Emergency Medicine 1st Edition -Dr.waleed (101 Papers) (5)

Internal & emergency medicine for FRCophth exam

1st edition

Organized by

Dr.Waleed Badr M.sc ophthalmology

Emergency medicine for the FRCophth exam 2011

2 Dr.Waleed Badr

INDEX

Cardiovascular

CPR for Cardiorespiratory arrest 3 Shock 10 Acute chest pain 15 Acute coronary syndrome (ACS) 17 Severe pulmonary oedema 20 Broad complex tachycardia 21 Narrow complex tachycardia 22 Venous thromboembolic diseases (DVT & PE) 24 Cardio-vascular drugs 28 Appendix : Basics & abnormalities of ECG 32

Chest

Bed side tests in chest medicine 37 Acute breathless patient 39 Acute severe asthma 42 Acute exacerbation of COPD 43 Pneumonia 45 Tension pneumothorax 47

Neurology

Headache D.D 49 Coma 51 Meningitis , Encephalitis & Cerebral abscess 54 Status epilepticus 56 Stroke 58 ICP 60

Endocrine

Coma in diabetic patients 61 Thyroid function tests 64 Thyroid emergencies 65 Addisonian crisis 66 Hypopituitary coma 67 Pheochromocytoma emergencies 67

GIT : Acute GIT bleeding 68

Haematology

An approach to bleeding disorders 73 Drugs affecting haemostasis 76 Hyperviscosity syndrome 79

Nephrology : Acute renal failure 80

Acute poisoning 82

Burns 85

Hypothermia 89

Needle-stick injuries 90

Perioperative care 91

Severe local anaesthetic toxicity 93

Choking in children 95


3 Dr.Waleed Badr

Cardiopulmonary Resuscitation (CPR) for cardiorespiratory arrest

Sudden cardiac arrest :

Sudden, unexpected loss of heart function, breathing & consciousness.

Usually results from an electrical disturbance in the heart e.g ventricular fibrillation, pulseless

ventricular tachycardia, Asystole or pulseless electrical activity that disrupts its pumping action &

causes blood to stop flowing to the rest of the body i.e loss of cardiac output.

Is different from a heart attack, which occurs when blood flow to a portion of the heart is blocked,

depriving the heart muscle of necessary oxygen. Like a heart attack, however, sudden cardiac arrest

almost always occurs in the context of other underlying heart problems, particularly coronary artery

disease.

Is a medical emergency. If not treated immediately, it is fatal, resulting in sudden cardiac death. With

fast, appropriate medical care, survival is possible. Administering cardiopulmonary resuscitation (CPR)

- or even just rapid compressions to the chest - can improve the chances of survival until emergency

personnel arrive.

Ventricular fibrillation (VF) :

These are the most common and most easily treatable cardiac arrest rhythms.

It produces rapid ineffective uncoordinated movement of the ventricles NO pulse.

ECG shows : rapid, bizarre & irregular ventricular complexes.

Pulseless (sustained) ventricular tachycardia (VT) :

Can cause cardiac arrest if the ventricular rate is so rapid that effective mechanical contraction &

relaxation cannot occur, especially if it occurs in the presence of severe LT ventricular impairment.

It may degenerate into VF.

Asystole :

This occurs when there is no electrical activity within the ventricles & is usually due to failure of the

conducting tissue or massive ventricular damage complicating MI.

When due to conducting tissue failure, permanent pacemaker implantation will be required if the

individual survives.

Pulseless electrical activity (PEA) : [[

This occurs when there is no effective cardiac output despite the presence of organised electrical activity

i.e electromechanical dissociation (EMD) .

It may be caused by reversible conditions, such as hypovolaemia, cardiac tamponade or tension

pneumothorax, but is often due to a catastrophic event such as cardiac rupture or massive pulmonary

embolism, and therefore carries an extremely poor prognosis.


4 Dr.Waleed Badr

Management of cardiorespiratory arrest

Chain of survival in cardiorespiratory arrest

Adult BLS Algorithm (UK) 2005

e.g

semilateral

position


5 Dr.Waleed Badr

In a second, confirm the diagnosis (unconscious, absent carotid pulse, apnoeic), then:

Shout for help (HOW? Ask someone to call the cadiac arrest team and bring the defibrillator (AED).

Note the time)

Then do by yourself Basic life support "BLS"

BLS aims to maintain a low level of circulation until more definitive treatment with advanced life support

"ALS" can be given.

BLS consists of ABC :

1. Prompt assessment & restoration of the airway.

2. Maintenance of breathing using rescue breathing ('mouth-to-mouth' breathing) .

3. Maintenance of the circulation using chest compressions

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 (10 sec max.) (look for chest movements,

listen to breath sounds & feel for the breath from the mouth).

If breathing is compromised, give high concentration O2 & manage

according to the findings e.g. relieve tension pneumothorax.

If no respiratory effort, treat as arrest, give 2 breaths after 1st set of

compressions

- Each inflation is 1s long.

- Use Ambu system (specialized bag& mask system; in place by thumbs pressing downwards

either side of the mouth-piece, palms against cheeks) if available and 2 resuscitators present.

Otherwise, mouth-to-mouth breathing.


6 Dr.Waleed Badr

C: Circulation (chest compressions)

Assess: check carotid pulse (in the next 10 seconds) if No pulse Start CPR immediately.

Check BP, capillary refill & look for evidence of haemorrhage. If shocked, treat accordingly.

Call for help again.

How to perform CPR ?

1. Start CPR on a firm surface.

2. Center over the lower 1/3 of the sternum.

3. Do 30 chest compressions to 2 breaths (30:2) .

4. Use the heels of hands placed one on top of the other with straight elbows

(directing the weight of your body through your vertical straight arms)

5. Aim for 4 cm chest depression at a rate of 100/min.

6. Allow the chest to recoil completely.

7. Interrupt infrequently as possible (only for DC and intubations).

8. Do 20 cycles (20 of 30:2) then recheck?

Then arrest team (not you except if you have the license) should have come to do: Advanced life

support "ALS" ALS aims to :

1. Restore normal cardiac rhythm by Electrical defibrillation "DC shock" when the cause of cardiac

arrest is due to a tachyarrhythmia .

2. Restore cardiac output by correcting other reversible causes of cardiac arrest.

3. ALS can also involve administration of IV drugs to support the circulation,

4. Endotracheal intubation to ventilate the lungs.

D: Disability :

Assess level of consciousness by AVPU score or Glasgow coma scale if time allows (see P.53)

Check pupils (size, equality and reaction). [

E: Exposure : Undress patient but cover to avoid hypothermia.

H: History from relatives and bystanders

Events surrounding onset of illness, evidence of overdose/suicide attempt, trauma .

Past medical history e.g. DM, asthma, COPD, drug abuse, epilepsy or recent head injury.

Medications.

Allergies.


7 Dr.Waleed Badr

Advanced life support "ALS"

Place defibrillator (monophasic) paddles on chest (apex and under Rt. clavicle) as soon as possible

and set monitor to read through the paddles if delay in attaching leads.

Assess rhythm: is it VF/pulseless VT or Asystole/PEA ?

1- VF/VT :

Immediate defibrillation must occur without delay: 360J monophasic or 150-360 J biphasic .

Immediately Resume CPR 30:2 for 2 minutes without attempting to confirm restoration of a pulse

(because restoration of mechanical cardiac output rarely occurs immediately after successful defibrillation).

If still VF/VT, repeat defibrillation . All shocks are 360J. Thereafter, additional shocks are given

every 2 minutes after each cycle of CPR .

2- A systole/PEA:

Immediately resume CPR 30:2 for 2 minutes continue until the victim starts to breathe normally .

Transverse cardiac pacing may be tried .

Correct reversible causes "4H, 4T" (see Algorithm) .

During CPR

Oxygen 100% .

Adrenaline 1mg/ml IV, every 3 min .

Amiodarone 300 mg IV . a futher 150 mg may be given, followed by an infusion of 1mg/min for

6h, then 0.5 mg/min for 6h (in resistant VF/VT) .

Atropine 3 mg IV (once) (in Asystole/PEA) .

Treat acidosis with good ventilation. Sodium bicarbonate may worsen intracellular acidosis &

precipitate arrhythmias, so use only in severe acidosis after prolonged resuscitation (e.g. 50 ml of

8.4 % solution by IVI).


8 Dr.Waleed Badr

Adult ALS Algorithm (UK) 2005


9 Dr.Waleed Badr

NB :

Send someone to check patients notes & usual doctor, these may give clues to the cause of the

arrest .

If IV access fails, give drugs down tracheal tube (2-3 times the IV dose diluted in 10ml 0.9% saline

followed by 5 ventilations to assist absorption).

(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 > 33C and pH and K+ are normal.

There was significant delay in starting CPR (BLS started after 5 min or ALS started after 30 min).

After 20 minutes if there is refractory Asystole/PEA .

When to not resuscitate?

The patient's condition is such that resuscitation is unlikely to succeed .

Mentally competent patient stated or recorded that he does not want to be resuscitated OR If

resuscitation is not in the patients interest as it would lead to a poor quality of life.

NB. Ideally, involve patients and relatives in the decision before the emergency. When in doubt,

resuscitate.

After successful resuscitation What to do?

