Emmergency Medicine

Emergency medicine for
the final FRCS exam

(Ophthalmology)
From Oxford Handbook Of Clinical Medicine
(Sixth Edition)
I hate this book, too crowded and too much complicated for us. In
these notes, I have tried to simplify it. I hope I have succeeded.
Please do not forget Kanski‟s chapter of systemic diseases. It is a
must. God bless you all and good luck.
2007
)Emergency medicine for the final FRCS exam (Ophthalmology 2007
Cardiopulmonary resuscitation (CPR) for

cardio respiratory arrest
 In a second, confirm the diagnosis (unconscious, apnoeic,

absent carotid pulse), then:
 Shout for help (how? Ask someone to call the
arrest team and bring the defibrillator. Note the time)
 Then do by yourself “Basic life support” which

consists of: ABC
A: Establish a patent Airway
 Protect cervical spine, if injury possible.
 Assess: any signs of obstruction?
Ascertain patency by:
 Head tilt (if no spinal injury is suspected).
 Chin lift.
 Jaw thrust.
 Clear the mouth.
B: Breathing
 Assess by Look, listen and feel
(determine respiratory rate, check bilateral
chest movement, percuss and auscultate).
 If no respiratory effort, treat as arrest, Intubate and
ventilate.
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 If breathing is compromised, give high concentration

oxygen and manage according to the findings e.g. relieve
tension pneumothorax.
 Give 2 breaths immediately (each inflation 2 seconds
long. Use Ambu system if available and 2 resuscitators
present, otherwise, mouth-to-mouth breathing).
C: Circulation (chest compressions)

 Assess: check carotid pulse  No pulse  Start CPR
immediately.
 Check BP, capillary refill and look for evidence of
hemorrhage.
 If shocked, treat accordingly.
 Call for help again.
 Start CPR on a firm surface.
 Do chest compressions 30:2 (new guidelines).
 Use the heel of hands with straight
elbows.
 Center over the lower third of the
sternum.
 Aim for 5 cm compression at 100/min.
 Allow the chest to recoil completely.
 Interrupt infrequently as possible (only for DC and
intubations).
 Do 20 cycles (20 of 30:2) then recheck?
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 Then arrest team (not you except if you have the

license) should have come to do: “Advanced
life support”
(Intubations and ventilation, IV access and monitoring)
D: Disability
 Assess level of consciousness (AVPU).
 Check pupils (size, equality and reaction).
 Glasgow coma scale if time allows.
E: Exposure
 Undress patient but cover to avoid hypothermia.
H: History from relatives and bystanders

 Events surrounding onset of illness.
 Past medical history e.g. DM, epilepsy or asthma.
 Medications.
 Allergies.
“Direct current cardio version”

“DC shock”
 Place defibrillator (monophasic) paddles on chest
(apex and under Rt. clavicle) as soon as possible and
set monitor to read through the paddles if there is delay
in attaching leads.
 Assess rhythm: is it VF/VT or pulseless VT
(asystole)?
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1- Ventricular fibrillation or tachycardia:

 Without delay: 200J; 200J; 360J.
 Adrenaline 1mg/ml IV, every 3 min.
 Still in VF/VT (by pulse), give 360J (3 times).
 Amiodarone 300 mg IV or Lidocaine 100 mg IV.
 Atropine 3 mg IV (once).
 Oxygen 100%.
2- A systole:
 Adrenaline 1mg/ml IV, every 3 min.
 Oxygen 100%.
 Atropine 3 mg IV (once).
 Amiodarone 300 mg IV or lidocaine 100mg IV.
 Give sodium bicarbonate 1 mmol/kg only in
severe acidosis after prolonged resuscitation (e.g. 50
ml of 8.4 % solution by IVI) because it may worsen the
acidosis and precipitate arrhythmias.
 Calcium chloride 10 ml 10%.
 In general, look for reversible causes of cardiac

arrest (MI, PE, tension pneumothorax, shock, hypoxia,
and electrocution) and treat accordingly.
 Send someone to check patient‟s notes and
doctor, searching for a clue as to the cause of the
arrest.
 If IV access fails, give drugs down tracheal tube
(2-3 times IV dose diluted in ≥ 10 ml 0.9 % saline
followed by 5 ventilations to assist absorption).
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 (Intracardiac injection in not recommended).

(PLEASE)
When to stop CPR?

No general rule, as survival is influenced by the
rhythm and the cause of the arrest. Stop only if:
 Normal rhythm occurs, core temperature is >
33°C and pH and potassium are normal.
 Basic life support started after 5 min or advanced
life support started after 30 min (there was significant
delay in starting CPR).
 >20 min with no rhythm.
 Exhaustion.
 The Patient is not for resuscitation (advanced
disease).
 Mentally competent patient stated or recorded
that he does not want to be rescued.
 Not in the patient interest as it would lead to a
poor quality of life.
 Involve patients and relatives.
 When in doubt, resuscitate.
“After successful resuscitation”

“What to do?”
 Transfer to CCU or ICU.
 Monitor vital sign.
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 Seek expert advice from a cardiologist.

 Consider ECG, CXR, glucose, blood gases,
CK/troponin.
 Explain to the patient‟s relatives what has
happened, whatever the outcome.
Shock
 Shock means circulatory failure resulting in inadequate
organ perfusion (systolic blood pressure < 90 mmHg) leading
to severe organ dysfunction.
 Signs: tachycardia, hypotension, capillary return ↓
(press a nailbed), air hunger and oliguria. If raised CVP, then
cardiogenic shock is most likely.
 Causes:
 Pump failure (Cardiogenic):
o Cardiogenic shock.
o Secondary: PE, tension pneumothorax, cardiac
tamponade.
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 Peripheral circulatory failure (Non

