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Ovid: Oxford Handbook of Accident and Emergency Medicine

Editors: Wyatt, Jonathan P.; Illingworth, Robin N.; Clancy, Michael J.; Munro, Philip T.; Robertson, Colin E. Title: Oxford Handbook of Accident and Emergency Medicine, 2nd Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 3 – Medicine Chapter 3 Medicine P.62
Chest pain Chest pain rightly frightens patients. It may reflect life-threatening illness: always take the complaint seriously. Triage patients with chest pain as ‘urgent’ and ensure that they are seen within the first few mins of arriving at hospital. The frequency of ischaemic heart disease is such that it is understandably the first diagnosis to spring to mind in the middle-aged or elderly. Remember that chest pain may result from a variety of other disease processes, many of which are also potentially life-threatening: The differential diagnosis of chest pain:

Common causes: Less common causes:
Musculoskeletal (eg costochondritis) Aortic dissection*
Myocardial ischaemia/infarction* Cholecystitis
Pneumothorax* Herpes zoster
Oesophagitis Oesophageal rupture*
Pneumonia Pancreatitis*
Pulmonary embolus* Vertebral collapse
Obscure origin (eg precordial catch) Tabes dorsalis (very rare)
* potentially rapidly fatal

With such a wide range of possible diagnoses, reaching the correct conclusion requires accurate interpretation of the history, examination and investigations, bearing in mind the recognised patterns of disease presentations. History Characterize the pain:

  • site (eg central, bilateral or unilateral)
  • severity
  • time of onset
  • duration
  • character (eg ‘stabbing’, ‘tight/gripping’, or ‘dull/aching’)
  • radiation (eg to arms and neck in myocardial ischaemia)
  • precipitating and relieving factors (eg exercise/rest/GTN spray)
  • previous similar pains

Enquire about associated symptoms Breathlessness, nausea and vomiting, sweating, cough, haemoptysis, palpitations, dizziness, loss of consciousness. Document Past history, drug history and allergies. Old notes and old ECGs are invaluable—request them at an early stage. Quickly exclude Contraindications for thrombolysis if MI appears likely (p75). Examination Evaluate Airway, Breathing, Circulation (ABCs) and resuscitate (O2, venous access, IV analgesia) as appropriate. Listen to both lung fields and check for tension pneumothorax and severe LVF. Continue to complete the full examination. Investigations These depend to a certain extent upon the presentation and likelydiagnosis, but both an ECG and CXR are usually required. Remember that these may initially appear to be normal in MI, PE and aortic dissection. Ensure that all patients receive ECG monitoring in an area where a defibrillator is readily available. P.63
ECG interpretation Interpreting ECGs requires an understanding of the considerable variation amongst normal ECGs. Some changes (eg LBBB) are always abnormal, others (eg RBBB) may not be. Follow a systematic approach (rate, axis, rhythm, QRS, ST and T-wave morphology). The ECG is recorded on standard paper such that a deflection of 10mm = 1mV. The recording rate = 25mm/sec. 1 small square = 0.04sec,1 large square = 0.2sec Rate The normal resting adult heart rate is 60-100/min. Calculate the rate by dividing 300 by the number of large squares in one R-R interval. Frontal plane axis Normally lies between -30° and +90°. QRS complexes in I and II should both be predominantly +ve. An axis more -ve than -30° is LAD (causes: left anterior hemiblock, inferior MI, ventricular pacing, VT, WPW syndrome). An axis more +ve than +90° = RAD (causes: PE, cor pulmonale, lateral MI, left posterior hemiblock, incorrectly placed leads). Longitudinal axis The transition zone between RV ‘Rs’ wave and LV ‘qR’ wave reflects relative dominance of each ventricle. It usually occurs in V3, but may shift (eg to V5 in RVH as ‘clockwise rotation’ around longitudinal axis). P wave Normally <0.12secs wide and <2.5mm tall. Normal P waves are upright in II and V4-6 and may be biphasic in V1. The alignment of lead II renders P waves prominent: choose it for rhythm strips or ECG monitoring. A tall peaked P wave in II may reflect right atrial hypertrophy; a widened bifid P wave left atrial hypertrophy. P waves are absent in AF. PR interval Normally 0.12-0.2secs. A short PR interval results from abnormally fast conduction between atria and ventricles, implying an accessory pathway (eg WPW). A prolonged PR interval = first degree heart block, which is usually abnormal (p78). In second degree heart block only a proportion of P waves are followed by a QRS complex, in complete heart block there is no association between P waves and QRS complexes (p78). QRS width Normally 0.05-0.11secs. A prolonged QRS complex represents abnormally slow intraventricular conduction and may be due to: RBBB (RsR’ in V1), LBBB (QS in V1, RsR’ in V6), tricyclic antidepressant poisoning (p189), ventricular rhythms and ectopics. QRS amplitude Due to the predominance of the left ventricle, the total QRS voltage can indicate LVH. ECG criteria suggesting LVH are: S in V2 + R in V5 > 35mm; R in I > 15mm; R in aVL > 11mm. Q waves May be normal in III, aVR and V1. Q waves in I, II, aVf and aVL are abnormal if >0.04s or >1/2 of the height of the subsequent R wave. ST segment Normally isoelectric (±1mm), merging imperceptibly with the proximal limb of the T wave. ST elevation is caused by: acute MI (concave down), pericarditis (concave up), ventricular aneurysm, Prinzmetal’s angina, LVH, hypertrophic cardiomyopathy, benign early repolarisation. ST depression is caused by: MI/ischaemia, digoxin, LVH with strain. P.65
QT interval = start of Q wave to end of T wave. Properly requires correction according to heart rate: QTc = QT/√R-R = 0.39sec ±0.04sec (Bazett’s formula). A useful rule is that at rates of 60-100/min, QT should be <1/2 R-R interval. A prolonged QTc predisposes to ‘torsades de pointes’ (p88). It occurs in: sleep, acute MI, hypothermia, hypocalcaemia, drugs (quinidine, tricyclic antidepressants), certain congenital diseases (eg Romano-Ward syndrome). A short QTc may be secondary to hypercalcaemia or digoxin. T waves Abnormal if inverted in V4-6. Peaked T waves are seen in early acute MI and hyperkalaemia (p158). Flattened T waves (sometimes with prominent U waves) occur in hypokalaemia.

Figure. T-Waves.

Calculating the R-R Interval To calculate the rate divide 300 by the number of big squares per R-R interval—if the uk standard ecg speed of 25mm/sec is used (elsewhere, 50mm/sec may be used: don’t be confused!)

R-R duration (sec) Big squares Rate (per min)
0.2 1 300
0.4 2 150
0.6 3 100
0.8 4 75
1.0 5 60
1.2 6 50
1.4 7 43

Angina Angina is defined as discomfort in the chest or adjacent areas due to myocardial ischaemia. It is usually brought on by exertion and associated with a disturbance of myocardial function without necrosis. It occurs when coronary artery blood flow fails to meet the O2 demand of the myocardium (eg during exercise, coronary artery spasm or anaemia). Ischaemia may produce ST depression on the ECG which resolves on recovery. T wave inversion commonly occurs in IHD, but is a non-specific finding. First presentation of angina Patients may come to A&E with angina as a first presentation of IHD. Always consider the possibility of MI. In particular, suspect myocardial cell death with any pain lasting >10mins (even if relieved by GTN). A normal examination, normal ECG and normal baseline cardiac enzymes do not exclude MI. If in any doubt, admit the patient. If considering discharge, discuss with senior A&E/medical staff. A patient might be discharged where the history is of exertional pains (classic triggers of angina are: walking uphill, climbing stairs, or walking in a cold wind) and where the pattern is predictable. Consider discharge in patients with <10mins chest pain duration if there is no worsening of symptoms, no pain at rest, no abnormal examination findings and no ECG abnormalities. Ensure that there is a clear plan for follow-up (a confirmed outpatient review date, usually with exercise testing). Counsel the patient about smoking, provide a GTN spray (with advice on its use). Start aspirin 75-150mg daily PO if no confirmed allergy or active peptic ulcer. Liaise with the GP and give the patient clear advice to return if symptoms worsen or if there is pain lasting >10mins. Unstable angina This covers a spectrum of severity between stable angina and acute MI. It can occur as worsening angina or a single episode of ‘crescendo’ angina, with a high risk of impending MI. Features include angina at rest, ↑frequency, duration and severity of pain (including ↓response to GTN). Refer urgently and meantime:

  • Provide high flow O2.
  • Attach to a cardiac monitor.
  • Obtain IV access and give IV opioid analgesia (±antiemetic) as required.
  • Give aspirin 300mg PO stat and clopidogrel 300mg PO stat, if not contra-indicated.
  • Start low molecular weight heparin (LMWH), eg dalteparin 120units/kg SC every 12hrs (max 10,000 units) or enoxaparin 1mg/kg (100units/kg) SC every 12hrs. LMWH is more effective than unfractionated heparin in reducing ischaemic events and the need for re-vascularization procedures. Bleeding complications are the same for both forms of heparin.
  • Commence GTN IVI (start at 0.6mg/h and ↑ as necessary) for pain which remains unrelieved, provided systolic BP is > 90mmHg.
  • Consider glycoprotein IIb/IIIa inhibitors (eg eptifibatide and tirofiban) for patients at high risk of developing MI according to local policy—seek expert advice.
  • If no contraindications, consider atenolol 25-50mg PO stat, according to local policy.
  • Note that some patients benefit from early revascularization procedures.

Prinzmetal’s or ‘variant’ angina Angina associated with ST elevation may be due to coronary artery vasospasm. This may occur with or without a fixed coronary abnormality and may be indistinguishable from an acute MI until changes resolve rapidly with GTN as pain is relieved. Atypical chest pain Patients with acute MI are occasionally sent home from A&E inadvertently. Cardiac chest pain may be poorly localized and may present with musculoskeletal features or gastrointestinal upset. In particular, patients with acute coronary syndromes commonly have chest wall tenderness. Some patients understandably play down symptoms in order to avoid admission to hospital. If the clinical history is suspicious of cardiac pain (especially in a patient with risk factors, such as family history of IHD, hypertension, smoking), then refer for admission. Do not be fooled by a normal ECG, normal examination or the fact that the patient is <30yrs old. Remember that oesophageal pain may improve with GTN and true cardiac pain may appear to improve with antacids. The decision whether or not to refer the patient for admission and investigation depends upon an assessment of the risk of MI. In general, refer those patients to exclude an MI (serial ECGs and cardiac enzymes) where chest pain lasting >15mins has some features of IHD. Also refer patients who look unwell, even if the chest pain lasts <15mins.

