Emergency Protocols Book Final

Emergency protocols - 2023
Copyright & Publishing Information
Copyright ©
All rights reserved. No parts of this book may be reproduced or used in any manner
without prior written permission from the copyright owner.
To request permissions, contact the publisher printlineoffset5@gmail.com
First paperback edition 2023.10.17
Chief editor Dr.Ganesha Gethamali Liyanarachchi
Co- Editors Dr.Harendra Karunathilake

Dr.Harsha Sathischandra
Dr.Upul Dissanayake
Dr.Rasika Ranaweerage
Dr.Kugananthan Nirujan
Cover art and Layout design
Dr.Kugananthan Nirujan
Dr.Rasika Ranaweerage
Dr.Chanuka Gunasekara
Dr.Sathilka Dissanayake
Printed by Print Line Offset Printers

877/1, Maradana Road,
Maradana,
Sri Lanka.
i
Authors / Contributors
Consultants
1. Dr. Ganesha Geethamali 8. Dr. Dhanapala Dissanayake

Liyanarachchi 9. Dr. Pradeep Kumarasinghe
2. Dr. Harsha Sathischandra 10. Dr. F. G. Sivagnanam
3. Dr. Harendra Karunathilake 11. Prof. Panduka Karunaratne
4. Dr. Ananda Jayanaga 12. Prof. Ariyaranee Gnanathasan
5. Dr. Upul Dissanayake 13. Prof. Prasad Katulanda
6. Dr. Hasith Wickramasinghe
7. Dr. Manohari Seneviratne
Senior Registrars
1. Dr. Rasika Ranaweerage 11. Dr. Nipun Ranaweera

2. Dr. Kithmal Jayasundara 12. Dr. M.N.S.K. Perera
3. Dr. Kugananthan Nirujan 13. Dr. Udani Dassanayake
4. Dr. Muditha Jayaweera 14. Dr. Devapriya Srikantha
5. Dr. Dulanjalie Bethmiarachchi 15. Dr. R.D.S. Gunarathne
6. Dr. Udeshan Eranthaka 16. Dr. Chamila Pradeep Lankaratne
7. Dr. Sadeve Walathararaachi 17. Dr. A.G.S.Nimesha
8. Dr. Pamini Ramanan 18. Dr. Aharani Kirubaharan
9. Dr. Gayathri Rajeevkumar 19. Dr. Dilushan Porawagamage
10. Dr. Anuke Edirisinghe
Other Contributors
1. Dr. Chanuka Gunesekara (Pre-intern)

2. Dr. Sathilka Dissanayake (Pre-intern)
Cover Page Design
1. Dr. Kugananthan Nirujan

2. Dr. Sathilka Dissanayake
ii
Preface
Towards the end of Covid19 pandemic in 2020 I felt that it would be very useful to have an easy
reference guide for junior doctors in managing medical emergencies. All my colleague consultant
physicians at National Hospital of Sri Lanka, Colombo agreed with me and helped to finalize this
guidance document.
This booklet gives a summary of how to diagnose and manage medical emergencies, in accordance
with the local & international guidelines, using the available resources in local set up. However, it is
emphasized that management need to be tailored to the needs of an individual patient.
As medical knowledge and technology is changing fast, the contents need to be updated at least
every two years.
I sincerely hope this booklet will help to reduce morbidity and mortality in patients admitted to the
medical units in Sri Lanka. Your feedback is much appreciated.
Dr. Ganesha Geethamali Liyanarachchi
MBBS, MD, MRCP (UK), FCCP, FRCP(Lond.)
Consultant Physician
National Hospital of Sri Lanka
ganeshaliyanarachchi@hotmail.com
31.08.2023
iii
Table Of Content
Copyright & Publishing Information ---------------------------------------------------------------------- i

Authors / Contributors--------------------------------------------------------------------------------------- ii
Consultants ---------------------------------------------------------------------------------------------------- ii
Preface --------------------------------------------------------------------------------------------------------- iii
Table Of Content --------------------------------------------------------------------------------------------- iv
Cardiovascular System Related Emergencies ------------------------------------------------------------ 1

Management of Acute Coronary Syndrome (ACS) ----------------------------------------------------2
Management of Acute Heart Failure ---------------------------------------------------------------------6
Management of Hypertensive Crisis ------------------------------------------------------------------- 10
Management of Tachycardia ---------------------------------------------------------------------------- 13
Management of Atrial Fibrillation ---------------------------------------------------------------------- 15
Management of Bradycardia ---------------------------------------------------------------------------- 18
Respiratory System Related Emergencies -------------------------------------------------------------- 19

Management of Acute Asthma Exacerbation -------------------------------------------------------- 20
Management of Exacerbation of COPD --------------------------------------------------------------- 22
Management of Pneumothorax ------------------------------------------------------------------------- 26
Management of Pulmonary Embolism ---------------------------------------------------------------- 30
Endocrine & Metabolism Related Emergencies ------------------------------------------------------- 35

Management of Diabetic Ketoacidosis (DKA) -------------------------------------------------------- 36
Management of Hyperosmolar hyperglycemic state (HHS) --------------------------------------- 40
Management of Hypoglycaemia ------------------------------------------------------------------------ 45
Management of Addisonian Crisis ---------------------------------------------------------------------- 47
Management of Thyroid Storm -------------------------------------------------------------------------- 49
Myxoedema Coma ----------------------------------------------------------------------------------------- 53
iv
Nervous System Related Emergencies ------------------------------------------------------------------ 56

Early Management of Acute Ischaemic Stroke ------------------------------------------------------- 57
Management of Bacterial Meningitis ------------------------------------------------------------------ 64
Management of Status Epileptics ----------------------------------------------------------------------- 67
Management of Myasthenic Crisis --------------------------------------------------------------------- 71
Emergencies Related to Infections ----------------------------------------------------------------------- 76

Management of Sepsis and Septic Shock ------------------------------------------------------------- 77
Management of Neutropenic Sepsis ------------------------------------------------------------------- 83
Toxicological Emergencies --------------------------------------------------------------------------------- 86

Management of Paracetamol Overdose in adults -------------------------------------------------- 87
Management of Organophosphorus poisoning ----------------------------------------------------- 92
Management of Warfarin Toxicity ---------------------------------------------------------------------- 94
Management of Snake Bite------------------------------------------------------------------------------- 97
Gastrointestinal System Related Emergencies-------------------------------------------------------- 100

Management of Hepatic Encephalopathy ---------------------------------------------------------- 101
Management of Upper Gastrointestinal Haemorrhage ----------------------------------------- 104
Management of Acute Liver Failure ------------------------------------------------------------------ 110
Emergencies Related to Electrolyte Imbalances ----------------------------------------------------- 115

Management of Hyperkalemia ------------------------------------------------------------------------ 116
Management of Hypokalemia ------------------------------------------------------------------------- 118
Management of Hyponatremia ----------------------------------------------------------------------- 119
Management of Hypercalcemia ----------------------------------------------------------------------- 123
Management of Hypocalcemia ------------------------------------------------------------------------ 127
v
Emergency protocols - 2023 Cardiovascular system
Cardiovascular System Related

Emergencies
Page | 1
Management of Acute Coronary Syndrome (ACS)

Management algorithm
Presentation
Acute central tightening
type chest pain
Workup
12 lead ECG
Troponin I
No
≥2 contiguous ST segment elevation Algorithm xxx
Yes
STEMI
General measures
1. SpO2 < 90% OR PaO2 < 60 mmHg – Give oxygen

2. Morphine 2-4mg slow IV push every 5-15 mins
3. A mild tranquillizer (usually a benzodiazepine)
should be considered in very anxious patients.
Time to PCI >120 min

≤120 min
(Wire crossing)
Primary PCI Eligible for thrombolysis

(Table 1)
• Aspirin 300mg • Aspirin 300mg

• A P2Y12 inhibitor (Clopidogrel 600mg • A P2Y12 inhibitor (Clopidogrel 300mg
/Ticagrelor 180mg/ Prasugrel 60mg) /Ticagrelor 180mg/ Prasugrel 60mg)
• Atorvastatin 40-80mg • Atorvastatin 40-80mg
No
Rescue PCI
Successful fibrinolysis Fibrinolysis therapy

• Further Mx
• Consider routine PCI Yes
Page | 2
Definitions
1. ST segment elevation
- ST-segment elevation is denoted by the difference between the onset of the Q wave
and the onset of the ST segment (J-point).
- It is considered suggestive of ongoing coronary artery acute occlusion in the following
cases,
a) At least 2 contiguous leads with ST-segment elevation ≥2.5 mm in men < 40 years,
≥2 mm in men ≥ 40 years in leads V2-V3.
b) ST-segment elevation of ≥1.5 mm in women in leads V2-V3 and/or ≥1 mm in the
other leads. (In the absence of LV hypertrophy or LBBB)
c) >= 0.5mm in V7-V9 and other leads.
2. Primary PCI
- Emergent PCl with balloon, stent, or other approved device, performed without
previous fibrinolytic treatment.
3. Rescue PCI
- PCl performed as soon as possible in the case of failed fibrinolytic treatment.
4. Routine PCI
- Coronary angiography, with PCl of the IRA if indicated, performed between 2 and 24
hours after successful fibrinolysis.
5. Successful fibrinolysis
- ST-segment resolution > 50% at 60–90min Algo xx- manage as
- Typical reperfusion arrhythmia relevant condition
- Disappearance of chest pain
Page | 3
Contraindications for fibrinolytic therapy
Table 1
Absolute Relative
Previous intracranial haemorrhage or stroke of Transient ischaemic attack in the preceding 6
unknown origin at any time. months.
Ischaemic stroke in the preceding 6 months. Oral anticoagulant therapy.
Central nervous system damage or neoplasms or Pregnancy or within 1 week postpartum.
arteriovenous malformation.
Recent major trauma/surgery/head injury Refractory hypertension (SBP >180 mmHg
(within the preceding month). and/or DBP >110 mmHg).
Known bleeding disorder (excluding menses). Advanced liver disease.
Aortic dissection. Infective endocarditis
Gastrointestinal bleeding within the past month. Active peptic ulcer.
Non-compressible punctures in the past 24 hours
(e.g. liver biopsy, lumbar puncture).
Fibrinolytic therapy and co-therapies
Table 2
Drug Regimen Remarks
Fibrinolytic therapy
Streptokinase 1.5 million units over 30—60 min IV Previous treatment with
streptokinase within 6 months
ia a contraindication.
Alteplase 15 mg IV bolus
0.75 mg/kg IV over 30 min (up to 50 mg)
then 0.5 mg/kg IV over 60 min (up to 35 mg)
Reteplase 10 units + 10 units iv bolus given 30 min
apart
Tenecteplase(TNK) Single IV bolus: It is recommended to reduce
30 mg (6000 IU) if <60kg to half-dose in patients ≥75
35 mg (7000 IU) if 60 to <70kg years of age.
40 mg (8000 IU) if 70 to <80kg
45 mg (9000 IU) if 80 to <90 kg
50 mg (10000 IU) if ≥90 kg
Antiplatelet co-therapies
Aspirin Loading dose of 150-300 mg orally or of 75-
250 mg IV if oral ingestion is not possible.
Followed by a maintenance dose of 75—100
mg/day.
Clopidogrel For primary PCI,
Loading dose of 600 mg orally, followed by a
maintenance dose of 75 mg/day.
For fibrinolytic therapy, In patients >75 years of age;
Loading dose of 300 mg orally, followed by a loading dose of 75mg
maintenance dose of 75 mg/day.
Page | 4
Prasugrel Loading dose of 60 mg orally, followed by a Contraindicated in patients

maintenance dose of 10 mg/day with
In patients with body weight <60 kg, a dose previous stroke.
of 5 mg/day is recommended. In patients >75 years, prasugrel
is generally not recommended.
Ticagrelor Loading dose of 180 mg orally, followed by a
maintenance dose of 90 mg bd.
Anticoagulant co-therapy
Enoxaparin In patients <75 years of age: The first two SC doses
30mg(0.5mg/kg) IV bolus followed 15min should not exceed 100 mg
later by 1mg/kg SC every 12 hours until per injection.
revascularization or hospital discharge for a Bolus dose of enoxaparin
maximum of 5 days. before thrombolysis has shown
to improve revascularisation
only with TNK.
In patients ≥75 years of age: In patients with eGFR <30
No IV bolus; start with 1st SC dose of 0.75 mL/min/1.73 m2, regardless of
mg/kg with a maximum of 75 mg per age, the SC doses are given
injection for the first two SC doses. once every 24 hours.
UFH 60 IU/kg IV bolus with a maximum of 4000
IU followed by an IV infusion of 12 IU/kg
with a maximum of 1000 IU/hour for 24-48
hours. Target aPTT: 50-70 s or 1.5 to 2.0
times that of control to be monitored at 3,
6, 12 and 24 hours.
References
2017 ESC Guidelines for the management of Acute coronary syndromes in patients
presenting with persistent ST segment elevation.
Page | 5
Management of Acute Heart Failure

Definition
❖ Acute Heart Failure refers to the rapid or gradual onset of symptoms and/or signs of Heart
Failure, severe enough for the patient to seek urgent medical attention, leading to an
unplanned hospital admission or an emergency department visit.
Presentation & Clinical Syndromes of AHF
Dry Wet
Warm
PCWP normal PCWP elevated
CI normal CI normal
PCWP low-normal PCWP elevated
Cold
CI decreased CI decreased
Wet & Warm Dry & Cold Wet & Cold
Acute Right
Pulmonary Cardiogenic
Decompensated Ventricular
oedema shock
HF Failure
Fluid Fluid Increased
redistribution accumulation, central venous Systemic
Main cause of to the lungs and increased pressure and hypoperfusion
symptoms acute respiratory intraventricular often systemic
failure pressure hypoperfusion
Onset Rapid (hours) Gradual (days) Gradual or rapid Gradual or rapid
Diuretics for
Diuretics peripheral
Inotropic agents or congestion
vasopressors Inotropic agents/
Inotropic
(if peripheral vasopressors
Main Treatment hypoperfusion/
agents/
(if peripheral
Diuretics hypotension) vasopressors
hypoperfusion/
Vasodilators Short-term MCS Short-term
hypotension)
or RRT if needed Short-term MCS MCS
or RRT if needed RRT
RRT – Renal Replacement Therapy CI – Cardiac Index

MCS – Mechanical Circulatory Support
PCWP – Pulmonary Capillary Wedge Pressure
Page | 6
Diagnostic evaluation of AHF
A patient suspected of AHF
Initial Investigations Specific evaluation

ECG Coronary angiography
Troponin , Serum
SpO2 (suspected ACS)
Creatinine, Electrolytes,
2D-Echocardiography D dimer/ CTPA
Blood Urea Nitrogen or
Chest X-ray (Suspected pulmonary
Urea, TSH, Liver
Lung USS embolism)
function, ABG, Serum
lactate
Natriuretic peptide testing
BNP <100 pg/mL BNP ≥ 100 pg/mL

NT-proBNP <300 pg/mL NT-proBNP ≥300 pg/mL
MR-proANP <120 pg/mL MR-proANP ≥120 pg/mL
Acute heart failure ruled out Acute heart failure confirmed
Comprehensive echocardiography
BNP = B-type natriuretic peptide

MR-proANP = mid-regional pro-atrial natriuretic peptide
NT-proBNP = N-terminal pro-B-type natriuretic peptide
CTPA = Computed Tomography Pulmonary Angiography
ABG = Arterial Blood Gas
Page | 7
Management of patients with acute decompensated heart failure
Congestion/Fluid overload
No Yes
Hypoperfusion
Loop diuretics (Frusemide)
Consider Inotropes
Loop diuretics (Noreadrenaline0.005 – 0.2mcg/kg/min /
(Frusemide) 20-400mg Dobutamine 5-20mcg/kg/min)
Yes Yes Hypoperfusion and

Congestion relief
congestion relief
No
No
Increase diuretic doses Medical therapy Consider vasopressors

and/or combine diuretics optimization (Norepinephrine)
Management of patients with pulmonary oedema
O2 or Ventilatory support
Yes No
SBP ≥110 mmHg
Loop diuretics Signs of

(Frusemide IV) hypoperfusion
and/or vasodilators (IV Yes No
GTN 10-200 mcg)
Loop diuretics and
Loop diuretics
inotropes/vasopressors
No Yes
Congestion relief
Consider RRT, MCS,

Medical therapy optimization
other devices
MCS = Mechanical Circulatory Support RRT = Renal Replacement Therapy

MCS
1. Ventricular assisting device.
2. Artificial heart
Page | 8
Management of patients with cardiogenic shock
Yes ACS and/or mechanical No

complications
Emergency PCI or Identify and treat other

surgical treatmenta specific causesb
Consider oxygen or Consider inotropes/

Consider short-term MCS
ventilatory support vasopressors
Yes Improvement of hypoperfusion No

and organ dysfunction
Weaning from inotropes/

vasopressors and/or MCS Mechanical Circulatory
Support
AND/OR
Continue aetiological Renal replacement
treatment if needed and therapy
medical therapy optimization
a
PCI in ACS, pericardiocentesis in tamponade, mitral valve surgery in papillary muscle rupture.
In case of interventricular septum rupture, MCS as RRT should be considered.
b
Other causes include acute valve regurgitation, pulmonary embolism, infection, acute
myocarditis, arrhythmia.
References
202
2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.
Page | 9
Management of Hypertensive Crisis

Management protocol for hypertensive emergency
SBP ≥ 180mmHg
AND/OR
DBP ≥ 110mmHg
No Hypertensive
Acute End organ damage
Urgency
Yes
Hypertensive Emergency
CVS Renal CNS

Presentation
Chest pain Haematuria Confusion
Back pain Reduced UOP Acute focal
Orthopnea neurological signs
PND Seizers
12 Lead ECG RFT,UFR/UPCR,

Workup Troponin I SE, Renal USS, NCCT Brain
BNP Renal artery MRI Brain
2D Echo doppler
DDs Acute cardiogenic

Aortic
pulmonary Ischaemic Intracranial Hypertensive
ACS AKI
dissection stroke haemorrhage encephalopathy
oedema
DOC Nitroglycerin Nitroprusside

Nitroglycerin Labetalol Nicardipine Labetalol
Nitroprusside Esmolol Labetalol
Labetalol Nitroprusside Labetalol Nitroprusside
Loop diuretics Labetalol
Target SBP <140 mmHg & ↓ MAP 20-25% Eligible for SBP <140 ↓ MAP
SBP <140 mmHg
HR < 60 bpm Over several Thrombolysi mmHg 20-25%
Immediately
Immediately hours s? over 1-2 h Immediately
No guideline)
Yes
BP <220/120 BP <185/110 BP
mmHg mmHg <180/105mm
Immediately Hg later
Immediately
Page | 10
Definitions
➢ Severe/ Grade 3 hypertension - SBP > 180 mmHg and/ or DBP > 120/110 mmHg
(No need for a second visit or ABPM; confirm with a repeated measure in 15 min)
➢ Hypertensive urgency - Severe hypertension without new or progressive

target organ damage.
➢ Hypertensive emergency - Severe hypertension with new or progressive target organ

damage. End organ damage with even BP <180/120 mmHg
can be considered.
Management of hypertensive urgency
• Target – <160/100 mmHg (in very high; 25 % reduction)

• Time duration – over 4 hours to days.
(Individual targets – those with a risk of imminent CV event, lower and
faster blood pressure reduction)
• Drugs – Oral drugs preferred
▪ Captopril – start 25 mg daily up to 150mg/day
▪ Amlodipine – 2.5 mg/day up to 10 mg/day
▪ Other first-line drugs (combinations are preferred)
• Other measures
▪ Explain to patient
▪ Keep in a quiet environment
▪ Salt restriction
• Monitoring
▪ For symptoms of target organ involvement,
▪ blood pressure, heart rate, lung auscultation, fluid balance
• Long term blood pressure target - 140/90 or 130/80 mmHg
• Plan discharge-
a. Antihypertensive
i. Those on treatment
- Reinstitution of prior medications (avoid drugs causing rebound
hypertension in non-adherents),
- Increase the dose of existing medications, and addition of
diuretics.
ii. Untreated hypertension
- Depending on intrinsic and extrinsic factors
- Start - BB/CCB/ACEI/ARB/diuretics etc.
- Combination of two drugs preferred.
b. Diet- low salt diet, keep in a quiet room
c. Review plan
Page | 11
Drug regimens for hypertensive crisis
Drug Regimen
Labetalol 10-20 mg bolus initially over 1 min. Then IV 2mg/min infusion (max 2.4
g/day). Repeated in 5 min, with increasing the dose (max 200)
Nicardipine IV 3-5 mg/hour, increase 1mg every 15 min
(Max-15mg/hour)
Nitroprusside IV 0.3-1.5 mcg/kg/min infusion,
Adjust 0.5 mcg/kg/min every 5 min (Max 10 mcg/kg/min)
Nitroglycerine IV 10-200mcg/min infusion
(Max per dose- 400 mcg/min)
Loop diuretics IV Bolus 50-100 mg, infusion start 5mg/hour,
(Max-1.5 g/day)
Metoprolol IV 5 mg over 5 min.
Repeated every 5 min to a max dose of 10-15 mg
Magnesium For prevention of seizures in preeclampsia
sulfate 4g (diluted in 250 mL NS/D5W) IV loading dose & 1-2 g/hr IV
May administer q4hr as necessary.
• If sympathetic overactivity is suspected.

o Eg: In following conditions,
1. Alfa 2 agonist/beta blocker withdrawal
2. Ingestion of sympathomimetic (methamphetamine, cocaine)
3. Pheochromocytoma
In sympathetic overactivity,
1. Avoid beta-blockers alone. (Except in beta-blocker withdrawal).

