Clinical features

History

1. (1) Sudden collapse

Examination

1. (1) Patient unresponsive

2. (2) Airway, breathing—no respiration or agonal breathing

• (3) Circulation—pulse not palpable

Immediate management

See Figs. 33.1.1 and 33.1.2

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Fig. 33.1.1

The adult basic life support algorithm for use of a single rescuer out of hospital. (Note—‘999’ is the telephone number for emergency services in the United Kingdom.)

Reproduced with permission from the Resuscitation Council UK.

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Fig. 33.1.2

The advanced life support algorithm.

Reproduced with permission from the Resuscitation Council UK.

Clinical features

• History

• A patient who is in extremis is unlikely to be able to give a lucid history and may die during (unwise) interrogation, but the following clues may be elicited and be very useful diagnostically:

  1. (1) Chest pain—suggests myocardial infarction or other cardiorespiratory catastrophe

  2. (2) Chest and back pain—dissection of thoracic aorta must be seriously considered

  3. (3) Abdominal pain—suggests ruptured abdominal aortic aneurysm or other intra-abdominal emergency

  4. (4) Recent surgery—pulmonary embolism likely

  5. (5) High fever/rigors—suggests infective cause

  6. (6) Recent travel to relevant area—malaria until proven otherwise

• Examination

• Airway and breathing:

  1. (1) Is the airway patent?

  2. (2) Is the patient making a respiratory effort, and is the chest expanding with it?

  3. (3) Is the chest expanding symmetrically? Could there be a tension pneumothorax? (trachea deviated, mediastinum shifted, absent breath sounds on hyperinflated side of the chest; see 2.3 below)

  4. (4) Widespread crackles in the chest—suggests pulmonary oedema in this context (see 1.8 below).

  5. (5) Does the patient look as though they could keep this breathing up for the next 10 min?—If not, the patient is very likely to need respiratory support. Call for assistance from the ICU immediately

Circulation

1. (1) Do the peripheries feel cold or warm?—if warm, sepsis is likely

2. (2) Pulse rate and rhythm—if rate <60/min or >120/min, consider whether arrhythmia is primary cause of hypotension

3. (3) Blood pressure (BP)

   • ◆ Is there severe postural dizziness, a postural rise in pulse rate (>30 beats/min) or postural drop in BP (>20 mmHg) if the patient is moved from lying to being propped up? These indicate significant intravascular volume depletion in this context.

   • ◆ Does BP fall substantially on inspiration? If so, indicates large intrathoracic pressure swings with breathing (likely in upper airway obstruction or asthma) or cardiac tamponade

4. (4) What is the jugular venous pressure (JVP)?

   • ◆ If low, indicates intravascular volume depletion or dilated circulation

   • ◆ If high, suggests primary cardiorespiratory problem

• General:

• 1. (1) Rash—purpura suggests meningococcal or other septicaemia

  2. (2) Temperature—high fever suggests infection

  3. (3) Loss of left radial pulse, or BP lower in left arm than right arm, indicates aortic dissection

  4. (4) Abdominal tenderness/peritonism—suggests ruptured abdominal aortic aneurysm or other intra-abdominal emergency

See Table 33.1.1 for further information

Immediate management

Airway and breathing:

1. (1) Ensure airway is clear: consider oropharyngeal airway

2. (2) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂ >92%

3. (3) If tension pneumothorax, decompress immediately (see Chapter 33.1.2, ‘Chest decompression’)

4. (4) Give intravenous (IV) naloxone (0.8–2.0 mg repeated at intervals of 2–3 min to a maximum of 10 mg) if there is any suspicion that patient has received opioids

5. (5) Consider elective intubation and ventilation

• Circulation:

• Obtain IV access using a safe technique (see Chapter 33.1.2)

• Also: begin resuscitation according to volume status as indicated in Table 33.1.2

  1. (1) Insert urinary catheter and monitor fluid input/output hourly in any patient with cardiorespiratory collapse.

  2. (2) Give broad spectrum antimicrobial cover to any patient with unexplained cardiorespiratory collapse, e.g. coamoxiclav 1.2g IV 6–8 hrly, as dictated by clinical suspicion of likely pathogen (see 7.7 below)

Key investigations

See Table 33.1.1

Further management

Determined by underlying condition

Clinical features

History

1. (1) Ischaemic chest pain

2. (2) Cardiorespiratory collapse

3. (3) May be nonspecific or silent, especially in elderly people or in diabetics

• Examination

• May be normal, but look for:

  1. (1) ‘Pump failure’—cool peripheries, hypotension

  2. (2) Pulmonary oedema—see section 1.8 below

  3. (3) Cardiac—gallop rhythm, murmurs

Immediate management

• If cardiorespiratory collapse, as described in 1.2 above

• Otherwise:

  1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂ >92%

  2. (2) Give aspirin 300 mg orally, chewed or dispersed in water (if not given before admission to hospital)

  3. (3) Give clopidogrel 300 mg orally

  4. (4) Analgesia—give adequate pain relief, e.g. (a) diamorphine by slow IV injection at 1 mg/min, usual maximum initial dose is 5 mg, but may be repeated if necessary, or (b) morphine by slow IV injection at 2 mg/min, usual maximum initial dose is 10 mg, but may be repeated if necessary. Both to be accompanied by appropriate antiemetic, e.g. metoclopramide 10 mg IV over 1–2 min, or cyclizine 50 mg IV over 1–2 min (caution in severe heart failure)

  5. (5) Reperfusion therapy—immediate triage to (a) primary percutaneous coronary intervention (PCI), if available in a timely manner (within 90 min of patient call) (Table 33.1.3), or (b) thrombolysis, if primary PCI not available (Table 33.1.4)

Key investigations

• To establish the diagnosis:

  1. (1) ECG—looking for ST segment elevation and/or (presumed or proven) new bundle branch block

  2. (2) Cardiac biochemical markers (troponins, CK-MB)

• Other important tests:

  1. (1) As indicated by clinical examination, e.g. chest radiograph to look for pulmonary oedema; echocardiography to assess LV function or cause of pansystolic murmur (?mitral valve dysfunction, ?ventricular septal defect)

  2. (2) Assess modifiable risk factors for ischaemic heart disease, e.g. cholesterol

Further management

Consider:

1. (1) Antiplatelet agents and anticoagulants

   • ◆ Aspirin (75–325 mg daily)—continue long term (if not contraindicated)

   • ◆ Clopidogrel (75 mg daily)—continue for at least 1 month after thrombolysis, or as determined by the type of stent implanted (if not contraindicated)

   • ◆ Glycoprotein IIb/IIIa inhibitors—e.g abciximab, eptifibatide, tirofiban—are indicated in patients managed with primary PCI, but not after fibrinolysis

   • ◆ Anticoagulants—patients treated with fibrinolytic therapy should receive low molecular weight heparin or fondaparinux (a factor Xa inhibitor)

2. (2) β-Blockade

   • ◆ Early—if no contraindication (e.g. hypotension, heart failure, heart block) give, e.g. atenolol 5 mg IV over 5 min, repeated after 10–15 min

   • ◆ Long term—if no contraindication continue oral β-blockade for at least 2–3 years

3. (3) Angiotensin converting enzyme (ACE) inhibition (or angiotensin receptor blockade)

   • ◆ Early—start within 24 h in patients who are normotensive and continue for at least 5–6 weeks

   • ◆ Long term—recommended for any patient with left ventricular dysfunction

4. (4) Lipid lowering—long-term treatment with statin will benefit most patients with coronary heart disease.