Figure. Normal lead II
Figure. Ischaemic changes in lead II

Myocardial infarction (MI) IHD is the leading cause of death in the Western world. Mortality from acute MI is believed to be 45%, with 70% of these deaths occurring before reaching medical care. Contributory risk factors for MI include smoking, hypertension, age, male sex, diabetes, hyperlipidaemia, family history. Pathology MI mostly affects the left ventricle. It usually results from sudden occlusion of a coronary artery or one of its branches by thrombosis over a pre-existing atheromatous plaque. Patients with IHD are at risk of sustaining an MI if additional stresses are placed upon their already critically impaired myocardial circulation (eg a high level of COHb following smoke inhalation during a fire). MI is also a feature of various vasculitic processes, including temporal arteritis, polyarteritis nodosa and Kawasaki disease. Diagnosis The diagnosis of acute MI requires two out of the following three features:

  • a history of cardiac-type ischaemic chest discomfort
  • evolutionary changes on serial ECGs
  • a rise and fall in serum cardiac markers

Note that 50-60% of patients will not have a diagnostic ECG on arrival and up to 17% will have an entirely normal initial ECG. Late presentation does not improve diagnostic accuracy of the ECG. History The classic presentation is of sudden onset, severe, constant central chest discomfort, which radiates to the arms, neck or jaw. The pain is similar in nature to previous angina pectoris, but is much more severe and unrelieved by GTN. The pain is usually accompanied by one or more associated symptoms: sweating, nausea, vomiting, breathlessness. Atypical presentation is relatively common, so adopt a high level of suspicion in order not to miss it. Many patients describe atypical pain, some attributing it to indigestion (be wary of new onset ‘dyspeptic’ pain inadulthood). Up to a third of patients with acute MI do not report any chest pain. These patients tend to be older, more likely to be female, have a history of diabetes or heart failure and have a higher mortality. These patients may present with:

  • LVF
  • collapse or syncope (often with associated injuries eg head injury)
  • confusion
  • stroke
  • an incidental ECG finding at a later date

In a patient who presents with possible MI, remember to enquire about past medical history (IHD, hypertension, diabetes, hyperlipidaemia) and contraindications to thrombolysis (see p75). Ask about drug history, including drugs of abuse (particularly cocaine). P.69
Examination As with other potentially life-threatening emergencies, examination and initial resuscitation (O2, IV cannula, analgesia) go hand in hand. The patient may be pale, sweaty and distressed. Specific physical signs are absent unless complications have supervened (eg arrhythmias, LVF). Direct initial examination towards searching for these complications and excluding alternative diagnoses:

  • check pulse, BP and monitor trace (?arrhythmia or cardiogenic shock)
  • listen to the heart (?murmurs or 3rd heart sound)
  • listen to the lung fields (?LVF, pneumonia, pneumothorax)
  • check peripheral pulses are present in all limbs (?aortic dissection)
  • check legs for evidence of DVT (?PE)
  • palpate for abdominal tenderness or masses (?cholecystitis, pancreatitis, perforated peptic ulcer, ruptured abdominal aortic aneurysm)

Investigations The diagnosis of MI within the first few hours is based upon history and ECG changes (serum cardiac enzymes may take several hrs to rise—see below).

  • Record an ECG as soon as possible, ideally within the first few minutes of arrival at hospital. Sometimes patients arrive at hospital with ECGs of diagnostic quality already recorded by paramedics. If the initial ECG is normal, but symptoms suspicious, repeat the ECG every 30mins and re-evaluate.
  • Request old notes (these may contain previous ECGs for comparison).
  • Ensure continuous cardiac monitoring and pulse oximetry.
  • Monitor BP and respiratory rate.
  • Get venous access and send blood for enzymes, U&E, glucose, FBC, lipids.
  • Obtain a CXR only if there is clinical evidence of LVF and if it will not delay thrombolysis.
  • ABGs are not routinely indicated as they rarely influence treatment and may cause bleeding during thrombolysis.

Cardiac enzymes Creatine kinase (CK), aspartate transaminase (AST) and lactate dehydrogenase rise and fall in a recognised sequence following MI. None of these can be used to identify acute MI in A&E—do not discharge a patient on the basis of a single normal blood test. CK-MB has a higher cardiac specificity than CK. CK-MB is 78-100% sensitive for acute MI at 6hrs after onset of pain. These tests may be employed as part of a strategy to rule out MI, but only after a minimum of 6hrs observation with serial ECGs and cardiac enzymes. Troponin T (cTnT) and Troponin I (cTnI) are proteins virtually exclusive to cardiac myocytes. They are highly specific and sensitive, but are only maximally accurate after 12hrs. Troponin T and I cannot be used to rule out MI in the first few hrs. Chest pain assessment units These units are becoming established in some A&E departments. A combination of ECGs, ST segment monitoring, cardiac enzymes and exercise testing is used to allow discharge of low to moderate risk patients within 6-12hrs. However, simply excluding an acute coronary syndrome is only part of the assessment of chest pain. P.70
Myocardial infarction—ECG changes 1 Infarction of cardiac muscle results in ECG changes which evolve over hours, days and weeks in a relatively predictable fashion. Hyperacute changes Frequently ignored, although often subtle. Some or all of the following may be observed within mins of infarction:

  • ↑ventricular activation time, since the infarcting myocardium is slower to conduct electrical impulses. The interval between the start of the QRS and apex of the R wave may be prolonged >0.045sec.
  • ↑height of R wave may be seen initially in inferior leads in inferior MI.
  • upward-sloping ST segment—having lost its normal upward concavity, the ST segment straightens, then slopes upwards, before becoming elevated.
  • tall, widened T waves develop.

Evolving acute changes In isolation, none of these changes are specific to MI. In combination and with an appropriate history, they provide the basis for ECG diagnosis of MI in A&E:

  • ST elevation—the most important ECG change. ST segments become concave down and are significant if elevated > 1mm in 2 limb leads, or >2mm in 2 chest leads.
  • Reciprocal ST depression may occur on the ‘opposite side’ of the heart.
  • Pathological Q waves (defined on p64) reflect electrically inert necrotic myocardium. ECG leads over a large transmural infarct thus demonstrate deep QS waves. Leads directed towards the periphery of a large infarct or over a smaller infarct may show a Qr complex or a loss of R wave amplitude.
  • T wave inversion—typically deeply inverted, symmetrical and pointed.
  • Conduction problems may develop. LBBB in a patient with acute cardiac chest pain makes interpretation of the ECG very difficult. LBBB does not have to be new to be significant. Do not delay intervention in patients with a good clinical history of MI in order to obtain old ECGs. Consider thrombolysis for all patients with LBBB who have symptoms consistent with MI.

Chronic changes In the months following an MI, ECG changes resolve to a variable extent. ST segments revert to becoming isoelectric, unless a ventricular aneurysm develops. T waves gradually become +ve again, but Q waves usually remain, indicating MI at some time in the past.

Figure. ECG changes following MI
Figure. Acute inferolateral infarction with “reciprocal” ST changes in I, aVL, and V2-V3.
Figure. Acute anteroseptal infarction with minimal “reciprocal” ST changes in III and aVF.

Myocardial infarction—ECG changes 2 Localisation of MI MI usually affects the LV, occasionally the RV, but virtually never the atria. The part of myocardium affected is implied by which leads show changes:

ECG leads Location of MI
V1-3 Anteroseptal
V5-6, aVL Anterolateral
V2-4 Anterior
V1-6 Extensive anterior
I, II, aVL, V6 Lateral
II, III, aVF Inferior
V1, V4R Right ventricle

Posterior MI No conventional electrode is directed over the posterior part of the heart, since the intervening tissues would result in an attenuated signal. ECG diagnosis of true posterior MI may be made from the use of V7-9 and from reciprocal changes seen in leads V1-3: tall, slightly widened R (reciprocal of Q), concave up ST depression (reciprocal of ST elevation), upright tall widened T (reciprocal of inverted T). Isolated posterior MI is unusual: it nearly always occurs as part of inferior (postero-inferior) or lateral (postero-lateral) MI. Right ventricular infarct This occurs as part of an inferior MI more often than is generally appreciated. In the presence of changes of acute MI in the inferior leads, ST elevation in V1 suggests RV involvement, particularly if this is greater than ST elevation in V2 or V3. In this case, record an ECG trace from lead V4R. The diagnosis of RV infarct helps determine treatment of ensuing cardiac failure: RVF requires IV fluids to maintain adequate filling pressure, LVF is treated with diuretics. Subendocardial infarct If myocardial damage is limited to the subendocardium, with sparing of the epicardium, Q waves do not develop. The changes of subendocardial MI are: ST depression and deeply inverted T waves. P.73

Figure. ECG of subendocardial infarct

Myocardial infarction—treatment Speed is of the essence—time really is muscle. Work efficiently as a team to ensure treatment is not delayed (eg one member takes the history whilst securing venous access, another gives aspirin and records an ECG).

  • Sit the patient up in a comfortable position.
  • Give O2 by face mask and attach cardiac monitor.
  • Obtain IV access and take samples for U&E, glucose, FBC, cardiac enzymes.
  • If it has not already been administered, try 1-2 puffs of GTN spray SL (beware sudden hypotension—if this occurs, lie the patient flat).
  • Provide small increments of IV opioid analgesia titrated to effect.
  • Give IV antiemetic (eg 10mg metoclopramide or 50mg cyclizine).
  • Give 300mg aspirin PO, unless already given prehospital, or contraindicated (allergy, active peptic ulcer).
  • Check for contraindications to thrombolysis (see below), explain the procedure and possible risks and ensure the patient understands and assents.
  • Administer thrombolysis and monitor carefully for hypotension or arrhythmias. Make sure that there is a defibrillator close at hand. Aim to give thrombolysis within 15mins of the patient’s arrival at hospital. Start LMWH (eg enoxaparin 1mg/kg IV stat) or heparin according to local protocols.
  • If pain continues, give IVI GTN (start at 0.6mg/h and ↑ as necessary), provided systolic BP is >90mmHg.
  • Consider atenolol (5mg slowly IV over 5mins, repeated once after 15mins), unless contraindicated (eg uncontrolled heart failure, hypotension, bradyarrhythmias, COPD).

