Clinical features

History

1. (1) Sudden collapse

Examination

1. (1) Patient unresponsive

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

3. (3) Circulation—pulse not palpable

Immediate management

See Figs. 30.1.1 and 30.1.2

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 ‘Upper airway obstruction’)

4. (4) Widespread crackles in the chest—suggests pulmonary oedema in this context (see ‘Pulmonary oedema’).

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 intensive care unit 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 30.1.1 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 oxygen saturations >92%

3. (3) If tension pneumothorax, decompress immediately (see Chapter 30.2, ‘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 30.2)

Also: begin resuscitation according to volume status as indicated in Table 30.1.2

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. co-amoxiclav 1.2 g IV 6–8-hrly, as dictated by clinical suspicion of likely pathogen (see ‘Septic shock’)

Key investigations

See Table 30.1.1

Further management

Determined by underlying condition

Hypotension

Peripheries cool and shut down

Intravenous fluid (0.9% saline or other crystalloid with sodium concentration in range 130–154 mmol/litre) given rapidly (0.5 litre boluses) until there is clear evidence that physical signs are being restored to normal, then slow rate infusion

Postural rise in pulse rate

Postural hypotension

Low jugular venous pressure

Lungs clear

Breathing difficulty

High jugular venous pressure

Do not give fluid

Gallop rhythm

Sit up

Basal crepitations

Consider intravenous loop diuretic and/or venodilator

Consider need for ventilation

Hypotension and breathing difficulty

Peripheries cool and shut down

Will almost certainly need urgent ventilation

High jugular venous pressure

Call for help from ICU/anaesthetist before the patient suffers cardiorespiratory arrest

May be gallop rhythm

Trial of fluid infusion may be appropriate: give 250 ml of 0.9% saline or other crystalloid with sodium concentration in range 130–154 mmol/litre, keeping patient under continuous observation and terminating infusion immediately in the event of clinical deterioration

Basal crepitations

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 ‘Pulmonary oedema’

3. (3) Cardiac—gallop rhythm, murmurs

Immediate management

If cardiorespiratory collapse, as described in ‘Cardiorespiratory collapse: the patient in extremis’

Otherwise:

1. (1) Oxygen—if needed, to achieve oxygen saturations >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 30.1.3), or (b) thrombolysis, if primary PCI not available or transfer times mean reperfusion may not be achieved within 120 min of symptom onset (Table 30.1.4)

Key investigations

To establish the diagnosis:

1. (1) ECG—looking for ST-segment elevation and/or (presumed or proven) new left 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)

   • • ADP receptor antagonists—e.g. 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 a statin will benefit most patients with coronary heart disease.

5. (5) Control of diabetes—some evidence supports the use of insulin in hospital to maintain blood glucose concentration <11 mmol/litre (but avoiding hypoglycaemia) 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 good control 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

Primary PCI is the best management for STEMI when it can be performed:^a

1. (1) Within 60–90 min of admission

2. (2) By individuals skilled in the procedure (>75 cases/year)

3. (3) In a high-volume centre (>200 cases/year)

Primary PCI is specifically indicated when there is:

1. (1) Contraindication to thrombolysis

2. (2) Haemodynamic compromise

Primary PCI should be considered as:

1. (3) Salvage procedure after failed thrombolytic therapy

Must satisfy three criteria:

1. (1) Typical chest pain at rest for >20 min

2. (2) ST elevation in two contiguous leads (≥1 mm inferiorly, ≥2 mm anteriorly), or (presumed or proven) new left bundle branch block

3. (3) Within 12 h of onset, but consider at 12–24 h if continuing pain

Absolute contraindications

1. (1) Bleeding—active internal bleeding; proven active peptic ulcer

2. (2) Brain—cerebrovascular accident within the past 6 months (or at any time if haemorrhagic stroke); known intracranial neoplasm or aneurysm

3. (3) Suspected aortic dissection

4. (4) Uncontrolled hypertension—SBP >180 mmHg or DBP >110 mmHg after pain relief and nitrates

5. (5) Pregnancy

Relative contraindications

1. (1) Recent (<6 weeks) major trauma/surgery/injury or traumatic resuscitation (>10 min or sufficient to fracture rib)

2. (2) Symptoms suggesting active peptic ulceration

3. (3) Defective haemostasis

4. (4) Lactation/peripartum

5. (5) Severe liver disease/oesophageal varices

6. (6) Severe renal disease

7. (7) Bacterial endocarditis

8. (8) Acute pancreatitis

9. (9) On warfarin with INR outside therapeutic range

Note that the following are not contraindications:

1. (1) Proliferative diabetic retinopathy

2. (2) Previous cardiopulmonary resuscitation, unless this is prolonged (>10 min) or associated with obvious trauma

3. (3) Therapeutic anticoagulation

Examples of agents

(1) Recombinant tissue-type plasminogen activator, e.g.

