage;
b. brain death is imminent;
c. put on mechanical ventilation;
d. GCS 3-5 / 15, both pupils fixed to light

Exclusion criteria:
 Age ≥ 71 (for kidney donors);
 Uncontrolled fulminant infection;
 Risk of transmission of disease caused by prions, including
Creutzfeldt-Jakob disease, rapid progressive dementia or
degenerative neurological disease;
 History of IV drug abuse;
 HIV +ve cases or has risk factors for HIV infection;
 Presence or previous history of malignant disease (except
primary basal cell carcinoma, carcinoma in-situ of uterine
cervix and some primary tumour of CNS)

Maintenance of organ perfusion of potential donor:

Aim:
Maintain SBP 100 - 140mmHg, AR 60-120 bpm
Maintain Mean BP > 80mmHg
Maintain CVP of 8-12cm H2O
Maintain hourly urine output ~100ml
Maintain intake and output balance and cover insensible loss
Maintain SaO2 >= 95%
Maintain body temperature> 36oC
Nephrology
 K2
a. Monitor BP, P, CVP, urine output, SaO2, ventilator status q1h,
body temperature q2h
b. Monitor electrolytes, RLFT, Ca/PO4 q6-8h, H’stix q2-4h
c. Set two good IV lines, preferably one central line
d. Monitor BP:
- If persistently hypertensive (MBP > 120mmHg), start
labetalol 5mg IV over 1 min and repeat at 5 min intervals if
necessary
- If persistently hypotensive (SBP ≤ 100mmHg)
: Start fluid replacement by infusing crystalloid or colloid
: Add dopamine 2.5 – 10 micrograms/kg/min if BP
persistently low despite adequate fluid replacement
: Add adrenaline 0.1 – 10 micrograms/kg/min
- If BP persistently low: start hydrocortisone 100mg stat &
100 mg q8h
e. Monitor urine output: If massive urine output ( > 200ml /hour )
: Control hyperglycaemia ( H’stix > 12mmol/L persistently) by
Actrapid HM hourly infusion at 2 – 6 units
: Control diabetes insipidus (serum Na ≥ 150mmol/L) by
dDAVP 2-6μg IV q6-8h
: Control hypothermia (body temperature ≤ 35oC) by apply
patient warming system
If oliguric (hourly urine < 30ml)
: check Foley patency
: oliguria with low or normal CVP, start fluid replacement
: oliguria with high CVP, start lasix 20 – 250mg IVI
f. Add prophylactic antibiotics after blood culture if fever > 38oC.

Routine arrangement:
a. Inform transplant coordinator via hospital operator at any time
b. Interview family for grave prognosis, do not discuss organ
donation with family until patient is confirmed brain death
c. Once the patient meets brain death criteria, arrange qualified
personnel to perform brain stem death test
Nephrology
 K 3

ELECTROLYTE DISORDERS
Hypokalaemia
Hints - Check drug history, most likely attributed to diuretic therapy;
- Usually associated with metabolic alkalosis;
- Start intravenous therapy if serum K < 2.5 mM;
- Consider magnesium depletion if hypoK is resistant to
treatment;
- Don’t give potassium replacement therapy in dextrose solution.
Ix: - serum RFT, total CO2 content, chloride, magnesium;
- simultaneous blood and urine x TTKG (trans-tubular potassium
gradient)
- check baseline ECG (esp. those patients on digoxin therapy)
Mx: If serum K > 2.5 mM & ECG changes are absent:
KCl 20-30 mmol/hour in saline infusion (up to 60-80 mmol/L)
as continuous IV infusion; may combine with oral KCl 30-40
mmoles (3-4 gm syr KCl) Q4H; maximum total treatment dose:
100 – 200 mmoles per day (~ 3 mmoles/kg/day).
If serum K < 2.5 mM &/or ECG changes present:
Consult ICU / cardiac monitor;
KCl 30-40 mmol/hour in saline infusion (concentration up to 80
mmol/L); may combine with oral KCl 30-40 mmoles (3-4 gm
syr KCl) Q4H; maximum total treatment dose: 100 – 200
mmoles per day (~ 3 mmoles/kg/day).
Hypokalaemia associated with metabolic acidosis

Give potassium citrate solution (1 mmole/mL) 15-30 mL QID

in juice after meals; start K replacement before bicarbonate
therapy in separate IV line if indicated.
Nephrology
 K4
Dosage form:
Syrup KCl ( 1 gram = 13.5 mmoles K );
Slow K ( 8 mmoles K / 600 mg tablet );
Potassium citrate ( 1 mL = 1 mmole K );
Phosphate-sandoz ( 3 mmoles K, 16 mmoles phosphate /
tablet ).

Pre-mixed K-containing solution for maintenance IV infusion

for HA Hospitals
0.9% NS with 10 mmoles K / 500 mL ( K conc: 20 mM)
0.9% NS with 20 mmoles K / 500 mL ( K conc: 40 mM)
5% D5 with 10 mmoles K / 500 mL ( K conc: 20 mM)
5% D5 with 20 mmoles K / 500 mL ( K conc: 40 mM)
Lactated Ringer’s with 2 mmoles K /500 mL (K conc: 4 mM)
Nephrology
 K 5
Hyperkalaemia
Hints: Exclude pseudohyerK e.g. haemolysis, esp. in those with
relatively normal renal function;
discontinue K supplement, NSAID, ACEI, K-sparing diuretic.
Ix: Repeat RFT CO2 chloride, ECG
Rx: For urgent cases ( serum K > 6 mM &/or ECG changes of
hyperK )
1. 10% Calcium gluconate 10 mL IV over 2-3 minutes with
cardiac monitoring; repeat if no effect in 5 minutes
(onset:1-3 min; duration: 30-60 min ). If digoxin toxicity is
suspected, omit calcium gluconate infusion.
2. Dextrose-insulin infusion: give 250 mL D10 or 50 mL D50
with 8-10 units Actrapid HM over 30 minutes; repeat every
4-6 hrs if necessary (onset: 30 minutes; duration: 4-6 hrs ).
3. Sodium bicarbonate 8.4% 100-150 mL over 30-60 min; to
be given after calcium infusion in separate IV line; watch
out for fluid overload (onset: 5-10 minutes; duration: 2 hrs).
4. Resonium C / A: 15-50 g orally Q 4-6 hrs or as retention
enema; may be given in 100-200 mL 10% mannitol as
laxative; one gm resonium will bind 1 mmole of K. (onset:
1-2 hrs; duration: 4-6 hrs).
5. Salbutamol 10-20 mg in 3 mL NS by nebulizer (onset:
15-30 minutes; duration: 2-3 hrs).
6. Diuretics: furosemide 40-80 mg IV bolus.
7. Emergency haemodialysis or peritoneal dialysis.
For chronic cases:
1. Low K diet (< 2 g/ day).
2. Diuretics: furosemide / thiazide
3. Correct acidosis with sodium bicarbonate 300-900 mg tds
(~10-30 mmoles/day).
4. Fludrocortisone 0.1-0.2 mg daily (for Type IV RTA).
Nephrology
 K6
Hypercalcaemia (Also see page PM 14 and GM 27)
Hints: calculated corrected serum calcium level based on serum albumin
concentration
Corrected calcium = 0.02 * (40 g/L – patient’s albumin (g/L)) + serum
Ca; commonly associated with dehydration.
Ix: check ionized calcium, PO4, RFT, ECG
Rx:
1. Off calcium / vitamin D supplement if any.
2. Volume repletion with NS at 100-500 mL/hr infusion ( guided by
CVP / urine output ); start furosemide after rehydration 20-40 mg
IV Q 2-12 H; aim at a urine output of ~ 200 mL/Hr; close
monitoring of Na K Ca Mg level.
3. Pamidronate 30-90 mg in 250-500 mL NS infused over 4-6 hrs;
maximum effect is not seen for several days; repeat another dose
after a minimum of 7 days if necessary.
4. Salmon calcitonin 4 units/kg IMI / SC Q 12 H; Ca level begins to
fall within 2-3 hrs; tachyphylaxis occurred within 2-3 days.
5. Mithramycin: 25 micrograms/kg IV in 500 mL D5 over 3-6 hrs
infusion; Ca begins to decrease in 12 hrs; peak action at 48 hrs;
repeat dose at 3-7 days interval if necessary (usually reserve for
malignancy-related hypercalcaemia ).
6. Hydrocortisone 5 mg/kg IV Q 8 H then prednisolone 40-100 mg
daily ( onset: 3-5 days; useful in haematological malignancy,
vitamin D intoxication, some CA breast).
7. Sandoz-phosphate 2-8 tablets per day; avoid if severe
hypercalcaemia or hyperphosphataemia.
8. Haemodialysis with zero or low Ca dialysate.
Nephrology
 K 7
Hypocalcaemia
Hints: usually due to chronic renal failure;
Ix: check ionized Ca level, PO4, ALP, Mg, RFT, amylase, CK,
ECG.
Rx: Symptomatic hypocalcaemia: 10% Calcium gluconate 20 mL
IV over 10-15 minutes then 30 mL 10% Ca gluconate in
500 mL NS/D5 Q 4-6 H /pint; monitor Ca level.
Chronic cases: ( add Vit D if no response after 2-4 gm
elemental Calcium )
1. Ca supplement: Caltrate=600 mg elemental Ca / tablet
Oscal=250 mg elemental Ca / tablet
Titralac=168 mg elemental Ca / tablet
Ca gluconate=27mg elemental Ca / tablet
2. Vit D: Calcitriol/1-αhydroxycholecalciferol: 0.25-2ug daily

Nephrology
 K8
Hypomagnesaemia
Hints: may be associated with hypoK, hypoCa, arrhythmia.
Ix: check RFT, K, Ca, ECG.
Fractional excretion (FE) of Mg
= 100 x (UMg x PCr) / (0.7 x PMg x UCr)
( if HypoMg, FE > 2.5% indicates renal loss of Mg).
Rx: Emergency:
4 mL 50% MgSO4 ( 8 mmoles ) solution IV in 20 mL NS/D5
infused over 15 minutes then 10 mL 50% MgSO4 ( 20 mmoles )
in 500 mL NS/D5 over 6 hrs.
Less urgent cases:
4 mL 50% MgSO4 ( 8 mmoles ) solution 500 mL NS/D5 Q 8
H/pint for 1 day ( up to 50% of the infused Mg will be excreted
in urine; slow and sustained correction of hypoMg is preferred)
Chronic cases:
Normal average daily intake of Mg ~ 15 mmoles ( ~ 1/3 is
absorbed )
1. Mg supplement : Mylanta / Gelusil : 3.5 mmoles/tablet
2. Amiloride: 5 – 10 mg daily PO ( decrease urinary loss of
Mg )
Nephrology
 K 9
Hypermagnesaemia
Hints: Uncommon in the absence of Mg administration or renal failure;
Mild cases ( < 1.5 mM ) usually require no treatment.

Rx: Take off Mg supplement if any;

Saline diuresis: NS 300 – 500 mL / hr infusion;
10% Calcium gluconate 10 – 20 mL in 100 mL NS over 15
minutes;
Furosemide 20 – 40 mg Q2-4 Hr ( aim at urine output ~ 200
mL/hr );
Haemodialysis if necessary.

Nephrology
 K 10
Hyperphosphataemia
Hints: Usually attributed to chronic renal failure;
Usually resolved in 6-12 hrs if RFT normal;
Aim at a serum phosphate level of ~ 1.4 mM for uraemic
patients.
Ix: RFT Ca PO4 CO2 ALP
Rx: 1. Low phosphate diet ( < 1 gm / 30 mmoles per day ).
2. Start phosphate-binder:
If serum phosphate < 2 mM:
Caltrate tab 1-2 tds with meal
Titralac tab 1-2 tds with meal
Ca acetate tab 1-2 tds with meal
If serum phosphate > 2 mM:
Alusorb tab 1-3 tds with meal
Alutab tab 1-3 tds with meal
3. Arrange dialysis if necessary.
Nephrology
 K 11
Hypophosphataemia
Hints: usually required no treatment if serum PO4 > 0.5 mM;
Replacement rate < 2 mg (0.067 mmoles)/kg per 6 hrs,
otherwise may be associated with metastatic
calcification.
Ix: check RFT serum Ca / PO4 ALP;
Fractional excretion (FE) of phosphate
FE = 100 x (Up x PCr) / (UCr x Pp)
(In the presence of hypoPO4, FE >5% indicates urinary loss)
Rx: IF serum PO4 < 0.5 mM with symptoms:
6 mL potassium di-phosphate solution in 500 mL D5 Q 12 H
infusion
(Potassium di-phosphate solution : 14.5 mmoles PO4 + 25
mmoles K per 10 mL solution)

Chronic therapy:
Sandoz-phosphate tab 1 QID PO (16 mmoles PO4; 20 mmoles Na; 3
mmoles K / per tablet)

Nephrology
 K 12
Hyponatraemia
Ix: RFT, serum / urine osmolarity, spot urine x Na.
1. Isovolaemia:
(urine Na > 20 mM: SIADH, hypothyroid, Addison’s disease;
urine Na < 10 mM: water intoxication )
Rx: restrict water intake < 1000 mL per day;
High salt diet (> 8 gm/day) ± sodium supplement:
Syr NaCl 2 gm tds (100 mmoles);
demeclocycline 600-1200 mg daily;
For symptomatic hypoNa: 100 mL 5.85% NaCl (1
mmole/mL) over 4-6 hrs + furosemide 40 mg IV; repeat if
necessary until serum Na > 120 mM or patient is
asymptomatic (rapid collection > 0.5 mM / Hr elevation in
serum Na may lead to central pontine myelinosis ).

2. Hypovolaemia:
(urine Na < 10 mM: fluid loss, hypotension, dehydration; urine Na
> 20 mM: diuretics, adrenal insufficiency, salt wasting)
NS 500 mL/hr till BP normal, then replace Na deficit with NS;
Sodium deficit = BW (kg) x 0.6 x (desired [Na] – measured [Na]);
replace first 50% of deficit over 4-6 hrs and the other 50% over
next 18-20 hrs till serum Na level reaches 120 mM or increase by
10-12 mM over 24 hrs.

3. Hypervolaemia:
( urine Na < 10 mM: CHF, cirrhosis; urine Na > 20 mM: acute /
CRF )
Rx: restrict water intake < 1000 mL per day;
Furosemide 40-80 mg IV / 20 – 500 mg PO daily.
Nephrology
 K 13
Hypernatraemia
Ix: serum / urine x osmolality.
Rx: Hypervolaemia:
(Primary Hyperaldosteronism, Cushing’s syndrome, acute salt
overload)
Start D5 infusion to correct water deficit;
Add furosemide 40-80 mg IV or PO Q12-24 H

Isovolaemia or Hypovolaemia:
(Diabetes insipidus, large insensible water loss, renal / GI loss )
 If volume is depleted, give NS 500 mL/hr infusion till no
orthostatic hypotension, then replace water:
Serum Na < 160 mM: give water PO
Serum Na > 160 mM: replace fluid with D5 or half half saline;
 body water deficit (L) = {0.6 x BW(kg) x (measured [Na] – 140)}
/ 140;
replace half of the body water deficit over first 24 hrs, then
remaining deficit over next 1-2 days ( correct Na at a rate < 0.5 –
1 mM/hr; rapid correction may lead to cerebral edema );
 For acute DI: give DDAVP 4-8 μg Q 3-4 H prn;
 For chronic central DI: DDAVP 10-40μg daily intranasally (in
one to two divided dose)
 For chronic nephrogenic DI: thiazide diuretic, e.g.
hydrochlorothiazide 25 mg daily, indapamide 2.5 mg daily,
amiloride 5 mg daily

Nephrology
 K 14

SYSTEMATIC APPROACH TO THE ANALYSIS OF

ACID-BASE DISORDERS

1. Hx and PE for causes of acid-base disturbance.

2. Identify the primary acid-base disturbance.
3. Assess adaptive response to primary acid-base disorder.
1o response Adaptive response
Metabolic
Acidosis ↓HCO3 ↓pCO2: 1.6 kPa per 10 mM ↓in HCO3
pCO2 =(1.5 x HCO3) +8 ±2 mmHg
Alkalosis ↑HCO3 ↑pCO2: 0.9 kPa per 10 mM ↑in HCO3
Respiratory
Acidosis ↑pCO2 acute: 0.77 mM ↑HCO3 per 1 kPa↑pCO2
chronic: 2.7 mM↑HCO3 per 1 kPa↑pCO2
Alkalosis ↓pCO2 acute: 1.5 mM ↓HCO3 per 1 kPa↓pCO2
chronic: 3 mM ↓HCO3 per 1 kPa↓pCO2
Suspect mixed metabolic / respiratory acid-base disorder if
compensation is not appropriate (common in clinical practice!).
4. Calculate serum anion gap ( Na  Cl  HCO3; normal 10  4 )
High AG metabolic acidosis:
- Treat underlying disorder, consider HCO3 therapy if serum HCO3 <
10.
Normal AG metabolic acidosis:
- Use IV NaHCO3 (1 mL = 1 mmoles of HCO3) if serum HCO3 < 10 (To
be given in large vein over 1-2 hrs, watch out for fluid / salt overload ).
- IV NaHCO3 required = (15 – measured HCO3) x BW (kg) x 0.5
(Correct to HCO3 > 15 mM is usually sufficient)
5. For patients with acidosis:
Compare AG with serum HCO3 (abnormal if discrepancy > 5):
AG >  serum HCO3: mixed metabolic acidosis / alkalosis
AG <  serum HCO3: mixed normal AG /↑AG metabolic acidosis
Nephrology
 K 15
6. Measure urine electrolytes / pH:
a) For patients with metabolic alkalosis
urine Cl < 15 mM – Cl responsive metabolic alkalosis, e.g.
vomiting
urine Cl > 15 mM – Cl resistant metabolic alkalosis, e.g.
mineralocorticol excess, during diuretic therapy.
b) For suspected renal tubular acidosis
urine anion gap : Na + K – Cl ( normal: negative )
urine osmolar gap: [urine osmolarity – 2(Na + K) – urea] / 2
(normal: >30)
abnormal value indicates low ammonium excretion, e.g. distal
RTA
*false positive conditions: - present of an unusual anion in urine,
e.g. ketone; excessive bicarbonaturia, urine pH > 6.5

Causes for high anion gap metabolic acidosis (MULEPAK)

M = methanol , U = uraemia,L = lactic acidosis,
E = ethylene glycol P = paraldehyde, A = aspirin,K = ketosis

Causes for normal anion gap metabolic acidosis (USEDCAR)

U = ureteroenterostomy, S = saline infusion, E = endocrinology
e.g.: Addison, D = diarrhoea, C = carbonic anhydrase inhibitor,
A = ammonium chloride R = renal tubular acidosis

Nephrology
 K 16
Therapeutic Options in patient with metabolic acidosis:
Hints: In order to avoid being misled by acute hyperventilation or
hypoventilation, plasma [HCO3] is, in general, a better guide
to the need of NaHCO3 therapy than systemic pH.

1. Correction of metabolic acidosis with HCO3

- Oral NaHCO3 : 300 mg ( 3.6 mmoles ) per tablet
- NaHCO3 required (mmoles) = (desired – measured HCO3 ) x
BW(kg) x 0.5
- Give over 1 – 2 hours as 8.4% NaHCO3 IVI ( 1 mL = 1 mmole
HCO3 )
- Overcorrection may increase CO2 production, which can
aggravate respiratory acidosis in a poorly ventilated patient.
Watch our for hypercapnia which may cause paradoxical increase
in acidaemia after NaHCO3 therapy
- Can worsen or precipitate hypokalaemia.
2. Hyperventilation:
If the patient with severe metabolic / respiratory acidosis is in
pulmonary oedema, one should consider ventilating the patient to
lower PCO2 appropriately to treat acidaemia.
Acidaemia responses much faster to lowering the PCO2 than to IV
NaHCO3 therapy.
3. Dialysis:
- Especially in those patients with volume overload;
- Use HCO3 bath for haemodialysis.
Nephrology
 K 17
Therapeutic options in patients with metabolic alkalosis:
Hints: Metabolic alkalosis is a disorder caused by mechanisms
whereby [HCO3] is elevated; and a renal basis, e.g.
hypovolaemia, to maintain an elevated [HCO3] level. Both
processes must be corrected if possible for an optimal response
to therapy.
Chloride-responsive metabolic alkalosis ( urine chloride < 15 mM ):
- give NS ± KCl to correct ECF volume;
- give H2 antagonist if alkalosis due to NG suction;
- acetazolamide 250 mg QID PO / IV ( may promote K loss ).
Chloride-resistant metabolic alkalosis ( urine chloride > 15 mM ):
- Block mineralocorticoid effect with spironolactone 100 – 400
mg daily PO.

Nephrology
 K 18

PERI-OPERATIVE MANAGEMENT IN
URAEMIC PATIENTS
1. Assess fluid status, BP control.
2. Check Na, K, urea, Creatinine, Ca/PO4, CBP, arterial blood gases,
CXR, ECG.
3. Consult renal team for need of peri-operative dialytic support.
HD: preferably 1 day before operation (pre-dilution / tight
heparin).
PD: continue CAPD. Cap off Tenckhoff catheter and drained out
PDF for abdominal operation.
Transplant recipient: continue usual dose of immunosuppressive
agents
4. Steroid cover for those patients on oral steroid.
5. Treatment of bleeding tendency: (arrange dialysis if available)
Dosage Onset time Remark
A) Blood -------- Hb > 8 g/dL,
Transfusion Hct >0.26.
fluid overload.
B) dDAVP 0.3 microgram/kg SC 1 hour for 2 days then off.
(Octostim: 15 micrograms/ml)
or 40 micrograms intranasally
BD
C) Cryoppt 10 bags 1 hour Major bleeding
D) FFP 5 units 1 hour Major bleeding
E) Premarin 0.6 mg/kg IV daily x 5/7 > 6 hour For major
surgery or long
lasting effect.
Nephrology
 K 19

RENAL FAILURE
Hints: Exclude pre-renal failure: Orthostatic hypotension,
congestive heart failure, cirrhosis
Exclude post-renal failure: PR exam, feel for bladder, bedside
USG
Ix: CBP, RLFT, CO2, Cl, Ca, PO4, amylase, urate, arterial blood
gases, CXR, ECG;
24 hr urine x Na K P Cr Cr Clearance;
MSU x RM C/ST, urine x dysmorphic RBC;
Autoimmune markers : ANF, DsDNA, C3/4, ANCA, anti-GBM,
etc ;
HBsAg/Ab, anti-HCV (urgent HBsAg if haemodialysis is
anticipated);
Urgent USG kidneys, KUB.
Treatment of suspected acute renal failure:
1. Fluid intake = 500 mL + urine output;
Fluid challenge: NS 500-1000 mL over 1-2 hrs for hypovolaemia;
Add frusemide 10 mg/hr IV infusion for fluid overload; metolazone
5-10 mg daily PO;
Dopamine 2.5 microgram/kg/min to improve renal blood flow.
2. Correct electrolyte disturbances: hyperkalaemia, metabolic acidosis.
3. Low salt diet (< 100 mmoles per day), low K (<20 mmoles/day),
low phosphorus diet (<800 mg day), low protein diet (40 g HBV).
4. Strict I/O chart, daily BW (< 1 kg increase in BW per day)
5. Emergency indications for dialysis: uncontrolled hyperkalaemia (>6
mmol/L); uncontrolled metabolic acidosis (HCO3 <10 mmol/L);
uncontrolled pulmonary oedema.
6. Less urgent indications for dialysis: uraemic pericarditis, uraemic
encephalopathy, intractable uraemic symptoms.
7. Inform on-call renal physician for acute HD support if indicated.
8. Avoid nephrotoxic drugs if possible, e.g. NSAID, aminoglycoside,
etc.
Nephrology
 K 20
Treatment of chronic renal failure:
1. Consult nephrologist for assessment of feasibility of long-term
renal replacement therapy.
2. No blood taking / BP measurement from AV fistula arm.
3. Monitor AV fistula daily / exit site dressing daily for CAPD
patients.
4. Strict I/O chart, daily BW ( < 1 kg increase in BW per day ).
5. Diet ( ± consult dietitian ):
Calorie 30-35 kcal/kg/day ( 500-700 kcal from PD already for
CAPD patients );
Protein: 0.6-0.75 gm/kg/day for CRF patients
1.2-1.3 gm/kg/day for CAPD patients
1-1.2 gm/kg/day for HD patients.
Na: < 100 mmoles per day for CRF / HD patients (except
salt-loser )
No restriction for euvolaemic CAPD patients.
K: < 1 mmole/kg/day.
PO4: <800 mg/day.
Vitamin: Ascorbic acid 100 mg/day (optional)
Folic acid 5 mg/day (optional)
Rocaltrol / Alfacalcidol: 0.25-2 μg /day ( For renal
osteodystrophy).
6. Control hypertension (<140/90 mmHg): long-acting calcium
channel blocker, beta-blocker, ACEI (monitor RFT, K ).
7. Correct metabolic acidosis, hyperK, hypocalcaemia.
8. Symptomatic anaemia: transfusion ( preferably during dialysis
using pack cell); give Lasix 20-80 mg IV before transfusion;
sustanon 250 mg IMI Q 3-4 week; consider EPO therapy for
refractory anaemia.
Nephrology
 K 21

EMERGENCIES IN
RENAL TRANSPLANT PATIENTS
Fever:
Both infection and acute graft rejection can present as fever;
a. Infection:
- Consider opportunistic infection if < 6 months post-transplant;
- Usual pattern of infection if > 6 months post-transplant;
- Search for infection: Hx, PE, culture from wound, urine, IV lines,
sputum, blood, viral culture & serology, CMV pp-65 Ag, CXR;
- Check CBP D/C, RLFT, CsA / Tacrolimus trough level, 24 hr urine x P
& Cr;
- Avoid macrolide antibiotics / fluconazole (may increase CsA /
Tacrolimus level)
b. Acute graft rejection:
- Acute increase in serum creatinine > 20% after excluding other causes;
- May present as oliguria, graft tenderness, fever, ankle edema,
hypertension;
- Check CBP, RLFT, CsA / tacrolimus trough level, 24 hr urine x P & Cr,
MSU;
- Arrange urgent USG kidney + Doppler study;
- Consider renal biopsy

Oligouria / Anuria:
- DDx: acute graft rejection
acute CsA, tacrolimus toxicity
obstructive uropathy
urinary leakage
acute tubular necrosis
acute vascular ( arterial or venous ) thrombosis.
- Treatment according to the cause
- Check CBP, RLFT, CsA / tacrolimus trough level, MSU RM C/ST, 24 hr
urine x P Cr
- Monitor I/O chart, hourly urine output
- Urgent USG graft kidney + Doppler study
- Arrange standby MAG-3 / DTPA scan
Nephrology

- Renal biopsy.
 K 22

DRUG DOSAGE ADJUSTMENT IN RENAL FAILURE

(D: reduce dose (in %), same interval as in normal; I: same dose as
normal, increase interval between 2 dose (in hrs))
Adjustment for Renal Failure Supplement
Name GFR (ml/min) for Dialysis
D/I >50 10-50 <10 or ESRF HD PD
Adriamycin D 100 100 75 ? ?
Allopurinol D 100 75 50 ? ?
I 8 8-12 12-24
Amiloride D 100 50 avoid ? ?
Atenolol D 100 50 25 + -
I 24 48 96
Azathioprine D 100 100 75 + -
Captopril D 100 75 50 - -
Carbamazepine D 100 100 75 - -
Chlorpropamide I 24 avoid avoid - -
Cimetidine D 100 50 25 - -
Colchicine D 100 100 50 - -
Cyclophosphamide D 100 100 50-75 + -
I 24 24 36
Digoxin D 100 25-75 10-25 - -
Disopyramide I none 12-24 24-40 + -
Gemfibrozil D 100 50 25 ? ?
Hydralazine I 8 8 8-16 - -
Insulin D 100 75 50 ? ?
Methyldopa I 6 8-12 12-24 + -
Nadolol D 100 50 25 + -
Neostigmine D 100 50 25 - -
Penicillamine D 100 avoid avoid ? ?
Probenecid D 100 avoid avoid ? ?
Procainamide I 4 6-12 8-24 + -
Spironolactone D 100 50 avoid ? ?
I 6-12 12-24 avoid
Sulindac D 100 100 50 ? ?
Nephrology
 K 23
Common Drugs not requiring dosage adjustment in Renal Failure
Barbiturates Benzodiazepines Bromocriptine Cefoperazone
Ceftriaxone Cholestyramine Cloxacillin Diltiazem
Erythromycin Furosemide Heparin Ketoconazole
Levodopa Lignocaine Minoxidil Nifedipine
Nitrates Prazosin Propylthiouracil Quinidine
Na valproate Steroids Streptokinase Theophylline
Tolbutamide Verapamil Warfarin

Drug interaction with calcineurin inhibitor (tacrolimus,

cyclosporine)
Increase drug level:
Imidazole: ketoconazole, fluconazole
Macrolide: erythromycin, clarithromycin
Calcium channel blocker: verapamil, diltiazam
Antidepressant: fluoxetine (Prozac)
Grapefruit juice
Decrease drug level:
Anti-TB drug: isonazid, rifampicin, ethambutol
Anti-convulsant: phenytoin
Lipid-lowering agent: cholestyramine
Sulfamethoxazole
Ethanol
Additive nephrotoxicity:
Aminoglycoside
Amphotericin B
Sulphonamide / Trimethoprim
Colchicine
NSAID
Others:
Hyperkalaemia with ACEI, K-sparing diuretics, NSAID
Myopathy / rhabdomyolysis with HMG-CoA reductase inhibitor
Estimation of Creatinine Clearance
Nephrology

Cr Cl (ml/min) = [(140-Age) x BW (kg)] / [0.82 x Cr (M)]

** value x 0.85 for women
 K 24

PROTOCOL FOR TREATMENT OF CAPD

PERITONITIS
(BASED ON RECOMMENDATION OF ISPD, 2010)

1. Treatment of peritonitis in CAPD patients

When patient have signs and symptoms of peritonitis S/S:
 Turbid fluid
 Abdominal pain
 Fever

a. Ask patient to come back immediately to dialysis unit for collection

of PDF
b. Send PDF :
 White cell count with differential, gram smear
 Culture
c. Rapid flushing of 3 bags of PDF with heparin 500 units per litre for
symptomatic relief
d. Adequate analgesia
e. Increase to 4 exchanges per day to improve ultrafiltration
f. Heparin: 500-1000 units/ L until signs and symptoms subsided or
until fibrin clots no longer visible
g. Preliminary antibiotics regime:
 Empiric antibiotics must cover both gram-positive and
gram-negative organisms.
 Gram-positive organisms may be covered by vancomycin or a
cephalosporin, and gram-negative organisms by a
third/forth-generation cephalosporin (ceftazidime, cefepime),
aminoglycoside or carbapenam.
Nephrology
 K 25
Suggested protocol
A. CAPD (intermittent dosing method)
 Daily urine output > 100 ml per day or deafness or recent
history of aminoglycoside in recent 3 months:
 Protocol 1
Loading dose:
Cefazolin 1 gram and Cefepime 1gram loading IP,
allow to dwell for at least 6 hours
Maintenance dose:
Cefazolin 1 gram + Cefepime 1gram into last bag
daily (at least 6 hours dwell) x 13 days
 Daily urine output < 100 ml per day and no recent history of
or contraindication to aminoglycosides:
Cefazolin 1 gram and Gentamicin 80 mg IP as loading
dose, then Cefazolin 1 gram and Gentamicin 40 mg IP into
last bag x 13 days.
 Substitute vancomycin (1gram iv or IP every 5-7 days) for
cefazolin if MRSE or MRSA suspected; no routine use of
Vancomycin to avoid emergence of VRE
 Change antibiotics regime once culture and sensitivity result
available
 For St. aureus or pseudomonas peritonitis, antibiotics should
be given x 21 days; otherwise 14 days of antibiotics are
adequate
 For refractory, recurrent or relapsing peritonitis, add Nystatin
oral suspension to prevent Candida peritonitis

B. CCPD (intermittent dosing method)

 Can convert to CAPD temporarily
 Intermittent dosing not recommended for severe cases
 Mild to moderate case: Cefazolin with Cefepime 1 gram into
long daytime dwell
Nephrology
 K 26
h. If patient has evidence of septicemia, admit patient and give
parenteral antibiotics
 Cefazolin 500 mg i.v.i. Q12Hr + Cefepime 1 Gm i.v.i. Q24H (if daily
urine > 100 ml per day)
 Cefazolin 500 mg i.v.i. Q12Hr + Gentamicin 100 mg Q48Hr (if anuria
and no recent aminoglycosides in 3 months)
i. Change antibiotics later according to culture and sensitivity result
and give adequate duration of antibiotics (14 – 21 days)
j. Repeat PDF x WCC and gram smear, culture on D4, reassess the S/S
k. Consider removal of Tenckhoff catheter if peritonitis fails to respond
to appropriate antibiotic within 5 days
l. Change transfer set after completion of antibiotics if patient
recovered

2. Treatment of fungal peritonitis

 Arrange removal of Tenckhoff catheter
 Arrange insertion of triple-lumen central venous catheter for
amphotericin B infusion and haemodialysis
 Continue CAPD until on call to OT, drain out the PDF before
going to OT
 Amphotericin B:
Test dose – 1 mg in 100 ml D5 over 1 hr
then 10 mg / 200 ml D5 over 6 hr on D1, 20 mg / 200 ml D5 over 6
hr from D2-21
alternative: Fluconazole: 200 mg loading and then 100 mg daily p.o.
x 3 weeks
Nephrology
 K 27
3. Antibiotic prophylaxis for procedure:
 For dental procedure, a single oral dose of amoxicillin (2 g) 2
hours before extensive dental procedures
 For patients undergoing colonoscopy with polypectomy –
Ampicillin (1 g) plus a single dose of an aminoglycoside (1.5
mg/kg, max 80 mg), with or without metronidazole, given IV just
prior to the procedure
 The abdomen should be emptied of fluid prior to all procedures
involving the abdomen or pelvis (such as colonoscopy, renal
transplantation, and endometrial biopsy)

Nephrology
 K 28

PROTOCOL FOR TREATMENT OF CAPD EXIT

SITE INFECTIONS
(BASED ON RECOMMENDATION OF ISPD, 2010)
Exit site infection:
1. Purulent discharge from exit site
Treatment:
1. Equivocal exit site infection
 Hibitane dressing TDS
 Local treatment: 0.1% Gentamycin cream, 2% mupirocin
cream or otosporin ear drops to exit wound TDS

2. Exit site infection

 Take exit site swab for microscopy and culture
 Empirical treatment depends on clinical appearance of the
exit site
 Oral penicillinase-resistant penicillin (Cloxacillin 500 mg
qid) or a first generation cephalosporin (Cephalexin 500 mg
bd to tds) x 14 days if gram positive organism was suspected
 Oral fluoroquinolones e.g. Ciprofloxacin 250 mg BD p.o. x
14 days if gram negative organism was suspected (avoids
medication contains multi-valent cations including
Sevelamer, Ca or Fe supplements , Mg-Al containing
antacids, sucralfate, milk; a minimal spacing of 2 hours from
ciprofloxacin if cannot discontinue). Treatment for 3 weeks
is probably necessary for exit site infection caused by P.
aeruginosa.
 Change antibiotics regime according to culture and
sensitivity result once available
 For slowly resolving or severe S. aureus exit site infection,
add Rifampicin 450 mg daily
 For Gram-ve organisms, if no improvement, parental
antibiotics may be needed
Nephrology

 If ESI + peritonitis: arrange early removal of Tenckhoff

catheter
 K 29
 Consult nephrologist for assessment if ESI is persistent
before further courses of antibiotics

 Refractory ESI:
- For double-cuffed Tenckhoff catheter, consider shaving
of external cuff if external cuff is eroded and extruded

 Recurrent ESI:
- Counsel on personal hygiene, review exit site care,
avoid excessive traction on TC
- Take nasal swab x R/M, c/st. If repeatedly grow S.
aureus, give mupirocin cream LA TDS x 1 wk to
eradicate nasal carriage

Nephrology
 Neurology
Neurology
 N1

Neurology
Coma
A medical emergency characterized by the absence of arousal and
awareness.

Timely identification and treatment of reversible cause can be

life-saving.

Mechanisms:
‐ Structural brain lesion.
‐ Diffuse neuronal dysfunction.
‐ Psychiatric (rare).

Approach:
Please refer to the flow chart.
Neurology
N2
 N3

Neurology
N.B. "head of bed": 30 degree for raised ICP; Flat for posterior circulation stroke

Supportive Care
a) Close monitoring of vital signs and neurological status
b) Proper positioning and turning to avoid aspiration, pressure nerve palsy,
contracture, pressure sore
c) Bladder catheterization
d) Adequate hydration, oxygenation and nutrition
e) Chest and limb physiotherapy
f) Hypromellose eyedrops and secure eyelids if no spontaneous blinking
 N4
Neurology

DELIRIUM
(Also refer to page PM 9-10 in Palliative Medicine)

An acute neuropsychiatric syndrome characterized by global cognitive

dysfunction and inattention. The diagnosis is clinical, based on bedside
observation. In the elderly, delirium is a common (and often sole)
manifestation of acute illness. It is not always transient and reversible
and can lead to long-term cognitive changes and mortality.
DSM V Diagnostic Criteria

 Disturbance in attention (i.e., reduced ability to direct, focus,

sustain, and shift attention) and awareness.
 Disturbance in cognition (e.g., memory deficit, disorientation,
language, visuospatial ability, perception)
 The disturbance develops over a short period (usually hours to
days) and tends to fluctuate during the course of the day
 Not better accounted for by another preexisting, established, or
evolving neurocognitive disorder and do not occur in the
context of a severely reduced level of arousal, e.g. coma
 There is evidence from the history, physical examination, or
laboratory findings that the disturbance is caused by a direct
physiologic consequence of another medical condition,
substance intoxication or withdrawal, exposure to a toxin, or
multiple etiologies

Other Associated Features: psychomotor disturbances (hyperactive,

hypoactive and mixed), altered sleep-wake cycle, emotional
disturbances
Choice of Ix according to the clinical presentation
a) CBP, ESR, RFT, LFT, Ca2+, thyroid function test, blood glucose,
ABG, urine analysis and culture, blood culture, ECG, CXR
b) in selected cases: CRP, troponin, serum B12, folate, syphilis
serology, HIV, autoantibodies, Mg, ammonia, cortisol, lumbar
puncture, toxicology screen, urinary porphyrins, EEG, CT brain
 N5

Neurology
Management
a) Prevention: orientation, early mobilization, visual and hearing
aids, avoid dehydration, psychoactive drugs and sleep deprivation
b) Identify and treat underlying causes (often multifactorial)
c) Review medications and remove potential harmful drugs
d) Protect airway, fluid and electrolytes balance, adequate nutrition
and vitamins, mobilization to prevent VTE, skin and bedsore
care, avoid physical restraints and Foley catheters.
e) Reassuring supportive nursing care in well illuminated, quiet
place. Normalize sleep-wake cycle.
f) Reserve pharmacologic management to agitated patients at risk
of causing harm to themselves or others
- Low dose haloperidol 1-3 mg daily in divided dose
- Atypical antipsychotics (risperidone, olanzapine, quetiapine) as
alternatives
- Lorazepam (second line agent): for withdrawal from
alcohol/sedatives
 N6
Neurology

ACUTE STROKE
It is essential to identify site, subtype, cause and risk factors of stroke.

1. Admit to designated acute stroke unit.

2. Initial assessment: vital signs including airway, respiration,
haemodynamics, conscious level & neurological impairment.
3. Ix : Urgent non-contrast CT brain, CBP, R/LFT, PT, aPTT, blood
glucose, lipid, CXR, ECG.
4. Special Ix (in selected cases): Magnetic resonance imaging (MRI),
magnetic resonance angiography (MRA), computer tomography
angiography (CTA), Echocardiography, Duplex study of carotid
arteries, Transcranial Doppler (TCD), cerebral angiography, VDRL,
hyper-coagulopathy assessment and autoimmune screening.
5. Supportive management:
a) Regular monitoring of neurological and vital signs
b) Swallowing assessment before feeding, positioning ± splinting to
avoid aspiration, contractures, pressure nerve palsy, shoulder
subluxation, pressure sores, etc
c) Ensure good hydration, nutrition and oxygenation
d) Meticulous control of blood sugar & pyrexia
e) Cautious and gradual lowering of elevated blood pressure
 In ischaemic stroke, lowering of blood pressure is considered:
 in case of hypertensive emergencies (eg: hypertensive
encephalopathy, aortic dissection, acute renal failure, acute
pulmonary edema or acute myocardial infarction)
 when the systolic blood pressure >220 mmHg, or the diastolic
blood pressure is >120 mmHg, according to repeated
measurements 20 minutes apart.
 when thrombolytic therapy is considered/given

 In hemorrhagic stroke, lowering of blood pressure is considered:

 if systolic blood pressure >200 mmHg or the mean blood
pressure is >150mmHg
 N7

Neurology
 if systolic blood pressure >180 mmHg or the mean blood
pressure is >130mmHg when there is no clinical evidence of
elevated ICP
 recent studies suggested that acute lowering of systolic BP to
less than 140mmHg is probably safe and associated with mild
improvement in functional outcome
f) Seizure should be treated promptly but prophylactic anticonvulsant
is not indicated for ischaemic or haemorrhagic stroke.
g) Early allied health therapists’ referral and assessment.