5. (5) Control of diabetes—evidence supports use of insulin in hospital and in the early post-hospital phase to maintain good control

Notes

1. (1) Treat complications, e.g. venodilator or diuretic for pulmonary oedema. Severe heart failure/shock may require ventilation, inotropes ± intra-aortic balloon pump

2. (2) Patients with diabetes will benefit from intensive insulin therapy during admission with acute myocardial infarction and afterwards

3. (3) For all patients: give advice regarding lifestyle issues before and after discharge from hospital—smoking, diet, exercise, management of obesity —also regarding resumption of normal activities. Consider referral to cardiac rehabilitation services

4. (4) Consider need for specialist cardiological opinion and/or investigation by cardiac stress test (e.g. treadmill exercise tolerance test) and/or coronary angiography

Clinical features

History

1. (1) Ischaemic chest pain at rest or on minimal exertion

2. (2) Chest tightness/breathlessness

• Examination

• ◆ sually no specific signs, but may be:

  1. (1) ‘Pump failure’—cool peripheries, hypotension

  2. (2) Pulmonary oedema—breathing difficulty, pulmonary crackles (see 1.8 below)

  3. (3) Cardiac—gallop rhythm, murmurs

Immediate management

Triage into high, intermediate, and low risk categories

• ◆ High risk—(1) typical clinical features of ischaemia and ST segment depression or transient ST segment elevation; (2) troponin elevation and a high risk score (risk calculator downloadable from http://www.outcomes.org/grace or http://www.timi.org/files/riskscore/ua_calculator.htm); (3) arrhythmias or haemodynamic compromise provoked by ischaemia

• ◆ Intermediate or low risk—clinical features of acute coronary syndrome and nonspecific ECG changes (T wave inversion, T wave flattening, minor conduction abnormalities)

• ◆ Low risk or an alternative diagnosis—normal electrocardiogram, normal biomarkers, normal cardiac examination and normal echo.

High risk category

1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂ >92%

2. (2) Give aspirin 300 mg orally immediately, chewed or dispersed in water (if not given before admission to hospital)

3. (3) Give clopidogrel 300 mg orally

4. (4) Give glycoprotein IIb/IIIa inhibitor—e.g abciximab, eptifibatide, tirofiban—probably benefits all high risk patients; definitely indicated in those undergoing revascularization.

5. (5) Give anticoagulation—low molecular weight heparin—e.g. enoxaparin 1 mg/kg (100 units/kg) every 12 h, or dalteparin 120 units/kg every 12 h (maximum 10 000 units twice daily)—or bivalirudin (a direct thrombin inhibitor). Continue for 48–72 h or after coronary angiography and revascularization.

6. (6) Give IV or oral β-blocker (see 1.3 above) unless contraindicated. Consider heart-rate-lowering calcium antagonist (e.g. diltiazem or verapamil) if β-blocker is contraindicated or not tolerated in patient without left ventricular dysfunction

7. (7) Nitrate—give if ongoing pain, e.g. (a) sublingual glyceryl trinitrate (GTN), 0.3–1 mg repeated as required; (b) buccal GTN, up to 5 mg, with tablet placed between upper lip and gum and left to dissolve; (c) IV infusion of isosorbide dinitrate at initial dose of 2 mg/h (increasing as necessary to maximum of 20 mg/h to relieve pain and as limited by hypotension)

8. (8) Analgesia—give adequate pain relief if ongoing pain not relieved by nitrate, e.g. (a) diamorphine by slow IV injection at 1 mg/min (usual maximum initial dose is 5 mg, but may be repeated if necessary), or (b) morphine by slow IV injection at 2 mg/min (usual maximum initial dose is 10 mg, but may be repeated if necessary). Both to be accompanied by appropriate antiemetic, e.g. metoclopramide 10 mg IV over 1–2 min, or cyclizine 50 mg IV over 1–2 min (caution in severe heart failure)

9. (9) Continuing ischaemia or haemodynamic instability—urgent PCI

Intermediate risk category

1. (1) As above for high risk, except do not give glycoprotein IIb/IIIa inhibitor.

   Patients who develop high risk features after initial presentation should be considered for urgent angiography and revascularization (within 24–72 h). Such patients also fulfill guideline criteria for GPIIb/IIIa inhibitors (initiated prior to angiography)

• Low risk category

• Clinically stable patients with minor or nonspecific ECG abnormalities and a low risk score (including negative repeat troponin) are at very low risk for in-hospital major cardiac events. Such patients may nevertheless have significant underlying coronary artery disease. They require stress testing or perfusion scanning, ideally prior to discharge

Key investigations

To establish the diagnosis

1. (1) ECG—looking for transient ST segment shift with pain; T wave changes are less specific and ECG may be normal

2. (2) Cardiac biochemical markers (troponins, CK-MB)

• Other important tests

• As for STEMI (see 1.3 above)

Further management

1. (1) Aspirin (75–325 mg daily)—continue long term (if not contraindicated)

2. (2) ACE inhibition (or angiotensin receptor blockade)—recommended for any patient with left ventricular dysfunction

3. (3) Lipid lowering—long-term treatment with statin will benefit most patients with coronary heart disease

   Consider:

4. (4) Clopidogrel (75 mg/day)—consider continuing for 1 year

Notes

1. (1) For all patients: give advice regarding lifestyle issues before and after discharge from hospital—smoking, diet, exercise, management of obesity—also regarding resumption of normal activities. Consider referral to cardiac rehabilitation services

2. (2) Consider need for specialist cardiological opinion and/or investigation by cardiac stress test (e.g. treadmill exercise tolerance test) and/or coronary angiography

Clinical features

History

1. (1) Syncope or presyncope

2. (2) Fatigue/breathing difficulty

3. (3) Drugs (especially β-blockers)

• Examination

• The most important immediate issue is to decide whether or not the circulation is compromised: is the patient cool peripherally? What are the rate, rhythm, and BP? Is there pulmonary oedema (see 1.8 below)?

• If seen in the presence of bradycardia, note rate and

  1. (1) Abnormal rhythm, e.g. dropped beats in second-degree AV block

  2. (2) Other cardiovascular abnormality, e.g. cannon waves in JVP in third-degree (complete) AV block

  3. (3) Temperature (hypothermia—see 9.4 below)

Immediate management

• Obtain ECG

• If the patient is haemodynamically compromised:

  1. (1) Give atropine, 0.3–1.0 mg IV, repeated as necessary

  2. (2) Consider isoprenaline, 0.5–10 µg/min by IV infusion

  3. (3) Consider temporary pacing (see Chapter 33.2, ‘Cardiac pacing (temporary’)

  4. (4) Consider glucagon 50–150 µg/kg IV in 5% glucose in cases of β-blocker overdose, with precautions to protect the airway in case of vomiting (NB unlicensed indication and dose)

Key investigations

• To establish the diagnosis:

• 12-lead ECG

Other important tests:

1. (1) Electrolytes (particularly potassium)

2. (2) Cardiac biochemical markers (depending on context)

3. (3) Chest radiograph—look at heart size and for evidence of pulmonary oedema

4. (4) 24 h ECG monitor (if symptoms intermittent and 12-lead ECG not diagnostic)

5. (5) Echocardiography (if clinical suspicion that heart is structurally abnormal)

Further management

Dependent on diagnosis. If not reversible, likely to require permanent pacing

Clinical features

History

1. (1) Syncope or presyncope

2. (2) Palpitations

3. (3) Fatigue/breathing difficulty

4. (4) Chest pain

• Examination

• The most important immediate issue is to decide whether or not the circulation is compromised: is the patient cool peripherally? What are the rate, rhythm, and BP? Is there pulmonary oedema (see 1.8 below)?