Alteplase

Accelerated regimen (within 6 h of AMI): 15 mg by IV injection, followed by IV infusion of 50 mg over 30 min, then 35 mg over 60 min (lower doses in patients <65 kg). This is the reference standard for comparison of other fibrinolytic agents/regimen

Standard regimen (6–12 h from AMI): 10 mg by IV injection, followed by IV infusion of 50 mg over 60 min, then 40 mg over 120 min (lower doses in patients <65 kg)

Tenecteplase

30–50 mg (6000–10 000 units, depending on body weight) by IV injection over 10 s. This does not require infusion pump or refrigeration and is particularly suited for prehospital administration as should be given within 6 h of symptom onset

Reteplase

10 units intravenously over not more than 2 min, followed 30 min later by another 10 units intravenously over not more than 2 min

(2) Streptokinase

1 500 000 units by IV infusion over 60 min. This remains the most widely used fibrinolytic agent internationally because it is relatively cheap

Common

Hypotension (SBP <90 mmHg)

Stop infusion until blood pressure recovers

Recommence infusion more slowly (to complete over 2 h) OR switch to rt-PA regimen (see Table 30.1.4)

Rigors

Stop infusion until rigor settles

Recommence infusion more slowly (to complete over 2 h) OR switch to rt-PA regimen (see Table 30.1.4)

Ventricular fibrillation

Cardiovert

Continue infusion at usual rate

Uncommon

Allergic reaction

Stop infusion

Recommence infusion more slowly if possible (to complete over 2 h) OR switch to rt-PA regimen (see Table 30.1.4)

Give hydrocortisone 100 mg IV and chlorpheniramine 10 mg IV

Haemorrhage (major)

Stop infusion

Consider fresh frozen plasma/cryoprecipitate

Stroke

Stop infusion

Urgent CT head

Clinical features

History

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

2. (2) Chest tightness/breathlessness

Examination

• • Usually no specific signs, but may be:

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

  2. (2) Pulmonary oedema—breathing difficulty, pulmonary crackles (see ‘Pulmonary oedema’)

  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 https://www.mdcalc.com/timi-risk-score-ua-nstemi); (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 ECG, normal biomarkers, normal cardiac examination and normal echo.

High-risk category

1. (1) Oxygen—to achieve oxygen saturations >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 ‘ST-segment elevation acute myocardial infarction (STEMI)’) 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 for high-risk category, 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 fulfil guideline criteria for glycoprotein IIb/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 ‘ST-segment elevation acute myocardial infarction (STEMI)’)

Further management

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

2. (2) Angiotensin-converting enzyme 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:

1. (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) Chest pain, particularly if of sudden onset, tearing in quality, and radiating to the back

2. (2) Collapse

Examination

1. (1) Patient will usually look very unwell and cool peripherally. BP may be low, normal, or raised. Pulse may be slow.

2. (2) Look for loss/reduction of one or more peripheral pulses: most likely is compromise of the left subclavian artery. Check left radial pulse in comparison with right; measure BP in both arms; any deficit on the left strongly supports the diagnosis of aortic dissection. Examine also for reduction of carotid or femoral pulse(s)

3. (3) Look for signs of new aortic regurgitation—note that the diastolic murmur may be very short

4. (4) Evidence of focal ischaemia, e.g. focal neurological deficit (‘stroke’)

5. (5) Could the patient have Marfan’s syndrome? (risk factor)

Immediate management

If cardiorespiratory collapse, as described in ‘Cardiorespiratory collapse: the patient in extremis’

1. (1) The key to correct management is a high index of clinical suspicion that aortic dissection might be the diagnosis. Most patients with chest pain and circulatory collapse have acute myocardial infarction, the management for which (thrombolysis) could clearly be fatal in the patient with aortic dissection