2. Use alfa blockers first line- (Phentolamine- 5 mg IV repeat if necessary q2-4hr up to 15
ml) and use labetalol or nitroprusside.
REFERENCES
1) 2020 AHA guideline- Global Hypertension Practice Guideline

2) 2018 ESC/ESH Guidelines for the management of arterial hypertension
Page | 12
Management of Tachycardia
Assess ABCD
• Give oxygen if SpO2 < 94%, IV assess
• Monitor ECG, SpO2, vitals
• Identify and treat reversible causes,
- Hypovolaemia
- Electrolyte imbalance
- Hyperthyroidism
- Hypoxia
- Hypotension
Life-threatening feature UNSTABLE

(Not sinus rhythm)
1. Shock Yes
2. Syncope Synchronized
3. Myocardial infarction DC shock (100J)
4. Severe heart failure Up to 3 shocks
No
No Is QRS narrow ? Yes
(<0.12s/3 small boxes)
Broad QRS Narrow
QRS
Regular Irregular Regular Irregular
Use vagal maneuvers Rate control (<110)

If VT If AF with BBB IV metoprolol 5-15 mg
Adenosine 6 mg rapid IV verapamil 5-10 mg
Amiodarone Tx as narrow IV bolus with Saline (Both over 2 min)
Procainamide
complex push.
If SVT If Polymorphic If unsuccessful, If heart failure
Same as regular give 12 mg IV Digoxin
VT (Load 0.75-1mg over 2 h
narrow complex If unsuccessful - give
IV Magnesium further 12 mg IV route)
(Verapamil) Amiodarone
2g over 10 min (CI- Hypotension, BA)
(Cautious- WPW)
Anticoagulation
If unsuccessful
Amiodarone If unsuccessful
or If unsuccessful IV verapamil
Procainamide or
DC shock (syn)
(If not given) IV metoprolol
CI- Contra Indications
Page | 13
Synchronized DC shock
▪ Sedation or anaesthesia if conscious
- Midazolam - 1mg IV every 3-5 minutes up to adequate sedation (maximum 5 mg)
- Fentanyl -1 mcg/kg/dose up to 50 mcg/dose every 3 minutes, titrating to effect
▪ Start with ~ 100 J initially (in AF/SVT 70- 120 J; VT with pulse 120- 150 L)
▪ Escalate by 50J subsequently
▪ If unsuccessful,
- Amiodarone 150mg IV over 15-20 min, or procainamide 15-18 mg/kg over 20 min
- Repeat synchronized shock
Vagal Stimulation
▪ Try at least 2 different maneuvers twice.
▪ Modified Valsalva
- Normal inspiration, strain in expiration for 15 sec
▪ Carotid sinus massage
- 5s on each side, R/S first, in front on C3
- Contra Indicated - in elderly, bruits, CVS disease
Adenosine
▪ The mean dose required is ∼6 mg.
▪ Dosing should then be incremental, starting at 6 mg in adults followed by 12 mg.
▪ Repeat administration is safe within 1 min of the last dose.
▪ To achieve efficient rhythm correction, injection should be as a rapid bolus with immediate
saline flush.
▪ Large, centrally located (e.g., antecubital) veins are likely to deliver more effective drug
concentrations to the heart than smaller distal veins
▪ Transient dyspnoea, facial flushing, increased skin temperature and chest pain (Ischaemic
or oesophageal origins) reported.
Procainamide
▪ Loading dose: 100-200 mg/dose or 15-18 mg/kg
▪ Infuse slowly over 25-30 min not to exceed 50 mg/min
Amiodarone
▪ Dose 5mg/kg ~ (150mg) in 5% dextrose 250 ml
▪ Infused over 15-20 min.
Digoxin
• 0.5mg repeated in 6hours. Max 1.5mg/24
• Load 0.75-1mg over 2 h IV route
Reference
1. 2019 ESC Guideline supraventricular tachycardia
Page | 14
Management of Atrial Fibrillation

A. Assessment and risk stratification
Yes
Is the patient unstable? Urgent ECV
No Start heparin/ NOAC as soon as possible.
UFH- 70 U/Kg bolus & 15 U/Kg/hr
Adequately anticoagulated >3 weeks LMVH 1mg/kg bd
Yes No
Valvular disease/ prior TE No Onset < 12 h

AND
(Can wait for delayed cardioversion)
onset > 48 h / unknown
No Yes
Yes
Onset 12-48h ago AND CHA₂DS₂-VASc < 1M/2F

(If < 24 h can wait for delayed cardioversion)
No Yes
Cleared by TOE
Safe Rhythm Control
Rate control
Start NOCA/Heparin as soon as possible.UFH- 70U/kg
bolus & 15U/kg/hr
IV Diltiazem-Bolus dose: 0.25 mg/kg LMVH-1mg/kg bd
(actual body weight) over 2 minutes Amiodarone - IV
(average dose: 20 mg) Dose 5mg/kg ~ (150mg) in 5% dextrose 250
IV Verapamil- Bolus: Initial: 5 to 10 mg over ≥2 ml, infused over 15-20 min
minutes; if there is inadequate response, dose may No Yes Procainamide - IV
be repeated after 15 to 30 minutes.
Loading dose: 100-200 mg/dose or 15-18
mg/kg; infuse slowly over 25-30 min not to
IV metoprolol- 2.5 to 5 mg over 2 minutes;
exceed 50 mg/min; may repeat q5min PRN
repeat dose every 5 minutes as needed.
not to exceed 1 g Maintenance: 1-4 mg/min
maximum total dose: 15 mg.
by continuous IV infusion
Propafenone- Oral
Yes 150 mg tds
Target < 110 Ablation
Symptoms
Symptoms Deteriorating LV function
Deteriorating LV function Target < 80
Cardiomyopathy
CRT Pacing not achieved in CRT
Valvular disease- Mitral stenosis (moderate-severe) TE- thromboembolism

TOE- transesophageal echo ECV-electrical cardioversion
NOAC- newer oral anticoagulants UFH-unfractionated heparin
CRT- cardiac resynchronization therapy LMVH-enoxaparin
Page | 15
B. Rate or Rhythm control
Rate control Rhythm control

Preferred in, Preferred in,
1. Young
1. Background Tx in all AF.
2. 1st AF
2. Firstline in minor/no
3. Tachycardia-mediated
symptoms. cardiomyopathy
3. After failure of rhythm control. 4. No/few comorbidities
4. When risks of restoring SR 5. Rate control difficult to achieve
outweigh the benefits. 6. AF precipitated by a temporary
event (acute)
7. Patient’s choice
Choice of drug for rate control
Assess None HFrEF Asthma/COPD Pre-excited AF

comorbidities
First line Beta blocker Beta NDCC Ablation

NDCC blocker (AV node)
Suboptimal response Rate>110/ symptomatic
Beta blockers
Digoxin
and/ or NDCC
and /or
Second line Digoxin and /or
Beta blockers
Digoxin Digoxin
and/ or
and /or
NDCC
Amiodarone
Combination of three drugs

Third line CRT
AV node ablation
1) Beta blockers
o IV Metoprolol-2.5-5mg over 2 min, 5 mg after 5 min if needed.
(total dose not to exceed 15mg)
o Bisoprolol- 2.5- 5 mg PO (Heart failure- 1.25mg)
2) NDCC (Non-dihydropyridine Calcium Channel Blockers)
o IV Verapamil-2.5-5mg over2 min, 5-10mg dose can be repeated after 15-30 min
Page | 16
3) Digoxin
- Loading dose-0.75-1mg IV given over at least 2 hours, following day maintenance dose
125- 250 mcg/day
4) Synchronized DC shock
- Sedation -Midazolam- 1mg IV every 3-5 minutes (max 5 mg/5 times) or Fentanyl -
1 mcg/kg/dose up to 50 every 3 minutes.
- Start with ~ 100 J initially (70- 120 J) Escalate by 50J subsequently
- If unsuccessful, - Amiodarone 150mg IV over 105-20 min, or procainamide 15-18 mg/kg
over 20 min.
C. Stroke Prevention
Long term OAC If OAC started,

For all CHA₂DS₂-VASc >1M/2F Initiate NOAC in ED.
AF with TIA/Stroke Warfarin if
AF-MS/mechanical valve/repair ▪ NOAC not available
▪ CrCl < 30
Short term (1month) OAC,
▪ Prosthetic valve
Post cardioversion if
CHA₂DS₂-VASc < 0M/1F
(Optional if AF < 24 hr)
D. Disposition and follow-up
❖ Hospital admission
- All patients specially; ACS, CHF not improved, Symptomatic.
❖ Discharge from ED
- Quickly after CV or effective rate control - send to ward
❖ Investigations and follow up
- Arranged to look for underlying cause, follow up for OAC and treatment.
References
1. 2020- ESC Guideline (AF)

2. 2019 ACC/AHA Guideline (AF)
Page | 17
Management of Bradycardia
Assess with ABCD approach
Give oxygen if SpO2 < 94% and IV access

Monitor ECG, BP, SpO2, 12 lead ECG
Identify and treat reversible causes (4H, 4T)
- hypoxia, hypothermia, heart block,
hyperkalaemia, hypothyroidism
- Poison-OP/Digitalis/Kaneru/BB/CCB
Life-threatening features
Yes Shock No
Syncope
Myocardial ischaemia
Severe heart failure
Atropine 0.6 mg IV Risk of asystole?

Recent asystole
Mobitz ii AV bloc
Yes
Satisfactory response? Complete heart block with
broad QRS
No
Ventricular pause > 3 s
Yes No
Consider interim measures:
1. Atropine 0.6 mg IV repeat to maximum of 3
mg
2. Isoprenaline 5 mcg/min IV- infusion
3. Adrenaline 2-10 mcg/min IV-infusion Observe
Alternative drugs
4. Glucagon: 5-10 mg over 1-2 min
5. Bolus dopamine: 2-5 mcg/Kg/min- infusion
1. ❖Transcutaneous pacing
Bradycardia work up
❖ Get EP/Cardiology opinion
References
1. 2018 ACC/AHA/HRS Guideline
2. 2021 UK resuscitation council- adult bradycardia
Page | 18
Emergency protocols - 2023 Respiratory system
Respiratory System Related Emergencies
Page | 19
Management of Acute Asthma Exacerbation

Assess the patient
Is it asthma?
Factors for asthma related death?
Severity of exacerbations?
Mild or Moderate Severe Life Threatening
▪ Talk in phrases ▪ Drowsy

▪ Talk in words ▪ Confused
▪ Prefers sitting
▪ Sit hunched forward, ▪ Silent chest
▪ Respiratory rate increased
▪ Agitated
▪ Accessory muscles not
▪ Respiratory rate >30/min
▪ used
▪ Accessory muscles in use
▪ pulse rate 100 120 bpm
▪ Pulse rate >120 bpm
▪ O2 saturation (on air) 90-
▪ O2 saturation (on air) <90%
95%
▪ PEF =< 60% predicted or best
▪ PEF >60% predicted or best
Start treatment Transfer to HDU/ Acute cubicle

▪ SABA 4 10 puffs by MDI + ▪ Nebulized bronchodilators Salbutamol
spacer. Worsening 5mg and ipratropium bromide 0.5 mg via
▪ Repeat every 20 mins for oxygen derived nebulizer (every 20 min
1hr. for 1st hour)
▪ Prednisolone 40-50mg oral ▪ Controlled low flow oxygen with target
▪ Controlled oxygen. SpO2 93-95%
▪ Target SpO2 93 95%. ▪ Oral prednisolone 40-50 mg or IV
hydrocortisone 200mg
Improving
▪ IV Mgso4 2g infusion over 20 min (single
dose only)
Continue treatment
Worsening
▪ With SABA as needed
▪ Assess response at 1hr
(or earlier)
Page | 20
Key Points
❖ Though nebulization is aerosol generating procedure and precipitate infection spreading it

is recommended as first line in severe and life-threatening asthma as SABA MDI has low
evidence in both situations.
❖ Oral and systemic glucocorticoid has similar efficacy in asthma management.
❖ IV glucocorticoid can specially use in patients with severe dyspnoea, swallowing difficulties,
vomiting and on non-invasive ventilation.
❖ Chest radiographs are only indicated when complication (pneumothorax) or alternative

diagnosis is suspecting.
❖ When PEF <50%, patient is not responding to initial treatments or deteriorating Arterial
blood gas (ABG) analysis should carried out.
❖ PaO2 <60mmhg and pCO2 >45mmHg consider as respiratory failure.
❖ Non-invasive ventilation has no or minimal place in asthma management.
❖ The decision to intubate and initiate mechanical ventilation is clinical.
❖ Aminophylline, IV salbutamol has no place in acute severe asthma management.
References
1. GINA 2021 update

2. UpToDate
Page | 21
Management of Exacerbation of COPD

Definition & Classification
An exacerbation of chronic obstructive pulmonary disease (COPD) is defined as an acute worsening

of respiratory symptoms that needs in additional therapy.
Symptoms
▪ Increased dyspnoea
▪ Increased sputum purulence
and volume
▪ Increased cough and wheeze
Exclude other DDs
▪ Pneumonia
▪ Pneumothorax
▪ Pleural effusion
▪ pulmonary embolism
▪ pulmonary oedema
▪ cardiac arrythmias
Acute respiratory failure Acute respiratory failure

No respiratory failure
Non-life threatening Life threatening
▪ RR 20-30 breaths per ▪ RR > 30 breaths per ▪ RR> 30 breaths per minute.
minute. minute. ▪ Using accessory respiratory
▪ No use of accessory ▪ Using accessory respiratory muscles.
respiratory muscles. muscles. ▪ Acute changes in mental
▪ No changes in mental ▪ No change in mental status.
status. status. ▪ Hypoxemia not improved
▪ Hypoxemia improved ▪ Hypoxemia improved with with supplemental oxygen via
with supplemental oxygen via Venturi mask > Venturi mask or requiring
oxygen given via 35% FiO2. FiO2 > 40%.
Venturi mask 24-35% ▪ PaCO2 increased compared ▪ PaCO2 increased compared
FiO2. with baseline or elevated with baseline or elevated > 60
▪ No increase in PaCO2. 50-60 mmHg. mmHg or the presence of
acidosis (pH ≤ 7.25)
Page | 22
Management of severe but not life-threatening exacerbations
1) Assess severity of symptoms, blood gases, chest radiograph.
2) Administer supplemental oxygen therapy.

• Obtain serial arterial blood gas, venous blood gas and oximetry measurements.
• Supplemental oxygen should be titrated to improve the patient’s hypoxemia with a target
saturation of 88-92%.
• Once oxygen is started, blood gases should be checked frequently to ensure satisfactory
oxygenation without carbon dioxide retention and/or worsening acidosis.
3) Bronchodilators
• Increase doses and/or frequency of short-acting bronchodilators
• Salbutamol 5mg and ipratropium 0.5mg by using air driven nebulizers
• Use spacers or air-driven nebulizers when appropriate (air driven prefer in more ill
patients)
4) Consider oral corticosteroids

• A dose of 40 mg prednisone per day for 5 days is recommended
• Therapy with oral prednisolone is equally effective to intravenous administration
5) Consider antibiotics when symptoms of bacterial infection are present

• 3 cardinal symptoms;1. increase in dyspnoea, 2.sputum volume, and 3.sputum
purulence.
• The recommended length of antibiotic therapy is 5-7 days.
• The choice of the antibiotic should be based on the local bacterial resistance pattern.
• Usually, initial empirical treatment is an aminopenicillin with clavulanic acid, macrolide,
or tetracycline.
• In patients with frequent exacerbations, severe airflow limitation and/or exacerbations
requiring mechanical ventilation, cultures from sputum or other materials from the lung
should be performed, as gram-negative bacteria (e.g., Pseudomonas species) or resistant
pathogens that are not sensitive to the above-mentioned antibiotics may be present.
• The route of administration (oral or intravenous) depends on the patient’s ability to eat
and the pharmacokinetics of the antibiotic, although it is preferable that antibiotics be
given orally.
6) Consider non-invasive mechanical ventilation (NIV)
7) At all times:
• Monitor fluid balance.
• Consider subcutaneous heparin or low molecular weight heparin for thromboembolism
prophylaxis.
Page | 23
8) Identify and treat associated conditions

• e.g., heart failure, arrhythmias, pulmonary embolism etc.
Indications for Non-invasive Mechanical Ventilation (NIV)
❖ At least one of the following:

1. Respiratory acidosis. (PaCO2 more than 6.0kPa or 45mmHg and arterial pH <7.35)
2. Severe dyspnoea with clinical signs suggestive of respiratory muscle fatigue, increased
work of breathing, or both, such as use of respiratory accessory muscles, paradoxical
motion of the abdomen, or retraction of the intercostal spaces.
3. Persistent hypoxemia despite supplemental oxygen therapy.
Indications for respiratory or medical intensive care unit admission
• Severe dyspnoea that responds inadequately to initial emergency therapy.

• Changes in mental status (confusion, lethargy, coma).
• Persistent or worsening hypoxemia (PaO2 < 5.3kPa or 40mmHg) and/or severe/worsening
respiratory.
• Acidosis (pH < 7.25) despite supplemental oxygen and non-invasive ventilation.
• Need for invasive mechanical ventilation.
• Hemodynamic instability – need for vasopressors.
Indications for invasive mechanical ventilation
• Unable to tolerate NIV or NIV failure.

• Status post respiratory or cardiac arrest.
• Diminished consciousness, psychomotor agitation inadequately controlled by sedation.
• Massive aspiration or persistent vomiting.
• Persistent inability to remove respiratory secretions.
Those who need ventilatory support due to respiratory distress and have one of the
following
1. Severe hemodynamic instability without response to fluids and vasoactive drugs.