Cardiogenic):
o Anaphylactic Shock.
o Hypovolaemic Shock:
 Bleeding: trauma, ruptured aortic aneurysm or ectopic
pregnancy.
 Fluid loss: vomiting (GIT obstruction), diarrhea
(cholera), burns or heat exhaustion.
o Septic Shock.
o Neurogenic shock: e.g. post spinal surgery.
o Endocrine failure: e.g. Addison‟s or
hypothyroidism.
o Iatrogenic: drugs e.g. anesthetics and antihypertensive
drugs.
 Management:
“If BP unrecordable, call the cardiac arrest team”
 Call for help + elevate the leg.
 A  Adequate ventilation.
 B  Oxygen 100%.
 C  Circulation (IV access x 2, wide bore, get help
if this takes > 2 min).
 Identify and treat underlying cause if clear (check
abdomen for signs of trauma or aneurysm. GIT bleeding
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and melaena). If unclear, ttt as Hypovolaemic (most

common cause).
 Infuse crystalloids: fast to raise BP (unless
cardiogenic shock) as dictated by BP, CVP, and urine
output.
 Vital sign monitoring: pulse, BP, temperature,
respiration and peripheral perfusion.
 Do some investigations: FBC, ABG, glucose, cross
matching, ECG.
 Consider: arterial line, central venous line and
bladder catheter (aim for a urine flow > 30 mL/h).
“Treatment according to the cause”

 Cardiogenic shock: Cold and clammy patient.
 Has high mortality. Can occur suddenly or after
progressively worsening heart failure. Ask a senior
physician‟s help both for exact diagnosis and treatment.
 Causes: arrhythmias, cardiac tamponade, tension
pneumothorax, MI, myocarditis or myocardial depression
(drugs, hypoxia, acidosis, sepsis), endocarditis and PE.
 Management:
o If cause is MI, prompt thrombolysis or acute
angioplasty.
o Manage in CCU or ICU if possible.
o Oxygen.
o Morphine (2.5 – 5 mg IV) for pain and anxiety.
o Investigations: ECG, CK, U&E, CXR, echo, ABG.
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o Close monitoring: CVP, BP, ABG, ECG and urine

output.
o Do 12 leads ECG every hour until diagnosis is
made.
o Consider Swan – Ganz catheter to assess
pulmonary wedge pressure and cardiac output and an
arterial line to monitor pressure.
o Correct arrhythmia, U&E and acid – base
imbalance.
o PCWP < 15 mm Hg: give plasma expanders (100
mL every 15 min IV), aim for 15 – 20 mm Hg.
o PCWP > 15 mm Hg: consider inotropes e.g.
dobutamine (2.5 – 10 ug/kg/min IVI), aim for systolic BP >
80 mm Hg.
o Look for and treat any reversible cause e.g. MI and
PE (thrombolysis). Consider surgery for valvular lesions.
Cardiac tamponade
 Pericardial fluid collection resulting in intrapericardial
pressure rise, heart cannot fill and the pumping stops.
 Causes: trauma, lung or breast cancer, pericarditis and
MI.
 Signs: Falling BP, rising JVP and muffled heart sounds
(Beck‟s triad), JVP increases on inspiration (Kussmaul‟s
sign), pulsus paradoxus (pulse fades on inspiration).
 Echo is diagnostic.
 CXR: globular heart, Lt. heart border convex or straight,
Rt. costophrenic angle < 90°.
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 ECG: electrical alternans.

 Management: very difficult. With actual senior help and
luck, prompt pericardiocentesis brings swift relief.
 While waiting, give oxygen, monitor ECG and set an IVI.
Take blood for group and save.
 Non Cardiogenic shock:

o Hypovolaemic:
 Treat underlying cause e.g. control obvious
hemorrhage, urgent laparotomy or thoracotomy, correct
electrolyte abnormalities and acidosis.
 Fluid replacement: saline or colloid initially; if
bleeding, use cross matched blood transfusion or group O
Rh – ve blood via large bore cannula.
 Titrate against BP, CVP and urine output.
o Anaphylactic shock:
 Type 1 IgE-mediated hypersensitivity reaction.
 Release of histamine and other mediators are involved.
 More common in atopic individuals.
 Look for any features suggestive of anaphylaxis
(history, urticaria, and wheeze).
 Anaphlactoid reaction involves direct release of
mediators from inflammatory cells without involving
antibodies e.g. with drugs.
 Causes: drugs e.g. penicillin and contrast mediators in
radiology. Stings and some kinds of food e.g. strawberries.
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 Signs and symptoms: tachycardia, hypotension,
redness, urticaria, wheezy chest, itching, laryngeal

obstruction and cyanosis.
 Treatment:
 Secure airway, give 100% oxygen. Intubate if
respiratory obstruction imminent.
 Remove cause, raise the feet.
 Adrenaline 0.5 mg (0.5 mL of 1:1000) IM repeated
every 5 min guided by BP, pulse and respiratory function
until better.
 Secure IV access.
 Antihistaminic e.g. chlorpheniramine 10 mg IV.
 Hydrocortisone 200 mg IV.
 IVI (0.9 % saline up to 2 L may be needed) titrated
against BP.
 Admit to ICU if still hypotensive, consider aminophylline
and nebulized salbutamol.
 Suggest a Medic-alert bracelet naming the allergen.
 Teach about self – injected adrenaline.
 Skin prick tests helps in identifying which allergens to
avoid.
 Note: if patient is severely ill or has no pulse,
consider IV adrenaline (1 mL of 1:10,000 solution per

minute). Stop as soon as a response has been obtained.
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o Septic shock:
 Endotoxin-induced vasodilatation with shock and coma
but with no signs of infection (fever and ↑ WCC).
 Warm and well perfused with bounding pulse.
 Antibiotics: if no clue, IV cefuroxime 1.5 g / 8h or
gentamycin + antipseudomonal.
 Give colloid or crystalloid by IVI.
 Monitor in ICU (central venous pressure and
pulmonary artery wedge pressure).
o Vasovagal attack:
 Cause: generalized vasodilatation.
 Clinical picture: bradycardia and hypotension.
 Treatment: Atropine 1mg IV and IVI fluids.
o Heat exposure (exhaustion):

 Tepid sponging and fanning.
 Avoid ice and immersion.
 IVI 0.9 % saline ± hydrocortisone 100 mg IV.
 Chlorpromazine to stop shivering.
 Stop cooling when core temperature < 39°C.
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Acute chest pain

 Causes:
o Acute myocardial infarction.
o Pulmonary embolism.
o Tension pneumothorax.
o Aortic dissection.
o Unstable angina / ACS.
o Esophageal rupture.
o Pneumonia, empyema and pleurisy.
o Chest wall pain e.g. muscular, rib fractures, bony
metastasis and costochondritis.
o Gastro-esophageal reflux.
o Pericarditis.
o Intra-abdominal e.g. cholecystitis and peptic ulceration.
o Sickle-cell crises.
 Management:
 Call for help.