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

3. (3) 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)

Key investigations

To establish the diagnosis:

1. (1) CT angiography of chest

2. (2) Transoesophageal echocardiography

3. (3) MRI of chest

Other important tests:

1. (1) Chest radiograph—look for widened mediastinum

2. (2) ECG—may have features of acute myocardial infarction (usually inferior) if dissection has compromised a coronary artery (usually right coronary artery)

3. (3) Cardiac biochemical markers—to exclude acute myocardial infarction, but note that elevation of troponin can occur

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

5. (5) Group and save/cross-match blood

Further management

1. (1) Reduce BP using agents that will not cause tachycardia or increase the rate of cardiac ejection, e.g. titrate IV labetalol (initial dose 50 mg bolus, followed by 1–2 mg/min) or esmolol (50–200 µg/kg/min) to achieve systolic BP <120 mmHg. If BP remains too high, add IV infusion of sodium nitroprusside (0.5–8 µg/kg/min) after β‎-blockade established (pulse <60/min)

2. (2) Obtain opinion from cardiothoracic surgeon: immediate surgical repair will usually be the best management for patients with dissection of the ascending aorta (Stanford type A) who are in reasonable condition, but medical treatment is generally recommended (as long as the dissection does not progress) when the ascending aorta is spared (type B)

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 ‘Pulmonary oedema’)?

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 ‘Hypothermia’)

Immediate management

Obtain ECG

If the patient is haemodynamically compromised:

1. (1) Give atropine, 0.5 mg IV (repeat to maximum of 3 mg)

2. (2) Consider isoprenaline, 1–10 µg/min by IV infusion

3. (3) Consider temporary pacing (see Chapter 30.2, ‘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 ‘Pulmonary oedema’)?

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 ‘Cardiorespiratory collapse: the patient in extremis’

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 30.1.6)

2. (2) Uncertain of the diagnosis of a broad complex tachycardia? See Table 30.1.7

3. (3) IV adenosine (administered as described later in this table)—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, 300 mg in 30–60 min followed by 900 mg/24 h until sinus rhythm restored (into central venous catheter), or

• • Sotalol, 2 mg/kg IV over 30 min

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

• • Adenosine, 6 mg by fast IV injection, if necessary followed by 12 mg (also by fast IV injection) after 1–2 min, and then by a further 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). Monitor/record ECG continuously.

• • 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 ‘Cardiac arrest’)

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

• • Lidocaine (lignocaine) 100 mg as IV bolus over a few min followed immediately by infusion of 1–4 mg/min

• • 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

AV dissociation—capture/fusion beats

The most reliable criterion for VT

Both occur rarely, but their presence usually secures the diagnosis of VT

Wide QRS complex

QRS width (s)

Predictive value for VT (%)

<0.12

14

0.12–0.14

43

>0.14

100

Concordance across chest leads

QRS complexes all positive or all negative is reliable pointer to VT

Extreme left axis deviation and/or a definite axis shift compared with previous ECGs

Strong indicator of VT

History

Myocardial infarction, ischaemic heart disease, or congestive heart failure present

VT

ECG

Features in Table 30.1.6 present

VT

Effect of adenosine

Inconclusive

VT

(Given as described in ‘Tachycardia’)

Reversion of tachycardia

AVNRT or AVRT (SVTs). May also reveal (but unlikely to revert) atrial flutter or fibrillation

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 ‘Cardiorespiratory collapse: the patient in extremis’

2. (2) Respiratory rate, cyanosis, peripheral circulation (cold, clammy), pulse rate and rhythm (?arrhythmia, see ‘Bradycardia’ and ‘Tachycardia’), 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 ‘Cardiorespiratory collapse: the patient in extremis’

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

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

3. (3) Give furosemide 40–80 mg IV

If not improving rapidly:

1. (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)

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

3. (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 (including troponin and NT-proBNP)

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 ‘ST-segment elevation acute myocardial infarction (STEMI)’

2. (2) Arrhythmia—see ‘Bradycardia’ and ‘Tachycardia’

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 pulmonary embolus (PE)

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

DVT:

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

PE:

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 ‘Cardiorespiratory collapse: the patient in extremis’. 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:

PE:

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

DVT and PE:

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 earlier in this table

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 30.1.8

• • PE—see Table 30.1.9

Further management

1. (1) Anticoagulation with low molecular weight heparin (typical dose 200 IU/kg subcutaneous once daily, but see manufacturer’s instructions) or standard (unfractionated) heparin (Table 30.1.10) until oral anticoagulation with warfarin (Table 30.1.11) or a direct oral anticoagulant (DOAC, Table 30.1.12) 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 (alteplase), 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 30.1.13

Active cancer

+1

Paralysis, plaster cast

+1

Bed rest >3 days, surgery within 4 weeks

+1

Tenderness along veins

+1

Entire leg swollen

+1

Calf swollen >3 cm

+1

Pitting oedema

+1

Collateral veins

+1

Alternative diagnosis likely

–2

Low

0

Moderate

1–2

High

≥3

0 or 1

Perform D-dimer^*

Negative

No further investigation

Positive

Perform ultrasonography

2 or more

Do not perform D-dimer^*

Perform ultrasonography

Negative

Withhold treatment and repeat ultrasonography in 1 week.

If serial ultrasonography is negative, PE rarely occurs

Positive

Diagnosis of DVT established

Clinical signs and symptoms of DVT (objectively measured leg swelling and pain with palpation in the deep vein system)

3.0

Heart rate >100/min

1.5

Immobilization ≥3 consecutive days (bed rest except to access bathroom) or surgery in previous 4 weeks

1.5

Previous objectively diagnosed PE or DVT

1.5

Haemoptysis

1.0

Malignancy (cancer patients receiving treatment within 6 months or receiving palliative treatment)

1.0

PE as likely or more likely than alternative diagnosis (based on history, physical examination, chest radiograph, ECG, and blood tests)

3.0

Low

<2

Unlikely

≤4

Likely

>4

High

>6

<2

Perform D-dimer

Negative

No further investigation

Positive

Perform CT pulmonary angiography (CTPA)

2 or more

Do not perform D-dimer

Perform CTPA

Negative

Positive

PE is excluded

Diagnosis of PE established

50

1.8

60

2.2

70

2.5

80

2.9

90

3.2

100

3.6

120

4.4

(4) Check APTT 6 h after start of treatment and then at least once daily, adjusting the infusion rate according to the APTT as follows:

>7.0

Stop for 30 min and then reduce by 1.0 ml/h (check APTT 4 h later)

5.1–7.0

Reduce by 1.0 ml/h (check APTT 4 h later)

4.1–5.0

Reduce by 0.6 ml/h (check APTT 4 h later)

3.1–4.0

Reduce by 0.2 ml/h

2.6–3.0

Reduce by 0.1 ml/h

1.5–2.5

No change

1.2–1.4

Increase by 0.4 ml/h

<1.2

Increase by 0.8 ml/h (check APTT 4 h later)

Direct thrombin inhibitor

Dabigatran

150 mg twice daily

Heparin given for first 5 days

Direct Xa inhibitors

Rivaroxaban

15 mg twice daily for 3 weeks, then 20 mg od

Heparin not required

Apixaban

10 mg twice daily for 1 week, then 5 mg twice daily

Heparin not required

Edoxaban

60 mg once daily (patient >60 kg)

30 mg once daily (patient <60 kg)

Heparin given for first 5 days

Standard (unfractionated) heparin

1. (1) Stop heparin

2. (2) Give protamine by slow IV injection: 1 mg neutralizes 100 units of heparin if given within 15 min of heparin. Give less if a longer time has elapsed because heparin is rapidly excreted. Maximum dose of protamine is 50 mg

1. (1) There is no point in giving FFP or other clotting concentrates: they do not contain heparin-neutralizing activity

2. (2) Excess protamine is anticoagulant

LMWH

1. (1) Stop heparin

2. (2) Administer protamine by slow IV injection, maximum 50 mg. This is less effective at neutralizing the effect of LMW heparin than it is for standard heparin. There is no good evidence on which to base dosage

1. (1) There is no point in giving FFP or other clotting concentrates: they do not contain heparin-neutralizing activity

2. (2) Excess protamine is anticoagulant

Warfarin

Immediate reversal (e.g. patient has major bleeding with high INR)

1. (1) Stop warfarin

2. (2) Vitamin K 5 mg (IV)

3. (3) FFP 15 ml/kg (IV), or PCC 50 IU/kg (IV).

