MEDICINE

EMERGENCIES
AFHDAAL & ZUMRA
1st Ed.

CONTENTS
General Measures of Emergency management
.......................................................................... 1
Adult basic life support ................................... 2
Adult advanced life support ............................ 2
Universal treatment algorithm ....................... 4
Acute coronary syndrome (ACS) .................... 6
Acute kidney injury (AKI) ............................. 12
Bradyarrhythmia’s post MI ........................... 18
Non-ST elevation myocardial infarction
(NSTEMI)/unstable angina (UA) ................. 18
Arrhythmias .................................................. 20
Atrial fibrillation ............................................24
Hypoglycaemia .............................................. 27
Diabetic ketoacidosis (DKA) ......................... 27
HHS: Hyperosmolar Hyperglycaemic State 29
Sepsis ............................................................. 30
Hypertensive emergencies ............................ 32
Pulmonary Embolism.................................... 34
Asthma ........................................................... 36
Anaphylaxis................................................... 40
Acute pneumothorax ..................................... 41
Tension pneumothorax .................................42
Stroke ............................................................. 43
Acute upper gastrointestinal (GI) bleeding . 45
Poisoning ....................................................... 47
Pulmonary Oedema ....................................... 52
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d. Check the GCS/AVPU

General Measures of 1. <8 – Intubate
e. Check for trauma/Fractures
Emergency management f. Cervical collar
4. Inform nurse to check CBS to exclude
hypoglycaemia
5. Administer the coma cocktail “DON’T F” to
address few common causes of
unconsciousness.

“DON’T F” Coma Cocktail

 D – Dextrose: For Hypoglycaemia
 O – Oxygen: For hypoxia
 N – Naloxone: For opiate overdose
 T – Thiamine: For Wernicke’s encephalopathy
 F – Flumazenil: For BDZ overdose

6. Treat if there is fever with

a. Paracetamol
1. Acute bed b. Cooling
2. Gather the team c. & BDZ
3. ABCD 7. Do a septic screen if infection is likely
a. Airway + Cervical spine protection a. FBC
1. Check patency: Talk to the patient b. ESR/CRP
2. Clear airway c. Cultures
3. Maintain airway 8. Supportive measures
4. Cervical collar a. Hydration
b. Breathing + With oxygen b. Nutritional support
1. Look/Listen/Feel c. Limb physiotherapy
2. High flow oxygen via face mask d. Nursing care
c. Circulation + IV cannulas e. Graduated Compression Stockings/TED
1. 2 Grey (Large bow) IV cannula 9. Definitive management depends on aetiology
2. Central line a. Primary brain problem
d. Disability 1. Ischemia
1. AVPU 2. H’r
4. Connect the patient 3. Hypoxia
a. Monitor 4. Meningitis
1. SPO2 b. Systemic illness
2. ECG leads 1. Toxins
3. PR 2. Metabolic: Na+↓, Glucose ↓
b. Urinary catheter 3. Organ failure: Liver, Kidney
c. NG tube 4. Endocrine: Adrenal insufficiency,
5. Monitor the vitals Myxoedema coma

Unconscious patient management Unconsciousness common aetiologias “5S”

Scenario: 55yr old male found unconscious at  Sugar ↓
home. Now BP is 90/60mmHg, PR: 96bpm  Stroke
 Seizure
1. Acute bed  SOL
2. Gather the team  Sepsis
3. Assess quickly ABCD
a. Oropharyngeal airway
b. High flow O2 via facemask
c. 2 Grey cannulas

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Adult basic life support Adult advanced life support

1. aim is to maintain adequate ventilation and 1. Attach cardiac monitor as soon as possible to
circulation until the underlying cause for the determine the cardiac rhythm
arrest can be reversed 2. Oropharyngeal (Guedel) or nasopharyngeal
2. 3-4min without adequate perfusion will lead to airways help maintain the patency of the airway
irreversible cerebral damage by keeping the tongue out of the way
3. Check whether the patient is responsive 3. Establish venous access
• Responds: recovery position • If venous access fails, drugs may be given
• Unresponsive: shout for help via an ET tube into the lungs
4. Airway assessment – (except for bicarbonate and calcium
• Open the airway salts)
– If starts breathing, roll the patient over – Double the doses- absorption is less
into the recovery position 4. Post-resuscitation care
– and try to keep the airway open until an • What precipitated the arrest?
orophyrangeal airway can be inserted • Record the notes
• Keep airway open, look, listen, and feel for – duration of the arrest
breathing – interventions and drugs (and doses
– not breathing or making occasional • Check
gasps or weak attempts – both lung fields are being ventilated?
– Start rescue breaths by giving two slow – broken ribs?
effective breaths
– cardiac murmurs?
5. Assessment of circulation
– Neck veins?
• carotid pulse
– Abdomen: aneurysm or signs of
– check for circulation every 10 breaths
peritonism?
(approximately every minute)
• Insert a urinary catheter
• If no signs of circulation → start chest
compression • Consider an NG-tube
• Still unconscious?
– Rate of 100 times per minute
– Glasgow Coma Score
– 30 compressions to 2 effective breaths
– brief neurological assessment
5. Investigations
• ECG: MI, ischaemia, tall T-waves (↑K+)
• ABG
– If mixed metabolic and respiratory
acidosis:
▪ adequate oxygenation and
ventilation
▪ bicarbonate
• CXR
– position of ET-tube
– pneumothorax
• U&Es
• Glucose
6. transferred to HDU
7. monitoring for 12-24h
8. talk to the relatives
• give a realistic (if bleak) picture of the
arrest and possible outcomes.

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Universal treatment • Resume CPR immediately and continue for

2min, then pause briefly to check the
algorithm monitor
• If VF/VT persists give adrenaline 1mg IV
1. Cardiac rhythms of cardiac arrest
followed by a 3rd shock of 150-360J
• VF/VT
biphasic (360J monophasic)
• Asystole and PEA
• Resume CPR immediately and continue for
VF/VT 2min, then pause briefly to check the
monitor.
• most common rhythms at the time of
• If VF/VT persists give amiodarone 300mg
cardiac arrest
IV followed immediately by a 4th shock of
• Precordial thump
150-360J biphasic (or 360J monophasic)
– a sharp blow with a closed fist on the • Resume CPR immediately and continue for
patient's sternum 2min
– may convert VF/VT back to a perfusing • Give adrenaline before alternate shocks
rhythm (approximately every 3- 5min): 1mg IV or
– effective if delivered within 30sec after 2-3mg via endotracheal route
cardiac arrest • check for a pulse:
– If present: start post-resuscitation care
– If pulse absent: switch to the non-
VF/VT side of the algorithm

Non-VF/VT (asystole and PEA)

1. Outcome is generally worse than for VF/VT
2. Management
• 30:2 for 2min
• Recheck the rhythm after 2min
• check for a pulse
– If present: start post-resuscitation care
– If absent: continue CPR
– If VF/VT: change to the VF/VT side of
the algorithm
1. Successful Mx of VF/VT • Give adrenaline
• prompt defibrillation – 1mg IV as soon as IV access is achieved
• single shock of 150- 200J biphasic (or 360J – and with alternate loops (every 3-5min)
monophasic) • Give atropine
• Shock is immediately followed by CPR – 3mg IV
without reassessing the rhythm or feeling – if there is asystole or if PEA is slow
for a pulse (<60/min)
2. Continuing Mx
• In asystole, if P waves are present on the
• 30 compressions: 2 breaths strip/monitor, pacing (external or
• Continue CPR for 2min and then pause transvenous) must be considered
briefly to check the monitor 3. Successful resuscitation
• If VF/VT persists give a futher (2nd shock) • = Identification of the cause and its
of 150-360J biphasic (or 360J monophasic) correction

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Acute coronary syndrome ▪ may be ↑acutely post MI, even in

non-diabetics, and reflects a stress-
(ACS) catecholamine response, which
may resolve without treatment.
Definition – Troponin I
1. two major groups on the basis of delivered – Lipid profile:
treatment modalities ▪ total cholesterol, LDL, HDL,
2. STEMI: triglycerides.
• chest discomfort and ST-segment elevation ▪ Serum cholesterol and HDL remain
on ECG close to baseline for 24-48h but fall
• Must undergo reperfusion therapy on thereafter and take ≥8 weeks to
presentation return to baseline.
3. NSTEMI and UA: – Portable CXR
• chest discomfort associated with transient ▪ Cardiac size
or permanent non-ST elevation ischaemic ▪ pulmonary oedema
ECG changes ▪ mediastinal enlargement
• If there is biochemical evidence → NSTEMI – General examination
• Else condition is termed UA ▪ peripheral pulses, fundoscopy,
• This group of patients is not treated with ▪ abdominal examination for
thrombolysis organomegaly, and aortic
aneurysm
Initial management of ACS
1. Suspected ACS:
• Enviorment
Conditions mimicking pain in ACS
– Continuous ECG monitoring
1. Pericarditis
– Defibrillator ready 2. Dissecting aortic aneurysm
• Drugs 3. Pulmonary embolism
– O. aspirin 300mg 4. Oesophageal reflux, spasm, or rupture
5. Biliary tract disease
– O. Clopidogrel 300mg
6. Perforated peptic ulcer
– No IM injections 7. Pancreatitis
▪ rise in total CK
▪ and risk of bleeding with ST elevation myocardial infarction
thrombolysis/anticoagulation
– O. Clopidogrel 600mg should be
(STEMI)
considered if planning to do immediate 1. ST-segment elevation/LBBB → immediate
PCI reperfusion
2. Clinical features: Chest pain
– Secure IV access
a. Nature = angina
– Give high-flow O2 (initially only 28% if b. greater severity
history of COPD). c. longer duration
– Diamorphine 2.5-10mg IV PRN for d. not relieved by SL GTN
pain relief e. Associated
– Metoclopramide 10mg IV for nausea 1. nausea and vomiting
– GTN spray 2 puffs (unless hypotensive) 2. sweating
• Further assessment 3. breathlessness
– exclude hypotension, murmurs 4. and extreme distress
f. Atypical pains
– identify and treat acute pulmonary
1. Epigastric or
oedema
2. Radiate through to the back
• Ix
– 12-lead ECG: within 10min
– FBC/U&Es:
▪ supplement K+ to keep it at 4-
5mmol/L
– Glucose:

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h. Ventricular septal defect