1. Transfer to CCU or ICU.

2. Monitor vital sign.

3. Consider ECG, CXR, glucose, blood gases, FBC, CK/troponin.

4. Seek expert advice from a cardiologist.

5. Explain to the patients relatives what has happened, whatever the outcome.


10 Dr.Waleed Badr

Shock

Definition: Circulatory failure inadequate organ perfusion .

Causes:

1) Cardiogenic shock : either due to pump failure or 2ry to PE,tension pneumothorax & cardiac

tamponade i.e obstructive shock .

2) Hypovolaemic Shock : due to loss of blood volume

Bleeding: trauma, ruptured aortic aneurysm or ectopic pregnancy.

Fluid loss: vomiting (GIT obstruction), diarrhea (cholera), burns

Heat exhaustion.

3) Anaphylactic Shock.

4) Neurogenic shock : i.e related to a nervous system injury e.g. post spinal surgery.

5) Septic Shock : due to toxins or poisons released by an infection .

6) Iatrogenic : drugs e.g. anesthetics and antihypertensives.

7) Endocrine failure : e.g. Addisons ds or hypothyroidism.

Clinical picture :

1. Vital signs :

- Temperature : commonly hypothermia .

- Heart rate : commonly tachycardia >100 beats/min

- Bl.P : in early stages of shock as COP but rapidly as shock progresses i.e hypotension .

- Respiratory rate : (compensatory tachypnea) in an attempt to remove excess acids in the

form of CO2.

2. CNS: Early : change in personality & may progress to restlessness. Late : confusion & ultimately coma

may occur.

3. CVS : Chest pain. with profound acidosis, abnormal heart rhythms (cardiac dysrhythmias) are more

prevalent and are potentially fatal.

4. GIT problems : arise most often from the shunting of blood away from this system. Symptoms include :

abdominal pain, nausea, vomiting, or diarrhea + GIT bleeding with black/tarry stool .

5. Skin : cold, pale, clammy & cyanosed (if extreme low blood O2 content) .

6. Renal problems : Oliguria & anuria (in severe cases) .


11 Dr.Waleed Badr

Management:

If BP unrecordable, call the cardiac arrest team

Call for help + make the patient lie on hard surface with raised legs.

A ensure patent airway (remove any obstruction, chin elevation, head tilt) & adequate

ventilation.

B O2 100%.

C Circulation (IV access x 2 wide bore, get help if this takes > 2 min).

Identify & treat underlying cause if clear ( e.g check abdomen for signs of trauma or aneurysm.

GIT bleeding and melena). If unclear, ttt as Hypovolaemic (most common cause).

Consider: arterial line, central venous line & Foley's catheter.

Infuse crystalloids: fast to raise BP (unless cardiogenic shock) as dictated by BP, CVP & urine output

(aim for a urine flow > 30 mL/h).

NB.Dont overload with fluids if cardiogenic shock (exclude PE & RV infarct 1st).

Vital sign monitoring: pulse, BP, temperature, respiration & peripheral perfusion.

Do some investigations: FBC, U&E, ABG, glucose, cross matching, ECG.

Treatment according to the cause

Cardiogenic shock: Cold & clammy patient.

Has a high mortality. Can occur suddenly or after progressively worsening heart failure.

Ask a senior physicians help both for exact diagnosis & treatment.

Causes:

1. MI, myocarditis or myocardial depression (drugs, hypoxia, acidosis, sepsis), endocarditis,

Arrhythmias .

2. 2ry to cardiac tamponade, tension pneumothorax &PE.

Management:

o If the 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 (every hour until diagnosis is made), Cardiac enzymes/troponins, U&E, CXR,

echo, ABG.

o Close monitoring: CVP, BP, ABG, ECG & urine output.

o Correct arrhythmia, U&E and acid base imbalance.


12 Dr.Waleed Badr

o Consider a Swan Ganz catheter to assess pulmonary capillary wedge pressure (PCWP) and

cardiac output & an arterial line to monitor pressure.

PCWP < 15 mm Hg: give plasma expanders (100 mL every 15 min IV), aim for 15 20 mm Hg.

PCWP > 15 mm Hg: consider +ve inotropes e.g dopamine OR 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.

Hypovolaemic shock:

Treat underlying cause e.g. control obvious hemorrhage, urgent laparotomy or thoracotomy.

Fluid replacement: Saline 0.9% or colloid initially; if bleeding, use cross matched blood transfusion or

group O Rh ve blood via large bore cannula.Titrate against BP, CVP & urine output.

Correct electrolyte abnormalities and acidosis.

Cardiac tamponade

Pericardial fluid collection intrapericardial pressure Heart cannot fill pumping stops.

Causes: trauma, lung or breast cancer, pericarditis and MI.

Signs:

BP, JVP & muffled heart sounds (Becks triad).

JVP on inspiration (Kussmauls sign) .

Pulsus paradoxus (pulse fades on inspiration).

Investigations:

ECG: electrical alternans.

CXR: globular heart, Lt. heart border convex or straight, Rt. costophrenic angle < 90.

Echo is diagnostic.

Management:

Very difficult. With actual senior help and luck, prompt pericardiocentesis brings swift

relief.

While awaiting, give oxygen, monitor ECG and set an IVI. Take blood for group & save.

Cardiothoracic surgery (e.g CABG, ventricular repair, or pericardial window) may have

a role


13 Dr.Waleed Badr

Anaphylactic shock:

More common in atopic individuals.

Pathophysiology: Type 1 IgE-mediated hypersensitivity reaction Release of histamine & other

mediators from mast cells increase in vascular permeability, vasodilatation & respiratory smooth

muscle contraction .

Causes: drugs e.g. penicillin and contrast mediators in radiology (e.g FA). Stings and some kinds of

food e.g. strawberries, eggs, fish .

NB. Anaphlactoid reaction involves direct release of mediators from inflammatory cells without involving

antibodies e.g. with drugs.

Clinical features : suggestive of anaphylaxis

- H/O previous allergy or atopy .

- Itching, sweating, erythema, urticaria .

- Tachycardia, hypotension,

- Wheezy chest, laryngeal obstruction (oedema), apnea & cyanosis.

- Vomiting, diarrhea & urinary incontinence .

- Syncope .

Differential diagnosis :

1. Causes of loss of consciousness :

Vasovagal attack (see below).

Hypoglycaemia .

MI .

2. Causes of respiratory distress : Acute asthma .

3. Causes of laryngeal obstruction : Idiopathic angioedema .

Treatment:

1. Remove cause, raise the feet + call for help .

2. ABC : Secure airway, 100% oxygen & Secure IV access.

3. Adrenaline 0.5 mg (0.5 mL of 1:1000) IM repeated every 5 min guided by BP, pulse and respiratory

function until better.

4. Antihistaminic e.g. chlorpheniramine 10 mg IV repeated every 6h if urticaria persists .

5. Hydrocortisone 200 mg IV (can be repeated if necessary) .

6. If hypotensive : IVI 0.9 % saline 500 ml over 15 minutes (up to 2 L may be needed), titrated against BP.

7. If severe bronchospasm : Consider aminophylline & nebulized salbutamol 2.5 mg . titrated against

respiratory function .

8. if laryngeal edema is worsening (stridor) : refer to ICU & Intubation/ventilation.

NB: 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.


14 Dr.Waleed Badr

9. After patient has come out of anaphylaxis patient is to be discharged only after 48hrs as

sometimes biphasic anaphylaxis reaction occurs which is even more severe.

Prophylaxis against anaphylactic shock :

Proper H/O atopy,drug allergy, hypersensitivity to insect bites or stings.

Family H/O anaphylaxis(AD inheritance) .

Skin- prick tests (showing specific IgE) helps in identifying which allergens to avoid.

Emergency tray equipped with Ambu bag with fascial fask, larnygyoscope, endotracheal tube,

oxygen cylinder & medicines (Adrenaline,hydrocortisone,antihistaminics,aminophylline, IV

glucose) .

Educated and trained Staff to deal in emergency.

Suggest a Medic-alert bracelet naming the allergen.

Teach about self injected adrenaline in case no help is available .

Septic shock:

Endotoxin-induced vasodilatation with shock & coma but with no signs of infection (fever and

WCC).

Warm and well perfused with bounding pulse.

Antibiotics: is given (preferably after blood culture). if no clue to source IV cefuroxime 1.5 g / 8h or

gentamycin + antipseudomonal.

Give colloid or crystalloid by IVI.

Monitor in ICU (CVP and pulmonary artery wedge pressure).

Vasovagal attack:

Cause: generalized vasodilatation.

Clinical picture: bradycardia & hypotension.

Treatment: raise legs, IVI fluids, Atropine 1mg IV & hydrocortisone 200 mg I.V .

Heat exposure (exhaustion):

Tepid sponging and fanning.

Avoid ice and immersion.

IVI 0.9 % saline hydrocortisone 100 mg IV.

Chlorpromazine 25mg IM to stop shivering.

Stop cooling when core temperature < 39C.


15 Dr.Waleed Badr

Acute chest pain

Causes:

Life-threatening :

ACS (unstable angina & Acute MI) .

Pulmonary embolism.

Aortic dissection.

Tension pneumothorax.

Esophageal rupture.

Others :

Pericarditis.

Pneumonia, empyema & pleurisy.

Gastro-oesophageal reflux , oesophageal spasm .