2. Severe ventricular or supraventricular arrhythmias.
3. Life threatening hypoxemia in patients unable to tolerate NIV.
Page | 24
Non-invasive Mechanical Ventilation (NIV)
• Non-invasive ventilation NIV is standard early therapy for hypercapnic ventilatory failure
during exacerbations of COPD.
• Ensure patients started on NIV have a plan in the event of deterioration.
(Agreed ceiling of care)
• NIV takes two forms CPAP and BiPAP (which may be more suitable for treating type II
respiratory failure in COPD)
• Both CPAP and BiPAP have been used to treat acute cardiogenic pulmonary oedema.
• The positive airway pressure is delivered by a tightly adhered face mask, which is sized to
fit the patient.
• The patient is awake and must be compliant with wearing the mask.
• Unlike tracheal intubation, NIV does not protect the airway, so coma and vomiting are
contraindications.
• Absolute contraindications include apnoea and cardiac arrest.
• Check CXR before starting (a pneumothorax will be converted into a tension pneumothorax
with NIV).
• Severe agitation may make effective NIV impossible.
• The patient should always be cared for by staff who are familiar with the ventilator and
mask.
• Start BiPAP at 10cmH2O inspiratory positive airway pressure (iPAP)/ 5cmH2O expiratory
positive airway pressure (EPAP) and titrate upwards.
• To treat persistent hypercapnia, increase IPAP by 2cmH2O at a time.
• To treat persistent hypoxia, increase IPAP and EPAP by 2cmH2O at a time.
• The maximum IPAP/ EPAP is 25/15cmH2O.
• For CPAP, commence treatment at 5-8cmH2O.
Reference
1. Gold report 2022
Page | 25
Management of Pneumothorax
• Air in the pleural space Pneumothorax
• In apparently normal lungs -primary pneumothorax
• In the presence of an underlying lung
disease-secondary pneumothorax
Spontaneous Traumatic
• Could be spontaneous or traumatic
• Risk factors—Smoking ,familial ,connective tissue
diseases related
Iry II ry
Clinical features
• Symptoms-Acute onset pleuritic type chest pain and/or breathlessness

• Signs-tachycardia, reduced chest expansion, hyper-resonant percussion note,
reduced breath sounds on the affected side, features of subcutaneous emphysema
Investigations
1. Chest x ray
▪ Diagnostic test.
▪ A visible lung edge and absent lung
markings peripherally.
▪ Size of pneumothorax is determined
according to the width of rim of air
surrounding the lung on CXR (measured
at the level of the hilum)
- If <2cm or 2cm - small
- If >2 cm - large
▪ CXR may also show features of the underlying lung disease.
2. CT chest
▪ To differentiate pneumothorax from bullous disease.
3. USS chest
▪ Acute trauma situations (decreased pleural sliding)
4. ABG
▪ Hypoxia and hypercapnia in secondary pneumothoraces.
Page | 26
Initial management
• Determine whether primary or secondary. (Patient with a lung disease, or age

more than 50 with significant smoking history).
• Management is determined by
I. The degree of breathlessness and hypoxia
II. Hemodynamic compromise
III. Presence and severity of underlying lung disease
IV. CXR pneumothorax size
Spontaneous Pneumothorax
Bilateral
Yes
AND / OR Chest drainage
Haemodynamically unstable
No
Look for features of

secondary causes
No ▪ Age > 50 Yes
▪ Significant smoking hx
▪ Evidence of underlying lung
disease
Primary Pneumothorax Secondary Pneumothorax
Size > 2 cm Size > 2 cm

Yes Yes
AND / OR Aspirate < 2.5L AND / OR
Breathless Breathless
No No
Size < 2 cm Yes
Aspirate < 2.5L Size 1-2 cm
AND
Breathing improved No
Yes
Yes No Size > 1 cm
No
Consider discharge. High flow O2

Review in OPD in 2-4 (Unless O2 sensitivity
Chest drainage
weeks. suspected)
Observe for 24h.
Page | 27
1) Aspiration
▪ Second intercostal space in midclavicular line, just above the upper border of the
rib, insert large bore 16G cannula, remove the inner needle, connect to a 3 way
tap via 50 ml syringe, with the tap turned on to the patient, aspirate air into
syringe, turn tap off and expel sir into atmosphere, repeat until resistance felt or
2.5L air aspirated.
▪ Halt if patient coughs excessively, do not aspirate more than 2.5 L of air, as it
suggests an air leak and aspiration is likely to fail.
▪ Aspiration is successful if the lung is fully or nearly re-expanded on CXR and if
patient feels symptomatically better.
▪ If initial aspiration of a primary pneumothorax fails, a chest drain is required.
2) Chest drainage
▪ Small(10-14 F) drains are sufficient in most cases.
▪ Large bore ones are considered in secondary pneumothorax with large air leak,
severe subcutaneous emphysema or in mechanically ventilated patients.
▪ Never clamp a bubbling chest drain. (Risk of tension pneumothorax)
▪ If the level in drain does not swing with respiration, the drain is either kinked,
blocked, clamped, or incorrectly positioned. (Check via CXR)
3) Oxygen
▪ All hospitalised patients should receive oxygen support (high flow- 10L per min)
except where CO2 retention is a problem(speeds up resolution of pneumothorax).
4) Surgical Management
▪ Indications for cardiothoracic referral,
- Second ipsilateral pneumothorax
- First contralateral pneumothorax
- Bilateral spontaneous pneumothorax
- Persistent air leak or failure of lung to re-expand (3-5 days of drainage)
- Spontaneous haemothorax
- Professions at risk after first pneumothorax (pilots, drivers)
Page | 28
5) Tension pneumothorax
▪ Presents with respiratory distress, agitation, hypotension, elevated JVP, tracheal
deviation.
▪ Give high flow oxygen.
▪ Do not wait for CXR.
▪ Insert large bore cannula into 2nd intercostal space in mid clavicular line on the side
of the pneumothorax.
▪ Aspirate until patient is less distressed and then insert chest drain in safe triangle.
6) Outpatient care
▪ Smoking cessation.
▪ Discuss risk of recurrence.
▪ Recommend not to fly for at least 1 week from the resolution of spontaneous
pneumothorax on CXR.
▪ Never to dive.
References
British Thoracic Society (BTS) guidelines on pneumothorax 2022.
Page | 29
Management of Pulmonary Embolism

Clinical Presentation
Dyspnoea
Chest pain Moderate risk factors
(Tightening or Pleuritic)
Presyncope or Syncope 1. Arthroscopic Knee Surgery
Strong risk factors 2. Auto-Immune Disease
Haemoptysis
1. Fracture of Lower Limb Shock 3. Central lines & IV cannulae
2. Heart Failure or Atrial 4. Chemotherapy
Fibrillation/Flutter 5. Congestive heart failure/
(Within 3 months) respiratory failure
3. Hip/Knee Replacement 6. Erythropoiesis stimulating
4. Major Trauma agents.
5. Myocardial Infarction 7. Hormone replacement
(within 3 months) therapy
6. Previous VTE 8. Oral contraceptive therapy
7. Spinal Cord injury 9. Cancer
Suspect Pulmonary 10. Pregnancy/Postpartum
Embolism period
11. IBD
Is there haemodynamic instability?

Cardiac arrest Obstructive shock Persistent hypotension
Systolic BP < 90 mmHg SBP < 90 mmHg or SBP drop > 40,
Need for cardiopulmonary And lasting longer than 15 min.
resuscitation. End-organ hypoperfusion (Not caused by new-onset arrhythmia,
(Altered mental status; cold, hypovolaemia, or sepsis.)
clammy skin; oliguria/anuria)
Present Absent
Suspected PE in a patient with Suspected PE in a patient

haemodynamic instability without haemodynamic
instability
Page | 30
Suspected PE in a patient with haemodynamic instability
Initial stabilization
• Advanced life support in cardiac arrest

• if SpO2 < 90% -> High flow nasal O2, mechanical ventilation if needed.
• Administer herapin 80 IU/kg i.v.
• ECG: exclude ACS, look for RV strain
• Ringer’s lactate or normal saline 200–500 ml IV over 15-30 min
Bedside 2D Echo
Absent Present
RV Dysfunction
Yes
Search for other causes of No CTPA immediately

shock or instability available and feasible
Yes
Confirmed PE
Reperfusion therapy CTPA
No PE
Search for other causes of

shock or instability
Page | 31
Suspected PE in a patient without haemodynamic instability
Clinical probability of PE
Modified Well’s criteria

(Table 1)
Low or intermediate clinical High clinical probability or

probability or PE unlikely PE likely
D-dimer CTPA
Test
Negative Positive
CTPA
No PE Confirmed PE No PE
No treatment No treatment or
Anticoagulation
investigate further.
Page | 32
Treatment modalities
1) Acute right ventricular failure
a) Volume optimization
- Cautious volume loading, saline or Ringer’s lactate <= 500ml over 15-30
minutes
b) Vasopressor and inotropes
- Norepinephrine 0.2 – 1.0 mg/kg/min
- Dobutamine 2 – 20 mg/kg/min
c) Mechanical circulatory support
- Veno arterial ECMO/extra corporeal life support
2) Reperfusion treatment
• Greatest benefits when initiated within 48 hours of symptom onset
• But still useful up to 6-14 days.
• Unsuccessful thrombolysis is judged by persistent clinical instability & unchanged RV
dysfunction on 2D ECHO after 36 hours.
Systemic thrombolysis
a) rtPA (Alteplase)
- 100mg over 2hours
- Accelerated regimen : 0.6mg/kg over 15min (maximum 50mg)
b) Streptokinase 250,000 IU – 30 min
- 100,000 IU/Hour over 12-24 hour
- Accelerated regimen : 1.5m IU over 2hour
Other modalities
c) Percutaneous catheter directed treatment
d) Surgical embolectomy
e) Venacava filters
3) Anti coagulation in acute stage

• High/ intermediate clinical probability of pulmonary embolism.
• Anticoagulation should be initiated while awaiting the diagnostic test.
a) Lower molecular weight heparin subcutaneous 1mg/kg bd
b) Fondaparinux – 7.5mg subcutaneous daily
c) Unfractionated heparin infusion
- Overt haemodynamic instability.
- Imminent haemodynamic decompensation in whom primary reperfusion
treatment will be necessary.
- Serious renal impairment CrCl < 30 ml/min
- Severe Obesity
Page | 33
d) Non vitamin K antagonist oral anticoagulant (NOAC)

- High dose Apixaban for 7 days 10mg orally bd followed by 5mg bd
- Rivaroxaban for 3 weeks – 15mg orally bd followed by 20mg daily
4) Vitamin K antagonist
• INR 2.0 – 3.0 for 2 consecutive days up to that parallel continue UFH, LMWH or
fondaparinux.
• Younger otherwise healthy < 60 Years warfarin 10mg can be started.
• Less than or equal to 5mg in patients more than 60 years.
Appendix
Table 1 – Modified Well’s criteria
Criteria Score
Clinical signs or symptoms of DVT 3
Alterative diagnosis less likely than PE 3
Clinical probability
Heart rate >100 bpm 1.5
Three-level score Two-level score
Immobilization (>3 days) or surgery in 1.5 Low 0-1 PE unlikely 0-4
last 4 weeks Intermediate 2-6 PE likely ≥5
Previous history of DVT or PE 1.5 High ≥7
Haemoptysis 1
Active cancer within the last 6 months 1
References
1. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism
2. American Society of Hematology 2020 guidelines for management of venous thromboembolism
3. British Thoracic Society guidelines for the management of suspected acute pulmonary
embolism
Page | 34
Emergency protocols - 2023 Endocrine & Metabolism
Endocrine & Metabolism Related

Emergencies
Page | 35
Management of Diabetic Ketoacidosis (DKA)
• Diabetic ketoacidosis is a state of uncontrolled catabolism associated

Patho-physiology
with marked insulin deficiency and elevated counter-regulatory

hormones, which accelerate the effects of insulin deficiency.
• The most important biochemical abnormality in DKA is uncontrolled
lipolysis in adipose tissue and uncontrolled ketogenesis in the liver.
1. Nausea, vomiting, and abdominal pain are general symptoms

Features
Clinical
2. Other symptoms include increased thirst and urination.

3. Kussmaul’s breathing(laboured deep breathing) and fruity odour are
specific signs.
Precipitating Factors
1. Inadequate insulin treatment or noncompliance

2. New-onset diabetes (20 to 25%)
3. Acute illness (Infection, Stroke or TIA, Myocardial infarction, Acute
pancreatitis)
4. Drugs (Clozapine or olanzapine, Cocaine, Lithium, SGLT2 inhibitors,
Terbutaline)
1. Capillary blood glucose level above 11 mmol/ L (200 mg/dL)

Diagnosis
2. Venous pH less than 7.3 / bicarbonate less than 15 mmol/L

3. Urine ketone ++ or more / capillary ketones above 3 mmol/L
* All three must be present.
The presence of one or more of the following may indicate severe DKA:
▪ GCS less than 12 or abnormal AVPU scale
Assessment of severity
▪ Oxygen saturation below 92% on air (assuming normal baseline

respiratory function)
▪ Systolic BP below 90 mmHg
▪ Pulse over 100 or below 60 bpm
▪ Venous/arterial pH below 7.0
▪ Bicarbonate level below 5.0 mmol/L
▪ Blood ketones over 6.0 mmol/L
▪ Hypokalaemia on admission (under 3.5 mmol/L)
▪ Anion gap above 16 [Anion Gap = (Na+ + K+) – (Cl- + HCO3-)]
A-Alert V-Voice P-Pain U-Unresponsive
Page | 36
Immediate Management (T =
Actions
1. Restoration of circulating volume. (T=0) (Box 1)
0 to 60 min) 2. Commence a fixed-rate intravenous insulin infusion (FRIII) (Box 2)
3. Potassium replacement (Box 3)
4. Assessment of the patient
5. Further investigations
▪ Blood ketones, venous plasma glucose, Urea and electrolytes, VBG,
FBC, inflammatory markers, blood cultures, urinalysis, and culture.
▪ ECG and Chest radiograph as clinically indicated.
Aims :
After Stabilization (T = 60 min to 6 hours)
1. Bicarbonate rise > 3 mmol/L/h or fall of blood glucose level > 3

mmol/L/h or fall of ketones at least 0.5 mmol/L/h.
2. Maintain potassium in normal range.
3. Avoid hypoglycaemia.
Actions :
1. Re-assess patient and monitor vital signs
2. Assess response to treatment
▪ Hourly blood glucose
▪ Hourly blood ketones
▪ VBG for pH and K+ at 60 minutes , 2 hours and 2 hourly thereafter.
3. Continue fluid replacement
4. Identify and treat the precipitating factors
5. Thromboprophylaxis with Low molecular weight heparin
Aims:
1. Ensure clinical and biochemical parameters are improving.
Subacute Management (T = 6 hours to 12 hours)
2. Continue IV fluid replacement.

3. Avoid hypoglycaemia.
4. Assess for complications. (e.g. fluid overload, cerebral oedema)
5. Treat precipitating factors as necessary.
Actions :
1. Re-assess patient, monitor vital signs.
2. Continue IV fluid via infusion pump at reduced rate;
▪ 0.9% sodium chloride 1L with KCl over 4 hours
▪ 0.9% sodium chloride with KCl over 6 hours
▪ Add 10% dextrose 125ml/h if the glucose falls below 14 mmol/L
▪ Consider reducing the rate of infusion to 0.05 units/kg/hour when
glucose falls below 14 mmol/L
▪ Reassess at 12 hours; further fluid may be required.
▪ Check for fluid overload.
3. Review biochemical and metabolic parameters
▪ At 6 hours check venous pH, HCO3-, potassium, capillary ketones and
glucose.
Page | 37
• By 24 hours the acidosis and ketonaemia should have resolved.
Intermediate Management (T = 12 hours to 24

• Resolution of DKA is defined as ketones less than 0.6 mmol/L and
venous pH over 7.3.
• Start oral feeding if the patient is tolerating. If not tolerating continue
IV.
 Do not rely on venous HCO-3 alone to assess the resolution of DKA due to the
possible hyperchloremic metabolic acidosis secondary to high volumes saline.
hours)
 Do not rely on urine ketone clearance to indicate resolution of DKA. (May

persist despite resolution of DKA)
Conversion to subcutaneous insulin

• FRIII should be converted to an appropriate subcutaneous regime when
biochemically stable (blood ketones < 0.6 mmol/L, pH > 7.3) and they
are ready and able to eat.
• Ensure that the S/C insulin is started before the IV insulin is
discontinued.
• Ideally give the S/C fast acting insulin at a meal and discontinue IV
insulin 30-60 minutes later.
Appendix
Box 1 - Restoration of circulating volume
Crystalloid fluid is recommended as the initial fluid of choice.
1. Systolic BP (SBP) less than 90 mmHg

• Give 500 ml of 0.9% sodium chloride solution over 10-15 minutes.
• If SBP remains below 90 mmHg this may be repeated whilst awaiting senior input.
• Hypotension is likely to be due to low circulating volume, but consider other causes
such as heart failure, sepsis, etc.
2. Systolic BP more than 90 mmHg

Fluid Volume
0.9% sodium chloride 1 L 1000 ml over 1st hour
0.9% sodium chloride 1 L with KCl 1000 ml over next 2 hours
 Cautious fluid replacement in young people aged 18 -25 years , elderly , pregnancy and
cardiac or renal failure.
 Add KCL according to box 3 .
Page | 38
Box 2 - Fixed Rate Intravenous Insulin Infusion (FRIII)
0.1 unit/Kg/h ( 6 units per hour if weight is 60 Kg)
The recommended targets are;

▪ Reduction of the blood ketone concentration by 0.5 mmol/L/hour
▪ Increase the venous bicarbonate by 3.0 mmol/L/hour
▪ Reduce capillary blood glucose by 3.0 mmol/L/hour (54 mg/dL)
Increase the insulin infusion rate by 1 unit/h increments hourly until the targets are reached.
If the glucose falls below 14.0 mmol/L (250mg /dL) , commence 10% glucose given at 125
ml/h alongside the 0.9% sodium chloride solution.
Consider reducing the rate of intravenous insulin infusion to 0.05 units/kg/h.
Box 3 – Potassium Replacement therapy

• Hypokalemia and hyperkalemia are life threatening complications in DKA.
• Serum potassium is often high on admission but falls with insulin treatment.
• Regular monitoring is mandatory.
• Maintain potassium between 4.0 and 5.5 mmol/L
Potassium level in first Potassium replacement in mmol/L of infusion

24 hours (mmol/L) solution
Over 5.5 Nil
3.5-5.5 40
Below 3.5 Senior review as additional potassium needs to
be given
References
1. The Management of Diabetic Ketoacidosis in Adults 2021, Joint British Diabetes Societies (JBDS)
for Inpatient Care Group.
Page | 39
Management of Hyperosmolar hyperglycemic state (HHS)
• HHS is an endocrine emergency commonly seen in type 2 diabetes

physiology
Patho-
mellites.
• Pathophysiology is similar to DKA but due to relative availability of insulin
compared to type 1 DM, ketonemia and acidemia is mild in HHS.
1 General appearance: generally ill-appearing with altered mental status

2 Cardiovascular: Tachycardia, orthostatic hypotension, weak and thready
Clinical Features
pulse
3 Respiratory: tachypnoea might be present if acidosis is profound
4 Skin: Delayed capillary refill, poor skin turgor, and skin tenting
5 Genitourinary: Decreased urine output
6 Central Nervous System (CNS): Focal neurological deficit, lethargy with
low Glasgow coma score, and in severe cases of HHS, the patient might
be comatose.
1 Discontinuation/ omission of antidiabetic medication.

2 Acute illness (Infection, Stroke or TIA, Myocardial infarction, Acute
pancreatitis)
3 Drugs (corticosteroids, thiazides, sympathomimetic agents and
conventional antipsychotics)
Diagnosed in the presence of,

1. marked hypovolaemia
2. measured or calculated serum osmolality usually ≥320 mOsm/kg
3. marked hyperglycaemia (≥30 mmol/L / 540mg/dl)
Diagnosis
Without significant
1. hyperketonaemia (ketones ≤3.0 mmol/L) or
2. acidosis (pH ≥7.3 and blood or serum bicarbonate ≥15.0 mmol/L)
Serum osmolality = Blood Urea Nitrogen (BUN) + 2(S.Na+) + S. Glucose

(mmol/l)
Serum = 2(Na) + Glucose(mg) + BUN(mg)
Osmolality 18 2.8
Normal Osmolality = 280-290mOsm/L
Page | 40
The presence of one or more of the following indicate the need for
admission to a High Dependency Unit.
1. Measured or calculated Osmolality >350 mOsm/kg
2. Sodium >160 mmol/L
Assessment of severity
3. Venous/arterial pH <7.1
4. Hypokalaemia (<3.5 mmol/L) or hyperkalaemia (>6 mmol/L) on
admission
5. GCS <12 or abnormal AVPU (Alert, Voice, Pain, Unresponsive) scale
6. SpO2 <92% on air (assuming normal baseline respiratory function)
7. Systolic blood pressure <90 mmHg or Pulse >100 or <60 bpm
8. UOP <0.5 ml/kg/h , Serum creatinine >200 µmol/L and/or acute
kidney injury
9. Hypothermia
10. Macrovascular event such as myocardial infarction or stroke
11. Other serious co-morbidity
1. Normalize the osmolality

Goals of Treatment
2. Replace fluid and electrolyte losses

3. Normalize blood glucose
Other goals include prevention of:

1. Arterial or venous thrombosis
2. Other potential complications e.g. Cerebral oedema/ central pontine
myelinolysis /osmotic demyelination syndrome
Page | 41
Management
0-60 minutes 1-6 hours 6-12 hours 12-24 hours 24-72 hours (Resolution)
Clinical assessment and monitoring
Clinical status History , Examination / NEWS / cardiac monitoring / UOP/ Check for continuous Clinical and cognitive status is back to
Severity assessment improvement premorbid status
Precipitating causes Assess for precipitating causes (MI, sepsis, vulnerable adult Treat precipitating
) factors Hypovolaemia is corrected
Osmolality Check hourly – target decline is 3-8 Check 2 hourly Check 4 hourly Osmolality < 300mOsm/kg
mOsm/kg/h (if no improvement
check 2 hourly) Blood glucose <15mmol/L
Blood glucose (BG) Check hourly - Target decline is 5mmol/L per hour
Interventions
Intravenous fluid 1 L over 1 hour Up to 2-3 L Up to 6L positive Rate depends on the Observe for fluid overload
(0.9% saline) positive balance balance by 12 hours fluid balance (to coverup Can be stopped if patient is eating and
by 6 hours the deficit of 220ml/kg) drinking
Insulin infusion Ketonemia >1 to Commence only if positive fluid Increase by 1U /h to If not eating > VRIII
0.05U/Kg/h < 3 mmol/L balance and BG plateaued on repeated achieve a BG target of If eating SC insulin
measurements ( >2 occasions ) 10-15mmol/L
Ketonaemia >
3mmol/L >DKA
guideline
Potassium Refer to Table 1
VTE prophylaxis LMWH used until discharged.
Page | 42
Management of osmolality changes during treatment of HHS
Calculated/ Measured Osmolality Sodium Fluid Status Action
Negative fluid
Decreasing by <3 mOsm/kg/hour Increasing balance & no signs of Increase rate of infusion of 0.9% saline
fluid overload
Decreasing by 3-8 mOsm/kg/hour