5. STEMI
Painless (‘Silent’) Infarcts And/Or Atypical a. history and ECG changes are normally
Infarction diagnostic
1. In diabetics, the elderly, and hypertensives
b. Give immediate reperfusion/medical
2. Presenting features
a. breathlessness from acute pulmonary treatment
oedema c. Biochemical markers
b. syncope or coma from arrhythmias 1. available later
c. acute confusional states 2. help reconfirm diagnosis
(mania/psychosis) 3. provide prognostic information
d. diabetic hyperglycaemic crises 6. ECG changes
e. hypotension/cardiogenic shock a. ST-segment elevation
f. CNS manifestations resembling stroke 2° 1. occurs within minutes
to sudden reduction in cardiac output
2. last for up to 2 weeks
g. and peripheral embolization
3. ≥2mm in adjacent chest leads and
≥1mm in adjacent limb leads is
3. Mx necessary to fulfil thrombolysis criteria
a. STEMI: 4. Persisting ST elevation after 1 month
1. Diagnosis made on presentation suggests formation of LV aneurysm
without delay 5. Infarction site
2. → rapid stabilization a. Anterior: ST elevation and/or Q-
3. → institution of reperfusion waves in V1-V4/V5
b. NSTEMI/UA b. Anteroseptal: ST elevation and/or
1. diagnosis made over period of 24-72h Q-waves in V1-V3
c. Stabilizing c. Anterolateral: ST elevation and/or
1. similar for all ACS patients Q-waves in V1-V6, I, and aVL
2. If suspected STEMI →continuous ECG d. Lateral: ST elevation and/or Q-
monitoring waves in V5-V6 and T- wave
3. immediate aspirin 300mg PO inversion/ST elevation/Q-waves in
4. clopidogrel 300mg PO I and aVL
5. analgesia e. Inferolateral: ST elevation and/or
6. O2 Q-waves in II, III, aVF, and V5-V6
7. exclude (sometimes I and aVL)
a. hypotension f. Inferior: ST elevation and/or Q-
b. murmurs waves in II, III, and aVF
c. acute pulmonary oedema g. Inferoseptal: ST elevation and/or
d. aortic dissection Q-waves in II, III, aVF, and V1-V3
d. Blood Ix h. True posterior:
1. FBC ⬧ Tall R-waves in V1-V2 with ST
2. Troponin I depression in V1-V3
3. Lipid profile ⬧ T-waves remain upright in V1-
4. Glucose V2
5. CXR – portable ⬧ This can be confirmed with
e. Dx based on electrodes on the back for a
1. History posterior ECG. Usually occurs
2. ECG (ST elevation/new LBBB) in conjunction with an inferior
3. biochemical markers or lateral infarct
4. Factors associated with a poor prognosis i. RV infarction:
a. Age >70 years ⬧ ST-segment elevation in the
b. Previous MI or chronic stable angina right precordial leads (V3R-
c. Anterior MI or RV infarction V4R)
d. LV failure at presentation ⬧ Usually found in conjunction
e. Hypotension (and sinus tachycardia) at with inferior infarction. This
presentation may only be present in the
f. Diabetes mellitus early hours of infarction
g. Mitral regurgitation (acute)

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1. low potassium and magnesium may be

arrhythmogenic
d. Strategies to limit infarct size
1. β-blockade, ACEI, and reperfusion.
9. Β blockade
a. Early Rx
1. Limiting infarct size
2. ↓ mortality
7. Cardiac troponins 3. Malignant arrhythmias
a. highly sensitive and specific markers of b. contraindications
cardiac injury 1. Absolute contraindications:
b. rise by 3h post MI and elevation may a. HR <60bpm
persist up to 7-14 days b. SBP <100mmHg
c. can also be elevated in non-ischaemic c. moderate to severe heart failure
myocyte damage such as d. AV conduction defect
1. myocarditis e. severe airways disease
2. cardiomyopathy 2. Relative contraindications:
3. and pericarditis a. Asthma
b. current use of calcium channel
blocker and/or β-blocker
c. severe peripheral vascular disease
with critical limb ischaemia
d. large inferior MI involving the right
ventricle
c. Management
1. metoprolol 1-2mg
2. 1-2-minute intervals
3. maximum dose of 15-20mg
4. Aim for a pulse rate of 60bpm and SBP
of 100-110 mmHg
5. If haemodynamic stability continues
8. STEMI: general measures 15-30min after last IV dose start
a. Immediate stabilizing measures metoprolol 50mg tds
b. Control of cardiac pain 10. ACEIs
1. Diamorphine 2.5-10mg IV + a. within the first 24h of presentation
metoclopramide 10mg IV 11. STEMI reperfusion therapy (thrombolysis)
a. is the drug of choice a. within 4h of onset of pain → best results
b. can repeat to ensure adequate pain b. presenting between 12-24h from onset of
relief pain should be thrombolysed
c. Nausea and vomiting should be c. results in reduction in
treated with metoclopramide 1. mortality
(10mg IV) or a phenothiazine 2. LV dysfunction
2. Oxygen 3. Heart failure
a. 2-5L/minute for at least 2-3h 4. cardiogenic shock
b. Beware of CO2 retention in 5. and arrhythmias
patients with COPD d. Indications for thrombolysis
3. Nitrates 1. Typical chest pain within previous 12h
a. CI: hypotension and ST elevation in two contiguous
b. MOA: venodilation ECG leads
⬧ may impair RV filling a. >1mm in limb leads or
⬧ precipitate hypotension b. >2mm in V1-V6
⬧ so used cautiously in inferior 2. Cardiac pain with new/presumed new
STEMI, especially with RV LBBB on ECG.
infarction 3. should not be given if the ECG is
c. no effect on mortality normal, or if there is isolated ST
c. Correction of electrolytes depression

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e. Choice of thrombolytic agent: rtPA 1. Absolute contraindication

1. has a greater reperfusion capacity a. Active internal bleeding
2. marginally higher 30-day survival b. Suspected aortic dissection
benefit than SK c. Recent head trauma and/or
3. but ↑ risk of haemorrhage. intracranial neoplasm
f. greatest benefit from thrombolysis d. Previous haemorrhagic stroke at
1. Anterior infarct any time
2. Marked ST elevation e. Previous ischaemic stroke within
3. Age >75 years the past 1 year
4. Impaired LV function or LBBB, f. Previous allergic reaction to
hypotensive fibrinolytic agent
5. SBP <100mmHg g. Trauma and/or surgery within past
6. Patients presenting within 1h of onset 2 weeks at risk of bleeding.
of pain. 2. Relative contraindications
g. Key points: STEMI a. Trauma and/or surgery more than
1. Reperfusion is marked by 2 weeks previously
normalization of ST segments on ECG. b. Severe uncontrolled hypertension
2. primary PCI and thrombolysis are the (BP>180/110) with/without
main reperfusion modalities. treatment
3. The best long-term outcome is achieved c. Non-haemorrhagic stroke over 1
with primary PCI. year ago
h. Alteplase (rtPA): Doses and administration d. Pregnancy or postpartum
1. GUSTO trial: accelerated rtPA is the e. Lumbar puncture within previous 1
most effective regimen month
2. Dose f. Menstrual bleeding or lactation
a. 15-mg bolus IV
b. then 0.75mg/kg over 30min (not to
exceed 50mg)
c. then 0.5mg/kg over 60min (not to Management key points: STEMI
1. Aspirin, clopidogrel, O2, continuous ECG
exceed 35mg).
monitoring.
d. followed by IV heparin 2. Analgesia: diamorphine (+ metoclopramide),
i. Tenecteplase GTN (monitor BP).
1. Injection over 10sec 3. Reperfusion therapy without delay:
2. at 30-50mg according to bodyweight a. primary PCI (gold standard) or
(500-600mcg/kg) b. thrombolysis.
3. Maximum dose is 50mg. 4. If primary PCI not available: carefully and rapidly
j. Complications assess indications and contraindications to
1. Bleeding thrombolysis.
5. IV heparin should be used with rtPA (and its
a. is seen in up to 10% of patients
derivatives) but not with streptokinase.
b. SK may be reversed by tranexamic 6. Early short-acting β-blockers e.g. metoprolol (if
acid (10mg/kg slow IV infusion) not contraindicated).
2. Hypotension 7. Correct low potassium and magnesium.
a. Lay patient supine 8. ACEI within the first 24h of presentation.
b. Slow/stop infusion until BP rises
3. Allergic reaction l. Primary PCI
a. Hydrocortisone 100mg IV 1. current gold standard reperfusion
b. Chlorphenamine 10mg IV strategy
4. Reperfusion arrhythmias 2. Indications: All patients with chest pain
a. short, self-limiting and ST-segment elevation or new LBBB
b. Due to metabolites are washed out m. Low molecular weight and unfractionated
of the ischaemia tissue heparin
5. Systemic embolization 1. LMWH
a. from lysis of thrombus within the a. use of LMWH and thrombolysis
left atrium, left ventricle, or aortic (e.g. enoxaparin 30mg IV bolus,
aneurysm then 1mg/kg SC q12h).
k. Contraindications

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b. LMWH can be used at a

prophylactic dose to prevent
thromboembolic events in patients
slow to mobilize as an alternative
to UFH.
2. UFH
a. There is no indication for ‘routine’
IV heparin following SK
b. IV heparin (4000U/max. IV bolus
followed by 1000U/hour max.
adjusted for an aPTT ratio of 1.5-
2.0 × control) should be used
routinely following rt-PA and its
derivatives for 24-48h.
n. STEMI: complications
1. Continuing chest pain
2. Fever
3. A new systolic murmur: VSD, acute
MR, or pericarditis
4. Arrhythmia: VT, AV block ectopics, and
bradycardia
5. Pump failure: hypotension, cardiac
failure, and cardiogenic shock.