Further management Arrhythmias Commonly occur after MI. Occasional ventricular ectopics or transient AF (lasting <30secs) require no treatment. Watch for sudden VT/VF and treat as on p52. Hypokalaemia Treat if K+< 4mmol/litre by IVI 20mmol KCl in 100mL 0.9% saline over 1h, together with Mg2+ 5mL 50% in 100mL 0.9% saline over 1h. Pulmonary oedema Treat as described on p98. Cardiogenic shock Defined as poor cardiac output with evidence of tissue hypoxia which does not improve with correction of intravascular volume. Mortality is ≈50-80%. Contact ITU and senior cardiologist. Echocardiography may be required to exclude conditions requiring urgent surgical repair (mitral regurgitation from papillary muscle rupture, aortic dissection, ventricular septum rupture, cardiac tamponade from ventricular wall rupture). Where these are excluded, early invasive cardiac re-vascularization may improve survival. Thrombolysis Thrombolysis can reperfuse infarcting myocardium and dramatically reverse ST changes. It significantly improves outcome: give it as soon as possible. Note that local protocol may be for angioplasty rather than thrombolysis. Ensure that the patient is involved in any decision to thrombolyse. Indications for thrombolysis

  • ST elevation of >1mm in 2 limb leads, or
  • ST elevation of ≥2mm in 2 or more contiguous chest leads, or
  • LBBB in the presence of a typical history of acute MI (NB: LBBB does not have to be new)

Contraindications to thrombolysis Most are only relative, but discuss with the patient and CCU before starting thrombolysis:

  • head injury, CVA or recent TIA, previous neurosurgery or cerebral tumour
  • recent GI or GU bleeding, menstruation or bleeding tendency(eg warfarin)
  • severe hypertension (eg systolic BP >200mmHg, diastolic BP >120mmHg), aortic dissection or pericarditis
  • puncture of non-compressible vessel (eg subclavian vein), traumatic CPR, ↓GCS post-arrest
  • major surgery within recent weeks
  • pregnancy

Strokes, intracranial haemorrhage and major bleeds are more common in patients given thrombolysis. Intracranial bleeding is more common in older patients, those with low body weight, hypertension on admission and those given tPA (rather than other thrombolytics). Choice of thrombolytic agents Streptokinase is a traditional thrombolytic agent. However, use tPA instead if: streptokinase was given >5days ago, or anterior MI in patient <75yrs old and <4hrs of onset of symptoms, or hypotensive (systolic BP <90mmHg). Give 1.5mega-units by continuous IVI over 1h. Streptokinase is allergenic (may require slow IV chlorphenamine 10mg and IV hydrocortisone 100mg) and frequently causes hypotension (↓IVI rate and tilt the bed head down—treament rarely needs to be discontinued). After a recent streptococcal infection, streptokinase may be ineffective due to the antibodies produced. Alteplase (recombinant tissue plasminogen activator- rtPA) is non-allergenic and non-antigenic. It is most effective given by an accelerated regimen, eg 15mg IV bolus, followed by 0.75mg/kg (max 50mg) IVI for 30mins, then 0.5mg/kg (max 35mg) IVI over 60mins. Give LMWH (eg enoxaparin 1mg/kg IV stat) or heparin concomitantly through a separate IV line (5000unit IV bolus, then 1000units/h IV), according to local protocols. Reteplase (modified tPA) can be given as two IV boluses of 10units each exactly 30mins apart. Give LMWH/heparin as for alteplase. Tenectaplase (modified tPA) is given as a single IV bolus over 10secs. Dose according to weight (<60kg = 30mg; 60-69kg = 35mg; 70-79kg = 40mg; 80-89kg = 45mg; >90kg = 50mg. Give LMWH/heparin as for alteplase. Failure to reperfuse Ensure that CCU staff see patients with acute MI who despite thrombolysis continue to have severe symptoms, ongoing evidence of myocardial dysfunction, or widespread ST elevation. They may require further investigation and in selected cases, further thrombolysis or transfer for urgent percutaneous transluminal coronary angioplasty. Primary angioplasty for acute MI Percutaneous transluminal coronary angioplasty is more effective than thrombolysis. Consider it particularly in patients in whom thrombolytics are contra-indicated and in cardiogenic shock. P.76
Pericarditis Acute inflammation of the pericardium characteristically produces chest pain, low grade fever and a pericardial friction rub. Pericarditis and myocarditis commonly coexist. Causes

  • myocardial infarction (including Dressler’s syndrome—see below)
  • viral (eg coxsackie B virus, HIV)
  • bacterial (pneumonia and/or septicaemia)
  • TB (especially in patients with HIV)—see p222
  • locally invasive carcinoma (eg bronchus or breast)
  • rheumatic fever—see p475
  • uraemia
  • collagen vascular disease (SLE, polyarteritis nodosa, rheumatoid arthritis)
  • after cardiac surgery or radiotherapy
  • drugs (hydralazine, procainamide, methyldopa, minoxidil)

Diagnosis Classical features of acute pericarditis are pericardial pain, a friction rub and concordant ST elevation on ECG. The characteristic combination of clinical presentation and ECG changes often allows a definite diagnosis. Chest pain is typically sharp, central, retrosternal and worse on deep inspiration, change in position, exercise and swallowing. Pericardial effusion may cause dysphagia by compressing the oesophagus. A pericardial friction rub is often intermittent, positional and elusive. It tends to be louder during inspiration and may be heard in both systole and diastole. Low grade fever is common. Appropriate investigations include: ECG, CXR, FBC, ESR, U&E. A pericardial effusion is most quickly and easily demonstrated by echocardiography: clinical evidence of cardiac tamponade is rare. ECG changes In acute pericarditis changes result from associated epicardial inflammation. Sinus tachycardia is usual, but AF, atrial flutter or atrial ectopics may occur. ST elevation is concave up (in contrast to MI—see p70) and present in at least 2 limb leads and all chest leads (most marked in V3-6). T waves are initially prominent, upright and peaked, becoming flattened or inverted over several days. PR depression (reflecting atrial inflammation) may occur in the same leads as ST elevation (this PR-ST discordance is characteristic). Pathological Q waves do not develop at any stage. Pericardial effusion causes ↓ QRS amplitude in all leads. Very occasionally, electrical alternans is also seen (and is diagnostic). Management Refer to the medical team/CCU for further investigation and treatment. The appropriate treatment depends on the underlying cause. Idiopathic pericarditis or viral pericarditis in young patients is usually benign and self-limiting, responding to symptomatic treatment (bed rest and NSAID). Occasionally, it follows a relapsing course before ‘burning itself out’. Dressler’s syndrome (autoimmune pericarditis ± effusion 2-14 wks after 3% of MIs) requires cardiology specialist care. P.77
Pericardial effusion may occur with any type of pericarditis. It is relatively common in acute bacterial, tuberculous and malignant pericarditis. Acute tamponade may occur following cardiac rupture with MI, aortic dissection or after cardiac surgery. Summon senior help and arrange immediate echocardiography for patients with signs of tamponade, with subsequent pericardiocentesis (preferably under ultrasound guidance) and depending upon the cause, with a definitive drainage procedure. Emergency ‘blind’ pericardiocentesis is described on p332.

Figure. ECG of pericarditis

Bradyarrhythmias Bradycardia is defined as a ventricular rate of <60/min in the adult. It is usually the result of influences on or disease of the SA node, or to AV block. Intraventricular conduction disturbances may progress to AV block. Sinus bradycardia may be physiological (eg athletes), the result of drugs(ß-blockers), or be pathological (hypothyroidism, hypothermia, hypoxia, ↑ICP, sick sinus syndrome, MI, myocardial ischaemia). Bradycardia also occurs in up to a third of patients with hypovolaemia (eg GI bleed, ectopic pregnancy). Sick sinus syndrome (or ‘sinus node disease’) is usually caused by ischaemia or fibrosis/degeneration of the SA node. It is characterized by sinus pauses (>2secs) or sinus arrest. Junctional or other escape beats may occur and occasionally a tachyarrhythmia may emerge (‘tachy-brady’) syndrome. The patient may present with dizziness, collapse, loss of consciousness or palpitations. A continuous 24h ECG tape may be useful to demonstrate the arrhythmias. Atrioventricular (AV) block is subdivided into three degrees. Each may result from a variety of causes, including IHD, drugs (eg excess digoxin) or cardiac surgery. First degree AV block Conduction from atria to ventricles occurs every time, but is delayed. The PR interval is >0.2sec (5 small squares on standard ECG). Second degree AV block Only a proportion of P waves are conducted to the ventricles. There are two main types:

  • Mobitz type I block (Wenckebach)—the PR interval becomesincreasingly lengthened until a P wave fails to conduct.
  • Mobitz type II block—failure to conduct P waves may occur regularly (eg 3:1) or irregularly, but the PR interval remains constant.

Third degree (complete) heart block Atrial activity is not conducted to the ventricles. With a proximal block (eg at the AV node), a proximal escape pacemaker in the AV node or bundle of His may take over, producing narrow QRS complexes at a rate of ≈50/min. With distal AV block a more distal escape pacemaker results in broad bizarre complexes at a rate of ≈30/min. If the escape pacemaker temporarily stops discharging, or a subsidiary pacemaker takes over, ventricular asystole may occur. Intraventricular conduction disturbances The intraventricular conducting system commences as the bundle of His and divides into right and left bundle branches—the latter subdivides further into antero-superior and postero-superior divisions. These two divisions and the right bundle branch are referred to as the ‘fascicles’. Blockage of 2 fascicles = bifascicular block.