 B  Oxygenation 100%.
 C  Circulation  IV line.
 Level of consciousness.
 Vital sign monitoring.
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Acute myocardial infarction

 Type of pain: Heavy pain > 15min, radiating to the arm,
neck and shoulder.
 Clinical picture: Dyspnea, sweating, palpitations,
nausea, dizziness, collapse and shock.
 Risk factors: DM, HTN, atherosclerosis and smoking.
 Chest x ray: ↑ in cardiac size.
 ECG: normal or elevated ST segment and pathological
Q.
 Cardiac enzymes:
 CK ↑ 8 – 12 h till 72 h.
 Lactate dehydrogenase ↑ 1 - 2 days till 7 days.
 Cardiac troponin.
 Aspartate transaminase.
 Investigate by echocardiography and coronary
angiography.
 Arrange for an emergency ambulance.
 Aspirin 300 mg PO chewed (unless clear
contraindication).
 Morphine 5 -10 mg IV.
 Metoclopramide 10 mg IV.
 Sublingual nitrate (2 puffs or 1 tablet) unless
hypotensive.
 B-blocker e.g. atenolol 5 mg IV (unless asthma or Lt.
ventricular failure).
 Attach ECG monitor and record a 12 lead ECG.
 High flow oxygen 100% by face mask.
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 IV access.
 Bloods for FBC, U&Es, glucose, lipids and cardiac
enzymes.
 Brief history: previous attack and risk factors for IHD or
any contraindications for thrombolysis.
 Examination: vital signs.
 Thrombolysis:
 Greatest benefit if given < 12 h of onset, up to 24 h.
 Indications: ST elevation > 2 mm in 2 or more chest leads.
 Contraindications: Internal bleeding, severe hypertension,
suspected aortic dissection, pregnancy, esophageal varices,
recent head trauma or hemorrhagic stroke.
 Streptokinase: 1.5 million units in 100 mL 0.9 % saline IVI
over 1h.
 Others thrombolytic agents that might be used in cases of
allergy to SK are alteplase and tenecteplase.
 Complications: failure to reperfuse, stroke, cardiogenic shock
and heart failure.
 If pain is uncontrolled especially with continuing ST
elevation, consider re-thrombolysis or rescue angioplasty.
 Consider DVT prophylaxis:
 Early post-op mobilization.
 Aspirin.
 Compression stocking.
 Low molecular weight heparin SC.
 Vena caval filter.
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Pulmonary embolism
 Always suspect PE in sudden collapse 1 – 2 wks after
surgery.
 Mechanism: venous thrombi, usually from DVT, pass
into the pulmonary circulation and block flow to lungs. The
source might be occult.
 Risk factors: malignancy, long immobilization following
surgery (pelvic), venous disease, obesity, THE PILL and
HRT.
 Prevention: see before (DVT prophylaxis).
 Signs and symptoms: acute dysnea, pleuritic chest
pain, haemoptysis, syncope, hypotension, tachycardia,
↑JVP, tachypnea, cyanosis, fever, AF and DVT (swollen leg).
 Type of pain: pleuritic chest pain.
 Investigations:
 U&E, FBC, baseline clotting.
 ECG:
o Normal 13 % or sinus tachycardia.
o Rt. ventricular strain pattern (V1 – 3).
o AF.
o Deep S waves in I (SI, QIII, TIII).
o Q wave in III (same).
o Inverted T wave in III (same).
 CXR: often normal, decreased vascular markings,
small pleural effusion, wedge shaped area of infarction.
 ABG: ↓ oxygen, ↓ carbon dioxide and ↑ PH.
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 D-dimer blood test: ↑ if thrombosis is present as it

indicates plasma level of fibrin product, so it helps to exclude
PE if (-ve).
 CT: Better with helical (spiral) CT. A ventilation-
perfusion (V/Q) scan can aid diagnosis. If equivocal,
pulmonary angiography or bilateral venogram may help.
 Doppler U/S for leg veins.
-------------------------------------------------------------------------
Management
 Oxygen 100 %.
 Morphine 10 mg IV.
 Antiemetic.
 If critically ill, consider immediate surgery.
 IV access and start heparin 10,000 U IV bolus then 15
– 25 U/Kg/h IVI.
 If systolic BP > 90 mm Hg, start warfarin 10 mg/24h
PO and confirm diagnosis.
 If systolic BP < 90 mm Hg, start rapid colloid infusion.
 If still hypotensive after 500 mL colloid, give
dobutamine 2.5 – 10 ug/kg/min IV (aim for 90 mmHg).
 If still hypotensive, consider noradrenalin.
 If still hypotensive after 30 – 60 min of standard
treatment with clinically definite PE and clinical improvement,
consider thrombolysis with streptokinase (loading dose
250,000 U IVI over 30 min, maintenance 100,000 U/h for 12
– 72 h according to response).
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Acute breathless patient

 Causes:
o Wheezy:
o Acute asthma.
o Acute exacerbation of COPD.
o Heart failure.
o Anaphylaxis.
o Stridor (upper air way obstruction):
o Tumor or FB.
o Acute epiglottitis.
o Laryngeal fracture.
o Crepitations:
o Heart failure.
o Pneumonia.
o Bronchiectasis.
o Clear chest:
o PE.
o DKA.
o Anemia.
o Shock.
o Central cause.
o Others:
o Pneumothorax.
o Pleural effusion.
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 Management:
 Call for help
 B  Oxygenation.
 C  Circulation  IV line.
 Level of consciousness.
 Vital sign monitoring.
Acute severe asthma