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c. Infections (Strep., Staph.,

Acute kidney injury (AKI) Leptospirosis, Brucella, G -ve
1. Syndrome of decreased renal function sepsis, Legionella)
occurring over hours–days, measured by 7. Calcium, urate, oxalate overload
a. serum creatinine or a. Tumour lysis syndrome
b. urine output
2. KDIGO criteria
a. ↑ creatinine >26μmol/L within 48h
b. ↑ creatinine >1.5 ≈ baseline (ie before the
AKI) within 7 days.
c. urine output <0.5mL/kg/h for >6
consecutive hours

4. Risk factors
a. pre-existing CKD
b. age
c. male sex
d. and comorbidity
3. Aetiology of AKI 1. DM,
a. Pre-renal Renal (parenchymal) 2. cardiovascular disease
1. Hypovolaemia 3. malignancy
2. Hypotension, shock 4. chronic liver disease
3. Renal artery emboli 5. complex surgery
4. Renal artery stenosis + ACEI 5. Commonest causes:
5. Hepatorenal syndrome a. Sepsis.
b. Post-renal (obstructive) b. Major surgery.
1. Renal vein thrombosis c. Cardiogenic shock.
2. ↑intra-abdominal pressure d. Other hypovolaemia.
3. HIV drugs (indinavir) e. Drugs.
4. Intratubular (uric acid crystals) f. Hepatorenal syndrome.
5. Ureteric g. Obstruction
a. Stones
b. Retroperitoneal fibrosis/tumour
6. Urethral
a. Prostatic hypertrophy
c. Renal (parenchymal)
1. Vasculitis (SLE, PAN)
2. Glomerulonephritis
3. Acute tubular necrosis
a. Ischaemia (e.g. hypotension)
b. Septicaemia
c. Toxins (myoglobin, BJ proteins)
d. Drugs (e.g. gentamicin) or radio
contrast media
e. Prolonged pre-renal oliguria
f. Malaria
4. Thrombotic microangiopathy
a. Accelerated hypertension
b. HUS/TTP/DIC
5. Scleroderma crisis
6. Sepsis
a. Interstitial nephritis
b. Drugs (NSAIDs, antibiotics)

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3. Septic fx?
a. Pyrexia
b. high CRP
c. leucocytosis
4. Hx
a. hypertension, diabetes, prostatism,
haematuria or vascular disease
b. H/O fluid loss
⬧ D: suggest
– hypovolaemia
– or haemolytic-uraemic
syndrome (HUS).
⬧ V
⬧ Diuretics
⬧ Bleeding
⬧ Fever
c. H/O sepsis
⬧ UTI
⬧ fever or hypothermia
⬧ bacterial endocarditis
d. H/O
⬧ Non-specific symptoms (e.g.
myalgia, arthralgia)
⬧ neurological signs
⬧ ophthalmic complications
⬧ sinusitis
⬧ haemoptysis
⬧ and skin rashes
e. DHx
⬧ NSAIDs
⬧ ACEI
6. Referring to the renal team ⬧ Antibiotics
a. not responding to treatment – aminoglycosides
b. complications: ↑K+, acidosis, fluid overload
– and amphotericin
c. Stage 3 AKI
⬧ drugs for HIV disease
d. difficult fluid balance (eg:
f. PMHx
hypoalbuminaemia, heart failure,
⬧ HTN
pregnancy)
⬧ DM
e. due to possible intrinsic renal disease
⬧ renovascular disease
f. AKI with hypertension
⬧ prostatism
7. Diagnosing the cause of AKI
⬧ or haematuria
a. 80% of AKI can be resolved by
g. symptoms or signs of liver disease?
1. adequate volume replacement
5. Urgent ultrasound scan to look for
2. treatment of sepsis, and
obstruction, blood flow, size, cysts, and
3. stopping nephrotoxic drugs
symmetry.
b. Causes of AKI that must be diagnosed early
6. Urinalysis and microscopy to look for
to a better outcome
red or white cell casts, myoglobinuria,
1. multisystem vasculitis or
and haematuria.
2. rhabdomyolysis
8. Assessment of severity
c. The priorities are
a. Fluid overload
1. Volume assessment and fluid challenge
1. PHTN: dyspnoeic
a. 1L of N/saline or Hartmann's
2. high JVP or CVP
solution
3. peripheral oedema
b. Give over 2h
4. gallop rhythm
c. assess urine output
5. dehydration (postural hypotension,
2. DHx: Stop all nephrotoxic drugs
tissue turgor)

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b. Hypotension 1. Anaemia suggests

c. Urine output: anuria occurs in a. chronic or acute on chronic renal
1. complete obstruction. e.g. prostate failure.
2. rapidly progressive glomerulonephritis 2. ↓platelets suggest
3. dissection of the aorta a. liver disease
d. Hyperkalaemia b. HELLP (haemolytic uraemic
1. ECG for signs syndrome, elevated liver enzyme,
2. serum potassium low platelet count)
e. Acidosis c. Sepsis
1. hyperventilation 3. ↑platelets:
2. cardiac instability a. vasculitis (e.g. Wegener's)
9. Poor prognostic features include eosinophilia
a. Age >50 years b. Churg-Strauss syndrome
b. Infection (esp. septicaemia) c. interstitial nephritis
c. Burns (>70% surface area) d. LFTs
d. Rising urea (>16mmol/24h) 1. Acute hepatitis, paracetamol overdose,
e. Oliguria for >2 weeks cirrhosis. Alkaline phosphatase often ↑
f. Multi-organ failure (>3) in vasculitis
g. Jaundice e. Blood cultures
10. Assessment of patients with AKI 1. Take BC in all patients with AKI (ARF)
a. Look for f. ESR/CRP
1. Is there life-threatening hyperkalaemia 1. CRP and ESR are elevated in vasculitis.
or pulmonary oedema? CRP may be normal in SLE.
2. What is the likely cause? g. Urine culture and ABST
3. Is the patient still passing urine? h. UFR
4. Does it look normal? 1. RBC casts → glomerular nephritis
b. Investigation 2. pigment casts → myoglobinuria
1. ECG 3. WBC casts suggest → acute
2. Urgent U&Es + ABGs pyelonephritis
3. CXR. 4. Excess eosinophils → interstitial
c. Pre-renal (75%) nephritis
1. Check postural BP, HR i. Coagulation
2. Assess volume status, measure CVP 1. Abnormal in
3. Sepsis screen. a. DIC
d. Renal (20%) b. liver disease,
1. Urinalysis and microscopy for c. SLE
blood/casts d. HELLP syndrome.
2. Vasculitis screen 2. PT and APTT are usually normal in
3. Drug history HUS.
4. CPK/myoglobin in urine. j. Urine Bence-Jones protein, present in 75%
e. Post renal (5%) of myeloma
1. May or may not have complete anuria k. USS
11. Investigations 1. exclude obstruction
a. U&Es 2. assess kidney size → acute-on-chronic
1. Urea is disproportionately raised in failure
a. -renal failure 3. blood flow with doppler
b. GI bleeds, l. CXR
c. catabolic states. 1. heart
2. Creatinine may be disproportionately a. size
elevated in b. dilated
a. Acute liver failure with renal failure c. pericardial effusion
b. Calcium, phosphate 2. pulmonary
1. Acidaemia increases ionized calcium. a. vasculature
2. Rhabdomyolysis may be associated b. pulmonary oedema
with high or low calcium. c. Kerley lines
c. FBC 3. lung fields

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a. ‘fluffy’ shadows: oedema ⬧ or 500mL 1.26% peripherally

b. haemorrhage of ANCA associated g. 250mg furosemide IV over 1h
vasculitis ⬧ or 5mg bumetanide.
m. ECG h. Calcium Resonium 30g
1. hyperkalaemia ⬧ Polystyrene sulphonate resin
a. tented T-waves enema (Calcium Resonium?)
b. QRS broadening ⬧ ↑gut losses of potassium
c. flattened P wave ⬧ Follow with 15g PO tds with
2. myocardial ischaemia regular lactulose
3. pericarditis ⬧ This takes 24h to work
12. Management i. Lactulose 20mL tds.
a. Resuscitate j. Monitor serum K+ frequently to
b. correct volume assess response to treatment.
c. Remove nephrotoxic drugs or agents b. Fluid balance
d. Sepsis: Identify and treat with ABX 1. Manage on HDU or ITU
e. Exclude obstruction or major vascular 2. Measure
injury a. Weight
f. Identify the minority (~5%) that have b. BP (supine and sitting or upright)
intrinsic renal disease since these are best c. HR
managed by a specialist centre. These 3. Assess hydration
include: a. dry axillae
1. Myeloma b. central skin turgor
2. Glomerulonephritis c. mucous membranes
3. Rhabdomyolysis (high CPK) d. JVP
4. Vasculitis 4. Measure CVP
5. Interstitial nephritis. 5. Examine fluid and weight charts
13. Mx c. If volume depleted
a. Hyperkalaemia 1. low or normal CVP ± postural
1. absolute K+ concentration is less hypotension give a trial of volume
important expansion (500mL of colloid or N
2. effect on the cardiac-conducting tissue saline) over 30min
is more important 2. Measure urine output
3. K+ is >7mmol/L → treat urgently 3. Inotropes
4. Rx a. If hypotension persists (MAP
a. 12-lead ECG <60mmHg) in spite of adequate
b. attach to cardiac monitor. volume replacement
c. ECG change +ve → 10mL of 10% b. i.e. CVP of >10cm
calcium gluconate IV over 10 d. fluid overloaded
minutes 1. Give O2
⬧ repeated every 10-20min until a. maintain SaO2 >95%.
ECG normalizes b. Consider CPAP
⬧ may require up to 50mL 2. Start IV nitrates (e.g. GTN 2-10mg/h
⬧ does not lower the potassium IV).
level 3. Give IV furosemide:
⬧ reduces cardiac a. 120mg-500mg
excitability b. then infuse 5-10mg/h.
d. nebulized salbutamol 5mg 4. Paracentesis if tense ascites is present
⬧ drive K+ intracellularly 5. Opiates
⬧ use lower doses in patients a. Avoid opiates
with ICH b. although a single dose (e.g. 2.5mg
e. 50mL 50% glucose with 5U diamorphine IV) may help relieve
soluble insulin over 15-30min anxiety and breathlessness.
⬧ monitor blood glucose 6. If no response, consider
⬧ lower K+ for several hours a. urgent haemofiltration
f. 50-100mL 8.4% bicarbonate IV b. dialysis
via central line over 30min

MEDICINE EMERGENCIES ZUMRA & AFDHAAL

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c. or venesection (remove 250-

500mL)
e. Correct other abnormalities
1. Acidaemia:
a. CFx: Kussmaul's breathing
b. may worsen hypotension
⬧ If pH is <7.2 → give 100mL of
8.4% bicarbonate
– via central line
– over 30min
– (or 500mL 1.26%
bicarbonate peripherally)
⬧ Arrange urgent dialysis
⬧ Correction can cause
symptomatic hypocalcaemia.
2. Hyponatraemia
a. Usually dilutional (relative water
excess)
3. Hyperphosphataemia
a. problem of chronic renal failure.
b. Give oral phosphate binders to
lower phosphate to <1.8mmol/L
c. e.g. calcium carbonate 300-
1200mg q8h PO
d. Phosphate levels decrease with
dialysis or haemofiltration.
4. Nutrition
a. no role for protein restriction.
b. If DM → insulin requirements fall
with renal impairment.