  • RBBB→ RsR′ in V1, deep delayed terminal S in lateral leads, QRS >0.12sec
  • Left anterior hemiblock→ LAD, ↑ventricular activation time, QRS <0.12sec
  • Left posterior hemiblock→ RAD, prominent Q inferiorly, QRS <0.12sec
  • LBBB→ QS in V1, RsR′ in V6, QRS >0.12sec
  • RBBB + left anterior hemiblock→ LAD, RBBB pattern, QRS >0.12sec
  • RBBB + left posterior hemiblock → RAD, RBBB pattern, QRS >0.12sec

In the context of recent MI, bifascicular block, if associated with first degree block (‘trifascicular block’) may lead to complete heart block and may require prophylactic pacing. P.79

Figure. ECG of first degree heart block
Figure. ECG of Mobitz type I Wenkebach block
Figure. ECG of Mobitz type II AV block
Figure. ECG of complete AV block

Treatment of bradyarrhythmias The emergency treatment of bradycardia depends upon two important factors: the clinical condition of the patient and the risk of asystole. Give O2, insert an IV cannula and follow the European Resuscitation Council Guidelines shown below (http://www.resus.org.uk). Atropine is the first-line drug. The standard dose is 500micrograms IV, which may be repeated to a total of 3mg. Further doses may result in toxic effects (eg psychosis, urinary retention). Epinephrine (adrenaline) can be used as a temporising measure prior to transvenous pacing if an external pacemaker is not available. Give by controlled infusion at 2-10micrograms/min, titrating up according to response (6mg epinephrine in 500mL 0.9% saline infused at 10-50mL per hour). External transcutaneous pacing is now available on many modern defibrillators. It allows a pacing current to be passed between 2 adhesive electrodes (eg placed over the front of the chest and the back). Select external demand pacing mode at a rate of 70/min, then gradually ↑ the pacing current from zero until capture is shown on the monitor. Clinically, capture will result in a palpable peripheral pulse at the paced rate and clinical improvement in the patient’s condition. Provide small doses of IV opioid if the patient finds external pacing very uncomfortable. Transvenous cardiac pacing is the treatment of choice for bradycardic patients who are at risk of asystole. The technique should only be performed by an experienced doctor. The preferred route of access is the internal jugular or subclavian vein. However, if thrombolysis has recently been given or is contemplated, or if the patient is taking anticoagulants, use the right femoral vein instead. Obtain a CXR to exclude complications. A correctly functioning ventricular pacemaker results in a pacing spike followed by a widened and bizarre QRS:

Figure. Paced rhythm

Permanent pacemakers and implantable defibrillators Increasingly sophisticated implantable devices are being used to manage arrhythmias. Occasionally, a patient will present to A&E with malfunction of one of these devices. Get urgent specialist advice. External transcutaneous pacing will provide temporary support whilst the problem is resolved. P.81

Figure. Algorithm for the management of bradycardia (http://www.resus.org.uk)

Narrow complex tachyarrhythmias This is almost always of supraventricular origin. Underlying rhythms include:

  • sinus tachycardia
  • paroxysmal AV re-entrant tachycardia (often referred to as ‘SVT’)
  • AF with fast ventricular response
  • atrial flutter
  • atrial tachycardia
  • junctional tachycardia

First determine whether the rhythm is regular or not. Treat irregular rhythms (AF) as outlined on p84. If the ventricular rate is exactly 150/min, atrial flutter with 2:1 block is likely. Give O2, insert an IV cannula and follow the algorithm shown below (http://www.resus.org.uk). Vagal stimulation Vagal stimulation may be achieved in various ways. The most effective is a Valsalva manoeuvre whilst supine. Instruct the patient to attempt to blow the plunger out of a 5mL syringe. If unsuccessful, in the young patient, massage the carotid sinus for 15secs (1 side only), by gently rubbing in a circular action lateral to the upper border of the thyroid cartilage. Carotid sinus massage may be dangerous (especially if there is a carotid bruit or previous CVA/TIA). Adenosine is a purine nucleoside with a very short half-life (10-15secs) which temporarily blocks conduction through the AV node. It may successfully terminate re-entrant tachycardias and may ‘unmask’ other conditions (eg atrial flutter) by temporarily producing a conduction block. Adenosine is contra-indicated in second degree or complete AV block and may exacerbate asthma. The effects are blocked by theophylline and it may be ineffective in patients already taking this or related drugs. Its effects are potentiated markedly (and hence dangerously) in the presence of dipyridamole, carbamazepine or in a denervated heart—seek advice. Give adenosine by fast bolus IV injection into an IV cannula in the antecubital fossa and flush with 0.9% saline (see below). Record a rhythm strip and warn the patient about transient flushing and chest discomfort. Synchronized cardioversion requires two doctors: one to perform cardioversion, the other (experienced in anaesthesia) to provide sedation or anaesthesia and manage the airway. Remember that the patient will not be fasted and is at risk of aspiration. The arrhythmia ↓cardiac output and ↑ circulation times, so IV anaesthetic agents take much longer to work than usual. If the anaesthetist does not appreciate this and gives additional doses of anaesthetic drugs, the result may be hypotension and prolonged anaesthesia after the arrhythmia has been corrected. Drug treatment of the uncompromised patient should follow Resuscitation Council guidelines and the advice of the CCU team and be tailored to individual circumstances.

Figure. Narrow complex tachycardia


Figure. Algorithm for the management of narrow complex tachycardia (http://www.resus.org.uk)

Atrial fibrillation Atrial fibrillation is rapid, irregular atrial activity and is associated with an irregular ventricular response. Acute onset is usually defined as within 48hrs. AF (together with atrial flutter) is one of the most common arrhythmias encountered in A&E. The incidence of AF increases with age, approximately doubling with each decade of adult life. It is rare in children except following cardiac surgery. Causes Acute AF may be associated with: IHD (33%), heart failure (24%), hypertension (26%) and valvular heart disease (7%). Other important cardiac causes include sick sinus syndrome, pericarditis, infiltrative heart disease, cardiomyopathy, myocardititis, congenital heart disease and post-cardiac surgery. Non-cardiac causes include: sepsis, PE, thyrotoxicosis, electrocution, lung or pleural disease, chest trauma, hypokalaemia, hypovolaemia, hypothermia, drug abuse (eg cocaine). Paroxysmal AF sometimes occurs in fit athletes. Holiday heart: binge drinking or occasionally alcohol withdrawal may cause acute AF in patients with no other predisposing factors. AF usually resolves spontaneously within 48hrs. The diagnosis of ‘holiday heart’ is one of exclusion after cardiac disease and other causes have been ruled out. Clinical features AF reduces cardiac output by 10-20% irrespective of underlying ventricular rate. Clinical presentation varies according to the cause and effect of the AF. Some patients are aysmptomatic, whilst others suffer life-threatening complications (heart failure, angina). Those patients with underlying IHD may develop ischaemia during periods of rapid ventricular rate. The onset of AF is associated with the development of cardiac thrombi with an ↑risk of embolism and stroke. Remember that in patients with chronic AF, a fast ventricular rate can also be due to fever, hypovolaemia, dehydration or drug toxicity. Treatment 50% of patients with acute atrial fibrillation revert spontaneously within 24-48hrs. Treat immediate threats to life according to the European Resuscitation Guidelines (http://www.resus.org.uk—see p86). Give O2, insert an IV cannula, treat pain, correct electrolyte abnormalities as necessary and refer to the medical team. High risk patients are those with a heart rate >150/min, ongoing chest pain and clinically impaired perfusion—seek expert help and give heparin (IV infusion or LMWH) with a view to synchronised cardioversion. For intermediate and lower-risk patients, a number of different options are available. Treatment depends upon local policy and individual circumstances. AF in Wolff-Parkinson-White syndrome This may result in an irregular, broad complex tachycardia. Impulses are conducted from the atria via the AV node and an accessory pathway. Do not give these patients AV-blocking drugs (digoxin, verapamil or adenosine) as this can result in acceleration of conduction through the accessory pathway, leading to cardiovascular collapse or VF. Seek expert help. See: http://www.resus.org.uk and http://www.clinicalevidence.com P.85

Figure. Algorithm for the management of atrial fibrillation (http://www.resus.org.uk)

Broad complex tachyarrhythmias May be caused by VT or rarely by SVT with aberrant conduction. In an emergency, do not spend time debating this: assume the diagnosis is VT and resuscitate the patient. Provide O2, insert an IV cannula and follow the European Resuscitation Council guidelines (http://www.resus.org.uk) below. The priorities in broad complex arrhythmias associated with tricyclic overdose are airway management, oxygenation, ventilation and correction of metabolic disorders: give IV bicarbonate, but avoid anti-arrhythmic drugs (p188).

Figure. Broad complex tachyarrhythmia

Evaluating the ECG: is it VT or SVT with aberrant conduction? VT is much more likely as a cause of the broad complex tachycardia if:

  • the patient is >60yrs
  • the patient has a history of IHD or cardiomyopathy
  • there is clinical evidence of AV dissociation (intermittent cannon ‘a’ waves seen on JVP, first heart sound of variable intensity)
  • inverted P waves in lead II
  • the frontal plane axis is bizarre (-90° to -180°)
  • the QRS is >0.13sec
  • there are ‘capture beats’ or ‘fusion beats’
  • the QRS is bizarre, not resembling a bundle branch block pattern
  • all chest leads (V1-6) are concordant (QRS complexes point the same way)
  • R > R′ (or r′) in V1
  • there is a deep S wave (either QS, rS or RS) in V6

Torsades de pointes This is a rare form of polymorphic VT, associated with hypomagnesaemia, hypokalaemia, long QT interval (congenital or drug related, eg sotalol, antipsychotics, antihistamines, antidepressants). A constantly changing electrical axis results in QRS complexes of undulating amplitude. Usually paroxysmal, it may degenerate to VF. Get expert help and treat with IV magnesium sulphate (5mL of 50% over 30mins). Refractory cases may require overdrive pacing.

Figure. Torsades de pointes.


Figure. Algorithm for the management of broad complex tachycardia (http://www.resus.org.uk)

Hypertensive problems Bear the following points in mind when contemplating the approach to a hypertensive patient in A&E:

  • Most patients with hypertension are asymptomatic.
  • Hypertension is an important risk factor for cardiovascular disease and stroke.
  • Most patients found to be hypertensive in A&E do not require any immediate intervention or treatment, but do require carefulfollow-up—usually by their GP.
  • Never intervene on the basis of a single raised BP measurement in the absence of any associated symptoms and signs.

Approach Approach patients found to be hypertensive as follows:

  • Those with no previous history of hypertension, but no other concerns or history of other conditions (eg diabetes, peripheral vascular disease, IHD or CVA)—arrange follow-up and monitoring with GP.
  • Those known to be hypertensive already on treatment—arrange follow-up and monitoring with GP.
  • Those with evidence of end organ damage (eg LV hypertrophy on ECG, retinal changes or renal impairment)—refer to the medical team.
  • Those with hypertension associated with pain, vasoconstriction(eg acute pulmonary oedema) or stroke—treat underlying cause where possible, but do not intervene in stroke associated hypertension except under the direction of a neurologist or stroke specialist.
  • Those with hypertension directly associated with symptoms orsigns – contact the medical team and consider whether intervention is appropriate (see below).