6. Specific therapy:
Ischaemic Stroke
a) Aspirin 75mg to 325 mg stat dose within 24 to 48 hours of onset of
acute ischaemic stroke. It should be withheld for the first 24 hrs if
thrombolytic therapy was given.
b) Thrombolytic therapy: in hospitals with stroke thrombolysis
program implemented, inform the thrombolysis team immediately
for urgent evaluation if a potential candidate is identified. (see
protocol for individual hospital for details)
Usual indication:
 Ischaemic stroke onset within 3 to 4.5 hr
 Good premorbid function
Usual contraindication for intravenous thrombolysis:
 Presence of extensive early infarct changes in CT
 Active internal bleeding
 Use of warfarin with INR > 1.7
 Prior intracranial haemorrhage
 Any intracranial surgery, serious head injury or previous
ischaemic stroke within 3 months
 Known intracranial AVM or aneurysm
 Clinical presentation suggestive of SAH
c) Immediate anticoagulation may be considered for acute ischaemic
stroke in:
- Arterial dissection
- Documented cardiac source of embolism
 N8
Neurology

- Cerebral venous thrombosis

Contraindications and precautions
e.g. BP > 180/110 mmHg, large infarct.
The use of anti-coagulation in acute stroke due to large artery thrombosis is
controversial.
d) Decompressive Hemicraniectomy: urgently consult neurosurgeon to
consider decompressive surgery in patient with malignant MCA syndrome
(massive middle cerebral artery territory infarct with eye deviation, dense
hemiplegia and progressive drowsiness +/- unequal pupil size. Serial CT
will show significant infarct with swelling and midline shift).

Intracerebral Haemorrhage
a) Urgent reversal of warfarin effect: for patients with elevated INR
due to warfarin:
 Give vitamin K1 5 to 10mg iv
 Give prothrombin complex concentrate (PCC) 25 to 50 units/kg
+/- FFP (PCC have shorter preparation/infusion time and much
less fluid volume. It is reasonable to consider as an alternative
to FFP since PCC can reverse warfarin effect much faster than
FFP. Fluid overload is not a concern for PCC). However, PCC
treatment is associated with 1% risk of thrombosis e.g. DVT,
PE, MI and ischeamic stroke. So it is contraindicated in
patients with active thrombosis or DIC and Transamine
(tranexamic acid) should not be given together with PCC.
 Give FFP as soon as possible if PCC is not available
b) Neurosurgical consultation:
 Cerebellar haematoma or large cerebellar infarct with
significant mass effect
 Large cerebral haematoma (> 30ml) with mass effect
 Impending or established hydrocephalus/ intraventricular
haemorrhage
 Subarachnoid haemorrhage

7. Rehabilitation:
All acute stroke patients should be assessed for rehabilitation
potential and admission to organized rehabilitation programmes
 N9

Neurology
8. Secondary prevention:
a) Risk factor modification for all types of stroke
b) Oral anticoagulation in cardioembolic stroke (including non-valvular
AF) and anti-phospholipid antibody syndrome
c) Aspirin 80-300mg daily for ischaemic stroke if anti-coagulation not
indicated. Aspirin + controlled release dipyridamole or clopidogrel
are other options for first line anti-platelet agents. Dual anti-platelet
agents may be considered in high risk TIA or minor stroke patients
on individual basis, preferably for a short course of 3 weeks.
d) Carotid Endarterectomy (CEA) or carotid stenting is indicated for
symptomatic extracranial carotid stenosis of 70-99%, depending on
the availability of expertise and their own track record of
peri-interventional complication. Intervention for symptomatic
stenosis of 50-69% can only be considered in centre with very low
complication rate (less than 3%). Carotid stenting will be preferable
in case of: (i) difficult surgical assess, (ii) medical co-morbidities
with high risk of surgery eg: IHD, (iii) radiation induced
arteriopathy, (iv) re-stenosis after CEA. (Please refer to individual
hospital logistic for referral of those patients for carotid intervention
to different involved specialties)
 N 10
SUBARACHNOID HAEMORRHAGE
Neurology

Investigations
1. CT brain as soon as possible
2. Lumbar puncture if CT is negative, to look for bloody CSF and send
CSF for xanthochromia. Xanthochromia is expected if LP is
performed > 12 hr after presumed SAH onset. If LP is performed
within 6 hr from headache onset, absence of xanthochromia is not
reliable to rule out SAH.
3. In patient with high clinical suspicion of CT negative SAH, if LP
result is inconclusive, it is reasonable to proceed to urgent CT
angiogram of brain.
4. Urgent cerebral angiogram if early surgery is considered. If DSA
cannot be arranged urgently, CT angiogram of brain should be
arranged. Most of the aneurysm with size > 5mm can be detected by
CTA.
Management
1. Correct any compromised airway, breathing and circulation
2. Confirm diagnosis (CT + LP) and consult neurosurgeons
3. Assess severity (Hunt and Hess1) and neurological status
4. Early surgery/endovascular coiling should be considered in patients
with grade 1, 2 and 3 SAH after aneurysm demonstrated by
DSA/CTA.
5. Begin nimodipine 60 mg po q4h, or 1 mg/hr iv infusion in grade 1,
2 and 3 patients (use of nimodipine should be individualized in
grade 4 and 5 patients) with BP check
6. Monitor BP closely and control high BP very carefully (exact level of
target BP is controversial, but avoid treating reactive HT due to raised ICP).
BP should be monitored and controlled to balance the risk of
hypertension-related rebleeding, and maintenance of cerebral
perfusion pressure.
7. Antifibrinolytic agent (Transamine): recent evidence suggests that
early treatment with a short course of antifibrinolytic agents (to
reduce rebleeding) combined with early aneurysm treatment
followed by discontinuation of the antifibrinolytic agent (to reduce
its side effect of aggravating ischaemic complication) may be
 N 11

Neurology
reasonable.
8. Monitor GCS, brainstem reflexes, neurological deficits
9. Correct for any abnormalities in To, fluid balance, electrolytes,
osmolality, blood glucose, SaO2 and cardiac rhythm. Dehydration
should be avoided, which might aggravate the severity of
vasospasm if developed subsequently
10. Anticonvulsant if seizures occur
11. Analgesics, sedatives, acid suppressants and stool softener prn
12. Prophylactic anti-convulsant may be considered (benefit
controversial)
1
Hunt & Hess Grading:
Grade 1 Asymptomatic/slight headache
2 Mod/severe headache and nuchal rigidity but no focal or lateralizing neurologic
signs except cranial nerve palsies
3 Drowsiness, confusion and mild focal deficit
4 Stupor, hemiparesis, early decerebrate rigidity and vegetative disturbances
5 Deep coma and decerebrate rigidity
 N 12
Neurology

TONIC-CLONIC STATUS EPILEPTICUS

Operational definition:
1. Two or more epileptic seizures without full recovery of
consciousness between attacks
2. Continuous seizure lasting more than 5 minutes.

High index of suspicious is needed for diagnosis of non-convulsive

status epilepticus. Consider EEG when patient has impaired
consciousness with no accountable cause.

General Management
1. Establish ABC, administer oxygen
2. Ensure good oxygenation and IV access
3. Check glucose and h’stix, electrolytes , NH3, ABG, anticonvulsant
level
4. Give D50 50 ml iv and/or 200 mg thiamine iv if chronic alcoholism
is suspected
5. Resume usual AED for known history of epileptic disorder
6. Suppress clinical seizures, identify complications and etiology
search
7. Consider special test like autoimmune NMDA antibodies when
indicated (like de novo SE)

(1) Stage 1: stage of early status (0–10 mins )

Treat with short acting anticonvulsants (benzodiazepine)

 Lorazepam IV: 4mg over 2 minute, repeat once in 5-10 min, if still
seizure, up to 8mg
 Diazepam IV: 5 – 10 mg over 1-2 minutes, up to 20 mg (if
lorazepam not available)
 Midazolam 0.2 mg/ kg imi, max. 10 mg if no iv access, repeat
once 5-10 mins if still seizure (if no iv access)

Note: total dose of benzodiazepine included those given pre-hospital.

 N 13

Neurology
(2) Stage 2: stage of established status (10-60 mins)

Treat with IV long acting antiepileptic drugs (usually give long

acting AED simultaneously when seizure develops)
 Phenytoin – iv loading dose 15mg/kg at a max. rate of 50mg per
minute. Undiluted (phenytoin precipitates with dextrose). To
consider giving 50% loading dose if patient is taking it before.
Monitor ECG and BP for cardiorespiratory depression,
hypotension and arrhythmias. Beware of purple glove syndrome.
Maintenance dose 5mg/kg/day (usually 100mg Q8H iv).
 Valproate: i.v. bolus 15-30 mg/ kg. Monitor LFT and NH3 level.
Maintenance dose: 30-60mg/kg /day in three to four divided
doses(usual dose : 4-8 mg /kg q8h)
 Levetiracetam: 30-70 mg /kg i.v.bolus over 15 mins,(usual dose :
1.5 -3 gm) then 2-12 gm/d iv divided to Q12H to Q6H (usual
dose:<1500 mg Q12H )
 Phenobarbital: i.v. infusion 10-20 mg/kg at a maximum rate of
100 mg/min. Give IV only when airway is protected due to risk of
respiratory suppression. Maintenance dose 2-3mg/ kg/ day in 2-3
divided doses

(3) Stage 3: stage of refractory status (Seizure despite

benzodiazepine and one anti-epileptic drug treatment)

Treat with general anesthesia, maintain for 12-24 hour before

gradual withdrawal. Use EEG as guideline for treatment response
If seizure recurs, escalate to higher dose and use for longer duration
 Midazolam Bolus 0.1-0.2 mg/kg → maintenance infusion 0.05- 3
mg/kg/hour
 Propofol Bolus 3-5 mg/kg → maintenance infusion 2 -15
mg/kg/hr.
 Thiopental Bolus 2-3 mg/kg → maintenance infusion 3-5
mg/kg/hr.
 N 14
Neurology

(4) Stage 4: stage of super-refractory status epilepticus

SE which has been continued or recurred despite therapy with
general anesthesia for 24 hours or more

 Consider use of ketamine, magnesium, immunotherapy, ketogenic

diet etc.
 N 15

Neurology
GUILLAIN-BARRÉ SYNDROME
Clinical Presentation

1. Subacute progressive polyneuropathy

2. Bilateral symmetric weakness of the limbs
3. Generalized areflexia or hyporeflexia
4. Monophasic illness pattern; clinical plateau by about 4 weeks
5. Miller Fisher syndrome: bilateral ophthalmoparesis, ataxia,
areflexia
6. Look for preceding infection e.g. Campylobactor jejuni,
Mycoplasma pneumonia, CMV/ EBV/ VZV; recent vaccination

Diagnosis

1. Should NOT have new-onset upper motor neuron signs or

sensory level.
2. Consider paralysis due to other acute neuropathies e.g. toxic
neuropathy (alcohol, heavy metals, insecticides, solvents, drugs
like cytotoxic agents), vasculitis, lymphomatous infiltration,
porphyria, critical illness polyneuropathy; or neuromuscular
junction disorders (e.g. myasthenic crisis, botulism)
3. Arrange nerve conduction study (may be normal in 1st week)
4. Perform lumbar puncture: look for cytoalbuminologic
dissociation [Raised CSF protein (may be normal in 1st week,
~80% abnormal in 2nd week, peak in 3rd to 4th week) and CSF
total white cell count < 50 cells/uL]
5. Anti-ganglioside antibodies:
GQ1b is closely associated with Miller-Fisher Syndrome
GM1 and GD1a are associated with acute motor or
motor-sensory axonal neuropathy.
.
 N 16
Neurology

Management

1. Monitor pulmonary dysfunction; consider mechanical ventilation

if:
- hypercarbia and/or hypoxaemia
- FVC < 15 ml per kg of BW
- inefficient cough, impaired swallowing, atelectasis
2. Watch for autonomic dysfunction (potentially fatal):
- cardiac monitoring (for arrhythmia and severe bradycardia)
- close BP monitoring (for extreme hypertension or hypotension)
3. Other supportive measures:
- monitor swallowing +/- temporary non-oral feeding
- DVT prevention
- urinary retention, constipation
- clear secretion
- early mobilization
- medical treatment for pain and paraesthesia
4. Immonotherapy (in severe cases):
- give intravenous immunoglobulin (IVIg) 0.4g/kg/day for 5 days
- alternatively start plasma exchange 50ml/kg/session of plasma for
5 exchanges over 2 weeks
6. Combination of IVIg and PE is not better than PE or IVIg alone.
Steroid treatment has no benefit.
 N 17

Neurology
MYASTHENIC CRISIS
Crisis: severe generalized weakness and need for respiratory support.
*Tensilon test - diagnostic test in untreated disease; not reliable in
differentiating myasthenic and cholinergic crisis and not without risk,
hence not recommended.

Management
1. Watch out for respiratory failure in any patient with progressive
weakness and bulbar symptoms
2. Closely monitor FVC, SaO2 and ABG. Consider mechanical
ventilation if:
- hypercarbia and/or hypoxaemia
- FVC < 15 ml per kg of BW
- inefficient cough, impaired swallowing, atelectasis
3. Stop anticholinesterase if patient is intubated
4. Give intravenous immunoglobulin (IVIg) 0.4g/kg/day for 5 days.
An alternative is plasma exchange 50ml/kg/session of plasma on
alternate days until adequate response achieved (usually after 5 - 6
exchanges)
5. Resume anticholinesterase at a smaller dose 48-72 hours after
stabilization and titrate accordingly
6. Start prednisolone 1 mg/kg/day; beware that early steroid-induced
deterioration may occur
7. Identify and treat any precipitating conditions (e.g. underlying
infection)
8. General supportive measures:
- monitor swallowing +/- temporary non-oral feeding
- DVT prevention
- urinary retention, constipation
- clear secretion
- early mobilization
9. Beware with the use of any drug that might worsen MG. e.g.
aminoglycosides, quinolones, quinine, quinidine, procainamide,
 N 18
Neurology

-blockers, muscle relaxants, phenytoin, penicillamine,

magnesium.
 N 19

Neurology
ACUTE SPINAL CORD SYNDROME
(Also refer to page PM15 and GM26)
It is of paramount importance to make an early diagnosis of acute
spinal cord compression, to provide the patient with the best chance for
neurological recovery. “Sensory level” can be falsely localizing and
imaging of spinal cord rostral to clinical sensory level is advisable.
Investigations to delineate level and nature of spinal cord lesion
1. XR spine
2. MRI spine of relevant level if immediately available; otherwise
myelogram and CT myelogram
3. Lumbar puncture if transverse myelitis is suspected; send CSF for
microscopy and cell counts, culture, AFB culture, biochemistry,
viral study and cytology; VDRL and oligoclonal band in selected
cases

Management
1. Correct any compromised airway, breathing and circulation
2. Immobilize relevant level of spine in case of traumatic spinal cord
injury or spine instability.
3. Initiate appropriate treatment for specific spinal cord lesions:
 neurosurgical / orthopaedic consultation for structural lesions
 antimicrobial therapy for abscess or other infections
 consider methylprednisolone (1 gram iv over one hour daily for 3 days,
with cardiac monitoring) in non-infectious transverse myelitis
4. Institute general supportive care:
 proper positioning & splinting
 adequate hydration and nutrition
 bladder catheterization
 prevent DVT
5. Close monitoring of respiratory function (FVC, respiratory rate)
and cardiac monitoring in case of high cord lesions
 N 20
Neurology

DELIRIUM TREMENS

 Characterized by hallucinations, agitation, confusion,

disorientation and autonomic overactivity including fever,
tachycardia and profuse perspiration in the setting of acute
reduction or abstinence from alcohol.
 Typically occurs 24-48 hours after the last drink and lasts one to
five days.
 Associated with a mortality of up to 5 %
 Diagnosis based on clinical features and exclusion of other causes
of delirium

Management
1. General supportive care
2. Monitor BP/P, I/O, To, cardiac rhythm
3. Correct fluid and electrolyte disturbance. Watch out especially for
hypomagnesaemia, hypokalaemia , hypoglycaemia and
rhabdomyolysis
4. Start benzodiazepine to treat psychomotor agitation
 chlordiazepoxide 10 mg – 20 mg TDS oral ( avoid in patients with
severe liver disease because of the risk of oversedation )
 lorazepam 2 mg TDS oral
 diazepam 5 mg TDS oral
 adjust dose according to severity. Reduce dose in elderly. Taper
dosage gradually over 5-7 days.
5. Concurrent use with IV thiamine. Give high dose thiamine in IV
form, e.g.100 mg IV Q8H
6. Ensure adequate nutrition and vitamins
7. Search out for and treat any concurrent illnesses
8. Reassuring nursing care in well-illuminated, quiet place.
 N 21

Neurology
WERNICKE’S ENCEPHALOPATHY

An acute or subacute neuropsychiatric disorder due to thiamine

deficiency which is underdiagnosed. Delayed diagnosis and treatment
can lead to irreversible brain damage (Korsakoff’s syndrome) and fatal
outcome.
The classical triad ophthalmoplegia, ataxia and confusion occurs only in
10% of patients. Difficult to differentiate from acute alcohol
intoxication.

Caine’s Criteria in Alcoholics

2 of the following 4 signs
‐ Dietary deficiency
‐ Oculomotor abnormalities
‐ Cerebellar dysfunction
‐ Either an altered conscious state or mild memory impairment

Predisposing Factors
‐ Alcoholics plus malnutrition
‐ GI surgery including bariatric surgery
‐ Repeated vomiting including hyperemesis gravidarum
‐ Chronic diarrhea
‐ Cancer
‐ Systemic illnesses (renal failure on CAPD or HD, AIDS, prolonged
infectious diseases, thyrotoxicosis)
‐ Dietary restriction e.g. anorexia nervosa, hunger strike, elder neglect

Investigations
WE is a clinical diagnosis which requires high index of suspicion
‐ EEG and CSF are normal or non-specific.
‐ MRI brain may show atypical features especially in non-alcoholics
‐ Pretreatment RBC transketolase is available locally but of limited
value in emergency diagnosis and treatment
‐ Serum magnesium (a co-factor for normal functioning of
thiamine-dependent enzymes)
 N 22
Neurology

Management
‐ Thiamine must be given immediately and in adequate amounts
‐ Oral thiamine is poorly absorbed and ineffective
‐ Intravenous 200-500mg thiamine in 100ml normal saline or 5%
dextrose over 30 minutes thrice daily for 2-3 days
‐ If improved, followed by 250mg thiamine IV/IM daily for 3-5 days,
or until improvement ceased
‐ Thiamine must be given before or concomitantly with any
carbohydrate
‐ Resuscitation facilities and adrenaline for rare occurrence of
anaphylaxis
‐ Monitor BP/P and temperature (hypo-/hyperthermia, hypotension
and tachycardia can occur)
‐ Monitor neurological signs (ophthalmoplegia can resolve within
hours)
‐ Correct any hypomagnesaemia
‐ Balanced diet
‐ Treat any concurrent illnesses (e.g. delirium tremens, hepatic
encephalopathy, traumatic subdural hematoma, sepsis)
 N 23

Neurology
PERI-OPERATIVE MANAGEMENT IN
PATIENTS WITH NEUROLOGICAL DISEASES
High risk of peri-operative pulmonary complications:
Parkinsonism, myasthenia gravis, other neuro-muscular disorders
affecting respiratory muscles and any neurological deficits
compromising respiratory effort.

Peri-operative management:
1. Comprehensive pulmonary assessment before operation
2. Optimal control of neurological conditions
3. Vigorous peri-operative chest physiotherapy
4. Regular monitoring of FVC, respiratory rate, SaO2, ABG
5. Continue anti-epileptic, anti-cholinesterase and anti-parkinsonism
drugs as close to normal schedule as possible.
Resume as soon as possible after operation.
Alternative preparation or drugs:
Anti-cholinesterase: Neostigmine 0.5 mg im/iv q4-6h
Anti-epileptic: phenytoin / sodium valproate/ levetiracetam /
lacosamide available in iv form
Transdermal patch of Rotigotine and parenteral apomorphine is
available if anti-parkinsonism drugs cannot be resumed quickly.
6a. Bridging therapy is recommended for patient with high risk of
thromboembolic event after anti-coagulant is stopped
6b. Discontinue anti-platelet agents 1 week before elective surgery, but
aspirin may be continued in the following procedures: (i) dental
procedure (ii) endoscopies with biopsies and polypectomies, (iii)
ophthalmologic procedures, (iv) peripheral vascular procedure, (v)
neuraxial anesthesia. Warfarin can be continued for most dental
procedures if INR is kept at a lower range before the procedure and
close monitoring in the day ward after the procedure is available.
7. Avoid aminoglycosides, quinolones, morphine, quinidine, β
-blockers, procainamide, penicillamine for myasthenia gravis
 N 24
Neurology

Risk of Peri-operative stroke

1. Increase in hypertension
2. Asymptomatic carotid bruit is not an independent risk factor.
Intervention to asymptomatic carotid stenosis before general surgery
(open heart surgery is excluded) might not be justified since the risk
of intervention would outweight its potential benefit.
3 Symptomatic severe carotid stenosis (> 70%) should be repaired
before non-emergency operation. Symptomatic large vessel stenosis
in the posterior circulation need to have aggressive intraoperative
maintenance of blood pressure to avoid prolonged hypotenion
4. Decreased by avoiding hypotension, hypovolaemia, polycythaemia
and anaemia.
5. Postpone elective procedures for at least 6 weeks after an ischaemic
stroke to allow healing at the infarct site; minor or lacunar stroke
may require shorter waiting period.
 Respiratory
Medicine
Respiratory
Medicine
 P1

MASSIVE HAEMOPTYSIS

Definition: Arbituary, expectorated blood ranging from

>100-200ml/day. Important management considerations include rate of

Respiratory
Medicine
bleeding and underlying lung function. Increased volume of bleeding
confers a much higher risk of death due to asphyxia than to
haemodynamic derangement. Airway protection is most important in
massive haemoptysis, close observation and treatment in ICU/HDU is
desirable.

Management objectives
Prevent asphyxia, localize bleeding site, stop bleeding, determine cause
of bleeding and treat underlying cause.

Management
1. Close monitoring of vital sign, i.e. BP/P, RR, SaO2
2. O2 supplement
3. Establish IV access
4. Take blood for CBP, clotting, ABG and X-match
5. Sputum for C/ST, AFB & cytology
6. Avoid sedation and cough suppressant
7. Antibiotic if infection is suspected, e.g. bronchiectasis, TB
8. Lie lateral on side of bleeding if lateralized
9. If depressed conscious state with risk of asphyxia, intubate for
suction and ventilation (single lumen ET if urgent airway access is
required; double lumen ET placement by anaesthetist is better for
isolation of bleeding side)
10. Early bronchoscopy to localize bleeding, diagnose endobronchial
lesion and for therapy

Persistent life-threatening haemoptysis

 Consult radiologist for bronchial arteriogram  bronchial artery
embolization if expertise available
 P2
 Consult surgeon for emergency lung resection if bleeding is
localized and adequate pulmonary reserve.
Respiratory
Medicine
 P3

SPONTANEOUS PNEUMOTHORAX
(Ref. BTS pleural disease guideline 2010)

Suspect tension pneumothorax if associated with cyanosis, sweating,

Respiratory
severe tachypnea, tachycardia and hypotension.

Medicine
Proceed to chest drain if bilateral pneumothorax / haemodynamically
unstable.

Definition
Size: visible rim between lung margin and chest wall at level of hilum.
Small < 2cm & large  2cm
Primary spontaneous pneumothorax (PSP): no underlying lung
disease
Secondary spontaneous pneumothorax (SSP): underlying lung
disease

Management
O2 and analgesic prn

Patients with PSP or SSP and significant breathlessness associated with

any size of pneumothorax should undergo active intervention.

PSP
1. Minimal symptoms
Observation is treatment of choice for small PSP without
significant breathlessness

2. Symptomatic
Needle aspiration (NA) or small-bore (< 14 F) chest drain

SSP
Small bore chest drain
 P4
Referral to thoracic surgeons for persistent air leak at day 2 for SSP
and day 3 to 5 for PSP
Chemical pleurodesis may be considered for patients with SSP but unfit
for surgery
Respiratory
Medicine

Indication for surgical advice

Second ipsilateral pneumothorax, first contralateral pneumothorax,
synchronous bilateral spontaneous pneumothorax, spontaneous
haemothorax, professions at risks (eg. pilots, divers), pregnancy.
 P5

PLEURAL EFFUSION

Diagnosis
1. Pleural tapping should not be done for bilateral pleural effusions in

Respiratory
Medicine
clinical setting strongly suggestive of a transudate unless presence
of atypical features or fail to respond to therapy
2. Diagnostic tapping with bedside USG guidance improves success
and reduces complications
3. Percutaneous pleural biopsy only diagnostically useful in areas
with high incidence of TB
4. Thoracoscopy is next investigation of choice in exudative pleural
effusions with inconclusive diagnostic pleural tap
5. Bronchoscopy can be considered if presence of haemoptysis or
clinical or radiologic features suggestive of endobronchial
obstruction

Indications for pleural fluid drainage in pleural infection

1. Frank pus or turbid/cloudy pleural fluid on diagnostic tapping
2. Loculation on CXR or pleural thickening with contrast
enhancement on CT thorax
3. Positive gram-stain +/- positive culture of pleural fluid
4. Pleural fluid biochemistry: pH <7.2, LDH >1000 IU/L or glucose
<2.2mmol/L
5. Large non-purulent effusions (> 40% of hemithorax)
 P6

Consider intrapleural fibrinolytic to decompress

multiloculated pleural collections in patients not fit for
surgery
Respiratory

Indication for chest drain insertion

Medicine

1. Empyema or complicated parapneumonic effusion

2. Symptomatic malignant pleural effusion (see below)
3. Haemothorax (surgical consultation is usually indicated)

Management of persistent/ recurrent malignant pleural effusion

1. Supportive care
2. Consult respiratory physician for difficult cases
3. Tube drainage and chemical pleurodesis
 Agent: Talc up to 5g in 100ml NS
 Must be performed under adequate analgesia +/- sedation
 Clamp drain for 1 to 2 hours post-sclerosant application, then
release clamp
 Chest tube kept unclamped thereafter for drainage until daily
output <150ml /day and CXR shows the lung to be re-expanded
with most of the effusion drained
4. Surgical pleurodesis (can be considered in patients with good
performance status)
5. Long term ambulatory indwelling pleural catheter drainage
(including patients with trapped lung)
 P7

OXYGEN THERAPY
The goal of O2 therapy: to deliver the minimum concentration
required for adequate tissue oxygenation with the least risk of toxicity.

Respiratory
Prescriptions should be precise and adequately monitored (e.g. by SpO2

Medicine
or ABG).
Device used should be safe, effective and with the greatest patient
comfort and acceptance at the least cost.

Common oxygen delivery methods

Variable performance devices
Actual FiO2 delivered not fixed, depends on multiple factors including
O2 flow, oropharyngeal geometry, tidal volume, respiratory rate &
pattern

1. Standard dual-prong nasal cannula

o FiO2 0.23 to 0.40 if O2 flow rate set at 1 to 6 L/min
o FiO2 non-specific roughly 20% + (4  oxygen litre flow per
minute)
o Most comfortable and cost-effective
o Higher flow (i.e. >6L/min), leading to wastage of O2 and dryness
of nasal mucosa

2. Simple face mask with no reservoir bag

o FiO2 up to 0.50 if O2 flow rate set at 6 to 10 L/min
o Actual FiO2 non-specific, depends on patient’s condition
o O2 flow rate set below <5L/min may cause CO2 rebreathing

3. Rebreathing mask with reservoir bag

o FiO2 0.70 if O2 flow rate set at 6 to 10L/min
o O2 flow must be  6 L/min to keep reservoir bag inflated
throughout inspiration & expiration
o No one way valve between reservoir bag and mask
 P8
4. Non-rebreathing mask with reservoir bag
o FiO2 0.60 – 1.00 if O2 flow rate set at 10 – 15 L/min
o Equipped with one-way valves to prevent exhalation into
reservoir bag and inhalation through mask exhalation ports (but
usually only one of the two valves on the mask exhalation ports
Respiratory
Medicine

is installed for safety reason)

Fixed performance devices

Delivery of oxygen at a fixed and pre-set concentration regardless of
patient’s clinical status (e.g. respiratory rate, tidal volume….)
1. Venturi mask
o Accurate FiO2 adjustable from 0.24 to 0.50 if O2 flow rate set at
3 – 15 L/min (O2 required to drive can be read off from the
Venturi device)

2. Humidified high flow nasal cannula, e.g. Optiflow, Airvo systems….

o Delivers humidified O2 at fixed FiO2 at high flow (up to
60L/min)
o Better patient’s tolerance to high flow O2 and the O2 is
humidified
o Actual FiO2 delivered can be set (by internal oxygen blender) or
determined (by sensor) depending on the device used

Other common oxygen delivery methods

1. T-piece to endotracheal or tracheostomy tube: O2 delivered through
the shorter end, open window by one-third if PCO2 is high
2. Thermovent to endotracheal or tracheostomy tube: watch out for
sputum blockage
3. Tracheostomy mask: consider to use humidification in
non-infectious situation (e.g. heated humidifier)
 P9
Indications for long-term O2 therapy in COPD
Start only when clinically stable for 3-4 weeks and after optimization of
other therapy

Continuous oxygen:

Respiratory
Medicine
1. Resting PaO2 ≤7.3 kPa (55 mm Hg) or SaO2 ≤88%: to maintain
PaO2 ≥8 kPa (60 mm Hg or SaO2 ≥90%)
2. Resting PaO2 7.4 to 7.9 kPa (56 to 59 mm Hg) or SaO2 ≥89% in the
presence of any of the following:
 Dependent oedema suggestive of cor pulmonale.
 P pulmonale on ECG (P wave >3mm in standard leads II, III, or
aVF)
 Erythrocythaemia (haematocrit >56%)

Noncontinuous oxygen:
Oxygen flow rate and number of hours per day must be specified
1. During exercise: PaO2 ≤7.3 kPa (55 mmHg) or oxygen saturation
≤88% with a low level of exertion
2. During sleep: PaO2 ≤7.3 kPa (55 mmHg) or oxygen saturation
≤88% with associated complications, such as pulmonary
hypertension, daytime somnolence, and cardiac arrhythmias.
 P 10

ADULT ACUTE ASTHMA

(Ref: GINA Guidelines 2014)

Definition of asthma exacerbations

Respiratory
Medicine

Episodes characterized by a progressive increase in symtoms of

shortness of breath, cough, wheezing or chest tightness AND
progressive decrease in lung function.
The decrease in expiratory airflow by PEF or FEV1 is more reliable
indicators of severity of the exacerbation than symptoms

Assessment
Initial assessment:
- Airway, Breathing, Circulation
- Life-threatening features
o Drowsiness, Confusion, Silent chest
- Consult ICU if any +ve
- Prepare for intubation

Further assessment
- According to worst feature identified  Moderate vs Severe
Exacerbation

Mild/Moderate Severe
Talks in phrases Talks in words
Prefers sitting to lying Sits hunched forwards
Calm Agitated
Increased respiratory rate RR >30/min
No use of Accessory muscles Use of Accessory muscles
Pulse rate 100-120/min Pulse rate >120/min
SpO2 (RA) 90-95% SpO2 (RA) <90%
PEF >50% predicted/best PEF ≤ 50% predicted/best
 P 11
Monitoring
- Vital signs, pulse oximetry, PFR/FEV1, ABG, electrolytes, CXR

Management
Moderate exacerbation

Respiratory
Medicine
 Controlled O2 aiming SpO2 93-95% by nasal cannulae or mask
 Short-acting 2-agonists
o Salbutamol 4 puff q4h with spacer + prn use
o Higher dose/more frequent dosing may be considered in
very symptomatic patients or those with severe exacerbation
 Oral corticosteroids
 ± Ipratropium bromide

Severe exacerbation
 Same as treatment for moderate episode plus
 Ipratropium bromide 3-4puffs with spacer
 Oral/IV corticosteroids
 Consider magnesium sulphate 1.2-2g iv over 20 minutes

Reassessment
- Clinical status and response to treatment
- Preferably with lung function measurement (PEF/FEV1)
- In ALL patients 1 hr after initial treatment

- If satisfactory response
 Controlled O2 aiming 93-95%, gradual weaning
 Prednisolone up to 50mg/d (or Hydrocortisone 200mg/d in
divided doses) for 5-7 day, adequate for most patients
 Continue inhaled 2 agonist q4h
- If unsatisfactory response
 Inhaled 2 agonist 6-10 puffs up to q15min
 Inhaled ipratropium bromide 3-4puffs then q6-8h
 P 12

Consider ICU admission if

- Life threatening features present
- Deterioration in PEF/FEV1
- Worsening or persistent hypoxia or hypercapnia
Respiratory
Medicine

- Respiratory failure requiring IPPV

- Respiratory or cardiorespiratory arrest

After improvement
- Stabilize in ward
- Discharge may be considered when symptoms have cleared, lung
function PEF/FEV1>60% predicted/best
- Actions recommended on discharge include
 Identifying & avoiding trigger factor(s) that precipitated
attack
 Prednisolone tablets (up to 50mg daily for 5-7 days)
 EARLY outpatient follow-up and review of long term
treatment plan especially inhalational steroids, AND
reviewing technique on use of inhaler and peak flow meter

Therapies NOT recommended during acute attacks:

- Sedatives (avoid strictly)
- Cough suppressant (avoid as far as possible)
- Mucolytic drug (may worsen cough)
- Chest physiotherapy (may increase patient discomfort)
- Antibiotics (unless strong evidence of lung infection)
- Hydration with large volumes of fluid
 P 13

LONG TERM MANAGEMENT OF ASTHMA

(Ref: GINA Guidelines 2014)
NOTE

Respiratory
Medicine
a. The goal of asthma care is to achieve and maintain symptoms
control; and to minimize future risks, such as exacerbations, fixed
airflow limitation and side effects of treatment.
b. Partnership between the patient and the health care providers is
needed for effective asthma management.
c. A continuous cycle of “assessment/treatment/review of response”
formed the basis of asthma management
d. Each patient is assigned to one of five “treatment steps”. Depending
on their current level of asthma control, treatment should be
adjusted (e.g. stepping up/down), taking into account of the
patient’s characteristics and preference
e. In treatment-naïve patients with persistent asthma, treatment should
be started at Step 2, or Step 3 if very symptomatic.
f. Reliever medication (rapid-onset bronchodilator) should be
provided for quick relief of symptoms at each treatment step.
g. Patients should avoid or control triggers at all times.
h. Patient education and treatment of modifiable risk
factors/comorbidities (e.g. smoking, obesity, anxiety) should be
included in every treatment step.

GINA assessment of Asthma control (2014)

1. Symptom control over past 4 weeks
- Daytime asthma symptoms > 2/week
- Nocturnal symptoms/awakening
- Reliever needed for symptoms > 2/week
- Activity limitation due to asthma
Well controlled: None
Partly controlled: 1-2 features
Uncontrolled: >3-4 features
2. Assessment on risk factors for poor asthma outcomes/ risk of
exacerbations
 P 14
- Uncontrolled symptoms
- Excessive SABA use
- Inadequate ICS: not prescribed, poor compliance, poor inhaler
technique
- Low FEV1, esp if <60% predicted/best
Respiratory
Medicine

- Major psychological/socioeconomic problems

- Exposures: e.g. smoking, allergen
- Comorbidities
- Sputum or blood eosinophilia
- Pregnancy
- History of intubation/ICU admission for asthma
- ≥ 1 severe exacerbation in last 12 months

TREATMENT
STEP 1: As-needed reliever medication
a. For untreated patients with occasional daytime symptoms
b. Short-acting bronchodilator as reliever: Inhaled 2-agonist prn
(but 2times/week).
c. Inhaled anticholinergic, short-acting oral 2-agonist or
therophylline NOT recommended for slower onset of action and
higher risk of side-effects.
d. Inhaled 2-agonist, leukotriene modifier may be considered
before exercise or allergen exposure.

STEP 2: Reliever medication plus a single controller

a. Reliever: Inhaled 2-agonist prn (but 2times/week).
b. Preferred daily controller medication: Low dose Inhaled
corticosteroids (ICS)
c. Alternatives: Leukotriene receptor antagonists (LTRA)
d. Not-recommended for routine use: Cromoglycate or
Nedocromil or Theophylline SR.
STEP 3: Reliever medication plus one or two controllers
a. Reliever: Inhaled 2-agonist prn (but 2 times/week).
b. Preferred daily controller medication:
 P 15

(i) Low dose ICS + long-acting inhaled 2-agonist (LABA),

OR
(ii) Combination of low dose ICS/Formoterol as both
maintenance and reliever treatment
c. Alternatives:

Respiratory
Medicine
(i) Medium dose ICS
(ii) Low dose ICS + LTRA
(iii) Low dose ICS + Theophylline SR
d. LTRA for aspirin sensitivity or exercise-induced asthma

STEP 4: Reliever medication plus two or more controllers

a. Reliever: Inhaled 2-agonist prn.
b. Preferred daily controller medications:
(i) Medium/high dose ICS + LABA
(ii) Combination of low dose ICS/Formoterol as both
maintenance and reliever treatment
c. Alternatives
(i) High dose ICS + LABA
(ii) Medium/high dose ICS + Theophylline SR/LTRA

STEP 5: Reliever medication plus additional controller options

a. As in Step 4 plus Specialist referral for investigation and
consideration of add-on treatment
(i) Options
a. Anti-IgE treatment
b. Sputum-guided treatment (sputum eosinophilia)
c. Bronchial thermoplasty
d. Low dose oral corticosteroid

Step-down
Review treatment every 3–6 months. If control has been sustained for >3
months, consider a gradual stepwise reduction.
Aim at finding the patient’s lowest treatment that controls both
symptoms and exacerbations.
 P 16
Step-up
If control is not achieved, consider stepping up AFTER reviewing
patient’s inhaler technique, compliance, environmental control
(avoidance of allergens/trigger factors), comorbidities and alternative
diagnoses.
Respiratory
Medicine

ICS dose
Drug Daily dose (mcg)
Low Medium High
Beclometasone 200-500 >500-1000 >1000
dipropionate (CFC)
Beclometasone 100-200 >200-400 >400
dipropionate (HFA)
Budesonide (DPI) 200-400 >400-800 >800
Ciclesonide (HFA) 80-160 >160-320 >320
Fluticasone 100-250 >250-500 >500
propionate (DPI)
Fluticasone 100-250 >250-500 >500
propionate (HFA)
Mometasone furoate 110-220 >220-440 >440
Triamcinolone 400-1000 >1000-2000 >2000
acetonide
 P 17

CHRONIC OBSTRUCTIVE
PULMONARY DISEASE (COPD)
Based on Global Initiative for Chronic Obstructive Lung Disease

Respiratory
Medicine
(GOLD) guidelines 2014

Treatment of acute exacerbation

1. Supplemental oxygen (start with 24% Venturi mask or 1-2L/min by
nasal prongs) to maintain SpO2 88-92%.
Check ABGs 30-60 mins later and modify flow rate according to
PaO2 and pH.
2. Short acting inhaled (with spacer) 2 agonist (Ventolin) +/-
ipratropium bromide (Atrovent)
3. If no response, consider iv aminophylline (second line therapy)
4. Corticosteroids (Hydrocortisone 100 mg iv Q6-8 hours or oral
Prednisolone 30-40 mg daily). Steroid should be discontinued after
the acute episode (e.g. 5-10 days)
5. Antibiotic in patients required invasive or non-invasive ventilation
(NIV), and/or at least two cardinal symptoms (one being  sputum
purulence):
  dyspnoea;
  sputum volume;
  purulent sputum
6. NIV – to relief dyspnoea by  work of breathing (WOB), improve
respiratory acidosis, avoid complications
Indications (NB also read contraindications in NIV chapter):
 Respiratory acidosis (pH ≤7.35 and/or PaCO2 >6.0kPa)
 Moderate to severe dyspnoea with signs of respiratory muscles
fatigue and  WOB, e.g. use of accessory muscles, paradoxical
abdominal motion, intercostal space retraction, RR > 25/min.
 Check ABG 30-60mins after initiation of NIV. Do not delay
intubation and mechanical ventilation if no improvement.
 P 18
7. Invasive mechanical ventilation (IMV)
For patients who are / have:
 Unable to tolerate or failed NIV
 Severe haemodynamic instability without response to fluid and
vasopressor.
Respiratory
Medicine

 Severe ventricular arrhythmia, respiratory or cardiac arrest.

 Impaired consciousness, massive aspiration, or unable to clear
secretions.