14. Indications for dialysis or haemofiltration

a. Persistent hyperkalaemia (K+ >7mmol/L)
b. Fluid overload (e.g. refractory pulmonary
oedema)
c. Pericarditis (heralds the risk of tamponade)
d. Acidosis (arterial pH <7.1, bicarbonate
<12mmol/L)
e. Symptomatic uraemia
1. Tremor
2. cognitive impairment
3. coma
4. fits
5. urea typically >45mmol/L

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Management key points: AKI

1. Treat hyperkalaemia (if ECG changes or K+
>7mmol/L):
a. 10mL of 10% calcium gluconate IV
b. 50mL 50% glucose with 5U soluble insulin
over 15min
c. Nebulized salbutamol
d. Contact renal team and arrange for
dialysis if appropriate.
2. Treat metabolic acidosis (if pH <7.2):
a. 50-100mL of 8.4% bicarbonate via central
line over 15-30min.
3. Treat pulmonary oedema:
a. O2, consider CPAP
b. IV GTN 2-10mg/h
c. IV furosemide: 250mg over 1h, followed
by infusion (5-10mg/h)
d. IV diamorphine (single dose of 2.5mg)
relieves anxiety and breathlessness
e. Haemofiltration or dialysis (venesect
~250-500mL if delay for dialysis).
4. Assess hydration and fluid balance: PR, lying
nd standing BP, JVP, skin turgor, chest
auscultation, ?peripheral oedema, CVP, fluid
and weight charts.
5. IV fluids if volume depleted: 500mL colloid or
0.9% saline over 30min, assess response, i.e.
urine output/CVP), continue fluids until CVP
~5-10cm. Inotropes if hypotension persists in
spite of CVP of >10cm.
6. Treatment of infection—remember to adjust
the dose of antibiotics in view of the renal
impairment.
7. Stop the nephrotoxic drugs (e.g. ACEI and
NSAIDs) and non-essential drugs.
8. Identify intrinsic renal disease and treat.
9. Relieve the obstruction e.g. urinary catheter,
nephrostomies.
10. Optimize nutritional support.
11. Identify and treat bleeding tendency—
prophylaxis with PPIs or H2 antagonist,
transfuse if required, avoid aspirin.

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Bradyarrhythmia’s post MI 3. Strict bed rest

4. O2
1. First-degree AV block 5. aspirin 300mg PO
a. Common and no treatment required. 6. SL nitrate
b. Significant PR prolongation (>0.20sec) is a 7. mild sedation if required
contraindication to β-blockade. 8. If pain:
2. Second-degree AV block a. diamorphine 2.5-5mg IV PRN
a. This indicates a large infarction affecting b. with metoclopramide 10mg IV
conducting systems and mortality is b. General investigations
generally ↑ in this group of patients. 1. FBC
b. Mobitz type I is self-limiting with no 2. markers of myocardial injury
symptoms. Generally, requires no specific 3. lipid profile
treatment. If symptomatic or progression 4. CRP
to complete heart block will need 5. TFT
temporary pacing. 6. portable CXR
c. Mobitz type II, 2:1, 3:1 should be treated a. LVF
with temporary pacing regardless of b. mediastinal abnormalities
whether it progresses to complete heart c. Confirm diagnosis
block. d. Risk stratification
3. Third-degree AV block e. Treatment
a. In the context of an inferior MI can be 1. Medical strategies:
transient and does not require temporary a. anti-ischaemic
pacing unless there is haemodynamic b. antiplatelet
instability or an escape rhythm of <40bpm. c. antithrombic
b. Temporary pacing is required with anterior 2. Invasive strategies
MI and unstable inferior MI. f. Secondary prevention and discharge

Non-ST elevation
myocardial infarction
(NSTEMI)/unstable angina
(UA)
1. General
a. NSTEMI: If biochemical evidence of
myocardial damage
b. UA: absence of damage.
2. 3 Clinical presentation
a. Rest angina
b. New-onset severe angina.
c. Increasing angina previously diagnosed
angina which has become
1. more frequent
2. longer in duration
3. or lower in threshold
3. Ex:
a. pulmonary oedema
b. haemodynamic stability
c. cardiac valve abnormalities
d. diaphoresis 5. medical management
4. Integrated management plan a. All patients should be treated with
a. Initial stabilization adequate analgesia, IV nitrates, β-blockers,
1. continuous ECG monitoring and statins
2. defibrillator facility

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b. Analgesia: diamorphine 2.5-5mg IV (with b. continued (75mg od) for at least 12

metoclopramide 10mg IV) months
1. Anxiolytic i. Antithrombotic therapy
2. Reduces pain and SBP 1. LMWHs
3. SE a. superior to UFH
a. hypotension b. reduction of mortality
b. and respiratory depression c. continued for 2-5 days after the last
4. AD: naloxone 400mcg-2mg IV episode of pain and ischaemic ECG
c. Nitrates: GTN infusion (50mg in 50mL changes
nitrate saline at 1-10mL/hour) d. advantages over UFH include
1. SE: ⬧ SC administration
a. headache ⬧ lack of monitoring
b. hypotension ⬧ reduced resistance
2. CI: sildenafil in the previous 24h ⬧ thrombocytopaenia
d. β-blockers e. Enoxaparin: 1mg/kg bd (100U/kg
1. Initially use a short-acting agent twice daily)
a. metoprolol 12.5-100mg PO tds 2. UFH infusion
2. Then converted to a longer-acting a. reduction of risk of death
agent b. continued for 2-5 days
a. atenolol 25-1000mg od c. Dose
3. CI ⬧ initial bolus of 60-70U/kg
a. Mild LVF is not an absolute (maximum 5000U)
contraindication ⬧ then infusion of 12-
b. overt heart failure 15U/kg/hour (≈1000U/hour)
⬧ β-blockade is contraindicated d. aPTT value of 1.5-2.0 × control
⬧ Use calcium antagonist: ⬧ initially every 6h after
amlodipine 5-10mg od) ⬧ 2 consistent values once every
e. Calcium antagonists 24h
1. Drugs and doses
a. diltiazem 60-360mg PO tds
b. verapamil 40-120mg PO tds
c. pulmonary oedema and in poor LV Management key points: NSTEMI
1. Continuous ECG monitoring
function
2. O2
⬧ Amlodipine/felodipine 5-10mg 3. Analgesia:
PO od a. diamorphine + (metoclopramide)
2. General b. GTN (monitor BP)
a. do not reduce mortality or risk of 4. Aspirin, clopidogrel, LMWH
MI 5. β-blockers:
f. Statins (HMG-CoA reductase inhibitors) a. initially short-acting agent, e.g. metoprolol
1. atorvastatin 80mg od 6. High-dose statins
2. high-dose statins to reduce mortality 7. Glycoprotein IIb/IIIa antagonists for high-risk
patients only.
and recurrent MI in the acute setting
g. ACEIs
h. Antiplatelet therapy
1. Aspirin (300mg PO)
a. administered immediately
b. continued indefinitely
c. reduce mortality and recurrent
ischaemic events
d. aspirin hypersensitivity or major
gastrointestinal intolerance
⬧ Give clopidogrel 75mg od
2. Thienopyridines:
a. Immediately → clopidogrel
(300mg od)

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Arrhythmias d. IHD
e. pericarditis;
1. Diagnosing: main distinctions 2. VT:
a. Tachy- (>120/min) versus brady- a. previous MI
(<60/min) arrhythmia b. LV aneurysm
b. Narrow (≤120ms or 3 small squares) versus 2. Ex
broad QRS complex a. BP
c. Regular versus irregular rhythm. b. heart sounds and murmurs
c. signs of heart failure
d. carotid bruits
3. Investigation
Arrhythmias common causes a. 12 lead ECG and rhythm strip
1. Underlying cardiac disease
1. Regular versus irregular rhythm
a. Ischaemic heart disease
b. Acute or recent MI 2. Narrow versus broad QRS complex.
c. Angina b. Blood tests:
d. Mitral valve disease 1. FBC, biochemistry, glucose (urgently)
e. LV aneurysm 2. Ca2+, Mg2+ (especially if on diuretics)
f. Congenital heart disease 3. Biochemical markers of myocardial
g. Abnormalities of resting ECG injury.
h. Pre-excitation (short PR interval) c. Where appropriate:
i. Long QT (congenital or acquired). 1. Blood cultures, CRP, ESR
2. Drugs
2. Thyroid function tests
a. Antiarrhythmics
b. Sympathomimetics (β2 agonists, cocaine) 3. Drug levels
c. Antidepressants (tricyclic) 4. Arterial blood gases.
d. Adenylate cyclase inhibitors aminophylline, d. CXR:
caffeine) 1. Heart size
e. Alcohol 2. Evidence of pulmonary oedema
3. Metabolic abnormalities 3. Other pathology
a. ↓ or ↑K+ a. Ca bronchus → AF
b. ↓ or ↑Ca2+
b. pericardial effusion →sinus
c. ↓Mg2+
tachycardia
d. ↓PaO2
c. hypotension ± AF
e. ↑PaCO2
4. Management
f. Acidosis.
4. Endocrine abnormalities a. Haemodynamically unstable
a. Thyrotoxicosis 1. Urgent correction usually with external
b. Pheochromocytoma defibrillation
5. Miscellaneous a. cardiac arrest
a. Febrile illness b. SBP <90mmHg
b. Emotional stress c. severe pulmonary oedema
c. Smoking d. evidence of cerebral hypoperfusion
d. Fatigue. 2. Sedate with midazolam 2.5-10mg IV
3. Analgesia: ± diamorphine 2.5-5mg IV +
Tachyarrhythmias heart rate (HR) metoclopramide 10mg IV
a. respiratory depression:
>120bpm
⬧ flumazenil
1. Hx
⬧ naloxone
a. General
4. Anaesthesia with propofol
1. Previous cardiac disease
a. prevent aspiration: e.g. cricoid
2. palpitations, dizziness
pressure, ET intubation
3. chest pain
5. Start at 200J synchronized shock and
4. symptoms of heart failure
increase as required.
5. recent medication
6. If tachyarrhythmia recurs or is
b. Associated conditions
unresponsive
1. AF:
a. Correct
a. alcohol,
⬧ ↓PaO2
b. thyrotoxicosis,
c. mitral valve disease ⬧ ↑PaCO2

MEDICINE EMERGENCIES ZUMRA & AFDHAAL

 21

⬧ acidosis, a. QRS width >120ms or >3 small squares.