• Physical examination is unlikely to aid diagnosis of the particular type of tachycardia, excepting for the presence of an irregularly irregular rhythm in atrial fibrillation (AF), but note the following:

  1. (1) Jugular venous pulse—absence of ‘a’ waves in AF; rapid flutter waves in atrial flutter; cannon waves in ventricular tachycardia

  2. (2) First heart sound—variable intensity in AF

  3. (3) A dilated heart increases the chance that tachycardia is ventricular in origin

Immediate management

• 1. (1) Obtain ECG

  2. (2) If cardiorespiratory collapse, as described in 1.2 above

  3. (3) For any tachycardia that is poorly tolerated, synchronized DC shock (under deep sedation or general anaesthesia) is the treatment of choice and usually provides rapid relief

  4. (4) Management otherwise depends upon clinical context and type of tachycardia

• General rule—do not give more than one antiarrhythmic drug to a patient without seeking specialist advice; if a first line antiarrhythmic drug fails, the appropriate treatment will often be to proceed to DC cardioversion

Key investigations

To establish the diagnosis:

1. (1) 12-lead ECG (see Table 33.1.6)

2. (2) Uncertain of the diagnosis of a broad complex tachycardia? See Table 33.1.7

3. (3) IV adenosine (administered as described below)—transient AV block may (a) reveal (but rarely terminate) atrial tachycardia/fibrillation/flutter; (b) terminate atrioventricular nodal re-entry (AVNRT) and atrioventricular re-entry tachycardias (AVRT); (c) usually have no effect on ventricular tachycardia

Other important tests:

1. (1) Electrolytes (particularly potassium)

2. (2) Cardiac biochemical markers (depending on context)

3. (3) Chest radiograph—look at heart size and for evidence of pulmonary oedema

4. (4) 24 h ECG monitor (if symptoms intermittent and 12-lead ECG not diagnostic)

5. (5) Echocardiography (if clinical suspicion that heart is structurally abnormal)

6. (6) Thyroid function tests (in atrial fibrillation)

Further management if severe haemodynamic compromise

• Atrial fibrillation/flutter

  • ◆ DC cardioversion, or

  • ◆ Amiodarone, 5 mg/kg over 20–120 min followed by 1200 mg/24 h until sinus rhythm restored (into central venous catheter), or

  • ◆ Sotalol, 1.5 mg/kg IV over 30 min

• Atrioventricular nodal re-entry (AVNRT) and atrioventricular re-entry tachycardias (AVRT) (supra-ventricular tachycardias, SVTs)

  • ◆ Adenosine, 3 mg by fast IV injection, if necessary followed by 6 mg (also by fast IV injection) after 1–2 min, and then by 12 mg (also by fast IV injection) after a further 1–2 min (NB contraindicated in those with asthma, and patients taking dipyridamole are very sensitive, requiring reduced initial dose of 0.5–1 mg)

  • ◆ Verapamil, 5–10 mg by slow IV injection over 2–3 min is an alternative in patients with asthma, but NOT in those who might have ventricular tachycardia, or in those who are receiving β-blockers

• Ventricular tachycardia

  • ◆ DC cardioversion (see 1.1 above)

Further management if no severe haemodynamic compromise

• Atrial fibrillation/flutter

  • Duration <48 h or transoesophageal echocardiography shows no intracardiac thrombus:

  • ◆ Consider prompt chemical or synchronized DC cardioversion

  • ◆ Flecainide (class 1 C) 2 mg/kg IV over 30 min if there is no evidence of ischaemic heart disease or left ventricular dysfunction

  • ◆ Amiodarone or sotalol (class III) can be used to restore sinus rhythm and maintain it

  • ◆ Digoxin is useful for rate control only but will not restore sinus rhythm. If digoxin is ineffective in controlling ventricular rate, and cardioversion is unsuccessful or inappropriate, consider adding verapamil or β-blocker

• Duration >48 h or thrombus on transoesophageal echocardiography:

  • ◆ Anticoagulate for 4–6 weeks before synchronized DC cardioversion

• Note

• Atrial fibrillation arising in the context of intercurrent illness is usually best managed by treatment of the underlying medical condition and with digoxin to control ventricular rate. The patient is likely to return to sinus rhythm when the underlying condition has resolved.

• Atrioventricular nodal re-entry (AVNRT) and atrioventricular re-entry (AVRT) tachycardias (supraventricular tachycardias, SVTs)

  • ◆ Vagal stimulation by respiratory manoeuvres (Valsalva), prompt squatting, or pressure over one carotid sinus (but not the latter in those with recent ischaemia, digoxin toxicity, or in elderly patients)

  • ◆ Adenosine if vagal stimulation fails

  • ◆ Other options include verapamil, β-blocker, flecainide, sotalol, or amiodarone

• Ventricular tachycardia

  • ◆ Consider synchronized DC cardioversion.

  • ◆ Lignocaine (lidocaine) 50–100 mg as IV bolus over a few min followed immediately by infusion of 4 mg/min for 30 min, 2 mg/min for 2 h, and then 1 mg/min up to 24 h.

  • ◆ Other antiarrhythmics that can be used include amiodarone, sotalol, procainamide and disopyramide—but seek expert help

• Torsade de pointes

• This form of ventricular tachycardia requires particular treatment:

  • ◆ Discontinue predisposing drugs and avoid empirical antiarrhythmic drug treatment

  • ◆ Give magnesium sulphate, 8 mmol of magnesium over 10–15 min, repeated once if necessary

  • ◆ If torsade is associated with bradycardia and pauses, consider isoprenaline infusion or overdrive atrial/ventricular pacing to increase heart rate

Clinical features

• History

  1. (1) Breathing difficulty

  2. (2) Orthopnoea, paroxysmal nocturnal dyspnoea

• Other cardiac symptoms:

  1. (3) Palpitations

  2. (4) Chest pain

  3. (5) Ankle oedema

  4. (6) Any previous cardiac history

• Examination

  1. (1) How unwell is the patient? If very ill, see 1.2 above

  2. (2) Respiratory rate, cyanosis, peripheral circulation (cold, clammy), pulse rate and rhythm (?arrhythmia, see 1.6 and 1.7 above), BP (often elevated, but may be normal or low), JVP (likely to be elevated), apex beat (displaced in congestive cardiac failure), heart sounds (gallop rhythm, murmurs), crackles and/or wheezes in chest, peripheral oedema (suggests biventricular failure in this context)

  3. (3) Pulse oximetry

Immediate management

If cardiorespiratory collapse, as described in 1.2 above:

1. (1) Position the patient ‘trunk up, legs down’

2. (2) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂ >92%

3. (3) Give furosemide 40–80 mg IV

4. If not improving rapidly:

5. (4) Give either:

   • ◆ Diamorphine by slow IV injection at 1 mg/min (usual maximum initial dose is 5 mg, but may be repeated if necessary), or

   • ◆ Morphine by slow IV injection at 2 mg/min (usual maximum initial dose is 10 mg, but may be repeated if necessary)

   • ◆ Both to be accompanied by appropriate antiemetic, e.g. metoclopramide 10 mg IV over 1–2 min (not cyclizine in severe heart failure)

6. (5) Unload with IV nitrate, e.g. isosorbide dinitrate 2–20 mg/h

7. (6) Consider continuous positive airway pressure (CPAP) mask, noninvasive ventilation, or tracheal intubation and intermittent positive pressure ventilation (IPPV)

Key investigations

• To establish the diagnosis:

• Chest radiograph

• Other important tests:

  1. (1) ECG—look for arrhythmia or acute myocardial infarction

  2. (2) Cardiac biochemical markers

  3. (3) Echocardiography—visualization of left ventricular size and function, also of other structural abnormalities, e.g. valve dysfunction

  4. (4) Invasive monitoring, e.g. pulmonary artery flow-directed (Swan Ganz) catheterization—to be considered only if the patient is failing to respond or when there is genuine doubt about cardiac filling pressures or diagnosis. A pulmonary capillary wedge pressure >18 mmHg supports the diagnosis of cardiogenic pulmonary oedema

Further management

Depending on clinical context:

1. (1) Acute myocardial infarction—see 1.3 above

2. (2) Arrhythmia—see 1.6 and 1.7 above

3. (3) Acute mechanical cause—e.g. aortic incompetence, mitral regurgitation, ventricular septal defect—may require surgical intervention

Clinical features

• History

• Deep venous thrombosis (DVT):

  1. (1) Calf/leg pain

  2. (2) Calf/leg swelling

  3. (3) Features to suggest PE

• Pulmonary embolus (PE):

  1. (1) Shortness of breath, developing over hours, days, or (sometimes) weeks

  2. (2) Pleuritic chest pain, haemoptysis (lung infarction, peripheral emboli)

  3. (3) Circulatory collapse (massive PE)

  4. (4) Features to suggest DVT

• Deep venous thrombosis and pulmonary embolus:

  1. (1) Previous episodes of DVT and/or PE

  2. (2) Risk factors—immobilization, recent surgery, previous episodes, malignancy, travel, family history, etc.