 Presentation: acute breathlessness and wheeze.
 History: ask about treatment, previous attacks, admission to
ICU.
 Investigations: Peak expiratory flow rate (PEFR), ABG,
CXR, FBC and U&E.
 Clinical picture:
 Severe attack: unable to complete sentences,
respiratory rate > 25/min, pulse >110/min, PEFR < 50%.
 Life threatening attack: PEFR < 33%, silent chest,
sweating, panic, speechless, using accessory muscles,
cyanosis, bradycardia, hypotensive, confusion, coma, ABG:
high carbon dioxide, low oxygen (<90%) + low pH.
 Treatment:
 Sit patient up and do not sedate.
 Give oxygen 100%.
 Salbutamol 5 mg (or terbutaline 10 mg) plus
ipratropium bromide 0.5 mg nebulized with oxygen.
 Hydrocortisone 100 mg IV or prednisolone 30 mg PO
or both if very ill.
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 If still PEFR < 75 %, repeat salbutamol every 15 min or

10 mg continuously per hour and give prednisolone 30 mg
PO if not already given.
 Monitor oxygen saturation (pulse oximeter), heart rate
and respiratory rate.
 CXR to exclude pneumothorax.
 If still not improving, consider aminophylline (5 mg/kg
IVI over 20 min) or give salbutamol IVI (3 – 20 ug/min).
 If still not improving, consider transfer to ICU to
intubate, give adrenaline and 500 mL colloid IVI.
 Once patient is improving:
o Wean and stop aminophylline over 12 – 24h.
o Switch to inhaled B-agonist and steroids.
o Continue to monitor PEFR with the above for 24h with
rate > 75% of predicted or best with diurnal variability < 25%
(beware of early morning dips in PEFR).
o Look for cause of acute exacerbation.
Acute exacerbation of COPD

 Common in winter and triggered by viral or bacterial
infections.
 Presentations: increasing cough, breathlessness or
wheeze with decreased exercise capacity.
 History: ask about treatment (home oxygen), smoking
and revise old notes.
 DD: asthma, pulmonary edema, upper respiratory tract
obstruction, pulmonary embolus and anaphylaxis.
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 Investigations: PEFR, ABG, CXR, ECG, blood culture if

pyrexial and sputum culture.
 Management:
 Look for the cause e.g. infection or pneumothorax.
 Controlled oxygen therapy (see below). Start at 24 - 28
% and vary according to ABG.
 Nebulized bronchodilator (salbutamol 5mg/4h and
ipratropium 500ug/6h).
 Hydrocortisone 200mg IV and oral prednisolone 30-
40mg.
 Antibiotics in evidence of infection.
 Physiotherapy to aid sputum expectoration.
 If no response, consider IV aminophylline.
 If no response, consider nasal intermittent positive
pressure ventilation (NIPPV) by a nasal mask and a flow
generator.
 Consider intubation and ventilation if pH decreasing
and CO2 rising.
 Consider respiratory stimulate drug e.g. doxapram
(only for patients not suitable for mechanical ventilation and
as a short term measure only).
 Stable COPD: stop smoking, encourage exercise,
proper nutrition, weight reduction and influenza vaccination.
Give short acting B2 agonist, ipratropium and corticosteroid
inhalations according to severity.
 Consider long term oxygen therapy.
 Surgery is indicated in selected cases e.g. recurrent
pneumothorax or isolated bullous disease.
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 Assess social circumstances and support required.

Identify and treat depression.
 Air travel is hazards if O2 saturation is low, check
availability of O2.
Oxygen therapy
 Don‟t leave patients hypoxic.
 Some patients rely on their hypoxic drive to breathe;
too much oxygen may lead to a reduced respiratory rate and
hypercapnia with a consequent fall in conscious level.
 In case of evidence of carbon dioxide retention, start
with 24 – 28 % O2. Reassess after 30 min.
 Monitor the patient carefully.
 Aim to raise O2 above 8.0KPa with a rise in CO2 <
1.5KPa.
 In case there is no retention, use 28-40% but still
monitor and repeat ABG.
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Hypoglycemic coma
 Call for help.

 A  Adequate ventilation.
 B  Oxygenation.
 C  Circulation  IV line.
 Level of consciousness  unconscious and
abnormal behavior (aggression).
 Vital sign monitoring (sweating, pulse ↑, seizures).
 Blood sample (gluco-sticks) glucose oxidase
strips.
 Treatment:
 Give 200 – 300 mL of 10% dextrose IV (20-30g)
OR
 Glucagon 1mg IV/IM. It will not work in drunk
patients.
 Once conscious, give sugary drinks and a meal.
 Give Thiamine if there is malnutrition or
suspicion of alcohol.
 If history of oral hypoglycemic ttt is +ve 
admission to the hospital to give 10% glucose over 1-2
hour to overcome another attack.
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 Clinical notes:
o Glucose level < 3.6 mmol/L  ↑ sympathetic activity  cold
and sweaty skin.
o Glucose level < 2.6mmol/L  neuroglycopenia  confused,
slurred speak.
o Glucose level < 1.5mmol/L  Coma.
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Diabetic ketoacidosis (DKA)
 Call for help.

 C  Circulation IV line.
 Level of consciousness.
 Vital sign monitoring.
---------------------------------------------------------------------------------
 DKA coma only occurs in type I diabetes; it may be the mode
of presentation.
 Precipitants include: surgery, MI, non-compliance, or wrong
insulin dose.
 The diagnosis requires ketosis and acidosis (pH < 7.3).
 Signs and symptoms: polyuria, polydipsia, lethargy,
anorexia, hyperventilation, ketotic breath, dehydration, vomiting,
abdominal pain and coma.
 Investigations: blood sample (gluco-sticks) glucose oxidase
strip, lab glucose, U&E, HCO3, ABG, urine for ketone, ECG to
exclude silent myocardial infarction.
 Treatment:
 Dehydration is more life-threatening than
hyperglycemia, so its correction takes precedence.
 IV access and start fluid (0.9% sodium chloride – saline
IVI) replacement immediately.
 Give one liter stat, then one liter over the next hour,
one liter over 2h, one liter over 4h, then one liter over 6h.
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 Use dextrose saline or 5% dextrose when blood