** These patients should be managed in intensive care unit (ICU); if

not available, then preferably in intermediate or special respiratory
care units with expertise in this area **
 P 19
Treatment of stable COPD

All patients should have smoking cessation, encouraged physical

activity and vaccination +/- rehabilitation.
Pharmacological treatment according to patient groups (A, B, C, D)

Respiratory
Medicine
based on symptom level and risks (airflow limitation and
exacerbation history)
A: Less symptom, low risk
B: More symptom, low risk
C: Less symptom, high risk
D: More symptom, high risk
 

 
 
(SABA, short acting beta-agonist; SAMA, short acting
anti-muscarinic agents; LABA, long acting beta-agonist; LAMA,
long acting anti-muscarinic agents; ICS, inhaled corticosteroid; CAT,
COPD Assessment Test; mMRC, modified Medical Research
Council breathless scale)
 P 20
Other points to note:
1. Steroid trial not predictive of response to inhaled steroid
2. Long-term oxygen therapy for chronic respiratory failure with
severe resting hypoxaemia
 Start only when clinically stable for 3-4 weeks after optimization
Respiratory
Medicine

of other therapy, in COPD patients who have:

A. Continuous oxygen therapy ( ≥15hours/day):
‐ Resting PaO2 ≤7.3 kPa (55 mm Hg) or SaO2 ≤88%: to maintain
PaO2 ≥8 kPa (60 mm Hg or SaO2 ≥90%); or
Resting PaO2 7.3 to 8.0 kPa (55-60 mm Hg) or SaO2 >88% with
evidence of peripheral oedema suggestive of CCF, pulmonary
HT( p pulmonale on ECG (P wave >3mm in standard leads II,
III, or aVF), or polycythaemia (haematocrit > 55%)
B. Non-continuous oxygen: Oxygen flow rate and number of hours per
day must be specified.
‐ During exercise: PaO2 ≤7.3 kPa (55 mmHg) or oxygen saturation
≤88% with a low level of exertion
‐ During sleep: PaO2 ≤7.3 kPa (55 mmHg) or oxygen saturation
≤88% with associated complications, such as pulmonary HT,
daytime somnolence, and cardiac arrhythmias”
 P 21

OBSTRUCTIVE SLEEP APNOEA

Suspect OSA if
(1) Snoring at night, PLUS

Respiratory
(2) Excessive daytime sleepiness (EDS)

Medicine
Mild: activity with little attention needed e.g. public transport
Moderate: activity with some attention e.g. conference
Severe: activity with much concentration e.g. phone call,
conversation; OR
(3) Any two out of the followings:
(i) Intermittent nocturnal arousal, (ii) Nocturnal choking, (iii)
Unrefreshed sleep at wakening, (iv) Daytime fatigue,
(v) Impaired daytime concentration

Indications for diagnostic sleep study

1. Suspect OSA
2. Unexplained pulmonary hypertension
3. Recurrent cardiovascular events e.g. CVA, angina, CHF; or poorly
controlled hypertension despite adequate medical therapy and
optimization of risk factors

Severity of OSA based on apnoea-hypopnoea index (AHI)

Mild: 5-15/hr Moderate: 15-30/hr Severe: > 30/hr

Indications for urgent arrangement of nasal CPAP

1. Pickwickian syndrome with daytime alveolar hypoventilation,
pulmonary hypertension or cor pulmonale.
2. Nocturnal malignant arrhythmia related to the OSA.
3. Nocturnal angina related to the OSA.
4. Severe EDS that may impose risk to the patient and/ or others e.g.
professional driver especially with history of road traffic accident.
 P 22

PREOPERATIVE EVALUATION OF PULMONARY

FUNCTION
Respiratory
Medicine
 P 23
High postoperative risk if :
1. Thoracic surgery: pre-op FEV1<1L or epo FEV1 < 40% predicted
2. ABG – Elevated PaCO2 >6kPa (45mmHg)
3. FEV1, FVC or MVV < 50% predicted
4. Evidence of pulmonary hypertension

Respiratory
Medicine
5. Preoperative cardiopulmonary exercise testing (CPET): VO2max <
15ml/kg/min.
Consult respiratory physician in high risk cases.
 P 24

MECHANICAL VENTILATION
1. Indications
 Respiratory failure not adequately corrected by other means
 Failure to protect the airway - (e.g. GCS<8)
Respiratory
Medicine

 Cardiac and/or respiratory arrest

 Clinical instability e.g. severe hypotension

2. Criteria suggesting the need of Mechanical ventilation

Laboratory Criteria:
Blood gas PaO2 < 7.3 kPa despite O2 supplement
PaCO2 > 6.7 kPa with pH < 7.32
Pulmonary funtion tests Vital Capacity < 10 ml/kg
FEV1 < 10ml/kg

Clinical Criteria:
Apnoea / hyponoea
Stridor
Depressed menal status
Remarks: Clinical assessment is more impotant than these criteria

3. Suggested initial ventilator settings

Disease Acute Resp distress Acute pulmonary *Obstructive Restrictive

condition syndrome (ARDS) oedema lung disease lung
(COPD/Asthma) disease
Tidal volume
(ml/kg 6 8 – 10 6–8 8 – 10
predicted BW)
Frequency or 10 – 12 10 – 12 8 – 10 10 – 12
RR(breath/min) Permissive Pressure control Ensure long To achieve
hypercapnia (keep (PC) +/- pressure enough desired pH
pH just > 7.25 as support (PS) expiratory time and ABG
“lung protective mode to achieve to avoid
strategy”) comfort air-trapping
PEEP (cmH2O) 8 – 15 High (8 – 15) 0–5 5
May need > 10 initially, can be
(open lung rapidly tailed
approach) down
*Peak pressure usually targeted at <35 cmH2O
 P 25

3 Monitoring during mechanical ventilation

a. General: vital signs, bowel motion, conscious level,
psychological status
b. P/E: Signs of upper airway obstruction (excessive inspiratory

Respiratory
efforts, inspiratory in-sucking of lower rib cage), ETT (patency,

Medicine
positioning), chest wall movement (especially asymmetry),
pressure sores, signs of DVT, hydration & nutritional status
c. Important parameters:
i. Cuff pressure: 20 – 30 cm H2O
ii. Ventilatory status:
 Volume-controlled mode or SIMV (VC + PS): avoid
excessive airway pressure
 Pressure-controlled mode or SIMV (PC + PS): monitor
tidal volume which varies with airflow obstruction or
lung compliance
 Pressure support mode: avoid excessive/inadequate tidal
volume and long/short inspiratory time
 Pause or plateau pressure (PP): Barotrauma risk  if PP
 35 cm H2O
 Auto-PEEP

4 Patient-ventilator asynchrony
Do not simply sedate a patient who is asynchronous with the
ventilator, look for possible underlying cause(s).

Checklist for trouble-shooting:

Problems Examples
a. Airway-related Inappropriate size/position (Normal 4-6 cm
above carina) of ET tube, leaky cuff/excessive
cuff pressure, blocked /kinked tube,
dislodgement
b. Ventilator-related Inadequate humidification, obstruction/ leak in
circuit, ventilator malfunction
 P 26

c. Inappropriate Inappropriate TV/ RR (or I:E) /sensitivity

ventilator settings settings, inadequate FiO2 and/or ventilation
with persistent hypoxaemia or hypercapnia
d. Underlying disease Stiff lungs, low cardiac output, poor cerebral
Respiratory
Medicine

perfusion, septic state

e. Complications of Atelectasis, ventilator-associated pneumonia,
mechanical pneumothorax, endobronchial intubation
ventilation
f. Others Fear, anxiety, pain, secretions in airway,
hunger, inability to open bowels/to move,
pressure sore
 P 27

NON-INVASIVE VENTILATION (NIV)

More evidence of efficacy in:
1. COPD with respiratory acidosis pH 7.25-7.35
2. Hypercapnic respiratory failure secondary to chest wall deformity

Respiratory
Medicine
or neuromuscular disease
3. Cardiogenic pulmonary edema
4. Weaning from tracheal intubation (esp COPD)
5. Acute respiratory failure in immunosuppressed states
6. Post-operative hypoxaemia (except in upper GI surgery)
7. Patients decided not for intubation

Less efficacious or even harmful in:

1. Acute severe asthma
2. Acute lung injury (ALI) or Acute respiratory distress syndrome
(ARDS)
3. Pneumonia, esp if copious secretions
4. Treatment of established post-extubation respiratory failure

Contraindications: respiratory arrest, medical instability, inability to

protect airway, excessive secretions, uncooperative or agitated status,
unfitting mask, and recent upper airway or gastrointestinal surgery
Practical aspects
1. Machine: sophisticated ICU ventilator (independent insp/exp limbs,
higher max flow); or smaller-sized ventilator dedicated for NIV
delivery (single limb only, with expiratory port which can be just a
hole or a dedicated device, e.g. Whisper-Swivel II valve); or a
hybrid type ventilator with function in between the above two types
2. Interface: nasal mask, oronasal mask, total full face mask, helmet,
nasal pillows (In acute respiratory failure, start with oronasal mask.)
3. Mode of delivery：Singel level (CPAP) or Bi-level (IPAP + EPAP)
 P 28
Factors associated with success: less sick (lower APACHE II score),
higher pH, lower respiratory rate (RR), lower PaCO2, subjective
improvement within one hour of start

Factors associated with failure: edentulous, pneumonia, excess

Respiratory
Medicine

secretions, mouth leaks, poor coordination, ARDS, PaO2/FiO2 ≤146,

sicker patient (Simplified Acute Physiology Score (SAPS II)≥35).
Common setting
1. Spontaneous/ timed (ST) mode or Spontaneous (S) mode
2. CPAP/EPAP: Pulmonary oedema: 8 to 12 cmH2O; COPD: 4-5
cmH2O. Normal lung: 5 cmH2O
3. IPAP: For COPD, start at 8-15 cmH2O, titrate up to 20 cmH2O.
Aim at tidal volume (Vt) around 7ml/kg BW and RR ≤ 25/min;
4. Backup RR: 6 to 12; with I:E ratio: 1:2 to 1:4 or Ti 0-8-1s

Points to note
1. Watch out for gastric distension
2. Monitor ABG: Within 1st 1-2 hours after start to determine success,
3. Consider invasive mechanical ventilation if there is no objective
signs of improvement after 1 hour of use
4. Consider repeat ABG at 4-6 hours if first set ABG show little
improvement. If still no response, consider intubation
5. Apply NIV for 4-6 hours, then remove mask for short periods every
few hours for meals, sputum clearance or bronchodilator inhalation
6. Stringent infection control measures should be taken during NIV
for patients with suspected respiratory infections (Single room with
airborne isolation might be needed, please refer to your hospital
guidelines).
Rheumatology &
Immunology
Rheumatology

Immunology
&
 R1

APPROACH TO INFLAMMATORY ARTHRITIS

Assessment
 Arthralgia – pain in a joint without demonstrable synovitis
 Inflammatory Arthritis (Synovitis) – joint swelling, warmth, pain
and tenderness
 Polyarthralgia/polyarthritis – 5 or more joints
 Chronic polyarthralgia/polyarthritis – more than 6 weeks

Rheumatology &
Immunology
Polyarthralgia/polyarthritis – common causes
 Bacterial arthritis (staphylococcal, streptococcal, gonococcal,
meningococcal)
 Bacterial endocarditis
 Viral arthritis
 Reactive arthritis
 Crystal–induced arthritis: gout, pseudogout
 Rheumatoid arthritis
 Seronegative spondyloarthropathies: ankylosing spondylitis,
psoriatic arthritis, inflammatory bowel disease
 Connective tissue diseases: SLE, systemic vasculitis, scleroderma,
Still’s disease
 Others: sarcoidosis, palindromic rheumatism, malignancy,
hyperlipoproteinemias, Lyme disease, rheumatic fever
Monoarthritis – common causes
 Septic arthritis
 Crystal-induced arthritis: gout, pseudogout
 Haemarthrosis / trauma / overuse
 Tuberculous arthritis
 Osteoarthritis
 Spondyloarthropathies: ankylosing spondylitis, psoriatic arthritis
 Monoarthritic onset rheumatoid arthritis
 Reactive arthritis
 Other uncommon causes: avascular necrosis, synovial metastasis
 R2

Relevant investigations
 CBP, ESR, CRP
 Renal / liver function, calcium, phosphate, urate
 Urinalysis
 ANA, RF (if SLE or RA is suspected)
 X-ray of the affected joints, USG & MRI if indicated
 Joint aspiration
 Synovial biopsy (in undetermined cases)
Rheumatology &
Immunology

Joint fluid analysis

Send fluid for:
 Gram stain (“urgent” if septic arthritis suspected)
 Bacterial culture
 AFB smear and culture (if indicated)
 White cell count
 Crystal microscopy

Joint fluid white cell count:

% of
Classification Clarity WBC/ml
Neutrophils
Normal Transparent < 200 < 25
Non-inflammatory Transparent < 2000 < 25
Inflammatory Translucent 2,000-100,000 25 – 75
Septic Opaque 50,000-300,000 > 90

Crystal microscopy:
 Urate crystals – slender and needle-shaped; strong negative
birefringence under polarized light
 Calcium pyrophosphate crystals – pleomorphic or
rhomboid-shaped; weakly positive birefringence under polarized
light
 R3

GOUTY ARTHRITIS
Clinical features
 Acute gout (monoarticular, polyarticular)
 Chronic tophaceous gout
 Uric acid calculi
 Gouty nephropathy
Diagnosis

Rheumatology &
Immunology
Definite gout
Intracellular negative birefringent urate crystal on joint fluid microscopy
Presumed gout
Classical history of episodic acute arthritis rapidly resolved with NSAID
(or colchicine) + history of hyperuricaemia
Management
Acute Gouty arthritis
1. NSAID/COX2 inhibitors (Note! Check patient’s drug allergy)
High dose, tapering over 5 days, reduce dose in renal impairment:
a) indomethacin 50mg tds  25mg tds  25mg bd
b) naprosyn 500mg stat  250mg tid  250mg bd
c) ibuprofen 800mg stat  400mg qid  200mg tid
2. Colchicine
0.5 mg tds for 1-2 days (stop if nausea/diarrhoea)
Renal impairment – caution and reduce frequency
Not recommend Q1H  Q2H for 10 doses regime
3. Corticosteroid
a) Intra-articular steroid injection after septic arthritis ruled out
b) Prednisolone 20 to 40 mg daily within 1 week, rapid tapering
(consider for patients with NSAID or colchicine
contraindications, or renal failure)

Urate lowering therapy

Low purine diet advisable but only attain small changes in serum uric
acid
 R4

Urate lowering therapy is indicated in patients with hyperuricaemia and

>2 acute gouty attacks of in 1 year (in terms of cost-effectiveness),
tophaceous gout or urate renal calculi.

1. Xanthine oxidase inhibitors (Do NOT use with azathioprine!)

a. Allopurinol (usual dose 300 mg daily)
 Start with low dose 100 mg daily; inform patients to stop if skin
reaction (~ 5%) and seek medical attention early
Rheumatology &
Immunology

 Further reduce dose in renal impairment

 Start allopurinol only when acute gout has subsided
 Prophylaxis: add regular colchicine 0.5 mg daily or bd, or NSAID,
for 3 to 6 months, to prevent acute gout attacks
 Titrate dose to target serum uric acid < 0.36 mmol/L
 FDA approved maximal dose is 800 mg daily
 Severe cutaneous adverse reations are associated with HLA B*5801
in Han Chinese (allele frequency ~7.3% locally). HA Expert Panel
(2012) opined that checking this gene before starting allopurinol is
not necessary
b. Febuxostat – a new non-purine selective xanthine oxidase inhibitor
 Alternative for patients with allopurinol cutaneous adverse reaction
 Usual dose 40 mg to 80 mg daily
 Caution in patients with high cardiovascular thromboembolic risks

2. Uricosuric drugs
Probenecid 250 mg bd to 1000 mg tds
(Contraindications: moderate renal impairment, urate renal stone,
tophaceous gout, and high 24-hour urine uric acid excretion)
Benzbromarone – licensed in HK but not under HA formulary
Sulfinpyrazone – not licensed in HK

3. Uricase
Rasburicase, a recombinant urate-oxidase enzyme, is for
pre-chemotherapy prevention of acute tumour lysis syndrome
 R5

SEPTIC ARTHRITIS
1. A hot, swollen and tender joint should be regarded as septic arthritis
until proven otherwise, even in the absence of fever, leucocytosis,
elevated ESR or CRP. Septic arthritis can present as monoarthritis
(80-90%), oligoarthritis or polyarthritis. Delay in diagnosis and
treatment can result in irreversible joint destruction or septicaemia.
2. Prompt aspiration of the joint is warranted. Synovial fluid should be

Rheumatology &
Immunology
sent for:
 Differential cell counts: Usually >50,000 WBC/ml and often
>100,000/ml, predominantly neutrophils.
 Gram stain
 Culture and sensitivity
 Polarising microscopy for crystals (septic arthritis may co-exist
with crystal arthropathies)
3. Other investigations: CBC with differentials, RFT, LFT, blood
culture, X-ray of the joint. Swabs of pharynx, urethra, cervix and
anorectum if gonococcal infection suspected.
4. Start empirical IV antibiotics immediately according to suspected
organisms and gram stain. Modify according to culture and
sensitivity results. Opinion from microbiologists is helpful. Refer to
IMPACT guideline (available as apps for mobile phone), or
(http://www.chp.gov.hk/files/pdf/reducing_bacterial_resistance_with
_impact.pdf)
5. Repeat aspiration of the joint to dryness.
6. Consult orthopaedic surgeon for drainage especially for infected
prosthetic joint. Open drainage is usually necessary for hip infection.
7. Start physiotherapy early.
8. NSAIDs for pain relief.
9. IV antibiotics for at least 2 weeks or until signs improved for
non-gonococcal arthritis, then orally for an additional 2-4 weeks.
 R6
Suggested choice of antibiotics: (Note! Check patient’s drug allergy)
Synovial fluid Organism IV Antibiotics
gram stain
Gram +ve Staph aureus Cloxacillin 1-2 g Q6H or
cocci (clusters) MSSA Cefazolin 1-2 g Q8H
Gram +ve Streptococcus Penicillin 2 megaunits Q4H
cocci (chains) or Cefazolin 1-2g Q8H
Gram –ve Enterobacteriaceae Ceftriaxone 2 g Q24H or
Rheumatology &
Immunology

Bacilli Cefotaxime 1g 8H
Pseudomonas Cefepime 2g Q12H or
Piperacillin 3g Q6H or
Imipenem 500 mg Q6H
+ gentamicin
Gram –ve Neisseria Ceftriaxone 2g Q24H or
diplococci gonorrhoeae** Cefotaxime 1g Q8H or
Ciprofloxacin 400mg Q12H

Empirical 1. No risk factors for Cloxacillin or

initial therapy atypical organisms Cefazolin or Ceftriazone
2. High risk for Cloxacillin +
Gram-ve sepsis Ceftriaxone or Cefotaxime
(elderly, frail, recurrent
UTI, recent abdominal
surgery,
immunocompromised)
3. Gonorrhoea Ceftriazone or cefotaxime or
suspected ciprofloxacin
4.MRSA suspected: Vancomycin 1g Q12H +
Ceftriaxone or Cefotaxime
** Treat possible concurrent Chlamydia trachomatis infection with doxycycline (100 mg
BD for 7 days) in patients with gonococcal infection.
 R7

RHEUMATOID ARTHRITIS
1. Diagnosis:
1987 ACR criteria for the classification of established RA
At least 4 of the following features
 Morning stiffness >1 hour
 Arthritis and soft tissue swelling of ≥3 joint areas
 Arthritis of hand joints

Rheumatology &
Immunology
 Symmetric arthritis
 Subcutaneous nodules in specific places
 Rheumatoid factor at a level above 95th percentile
 Radiographic changes suggestive of joint erosion
Clinical symptoms must be present for at least 6 weeks.

2010 ACR/EULAR classification criteria for RA

6/10 points – classified as having definite RA
 Joint involvement
1 large joint (0)
2-10 large joints (1)
1-3 small joints (with or without large joints) (2)
4-10 small joints (with and without large joints) (3)
>10 joints (at least 1 small joint) (5)
 Serology
Negative RF and negative anti-CCP (0)
Low positive RF or low positive anti-CCP (2)
High positive RF or high positive anti-CCP (3)
 Acute phase reactants
Normal CRP and normal ESR (0)
Abnormal CRP or ESR (1)
 Duration of symptoms
< 6 weeks (0)
≥ 6 weeks (1)
 R8
2. Investigations
 ESR and C-reactive protein (CRP)
 RF (sensitivity ~70%)
 Anti-cyclic citrullinated peptide antibody (anti-CCP) – highly
specific for RA, helpful in undetermined situations
 Plain X-ray of the hands and feet for erosion
 MRI or USG may be useful for detecting early bony erosion
Rheumatology &

3. Clinical assessment
Immunology

Includes: subjective & objective evidence of active synovitis;

efficacy, tolerability & need for adjustment of present Rx;
associated comorbidities (cardiovascular / osteoporosis) &
extra-articular problems
Useful parameters:
 degree of joint pain
 duration of morning stiffness
 number of tender and swollen joints
 functional status (Health Assessment Questionnaire)
 patient’s and physician’s global assessment
 ESR or CRP (if persistently raised without obvious synovitis
– beware of infection)
 radiographic progression

4. Management overview:
Goals:
 Treat-to-target: aim at low disease activity or remission
 Treat RA early: best outcome in first 2 years from onset
 Prevent joint damage and preserve daily function
 Patient education / counseling; rheumatology nursing
 Medications (plain analgesic / NSAID / DMARDs / biologics /
judicious use of steroid)
 Non-pharmacological: physiotherapy, occupational therapy,
podiatrist, dietitian (multi-disciplinary team care)
 Orthopaedic operations
 Management of associated comorbidities & their risk factors
 R9

5. EARLY aggressive use of DMARDs is especially indicated for

patients with poor prognostic factors
 High disease activity at onset (≥ 18 joints)
 High baseline joint damage (erosive disease)
 Persistently high CRP level
 Positive IgM rheumatoid factor or anti-CCP (esp. high titer)
 Positive family history of RA
 Nodular disease

Rheumatology &
Immunology
 Extra-articular manifestations

6. Conventional DMARDs
 Start DMARDs early! All take time to act.
 Usually start with monotherapy, but step-up combination may be
considered early in patient with severe disease
 Titrate up to optimal doses according to RA disease activity
 Switch or add-on another DMARD promptly if target not met
 Counsel patients on DMARD effects and side effects and their
slow action
 Anchor drug is methotrexate
 Other examples: sulphasalazine, hydroxychloroquine,
leflunomide, low dose prednisolone (less than 10mg/day),
cyclosporin A, azathioprine, intramuscular gold

7. Biologics
 Should be prescribed by rheumatologist with reference to local &
international guidelines
 E.g. anti-TNF (Etanercept, Adalimumab, Infliximab,
Golimumab, Certolizumab), IL-6 receptor blocker
(Tocilizumab), co-stimulation molecule blocker (Abatacept),
anti-CD 20 (Rituximab)
 Safety Net available for many of them. Check HAHO intranet
site for updated details under Samaritan fund: ha.home >
Guidelines > Non-clinical Manual / Guidelines > Samaritan Fund
 Need to screen for hepatitis carrier and latent TB before use
 R 10

Response criteria

1. ACR response criteria

ACR20/50/70 responses
≥ 20%/50%/70% improvement in
(a) Swollen joint count
(b) Tender joint count
(c) Improvement in at least 3 of the following 5 measures:
Rheumatology &
Immunology

 Patient’s global assessment of disease activity

 Physician’s global assessment of disease activity
 Patient’s assessment of pain
 Acute-phase reactant (ESR, CRP)
 Functional scores (HAQ)

2. EULAR response criteria

Disease activity score (DAS)
DAS44 and DAS28 (more convenient in daily clinical practice)
DAS28 = 0.56 • √(t28) + 0.28 • (sw28) + 0.70•Ln(ESR) +0.014•GH
 Number of tender joints among 28 joints (t28)
 Number of swollen joints among 28 joints (sw28)
 Erythrocyte sedimentation rate (ESR, mm/hour)
 General health status (GH) using a 100-mm visual analog scale

Disease status: High disease activity > 5.1

Low disease activity ≤ 3.2
Remission < 2.6

Response criteria (Good / Moderate / No):

Final score Decrease in DAS28
> 1.2 0.6 to 1.2 < 0.6
< 3.2 Good Moderate No
3.2 – 5.1 Moderate Moderate No
> 5.1 Moderate No No
 R 11

ANKYLOSING SPONDYLITIS
1. Modified New York criteria for definite AS (1984)
a. Radiological criterion
Sacroiliitis: ≥ grade II bilateral or grade III to IV unilaterally
b. Clinical criteria (at least 1 out of 3)
 Low back pain & stiffness for > 3 months that improve with
exercise but not relieved by rest

Rheumatology &
 Limitation of motion of lumbar spine in both sagittal &

Immunology
frontal planes
 Limitation of chest expansion relative to normal correlated for
age & sex

2. ASAS criteria for axial spondyloarthritis (SpA) (2009):

a. Imaging evidence of sacroiliitis (XR, MRI or CT) plus one SpA
features*
b. HLA-B27 positivity plus 2 other SpA features*
SpA features:
 Inflammatory back pain age of onset < 40
 Arthritis
 Enthesitis
 Psoriasis
 Uveitis
 Dactylitis
 Crohn’s/colitis
 Good response to NSAIDs
 Family history for SpA
 Elevated C-reactive protein (CRP)
 HLA-B27
3. Other extra-skeletal features – apical fibrosis, aortic insufficiency
4. Measurements
a. Modified Schober test – spinal forward bending (excursion of
two points: PSIS level and 10 cm above; normal > 10 cm). Note:
finger floor distance may be apparently normal when good hips
flexion compensates limited spinal flexion
 R 12

b. Occiput to wall distance, tragus to wall distance

c. Chest expansion
d. Lumbar lateral flexion
e. Cervical spine rotation
f. Intermalleolar distance
5. Investigations
a. XR sacroiliac joints and spine
b. MRI / CT SI joints in doubtful cases
Rheumatology &
Immunology

c. HLA-B27 (role refers to ASAS criteria)

6. Disease assessment
a. BASDAI (Bath Ankylosing Spondylitis Disease Activity Index),
active disease defined as ≥ 4 (out of 10)
b. BASFI (Bath Ankylosing Spondylitis Functional Index)
c. BAS-G (Patient’s / Physician’s Global score)
d. BASMI (Bath Ankylosing Spondylitis Metrology Index)
e. Acute phase reactants (ESR/CRP) can be normal in patients with
predominant axial involvement
7. Treatment
a. Education, stretching exercise & physiotherapy
b. NSAIDs for pain and stiffness at optimal tolerated dose
c. Addition of gastroprotective agents or use selective COX-2
inhibitor in patients with high GI risks (elderly, history of peptic
ulcer, comorbidity)
d. Analgesics such as paracetamol and tramadol for patients in
whom conventional NSAIDs or COX-2 inhibitor are insufficient,
contraindicated or intolerated
e. Sulphasalazine for patients with peripheral arthritis
f. Anti-TNF therapy for patients with persistent high disease
activity despite adequate trial of the above treatment including
2-3 NSAIDs (at least 2 months for each unless contraindicated).
Refer rheumatologist for assessment of disease activity and
indications for anti-TNF therapy
8. ASAS 50 Response criteria:  BASDAI by 50%
 R 13

PSORIATIC ARTHRITIS
Diagnostic criteria
1. Moll & Wright criteria 1973:
 Inflammatory arthritis (peripheral arthritis and/or sacroiliitis or
spondylitis)
 The presence of psoriasis
 The absence of rheumatoid factor

Rheumatology &
Five types: asymmetrical oligoarthritis, predominant DIP,

Immunology
symmetrical polyarthritis, axial AS like, arthritis mutilans

2. The Classification of Psoriatic Arthritis criteria (CASPAR):

Mandatory: Inflammatory articular disease (joint, spine or

entheseal)
With 3 or more points from the following:
1. Current psoriasis (scores 2 points)
2. Personal history of psoriasis (if current psoriasis absent)
3. Family history of psoriasis (if personal history of psoriasis
or current psoriasis absent)
4. Psoriatic nail dystrophy
5. A negative test for rheumatoid factor
6. Current dactylitis
7. History of dactylitis (if current dactylitis absent)
8. Radiological evidence of juxta-articular new bone formation

Clinical features
 30% psoriasis population has arthritis
 60% psoriasis preceeds arthritis, 20% arthritis preceeds
psoriasis, 20% concurrent
 Also watch out for associated metabolic syndrome e.g.
overweight, diabetes mellitus, hypertension, hyperlipidaemia,
hyperuricaemia etc
 R 14

Features distinguishing PsA from RA

 Presence of psoriasis
- Hidden lesions common, e.g. scalp, hairline, behind the ear and
inside ear cannel, guttate lesions on back, under the breasts,
around umbilicus, around the perineum or even natal cleft
 Nail dystrophy
- Onycholysis, pitting, ridging, etc
 Distal phalangeal joint involvement
Rheumatology &
Immunology

 Spondylitis or sacroiliitis
 Enthesitis (inflammation of junction of tendon and bone)
 Dactylitis

Treatment
Oral steroid – risk of psoriasis flare up upon tapering, and hence steroid
dependency. So be cautious with starting oral steroid.
Early DMARD treatment for psoriatic arthritis
 Active arthritis (> 3 tender/ swollen joints, dactylitis counted as one
active joint)
DMARD. Methotrexate, sulphasalazine, leflumomide, cyclosporin
Anti-TNFα therapy (refer to rheumatologist)
 For skin psoriasis
(a) Topical steroid (potency)
- Fluocinolone < betamethasone < clobetasol (to be used by
specialist)
- Lotion < cream < ointment < occlusive dressing
- Common e.g.: 0.1% betamethasone cream, Diprosalic
(betamethasone + salicylate)
(b) Topical Tar products, e.g. shampoo, bathing soap
(c) Vit D analogues: e.g. Dovonex (calcipotriol) (to be used by
dermatologist)
(d) UVA or UVB (to be used by dermatologist)
(e) Anti-TNFα therapy, anti-IL 12/23, anti-IL 17 and other
biologics (to be used by specialist)
 R 15

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

American College of Rheumatology (ACR) criteria for the

classification of SLE (Tan et al. 1982, revised 1997, Hochberg et al.)
≥ 4 criteria, serially or simultaneously = classified as SLE (specificity = 96%)
1. Malar rash
2. Discoid rash
3. Photosensitivity

Rheumatology &
Immunology
4. Oral ulcers
5. Arthritis
6. Serositis (pericarditis, peritonitis, pleuritis)
7. Renal disease (proteinuria > 0.5 g/day, or +++ by dipstick, or
cellular casts)
8. Neurological (seizure, or psychosis)
9. Haematological (haemolytic anaemia, or leucopenia < 4×109/L,
lymphopenia < 1.5×109/L, on two or more occasions, or
thrombocytopenia < 100×109/L)
10. Immunological (anti-dsDNA, or anti-Sm, or false +ve VDRL for
more than 6 months, or the presence of the antiphospholipid
antibodies)
11. Positive anti-nuclear antibody (ANA)

SLICC (Systemic Lupus International Collaborating Clinics)

Classification criteria for SLE (Petri et al. 2012)
≥ 4 criteria (at least 1 clinical + 1 immunologic criteria) OR
biopsy-proven lupus nephritis with positive ANA or anti-DNA
Clinical Criteria
1. Acute or subacute cutaneous lupus
2. Chronic cutaneous lupus
3. Oral/Nasal ulcers
4. Non-scarring alopecia
5. Inflammatory synovitis with physician-observed swelling of two or
more joints OR tender joints with morning stiffness
6. Serositis
 R 16

7. Renal: Urine protein/creatinine (or 24 hr urine protein) representing

at least 500 mg of protein/24 hr or red blood cell casts
8. Neurologic: seizures, psychosis, mononeuritis multiplex, myelitis,
peripheral or cranial neuropathy, cerebritis (acute confusional state)
9. Haemolytic anaemia
10. Leukopenia (<4×109/L at least once) OR Lymphopenia (<1×109/L
at least once)
11. Thrombocytopenia (<100×109/L) at least once
Rheumatology &
Immunology

Immunologic Criteria
1. ANA above laboratory reference range
2. Anti-dsDNA above laboratory reference range (except ELISA:
twice above laboratory reference range)
3. Anti-Sm
4. Antiphospholipid antibody: e.g. lupus anticoagulant, false-positive
test for syphilis, anticardiolipin antibody (at least twice normal or
medium-high titre), anti-β2 glycoprotein 1 antibody
5. Low complement: e.g. low C3, low C4, low CH50
6. Direct Coombs test in absence of haemolytic anemia

Anti-ENA antibodies
 Anti-Ro: associated with photosensitivity and an increased risk of
congenital heart block (~2% incidence). Pre-pregnancy counseling
and ultraviolet light protection should be advised.
 Anti-ENA antibodies seldom sero-convert and repeating tests is not
necessary.

Anti-phospholipid antibodies
 Lupus anticoagulant (LAC) and anti-cardiolipin (aCL) antibody
(IgG) are available in most HA hospitals.
 They are strongly associated with cerebro-vascular accidents in
Chinese SLE patients. Other associations: thrombocytopenia,
livedo reticularis, valvular heart lesions, recurrent miscarriages and
venous thrombosis.
 R 17

 Twice positive tests 12 week apart are necessary for the diagnosis of
antiphospholipid syndrome. Only strongly positive aCL is
clinically relevant.
 Because of the association with recurrent abortions and miscarriages,
these antibodies have to be checked before pregnancy.
 Anti-β2-GPI antibody is more specific than aCL for thrombosis.
Because of its limited sensitivity, anti-β2-GPI should only be
considered in patients in whom antiphospholipid syndrome is

Rheumatology &
Immunology
suspected but yet aCL and LAC is negative.

Monitoring of disease activity

 Clinical assessment (signs and symptoms of disease flares)
 Serology: C3 and C4 level, anti-dsDNA titer

Points to note
 The ANA titer only correlates with disease activity very roughly
and is not reliable for disease monitoring. Thus, there is no need
to repeat ANA every visit.
 C-reactive protein (CRP) is usually not elevated in patients with
active SLE. An elevated CRP in SLE may indicate persistent
synovitis / arthritis, serositis or infection. Infection has always to
be considered before augmentation of immunosuppressive therapy.

Disease activity scoring system

The ACR SELENA-SLEDAI is most widely used disease activity index.
Items can be used as a checklist for disease flares:
Seizure (8) Cerebrovascular accident (8)
Psychosis (8) Retinal hemorrhage / infarct /
Organic brain syndrome (8) optic neuritis (8)
Lupus headache (8) Vasculitis (8)
Cranial nerve disorder (8)
Arthritis (> 2 joints) (4) Oral ulcer (2)
Myositis (4) Pleuritis (2)
 R 18

Proteinuria (4) Pericarditis (2)

Urine cast (4) New skin rash (2)
RBC cast in urine (4) Alopecia (2)
Sterile pyuria (4)  anti-dsDNA titre (2)
 C3 (2)
Fever (1) Leukopenia (< 3×109/L) (1)
Thrombocytopenia (1)
* Only new features or manifestations are scored
Rheumatology &
Immunology

Treatment of SLE
General: Patient education and counseling, sun-screening (avoid strong
sunlight, frequent application of SPF 15+ sun lotion), screening and
treatment of cardiovascular risk factors and osteoporosis, vaccination
and infection prevention, early recognition and prompt treatment
Hydroxychloroquine should be considered for every lupus patient:
 Overall stabilizing SLE
 Decreases infection, some anti-thrombotic and lipid lowering
effect
 Stabilises pregnant SLE patients and improves foetal outcome
 Recommend < 6.5 mg/kg/day

Mild SLE manifestations

 NSAIDs – arthritis, serositis, fever
 Hydroxychloroquine – arthritis, skin lupus
 Methotrexate – persistent and refractory arthritis and skin
 Topical steroid – skin lupus
 Small to moderate doses of prednisolone – fever, systemic upset,
mild cytopenias, more severe serositis and skin lupus
 Azathioprine – haematological, mild renal disease, steroid sparing
 R 19

Severe SLE manifestations

Glomerulonephritis, neuropsychiatric lupus, severe cytopenias,
thrombotic thrombocytopenic purpura, pulmonary haemorrhage,
myocarditis, pneumonitis, pulmonary hypertension
 Moderate to high doses of prednisolone
 Intravenous pulse methylprednisolone
 Azathioprine
 Cyclophosphamide (intravenous pulse or oral)

Rheumatology &
Immunology
 Mycophenolate mofetil (MMF)
 Cyclosporin A and Tacrolimus
 Plasma exchange
 Intravenous immunoglobulin
 Rituximab
 Vasodilatation (bosentan, inhaled iloprost, sildenafil)
 Anticoagulation
Lupus nephritis (ISN/RPS Classification 2003)
Class I: Minimal mesangial lupus nephritis
Class II: Mesangial proliferative lupus nephritis
Class III: Focal proliferative lupus nephritis
Class IV-G: Diffuse global proliferative lupus nephritis
Class IV-S: Diffuse segmental proliferative lupus nephritis
Class V: Membranous lupus nephritis
Class VI: Advanced sclerotic lupus nephritis

MMF is increasingly used as first line treatment for proliferative lupus

nephritis because of lower frequency of adverse effects compared to
cyclophosphamide e.g. premature ovarian failure and haemorrhagic
cystitis. However, cyclophosphamide remains the conventional
treatment for those with rapidly progressive crescentic GN and those
with impaired renal function.
 R 20

Neuropsychiatric lupus
19 Neuropsychiatric syndromes according to the 1999 ACR
classification
Central nervous system Peripheral nervous system
Aseptic meningitis Guillain-Barre syndrome
Cerebrovascular disease Autonomic neuropathy
Demyelinating syndrome Mononeuropathy
Headache (single/multiplex)
Rheumatology &
Immunology

Movement disorder Myasthenia gravis

Myelopathy Cranial neuropathy
Seizure disorder Plexopathy
Acute confusional state Polyneuropathy
Anxiety disorder
Cognitive dysfunction
Mood disorders
Psychosis

Diagnosis
 Till now, no specific confirmatory serological & imaging tests
 A diagnosis by exclusion (to rule out CNS infections, metabolic
encephalopathy, effects of drugs / toxins including corticosteroids,
electrolyte disturbances, rarely brain tumour)
 Lupus activity in other systems increases likelihood of active
neuropsychiatric lupus but CNS infection may coexist with active
neuropsychiatric lupus
 CT brain, MRI brain / spinal cord for anatomical diagnosis
 Lumbar puncture to rule out CNS infection
 EEG
 Antiphospholipid antibodies
 Anti-ribosomal P antibody (private laboratory) is associated with
lupus psychosis but its usefulness is limited by the low sensitivity
 R 21

Treatment

 Symptomatic: anti-convulsants, anti-psychotics, anti-depressants,

sedatives
 Secondary prophylaxis for atherosclerotic vascular disorders:
aspirin / warfarin
 Immunosuppressive or immunomodulating treatment (eg. high dose
corticosteroids, pulse methylprednisolone, cyclophosphamide, IVIG,

Rheumatology &
Immunology
rituximab): severe psychosis, acute confusional state, myelopathy,
myasthenia gravis, neuropathies, demyelinating syndrome.

Novel / investigational therapies for SLE

 Belimumab – for “sero-positive” SLE, steroid sparing effect
 Rituximab – efficacy shown in cohort series
 Other novel agents: Sirolimus, Ocrelizumab, Epratuzumab,
Abatacept, anti-type I interferons
 Immunoablative cyclophosphamide  stem cell rescue
 Mesenchymal stem cell therapy

Useful apps: RheumaHelper – for Classification criteria and Disease

Activity scoring of many rheumatic diseases. Available free from iTune
App Store and Google Play Store.
 R 22

RHEUMATOLOGICAL EMERGENCIES
CERVICAL SUBLUXATION
 Suspect in RA patients with long standing and severe disease
 Commonly presents with neck pain radiating towards the occiput,
clumsiness, abnormal gait, spastic quadriparesis, sensory and sphincter
disturbances. May cause cord compression and death.
 4 forms in descending order of frequency: anterior, posterior, lateral,
Rheumatology &
Immunology

vertical
Investigations:
 Plain AP and lateral XR of cervical spine with flexion and extension
views
 Anterior subluxation: distance between the posterior aspect of the
anterior arch of the atlas and the anterior aspect of the odontoid process
(Atlanto-dens interval, ADI) ≥ 4mm
 Dynamic (flexion-extension) MRI (if surgery indicated)
Management:
Medical
 High-impact exercises and spinal manipulation are contraindicated
 Soft collars may serve as reminder for patients and physicians but
provide little structural support
 Stiff cervical collars may provide marginal benefit but compliance is a
problem
 Neuropathic pain relief
Surgical
 Urgent referral to orthopaedic surgeons or neurosurgeons if signs of cord
compression
 Patients with severe subluxation but without signs of cord compression
are at risk for severe injury and perhaps death due to a variety of insults
including falls, whiplash injuries, and intubation. Surgical decision
should be individualized.
 Surgical options: craniocervical decompression, cervical or
occipito-cervical fusion (alone or in combination)
 R 23

GIANT CELL ARTERITIS (GCA)

Presentation: At least 3 of the following 5 criteria

1. Age ≥ 50 years
2. Localized headache of new onset
3. Tenderness or decreased pulse of the temporal artery
4. ESR > 50 mm/hr
5. Biopsy revealing a necrotizing arteritis with a predominance of

Rheumatology &
Immunology
mononuclear cells or a granulomatous process with
multinucleated giant cells.
 Polymyalgia Rheumatica (PMR) is characterized by aching and
morning stiffness in the shoulder and hip girdles, occurring in
40-50% of GCA patients.
 Other presentations: jaw or arm claudication, weight loss, PUO
 Complications: Ischaemic optic retinopathy (visual loss 15-20%).
Blindness is abrupt and painless, may be preceded by amaurosis
fugax.
 Aneurysms, dissections, stenotic lesions of the aorta and its major
branches
Investigations
 Elevated ESR, often >100mm/hr (5% of GCA has ESR<
40mm/hr)
 Temporal artery biopsy of the affected side
Treatment
 High dose prednisolone (1mg/kg/day)
 For visual symptoms or signs (eg, amaurosis fugax, partial or
complete visual loss), start empirical steroid before temporal
artery biopsy result
 Acute visual changes - consider IV pulse methylprednisolone
(250-1000mg) daily for 3 days

SEPTIC ARTHRITIS (see page R5-6)

 R 24

ANCA VASCULITIS – Pulmonary Renal syndrome

Presentation:
 Acute renal failure, signs of acute glomerulonephritis, or
 Acute pulmonary haemorrhage
Investigations
 ANCA (anti-neutrophil cytoplasmic antibody) +ve
Rheumatology &

Cytoplasmic (c-ANCA) or Perinuclear (p-ANCA) pattern

Immunology

 Anti-PR3 (proteinase 3) +ve or anti-MPO (myeloperoxidase) +ve

respectively
 Raised ESR/CRP
 Renal biopsy to show pauci-immune glomerulonephritis
 CXR, HRCT, bronchoscopy etc for pulmonary haemorrhage
Treatment
 Organ support: dialysis and ventilator care (consult ICU if needed)
 Intravenous pulse steroid or high dose steroid
 Cyclophosphamide or rituximab in refractory patients
 Plasma exchange possibly useful in:
 Patients with acute renal failure requiring dialysis support
 Pulmonary haemorrhage
 Concomitant anti-GBM +ve patients
 R 25

NON-STEROIDAL ANTI-INFLAMMATORY DRUGS

(NSAIDS)
o Do not use > 1 NSAID at a time
o Use the lowest possible dosage and frequency sufficient for pain
relief
o Efficacy is similar among various NSAIDs. Conventional ones
such as naproxen, ibuprofen and indomethacin are equally

Rheumatology &
effective.