⬧ ↓K+ 2. Steps
b. Give a. STEP ONE: Rhythm strip
⬧ Mg2+ 8mmol IV stat 1. Regular
⬧ shock again a. VT (mono/polymorphic)
⬧ Amiodarone 150-300mg bolus b. SVT or atrial flutter with bundle
IV branch block
7. Give specific antiarrhythmic therapy c. Atrial flutter or SVT with pre-
b. Haemodynamically stable patients excitation (e.g. WPW).
1. continuous ECG monitoring and 12- 2. Irregular
lead ECG a. AF, atrial flutter, or multifocal
2. vagotonic manoeuvres atrial tachycardia with bundle
a. Valsalva branch block
b. carotid sinus massage b. Pre-excited AF (e.g. WPW)
3. If doubt regarding diagnosis c. Torsades de pointes (PVT)
a. give adenosine b. STEP TWO: any features help distinguish
⬧ 6mg as fast IV bolus VT from SVT with aberrancy?
⬧ followed by 5mL saline flush. 1. Factors favouring SVT
⬧ If no response, try 9, 12, and a. A grossly irregular broad complex
18mg tachycardia with rates ≥200/min
b. continuous ECG rhythm strip. suggests AF with conduction over
4. Definitive treatment should start as an accessory pathway.
soon as diagnosis is known b. Slowing or termination by
vagotonic manoeuvres.
c. Evidence of atrial and ventricular
coupling (e.g. with 1:2 AV block)

2. Factors favouring or diagnostic of VT

a. Cycle length stability
(<40ms R-R variation).
b. QRS >140ms (3.5 small squares)
⬧ especially with normal
duration when compared with
previous ECG in sinus rhythm.
c. Marked left axis deviation
(negative in lead II).
d. QRS concordance in chest leads.
⬧ If the predominant deflection
of the QRS is positive this is
highly suggestive of VT.
e. In patients with previous LBBB or
RBBB, it is difficult to distinguish
VT from SVT with aberrancy. A
different QRS morphology in
Broad complex tachycardia: diagnosis
1. Definition

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tachycardia suggests VT (other

clues are given in Table 1.4).
f. Fusion or capture beats. Morphology rules
g. Independent atrial activity (seen in RBBB LBBB
~25%) Lead  rSR' with R' >r  rS or QS with
V1  RS with R >S time to S-wave
nadir <70ms
Lead  If a Q-wave is  R-wave with no
V6 present, it Q-wave
must be 40ms
and <0.2mV

c. STEP THREE: What are the effects of

adenosine?
The transient AV block produces one of
three results:
1. The tachycardia terminates.
a. This suggests an SVT with
aberrancy or RVOT tachycardia
(technically a form of VT).
2. The ventricular rate slows unmasking
atrial activity.
a. Either ‘flutter’ waves (atrial flutter
with block or intra-atrial
tachycardia) or AF.
b. The tachycardia typically continues
after a few seconds once the
adenosine wears off.
3. No effect on the rhythm.
a. Check that the patient received a
therapeutic dose of adenosine (and
experienced chest tightness with
the injection).
b. Higher doses are required in
patients on theophyllines.
c. The diagnosis is most likely to be
VT.
d. is any doubt about diagnosis → treated as
VT until proven otherwise
3. Morphologic rules

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Monomorphic ventricular tachycardia

(MVT) Doses
 NaHCO3
o 8.4% 50ml via central line over 20mins
 Amiodarone
o 300mg IV over 1 hour via central line
o 900mg IV over 23 hours
o 200mg PO tds for 1 week
o 200mg PO bd for 1 week

Supraventricular tachycardia
1. General measures
a. Acute bed
b. ABC
c. Haemodynamically stable or not
1. Management 2. If Haemodynamically unstable
a. ABC a. Emergency trolley
b. Haemodynamically unstable b. Anaesthetic help and be ready to intubate
1. Precordial thumb c. Sedate
2. unsynchronized external defibrillation 1. IV midazolam 2.5-5mg
(200J, 200J, 360J) d. Synchronized biphasic DC cardioversion
c. Haemodynamically stable 1. 50-100J
1. Chemical cardioversion with 3. If haemodynamically stable
a. First line: Amiodarone, sotalol a. Vagal manoeuvre
b. Second line: Lignocaine, beta 1. Valsalva
blocker 2. Carotid sinus massage
2. IV Mg2+ for all patients. b. IV medications
a. 8mmol bolus over 2-5mins 1. IV adenosine
b. 60mmol in 50ml glucose infusion a. 6mg fast IV bolus via large
over 24 hour proximal vein near to the heart
b. Followed by 5ml saline flush
⬧ t1/2 = 7 Seconds
c. If no response try: 9mg → 12mg →
18mg
d. CI
⬧ Bronchial asthma
e. Monitor
⬧ 12 lead ECG
⬧ Bronchospasm
2. IV verapamil
3. IV metaprolol

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Atrial fibrillation
1. Presentation a. Hypokalaemia
a. Palpitations b. hypomagnesaemia.
b. chest pain d. Acidosis
c. breathlessness 1. If severe acidosis (pH ≤7.1) give
d. collapse NaHCO3
e. or hypotension 2. NaHCO3 50mL of 8.4% slowly IV over
f. embolic event – less common 20min
2. Hx e. To confirm diagnosis
a. establish the duration of the AF 1. CSM or IV adenosine may help
3. Causes 2. CSM or adenosine will slow the
a. Underlying cardiac disease ventricular rate and reveal flutter waves
1. Ischaemic heart disease 3. Particularly helpful if PR is ~ 150bpm
2. Mitral valve disease where atrial flutter should always be
3. Hypertension considered
4. Heart failure f. Does the ECG in AF show intermittent or
5. Cardiomyopathy constant delta waves? This suggests WPW
6. Pericarditis and digoxin and verapamil are
7. Endocarditis contraindicated
8. Myocarditis g. Treat reversible causes
b. Separate intrathoracic pathology 1. Thyrotoxicosis
1. Pneumonia 2. chest infection
2. Malignancy (1° or 2°) 6. Management: Haemodynamically unstable
3. Pulmonary embolus patients
4. Trauma a. DC cardioversion (under GA or sedation)
c. Metabolic disturbance b. All hypotensive patients
1. Electrolytes (↓K+, ↓Mg2+) 1. should undergo external defibrillation
2. Acidosis 2. using a synchronized shock of initially
3. Thyrotoxicosis 200J
4. Drugs (alcohol, sympathomimetics) c. Do not attempt to defibrillate hypotensive
4. Investigations patients with known chronic AF or a known
a. ECG: underlying cause driving a fast ventricular
1. Broad QRS if aberrant conduction response.
2. ST-T-wave changes d. Relative contraindications to defibrillation
b. CXR: → optimize clinical picture before
1. Cardiomegaly cardioversion, if possible:
2. pulmonary oedema 1. Hypokalaemia
3. intrathoracic precipitant a. Give 20mmol over 1h in 100mL
4. valve calcification (MS) nitrate saline
c. RFT & SE: b. via a central line
1. Hypokalaemia 2. If digitoxicity is a possibility
2. renal impairment a. ensure K+ is 4.5-5mmol/L
d. Troponin I: Small rise after DC shock b. and give magnesium sulphate
e. TFT 8mmol in 50mL nitrate saline over
f. Mg2+, Ca2+ levels 15min, before attempting
g. ABG: if hypoxic, shocked, or ?acidotic defibrillation at low energies
h. Echo ±TOE: for LV function and valve initially (e.g. 20- 50J).
lesions and to exclude intracardiac 3. AF >48h' duration
thrombus prior to version to SR. a. carries a significant risk of
5. Management: Immediate thromboembolic complications
a. General measures of arrhythmia unless patient is on long-term
b. IV access anticoagulation and INR has been
c. Electrolyte abnomalities therapeutic.
1. Immediately check K+ levels b. Consider performing a TOE first
2. Correct any electrolyte abnormalities e. If DC shock fails initially:

MEDICINE EMERGENCIES ZUMRA & AFDHAAL

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1. Give IV amiodarone of 2-3) until warfarinization is

a. 300mg over 60min via a central adequate (aim for an INR of 2-3).
line c. AF <48h' duration:
b. followed by IV infusion of 900- 1. Consider ‘pill-in-pocket’ strategy for
1200mg over 24h cardioversion.
2. Correct hypokalaemia (aim for K+ 4.5- 2. Chemical (e.g. flecainide or
5.0mmol/L). amiodarone) or DC cardioversion.
3. Attempt further DC shock. a. Flecainide
7. Management: Haemodynamically stable ⬧ 2mg/kg IV over 10min (max.
patients dose 150mg).
a. initial aim ⬧ Must be avoided in patients
1. rapid pharmacological rate control with known IHD and/or poor
2. followed by a decision regarding LV function.
restoration of sinus rhythm if b. Amiodarone
appropriate ⬧ may be used IV/PO.
b. AF >48h duration: ⬧ Dosing requires central line
1. Control ventricular rate (digoxin, β- ⬧ and it may take 24-48h for
blockers, verapamil, diltiazem). sinus rhythm to be achieved.
2. Consider anticoagulation 3. If cardioversion is inappropriate or
a. start LMWH/UFH (UFH: give unsuccessful: rate control.
bolus of 5000U followed by 4. Consider anticoagulation
infusion aiming for an aPTT ratio
5.

MEDICINE EMERGENCIES ZUMRA & AFDHAAL

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MEDICINE EMERGENCIES ZUMRA & AFDHAAL

 27

Hypoglycaemia b. RR
c. Smell of ketones
Scenario: 40yr old male found to be unconscious 4. Investigation
has a CBS of 40mg/dl. a. CBS: Did patient take insulin?
b. ABG: Degree of acidosis
1. General measures of unconscious patient
c. RFT: Renal function
2. Give IV thiamine 300mg stat
d. SE:
3. Give dextrose 25% 50ml dextrose bolus
1. Serum K+ level
4. Maintenance drip of dextrose 10% infusion
2. Corrected Na+
a. 1 litre 8 hourly
b. CBS hourly or 2 hourly
5. If still not responding
a. 50% dextrose via central or large vein 𝒙 − 55
b. Glucagon 1mg IM or S/C 𝑪𝒐𝒓𝒓𝒆𝒄𝒕𝒆𝒅 𝑵𝒂+ = 𝑁𝑎+ + ൜1.6 × ൤ ൨ൠ
5.5
6. Find out aetiology for the hypoglycaemia with 𝒙 = 𝑝𝑙𝑎𝑠𝑚𝑎 𝑔𝑙𝑢𝑐𝑜𝑠𝑒 𝑚𝑚𝑜𝑙/𝑙
Hx and thorough Ex
e. Urine ketone bodies:
1. Strongly positive?
2. On captopril/Sulphydryl drugs?
f. FBC
1. Nutrophilia?
g. Septic screening: UC & BC
h. CXR: infection evidence?
i. Amylase
1. Acute pancreatitis?
j. Serum osmolality