Increasing Continue same rate of infusion
(Appropriate rate)
Consider reducing infusion rate of IV flids

Decreasing by >8 mOsm/kg/hour and/or insulin
(If already commenced)
Negative fluid
Increasing balance & no signs of Increase rate of infusion of 0.9% saline
fluid overload
Increasing
Adequate fluid Consider switching to .45% saline of same
balance rate
Osmolality (mOsm/kg) = (2xNa+) + glucose(mmol) + urea

18 2.8
Page | 43
Management of blood glucose
Fall of blood glucose at a rate of up to 50mg/dl per hour is ideal.
Potassium replacement – Table 1

Potassium level in first 24 hours Potassium replacement in infusion
(mmol/L) solution
≥ 6.0 Senior review/ ICU/ Outreach
5.5 – 5.9 Nil
3.5 – 5.5 40 mmol/L
< 3.5 Senior review/ ICU/ Outreach
Additional Potassium is required.
References
1. The Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults, February 2022- Joint
British Diabetes Societies (JBDS) for Inpatient Care group.
Page | 44
Management of Hypoglycaemia
Definition of hypoglycemia
Capillary blood sugar < 70mg/dl
Level Capillary blood sugar

Level 1 CBS <70mg/dl but >54mg/dl
Level 2 CBS <54mg/dl
Level 3 Sever cognitive impairment requiring
assistance for recovery
Symptoms
Neuroglycopenia Autonomic manifestations

Confusion/drowsiness/coma Tremor
weakness Palpitations
Visual impairment Sweating
Anxiety, hunger
Conscious, alert Unconscious /

and able to drowsy/unable
swallow to swallow
(LEVEL 1,2) (LEVEL 3)
Yes
Yes
Oral glucose IV access

25% 75ml
Yes No
(15-20g)
Orloooooo -Iv Glucose
50% 5ml 50% 50ml with saline
infusion
-25% dextrose 75ml IM Glucagon 1mg
-10% Dextrose 150-
200ml over 15 minutes
Page | 45
CBS 10-15
minutes later
If < 70mg/dl
Repeat 25% Dextrose 75 ml orally
50% Dextrose 50ml
If after 3 cycles
or in 30-45
minutes CBS -Iv Glucose 50% 50ml with
remains < saline push
70mg/dl 50% 50ml with saline infusion
-25% dextrose 75ml
Yes -10% Dextrose 150-200ml over
15 minutes
IV access
No
IM Glucagon 1mg
References
UpToDate
Page | 46
Management of Addisonian Crisis
• Addisonian crisis, (adrenal crisis), is an endocrinologic emergency with a

Definition
high mortality rate secondary to physiologic derangements from an

acute deficiency of the adrenal hormone cortisol.
• Fatigue, Nausea, Vomiting, Abdominal pain, Muscle cramps

Features
Clinical
• Hypotension, Hypovolaemic shock and coma.
• Gastroenteritis/ fever
Precipitating factors
• Trauma/ surgery/ dental procedure

• Major psychological distress.
• Not adjusting glucocorticoid dose appropriately.
• Other risk factors (Diabetes mellitus, Diabetes insipidus, Asthma,
Premature ovarian failure)
• Serum electrolytes (SE) and glucose

Investigations
- Hyponatraemia, Hyperkalaemia, Hypercalcemia, hypoglycaemia

• Routine measurement of plasma cortisol and ACTH.
• Establish intravenous access with a large-gauge needle.

• Infuse 1- 3L of isotonic saline or 5% dextrose as quickly as possible.
General measures
- Frequent hemodynamic monitoring

- Avoid iatrogenic fluid overload.
- Monitor electrolytes.
- Hyponatremia is rapidly corrected with volume repletion and
cortisol therapy.
Page | 47
Cortisol Therapy • Hydrocortisone 100 mg IV bolus, followed by 50 mg IV every 6 hours.

• Or 200mg/24 hours as a continuous intravenous infusion for the first 24
hours.
• If hydrocortisone is unavailable, alternatives include
Methylprednisolone and Dexamethasone.
• Saline must be administered if dexamethasone is given instead of
hydrocortisone.
• Continue IV N/S at a slower rate for next 24-48 h.

• Search for & treat possible precipitating causes.
Subacute & Long-term
• Find the type of insufficiency and its cause.

Management
• Taper parenteral glucocorticoid over 1 to 3 days, if precipitating or

complicating illness permits, to oral glucocorticoid maintenance dose.
• Arrange short Synacthen test if necessary
• For patients with primary adrenal insufficiency, begin mineralocorticoid
replacement with fludrocortisone, 50-100 microgram by mouth daily,
when saline infusion is stopped.
❖ Education for patients and relatives must include information about correct adjustment of
glucocorticoid replacement, symptom awareness, and use of steroid emergency cards and
medical alert bracelets.
❖ Emergency self-administration of hydrocortisone is of key importance to prevent crisis-related
morbidity and mortality.
References
UpToDate
Page | 48
Management of Thyroid Storm

Introduction
Thyroid storm, also known as thyrotoxic crisis, is an acute, life-threatening
complication of hyperthyroidism. It is an exaggerated presentation of
thyrotoxicosis. It comes with sudden multisystem involvement.
1 General : Fever, Excessive sweating, Orbitopathy, hand tremors, moist

& warm skin
Clinical Features
2 CVS : Tachycardia, Hypotension, Arrhythmia, Heart failure with

pulmonary and peripheral oedema
3 CNS : Hyperreflexia, Agitation, Delirium, Anxiety, Psychosis, or Coma.
4 GI : Nausea, Vomiting, Diarrhoea, Abdominal pain, Intestinal
obstruction, and Acute hepatic failure
1 Abrupt discontinuation of antithyroid medicine

2 Thyroid surgery/ Non-thyroid surgery/ Trauma
3 Acute illnesses (infections, diabetic ketoacidosis, acute myocardial

infarction, cardiovascular accident, cardiac failure, and drug reactions)
4 Recent use of Iodinated contrast medium, Radioiodine therapy (rare)
5 Stroke or traumatic brain injury
6 Medication side effects (amiodarone, anaesthetics, salicylates)
7 Hyperemesis gravidarum in pregnancy, Parturition
8 Burns
Diagnosi
• Apply for Burch-Wartofsky Point Scale (Figure 1)

s
• (≥ 45 Thyroid storm ,25–44 -Impending storm)
1 ICU admission if APACHE2 score more than 9

2 PCM and cooling blanket
General Management
3 Potassium iodide 200mg or equivalent dose of lugols solution

4 IV hydrocortisone 300mg/daily or Dexamethasone 8mg daily
5 Beta blocker: Commonly used is propranolol 60-80mg PO every 4-6
hours But depending on the patient short acting I.V beta blockers may
be preferred.
6 Look for the precipitating cause and treat.
Page | 49
Antithyroid medication
Management
Specific
01) Methimazole 30mg/daily in divided doses(IV/Oral/NG)
OR
02) Propylthiouracil 600mg po/NG OR
03) Carbimazole 30mg/daily in divided doses
Management of organ involvement
• Killip class ≤ III and ≥150 bpm- IV Esmolol and landiolol as

1st line.
- Esmolol 1 mg/kg for 30 seconds initial dose and
subsequent dosage should be controlled appropriately
while monitoring the heart rate (~150 μg/kg/min)
Tachycardia/ AF • When HR less than 130 change to a oral beta blocker
In a case of AF • Digitalis can be used in AF
anticoagulation
according to AF
guidelines
• If the heart rate of patients classified as Killip class IV is
≥150 bpm, the use of landiolol or esmolol may be
considered.
Killip class III

- I.V Furosemide
- Nitrates (I.V/Sublingual)
Heart failure - Beta blockers for the
tachycardia
Should be treated according to - Digoxin if AF
the Guidelines for the treatment
of acute heart failure guidelines
Respiratory support – Oxygen, Killip class IV
NIV or Intubation accordingly. - Inotrope and vasopressor
support
- The short-acting beta1-selective
adrenergic antagonists landiolol
or esmolol may be considered
when heart rate is ≥150 bpm.
- digitalis When AF is present,
Page | 50
• GI symptoms, including diarrhea, nausea, and vomiting,

are associated with thyrotoxicosis, heart failure,
neurological disorders, and gastrointestinal infection.
Gastrointestinal • Treatment for GI infection should be performed when
disorders and hepatic necessary.
damage in thyroid storm • Acid-suppressive drugs such as proton pump inhibitors
(PPIs) or histamine-2 receptor antagonists.
• Hepatotoxicity with or without jaundice in thyroid storm
can be caused by hepatocyte damage due to
thyrotoxicosis, heart failure, precipitating hepatic-biliary
infection, or drug-induced liver damage.
• Differential diagnosis for the origin of hepatic dysfunction
and appropriate treatment based on its origin should be
performed, including TPE for acute hepatic failure.
-
Appendix
Figure 1 - Burch-Warsofsky Point scale
Page | 51
APACHE ⅱ Score
Killip classification
Class I No evidence of heart failure

Class II Findings consistent with mild to moderate heart failure (eg, S3 gallop, lung
rales less than one-halfway up the posterior lung fields, or jugular venous
distension)
Class III Overt pulmonary edema
Class IV Cardiogenic shock
References
UpToDate
Page | 52
Myxoedema Coma
• Severe hypothyroidism leading to decreased mental status,

Introduction
hypothermia, and other symptoms related to slowing of function in

multiple organs
• The condition usually occurs in patients with long-standing,
undiagnosed hypothyroidism
1. Usually presents with confusion, hypothermia, hypoventilation,

Features
Clinical
hypotension, bradycardia and come.

2. See box 1 for more signs and symptoms.
1. Infection (Pneumonia, Influenza, UTI, Sepsis)

2. Medications (Amiodarone, Anesthetic agents, Barbiturates, Beta

blockers, Lithium, Narcotics, Phenothiazines, Phenytoin, Rifampin)
3. Hypoglycemia, Hypothermia, CO2 retention
4. Congestive cardiac failure, Stroke
5. Surgery/ Trauma/ Burns
6. Intravascular volume contraction (GI Bleeding, Diuretics)
The diagnosis of myxedema coma is initially based upon the history,

Diagnosis
physical examination, and exclusion of other causes of coma. In patients in

whom the diagnosis is suspected, thyroid function tests confirm the
diagnosis.
• TSH
•
Investigations
Free thyroxine (T4)

• Cortisol
• Serum electrolytes- look for hyponatremia
• ABG
• Other investigations looking for underlying precipitating cause
Page | 53
1. Ideally should be admitted to ICU.

2. Assisted ventilation if needed.
3. Hemodynamic support
- Judicious administration of intravenous fluids and correction of
General Management
electrolytes and glucose.

- Severe hypotension that does not respond to fluids should be
treated with a vasopressor until the T4 has had time to act.
4. Passive rewarming with a blanket is preferred for correction of
hypothermia
5. Monitor for Hyponatremia and correct.
6. Start stress doses of glucocorticoids
- IV hydrocortisone 100mg every eight hours
7. Treat the underlying precipitating cause. Empiric antibiotic therapy
until cultures are negative should be considered.
• Combined therapy with T4 (Levothyroxine) and T3 (Liothyronine)

- Initial dose of 200-400 mcg T4 intravenously, followed by daily IV
doses of 50-100 mcg until the patient can take T4 orally. (Use lower
doses in elderly, patient with cardiac impairment/arrythmias.)
- IV T3 at the same time; the initial dose is 5-20 mcg, followed by 2.5-10
mcg every 8h (lower doses for older patients and those with
coexisting cardiovascular disease)
Specific Management
- T3 is continued until there is clinical improvement and the patient is

stable.
- When IV T3 and T4 is not available thyroxine can be administered via
NG, Initial loading dose is 500mcg.
- Daily maintenance dose is 1.6mcg/kg per day when given orally.
- Same dose can be used with per rectal route also.
• Serum T4 and T3 should be measured every one to two days to confirm

that the therapy is working and that very high levels of T3 are avoided.
• Serum T3 should be measured at least one hour after dosing .
• Once there is improvement (regained consciousness, improved mental
status, improved pulmonary and cardiac function), the patient can be
treated with oral T4 alone.
Page | 54
Appendix
Box 1 – Signs & Symptoms of Myxedema Coma

• Hypothermia
• Hypotension
• Bradycardia
• Decreased pulse pressure
• Decreased respiratory rate
• Periorbital puffiness
• Macroglossia
• Coarse or thinning hair
• Thyroid is commonly small
• Slow respiratory rate
• Signs of pleural effusion
• Soft or distant heart sounds, diminished apical impulse, pericardial effusion
• Abdominal distention due to ascites
• Diminished or absent bowel sounds due to ileus
• Bladder distension
• Cold extremities, nonpitting edema of the upper and lower extremities
• Cool, pale, dry, scaly, and thickened skin
• Dry, brittle nails
• Ecchymoses, purpura
• Confusion, stupor, slow speech, delayed reflexes, seizures, coma, prominent psychotic
features, seizures
References
UpToDate
Page | 55
Emergency protocols - 2023 Nervous system
Nervous System Related Emergencies
Page | 56
Early Management of Acute Ischaemic Stroke
Stroke Algorithm
Clinically Acute Stroke
Immediate general assessment and stabilization

• Assess ABCDE
• Connect to cardiac monitor- assess vital signs and stabilize.
• If SpO2<95% -start 5L/min O2 via face mask and titrate; maintain SpO2>94%
• Check CBS, if <60mg/dl, IV 50% dextrose 50ml.
• Recheck in 15 minutes, if still <60mg/dl repeat IV dextrose as necessary.
• History and physical examination to differentiate from stroke mimics.
• Establish time of symptom onset or last known normal (< 4.5 hours)
• Perform neurologic examination (NIHSS)
• Obtain IV access and perform lab tests.
(CBC, PT/INR, APTT, SE, S. Creatinine, Troponin)
• Obtain 12 lead ECG.
• Perform urgent NCCT brain
Does CT scan show haemorrhage?

No Yes
Acute ischaemic stroke Haemorrhagic stroke
• Consult a neurosurgeon if indicated.

1. Acute Cerebellar ICH >3cm diameter or
causing brainstem compression.
2. IVH with obstructive hydrocephalus and
neurologic deterioration.
3. Lobar haemorrhage causing life threatening
mass effect / herniation or obstructive
hydrocephalus.
Page | 57
Acute ischaemic stroke
Consider fibrinolytic therapy

Check eligibility and exclude
contraindications (see box 1)
Inclusion criteria
1. Clinical diagnosis of ischemic
Yes stroke causing measurable
No
neurologic deficit
2. Time window – within 4.5
hours of onset
3. Age ≥ 18
Candidate Not a candidate
Review risks/benefits with patient & Minor stroke (NIHSS ≤ 5) Major stroke
family. If acceptable: High risk TIA (ABCD2 score≥4) (NIHSS > 5)
• Aspirin 300mg
• Aspirin 300mg stat
stat
• Clopidogrel 300mg stat
• Give rtPA (Alteplase) Infusion 0.9mg/kg
(maximum dose 90mg) over 60min, with • Aspirin 75mg
• Aspirin 75mg nocte
10% of the dose as a bolus over 1min. nocte or
• Clopidogrel 75mg
• No anticoagulants or antiplatelets • Clopidogrel
nocte for 21 days
treatment for 24 hours. 75mg nocte
Urgent admission to stroke unit / ICU & Look for neurologic complications
aggressively monitor:
• Cerebral oedema with mass
• Vitals in effect (decreased arousal,
- Every 15 min for 2hrs ipsilateral pupillary dilation and
- Every 30 min for 6hrs worsening of motor responses)
- Every 1hrly for 16 hrs • Haemorrhagic transformation
• For neurologic deterioration
• Mannitol (1g/kg bolus→0.25- 0.5g/kg every 6

hours)
• Hypertonic saline (3% 150ml with serum Na goal
of 145-155 mEq/L)
• Hyperventilation (PaCO2 goal; 30 to 35mmHg)
• Decompressive hemicraniectomy.
Page | 58
Blood Pressure control in Acute Ischaemic Stroke (AIS)
Acute ischemic stroke

& elevated BP
Candidate for fibrinolytic No fibrinolytic therapy

therapy
BP ≤ 220/120 mmHg SBP>220 mmHg/

DBP >120 mmHg
Presence of hypertensive
comorbid disease?
• Acute coronary event

• Acute heart failure
• Hypertensive encephalopathy
Yes No
Do not initiate
antihypertensive therapy
within 1st 48-72 hours
• IV Labetalol 10mg
• IV Labetalol 10 mg,
• IV Labetalol 10-20mg followed by a continuous
followed by a
Drug over 1-2 minutes infusion of 2-8 mg/ min.
continuous
regimen before Alteplase
infusion of 2-8mg
• May repeat one time. • IV GTN 5-400mcg/min in
/minute
acute heart failure.
Maintain BP ≤ 180/105 Lower the MAP by 15%

Goal
mmHg or less for 1st 24h within 24 hours.
MAP- Mean Arterial Pressure
Page | 59
Box 1
Exclusion criteria for IV Alteplase Warnings
• Minor non- disabling Stroke • Recent major trauma or
• Known history of ICH surgery (within 14 days)
• Other stroke or serious head trauma within past 3 months • Moderate to severe stroke
• Intracranial or intraspinal surgery within past 3 months with early improvement.
• Intra-axial intracranial neoplasm • Seizure at onset.
• Sustained SBP > 185 or DBP >110 mmHg even after BP lowering • Arterial puncture at a non-
treatment. compressible site within
• Symptoms suggestive of SAH past 7 days.
• Aortic arch dissection • Genito-Urinary tract
• Active internal bleeding (Gastrointestinal bleeding within past hemorrhage within past 21
21 days) days.
• Patient received heparin within the last 48 hours and has • Serum glucose < 50mg/dl.
elevated APTT (40s) • Myocardial infarction in
• Patient received full treatment dose of LMWH within previous past 3 months.
24 hours. • Pregnancy.
• Platelet count < 100 000/μl
• Vitamin K antagonist use and INR > 1.7
• Symptoms consistent with infective endocarditis
General measures
❖ Head of bed elevation to 300in selected patients at risk for; elevated intracranial pressure
(cerebral oedema) or aspiration (dysphagia/ diminished consciousness) or cardiopulmonary
decompensation or oxygen desaturation.
❖ Hyperthermia - treat with antipyretics and determine the source.
❖ Fluids- correct intravascular volume depletion with isotonic saline
❖ Hyperglycaemia - treat and achieve target of 140 – 180mg/dL
❖ Dysphagia screening before eating, drinking and oral medications.
❖ Nutrition- enteral nutrition within 7 days (If can’t swallow NG tube, if anticipated duration
of swallowing inability > 2-3 weeks; PEG)
❖ DVT prophylaxis with pneumatic calf compression recommended. No definite benefit of
LMWH.
❖ Skin and pressure point care.
❖ Early rehabilitation with an intensity acceptable for the patient’s tolerance and anticipated
outcome.
❖ Screen for post stroke depression and if indicated treat with antidepressants.
❖ Functional assessment prior to discharge.
Page | 60
Antithrombotic treatment
ASA guidelines NICE
Immediate • For moderate to higher strokes, • Aspirin 300mg for 2
antithrombotic (NIHSS score > 5) weeks/ until initiation
treatment - Aspirin 300mg monotherapy (162- of long-term
325mg) antiplatelet
• For minor stroke (NIHSS score ≤ 5 ) and high risk treatment.
TIA
- DAPT with Aspirin 300mg and
Clopidogrel 300mg stat.
- Aspirin 75mg and Clopidogrel 75mg daily
for 21 days.
• Intracranial large artery atherosclerosis
- DAPT for 90 days
• For patients on single antiplatelet at the time
of stroke
- Switch to DAPT if it is a minor stroke or
continue the same agent if it is a major
stroke
Long term • Choice of antiplatelet should be individualized. • Aspirin/ clopidogrel

antithrombotic • GI disturbances and other bleeding 75mg nocte
treatment complications; Clopidogrel 75mg is best over
aspirin.
Treatment of Hyperlipidaemia
Timing of statin
1. According to AHA/ASA guidelines

- Already on statin, continuation of statin is reasonable.
- If patient qualify for statin, in-hospital initiation of statin therapy is reasonable.
2. According to NICE
- Continue statin if patient already taking.
- Immediate initiation is not recommended.
- It is safe to start statins after 48 hours.
DAPT- Dual Anti Platelet Therapy
Page | 61
NIHSS Score – National Institute of Health Stroke Scale
Page | 62
Choice of statin
1. High intensity statin