4. (4) Recheck INR

1. (1) Large volumes of FFP (up to 2 litres) can be required to effect complete reversal of warfarin

2. (2) PCC should be used for life-threatening bleeding

3. (3) Continue warfarin in lower dose if risk/benefit considerations indicate that continued anticoagulation is justified when INR back in therapeutic range

Controlled reversal (e.g. high INR but patient is not bleeding or has minor bleeding only)

1. (1) INR <8. Stop warfarin. Re-check INR in 3 days

2. (2) INR 8–12. Stop warfarin. Give vitamin K 2.5 mg PO or 0.5 mg IV. INR rechecked in 24 h should show a fall

3. (3) INR >12. Stop warfarin. Give vitamin K 5 mg PO or 1 mg IV. INR rechecked in 24 h should show a fall

Dabigatran

Idarucizumab 2.5 g IV; two doses within no more than 15 min (total 5 g)

Rivaroxaban

Apixaban

Edoxaban

Andexanet alfa—granted final approval by FDA in January 2019 and conditional marketing authorisation in EC in April 2019 but robust evidence of efficacy is lacking (main clinical trial gave bolus 400–800 mg over 15–30 min followed by infusion of 480–960 mg over 2 h)

Clinical features

History

1. (1) Shortness of breath or circulatory collapse, but there are no specific symptoms

2. (2) Can follow acute myocardial infarction, aortic dissection, cardiac trauma (including iatrogenic with cardiac catheterization)

3. (3) There may be evidence of a condition that can cause pericardial effusion, e.g. tuberculosis, cancer, advanced renal failure

Examination

The key to making this rare but very important (because treatable) diagnosis is to consider it in any patient with unexplained cardiorespiratory collapse. Signs of tamponade are:

1. (1) Grossly elevated JVP—which may rise further on inspiration (Kussmaul’s sign)

2. (2) Pulsus paradoxus—an exaggerated fall in systolic BP on inspiration (normal <10 mmHg), but a rapid screening test for severe cases is to ask ‘Does the radial pulse disappear on inspiration’?

   Evidence of a (large) pericardial effusion, although these will not be present unless there is a pre-existing effusion

3. (3) Increased area of cardiac dullness

4. (4) Quiet heart sounds

Immediate management

If the patient is in extremis proceed as in ‘Cardiorespiratory collapse: the patient in extremis’

1. (1) Give sodium chloride 0.9% 500 ml by rapid IV infusion, to support BP

2. (2) Perform or arrange for immediate/urgent pericardial aspiration (see Chapter 30.2, ‘Pericardiocentesis’)

Key investigations

To establish the diagnosis:

1. (1) Echocardiography

   • • The most sensitive test for the presence of pericardial fluid

   • • Diastolic collapse of right ventricle or right atrium indicates severe circulatory embarrassment

2. (2) Cytology and culture of pericardial fluid

Other important tests:

1. (1) Chest radiograph—look for globular heart (almost invariably with clear lung fields)

2. (2) ECG—look for low voltage QRS complexes and electrical alternans (in large pericardial effusion) and for evidence of acute myocardial infarction

Further management

As determined by underlying condition

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 ‘Pulmonary oedema’

2. (5) Aortic dissection—see ‘Dissection of the thoracic aorta’

3. (6) Scleroderma—scleroderma renal crisis

Immediate management

In an uncomplicated case:

1. (1) Admit to hospital, or commence treatment, initiate investigations and follow-up within a few days in an ambulatory care setting

2. (2) Avoid strenuous activity

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. (1) Admit to hospital

2. (2) Bed rest

3. (3) No smoking

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

   • • Labetalol, initial bolus of 20 mg IV, then at 0.5–2 mg/min, or

   • • Sodium nitroprusside (IV) at initial dose of 0.25–0.5 µg/kg per min, increasing up to 8–10 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 ‘Dissection of the thoracic aorta’)

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 oxygen saturations >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 0.9% saline or other crystalloid with sodium concentration in range 130–154 mmol/litre, 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):

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

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

7. (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)

8. (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) Chronic respiratory condition—usually chronic obstructive pulmonary disease