Musculoskeletal : e.g. muscular, rib fractures, bony metastasis and costochondritis.

Cholecystitis, peptic ulceration & pancreatitis .

Cervical spondylosis .

Sickle-cell crises.

Management:

Call for help.

ABC .

Level of consciousness.

Vital sign monitoring.


16 Dr.Waleed Badr

Workup of chest pain

Ischaemic

cardiac

Aortic

dissection

Pericarditis/

Pleurisy

Oesophageal Musculo-

skeletal

Site Central,diffuse Between

shoulder

blades

Retrosternal

Radiation Jaw/neck/shoul

der/arm/occasi

onally back

Back

Character Dull,constricting,

choking,

squeezing,

crushing or

pressure

Sharp &

tearing

Sharp Can mimic

anginal pain i.e

constricting

Precipitated

by

Exercise,

emotion, cold,

after a large

meal

Breathing,

coughing or

lying flat

Food,lying flat,hot

drinks,alcohol

Movement

(bending,

stretching,

turning)

Relieved by Rest, nitrates leaning

forwards

Nitrates,antacids

Associated

symptoms &

signs

Autonomic disturbance e.g

sweating, nausea & vomiting

Breathlessness

Local tenderness

over a rib or

costal cartilage


17 Dr.Waleed Badr

Acute coronary syndrome (ACS)

ACS includes :

Unstable angina

Non ST elevation MI (NSTEMI) = non Q wave or subendocardial MI.

ST elevation MI (STEMI) = acute MI . [[

STEMI (Acute MI)

Risk factors: DM, HTN, atherosclerosis & smoking.

Clinical picture:

Heavy chest pain > 15min, radiating to the arm, neck and shoulder.

Dyspnea, sweating, palpitations, nausea, dizziness, collapse and shock.

Epigastric pain & vomiting (inferior MI) .

May present without chest pain (Silent MI) e.g in elderly or diabetics .

Investigations :

o Bloods for FBC, U&Es, glucose, lipids and cardiac enzymes.

- CK : 8 12 h till 72 h.

- Lactate dehydrogenase : 1 - 2 days till 7 days.

- Cardiac troponin & Aspartate transaminase.

o Chest x ray: in cardiac size.

o ECG: normal or elevated ST segment & pathological Q.

o Echocardiography and coronary angiography.

Management :

Arrange for an emergency ambulance.

Attach ECG monitor and record a 12 lead ECG.

High flow oxygen 100% by face mask.

IV access.

Brief assessment :

Brief history: previous attack & risk factors for IHD or any contraindications for thrombolysis.

Examination: vital signs.

Medications :

Morphine 5 -10 mg IV + antiemetic e.g Metoclopramide 10 mg IV.

Sublingual nitrate (2 puffs or 1 tablet) unless hypotensive.

Aspirin 300 mg PO chewed (unless clear contraindication).


18 Dr.Waleed Badr

B-blocker e.g. atenolol 5 mg IV (unless asthma or Lt. ventricular failure).

Restore coronary perfusion either primary percutaneous coronary intervention (PCI) e.g angioplasty

(if available) or thrombolysis .

Primary PCI:

The treatment of choice if ongoing ischaemia & presentation is within 12h.

More effective than thrombolysis, with a greater reduction in the risk of death, recurrent MI or

stroke .

Not available in all locations .

Thrombolysis:

Greatest benefit if given < 12 h of onset, up to 24 h. thrombolysis is contraindicated beyond 24h

from the time of onset of symptoms .

Indications: ECG criteria for thrombolysis

1. ST elevation > 1 mm in 2 or more limb leads OR > 2 mm in 2 or more chest leads.

2. LBBB (unless known to have LBBB previously) .

3. Posterior changes : deep ST depression & tall R waves in leads V1 to V3 .

NB. Dont thrombolyze ST depression alone, T-wave inversion alone or normal ECG .

Contraindications: Internal bleeding, suspected aortic dissection, esophageal varices, active

peptic ulcer, recent surgery, trauma or hemorrhagic stroke. severe hypertension, pregnancy .

Choice of agent :

- Streptokinase (SK): 1.5 million units in 100 mL 0.9 % saline IVI over 1h.

- In cases of allergy to SK (rare) : Tissue plasminogen activator might be used e.g Alteplase

(human tPA), Tenecteplase & Reteplase ( tPA analogues) .

Complications:

- Recurrent ischaemia or Failure to reperfuse (persistent pain with continuing ST-segment

elevation) consider re-thrombolysis or rescue angioplasty

- Stroke .

- Pericarditis, cardiogenic shock & heart failure.


19 Dr.Waleed Badr

NSTEMI

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).

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 O2.

Analgesia: Morphine (5 10 mg IV) + metoclopramide (10 mg IV).

Nitrates: GTN spray or sublingual tablets as required.

Aspirin 300 mg PO followed by 75mg/d (unless contraindicated) .

BBlockers e.g. metoprolol 50-100 mg/8h . If contraindicated (asthma, COPD, LVF, bradycardia &

coronary artery spasm), give calcium channel antagonist e.g verapamil 80-120 mg/8h .

Low molecular weight (LMW) heparin SC with monitoring APTT.

IV nitrate if pain continues e.g GTN 50 mg in 50mL 0.9% saline .

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 & angiogram).


20 Dr.Waleed Badr

Severe pulmonary edema

Causes:

Cardiovascular (LV failure post MI or IHD, mitral stenosis, arrhythmias & malignant hypertension).

ARDS from trauma, post-op, sepsis.

Fluid overload.

Neurogenic e.g. head trauma.

Symptoms: Dyspnea, orthopnea, pink frothy sputum.

Signs: distressed, pale, sweaty, pulse, tachypnea, pink frothy sputum, fine lung basal crackles &

wheeze. Usually sitting up and leaning forward.

DD:

1. asthma/COPD.

2. Pneumonia & pulmonary edema are often hard to distinguish especially in the elderly where they

may co-exist. Do not hesitate to treat all three simultaneously.

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).

Diamorphine (2.5 5 mg IV slowly).

Diuretics e.g. frusemide 40-80 mg IV slowly.

GTN spray or SL.

Start nitrate infusion e.g isosorbide dinitrate 2-10 mg/h IVI 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.


21 Dr.Waleed Badr

Broad complex tachycardia

ECG shows rate of > 100bpm and QRS complexes > 120 ms (> 3 small squares done at the standard UK rate

of 25 mm/s).

Management :

If in doubt, treat as ventricular tachycardia (the commonest cause).

Identify the underlying rhythm and treat accordingly.

If 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-arrhythmic therapy, surgical isolation of arrythmogenic

area or implantable cardioverter defibrillator (ICD) may help.

Treatment of ventricular fibrillation: use non-synchronized DC shock (no R wave to trigger

defibrillation).

Treatment of ventricular extrasystoles (ectopics): common after MI, seen in healthy, no need for anti-

dysrhythmic drugs, seek expert advice.


22 Dr.Waleed Badr

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, sawtooth baseline, ventricular rate 150 bpm (2:1 block)) .

Multifocal Atrial tachycardia

Junctional tachycardia

Atrial fibrillation (AF)

Causes:

Cardiac :

- Coronary artery disease (including acute MI) .

- Valvular heart disease (especially Mitral valve disease) .

- Hypertension .

Non-cardiac : Pneumonia, pulmonary embolism & Hyperthyroidism .

Idiopathic (lone AF) .

Symptoms : may be asymptomatic or present with chest pain, palpitations & dysnea.

Signs :

Pulse : irregularly irregular* ( apical pulse rate (300-600 bpm) is greater than the radial rate) .

First heart sound is of variable intensity.

hypotension & pulmonary embolism.

Complications: embolic stroke, CRAO.

Investigations:

U&E, cardiac enzymes , thyroid function tests , D-dimer (if the patient has risk factors to pulmonary embolism)

ECG : absent P wave, irregular QRS complexes .

ECHO : (LA enlargement, mitral valve disease, poor LV function).


23 Dr.Waleed Badr

Treatment: of Acute AF (< 72h)

Goals of treatment :

1. Hemodynamic stabilization

2. Ventricular rate control

3. Prevention of embolic complications .

Treat any associated acute illness e.g. MI.

Control ventricular rate with B-blocker (Esmolol) or digoxin PO or IV.

- PO : Loading dose 0.5mg 6-hourly for 2 doses, then 0.125-0.25 mg daily .

- IV : 0.75-1 mg in 0.9% NACL over 1 hr .

If AF does not resolve, consider drug or electrical cardioversion.

- Drug cardioversion: Amiodarone IVI 5 mg/kg over 1hr then up to 15 mg/kg/24h .

- DC cardioversion: indicated in electively following a first attack with an identifiable cause

OR as an emergency if patient is compromised. Protocol: 200J, 360J, 360J (DO ECHO FIRST; is

heart structurally normal?).

Anticoagulation is not required if AF of recent onset with normal echo but aspirin 300 mg PO

maybe given. Otherwise, give warfarin 3 wks before and 4 wks after DC cardioversion.


24 Dr.Waleed Badr

Venous thromboembolic disease (VTE)

The most common presentation is Deep vein thrombosis (DVT) of the leg and/or pulmonary embolism (PE) .