glucose is < 15 mmol/L.
 Use saline more cautiously in elderly and heart failure
patients.
 Check plasma glucose: usually > 20mmmol/L (give 4
– 8 U soluble insulin (neutral insulin) IV / h) OR 50 unit
insulin in 500 ml hemacele solution.
 Aim for a fall in glucose of 5 mmol / h.
 Continue on insulin sliding scale.
 K+ replacement.
 NG tube only if nauseated/vomiting/unconscious.
 Monitor potassium, glucose and HCO3 hourly initially.
 Urinary catheter if no urine passed for > 4h.
 Monitor CVP (fluid therapy guidance).
 Treat infection if present.
 Give heparin 5000U/8h SC until mobile.
 Change to SC insulin when ketones are ≤ 1+ and
eating.
 If acidosis is severe (pH < 7), give IV bicarbonate after
discussing with seniors because of its effects on Hb -
dissociation and cerebral circulation.
 Potassium administration (KCL 10 - 20mmol/L of IV
fluid) because total body potassium is low and plasma
K+ falls as it enters cells with treatment. Don’t add K+ to
the first bag, check U&Es hourly initially and replace as
required.
 If cerebral edema occurs, consider giving mannitol
and hydrocortisone.
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Hyperglycemic hyperosmolar non ketotic

coma (HONK)
 Only in those with type II diabetes are at risk of this.
 The history is longer (e.g. 1wk), old patient, presenting
for the first time, focal CNS signs may occur.
 There is marked dehydration and glucose > 35 mmol/L.
 Acidosis is absent (no switch to ketone
metabolism).
 Risk of DVT is high.
 Treatment:
 Rehydration over 48h with 0.9% (0.45%) saline IVI at
half the rate used on DKA.
 Wait an hour before giving insulin, it may not be
needed.
 If needed, give 1U/h (3U/h) (aim for 3 - 5mmol / h fall in
blood glucose followed by sliding scale insulin).
 Potassium administration 0 – 5 mmol / L / h.
 Heparin administration  risk for thrombosis.
 Look for the cause e.g. MI or infection.
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Coma
 Definition: unarousable, unresponsiveness.
 Causes:
 Metabolic: drugs, poisoning, DM, hypoxia, septicemia,
hepatic, uremic and CO2 narcosis.
 Neurological: trauma, meningitis, encephalitis, tumors,
hemorrhage, HTN, stroke and epilepsy.
Management of coma
 Call for help.
 B  Oxygenation 100%.
 C  Circulation  IV line and support circulation if
required.
 Consider intubation if GCS < 8.
 Stabilize cervical spine.
 Level of consciousness  (document).
 Blood glucose in all patients; give 50 mL 50% dextrose
IV immediately if presumed hypoglycemia.
 Control seizures.
 Consider IV glucose, IV thiamine (alcohol, Wernicke‟s
encephalopathy), IV naloxone (opiate intoxication) and IV
29
flumazenil (benzodiazepine intoxication if airway

compromised).
 Brief examination: pupils every few minutes particularly
if trauma is the likely cause „localizing sign‟, signs of trauma,
other diseases e.g. liver disease, DM, examine skin for
injection marks, smell breath „alcohol, hepatic fetor, ketosis,
uremia‟, meningism, heart and lung, abdomen and rectum,
foci of infection.
 Obtain history from family, ambulance staff and
bystanders.
 Investigations: ABG, FBC, CXR, U&E, LFT, toxin
screen, ethanol and drug levels, CT and lumbar puncture,
urine analysis: save the first few for drug levels, monitor the
outflow and check for glucose and ketones.
 Eye examination (don't dilate):
 Eye movement.
 Visual fields in light coma, test fields with visual
threat.
 Reflex  vestibulo-ocular reflex (doll‟s head
maneuver or ice water calorics).
 Pupil size:
o Dilated  3rd nerve.
o Pin point  opiate poisoning or pontine lesion.
o Horner‟s syndrome.
 Fundus:
o Papilloedma  ↑ ICT.
o Hemorrhage: subhyaloid & subarachnoid in Terson‟s
syndrome.
31
o HTN and DM.

 Motor signs: Tone, tendon reflex, planter reflex.
 Mannitol 20% ± hydrocortisone in case of cerebral
edema.
 Monitor the neurological signs and coma scale.
 General care of comatose patients.
Glasgow coma scale

 This gives a reliable, objective way of recording the
conscious state of a person. It is used for initial and
continuing assessment. It also has value in predicting
ultimate outcome.
 Best motor response: obeying command(6),
localizing response to pain (5), withdrawal to pain (4), flexor
response to pain (3), extensor response to pain(2), no
response to pain (1). Note that it is the best response of any
limb which should be recorded.
 Best verbal response: oriented (5), confused
conversation (4), inappropriate speech (3), incomprehensive
speech (2), none (1). Record level of best speech.
 Eye opening: spontaneous eye opening (4), eye
opening in response to speech (3), eye opening in response
to pain (2), no eye opening (1).
 Severe injury (GCS ≤ 8).
 Moderate injury (GCS 9 - 12).
 Minor injury (GCS 13 - 15).
30
 Primary scale (AVPU):

 A alert.
 V responds to vocal stimuli.
 P responds to pain.
 U unresponsive.
Status epilepticus
 Definition: seizures lasting > 30 min or repeated
without intervening consciousness. Mortality and risk of
permanent brain damage increase with the length of attack.
Aim to terminate in < 20 min.
Management
 Call for help.
 A  Adequate ventilation. Open and maintain the
airway. Remove false teeth. Insert oral/nasal airway. Intubate
if necessary.
 B  Oxygenation. (100% + suction, as required).
 C  Circulation. IV access and take blood.
 Investigations: U&E, LFT, glucose, ABG, ECG, LP,
EEG, CT, pulse oximeter, cardiac monitor, calcium,
toxicology screening if indicated and anticonvulsant levels.
 Protect from injury.
 Admit in ICU with vital signs monitoring.
 Treatment:
32
 Lorazepam 4 mg as a slow bolus (≤ 2 min) into a large