Immunology
o If one NSAID is not working despite 2-3 week of treatment at full
dosage, shifting to another NSAID may be considered.
o Coexisting hypertension, fluid retention and/or renal impairment –
consider sulindac

Adverse Effects
Beware of cross allergy between NSAIDs and COX-2 inhibitors
o GI: dyspepsia, peptic ulcer, GI bleeding and perforation
o Renal: renal impairment
o CVS: fluid retention, worsening of hypertension, increased
cardiovascular events
o Liver: raised transaminases
o CNS: headache, dizziness and cognitive impairment, especially use
of indomethacin in elderly
o Skin: may range from mild rash to Steven Johnson’s Syndrome
o Resp: may precipitate or exacerbate bronchospasm in aspirin
sensitive individuals

Risk factors for gastrointestinal toxicity:

a. Chronically disabled
b. Age > 60 years
c. Previous history of proven peptic disease
d. Co-administration of high dose prednisolone or anticoagulation
e. Higher dosage of NSAIDs
f. Extent of inflammatory disease for which NSAIDs is prescribed
 R 26

COX-2 inhibitors
Efficacy: similar to non-selective conventional NSAIDs
Advantages:
o Reduce gastrointestinal toxicity.
o Less effect on platelet function, hence less bleeding risk.
o Less risk of precipitating bronchospasm
Adverse effects:
o Increase risk of cardiovascular events (MI, stroke). Risk proportional
Rheumatology &
Immunology

to dosage. May worsen BP control and heart failure

o Nephrotoxicity, hepatotoxicity, cardiotoxicity similar to conventional
NSAIDs
o Celecoxib should be avoided in patients with sulphonamide allergy

Current recommendations for patients receiving NSAIDs

1. Prescribe lower-risk agents. Weigh GI against CV risk in individual
patient:
o If estimated risk of life-threatening GI bleeding > risk of CV events,
consider use of NSAIDs with gastroproection or the COX-2
inhibitors.
o If risk of CV events > the risk of GI bleeding, COX-2 inhibitors
should be avoided.
2. Limit duration, frequency and dosage.
3. Patients with known H pylori infection should undergo eradication
before NSAID therapy.
4. For patients at higher risk for GI complications, consider assessing
for and treating H pylori if present and co-therapy with
gastroprotective agents.
5. Gastroprotection:
o Proton pump inhibitors (PPIs)
o Misoprostol
o COX-2 inhibitor alone is beneficial in reducing GI risks, but with
the possible trade-off of increasing CV risk.
o COX-2 inhibitor with concurrent PPI therapy may be considered
in ultra-high risk patients eg. recurrent ulcer bleeding.
Infections

Infections
 In 1

COMMUNITY-ACQUIRED PNEUMONIA

Definition of pneumonia
• Clinical: syndrome of fever, chills, dyspnoea, cough with sputum and
pleurisy etc.
• Radiological: consolidation on X-ray imaging Causative agents
• Pathological: a form of acute respiratory infection that alveoli are
filled with pus and fluid, which makes breathing painful and limits
oxygen intake

Bacteria Others

Typical
• Streptococcus pneumoniae
• Haemophilus influenzae
• Moraxella catarrhalis
• Klebsiella pneumoniae & other
gram -ve organisms (DM,
Alcoholic, those with risk of
aspiration)
Infections
• Mycobacterium tuberculosis
• Viruses (Influenza, RSV, VZV,
Measles)
• Emerging agents (MERS, Avian
influenza)
• Pneumocystis jirovecii

Atypical
• Legionella pneumophila
• Mycoplasma pneumoniae
• Chlamydophila pneumoniae

General principles
• Tuberculosis is endemic in Hong Kong
• Aware host factors like immunocompromised status
• Aware risk factors and exposure history for atypical pathogen
infection
• Early isolation of patients with suspected or confirmed air-borne
pathogens (tuberculosis, measles), or infectious diseases with special
significance (MERS, avian influenza)
 In 2
• Due to high prevalence of macrolide resistance in Mycoplasma
pneumoniae in Asia, early substitution of macrolide to doxycycline is
recommended when clinical suspicion arises

Empirical treatment
1. Patients who are stable for management in outpatient setting
• PO Amoxicillin-clavulanate (beta-lactam with beta-lactamase
inhibitor) +/- macrolide or doxycycline

2. Hospitalized patients with mild to moderate pneumonia

• PO/IV Amoxicillin-clavulanate +/- macrolide or doxycycline
• Alternatives: IV ceftriaxone, cefotaxime +/- macrolide or
doxycycline
Infections

• With chronic lung condition like bronchiectasis

• Anti-pseudomonal antibiotics (e.g. IV piperacillin-tazobactam,
cefepime) +/- macrolide or doxycycline

3. Hospitalized patients with severe pneumonia, defined as having any 1

in 3 major criteria OR 2 in 6 minor criteria:
• Major criteria: need of mechanical ventilation, septic shock, acute
renal failure;
• Minor criteria: multilobar involvement, mental confusion,
respiratory rate >30 bpm, PaO2/FiO2 <250, SBP < 90mmHg/ DBP
< 60mmHg, serum urea level > 7 mmol/L)
• IV piperacillin-tazobactam or ceftriaxone or cefepime +/-
macrolide or doxycycline +/- oseltamivir

Remarks:
1. In Hong Kong, macrolide/azalide, tetracycline or cotrimoxazole should not be
used alone for empiric treatment of CAP. Locally, 50−70% pen-sensitive and
pen-resistant Streptococcus pneumoniae isolates are multi-resistant to these
agents (Interhospital Multi-disciplinary Programme on Antimicrobial
Chemotherapy (IMPACT), Fourth Edition (2012, version 4.0))
2. Caution required as unique groups of COPD patients appears to be the main
reservoir of levofloxacin-resistant Streptococcus pneumoniae (IMPACT,
Fourth Edition (2012, version 4.0))
 In 3

HOSPITAL ACQUIRED PNEUMONIA (HAP)

Pneumonia occurring ≥ 48 hr after admission and excluding any infection
that is incubating at the time of admission
There are two principles guiding the strategy of antibacterial therapy for
HAP:
• Initial administration of adequate treatment with an antibacterial
agent(s) active against the causative pathogen(s).
• De-escalation once the causative pathogen is known.
2 empiric Rx categories :
1. Early-onset pneumonia (≤ 4 days admission) with no risk factors
for multidrug-resistant (MDR) pathogens & any disease severity
3rd generation cephalosporin OR

Infections
β-lactam/β-lactamase inhibitor
(Amoxycillin-clavulanate/ Ampicillin-sulbactam)
2. Late-onset pneumonia (> 4 days admission) OR risk factors for
MDR pathogens and all disease severity
Antipseudomonal β-lactam/β-lactam inhibitor OR
Antipseudomonal cephalosporin OR
Antipseudomonal carbepenem
± aminoglycoside OR fluoroquinolone
± Vancomycin after careful assessment of indication

Risk factors for MDR pathogens (Pseudomonas aeruginosa,

ESBL-producing Enterobacteriaceae, Acinetobacter species and
MRSA)
• Antimicrobial therapy in preceding 90 days
• High frequency of antibiotic resistance in the community or in the
hospital
• Hospitalization for ≥ 2 days in the preceding 90 days
• Residence in a nursing home or extended care facility
• Chronic dialysis within 30 days
• Home wound care
• Family member with multi-resistant pathogen
• Immunosuppressive disease and/or therapy
 In 4
Empiric antibiotic may need modification/de-escalation once the results of
blood or respiratory tract cultures become available

Organisms Antibiotics

Onset <4 days after • S. pneumoniae, • IV/PO

admission with no • H influenzae Amoxicillin-clavulanate
previous antibiotics • M. Catarrhalis or
• S. aureus • Cefuroxime if penicillin
allergy (non-type I
hypersensitivity)
Onset ≤ 4 days after • MRSA; • IV
admission + had • P aeruginosa, cefoperazone-sulbactam,
Infections

received antibiotic • Acinetobacter, • Cefepime or

recently, OR • Klebsiella spp., • piperacillin-tazobactam
onset ≥ 5 days after  an aminoglycoside
• Enterobacter spp.
admission OR  Vancomycin after careful
mechanical assessment of indications
ventilation
 In 5

PULMONARY TUBERCULOSIS
Recommendations
* Directly observed treatment (DOT) should be given as far as possible.
1. Uncomplicated new cases – 6 months in total
• 2 HRZ + (E or S)/ 4 HR (When Rx started in hospital or when
3x/week regimen not tolerated)
• 2 HRZ + (E or S)/ 4 HR3
• 2 HRZ + (E or S)3/ 4HR3 (Government Chest Clinic regimen)
2. Retreatment cases – 9 months in total.
• 3 (or 4) HRZES/ 6 (or 5) HR ± E
Notations:
• Figures in front of drug combinations = duration in months.

Infections
• Subscript ‘3’ = thrice weekly & absence of subscript indicates
daily.
• The slash “/” is used to separate different phases of Rx.

Drugs and dosages

Daily 3x/week
BW Dose BW Dose
H = Isoniazid -- 300 mga -- 10-15 mg/kg
<50 kg 450 mg
R = Rifampicin -- 600 mg
>50 kg 600 mg
<50 kg 1-1.5 g <50 kg 2g
Z = Pyrazinamide
≥50 kg 1.5-2 g ≥50 kg 2.5 g
E = Ethambutolb -- 15 mg/kg -- 30 mg/kg
<50 kg 500-750 mgc <50 kg 500-750 mg
S = Streptomycin
≥50 kg 750 mg ≥50 kg 750-1000 mg
a) i) Some elderly and/or malnourished can only tolerate 200 mg.
ii) Vitamin B6 10 mg/d for malnutrition, alcoholism, pregnancy.
 In 6
iii) May cause peripheral neuropathy, encephalopathy and convulsions
especially in renal impairment.
iv) Drug interaction with phenytoin & carbamazepine.
b) Assess baseline visual symptoms & acuity before starting Rx with close
monitoring during therapy & consult ophthalmologist prn
c) Lower dose for > 60 years old.

Reference: Chemotherapy of TB in HK – updated in 2006.

www.info.gov.hk/tb_chest
Infections
 In 7

CNS INFECTIONS
Consider CNS infections in the presence of sepsis and one or more of the
followings: meningism, seizures, headache, impaired consciousness,
photophobia, confusion, signs of increased intracranial pressure (↑ ICP),
focal neurological deficits, presence of parameningeal focus of sepsis.
Signs and symptoms may be subtle or absent in elderly or
immunocompromised host.

1. CSF examination is crucial in the diagnosis of meningitis

2. Watch out for signs of ↑ ICP and do urgent CT brain before LP. If LP
is contraindicated, likely to be delayed or fails, empirical antibiotics
can be started after taking blood cultures

Infections
3. CSF analysis: cell count, protein, glucose (simultaneous blood
sugar), gram stain, culture, AFB (smear and C/ST), Cryptococcus
(India ink smear, Ag and culture), viral studies. Do not wait for C/ST
results before starting Rx
4. Other Ix: CBP, RFT, LFT, CXR, EEG, XR skull, sinuses and
mastoid
5. Look for any predisposing factors: sinusitis, endocarditis, otitis
media, skull fracture, immunocompromised state, etc

Typical CSF findings in meningitis

Normal Viral Bacterial TB / Cryptococcal

Appearance clear clear turbid turbid/viscous

Mononuclear
cells (/mm3)
<5 10-100 <50 100-300

PMN (/mm3) nil nil 200-3000 0-200

Protein (g/l) 0.2-0.4 0.4-0.8 0.5-2.0 0.5-3.0
CSF/blood
glucose
>1/2 >1/2 <1/2 <1/2
 In 8
Initial empirical anti-microbial regimes
Bacterial Ceftriaxone 2 g q12h OR Cefotaxime 1.5-2 g iv q4h iv +
meningitis Vancomycin$ 500 -1000 mg q6-12h +
Ampicillin 2g iv q4h (if risk of listeriosis anticipated@)

Brain abscess Ceftriaxone 2 g q12h OR Cefotaxime 1.5-2 g iv q4h iv +

Metronidazole 500 mg iv q8h

TB meningitis INAH 300-600 mg daily

Rifampicin 450-600 mg daily
Pyrazinamide 1.5-2 g daily
Ethambutol 15 mg/kg/d daily (25 mg/kg/d for first 2/12)
Pyridoxine 100 mg daily
± Streptomycin 0.75 g im daily
Infections

Cryptococcal Amphotericin B 0.7 – 1 mg/kg iv infusion over 4-6 hrs +

meningitis 5-Flucytosine 25 mg/kg q6h po for 2 weeks, then
fluconazole at least 400mg/d for a minimum of 8 weeks
(immunocompetent patients)

Viral Acyclovir 10 mg/kg iv q8h (or 500mg iv q8h)

encephalitis

$ Aim at trough concentration 15-20 micrograms/ml

@ Immunocompromized, pregnancy and elderly

• Dexamethasone 4 mg q6h in complicated TB meningitis or brain abscess with

significant cerebral oedema.
• Dexamethasone (0.15 mg/kg q6h for 2-4 days with the first dose administered
10-20 min before, or at least concomitant with, the first dose of antimicrobial
therapy) in adults with suspected or proven pneumococcal meningitis
• Prophylactic anti-convulsant may be considered in cerebral abscess and subdural
empyema
• Duration of Rx for brain abscess 6-8 weeks
• Duration of Rx for meningitis: ≥ 7days for H. influenzae, 10-14 days for S.
pneumoniae, 14-21 days for L. monocytogenes and S. agalactiae, and 21 days for
Gram negative bacilli. DO NOT change to oral therapy.
• Consider prophylaxis for contacts in cases of meningococcal meningitis:
ciprofloxacin 500mg stat, ceftriaxone 250mg IM stat
 In 9

URINARY TRACT INFECTION

Diagnosis Organisms (a) Antibiotics

Cystitis E. coli; • PO Nitrofurantoin(b, c)
S. saprophyticus; • Amoxicillin-clavulanate(c)
Gp B streptococcus; • TMP-SMX(d)
Proteus spp; • Fluoroquinolone (d)
klebsiella spp.

Acute E. coli; • IV Amoxicillin-clavulanate

pyelonephritis other • 3rd cephalosporins (e) 
enterobacteriacea; Aminoglycoside (f)
enterococcus

Infections
• Piperacillin-tazobactam or
(Pseudomonas in carbapenem if suspect
Catheter related, Pseudomonas infection
obstruction or
transplant related
infection)

Remarks
a. Escherichia coli is the most common causative pathogen. ESBL
strain is not uncommonly seen in Enterobacteriaceae. Empiric
Carbapenem may be considered for severe clinical cases.
b. Nitrofurantoin is well tolerated, and demonstrates a consistently low
level of resistance among E. coli, gram-positive cocci (including
Enterococcus and S. saprophyticus), but inactive against most
Proteus, and Klebsiella strains. Nitrofurantoin should not be used to
treat pyelonephritis since it does not achieve reliable tissue levels.
c. Give 5-7 day of amoxicillin-clavulanate or Nitrofurantoin as 3-day
course may not be as effective as ciprofloxacin and TMP-SMX.
d. There is the increasing problem of resistance to TMP-SMX and
fluoroquinolone.
e. For example ceftriaxone and cefotaxime. A 14-day regimen is
generally recommended for upper UTI.
f. Aminoglycosides achieve higher tissue levels, relative to serum
levels, than do beta-lactams.
 In 10

ENTERIC INFECTIONS
Acute infective diarrhoea may be due to viruses e.g. Norovirus, bacteria
and their toxin, and sometimes protozoa. Most are self-limiting.

Clinical presentation

1. Secretory diarrhoea (Non-inflammatory enteritis)

• Commonly caused by salmonellosis
• Norovirus: pronounced vomiting
• Cholera classically presents as acute painless profuse rice water
diarrhoea without blood or mucus
Infections

2. Invasive diarrhoea (Inflammatory enteritis)

• Presents as dysenteric syndrome i.e. transient diarrhoea followed by
abdominal colic, tenesmus, fever, blood and mucus in stool
• Commonly caused by shigellosis (bacillary dysentery), non-cholera
vibrios (Vibrio parahaemolyticus and Plesiomonas shigelloides)
and occasionally Entamoeba histolytica (amoebic dysentery).
3. Typhoid and paratyphoid fever (enteric fever)
• Caused by Salmonella typhi (typhoid fever) and Salmonella
paratyphi (paratyphoid fever)
• Suspect in patient of high fever with relative bradycardia, ↓platelet,
N to ↓WCC, no localized focus of infection.

4. Clostridium difficile infection (CDI)

• Common cause of hospital acquired diarrhoea.
• Clinical presentation can range from mild diarrhoea to
pseudomembranous colitis (PMC). Fulminant colitis can result in
toxic megacolon and death
• Common risk factors: use of broad spectrum antibiotics, e.g.
cephalosporins, fluoroquinolones and clindamycin, use of
immunosuppressants and prolonged hospitalisation
 In 11
5. Enteric infections associated with systemic complications
• E coli O157:H7 — haemolytic-uraemic syndrome
• Campylobacter enteritis — Guillain-Barré syndrome
• Non-polio enteroviruses — Hand-foot-mouth disease, myocarditis,
encephalitis, etc.
6. Enteric infections are often more severe in immuno-compromised
patients, e.g. elderly, diabetes mellitus, cirrhosis, anatomical or
functional hyposplenism, concurrent immunosuppressant therapy

Management for enteric fever

1. Enteric fever is diagnosed by compatible clinical features and positive

culture from bone marrow aspirate, blood or stool. Widal serology is

Infections
neither sensitive nor specific.
2. Antibiotics treatment:
• Levofloxacin 750mg daily iv/po OR ciprofloxacin 500mg bd po x
7d (10-14d for severe disease).
• Alternative: Ceftriaxone 2g iv q24h x 10 – 14 days
• Strains with nalidixic acid resistance (a surrogate marker
predicting clinical failure with fluoroquinolone therapy):
Azithromycin 500mg daily x 7 days or Ceftriaxone 2g iv q24h x
10 – 14 days

Management for other bacterial enteric infections

1. Adequate fluid and electrolyte supplement

2. Routine antibiotic not recommended for mild to moderate
gastroenteritis
3. Consider fluoroquinolone e.g. ciprofloxacin 500mg bd for 3 days or
azithromycin 500mg daily for 3 days, for cases of febrile
dysentery, especially for toxic patients.
4. Use of antibiotics as adjuvant therapy, e.g. doxycycline 300mg for
single dose, tetracycline 500mg qid for 3 days, or ciprofloxacin
500mg bd for 3 days, can reduce duration and severity of diarrhoea in
cases of cholera
 In 12
NOTE: If Campylobacter enteritis is suspected and antimicrobial is
indicated on clinical grounds, a macrolide (e.g. clarithromycin
or azithromycin) is preferred because of increasing report of
fluoroquinolone resistance.

Management of Clostridium difficile infection

1. Diagnosed by detection of C. difficile toxin or PCR in stool

2. Discontinuation of inciting and unnecessary antimicrobial therapy
3. Specific antimicrobial therapy
• For mild case: oral metronidazole 400mg tds for 10-14 days
• For severe case: oral vancomycin 125mg qid for 10-14 days
- add IV metronidazole 500mg q8h for cases complicated with
Infections

ileus or megacolon, surgery may be necessary

- consider rectal instillation of vancomycin for case of complete
ileus
• For relapsed case: can repeat course of oral vancomycin; can
consider oral vancomycin with gradual tapering regimen for case
of repeated relapse or fecal transplant for refractory case
Reference
1. HA fact sheet on typhoid and paratyphoid fever (Jul 2011)
2. HA factsheet on cholera (Jul 2011)
3. HA fact sheet on Management of E coli O157: H7 (Jun 2011)
4. HA infection control guideline on Clostridium difficile infection
(Oct 2012)
 In 13

ACUTE CHOLANGITIS
1. Investigations
a) CBP, LFT, RFT
b) PT, APTT, Glucose
c) Blood culture
d) Abdominal USG

2. Management
a) Active resuscitation and monitor vital signs
b) IV antibiotics for mild to moderate cases:
- Amoxicillin-clavulanate (Augmentin) (± Aminoglycoside)
- Cefuroxime + metronidazole (± Aminoglycoside)

Infections
- If penicillin allergy, Levofloxacin + metronidazole
- IV antibiotic can be switched to oral formulary for completion
of therapy if clinically stable.
c) IV antibiotics for severe cases: Consider Tazocin, carbapenems,
3rd generation cephalosporin or levofloxacin + metronidazole.
d) Duration of Rx: 4-7d unless difficult to achieve biliary
decompression.
e) Early decompression of biliary obstruction by ERCP or PTBD.

3. Preparation for ERCP

a) Indications for emergency ERCP
- Increasing pain and guarding in epigastrium or RUQ
- Hypotension despite resuscitation
- High fever (> 39oC)
- Mental confusion, which is a predictor of poor outcome
b) Correct coagulopathy
c) Fast patient

4. Care for patients who have nasobiliary or percutaneous (PTBD)

drainage of obstructed biliary tract
a) Check input/output chart (including NB drain) daily
b) Check hydration status, RFT, HCO3 and correct fluid and
electrolyte derangement as necessary
 In 14

SPONTANEOUS BACTERIAL PERITONITIS

High index of suspicion is necessary

1. Cirrhotic patients may have an insidious onset of fever and lack of

peritoneal signs, perform diagnostic paracentesis, send ascitic fluid
for:
 Cell count (EDTA bottle to haematology laboratory, request
differential WBC)
 Low protein level is consistent with spontaneous bacterial
peritonitis
 Fluid for bacterial culture in blood culture broth
Infections

 Cytology

2. Diagnostic criteria:
 ascitic fluid WCC > 500/mm3 or neutrophil > 250/mm3
(In traumatic tap, subtract 1 PMN for every 250 RBCs)

3. Perform blood culture

4. Common organisms: E.coli, Klebsiella sp, Pneumococcus,

Enterococci.

5. Empirical treatment:
 IVI Ceftriaxone 2gm q24h OR IVI Cefotaxime 2 gm q8h (q4h if
life-threatening)
 May consider reassessment by repeating paracentesis 48 hours
later.
 Usual duration of treatment : 5-10 days
 Consider IV albumin 1.5gm/kg at diagnosis and 1gm/kg on day 3,
especially in patients with renal impairment

Watch out for hepatic encephalopathy.

 In 15

NECROTIZING FASCIITIS

Necrotizing Fasciitis is a deep seated infection of the subcutaneous tissue

that results in progressive destruction of fascia and fat, but may spare the
skin. Early Recognition is important because there may be a remarkably
rapid progression from an inapparent process to one associated with
extensive destruction of tissue, systemic toxicity, loss of limb or death.
Diagnosis and Management:
1. Difficult to distinguish from cellulitis in early stages.
2. Excruciating pain and presence of systemic toxicity out of proportion
to the local findings.
3. Skin breakdown with bullae and frank cutaneous gangrene can be

Infections
seen.
4. Risk factors assessment and urgent Gram stain may guide choice of
antibiotics.
5. Immediate surgical intervention and antibiotic therapy are the
mainstay of treatment.

Risk Factors Organisms Antibiotics

Following exposure • IV Levofloxacin
• Aeromonas spp.
to freshwater, Plus
seawater or seafood • Vibrio vulnificus • IV Amoxicillin-clavulanate
Following • Polymicrobial
intraabdominal, • Enterobacteriacea
Imipenem or Meropenem
gynecological or • Streptococci
perineal surgery • Anaerobes
• IV penicillin G 4 megaunits
Following cuts, Q4H Plus
abrasion, recent • Group A • IV Linezolid 600mg Q12H
chickenpox, IVDU, Streptococcus •  IVIG (1-2g/kg for 1 dose)
healthy adults for streptococcal toxic shock
syndrome
 In 16
Infections

If culture showed
MRSA, please notify
Department of
Health.
 In 17

SEPTIC SHOCK
Terminology:
Systemic inflammatory response syndrome (SIRS): manifests by 2 or
more of the following conditions:
• Temperature > 38°C or < 36°C
• Heart rate > 90 bpm
• Respiratory rate > 20 bpm or PaCO2 < 4.3kPa
• WBC > 12,000/µL, < 4000/µL, or 10% immature (band) forms

Sepsis: SIRS due to a documented infection. With sepsis, at least 1 of

the following manifestations of inadequate organ function/perfusion
also must be included:
• Alteration in mental state
• Hypoxaemia

Infections
• Elevated plasma lactate level
• Oliguria (urine output <30 mL or 0.5 mL/kg for at least 1 h)

Septic shock: A subset of severe sepsis with hypotension despite

adequate fluid resuscitation, along with the presence of perfusion
abnormalities.

Principles of management
• Early recognition: high index of suspicion and perform sepsis
work-up whenever appropriate
• Early and adequate antibiotic therapy: choice based on the suspected
primary site of infection and risk factor(s) for drug resistant pathogens
• Source control: e.g. removal of indwelling devices, drainage of
abscess
• Early haemodynamic resuscitation and continued support: targeted
MAP ≥ 60 mmHg. Fluid resuscitation initially. Start vasopressor (e.g.
dopamine, noradrenaline) if patient does not respond to fluid
resuscitation (e.g. ≥ 4L of crystalloid) or evidence of fluid overload is
present
• Proper ventilator management with low tidal volume in patients with
ARDS
• Target blood glucose level ≤ 10mmol/L
• Strategies with less clear value:
- Corticosteroids (refractory vasopressor-dependent shock)
 In 18

ANTIBIOTICS FOR FEBRILE NEUTROPENIC

PATIENTS
1. Definition:
 Neutropenia: Neutrophil (ANC) ≤ 0.5 x 109/L or ≤ 1 x 109/L
with a predictable decline to ≤ 0.5 x 109/L in 24 - 48h
Note: Neutropenia can occur either from disease or treatment.
• Fever: Pyrexia > 38.3oC or > 38oC for > 1 hour
2. Work up:
• Assess localizing signs & symptoms for infection, sepsis &
shock
• Initially blood, sputum & urine cultures, CXR; other
specimens if clinically indicated
3. Risk assessment:
Infections

• Low risk: Neutropenic period ≤ 7 days, no or few co-morbidities

• High risk: ANC ≤ 0.1 x 109/L for > 7 days, shock, pneumonia,
newly onset abdominal pain or CNS signs
4. Empirical antibiotic therapy for neutropenic fever:
• Give antibiotics as soon as possible (after immediate
sepsis workup)!
• Low risk:
• Ciprofloxacin 750mg BD PO + Augmentin 1g BD PO
• Levofloxacin 750mg daily PO if penicillin allergy
• If Fluoroquinolone has been used for prophylaxis, use regime as
for high risk
• High risk:
Possible IV regimes for high risk cases
Ceftazidime 1-2 g q8h IV Cefepime 2 g q12h or 1g q8h IVI
Imipenem 500 mg q6h IVI Meropenem 500mg q6-8h to 1 g q8h
IVI
Tazocin 4.5 g q6-8h IVI Sulperazon 1-2g q8-12h IV
• + Aminoglycoside for ill cases (e.g. IVI Amikacin 15mg/kg over 1h q24h,
750mg q24h or 375mg q12h)
 In 19
• + Vancomycin 500 mg q6h or 1gm Q12H if culture +ve or highly suggestive of
MRSA/skin/catheter infection
• + Amphotericin B 0.5 – 1.0 mg/kg/day if no response after 5d & culture –ve
Reference: Freifeld AG, Bow EJ, Sepkowitz KA, et al. Clinical Practice Guideline for the
Use of Antimicrobial Agents in Neutropenic Patients with Cancer: 2010 Update by the
Infectious Diseases Society of America. Clinical Infectious Diseases 2011:52(4);427-31.

Additional notes by Medical Oncology:

Neutropenia can be resulted from either the disease or treatment e.g.

chemotherapy

Prompt initiation of broad-spectrum antibiotics after immediate sepsis

Infections
workup is important as patients with febrile neutropenia can rapidly
deteriorate
 In 20

MALARIA
Management of Acute Attack
1. Anti-malarial chemotherapy should be administered as soon as the
diagnosis is made
2. Monitor blood for parasites and repeat testing is needed if the
diagnosis is strongly suspected
3. Maintain fluid and electrolytes balance; avoid over-hydration
4. Renal failure regime for blackwater fever; treat hypoglycaemia
and/or shock if present
5. Pulmonary oedema may develop, treated by prop up, oxygen, loop
diuretic, veno-dilator; if hypoxic may need positive pressure
Infections

ventilation
6. Avoid sedatives and corticosteroids
7. Watch for relapse (usually within 2 months) and signs of peritoneal
irritation (splenic rupture).
Anti-malarial Chemotherapy
A. Uncomplicated P. vivax, P. malariae and P. ovale
Chloroquine 600 mg base po stat
and 300 mg base 6 hours later
then 300 mg base daily for 2 more days
plus Primaquine 15 mg base (0.25 mg/kg) po daily taken with food
for 14 days in P. vivax and P. ovale infection to eradicate hypnozoites
in the liver.

NOTE 1 Chloroquine-resistant P. vivax reported from Oceania, Indonesia

and South America, treatment similar to that of P. falciparum
malaria is required.
NOTE 2 Primaquine-resistant P. vivax reported in South-east Asia and
Western Pacific. An increased of the dose to 22.5 – 30 mg daily
(or 0.5 mg/kg) is effective
NOTE 3 Primaquine is contraindicated in pregnancy. In G6PD deficiency,
primaquine is safe in dosage of 0.75mg/kg once a week for 8
weeks. Monitor Hb level.
 In 21
B. Uncomplicated P. falciparum malaria
1. Definition: symptomatic malaria without signs of severity or evidence
of vital organ dysfunction
2. Treatment:
a. Artesunate 200 mg (4 mg/kg) po daily for 3 days
plus Mefloquine 1000 mg base po on day 2, then 500 mg po on day
3
b. Quinine 600 mg salt (10 mg/kg) po 8 hourly for 7 days
plus Doxycycline 100 mg po BD for 7 days

C. Severe P. falciparum malaria

1. Definition: presence of one or more of the following clinical or
laboratory features, after excluding other obvious cause of their

Infections
symptoms:
a. Clinical: Prostration, Impaired consciousness, Respiratory distress
(acidotic breathing), Multiple convulsions, Circulatory collapse,
Pulmonary oedema (radiological), Abnormal bleeding, Jaundice,
Haemoglobinuria
b. Laboratory: Severe anaemia, Hypoglycaemia, Acidosis, Renal
impairment, Hyperlactataemia, Hyperparasitaemia (>5%)

2. Treatment:
a. Artesunate 2.4 mg/kg i.v. or i.m. given on admission (time = 0), then
at 12 h and 24 h, then once a day until oral medication could
be taken, treat for a total of 7 days
plus Doxycycline 100 mg po bid for 7 days once oral medication
could be taken or Mefloquine as in above section B2a
b. Quinine dihydrochloride 20 mg/kg loading dose in 5% dextrose
infused over 4 hours, maintenance dose 10 mg/kg infused over 2 – 4
hours every 8 hours. Change to oral dose when feasible to
complete a 7-day course
plus Doxycycline as in above section C2a

Note 1 Consider Primaquine 45 mg single dose to eradicate gametocytes in

blood at the end of treatment of falciparum malaria
Note 2 Do not use loading dose if patient has received quinine, quinidine, or
mefloquine in preceding 24 hours.
 In 22

CHICKENPOX / HERPES ZOSTER

Diagnosis
1. Acute illness of typical generalised papulovesicular rash without
other apparent cause (the rash may be atypical with few or no
vesicle in vaccinated persons)
2. Confirmed by laboratory test
• Virus detected by DIF, PCR or culture from clinical
specimens
• Paired serology in acute and convalescent phases

Management
1. Keep patients from school / work for at least 5 days after onset of
Infections

eruption or until vesicles become dry

2. Airborne and contact precautions for chickenpox/ disseminated zoster
when in hospital
3. Give acyclovir 10 – 12 mg/kg q8h IV infusion for 7 days for severe
zoster or chickenpox in elderly or immuno-compromised patients
4. Therapy for neuralgia usually required for zoster
5. Watch for development of severe secondary skin infection
(Staphylococcus/Streptococcus) and consider antibiotics (e.g. oral
cloxacillin) if necessary.
6. For herpes zoster with ophthalmic involvement, urgent eye
consultation is recommended.
7. Varicella-zoster immunoglobulin (VZIG) should be administrated as
soon as possible after exposure and within 10 days for high risk
patients, e.g. immunocompromised persons and pregnant women.
8. VZV vaccination should be given within 3 to 5 days after exposure as
PEP in persons who i) do not have evidence of immunity, ii) eligible
for vaccination, e.g. immunocompetent, non-pregnant and >12
months of age, and iii) are not indicated for VZIG

Reference:
HA Guideline on varicella zoster virus infections. CCIDER. 8 Nov 2013.
Prevention of Varicella. Centres of Disease Control and Prevention. 22
Jun 2007.
 In 23

HIV / AIDS
Diagnosis of HIV infection and AIDS:
1. HIV infection: Screening test (ELISA) followed by confirmatory test
(Western Blot or Line Immunoassay)
2. AIDS: Laboratory evidence of HIV infection plus indicator diseases
for AIDS
3. Obtain informed consent before performing HIV test
4. Counselling is crucial because of major psychological and social
implications of a positive result. Patient confidentiality should be
respected and protected.
5. Referral for counselling and medical consultation available from
a. PMH Infectious Diseases Special Medical Clinic (IDSM)

Infections
(Tel: 6461 0613)
b. QEH Special Medical Service (Tel: 3506 5855)
c. CHP Kowloon Bay Integrated Treatment Centre (ITC)
(Tel : 2116 2888)
6. Voluntary reporting of HIV infection and AIDS to Department of
Health (DH 2293 form) is encouraged for epidemiological purpose.
Clinical management of HIV/AIDS
1. Baseline assessment:
• CD4/CD8 count
• HIV RNA level
• Consider baseline genetic resistance testing (GRT)
• Serological evidence of HBV and HCV coinfection
• Syphilis serology and screen for other STIs
• Toxoplasma and CMV serology
• CXR for evidence of tuberculosis and tuberculin skin test
• G6PD status
• Baseline CBP, RFT with eGFR, LFT, CaPO4, fasting lipid and
glucose, ECG
• Urine dipstick analysis
2. For patients with respiratory symptoms:
• CXR, ABG, LDH +/-β1,3 glucan
 In 24
• Sputum for C/ST, AFB smear and C/ST +/- TB PCR, staining for
Pneumocystis jirovecii +/- PCP PCR (if available)
• Consider empirical Rx for PCP if hypoxaemia present
• Bronchoscopy for non-responsive cases
3. For patients with GI symptoms:
• Stool for microscopy and C/ST
• Stool for Cryptosporidia /Cyclospora/Isospora / Microsporidia
• Stool for AFB smear and culture
• Workup for the GI pathogens (e.g. Norovirus infection, and
Clostridium difficile infection etc.)
• OGD for dysphagia, colonoscopy for chronic diarrhoea,
• USG abdomen & check viral hepatitis serology for deranged LFT
4. For patients with neurological symptoms:
Infections

• CT / MRI brain, CSF examination

• Toxoplasma serology, cryptococcal Ag
• Consider PML or HIV Associated Neurocognitive Disorders
(HAND) as DDx
• Nerve conduction studies for neuropathy
5. For patients with haematological problems:
• Marrow biopsy for histology, AFB smear and culture, Parvovirus
B19 antibody and consider marrow for Parvovirus B19 DNA
6. For patients with PUO:
• Blood +/- marrow for bacterial, fungus and mycobacteria culture
• Blood for CMV pp 65 antigen, cryptococcal Ag and penicillium
serology/ galactomannan
• CXR, CT thorax and abdomen/pelvis +/- PET scan

Antiretroviral therapy
Nucleoside/Nucleotide reverse transcriptase inhibitors (NRTIs):

Zidovudine (Retrovir, AZT, ZDV) 250 – 300 mg bd

Didanosine (Videx, ddI) 250 – 400 mg daily

Lamivudine (Epivir, 3TC) 150 mg bd

 In 25

Stavudine (Zerit, d4T) 30 – 40 mg bd

Abacavir (Ziagen, ABC) 300 mg bd (check HLA B*5701

before initiation)

Tenofovir (Viread, TDF) 300 mg daily

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Nevirapine (Viramune, NVP) 200 mg daily for 2 weeks, then

200 mg bd (*avoid in female with
CD4 > 250 and male with CD4 >
400)

Nevirapine XR (Viramune XR) Can replace NVP 200 mg bd

Infections
Efavirenz (Stocrin, EFV) 600 mg nocte (*avoid in women
of child-bearing age)

Rilpivirine (Edurant, RPV) 25 mg daily

Etravirine (Intelence, ETR) 200 mg bd

Protease inhibitors (PIs)

Indinavir (Crixivan, IDV) 800 mg (with RTV 100 mg) bd

Saquinavir (Invirase, SQV) 1000 mg (with RTV 100 mg) bd

Lopinavir /Ritonavir 2 tab bd or 4 tab daily (naïve pt)

(Kaletra, LPV/RTV) (400/100 mg)

Atazanavir (Reyataz, ATV) 300 mg (with RTV 100 mg) daily

or 400 mg daily

Darunavir (Prezista, DRV) 600 mg (with RTV 100 mg) bd

800 mg (with RTV 100 mg) daily
(for treatment naïve patients)

Tipranavir (Aptivus, TPV) 500 mg (with RTV 200 mg) bd

 In 26

Ritonavir (Norvir, RTV) Used in low-dose (100 mg) for

boosting level of other PIs

Integrase inhibitor (II)

Raltegravir (Isentress, RAL) 400 mg bd

Entry inhibitor (CCR5 antagonist)

Maravoric (Celsentri, MVC) 300 mg bd (dose adjustment

needed for drug interaction)

Fusion inhibitor

Enfuvirtide (Fuzeon, ENF, T20) 90 mg SC q12h

Infections

Combination formulations

Combivir AZT + 3TC

Kivexa ABC + 3TC

Truvada TDF + emtricitabine (FTC)

Atripla TDF + FTC + EFV

Stribild Elvitegravir (EVG) + cobicistat

(COBI) + TDF + FTC

1. Patients should be prescribed combination anti-retroviral therapy

(cART) consisting of three active drugs.
 The first-line regimen usually consists of
- 2 NRTIs + 1 PI (usually boosted with RTV),
- 2 NRTIs + 1 NNRTI or
- 2 NRTIs + 1 II.
 The other classes of drugs are generally reserved for patients with
HIV drug resistance.
 In 27
2. cART is recommended for all HIV-infected individuals to reduce the
risk of disease progression unless contraindicated. The strength and
evidence for this recommendation vary by pretreatment CD4 count
3. cART is also recommended for HIV-infected individuals for the
prevention of transmission of HIV
4. Drug adherence should be regularly assessed and reinforced to
prevent emergence of viral resistance
5. CD4 count and HIV RNA level should be monitored regularly and
therapeutic drug level monitoring and genotypic resistance assay
should be arranged for patients with non-suppressed viral load
6. Cautious about drug interactions especially when patient is receiving
PI or NNRTI

Infections
Opportunistic Infection Prophylaxis
1. Pneumocystis jiroveci pneumonia (PCP)
Indications: a. after an episode of PCP
b. when CD4 count falls below 200/ul
First line: Septrin 480 mg to 960 mg daily
Second line: Aerosolised pentamidine 300 mg every 4 weeks
(*should be conducted in facilities with adequate
ventilation to prevent transmission of TB)
Dapsone 100 mg daily

2. Mycobacterium avium complex (MAC)

• Indication: CD4 <50/ul
• Azithromycin 1000 mg once weekly OR clarithromycin 500 mg BD

Treatment of Opportunistic Infections

1. Pneumocystis jiroveci pneumonia
a) Consider in patients with fever, dry cough and dyspnoea
b) May have normal CXR during early stage
c) Diagnosis by sputum induction with hypertonic saline/ BAL/
transbronchial lung biopsy for staining for Pneumocystis jirovecii
+/- PCP PCR, hypoxaemia on ABG
 In 28
d) Oxygen supplement
e) Drugs:
▪ Septrin at TMP 15 mg/kg/d po/IV (3-4 tab qid) for 3 Wks
▪ If acutely ill or PaO2 <8: add Prednisolone 40 mg bd for 5 days,
then 40 mg daily for 5days, then 20 mg daily for 11 days
▪ Alternative regimen:
i. Clindamycin 600 mg IV q8h + Primaquine 30 mg daily po for
3 Wks
ii. Pentamidine isethionate 4 mg/kg/d IV for 3 weeks
2. Tuberculosis Combination therapy (DOTS): isoniazid,
rifampicin, pyrazinamide and ethambutol;
levofloxacin and streptomycin for patients with
adverse reaction or intolerable to first-line drugs
Infections

3. MAC Combination therapy with 3 - 4 drugs:

Ciprofloxacin 750mg bd/ levofloxacin 500mg/d
Clarithromycin 500mg bd/azithromycin
500mg/d
Ethambutol 15 mg/kg/d
Rifabutin 300 mg daily
Amikacin 10 - 15 mg/kg/d IV

4. Candida Fluconazole 100 mg/d (higher dose up to 400

oesophagitis mg/d for refractory cases) or
Itraconazole solution 200 mg daily for 2 – 3
weeks Can consider echinocandin

5. Cryptococcosis Amphotericin B 0.7 mg/kg/d IV (Max 1.5

mg/kg/d) or liposomal amphotericin B 3-4
mg/kg/d IV for 2 weeks + flucytosine 25 mg/kg
q6h for 2 weeks, then fluconazole 400 mg/d po
for total of at least 10 weeks
 In 29

6. Penicilliosis Induction: amphotericin B 0.5-1 mg/kg/d IV or

liposomal amphotericin B 3-5 mg/kg/d IV for 2
wks
Maintenance: itraconazole 200 mg bd

7. Toxoplasmosis Pyrimethamine 200 mg po x 1 then 50-75 mg/d +

clindamycin 600 mg qid + folinic acid 10-20 mg
daily for 6 wks
Maintenance: Pyrimethamine 25-50 mg/d +
clindamycin 300-450 mg qid + folinic acid 10-20
mg daily

Infections
8. CMV retinitis Ganciclovir 5 mg/kg IV q12h, foscarnet 60
mg/kg IV q8h or valganciclovir 900 mg po bd for
3 wks
Maintenance: Valganciclovir 900 mg daily po

9. Cryptosporidiosis Nitazoxanide 500 mg bd po for 2 wks

10. Cyclosporiasis Septrin 960 mg bd for 3-4 wks

11. Isosoporiasis Septrin 960 mg qid for 10 days

12. Microsporidiosis Albendazole 400 mg bd for 3 wks

Reference:
1) EACS guideline 2013
2) Panel on Antiretroviral Guidelines for Adults and Adolescents.
Guidelines for the use of antiretroviral agents in HIV-1-infected
adults and adolescents. Department of Health and Human Services.
Available at
http://aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL.pdf
Accessed in June 2014
 In 30
3) Panel on Opportunistic Infections in HIV-Infected Adults and
Adolescents. Guidelines for the prevention and treatment of
opportunistic infections in HIV-infected adults and
adolescents:recommendations from the Centers for Disease Control
and Prevention, the National Institutes of Health, and the HIV
Medicine Association of the Infectious Diseases Society of America.
Available at
http://aidsinfo.nih.gov/contentfiles/lvguidelines/adult_oi.pdf
Accessed in June 2014
Infections
 In 31

RICKETTSIAL INFECTION

Rickettsiae are obligate intracellular bacteria. They are maintained in

nature through cycle involving reservoir mammals and arthropod vectors
except louse borne typhus. Humans are incidental hosts via arthropod
vector. In Hong Kong, majority of the reported cases contracted the
diseases locally and mostly related to outdoor activities. Vasculitis of
small vessels is basic underlying pathology. The severity of disease can
range from mild to multi-organ failure and even fatal outcome. Patients
usually present with triad (i.e. fever, skin rash/eschar and headache).