Deep vein thrombosis (DVT)

DVTs occur in 25-50% of surgical patients, and many non-surgical patients.

Risk factors (of DVT/PE) :

1. Patient factors : Age,obesity,varicose veins, previous DVT/PE, family history, pregnancy, oestrogen-

containing oral contraceptives & HRT.

2. Immobility : especially long flights (> 4hours) or associated with illness / hospital admission) .

3. Surgical conditions : recent major surgery (especially pelvic or orthopaedic) .

4. Medical conditions : MI/heart failure, inflammatory bowel disease, pneumonia & malignancy .

5. Haematological disorders : thrombophilic states, hyperviscosity syndromes & Myeloproliferative

disease

Signs :

Calf warmth/tenderness/swelling/erythema

Pitting oedema.

Mild fever .

Homans' sign ( resistance/pain on forced foot dorsiflexion) : should not be tested for as it may

dislodge thrombus.

Differential diagnosis :

Ruptured knee (Bakers Cyst) : Usually occur in patients with rheumatoid arthritis .

Cellulitis : Infective cellulitis is usually distinguished by marked skin erythema & heat which is localised

within a well-demarcated area of the leg and may be associated with an obvious source of entry of

infection (e.g. an insect bite or leg ulcer).

Investigations :

1. FBC (WCC to help find infection; Hb to look for polycythaemia; platelet count look for

thrombocytosis) .

2. D-dimer blood tests (evidence of clot lysis) : High sensitivity but low specificity ( if thrombosis,

infection, malignancy & post-op) .

3. Compression U/S of calf & leg (ideally doppler U/S) : if ve, repeat at 1wK to catch those with

early but propagating DVTs ; this should also rule out ruptured knee

4. ECG; CXR; ABG; V/Q scan & CT pulmonary angiography (If pulmonary embolus a serious

concern).

NB.Both may coexist with a DVT .


25 Dr.Waleed Badr

5. Thrombophilia tests : before commencing anticoagulant therapy if there are no predisposing

factors, in recurrent DVT, or if there is a family history of DVT.

Complications :

1. Pulmonary embolism : range of severity from asymptomatic, to symptomatic, to sudden death

2. Chronic post-phlebitic leg problems (10-30%) : due to damage of venous valves by the

thrombus . it results in pain, swelling, eczema, itch & ulceration .

3. Stroke or other arterial embolus : via mechanism of paradoxical embolus through cardiac defect

4. Complications of anticoagulants e.g haemorrhage (intra-cranial, ocular, GI & other)

Prophylaxis : (against DVT/PE)

Early post-op mobilization (the simplest method) .

Compression stockings (to prevent further thrombosis) .

Low M.W heparin e.g enoxaparin 20 mg/24h SC .

Aspirin .

Avoid contraceptive pill if at risk e.g major or orthopaedic surgery.

Vena caval filters (of limited use) .

Management :

Graded support stocking .

Treatment of any underlying risk factors .

Anti-coagulants :

- Assessment of risk factors for haemorrhage .

- Initially with heparin e.g LMWH (enoxaparin 1.5mg/kg/24h SC) .

- Start warfarin simultaneously with LMWH (as it is prothrombotic for the first 48h) .

- Stop heparin when INR is 2-3

- Treat for 3 months if post-op; 6 moths if no cause is found;malignancy or recurrent DVT.

Vena caval filters : may be used in active bleeding, or when anticoagulants fails, to minimize risk

of pulmonary embolus.

When is there a high probability of a DVT ? (WELLS Score)

Calf swelling > 3cm compared to the other leg (measured 10cm below tibial tuberosity)

Immobile (e.g in bed, in plaster or paralysed) .

Local tenderness over deep venous system .

Active malignancy .

Family history of DVT ( 2 close relatives).

Others : pitting edema & dilated superficial veins .


26 Dr.Waleed Badr

Pulmonary embolism (PE)

Always suspect PE in sudden collapse 1-2 wks after surgery.

Mechanism: Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood

flow to lungs. The source is often occult.

Risk factors: malignancy, long immobilization following surgery (especially pelvic), venous disease,

obesity, the PILL & HRT.

Signs and symptoms:

Acute dyspnea , tachypnea , pleuritic chest pain .

Hypotension, tachycardia, gallop rhythm, loud P2, JVP .

Haemoptysis, syncope, Cyanosis, AF and DVT (swollen leg).

Investigations:

U&E, FBC, baseline clotting.

ECG:

- Normal or sinus tachycardia (the commonest)

- Rt. ventricular strain pattern (V1 3), Rt. Axis deviation, RBBB .

- AF.

- Rarely, SI,QIII,TIIII pattern occurs : deep S waves in I, pathological Q waves in III, inverted T waves

in III.

CXR: often normal, vascular markings, small pleural effusion, wedge shaped area of infarction.

ABG: O2, CO2 and PH.

D-dimer blood test:

- if thrombosis is present as it indicates plasma level of fibrin product, so it helps to exclude PE if

Normal.

- High sensitivity but low specificity as it also in infection, malignancy & post-op .

- CT pulmonary angiography (CTPA): Better with helical (spiral) CT. It is sensitive & specific in

determining if emboli are in pulmonary artery. If unavailable, a ventilation-perfusion (V/Q) scan can

aid diagnosis. If equivocal, pulmonary angiography or bilateral venograms may help.

- Doppler U/S for leg veins.


27 Dr.Waleed Badr

Management

Prevention: see DVT prophylaxis P.25

Immediate management :

Oxygen 100 %.

Morphine 10 mg IV (if pain) + antiemetic.

If critically ill, consider immediate thrombolysis or surgery.

IV access and start LMWH or Unfractioned heparin (faster onset & rapid reversal of anticoagulation)

10,000 U IV bolus then 15 25 U/Kg/h IVI as guided by APTT.

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 BP after 500 mL colloid, give dobutamine 2.5 10 ug/kg/min IV (aim for BP > 90 mmHg).

If still BP, consider noradrenaline.

If still BP 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).

TTT of underlying risk factors .


28 Dr.Waleed Badr

Cardiovascular drugs

1. B-blockers :

Classification :

1. 1st generation

(Non-selective blockers)

Propranolol Sotalol Timolol Levobunolol Metipranolol

2. 2nd generation

(selective B1 blockers)

(cardioselective)

Atenolol Metapralol Bisoprolol Betaxolol

3. 3rd generation

(blockers with V.D action)

Dilevalol Nebivolol

Mechanism of action : Block B-adrenoceptors, thus antagonizing the sympathetic nervous system. Blocking

B1-receptors is negatively inotropic and chronotropic (Pulse by firing of sinoatrial node), and B2-

receptors induce peripheral vasoconstriction and bronchoconstriction.

Indications :

1. Hypertension (2nd line).

2. Ischaemic heart diseases : Angina, post MI (mortality).

3. Cardiac arrythmias (antidysrhythmic).

4. Hyperthyroidism .

5. Prophylaxis of migraine .

6. Anxiety & tremors .

7. Glaucoma .

Side effects :

1. Bronchospasm (in susceptible patients) .

2. Hypotension & bradycardia (antidote to bradycardia is Atropine up to 3mg IV. Give glucagon 2-

10mg IV bolus + 5% dextrose if atropine fails ( an atropine infusion of 50g/kg/h). If unresponsive,

consider pacing or an aortic balloon pump).

3. Peripheral ischaemia, intermittent claudication & cold extremities .

blood flow to liver & kidney metabolism & excretion of drugs .

4. Potentiation of the hypoglycaemic effect of insulin & oral hypoglycaemic drugs & masking of the

hypoglycaemic symptoms .

5. Hyperkalaemia in diabetic & uraemic patients .


29 Dr.Waleed Badr

6. Miscellaneous S/E : night mares, depression, headache, nausea, vomiting, lipido & possible of

plasma HDL level .

Contraindications :

Congestive heart failure .

heart Block

Asthma/COPD .

Hypotension & bradycardia .

Prinzmetal's angina (angina due to coronary spasm caused by hyperactivity of receptors in the

coronaries) .

Peripheral vascular disease .

2. Diuretics :

Loop diuretics

(Furosemide)

Thiazide diurectics

(hydrochlorothiazide)

K+ sparing diuretics

(Spironolactone)

Mechanism

of action

Act mainly at limb of loop of henle .

Inhibit Na+/K+/2CL- cotransport Na+ & CL- reabsorption .

Act mainly at proximal part of DCT.

Inhibit Nacl cotransport Na+ & CL- reabsorption.

Act mainly at distal part of DCT & upper part of

collecting tubules .

Competitive inhibition with aldosterone .

Indications Acute pulmonary edema Hypertensive

emergencies .

Hyper Ca2+ & Hyper K+ .

Congestive heart failure Essential hypertension . Diabetes insipidus .

Given with other diuretics (to balance K+

loss) .

Hyperaldosteronism Side effects Hypokalaemia .

Hypomagnesaemia . Hyponatraemia . Hypocalcaemia . Hyperuricaemia .

Ototoxicity .

Hyperkalaemia . Gynecomastia &

impotence in males .

Menstrual disorders & hirsutism in females

3. Calcium channel blockers :

Classification :

Drugs CVS pharmacological effects Indications

1. Dihydropyridines

Nifedipine Amlodipine Lacidipine Nimodipine Nicardipine Felodipine

Peripheral V.D . Coronary V.D . Tachycardia (can be used with

B-blockers) .