2. (2) Recent increase in breathlessness

3. (3) Evidence of infection—fever, sweats, increased sputum production, increased sputum purulence

4. (4) ‘Cor pulmonale’—worsening ankle oedema

Examination

1. (1) Cyanosis

2. (2) Respiratory rate

3. (3) Temperature

4. (4) Evidence of CO₂ retention—drowsiness, asterixis, metabolic flap

5. (5) Chest signs—of chronic respiratory condition, of infection, and exclude pneumothorax

6. (6) Signs of cor pulmonale—elevated JVP, right ventricular heave, right ventricular gallop, loud P2, congested liver, ascites, peripheral oedema

7. (7) Check peak expiratory flow rate if patient is able to use peak expiratory flow recorder

8. (8) Check pulse oximetry. Is the patient getting exhausted? Remember that a ‘normal’ respiratory rate in the patient who looks very tired may mean that they are close to death

Immediate management

The patient who is extremely ill

If the patient is in extremis, proceed as in ‘Cardiorespiratory collapse: the patient in extremis’, with the exception that a high concentration of inspired oxygen should NOT be given to patients who are KNOWN to have acute on chronic respiratory failure. If the patient is known to have chronic respiratory failure:

1. (1) Give controlled oxygen (24–28% or 1–2 litres/min by nasal prongs), aiming to achieve Pao₂ >8 kPa (60 mmHg) or Sao₂ >90% without CO₂ retention or acidosis

2. (2) Initiate other aspects of management listed later in this table

3. (3) Check arterial blood gases, adjusting inspired oxygen concentration if allowed by clinical response, Pao₂, Paco₂, and pH (pH, not hypoxia, is the most important factor related to survival in patients with acute on chronic respiratory failure)

   Consider need for ventilatory support:

   • • Noninvasive positive pressure ventilation (NIV)—particularly in patients with exacerbation of chronic obstructive pulmonary disease who have persistent respiratory acidosis (pH <7.35) despite controlled oxygen therapy and maximal medical therapy—proceeding if required and if appropriate to

   • • Endotracheal intubation and intermittent positive pressure ventilation

Note—if it is uncertain whether or not a patient has acute on chronic respiratory failure, then high concentration oxygen should be given to all patients who are extremely ill. All such patients require continued close monitoring of their clinical state and arterial blood gases, allowing (among other things) detection of the few who will have acute on chronic respiratory failure and lose their respiratory drive in response to high concentration oxygen

The patient who is moderately unwell

1. (1) Give controlled oxygen (24–28% or 1–2 litres/min by nasal prongs), aiming to achieve Pao₂ >8 kPa (60 mmHg) or Sao₂ >90% without CO₂ retention or acidosis. Check arterial blood gases after 30–60 min

2. (2) Give nebulized β‎₂-agonist, e.g. salbutamol 2.5–5 mg, terbutaline 5–10 mg, using air as the driving gas, repeated as required, while continuing to deliver oxygen by nasal prongs at 1–2 litre/min

3. (3) Give nebulized anticholinergic, e.g. ipratropium bromide 500 µg (can be combined with β‎₂-agonist), repeated as required

4. (4) Give corticosteroid, e.g. hydrocortisone 100 mg IV twice daily or prednisolone 30 mg orally once daily (continued for 7–14 days)

5. (5) Give antibiotic that will cover likely respiratory pathogens if two of the following symptoms are present—increased breathlessness, increased sputum volume, or increased sputum purulence, e.g. amoxicillin 250 mg orally three times daily or (if allergic to penicillin) clarithromycin 250–500 mg orally twice daily (IV if oral administration not possible)

6. (6) Give diuretic, e.g. furosemide 40–80 mg IV, if evidence of fluid overload

7. (7) 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

8. (8) Consider need for ventilatory support, usually by NIV, if patient does not improve

Note—use IV fluids to correct and prevent dehydration

Key investigations

To establish the diagnosis:

1. (1) Chest radiograph—looking for focal consolidation and to exclude pneumothorax

2. (2) Sputum culture

   To determine severity and monitor response to treatment:

3. (3) Arterial blood gases

4. (4) Serial measurements of peak flow

Other important tests:

1. (1) Full blood count

2. (2) Electrolytes, renal and liver function

3. (3) ECG

Further management

1. (1) Optimization of treatment for chronic pulmonary condition, usually chronic obstructive pulmonary disease