𝑺𝒆𝒓𝒖𝒎 𝑶𝑺𝑴 = 2𝑆𝐸 + 𝐵𝑈 + 𝑅𝐵𝑆

= 2ሺ𝑁𝑎+ + 𝐾 + ሻ + 𝐵𝑈 + 𝑅𝐵𝑆

5. Management
a. General measures to all patients
1. Rehydration – without delay
Diabetic ketoacidosis (DKA) 2. Insulin therapy – without delay
a. Infusion: Because t1/2 of insulins is
1. General short
a. In insulin dependent (T1DM) 3. 2 Large bore IV cannulas
b. Not in non-insulin dependent DM a. In each arm
c. In some type 2 DM b. Away from major veins in the wrist
d. average fluid loss in DKA is 100mL/kg – for AV fistula
2. Hx 4. Start IV N/S
a. Dehydration: 5. NBM – at least 6h (Gastroparesis)
1. Polyuria b. General measures in addition
2. Polydipsia 1. NG tube: if unconscious
3. Vomiting a. Aspiration/ Vomiting
b. Weight loss 2. Urinary catheter: If oliguria/ ↑S.Cr
c. Weakness
3. Broad spectrum ABx: If infection
d. Dyspnoeic/ Hyperventilation
suspected
i.e Kussmaul’s respiration
4. Enoxaparin: DVT prophylaxis
e. Abdominal pain: Acute abdomen
c. Fluid replacement: 0.9% N/S
f. Confusion
1. Hypotension: 500ml N/S
g. Coma
a. IV over 15-20mins
3. Ex
b. Repeat until SBP > 100mmHg
a. Hydration
c. Max 3 doses

MEDICINE EMERGENCIES ZUMRA & AFDHAAL

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2. Once normotensive (Next 15h) 2. 4-hourly

a. 1st: N/S 1L + K+ 2hourly a. RFT
b. 2nd: N/S 1L + K+ 2hourly b. SE
c. 3rd: N/S 1L + K+ 2hourly c. VBG
d. 4th: N/S 1L + K+ 3hourly
e. 5th: N/S 1L + K+ 3hourly
f. 6th: N/S 1L + K+ 3hourly
OGyG in PBU
d. “No First KCl” rule  14: O - Orange
1. 1st litre of fluid  16: Gy – Grey
2. K+ > 5.5mmol/l ▪ 17: White (in between two G’s)
3. UOP < 30ml/hr  18: G - Green
 20: P - Pink
 22: B - Blue
 24: U – Yellow
“No First KCl” rule (In PBU yellow cannula is mostly used)
 No UOP
 First N/S
 K+ > 5.5mmol/l

Serum K+(mmol/L) Amount of K+ (mmol)

to add to each litre of
fluid
>5.50mmol/L Nil
2.5-5.5mmol/L 40mmol/L
<2.5mmol/L 60-80mmol/L
Get senior opinion

e. Insulin therapy
1. K+ < 3.3mmol/l
a. Delay insulin only if K+ <
3.3mmol/l
b. Correct with N/S + K+
2. IV insulin infusion via infusion pump
a. 50U S.insulin into 50ml 0.9%
normal saline
b. Infusion at fixed rate: 0.1U/kg/hr
3. Review in 1 hour
a. Target
⬧ Blood glucose drop by 5mmol/l
⬧ Capillary ketones drop by
1mmol/l
b. If target is not reached
⬧ Increase infusion by 1U/hr
4. Fixed rate insulin is continued till
a. Capillary ketones < 0.3
b. Venous pH > 7.3
c. Venous HCO3- > 18
5. At blood glucose 15mmol/l
a. Stop IV insulin
b. Start 5% dextrose infusion
f. Monitor
1. Hourly
a. Blood glucose
b. Capillary ketones
c. UOP

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HHS: Hyperosmolar .

Hyperglycaemic State
1. General measure of unconscious patient
2. CBS: 900mg/dl
3. Management
a. General measures to all patients
1. Rehydration – without delay
2. Insulin therapy – without delay
a. Infusion: (Not IV, because t1/2 of
insulins is short)
3. 2 Large bore IV cannulas
a. In each arm
b. Away from major veins in the wrist
– for AV fistula
4. Start IV N/S
5. NBM – at least 6h (Gastroparesis)
b. General measures in addition
1. NG tube: if unconscious
a. Aspiration/ Vomiting
2. Urinary catheter: If oliguria/ ↑S.Cr
3. Broad spectrum ABx: If infection
suspected
4. Enoxaparin: DVT prophylaxis
c. Fluid replacement: 0.9% N/S
1. 1st: N/S 1L/1hr
2. 2nd: (N/S 1L + K+)/2h
3. 3rd: (N/S 1L + K+)/2h
4. 4th: (N/S 1L + K+)/ 6h
5. 5th: (N/S 1L + K+)/ 6h
6. 6th: (N/S 1L + K+)/ 6h
7. …... continued till rehydrated ~ 48
hours
d. “No First KCl” rule
1. 1st litre of fluid
2. K+ > 5.5mmol/l
3. UOP < 30ml/hr
e. Insulin therapy
1. K+ < 3.3mmol/l
a. Delay insulin only if K+ <
3.3mmol/l
b. Correct with N/S + K+
2. Up to blood glucose reaches 15mmol/l
a. IV insulin infusion at 2- 4U/h
3. At blood glucose 15mmol/l
a. Stop IV insulin
b. Start 5% dextrose infusion
4. If patient is eating and drinking
normally, consider starting
a. SC insulin
b. or oral hypoglycaemic agents
f. Monitor
1. Glucose: 1 hourly
2. Electrolytes: 2 hourly
3. RFT
4. & osmolality

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Sepsis b. Obtain blood cultures

c. Administer BSABx
d. Administer 30 mL/kg crystalloid
(for hypotension or lactate 24 mmol/L)
Definitions 2. TO BE COMPLETED WITHIN 6 HOURS:
a. Apply vasopressors to maintain a MAP
1. SIRS: ≥2 of the following: ≥65 mmHg
a. Temperature > 38°C or < 36°C
(for hypotension that does not respond to
b. Heart rate > 90 beats/min
c. Respiratory rate > 20 breaths/min or initial fluid resuscitation)
Paco2 < 32 mmHg b. Measure CVP if
d. Leukocytes > 12,000, < 4,000/mm3 1. persistent arterial hypotension despite
2. Sepsis: volume resuscitation (septic shock)
a. SIRS with documented/Suspected infection 2. or initial lactate 24 mmol/L :
3. Severe sepsis: c. Remeasure lactate
a. sepsis associated with 1. if initial lactate was elevated
1. organ dysfunction
2. hypoperfusion
a. Confusion
b. Oliguria Surviving Sepsis “CALF CiViL”
c. Ischemic changes: ↑ troponin I  C - Culture
d. ↑ Lactate levels  A - ABx
e. CRFT > 2s  L - Lactate
3. or hypotension  F - Fluid
4. Septic shock:  C - CVP
a. sepsis with hypotension  V - Vasopressor
b. despite adequate resuscitation  L - Lactate
c. along with the presence of perfusion
abnormalities
5. MODS:
a. a state of altered organ function in an acutely
ill patient
b. such that homeostasis cannot be maintained
without intervention

Surviving Sepsis Campaign Bundles

1. TO BE COMPLETED WITHIN 3
HOURS:
a. Measure lactate level

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Hypertensive emergencies 6. CXR:

a. cardiac enlargement
b. Pulmonary oedema
7. ECG: LVH
b. Diagnostic Ix
1. 24-hour urine
a. Creatinine clearance
b. Free catecholamines,
metanephrines, or VMA
2. Echo
a. LVH
b. aortic dissection
3. Renal USS and Doppler:
a. size of kidneys
b. renal artery stenosis
4. MR renal angiogram: renal artery
stenosis
Scenario: 60-year-old male, known patient with 5. CT/MR brain: intracranial bleed
hypertension presents with severe headache. On 6. Drug screen: cocaine, amphetamine,
admission, the blood pressure is 210/120mmHg. others.
How will you approach? 5. Mx
a. Avoid rapid reduction of BP:
1. General measures !Cerebral and cardiac hypoperfusion
2. Hx b. Reduction goal:
a. previous BP recordings 1. 25% reduction over 1 to 4 hours
b. previous and current treatment 2. Less rapid reduction over 24 hours
c. sympathomimetics 3. To a DBP of 100mmHg
d. antidepressants
e. non-prescription drugs
f. recreational drugs Rapid BP Correction: Indications
3. Ex The only two situations where BP must be lowered
a. Check the BP yourself rapidly are in the context of ,
1. in both arms 1. aortic dissection and
2. after a period of rest 2. MI
3. and if possible on standing
b. Monitor the patient's BP regularly c. If alert and well → Oral therapy,
c. Look for evidence of Else IV therapy
1. cardiac enlargement d. Oral
2. heart failure 1. First-line treatment:
3. peripheral pulses a. β-blocker + thiazide diuretic
4. renal masses b. or β-blocker + low-dose CCB (DP)
5. or focal neurological deficit 2. Oral drugs
d. Always examine the fundi: dilate if a. Atenolol 50-100mg PO od
necessary b. Or Labetalol 100-400mg bd
4. Ix c. Nifedipine 10-20mg tds
a. Basic Ix e. IV drugs
1. FBC: 1. GTN 1-10mg/hr IV infusion
a. MAHA (microangiopathic 2. Labetalol
haemolytic anaemia) with a. 20-80mg IV bolus q10 min
malignant HT b. 20-200mg/min by IV infusion
2. UFR: increasing every 15 min
a. Protein 6. Mx of accelerated and malignant HTN
b. red cells ± casts a. Basic
3. RFT: Renal impairment 1. General measures
4. SE: Hypokalaemia 2. Transfer to HDU
5. PT/INR & APTT: DIC with malignant 3. Bed rest
HT

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4. Insert an arterial line

5. Urinary catheter
6. Monitor
a. BP: ½ hourly
b. Neurological state
c. ECG
d. Fluid balance
7. Aim to lower the DBP
a. 100mmHg
b. Or by 15-20mmHg
whichever higher over first 24 hours
8. Early fx → Oral thx
9. Late fx/Haemodynamically unstable →
IV thx
10. Consider ACEI
a. 2.5 mg orally once a day
b. Captopril 25mg tds
b. Special circumstances
1. Furosemide 40-80mg IV, if:
a. Pulmonary oedema or
b. Encephalopathy
2. IV therapy, if:
a. LVF+ → Nitroprusside or
hydralazine
b. LVF° → Labetalol
3. AKI: Nephrology referral
7. Causes
a. Primary/Essential HTN
b. Secondary HTN
1. Renal
a. Renal artery stenosis
b. Renal parenchymal disease: AGN
2. Endocrine
a. Pheochromocytoma
b. Cushing’s
c. Thyrotoxicosis
3. Vascular
a. Vasculitis
b. Coarctation of aorta
4. Drugs
a. Cocaine
b. Amphetamine
5. Pregnancy
a. Eclampsia
b. Pre-eclampsia

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Pulmonary Embolism

Scenario: 40year old women presented with SOB 2. Classic changes:

of acute onset, pleuritic chest pain and a. S1Q3T3
haemoptysis. How would you approach?