Bl.P lowering effect

Hypertension &

angina

2. Non-

dihydropyridines

Verapamil Diltiazem

A-V & S-A conduction delay Bradycardia (Don't give with B-

blockers " risk of bradycardia LVF").

Peripheral & Coronary V.D . Bl.P lowering effect .

Hypertension, angina

& arrhythmias .


30 Dr.Waleed Badr

Mechanism of action : Work by blocking voltage-gated ca2+ channels in cardiac muscle & blood vessels. This

intracellular Ca2+ leading to a reduction in muscle contraction, thereby promoting coronary & peripheral

vasodilatation & reducing cardiac contractility and myocardial oxygen consumption (Bl.P ) .

Side effects :

1. Aggravation of congestive heart failure .

2. A-V block in patients with pre-existing disease .

3. Dizziness, fatigue, headache & flushing .

4. Ankle oedema .

5. Gigival hyperplasia .

6. Nausea, vomiting & constipation

Contraindications: heart failure & heart block.

4. Digitalis (Digoxin) :

Mechanism of action :

1. +ve inotropic action (Blocks the Na+/K+ pump free intracellular ca2+) improves myocardial

contractility & COP .

2. Slow the heart rate (used in fast AF to control ventricular rate. aim for pulse


31 Dr.Waleed Badr

Precautions for digitalis therapy :

Never give I.V digitalizing dose before being sure that the patient has not received any digitalis

during previous 14 days to avoid digitalis toxicity .

Make sure that K+ level is normal .

Use lower digitalizing dose with elderly people , since toxic effects may be pronounced after

administration of the normal adult dose of digitalis .

If on digoxin, Avoid/or use less energy in cardioversion.

If on amiodarone , halve the dose of digoxin.

SE (digitalis toxicity)

Cardiac : Any arrhythmia (particularly AV block & ventricular tachycardia/fibrillation) .

Ocular : white halos, yellow/green chromatopsia, diplopia .

Nausea , vomiting & appetite .

Hypokalaemia .

Headache, confusion , delirium & hallucinations (digitalis delirium) .

Gynaecomastia & galactorrhea .

Management of digitalis toxicity :

Stop digitalis administration .

Check & correct hypokalaemia .

Treat any arrhythmia .

Digoxin-specific antibody fragments IVI (Digibind) : specific antibodies that permits high renal

clearance of digitalis complex by glomerular filteration .

5. Antiarrhythmic drugs

Classification :

1. Class I

Ia : Quinidine, Disopyramide, Procainamide Ib : Lidocaine Ic :Flecainide

2. Class II B blockers 3. Class III Amiodarone * 4. Class IV Calcium channel blockers (Verapamil & diltiazem) 5. Class V Adenosine .

Digoxin

* S/E of amiodarone : vortex keratopathy ,cataract, optic neuropathy, peripheral neuropathy, myopathy,

alteration of thyroid function & hepatotoxicity .


32 Dr.Waleed Badr

Appendix1 : Basics & abnormalities of ECG

ECG: A methodical approach

First confirm the patient's name and age, and the ECG date. Then:

Rate: - At usual speed (25mm/s) each "big square" is 0.2s; each "small square" is 0.04s.

- To calculate the rate, divide 300 by the number of big squares per R-R interval .

Rhythm: - If the cycles are not clearly regular, use the "card method": lay a card along ECG, marking

positions of 3 successive R waves. Slide the card to and fro to check that all intervals are equal. If

not, note if different rates are multiples of each other (i.e varying block), or is it 100% irregular (AF

or VF)?

- Sinus rhythm is characterized by a P wave (upright in II, III, & aVF; inverted in aVR) followed by a

QRS complex.

- AF has no discernible P waves and the QRS complexes are irregularly irregular.

- Atrial flutter has a "sawtooth" baseline of atrial depolarization (~300/min) and regular QRS

complexes.

- Nodal rhythm has a normal QRS complex but P waves are absent or occur just before or within

the QRS complex.

- Ventricular rhythm has QRS complexes >0.12s with P waves following them.

Axis: - The mean frontal axis is the sum of all the ventricular forces during ventricular depolarization.

- The axis lies at 90 to the isoelectric complex (ie the one in which positive and negative

deflections are equal).

- Normal axis is between -30 and +90 .

- As a simple rule of thumb, if the complexes in leads I and II are both "positive", the axis is normal.

- Left axis deviation (LAD) is -30 and -90. Causes: left anterior hemiblock, inferior MI, VT from LV

focus, Wolff- Parkinson-White (WPW) syndrome (some types).

- Right axis deviation (RAD) is +90 and +180 . Causes: RVH, PE, anterolateral MI, left posterior

hemiblock (rare), WPW syndrome (some types).

P wave: - Normally precedes each QRS complex.

- Absent P wave: AF, sinoatrial block, junctional (AV nodal) rhythm.

- Dissociation between P waves and QRS complexes indicates complete heart block.

- P mitrale: bifid P wave, indicates left atrial hypertrophy.

- P pulmonale: peaked P wave, indicates right atrial hypertrophy (Pseudo-P-pulmonale seen if K+ ) .

P-R interval: - Measure from start of P wave to start of QRS.

- Normal range: 0.12- 0.2s (3-5 small squares).

- A prolonged P-R interval implies delayed AV conduction (1st degree heart block).

- A short P-R interval implies unusually fast AV conduction down an accessory pathway e.g WPW .


33 Dr.Waleed Badr

QRS complex: - Normal duration: 0.12s suggests ventricular conduction defects, e.g a bundle branch block .

- Large QRS complexes suggest ventricular hypertrophy.

- Normal Q wave 0.5mm) in ischaemia .

T wave: - Normally inverted in aVR, V1 and occasionally V2.

- Abnormal if inverted in I, II, and V4-V6.

- Peaked in hyperkalaemia & flattened in hypokalaemia.

ECG additional points

Where to place the chest leads ?

V1: right sternal edge, 4th intercostal space

V2: left sternal edge, 4th intercostal space

V3: half-way between V2 and V4

V4: the patient's apex beat (p64); all subsequent leads are in the same horizontal plane as V4

V5: anterior axillary line

V6: mid-axillary line (V7: posterior axillary line)

Finish 12-lead ECGs with a long rhythm strip in lead II.

Disorders of ventricular conduction

Bundle branch block

Delayed conduction is evidenced by prolongation of QRS >0.12s. Abnormal conduction patterns

lasting 0.12s, "RSR" pattern in V1, dominant R in V1, inverted T

waves in V1-V3 or V4, deep wide S wave in V6. Causes: normal variant (isolated RBBB), pulmonary

embolism, cor pulmonale.


34 Dr.Waleed Badr

In LBBB, the following pattern is seen: QRS >0.12s, "M pattern" in V5, no septal Q waves, inverted T

waves in I, aVL, V5-V6. Causes: IHD, hypertension, cardiomyopathy, idiopathic fibrosis. NB: If there is

LBBB, no comment can be made on the ST segment or T wave.

Bifascicular block : is the combination of RBBB and left bundle hemiblock, manifest as an axis

deviation, eg LAD in the case of left anterior hemiblock.

Trifascicular block : is the combination of bifascicular block and 1st degree heart block.

Ventricular hypertrophy

There is no single marker of ventricular hypertrophy: electrical axis, voltage, and ST wave changes

should all be taken into consideration. Relying on a single marker such as voltage may be unreliable

as a thin chest wall may result in large voltage whereas a thick chest wall may mask it.

Suspect left ventricular hypertrophy (LVH) if the R wave in V6 >25mm or the sum of the S wave in V1

and the R wave in V6 is >35mm .

Suspect right ventricular hypertrophy (RVH) if dominant R wave in V1, T wave inversion in V1-V3 or V4,

deep S wave in V6, RAD.

Other causes of dominant R wave in V1: RBBB, posterior MI, some types of WPW syndrome .

Causes of low voltage QRS complex: (QRS 100) : Causes: Anaemia, anxiety, exercise, pain, fever, sepsis, hypovolaemia, heart failure, pulmonary embolism, pregnancy, thyrotoxicosis, beri beri, CO2 retention, autonomic

neuropathy, sympathomimetics, e.g caffeine, adrenaline, and nicotine (may produce abrupt changes

in sinus rate, or other arrhythmia).

Sinus bradycardia (Rate 0.20s). It rarely causes

symptoms.

- 2nd degree: In this condition dropped beats occur because some impulses from the atria fail to

conduct to the ventricles.

Mobitz type I : there is progressive lengthening of successive PR intervals, culminating in a

dropped beat. The cycle then repeats itself. It is usually due to impaired conduction in the

AV node itself.

Mobitz type II : the PR interval of the conducted impulses remains constant but some P

waves are not conducted (2:1or 3:1). it is usually caused by disease of the His-Purkinje

system and carries a risk of asystole.

Causes of 1st & 2nd degree: Normal variant, athletes, sick sinus syndrome, IHD, acute

carditis, drugs (digoxin, B-blockers).


35 Dr.Waleed Badr

- 3rd degree (complete): When AV conduction fails completely, the atria and ventricles beat

independently (AV dissociation). Ventricular activity is maintained by an escape rhythm arising in

the AV node or bundle of His (narrow QRS complexes) or the distal Purkinje tissues (broad QRS

complexes).