• Examination

• Deep venous thrombosis:

  1. (1) Calf/leg swelling—measure circumference 10 cm below tibial tuberosity: difference between sides of >1.5 cm likely to be significant

  2. (2) Calf tenderness; palpable cord; positive Homan’s sign

  3. (3) Dilated superficial veins; leg feels warmer than the other

  4. (4) Check for signs of PE

  5. (5) Consider alternative diagnoses—especially Baker’s cyst, cellulitis, haematoma in muscle

• Pulmonary embolus:

  1. (1) May be no abnormal signs

  2. (2) Tachypnoea (50–70% of cases), crackles (18–50%), tachycardia (24–30%), pleural rub (<10%)

  3. (3) Circulatory collapse with cool peripheries, hypotension, and cyanosis. Look particularly for signs of right heart strain: elevated JVP, parasternal heave, S3 over right ventricle, loud P2

  4. (4) Check for signs of DVT

  5. (5) Consider alternative diagnoses—especially pneumonia, musculoskeletal pain, pneumothorax

• Notes

  1. (1) Low-grade fever is common in both DVT and PE

  2. (2) In cases of DVT or PE—perform rectal/pelvic examination (before discharge from hospital)

Immediate management

1. (1) If cardiorespiratory collapse, as described in 1.2 above. Note that patients with massive PE require volume expansion even though their JVP is elevated

2. (2) If index of clinical suspicion for PE is high, give treatment dose of low molecular weight heparin pending the results of investigation

Key investigations

• To establish the diagnosis:

• Tests commonly used to demonstrate the presence of thrombus/embolus are as follows:

  • ◆ DVT—venous ultrasonography, (contrast venography)

  • ◆ PE— contrast enhanced spiral CT scan, (lung ventilation/perfusion [VQ] scan, pulmonary angiogram)

• Other important tests:

• Pulmonary embolus:

  1. (1) ECG—commonest abnormality is sinus tachycardia and/or nonspecific ST segment or T wave abnormalities. Look for signs of right heart strain, e.g. T wave inversion in V1/V2, S1Q3T3, axis shift

  2. (2) Chest radiograph—look for atelectasis or pulmonary parenchymal abnormality, also pleural effusion. May be normal

  3. (3) Arterial blood gases—look for hypoxia; but normoxia does not exclude PE

• Deep venous thrombosis and pulmonary embolus:

  1. (1) Full blood count, electrolytes, renal and liver function tests—may give a lead to an underlying medical condition and will establish baseline

  2. (2) At a later stage a thrombophilia screen may be appropriate, also investigations dictated by clinical findings or investigations detailed above

Clinical decision-making

Many patients referred for medical opinion have a low probability of having DVT or PE and not all require imaging to exclude DVT or PE. Follow management algorithms as follows:

• ◆ DVT—see Table 33.1.8

• ◆ PE—see Table 33.1.9

Further management

1. (1) Anticoagulation with low molecular weight heparin (typical dose 200 IU/kg subcutaneous o.d., but see manufacturer’s instructions) or standard (unfractionated) heparin (Table 33.1.10) until oral anticoagulation (usually with warfarin, Table 33.1.11) is established

2. (2) In cases with circulatory collapse consider thrombolysis, e.g.:

   • ◆ Streptokinase by IV infusion of 250 000 units over 30 min, then 100 000 units/h for 24 h, or

   • ◆ Tissue plasminogen activator, 10 mg by IV infusion over 1–2 min, followed by 90 mg over 2 h (maximum 1.5 mg/kg in patients of <65 kg)

3. (3) In cases with circulatory collapse and contraindication to thrombolysis, consider catheter extraction or fragmentation of embolus, or surgical embolectomy

Notes

1. (1) No monitoring of low molecular weight heparin treatment is required, excepting if used in patients with chronic kidney disease when monitoring of anti-Xa levels is required.

2. (2) Methods of reversing anticoagulation are shown in Table 33.1.12

Clinical features

History

1. (1) Headache

2. (2) Blurring of vision

3. (3) Drowsiness

4. (4) Epileptic fits

• Examination

  1. (1) BP—will usually be grossly elevated with diastolic pressure >130 mmHg, but note that accelerated hypertension can occur at lower pressures than this and the diagnosis is established not by a particular elevation of BP but by signs of fibrinoid necrosis

  2. (2) Ocular fundi

     • ◆ Grade III retinopathy: flame-shaped superficial haemorrhages, ‘dot and blot’ haemorrhages, cotton wool spots (retinal microinfarcts), hard exudates

     • ◆ Grade IV retinopathy: as grade III + papilloedema

     • ◆ Note that there is no difference in management or prognosis of patients with grade III or grade IV disease

  3. (3) Urine—stix testing shows proteinuria and haematuria, microscopy may show red blood cell casts

• Also look for signs of:

  1. (4) Pulmonary oedema—see 1.8 above

  2. (5) Aortic dissection—see 1.5 above

  3. (6) Scleroderma—scleroderma renal crisis

Immediate management

• In an uncomplicated case:

  1. (1) Admit to hospital

  2. (2) Bed rest

  3. (3) No smoking (causes an acute rise in BP)

  4. (4) Aim to lower diastolic pressure into range 100–105 mmHg over 2–3 days using:

     • ◆ Atenolol 25–50 mg orally, or

     • ◆ Nifedipine 10–20 mg of modified release preparation orally (tablets, not sublingual)

     • ◆ Further dosing determined by response

     • ◆ Maximum initial fall in BP should not exceed 25% of presenting value

• In a complicated case (aortic dissection, epileptic fitting, acute pulmonary oedema, oral medication not possible):

• (1), (2), and (3)—as above

  1. (4) Aim to lower diastolic pressure to less than 100–110 mmHg over several hours (depending on clinical context) using:

     • ◆ Labetolol, initial bolus of 20 mg IV, then at 20 mg/h, increased as necessary every 30 min to maximum of 120 mg/h, or

     • ◆ Sodium nitroprusside (IV) at initial dose of 0.25–0.5 µg/kg per min, increasing up to 8 µg/kg per min. This must only be given to patients with aortic dissection after β-blockade has been established with, e.g. esmolol (50–200 µg/kg per min)

Key investigations

• To establish the diagnosis:

• Accelerated hypertension is a clinical diagnosis

• Other important tests:

  1. (1) ECG—looking for evidence of left ventricular hypertrophy and acute myocardial ischaemia

  2. (2) Chest radiograph—looking for heart size, pulmonary oedema, and (if chest/back pain) for aortic dissection

  3. (3) Electrolytes and renal function—if serum creatinine >250 µmol/litre renal function is likely to deteriorate further (at least in the short term)

  4. (4) ‘Autoimmune/vasculitic’ serology—ANCA, ANA, etc.—for evidence of multisystem disorder that can present with accelerated phase hypertension and which (if present) will require specific treatment

  5. (5) CT angiography of chest if aortic dissection suspected (or other imaging, see 1.5 above)

Further management

When acute emergency is controlled, all patients who have suffered from accelerated phase hypertension require thorough investigation for secondary causes of hypertension

Clinical features

History

1. (1) Premonitory aura—apprehension, light-headedness, dizziness, tingling or itching of skin

2. (2) Facial, tongue or throat swelling

3. (3) Stridor or wheeze

4. (4) Syncope or collapse

5. (5) Exposure to precipitant—foodstuffs (e.g. peanuts), hymenopteran stings, drugs (e.g. parenteral penicillins)

Examination

1. (1) Cyanosis

2. (2) Hypotension

3. (3) Facial, tongue, or throat swelling

4. (4) Stridor or wheeze

5. (5) Urticaria, angio-oedema, skin erythema, or extreme pallor

Immediate management

• 1. (1) Stop any potential causative agent immediately

  2. (2) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂ >92%

  3. (3) Adrenaline (epinephrine)

     • ◆ Give 0.3–0.5 ml of 1:1000 adrenaline (0.3–0.5 mg) intramuscularly into lateral thigh, repeated every 5–10 min as needed

     • If this is ineffective, or if the patient is about to die:

     • ◆ Give 5 mg adrenaline (5 ml of undiluted 1:1000 adrenaline) nebulized with oxygen, and

     • ◆ Make up 1:100 000 preparation of adrenaline by diluting 0.5 mg adrenaline (0.5 ml of 1:1000 adrenaline) to total of 50 ml with 0.9% saline and give at 0.5–1.5 ml/min, titrated according to clinical response