Commence high intensity statin on patients with very high/High risk of Atherosclerotic
cardiovascular disease (ASCVD)risk factors.
High intensity statins- Atorvastatin 40-80mg, Rosuvastatin- 20-40mg(Capable of reducing LDL
by 50%)
2. Moderate-intensity statin
- Patient with Clinical ASCVD
➢ had side effects from high-intensity statins or
➢ for whom high-intensity statins are Contraindicated
3. Clinical ASCVD with very high risk and on maximally tolerated statin and have LDL-C >
70mg/dL or non-HDL- C >100mg/dl other lipid lowering medications should be considered.
a. Ezetimibe b. PCSK9 inhibitor
Very High-Risk Future ASCVD events
Very high risk includes a history of multiple major ASCVD events or 1 major ASCVD event and multiple high risk
conditions
Major ASCVD events
• History of ischaemic stroke
• Recent acute coronary syndrome (within past 12 hours)
• History of MI other than recent ACS event listed above
• Symptomatic peripheral arterial disease (History of claudication with ankle brachial index <0.85 or
previous amputation
High-risk conditions
• Age ≤ 65y
• Heterozygous familial hypercholesterolemia
• History of coronary artery bypass surgery or percutaneous coronary intervention outside of the
major ASCVD events
• Diabetes
• Hypertension
• Chronic kidney disease (eGFR =15-59ml/min-1.73m-2
• Current smoking
the information in this table is from 2018 AHA/ACC guideline on Management of Blood Cholesterol. For high intensity
statin therapy, the guidekine recommends atorvastatin 80mg daily or rosuvastatin 20mg daily.
Please refer to the guideline for contraindications to high intensity statin therapy and recommendations for moderate
intensity statin theraoy. ACS indicates acute coronary sumptaoms; ASCVD, atherosclerotic cardiovascular disease; and
MI, mayocardial infarction.
References
1. Guidelines for the Early Management of Patients with Acute Ischemic Stroke: 2019 Update to
the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for
Healthcare Professionals from the American Heart Association/ American Stroke Association.
(AHA/ ASA stroke guideline)
2. Stroke and transient ischaemic attack in over 16s: diagnosis and initial management NICE
guideline (2019)
3. UpToDate
Page | 63
Management of Bacterial Meningitis
Clinical Syndrome of meningitis
History of CNS disease

No New onset seizure Yes
Papilledema
Focal neurological deficit
Blood culture
Lumbar puncture Blood culture
(After senior opinion) FBC, ESR, CRP, RBS, S/E, S.Cr
FBC, ESR, CRP, RBs, S/E, S.Cr NCCT Brain
Dexamethasone Dexamethasone
Empirical antibiotic therapy Empirical antibiotic therapy
CSF finding meningitis Negative CT head or MRI
Bacterial Viral Perform a lumbar puncture
Dexamethasone Omit Antibiotics

Antibiotic Acyclovir
Therapy Supportive care
Page | 64
Indications for NCCT Brain before LP Indications for repeat LP

• Immunocompromised state • Persisting fever/ high inflammatory markers
(eg, HIV infection, immunosuppressive • New neurological signs
therapy, solid organ or hematopoietic cell • Clinical Deterioration
transplantation)
• History of central nervous system disease
(mass lesion, stroke, or focal infection)
• New-onset seizure
(within one week of presentation)
• Papilledema
• Abnormal level of consciousness
• Focal neurologic deficit
Empirical antibiotic therapy according to the risk factors
Condition Primary Therapy Alternative Therapy Additional Information

Acute bacterial meningitis
Normal Cefotaxime / In immediate Dexamethasone (0.15mg/kg) 8-10
healthy adults Ceftriaxone +/- penicillin or mg IV, starting before or with the
Vancomycin cephalosporin first dose of antibiotic, then 6
hypersensitivity hourly for 2-4 days.
Chloramphenicol +/- Antibiotic therapy should not be
Vancomycin delayed if corticosteroids are not
available.
Age >50, Cefotaxime / In immediate
alcoholics, Ceftriaxone + hypersensitivity,
Debilitating Ampicillin +/- Chloramphenicol +/-
disease Vancomycin Vancomycin
Immune- Ampicillin + In hypersensitivity Listeria suspected – Cephalosporin
compromised Cefotaxime / Chloramphenicol + Hypersensitivity – Trimethoprim-
patients Ceftriaxone + Vancomycin Sulfamethoxazole
(Severe Vancomycin
neutropenia,
HIV
Penetrating Vancomycin + Vancomycin +
trauma, post- Ceftazidime Meropenem
neurosurgery
CSF shunt Vancomycin + Vancomycin + Removal of infected shunt with
infections Ceftazidime Meropenem appropriate antimicrobial therapy
is the most effective treatment.
Contact microbiologist for doses
and duration of antibiotic therapy
and timing of shunt reimplantation.
Page | 65
Duration of antibiotic treatment for specific pathogens
Microorganism Duration (days )

Unconfirmed Organism 10
Streptococcus Pneumoniae 10- 14
Haemophilus Influenzae 7
Neisseria meningitidis 7
Group B Streptococcus Listeria 21
Monocytogenes, Escherichia coli and other
coliforms
Staphylococcus Aureus/ Staphylococcus 14-28
Epidermidis
Doses, route, and frequency of antibiotics for CNS infections – Adults

Antibiotic Dose
Cefotaxime 2g IV 4-6 hourly
Ceftriaxone 2g IV 12 hourly
Ceftazidime 2g IV 8 hourly
Ampicillin 2g IV 4 hourly
Meropenum 2g IV 8 hourly
Penicillin G 4 MU IV 4 hourly
Vancomycin 500mg -750mg IV 6 hourly or 15mg/kg IV 8 hourly
Chloroampenicol 12.5mg-25mg/kg IV 6 hourly
Acyclovir 10mg/kg IV 8 hourly
References
1. Up to Date
2. Empirical & prophylactic use of antibiotics- National Guideline-2016 Sri Lanka College of
Microbiologists
3. IDSA (Infectious disease society of America) Guideline
4. NEJM- Dexamethasone in adults with Bacterial Meningitis (2002)
Page | 66
Management of Status Epileptics
0-5 Minutes Initial assessment & management

• ABCD assessment
• Administer O2, if needed. Keep at Left lateral position.
• Check for CBS & correct hypoglycemia.
(If alcohol related, administer IV Thiamine 100mg,
Stabilization followed by 10% Dextrose 150-200ml)
• Check Temperature & Meningism.
• IV access- Send blood for SE, Ca, Mg, FBC, RFT, LFT, CPK
• Prepare for the first Antiepileptic medication.
5- 15 Minutes Seizure continues
Benzodiazepine 1st Dose

IV Access No IV Access
IV Midazolam 0.1- IM Midazolam 0.2mg/kg
0.2mg/kg (10mg/dose) (max 10mg/Dose)
or or
IV Lorazepam 0.1mg/kg Buccal Midazolam
(4mg/ dose) 0.3mg/k (max10mg/Dose)
Initiation of first line or or
Therapy IV Diazepam 0.1 mg/kg Rectal Diazepam 0.2-0.5
(5-10mg/dose) mg/kg (10mg)
Seizure 5 minutes after 1st dose
Benzodiazepine 2nd Dose

Seizure 5 minutes after 2nd dose
15-30minutes IV Phenytoin 20mg/kg over 20 minutes (Max1.5g)

Second line Therapy (Infusion rate 50mg/min, 25mg/min in elderly & cardiac
disease, Avoid in myoclonic fits, cardiac monitoring)
Consider
or
Neuroimaging & EEG
IV Levetiracetam 60mg/kg over 15 minutes (Max 4.5g)
Treat the potential
IV phenobarbital 20mg/kg over 20 minutes (Max 1g)
cause
IV Valproate 30-40mg/kg (Max 3000mg) over 20min
More than 30 minutes
Anesthetic agents
Third line Therapy Need ICU care
Consider Immunotherapy & alternative treatment
Page | 67
First line Therapy- Benzodiazepines

Route Lorazepam Midazolam Diazepam
IV 0.1mg/kg ( or 4mg) 0.1-0.2mg/kg or 10mg 0.15-0.2 (or 5 -10mg )
IM - 0.2mg/kg or 10mg -
Intra Nasal - 0.2mg/kg or 10mg -
Buccal - 0.3mg/kg or 10mg -
PR - - 0.2-0.5mg/kg
Second line Agents

Maintenance
Drug Initial dose Infusion rate Considerations
doses
Phenytoin 15-20mg/kg 50mg/min 100mg IV 8h Monitor ECG & BP.
(Max 1500mg) (6-8 hours after Cautions on patient
loading dose) already on phenytoin
Contraindications - AV
blockage, severe
hypotension.
Avoid in myoclonic fits.
Levetiracetam 60mg/kg 2-5mg/kg/min 500-1000mg Reduce dose in severe
(Max 4500mg) in 100ml of IV/po 12h renal failure.
N/S over 15 (10-14h after Avoid in mood or
minutes loading dose) behavioural disorders.
Sodium 30-40mg/kg 10mg/kg/min 500mg IV/po 12h Contraindicated in
Valproate (Max 3g) over 10- (10-14h after severe liver
20min loading dose) dysfunction.
Phenobarbital 20mg/kg 50mg/min 1mg/kg IV 12h Need cardiorespiratory
(Max 1 g) monitoring.
Contraindicated in liver
failure & Respiratory
depression.
Lacosamide 200mg-400mg 5-10mg/min 200mg IV 12h
(Max 600mg) (over 15-30
minutes)
Topiramate 200-400mg po 300mg po 6h
Gabapentin 300-900mg po 300-900mg po
Page | 68
Anaesthetic Agents for refractory SE

Drug Loading dose Maintenance infusion Adverse effects
rates
Midazolam 0.2-0.4mg/kg every 5 min until 0.1-2mg/kg/h Respiratory depression
seizure controlled Hypotension
(Max dose 2mg/kg )
Propofol 2mg/kg IV every 5 min until 5-10mg/kg/h Respiratory depression
seizure controlled
Thiopental 100-250mg/kg 3-5mg/kg/min Arrhythmias
Hypertension
Super Refractory SE- Treatment options

1. Magnesium sulphate 2-6g/h
2. Lidocaine IV
3. Immunological Therapy
4. Neurosurgery & neurostimulation
Definitions of Status Epileptics

1) Status epilepticus
❖ Condition resulting either from failure of mechanisms responsible for seizure formation or
from the initiation of mechanisms which leads to abnormal prolong seizures.
o GTC seizure- 5 minutes
o Focal seizure- 10 minutes
o Absence 10- 15 minutes
2) Refractory status
❖ SE refractory to early benzodiazepines & additional first line anti-seizure medication.
3) Super refractory status

❖ If seizure cannot be terminated with the use of an anaesthetic in addition to the
benzodiazepines & standard anticonvulsants after 24 hours.
Predictors of autoimmune cause

1. Status epileptics as presentation of new onset seizure
2. Progression to refractory or super refractory status epileptics
3. Relatively recent but explosive onset of seizure
4. Absence of establish epilepsy history
5. Presence of other neurological problems such as memory loss, autonomic dysfunction,
ataxia or movement disorder
6. New psychiatric symptoms of behaviour changes
7. History of Cancer
8. Lymphocytic pleocytosis on CSF examination
Page | 69
References
1. ILAE Guidelines
Page | 70
Management of Myasthenic Crisis

Definitions
❖ Myasthenic crisis
- Life-threatening maximal manifestation of myasthenia gravis (MG) necessitating
mechanical ventilation, supportive feeding, and intensive care.
- Weakness may develop within minutes to days and encompass flaccid tetraparesis
with immobility, severe dyspnea, respiratory insufficiency, and aspiration.
❖ Impending myasthenic crisis

- In patients with a known diagnosis of myasthenia gravis, " Impending myasthenic
crisis" is defined as rapid clinical worsening of myasthenia gravis that, in the
opinion of the treating clinician, could lead to crisis in the short term (days to
weeks).
Algorithm for Management of MC
Clinical features
• Dyspnea that occurs or worsens when the patient lies supine.
• Severe dysphagia with weak cough and difficulty clearing secretions.
• Poor neck muscle power, Inverse aspiration
• Signs of respiratory muscle weakness
- Hypophonia
- Pausing during speech to take a breath
- Poor respiratory effort
- Increased respiratory rate with shallow breaths
- Use of accessory muscles of respiration, and paradoxical abdominal
breathing.
- Low baseline vital capacity (VC) that is <30 ml/kg of ideal body weight,
even if the patient is breathing without distress.
- Generalized weakness can mask the usual signs of respiratory distress,
such as accessory muscle use.
- ventilatory failure may be the only clinically overt manifestation
Diagnosis
• Look for precipitants.
- Concurrent infection.
- Surgical intervention, pregnancy, childbirth, or tapering of
immunosuppressive medications.
- Concurrent medications. (Box 1)
• Exclude other DDs
- Guillain-Barré syndrome, amyotrophic lateral sclerosis and other
myasthenic syndromes.
Page | 71
Evaluation & Management

• Admit to ICU
• Frequently monitor respiratory muscle strength 2 hourly. (Box 2)
• Electively intubation if clinical evaluation or tests of respiratory muscle strength
suggest impending respiratory failure. (Box 3)
• Temporarily stop anticholinesterase medications for intubated patients.
• Cardiac monitoring.
• Begin rapid therapy with plasma exchange or IVIG. (Box 4)
• Begin immunomodulating therapy (Box 5)
• Treat Intercurrent infections and address precipitating factors.
• Initiate weaning from mechanical ventilation when respiratory muscle strength is
improving,
- should be individualized for each patient.
- Median duration is approximately two weeks .However, particular
attention should be paid to measuring indices of respiratory muscle
strength and secretion clearance.
- Some patients may require a tracheostomy for prolonged weaning.
• Watch out for Cholinergic crisis due to excessive anticholinesterase medication
causing weakness. Rare phenomenon.
Appendix
Box 1
Commonly used drugs which may worsen myasthenia gravis
Antimicrobials Aminoglycosides : Amikacin, Gentamicin, Streptomycin
Macrolides : Erythromycin, Azithromycin

Tetracyclines : Tetracycline, Doxycycline
Quinolones : Ciprofloxacin, Ofloxacin, Norfloxacin
Antimalarials : Chloroquine, Hydroxychloroquine, Quinine
Urinary antiseptics: Nalidixic acid
Anticonvulsants : Phenytoin, Carbamazepine
Antipsychotics : Phenothiazines, Clozapine
Cardiovascular : All Beta blockers including topical agents.
agents : Calcium channel blockers (Verapamil, Nifedipine)
: Class I antiarrhythmic drugs (Quinidine, Procainamide)

Page | 72
Others : Neuromuscular blocking agents

Box 2
Objective Measurement of respiratory muscle function
• The Vital Capacity (VC) and the Maximal Inspiratory Pressure (MIP) are used.
• The VC reflects the mechanical function of both inspiratory and expiratory muscle
strength. It can be performed easily at the bedside. The patient is instructed to
take a deep breath in and then to exhale maximally into a respirometer (usually a
slow VC maneuver).
• If a respirometer is not available, Single breath count (SBC) can be used as a
surrogate. Usually, SBC less than 20 would warrant consideration of NIV and SBC
less than 15 warrants intubation- but this should be done in correlation with the
clinical assessment.(Eg-Rapidity of SBC decline, Neck muscle power).
• Oxygenation should be monitored continuously, although abnormalities of arterial
blood gases (eg: hypoxemia and hypercarbia) are insensitive measures of
respiratory muscle weakness, because they often develop only after the onset of
life-threatening respiratory failure.
Box 3
Ventilatory support
• Ideally, endotracheal intubation should be performed electively rather than as an

emergent response to precipitous respiratory collapse.
• Elective intubation should be considered.
1. VC falls below 15 to 20 mL/kg
2. Additional indications for mechanical ventilation include clinical signs of
respiratory distress, progressive respiratory acidosis despite therapy, and
inadequate secretion clearance.
• In general, we use assist control modes of volume-controlled ventilation and low
levels of positive end-expiratory pressure (PEEP) with subsequent adjustments to
achieve adequate gas exchange. It is important to avoid overventilation.
• For intubation, succinylcholine is safe in myasthenia gravis, but increased doses
are needed.
• After intubation, cholinesterase inhibitor therapy used for myasthenia gravis is
usually withdrawn temporarily to avoid the excess secretions that may complicate
pulmonary management. These agents can be reintroduced after successful
extubation and once dysphagia has largely resolved.
• Non-invasive positive pressure ventilation (NPPV) may be used on a case-by-case
basis in those expected to resolve quickly who have adequate cough and can
tolerate the mask.
Page | 73
Box 4 - Rapid therapies

• The main therapies for myasthenic crisis are plasma exchange and IVIG.
• These start to work within several days, but the benefits last only a few weeks.
Therefore, initiation of immunosuppressive therapy is also necessary for most patients.
1) Plasma exchange
▪ Directly acetylcholine receptor antibodies from the circulation, and its clinical
efficacy roughly correlates with the reduction in antibody levels.
▪ Treatment for seriously ill patients in the midst of myasthenic crisis, although
it has never been studied in a randomized, controlled trial for this indication.
The beneficial clinical effect usually lasts only three to four weeks. In addition,
the acetylcholine receptor antibody levels rebound within weeks if
concurrent immunotherapy (eg, glucocorticoids) is not used.
▪ A typical course of treatment consists of five exchanges (3-5L of plasma each)
over 7-14 days.
2) Intravenous immune globulin —

▪ IVIG is used in the same setting as plasma exchange to quickly reverse an
exacerbation of myasthenia.
▪ The total dose of IVIG is 2 g/kg, usually over two to five days (eg, 400 mg/kg
per day over five days).
▪ Spreading the IVIG dose over more days may be preferable in those who have
renal disease or heart failure and in older adults.
 Choosing rapid therapy —No significant advantage of one over the other.
Box 5 - Immunosuppressive therapy

• Oral or nasogastric glucocorticoids are started at moderate to high dose (eg, prednisone
60 to 80 mg daily) for most patients with myasthenic crisis in order to provide a longer
period of benefit. The onset of benefit with glucocorticoids for myasthenia gravis
generally begins within two to three weeks and peaks after a mean of 5.5 months.
• The initiation of high-dose glucocorticoids is associated with a transient worsening of

weakness and myasthenic symptoms that is serious in up to 50 %, and additionally with
respiratory failure requiring mechanical ventilation in up to 10 percent.
• The transient worsening usually occurs 5-10 days after the initiation of glucocorticoids
and lasts approximately 5-6 days. However, concern regarding initial worsening of
myasthenia gravis with high-dose glucocorticoids is ameliorated when the patient is
receiving concurrent treatment with plasma exchange or IVIG. The quick onset of action
of these rapid therapies helps to prevent the transient worsening that would otherwise
occur due to the glucocorticoids.
• Other immunosuppressive treatments for myasthenia gravis,

▪ Azathioprine
▪ mycophenolate mofetil
▪ cyclosporine
Page | 74
References
UpToDate
Page | 75
Emergency protocols - 2023 Infections
Emergencies Related to Infections
Page | 76
Management of Sepsis and Septic Shock
Management of Sepsis &

Septic Shock
Sepsis Septic Shock

Sepsis is life threatening organ dysfunction Persistent hypertension requiring
by a dysregulated host response to vasopressors to maintain a mean arterial
infection. pressure > 65mmHg or serum lactate >
2mmol/L despite adequate fluid
resuscitation in sepsis
Screening Tools for sepsis Clinical presentation

1. SIRS 1. Hyper/hypothermia
2. NEWS 2. Tachypnoea
3. MEWS 3. Tachycardia
4. SOFA score 4. Hypotension
5. Evidence of Infection
Page | 77
A: Airway B: Breathing
df
1. Spo2 target 94-98%
1.Ensure clear airway & airway
maintenance
2. Suck out secretions
3.If low GCS, secure the airway with

positioning, maneuvers & airway adjuncts
Initial Assessment
C: Circulation
1.Intravenos access with two wide bore

cannula
2. IV crystalloid fluid 30mL/ kg within the Additional Therapies

first 3hr of resuscitation for hypotension
or lactate > 4mmol/L
3. Mean arterial pressure target: 1. IV hydrocortisone at a dose of