vein. Beware of respiratory arrest during the last part of the
injection. Have full resuscitation facilities around.
Alternatively use diazepam. While waiting for this to work,
prepare other drugs. If fits continue …
 Phenytoin infusion (15mg/Kg IVI at a rate of ≤
50mg/min). Beware of hypotension and don‟t use in case of
bradycardia and heart block. Requires BP and ECG
monitoring. If fits continue …
 Diazepam infusion (100mg in 500mL of 5% dextrose at
about 40 mL/h). Monitor respiratory function.
 Dexamethasone 10 mg IV if vasculitis or cerebral
edema possible.
 General anesthesia.
 Start oral drugs as soon as seizures are controlled.
 Search for the cause.
 Suspect eclampsia in pregnant ladies (check urine and
BP, call obstetrician for immediate delivery).
 Give thiamine if alcoholism and malnourishment
suspected.
 IV glucose 50 mL 50% unless glucose known to be
normal.
 Correct hypotension with fluids.
33
Stroke
 Stroke result from ischemic infarction or bleeding into
any part of the brain. It manifests by rapid onset (over
minutes) of focal CNS signs and symptoms.
 Causes: thrombosis, emboli, CNS bleed
(hypertension, trauma and aneurysm rupture).
 Risk factors: hypertension, smoking, DM, heart
disease (AF) and hypercholesterolemia.
Management
 Call for help.
 C  Circulation  IV line.
 Level of consciousness (document).
 Vital sign monitoring  for hypertension, admit and
control over days not hours.
 Admission to stroke units for nursing/physio saves lives
and is a great motivation.
 Investigations: urgent CT/ MRI within a few days of
stroke to differentiate hemorrhagic from ischemic if
considering anticoagulation.
 Pointers to hemorrhagic strokes are meningism,
severe headache, and coma within hours.
 Pointers to ischemic strokes are carotid bruit, AF
and past TIA.
34
 Treatment:
 Unless there is strong suspicion of CNS bleeding,
acute aspirin (300mg/24h PO) has a worthwhile effect.
 Nil by mouth if swallowing is a problem.
 Maintain hydration. Don‟t over hydrate (cerebral
edema).
 Turn regularly and keep dry (consider catheterization)
to stop bed sores.
 Monitor and treat ↑ BP.
 If cerebellar hemorrhage possible, refer for immediate
evacuation.
 Passive limb movements, subcutaneous heparin and
compressing stocking (DVT prophylaxis).
 Emotional support and rehabilitation.
 Do complete investigations: FBC, CXR, CT of head,
ECG, carotid Doppler, ESR, U&E, lipids, blood glucose,
echo, carotid angiography and clotting tests.
 Brain attacks: some randomized trials suggest
thrombolysis with alteplase within 3h of onset of symptoms
might decrease risk of adverse outcome. These hospitals
have CNS thrombolysis teams with a dedicated imaging
service on 24h call. Howerever, this is still not recommended
yet in the UK.
35
Atrial fibrillation
 Narrow complex tachycardia: ECG shows rate > 100 bpm
and QRS complex duration of < 120 ms (< 3 small squares on
ECGs done at the standard UK rate of 25 mm/s).
 DD:
 Sinus tachycardia: normal P wave followed by normal QRS.
 Atrial fibrillation: absent P wave, irregular QRS complexes.
 Atrial flutter: rate 300 bpm, saw tooth base line, ventricular
rate 150 bpm (2:1 block).
 Causes of AF: MI, ischemic heart disease, mitral stenosis,
hyperthyroidism, hypertension, Lone AF = no cause.
 Complication: embolic stroke, CRAO,pulmonary embolism.
 ECG: absent P wave, irregular QRS complexes.
 Signs and symptoms: may be asymptomatic or present with
chest pain, palpitations and dysnea. On examination, the
pulse is irregularly irregular, the apical pulse rate (300-600
bpm) is greater than the radial rate and the first heart sound is
of variable intensity. May also present with hypotension,
collapse and pulmonary embolism.
 Investigations: U&E, cardiac enzymes, thyroid function tests
and echo (LA enlargement, mitral valve disease, poor LV
function).
 Treatment:
 Acute AF (< 72h):
 Treat any associated acute illness e.g. MI.
 Control ventricular rate with digoxin PO or IV.
36
 If still too fast and LV function is adequate, consider low dose

B-blocker. If AF does not resolve, consider drug or electrical
cardioversion.
 Drug cardioversion: Amiodarone IVI or PO.
 DC cardioversion is indicated in: electively following a first
attack with an identifiable cause OR as an emergency if
patient is compromised. Protocol: 200J, 360J, 360J (100J
may be tried first but is successful in < 20%). (DO ECHO
FIRST; is heart structurally normal?).
 Anticoagulation is not required if AF of recent onset with
normal echo but aspirin maybe given. Otherwise, give warfarin
3 wks before and 4 wks after DC cardioversion.
 Chronic AF:
 Control rate with Digoxin PO.
 If rate is still too fast, check compliance and serum level.
Cautiously increase dose or consider low dose B blocker.
Alternatively, give Amiodarone 300mg PO.
 Anticoagulant with warfarin if > 65 years unless
contraindicated. Aim for INR 2.5 - 3.5. For those aged < 65
with no other risk factors (e.g. HTN, DM, MI) or those in whom
warfarin is contraindicated, aspirin (300 mg PO) is an
alternative.
 Paroxysmal AF:
 B – Blocker (sotalol). Monitor QT interval.
 Alternatively give Amiodarone PO.
 Anticoagulant with warfarin.
37
ECG
 First confirm the patient‟s name, age, and the ECG date.
 Rate: (300/R-R). Divide 300 by the number of big squares
per R – R interval. (Big square 0.2s, small square 0.04s).
 Rhythm: use the card method.
 P wave: p mitrale (bifid and indicates Lt. atrial
hypertrophy), p pulmonale (peaked and indicates Rt. atrial
hypertrophy).
 P - R interval: from start of P to start of QRS (3 -5 small
squares). Prolonged in heart block and short in WPW
syndrome.
 QRS complex: normally less than 3 small squares.
Prolonged QRS suggest BBB. Large QRS suggest ventricular
hypertrophy. Pathological Q in acute MI is deep (>2mm) and
wide (>0.04s).
 QT interval: from start of QRS till end of T. Varies with
rate. Prolonged in myocardial ischemia and myocarditis.
 ST segment: usually isoelectric. Elevated (>1mm) in
infarction and depressed (>0.5mm) in ischemia.
 T wave: abnormal if inverted in I, II and V4 – V6. Peaked
in hyperkalaemia and flattened in hypokalaemia.
38
ECG abnormalities
 Sinus tachycardia: rate > 100 e.g. anxiety, exercise,
sepsis and pregnancy.
 Sinus bradycardia: rate < 60 e.g. vasovagal attack,
acute MI and B – Blockers.
 AF: see before.
 Heart block: IHD, congenital and drugs.
 ST elevation: acute MI and acute pericarditis (saddle
shaped).
 ST depression: digoxin (downward sloping), ischemia
(horizontal).
 T inversion: PE and BBB.
 ST and T wave changes are often non specific and
must be interpreted in the light of the clinical context.
----------------------------------------------------------------------------------
 Tachycardia (> 100 bpm):