  4. (4) Fluid—give balanced salt solution or 0.9% saline, 10–20 ml/kg, as rapid IV infusion if patient is hypotensive

• Second line therapy—can be considered after cardiorespiratory stability has been achieved (but no strong evidence that they are required):

  1. (5) H₁-blocker, eg. chlorpheniramine 10–20 mg IV, repeated up to 40 mg in 24 h (change to oral when patient tolerates)

  2. (6) H₂-blocker, e.g. ranitidine 50 mg IV three times daily (change to oral when patient tolerates)

  3. (7) Steroid, e.g. hydrocortisone 1.5–3 mg/kg IV, then repeated four times daily (change to oral prednisolone 40 mg daily when patient tolerates)

  4. (8) β₂-Agonist, e.g. salbutamol 5 mg (repeated as necessary) via oxygen-driven nebulizer if bronchospasm is a persistent problem

Key investigations

To establish the diagnosis:

1. (1) Anaphylaxis is a clinical diagnosis

2. (2) Mast cell tryptase—immediately after resuscitation, after 1–2 h, and after 24 h (or convalescent)

• Other important tests:

• ECG, chest radiograph, electrolytes, renal function, arterial blood gases (depending on context)

Further management

1. (1) Patients must be observed for 4–6 h after full recovery before discharge from immediate medical care

2. (2) Determination of allergen (if any)—refer to allergy services; advice regarding avoidance; MedicAlert bracelet

3. (3) Instruction regarding self-injection of adrenaline and supply of appropriate medication, e.g. EpiPen

Clinical features

History

1. (1) Collapse with extreme difficulty in breathing

Examination

1. (1) Patient looks as though they are about to die

2. (2) Gasping respiratory effort

3. (3) Cyanosis

4. (4) Chest looks asymmetrical, being prominent on side of tension

5. (5) Tracheal deviation, away from side of tension

6. (6) Mediastinal shift, away from side of tension, most reliably detected by percussion of cardiac dullness

7. (7) Chest is silent on side of tension, the only breath sounds being heard in the opposite axilla

Immediate management

Insert needle to decompress chest; see Chapter 33.2, ‘Chest decompression’

Key investigations

To establish the diagnosis

1. (1) Tension pneumothorax is a clinical diagnosis to be treated immediately without delay for investigation

Note:

• ◆ The signs of tension pneumothorax are not subtle, but you will not make the diagnosis unless you consider it and seek the presence of the signs listed above

• ◆ If a patient appears to be dying and you think that they might have a tension pneumothorax, then—after calling for help and initiating resuscitation (see 1.1 above)—there is nothing to be lost (and potentially much to be gained) from an attempt at chest decompression

• Other important tests:

• Chest radiograph will confirm diagnosis of pneumothorax after decompression

Further management

Insertion of chest drain (see Chapter 33.2, ‘Chest drain’) after tension has been relieved

Clinical features

History

1. (1) Worsening asthma

2. (2) Increasing difficulty breathing

3. (3) Decrease in exercise tolerance

4. (4) Increasing wheeze

5. (5) Chest tightness

6. (6) Cough

7. (7) Difficulty in speaking

8. (8) Fall in self-monitored peak flow

9. (9) Failure to obtain improvement with use of regular β₂-agonist

10. (10) Precipitating factor—exposure to known precipitant, e.g. exercise, cold air, dusty environment, upper respiratory tract infection

• Examination

• Moderate uncontrolled acute asthma:

  1. (1) Breathlessness

  2. (2) Wheeze

  3. (3) Chest tightness

  4. (4) Peak flow 50–70% of predicted or personal best

• Acute severe attack:

  1. (1) Cannot complete sentences in one breath

  2. (2) Increased respiratory rate (>25 breaths/min)

  3. (3) Use of accessory muscles of respiration

  4. (4) Tachycardia (>110/min)

  5. (5) Peak flow <50% of predicted or personal best

• Life-threatening asthma:

  1. (1) Exhaustion, confusion, or coma

  2. (2) Inability to speak

  3. (3) Cyanosis

  4. (4) Bradycardia or hypotension

  5. (5) Silent chest

  6. (6) Peak flow <33% of predicted or personal best (or unrecordable)

Notes

1. (1) A ‘normal’ respiratory rate is consistent with the patient being near to death if they are exhausted

2. (2) Always check carefully for signs of pneumothorax

3. (3) Always check pulse oximetry

4. (4) Asking the patient to count out loud as far as they can on a single breath provides a rapid, quantitative, and repeatable measure of respiratory function

Immediate management

• If cardiorespiratory collapse, as described in 1.2 above

• Moderate uncontrolled acute asthma:

  1. (1) β₂-Agonist via spacer and mask or nebulizer (see below)

  2. (2) Oral prednisolone 30 mg once daily

  3. (3) Inhaled steroids—commence or increase dose

• Acute severe attack:

  1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂>92%

  2. (2) Salbutamol 2.5–5 mg or terbutaline 5–10 mg via oxygen-driven nebulizer, repeated up to every 15–30 min as needed, and then 4 hourly

  3. (3) Steroids—hydrocortisone 200 mg IV four times daily or prednisolone 30–60 mg orally once daily

• Life-threatening attack or patient failing to improve:

• (1), (2), and (3) As for acute severe attack

  1. (4) Add ipatropium 0.5 mg to nebulized β₂-agonist

  2. (5) Consider magnesium sulphate 1.2–2 g IV over 20 min

  3. (6) Consider aminophylline, loading dose (in patient not previously treated with theophylline) of 5 mg/kg given IV over 20 min, then an infusion of 0.5 mg/kg per h aiming for serum concentration in the range 10–20 mg/litre. Omit loading dose if patient already taking oral theophylline

  4. (7) Consider IV salbutamol (3–20 µg/min) or terbutaline (1.5–5 µg/min) infusion

Notes

1. (1) Mechanical ventilation—if the patient is deteriorating, call for help from the ICU sooner rather than later. Elective endotracheal intubation and positive pressure ventilation is better than that done after cardiorespiratory arrest—indications are hypoxia (Pao₂ <8 kPa) despite Fio₂ 60%, hypercapnoea (Paco₂ >6 kPa), exhaustion with feeble respiratory effort, confusion/drowsiness, unconsiousness, respiratory arrest (to be avoided if possible)

2. (2) Fluids—give IV fluids to correct and prevent intravascular volume depletion/dehydration

Key investigations

To establish the diagnosis:

Acute asthma is a clinical diagnosis

Other important tests:

1. (1) Chest radiograph—exclude pneumothorax

2. (2) Arterial blood gases—markers for life-threatening asthma being normal or high Paco₂ (>5 kPa), low pH or high H⁺, severe hypoxia (Pao₂ <8 kPa) in spite of high flow oxygen treatment

3. (3) Electrolytes, renal and liver function, full blood count

Further management

1. (1) Optimization of long-term asthma management

2. (2) Education regarding how to recognize severe attacks and how to respond when they develop

Clinical features

History

1. (1) Breathing difficulty

2. (2) Flu-like prodrome

3. (3) High fever, sweats, rigors

4. (4) Pleuritic chest pain

5. (5) Sputum production (but note that this is not expected in atypical pneumonia)

6. (6) Travel

7. (7) Pet birds

Examination

1. (1) Severity of illness—exhaustion, use of accessory muscles and inability to talk in sentences all indicate severe illness and probable need for management on HDU/ICU

2. (2) Vital signs—temperature, pulse, BP—also peripheral perfusion (hot or cold)

3. (3) Respiratory —cyanosis, respiratory rate, focal lung signs (consolidation, pleural rub, pleural effusion)

4. (4) Sputum—inspect if any produced

5. (5) Pulse oximetry

Determination of severity

1. (1) Can be estimated using the six-point CURB-65 score, with one point scored for each of (a) Confusion; (b) Urea >7 mmol/litre; (c) Respiratory rate >30/min; (d) Systolic blood pressure <90 mmHg; (e) Diastolic Blood pressure <60 mmHg; (f) age >65 years.