Diagnosis

Infections
1. Weil-Felix test: non-sensitive and non-specific
2. Indirect immunofluorescence assay (sent to PHLC):
• Spotted fever group
• Typhus group
• Scrub typhus
Management
1. All beta-lactams and aminoglycosides are not effective.
2. Doxycycline is the most effective drug
3. The usual adult oral dose of doxycycline is 100mg twice daily for
7-14 days.
4. Azithromycin is an option for those who are contraindicated for
tetracycline such as pregnant women and children.
5. Notify to CHP
 In 32

INFLUENZA
An acute viral disease of the respiratory tract caused by the influenza A
(H3N2, H1N1, H5N1, H7N9 etc.), B and C viruses, with fever, headache,
myalgia, prostration, coryza, sore throat and cough.

Diagnosis

1. Nasopharyngeal aspirates/ tracheal aspirates/ broncho-alveolar

lavage specimens for direct antigen detection (immunofluorescence
or EIA), AND viral culture; PCR in selected cases (consult clinical
microbiologist).
2. Acute and convalescent sera for specific Ab rise
Infections

Complications
Primary viral pneumonia, secondary bacterial pneumonia, myocarditis,
myositis, rhabdomyolysis, Guillain-Barré syndrome, transverse myelitis,
Reye’s syndrome (associated with use of aspirin in children)

Management

1. Droplet precautions
2. Treatment
• Effective against influenza A and B
- Oseltamivir 75 mg bd po x 5 d
- Zanamivir 10 mg bd inhaler puff x 5 d

N.B.
• Beneficial effects of treatment are most apparent if started early (i.e. within 48
hrs of symptom onset). However, in severe, hospitalized cases, therapy should
still be considered beyond the 48-hr window period.
• In complicated cases (e.g. viral pneumonia), increased dose of oseltamivir
(150 – 300mg bd for ≥5 days) may be considered.
• Seasonal influenza A/H1N1 virus exhibits a high level of oseltamivir
resistance (except for the influenza A/ H1N1 (2009) virus, which caused
pandemic in 2009 – 2010.)
• Intravenous preparations of zanamivir and peramivir may be considered as
salvage therapy for critical cases.
 In 33
Special points on Novel Influenza A
1. A statutory notifiable disease
2. Influenza A/H5N1 virus is a highly pathogenic form of
avian influenza that caused outbreak in various countries.
3. Since 2013, outbreaks of infection due to influenza
A/H7N9 have occurred in Mainland China
4. Pay attention to epidemiological link (Travel/ Occupation/
Contact/ Clustering) in evaluation of patients with fever
+/- URTI.
5. In general, neuraminidase inhibitors remain effective as a
treatment for novel influenza A/H5N1 and A/H7N9.
Prolonged duration and/ or increased dose of of therapy
may be necessary.

Infections
6. Intravenous preparation of zanamivir and peramivir may
be considered for critical cases.

Reference
1. HA fact sheet on antiviral therapy against influenza (Jan
2009)
2. HA fact Sheet on H5N1 Avian Influenza (Jan 2009)
3. HA Interim Guidance on Clinical Management of Human
Infection due to Avian Influenza A (H7N9) (May 2013)
4. HA Interim Recommendation on Antiviral Therapy for
Human Infection due to Avian Influenza A (H7N9) (May
2013)
 In 34

INFECTION CONTROL
Hand Hygiene (HH)
Good hand hygiene practices is utmost important to prevent healthcare
associated infections.
“Five moments” for HH (WHO recommendations):
1. Before patient contact
2. Before aseptic task
3. After body fluid exposure risk
4. After patient contact
5. After contact with patient surroundings

Precautions to prevent transmission of infectious agents

Infections

2 tiers of precautions:

1. Standard precautions (SP)

Applied to all patients in all healthcare setting, regardless of suspected
or confirmed presence of an infectious status. HCWs should apply SP
when contact with
• blood;
• all body fluids, secretions, and excretions except sweat, regardless of
whether or not they contain visible blood;
• non-intact skin; and
• mucous membranes.

2. Transmission-based precautions
Applied to patients who are known or suspected to be infected or
colonized with infectious agents, including epidemiologically important
pathogens which require additional control measures to effectively
prevent transmission. These composed of droplet, contact and airborne
precautions.
 In 35

Precautions Prevent transmission of infectious agents

Contact spread by direct/ indirect contact with patients or

patient’s environment
e.g. Norovirus, RSV, C. difficile, MRSA

Droplet spread through close respiratory or mucous

membrane contact with respiratory secretions
e.g. Influenza, N. meningitides, B. pertussis

Airborne that remain infectious over long distance when

suspended in air
e.g. Measles, Chickenpox, M. tuberculosis

Infections
3. Syndromic and empiric applications of transmission-base
precautions
Clinical syndrome Potential Empiric
pathogens precautions
Acute diarrhoea with likely Enteric Contact
infectious cause in an pathogens
incontinent/diapered patient
Abscess/draining wound MSSA, MRSA, Contact
that cannot be covered Group A
Streptococcus
Vesicular rash Varicellar-zoster, Airborne + Contact
variola
Petechial/ecchymotic with N.meningitides Droplet (for 24
fever; meningitis hrs.of antimicrobial
therapy); mask and
face protection for
intubation
Maculopapular rash with Measles airborne
cough, coryza and fever
 In 36

Cough/ fever/ pulmonary M. tuberculosis airborne

infiltrate and other clinical
features suggestive of TB

Diagnosis of many infections require laboratory confirmation.

Appropriate Transmission-based precautions should be implemented
when test results are pending based on the clinical presentation and
likely pathogens. Examples:
Infections
 In 37

NEEDLESTICK INJURY OR MUCOSAL CONTACT

TO HIV, HBV AND HCV
Prevention of transmission of HIV, HBV and HCV in healthcare setting is
based on the principle of Standard Precautions.
1. Avoid recapping needles
2. Dispose of sharps immediately after use
3. Plan for safe handling and disposal before beginning any procedures
using sharps
4. Use safety devices, if available

Measures that involve exposure to blood, body fluids, and tissues:

Infections
Gown / plastic Eye
Procedures Handhygiene Gloves Mask
apron Protection

1. Suctioning + + * * *
2. Inserion of
+ + * * *
airways
3. Artificial
Airway care
+ + * * *

4. CPR + + * * *
5. Assisting with
- intubation + + * + +
- bronchoscopy + + + + +
- tracheotomy + + + + +
6. ABG punctures + + * * *
7. Cleansing
surfaces or + + * * *
equipment
8. Blood taking + + * * *

+ Routinely *if soiling or spluttering likely

 In 38

Management of needle-stick injuries or mucosal contact with

blood and body fluids

1. First Aid (of utmost importance for lowering the risk of

infection)
• Express blood gently and wash immediately and thoroughly with soap
and water.
• In case of mucosal contact such as spillage into the eyes, wash
immediately and liberally with running water
• wound should be disinfected and dressed
• Attend A & E
2. Reporting: Injured staff should report to his unit head or physician i/c
and Infection Control Team.
Infections

3. Counselling
4. Management of occupational exposure to HIV:
• Risk of HIV transmission is about 0.3% after needlestick injury and
0.1% after mucosal exposure.
• Source patient should be assessed for risk of HIV infection. Counselling
and HIV testing with consent should be offered where appropriate.
• The injured staff should be encouraged to undergo HIV testing at 0, 3
and 6 months; additional test at 12 months for those who have taken
PEP; or have become infected with HCV after exposure to source
co-infected with HIV and HCV to detect delayed HIV conversion.
• Post-exposure prophylaxis with a 4-week course regimen containing 3
antiretroviral drugs should be initiated as soon as possible, preferably
within 2 hours after the exposure.
• PEP can be initiated at any A&E department followed by referral to the
Therapeutic Prevention Clinic, at
.1. IDSM, PMH (Tel:6461 0613),
.2. Special Medical Service, QEH (Tel:2958 5855), or
.3. ITC, CHP (Tel:2116 2929), for counselling, follow up and HIV
testing.

Reference :
1) Updated US Public Health Service guidelines for the management of occupational exposures
to human immunodeficiency virus and recommendations for postexposure prophylaxis.
2) EACS guideline 2013
 In 39
5. Post-exposure prophylaxis against hepatitis B infection
• Save blood for HBV status of source and injured staff, if status
unknown.
• If source person can’t be traced, may treat as if he is HBsAg +ve
• No treatment is required if injured staff is anti-HBs is +ve
• HBIG and HB Vaccine can be offered to injured staff if anti-HBs is
negative (depends on HBsAg status of source and vaccination
history of injured staff)

POST-EXPOSURE PROPHYLAXIS

Previously Vaccinated Unvaccinated

Infections
Source Known Known Unknown HBV HBV
HBsAg Responders Non-respo Response markers markers
status nders -ve +ve

HBsAg Nil HBIG Depends HBIG + Nil

+ve within 24 on anti- HB Vac
hrs,rept HBs status
after 1/12 of exposed

HBsAg Nil Nil Nil HB Vac Nil

-ve

HBsAg Nil Depends Depends HBIG + Nil

unknown on source on anti- HB Vac
HBsAg HBs status or
status of exposed HBVac,
person depending
on source
HBsAg
status
 In 40
φ means HBsAg -ve AND anti-HBs -ve
ψ means HBsAg +ve OR anti-HBs +ve
• Where indicated, one dose of HBIG (0.06 ml/kg) should be
given within 24 h of exposure, and preferably within 7 days
• If HBIG has been given, the first dose of vaccine can be delayed for
up to 1 week after exposure.
• HBIG and HB vac can be given together but at a different sites
• Injured staff can be referred to the Viral Hepatitis Preventive Service
of DH (Tel: 21129911) for vaccination.

6. Post-exposure management against Hepatitis C infection

• There is no universally accepted effective therapy for preventing
HCV infection after accidental occupational exposure. Early
Infections

identification of acute HCV infection and treatment with Interferon

plus ribavirin may prevent chronic HCV.
• Check anti-HCV of source patient after informed consent.
• Check anti-HCV and aminotransferase (ALT) of exposed person
soon after exposure and again at 6 months. Repeat at 12 month if
source is HIV-HCV co-infected.
• If source is HCV infected /IV drug addict /unknown HCV status,
arrange follow-up in 6-8 weeks to test for anti-HCV, ALT and
HCV RNA. Refer the injured to specialist if HCV-RNA positive.
 In 41

Middle East Respiratory Syndrome (MERS)

Background
• Caused by MERS-coronavirus (MERS-CoV), first reported in
Middle East in 2012.
• Most cases occur in Arabian Peninsula
• Suspected source for human infection : Dromedary camels and bats
• Incubation period : 2 to 14 days
• Case fatality rate : around 30%

Clinical manifestation
• Can be asymptomatic
• Common presentation : pneumonia presenting with fever, cough, and
shortness of breath

Infections
• Other symptoms : gastrointestinal symptoms, including diarrhoea
• Severe illness : Organ failure e.g. respiratory failure, renal failure, or
septic shock

Investigations
• Upper respiratory tract specimens (NPA, NPS), or lower respiratory
tract specimens (sputum, tracheal aspirate, BAL) in patients with
pneumonia, for MERS-CoV PCR (lower respiratory tract specimens
may have a better diagnostic yield)
• Repeated testing may be necessary to exclude the diagnosis.
• Stool for MERS-CoV PCR in patients with epidemiological link
presenting with diarrhoea.
• Microbiological workup to exclude other infections

Clinical management
• Isolate the patient(s) in airborne infection isolation room (AIIR) with
standard, contact, droplet and airborne precautions
• Start empirical antimicrobial agents
• β-lactam/β-lactamase inhibitor combination OR 3rd generation
cephalosporin + macrolide
• Respiratory fluoroquinolones for patient with β-lactam allergy
• Liaise with lCU early for intensive care if anticipate clinical
deterioration
 In 42
• Provide supportive treatments : Oxygen, IV fluid, Inotropic support
+/- steroid* (septic shock), Mechanical ventilation +/- ECMO
(respiratory failure), Renal dialysis (renal failure)
* Avoid high-dose systemic corticosteroids for viral pneumonitis;
consider administration of intravenous hydrocortisone (up to 200
mg/day) or prednisolone (up to 75 mg/day) to patients with
persistent shock who require escalating doses of vasopressors
• Based on the current scientific evidence, no specific anti-viral
treatment can be recommended at the moment
• Continue isolation and infection control measures till asymptomatic
and specimens negative for novel coronavirus.

Reference:
Interim Recommendation on Clinical Management of cases of Middle
Infections

East Respiratory Syndrome. HA CCIDER.

 In 43

Viral haemorrhagic fever (VHF)

Background
• VHF can be caused by four families of enveloped RNA viruses -
Arenaviruses, Bunyaviruses, Filoviruses and Flaviviruses
• VHF in general refers to severe febrile illnesses with abnormal
vascular regulation and vascular damage but not all patients infected
with a VHF agent develop this syndrome
• The routes of transmission are variable :
• Most are zoonotic with spread via arthropod bites or contact with
infected animals
• Human to human transmission possible e.g. in Ebola virus,
Marburg virus, Lassa virus and CCHF virus infection - usually
occur through direct contact with contaminated blood or body

Infections
fluids via mucous membrane during care of sick patients or
handling of dead bodies in burial ritual

Summary of common VHF agents are listed below

Source of
Natural Incubation
Disease (Virus) Family Human
Distribution (Days)
Infection

Lassa fever Arenaviridae W. Africa Rodent 5-16

Argentine HF Arenaviridae S. America Rodent 7-14

Rift Valley Africa, Middle
Bunyaviridae Mosquito 2-5
fever East
Crimean- Europe, Asia,
Bunyaviridae Tick 3-12
Congo HF Africa
Hantavirus Bunyaviridae worldwide Rodent 9-35
Marburg virus Filoviridae Africa Fruit Bats 2-21
Ebola virus Filoviridae Africa Fruit Bats 2-21
Africa, South &
Yellow fever Flaviviridae Mosquito 3-6
Central America
Asia, Africa,
Dengue HF Flaviviridae Mosquito 3-15
American
 In 44
Clinical features
• Vary according to specific viral infection, range from minimally symptomatic
to fulminant presentations
• Common presenting features : fever, myalgia, headache and prostration,
conjunctival injection, mild hypotension, flushing and petechial haemorrhages

• GI symptoms e.g. nausea, vomiting, diarrhoea and abdominal pain are often
present in the pre-haemorrhage stage
• Severe haemorrhagic manifestations in later stage: bruising, ecchymoses,
bleeding at injection sites, gingival haemorrhage and GI bleeding. It is often
accompanied by renal failure, hepatic damage, multi-organ failure and shock.

Diagnosis
• Suspect VHF based on clinical assessment and travel history
• Need to exclude other differential diagnosis e.g. malaria, meningococcemia
Infections

• Diagnosis of VHF can be confirmed by blood test using PCR method to detect
specific virus

Management
• Infection control (those with possible human to human transmission) : i) Single
room (in practice, use an Airborne Infection Isolation Room (AIIR) with toilet
facility); ii) Standard, Contact and Droplet precautions; iii) Prevention of
sharps injury and mucocutaneous exposure to blood, body fluids, secretion and
excretions; and iv) Meticulous Hand Hygiene
• Mainly supportive care: i) Fluid and electrolyte management; ii)
Hemodynamic monitoring; iii) Ventilation and/or dialysis support; iv) Treat
secondary bacterial infections; v) Manage severe bleeding complications
• Anticoagulants, aspirin, NSAIDS and intramuscular injections are
contraindicated
• Ribavirin can be considered in VHF caused by Arenavirus or Bunyavirus
• ZMapp and Favipiravir have been investigated in the management of Ebola
virus disease (EVD).

Vaccination
• Yellow fever vaccine is recommended and required for travelers to some
countries in Africa and South America (refer to CDC/WHO website for
details)
• Vaccines for other VHF agents e.g. Ebola virus are under investigation.
Reference:
Guidelines on Management of Patients with Suspect Viral Haemorrhagic Fever. HA CCIDER
Palliative
Medicine

Medicine
Palliative
 PM 1

ANOREXIA
Anorexia can be due to multiple causes, leading to early satiety or loss
of desire to eat; may or may not be associated with cachexia.

Causes:
1. Concomitant symptoms: pain, depression, constipation, dyspnoea,
dysphagia, nausea, vomiting, anxiety
2. Oral problems: dry mouth, candidiasis, ulcers, ill fitting denture,
change in taste
3. Delayed gastric emptying: hepatomegaly, autonomic neuropathy
4. Medications: opioids, antibiotics
5. Odour: foul smelling discharge, fungating mass, incontinence

Management:
1. Treat reversible causes and optimize symptom palliation
2. Maintain good oral hygiene

Medicine
Palliative
3. Provide frequent small meals or food on demand, allow patient to eat
what they wish, keep company during eating
4. Acknowledge concerns on prognosis, body image, social impact
5. Proper mood assessment and psychological support

Appetite stimulating agents:

1. Corticosteroids: e.g. dexamethasone 2-4 mg daily
 Rapid onset, but effect tails off after 4 weeks
 Increase food intake, but no weight gain
 May reduce nausea and improve sense of well being
 Discontinue after 1 week if no benefit; if effective, keep minimum
effective dose; tail off if effect wears off
 Look out for DM, TB before starting; give OM or before noon to
avoid disrupting diurnal rhythm; monitor mouth condition for oral
candidiasis.
 PM 2
2. Progestogen: e.g. megestrol acetate 160 mg daily to Qid
 Improve appetite and has a small effect on weight gain
 Less rapid onset but action lasts longer than corticosteroid
 S/E: Oedema, thromboembolism and deaths are more frequent
 Potential application in anorexia-cachexia syndrome related to
cancer, AIDS, advanced COPD.
3. Prokinetics e.g. metoclopramide 5-10mg tid
 For early satiety, delayed gastric emptying, gastroparesis

PRACTICAL POINT:
Appetite stimulating agents does not reverse cachexia.
Palliative
Medicine
 PM 3

NAUSEA & VOMITING

Causes:
1. GI related: GI obstruction, constipation, gastroenteritis, gastric
irritation, GERD, autonomic neuropathy
2. Metabolic: hypercalcaemia, uraemia, liver failure
3. Drugs: opioids, antibiotics
4. Cancer treatment: chemotherapy, radiotherapy
5. CNS: increased ICP, brain stem disease, vestibular dysfunction

Management:
1. Elucidate and remove cause of nausea and vomiting if possible (e.g.
constipation, hypercalcaemia).
2. Pay attention to environment, odour, food presentation.
3. Antiemetics (If oral absorption is in doubt, use other routes)
 Prokinetic: e.g. metoclopramide 5-10mg tid, domperidone 10mg
tid.
 Central anti-dopaminergic drugs e.g. haloperidol 0.5-5 mg bid (e.g.

Medicine
Palliative
uraemia, opioid-induced).
 Dexamethasone 16 mg OM initially for brain tumour while
pending tumour targeted treatment; 8 mg OM initially for reducing
compression on gut by tumour masses.
 For emetogenic chemotherapy related nausea and vomiting,
consider 5HT3 antagonists e.g. granisetron, ondansetron,
tropisetron, and neurokinin-1 (NK-1) antagonist e.g. aprepitant

PRACTICAL POINTS:
1. Do NOT use metoclopramide in complete GI obstruction.
2. Dosage adjustment of metoclopramide is required in renal failure.
 PM 4

CANCER PAIN MANAGEMENT

Optimum management of cancer pain requires a multidisciplinary
approach. The Basic General Principles are:
1. By the Mouth: oral route the preferred route.
2. By the Clock: regular analgesics.
3. By the Ladder (WHO Analgesic Ladder)  adjuvants.
Start appropriate analgesic according to the intensity of pain
WHO analgesic ladder step Analgesics of choice
1 ( mild pain) Paracetamol and/or NSAIDs
2 (mild to moderate pain) Weak opioids (e.g codeine,
dihydrocodeine, tramadol) ±
paracetamol and/or NSAIDs
3 ( moderate to severe pain) Strong opioids (e.g morphine,
methadone, fentanyl) ±
paracetamol and/or NSAIDs
Adjuvants: antidepressants (e.g amitriptyline and imipramine) and
Palliative
Medicine

anticonvulsants (e.g gabapentin and pregabalin)

PRACTICAL POINTS:
1. Consult palliative care or cancer pain specialist when patient in severe pain
crisis.
2. Pethidine NOT recommended because of adverse S/E profile.
3. FDA recommended withdrawal of propoxyphene in 2010.
4. Potency of Tramadol is between weak and strong opioids; similar S/E
profile; watch out for drug-drug interaction e.g. SSRI, TCA, warfarin.
5. Fentanyl patch is NOT for opioid naïve patients, acute pain or initial
titration. Consult specialists.
6. Caution was recommended on chronic use of NSAIDs, as many cancer
patients are at high risk of GI, renal, cardiac toxicities or bleeding
disorders.
7. In ESRD, paracetamol is the first line drug. Weak opioids, morphine,
NSAID, COX-2 inhibitor should be AVOIDED. Methadone and fentanyl as
suitable strong opioids, consult specialist.
8. COX-2 inhibitor is no different from NSAID in renal toxicity.
 PM 5

GUIDELINES ON USE OF MORPHINE FOR CHRONIC

CANCER PAIN CONTROL

1. Morphine is the strong opioid of choice for moderate to severe

cancer pain.
2. Morphine has no standard upper dose range. The optimal dose is the
dose providing adequate pain relief with minimal or tolerable S/E.
3. Oral route is preferred unless not feasible e.g. GIO, dysphagia
4. Use immediate release morphine i.e. syrup morphine for titration.
5. Start with syrup morphine 5mg Q4H regularly, not PRN. Some
prefer to double the dose at bedtime to avoid waking the patient up at
4 am.
6. Consider a lower starting dose of 2.5mg for patients susceptible to
S/E e.g. old age, COPD, frailty, sleep apnoea.
7. Dose increment: e.g. 5mg7.5mg10mg15mg20mg30mg
etc.
8. For breakthrough pain, prescribe the SAME dose as the one for
regular use in between the regular intervals, given up to hourly.

Medicine
Palliative
Review within 24 hours and adjust the regime according to
breakthrough requirement.
9. AVOID morphine in renal failure as active metabolites are excreted
by renal route.
10. Side effect of opioids and their management:
GI Nausea, vomiting, constipation
ANS Dry mouth, urinary retention, postural hypotension
CNS Sleepiness, cognitive impairment, delirium, hallucination,
respiratory depression, myoclonus, seizure, hyperalgesia
Skin Itchiness, sweating
a. Good explanation is important.
b. Ensure adequate hydration of patient.
c. Give laxatives CONCURRENTLY if not contraindicated,
preferably a combination of stimulant and stool softener e.g.
Senna 15mg Nocte and lactulose 10ml tid.
d. Nausea may occur initially. May prescribe antiemetic PRN
e.g.metoclopramide 5-10mg tid, haloperidol 0.5-5mg daily.
e. May consider methylphenidate 5 – 20mg daily for sleepiness
 PM 6
f. Consider reduce dose of morphine if pain is well controlled;
abrupt discontinuation may precipitate withdrawal symptom.
g. Consider adjuvant analgesics.
h. Consult specialist to switch to another strong opioid.

Dose conversion of oral morphine to parenteral route

1. Parenteral route has NO special advantage over oral route.
2. SC route is the preferred alternate route, or IV if access available.
No indication for IMI generally.
3. Dose conversion
 Oral daily dose of morphine÷2 = daily dose of morphine SC
 Oral daily dose of morphine÷3 = daily dose of morphine IV
 E.g. Morphine 60mg PO = 30mg SC = 20mg IV

PRACTICAL POINTS ON PARENTERAL DRUGS:

Generally, parenteral drugs for symptom control can be given by:
1. Syringe driver (10ml syringe or specified syringe) OR
Palliative
Medicine

2. Infusion pump by adding drugs to parenteral fluid to be given SC

(NS only for SC) or IV.

PRACTICAL POINTS ON LAXATIVES:

1. Metamucil requires good fluid intake and has high K content; NOT
for frail patients with reduced water intake.
2. Mg Trisilicate has high Mg content; NOT for ESRD.
3. Fleet enema contains high phosphorus content; NOT for ESRD.
 PM 7
DYSPNOEA
Causes:
Dyspnoea is a subjective experience of the patient and is usually
multifactorial in advanced cancer.
Common Cardiorespiratory Causes Common Systemic
Causes
Malignancy Lung masses, Pleural effusion, Chest Anaemia, Cachexia,
related infection, Major airway obstruction, Muscle weakness, Gross
SVCO, Lymphangitis carcinomatosis, hepatomegaly or Tense
Pneumothorax, Pericardial effusion, ascites, Metabolic
Pulmonary embolism, acidosis
Post-irradiation or
post-chemotherapy Pneumonitis.
Non-mlignant Co-existing COPD, Asthma, Heart Anxiety
failure

Management:

Medicine
Palliative
1. Identify and treat as many reversible causes as possible e.g. pleural,
pericardial or abdominal tapping, chest drain insertion, antibiotics,
anticoagulation, blood transfusion, bronchodilators, diuretics.
2. Oxygen for hypoxic patients, nasal prong better tolerated than face
mask.
3. Dexamethasone 4-8 mg daily for lymphangitis carcinomatosis,
post-irradiation or post-chemotherapy pneumonitis; 16mg daily for
SVCO, major airway obstruction.
4. Opioid:
 For opioid naïve patients, start with morphine 1-2 mg Q4H PO or
SC. Increment of 25% of baseline dosage for patient on
morphine
 Monitor mental state, RR, SaO2. Withhold opioids if there is
sign of respiratory depression.
 Titrate up in steps according to effect: e.g. 1 mg 2 mg  3mg
5mg…
 PM 8
 Dyspnoea in the terminal phase: In opioid naïve patients, start
with morphine 5mg SC infused over 24 hours; for patients with
CRF, start with fentanyl 50-100 microgram SC infused over 24
hours. For intermittent/ breakthrough dyspnoea, add morphine
1-2mg SC q2h prn; or fentanyl 12.5microgram SC q2h prn for
CRF.
5. Anxiolytic: indicated for patient with strong anxiety or panic.
6. Non-drug measures: prop up, face fan / good air circulation.
7. For severe dyspnoea refractory to above treatment, consult PC
specialist. The use of palliative sedation should ONLY be
prescribed by PC specialist for refractory dyspnoea. Patient and
family should be informed about the purpose, possible impairment in
communication, and this is not euthanasia.

PRACTICAL POINTS:
1. CXR is useful in elucidating most underlying causes.
2. SaO2 / lung function parameters do NOT correlate with intensity of
Palliative
Medicine

dyspnoea.
3. Look out for trapped lung in chest tapping, stop if patient coughing
or develop chest pain; document in patient’s record to guide decision
on chest tapping in subsequent admission.
4. USG guidance is helpful in chest tapping especially in the presence
of loculations.
5. Before abdominal tapping, watch out for coagulopathy; for patients
with suspected haemoperitoneum, consider the risk of removing the
tamponade effect on a ruptured tumour with release of
intra-abdominal pressure upon tapping.
 PM 9
DELIRIUM

Delirium is an acute confusional state with fluctuating course,

characterized by altered consciousness and cognitive deficits.
Manifestations can be hyperactive, hypoactive, or mixed.
Delirium is common at terminal stage, but can have easily remediable
causes.
Common causes:
1. Drugs : opioid, anticholinergic, steroid, antidepressant, sedatives
2. Uncontrolled symptoms: eg pain, faecal impaction, urine retention
3. Infections
4. Metabolic : hypercalcaemia, electrolytes disturbance,
hyper/hypoglycaemia, liver failure, uraemia, dehydration, hypoxia,
CO2 retention
5. Organic brain disorder : brain tumour or metastases, cerebrovascular
events
Exacerbating factors:

Medicine
Palliative
1. Change of environment or excessive stimuli – temperature, noise,
lighting
2. Insomnia, anxiety, depression, fear
Management:
1. Calm reassurance and explanation to patient and family
2. Reduce environmental stimuli, avoid restraints and keep patient
accompanied.
3. Identify reversible causes and treat accordingly.
 Bedside examination – include assessing the hydration status,
neurological exam, PR exam, palpating for urinary bladder,
checking temperature, SaO2 and H’stix
 Take blood for CBP with d/c, RLFT, Ca2+, cultures as
appropriate and treat accordingly
 Review drug charts – if drug-related delirium is suspected, stop
the drug if possible or switch to alternatives where available; if
opioid toxicity, reduce dose by one-third to half. Ensure adequate
hydration.
 +/- CT brain if suspected remediable CNS causes
 PM 10
4. Drug treatment for delirium is indicated if the symptoms are
distressing (lower doses for frail elderly with caution):
 Haloperidol po/sc 1 – 3mg stat (start at 0.5 in elderly) THEN q4
– 6h; or sc infusion 5 – 20mg q24h via a syringe driver ; shown
to be effective in hyperactive, hypoactive and mixed types of
delirium
 Chlorpromazine po 25 – 50 mg q8h is an alternative and has
similar efficacy to haloperidol.
 Benzodiazepine may aggravate agitation; use judiciously in
combination with haloperidol for sedation in terminal delirium or
if symptoms remain refractory. Midazolam sc 2.5 – 5mg stat for
acute control then 5 – 30mg q24h via syringe driver.
Palliative
Medicine
 PM 11

MALIGNANT BOWEL OBSTRUCTION (MBO)

1. Assess if surgery is feasible, more likely for patient with single level
obstruction with good performance status. Surgical intervention also
depends on other prognostic criteria (age, comorbidities, nutritional
status and history of radiotherapy to abdomen)
2. For inoperable cases, symptomatic medical treatment (should be
individualized):
a. Fasting, IV/SC rehydration
b. Antiemetics:
- Haloperidol SC: 5-15 mg/24 h
- Metoclopramide SC 30-60 mg/24 h (contraindicated in
complete obstruction)
- Ondansetron IV: 4-8 mg/24h in refractory cases
c. Anticholinergic antisecretory:
- Hyoscine-N-butylbromide SC 40-120 mg/24 h
d. Antisecretory somatostatin analogue:
- In refractory MBO with high output, consider Octreotide

Medicine
Palliative
SC/IV 300 micrograms/24 h for 3 days, up to 600
micrograms/24h (total duration <7 days)
e. Gastric antisecretory:
- Pantoloc 40 mg IV over 24 h or single injection
f. Steroids:
- Dexamethasone IV/SC 0.25-1 mg/kg/24 h or in one single
injection, short course 5-10 days
g. Analgesics:
- IV/SC morphine or fentanyl (dose titration as in pain
management)
h. Nasogastric tube (NG tube)
- Necessary if abundant vomiting and/or significant gastric
distention (> 1 litre/day)

PRACTICAL POINTS:
1. Surgery carries high mortality, complication rates and substantial
hospitalization relative to the patient’s remaining survival time.
Consider stenting in individual cases.
 PM 12
2. Stop stimulant laxatives and prokinetic agents if complete MBO.
3. NG tube is no longer used routinely and should instead be decided
on a case-by-case basis. Aim to remove the NG tube as soon as
possible to minimize patient discomfort.
4. Consider venting gastrostomy in refractory high output MBO.
5. MBO may be reversible under symptomatic medical treatment.
Palliative
Medicine
 PM 13

PALLIATIVE CARE EMERGENCIES:

MASSIVE HAEMORRHAGE
Anticipation:
Important for care planning or advance directives; identify any
underlying causes e.g. coagulopathy or thrombocytopenia and /or
potential lesions e.g. H&N tumour eroding carotid artery; repeated
episodes of haemoptysis; invasion into internal structures e.g. aorta;
tumour rupture e.g. HCC.
Management:
If indicated, haemodynamic stabilization with transfusions and volume
replacement should be given. Repeated transfusion is warranted only if
clear benefit was obtained following the last transfusion. In case of
massive haemorrhage that occurs at the end- of-life with a DNACPR
directive, comfort measures should be taken.
1. Apply direct pressure with adrenaline (1 in 1000) soaked dressing to

Medicine
Palliative
any external bleeding point.
2. Use green surgical towels to reduce the frightening visual impact of
the bright red blood.
3. Sedate with midazolam 5-10 mg SC or diazepam 5-10 mg per rectal
stat to relieve panic and fear.
4. Address emotional impact on family and staff.
 PM 14

MALIGNANT HYPERCALCAEMIA
(Also see page K6 and GM27)
Presentation: delirium, malaise, thirst, nausea, constipation
Common primary: myeloma, breast, lung, head & neck, kidney
Management:
1. Monitor Ca, P, RFT, urine output.
2. Withdraw drugs that promote hypercalcaemia (thiazide diuretics,
lithium, ranitidine, vitamins D and preparations containing calcium)
3. Rehydration with NS 2-3 litres/day, to keep adequate urine output e.g. >
2 L/day.
4. Bisphosphonate infusion after correction of dehydration
 Pamidronate infusion
3.0-3.25 mmol/L - 60mg in 500ml NS over 2-4hrs
>3.25 mmol/L - 90mg in 500ml NS over 2-4hrs
 Zoledronic acid 4mg iv infusion over 15 min
 Adjust dose or infusion rate in renal impairment.
 Longer infusion in pamidronate (i.e., >2 hrs and up to 24 hrs) may
reduce the risk for renal toxicity, particularly in patients with
preexisting renal insufficiency.
 Dose reduction in zoledronic acid
Palliative
Medicine

CrCl ml/min Dose

>60 4mg
50-60 3.5mg
40-49 3.3mg
30-39 3mg
 Bisphosphonate is generally contraindicated if CrCl<30
5. Consider steroid e.g. Prednisolone 30mg or hydrocortione 100mg iv q6h
for hypercalcaemia in myeloma and lymphoma
6. Haloperidol 0.5-5mg daily for delirium.
7. Maintain IV hydration till patient can maintain oral hydration.

PRACTICAL POINTS:
1. Allow time to achieve full treatment effect: check calcium level at day 5
to assess effectiveness. Do NOT repeat bisphosphonate infusion until
day 7.
2. Patient may look exceptionally ill with hypercalcaemia, on the other
hand, bisphosphonate may not be appropriate at EOL, if in doubt,
consult.
3. Effect of bisphosphonate lasts for 2-4 weeks, plan accordingly.
 PM 15

METASTATIC SPINAL CORD COMPRESSION

(Also see page N19 and GM26)

Common primary: breast, lung, prostate (15-25%); myeloma, kidney,

lymphoma (5-10%); GI, melanoma, sarcoma, unknown primary (<5%)
Site of Compression: thoracic (70%), lumbosacral (20%), cervical
(10%)

Presentation:
1. Back pain aggravated by coughing or lying down; neuropathic pain
radiating from back to thigh or around the trunk; motor weakness or
impaired sensation; sphincter disturbance is a late sign with poor
prognosis in functional outcome
2. Perform a FULL neurological examination in ANY cancer patient
with the slightest suspicion
3. Can be the first presentation of cancer
4. Site of pain may not correlate with level of compression

Medicine
Palliative
Investigation & management:
1. Plain X ray may not show bone lesion till bone loss is considerable.
2. Urgent MRI of the whole spine.
3. Start dexamethasone 16mg per day PO or IV
4. Urgent referral for RT; tail down steroid after RT
5. Consult O&T for surgical intervention which may be appropriate in
selected cases (uncertain cause, radioresistant tumour, failed
radiotherapy, unstable spine, major structural compression, cervical
cord lesion, solitary vertebral metastasis)

PRACTICAL POINTS:
1. Functional status at the time of treatment is the most important factor
in determining the prognosis and outcome; early diagnosis important
2. CNS examination can be normal to begin with; keep monitoring
 PM 16

LAST DAYS OF LIFE

1. Recognizing a patient is approaching end-of-life is important in
triggering the care planning and communication with patient and
family.
2. Inappropriate interventions, investigations and medications should
be withheld to focus on comfort measures.
3. Anticipatory prescription facilitates timely symptom control e.g.
pain, delirium, dyspnoea, death rattle, myoclonus. Medications must
be regularly reviewed and adjusted. Dose reduction in elderly and
frail is needed.
Pain: Morphine 2.5-5mg SC prn hrly or fentanyl 12.5 microgram SC
prn hrly if not on regular opioid; step up the regular dose of opioid if
already on opioid and change to SC route.
Nausea / vomiting: Haloperidol 0.5-1 mg SC prn hourly.
Agitation / anxiety: Haloperidol 2.5mg sc prn hrly, or Midazolam
2.5mg SC prn hourly.
Palliative
Medicine

Myoclonus: Midazolam 2.5mg SC prn hourly.

DEATH RATTLE & TERMINAL DYSPNOEA

1. Due to excessive respiratory secretions, the noise of which can be
distressing for relatives; explain that patient is not choking.
2. Avoid excessive fluid.
3. Gentle suction.
4. Hyoscine butylbromide (Buscopan) 20-60 mg q24h SC.
5. For terminal dyspnoea, please refer to DYSPNOEA session
PRACTICAL POINTS:
1. Do NOT use morphine for sedation.
2. Poor circulation may not give accurate SaO2; upward titration of
oxygen with plateau of dyspnoea relief or oxygen saturation is not
indicated. High oxygen flow may cause more discomfort to patient.
 General Internal
Medicine
Medicine
Internal
General
 General Internal
Medicine
GM 1

ANAPHYLAXIS
 GM 2

ACUTE POISONING
The guidelines below are very general and treatment options may not
apply to all patient. For specific poisoning patient management, please
call Hong Kong Poison Information Centre (HKPIC) – 27722211 or
26351111. (Note: all dosages quoted are for adult.)

General management of acute poisoning

(1) General measures
- Maintain ABC with precaution of secondary contamination
- Close monitor vital signs + neurological status
- Watch out and treat concomitant injuries; eg. head injury
- Obtain history of offending poison, dose, timing of ingestion
- Ix: Blood gas, CBP, L/RFT, glucose, H’stix,
Urine, blood, +/-gastric contents for toxicology
Specific drug level: Panadol, ethanol, salicylate, as indicated
ECG (assess for HR, QRS, QTc, arrhythmia)
- Correct fluid, electrolyte disturbance and treat arrhythmia.
- Psychiatry consultation, suicidal precautions as appropriate.

(2) Consider GI decontamination

General Internal
Medicine

Activated Charcoal (AC)

- Within first 1-2 hr after a toxic ingestion, Dose: 1g / kg PO.
- Not for small molecules (Fe, Li, toxic alcohols), caustic, hydrocarbon.