Mild/moderate hypertension (diastolic 100–125mmHg) Ascertain if the patient has a past history of hypertension and is taking drug therapy for this. Examine for retinal changes and evidence ofhypertensive encephalopathy (see below). Investigate as appropriate (consider U&E, urinalysis, CXR, ECG). Deciding how to proceed will depend upon the BP and the exact circumstances. Refer to the medical team if there is evidence of hypertensive encephalopathy or if the BP is moderately ↑(ie diastolic BP: 110-125mmHg). P.91
Severe hypertension (diastolic >125mmHg) Patients with a diastolic BP > 125mmHg require urgent assessment. Search for evidence of hypertensive encephalopathy: headache, nausea, vomiting, confusion, retinal changes (haemorrhages, exudates, papilloedema), fits, focal neurological signs, ↓conscious level. Ask about recent drug ingestion (eg ecstasy or cocaine—p206). Investigations Insert an IV cannula and send blood for U&E, creatinine and glucose. Obtain a CXR and ECG and perform urinalysis. If there is ↓conscious level, focal signs or other clinical suspicion that the hypertension may be secondary to CVA/subarachnoid haemorrhage, arrange an urgent CT scan. Management

  • Refer patients with a diastolic pressure >125mmHg or evidence of hypertensive encephalopathy to the medical team and involve ITU if necessary. Resist commencing emergency treatment until consultation with an expert. There is a significant risk of complications (CVA or MI) if the BP is reduced rapidly. In many cases it is appropriate to commence oral antihypertensive therapy using a ß-blocker (eg atenolol or labetolol) or calcium channel blocker (eg nifedipine).
  • If treatment is considered to be appropriate, commence oral treatment or commence an IVI of sodium nitroprusside or labetolol withcontinuous BP monitoring via an arterial line. Sodium nitroprusside has a very short half-life (≈1-2mins) and acts as a vasodilator of botharterioles and veins. IV labetolol may be the preferred option ifaortic dissection (p92) or phaeochromocytoma are suspected.

Hypertension in pregnancy If the hypertension is part of pre-eclampsia or eclampsia (diastolic BP ≥90mmHg, provided that it was <90mmHg at booking visit; or diastolic BP >25mmHg above booking level) urgently involve an obstetrician(see p566). P.92
Aortic dissection Remember: hypertensive patients with sudden, severe chest and/or back pain may have acute aortic dissection. Pathology Aortic dissection is longitudinal splitting of the muscular aortic media by a column of blood. The dissection may spread proximally (possibly resulting in aortic incompetence, coronary artery blockage, cardiac tamponade), distally (possibly involving the origin of various arteries), or rupture internally back into the aortic lumen, or externally (eg into the mediastinum resulting in rapid exsanguination). More than 70% of patients have a history of hypertension. It occurs more frequently in those with bicuspid aortic valve, Marfan’s syndrome or Ehlers-Danlos syndrome. Up to 20% follow recent cardiac surgery or recent angiography/angioplasty. Each dissection may be classified Stanford type ‘A’ or ‘B’, according to whether the ascending aorta is involved or not, respectively. Overallmortality is ≈30% (35% for type A and 15% for type B). History Aortic dissection may mimic the presentation of an MI, requiring a high index of suspicion. It typically presents with abrupt onset sharp, tearing or ripping pain (maximal at onset) in anterior or posterior chest. Migration of the pain may reflect extension of the dissection. Syncope occurs in ≈10% of patients, sometimes in the absence of any pain. Occasionally, patients can present with neurological deficit associated with chest pain. Examination The patient is usually apprehensive and distressed, with pain which is difficult to alleviate, even using IV opioid. Clues to the diagnosis include:

  • an aortic regurgitation murmur (30%)
  • asymmetry or absence of peripheral pulses or a pulse deficit (15-20%)
  • hypertension
  • hypotension with features of tamponade or neurological signs in association with pain (eg secondary to spinal/carotid artery involvement)

Investigations Send blood for U&E, glucose, FBC, coagulation and X-matching. Obtain an ECG and CXR. Thoracic aortic dissection usually results in an abnormal CXR. One or more of the following changes may be seen:

  • an widened or abnormal mediastinum (present in ≈75%)
  • a ‘double knuckle’ aorta
  • left pleural effusion (≈20%)
  • deviation of the trachea or NG tube to the right
  • separation of two parts of the wall of a calcified aorta by >5mm (the ‘calcium sign’)

The ECG may demonstrate an MI, LVH or ischaemia. Note that ≈12% of patients with aortic dissection have a normal CXR and ≈30% have a normal ECG. Trans-oesophageal echo, CT/angiography provide the definitive diagnosis. P.93
Management On suspicion of aortic dissection:

  • provide O2 by face mask
  • insert 2 large-bore (14G) IV cannulae and X-match for 6 units (inform blood bank of suspected diagnosis)
  • give IV opioid and titrate according to response (eg total of 10mg morphine)
  • give IV anti-emetic (eg cyclizine 50mg)
  • call cardiothoracic team and cardiologist at an early stage
  • insert an arterial line and discuss with specialist teams how to control the BP (eg labetalol infusion)
  • arrange further investigation based upon specialist advice and available resources (eg aortography, echocardiography, CT scan, MRI)

Type A dissections are usually treated surgically, whereas type B lesions are usually treated medically. P.94
Haemoptysis Haemoptysis may be the chief or sole complaint of patients presenting to A&E. It is a very important symptom and always warrants investigation. Causes of haemoptysis

Respiratory – infection (URTI, pneumonia, TB, lung abscess)
– carcinoma (bronchial or laryngeal)
– bronchiectasis
Cardiovascular – pulmonary oedema
– PE
– ruptured aortic aneurysm (aorto-bronchial fistula)
Coagulation disorder – drugs (eg warfarin, heparin)
– inherited (eg Christmas disease)
Trauma – penetrating or blunt (p330)
Other (rare) – Goodpasture’s syndrome, Wegener’s granulomatosis

Presentation Try to ascertain the exact nature of the material coughed up (eg ‘bright red streaks’ or ‘dark brown granules’) and how much of it there was. Patients sometimes have surprising difficulty distinguishing vomited blood from that coughed up. However, if the material produced is frothy and alkaline on testing, it is likely to be haemoptysis. Enquire about associated symptoms and take a drug history. Assess ‘ABCs’ and examine with particular regard to possible causes implicated by the history. Investigation

  • send blood for FBC, coagulation screen, U&E, LFTs
  • request Group and Save, or X-match if evidence of significant haemorrhage
  • check O2 saturation by pulse oximetry
  • check ABG
  • obtain CXR and ECG
  • perform urinalysis—if shocked, insert catheter and monitor urine output
  • collect sputum samples and send for microscopy, culture and sensitivity
  • initiate further investigations according to the likely diagnosis

Treatment The first priority is resuscitation

  • Airway: clear and secure as clinically indicated (coughing/suction). Massive haemorrhage may require emergency GA and tracheal intubation. Whilst preparing for this, tilt the trolley so that the patient is head-down.
  • Breathing: provide O2. If ventilation is inadequate or the patient is apnoeic, assist with bag and mask or tracheal tube.
  • Circulation: insert a large bore (14G) IV cannula (use 2 if hypovolaemic). Give IV fluids/blood/clotting factors as clinically indicated (p166).

Further treatment Commence specific treatment measures aimed at life-threatening underlying cause (eg LVF, PE, infection, coagulopathy). Refer for admission and further investigation (including bronchoscopy). P.95
The dyspnoeic patient The normal adult respiratory rate is 11-18/min, with a tidal volume of 400-800mL. Acute dyspnoea is the predominant presenting symptom of a number of emergency problems and is a feature of even more. Common causes of acute dyspnoea Cardiac

  • LVF (p98)
  • MI (p68)
  • PE (p118)
  • arrhythmias (p78)


  • asthma (p102)
  • exacerbation of COPD (p106)
  • pneumonia (p108)
  • pleural effusion (p101)
  • pneumothorax (p112)


  • aspiration of FB or vomit (p110)
  • pneumothorax/haemothorax (p326)
  • flail chest (p324)
  • near drowning (p246)


  • hypovolaemia (from any cause)
  • hyperventilation syndrome (p97)
  • fever from any cause
  • respiratory compensation for metabolic acidosis (DKA, salicylate overdose)

Approach Follow the ABC approach and resuscitate as necessary. The main aim of treatment is to correct life-threatening hypoxia. Although the differential diagnosis is potentially huge, the history often points to the diagnosis. Enquire particularly about speed of onset of dyspnoea, past medical history and associated symptoms (cough, haemoptysis, fever, wheezing, chest pain). Examine carefully, paying attention to the respiratory rate, depth and pattern. Apply a pulse oximeter. Pulse oximetry This simple, rapid, safe and non-invasive technique is based on the difference in light absorption between oxyhaemoglobin and deoxyhaemoglobin. It provides a continuous means of determining arterial oxygen saturation. It does not provide information about ventilation or pCO2—a normal oxygen saturation does not exclude significant lung pathology (eg PE). Pulse oximetry may be inaccurate or misleading in:

  • poor peripheral perfusion/shock
  • methaemoglobinaemia (falsely ↓ when SaO2> 85%; falsely ↑ when <85%)
  • hypothermia
  • CO poisoning (falsely high reading as COHb reads as oxyhaemoglobin)
  • nail varnish/synthetic fingernails (if a finger probe is used)
  • excessive movement

Oximetry can use a finger, toe, ear or nose. Correlate readings with clinical findings: a non-pulsatile trace (or heart rate different from that on the cardiac monitor) suggests the saturation reading is probably inaccurate. P.97
Hyperventilation Hyperventilation is breathing occurring more deeply and/or more rapidly than normal. CO2 is ‘blown off’, so that arterial pCO2↓. Hyperventilation may be primary (‘psychogenic’) or secondary. A classical secondary cause is DKA—Küssmaul’s respiration represents involuntary respiratory compensation for a metabolic acidosis. Secondary causes of hyperventilation