o With narrow QRS:
Regular  sinus tachycardia.
Irregular  AF, A flutter.
o With wide QRS: Ventricular tachycardia.
 Bradycardia (< 60 bpm): B blockers, Ca channel

blockers, myocardial infarction.
39
 A-V block:
 1st degree  fixed prolonged P - R interval > 0.2
sec.
 2nd degree:
 I: progressive prolongation.
 II: 2:1, 3:1 AV block.
 3rd degree  AV dissociation with wide QRS.
 Nodal bradycardia  digitalis toxicity.
 QRS complex:
 Acute myocardial infarction:
 ST elevation.
 T inversion.
 Pathological Q  deep, wide.
 ST depression  ischemia, hypotension, digoxin.

 ST elevation  MI.
 Peaked T wave  hyperkalaemia.
 Flat T  hypokalaemia.
41
Synopsis to minimize “I don’t know”

 You were giving local anesthesia  breathlessness?
What to do?
 Call for help.
 C  Circulation IV line.
 Level of consciousness.
 Causes:
 Brain stem anesthesia  midazolam IV.
 Anaphylaxis  Adrenaline 1mg 1:1000 IM.
 Toxic reaction.
 Pulmonary embolism.
--------------------------------------------------------------------------------------
Acute coronary syndrome (ACS)

(Without ST - elevation)
 ACS includes unstable angina, evolving MI and non Q wave

or subendocardial MI.
 Patients should be managed medically until symptoms settle
and then investigated by angiography with a view to possible
angioplasty or surgery (CABG).
 Assessment: brief history (previous attack, relief with
rest/nitrates, risk factors for IHD, history of cardiovascular
diseases), examination (vital signs, signs of heart failure).
40
 Investigations: ECG (ST depression, flat or inverted T or

normal), cardiac enzymes, CXR, glucose, lipids, U&E, FBC.
 NB: measurement of cardiac troponin helps predict which
patients are at risk of a cardiac event and who can be
discharged early (2 different forms: troponin T and troponin I).
 Management:
 Admit to CCU and monitor closely.
 High flow oxygen.
 Analgesia: morphine (5 – 10 mg IV) + metoclopramide
(10 mg IV).
 Nitrates: GTN spray or sublingual tablets as required.
 Aspirin (300 mg PO) unless contraindicated.
 B – Blockers e.g. metoprolol or atenolol. If
contraindicated (asthma, COPD, LVF, bradycardia and
coronary artery spasm), give calcium channel antagonist
(verapamil).
 Low molecular weight heparin SC with monitoring
APTT.
 IV nitrate if pain continues.
 If symptoms fail to improve, refer to a cardiologist for
urgent angiography ± angioplasty or CABG.
 If improving (no further pain, normal ECG and negative
troponin), treat medically, address risk factors (DM, HTN,
smoking), gentle mobilization and arrange further
investigations (stress test and angiogram).
42
Severe pulmonary edema

 Causes:
 Cardiovascular (Lt. ventricular failure – post MI or IHD,
mitral stenosis, arrhythmias and malignant hypertension).
 ARDS from trauma, post-op, sepsis.
 Fluid overload.
 Neurogenic e.g. head trauma.
 DD: asthma/COPD, pneumonia and pulmonary edema
are often hard to distinguish especially in the elderly where
they may co-exist. Do not hesitate to treat all three
simultaneously.
 Symptoms: Dyspnea, orthopnea, pink frothy sputum.
 Signs: distressed, pale, sweaty, ↑pulse, tachypnea,
pink frothy sputum, fine lung crackles and wheeze. Usually
sitting up and leaning forward.
 Investigations: begin treatment before investigations.
 CXR: cardiomegaly, signs of pulmonary edema
(bilateral shadowing, small effusions at Costophrenic angles,
fluid in lung fissures and Kerley B lines “linear opacities”).
 ECG (MI), U&E, cardiac enzymes, ABG, consider
echo.
 Treatment:
 Sit the patient upright.
 Oxygen 100%.
 IV access and monitor ECG, treat arrhythmias (AF).
43
 Diamorphine (2.5 – 5 mg IV slowly).

 Diuretics e.g. frusemide IV slowly.
 GTN spray or SL.
 Start nitrate infusion if systolic BP ≥ 100 mmHg.
 If patient is worsening, give further dose of frusemide.
 Consider ventilation or venesection (get help).
 If systolic BP < 100 mmHg, treat as Cardiogenic shock
(inotropes support).
 Once stable and improving, do all investigations again
and treat permanently accordingly.
--------------------------------------------------------------------------------------
Broad complex tachycardia

 ECG shows rate of > 100 bpm and QRS complexes >
120 ms (> 3 small squares).
 If in doubt, treat as ventricular tachycardia (the
commonest cause).
 Identify the underlying rhythm and treat accordingly.
 No pulse, treat as arrest.
 Treatment of ventricular tachycardia: oxygen, IV
access, if unstable (sedation, DC shock, correct
hypokalaemia and hypomagnesaemia, amiodarone or
lidocaine), if stable (correct hypokalaemia and
hypomagnesaemia, amiodarone or lidocaine, sedation, DC
shock).
 After correction of VT: find the cause, anti-arrhythmias
therapy, surgical isolation of arrythmogenic area or
implantation of tiny automatic defibrillators may help.
44
 Treatment of ventricular fibrillation: use non-