Causes of 3rd degree: Idiopathic (fibrosis), congenital, IHD, aortic valve calcification,

cardiac surgery/trauma, digoxin toxicity, infiltration (abscesses, granulomas, tumours,

parasites).

Q waves: Pathological Q waves are usually >0.04s wide and >2mm deep. Usually as sign of infarction, and may occur within a few hours of an acute MI.

ST elevation: Normal variant (high take-off), acute MI, Prinzmetal's angina , acute pericarditis (saddle-shaped), left ventricular aneurysm.

ST depression: Normal variant (upward sloping), digoxin (downward sloping), ischaemic (horizontal).

T inversion: In V1-V3: normal (Blacks and children), right bundle branch block (RBBB), pulmonary embolism. In V2-V5: subendocardial MI, HOCM, subarachnoid haemorrhage, lithium. In V4-V6 and aVL:

ischaemia, LVH, associated with left bundle branch block (LBBB).

NB: ST and T wave changes are often non-specific, and must be interpreted in the light of the clinical

context.

MI: - Within hours, the T wave may become peaked and ST segments may begin to rise.

- Within 24h, the T wave inverts, as ST segment elevation begins to resolve. ST elevation rarely

persists, unless a left ventricular aneurysm develops. T wave inversion may or may not persist.

- Within a few days, pathological Q waves begin to form. Q waves usually persist, but may resolve

in 10%.

- The leads affected reflect the site of the infarct: inferior (II, III, aVF), anteroseptal (V1-4),

anterolateral (V4-6, I, aVL), posterior (tall R and ST in V1-2). - "Non Qwave infarcts" (formerly called subendocardial infarcts) have ST and T changes without Q

waves.

Pulmonary embolism: - Sinus tachycardia is commonest.

- There may be RAD, RBBB , right ventricular strain pattern (R-axis deviation. Dominant R wave and T

wave inversion/ST depression in V1 and V2. Leads II, III and aVF may show similar changes).

- Rarely, the SIQIIITIII pattern occurs: deep S waves in I, pathological Q waves in III, inverted T waves

in III.

Metabolic abnormalities:

- Digoxin effect: ST depression and inverted T wave in V5-6 (reversed tick). In digoxin toxicity, any

arrhythmia may occur (ventricular ectopics and nodal bradycardia are common).

- Hyperkalaemia: Tall, tented T wave, widened QRS, absent P waves, "sine wave" appearance .

- Hypokalaemia: Small T waves, prominent U waves.

- Hypercalcaemia: Short QT interval.

- Hypocalcaemia: Long QT interval, small T waves.


36 Dr.Waleed Badr

Exercise ECG testing

The patient undergoes a graduated, treadmill exercise test, with continuous 12- lead ECG and blood

pressure monitoring.

Indications:

To help confirm a suspected diagnosis of IHD.

Assessment of cardiac function & exercise tolerance.

Prognosis following MI. Often done pre-discharge (if +ve, worse outcome).

Evaluation of response to treatment (drugs, angioplasty, coronary artery bypass grafting, CABG).

Assessment of exercise-induced arrhythmias.

Contraindications:

Unstable angina

Recent Q wave MI (2mm (with or without chest pain).

Atrial or ventricular arrhythmia (not just ectopics).

Fall in blood pressure, failure of heart rate or blood pressure to rise with effort, or excessive rise in

blood pressure (systolic >230mmHg).

Development of AV block or LBBB.

Maximal or 90% maximal heart rate for age is achieved.

Interpreting the test:

A positive test only allows one to assess the probability that the patient has IHD. 75% with significant coronary

artery disease have a positive test, but so do 5% of people with normal arteries (the false positive rate is even

higher in middle-aged women, eg 20%). The more positive the result, the higher the predictive accuracy.

Down-sloping ST depression is much more significant than up-sloping, e.g 1mm J-point depression with down-

sloping ST segment is 99% predictive of 2-3 vessel disease.


37 Dr.Waleed Badr

Bed side tests in chest medicine

Peak expiratory flow rate (PEFR) : is measured by a maximal forced expiration through a peak flow meter.

It correlates well with the forced expiratory volume in 1 second (FEV1) and is used as an estimate of

airway calibre. Peak flow rates should be measured regularly in asthmatics to monitor response to

therapy and disease control.

Pulse oximetry : allows non-invasive assessment of peripheral O2 saturation . It provides a useful tool for

monitoring those who are acutely ill or at risk of deterioration. On most pulse oximeters, the alarm is set at

90%. A PaO2 80% is clearly abnormal and action is required (unless this is normal for the patient e.g in

COPD).

Arterial blood gas (ABG) analysis :

Heparinized blood is taken from the radial, brachial, or femoral artery & pH, PaO2, and PaCO2 are

measured using an automated analyser.

Normal pH is 7.40 0.05.

A pH < 7.35 indicates acidosis & a pH > 7.45 indicates alkalosis.

What is the difference between metabolic & respiratory acidosis & alkalosis ? SIMPLE RULES

- CO2 is an acidic gas (N: 4.5-6.0 kPa).

- HCO-3 alkaline (N: 22-28 mmol/L).

- 1 changes in HCO-3 are termed metabolic, and of CO2 respiratory.

1 Look at the pH: is there an acidosis or alkalosis?

2 Is the CO2 abnormal? If so, is the change in keeping with the pH ( i.e if there is an acidosis, is

CO2 raised)? If so it is a respiratory problem. If there is no change, or an OPPOSITE one, then

the change is compensatory.

3 Is the HCO-3 abnormal, and if so, is the change in keeping with the pH? If so the problem is a

metabolic one.

An example

pH 7.05, CO2 2.0 kPa, HCO-3 8.0 mmol/L.

There is an acidosis, and the CO2 is low, and so is a compensatory change. The HCO-3 is low,

and is thus the cause; ie a metabolic acidosis.


38 Dr.Waleed Badr

Acidosis Alkalosis

Metabolic pH HCO-3 Lactic acid

(shock,infection,hypoxia) .

Urate (renal failure) .

Ketones (D.M, alcohol) .

Salicylate poisoning .

pH HCO-3 Vomiting .

Burns .

K+ depletion (Diurectics) .

Ingestion of base .

Respiratory

pH CO2

Respiratory failure

pH CO2 A result of hyperventilation

CNS : stroke, subarachnoid

hge,meningitis.

Others : anxiety, fever,

pregnancy, salicylate poisoning.

Normal PaO2 is 10.5-13.5 kPa.

Causes of Hypoxia : ventilation/perfusion (V/Q) mismatch "the commonest cause",

hypoventilation, abnormal diffusion, right to left cardiac shunts.

Severe hypoxia is defined as a PaO2 < 8kPa .

Normal PaCO2 is 4.5-6.0 kPa.

PaCO2 is directly related to alveolar ventilation.

A PaCO2 < 4.5 kPa indicates hyperventilation and a PaCO2 > 6.0kPa indicates hypoventilation.

Type 1 respiratory failure is defined as PaO2 < 8 kPa and PaCO2 < 6.0 kPa, whereas type II respiratory

failure is defined as PaO2 < 8 kPa and PaCO2 > 6.0 kPa.

When to consider arterial blood gas (ABG) measurement In these clinical scenarios:

Any unexpected deterioration in an ill patient.

Anyone with an acute exacerbation of a chronic chest condition.

Anyone with impaired consciousness.

Anyone with impaired respiratory effort.

Or if any of these signs or symptoms are present:

Signs of CO2 retention : bounding pulse, drowsy, tremor (flapping), headache, pink palms,

papilloedema .

Signs of hypoxia : cyanosis, confusion, visual hallucinations .

Or to monitor the progress of a critically ill patient:

Monitoring the treatment of known respiratory failure.

Anyone ventilated on ITU.

After major surgery.

After major trauma.

To validate measurements from transcutaneous pulse oximetry:

Pulse oximetry sometimes suffices when it is not critical to know PaCO2.


39 Dr.Waleed Badr

Acute breathless (dyspnea) patient

Causes:

Wheezy:

Acute asthma.

Acute exacerbation of COPD.

Heart failure.

Anaphylaxis.

Stridor (upper air way obstruction):

Tumor or FB.

Acute epiglottitis.

Trauma e.g Laryngeal fracture.

Crepitations:

Heart failure.

Pneumonia.

Bronchiectasis.

Clear chest:

PE.

Metabolic acidosis e.g DKA.

Anemia.

Shock.

CNS causes.

Drugs e.g salicylates

Others:

Pneumothorax.

Pleural effusion.

Workup:

History

Rate of onset & severity of the breathlessness

H/O Associated cardiovascular symptoms (chest pain, palpitations, sweating and nausea) or

respiratory symptoms (cough, wheeze, haemoptysis, stridor) .

A previous history of repeated episodes of left ventricular failure, asthma or exacerbations of

COPD.

In the severely ill patient it may be necessary to obtain the history from accompanying relatives.


40 Dr.Waleed Badr

In children, the possibility of inhalation of a foreign body or acute epiglottitis should always be

considered.

Clinical assessment :

Level of consciousness

Degree of central cyanosis

Evidence of anaphylaxis (urticaria or angioedema)

Patency of the upper airway

Ability to speak (in single words or sentences)

Cardiovascular status (heart rate and rhythm, BP and degree of peripheral perfusion).