  • metabolic acidosis (including DKA, uraemia, sepsis, hepatic failure)
  • poisoning (eg aspirin, methanol, CO, cyanide, ethylene glycol)
  • pain/hypoxia
  • hypovolaemia
  • respiratory disorders (eg PE, asthma, pneumothorax)

Primary (psychogenic or inappropriate) hyperventilation Typically, the patient is female, agitated and distressed and has a past history of panic attacks or episodes of hyperventilation. She may complain of dizziness, circumoral paraesthesia and carpopedal spasm and occasionally sharp or stabbing chest pain. Initial examination reveals tachypnoea with equal air entry over both lung fields and no wheeze or evidence of airway obstruction. Although the presentation may appear to be very convincing of primary hyperventilation, it is important to exclude secondary causes. Therefore perform the following investigations:

  • SaO2 (pulse oximetry) on presentation
  • ECG
  • ABG if SaO2↓, or if symptoms do not completely settle in a few mins
  • BMG

If symptoms do not completely settle in a few mins, obtain:

  • ABG
  • CXR
  • U&E, blood glucose, FBC

Treatment Do not sedate a patient with hyperventilation. Once serious diagnoses have been excluded, use this information to help reassure the patients with primary hyperventilation. Often this is all that is required, but it may be helpful to try simple breathing exercises (breathe in through nose—count of 8, out through mouth—count of 8, hold for count of 4 and repeat). Discharge the patient with arrangements for GP follow-up. If these simple measures fail, reconsider the diagnosis and refer the patient to the medical team for subsequent observation and treatment. P.98
Cardiogenic pulmonary oedema Pulmonary oedema may be classified according to whether or not it is due to a cardiac cause. Non-cardiogenic pulmonary oedema is considered on p100. In cardiogenic pulmonary oedema failure of the left heart causes ↑left ventricular end-diastolic pressure, producing ↑pulmonary capillary hydrostatic pressure. Fluid collects in the extravascular pulmonary tissues faster than the lymphatics can clear it. Causes of cardiogenic pulmonary oedema Often an acute complication of MI and IHD, or an exacerbation of pre-existing cardiac disease (eg hypertension, aortic/mitral valve disease). Other causes are:

  • arrhythmias
  • failure of prosthetic heart valve
  • ventricular septal defect
  • cardiomyopathy
  • negatively inotropic drugs (eg ß-blockers)
  • acute myocarditis
  • left atrial myxoma (may produce syncope, fever, ↑ESR, but is very rare)
  • pericardial disease

The history is frequently dramatic. Dyspnoea and distress may prevent a full history from being taken. Find out the length of the history and whether there is any chest pain. Check current drug therapy/allergies and establish what emergency prehospital treatment has been administered. Examination usually reveals a tachypnoeic, tachycardic and anxious patient. If the pulmonary oedema is severe, the patient may be cyanosed, coughing up frothy pink sputum and unable to talk. Check pulse and BP and auscultate the heart for murmurs and 3rd/4th heart sounds of gallop rhythm (difficult in a noisy department). Look for ↑JVP (also a feature of PE and cardiac tamponade). Listen to the lung fields: fine inspiratory crepitations (crackles) may be limited to the bases or be widespread. In some patients, wheeze may be more prominent than crepitations. Cardiogenic pulmonary oedema is associated with evidence of ↓cardiac output (peripherally cool and pale). Consider other diagnoses (eg sepsis) in patients who have warm, flushed extremities. Investigation Commence treatment before completing investigations:

  • attach a cardiac monitor and check SaO2 with pulse oximeter
  • obtain ECG to check for arrhythmias, LAD, LVH, LBBB, recent or evolving MI.
  • send blood for U&E, glucose, FBC
  • if severely ill or SaO2 < 90% obtain ABG
  • request old hospital notes/ECGs
  • obtain a CXR and look for features of cardiogenic pulmonary oedema:
    • upper lobe diversion (distension of upper pulmonary veins)
    • cardiomegaly (LV and/or LA dilatation)
    • Kerley A, B or C septal lines
    • fluid in interlobar fissures
    • peribronchial/perivascular cuffing and micronodules
    • pleural effusions
    • bat’s wing hilar shadows

Treat urgently. Provide the following within the first few mins:

  • Check that the airway is clear.
  • Sit the patient up, supported comfortably by pillows and raised back.
  • Provide high flow O2 by tight-fitting face mask.
  • If systolic BP > 90mmHg, give 2 puffs of GTN SL (800micrograms) and commence GTN IVI, starting at 10micrograms/min, increasing every few mins according to clinical response (monitor BP closely and take special care to avoid hypotension). An alternative to GTN IVI is buccal GTN (3-5mg).
  • Give IV frusemide 50-100mg.
  • If the patient has chest pain or is distressed, give very small titrated increments of IV opioid (+antiemetic). Do not give opioids to patients who are drowsy, confused or exhausted as this may precipitate respiratory arrest.
  • Consider inserting a urinary catheter and monitor urine output.
  • Treat underlying cause and associated problems (arrhythmias, MI, cardiogenic shock, acute prosthetic valve failure).

Monitor the SaO2 and the clinical response to this initial treatment. Rapid improvement may occur, due to venodilatation and reduction of preload. If the patient does not improve, recheck ABG and consider the following measures:

  • If ABG reveals hypoxia (pO2 < 9kPa) or hypercarbia (pCO2 > 7kPa), involve ITU to consider CPAP or tracheal intubation/IPPV. CPAP appears safe and effective in acute cardiogenic pulmonary oedema and may avoid the need for intubation.
  • Rapid sequence intubation in the presence of cardiogenic pulmonary oedema may be associated with cardiovascular collapse. Stop nitrates prior to administering anaesthesia and be ready to give pressors ±fluids immediately post-induction.
  • If the patient is hypotensive refer to ITU for treatment of cardiogenic shock (p74). An intra-arterial line, Swan-Ganz catheter and inotropic support (dobutamine) are likely to be required. Echocardiography may be helpful to exclude valve or septal rupture and guide treatment.

Prosthetic valve failure Always consider valve failure in patients with prosthetic valves. A large variety of prosthetic heart valves are in common use. All are associated with some risks (eg embolism, failure, obstruction, infection, haemorrhage from associated anticoagulation), which vary according to the design. Acute failure of a prosthetic aortic or mitral valve results in dramatic acute onset pulmonary oedema with loud murmurs. The patient may deteriorate rapidly and not respond to standard drug treatment. If suspected, resuscitate as described above and urgently call for expert help (ITU team, cardiologist and cardiothoracic surgeon). Emergency transthoracic or transoesphageal echocardiography confirms the diagnosis. Immediate valve replacement is required. P.100
Non-cardiogenic pulmonary oedema Pulmonary oedema may occur in the absence of ↑pulmonary venous pressure. One or more of the following mechanisms may be responsible:

  • ↑capillary permeability
  • ↓plasma oncotic pressure
  • ↑lymphatic pressure

Changes in capillary permeability, secondary to a variety of triggers, is the mechanism most frequently implicated in non-cardiogenic pulmonary oedema, when it occurs as the Adult Respiratory Distress Syndrome (ARDS). Since the mechanisms producing cardiogenic and non-cardiogenic pulmonary oedema differ, so the approach to treatment differs. Causes of non-cardiogenic pulmonary oedema

  • ARDS (sequel to sepsis, trauma, pancreatitis)
  • intracranial (especially subarachnoid) haemorrhage
  • IV fluid overload
  • hypoalbuminaemia (liver failure, nephrotic syndrome)
  • drugs/poisons/chemical inhalation
  • lymphangitis carcinomatosis
  • smoke inhalation
  • near drowning

Approach Distinguishing non-cardiogenic from cardiogenic pulmonary oedema is usually apparent from the history. Evaluate the patient as described on p98 and resuscitate according to ABCs. Treatment needs to be directed towards the underlying cause and according to the physiological disturbance. To estimate the latter, invasive monitoring may be required (urinary, intra-arterial, central venous and Swan-Ganz catheters). Refer to ITU, to provide appropriate IV fluids, inotropes, tracheal intubation, IPPV and PEEP. P.101
Pleural effusion Under normal circumstances, each pleural cavity contains < 20mL fluid. Accumulation of fluid unilaterally or bilaterally occurs in numerous disease processes. Causes Pleural effusions are classified according to their protein content as exudates (>30g/L) or transudates (<30g/L). Exudates

  • pneumonia (bacterial, viral, mycoplasma)
  • malignancy (bronchial carcinoma, mesothelioma, lymphoma)
  • TB
  • PE with pulmonary infarction
  • collagen vascular disease (SLE, rheumatoid arthritis)
  • subphrenic abscess
  • amoebic liver abscess
  • pancreatitis
  • chylothorax (thoracic duct injury—rare)


  • cardiac failure
  • nephrotic syndrome
  • hepatic failure
  • ovarian fibroma (Meig’s syndrome—rare)

Clinical presentation Symptoms are usually due to the underlying disease process, rather than the effusion itself. Occasionally, the former may be asymptomatic and the latter large, causing dyspnoea (initially only on exercise, later also at rest) and a mild dull ache. Signs of an effusion are not apparent until >500mL is present. Dyspnoea, stony dullness to percussion, with absent breath sounds over the effusion are characteristic. Bronchial breathing may be heard just above the effusion. Very large unilateral effusions may produce evidence of mediastinal shift (away from the collection of fluid). Investigations CXR can demonstrate pleural effusions as small as 250mL, as blunting of the costophrenic angle. Other investigations will be required (eg SaO2, ABG, U&E, LFTs, FBC), but depend upon the likely underlying cause. Treatment Provide O2 and resuscitate as necessary, according to the underlying pathology. Emergency therapeutic pleural aspiration is rarely required in A&E, except where haemothorax is suspected. Refer to the medical team for further investigation (including diagnostic/therapeutic pleural aspiration). P.102
Acute asthma—assessment Follow the British Thoracic Society guidelines1 incorporated in pp104-5 to assess and manage adults presenting with asthma. The guidelines are essentially self-explanatory and reflect continuing concern over deaths from asthma. Patients with severe asthma and one or more adverse psychosocial factors (psychiatric illness, alcohol or drug abuse, denial, unemployment) have ↑ mortality. Measure the peak expiratory flow rate and compare it against that expected (see below). The peak flow acts as an immediate triage tool: remember that some patients with life-threatening airways obstruction may be too dyspnoeic to register a peak flow. Make an initial assessment of the severity of acute asthma based upon a combination of clinical features, peak flow measurement and pulse oximetry as outlined below. Moderate exacerbation of asthma