2. (2) Depending on CURB-65 score, the risk of mortality or need for ICU admission is as follows: score 0, 0.7%; score 1, 3.2%; score 2, 13%; score 3, 17%; score 4, 41.5%; score 5, 57%

Immediate management

• If cardiorespiratory collapse, as described in 1.2 above

  1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂>92%

  2. (2) Appropriate antimicrobial agent

• British Thoracic Society guidelines for treatment of community-acquired pneumonia:

  • ◆ Mild/moderate pneumonia (CURB-65 score of 0–2)—oral therapy with extended spectrum penicillin (e.g. amoxicillin 250–500 mg three times daily) alone or with a macrolide (e.g. clarithromycin 250–500 mg twice daily). Omit the penicillin in patients with penicillin allergy

  • ◆ Severe pneumonia (CURB-65 score of 3 or more)—IV therapy with a second- or third-generation cephalosporin (e.g. cefotaxime 1 g twice daily) plus a macrolide (e.g. erythromycin 500 mg four times daily)

  • ◆ Suspected legionnaire’s disease—high-dose IV erythromycin (1 g four times daily) plus consider adding oral rifampicin (0.6–1.2 g daily in two to four divided doses)

• In areas/countries where there is serious concern that Strep. pneumoniae may be resistant to penicillin and other agents:

  • ◆ Mild/moderate pneumonia (CURB-65 score of 0–2)—second- or third-generation cephalosporin (e.g. cefotaxime 1 g IV twice daily) plus macrolide (e.g. erythromycin 500 mg orally or IV four times daily), or fluoroquinolone (e.g. levofloxacin 500 mg orally or IV once or twice daily) alone

  • ◆ Severe pneumonia (CURB-65 score of 3 or more)—second/third-generation cephalosporin (e.g. cefotaxime 1 g IV twice daily) plus macrolide (e.g. erythromycin 500 mg IV four times daily), or second-/third-generation cephalosporin (e.g. cefotaxime 1 g IV twice daily) plus fluoroquinolone (e.g. levofloxacin 500 mg IV twice daily)

Notes

1. (1) If staphylococcal pneumonia is suspected, add flucloxacillin 1 g IV four times daily (or vancomycin if methicillin-resistant Staph. aureus is proven or suspected)

2. (2) See Chapters 18.4.3 and 18.4.4 for discussion of antimicrobial treatment of patients with hospital-acquired pneumonia or pneumonia in immunocompromised patients

3. (3) Give IV fluids to maintain adequate intravascular volume/hydration

Key investigations

To establish the diagnosis:

1. (1) Chest radiograph—looking for focal consolidation (lobar pneumonia) or more widespread interstitial shadowing

2. (2) Blood culture

3. (3) Sputum culture

4. (4) Urinary pneumococcal antigen and legionella antigen tests

• To establish severity:

• Arterial blood gases—if patient is very ill or pulse oximetry shows Pao₂ <92%

• Other important tests:

• Full blood count, electrolytes, renal and liver function

Further management

Follow-up chest radiograph to ensure complete resolution

Clinical features

History

1. (1) Haematemesis or ‘coffee-ground’ vomiting

2. (2) Melaena

3. (3) Presyncope

4. (4) Indigestion or reflux or medication for these symptoms

5. (5) Retching before haematemesis (consider Mallory–Weiss tear)

6. (6) Previous upper gastrointestinal investigation or surgery

7. (7) To suggest recent development of anaemia

8. (8) Drugs that predispose to upper gastrointestinal haemorrhage—aspirin, nonsteroidal anti-inflammatory agents (NSAIDs), anticoagulants

9. (9) Risk factors for, or presence of, chronic liver disease (consider varices)

10. (10) Anorexia and weight loss (consider malignancy)

Examination

1. (1) State of circulation—temperature of peripheries, pulse rate, BP, JVP

2. (2) Mucous membranes—chronic anaemia

3. (3) Evidence of chronic liver disease—jaundice and other manifestations (consider varices)

4. (4) Evidence of portal hypertension—especially splenomegally (consider varices)

5. (5) Lymphadenopathy—especially in left supraclavicular fossa (consider malignancy)

6. (6) Abdomen—for epigastic mass (consider malignancy)

7. (7) Rectal examination—for blood/melaena

Notes

1. (1) The most reliable signs of intravascular volume depletion are severe postural (sitting vs lying, if standing not possible) dizziness, a postural rise in pulse rate of >30 beats/min, postural hypotension (>20 mmHg fall in systolic BP) and a low JVP

2. (2) Clinical assessment of severity, see Table 33.1.13

3. (3) Most likely diagnoses are peptic ulcer (35–50%), erosive disease (10–15%), oesophagitis (10%), Mallory–Weiss tear (5–10%) and oesophageal varices (5–10%). No cause can be established in 5–15% of cases

Immediate management

• If cardiorespiratory collapse, as described in 1.2 above

  1. (1) Establish IV access with one or more large-bore peripheral venous cannulae (look in the antecubital fossae in the patient who is shut down). If you cannot do this, then insert a femoral venous catheter (see Chapter 33.2, ‘Femoral vein cannulation’). DO NOT ATTEMPT TO INSERT AN INTERNAL JUGULAR OR SUBCLAVIAN VENOUS CATHETER INTO A PATIENT WHO OBVIOUSLY HAS SEVERE INTRAVASCULAR VOLUME DEPLETION (see Chapter 16.1 for discussion)

  2. (2) If clinical evidence of intravascular volume depletion, give 1000 ml of IV fluid (colloid, e.g Gelofusin, or 0.9% saline) as fast as possible. Repeat clinical examination. If the patient still has intravascular volume depletion, give further 500 ml of fluid as fast as possible. Repeat cycle until arterial pressure and JVP restored towards normal, then slow down rate of infusion. Use blood instead of colloid/saline as soon as it is available

  3. (3) Cross-match blood for transfusion

  4. (4) Consider need for urgent upper gastrointestinal endoscopy

  5. (5) If oesophageal varices—see Table 33.1.14

• Also:

  1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂>92%

  2. (2) Insert urinary catheter and monitor fluid input/output hourly in any patient with substantial gastrointestinal haemorrhage—a satisfactory urine output is the best gauge of adequate resuscitation

  3. (3) Correct any coagulopathy—see 1.9 above, Table 33.1.3 (iatrogenic overanticoagulation) and 9.1 below (disseminated coagulation)

  4. (4) Nurse to avoid aspiration, and do not insert nasogastric tube, which makes this more likely

Key investigations

• To establish the diagnosis (and also potentially therapeutic):

• ◆ pper gastrointestinal endoscopy:

  • ◆ Within 24 h of admission in anyone with a substantial gastrointestinal bleed

  • ◆ Urgently if oesophageal varices are suspected or the patient is actively bleeding

  • ◆ See Table 33.1.13 for assessment of risk of rebleeding and mortality after endoscopy

Other important tests:

1. (1) Full blood count—but remember that the initial haemoglobin concentration is a poor estimate of the volume of acute blood loss

2. (2) Electrolytes, renal and liver function tests

3. (3) Coagulation screen

4. (4) To pursue possibility and causes of chronic liver disease (if clinically indicated)

Further management

1. (1) Immediately inform surgical colleagues of all cases of substantial gastrointestinal haemorrhage

2. (2) Dependent on cause of haemorrhage, e.g.:

   • ◆ Acid suppression for ulcer healing—high-dose IV proton pump inhibitor, e.g. omeprazole 80 mg bolus followed by 8 mg/h for 72 h

   • ◆ Eradication of H. pylori

Clinical features

• History

• 1. (1) Haemorrhoids

  2. (2) Abdominal pain—if long-standing and intermittent may suggest diverticular disease, if severe may indicate mesenteric ischaemia

  3. (3) Previous lower gastrointestinal investigation or surgery

  4. (4) To suggest recent development of anaemia

  5. (5) Anorexia, weight loss, recent alteration in bowel habit (consider malignancy)

  6. (6) Drugs that predispose to gastrointestinal haemorrhage—aspirin, NSAIDs, anticoagulants

  7. (7) Risk factors for, or presence of, chronic liver disease (consider rectal varices)

  8. (8) Family history—colonic polyps/neoplasia, hereditary haemorrhagic telangiectasia

Examination

1. (1) State of circulation—temperature of peripheries, pulse rate, BP, JVP

2. (2) Mucous membranes—chronic anaemia

3. (3) Jaundice—suggests malignancy or chronic liver disease

4. (4) Lymphadenopathy—suggests malignancy

5. (5) Abdomen—for localized tendeness, peritonism, or palpable mass

6. (6) Rectal examination—for piles and blood

7. (7) Peripheral vasculature—generalized disease increases likelihood of mesenteric ischaemia

8. (8) Telangiectasiae on skin or mucosae

Notes

1. (1) The most reliable signs of intravascular volume depletion are severe postural (sitting vs lying, if standing not possible) dizziness, a postural rise in pulse rate of >30 beats/min, postural hypotension (>20 mmHg fall in systolic BP) and a low JVP

2. (2) Most likely diagnoses are diverticulosis (35%), colonic polyp or cancer (15%), inflammatory bowel disease (15%), benign anorectal conditions (10%), and angiodysplasia (10%).