2. (2) Emphasize need to stop smoking

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 30.2, ‘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 earlier in this table

• • 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 ‘Cardiac arrest’)—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 30.2, ‘Chest drain’) after tension has been relieved

Clinical features

History

1. (1) Extreme difficulty in breathing

2. (2) Coughing/choking

3. (3) Noisy breathing

4. (4) Difficult/unable to speak

5. (5) ‘Something stuck’

Examination

1. (1) Extreme but ineffective respiratory effort

2. (2) Cyanosis

3. (3) Drooling (cannot swallow saliva)

4. (4) Stridor

Immediate management

1. (1) If cough ineffective, give five back blows with patient leaning forward (to ensure object is projected from mouth rather than forced further down the airway if it moves).

2. (2) If back blows ineffective then give five abdominal thrusts (Heimlich manoeuvre) if the patient has inhaled a foreign body:

   • • Patient sitting or standing—rescuer stands or kneels behind patient, encircling the patient’s waist with their arms, placing one fist just above the navel (well below xiphoid process) and using their other hand to press the fist into the patient’s abdomen with a quick upward thrust. Repeat as necessary

   • • Patient lying—place patient on their back. Rescuer kneels astride patient and puts the palm of one hand between the navel and xiphisternum, places their other hand on top of this, and pushes upwards and inwards

3. (3) If abdominal thrusts (Heimlich manoeuvre) is inappropriate or has failed, continue to alternate back blows and chest thrust or:

   • • If there is time and you have the expertise—spray the pharynx with local anaesthetic (e.g. 5% cocaine and adrenaline) and examine the pharynx and upper airway by indirect laryngoscopy to establish the cause of obstruction and allow (if possible) its removal (with finger sweep under direct vision or long-handled forceps) or passage of an endotracheal tube

   • • If there is time and you are not experienced in upper airway management—call immediately for help from anaesthetic or ear, nose, and throat (ENT) colleagues

   • • If there is no time—call cardiac arrest team

Key investigations

To establish the diagnosis:

• • Upper airway obstruction is a clinical diagnosis

Other important tests:

As dictated by cause of obstruction

Further management

As dictated by cause of obstruction; see Chapter 30.2, ‘Cricothyroidotomy’

Clinical features

History

1. (1) Worsening asthma

2. (2) Increasing difficulty in 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 ‘Cardiorespiratory collapse: the patient in extremis’

Moderate uncontrolled acute asthma:

1. (1) β‎₂-Agonist via spacer and mask or nebulizer (see later in this table)

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 oxygen saturations >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-hrly

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

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

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

6. (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

7. (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 intensive care unit 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, unconsciousness, 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 high dependency unit/intensive care unit

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 intensive care unit 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 ‘Cardiorespiratory collapse: the patient in extremis’

1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve oxygen saturations >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 500 mg three times daily) alone or with a macrolide (e.g. clarithromycin 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 broad-spectrum β‎-lactamase stable antibiotic (e.g. co-amoxiclav 1.2 g three times daily) plus a macrolide (e.g. clarithromycin 500 mg twice daily). In penicillin-allergic patients, a second- (e.g. cefuroxime) or third-generation (e.g. ceftriaxone) cephalosporin can be used instead of co-amoxiclav

   • • Suspected legionnaire’s disease—fluoroquinolone (e.g. ciprofloxacin 500 mg twice daily PO) and macrolide (e.g. clarithromycin 500 mg twice daily PO) 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 Streptococcus 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 clarithromycin 500 mg IV twice 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 clarithromycin 500 mg IV twice 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 Staphylococcus aureus is proven or suspected)

2. (2) See Chapters 18.4.3 and 18.4.5 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 oxygen saturations <92%

To establish risk of empyema:

Sampling of parapneumonic effusion—empyema or clear fluid with pH <7.2 require early and effective drainage of pleural fluid

Other important tests:

Full blood count, electrolytes, renal and liver function, C-reactive protein

Further management

Follow-up chest radiograph to ensure complete resolution at 6 weeks

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 or vomiting 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 splenomegaly (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; haemorrhoids (as evidence of portal hypertension)

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 30.1.14

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 ‘Cardiorespiratory collapse: the patient in extremis’