NB.Pulmonary oedema is suggested by pink frothy sputum and bi-basal crackles, asthma or COPD by

wheeze and prolonged expiration, pneumothorax by a silent resonant hemithorax, and pulmonary

embolus by severe breathlessness with normal breath sounds. The peak expiratory flow should be

measured whenever possible. Leg swelling may suggest cardiac failure or, if asymmetrical, venous

thrombosis.

Investigations : ABG, CXR & ECG ( to confirm the clinical diagnosis).

Management : look chest pain


41 Dr.Waleed Badr

Differential diagnosis of acute breathlessness

Condition History C/P CXR ABG ECG Pulmonary

oedema

Chest pain,

palpitations,

orthopnoea,

cardiac history*

Central

cyanosis, JVP, sweating, cool

extremities, pink

frothy sputum

,basal crackles*

Cardiomegaly,

oedema/pleural

effusions*

PaO2 PaCO2

Sinus

tachycardia,

ischaemia*,

arrhythmia

pulmonary

embolism

Risk factors,

chest pain,

pleurisy,

syncope*,

dizziness*

Central

cyanosis, JVP*, absence of signs

in the lung*,

shock

(tachycardia,

hypotension)

Often normal

Prominent hilar

vessels,

oligaemic lung

fields*

PaO2 PaCO2

Sinus

tachycardia,

RBBB, S1Q3T3

pattern

T (V1-V4)

Acute severe

asthma

History of

asthma,

asthma

medications,

wheeze*

Tachycardia,

pulsus

paradoxus,

cyanosis (late),

JVP *, peak flow, wheeze*

Hyperinflation

only (unless

complicated by

pneumothorax)*

PaO2 PaCO2 (PaCO2 in extremis)

Sinus

tachycardia

(bradycardia in

extremis)

Acute

exacerbation

of COPD

Previous

episodes*,

smoker. If in

type II

respiratory

failure may be

drowsy

Cyanosis,

hyperinflation*,

signs of CO2

retention

(flapping tremor,

bounding

pulses)*

Hyperinflation*,

bullae,

complicating

pneumothorax

or PaO2 PaCO2 in type

II failure H+, HCO3 in chronic type II

failure

Normal, or signs

of right

ventricular

strain

Pneumonia Prodromal illness*, fever*,

rigors*, pleurisy*

Fever, confusion,

pleural rub*,

consolidation*,

cyanosis (if

severe)

Pneumonic

consolidation*

PaO2 PaCO2 ( in extremis)

Tachycardia

Metabolic

acidosis

Evidence of

DM or renal

disease, aspirin

or ethylene

glycol

overdose

Fetor (ketones),

hyperventilation

without heart or

lung signs*,

dehydration*, air

hunger

Normal PaO2 normal

PaCO2, H+

Psychogenic Previous episodes,

digital or peri-

oral

dysaesthesia

No cyanosis, no

heart or lung

signs,

carpopedal

spasm

Normal PaO2 normal*

PaCO2, H+*


42 Dr.Waleed Badr

Acute severe asthma

Presentation: acute breathlessness and wheeze.

History: Ask about usual treatment, previous attacks, if admitted to ICU.

Clinical picture:

Severe attack: Unable to complete sentences, respiratory rate > 25/min, pulse >110 beats/min, PEFR <

50% of predicted.

Life threatening attack: PEFR < 33% of predicted, silent chest, sweating, panic, speechless, using

accessory muscles, cyanosis, bradycardia, hypotension, confusion, coma.

Investigations: Peak expiratory flow rate (PEFR), ABG (high CO2, low O2 (


43 Dr.Waleed Badr

If still not improving, consider transfer to ICU to intubate, give adrenaline and 500 mL colloid IVI.

Once patient is improving:

- Wean and stop aminophylline over 12 24h.

- Switch to inhaled B-agonist bronchodilator and steroids.

- 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).

- Look for cause of acute exacerbation.

Acute exacerbation of COPD

Common in winter & triggered by viral or bacterial infections.

Presentations: cough, breathlessness or wheeze with exercise capacity.

History: ask about usual treatment (home oxygen), smoking and exercise capacity.

Investigations: PEFR, ABG, CXR, ECG, blood culture (if pyrexial) & sputum culture.

Management:

Look for the cause e.g. infection or pneumothorax.

Controlled oxygen therapy :

- Dont leave patients hypoxic. However,in some patients, who 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 CO2 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% O2 but still monitor and repeat ABG.

Nebulized bronchodilator (salbutamol 5mg/4h & ipratropium 500ug/6h).

Hydrocortisone 200mg IV & oral prednisolone 30-40mg.

Antibiotics if evidence of infection.

Physiotherapy to aid sputum expectoration.

If no response, consider IV aminophylline.

If no response, consider nasal intermittent positive pressure ventilation (NIPPV) delivered by a nasal

mask and a flow generator.

Consider intubation and ventilation if pH and CO2 .


44 Dr.Waleed Badr

Consider respiratory stimulant drug e.g. doxapram (only for patients not suitable for mechanical

ventilation and as a short term measure only).

TTT of 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.

Assess social circumstances and support required. Identify and treat depression.

Air travel is hazards if O2 saturation is low, check availability of O2.


45 Dr.Waleed Badr

Pneumonia

Definition: an infection of the lung parenchyma.

Incidence: 12 per 1000 adults & mortality rate is 10% .

Causative organisms:

Strept. pneumoniae (the commonest) 60-75% .

Mycoplasma pneumoniae 5-18% .

Others : staph.aureus, haemophilus influenza, legionella & chlamydia psittaci, G-ve bacilli e.g

pseudomonas (often hospital-acquired or immunocompromised) .

Symptoms : fever, rigors, malaise, anorexia, dyspnea, cough, purulent sputum, haemoptysis & pleuritic

chest pain.

Signs :

Fever, cyanosis, herpes labialis, confusion .

Tachypnoea, tachycardia, hypotension .

Signs of consolidation (diminished expansion, dull percussion note, tactile vocal fremitus/vocal

resonance, bronchial breathing) .

Pleural rub .

Severity :

Calculate the core adverse features CURB-65 score

Confusion .

Urea > 7mmol/L .

Respiratory rate 30/min .

BP < 90/60 .

Age 65 .

Score : 0-1 home treatment if possible; 2 hospital therapy; 3 severe pneumonia.


46 Dr.Waleed Badr

Management :

A Adequate ventilation (may need intubation) .

B Oxygenation.

C Circulation IV line. Treat hypotension & shock

Investigations : CXR, ABG, FBC, U&E, LFT, CRP, blood culture, aspiration of pleural fluid for culture

& bronchoscopy (if immunocompromised)

Empirical antibiotics :

o Cefuroxime 1.5g/8h IV + clarithromycin 500 mg/12h IVI .

o If atypical :

- Legionella : add levofloxacin + rifampicin .

- Chlamydia : add tetracycline .

o If hospital acquired/immunocompromised : gentamicin IV + antipseudomonal penicillin .

Intravenous fluids : may be required .

Analgesics : for pleuritic chest pain .

Some patients may need intubation & a period of ventilatory support .

Complications : Pleural effusion, empyema, lung abscess, respiratory failure, septicaemia, pericarditis,

myocarditis, cholestatic jaundice & renal failure .


47 Dr.Waleed Badr

Tension pneumothorax

This is a medical emergency, requires immediate relief. Do not delay management for obtaining a CXR.

Causes:

1ry (Spontaneous) : esp.in young thin men.

2ry : to underlying lung disease e.g asthma, COPD, TB, pneumonia, lung abscess, lung fibrosis &

carcinoma .

Trauma, iatrogenic (subclavian CVP line insertion, pleural aspiration or biopsy, percutaneous liver

biopsy & +ve pressure ventilation).

Pathophysiology : 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.

Clinical picture:

Symptoms : may be asymptomatic or sudden onset of dyspnea and/or pleuritic chest pain.

Signs:

- Tachycardia & hypotension .

- Distended neck veins .

- Reduced expansion, Hyper-resonance on percussion and diminished breath sounds on the

affected side.

- Trachea deviated away from the affected side.

Investigations: CXR, ABG.


48 Dr.Waleed Badr

Management: depends on whether it is 1ry or 2ry, size & symptoms

Aspiration of pneumothorax :

After infilterative anaesthesia, Insert a large bore (14 - 16 G) cannula (venflon) into the 2nd

intercostal space in the mid-clavicular line on the side of the suspected pneumothorax.

Connect the cannula to a 3-way tap and 50mL 0.9% saline. Aspirate up to 2.5 litres of air.

Request CXR to confirm resolution.if successful repeat CXR after 24h to exclude recurrence .

Advice to avoid air travel for 6 weeks after normal CXR. Diving should be permanently avoided.

If unsuccessful, insert an intercostal drain.

Chest (intercostal) drain :

Inserted in 4th 6th intercostal space, anterior to mid-axillary line .

Use a small tube unless blood/pus is also present.

May be removed 24h after the lung has re-expanded & air leak has stopped (i.e the tube stops

bubbling). This is done during expiration or a Valsalva manoeuvre.

If failed to re-expand lung (within 48h), suction or surgical intervention may be required

Arrange for surgical advice if :

Bilateral .