  • increasing symptoms
  • peak flow >50-75% best or predicted
  • no features of acute severe asthma (below)

Acute severe asthma Any 1 of:

  • peak flow 33-50% best or predicted
  • respiratory rate ≥25/min
  • heart rate ≥110/min
  • inability to complete sentences in 1 breath

Life-threatening asthma A patient with severe asthma with any 1 of:

  • peak flow <33% best or predicted
  • SaO2< 92%
  • pO2 < 8kPa
  • normal pCO2 (4.6-6.0kPa)
  • silent chest
  • cyanosis
  • feeble respiratory effort
  • bradycardia, arrhythmia hypotension
  • exhaustion, confusion, coma

Near fatal asthma

  • ↑ pCO2 and/or requiring mechanical ventilation with ↑inflation pressures

Other investigations Obtain ABG if SaO2 <92% or if there are other features of life-threatening asthma. Obtain a CXR if there is:

  • suspected pneumomediastinum or pneumothorax
  • suspected consolidation
  • life-threatening asthma
  • failure to respond to treatment satisfactorily
  • requirement for ventilation

Footnote 1 British Thoracic Society 2003 Thorax 58 (suppl 1). See also http://www.sign.ac.uk and/or http://www.brit-thoracic.org.uk P.103

Figure. Peak expiratory flow rates in normal adults

Acute asthma—management Initial treatment Follow BTS/SIGN guidelines1 summarized as follows:

  • Provide high flow O2.
  • Administer high dose nebulized ß2 agonist (eg salbutamol 5mg orterbutaline 10mg). In severe asthma or asthma that is poorly responsive to the initial nebulizer, consider continuous nebulization.
  • Give a corticosteroid: either prednisolone 30-60mg PO or hydrocortisone (preferably as sodium succinate) 200mg IV.
  • Add nebulised ipratropium bromide (500micrograms) to ß2 agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to ß2 agonist therapy.
  • Consult with senior medical staff to consider a single dose of IV magnesium suphate (1.2-2g IVI over 20mins) for patients with acute severe asthma without a good initial response to inhaled bronchodilator therapy or for those with life-threatening or near-fatal asthma. Note that this is at present an unlicensed indication—see BNF.
  • Avoid ‘routine’ antibiotics.
  • IV aminophylline is no longer part of initial therapy. Use it only after consultation with senior medical staff. It is possible that some individual patients with near-fatal or life-threatening asthma with a poor response to initial therapy may gain additional benefit from IV aminophylline. The loading dose of IVI aminophylline is 5mg/kg over 20mins unless on maintenance therapy, in which case check blood theophylline level and start IVI of aminophylline at 0.5-0.7mg/kg/hr.
  • No benefit for leukotriene receptor antagonists or heliox (helium/oxygen mixture) has been shown in acute asthma.
  • Some patients with acute asthma require rehydration and correction of electrolyte imbalance. Hypokalaemia may be caused or exacerbated by ß2 agonist and/or steroid therapy.

Criteria for admission Admit patients with any features of

  • a life-threatening or near-fatal attack
  • severe attack persisting after initial treatment

Consider for discharge those patients whose peak flow is >75% best or predicted 1hr after initial treatment. Referral to ITU Refer any patient requiring ventilatory support or with acute severe or life-threatening asthma failing to respond to therapy, evidenced by:

  • deteriorating peak flow
  • persisting or worsening hypoxia
  • hypercapnoea
  • ABG showing ↓pH or ↑H+
  • exhaustion, feeble respiration
  • drowsiness, confusion
  • coma or respiratory arrest

Footnote 1 British Thoracic Society 2003 Thorax 58 (suppl 1).See also http://www.sign.ac.uk P.105
Cardiac arrest in acute asthma The underlying rhythm is usually PEA. This is usually secondary to prolonged severe hypoxia or (rarely in a self-ventilating patient) to tension pneumothorax. Give advanced life support according to the standard guidelines on p45 and treat tension pneumothorax if present (p320). P.106
Chronic obstructive pulmonary disease (COPD) Definition, causes and manifestations COPD is characterized by chronic airflow limitation resulting from impedance to expiratory airflow, mucosal oedema, infection, bronchospasm and bronchoconstriction due to ↓lung elasticity. Smoking is the main cause, but other causes, including chronic asthma, α-1 antitrypsin deficiency and chronic infection (eg bronchiectasis) may be responsible. Common manifestations are chronic bronchitis (defined clinically as a productive cough for >3 months for 2 consecutive yrs) and emphysema (defined pathologically as permanent dilatation of airways distal to terminal bronchioles). COPD rarely exists as a single entity and usually a combination of various processes is present. This results in ventilatory compromise, ↑work of breathing and eventually hypoxaemia and sometimes hypercarbia. History Exertional dyspnoea, cough and sputum production are the usual complaints. Find out from the patient (or relatives) relevant past medical history:

  • Present treatment including inhalers, steroids, antibiotics, theophyllines, nebulizers, home O2 treatment.
  • Past history—enquire about previous admissions (including to ITU) with similar complaints. Ask about other illnesses.
  • Exercise tolerance—how far can he/she walk on the flat without stopping? How many stairs can he/she climb? How independent is he/she?
  • Recent history—is this presentation due to a rapid deterioration (eg ↑wheeze or breathlessness). Ask if there has been an ↑volume of sputum or if it has become purulent. Remember that chest injuries, abdominal problems and other infections may cause respiratory decompensation.

Examination Examine for dyspnoea, tachypnoea, accessory muscle use and lip-pursing. Look for hyperinflation (‘barrel chest’) and listen for wheeze or coarse crackles (large airway secretions). Cyanosis, plethora (due to secondary polycythaemia) and right heart failure (cor pulmonale) suggest advanced disease. Look for evidence of hypercarbia: tremor, bounding pulses, peripheral vasodilatation, drowsiness or confusion. Check for evidence of other diagnoses in an acutely breathless patient, particularly: asthma (p102), acute LVF (p98), pneumothorax (p112), PE (p118). Remember that these conditions may coexist with COPD. Investigations

  • SaO2, respiratory rate, pulse rate, BP, T° and peak flow (if possible)
  • CXR (look for pneumothorax, hyperinflation, bullae, heart failure and pneumonia)
  • ECG
  • ABG (or capillary blood gas), documenting the FiO2
  • FBC, U&E, glucose and if pneumonia is suspected, blood cultures, CRP and pneumococcal antigen
  • Theophylline level if taking theophylline
  • Send sputum for microscopy and culture if purulent
  • Take blood cultures if pyrexial

Treatment1 Give O2—remember that hypercapnoea with O2 is multifactorial, but ↑ventilation/perfusion mismatch accompanied by ↑dead space ventilation appear to be more important than suppression of hypoxic drive. The general aim of O2 therapy is to maintain SaO2 > 90% without precipitating respiratory acidosis or worsening hypercapnoea.

  • If the patient is known to have COPD and is drowsy, or has a documented history of previous hypercapnoeic respiratory failure, give an FiO2 of 24-28% via a Venturi mask and obtain ABG immediately. Titrate up the FiO2 with serial ABG sampling until the minimum FiO2 that achieves clinical improvement (or SaO2 90-92%) is reached. Watch for ↑drowsiness or worsening acidosis and respond accordingly (see steps outlined below).
  • For all other patients, including those where the diagnosis is unclear, provide 40% O2 by mask until the history is clarified and ABG result obtained.

Give bronchodilators and steroids

  • Give nebulized salbutamol 2.5-5mg or terbutaline 5-10mg.
  • Consider adding nebulised ipratropium 0.5mg.
  • Use O2 driven nebulizers unless the patient has hypercapnoeic, acidotic COPD, in which case use nebulizers driven by compressed air, supplemented by O2 via nasal prongs at 1-4L/min.
  • Give steroids (eg prednisolone 30mg PO stat or hydrocortisone 100mg IV if unable to swallow).

Other drug treatments

  • Give antibiotics (eg amoxicillin, tetracycline or clarithromycin) if the patient reports ↑purulent sputum or there is clinical evidence of pneumonia and/or consolidation on CXR.
  • Only consider IV aminophylline if there is an inadequate response to nebulised bronchodilators.
  • Only consider doxapram if non-invasive ventilation is unavailable or inappropriate (seek specialist advice).

Non-invasive ventilation If the patient has a pH < 7.35, pCO2> 7kPa, or is becoming increasingly exhausted, agitated or confused, call senior medical and/or ITU staff immediately. Non-invasive ventilation is the treatment of choice for persistent hypercapnoeic ventilatory failure during exacerbations despite optimal medical therapy. Contraindications include apnoea, pneumothorax, severe agitation and inability to tolerate or fit the face mask. Invasive ventilation Formal intubation and ventilation may be indicated depending upon various factors (eg co-morbidity, functional status). Sometimes ventilation is not appropriate, particularly in severe chronic disease. A decision not to ventilate should only be made by experienced staff following careful consideration of the patient’s presentation, past history and degree of disability, after discussion with the patient and their family and if possible, the GP. Keep these patients comfortable with appropriate nursing care and document decisions and reasoning in the case notes. Footnote 1 See National Institute for Clinical Excellence guideline on COPD, 2004 (http://www.nice.org.uk) P.108
Pneumonia Pneumonia involves symptoms and signs of lower respiratory tract infection (breathlessness, productive cough and fever) usually associated with CXR abnormalities. Pneumocystis pneumonia may occur with minimal or no CXR changes. Consider pneumonia in patients with septicaemia or acute confusional states. Causes Bacterial (80–90%) Streptococcus pneumoniae is a frequent cause of community acquired pneumonia. Others include Mycoplasma pneumoniae, Haemophilus influenzae, Legionella, Chlamydia psittaci, Staphylococcus aureus (can cause fulminant pneumonia in patients with influenza). Gram -ve and anaerobic infections are rare. Always consider TB, particularly in chronic alcoholism, poor social circumstances, immigrants and those travelling to developing countries or individuals not BCG vaccinated. Immunosuppressed patients (including those with HIV) are at ↑risk of TB and Pneumocystis carinii pneumonia (PCP). Viral (10–20%) Predominantly influenza and RSV. Rickettsial (1%) Rarely, Coxiella burnetti. Signs and symptoms Fever, cough and production of sputum are the commonest complaints. Breathlessness, pleuritic chest pain, myalgia, rigors or haemoptysis may occur. Note that pneumonia can present without obvious chest signs: Mycoplasma pneumonia may present in children and young adults with sore throat, headache, nausea, abdominal pain and diarrhoea. Legionella can present with constitutional upset, diarrhoea or confusion, particularly in the elderly. Pneumocystis pneumonia in immunosuppressed patients may present with cough, dyspnoea and marked hypoxia, with relatively few other findings. Examination and investigation

  • Check respiratory rate, pulse and BP.
  • Clinically assess oxygenation and perfusion.
  • Look for evidence of dehydration, anaemia or underlying malignant disease.
  • Auscultation usually reveals a patch of inspiratory crackles signs of consolidation (dullness to percussion and bronchial breathing) are present in <25%.
  • Check BMG, SaO2 (obtain ABG if <96%).
  • Check peak flow, if possible, as this may reveal coexisting airway obstruction (eg asthma or COPD).
  • Obtain CXR. Look for patchy or lobar opacification, mass lesions or an air bronchogram. Note that CXR changes may take up to 6wks to resolve following an episode of pneumonia.