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 30.2, ‘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 17.1 for discussion)

2. (2) If clinical evidence of intravascular volume depletion, give 1000 ml of IV fluid (0.9% saline) as fast as possible. Repeat clinical examination. If the patient still has intravascular volume depletion, give a 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 saline as soon as it is available

3. (3) Cross-match blood for transfusion

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

5. (5) If oesophageal varices—see Table 30.1.15

Also:

1. (1) Oxygen—high flow, with reservoir bag if needed, to achieve oxygen saturations >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 ‘Deep venous thrombosis and pulmonary embolus’, Table 30.1.3 (iatrogenic over anticoagulation) and ‘Disseminated intravascular 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):

Upper gastrointestinal endoscopy:

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

• • Urgently (once resuscitated) if oesophageal varices are suspected or the patient is actively bleeding

See Table 30.1.14 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

Resuscitation

As described in ‘Upper gastrointestinal haemorrhage’

Coagulopathy

Correct if present:

Give vitamin K, 1 mg IV

Maintain platelet count >25 × 10⁹/litre

Give 2 units of FFP for every 4 units of blood or packed cells

Pharmacological measures to reduce haemorrhage

Consider:

• •  Vasopressin, 20 units IV over 15 min, followed by 20 U/h IV

• •  Terlipressin, 2–4 mg IV bolus, followed by 1–2 mg IV every 4–6 h as needed for up to 72 h

• •  Octreotide 50 µg IV bolus, followed by 50 µg/h IV for 5 days

Note:

Nitrates are often given (sublingually, as transdermal patch, or intravenously) concurrently with vasopressin to reduce side-effects

Urgent endoscopy

Banding or sclerotherapy can stop bleeding, hence immediate liaison with specialist gastroenterological/hepatological services is essential in cases of suspected variceal haemorrhage

Sengstaken–Blakemore tube

Consider if:

Haemorrhage is torrential

Other factors prevent safe emergency endoscopy

Antibiotics

Prophylactic antibiotics for patients with suspected or confirmed variceal bleeds

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 tenderness, 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) Telangiectasias 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 ‘Cardiorespiratory collapse: the patient in extremis’

1. (1) Establish IV access—as in ‘Upper gastrointestinal haemorrhage’

2. (2) If clinical evidence of intravascular volume depletion, resuscitate as described in ‘Upper gastrointestinal haemorrhage’

3. (3) Cross-match blood for transfusion

Also:

1. (4) Oxygen—high flow, with reservoir bag if needed, to achieve oxygen saturations >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 ‘Deep venous thrombosis and pulmonary embolus’, Table 30.1.3 (iatrogenic overanticoagulation) and ‘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 Clostridium 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 ‘Cardiorespiratory collapse: the patient in extremis’

1. (1) Fluid and potassium resuscitation as necessary—see ‘Upper gastrointestinal haemorrhage’ and ‘Hypokalaemia’

2. (2) Consider giving antibiotics—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) Consider C. difficile colitis—if this is likely (e.g. patient has recently been exposed to antibiotic treatment and no other cause of colitis apparent), consider starting vancomycin (125–500 mg orally four times daily) until results of testing for C. difficile toxin are available.

3. (3) In cases of known ulcerative or Crohn’s 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 30.1.16)

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, also for ova, cysts, and parasites if relevant travel history

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

Bowels

Open >6 times per day, with blood in the motions

Pulse

>100/min

Fever

>38° C

Albumin

<30 g/litre

C-reactive protein

>45 mg/dl

Abdominal radiograph

Toxic megacolon

Mucosal islands

Dilated small bowel

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 specify 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 ‘Cardiorespiratory collapse: the patient in extremis’

Acute hepatic failure:

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

2. (2) Treat/prevent hypovolaemia—give 4.5% serum albumin IV to keep central venous pressure 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 20% glucose IV (central line) at 10–20 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:

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

8. (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

9. (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-hrly (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 (alanine aminotransferase, aspartate aminotransferase, γ‎-glutamyl transferase)

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 30.1.17): urgent orthotopic liver transplantation may be required and appropriate

2. (2) Dependent on cause of hepatic failure

Arterial pH <7.3—regardless of presence or absence of hepatic encephalopathy

A patient satisfying any one of the three criteria should be considered for transplant listing