1. Ix
a. ABG:
1. Mild respiratory alkalosis
2. Low PaCO2
b. ECG:
1. MC: Sinus tachycardia with/without
nonspecific ST and T changes
b. Right axis deviation

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c. RBBB
c. CXR
1. Westermark’s sign: Focal pulmonary Breathlessness/dyspnoea causes
oligemia 1. Acute (seconds)
2. Raised hemidiaphragm a. PE
3. Small pleural effusion b. Pneumothorax
4. Wedge shaped shadows c. Foreign body
d. Anaphylaxis
d. FBC
e. Anxiety
1. Neutrophil leucocytosis
2. Subacute (minutes-hours)
e. Troponin mildly elevated a. Acute left ventricular failure (pulmonary
f. D-dimer oedema)
1. Highly sensitive, but non-specific b. Asthma exacerbation
2. Use to rule out PE in low risk patients c. COPD exacerbation
d. Pneumonia (bacterial, viral, fungal, TB)
e. Metabolic acidosis
3. Chronic (days-weeks)
a. Anaemia
b. Thyrotoxicosis
c. Recurrent pulmonary emboli
d. Cardiac disease (chronic cardiac failure,
arrhythmias, valvular heart disease)
e. Asthma
f. COPD
g. Non-resolving pneumonia
h. Bronchiectasis
i. Lung cancer

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Asthma
Scenario: 26year old male presented with sudden
onset SOB worsening over 2 hours with wheeze.
How will you approach this patient?

1. Initial Mx
a. Sit the patient up
b. O2
1. High flow
2. Via facemask
3. SpO2 target >92%
c. Nebulize bronchodilators
1. Salbutamol 5mg administered via O2
2. Repeat up to every 15-30mintues if
required
3. Continuous nebulization if inadequate
response
a. Salbutamol 5-10mg/h
d. Add ipratropium bromide
1. 0.5mg, 4-6 hourly
2. Given if response to beta 2 agonist is
poor.
e. IV access
f. Steroids
1. 200mg hydrocortisone IV
2. Continue
a. Hydrocortisone 100mg qds IV
b. Or Prednisolone 30-50mg daily
g. Antibiotics
1. If evidence of chest infection
h. Adequate hydration
1. Prevents mucus plugging
2. IV or PO 2-3l/day
2. Monitor
a. Pre and post nebuliser peak flow
b. ABG 1-2 hourly
c. Serum K+ daily
3. Continued Management: If condition
deteriorating
a. Continue O2
b. Nebulize salbutamol every 15 minutes
c. Give IV MgSO4 single dose:
1. Dose: 1.2-2g over 20 minutes
2. Repeated dose note given
d. Consider IV aminophylline infusion
e. Consider IV salbutamol infusion
f. Get anaesthetic help
1. NPPV (Noninvasive Positive-Pressure
Ventilation)
a. CPAP
b. BIPAP
2. Intubate and ventilate
4. Complications
a. Urgent CXR:
1. Pneumothorax – MC
2. PE

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Anaphylaxis

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Acute pneumothorax
1. Mx
a. General measures
1. Prop up
2. Oxygen
2. Causes
a. Primary/spontaneous pneumothorax
1. healthy subjects
2. no known underlying lung disease
3. More common in tall, young men who
smoke, aged 20-40 years
4. Probably due to rupture of apical
subpleural blebs/bullae.
b. Secondary pneumothorax
1. pleural rupture due to underlying lung
disease:
a. emphysema
b. fibrosing alveolitis
c. cystic fibrosis
d. sarcoidosis
c. Infection:
1. cavitating pneumonia, e.g.
staphylococcal
2. lung abscess
3. tuberculosis
4. PCP.
d. Trauma: particularly chest trauma in RTA.
e. Iatrogenic:
1. after pleural biopsy or aspiration
2. transbronchial biopsy
3. percutaneous lung biopsy
4. subclavian vein cannulation
5. mechanical ventilation with high
airway pressures
3. Ix
a. CXR
1. Hyperlucency of one lung field
2. Clear heart border
4. Signs of tension pneumothorax
a. Hypotension
b. Tachycardia
c. Trachea deviated to opposite side
d. ↑ JVP

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Tension pneumothorax
1. Do not leave the patient unattended.
2. Give maximal inspired O2 to reverse hypoxia.
3. Insert an 18G (green) or pink cannula (or the
largest available) perpendicular to the chest
wall into the second intercostal space in the
midclavicular line on the side with the
pneumothorax on clinical examination
(reduced breath sounds and trachea deviated
away).
4. Relief should be almost immediate.
5. Leave the cannula in place until the air ceases
to rush out.
6. Insert a chest drain as soon as possible.
7. If no air rushes out when the cannula is
inserted, the patient does not have a tension
pneumothorax and the cannula should be
removed.

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Stroke

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1. Presentation e. Patients should be mobilized as soon as

a. MC: focal deficit of cerebral function possible.
b. confusion (e.g. due to dysphasia or
visuospatial impairment)
c. seizures
d. declining levels of consciousness or
e. global loss of brain function and coma
2. Conditions mimic stroke
a. Cerebral tumour (1° or 2°)
b. Brain abscess
c. Demyelination
d. Focal migraine
e. Subdural haematoma
f. Todd's paresis (post seizure)
g. Hypoglycaemic attack
h. Encephalitis
3. Hx
a. Risk factors
1. General
a. Increasing age
b. Hypertension
c. Diabetes
d. Family history
e. ↑lipids
2. Lifestyle
a. Drug abuse (cocaine)
b. Smoking
c. Oral contraceptive pill
d. Hormone replacement therapy
e. Neck trauma/manipulation
3. Cardiac
a. Atrial fibrillation
b. Myocardial infarction
c. Ischaemic heart disease
4. Thrombolysis
a. BP control
1. BP must be <185/110mmHg prior to
thrombolysis
2. maintained below 180/105mmHg for
24h after thrombolysis
3. avoid excessive BP lowering which may
worsen blood flow and cerebral
ischemia
5. Management
a. Exclude hypoglycaemia.
b. Brain imaging should be undertaken as
soon as possible, within 24 hours of onset.
c. Assess swallowing before giving oral foods,
fluid or oral medication on admission. If
impaired: specialist assessment of within
24-72 hours of admission.
d. If surgical referral for decompressive
craniectomy is indicated*: refer within 24
hours of onset of symptoms and treat
within a maximum of 48 hours.

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Acute upper gastrointestinal 1. 2 large bore (14G-16G) cannulae.

2. Insert a central line if peripheral access
(GI) bleeding is difficult.
c. Grouping and save + cross match 4-8U.
1. Presentation d. IV fluids:
a. Haematemesis 1. if haemodynamically compromised,
b. Melaena a. initially give 500mL-1L colloid over
c. Weakness/sweating and palpitations. 1h,
d. Postural dizziness and fainting b. then crystalloid and continue until
2. Causes compatible blood is available.
a. Peptic ulcer: 35-50% 2. If there is massive haemorrhage,
b. Gastroduodenal erosions: 8-15% a. give ‘O’- negative blood
c. Oesophagitis: 5-15% 3. if haemodynamically stable:
d. Varices: 5-10% a. give slow infusion of 0.9% saline to
e. Mallory-Weiss tear: 15% keep the IV line patent and for
f. Upper GI malignancy: 1% maintenance fluids.
3. Hx e. Consider central line insertion and CVP
a. Dyspepsia monitoring if initial Rockall score is ≥3.
b. Alcohol f. If ulcer haemostasis needed
c. drug history (e.g. NSAIDs, anticoagulants) 1. Commence IV PPI (80mg IV, followed
d. risk factors for liver disease by 8mg/h) pre-endoscopy and for 72h
e. normal vomit prior to haematemesis after endoscopy
(Mallory-Weiss tear, variceal bleed) g. Monitor
f. previous GI bleeds, ulcers or surgery 1. pulse rate
4. Ex 2. BP
a. look for stigmata of chronic liver disease 3. urine output
(including hepatomegaly and 4. and CVP
splenomegaly) h. Keep the patient NBM for the endoscopy.
b. scars of previous surgery 7. Management key points: variceal Haemorrhage
c. telangiectasia (Osler-Weber-Rendu a. Initial resuscitation: Transfuse with blood,
syndrome) FFP, and platelets as necessary
d. abdominal bruit b. Vitamin K (10mg IV once).
e. bruises c. Prophylactic antibiotics (for 5 days):
f. Rectal examination may reveal melaena or 1. a 3rd-generation cephalosporin (e.g.
semi-fresh blood ceftriaxone)
5. Severity 2. or ciprofloxacin and amoxicillin
a. Rockall score d. Terlipressin
1. Score <3 = excellent prognosis 1. 2mg initially
2. Score >8 = high risk of death 2. then 1-2mg every 4-6h for up to 72h
e. UGIE:
1. band ligation
2. or sclerotherapy
f. If bleeding is not controlled,
1. balloon tamponade (e.g. a Sengstaken-
Blakemore or Linton tube)
2. TIPS or
3. surgery
8. General measures to stop the bleeding
a. Correct any coagulopathy
1. Plt < 50,000/mm3 → platelet support
(6-12U of platelets).
6. Management key points: initial management of 2. Cryoprecipitate → if the fibrinogen
upper GI bleed* levels are low.
a. Protect the airway: position the patient on b. Serum calcium
side. 1. may fall after several units of citrate-
b. IV access: containing blood transfusion.

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2. Give 10mL (4.5mEq) of calcium

gluconate for every 3-4U transfused
c. Ulcer healing agents: give an IV PPI such as
1. pantoprazole (40mg IV daily)
2. or omeprazole (80mg IV, followed by
8mg/h for 72h).
d. Tranexamic acid
1. 0.5-1g IV tds or 1-1.5g PO tds
2. increases the levels of fibrinogen
9. Key points
a. Peptic ulcer
1. IV PPI infusion was almost as effective
as therapeutic endoscopy in bleeding
peptic ulcer disease.