Immediate management

If cardiorespiratory collapse, as described in 1.2 above

1. (1) Establish IV access—as in 3.1 above

2. (2) If clinical evidence of intravascular volume depletion, resuscitate as described in 3.1 above

3. (3) Cross-match blood for transfusion

Also:

1. (4) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂ >92%

2. (5) Insert urinary catheter and monitor fluid input/output hourly in any patient with substantial gastrointestinal haemorrhage—a satisfactory urine output is the best gauge of adequate resuscitation

3. (6) Correct any coagulopathy—see 1.9 above, Table 33.1.3 (iatrogenic overanticoagulation) and 9.1 below (disseminated intravascular coagulation)

Key investigations

• To establish the diagnosis:

• In all patients:

  1. (1) Proctoscopy and rigid sigmoidoscopy

As required:

1. (2) Colonoscopy

2. (3) Mesenteric angiography

Other important tests

1. (1) Full blood count

2. (2) Electrolytes, renal and liver function tests, coagulation screen, inflammatory markers

3. (3) To pursue possibility and causes of chronic liver disease (if clinically indicated)

Further management

1. (1) Inform surgical colleagues of all cases of substantial gastrointestinal haemorrhage immediately

2. (2) Dependent on cause of haemorrhage

Clinical features

History

1. (1) Bowel motions—frequency and type (blood, mucus, pus)

2. (2) Abdominal pain

3. (3) Rapidity of onset

4. (4) Systemic features—fever, malaise, anorexia

5. (5) Previous episodes/known colitic disease

6. (6) Recent diet (contaminated or infected food)

7. (7) Have close contacts also been ill?

8. (8) Recent antibiotic treatment (consider C. difficile)

9. (9) Use of NSAIDs

10. (10) Associated vomiting

11. (11) Travel

12. (12) Risk factors for HIV (in some cases)

Examination

1. (1) State of circulation—temperature of peripheries, pulse rate, BP, JVP

2. (2) Signs of toxicity—fever

3. (3) Mucous membranes—chronic anaemia, ulceration, candida

4. (4) Abdomen—for distension, localized tenderness, peritonism or palpable mass, or altered bowel sounds (absent, reduced)

5. (5) Rectal and perineal examination—for fistulas and nature of stool (blood, pus)

6. (6) Peripheral vasculature—generalized disease increases likelihood of ischaemic colitis

7. (7) Peripheral oedema—suggests hypoproteinaemia and chronic disease in this context

• Notes

• The most reliable signs of intravascular volume depletion are severe postural (sitting versus lying, if standing not possible) dizziness, a postural rise in pulse rate of >30 beats/min, postural hypotension (>20 mmHg fall in systolic BP) and a low JVP

Immediate management

• If cardiorespiratory collapse, as described in 1.2 above

  1. (1) Fluid and potassium resuscitation as necessary—see 3.1 above and 5.5 below

  2. (2) Most cases of acute colitis do not require antimicrobial therapy and settle with rehydration and time, the results of stool culture and rectal biopsy (which should be available in 24–48 h) being used to guide further treatment decisions. However, patients who are very ill with marked systemic symptoms and bloody diarrhoea (indicating probable colitis) should be given antimicrobial therapy pending culture results. Treat empirically with, e.g. ciprofloxacin (500–750 mg orally twice daily, or 200–400 mg IV twice daily) and metronidazole (400 mg orally three times daily or 500 mg IV three times daily), or—in parts of the world where gastrointestinal pathogens are likely to be resistant to fluoroquinolones—with azithromycin 250–500 mg four times daily

  3. (3) Also, in cases of known colitis (and to be considered in those with new and undiagnosed presentations of colitis), give steroids to those who are very ill, e.g. hydrocortisone 100 mg IV every 6 h and 100 mg as rectal drip twice daily

• Note the features of a severe acute attack of ulcerative colitis (Table 33.1.15)

Key investigations

• To establish the diagnosis:

• In all patients:

  1. (1) Abdominal radiograph—to assess extent of inflammation and to exclude toxic megacolon (required before proctoscopy/sigmoidoscopy), and erect chest radiograph—looking for air under diaphragm (perforation)

  2. (2) Flexible or rigid sigmoidoscopy and rectal biopsy

  3. (3) Stool—microscopy, culture, and testing for C. difficile toxin

  4. (4) Blood cultures

Other important tests

1. (1) Full blood count

2. (2) Group and save or cross-match blood

3. (3) Electrolytes, renal and liver function tests, inflammatory markers, coagulation screen

Further management

1. (1) Inform surgical colleagues of all cases of acute colitis, urgently if radiography shows perforation or toxic dilatation

2. (2) Nurse with appropriate barrier precautions (if possible) until infective cause excluded

3. (3) Further management dependent on cause of colitis

4. (4) Note that suspected or proven food poisoning and typhoid are notifiable diseases in the UK

Clinical features

Definitions

1. (1) Acute hepatic failure is hepatocellular jaundice, hypertransaminasaemia, and prolongation of the prothrombin time associated with an acute liver disease

2. (2) Fulminant hepatic failure is acute liver failure with hepatic encephalopathy, most definitions specifying that this must occur within a particular time (variable) from the onset of clinical evidence of liver disease (usually jaundice)

History

1. (1) Jaundice—not always present in fulminant hepatic failure

2. (2) Confusion/drowsiness—note timing of onset of mental changes in relation to jaundice

3. (3) Relevant to cause of acute liver failure, e.g. paracetamol overdose, full drug history (prescribed and nonprescribed), risk factors for viral hepatitis

4. (4) Is there a background of chronic liver disease?—alcohol, risk factors for viral hepatitis

5. (5) Autoimmune conditions (associated with autoimmune chronic active hepatitis)

6. (6) Family history (Wilson’s disease is a rare cause of fulminant hepatic failure)

Examination

1. (1) State of circulation—vital signs are normal in the early stages. Tachycardia and hypotension occur later. Hypertension and bradycardia are very late and sinister signs of cerebral oedema

2. (2) Jaundice

3. (3) Liver—usually tender, but normal size or only slightly enlarged in acute hepatic failure. If hepatomegaly consider hepatic venous obstruction (Budd–Chiari), malignant infiltration, chronic liver disease

4. (4) Ascites—if substantial consider Budd–Chiari syndrome

5. (5) Encephalopathy

   • ◆ Grade 1—mild confusion, irritability, decreased attention

   • ◆ Grade 2—drowsiness, lethargy, inappropriate behaviour

   • ◆ Grade 3—somnolent but rousable, disorientated

   • ◆ Grade 4—coma

6. (6) Signs of chronic liver disease

• Notes

• Focal neurological signs are not expected in acute hepatic failure. If present they suggest a focal cerebral lesion, most likely haemorrhage in this context

Immediate management

• If cardiorespiratory collapse, as described in 1.2 above

• Acute hepatic failure:

  1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve Pao₂>92%

  2. (2) Treat/prevent hypovolaemia—give 4.5% serum albumin IV to keep CVP at +10 cmH₂O. Give systemic vasopressor support (e.g. epinephrine, norepinephrine, dopamine) if fluid replacement fails to maintain mean arterial pressure of 50–60 mmHg.