200mg/d given as 50mg
> 65mmHg intravenously every 6 hours or as
4. First line vasopressor: norepinephrine a continuous infusion
2. Glycemic target: 144-180mg/dl,
RBS >180mg/dl manage with
Antimicrobials insulin
3. DVT prophylaxis with S/C
enoxaparin if no
1. Blood cultures prior to antibiotics & contraindications
relevant other cultures 4. Early enteral feeding
2. Broad spectrum antimicrobial 5. Stress ulcer prophylaxis
administration within one hour of 6. PH < 7.2 IV sodium bicarbonate
diagnosis of sepsis
3. Source control
Page | 78
Treatment Modalities
1. Hemodynamic Management
Mean arterial pressure (MAP): initial target MAP > 65mm Hg
1.1 Fluids
Sepsis induced hypoperfusion or septic shock: at least 30mL/ kg of IV crystalloid fluid should
be given within the first 3hr of resuscitation.
• Balanced crystalloids instead of normal saline for resuscitation.
• Blood lactate should be measured
• Use dynamic measures to guide fluid resuscitation e.g POCUS with IVC assessment and
cardiac output assessment
• Guiding resuscitation to decrease serum lactate in patients with elevated lactate level.
• Detailed initial assessment and ongoing re-evaluation of the response to treatment to avoid
over- and under-resuscitation.
• Invasive monitoring of arterial blood pressure over non-invasive monitoring
1.2 Vasopressors
Start vasopressors peripherally to restore MAP rather than delaying initiation until a central
venous access is secured.
• Norepinephrine as the first-line agent over other vasopressors.
• Septic shock on norepinephrine with inadequate mean arterial pressure levels, suggest
adding vasopressin instead of escalating the dose of norepinephrine.
• Inadequate MAP despite norepinephrine and vasopressin, suggest adding epinephrine.
1.3 Inotropes
SepticIn
shock and cardiac dysfunction with persistent hypoperfusion despite adequate volume
status and arterial blood pressure, suggest either adding dobutamine to norepinephrine or
using epinephrine alone.
• Norepinephrine dose: 0.01Mg/kg/min – 1Mg/kg/min
• Epinephrin dose:0.01Mg/kg/min- 1Mg/kg/min
• Dobutamine dose: max 20Mg/kg/min
Page | 79
2. Antimicrobial treatment
• Administer antimicrobials immediately, ideally within 1 hour of recognition of sepsis
• Use empiric antimicrobials with MRSA coverage for patients at high risk of MRSA
infections
• Use two antimicrobials with gram-negative coverage for empiric treatment for patients at
high risk of sepsis with multidrug resistant (MDR) organisms
• Empiric antifungal therapy if high risk of fungal infection
• Prompt identification of site of infection & source control (e.g: drainage of an abscess,
debriding infected necrotic tissue, removal of a potentially infected device, or definitive
control of a source of ongoing microbial contamination)
• Daily assessment for de-escalation of antimicrobials
• Optimal duration of antimicrobial therapy following adequate source control should be

guided by clinical evaluation & procalcitonin levels.
3.Admission to intensive care
• For adults with sepsis or septic shock who require ICU admission, suggest admitting the
patients to the ICU within 6 hours of diagnosis of sepsis
4.Ventilation
• SPO2 target: 94%-98%
• Sepsis-induced hypoxemic respiratory failure, suggest the use of high flow nasal oxygen
over non-invasive ventilation.
• Sepsis-induced ARDS, recommend using a low tidal volume ventilation strategy (6mL/kg),
over a high tidal volume strategy (> 10mL/kg)
• Sepsis-induced respiratory failure (without ARDS), suggest using low tidal volume as
compared with high tidal volume ventilation.
Page | 80
• Sepsis-induced moderate severe ARDS, we suggest using traditional recruitment

maneuvers.
• Sepsis-induced moderate-severe ARDS, recommend using prone ventilation for greater

than 12hour daily
5.Additional therapies
•Steroids: septic shock and an ongoing requirement for vasopressor therapy
IV hydrocortisone at a dose of 200mg/d given as 50mg intravenously every 6 hours

or as a continuous infusion until weaned off from vasopressors.
It is suggested that this is commenced at a dose of norepinephrine or epinephrine
≥ 0.25 mcg/kg/min at least 4 hours after initiation.
• Blood transfusion:
Restrictive (over liberal) transfusion strategy: Hb transfusion trigger of 7g/dl
(However, assessment of a patient’s overall clinical status and consideration of
circumstances such as acute myocardial ischemia, severe hypoxemia or acute
hemorrhage is required)
• Stress ulcer prophylaxis: with IV PPI
• Thromboembolism (VTE) prophylaxis: unless a contraindication to such therapy exists

with LMWH
If pharmacotherapy contraindicated, such patients may benefit from mechanical VTE
prophylaxis e.g intermittent pneumatic compression (IPC) and/or graduated
stockings.
• Glycemic control: initiate insulin therapy at a glucose level of ≥ 180mg/dL (10 mmol/L)
with a glycemic target of 140−180mg/dL (8−10 mmol/L)
Monitor CBS 4 hourly until stabilization
• Acidosis: for severe metabolic acidemia (pH ≤ 7.2) and acute kidney injury (AKIN score 2
or 3), suggest using IV sodium bicarbonate therapy
Page | 81
• Feeding: suggest early (within 72hr) initiation of enteral nutrition.
• AKI: suggest using either continuous or intermittent renal replacement therapy. CRRT
will be better tolerated with hemodynamic instability than intermittent RRT.
6. References
Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic
Shock 2021 Critical Care Medicine.
Page | 82
Management of Neutropenic Sepsis

A patient with risk factors presenting with fever OR
signs and symptoms suggestive of sepsis
1. Post-chemotherapy
2. Post-transplantation
3. Chronic granulomatous disease
4. Clozapine-induced agranulocytosis
5. Haemato-oncology patient who has received
chemotherapy within the last 14 days or has a history of
recurrent neutropenia.
Emergency Assessment
Investigations
Brief history
Initial investigations
1. What are the underline Examination (head to toe)
1. FBC
malignancy/ 1. To find septic focus.
2. Renal & liver function tests
immunocompromised 2. look for hidden areas-
3. CRP, Lactate
state? oral cavity, ears, sub
4. Peripheral blood culture
2. When was the last mammary area, genital
before starting antibiotics.
chemotherapy date? and perineal, bedsore.
Additional investigation
3. What are the previous 3. Septic arthritis
1. Central line blood culture
co-morbidities? 4. Meningitis
2. Chest x-ray
4. What are the presenting 5. Features of infective
3. Urinalysis
symptoms? endocarditis)
4. CSF analysis
5. 2D Echo ect.
Diagnosis
Absolute neutrophil count of less than 0.5 x 109/L, or < 1x109/L & “falling”
And
A temperature higher than 38oC
OR
Other signs or symptoms consistent with clinically significant sepsis.
 Neutropenic patients with sepsis or severe sepsis may not have a fever.
(e.g. elderly, patients on corticosteroids)
Page | 83
Emergency Management
• Follow surviving sepsis campaign guideline for sepsis management in general.
• Calculate qSOFA.
• Initial resuscitation→ I.V fluid and vasopressors.
• Start antibiotics within 1 hour of making diagnosis of neutropenic sepsis
(Starting antibiotics should not be delayed because of waiting for investigations).
Yes Is the patient critically ill or hemodynamically No

unstable?
Low-risk group
Primary therapy Primary therapy 1. Outpatient status at the time of

Meropenem 1g IV 8h Piperacillin-tazobactam development of fever.
+ 4.5g IV 6h 2. Anticipated short duration of severe
Vancomycin 1g IV 12h OR No neutropenia (≤100 cells/mm3 for <7d)
(Infusion over 100min) Ceftazidime 1-2g IV 8h 3. Good performance status. (ECOG 0-1)
+/- +/- 4. No comorbidities.
Amikacin 15mg/kg IV 5. No hepatic insufficiency.
Amikacin 15mg/kg IV
once daily. 6. No renal insufficiency.
once daily
7. MASCC risk index score of equal to or
greater than 21.
Suspected MRSA infection? Yes
1. Patients colonized with MRSA.

Co-amoxiclav 1.2g IV 8 hourly
2. Clinical evidence of a vascular catheter
+
related infection. Ciprofloxacin 400mg IV 12 hourly
3. Skin and soft tissue infection.
4. Pneumonia in a unit with a high incidence No
of MRSA infection.
Yes
Primary therapy Persistent or recurrent fever after 4-7 days of

AddYES
vancomycin 1g IV 12 hourly
broad-spectrum antibiotics.
(infusion over 100 minutes) in
Overall duration of neutropenia for>7 days
addition to above antibiotics.
and no identified source of fever.
Empirical antifungal therapy

Fluconazole 400mg IV/po once
daily.
Page | 84
Environmental precautions
• Protective isolation (reverse barrier nursing care)
• Hand hygiene
• Full barrier precautions (e.g. Mask, gown, gloves, overshoes)
References
1. NICE guideline on neutropenic sepsis: prevention and management of neutropenic sepsis in
cancer patients-2020 update
2. National antibiotic guideline 2016 by Sri Lankan collage of microbiologist.
Page | 85
Emergency protocols - 2023 Toxicology
Toxicological Emergencies
Page | 86
Management of Paracetamol Overdose in adults

Definitions
❖ Acute overdose
- Excessive amounts of paracetamol ingested over a period of less than 1 hour; usually
in the context of self-harm.
❖ Staggered overdose
- Excessive amounts of paracetamol ingested over longer than 1 hour; usually in the
context of self-harm.
❖ Therapeutic excess: (RSTI-repeated supratherapeutic ingestion)

- Excessive paracetamol taken with intent to treat pain or fever and without self- harm
intent.
- Paracetamol ingested at a dose greater than the licensed daily dose AND more than or
equal to 75 mg/kg/24 hours.
- Can involve use of excessive doses of the same paracetamol product or inadvertent
use of more than one paracetamol-containing product at the same time.
Management – Acute/ Staggered overdose
Gastrointestinal decontamination
▪ In all patients who present within four hours of a known or suspected

acetaminophen ingestion.
▪ Activated charcoal (AC), 1 g/kg (maximum dose 50 g) by mouth.
Investigations
▪ Do LFT, SE, SCr, RBS,

▪ Serum Paracetamol level if after 4 hrs / <24 hrs/ unknown time of ingestion
Page | 87
Antidote- N-acetylcysteine
Indications
1. Serum acetaminophen concentration drawn at four hours or more following

acute ingestion of an immediate-release preparation is above the "treatment"
line of the treatment nomogram for acetaminophen poisoning.
2. A suspected single ingestion of greater than 150 mg/kg (7.5 g total dose
regardless of weight (15 tablets)) in a patient for whom the serum
acetaminophen concentration will not be available until more than eight hours
from the time of the ingestion.
3. Patient with an unknown time of ingestion and a serum acetaminophen
concentration >10 mcg/mL.
4. Patient with a history of acetaminophen ingestion and any evidence of liver
injury.
5. Patients with delayed presentation (>24 hours ) and evidence of liver injury.
Method of administration
1. 20-hour intravenous (three bag) IV protocol - used most often

2. Simplified 20-hour (two-bag) IV protocol - nonallergic anaphylactic reactions
(NAAR) during treatment with IV N-acetylcysteine can be reduced by using a two-
bag regimen instead of the traditional three-bag regimen.
3. 72-hour oral protocol.
Check the annexures for three bag protocol and two bag protocol.
Indications to stop/prolong NAC
• Check the serum ALT and acetaminophen concentrations as the patient is

approaching the end of the protocol (approximately 18 hours after starting
treatment). If the serum ALT is elevated OR if the serum acetaminophen
concentration is detectable, continue treatment with N-acetylcysteine at 6.25
mg/kg per hour (for IV protocol) or 70 mg/kg every four hours (for oral
protocol) and obtain a serum acetaminophen concentration and ALT
measurement every 12 hours thereafter. If the ALT is elevated, also measure
the international normalized ratio (INR).
• Treatment can be stopped when the serum acetaminophen concentration is
undetectable, the ALT is clearly decreasing or in the normal range, and the INR
is less than two.
Page | 88
Other treatment options
1. Cimetidine
- It is an inhibitor of acetaminophen metabolism ? no evidence
2. Fomepizole
- In addition to inhibiting alcohol dehydrogenase, fomepizole is a potent inhibitor of
CYP 2E1. Animal studies report that early administration of fomepizole prevents
acetaminophen oxidation and limits hepatic injury
3. Methionine
- No benefit
4. Extracorporeal removal
- When severe acetaminophen poisoning is complicated by acute kidney injury (acute
renal failure), hemodialysis is necessary. For patients with a massive overdose and
evidence of mitochondrial dysfunction (such as severe lactic acidosis without liver
failure), some experts advocate early hemodialysis in addition to acetylcysteine
Special situations
1. Hepatic failure
All patients should receive IV therapy. The dosing protocol is the same as the 20-hour regimen
used for the prevention of hepatic injury, except the final infusion rate (6.25 mg/kg per hour) is
continued until the patient receives a liver transplant OR the hepatic encephalopathy resolves
or INR<2.
Patients should be considered for liver transplant and referred to a specialized care in,
(king’s college criteria)
a. PH <7.3 (irrespective of degree of hepatic
encephalopathy) OR
b. Grade 3 or 4 hepatic encephalopathy AND
c. Prothrombin time>100 seconds
d. Serum creatinine>3.4mg/dL
Massive overdose >50g
• Early treatment with IV N-acetylcysteine using the standard 20-hour protocol.
• Approach is to double the final infusion rate of the 20-hour IV protocol to 12.5 mg/kg per
hour and continue the infusion until the serum acetaminophen concentration is
undetectable.
Page | 89
2. Treatment in pregnancy
The essential elements of treating overdose do not differ significantly in the pregnant patient.
Pre-pregnancy weight is used for dose calculation.
3. Repeated supratherapeutic ingestion (RSTI)
Acetaminophen serum concentrations are frequently at therapeutic levels in the chronic
overdose or RSTI population, and concentrations do not correlate with toxicity as with the
acute overdose.
Indications for NAC in RSTI
a. Ingestion of greater than 7.5 to 10 g of acetaminophen over 24 hours, or ingestion of
greater than 4 g over 24 hours and an increased susceptibility to hepatotoxicity (eg,
chronic alcohol use, fasting, use of P450-inducing drugs.
b. Abdominal pain or liver tenderness, nausea, vomiting, jaundice, or are ill appearing.
c. Supratherapeutic serum acetaminophen concentrations (greater than 20 mcg/mL, or

130 micromol/L) with or without ALT elevation.
d. Elevated ALT or AST concentration (≥50 U/L) on presentation.
Annexure
1. Method of administration
a. Three bag method

- Administer an initial loading dose of 150 mg/kg IV over 15 to 60 minutes.
(we recommend 60 minutes)
- Next, administer a dose of 50 mg/kg over four hours.
(ie, infusion at 12.5 mg/kg per hour IV for four hours)
- Finally, administer a dose of 100 mg/kg over 16 hours.
(ie, infusion at 6.25 mg/kg per hour IV for 16 hours)
b. Two bag method

- Firstly, administer a four-hour infusion at 50 mg/kg per hour IV
(ie, total of 200 mg/kg over four hours)
- Next, administer a 16-hour infusion at 6.25 mg/kg per hour IV
(ie, total of 100 mg/kg over 16 hours)
Page | 90
2. Rumack-Matthew Normogram
▪ This nomogram should only be used after a

single acute acetaminophen ingestion.
▪ The line indicates the level at which toxicity is
possible after acetaminophen overdose.
▪ A serum acetaminophen level should be
obtained four or more hours after an
ingestion to ensure that a peak level has
occurred.
▪ Patients who ingest extended-release
preparations should have a second level
drawn four hours after the first level to assess
for an additional rise in serum concentration.
▪ The level should be plotted in relationship to
the time of ingestion to determine the
likelihood of toxicity and the need for
treatment.
▪ Caution should be used in assessing the
reliability of the time of ingestion.
▪ This nomogram cannot be used for ingestions
that occurred greater than 24 hours prior to
presentation, repeated supratherapeutic oral
ingestions, or iatrogenic intravenous
overdose.
References
1. Bestpractice.bmj article on paracetamol overdose in adults 6 Aug 2022

2. The National Poisons Information Service (NPIS) in the UK
3. Lancet article on efficacy of a two bag acetylcysteine for management of paraceramol overdose
4. Upto- date
Page | 91
Management of Organophosphorus poisoning

Check ABC
Decontamination
1. Remove any contaminated clothes.
2. Wash exposed skin with soap and water
3. Irrigate eyes if exposed
4. If ingested:
a. Perform gastric lavage if presenting within
two hours of ingestion via NG tube.
b. If unconscious intubates prior to lavage:
avoid succinylcholine
c. After lavage give activated charcoal 1g/kg
via NG tube
Look for features of cholinergic syndrome
1. Bronchospasm or crepitations
2. Excessive sweating If absent can be
3. Miosis – usually pinpoint pupils carefully monitored
4. Hypotension
If present give atropine
1. IV atropine 2-5mg given.

2. Check for features of cholinergic syndrome in five mins.
3. If still present give double the dose of atropine every 5
mins till features of adequate atropinization. If presenting within 24
(tachycardia and mydriasis are not contraindications) hours
a. Clear lungs IV Pralidoxime 30mg/kg
b. Heart rate > 80 over 20 mins then
c. Systolic blood pressure > 80 mmHg 10mg/kg/hour till clinical
d. Dry axillae recovery.
e. Pupils no longer pinpoint (Avoided in Carbamate
4. Calculate the total dose of atropine given and give 20% poisoning)
of the total dose hourly as an infusion.
5. Check for features of cholinergic syndrome every fifteen
mins and adjust the dose of atropine infusion
appropriately.
Page | 92
❖ Look for features of atropine poisoning.

1. Confusion
2. Urine retention
3. Hyperthermia
4. Tachycardia
5. Paralytic ileus
❖ If so, omit atropine infusion and monitor every 30 min still they resolve and restart infusion
at 80% of previous rate.
❖ If patient is agitated give iv Diazepam 10mg.
References
UpToDate
Page | 93
Management of Warfarin Toxicity

Major bleeding Non-bleeding
Non-major bleeding
Limb or life threatening INRs >5·0 and >8·0
Emergency anticoagulation Anticoagulation reversal INR >5·0 but who are not
reversal with 25–50 U/kg four- with 1–3 mg IV vitamin K. bleeding should have 1–2
factor prothrombin complex doses of warfarin withheld,
concentrate (PCC) and 5mg IV Patients bleeding at
and their maintenance dose
vitamin K. therapeutic levels of
should be reduced.
anticoagulation should be
If PCC not available, use Fresh investigated for the INR >8·0 should receive 1–5
Frozen Plasma (FFP). source of bleeding. mg of oral vitamin K
Recombinant factor VIIa is not The cause of the elevated
recommended. INR should be investigated.
Special situations
1) Emergency surgery for patients on warfarin
• For surgery that requires reversal of warfarin and that can be delayed for 6–12 h,
the INR can be corrected by giving intravenous vitamin K.
• For surgery that requires reversal of warfarin and which cannot be delayed, INR
can be corrected by giving PCC and intravenous vitamin K.
2) Head Injury in Patients on Warfarin

• All patients on warfarin presenting to accident and emergency departments with
head injuries, however minor, should have their INR measured.
• Individuals with loss of consciousness, amnesia, or reduced Glasgow Coma scale
(GCS) should have an immediate head CT scan.
• Patients on warfarin with a strong suspicion of intracerebral haematoma after a
clear head injury should have their INR reversed with PCC immediately and before
the CT and INR results are available.
• Delayed intracranial bleeding can occur in patients on warfarin even when the
initial CT scan is normal. In view of this, patients with a supra-therapeutic INR
should have this corrected into the therapeutic range with oral vitamin K. It is
suggested that the INR is maintained as close to 2.0 as possible for the 4 weeks
after a significant head injury and a normal CT scan.
Page | 94
3) Patient with mechanical heart valve

Bleeding
4)
Yes
5) No
1. Evaluate
6) Bleeding Risk in Mechanical Valve INR >5 and ≤10
Patients
7)
8) major bleeding risk (uncontrolled, life- - Temporarily discontinue VKA
Assess for non- bleeding patients in
9)
threatening, causing hemodynamic instability) this INR range.
10) valve thrombosis risk.
against
11) - Monitor INR closely for a
2. Identify
12) and Treat Underlying Cause gradual reduction and restart
13)
3. Anticoagulation Reversal Strategy VKA when INR is within the
14) therapeutic range.
Assess severity of bleeding and risk of worsening.
15) - Low-dose vitamin K is not
For 16)
life-threatening bleeding inaccessible to local routinely administered in this
17) consider,
control, scenario.
18)
• Administer Vitamin K (IV dose
19)
ranging from 2.5 to 10 mg).
20)
• Use Four-Factor PCC preferred
21) over Three-Factor PCC or FFP, if
22) available, for rapid and low- INR >10
23) volume reversal of VKA effects.
24) • Monitor INR frequently (e.g., 30 - Temporarily halt VKA if INR is
25) minutes, then every 4-6 hours) >10 without bleeding.
26) until normalization.
27) • Consider repeating vitamin K - Consider 1 to 2.5 mg oral
28) doses at 12-hour intervals if vitamin K if high bleeding risk,
29) necessary. with close INR monitoring (daily
•
30) Caution against repeated PCC dosing due for at least two weeks).
31) to unstudied risk of thrombosis.
- Low-dose vitamin K rapidly
32) reduces excessive anticoagulation
without causing temporary
resistance to VKA therapy.
- Oral vitamin K is preferred

over intravenous for a gradual
INR decrease, reducing the risk of
subtherapeutic INR and
thromboembolism.
Page | 95
Management of Other Bleeding Types