Gastric Lavage (GL)

- For potentially life-threatening poisonous ingestion
- Preferably within first hour post ingestion
- Intubation needed for confused, comatose patient
- Conscious patient must be cooperative, consent signed, lying head
down left lateral position, with powerful suction standby
- 36-40 F oro-gastric tube, 200-250ml water each time for at least 4-6L
or until return fluid is clear
 GM 3
Multiple dose activated charcoal (MDAC)
- 1g/kg PO, follow by 0.5g/kg q2-4hr for 1-2 days.
- Consider for Theophylline, Phenobarbital, Phenytoin, Digoxin,
Carbamazepine, Dapsone, GI concretion forming drug; aspirin and
sustained release (SR) preparation

Whole bowel irrigation (WBI)

- Toxic dose of SR preparation, body packers, and drugs not adsorbed
to AC
- PEG 1-2 L/hr till clear rectal effluent (orally or via a NG tube)

(3) Consider use of specific Antidotes

Level I, II, III antidotes kept at acute hospitals, cluster hospitals and
HKPIC respectively

(4) Enhanced Elimination as needed

Urinary Alkalinization
- Useful in Aspirin, Phenobarbital, Chlorpropamide, Formate,
Methotrexate
- 1-2 mEq/kg NaHCO3 IV bolus, then 50mEq NaHCO3 (8.4%) in 500ml
D5 Q4-6hr IV infusion

General Internal
Medicine
- Works by ion trapping, must get urine pH>7.5 to be effective
- Monitoring serum pH, avoid >7.55, avoid hypokalaemia
Haemodialysis / Haemoperfusion
Haemodialysis Hemoperfusion
Strong Methanol / Ethylene Glycol Theophylline
Indication Lithium, Aspirin

Rarer Ethanol / Isopropanol Carbamazepine, Phenytoin

Indication Phenobarbital
 GM 4
Treatment of specific drug poisoning
Benzodiazepine overdose
- Supportive measure is the mainstay of treatment
- Flumazenil is an effective antidote indicated in selected case
- Start with 0.2 mg IV over 30 sec and titrate up to 1-2 mg in total
C/I : patient with undifferentiated coma, epilepsy, benzodiazepine
dependence, co-ingestion of pro-convulsion poisons; eg.TCA.
Opioid overdose
- Supportive measure is the mainstay of treatment
- Naxolone: 0.4 mg – 2 mg as an IV bolus & repeated as needed.
- For chronic user, start with low dose of 0.1 mg.
- Naxolone infusion if repeated dose of naxolone needed.
(2/3 of initial effective naloxone bolus on an hourly basis:
ie. 4X initial effective dose + 500ml NS, Q 6 hour).
Amphetamine / Cocaine overdose
- Agitation, Hyperthermia - Rapid cooling, IV benzodiazepine
- HT- Phentolamine 1-5mg IV & repeat every 10 minutes or
Nitroglycerin 0.25-0.5 microgram/kg/min
- Cocaine (Na channel blocking effect) – NaHCO3 1-2mEq/kg IV bolus
till QRS <100ms or pH >7.55.
General Internal
Medicine

Paracetamol overdose
- Acute toxic dose: >150mg/kg.
- Check paracetamol level at 4 hour, LRFT.
- AC if within 1st hour, NAC if toxic level above Tx line.
- NAC has full protection if given within 8 hr post-ingestion, useful
even on late administration.
NAC dose In D5 Rate
Loading 150mg/kg 200ml in 1hr
then 50mg/kg 500ml D5 in 4 hr
then 100mg/kg 1000ml D5 in 16 hr
- With evidence of liver injury, check prognostic markers:
PT, APTT, L/RFT, blood gas, lactate, PO4, FP.
 GM 5
Salicylate overdose
- >150mg/kg acetylsalicylate (aspirin) – potentially toxic
- Pure methyl salicylate (oil of wintergreen): 10ml  14g salicylate
- Ix: R/LFT, blood gas, serial salicylate level, glucose, urine ketone
- Consider GL, AC, MDAC, WBI (depend on amount / formulation)
- Hydration, urine alkalinization if ASA >40mg/dL (>2.9mmmol/L)
- HD if end organ failure or ASA >100mg/dL (>7.3mmol/L)

Anti-cholinergic poisoning
- Physostigmine in selected case – 0.5-1mg slow IV, repeat up to 2 mg
C/I: TCA, widen QRS, CV disease, asthma, gangrene.

Beta-blocker overdose / Calcium channel blocker overdose

- GI decontamination, haemodynamic and cardiac monitoring
- Treatment options for hypotension and bradycardia:
 Atropine: 0.6mg IVI (up to 3mg) and iv fluid.
 Glucagon: 2-5mg IVI over 1 min (up to 10mg) follow by 2-5mg/hr
in D5 (for  blocker poisoning)
 CaCl2 1g or Ca gluconate 3g slow IV, repeat Q10min
(For CCB poisoning, 2-3 doses can be safely given without check Ca level)
 High Dose Insulin / Dextrose – Start with 0.5 - 2 units/kg/hr, titrate

General Internal
up to 10 units/kg/hr (Start early for the treatment takes time to be effective)

Medicine
 Inotropes: Adrenaline - 0.02 microgram/kg/min and titrate up
Noradrenaline - 0.1microgram/kg/min and titrate up
Dobutamine - 2.5 microgram/kg/min and titrate up
Isoproterenol - 0.1 microgram/kg/min and titrate up
(Dopamine not suggested due to its indirect effect)
 NaHCO3 1-2 mEq/ kg IV bolus for propanolol poisoing if QRS >
100ms, repeat as indicated.
(Co-administration of calcium and glucagon is useful in refractory or mixed cases)
 GM 6
Digoxin overdose
- Ix : RFT, digoxin level, ECG
- GI decontamination : consider GL, AC, MDAC
- Bradydysrhythmias – atropine
- Tachydysrhythmia – Tx hypoK, hypoMg, lignocaine,amiodarone
- Cardioversion – may precipitate refractory VT, VF, start with low
dose: 10-25J, pre-Tx with lignocaine or amiodarone
- Digoxin Immune Fab fragments (Digifab® in HA) indications:
 Brady or Vent arrhythmia not responsive to atropine
 Serum K+ > 5mEq/dL in acute DO
 Digoxin level: 10-15ng/mL (13-19.5nmol/L) in an acute DO
 Digoxin ingestion of > 10 mg
- The recommended dosage of Digifab® can be calculated by any one
of the below formulas:
Known ingestion amount No. of vial = Amount ingested in mg x 1.6

Known digoxin level No. of vial = (digoxin level (ng/mL)) x (wt in kg)
100

Empiric dosing Acute overdose: 10 vials

Chronic overdose: 4 vials
General Internal
Medicine
 GM 7
Warfarin or superwarfarin rodenticide overdose

Asymptomatic Symptomatic, check INR stat

INR at ~ 48 hours
No severe bleeding Severe/ life threatening
bleeding

Normal Prolonged INR

Not poisoned
FFP, Vit K1
No Vit K1 (oral, sc, iv - 10mg)
Oral Vit K1
(<1mg/min if IV)
(5-10mg for warfarin,10-25mg for
superwarfarin)

Monitor INR until plateau

Vit K1 has short duration of action

FU, may need months tds/QID dose needed
for superwarfarins

Mx guideline for warfarin patient with over anti-coagulation

INR Bleeding Recommendation/Action

General Internal
Medicine
<5 No Reduce dose or omit next few doses
> 5 but < 9 No If no risk factors for bleeding, omit next few doses; if risk
factors for bleeding, administer 1.0-2.5 mg oral vitamin K
>9 No 3.0-5.0 mg oral vitamin K
> 20 Yes (serious) 10 mg IV vitamin K and FFP or PCC
Any Yes (life-threatening) 10 mg IV vitamin K and PCC
1998 and 2001 ACCP Recommendations for Reversing Excessive Warfarin-Associated
anti-coagulation

Theophylline poisoning
- Ix : Theophylline level, electrolytes, ECG
- ABC monitoring and supportive measures.
- GI decontamination: GL / MDAC
- Patient died from tachyarrhythmia, hypotension and seizure
- Hypotension – IV fluid, -agonist (Phenylephrine, Noradrenaline)
 GM 8

- Tachyarrhythmia – diltiazem or -blockers (esmolol, propranolol)

- HP indication: Ileus / IO prevents use of MDAC
Theophylline level >80mg/L (acute) or 60mg/L
(chronic)
Elderly with level > 40mg/L with severe symptoms

Psychiatric Drugs
Antipsychotics poisoning
- Supportive care, ECG, GI decontamination as indicated
- Hypotension – IV fluid, inotropes (-adrenergic agonists)
- Cardiotoxicity, widen QRS – treat like TCAs
- Dystonia – diphenhydramine or cogentin
- Look out for neuroleptic malignant syndrome

Tricyclic antidepressant overdose

- Ix : Blood gas, ECG[ sinus tachycardia, widen QRS; > 100msec,
terminal 40ms right axis deviation (R in aVr)]
- Ensure ABC with intensive monitoring
- Consider GL and AC 1g/kg if < 1-2 hr post ingestion, MDAC
- Aggressive supportive care & early serum alkalization
- Physostigmine & Flumazenil are contraindicated
General Internal
Medicine

- Serum alkalization by NaHCO3

Indications QRS > 100ms Vent arrhythmia Hypotension
Dose 1-2 mEq per kg IV bolus
May need repeated bolus or infusion to meet endpoints

End points QRS <100ms* or Reversal of Correction of BP or

pH 7.5-7.55 arrhythmia or pH pH 7.5-7.55
7.5-7.55
Contra- pH > 7.55 [Consider hypertonic saline]
indications Intolerable to Na/fluid load [Consider hyperventilation]

*QRS endpoint with reference to patient baseline ECG

 GM 9
SSRI (selective serotonin reuptake inhibitors) and others
- Supportive care, ECG, GI decontamination as indicated
- Treatment for serotonin syndrome (SS) if present
Remove offending drugs, benzodiazepine, hydration, cooling,
cyproheptadine (8-12mg, then 2mg Q2hr, up to 32mg in 1st 24 hr),
neuromuscular blockage.
- Citalopram – observe for > 24 hr, cardiac monitoring for prolonged
QT, Tdp (especially with dose >400mg) 
- Venlafaxine – seizure; esp with dose >1.5g, prolonged QRS

Lithium poisoning
- Ix: RFT, serial Lithium level (Q4hr), AXR
- GI decontamination: GL, WBI
- Volume replacement and correction of hyponatraemia
- Haemodialysis if↑level esp. >4mEq/L, sig DO +/- neuro-toxicity

Valproic acid poisoning

- Ix: LFT, valproic acid level, ammonia
- ABC monitoring and supportive measures.
- GI decontamination: AC , GL / MDAC / WBI
- L-Carnitine for VPA induced↑ammonemia, encephalopathy ,hepatotoxicity.

General Internal
Medicine
- IV Naloxone (0.4mg-2mg) for CNS and respiratory depression
- Haemodialysis / Haemoperfusion: rarely considered

Carbamazepine poisoning
- Ix: Carbamazepine level, ECG (widen QRS)
- ABC monitoring and supportive measures.
- GI decontamination: AC / MDAC
- NaHCO3 for widen QRS>100ms (theoretically beneficial)
- Haemoperfusion
 GM 10
Non-Pharmaceutical
Organophosphate poisoning
- Decontamination and staff protection, supportive care
- Ix: plasma cholinesterase, ABG
- Atropine - Initial dose of 0.6-1.2 mg IV, repeat and double the dose
every 5 min until lungs clear (huge dose may be used)
- Pralidoxime - 1-2 g to 100ml NS IV over 30 min, follow by infusion
at 8-10 mg/kg/hr, can be titrated up to 20 mg/kg/hr.

Carbamate poisoning
- Similar to organophosphate poisoning
- Atropine - 0.6-1.2 mg IV, repeat and double the dose Q5min until
lungs clear.
- Pralidoxime – not usually recommended

Paraquat poisoning
- More than 10ml 20% paraquat ingestion is potentially fatal
- GI decontamination: GL in early presentation, AC
- Largely supportive treatment, use lowest FiO2 as possible
- Contact HKPIC for option of anti-inflammation therapy in severe
paraquat poisoning.
General Internal
Medicine

Household products
- Disinfectants and multi-purpose cleaners ( Dettol®, Salvon®,
Swipe® , Green water, Household hypochlorite bleach, etc )
- No antidote, mainstay of treatment is supportive
- GI decontamination is potential harmful
- Mainly irritant effect, upper endoscopy is not routinely indicated
- Can be caustic if large quantity & high concentration are ingested
- Need OGD if caustic ingestion (drain opener)

Methanol / Ethylene glycol [EG] poisoning

Ix: Blood: CBP, LRFT, ethanol level, anion gap, osmolar gap,
methanol or ethylene glycol level
Urine for Ca oxalate and fluorescence [in EG poisoning]
 GM 11
Management:
- Consider NG suction, IV NaHCO3 to correct acidosis
- IV ethanol (16g/20ml), diluted to 10% solution
 Loading: 0.8g/kg in 30min
 Maintenance: start at 0.1g/kg/hr, titrate upwards prn
- IV folinic acid 1mg/kg q4-6hr (for methanol poisoning)
- Thiamine 100mg and pyridoxine 50mg q4-6hr (for Ethylene glycol)
- Fomepizole is available as Level III antidote.
[Contact HKPIC for its indication and mobilization if needed]

- HD indication:
 Methanol or ethylene glycol level >250mg/L
 High osmolar gap without other cause
 Acid/base abnormality, End-organ toxicity

General Internal
Medicine
 GM 12
Cyanide poisoning

- ABC monitoring and supportive measures.

- Surface decontamination and staff protection
- Treat seizure and correct metabolic acidosis
- GI decontamination: consider AC +/- GL if within 1 hr
- Ix : RFT, ABG, lactate, AV O2 gradient (PaO2 – PvO2),
CO-Hb, met-Hb, Cyanide level
- Early use of antidotes
General Internal
Medicine

Urgent use of antidote:

- Hydroxocobalamin: 5g IV in 15-30 min (can be repeated at 2-4 hr)
- Sodium nitrite - 10ml of 3% (300mg) IV over 5 min
(Adverse effects: hypotension, methaemoglobinemia)
- Sodium thiosulphate- 50ml of 25% (12.5g) IV
(Thiosulphate can be repeated if there is no response in 30 min)
 GM 13
Carbon monoxide poisoning
- Pulse oximeter cannot detect CO-Hb; can be misleading
- Hyperbaric oxygen treatment (HBO)
 Usefulness remains controversial
 Potential risk for patient and medical staffs (during transfer / in the chamber)
 No definite evidence to support routine use
 Referral is a case to case individual decision by the in-charge physician

Suggested guideline for CO poisoning

Acute CO exposure with symptoms

100% O2, CO-Hb level, ABG, ECG

Syncope, coma, seizure, cardiac ischaemia or vent. arrhythmias

No Yes

Yes
CO-Hb > 25% Consider ICU care
Pregnancy with CO-Hb > 15% Monitor acidosis
No

Continue 100% O2 therapy Consider HBO*

Yes

General Internal
Medicine
Symptomatic (headache,nausea), abnormal mental or neuropsychiatric status

No

Discharge when CO-Hb < 10%

 GM 14
Pulmonary irritant inhalation
- Highly water solubility: SO2, Ammonia, HCl, and Chloramine
(Cause upper airway, eye and nose irritation, rapid onset)
- Intermediate water solubility: Chlorine
(Delayed irritation, potential prolonged exposure, acute lung injury)
- Low water solubility: Phosgene, Nitrogen dioxide
(Non-irritating, affect lower airway, lack of noticeable effects  prolonged exposure
and acute lung injury)

Clinical effects ranging from:

Stridor, bronchospasm  lung injury, bronchiolitis obliterans
High water solubility irritant  Low water solubility irritant

Monitoring / Ix
- Vital sign / SaO2 / PFR / FEV1/ FVC / voice quality
- ABG, ECG, CXR, Lung function test, fibreoptic bronchoscopy

Treatment
- Remove from exposure, ABC monitoring, O2 and supportive care
- Nebulized β-agonists for bronchospasm
- No role for steroids, other than for bronchospasm
- Nebulized bicarbonate for Cl2, HCl or other acidic gas
General Internal

[2ml NaHCO3 8.4% + 2ml water/saline]

Medicine

Observation
- SO2, NH3, NH2Cl, HCl exposure have no delayed toxicity.
(Improving patients will continue to do well; only need to be observed
for the duration of their symptoms)
- Cl2, COCl2, NO2; Low and intermediate water solubility agents
(Potential for acute lung injury with delayed onset of symptom.
Observe all patients with any symptoms for at least 24 hour
Aware of risk of bronchiolitis obliterans)
 GM 15

Smoke inhalation management flow-chart

Unconsciousness, stridor, resp distress, PaO2<8kPa

No Yes

History of unconsciousness Intubation

Close space exposure Use adequate-sized ET tube
Carbonaceous sputum Humidified O2
Facial burn or singed nasal hair Frequent suction
Hoarseness
Oropharyngeal burn, swelling
Upper airway edema

Yes

No
Nasopharynoscopy / Bronchoscopy

No clinically important edema

Close monitoring Worsen airway / pulmonary status

General Internal
Medicine
 GM 16
Snake Bite

Local venomous Snake Toxicity

Viper蝮蛇
Bamboo Snake 青竹蛇 Local pain swelling +/- bruising,
Chinese Habu 烙鐵頭 Systemic coagulopathy, DIC
Mountain Pit Viper 山烙鐵頭 Hypotension
Elapidae眼鏡蛇
Banded Krait 金腳帶
Paralysis, minimal local reaction
Many Banded Krait 銀腳帶
Chinese Cobra 飯鏟頭 Early local necrosis
(severe pain and swelling)
King Cobra 過山烏 Rhabdomyolysis, Paralysis
Coral snake 珊瑚蛇 Neurotoxicity with paralysis
Colubridae游蛇
Prolonged bite required for effective
Red-necked Keel Back snake 紅脖游蛇
envenomation to cause DIC
Hydrophiidae海蛇
Mangrove Water snake 黑斑水蛇
Neurotoxic, myotoxic with
Chinese Water snake中國水蛇
rhabdomyolysis
General Internal

Plumbeous Water snake 鉛色水蛇

Medicine

Investigation
- CBP, APTT, PT (esp. whole blood clotting time), RFT, CPK
- Urine for myoglobin and haemoglobinuria
- ECG, Bed side spirometry for FVC if available, serial PFR, CXR
Investigations should be repeated in the following situations
- Progression of local or systemic symptoms.
- Abn result from initial test until normal or other cause identified
- After anti-venom administration
- Snake identification is useful (Photographing at safe distance)
[head, tail, dorsal, ventral feature important for identification]
(Consult HKPIC for urgent contact with biologist for snake
identification and advice on anti-venom use)
 GM 17
Treatment
- Supportive care, analgesic, Tetanus prophylaxis
- Q1/2 hour assessment for local / systemic S/S for first few hours
- Antivenoms should be considered for
 Local progression, necrosis, compartment syndrome.
 Systemic toxicities, i.e. coagulopathies, weakness,
rhabdomyolysis, hypotension etc.
 First S/S of neurotoxicity after krait bite
Starting
Antivenoms available in HA Snake bite in HK
Dose
Green Pit Viper (Thailand) 3 vials Bamboo snake 青竹蛇
Agkistrodon halys (China) 1-2 vials Bamboo snake 青竹蛇
抗蝮蛇毒血清 6000U/vial Chinese Habu 烙鐵頭
Mountain Pit Viper 山烙鐵頭
Antivenin of B. multicinctus and N. atra 1 vial Chinese Cobra飯鏟頭
(Taiwan) Many Banded Krait銀腳帶
1000U/vial
Naja Naja (China) 2 vials Chinese Cobra飯鏟頭
抗眼鏡蛇毒血清 1000U/vial
Cobra (Thailand) 10 vials Cobra飯鏟頭
Bungarus multicinctus (China) 1 vial Many Banded Krait銀腳帶
抗銀環蛇毒血清 10000U/vial King Cobra過山烏

General Internal
Banded krait (Thailand) 5 vials Banded Krait金腳帶

Medicine
King cobra (Thailand) 5 vials King Cobra過山烏
Agkistrodon acutus (China) 4 vials Hundred Pacer 百步蛇
抗五步蛇毒血清 2000U/vial
Russel’s Viper (Thailand) 3 vials Russell’s viper 鎖鍊蛇
Australian Tiger Snake (Australia) 1 vial Probably for sea snakes

Precautions and pre-treatment in anti-venom administration

- Resuscitation equipment stand-by
- Pre-treatment with anti-histamine and hydrocortisone is advised
- 1st dose to 500 ml NS, give at 100ml/hr.
- If no allergy after 5-10min., fasten rate, dose finish in 30 min.
- May need further doses if clinically indicated
- No evidence to support routine prophylactic antibiotic use
- Debridement and surgery for compartment syndrome as indicated
 GM 18

ACCIDENTAL HYPOTHERMIA
(Use low temp thermometer for core temp)
Avoid rough handling of geriatric hypothermia patient as this may provoke
cardiac arrhythmia.

Ix - CBP, RFT, blood glucose, h’stix, ABG, amylase, cardiac enzymes,

coagulation profile, TSH, blood culture (esp in elderly), CXR, ECG,
toxicology screen and SXR in comatose patient
General Internal
Medicine
 GM 19

HEAT STROKE / EXHAUSTION

HEAT STROKE is caused by over-heating of the body core when
sweating is limited.
HEAT EXHAUSTION is caused by sustained heat stress that causes
water and salt depletion (may be complicated by heat stroke in
advanced stage).
Heat Stroke Heat Exhaustion
Risk Factors: Drugs or diseases causing
limited sweating esp in
elderly, infants
Skin: Hot and dry in Warm and wet.
non-exertional heat stroke.
Sweating can occur in
exertional heat stroke.
Core body temp: 40 – 41 ºC 38 – 39 ºC
Central nervous Significant Insignificant
system features:

General Internal
Acid-base disorder: Respiratory alkalosis

Medicine
Lactic acidosis
Acute renal injury Common Pre-renal failure

Management
1. Check CBP, RLFT, ABG, coagulation profile, CPK, urine
myoglobin
2. Monitor vital signs (esp urine output) and core temp
3. Cooling of body by removing all clothing, tepid water sponging,
fanning
4. Oral fluid and salt replacement in heat exhaustion (25 g NaCl in 5
litres of water)
5. Correction of electrolyte disturbances and hypovolaemia
 GM 20
6. Lactic acidosis not responding to volume expansion should be
treated with bicarbonate
7. Convulsion should be treated with anticonvulsive therapy
8. Look out and support multiorgan failure in heat stroke

Remark:
1. Avoid alpha-adrenergic agonist (as vasoconstriction will impair
cooling).
2. In Exertional Heat Stroke: paracetamol or NSAID can
exacerbate acute kidney injury or liver derangement.
General Internal
Medicine
 GM 21

NEAR DROWNING
The most important consequence of near-drowning is asphyxia which
leads to hypoxaemia, hypercapnia and metabolic acidosis.

1. Monitor and maintain ABC. Clear airway and CPR if necessary.

Look for cardiac arrhythmia.
2. Ix: ABG, RFT, ECG, CXR, SXR and X ray cervical spine, cardiac
monitoring and body temperature monitoring. Maintain euglycaemia.
3. Beware of head and cervical spine injury and hypothermia.
4. Correct hypoxia and metabolic acidosis. Give O2 therapy (PEEP
may be necessary for severe hypoxia). Treat bronchospasm with
2-agonist. Bronchoscopy may be necessary if persistent atelectasis
or localized wheezing.
5. Treat seizure with anticonvulsant. Watch out for cerebral oedema.
6. Consider antibiotics for pneumonia.
7. Rule out drug effects e.g. alcohol, hypnotics, narcotics.

ELECTRICAL INJURY
Electrical injuries cause cardiopulmonary arrest, burn, acute renal

General Internal
failure due to hypovolaemia or myoglobinaemia, injuries to nervous

Medicine
system, damages to vessels causing thrombosis or haemorrhage.
Extent of external injury may not correlate with severity of internal
injury. Alternate current (AC) is more dangerous than direct current
(DC). Current with frequency of 50-60 cycles/sec is more dangerous.

- Ix : ECG, ABG, RFT, CPK, LDH, urine myoglobin

- Monitor: Vital signs, cardiac rhythm, neurological status, urine output
and colour
- Look for fracture, spinal injury and internal organs damage
- CPR if necessary
- Antiarrhythmic drugs depend on nature of arrhythmia
- IV fluid replacement
- Treat burn and compartment syndrome as appropriate
 GM 22

RHABDOMYOLYSIS
Dx:
Red or brown urine +ve for blood but no RBC under microscopy
Urine +ve for myoglobin
Pigmented granular casts in the urine
 CK level
Others: hyperkalaemia, hypocalcaemia, hyperphosphataemia,
hyperuricaemia, DIC, Acute Kidney Injury.

Mx:
Aim: correction of hypovolaemia, enhance clearance of heme proteins,
mitigate the adverse consequences of heme proteins on the
proximal tubular epithelium
 NS infusion 1-1.5 L/hr
 Monitor urine output & haemodynamic parameters
 Continue IV infusion with 500ml NS alternating with D5 1 L/hr after
satisfactory BP and urine output achieved
 Keep urine output at 300ml/hr until myoglobinuria ceased
 Add NaHCO3 50meq/L to each 2nd or 3rd bottle of D5 to keep
General Internal

urinary pH > 6.5. Monitor arterial pH and serum calcium every 2

Medicine

hours. Stop NaHCO3 if arterial pH > 7.5, or serum HCO3 >

30meq/L, or symptomatic hypocalcaemia.
 Add 20% mannitol at a rate of 1-2g/kg BW over 4 hr with plasma
osmolar gap kept below 55 mosm/kg
 Withhold mannitol and HCO3 if marked diuresis not achieved.
 May try furosemide & renal dose dopamine for anuric patients
 Extracorporeal elimination of heme protein is controversial
 Look out and treat significant compartment syndrome
NB:
 Regimen is less effective if began after the first 6 hrs when renal
failure may have already established.
 Elderly patient may require slower volume replacement.
 Look out for hypercalcaemia in recovering phase of AKI.
 GM 23

SUPERIOR VENA CAVA SYNDROME

Causes: ≥ 80% due to malignancy
*Non-malignancy aetiologies: e.g. central venous catheter;
pacemaker wire, indwelling cardiac device; infection (e.g. TB, fungal);
aortic aneurysm; post-irradiation.

P/E: Dilated superficial veins over anterior chest wall

Engorged jugular veins  facial and arm veins
Oedema of face, neck, and upper extremities with cyanosis

DDx: Pericardial effusion with tamponade

Ix: CXR, Duplex ultrasonography, CT, digital subtraction venography,

bronchoscopy
Look for secondary pulmonary embolism.

Tx Look out for upper airway obstruction (stridor) - may be

life-threatening
Malignant SVC syndrome - see pages GM24-25
Central venous catheter - removal under anticoagulation 

General Internal
Medicine
regional fibrinolytic therapy
SVC stenting – consult interventional radiologist for feasibility
 GM 24

Medical Oncology
MALIGNANCY-RELATED SUPERIOR VENA CAVA
SYNDROME
(cross-reference from SVC SYNDROME)
Malignancy accounts for 80% of SVC syndrome
Non-small cell lung carcinoma (50%)
Small cell lung carcinoma (25%)
Non-Hodgkin lymphoma (10%)
Others e.g. germ cell neoplasms, breast carcinoma, thymoma etc

Treatment is tailored to the specific neoplasm, therefore tissue diagnosis

is essential prior to empirical treatment, which could jeopardize
histological evaluation, e.g. corticosteroid in lymphoma.

Ix
For immediately life-threatening situations e.g. upper airway
obstruction due to tumour compression or severe laryngeal edema,
impaired conscious state due to cerebral edema
Stabilize airway, breathing, circulation
General Internal

Urgent Oncology consultation for immediate treatment

Medicine

Urgent endovascular stenting can provide the most rapid relief

without affecting subsequent tissue diagnosis. Total SVC occlusion
and SVC thrombus are not absolute contraindications for stenting.
Post stenting short-term anti-thrombotic therapy recommended e.g.
dual antiplatelets for 3 months.
For stable /stabilized patients
Clinical examination and investigations targeted to establish tissue
diagnosis by minimally invasive methods.
Sputum cytology, serum AFP, βHCG levels, LN biopsy, pleural fluid
cytology/pleural biopsy, bone marrow biopsy, endoscopic biopsy,
image-guided biopsy. For suspected lymphoma, excisional biopsy of
enlarged lymph node is essential.
Watch out for coexisting pericardial effusion/cardiac tamponade.
 GM 25
Tx
Empirical
Prop up for head elevation
Oxygen supplement
Dexamethasone 4mg q6h iv
Disease-specific (Consult Oncology)
Chemotherapy
Radiotherapy.
Targeted therapy

Presence of SVC thrombus

Long term anticoagulation, if not contraindicated, for 6 months AND
preferably continued beyond 6 months in those with active cancer or
receiving chemotherapy (ASCO guideline 2013 update). LMWH is
preferred over warfarin in malignancy-related thrombosis (and CrCl >
30 ml/min) for its lower rate of recurrent thromboembolism and less
drug interaction with subsequent systemic cancer therapy. Both have
similar bleeding risks.

General Internal
Medicine
 GM 26

NEOPLASTIC SPINAL CORD/CAUDA EQUINA

COMPRESSION
(Also see page N19 and PM15)
Etiologies
Prostate cancer (20%)
Breast cancer (20%)
Lung cancer (20%)
Others : non-Hodgkin lymphoma, multiple myeloma/plasmacytoma,
renal cell carcinoma etc

Prompt diagnosis and immediate treatment important in maximizing

neurological outcome

Ix
Diagnosis confirmed with MRI of entire thecal sac since multiple level
involvement present in 33% of patients (CT myelography if
contraindicated for MRI)
For patients without known malignancy, actively search for potential
primary. Tissue diagnosis is essential for subsequent management.
General Internal
Medicine

Tx
General
dexamethasone 4mg q6h iv
adequate pain control
bowel care
bladder catheterization for retention of urine
compression stockings
Specific (Consult Oncology)
RT for most metastatic cancers
Chemotherapy for chemosensitive tumours
Hormonal therapy for selected cases
Surgery for suspected malignancy without tissue diagnosis and no
alternative site for biopsy, presence of spinal instability or
radiotherapy/chemotherapy-resistant tumours.
 GM 27

HYPERCALCAEMIA OF MALIGNANCY
Aetiologies (in decreasing order of frequency)
Humoral hypercalcaemia of malignancy (PTHrP) e.g. squamous
cell/renal cell/transitional cell carcinomas, breast/ovarian cancers etc
Osteolysis from bone metastases
Calcitriol-secreting lymphoma
Ectopic PTH secretion

**Initial approach to and control of hypercalcaemia covered in

Electrolye Disturbances section on page K6 and PM14)

Oncology specific aspects:

Ensure adequate pain control
Workup for the cause of hypercalcaemia e.g. previously undiagnosed
malignancy, new development of bone metastasis, recurrence of cancer
etc
Consult Oncology for disease control of the underlying cancer
Systemic corticosteroid can be helpful for calcitriol-secreting lymphoma
in some circumstances, but to be avoided if the specific tissue diagnosis
has not been made yet, please discuss with oncologist first.

General Internal
Medicine
 GM 28

TUMOUR LYSIS SYNDROME

TLS can occur after cytotoxic therapy or spontaneously in high-grade
malignancy or high tumour burden, most commonly lymphoblastic
leukaemia/high-grade lymphomas especially Burkitt’s.

Ix/monitoring
Fluid input/output, ECG/cardiac monitoring, serum potassium, calcium,
phosphate, urate, creatinine, LDH, G6PD level

Diagnosis
Laboratory TLS – At least 2 of the following abnormal serum
biochemistries occurring within 3 days before/7 days after beginning
chemotherapy despite adequate prophylaxis :
potassium ≥6mmol/L or 25% increase from baseline
urate ≥ 0.5mmol/L or 25% increase from baseline
phosphate ≥1.45mmol/L or 25% increase from baseline
calcium ≤1.75mmol/L or 25% decrease from baseline
Clinical TLS – laboratory TLS AND any of the following :
increased serum creatinine to ≥1.5 times ULN
seizure
cardiac arrhythmia
General Internal
Medicine

sudden death

Prophylaxis
Adequate hydration 3-4L/day, aim for urine output ~150ml/hr, +/- diuretics
Hypouricaemic agents : allopurinol adjusted for renal function, (or
rasburicase if the patient is of high risk of TLS, please note rasburicase is
contraindicated in patients with G6PD deficiency)

Tx
Correct electrolytes disturbances (see Electrolyte Disturbances section)
Maintain I/O balance
Monitor and treat arrhythmias
For persistent hyperkalaemia, hyperphosphataemia, hyperuricaemia,
hypocalcaemia or oliguria, Nephrology consultation with a consideration of
dialysis support.
 GM 29

EXTRAVASATION OF
CHEMOTHERAPEUTIC AGENTS
Definition: escape of an irritant (causing tissue inflammation) or vesicant
(causing tissue necrosis) drug into the extravascular space.
Commonly used vesicants :
Anthracyclines e.g. doxorubicin, epirubicin, daunorubicin, idarubicin
Vinca alkaloids e.g. vinblastine, vincristine, vinorelbine

Prevention of extravasation is the best strategy against extravasation injury

Proper infusion technique is of paramount importance
Consider the use of central venous catheter for vesicant infusion
For peripheral infusion of chemotherapy, use a newly set IV line in a large
peripheral vein with close monitoring of any evidence of extravasation.

When extravasation is suspected

Stop the infusion immediately
Leave the catheter in place
Aspirate fluid from the extravasation area
DO NOT flush the line or apply local pressure.
Administer antidote if applicable before removal of catheter.

General Internal
Access the extravasation kit for specific antidote

Medicine
Anthracyclines topical DMSO, consider IV
dexrazoxane if available
Mitomycin topical DMSO
Mechlorethamine, (bendamustine, SC sodium thiosulphate
dacarbazine, cisplatin, carboplatin)*
Vinca alkaloids, (etoposide, taxane)* SC hyaluronidase
*(specific antidote recommendation is less consistent for drugs in bracket)
Elevate the extremity with extravasation.
Apply heat locally for vinca alkaloids and epipodophyllotoxins (e.g.
etoposide); apply cold locally for other agents.

Take clinical photos of the extravasation injury.

Document the extravasation process and measures taken.
Monitor the healing process, full-thickness skin or surrounding tissue
necrosis may necessitate surgical intervention.
GM 30

BRAIN DEATH
(Please refer to a revised set of Guidelines on Diagnosis of Brain Death
issued on 15 November 2017 with link provided below.
http://ha.home/circular2/Ops-2017-32.pdf)

(Based on HA Guidelines on Diagnosis of Brain Death, 4 October 2010,

ref: HA752/10/1/3)
Use updated Brain Death Certification Form HA0090/MR.
- For patients who are 5 yrs of age or older
Concept: Brain death equates with death both medically and legally.
1. Pre-conditions and exclusions for considering diagnosis of brain
death
* All the following should coexist
a) Diagnosis of severe irremediable brain injury which is consistent
with progression to brain death (the clinical diagnosis is usually
confirmed by neuro-imaging). The diagnosis of a disorder
which can lead to brainstem death should have been fully
established.
b) Apnoeic patient on a ventilator
- Muscle relaxants and other drugs should have been excluded
as a cause of such findings
c) Exclusion of potentially reversible causes of coma
- Depressant drugs or poisons; peripheral nerve stimulator to
confirm intact neuromuscular conduction.
- Primary hypothermia: core temp >35C before diagnostic
tests of brain stem death are carried out
- Metabolic and endocrine disturbances (e.g. severe electrolyte
or endocrine disturbances)
- Arterial hypotension as the cause for the coma should be
excluded.

2. Tests for confirming brain death

* All brainstem reflexes must be absent.
* The testing of all the following is considered sufficient
a) Both pupils - fixed in diameter and non-reactive to light
b) Absence of bilateral corneal reflexes
 GM 31

c) Absence of vestibulo-ocular reflexes - no eye movement occurs

during or after the slow injection of at least 20 ml ice-cold water
into at least one external auditory meatus, or preferably into each
external auditory meatus in turn. Clear access to the tympanic
membrane should be established by direct inspection. This test
may be contraindicated on one or other side by local trauma
d) No motor responses within the trigeminal nerve distribution can
be elicited by adequate pain stimulation of any somatic area
e) Absence of gag reflex
f) Absence of cough reflex
g) Testing for apnoea: should be done last. No respiratory
movements occur when the patient is disconnected from the
mechanical ventilator for long enough to ensure that the PaCO2
rises above the threshold for stimulating respiration (ie PaCO2 >
8.0 kPa and arterial pH < 7.30). ABG must be available for this
test to be performed. The patient should be disconnected from
mechanical ventilator when PaCO2 is close to normal.
Hypoxaemia during disconnection should be prevented by

General Internal
preoxygenation and administration of oxygen during the test, e.g.

Medicine
by delivering O2 through a catheter into the trachea
* Period of observation and repetition of tests: 2 full separate
examinations should be performed. The first examination should be
performed after all pre-conditions met, and after at least 4 hrs of
observation of coma (Glasgow Coma Scale of 3) with absent
brain-stem function. The second examination can be performed any
time after the first examination, so that total period of observation is at
least 4 hours. The minimum period of observation need to be totally
24 hours after cardiorespiratory arrest.
* Medical practitioners:
- One of the doctors must be a specialist recognised by the appropriate
College as having demonstrated skill and knowledge in the
 GM 32

certification of death following irreversible cessation of brainstem

function (usually an Intensivist, Critical Care Physician, Neurologist
or Neurosurgeon).
- The other doctor should preferably be of the same qualification but
should be at least 6 years after registration and possess the skill and
knowledge in the certification of death following irreversible cessation
of brainstem function
- The person authorizing removal of tissues and the person removing
tissues MUST NOT be responsible for determining brainstem death.
* Confirmatory Ix
If the preconditions for clinical diagnosis and confirmation of
brainstem death cannot be satisfied, objective demonstration of
absence of intracranial blood flow is required (after the 4 hour period
of observation of coma and of absent brainstem responses, where
these can be tested).
* Time of death - the time when certification of brain death has been
completed (ie following the second confirmatory examination) or if a
confirmatory investigation is used, then the time of death should be
after the confirmatory investigation.
* Clinical observations compatible with diagnosis of brain death
- movements of limbs in response to a stimulus outside the
General Internal
Medicine

distribution of cranial nerves

- sweating, blushing, tachycardia
- normal BP without pharmacologic support
- absence of diabetes insipidus
- deep tendon reflexes
- extensor plantar reflex
* Features NOT COMPATIBLE with brainstem death:
- decerebrate or decorticate posturing.
- seizure.
 Procedures

For all procedures,

INFORMED CONSENT
Must be obtained except
in an emergency life-saving
situation Procedures

Always mark the correct side

before procedure
 Pr 1

ENDOTRACHEAL INTUBATION
Indications
1. Respiratory / ventilation failure, including CPR
2. To protect airway against aspiration
3. To manage excessive airway secretions
Equipment
1. Bag-Mask-Valve device (BMV)
2. IV access* as far as possible
3. Cardiac monitor & pulse oximeter
4. Oropharyngeal / nasopharyngeal airways
5. Direct laryngoscope (Macintoch) with functioning light bulb and
blade of appropriate size (start with size 3, usually size 3-4 for
adults)
6. Endotracheal tube (Male 8-8.5 mm, female 7-8 mm internal
diameter) with low pressure cuff
 with syringe for cuff inflation, check cuff for leakage
(Inflate with 10 ml syringe, then deflate completely)
 If stylet used, lubricate and insert into ETT. Its tip must be
recessed > 1 cm from distal end of tube
7. End-tidal CO2 monitor if available
8. Yankauer sucker
9. Bougie if indicated
10. A spare endotracheal tube with size 0.5 – 1mm smaller
Note

Procedures
1. Consult anaesthetists in expectedly difficult case
2. In patients with suspected unstable cervical spine, leave intubation
to expert hands if possible, otherwise, do in-line stabilization during
intubation
3. Do not attempt intubation for >15 sec at a time. Achieve adequate
oxygenation before the next attempt
 Pr 2
Procedure
1. Position patient supine
2. Place patient in sniffing position (neck flexed and head extended),
Open airway by head tilt-chin lift / jaw thrust
3. Remove dentures and other foreign bodies
4. Fit a face mask tightly on patient’s nose and mouth and ventilate
using a BMV connected to O2 (bag should be inflated with O2)
5. Pre-oxygenate for 5 minutes
6. (Optional) Apply cricoid pressure (Sellick’s manoeuvre)
7. Perform Rapid Sequence Induction (RSI)
 Give a short acting sedative (e.g. midazolam or propofol)
 followed immediately by a paralytic agent such as
suxamethonium or rocuronium
8. Insert direct laryngoscope: Push tongue to the left, expose larynx by
pulling jaw towards ceiling (Do not lever laryngoscope at the teeth)
9. Gently slide ETT in between cords and immediately remove stylet.
Advance ETT till marking at incisor is 22-24 cm for males, 20-22
cm for females (Or visualizing the thick black line in ETT entering
vocal cord)
10. For more difficult case, consult anesthetist / senior. In selected case,
may consider the use of bougie or McCoy blade for assistance:
insert bougie as a guidewire, then thread ETT through afterwards
11. Inflate cuff (4-6 mls air to achieve cuff pressure 20 - 24 cm H2O)
12. Connect ETT to BMV
13. Confirm ETT position by end-tidal CO2 device if available. Observe
lung expansion, auscultation (bilateral chest and epigastrium (for
the absence of gurgling sound)).
Procedures

14. Off cricoid pressure AFTER endotracheal intubation is confirmed if

using Sellick’s manoeuvre
** In case of failed intubation, maintain mask ventilation and summon
help. DO NOT inject second dose of muscle relaxant for another
attempt.