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Poisoning 1. 50g every 4h

2. Accelerate whole body clearance of
General management some drugs by interrupting
1. General measures enterohepatic cycling, e.g.
a. A phenobarbital, phenytoin,
1. Remove foreign bodies, secretions, carbamazepine, digoxin, paraquat and
vomitus and dentures. slow- release preparations such as
2. Maintain patient in head low and semi- theophylline
prone position
3. Insert airway if respiration is impaired
b. B
1. High flow O2
c. C
1. BP
2. 2 wide bore (Orange or Grey) cannula
3. IV N/S infusion
4. Head low position
5. Inotropes when necessary
2. Supportive therapy
a. IP/OP chart
1. ensuring an adequate urine output
2. adequate amount of oral and IV fluids
b. Hypothermia
1. Cover with blankets
c. Cardiac arrhythmias
1. Do ECG
d. Treat associated conditions accordingly
1. Cardiac arrhythmias
2. Seizures
3. Pulmonary oedema
4. Acute renal failure
e. Monitor
1. Breathing
2. BP
3. Temperature
4. acid-base
5. and electrolyte
f. Intubate if GCS <8
g. Remove contaminated clothing and wash
the skin thoroughly with soap and water
Acute Organophosphate Poisoning
3. Measures to reduce gut absorption 1. Clinical features: Due to overstimulation of,
a. Gastric lavage a. muscarinic acetylcholine receptors in the
1. only effective if used up to 1h post OD parasympathetic system
2. CI: if corrosive substances or 1. Bronchospasm
hydrocarbons have been ingested 2. Bronchorrhoea
b. Activated charcoal 3. Miosis
1. 50g as a single dose 4. Lacrimation
2. Suspend 50 g in 200 ml of water. 5. Salivation
Recommended dose is 1 g/kg 6. Diarrhoea
3. will adsorb many drugs if given within 7. Hypotension
1h of ingestion 8. Bradycardia
4. Drugs not adsorbed by charcoal: iron, 9. Vomiting
lithium, salts, alkalis, acids, ethanol, b. nicotinic and muscarinic acetylcholine
methanol, ethylene glycol, and organic receptors in the CNS
solvents 1. Confusion
c. Multiple-dose activated charcoal 2. Coma
3. Agitation

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 48

4. Respiratory failure 4. Maintenance infusion: Once the patient

c. acetylcholine receptors in the sympathetic is stable
system a. 5% dextrose containing 10 - 20% of
1. Excessive sweating the total initial dose of atropine on
2. Mx: General an hourly basis
a. Assess airway, breathing and circulation 5. Atropine toxicity
b. Monitor a. CFx:
1. cardiac rhythm ⬧ agitation, flushing, pyrexia
2. SpO2 b. Stop atropine infusion
c. ECG c. wait for 30 - 60 minutes
d. Every 15 min assess d. Restart infusion at a lower rate
1. level of consciousness and e. Pralidoxime:
2. pulmonary oedema 1. Loading dose: 30 mg/kg IV over 10 - 20
3. cyanosis minutes
4. axillary sweating 2. Then continuous infusion of 8 -10
5. and pupillary size mg/kg/hr until clinical recovery
e. Look for muscle fasciculations, paralysis or a. for 7 days
convulsions b. or 12 - 24 hours after atropinisation
f. Obtain and maintain IV access with as low is no longer required
infusion of 5%dextrose c. or whichever is later
g. Give diazepam 5-10 mg IV if convulsions f. Review response at regular intervals
occur g. Watch for Intermediate Syndrome once the
h. Give frusemide 40-80mg IV in pulmonary patient recovers from the initial cholinergic
oedema, Consider ventilation in refractory crisis
cases
i. If respiratory failure is imminent, prompt
endotracheal intubation and mechanical
ventilation are life-saving
3. Mx: Elimination of the poison
a. remove contaminated clothes
b. wash the skin thoroughly with soap and
water
c. Gastric decontamination
1. within 2 hours of ingestion of poison
2. Give activated charcoal 50 g suspended
in 200 ml of water
d. IV atropine: immediately
1. 1.8- 3.0 mg fast IV bolus
(3 - 5 of 0.6 mg atropine ampoules)
2. atropine therapy should be guided by
a. Poor air entry into the lungs due to
bronchial secretions and
bronchospasm
b. Excessive sweating
c. Bradycardia (HR< 60/pm)
d. Hypotension
e. Miosis
3. Double the dose of atropine every 5
minutes, until most (at least 3 of the 5)
parameters are corrected
a. Clear chest with no wheeze
b. Dry axillae
c. Heart rate between 8O- 100 bpm
d. SBP>90 mmHg
e. Pupils no longer pin point

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Paracetamol Poisoning b. enzyme-inducing drugs

1. carbamazepine
2. phenytoin
3. phenobarbitone
4. primidone
5. and rifampicin
c. Conditions causing glutathione depletion
1. malnutrition
2. eating disorders
3. malabsorption states and
4. HIV infection
4. Toxic dose
a. Fatal single overdose
1. 10g (20 tablets of 500 mg each)
2. or 200 mg/kg body weight
b. Repeated supratherapeutic doses →
hepatotoxicity
1. exceeding 100 mg/kg/day
5. CMLx
a. Acute liver failure
b. Severe metabolic (lactic) acidosis
c. Pancreatitis
d. AKI
6. Ix
a. Blood for PCM level
1. after 4 hours of ingestion
2. Plasma levels after 15 hours are less
1. Pathophysiology reliable
a. In therapeutic doses b. LFTs (ALT > 1000 IU/L)
1. only a minor fraction is oxidized to the 1. Transaminases rise by 24h.
reactive/toxic species (NABQI) c. U&Es
2. NABQI is detoxified by conjugation 1. S. Cr
with glutathione. 2. Renal failure generally occurs on day 3
b. In overdose d. PT/INR
1. normal metabolic routes become 1. May be normal despite high
saturated transaminases.
2. therefore an ↑ fraction is metabolized 2. The PT is the best indicator of the
via the cytochrome p450 system to severity of liver failure.
toxic metabolites e. FBC
3. whose detoxification rapidly depletes 1. Thrombocytopenia seen in severe
hepatic glutathione stores overdoses.
2. Clinical features f. RBS:
a. first 24 hours 1. Hypoglycaemia progressive liver
1. commonly asymptomatic failure.
2. nausea and vomiting 2. Give IV glucose (25- 50ml of 50%
b. >24 hour dextrose) if necessary
1. right hypochondrial pain g. ABGs: To assess degree of acidosis.
2. jaundice h. IP/OP chart
3. oliguria 7. Mx
4. hypoglycaemia a. Determine the time of ingestion as
5. AKI – day 3 accurately as possible
6. Encephalopathy - 72h b. activated charcoal 50g < 1-2 hour
7. Lactic acidosis: either <12h (very rare) c. NAC
or late 1. Indication
3. Higher risks patients: a. more than 10 g (20 tablets of 500
a. Regular alcohol excess mg each)

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b. dose exceeding 200mg/kg is 3. PT

ingested and the time of ingestion 4. LFTs
is not reliable 5. RBS – 6hourly
2. Mild reactions effectively treated by 6. and ABGs daily
antihistamines g. Pt is the best indicator of the severity of
a. Up to 10% of patients have liver failure
⬧ rash 1. Give vitamin K IV 10mg (as a single
⬧ bronchospasm dose, in case body stores are deficient)
⬧ or hypotension. 2. avoid giving FFP unless there is active
b. Stop the IVI bleeding
c. and give chlorphenamine 10mg IV,
Hydrocortisone 200mg IV
d. Start slow infusion
3. Graph
a. Measure paracetamol levels at least
4h post ingestion and ideally 4h
later, and plot on the graph
b. All patients on or above the
‘normal’ treatment line should be
given NAC
4. Infusion rate if features of liver damage
a. 150 mg/kg/24hr in 1500ml of 5%
dextrose
b. continued until liver damage is
seen to recover
d. NAC infusion:
1. 150mg/kg in 200mL 5% glucose over
15min, followed by
2. 50mg/kg in 500Ml 5% glucose over 4h,
and finally
3. 100mg/kg in 1L 5% glucose over 16h.
e. Oral methionine:
1. Only use if patient is allergic to NAC.
2. Give 2.5g stat and 3 further doses of
2.5g every 4h.
3. less effective unless given within 8
hours of overdose
f. Monitor
1. U&Es,
2. FBC

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Pulmonary Oedema a. continuously monitored with resuscitation

facilities
1. Presentation b. Sit the patient upright
a. Acute breathlessness c. O2
b. Cough 1. Give high flow oxygen by face mask:
c. frothy blood-stained (pink) sputum Give 60-100% O2
d. Collapse 2. Caution: Start with 24% in COPD
e. cardiac arrest d. Gain IV access
f. or shock 1. Urgent: RFT, SE, FBC, ABG & trop I
2. Causes e. Connect to a cardiac monitor: arrhythmias
a. Cardiac: f. Insert a urinary catheter to monitor urine
1. LVF due to any cause output
2. Mitral stenosis g. Perform 12 lead ECG and arrange an urgent
b. Non-cardiac: portable CXR
1. ARDS (smoke inhalation, pulmonary h. Give frusemide
vasculitis, sepsis, DIC, drowning) 1. 40 -120 mg slow IV injection
3. Clinical features 2. Larger doses are required in renal
a. Onset: Usually acute failure
b. Dyspnoea i. Give diamorphine
c. orthopnoea 1. 2.5 - 5 mg slow IV (2mg per min.)
d. PND 2. Caution: respiratory depression.
e. Frothy blood-stained sputum j. Give metoclopramide
f. Bilateral fine pulmonary crepitations 1. 10 mg IV
g. Evidence of the underlying condition such 2. to prevent nausea/ vomiting
as chest pain in MI may be apparent k. If the SBP is ≥90mmHg (CI: aortic
4. Investigations stenosis):
a. Monitor 1. Give sublingual GTN spray (2 puffs)
1. cardiac rhythm 2. Start IV GTN infusion
2. pulse a. 1-10mg/hour,
3. BP b. increase the infusion rate every 15-
b. ECG: 20min,
1. Arrhythmia c. titrating against BP
2. Ischaemia 3. or ISDN 2 -10 mg/h IV infusion.
3. MI 4. Caution: Avoid when initial SBP is <90
c. CXR: Cardiomegaly and signs of failure mmHg
1. pleural effusions 5. (aiming to keep SBP ~100mmHg)
2. fluid in horizontal fissure l. If the patient is showing fatigue, consider
3. 'bat's wing’ appearance intubation and ventilation or NIV where
4. upper lobe blood diversion available
d. ABG m. Catheterise the bladder and maintain fluid
1. Type 1 respiratory failure balance
e. FBC: n. If the patient is hypotensive (SBP<90) with
1. Severe anaemia pulmonary oedema, treat as cardiogenic
2. evidence of infection shock.
f. U&E: Changes due to AKI o. Identify the underlying cause and institute
g. Echo: specific treatment
1. Impaired LV function p. If dyspnoea cannot be significantly
2. Valvular abnormalities improved by acute measures may require
h. Troponin I CPAP or mechanical ventilation.
5. Principles of management q. Repeat ABG and K+ if the clinical condition
a. Stabilize the patient: relieve distress and deteriorates or after 2h if there is
begin definitive treatment. improvement and the original sample was
b. Look for an underlying cause. abnormal
c. Address haemodynamic and respiratory
issues.
d. Optimize and introduce long-term therapy.
6. Management:

MEDICINE EMERGENCIES ZUMRA & AFDHAAL