• Tailor management based on bleeding severity, control accessibility, and
risk of exacerbation.
• For minimal bleeding, temporarily withhold VKA. Decide on low-dose
vitamin K and aggressive measures based on bleeding risk.
Resumption of Anticoagulation
Determine optimal timing for resuming anticoagulation, considering bleeding site, cause,
and interventions. Individualize decisions in consultation with cardiologists or cardiac
surgeons.
Reference
1. Guidelines on oral anticoagulation with warfarin – 4th Edition
2. British Society for Haematology (BSCH)
3. UpToDate
Page | 96
Management of Snake Bite

Identify the
Patient with confirmed or suspected snake bite
snake
Admit, reassure, and assess for local and

systemic envenomation.
Give Tetanus Prophylaxis subcutaneously 0.5 ml
Local envenomation Systemic envenomation
Give Anti Venom if;

Local • Cobra
Swelling
envenomation
Blistering • Russell’s Viper
following a
Tissue necrosis
cobra bite • Saw scaled viper
• Krait
Observe for 24 hours

Spontaneous Bleeding
Respiratory failure
No Systemic Ptosis
envenomation Ophthalmoplegia
+ 20 min Whole blood clotting time
Discharge
Premedicate with S/C
Other snakes
Adrenaline (1:1000) 0.25 ml
10-20 ampoules of Indian poly specific Anti

Snake Venom in 400 ml of N/S over 1 hour
If coagulopathy persists in 6 hours Anti Treat

Snake Venom can be repeated but not coagulopathy with
for persisting neurotoxicity. FFP 15 ml/kg
Page | 97
Antivenom Therapy: Indian manufactured polyvalent antivenom

Indications for Antivenom therapy:
1. Russell’s Viper
▪ If coagulopathy is presents.
▪ If no demonstrable coagulopathy
- but proven Russell’s viper bite with fang marks, abdominal pain and
some local effects.
- Or any one or more systemic effects such as visual disturbances,
dizziness, faintness, collapse, shock, hypotension, cardia arrythmias or
myocardial damage.
2. Cobra
▪ Any evidence of systemic envenoming or local envenoming.
▪ As dry bites are common, in the presence of fang marks without symptoms of
envenoming observe for 48 hours and if any swelling appears give the first dose of
AV. (10 vials)
3. Kraits
▪ If neurotoxic effects are presents.
▪ If severe abdominal pain in the absence of neurotoxic effects.
4. Saw Scaled Viper
▪ Only if coagulopathy present.
Antivenom Dose and preparation
❖ Russell’s Viper bite- the first dose is 200ml (20 ampoules): subsequent doses should be
100ml (10 ampoules) to a maximum of 40 ampoules.
❖ All other species- the first and any subsequent doses, is 100ml.
❖ Administer antivenom as intravenous infusion over one hour, the required dose being
dissolved in water and made up to 500ml with normal saline.
❖ Observe for signs of anaphylaxis and monitor pulse, respiratory rate, and blood pressure.
Treat anaphylaxis immediately.
Management of Antivenom Reaction
• Epinephrine (adrenaline) is given intramuscularly (ideally into the upper lateral thigh) in an
initial dose of 0.5 mg for adults, repeat every 5 minutes if needed.
• If bronchospasms developed
- Oxygen driven nebulization with salbutamol 5mg.
- Intravenous chlorpheniramine 10mg bolus and intravenous hydrocortisone 200mg
bolus.
• If unresponsive for intramuscular adrenaline and remain hypotensive and shocked
- Lay supine with leg elevated to 45 degrees
- Rapid administration of 0.9% saline boluses 1-2 liters
- IV adrenalin infusion (1mg of 0.1% solution in 250ml of 0.9% saline or 5%
dextrose, infused at a rate of 15-60 drops /min (0.1mcg/kg/min)
Page | 98
References
1. SLMA Guideline on management of snake bite 2017
2. WHO Guideline on snake bite management 2016
Page | 99
Emergency protocols - 2023 Gastrointestinal system
Gastrointestinal System Related

Emergencies
Page | 100
Management of Hepatic Encephalopathy
Classification of Hepatic Encephalopathy (HE)
Diagnosis
• Mainly a clinical diagnosis

• Covert HE can be assessed with bedside psychometric tests (eg. Number connection test)
• Normal serum ammonia value questions the diagnosis of HE but won’t exclude it. It’s not
routinely performed.
• Brain imaging by CT scan or MRI should be performed in case of diagnostic doubts or non-
response to treatment.
• EEG: High-amplitude low-frequency waves and triphasic waves may be observed. But
they’re not specific for HE
Classification HE
1. Severity based: West Haven criteria
Classification Clinical features
Minimal Covert Abnormal results on psychometric or neurophysiological

testing without clinical manifestations
Grade I Changes in behavior, mild confusion, slurred speech,
disordered sleep
Grade II Overt Lethargy, moderate confusion, asterixis
Grade III Marked confusion (stupor), incoherent speech, sleeping
but arousable
Grade IV Coma, unresponsive to pain
2. Time course
• Episodic
• Recurrent - more than one episode over a period of 6 months
• Persistent - no return to normal/baseline neuropsychiatric performance
in between episodes
3. Precipitating factors
• Non-precipitated
skfnsfksff
• Precipitated
Page | 101
Precipitating factors of hepatic encephalopathy

• Gastrointestinal bleeding • Sedative or benzodiazepine use
• Infection (including spontaneous bacterial • Hypoglycaemia
peritonitis and urinary tract infections) • Constipation
• Hypokalemia and/or metabolic alkalosis • Hepatocellular carcinoma and/or
• Renal failure vascular occlusion (hepatic vein or portal
• Hypovolemia vein thrombosis)
• Hypoxia
Management
Treat precipitating Factors

• Infections
• Electrolyte imbalances
• Constipation
Definitive Management
• Supportive care: Avoid dehydration, correct electrolyte abnormalities.

• Patients with overt HE grade 3 and 4 are at risk of aspiration and should be
treated in the ICU.
• Nutritional support: Daily energy intake of 35 to 40 kcal/kg/day, protein intake
1.2 to 1.5 g/kg/day.
Substitution of animal proteins with vegetable proteins may improve nitrogen
balance and mental status. Addition of branched-chain amino acids (BCAA) to a
low protein diet in patients whose symptoms worse with protein intake
Once the patient improves standard diet can be given
If there is demonstrated or suspected vitamin/ micronutrient deficiencies it
should be treated, as they can compound HE
• Correction of precipitating causes
• Drug therapy to lower blood ammonia concentration
Lactulose (30 to 45 mL orally two to four times per day) should be titrated to
achieve two to three soft stools per day
For patients without improvement in mental status within 48 hours or who
cannot take lactulose, rifaximin is 550 mg orally two times daily or 400 mg
orally three times daily can be given.
• L-ornithine-L-aspartate (6-18 grams by mouth daily)
• MARS- Molecular adsorbing recirculating system
• Evidence for use of Flumenazil and Na Benzoate are sparce.
Page | 102
Reference
• EASL Clinical Practice Guidelines on the management of hepatic encephalopathy, 2022

• UpToDate
Page | 103
Management of Upper Gastrointestinal Haemorrhage
Sources of UGI Bleeding
Non- portal hypertensive bleeds Portal Hypertensive bleeds
▪ Ulcer bleeds ▪ Oesophageal varices

▪ Mallory-Weiss tears ▪ Cardo-fundal varices
▪ Neoplasms ▪ Ectopic varices
▪ Oesophagitis ▪ Portal hypertensive gastropathy
▪ Gastric antral vascular ectasia
Risk Assessment
▪ Rockall Score (Pre-endoscopic)
▪ Glasgow Blatchford Score
▪ AIM65
For initial triage
High Risk: Intensive monitoring & early endoscopic intervention
Low Risk: Fast tracked towards early hospital discharge
Check the Appendix for scoring.
Suspected Variceal Bleeding

▪ Hemodynamic resuscitation – initially using IV crystalloid fluids
▪ Use restrictive RBC transfusion policy
▪ Start vasoactive medication
▪ Give antibiotic prophylaxis
▪ Temporarily withhold antiplatelet agents and anticoagulants*
▪ Consider endotracheal intubation in selected at-risk patients **
(GCS <8 or Upper airway compromised)
▪ Consider giving an IV promotility agent prior to upper
gastrointestinal endoscopy
Perform EGD within 12 hours of patient presentation once

adequately hemodynamically resuscitated
Page | 104
• Oesophageal variceal bleeding confirmed

• Perform risk stratification
• Perform EBL (Endoscopic band ligation)
EVH controlled Persistent EVH Recurrent EVH

within the first
Low risk of recurrent bleeding: ▪ Consider urgent ▪5 days
Second attempt
TIPS or at endoscopic
▪ continue vasoactive haemostasis or
▪ oesophageal stent
medication for up to 5 days ▪ Perform salvage
(if available) or
▪ initiative/resume NSBB TIPS
▪ tamponade balloon
▪ schedule follow-up
as a temporizing
endoscopy within 1–4 weeks
measure followed
for repeat EBL for secondary
by rescue TIPS
prophylaxis
High risk of recurrent

bleeding:
▪ consider pre-emptive TIPS

within 72 hours (preferably
within 24 hours)
EGD-esophagogastroduodenoscopy EVH- Endoscopic Variceal Haemorrhage
EBL-endoscopic band ligation
IV-intravenous
NSBB-nonspecific beta blocker
RBC-red blood cell
TIPS-trans jugular intrahepatic portosystemic shunt.
* The restarting of antiplatelet agents and/or anticoagulants should be guided by the

patient’s risk of rebleeding versus their risk of thrombosis.
** Extubation should occur as soon as clinically safe following upper gastrointestinal endoscopy
Page | 105
Gastric Variceal Haemorrhage (GVH)
▪ Perform endoscopic cyanoacrylate injection

▪ Cyanoacrylate injection or EBL in patients with
Gastroesophageal varices type 1; specific bleeding
▪ EUS-guided injection of coils + cyanoacrylate may be
used in centres with expertise
GVH controlled Persistent GVH Recurrent GVH within the

first 5 days
▪ Continue vasoactive ▪ Urgent rescue TIPS or ▪ TIPS or BRTO or

medication for up to 5 days BRTO or ▪ may consider relook
▪ initiative/resume NSBB ▪ tamponade gastric endoscopy with
▪ For secondary prophylaxis, an balloon as a temporizing EUS-guided
individualized patient approach measure followed by injection of coils +
should be used based upon rescue TIPS or BRTO cyanoacrylate in
patient factors and local (balloon retrograde centres with
expertise. transvenous expertise
▪ If patient is at high risk for obliteration)
rebleeding, consider pre-
emptive TIPS
Treatment modalities in Variceal bleeding in chronic liver disease

Red cell transfusion
▪ A restrictive red blood cell (RBC) transfusion strategy: with a haemoglobin threshold of ≤
7g/dL prompting RBC transfusion (in hemodynamically stable patients with acute upper GI
haemorrhage and no history of cardiovascular disease)
▪ A post-transfusion target haemoglobin of 7–9g/dL is desired.
▪ In patients with a history of cardiovascular disease: haemoglobin threshold < 8g/dl
▪ If hemodynamically unstable with hypotension despite fluid resuscitation red cell transfusion
is recommended.
Page | 106
Vasoactive drugs
▪ IV Terlipressin 1mg 6H
▪ IV octreotide 50-100mg stat followed by 25-50mg infusion
▪ Initiated at the time of presentation in patients with suspected acute variceal bleeding and
be continued for a duration of 3- 5 days.
Antibiotic prophylaxis
▪ IV Ceftriaxone 1 g/day for up to 7 days or oral norfloxacin 400mg bd
▪ Significantly reduces rebleeding, infections and mortality
▪ Maximum duration of 7 days
▪ Consider discontinuing when haemorrhage has resolved and vasoactive drugs are
discontinued.
Intravenous Prokinetic
▪ IV Erythromycin 250mg given 30–120 minutes prior to upper GI endoscopy in patients with
suspected acute variceal haemorrhage.
▪ Improve visibility, increase chances of diagnosis at first UGIE, reduce 2nd look UGIE and
hospital stay.
Endoscopic evaluation
▪ In patients with suspected variceal haemorrhage, endoscopic evaluation should take place
within 12 hours from the time of patient presentation provided the patient has been
hemodynamically resuscitated.
Non-selective beta blockers
▪ Carvedilol/propanol should be started when vasoactive drugs are discontinued.
Do nots in Variceal bleeding in chronic liver disease
▪ Transfusion of fresh frozen plasma for elevated INR

▪ Transfusion of tranexamic acid for bleeding
▪ Don’t transfuse RCC aiming at Haemoglobin > 9g/dl
Secondary prophylaxis
▪ Patients who have undergone EBL for acute EVH should be scheduled for follow-up EBLs at
1- to 4-weekly intervals to eradicate oesophageal varices.
▪ Use of NSBBs (propranolol or carvedilol) in combination with endoscopic therapy.
Page | 107
Appendix
1. Rockall Score
AIM65 Score
Criteria Score
Risk factor Score
Age
Albumin <3mg/dl 1
<60 yrs 0 INR >1.5 1
60-79 yrs 1 Altered mental status 1
> 80yrs 2 SBP< 90mmHg 1
Schock Age>65 yrs 1
Score > 2 considered high risk
SBP> 100, pulse <100 0
SBP > 100, Pulse >100 1
SBP<100 2 Rockall Score Risk Category
Comorbidity No major comorbidity 0
No major comorbidity 0
IHD, HF, Any major 2
IHD, HF, Any major 2 comorbidity
comorbidity
Renal failure, Liver Failure, 3 Renal failure, Liver Failure, 3
disseminated malignancy disseminated malignancy
High risk >6
Management of Ulcer Bleeding
• IV PPI Bolus+ Infusion

IV Pantoprazole 80mg stat followed by 8mg/hour infusion
• Once hemodynamically stable, arrange endoscopy
Active bleeding/ non bleeding Adherent clot Flat spot/ clean base
visible vessel
• Endoscopic therapy • May consider endoscopic • No endoscopic

• IV PPI bolus+ therapy therapy
infusion • IV PPI bolus+ infusion • Oral PPI
Page | 108
Endoscopic Therapy
▪ Thermal therapy
▪ Injection (adrenaline/ sclerosant e.g., Ethanol)
▪ Clips through scope
Post Endoscopic Medical Therapy
▪ Active bleeding, visible vessel, clot

High dose PPI continuously or intermittently for 3 days after successful endoscopic
haemostasis a bleeding ulcer
-IV pantoprazole/omeprazole 80mg bolus and 8mg/hour infusion
-IV pantoprazole /omeprazole 80mg bolus and 40mg 2-4 times daily
▪ Flat spot, clean base
Standard oral PPI once daily
Secondary Prevention
▪ Treat the aetiology

▪ H pylori therapy
▪ Avoid NSAIDS
▪ Aspirin for secondary prevention: resume soon after haemostasis achievement with
PPI
▪ Aspirin for primary prevention: do not resume aspirin in most patients
▪ Idiopathic: maintenance PPI therapy
References
• Gralnek Ian M et al, Endoscopic diagnosis and management of esophagogastric variceal

haemorrhage: European Society of Gastrointestinal Endoscopy (ESGE).54: 1094–1120 |
2022.
• Up to date
• Managing Upper GI bleeding: What’s changed and what’s still the same, Prof. Madunil A
Niriella
Page | 109
Management of Acute Liver Failure

Definition
Severe acute liver injury defines a syndrome characterized by markers of liver damage
(elevated serum transaminases) and impaired liver function (jaundice and INR >1.5) which
usually precedes clinical encephalopathy in a patient without a chronic liver disease except
those who present with an acute presentation of chronic autoimmune hepatitis, Wilson
disease and Budd-Chiari syndrome.
Classification
• Hyperacute liver failure - patients developing HE within 7 days of noting jaundice

• Acute liver failure - patients develops, HE between 8 and 28 days of noting jaundice
• Subacute liver failure - HE occurring within 5–12 weeks of jaundice
• Chronic liver disease - Disease duration of greater than 28 weeks before the onset of
encephalopathy
Causes
Infections Autoimmune Other

Malignant
• Breast • Wison’s
• Viral Toxins • Small cell • Budd-Chiari
hepatitis
• PCM lung cancer • Venoo-occlusive
• Sepsis • Lymphoma
• Idiosyncratic • Acute fatty liver of
• Mushroom • Melanoma pregnancy/HELLP
poisoning • myeloma syndrome
• Partial hepatectomy
HELLP – Haemolytic, elevated Liver Enzymes, Low platelets
Assessment
Investigations
For complications
• Lipase and Amylase
Page | 110
For Aetiology
• Toxicology screen in Urine and Paracetamol serum level
• Serological screen for virus infections
• HBsAg, anti-HBc IgM (HBV DNA), delta if positive for HBV
• Anti HAV IgM
• Anti-HEV IgM
• Anti-HSV IgM, anti VZV IgM, CMV, HSV, EBV, parvovirus and VZV PCR
• Autoimmune markers: ANA, ASMA, anti-soluble liver antigen,
• globulin profile, ANCA, HLA typing
For Severity
• PT, INR or factor V and full coagulation screen including fibrinogen
• Liver blood tests including LDH and conjugated and unconjugated
• bilirubin and creatinine kinase
• Assessment of renal function:
Urine output: hourly
Low urea is a marker of severe liver dysfunction.
Creatinine may be difficult to assay in the context of elevated bilirubin.
• Arterial blood gas and lactate
• Arterial ammonia
Acute management
Management
Monitor
• Vitals – BP, PR, RR, UOP, SPO2

• Nutritional status and fluid balance
• Glucose infusions (10–20%): glycemic target ± 140 mg/dl,
• Na 135–145 mmol/L
• Restrict clotting factors unless active bleeding

• Stress ulcer prophylaxis
Page | 111
Treat the aetiology
• N-acetylcysteine in early stage, even in non-paracetamol cases (In

non-paracetamol ALF NAC did not improve survival overall, but did
improve outcome in adults with mild grades of HE
• Acetaminophen toxicity — N-acetylcysteine
• Hepatitis B infection — Antiviral therapy with a nucleos(t)ide
analogue may be beneficial
• Mushroom poisoning — Early administration of activated charcoal,
additional administration of silibinin and penicillin G
• Budd-Chiari syndrome — Transjugular intrahepatic portosystemic
shunt placement, surgical decompression, or thrombolysis
• Herpes simplex virus infection – Acyclovir
• Autoimmune hepatitis – Trial of glucocorticoids in patients without
encephalopathy. Transplant workup if they develop encephalopathy
• Wilson disease – Therapeutic plasma exchange
• Acute fatty liver of pregnancy – Prompt delivery of the fetus
Monitor for Hepatic Encephalopathy - mental alterations
In case of hepatic encephalopathy
• Transfer to an appropriate level of care (ideally critical care) at the first

symptoms of mental alterations
• Quiet surrounding, head of bed >30°, head in neutral position and
intubate, ventilate, and sedate if progresses to ≥3 coma.
• Low threshold for empirical start of antibiotics if hemodynamic
deterioration and/or increasing encephalopathy with inflammatory
phenotype
• In case of evolving HE intubation and sedation prior to the transfer
• Ensure volume replete and normalize biochemical variables (Na, Mg, PO4,
K)
• Mannitol or hypertonic saline should be administered for surges of ICP
• Consider short term hyperventilation
• Mild hypothermia and indomethacin may be considered in uncontrolled
Page | 112
Antibiotics
• Prophylactic antibiotics, non-absorbable antibiotics, and antifungal have not been

shown to improve survival in ALF
• Early antibiotic treatments should be introduced upon appearance of progression
of hepatic encephalopathy, clinical signs of infections, or elements of SIRS
Fresh frozen plasma
• The routine use of fresh frozen plasma and other coagulation factors is not
recommended.
• It has a place if there is active bleeding or before invasive procedures like central
venous line insertion.
Lactulose in acute liver failure
• Whereas lactulose is commonly used in patients with hepatic encephalopathy due

to chronic liver disease, its use in acute liver failure is controversial.
• One study found a small increase in survival time among patients with acute liver
failure who received lactulose. However, there was no difference in the severity
of encephalopathy or in overall outcomes.
• One concern with the use of lactulose is that it may lead to bowel distension that
could result in technical difficulties during liver transplantation.
•
Proton Pump Inhibitor (PPI) in acute liver failure
• PPI administration should be balanced against the risk of ventilator associated

pneumonia and Clostridium difficile infection.
• Consider stopping PPI when enteral feeding has been established.
Criteria for transfer to a special unit
Page | 113
complications of acute liver failure
Indications for emergency referral for liver transplantation
Source
• EASL Clinical Practical Guidelines on the management of acute (fulminant) liver failure
2017
• UpToDate
Page | 114
Emergency protocols - 2023 Electrolyte Imbalance
Emergencies Related to Electrolyte