  3. (3) Treat/prevent hypoglycaemia—give 50% glucose IV (central line) at 5–10 ml/h (monitor BM stix regularly)

  4. (4) Give prophylactic broad-spectrum antibiotic, e.g. cefotaxime 1 g IV twice daily

  5. (5) Give prophylaxis against gastrointestinal stress ulceration, e.g. ranitidine (150 mg orally twice daily, 50 mg IV three times daily)

  6. (6) Give N-acetylcysteine by IV infusion:

     • ◆ Paracetamol overdose: 150 mg/kg in 200 ml 5% dextrose over 15 min, then 50 mg/kg in 500 ml 5% dextrose over 4 h, then 100 mg/kg in 1000 ml 5% dextrose over 16 h

     • ◆ Other diagnosis: 150 mg/kg in 1000 ml 5% dextrose over 24 h

  7. (7) Give corticosteroids, e.g. prednisolone 40–60 mg/day, if acute liver failure is due to autoimmune hepatitis.

• Hepatic encephalopathy:

• To prevent or treat:

  1. (1) Removal or correction of precipitating factors

     • ◆ Drugs—stop all if possible, particularly sedatives/hypnotics and diuretics

     • ◆ Fluid and electrolyte balance—maintain carefully. Avoid/treat dehydration, hypoglycaemia, hypokalaemia, hypophosphataemia

  2. (2) Minimize absorption of nitrogenous substances. The following treatments may be given:

     • ◆ Enemas (MgSO₄ or phosphate) to encourage bowel emptying

     • ◆ Disaccharide laxative, e.g. lactulose 30–50 ml three times daily, dosage then adjusted to produce 2–3 soft stools daily

     • ◆ Broad-spectrum poorly-absorbed antibiotic, e.g. neomycin 1 g four times daily by mouth

  3. (3) If grade 3 or 4 encephalopathy, also

     • ◆ Intubate and ventilate

     • ◆ Give parenteral feeding

Notes

1. (1) Hyponatraemia is common and due to water excess rather than sodium deficiency. It should be treated with fluid restriction and not by infusion of saline

2. (2) If there is a history of chronic high alcohol intake or malnourishment, give thiamine IV BEFORE giving glucose to avoid risk of precipitating Wernicke’s encephalopathy, e.g. Pabrinex IV high-potency injection, 10 ml (2 ampoules) over 10 min (repeated three times daily)

3. (3) Insert urinary catheter and monitor fluid input/output hourly in any patient with acute hepatic failure

4. (4) Cerebral oedema:

   • ◆ Avoidance—avoid overfilling with IV fluids

   • ◆ Treatment—nurse in quiet room with trunk and head elevated at 40°; consider transfer to facility where intracranial pressure can be monitored; consider mannitol 1 g/kg as IV bolus of 20% solution (if plasma osmolality <315 mosmol/kg and the patient is not oliguric), repeated 4 hourly (0.5 g/kg) if previous infusion induced a diuresis

Key investigations

To establish the presence of acute liver failure:

1. (1) Liver blood tests—bilirubin, transaminases (ALT, AST, gGT)

2. (2) Prothrombin time/coagulation screen

• To establish the cause of liver disease:

• If no history of paracetamol overdose

  1. (1) Hepatitis B core IgM, hepatitis A IgM, liver autoantibodies, immunoglobulins

  2. (2) Abdominal ultrasound and Doppler of hepatic veins—looking for size/echogenicity of liver, splenomegaly, signs of Budd–Chiari

  3. (3) If <40 years: serum copper and caeruloplasmin; ophthalmic examination for Kayser–Fleischer rings (Wilson’s disease)

Notes

1. (1) Tap ascites if present—microscopy, culture, and sensitivity. Culture/swab blood, urine, nasal, high vagina

2. (2) Do not correct coagulopathy unless the patient is bleeding: the prothrombin time is an important prognostic indicator. If bleeding, or to cover invasive procedures, give vitamin K 10 mg IV, fresh frozen plasma and platelets, and maintain haematocrit 30–35% by blood transfusion.

3. (3) Where the prothrombin time (in s) is greater than the time after a paracetamol overdose (in h), there is a substantial risk of developing acute liver failure

Other important tests:

1. (1) Full blood count

2. (2) Glucose, renal function tests, amylase

3. (3) Arterial blood gases

Further management

1. (1) Discuss all cases of acute hepatic failure with a specialist (transplant) centre (see Table 33.1.16): urgent orthotopic liver transplantation may be required and appropriate

2. (2) Dependent on cause of hepatic failure

Clinical features

• History

• 1. (1) Abdominal pain—duration, constant or colicky, where is it worst (point with one finger), radiation

  2. (2) Gastrointestinal symptoms—anorexia, nausea, vomiting, diarrhoea, constipation (precisely when were the bowels last open), blood in vomit or stool

  3. (3) Urinary symptoms—frequency, pain on micturition, haematuria

  4. (4) Gynaecological symptoms—last menstrual period, vaginal discharge

  5. (5) To suggest sepsis—sweats, fevers, rigors

  6. (6) History of gastrointestinal problems—indigestion, peptic ulceration, gallstones, pancreatitis

  7. (7) History of atheromatous vascular disease—ischaemic heart disease, cerebrovascular disease, peripheral vascular disease (increase the likelihood of bowel ischaemia or of abdominal aortic aneurysm, also relevant to surgical risk)

Examination

1. (1) State of circulation—temperature of peripheries, pulse rate, BP, JVP

2. (2) Signs of toxicity—fever

3. (3) Foetor

4. (4) Abdomen:

   • ◆ Inspection—distension, movement on respiration

   • ◆ Palpation—tenderness, guarding, rigidity, rebound tenderness, palpable mass

   • ◆ Auscultation—bowel sounds

   • ◆ Check all hernial orifices and abdominal aorta

5. (5) Rectal examination—for tenderness and nature of stool, blood in stool

6. (6) Vaginal examination—tenderness, pelvic mass

7. (7) Test urine for blood

• Note

• The likely cause of abdominal pain depends on the context. Cases presenting in the community that require assessment in hospital will generally be referred directly to surgical services, and many will have ‘obvious’ diagnoses such as appendicitis. Patients presenting to medical services or who develop abdominal pain when already on a medical ward will generally be older and with multiple comorbidities, and are much more likely to have intestinal vascular events or obstruction due to malignancy

Immediate management

If cardiorespiratory collapse, as described in 1.2 above

1. (1) Establish IV access—as in 3.1 above

2. (2) If clinical evidence of intravascular volume depletion, resuscitate as described in 3.1 above

3. (3) Urgent liaison with surgical colleagues

4. (4) Analgesia—give adequate pain relief, e.g.:

   • ◆ NSAID: e.g. diclofenac 75 mg intramuscularly, repeated after 30 min if necessary

   • ◆ Opioid: e.g. morphine 5 mg subcutaneously plus 5 mg intramuscularly, repeated if necessary and accompanied by appropriate antiemetic, e.g. metoclopramide 10 mg IV over 1–2 min, or cyclizine 50 mg IV over 1–2 min

5. (5) Nasogastric tube—when there is continued vomiting and/or suspected intestinal obstruction

6. (6) Urinary catheter

Key investigations

To establish the diagnosis:

1. (1) Supine abdominal radiograph—is there intestinal obstruction (seldom indicates cause)? Is there a urinary stone (CT preferred imaging technique)?

2. (2) Erect chest radiograph—is there gas under the diaphragm indicating intestinal perforation?

3. (3) Serum amylase—a substantial increase suggests pancreatitis

4. (4) Abdominal CT scan—increasingly used in the management of patients with acute abdominal pain

5. (5) Abdominal ultrasound—when acute gallbladder disease is suspected

• Note

• Patients with generalized peritonitis require an urgent laparotomy provided that pancreatitis has been excluded. Do not delay: if the patient requires resuscitation, then make arrangements for theatre whilst initiating resuscitation and continue to resuscitate in the anaesthetic room. Do not wait ‘until the patient is a bit better’ before involving anaesthetic and surgical colleagues

Other important tests:

1. (1) Full blood count

2. (2) Group and save or cross-match blood

3. (3) Electrolytes, renal and liver function tests

4. (4) Coagulation screen

Further management

Dependent on the cause of the acute abdomen