After-care
Urgent CXR to check ETT position (ETT tip 4 ± 2cm from carina,
exclude pneumothorax/pneumomediastinum)
 Pr 3

SETTING CVP LINE

Indications
1. Haemodynamic monitor
2. Administration of TPN, vasopressors
Contraindications
1. Bleeding tendency
2. Ipsilateral carotid artery aneurysm
Internal Jugular Vein (IJV) Puncture
- Aseptic technique, use Gauge 14 or 16 angiocatheter
- Preferably US-guided
- IJV runs behind the sternocleidomastoid (SCM) close to the lateral
border of the carotid artery
- Place patient in a 20° head-down position with the head turned to the
opposite side
- Right side preferred to avoid injury to the thoracic duct
(1) Anterior approach: Insert angiocath 0.5cm – 1cm lateral to carotid
pulse at midpoint of the sternal head of SCM.
(2) Central approach: Insert angiocath at apex of triangle formed by
two muscle bellies of SCM and clavicle.
- Advance angiocath towards ipsilateral nipple with the syringe at
30-45° above the skin. Maintain gentle aspiration till a gush of blood
(dark red) is aspirated
- Gently withdraw stylet of angiocath while pushing angiocath into
position, connect infusion set to angiocatheter

Procedures
- If the artery is punctured (bright red blood), withdraw everything and
apply firm pressure for at least 5 minutes
- (Never advance beyond clavicle. Pneumothorax can kill)
 Always make sure that the catheter is in vascular space
(Check siphoning: Venous blood backflows upon lowering
infusion set below the patient &blood level should oscillate with
respiration)
 Read the first CVP reading yourself
 Always take a CXR afterwards to exclude pneumothorax
 Maintain catheter patency with infusion of fluid
 Pr 4

DEFIBRILLATION
The speed with which defibrillation performed is the major determinant
of the resuscitation success. Rapid diagnosis of VF and pulseless VT
followed by immediate defibrillation is important.

1. CPR before defibrillator available.

2. Attach and turn on defibrillator when available.
3. Check rhythm and identify shockable rhythm (VF and pulseless VT).
4. Apply appropriate conductive material to hand-held paddles or use
defibrillator electrode pads. Do not rub the 2 paddles together.
5. Select energy level
Monophasic defibrillator – 360J
Biphasic defibrillator – device specific; if waveform type unknown,
use 200J
(150J to 200J for biphasic truncated exponential waveform or 120J
for rectilinear biphasic waveform).
6. Press charge button on machine or paddle.
7. Apply firm pressure with one paddle at cardiac apex, the other over
base of heart (if paddles are used)*
8. Warn everybody to stay clear of the patient.
9. Deliver the shock by pressing both discharge buttons simultaneously.
10. Resume CPR immediately after the shock and give 5 cycles of CPR
(one cycle of CPR: 30 compressions then 2 breaths). Then check
rhythm.
Procedures

* For patient with permanent pacemaker, anterior-posterior orientation is

preferred or with paddles > 10cm from pacemaker. Interrogate pacemaker
after defibrillation to ensure normal functions.
 Pr 5

TEMPORARY PACING
1. Equipment: Venous puncture set, temporary pacing wire and
pacemaker, cardiac monitor, defibrillator/transcutaneous pacing
standby.
2. Select venous access (femoral, internal jugular or subclavian).
3. Give local anaesthesia and perform venipuncture under aseptic
technique.
4. Manipulate pacing wire to RV apex  fluoroscopic guidance.
5. Connect pacing wire to temporary pacemaker.
6. Test pacing threshold with a pacing rate above the patient’s own rate.
Accept site if threshold <1 volt. Set output at >3x threshold or 3V
whichever is higher.
7. Test for sensing threshold with pacing rate less than patient’s own
rate if clinically feasible. Set sensitivity to 1/2 of sensing threshold
(i.e. more sensitive than the sensing threshold).
8. Set desirable pacing rate, eg. 70-80/min.
9. Secure pacing wire at insertion site and cover with dressing.
10. Record the rhythm.

Aftercare
 Full lead ECG and portable CXR.
 Continue cardiac monitoring.
 Check pacing threshold daily and adjust output accordingly.
 Watch out for complications (infection, bleeding, haematoma,
pneumothorax, thrombophlebitis, etc).

Procedures
Transcutaneous Pacing (TCP)
 As interim measure before transvenous pacing.
 Anterior TCP patch at cardiac apex and posterior patch over left
infrascapular region. Turn the pacer ON  consider analgesia.
 Set the rate to ~60/min (adjusted to clinical condition). Set the
current output 2mA above the level with consistent mechanical
capture (safety margin). (Do not assess carotid pulse to confirm
mechanical capture as muscular jerking may mimic carotid pulse.)
 Pr 6

LUMBAR PUNCTURE
Indications
1. To check intracranial pressure (ICP) and obtain cerebrospinal fluid
(CSF) for diagnosing a wide variety of neurological and
neurosurgical conditions
2. To drain CSF
3. To give intrathecal injection

Precautions
Always examine the patient for evidence of raised intracranial
pressure and focal cerebral lesion before performing LP
(papilloedema, false localising signs)
1. LP may be performed in some exceptional circumstances if such
evidence is present. Always consult the Neurology Team
(Medicine) or Neurosurgery Department before making a decision
under such circumstances.
2. In case of doubt, a CT scan of the brain should be performed first to
exclude contraindications of LP. Perform blood culture and start
antibiotic for bacterial meningitis if such diagnosis is suspected and
CT brain cannot be done shortly.
3. Do not perform LP if there is uncorrectable bleeding tendency or
local infection in the area of needle insertion.

Procedures
Procedures

1. Lie patient in left lateral position with back and knees flexed (may
try sitting position if failure after 2-3 attempts)
2. Aseptic technique
3. Infiltrate skin with local anaesthetic
4. Advance LP needle between spinous processes of L3/4 or L4/5.
Use fine-bore (# 23) needle if raised ICP suspected
5. At about 4-5 cm, a ‘give’ sensation indicates that the needle has
pierced through ligamentum flavum
6. Remove stylet to allow CSF fluid to come out
7. Note the appearance of the CSF and measure CSF pressure
 Pr 7
8. Lie patient flat for 4-6 hours after LP (24 hours if ICP increased)
9. Depending on provisional clinical diagnosis, send CSF fluid for:
- Biochemistry (use fluoride bottle for CSF glucose, check
simultaneous blood glucose)
- Microscopy and cell count, cytology
- Gram stain and culture, CIE for bacterial antigen (patient already
on antibiotics)
- AFB smear and culture ± PCR, VDRL / FTA
- Indian Ink preparation, fungal culture and cryptococcal antigen
- Viral isolation and antibody titre ± PCR
- IgG / albumin ratio and oligoclonal bands (with serum)

Procedures
 Pr 8

BONE MARROW ASPIRATION &

TREPHINE BIOPSY
Bone Marrow (BM) Aspiration & Trephine Biopsy
1. Obtain informed consent
2. Use either a reusable BM Biopsy needle supplied by CSSD or a
disposable one e.g. Jamshidi or ‘J’ style BM Biopsy needle
3. Site: Posterior superior iliac crest (patient in lateral recumbent or
prone position)
4. Clean the skin overlying the posterosuperior iliac crest with aseptic
technique
5. Infiltrate overlying skin and periosteum with local anesthetics.
6. Incise skin with a scalpel (2-3 mm incision)
BM Aspiration
1. Hold needle at right angle to iliac crest
2. Advance needle with firm pressure in a clockwise-
anticlockwise motion till a decrease in resistance is felt
3. Remove the stylet
4. Apply gentle suction with a 10-20 ml syringe, aspirate 0.2 to 2ml
bloody fluid, reinsert the stylet
5. Make marrow smear on clean slides before the specimen clots, and
send marrow clot in a EDTA specimen bottle for section
6. Put additional material in appropriate media for special tests e.g.
cytogenetic study, microbiological culture
BM Trephine Biopsy
Procedures

1. Following the BM aspiration, with the stylet locked in the needle,

push out the needle to the periosteal surface, and advance needle
with firm pressure in a clockwise-anticlockwise motion in a
slightly different angle (not the same track as that of BM aspiration)
till a decrease in resistance is felt
2. Push, rotate and advance the needle till the needle reaches the
trabecular bone
 Pr 9
3. Remove the stylet, advance further for 1-1.5 cm using a circular
rotating motion of the needle along its long axis to include a core
of marrow within the needle. The biopsy specimen should measure
at least 1.6cm.
4. Withdraw needle by 2-3 mm, then with less pressure advance 2-
3 mm in a different direction to break specimen
5. Withdraw needle by rotation with quick full twists
6. Imprints from biopsy specimen can be obtained ( by gently
touching glass slides to specimen ), epseically if no bone marrow
aspirates obtained ( dry tap )
7. Push the specimen from needle by inserting the stylet at the tip and
put the specimen in a formalin bottle

N.B. For patients with hematological malignancies or myelodysplastic

syndrome, arrange with laboratory haematologist beforehand for
cytogenetic, cytochemistry and immunophenotyping studies (if
available)

Procedures
 Pr 10

CARE OF HICKMAN CATHETER

Hickman Catheter Irrigation & Heparin Lock
1. Wash hands thoroughly with anti-microbial soap and water.
2. Put on non-sterile latex gloves.
3. Draw 5 ml of heparin-saline (50unit / 5 ml) into a 10ml syringe and
10 ml Normal Saline in another 10 ml syringe. Eliminate air from
the syringes.
4. Swab end one-inch of catheter and the junction (catheter with
Heparin cap or with IV tubing) with alcohol wipe vigorously with
friction for at least 3 times. Allow the antiseptic to air dry.
5. Ensure that the catheter clamp is closed.
6. Disconnect the heparin block or IV tubing and swab the hub
vigorously with friction for at least 3 times with Alcohol wipe.
Allow the antiseptic to air dry.
7. Perform each catheter irrigation and catheter cap:
Weekly heparin-saline flushing
 Connect an empty 10 ml syringe.
 Release clamp, and aspirate 5 ml of blood (3 times the catheter
volume) to clear the catheter.
 Reclamp catheter. Remove and discard the blood syringe
 Inject 10ml normal saline, then 5ml heparin saline
 Swab the hub with Alcohol wipe and insert a new catheter cap

Clearing of Blocked Hickman Catheter

Procedures

Stage I – If infusion rate is slow:

1. Wash hand thoroughly with soap and water.
2. Put on non-sterile latex gloves.
3. Prepare 10ml Normal Saline in a 10ml syringe.
4. Wipe end one-inch of catheter and the junction (catheter with
Heparin block or with IV tubing) with alcohol wipe vigorously
with friction for at least 3 times. Allow the antiseptic to air dry.
5. Ensure catheter clamp is closed.
 Pr 11
6. Disconnect the heparin block or IV tubing. Swab the hub
vigorously with friction for at least 3 times with alcohol wipe.
Allow the antiseptic to air dry.
7. Verify catheter occlusion by attaching an empty syringe to catheter
and attempt to aspirate. If all clots in the catheter can be aspirated
successfully, follow with catheter irrigation and heparin block or
resume IV infusion.
8. If catheter is still occluded, attempt clearing by using a gentle
alternating irrigation and aspiration (push and pull) with a 20 ml
syringe half filled with normal saline. If this fails, try with
heparinised-saline.
N.B. 1. Do not force fluid as catheter damage may result.
2. If necessary, obtain an X-ray image of catheter to check it is
in-situ
Stage II – If the first procedure has failed or the catheter has been
blocked for over 2 hours:
Repeat procedure in stage I but with 3 ml pure heparin (1000 units/ml)
by Doctor
Stage III – If stage I & II have failed:
A fibrinolytic agent e.g. Urokinase can be used. Please contact
haematologist or haematology nurse

Procedures
 Pr 12

RENAL BIOPSY
Relative contraindications:
1. Active infection e.g. acute pyelonephritis
2. Very small kidneys (<8 cm)
3. Single kidney
4. Uncontrolled hypertension
5. Bleeding tendency

Preparation:
1. Check CBP, platelets, PT, aPTT, bleeding time
2. Type and screen/X-match 1 pint packed cells
3. Trace film / report of USG or IVP
4. USG for localization

Biopsy:
(Preferably done in early morning on a weekday)
1. Platelet count should be >100 x 109 /L, PT, aPTT normal
2. Check baseline BP/P
3. Fresh biopsy specimen put into plain bottle with NS and send for
histology, immunofluorescence  electron microscopy

Post-Biopsy Care:
1. Encourage fluid intake
2. Complete bed rest for 24 hours
Procedures

3. BP/P monitoring at least hourly for 4 hrs (every 15 mins for one
hour), then q4h if stable
4. Save all urine samples for inspection and for RBC
5. Appropriate oral analgesics
6. Inform if gross haematuria, falling BP (SBP<100 mmHg),
increasing pulse rate (>100/min), oozing of blood or severe pain at
biopsy site
 Pr 13

INTERMITTENT PERITONEAL DIALYSIS

I. Tenckhoff catheter in-situ

1. Use automatic peritoneal dialysis machine
- Regular Rx once to twice a week
- Heparinisation (optional): during IPD 100 - 500 units/L
Post-dialysis up to 5,000 units IP
2.
Duration of Medication
PD (per litre
PD Dialysis Drain fluid)
programme
1st 20-80 L 1L/cycle 30 mins 20 mins Heparin
100-500 units
(optional)
Subsequently 2L/cycle 30 mins 20 mins Optional

II. Acute PD catheter insertion for patients without a Tenckhoff

Catheter
1. Empty bladder
2. Prime abdomen with 2 litres 1.5% PD Fluid via a #16
angiocatheter at 2 cm below umbilicus
3. Ensure smooth flow. Watch out for extraperitoneal infusion in

Procedures
obese patients
4. Give local anaesthesia
5. Aseptic technique
6. Insert catheter for acute PD at 2-3 cm below umbilicus in
midline, with catheter tip towards rectovesical pouch
7. Bed cage to protect catheter after insertion
 Pr 14
8. IPD order: Total duration 40 hours
2 litres 1.5%* PD fluid per shift
Add heparin 100-500 units/litre
Add 4 mEq KCl /litre if serum K < 4 mmol/l
Inflow + indwelling 40 mins; outflow 20 mins
(* may adjust % of PD fluid as required e.g. use 4.25% PD
fluid if fluid overload)
(* Use 1 litre exchanges if in respiratory distress)
9. Monitor inflow/outflow, if poor, reposition patient / give
laxatives/ adjust or replace catheter
10. Add soluble insulin (4-6 units/bag for 2L of 2.5% PD fluid) for
diabetics. Monitor h'stix q4-6 hours, aim at sugar 10 mmol/l
Relative contraindications to peritoneal dialysis:
1. Severe bleeding tendency
2. Multiple lower abdominal scar, recent abdominal surgery
3. Suspicion of abdominal pathology
4. Respiratory failure
5. Pleuroperitoneal leak
6. Aortoiliac graft
7. Burns or other hypercatabolic state or life threatening
hyperkalaemia (not efficient enough)
Preparation for Tenckhoff Catheter Insertion
1. Give laxatives the night before T.C. insertion
2. Transfuse if Hb <8 g/dl, or Hct <0.26
Procedures

3. Give dDAVP to correct bleeding tendency

4. Antibiotics prophylaxis (optional) :
Regime 1 :
Ampicillin 500 mg iv + cloxacillin 500 mg iv before insertion, then
Ampicillin 500 mg and Cloxacillin 500 mg qid
Regime 2 :
Vancomycin 1 g in 100 ml NS, infuse over 1 hr
5. Empty urinary bladder before Catheter insertion
 Pr 15

PERCUTANEOUS LIVER BIOPSY

Before liver biopsy, educate the patients about their liver disease and
investigations other than liver biopsy. Carefully inform the patients
about the procedure, risks and benefits, limitations and alternatives (if
any) before obtaining consent

Contraindications

1. PT > 3 secs prolonged; platelet count < 60x 109/L; bleeding time >
10 mins; haematocrit < 25%
(Consider safer approach like USG-guided plugged liver biopsy or
transvenous liver biopsy)
2. Gross ascites
3. Patient unable to hold breath or cooperate
4. Extrahepatic biliary obstruction, cholangitis
5. Vascular tumour, hydatid cyst, subphrenic abscess
6. Amyloidosis
7. Morbid obesity

Procedure
(Biopsy preferably done on a weekday in the morning)

1. If no contraindication, discontinue anti-platelet agents, warfarin or

new oral anticoagulants for adequate period before procedure.

Procedures
Consider bridging therapy with heparin in high thrombotic risk
patients. Risk of stopping antiplatelet agents or anticiagulants
should be weighed against the benefit of liver biopsy. Consult
relevant specialist(s) if indicated. In general, stop warfarin for 5
days prior to liver biopsy. Withold heparin for 12-24 hours.
2. Check CBP, platelet, INR, APTT +/- bleeding time in patients with
renal impairment or chronic liver disease
3. X-match 2 pints whole blood for reserve and consider antibiotic
prophylaxis in selected cases
4. Check BP/P before procedure
 Pr 16
5. Instruct patient on how to hold breath in deep expiration for as long
as he can
6. Palpate the abdomen and percuss for liver dullness in the
mid-axillary line
7. Perform ultrasound for guidance immediately before the liver
biopsy, with marking of the optimal biopsy site. Ultrasound
examination by the individual performing biopsy is preferred
8. Choose rib space with maximum liver dullness (ascertain puncture
site with USG is preferred if available)
9. Aseptic technique, anaesthetise skin, make a small incision
10. Use the Hepafix needle or spring loaded cutting needle. Follow
instructions in the package.
Make sure that the patient is holding his breath in deep
expiration before introducing the biopsy needle into liver.
Avoid lower border of ribs.
11. Send specimen for histology in formalin or formalin-saline
12. One pass is usually enough

Post-biopsy Care

1. BP/P every 15mins for 1 hr, then every 30mins for 1 hr then hourly
for 4 hrs, then q4h if stable
2. Watch out for fall in BP, tachycardia, abdominal pain, right
shoulder pain, pleuritic chest pain or shortness of breath
3. Complete bed rest for 8 hrs; patient may sit up after 4 hrs.
Procedures

4. Simple analgesics prn

5. Diet: full liquid for 6 hrs, then resume regular diet
6. Avoid lifting weights greater then 5 kg in the first 24 hours.
7. Anti-platelet agents may be restarted 48-72 hours after biopsy
8. Warfarin may be restarted the day following biopsy
 Pr 17

ABDOMINAL PARACENTESIS
1. Routine prophylactic use of fresh frozen plasma or platelets before
paracentesis is not recommended because bleeding complications
are infrequent.
* However, abdominal paracentesis should be avoided in patient
with disseminated intravascular coagulation and hyperfibrinolysis
2. Site: left lower quadrant preferred - 2 finger breaths (3cm) cephalad
and 2 finger breaths medial to the anterior superior iliac spine. Right
lower quadrant is suboptimal in the setting of dilated caecum or an
appendectomy but it is preferred in case of gross splenomegaly.
3. Aseptic technique
4. May infiltrate with 1% lignocaine
5. Insert needle (#19 or 21) and aspirate fluid or use commercial
paracentesis set
6. Send for microscopy and C/ST (use blood culture bottle), white cell
count (total and PMN), biochemistry (albumin and protein) for
initial screening. Check serum albumin and calculate SAAG –
serum-ascites albumin gradient
7. Albumin infusion may not be necessary for a single paracentesis of
less than 4-5L. On the other hand, for large volume paracentesis,
consider albumin infusion of 6-8 g/litre after every 5L ascitic fluid
removed

Procedures
 Pr 18

PLEURAL ASPIRATION

 Review latest CXR to confirm diagnosis, location and extent of

effusion. (Pitfall: Be careful NOT to mistake bulla as pneumothorax
or collapsed lung as effusion). Correct side marking is essential
before procedure.
 Patient position: A) 45o Semi-supine with hand behind head. Or B)
Sitting up leaning over a table with padding
 Use ultrasound guidance if available
 Best aspiration site guided by percussion. Aseptic technique.
Puncture lateral chest wall, preferably at safety triangle, along mid-
or posterior axillary line immediately above a rib. (The “triangle
of safety” is bordered anteriorly by the lateral edge of pectoralis
major, laterally by the lateral edge of latissimus dorsi, inferiorly by
the line of the fifth intercostal space and superiorly by the base of
the axilla)
 Anaesthetise all layers of thoracic wall down to pleura
 Connect a fine-bore needle (21G)/angiocath to syringe for simple
diagnostic tap. 3-way tap may be used if repeated aspiration is
expected.
 Avoid large bore needle.
 Throughout procedure, avoid air entry into pleural space. (If 3-way
tap is used, ensure proper sealing of all joints of the tap)
 Withdraw 20-50 ml pleural fluid and send for LDH, protein, cell
count & D/C, cytology (yield improves if larger volume sent),
Procedures

gram stain & C/ST, AFB smear & culture. Check fluid pH & Sugar
(contained in fluoride tube) if infected fluid/empyema is suspected.
Check concomitant serum protein and LDH
 For therapeutic tap, connect 3-way tap (+/- connect to bed side bag)
and aspirate slowly and repeatedly. Do not push any aspirated
content back into pleural cavity. DO NOT withdraw more than
1-1.5 L of pleural fluid per procedure to avoid re-expansion
pulmonary oedema.
 Take CXR and closely monitor patient to detect complications
 Pr 19

Complications
1. Commonest: Pneumothorax(2-15%), Procedure failure,
Bleeding(haemothorax, haemoptysis), Pain, Visceral damage(liver
and spleen)
2. Others: Re-expansion pulmonary oedema from too rapid removal of
fluid, pleural infection/empyema, vagal shock, air embolism,
seeding of mesothelioma (avoid biopsy if this is suspected)

Procedures
 Pr 20

PLEURAL BIOPSY
Contraindications:
1. Uncooperative patient
2. Significant coagulopathy

Procedure:
Correct side marking is essential before procedure.
1. Ensure there is pleural fluid before attempting biopsy. Assemble
and check the Abrams needle before biopsy. A syringe may be
connected to the end hole of Abrams needle.
2. Preparation as for Steps 1 to 4 of Pleural Aspiration
(NB: If fluid cannot be aspirated with a needle at the time of
anesthesia, do not attempt pleural biopsy)
3. After skin incision (should be made right above a rib), advance a
CLOSED Abrams needle (with inner-most stylet in situ) through
soft tissue and parietal pleura using a slightly rotary movement
4. Once the needle is in the pleural cavity, rotate the inner tube
counter-clockwise to open biopsy notch (spherical knob of inner
tube will click into position in the upper recess of the groove of the
outer tube)
(Aspiration of fluid by the connected syringe confirm pleural
placement of the Abrams needle)
5. Apply lateral pressure on the notch against the chest wall anteriorly,
posteriorly or downwards (but NOT upwards to avoid injuring the
Procedures

intercostal vessels and nerve) with a forefinger, at the same time

slowly withdraw the needle till resistance is felt when the pleura is
caught in the biopsy notch
6. Hold the needle firmly in this position and sharply twist the grip of
inner tube clockwise to take the specimen
7. Repeat Steps 4 to 6 above in the remaining two directions, totally
take at least 3 specimens if possible
8. Firmly apply a dressing to the wound and quickly remove the
needle when the patient is exhaling
 Pr 21
9. While an assistant presses on wound, remove stylet of needle, open
inner tube and flush specimen(s) out with NS
10. If tapping is necessary, aspirate as for Steps 5-8 of Pleural
Aspiration
11. Take CXR to detect complication(s)
Complications: As for Pleural Aspiration

Procedures
 Pr 22

CHEST DRAIN INSERTION

Correct side marking is essential before procedure.

1. Preparation as for Pleural Aspiration. (Preferred patient position in

BTS guideline: Semi-supine on the bed, slightly rotated, with arm
on the side of the lesion behind his/her head to expose axillary
area.)
2. Always check the number of rib space from sternal angle.
Re-confirm insertion site by percussion, incise skin right above the
rib at anterior or mid-axillary line in 5th or 6th intercostal space.
(Alternate site: 2nd intercostal space, mid-clavicular line, is
uncommonly used nowadays)
3. USG guidance is strongly recommended if available
4. Insertion site should be within the “safe triangle.” (A space
bordered by anterior border of latissimus dorsi, lateral border of
pectoralis major and a horizontal line superior to nipple or 5th
intercostal space.)
5. Anaesthetise all layers of thoracic wall including pleura. (Do not
proceed if needle for anaesthesia cannot aspirate free gas/ fluid).
6. Proceed with blunt dissection of intercostal muscle with artery
forceps down to parietal pleura.
7. Preferred insertion method: Double-clamp outer end of Argyle
drain (24 Fr to drain air/fluid, 28 Fr to drain blood/pus). Apply
artery forceps in parallel with tip of drain. Breach pleura with
Procedures

finger. Insert drain tip, release forceps & use them to direct drain
into place.
8. Alternate method: Insert Argyle drain with inner trocar.
Withdraw trocar by 1 cm into drain immediately after puncturing
pleura. Match every 1 cm advancement of drain with 1-2 cm
trocar withdrawal. Double-clamp chest drain when trocar tip
appears outside chest wall
9. Direct drain apically to drain air and basally to drain fluid
10. Attach chest drain to 2 cm underwater seal. Ensure fluid level
swings with respiration and coughing.
 Pr 23

11. Apply a skin suture over the wound and make a knot, leaving
appropriate length on both sides. Form a 2 cm “sling” by tying
another square knot 2 cm from previous knot. Tie the “sling” to
the drain; make several knots using remaining threads to prevent
slipping.
12. Apply dressing.
13. Take CXR to confirm tube position and detect complication(s)
Complications: As for Pleural Aspiration

Procedures
 Geriatrics
Medicine
(Insert to electronic version only)
(This is a blank page)
 Gr 1

ALTERED RESPONSIVENESS OR “DECREASED GC”

may represent the hypoactive form of delirium (DSM-5 major
neurocognitive disorder)

History
Obtain from OAH staff/ family as far as possible
Do not assume the patient non-communicable unless proven otherwise
Be cautious about sinister conditions if there is an abrupt change in
consciousness level

Medication history (CMS / private drugs) reviewed to identify sedative

drugs or recently added or withdrawn drugs

P/E
Vitals

 GCS or level of consciousness documentation

 BP/pulse, temperature, RR, SpO2, hydration status
 Colour – cyanosis, pallor, jaundice

Abdominal exam

 rule out acute abdomen – ischaemic bowel can be subtle

 bladder size
 PR - loaded rectum, melena

Examine 4 limbs for any focal signs and nuchal rigidity (can be difficult
to differentiate from neck contracture)

Examine covered parts of body for any wound, rash, pressure ulcers
and peripheral ischaemia / gangrene

Move 4 limbs to detect unknown fractures / acute arthritis (crystal or

septic arthritis)
Gr 2

Ix
 Hemoglucostix and urine multistix
 Read CXR from AED
 routine blood tests including electrolytes, RG, WCC, Hb
 Septic workup
 Consider AXR for high faecal impaction or IO
 Judicious use of urgent CT brain

Mx
 Search and treat underlying causes (delirium in older adult is not
uncommonly multifactorial)
 Cautiously order NPO on admission and remember to resume
feeding later
 Keep good hydration and oxygenation
 Withhold some regular medications if not absolutely and
immediately necessary.
e.g. statin, vitamins, Ca
 Withhold or tapering medications that may give rise to altered
consciousness
 sedatives and other psychotropic drugs,
 anti-hypertensives if BP is low
 diuretics if dehydrated or poor intake
 Review OHA/insulin regimen according to hemstix
 consider splitting long acting insulin into short-acting
insulin to avoid hypoglycaemia in fluctuating oral intake
 withhold metformin if ill or poor intake
 Remember to resume medications when condition improves and
feeding satisfactory
 Consider empirical antibiotic
 Gr 3

ASSESSMENT OF MENTAL COMPETENCE

Mental competence refers generally to an individual’s ability to make an

informed choice with respect to a certain decision. It is an essential step
of obtaining informed consent, advance directive and advance care plan.

Four key elements of informed consent

1. Competence (be aware of cognitive function and consciousness)
2. Voluntariness (free will, independent decision making)
3. Disclosure of information: pros and cons of choices including
alternatives
4. Understanding and acceptance of information and consequence

Key steps in assessing mental competence

1. Patient receive and understand information(s) - capable to
comprehend
2. Patient is asked to paraphrase -in order for the clinician to evaluate
his/her understanding of the information, and correct any
misconceptions
3. Capable to analyze the decision(s) to make - seeing both sides of
argument and appreciating consequence(s)
4. Patient make his/her own choice(s) with reasoning
5. Patient has to express his decision(s) by means of communication
understandable by others
6. Capable to retain the information and decision , at least for a short
period

Clinical assessment
Rule out delirium
Rule out depression
Facilitate communications, e.g. correction of hearing deficit, presence of
translator (for dialect speaker) and writing in place of speech (for
patients with expressive aphasia)
Gr 4

CARE OF DYING
Geriatric patients need different EoL care approach because:

a. high unpredictability of complex disease trajectories

b. high prevalence of non-cancer co-morbidities, frailty and dementia.
c. tendency of rapid clinical deterioration and slow recovery in acute
illnesses.

The diagnosis of dying is more of a process than an event. The

Ellershaw’s criteria would not be adequate for diagnosing dying in
non-cancer older patients while geriatric multidisciplinary assessment
together with patients/ families as team members is mandatory for
individual care planning, including DNACPR, AD and ACP.

It is prudent and sometimes necessary to combine both life sustaining

therapy (LST) and palliative care therapy in the initial dying process.
The art is to strike the balance of allowing recovery where potential
exists and avoiding futile interventions resulting in prolonging the dying
process.

Stop LST and shift focus to comfort care and support to the families
when death is imminent and inevitable. Make sure to take off
unnecessary and inappropriate medications, monitoring and
interventions. Keep reasonable artificial fluid therapy which is regarded
as basic care in Chinese culture.

Aggressive symptomatic control with the use of opiates and sedatives

could sometimes be misinterpreted as hastening death. Side effects of
these medications can be difficult to differentiate from the dying process.
Reassessment, education, effective communication between the health
care team and the family are the keys to achieve a good death with
effective symptom control.
 Gr 5
Practical tips to avoid misinterpretation as “euthanasia”:

a. Start low in the opiates naïve patients.

Beware of opioid overdose in some commonly used regimen:

“10mg morphine (+/- haloperidol / buscopan) in 500ml NS Q24hr
intravenously.” 10mg iv morphine is equivalent to 30mg oral
morphine which can be an overdose in opiate naïve older patients,
especially in those with COPD.

Suggest starting with 3 mg morphine(+/- haloperidol/ buscopan)

in 500ml NS Q24h and titrate up with 0.5mg-2.5mg SC
morphine q2hourly prn.

b. Make sure to document the failure to control symptoms at current

doses before increasing the dose and/or switching to more potent
medications.

c. If suspected overdose, allow trial of decreasing/ withholding

medications to see for any clinical improvement in cognition and
respiration vs any recurrence of distressing symptoms.

d. Repeated and continuous assessment and communication can never

be overemphasized.
Gr 6
Drug Prescribing in End-of-life Care of Older Adults

Symptom Condition Recommended Medications

Starting regimen Maintenance

(CSCI = continuous
subcutaneous infusion)

Dyspnoea Usual Morphine sc 0.5mg q2-4h If 3 doses in 24hr: CSCI

prn Morphine 2-5mg q24h
ESRD Fentanyl sc 12.5mcg If 3 doses in 24hrs: CSCI
q2-4h prn Fentanyl 25-75mcg q24h
Agitation Haloperidol sc 1mg q2-4h If 2 doses in 24hrs: CSCI
prn Haloperidol 2-10 mg q24h
Death rattle Usual Buscopan sc 20mg q8h If 2 doses in 24hrs: CSCI
prn Buscopan 40-120mg q24h
CHF Furosemide sc 10-20mg
q4h prn
Nausea/vomting Usual Maxolon iv 10mg q8h prn If 2 doses in 24hrsI: CSCI
Maxolon 30mg q24h
Alternative Haloperidol sc 1-2mg q8h If 2 doses in 24hrs: CSCI
prn Haloperidol 2-10mg q24h
ESRD Haloperidol sc 0.5-1.5mg If 2 doses in 24hrs: CSCI
q8h prn Haloperidol 1-3mg q24h
Pain Usual Morphine sc 2.5mg q2-4h If 3 doses in 24hr: CSCI
prn Morphine 5-15mg q24h
ESRD Fentanyl sc 12.5-25mcg If 3 doses in 24hrs: CSCI
q2-4h prn Fentanyl 25-75 mcg q24h
 Gr 7

DIABETES MELLITUS IN OLD AGE

Assessment of DM older adults
Comprehensive geriatric assessment approach in particular
Cognition
Gait and balance
Frailty syndrome – gait speed and muscle strength
Vision
Mood
Social reserve
Hand dexterity
And other standard complication assessment in adults in the absence of
established complications

Glycaemic targets
Glycaemic control in older adults is highly individualized with various
targets, and is particularly loosened in those with established
complications and co-morbidities

American Diabetes Association / American Geriatrics Society (2012) consensus guideline 
for glycaemia goal in elderly people with diabetes 
Fasting /
Bedtime
Patient characteristics / HbA1c preprandial
Patient type glucose
health status target glucose
(mmol/L)
(mmol/L)
Few coexisting chronic
Healthy (longer life
illness, intact cognitive and <7.5% 5-7.2 5-8.3
expectancy)-
functional status
Complex/ intermediate
Multiple coexisting chronic
(intermediate remaining
illness or >2 instrumental
life expectancy, high
ADL imparment or mild to <8% 5-8.3 5.6-10
treatment burden,
moderate cognitive
hypoglycaemia
impairment
vulnerability, fall risk)c
Very complex/poor
Long term care/end-stage
health
chronic illness, moderate to
(Limited remaining life <8.5% 5.6-10 6.1-11.1
severe cognitive impairment,
expectancy makes
>2 ADL dependencies
benefit uncertain)
Gr 8
Treatment principles:
1. Prevent acute complications of profound hyperglycemia
2. Avoid hypoglycaemia
3. Delay chronic complications but not applicable if already
established or in the presence of limited life expectancy

Management
Diet and weight control
Aim at weight stabilization
Weight reduction should not be loosely advised to balance against
compromising quality of life

SBMG
SMBG (usually by OAH staff or family) should not be routinely advised
to monitor post-prandial hyperglycaemia but sometimes indicated to
detect fasting or pre-meal hypoglycemia.
Pharmacotherapy
1. metformin is the preferred initial therapy if no contraindications
(eGFR <30ml/min per 1.73m2 or at risk of lactic acidosis)

2. short-acting sulphonylurea to minimize the risk of hypoglycaemia

3. α-glucosidease inhibitor is safe for hypoglycaemia and good for

postprandial hyperglycaemia but potency is low

4. adverse profile of thiazolidinedione with particular concerns in old

age are: water retention, edema and heart failure, fragility fractures
and possible bladder cancer

5. incretin-based therapies such as dipeptidyl peptidase-IV inhibitors

and glucagon-like peptide receptor agonists have low risk of
hypoglycaemia and are good to counteract post-prandial
hyperglycaemia
 Gr 9
6. In general, insulin therapy for frail older adults should be simple and
once or twice daily dose of intermediate acting insulin is sufficient.
Consider long-acting basal insulin analogue (glargine and detemir)
with or without pre-prandial rapid-acting insulin analogue (lisopro
and aspart), which are reserved only for those with wide glycaemic
excursion. (profound post-prandial hyperglycaemia and recurrent
nocturnal or pre-meal hypoglycaemia)

7. The safety profile of SGLT2 inhibitor in old age is awaited

Practical notes to avoid hypoglycaemia

1. Preferred therapy
a. Metformin
b. Incretin-based therapy
c. Glucosidase inhibitor (low potency)
d. Long-acting basal insulin analogue

2. Hypoglycaemia can blunt glucose counter-regulatory response

to subsequent hypoglycaemia, leading to recurrent
hypoglycaemia. Loose control for 2-3 weeks is advised for
restoring the counter-regulatory response.

3. Infection related hyperglycemia may need escalation of insulin

therapy to counteract the activation of stress hormones. This
phase can be prolonged beyond the resolution of the crisis and
therefore it is not uncommon that a patient is discharged with a
higher insulin dosage. Prompt scaling down of insulin at
post-discharge can avoid hypoglycemia. It is safer to allow a
loose control on discharge.

4. Consider continuous glucose monitoring study when

asymptomatic hypoglycaemia, which is common in old age, is
suspected.
Gr 10

FALLS

Defined as an event that results in the patient or a body part of the

patient coming to rest inadvertently on the ground or other surface lower
than the body. Fall results in injuries, more hospitalizations, clinic
visits and emergency attendance. Moreover, fear of falling, loss of
confidence in walking, social isolation and depression can occur.

Approach to falls: do not just treat the consequences of falls. Find out
the causes of falls. Falls in older people are often due to interaction
between multiple risk and precipitating factors. One practical way is to
use a mnemonic as below:

Risk and precipitating factors for falls

Mnemonic (A E I O U, A B B C C C D) of risk or precipitating factors for

falls
A Anti-depressants, antipsychotics, anticholinergics, antiepileptics,
anti-hypertensives
E Environmental hazards e.g. home, outdoors
I Infectious diseases e.g. urinary tract infection, chest infection and others
O Osteoarthritis and musculoskeletal problems
U Unwell patients are more prone to falls
B Blindness and visual impairment e.g. refractive, cataract, macular
degeneration, glaucoma, visual field defect, hemi-spatial neglect after
cortical stroke
B Biochemical abnormalities e.g. hyponatraemia, hypokalaemia,
hypoglycaemia
C Cardiovascular problems e.g. postural hypotension, heart block,
arrhythmias, carotid sinus hypersensitivity
C Central nervous system or peripheral nervous system disorders,
Parkinsonism
C Cognitive impairment e.g. dementia, delirium
D D vitamin deficiency
Adopted from Chan’s Practical Geriatrics, 3rd Edition
 Gr 11
Fall assessment
 Obtain history on circumstances of fall, precipitating factors and
consequences. Ask a witness if available.
 Ask relevant history e.g. living environment, social support, past
medical illnesses, medications, history of falls or near falls,
mobility and functional status.
 Testing gait, balance, lower limb and joint function, cardiovascular
and neurologic examination, if relevant.
 Perform Timed up-and-go test (TUGT)
A simple test in which older patients are timed while rising from a
46 cm high armchair, walking 3 metres, turning around and
returning to sit in the chair (total 6 metres). Walking aids are
allowed and patients who require more than 20 seconds to
complete are at risk for falls.
 Perform ECG and other investigations as guided by history and
examination.

Management of Falls – usually multi-modalities

1. Medication review and minimization
 Minimize medications and in particular psychotropic drugs
 Use standardized tool such as the Beers Criteria for Potentially
Inappropriate Medication Use in Older Adults and STOPP
(Screening Tool of Older Person’s potentially inappropriate
Prescriptions) for drug reconciliation.
2. Treatment of cardiovascular risk factors
 Treat underlying cardiovascular causes e.g. carotid sinus
hypersensitivity, vasovagal syndrome, orthostatic hypotension,
postprandial hypotension), arrhythmias.
3. Strength and balance training (including Tai Chi)
 Beware that prescribing inappropriate exercise may on the contrary
increase falls in older people.
4. Home and environmental hazard modification
5. Foot and footwear check and modifications
6. Vitamin D and Calcium supplementation
 Vitamin D3 800 IU per day with or without calcium supplement is
Gr 12
recommended for fall prevention.
7. Correction of vision
 Early cataract surgery reduces falls.
 Beware of multifocal lens which may increase fall risk.
8. Strengthen bone to reduce fracture even when falls occur
9. Hip protectors
 Evidence not concrete except in residential care homes and
compliance is the usual limiting factor for its effectiveness.
10. Safety alarms

Interventions that may be ineffective yet harmful

 Restraints do not reduce risk of falling. On the contrary, patients
may fall more frequently and sustain more serious injuries after
using restraints.
 Restraints increase the risk of delirium in the hospital and the
resulting immobilization are associated with pressure ulcer
occurrence, respiratory complications, and death via strangulation
and asphyxia.
 Bed rails may lead to serious injury e.g. limbs snag on metal bars
or older patients climb over the rail, falling even greater distance
onto the floor.
 Gr 13

HYPERTENSION IN OLD AGE

Difference in hypertension between older adults and younger adults:
1. Isolated systolic hypertension (SBP > 160 while DBP <90 mmHg)
mostly occurs in older patients.
2. Older adults have reduced baro-reflex sensitivity resulting in
reduced heart rate and vasoconstrictor response to sympathetic
activation. In addition, they have marked variability in blood
pressure and are more vulnerable to hypotension during common
daily activities e.g. postural change or meal ingestion; in response to
medications; and during volume contraction.
3. Antihypertensive medications can worsen postural hypotension and
put vulnerable older adults at a greater fall risk.
4. Possible and controversial beneficial effects of having higher blood
pressure are consistently observed in ‘survivors’ older than 85 years
in various observational studies.

Hypertension treatment consideration in older adults:

1. Life style modification, in particular about diet and weight control
is difficult to achieve in older persons and has to be balanced
against compromising quality of life.