Imbalances
Page | 115
Management of Hyperkalemia
• Assess using ABCDE approach
• 12-lead ECG and monitor cardiac rhythm if serum K+ ≥ 6.5mmol/L
• Exclude pseudohyperkalaemia
• Give empirical treatments for arrythmia if hyperkalaemia is suspected
Mild Moderate Severe

K+ 5.5 – 5.9 mmol/L K+ 6 – 6.4 mmol/L K+ ≥ 6.5mmol/l
Consider cause and need for Treatment guided by clinical Consider cause and need for
treatment condition, ECG and rate of treatment
rise
ECG Changes?
Peaked T waves Broad QRS Bradycardia

Flat/ absent P Sine wave VT
waves
IV Calcium
10ml 10% Calcium chloride IV or
30ml 10% Calcium Gluconate IV
Protect the
• Use large IV access and give over 5min
heart
• Repeat ECG
• Consider further dose after 5 min if ECG changes
persistent
Insulin – Glucose IV Infusion

Shift K+
Into cells Glucose 25g with 10 units soluble insulin over 15-30min IV
(25-50ml 50% glucose; 125ml 20% glucose, 250ml 10% glucose)
If pre treatment blood glucose < 7mmol/L
Start 10% glucose infusion at 50ml/hour for 5 hours (25g)
Remove K+ Salbutamol 10-20 mg nebulised

From the
body
Sodium zirconium cyclosilicate
Sodium zirconium cyclosilicate
10g x3/day oral for 72hrs or
10g x3/day oral for 72hrs or
Monitor K+ Patiromer 8.4G/day oral or
Patiromer 8.4G/day oral
And blood Calcium resonium 15g x3/ day oral
glucose Consider dialysis
Monitor serum K+ and blood glucose
K+ ≥ 6.5mmol/l
Despite medical therapy
Prevention Consider cause of hyperkalaemia and prevent recurrences
Page | 116
Source
• European Resuscitation Council Guideline
Page | 117
Management of Hypokalemia
Hypokalaemia
Serum potassium
<3.5 mmol/L
Identify and treat the underlying cause of hypokalaemia. Hypokalaemia is often

resistant to treatment when hypomagnesaemia is present so treat both
Discontinue drugs which may reduce serum potassium concentration if possible

(e.g. Thiazides, loop diuretics etc)
Mild Moderate Severe

3.0-3.5 mmol/L 2.5-2.9 mmol/L <2.5 mmol/L
KCL 2 tabs BD KCL 2 tabs TDS IV replacement
(IV replacement may be used (IV replacement may be used 40mmol KCI in 0.9%
if the patient is NBM if the patient is NBM NaCl 1L over 6 hours
20-40mmol KCI in 0.9% NaCl
20-40mmol KCI in 0.9% NaCl
1L over 8 hours) NBM-Nill by
1L over 8 hours)
mouth
Monitor serum potassium Monitor serum potassium Monitor serum

at least twice weekly until daily until >2.9 mmol/L potassium after 6 hours
stable or >4.5 mmol/L, then and repeat infusion if
then re-assess manage as for mild appropriate
hypokalaemia
Potassium level may rise initially then fall as potassium uptake into cells increases.
For ongoing renal loss, potassium sparing diuretics may be used,
e.g. Amiloride or Spironolactone
References
• Guidelines for the management of acute hypokalaemia in adults – NHS foundation
trust
Page | 118
Management of Hyponatremia
Classification
Mild: 130-134 mmol/L

Moderate: 125-129 mmol/L
Severe: < 125 mmol/L
Acute : <48hours Chronic : >48hours or unknown duration
Symptoms
Asymptomatic Mild to Moderate Severe

▪ Nausea ▪ Confusion
▪ Vomiting ▪ Drowsiness
▪ Headache ▪ Seizures
▪ Lethargy ▪ Coma
▪ Fatigue
▪ Muscle cramps
Management
Severe symptoms (Acute or chronic moderate symptoms
(a) 150ml 3%Nacl over 20min • Single IV infusion of 150ml of 3%

Repeat SE NaCl over 20 minutes
(b) Repeat 150ml 3% NaCl over 20min • Aim 5mmol/l/day increase in
Repeat (a) & (b) steps until achieving serum Na
5mmol/l increase in serum Na • Check Na after 1hr, 6hr,12hr
Improvement of symptoms after

5mmol/l rise
No
Yes
Page | 119
Yes No
• Stop infusion of 3%NaCl and keep IV line • 3% NaCl IV infusion for additional
open by smallest feasible volume of 1mmol/l increase in Na
normal saline • Stop infusion if symptoms improve or
• Check Na 6hrly and 12 hrly and daily serum Na level increase 10mmol/l in total
• Increase in Serum Na by 10mmol/l during or serum Na 130mmol/l which ever occur
1st 24 hrs and after that 8mmol/l/day first
until serum Na is 130mmol/L • Check serum Na every 4 hrs as long as
• Start diagnostic specific treatment if 3%NaCl continue
available
Hyponatraemia without severe or moderately severe symptoms
Acute Chronic
• If Acute decrease in Serum Na • Stop non-essential fluid/medications
exceeds 10mmol/l • Cause specific treatment
• Mild hyponatraemia: No treatment
• Single IV infusion of 150ml 3% • Moderate or profound hyponatraemia:
saline over 20min Avoid increase in serum Na
• Check Na 4hrs after that >10mmol/l/day and >8mmol/l every
24hrs there after
• Check serum Na 6 hrly
Page | 120
Hypotonic Hyponatremia
Serom Osmolality < 275mOsm/Kg
Urine Spot Osmolality> 100mOsm/Kg
Hypovolemic Euvolemic Hypervolemic

Spot U.Na >30mmol/L Spot U.Na >30mmol/L Spot U.Na < 30mmol/L
▪ Renal: • SIADH ▪ Heart failure
• Diuretics ▪ Cirrhosis
▪ Nephrotic
• Addison’s disease Treatment of SIADH
syndrome
• Tubular interstitial disorders • First line- fluid
▪ Renal failure
• Osmotic diuresis Cerebral salt restriction
Treatment
• wasting • Second line- low
▪ Not to treat with
dose loop diuretic
sole aim of
Spot U.Na < 30mmol/L and oral salt
increasing serum
▪ Extra renal: • Treat the aetiology
Na
• GI losses- vomiting, diarrhea ▪ Fluid restriction
• Burns ▪ Vaptans e.g
• Third space losses Tolvaptan are
Treatment recommended in
• IV NaCl 0.9% 0.5ml-1ml/kg/hour US guidelines.
• Haemodynamic instability IV fluid
resuscitation overrides the risk of
rapid increase in serum Na
• Treat the aetiology
Rapid overcorrection of Na
• Discontinue ongoing active treatment

• 5%dextrose 10ml/kg/hr
• Iv desmopressin- 2mg
Page | 121
Treatment of hyponatremia
Goal – raise serum Na by 0.5-1meq/l/hour and not more than 10-12meq/day to bring up Na
to 125-130meq/l
Step 1: Calculation of Na deficit

Na deficit= (derived Na – Measured Na) ×0.6male/0.5female×weight in kg
Eg: 60kg male patient with serum Na 112
Na deficit= (120-112) ×0.6×60kg
Step 2 Step 3
volume of 3%saline needed rate= 561cc/24hrs

= Na deficit = 23cc/hr
513 meq/l
= 288/513
= 0.561
0.561L or 561 ml 3% saline
References
1. Medscape
2. Joint european clinical practice guidelines 2019 june update
Page | 122
Management of Hypercalcemia
Clinical features
• Groans: Gastrointestinal symptoms like pain, nausea, and vomiting.

Hypercalcemia can lead to peptic ulcer disease and pancreatitis.
• Bones: Bone pain. Hypercalcemia can lead to osteoporosis, osteomalacia,
arthritis and pathological fractures.
• Stones: Renal stones.
• Moans: Refers to fatigue and malaise.
• Thrones: Polyuria, polydipsia, and constipation.
• Psychic overtones: Lethargy, confusion, depression, and memory loss.
Severe hypercalcemia inhibits neuromuscular and myocardial depolarization

leading to muscle weakness and arrhythmias. It can cause prolonged PR interval,
short QT interval, widened QRS complex, and bradycardia
Causes
Parathyroid mediated Non-parathyroid mediated Medications

• Primary hyperparathyroidism • Hypercalcemia of malignancy • Thiazide diuretics
(sporadic) • Secretion of PTHrP • Lithium
• Multiple endocrine neoplasia • Increased calcitriol (activation of • Excessive vitamin A
(MEN) syndromes extrarenal 1-alpha-hydroxylase)
• Hyperparathyroidism-jaw • Osteolytic bone metastases and Miscellaneous
tumor syndrome local cytokines
• Familial hypocalciuric • Vitamin D intoxication • Hyperthyroidism
hypercalcemia • Chronic granulomatous disorders • Acromegaly
• Tertiary hyperparathyroidism or other illnesses characterized by • Pheochromocytoma
(renal failure) granuloma formation • Adrenal insufficiency
• Increased calcitriol (activation of • Immobilization
extrarenal 1-alpha-hydroxylase) • Parenteral nutrition
• Milk-alkali syndrome
Classification
Mild hypercalcemia Moderate hypercalcemia Severe hypercalcemia

Calcium above the upper A moderately elevated serum
Calcium >14 mg/dL [3.5
limit of normal but <12 calcium of 12 to 14 mg/dL (3 to
mmol/L])
mg/dL [3 mmol/L]) 3.5 mmol/L)
Page | 123
Management
Mild hypercalcemia Moderate hypercalcemia Severe hypercalcemia

• Adequate hydration (at • Asymptomatic or mildly
least six to eight glasses • Volume expansion with
symptomatic individuals
of water per day) is isotonic saline
with chronic moderate
recommended to • Administration of isotonic
hypercalcemia may not saline at an initial rate of 200
minimize the risk of require immediate therapy.
nephrolithiasis to 300 mL/hour that is then
However, they should adjusted to maintain the urine
• Avoid factors that can
follow the same output at 100 to 150 mL/hour
aggravate hypercalcemia
like, Thiazide diuretics, precautions described in patients without edema
lithium carbonate, above for mild • The rate of infusion depends
Calcium supplements, hypercalcemia. upon severity of
Vitamin D supplements in • However acute rise of hypercalcemia, the age of the
excess of 800 patient, and presence of
calcium to this range might
international units/day comorbid conditions,
need treatment with
and Multivitamins particularly underlying cardiac
normal saline hydration or renal disease
containing calcium and bisphosphonates as in • Saline therapy rarely
for severe hypercalcemia. normalizes the serum calcium
concentration in patients with
severe hypercalcemia.
Concurrent treatment with
bisphosphonates with or
without calcitonin is typically
required to treat moderate to
severe hypercalcemia
Calcitonin
• MOA- Decreases bone resorption via interference with osteoclast function and increases
renal calcium excretion.
• The initial dose is 4 units/kg and it is administered intramuscularly or subcutaneously.
The serum calcium is repeated in four to six hours. If a hypo calcemic response is noted,
then the patient is calcitonin sensitive and the calcitonin can be repeated every 12 hours
for a total duration of 24 to 48 hours. If the response is not satisfactory, the dose may be
increased to 8 units/kg every 6 to 12 hours.
• The duration of treatment is limited to the first 48 hours because of the development of
tachyphylaxis.
• It has a rapid onset of action and lowers the serum calcium concentration by a maximum
of 1 to 2 mg/dL beginning within four to six hours
Page | 124
Bisphosphonates
• It is useful for longer-term control of hypercalcemia in patients with more severe
(calcium >14 mg/dL) or symptomatic hypercalcemia
• MOA- Bisphosphonates attach to hydroxyapatite binding sites on bony surfaces,
especially surfaces undergoing active resorption. When osteoclasts begin to resorb
bone that is impregnated with bisphosphonate, the bisphosphonate impairs the
ability of the osteoclastic resorption. It also reduces osteoclast activity by decreasing
osteoclast progenitor development and recruitment and by promoting osteoclast
apoptosis.
• Zoledronic acid (4 mg IV over 15 minutes) is preferred over pamidronate (60 to 90
mg over 2 hours) because it is superior to pamidronate in reversing hypercalcemia
related to malignancy
• In patients with impaired renal function (creatinine >4.5 mg/dL) a reduced dose
and/or slower infusion rate (2 to 4 mg zoledronic acid over 30 to 60 minutes, 30 to 45
mg pamidronate over 4 hours) may minimize risk. The renal tubular toxicity is related
to the rate of infusion.
• Side effects - Flu-like symptoms (fever, arthralgias, myalgia, fatigue, bone pain),
ocular inflammation (uveitis), hypocalcemia, hypophosphatemia, and impaired renal
function, including proteinuria.
• Check serum creatinine and vitamin D level before giving bisphosphonates
• Bisphosphonate
Cs contraindications (eg. Severe renal impairment, allergy) or
refractory hypercalcemia:
•
Denosumab
• given as an initial dose of 60 mg subcutaneously in patients contraindicated for
bisphosphonates and 120mg SC who are refractory for Zoledronic acid. In case reports it
improved serum calcium within two to four days.
• MOA- Denosumab is a monoclonal antibody with affinity for nuclear factor-kappa ligand
(RANKL). Denosumab binds to RANKL, blocks the interaction between RANKL and RANK
(a receptor located on osteoclast surfaces), and prevents osteoclast formation, leading
to decreased bone resorption.
Denosumab
• Hemodialysis with little or no calcium in the dialysis fluid is considered treatment of last
resort. Dialysis may be indicated in patients with severe malignancy-associated
hypercalcemia and renal insufficiency or heart failure, in whom hydration cannot be
safely administered.
Page | 125
What is the place for loop diuretics in the management of hypercalcemia?

• In the absence of renal failure or heart failure, loop diuretic is not recommended, as it
can cause the potential for fluid and electrolyte complications (eg, hypokalemia,
hypomagnesemia) and volume depletion resulting from a massive saline infusion and
furosemide-induced diuresis.
• However, in individuals with renal insufficiency or heart failure, careful monitoring,
and judicious use of loop diuretics (after intravascular volume has been repleted) may
be required to prevent fluid overload.
Preventing recurrence
• In patients with hypercalcemia of malignancy, the underlying disease causing the

hypercalcemia should be treated, if at all possible.
• In patients with renal insufficiency and history of hypercalcemia, calcium intake
should be limited to 1000 mg per day (total diet plus any supplements). Excessive
vitamin D supplements should be avoided.
• In patients with normal renal function and history of hypercalcemia, excessive
amounts of calcium and vitamin D supplements should also be avoided.
Reference
• UpToDate
Page | 126
Management of Hypocalcemia
Definition
Hypocalcemia is defined as a total serum calcium concentration < 8.8 mg/dL (< 2.20
mmol/L) in the presence of normal plasma protein concentrations or as a serum
ionized calcium concentration < 4.7 mg/dL (< 1.17 mmol/L).
Clinical features
Acute Chronic
• Neuromuscular irritability (tetany) • Ectopic calcification (basal ganglia)
• Paresthesia (perioral, extremities) • Extrapyramidal signs
• Muscle twitching • Parkinsonism
• Carpopedal spasm • Dementia
• Trousseau's sign • Subcapsular cataracts
• Chvostek's sign • Abnormal dentition
• Seizures • Dry skin
• Laryngospasm
• Bronchospasm
• Cardiac
• Prolonged QT interval
• Hypotension
• Heart failure
• Arrhythmia
• Papilledema
Aetiology
• Acute pancreatitis
• Hypoparathyroidism • Osteoblastic metastases
• Vitamin D deficiency or resistance • Sepsis or acute severe illness
• PTH resistance • Drugs - Inhibitors of bone
• Pseudohypoparathyroidism resorption (bisphosphonates,
• Hypomagnesemia calcitonin, denosumab),
• Renal disease especially in vitamin D deficiency
• Tumor lysis • Cinacalcet
• Calcium chelators (EDTA, citrate,
phosphate)
Page | 127
Management
Severe symptomatic and/or acute hypocalcemia
• Patients with symptoms (eg, carpopedal spasm, laryngospasm,

bronchospasm, seizures) or A prolonged QT interval or asymptomatic
patients with an acute decrease in serum corrected calcium to ≤7.5
mg/dL (≤1.9 mmol/L)
• IV calcium 1 or 2 g of calcium gluconate (90 or 180 mg elemental
calcium), in 50 mL of 5% dextrose or normal saline) can be infused
over 10 to 20 minutes. The bolus may be repeated after 10 to 60
minutes, if needed to resolve symptoms.
• IV calcium should be continued until the patient is receiving an
effective regimen of oral calcium and vitamin D.
• In patients with hypomagnesemia, IV MgSO4 2 g should be infused as
a 10% solution over 10 to 20 minutes, followed by 1 gram in 100 mL of
fluid per hour. Magnesium repletion should be continued as long as
the serum magnesium concentration is less than 0.8 mEq/L (1 mg/dL).
How does hypomagnesemia cause hypocalcemia?
• Induces resistance to parathyroid hormone (PTH) and diminishes its

secretion.
Mildly symptomatic or chronic hypocalcemia

• For patients with serum corrected calcium concentration above 7.5 to 8.0
mg/dL or a serum ionized calcium concentration above 3.0 mg/dL [0.8
mmol/L]) or for chronic hypocalcaemia, oral calcium supplementation is
preferred.
Page | 128
Aetiology Based Treatment
• Hypoparathyroidism • Lifelong calcium and vitamin D supplementation

• Vitamin D deficiency • Nutritional vitamin D deficiency with 50,000
international units of vitamin D2 or D3 weekly for
six to eight weeks.
• High doses of vitamin D of 10,000 to 50,000
international units may be necessary to treat
patients with gastrectomy or malabsorption.
• Chronic kidney disease • Active form of vitamin D supplementation

• Autosomal dominant • Many are asymptomatic and require no therapy.
hypocalcaemia Recombinant human PTH and calcilytics can be
used if therapy is needed.
• Pseudohypoparathyroidism • Patients with PHP infrequently develop
hypercalciuria with calcium and vitamin D
therapy. Therefore, the goal of treatment with
calcium and vitamin D is to maintain
normocalcemia (rather than low-normal serum
calcium as for other forms of
hypoparathyroidism).
Reference
• UpToDate
Page | 129

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First paperback edition 2023.10.17

Chief editor Dr.Ganesha Gethamali Liyanarachchi

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Cover art and Layout design

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Copyright & Publishing Information ---------------------------------------------------------------------- i

Cardiovascular System Related Emergencies ------------------------------------------------------------ 1

Respiratory System Related Emergencies -------------------------------------------------------------- 19

Endocrine & Metabolism Related Emergencies ------------------------------------------------------- 35

Nervous System Related Emergencies ------------------------------------------------------------------ 56

Emergencies Related to Infections ----------------------------------------------------------------------- 76

Toxicological Emergencies --------------------------------------------------------------------------------- 86

Gastrointestinal System Related Emergencies-------------------------------------------------------- 100

Emergencies Related to Electrolyte Imbalances ----------------------------------------------------- 115

Cardiovascular System Related

Management of Acute Coronary Syndrome (ACS)

1. SpO2 < 90% OR PaO2 < 60 mmHg – Give oxygen

Time to PCI >120 min

Primary PCI Eligible for thrombolysis

• Aspirin 300mg • Aspirin 300mg

Successful fibrinolysis Fibrinolysis therapy

Contraindications for fibrinolytic therapy

Prasugrel Loading dose of 60 mg orally, followed by a Contraindicated in patients

Management of Acute Heart Failure

Presentation & Clinical Syndromes of AHF

Onset Rapid (hours) Gradual (days) Gradual or rapid Gradual or rapid

RRT – Renal Replacement Therapy CI – Cardiac Index

Diagnostic evaluation of AHF

A patient suspected of AHF

Initial Investigations Specific evaluation

Natriuretic peptide testing

BNP <100 pg/mL BNP ≥ 100 pg/mL

Acute heart failure ruled out Acute heart failure confirmed

BNP = B-type natriuretic peptide

Management of patients with acute decompensated heart failure

Yes Yes Hypoperfusion and

Increase diuretic doses Medical therapy Consider vasopressors

Management of patients with pulmonary oedema

Loop diuretics Signs of

Consider RRT, MCS,

MCS = Mechanical Circulatory Support RRT = Renal Replacement Therapy

Management of patients with cardiogenic shock

Yes ACS and/or mechanical No

Emergency PCI or Identify and treat other

Consider oxygen or Consider inotropes/

Yes Improvement of hypoperfusion No

Weaning from inotropes/