synchronized DC shock (no R wave to trigger defibrillation).
 Treatment of ventricular extrasystoles: common after
MI, seen in healthy, no need for anti-dysrhythmic drugs, seek
expert advice.
Tension pneumothorax
 This is a medical emergency, requires immediate relief.
Do not delay management for obtaining a CXR.
 Causes: spontaneous (young thin men), asthma,
COPD, trauma, iatrogenic (CVP line and positive pressure
ventilation).
 Clinical picture: may be asymptomatic or sudden
onset of Dyspnea and/or pleuritic chest pain. Signs include
reduced expansion, hyper-resonance on percussion and
diminished breath sounds on the affected side. With tension
pneumothorax, the trachea will be deviated away from the
affected side and the patient will be very unwell.
 Investigations: CXR, ABG.
 Treatment:
 Chest drain.
 Arrange for surgical advise if bilateral, lung fails to
expand after intercostals drain insertion, 2 or more episodes
on the same side or history of pneumothorax on the opposite
side.
45
 Tension pneumothorax:
 Air drawn inside the pleural space with each inspiration
has no route to escape during expiration, pushing the
mediastinum to the opposite side, kinking and compressing
great veins. Unless the air is rapidly removed, cardio
respiratory arrest will occur.
 Treatment: insert a large bore (14 - 16 G) needle
(venflon) with a syringe, partially filled with 0.9% saline into
the second intercostal space in the mid-clavicular line on
the side of the suspected pneumothorax. Remove plunger to
allow the trapped air to bubble through the syringe with the
saline as a water seal until a chest tube can be placed.
 Aspiration of pneumothorax: through the second

intercostal space in the mid-clavicular line with a 16 G
cannula after infiltrative anesthesia. Connect to a 3 way tap
and 50 mL syringe. Request CXR to confirm resolution.
Advice to avoid air travel for 6 weeks after normal CXR.
Diving should be permanently avoided. If unsuccessful,
insert an intercostal drain.
 Intercostal tube drainage: use small tube, removed

during expiration or valsalva. If failed to re-expand lung,
suction or surgical intervention may be required.
46
Acute upper gastrointestinal bleeding

 Causes: gastric/duodenal ulcer, esophageal varices,
portal hypertension gastropathy, drugs (NSAIDs, aspirin,
thrombolytic, anticoagulants).
 Signs and symptoms: haematemesis or melaena,
fainting, postural dizziness or hypotension, tachycardia, cool
and clammy, jaundice.
 Management:
Assess whether patient is in shock

 Cool and clammy.
 Pulse > 100 bpm.
 JVP < 1 cm H2O.
 Systolic BP < 100 mm Hg.
 Urine output < 30 mL/h.
 If not in shock:
 Insert 2 big cannulae, start slow saline IVI, check
bloods, vital signs + urine output.
 If shocked:
 Protect airway.
 Insert 2 big cannulae.
 Draw bloods for investigations.
 Cross match 6 unites.
47
 High flow oxygen.

 Rapid IV colloid infusion up to 1 L.
 If still shocked, give group specific blood or group O
Rh – ve until cross matching is done.
 Otherwise slow saline infusion as dictated by hemodynamic.
 Correct clotting abnormality (vit k, FFP, platelet concentrates).
 Set up CVP line to guide fluid replacement.
 Catheterize and monitor urine output (aim for > 30 mL/h).
 Vital signs monitoring.
 Notify surgeons of all severe bleeds.
 Urgent endoscopy for diagnosis ± control of bleeding
(banding or sclerotherapy).
 Pass a Sengstaken - Blakemore tube.
 Proton pump inhibitors to prevent stress ulcers.
 Care for rebleeds. Very serious events. 40 % of those
patients will die.
-----------------------------------------
GOOD LUCK
48

Emmergency Medicine

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Emergency medicine for

the final FRCS exam

Cardiopulmonary resuscitation (CPR) for

 In a second, confirm the diagnosis (unconscious, apnoeic,

 Shout for help (how? Ask someone to call the

arrest team and bring the defibrillator. Note the time)

 Then do by yourself “Basic life support” which

 If breathing is compromised, give high concentration

C: Circulation (chest compressions)

 Then arrest team (not you except if you have the

H: History from relatives and bystanders

“Direct current cardio version”

1- Ventricular fibrillation or tachycardia:

 In general, look for reversible causes of cardiac

 (Intracardiac injection in not recommended).

When to stop CPR?

“After successful resuscitation”

 Seek expert advice from a cardiologist.

 Peripheral circulatory failure (Non

and melaena). If unclear, ttt as Hypovolaemic (most

“Treatment according to the cause”

o Close monitoring: CVP, BP, ABG, ECG and urine

 ECG: electrical alternans.

 Non Cardiogenic shock:

 Signs and symptoms: tachycardia, hypotension,

redness, urticaria, wheezy chest, itching, laryngeal

 Note: if patient is severely ill or has no pulse,

consider IV adrenaline (1 mL of 1:10,000 solution per

 Clinical picture: bradycardia and hypotension.

 Treatment: Atropine 1mg IV and IVI fluids.

o Heat exposure (exhaustion):

Acute chest pain

 Call for help.

Acute myocardial infarction

 D-dimer blood test: ↑ if thrombosis is present as it

Acute breathless patient

Acute severe asthma

 If still PEFR < 75 %, repeat salbutamol every 15 min or

Acute exacerbation of COPD

 Investigations: PEFR, ABG, CXR, ECG, blood culture if

 Assess social circumstances and support required.

 Call for help.

Diabetic ketoacidosis (DKA)

 Call for help.

 Use dextrose saline or 5% dextrose when blood

Hyperglycemic hyperosmolar non ketotic

flumazenil (benzodiazepine intoxication if airway

o HTN and DM.

Glasgow coma scale

 Primary scale (AVPU):

 Lorazepam 4 mg as a slow bolus (≤ 2 min) into a large

 If still too fast and LV function is adequate, consider low dose

 Tachycardia (> 100 bpm):

 Bradycardia (< 60 bpm): B blockers, Ca channel

 ST depression  ischemia, hypotension, digoxin.

Synopsis to minimize “I don’t know”

Acute coronary syndrome (ACS)

 ACS includes unstable angina, evolving MI and non Q wave

 Investigations: ECG (ST depression, flat or inverted T or

Severe pulmonary edema

 Diamorphine (2.5 – 5 mg IV slowly).

Broad complex tachycardia