Lung fails to expand after intercostal drain insertion .

2 or more previous episodes on the same side.

History of pneumothorax on the opposite side.


49 Dr.Waleed Badr

Headache D.D

A. Life- or Vision-Threatening

1. Subarachnoid hemorrhage : Extremely severe headache, stiff neck, conscious level; rarely, subhyaloid

hemorrhages seen on fundus examination, usually from a ruptured aneurysm.

2. Structural abnormality of the brain e.g tumor, aneurysm, AV malformation ( conscious level, signs of

ICT, or neurologic signs during, and often after, the headache episode).

3. Epidural or subdural hematoma (follows head trauma; altered level of consciousness; may produce

anisocoria.).

4. Infectious CNS disorder e.g meningitis, encephalitis, brain abscess (fever, stiff neck, conscious level,

photophobia, neurologic signs).

5. Giant cell arteritis (GCA) : Age >50 years, ESR & CRP, scalp tenderness, ..etc

6. Acute angle-closure glaucoma

7. Ocular ischemic syndrome

8. Malignant hypertension

9. ICT e.g Papilloedema & ICH (headaches usually worse in the morning & worsened by Valsalva) .

B. Others

Migraine

Cluster headache

Tension headache

Herpes zoster ophthalmicus : headache or periocular pain may precede the herpetic vesicles .

Sinus headache : may be a serious headache in diabetic patients and immunocompromised hosts

because mucormycosis may be responsible .

Vertebral artery dissection (neck pain & cerebellar/medullary signs) .

Cervical spine disease .

Pagets disease ( Alk phos)

Trigeminal neuralgia :

- Brief attacks of severe paroxysmal & sharp pain (like an electric shock) lasting a few seconds that

start in the distribution of one of the divisions of the trigeminal nerve

- Normal facial sensation


50 Dr.Waleed Badr

Raeder paratrigeminal neuralgia :

- Occurs in middle aged men

- Severe unilateral headache with periocular pain in the distribution of the 1st division of trigeminal

nerve .

- Lasts from hours to weeks before it resolves spontaneously .

- Associated with ipsilateral postganglionic horner syndrome .

Tolosa-Hunt syndrome .

Convergence insufficiency & Accomodative spasm .

Drugs e.g nitrates, CCB & Carbon monoxide poisoning .


51 Dr.Waleed Badr

Coma

Definition: unarousable, unresponsiveness.

Causes:

Metabolic Neurological

- Drugs, poisoning e.g CO1, alcohol

- Hypoglycaemia, Hyperglycaemia .

- Hypoxia, CO2 narcosis (COPD)

- Septicaemia .

- Hypothermia .

- Myxoedema, Addisonian crisis .

- Hepatic/uraemic encephalopathy .

- Trauma .

- Infection : e.g meningitis,

encephalitis .

- Tumours .

- Stroke .

- Epilepsy .

Management of coma

Call for help.

ABC .

Consider intubation if GCS < 8.

Stabilize cervical spine.

Vital signs monitoring.

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, Wernickes encephalopathy), IV naloxone (opiate

intoxication) and IV flumazenil (benzodiazepine intoxication if airway compromised).

Brief examination:

Signs of trauma e.g haematoma, laceration, fracture .

Signs of other diseases e.g. liver disease, DM .

Skin : for needle marks, cyanosis, pallor, .etc

Smell breath alcohol, hepatic fetor, ketosis, uremia .

Meningism, heart and lung, abdomen and rectum exam .

Eye examination (see below) .

Foci of infection e.g abscesses .

Examine for CNS asymmetry e.g tone, spontaneous movements, reflexes.


52 Dr.Waleed Badr

Quick 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.

Mannitol 20% hydrocortisone in case of cerebral edema.

Monitor the neurological signs and coma scale.

General care of comatosed patients.

Eye examination in coma (don't dilate)

1. Eye opening (see glasgow coma score)

2. Blinking reflex in light coma, test fields with visual threat. No blink in 1 field suggests hemianopia &

contralateral hemisphere lesion .

3. Eye movements & Vestibulo-ocular reflex (dolls head maneuver or ice water calorics .

4. Pupil size: checked every few minutes during the early stages, particularly if trauma is the likely cause

localizing sign.

a) Fixed, dilated pupil :

Unilateral 3rd nerve palsy with transtentorial herniation.

Bilateral atropine or barbiturate poisoning .

b) Marcus Gunn pupil ON or chiasm damage, pit. Apoplexy

c) Pin point

Unilateral Horners syndrome.

Bilateral pontine haemorrhage, opiate poisoning

5. Fundus:

Papilloedma ICT.

Hemorrhage: subhyaloid & subarachnoid in Tersons syndrome.

Signs of other disease e.g HTN and DM.


53 Dr.Waleed Badr

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. 3 types of response are

assessed

1) Best motor response:(6 grades) Obeying commands(6), Localizing response to pain (5), Withdrawal

to pain* (4), Flexor response to pain (decorticate posture)** (3), Extensor response to pain

(decerebrate posture)*** (2), No response to pain (1). Note that it is the best response of any limb

which should be recorded.

* omitted in some centers so GCS is 14 not 15 .

** Damage above the level of red nucleus in midbrain

*** damage below the level of red nucleus in midbrain

2) Best verbal response (5 grades): Oriented (5), Confused Conversation (4), Inappropriate speech (3),

Incomprehensive speech (2), None (1). Record level of best speech.

3) Eye opening (4 grades) : Spontaneous eye opening (4), Eye opening in response to speech (3), Eye

opening in response to pain (2), No eye opening (1).

An overall score is made by summing the score in the 3 areas assessed:

Severe injury (GCS 8).

Moderate injury (GCS 9 - 12).

Minor injury (GCS 13 - 15).

Primary scale (AVPU): is sometimes used in the initial assessment primary survey

A alert.

V responds to vocal stimuli (voice) .

P responds to pain.

U unresponsive.


54 Dr.Waleed Badr

Meningitis

Organisms: Meningococcus or pneumococcus. Less commonly Haemophilus influenza; listeria; CMV;

cryptococcus or TB .

Clinical features :

Early : headache, leg pains, cold hands and feet, abnormal skin colour .

Later :

Signs of Meningism : neck stiffness, photophobia, kernigs sign (pain + resistance on passive knee

extension with hip flexed) .

conscious level & coma .

Seizures focal CNS signs opisthotonus .

Petechial rash (non blanching) .

Signs of septicaemia (capillary refill; DIC; BP) .

Investigations :

U&E, FBC, LFT, glucose, coagulation screen .

Blood culture & serology .

Lumbar puncture(LP): for opening pressure ( in meningitis) & CSF sample for microscopic

examination .

CSF PCR (in aseptic meningitis) .

CXR (for TB meningitis) .

Management :

A Adequate ventilation.

B Oxygenation.

C Circulation IV line.

Start antibiotics immediately :

o < 55Y : Cefotaxime 2g/6h slow IV .

o > 55Y : Cefotaxime + ampicillin 2g/4h IV (for listeria).

o Aciclovir (if viral encephalitis suspected) .

If septicaemic signs :

o Dont attempt LP .

o Get help from critical care team .

o Treat shock (if present) & careful monitoring .

If meningitic signs :

o Dexamethasone 4-10 mg/6h IV (avoid if immunocompromised) .

o If signs of ICP take to ITU & dont do LP .


55 Dr.Waleed Badr

o If no shock or ICP signs do LP .

o If not sure , get senior help .

Subsequent therapy :

o Cefotaxime 2g/8h IVI for 10 days ( dose in renal failure) .

o Maintenance fluids .

o Isolation for the 1st 24h.

o If poor response, consider intubation & ventilation inotropic/vasopressor support .

Encephalitis

Organisms:

Viral : HSV-1&2, arboviruses, CMV, EBV, VZV, HIV, measles, mumps,rabies, japanese B encephalitis,

west nile virus, tick-borne encepahlitis .

Non-viral : any bacterial meningitis, TB, malaria, listeria, lyme disease, legionella, leptospirosis,

aspergillosis, cryptococcus, schistosomiasis .

Signs & symptoms: Confusion, coma, seizures, fever, headache, focal neurological signs history of

travel or animal bite .

Investigations:

U&E, FBC, LFT, glucose, coagulation screen .

Blood culture & serology .

CT (contrast-enhanced) or MRI :

- Focal bilateral temporal lobe involvement HSV encephalitis

- Meningeal enhancement meningoencephalitis .

Lumbar puncture (LP) & CSF PCR : CSF protein & lymphocytes and glucose

EEG

Management: mortality in untreated viral encephalitis is 70%

Symptomatic ttt e.g phenytoin for seizure .

Aciclovir 10 mg/kg/8h IV over 1h for 14 days .

Cerebral abscess

Causes: it may follows ear, sinus, dental of periodontal infection; skull fracture; congenital heart disease;

endocarditis; bronchiectasis .

Signs & symptoms: seizures, fever, signs of ICP & signs of sepsis elsewhere

Investigations: CT/MRI, WBC, ESR .

Management: referral to neurosurgery treat the source infection + treat ICP .


56 Dr.Waleed Badr

Status epilepticus

Definition: Seizures lasting > 30min or repeated with

Documents

Emergency Medicine 1st Edition -Dr.waleed (101 Papers) (5)