2. Clinical trials of hypertension, exclusively recruiting or also

including patients over the age of 80 years have consistently
demonstrated mortality and cardiovascular benefit. However,
participants in clinical trials are usually healthier than the other
older adults. Old and frail individuals with multiple chronic
conditions are usually not included and the balance of risks and
benefits in these patients is particularly unclear.

3. While benefits are clear for SBP <150 mmHg (strong evidence),
stricter control in older adults of SBP < 120 mg Hg has recently
been shown to be beneficial in terms of mortality and morbidity.
(SPRINT, NEJM 2015) In general, if lower than conventional
targets (< 140/90 mmHg) can be achieved with good tolerance,
treatment does not need to be adjusted (expert opinion).
Gr 14

4. Diastolic blood pressure should be targeted < 90 mmHg (strong

evidence). An increased risk of ACS is associated with DBP
between 61 to 70 mmHg and increased further at DBP ≤ 60 mmHg,
likely due to myocardium hypo-perfusion which is diastolic phase
dependent. In general, a DBP of not < 60 mmHg or in the presence
of coronary artery disease, not < 65 mmHg, is recommended.

5. Be aware that the first one to two months of anti-hypertensive

therapy in older patients is associated with increased risk of falls
and hip fracture. Therefore start low (initial doses approximately
one-half that in younger adults) and go slow (to achieve target BP
over a period of weeks to months) unless in hypertensive
emergency to minimize the risk of postural hypotension. The
prevalence exceeds 30% after 80 years of age.

6. Exercise clinical judgement rather than clinical guideline in

treating blood pressure in frail older adults with limited life
expectancy, where immediate risk associated with treatment may
outweigh long term benefit. Slow walking speed (inability to walk
6 meters in less than 8 seconds), as a measure of frailty, may
identify patients at risk of adverse effect.
 Gr 15

MUSCULOSKELETAL PAIN
Musculoskeletal pain is common, under-recognized and under-treated in
older people.

Pain Assessment in Older People

- to distinguish the cause of musculoskeletal pain,

- to identify comorbid diseases influencing pain management
- to recognize complicating psychosocial issues
- repeated assessment of pain levels and functional status is crucial for
optimal pain management
- Mnemonics for pain assessment (PQRSTUVA)
Precipitating / Palliating factors Timing
Quality Upsetting ADL
Radiation Vital sign changes
Severity Associated symptoms
- for cognitively intact older people, self-reported measures can be
used (e.g. numerical and graphic rating scales).

 Figure: Numerical Rating Scale  Figure: Wong-Baker Faces Pain Scale

- For cognitively impaired older people, non-verbal pain assessment

tools can be used (e.g. Abbey Pain Scale) by observing patient’s
facial expressions, behaviors and activities.
Gr 16

Table: Non-Specific Symptoms and Signs of the Presence of Pain in Older People
Vocalization Moaning, sighing, groaning
Facial expression Frowning, grimacing, fearful facial expressions

Change in body language Fidgeting, guarding, bracing, withdrawn

Mental status change Increasing restlessness or agitation, depressed affect of

sudden onset
Behavioral change Refusing to walk, eat or sleep, paucity of speech and
interaction, resisting certain movements during care
Physiological change Temperature, blood pressure or pulse outside normal limits,
tachypnea

Common Musculoskeletal Disorders in Older People

- Joints: osteoarthritis of knees, hips, hands; inflammatory arthritis
(rheumatoid arthritis), crystal-induced arthropathy (gout and
pseudogout)
- Bones: osteoporotic fractures
- Soft tissues (tendons, bursae, ligaments, muscles): rotator cuff
syndrome, adhesive capsulitis, tendonitis, bursitis and myopathy
- Chronic low back pain (CLBP) due to multiple etiologies (e.g.
lumbar spondylosis and spondylolisthesis, disk disease, osteoporotic
vertebral fracture, spinal stenosis, paraspinal muscle spasm, referred
pain from hip and sacroiliac joint diseases)

Management
- Management should be individualized and requires a
multidisciplinary approach with a combination of
non-pharmacological and pharmacological modalities addressing
physical, psychological, social and spiritual components of pain.
- Aims: to relieve pain, restore function and maintain quality of life.
- Drug review for iatrogenic rheumatic syndromes (e.g.
diuretic-induced gout).
 Gr 17

Non-Pharmacological

- Physical therapy (weight-bearing exercise for osteoporosis, Tai Chi

for arthritis, physical modalities e.g. TENS, ultrasound, heat or ice
for pain relief), occupational therapy (for patients’ independence and
hazard reduction with assistive devices, joint rest with splinting for
synovitis), patients’/caregivers’ education (self-management, drug
use), lifestyle advice (weight reduction for osteoarthritis, dietary
advice for osteoporosis and gout), alternative medicine (herbs and
acupuncture), psychosocial and spiritual support.

Pharmacological

- Older people are vulnerable to adverse drug reactions. Drug choice

should be based on individual profiles of renal, liver functions,
cardiovascular risk factors and gastrointestinal disorders with
alertness to drug-drug and drug-disease interactions.

- A stepwise pharmacological approach can be used in the pain

management of osteoarthritis and CLBP:
[1] Acetaminophen as first-line therapy for mild-to-moderate pain.
[2] NSAIDs as added-on if pain is not relieved or for inflammatory
pain. However, NSAIDs can cause gastrointestinal bleeding, fluid
retention, renal, liver impairment and precipitate heart failure in
older people. The lowest effective dose should be used for the
shortest period of time. COX-2 inhibitors also have cardiotoxicity,
nephrotoxicity and hepatotoxicity similar to NSAIDs.
[3] Weak and strong opioids for moderate-to-severe pain.
Gr 18
- Because of increased toxicities of NSAIDs and colchicine in old age,
corticosteroids have been used more often in treating acute attacks of
gout.

- Others: topical analgesics (topical NSAIDs, anesthetics), adjuncts

(anti-convulsants, anti-depressants)

Injection Therapy: Intra-articular injection (e.g. hyaluronic acid for

osteoarthritis, corticosteroid for inflammatory arthritis, adhesive
capsulitis), epidural injection of local anesthetics or corticosteroid for
CLBP

Surgery: Joint replacement and spinal surgery are reserved for people
not responding to medical therapy and with impaired daily activities.
 Gr 19

NEUROCOGNITIVE DISORDER
History (collect history from someone who knows the patient well)
Past or current occupation
Years of education
Smoking and alcohol habit

Chief complaint
Cognitive deficits / Memory loss
Duration / onset / course / initial symptom (memory first or other
cognitive domain first)
Onset - insidious / sudden / progressive

Suggested list of questions:

Short term memory became worse?
Stocking repeated items in refrigerator?
Forgot meals?
Forgot turning off stove?
Got lost in neighbourhood?
Cannot recognise family persons?

Functional assessment for staging (suggested items)

Basic ADL – suggested questions: selection of appropriate clothes,
continence status
Instrumental ADL – telephone, finance (banking, paying bills), shopping,
cooking, medication management, travelling alone
Social activities and hobbies

Behvioural and psychological symptoms of dementia (BPSD)

Apathy, sleep disturbances, irritability/ agitation, wandering, mood
disorders (depression), psychotic symptoms, eating/ appetite disorders
Common examples:
Delusion of theft by domestic maid
Visual hallucination - seeing many small people or deceased relatives
Sleep and nighttime behaviour disturbance
Gr 20
Lost interest in past hobbies (e.g. playing Mahjong, watching TV,
reading newspaper)

Past health : diabetes mellitus, hypertension, stroke, atrial fibrillation

Drug history
Sexual history – HIV, Syphilis
Family history of neurocognitive disorder

Physical examination
General impression – Apathetic / agitated / sociable
Pulse regular or in AF, bruits, murmur
Focal neurological sign, muscle tone, muscle power, tendon reflexes
Frontal release signs
Gait and parkinsonian sign
Do not omit other systemic examination (you could miss a
para-neoplastic syndrome presenting as dementia)

Investigations
Renal and liver function, complete blood picture
Blood Glucose, lipid profile
Thyroid function
Serum vitamin B12 and folate level
Syphilis serology (optional)
HIV Ab (if suspicious)
ECG – note AF (vascular dementia), long QT interval (neuroleptic
treatment precaution), bradycardia (cholinesterase inhibitor treatment
precaution)
Neuroimaging / Plain CT brain is basic
Other potentially useful tests:
MRI brain, EEG (esp. for CJD), CSF examination for biomarkers,
functional imaging (FDG-PET, SPECT) ± pathological imaging
(Pittsburgh Compound B)
 Gr 21
Reference to Diagnostic Criteria (DSM-5) when making diagnosis
1. Dementia (major neurocognitive disorders).
a. Significant cognitive decline from a previous level of
performance in ≥1 cognitive area (memory, language, attention,
executive function, perceptual-motor and social recognition).
b. Interference with independence in everyday activities.
2. Mild cognitive impairment (MCI) or mild neurocognitive disorder.
1(a) + no impairment in independence in everyday activities.
3. Not in the context of active delirium.
Gr 22
Patterns in different types of NCDs

Subtypes of Dementia Main features

Alzheimer’s disease (AD) Episodic memory impairment
Vascular dementia (VAD) Stepwise deterioration and history of stroke
Lewy body dementia Parkinsonism (within 1 year of cognitive
(LBD) symptoms onset), vivid visual hallucination,
fluctuation of consciousness, severe autonomic
dysfunction, neuroleptic sensitivity, REM sleep
behavioral disorder
Parkinson’s disease Cognitive symptoms after at least one year of PD
dementia motor features (1-year rule), some shared features
with LBD but less prominent, executive
dysfunction most prominent
Behavioral variant of ( ≥ 3 of the following)
frontotemporal dementia Behavioral disinhibition, apathy or inertia, loss of
sympathy or empathy, stereotyped or compulsive/
ritualistic behavior, hyperorality or dietary
changes, executive dysfunction
Primary progressive Agrammatism, speech apraxia, impairment in
aphasia object naming, impairment in object knowledge,
dyslexia, dysgraphia, asymmetric atrophy of
dominant hemisphere
Normal pressure Development of apraxic gait  then urinary
hydrocephalus incontinence (urge)  dementia
Alcoholic dementia Heavy drinker, amnesia and frontal lobe features,
± cerebellar signs and chronic liver disease signs
Traumatic brain injury History of chronic repetitive head injury e.g.
boxer.
Creutzfeldt-Jakob disease Rapidly progressive dementia (over months or
(CJD) weeks), pyramidal/extrapyramidal symptoms,
visual or cerebellar disturbance, myoclonus, or
akinetic mutism
HIV infection, Sexual history
neurosyphilis
 Gr 23
Management
Social
Prognosis information
Financial arrangement
Advance care planning
Enduring power of attorney
Community and Day care resource

Medical
Vascular risk factors control
Non-pharmacological treatment (it may be the most and do not ignore
this)
Pharmacological

1. Drugs retarding cognitive deterioration /delaying institutionalization:

Cholinesterase inhibitor Donepezil Starting with 5 mg daily
 For mild to moderate (increase to 10 mg daily po after
AD. 4 to 6 weeks)
 Major side effects: Galantamine Immediate release: Starting with
anorexia, nausea, (max dose 16 mg 4 mg BD (increase to 8 mg BD
vomiting, diarrhea, for moderate after 4 weeks  12 mg BD after
bradycardia renal impairment) another 4 weeks)
Extended release: start with 8 mg
daily (increase to 16 mg daily
after 4 weeks  24 mg daily
after another 4 weeks)
Rivastigmine Starting with 1.5 mg BD
(increase to 3 mg BD after 4
weeks  4.5 mg BD after
another 4 weeks)
Rivastigmine Start with 4.6 mg/24 hr (increase
(transdermal to 9.5 mg/ 24 hr after 4 weeks)
patch)
NMDA antagonist Memantine (max Start with 5 mg daily (increase to
 Major side effects: dose 10 mg daily 5 mg BD after 1 week, then 5 mg
headache, dizziness, if CrCl < 30 OM & 10 mg PM after another 1
sedation, agitation, ml/min) week, then 10 mg BD after
constipation another 1 week)*
*
For Asians and older adults, dose escalation may need to be
slower and the maximum dose tolerated may be lower
Gr 24

2. Management of BPSD (must always use non-pharmacological

method first)

Behavioral symptoms Non-pharmacological intervention

Apathy Offer simple tasks, stimulation or activities
Sleep disturbances Good sleep hygiene, more stimulation/ exercises in
day time
Irritability/ agitation Avoid difficult tasks, distraction
Wandering Offer safe place to wander, visual cues
Mood disorders Exercise
Psychotic symptoms Reassurance, distraction, removal of confusing
items e.g. mirror
Eating/ appetite Removal of distraction during eating, use flavor
disorders enhancers, consider food preferences/ cultural
factors
Use antipsychotic only when BPSD is potentially harmful to
patient/ caregivers: e.g. haloperidol 0.5 mg nocte po
(contraindicated for LBD), quetiapine 12.5 mg/ 25 mg nocte po as
starting dose.
 Gr 25

NURSING HOME-ACQUIRED PNEUMONIA (NHAP)

Aspiration plays an important role in the causation of NHAP. Risk

factors include advanced dementia, old CVA, GERD and poor oral
hygiene.

Causative agents
Respiratory viruses (Influenza A and B viruses, and RSV), Gram
negative bacilli (GNB) and Staphylococcus aureus are more frequently
isolated in NHAP compared with CAP.
Mycobacterium tuberculosis should be considered in view of its
endemicity in HK.
Streptococcus pneumoniae and Haemophilus influenzae are also
common bacterial culprits.
Atypical pathogens are less commonly implicated in NHAP than CAP.

History
The symptoms are similar to those of community-acquired pneumonia
(CAP).
An episode of aspiration may or may not be witnessed.
Onset of respiratory symptoms occurring shortly after the meal suggests
that aspiration is the likely cause.

Investigations
CXR: a clear image indicates simple aspiration without pneumonitis
(chemical inflammation of lung parenchyma without infection) or
pneumonia (infection).
Sputum: routine bacterial cultures, and AFB smear and cultures.
Gr 26
NPA: a rapid test, such as by IF, should always be considered for
infection control and discharge planning.

Treatment
Non-pharmacological treatments
Keep good oral hygiene, e.g. regular mouth treatment with normal saline
or oral disinfectants.
Consult dental surgeon for dental caries or dental abscess.
Prop up patients during feeding. Add thickener if appropriate.
Physiotherapy for chest exercise, drainage and collection of sputum
specimens.

Empirical antibiotic treatments

The recommendations are in line with those for CAP.
Empirical broad-spectrum antibiotics may be used with caution in
patients with history of MDR bacterial pneumonia, e.g. vancomycin for
MRSA and ertapenem for ESBL-producing GNB.
Empirical anti-viral agents, such as oseltamivir and amantadine, should
be considered when viral infection is suspected, especially if outbreak of
influenza-like illnesses in nursing home is reported.
Report to the Community Geriatric Assessment Team (CGAT) if
outbreak of viral infection in nursing home is suspected or confirmed.
 Gr 27

ORTHOSTATIC HYPOTENSION
Orthostatic (postural) hypotension (OH) is a common, remediable and
yet an under-diagnosed condition, which may result in disability and
even death.

Definition:
A drop in systolic blood pressure (BP) of ≥20 mmHg or diastolic BP of
≥10 mmHg within 3 minutes of standing

Measurement of orthostatic BP (with/without associated symptoms):

- Active standing test: measure baseline BP after 5-minute rest in a
supine position, then measure BPs at 1-minute and 3-minute standing
(or in an upright position if unable to stand).
- Passive head-up tilt test is recommended if the active standing test is
negative.

Clinical presentation:
- Dizziness on standing, syncope or near syncope, falls, inability to
stand or walk
- Atypical presentation: stroke or transient ischemic attack,
seizure-like symptom, cognitive impairment, angina or myocardial
infarction, heat or meal-related symptom, chronic fatigue

Causes:
- Prolonged immobility
- Hypovolaemia
- Drug-induced: anti-hypertensives, anti-anginal, vasodilators,
diuretics, anti-adrenergics, anti-cholinergics, anti-parkinsonian drugs,
anti-psychotics, anti-depressants, sedatives and narcotics
- Neurological diseases: Parkinson’s disease, Lewy’s body dementia,
multi-system atrophy, pure autonomic failure, peripheral neuropathy
(e.g. diabetic, alcoholic, paraneoplastic autonomic neuropathy)
- Cardiovascular diseases with low cardiac output: aortic stenosis,
hypertrophic cardiomyopathy, mitral valve prolapse, varicose veins
Gr 28
- Endocrine disorders: adrenal insufficiency, pheochromocytoma,
diabetes insipidus
- Baroreceptor destruction (e.g. neck radiation or surgery)

Notes: OH is more prominent in early morning or after meals.

Supine hypertension and a loss of diurnal variation in BP are
commonly associated in OH due to autonomic dysfunction.

Management:
- Aims: to improve symptoms and functional status, to reduce fall
injuries, neurovascular and cardiovascular complications
- Identify and treat underlying causes
- Medication review

Non-pharmacological
- Patients and caregivers education
- Adequate salt (>10 g per day or 24 hours urine Na >170 mmol) and
water (1.5-2.5 L per day) intake
- Water-bolus treatment before standing
- Avoid triggers (e.g. immobility, abrupt posture change, heavy meals,
hot environment)
- Physical counter maneuvers (exercise before standing)
- Compression therapy (abdominal binders, stockings)
- Elevate the head of the bed during sleep to reduce supine
hypertension and nocturnal diuresis

Pharmacological
- Fludrocortisone (synthetic mineralocorticoid, first line monotherapy):
initial dose: 50 microgram daily orally, increasing up to 100-600
microgram daily orally or till mild pedal edema
Adverse effects: supine hypertension, hypokalemia, peripheral
edema, precipitate heart failure
- Midodrine (alpha 1 adrenoceptor agonist): initial dose: 2.5 mg bd or
tds orally, increasing up to 10 mg tds orally
Adverse effects: supine hypertension, piloerection, pruritus or
 Gr 29
paresthesia, urinary retention
Contraindicated in severe heart disease, acute kidney injury, urinary
retention, pheochromocytoma and thyrotoxicosis
- Pyridostigmine (cholinesterase inhibitor) 30-60 mg bd or tds orally
- Droxidopa (norepinephrine precursor) 100-600 mg tds orally as a
short-term treatment of neurogenic orthostatic hypotension
Gr 30

PHARMACOTHERAPY IN OLD AGE

Adverse drug reaction (ADR):
‐ Identify patients at risk of or suffering ADR (polypharmacy,
high-risk medications)
‐ Always think of ADR if new symptom develops, rather than
prescribing a new medication to treat the new symptom (prescribing
cascade)

Medication adherence:
‐ Simplify administration regime (aim at once daily)
‐ Assess patient’s hand function, cognitive function, vision, literacy,
swallowing
‐ Use assistive tools (e.g. pillbox, calendar)
‐ Empower reliable caregiver to manage medications in patients with
cognitive impairment
‐ Refer CNS for medication management if necessary

Prescribing:
‐ Beware of change in pharmacokinetics and pharmacodynamics in
older patients
‐ “Start low, go slow” and optimize dosage
‐ Define overall goals of care (symptom relief, optimize physical /
cognitive function, preventive)
‐ Estimate time to benefit and life expectancy
‐ Determine absolute benefit-harm thresholds of medications
‐ Comprehensive geriatric assessment could help identify complex
interactions and impacts between medications and patient’s
co-existing diseases, function and social problems
‐ Beware of drug-drug or drug-disease interactions

Medications review:
‐ Accurately ascertain all current medication use (in HA, private
sector, GOPC, over-the-counter, traditional Chinese medicine)
‐ Verify current indications for ongoing treatment
 Gr 31
‐ Stop medications that are without net benefits (or gradually wean
off medications that are likely to cause adverse withdrawal events
(e.g. benzodiazepines, β-blocker, steroid)

Iatrogencity - Relationship between geriatric conditions and

causative medications:

Geriatric conditions Causative medications

Fall Hypnotics, sedatives, antipsychotics,
antidepressants, antihistamines
Urinary incontinence Diuretics, cholinesterase inhibitors
Delirium Anticholinergics, benzodiazepines
Syncope Cholinesterase inhibitors, tricyclic
antidepressants, α-blockers
Anorexia / Weight loss Metformin, cholinesterase inhibitors
Gr 32

POST-OPERATIVE DELIRIUM
Post-operative delirium occurs in 20-40% of older patients undergoing
surgery. Risk factors include advanced age, multiple co-morbidities,
disability and pre-existing cognitive impairment. One of the purposes of
assessment and treatment is the prevention and early detection of
post-operative complications.

Physical examination

Pneumonia: sputum sound and crepitation

Fluid overload/ CHF/ ACS: lower limb edema, elevated JVP, murmur
(AS or MR) and crepitation

UTI/ urine retention: palpable urinary bladder and suprapubic tenderness

Acute CVA: facial asymmetry, dysarthria, dysphasia, hemiparesis or

hemi-sensory loss

DVT: calf swelling and tenderness

Rectal examination - GI bleeding and loaded rectum

Investigations (according to the clinical suspicion)

Capillary glucose (poor glycemic control)

Blood tests: CBC D/C, CRP, R/LFT/CaPO4, RG, cardiac biomarkers

and ABG (anemia, sepsis, acute renal or liver failure, poor glycemic
control, fluid overload, acute cardiac event)

Urine analysis and culture (UTI)

 Gr 33
Post-void residual urine by bladder scan (urine retention)

ECG (ACS/ CHF)

CXR (pneumonia)

CT brain (acute CVA)

USG Doppler or CT pulmonary angiogram (thromboembolism)

Treatments

The principle of treatments of post-operative delirium is keeping with

those of delirium, with the emphasis on the following areas.

Optimize the physical conditions and treat the underlying causes

Early mobilization if no surgical contra-indications

Stop or reduce the dose of psychotropic drugs in patients with

hypoactive delirium

Temporary use of psychotropic drugs, such as trazodone, quetiapine or

risperidone, for hyperactive patients

Observe cognitive status after discharge (dementia is more likely in

patients with post-operative delirium)
Gr 34

PRESSURE ULCERS
General Management
 To assess the co-morbid illness and functional status
 Maintain good hydration, nutrition, oxygenation and optimize
glycaemic control
 Provide appropriate pressure reliving bed and avoid inappropriate
bed elevation or sitting
 Control excessive moisture and contamination due to urinary or
fecal incontinence
 Look for complications, cellulitis, osteomyelitis or septicaemia
 Antibiotics if:
 local infection (cellulitis, lymphangitic streaking, purulence,
malodour, wet gangrene, osteomyelitis, etc)
 systemic symptoms (fever, chills, nausea, hypotension,
hyperglycemia, leukocytosis, delirium)
 Pain Control
 Systemic analgesics, like paracetamol, opioids and/or
non-steroidal anti-inflammatory drugs, can be used 30
minutes prior to dressing and afterwards
 Assess life expectancy and chance of wound healing to arrive at an
overall goal of management – healing, symptomatic relief, or odour
reduction only.

Wound Assessment and Staging

 Evaluated for length, width, and depth, presence of sinus tracts,
exudate, and presence of necrotic or granulation tissue.
 Staged according to The National Pressure Ulcer Advisory Panel
(NPUAP).
 Gr 35

Stage Description
1 Non-blanchable erythema (over a bony prominence)
2 Erosion (epidermal base) or superficial ulcer (dermal base)
3 Ulcer (subcutaneous fat base)
4 Ulcer (muscle, fascia, bone base)
SDI sDTI (suspected deep tissue injury)
Unstageable (slough or eschar in the base obscuring the actual
US depth

Local Wound Management (in general)

 Stage 1 pressure ulcers can be covered with transparent film for
protection.
 Stage 2 pressure ulcers require a dressing that maintains a moist
wound environment. A semiocclusive (transparent film) or
occlusive dressings (hydrocolloids or hydrogels) can be used
unless there is infection
 Stage 3 and 4 pressure ulcers generally require debridement of
necrotic tissue and coverage with appropriate dressings, and
possibly treatment of infection

Wound Debridement
 Ways to remove the necrotic tissues include: irrigation, surgical
debridement, autolytic debridement, enzymatic debridement, and
biologic debridement
 Do not debride stable, hard, dry eschar in ischemic limbs
 Immediate surgical debridement to remove the eschar and necrotic
tissue in the presence of advancing cellulitis, crepitus, fluctuance,
and/or sepsis secondary to ulcer-related infection.
 Non-surgical debridement is preferred when there is no urgency
 Autolytic debridement using body own enzymes to degrade
dead tissues by placing an occlusive dressing.
Gr 36

 Enzymatic debridement uses proteolytic enzymes that act by

decomposing collagen and liquefying necrotic debris without
damaging granulation tissue.

Wound Dressing
 To protect the wound from contamination, and facilitate healing by
absorbing exudate and protecting healing surfaces.
 Dressings are selected based on wound characteristics, including
the presence of heavy exudate, desiccation, or necrotic tissue
 An absorptive dressing, like foams and alginates, should only be
used to absorb excessive wound discharge
 A moisture retaining dressing, including saline moistened gauze,
transparent films, hydrocolloids, and hydrogels, should be used to
keep moisture for desiccated ulcers
 Hydrogels to keep moisture for autolytic debridement
 Foam and low-adherence dressings for the granulation stage
 Hydrocolloid and low-adherence dressings for the epithelialization
stage

Antiseptics and antimicrobial agents

 Most topically-applied antiseptic and antimicrobial products are
irritating, partially cytotoxic leading to delayed healing
 Two of these agents may have potential benefits, including
Cadexomer iodine and Silver-based dressing
 Use only in the presence of heavy local contamination.

Negative pressure wound therapy (NTWT)

 Enhances wound healing by reducing edema surrounding the
wound, stimulating circulation, increasing the rate of granulation
tissue formation and wound closure
 Can be considered as an early adjuvant for the treatment of Stage
III and IV pressure ulcers
 The pressure ulcer should be debrided of necrotic tissue prior to the
use of NPWT and covered with a foam dressing
 Gr 37

End of Life Care

 Pressure ulcers are common in frail immobilized older patients at
the last stage of their life and the wound is not likely to heal
 Pain management, odour control, and exudate control are indicated
for comfort care
 Conservative debridement of slough can, however, be undertaken to
control the bioburden
Gr 38

SPASTICITY
Assessment:
Identify muscles/muscle group
Involved muscles may demonstrate spontaneous or elicited clonus,
increase tendon reflexes
DDX: distinguish from parkinsonism

P/E:
1. New onset spasticity
i. History, P/E, EMG, NCV, imaging studies of head, neck and
spine
2. Past history of neurological insults, need to rule out factors that
exacerbate spasticity
i. Eg. Medication changes, noxious stimuli, increase in ICP
3. Modified Asthworth Scale to assess degree of spasticity
i. 0-4 (normal to rigid tone)
Management
1. Identity goal first
i. Does the patient need treatment? Pay attention to patient’s
wish
ii. Aim of treatment - need to balance the pros and cons of
treatment
iii. Will the treatment affect the quality of life of patient and
carers?
2. Therapy
i. Removal of noxious stimuli
ii. Proper positioning,
iii. Preventive measures
iv. Therapeutic interventions: physical and occupational therapy
v. Drugs: oral or injection therapy
vi. Surgery: dorsal rhizotomy, tendon release
 Gr 39
Need to consider the following before initiation of treatment
a. Duration of spasticity
b. Severity of spasticity
c. Location of spasticity
d. Prior successful intervention
e. Current functional status and future goal
f. Underlying diagnosis and comorbidities
g. Ability to comply with treatment
h. Availability of carer and follow up therapy

Drugs treatment
1. Benzodiazepam
a. Diazepam: start at 5mg N, can increase slowly up to 60mg /d
in divided dose
b. Clonazepam: 0.5mg N, up to 20mg/d in divided dose
Side effects: sedation, weakness, hypotension, memory impairment,
tolerance and dependency
2. Baclofen
i. Dosage range from 30-100mg/d in divided dose
ii. Side effects: nausea, vomiting, tolerance, seizure,
hallucination, cautious use in renal insufficiency
3. Dantrolene
i. For supraspinal cause e.g. cerebral palsy/ traumatic brain
injury
ii. Dosage range 25-400mg /d
iii. Side effects: drowsiness, dizziness, fatique, weakness, impair
LFT
4. Injection therapy
a. Phenol
i. Degeneration of neurons last ~ 6 months
ii. Do not cause permanent reduction of spasticity
iii. Need stretching, serial casting
Gr 40
b. Botulinium toxin
i. Effect last ~2-6 months
ii. After injection, need therapeutic intervention such as
retraining of gait, increase range of movement, improve
fit and tolerance of orthosis
iii. Warning: spread from the area of injection to other areas
of the body, causing life-threatening, and sometimes
fatal, swallowing and breathing difficulties. Do not
exceed a total dose of 400 Units administered in a 3
month interval
 Gr 41

SYNCOPE
Syncope is a T-LOC due to transient global cerebral hypoperfusion
characterized by rapid onset, short duration, and spontaneous recovery.

Diagnos c flowchart in pa ents with suspected T‐LOC

T‐LOC – suspected syncope

Ini al evalua on*

Syncope T‐LOC – non‐syncopal

Confirm with specific test

Certain Uncertain diagnosis or specialist consulta on
diagnosis
Treatment
Treatment Risk stra fica on

High risk ** Low risk, recurrent Low risk, single

syncopes or rare

Early Cardiac or neurally‐

No further
evalua on & mediated tests as
evalua on
treatment appropriate

* Initial evaluation = Careful history + physical exam (esp. CVS +neuro

exams) + orthostatic BP measurements + 12-lead ECG

Careful history:
Prior to attack: 3Ps: Provokers (activities), Posture, Prodrome
During the attack (±witness): duration, skin colour, movements,
tongue-biting
End of attack: autonomic symptoms, confusion, drowsiness
Background: Number and details of previous attack(s), Family history,
previous cardiac disease, neurological history, metabolic disorder,
medications.
Gr 42
** Short-term high-risk criteria which require prompt hospitalization or
intensive evaluation
History: Abnormal ECG:
• Syncope during supine • NSVT
• Syncope during exertion • Bifascicular block
• Palpitations at the time of • Intraventricular conduction
syncope abnormalities (QRS ≥ 120ms)
• History of MI, CHF, low • Inadequate sinus bradycardia
LVEF (<50bpm) or SA block in the
• Family history of sudden absence of -ve chronotropic drugs
cardiac death or physical training
Important co-morbidities: • Pre-excited QRS complex
• Severe anaemia • Long or short QT interval
• Electrolyte disturbance • RBBB w/ STE in V1-3 (Brugada
• Orthostatic hypotension of pattern)
acute onset • ARVC: -ve T waves in Rt
precordial leads, epsilon waves,
ventricular late potentials

Choice of Ix following initial evaluation

• CBP, LFT, RFT, CaPO4, cortisol, cardiac enzymes
• Neurally-mediated tests: tilt-table test, carotid sinus massage
(>40y/o), active standing
• Cardiac tests: prolonged ECG monitoring, electrophysiological
study, echocardiogram, exercise testing, carotid doppler
• Neurological evaluation: CT brain, EEG, MRI +MRA head and
neck, autonomic function test

Treatment:
Neurocardiogenic syncope:
• Counsel patients to take precautionary steps to avoid injury by
being aware of prodromal symptoms and maintaining a horizontal
position at those times
 Gr 43
• Avoid known precipitants and triggers (e.g. hot crowded
environments, volume depletion, cough suppression in cough
syncope)
• Maintain adequate hydration
• Employ isometric muscle contraction (e.g. hand-grip, leg crossing)
during prodrome to abort episode
• Fludrocortisone 50 – 300μg daily (S/E: supine HT, hypokalemia,
Na and fluid retention)
• Midodrine 2.5mg bd -15mg tds for frequent hypotensive symptoms
(>1 syncope/mth) (S/E: supine HT, bradycardia, piloerection,
caution if prone to urinary retention)
• SSRI antidepressant (e.g. paroxetine)for refractory vasovagal
syncope
• Dual-chamber cardiac pacing: for cardioinhibitory carotid sinus
syncope
• Betablockers are relatively contraindicated in most cases of
neurocardiogenic syncope

Orthostatic hypotension:
• Adequate hydration and elimination of offending drugs
• Salt supplementation, compressive stockings, and counseling on
standing slowly
• Midodrine and fludocortisone (as above)

Cardiac syncope:
• Treat the underlying disorder
• Cardiac pacing for sinus node dysfunction or high-degree AV
block
• Discontinue QT-prolonging drugs
• Catheter ablation: selected patients with syncope associated with
SVT
• ICD for documented VT without correctable cause

Ref: ESC Guidelines for the diagnosis and management of syncope (ver.
2009)
Gr 44

URINARY INCONTINENCE

 A syndrome characterized by complaint of involuntary loss of urine.

 Common in people with chronic physical disabilities, cognitive
impairment and frailty especially in hospital and residential care
 The goal of assessment is to determine transient, persistent and
reversible causes. Some of the underlying conditions are uncommon
but serious (e.g. spinal cord lesion, carcinoma or bladder and
prostate, bladder stones and low compliance bladder)

History
 Types (urge/overactive bladder, stress, overflow, functional or
mixed)
 Urinary symptoms (storage, voiding and post micturition)
 Associated symptoms (e.g. haematuria, passage of stones,
dysuria and pelvic pain)
 Bowel symptoms and sexual function
 Significant past health including medical, urological,
gynecological and neurological conditions (e.g. diabetes,
malignancy, recurrent urinary tract infections, pelvic or lower
urinary tract surgery and radiotherapy). Outcome of previous
medical or surgical interventions
 Medication history (e.g. psychotropic, anti-hypertensive,
diuretic, nasal decongestant)
 Functional and mental state
 Dietary (caffeinated drinks, alcohol)
 Environment and social support
 Impact on the individual and care giver

Physical examination
 General (peripheral oedema, diabetes)
 Abdominal (bladder distension after voiding)
 Pelvic (gynaecological abnormalities, mass, fistula, and skin
condition)
 Gr 45

 Rectal (perineum sensation, rectal tone, faecal impaction,

prostate and mass)
 Neurological (dementia, delirium, stroke, parkinson’s disease,
cord compression, autonomic neuropathy, peripheral
neuropathy)

Investigations
 3-Days bladder diary
 Urinalysis and renal function
 Post void residual
o Indicated if symptoms suggestive of voiding dysfunction
and recurrent urinary tract infection
o Bladder scan is preferable then catheterization
 Other optional tests (urine cytology, imaging, cystoscopy,
uroflowmetry, urodynamic study)

Management
 Etiology of urinary incontinence in elderly is complex. An
intact micturition pathway is vital but it also depends on patient
and environmental factors.
 The mnemonic DIAPPERS (Resnick 1984) is helpful in
management on reversible causes
D: Delirium
I: Infection of urinary tract or other infection
A: Atrophic urethritis and vaginitis
P: Pharmaceutical (diuretics, anticholinergic, antihistamine, CCB)
P: Psychological problems, especially depression
E: Excess urine output (eg. CHF, hyperglycaemia)
R: Restricted mobility
S: Stool impaction
Gr 46

 Non pharmacological
o Toileting regime, bladder training, pelvic floor exercise,
fluid management, environmental measures
 Pharmacological
o Anti-cholinergic drugs (oxybutynin, tolterodine,
solifenacin, darifenacin, trospium
o Beta-adrenoceptor antagonist (mirabegron)
o Alpha-adrenoceptor antagonist (prazosin, terazosin,
alfuzosin, doxazosin, tamsulosin)
o 5-Apha reductase inhibitor (finasteride, dutasteride)
o Anti-cholinesterase inhibitor (distigmine)
o Others (botulinum toxin, duloxetine)

Referral to specialist care

 If visible or microscopic haematuria, recurrent urinary tract
infections, suspected malignancy of urinary tract
 Failed empirical treatment
 Gr 47

URINARY RETENTION
Urinary retention can be acute or chronic. Acute urinary retention (AUR)
is defined as a generally (but certainly not always) painful, palpable or
percussable bladder (150-200ml), when the patient is unable to pass any
urine when the bladder is full. The risk of AUR is 1/10 in aged above
70.

Causes

 Bladder outflow obstruction

o Mechanical: BPH, malignancy, infection, stones, urethral
stricture
o Dynamic: Drugs, pelvic floor dysfunction
 Bladder over-distension
o Immobility, constipation, pain, drugs
 Neuropathic
o Spinal cord or cauda equina lesion, peripheral neuropathy

Assessment

 Mental state, mobility, pain, constipation, signs of urinary tract

infection, bladder stones or malignancy, neurological
examination including digital rectal examination (DRE)
 Drug history
 In men, DRE to assess prostate size and characteristics
 In women, perineal examination for genital prolapse

Investigation

 Urinalysis and renal function test

 Imaging of urinary tract (KUB, USG, MRI/CT, cystoscopy, etc.)
should be arranged only if history recurrent urinary tract
Gr 48
infections or suspicious of renal stones, malignancy or other
anatomical abnormalities
 PSA testing could be arranged if symptoms suggestive of
bladder outflow obstruction or if the prostate feels abnormal
during DRE, or there is concerns about prostate cancer. PSA
based screening for healthy elderly men is not recommended
 Do not routinely arrange post void residual (PVR)
measurement, uroflowmetry or urodynamic study at initial
assessment


Management

 to prevent damage to the upper urinary tract by

normalizing voiding and urethral pressures
 no consensus on normal value of PVR. Some advocate the
upper cutoff at 150-250ml.
 In general, urinary drainage by catheter is recommended in
patient with acute urinary retention and
suspected/established spinal cord injury
 The optimal time of trying to wean off catheter (TOWC) is
not clear. Factors including underlying causes, prior
detrusor damage due to over-distension and risk of catheter
related urinary tract infections should be considered
 Numerous drugs have been implicated with urinary
retention (Table).
 Referral for surgical or gynaecological assessment if
suspected underlying malignancy, urethral stricture or
renal stone
 Gr 49
General measures

 Encourage early mobilization and proper toileting

environment
 Adequate pain control and bowel routine
 Medications review

Pharmacological

 Alpha blockers and 5 Alpha reductase inhibitors

 Parasympathomimetics
o Distigimine (Ubretid 5-10mg daily)
 Taken >30 minutes before breakfast
because of the poor absorption and low
bioavailability

Non pharmacological

 Chronic intermittent self catheterization (CISC)

 Long term Foley
 Supra-pubic catheterization
 Surgical intervention
Gr 50
Class Type Examples Mechanisms
Drugs with Anti Anti Psychotic Phenothiazines
cholinergic Thioxanthenes
properties Clozapine
Risperidone
Class I Antiarrhythmic Disopyramide
Flecainide
Antispasmodic Hyoscine
Antiparkinsonian Artane Blockade of
Anti Histamine (H1) Chlorphenamine parasympathetic
Diphenhydramine pathway which
Hydroxyzine impaired detrusor
Promethazine contractility
Loratidine
Bronchodilators Ipratropium
Thiotropium
Drugs for detrusor Oxybutynin
overactivity Tolterodine
Solifenacin
Darifenacin
Anti depressant Tricyclics Amitriptyline Competitive
Imipramine antagonist of
muscarinic receptor
which impaired
detrusor contractility
SSRI Fluoxetine Increase external
Citalopram sphincter activity
SNRI Venlafaxine Increase
Desvenlafaxine external/internal
sphincter activity
Anxiolytics Benzodiazepine Clonazepam Muscle relaxation
Diazepam
Analgesic Opiates Impair bladder
Opioids analogues sensation
Increased sphincter
activity
Alpha agonist Nasal decongestant Phenylephrine Increase internal
Ephedrine sphincter activity
Pseudoephedrine
NSAIDs COX/COX2 inhibitors Naprosyn Inhibit PGE2
Celecoxib synthesis which
suppress micturition
reflex
Calcium Channel Nifedipine Reduce detrusor
blockers Amlodipine contractility
Acknowledgement

Acknowledgement
The Editorial Board would like to thank the Coordinating
Committee (COC) in Internal Medicine for their support and
generous contribution to the publication of this Handbook.

We would also like to extend the heartfelt thanks to all the

colleagues who have made invaluable suggestions to the contents
of Seventh Edition of this Handbook.

Finally, we express our special gratitude to the following

colleagues for their efforts and contribution to the Handbook

Prof Anthony Chan Dr Edwin Hui* Dr KL Lui*

Dr KH Chan* Dr KF Hui Dr Colin Lui*
Dr KK Chan Dr WM Hui* Dr WF Luk*
Dr KH Chan Dr YT Hui* Dr Flora Miu*
Dr KS Chan* Dr Bonnie Kho* Dr CC Mok
Dr NY Chan* Dr Emily Kun Dr Carmen Ng*
Dr YH Chan* Dr Patrick Kwan Dr PW Ng
Dr TN Chau Dr MS Lai * Dr WL Ng
Dr KS Cheng* Dr WC Lao* Dr Winnie Sin*
Dr CM Cheung Dr TW Lam* Dr Loletta So*
Dr Nelson Cheung* Dr ST Law* Dr SF Sze*
Dr Tommy Tang* Dr WS Leung * Dr Owen Tsang*
Dr CH Choi* Dr YY Leung Dr Doris Tse
Dr KW Choi* Dr L Li Dr Winnie Wong
Dr CC Chow Dr KK Li* Dr TC Wu*
Dr MY Chu* Dr Herman Liu* Dr Jonas Yeung*
Dr WC Fong* Dr Patrick Li Dr CW Yim
Dr James Fung* Dr HY Lo Dr Shirley Ying
Dr CP Ho* Dr YT Lo* Prof MF Yuen*
Acknowledgement

Hong Kong Poison Information Centre : Dr Fei Lung Lau*, Dr Yiu Cheung
Chan*

* Doctors involved in updating contents for the 7th edition.

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