Assessment: admit or discharge Of those who present to A&E, some patients with ‘mild’ illness, good social circumstances and no significant co-morbidity may be safely discharged with appropriate antibiotics (eg amoxicillin 0.5-1g PO tds), simple analgesia for pleuritic pain to aid deep breathing/coughing and GP follow-up. Do not discharge patients with any of the following: confusion, urea >7mmol/L, respiratory rate >30/min, systolic BP < 90mmHg, diastolic BP ≤ 60mmHg, age ≥ 65yrs (see: http://www.brit-thoracic.org.uk). If in doubt, discuss with a senior/expert. P.109
Treatment1 Patients deemed suitable for discharge Provide simple analgesia, oral antibiotics and GP follow-up as outlined opposite. Patients admitted, but not severely unwell Start either oral or IV antibiotics, as follows:

  • either amoxicillin 0.5-1g PO tds + erythromycin 500mg PO qds (or clarithromycin 500mg bd)
  • or if IV therapy is needed: ampicillin 500mg IV qds + erythromycin 500mg IV qds (or clarithromycin 500 mg bd)
  • Monitor SaO2 and provide O2 accordingly.
  • Provide simple analgesia.

Acutely unwell Treat patients who are breathless at rest, dehydrated, or with severe constitutional upset with high flow O2 (beware CO2 retention in known severe COPD), IV fluids (±analgesia) and IV antibiotics (eg co-amoxiclav 1.2g IV tds + erythromycin 500mg IV qds). Treat airflow obstruction (eg with nebulised salbutamol), in addition to the above measures. Differential diagnosis Pneumonia-like presentations can occur with pulmonary oedema, pulmonary infarction, pulmonary vasculitis (eg SLE, PAN, Churg-Strauss and Wegener’s), aspergillosis, allergic alveolitis, bronchial or alveolar cell carcinoma, acute pancreatitis and subphrenic abscess. Also, do not forget TB. Footnote 1 See British Thoracic Society guideline, 2004: http://www.brit-thoracic.org.uk P.110
Pulmonary aspiration Aspiration of solid or liquid material into the upper and lower airways is likely when one or more of the following features are present:

  • altered conscious state: head injury, CVA, overdose, sedation, anaesthesia
  • ↓cough and/or gag reflexes: related to above factors and/or bulbardysfunction, intubation/extubation, Guillain-Barré syndrome, multiple sclerosis, myasthenia gravis
  • susceptibility to regurgitation/vomiting: alcohol, full stomach, upper GI tract pathology (including hiatus hernia, oesophageal obstruction, pregnancy, NG tube)

Clinical features Large food particles sufficient to cause complete airway obstruction cause choking, inability to speak, respiratory effort, cyanosis, loss of consciousness and death. Smaller particles may pass through the vocal cords causing coughing, stridor, tachypnoea and wheeze. 80% of patients are aged <4yrs, with peanuts being the classic inhaled objects. Delayed presentation with cough, wheeze, haemoptysis, unresolved pneumonia, abscess formation or empyema occurs in ≈30% often days/wks later. Vomiting/regurgitation is often witnessed and pulmonary aspiration confirmed by seeing gastric contents in the oropharynx or trachea during intubation or following suction. Gastric content is a mixture of semi-solid and liquid material: aspiration leads to a sudden onset of severe dypsnoea, wheeze and cyanosis. Its acid nature causes severe damage to the alveolar-capillary membrane, with denaturation of pulmonary surfactant, ↑pulmonary permeability with oedema and atelectasis. Hydrocarbons (eg petrol, paraffin) cause severe pulmonary toxicity ifaspiration occurs during ingestion or following regurgitation/vomiting. Investigations ABG These show hypoxaemia within mins of acid aspiration. Initially, patients may hyperventilate with ↑pCO2 until pulmonary compliance ↑ work of breathing sufficient to result in hypoventilation. CXR Abnormalities develop in >90% of patients, but this may take hours/days. Appearances depend upon the nature of the aspirated material and the patient’s position at the time of the episode (right lower lobe is most frequently and severely affected, followed by left lower lobe and right middle lobe). In severe aspiration, diffuse bilateral infiltrates and pulmonary oedema similar to ARDS appearances are present. Less severe episodes produce atelectasis followed by alveolar infiltration. Intrapulmonary FBs These (including peanuts) are rarely radio-opaque. The resulting collapse, hyperinflation or consolidation is usually obvious and depends upon whether the obstruction is complete or partial and if supervening infection is present. If the history strongly suggests an inhaled FB but the CXR is normal, consider obtaining an expiratory CXR which may show evidence of air trapping distal to the obstruction. P.111
Prevention Prevention is everything. Pay meticulous attention to airway protection. This may involve positioning (tilt head down on the right hand side), suction to the oropharynx (Yankauer catheter avoiding stimulation of the gag reflex) and if necessary, tracheal intubation. Note that intubationprotects the lower airway against large volume aspiration, but fluidsaccumulating above the cuff can trickle through the held-open cords to the lungs. In at-risk patients, pass a NG tube to empty the stomach. However NG tubes can also predispose to aspiration by preventing closure of the oesophageal sphincters and interfering with coughing and clearing the pharynx. Treatment Correct hypoxia with high FiO2, and give nebulised salbutamol for associated bronchospasm (p104). If particulate aspiration is present, refer for urgent bronchoscopy. Although secondary infection is common, the routine use of antibiotics or steroids is not indicated. P.112
Spontaneous pneumothorax 1 Pneumothorax may occur spontaneously, in the absence of trauma. The management of tension pneumothorax and pneumothorax following trauma is considered on p320 and p326. Spontaneous pneumothorax may occur in previously healthy young individuals or in older patients with ruptured emphysematous bullae. Spontaneous pneumothorax may occasionally be secondary to other underlying disease, including asthma, bronchial carcinoma, Marfan’s syndrome, infection (pneumonia, TB, lung abscess), cystic fibrosis, and oesophageal rupture. Presentation Spontaneous pneumothorax may be heralded by sudden onset unilateral pleuritic chest pain, dyspnoea and sometimes a cough. Classical physical signs may or may not be present (depending upon the size of the pneumothorax): tachypnoea, tachycardia, normal/hyper-resonant percussion note with ↓air entry on the affected side. Rarely, there may be a systolic ‘crunch’ heard at the left parasternal edge with a small left pneumothorax (Hamman’s SIGN). Tension pneumothorax causes tracheal deviation, tachypnoea, tachycardia and hypotension. It requires immediate decompression using a needle in the second intercostal space in the mid-clavicular line (p320). Investigations CXR—look for a rim of lung edge. Pneumothoraces are classified for treatment purposes into small or large, according to whether the visible rim is <2cm or >2cm from the chest wall (see below). Do not mistake an emphysematous bulla or the medial edge of the scapula for a pneumothorax. Remember that on supine X-rays, lung markings may extend to the chest wall, despite a large pneumothorax. This is because in the supine position, air in the pleural cavity moves anteriorly (see p326). An additional lateral decubitus or upright X-ray may help to identify small pneumothoraces. ABG and SaO2 (pulse oximetry) may reveal hypoxia. ECG may show sinus tachycardia and other non-specific features (right axis deviation, T-wave inversion in anterior leads). Treatment1 Provide O2, insert an IV cannula and follow the British Thoracic Society guideline algorithms on pp114-5. These guidelines base treatment upon a categorization of patients according to whether the spontaneous pneumothorax is ‘primary’ (no associated underlying lung disease) or ‘secondary’ (associated with underlying lung disease). Some patients with ‘primary’ pneumothorax may be discharged from A&E with early chest clinic follow-up (if aspiration has been performed, observe for a period first to ensure clinical stability). Advise patients to avoid diving and air travel and to return immediately if they develop breathlessness. Admit all patients with ‘secondary’ pneumothorax to hospital, irrespective of whether they are treated with aspiration and/or intercostal tube drainage. Footnote 1 Henry et al. Thorax 2003; 58 (suppl II): ii:39-52. See: http://www.brit-thoracic.org.uk P.113
Aspiration technique Infiltrate local anaesthetic (eg 1% lidocaine/lignocaine), then insert a 16G IV cannula (consider a special pig-tail cannula) just above the 3rd rib (ie in the 2nd intercostal space) in the mid-clavicular line, or in the axilla as for intercostal drainage. Remove the needle, attach a three-way tap, then aspirate air with a 50mL syringe. Continue aspiration until the patient coughs excessively, or until 2.5 litres of air is removed. Intercostal (chest) drain insertion For cosmetic reasons and to avoid transfixing the pectoral muscles, use an axillary approach (just anterior to the mid-axillary line in the 5th intercostal space). Adopt an open technique as described on p327, with a smaller tube size (eg 10-14 FG). Having sutured the tube in place, obtain a CXR, then refer to the medical team. Note Catheter over guidewire systems (Seldinger technique) may be as safe and effective as small calibre tubes. P.114
Spontaneous pneumothorax 2

Figure. Treatment algorithm for primary pneumothorax1

Footnote 1 Henry et al. Thorax 2003; 58 (suppl II): ii:39-52. See: http://www.brit-thoracic.org.uk P.115

Figure. Treatment algorithm for secondary pneumothorax1

Footnote 1 Henry et al. Thorax 2003; 58 (suppl II): ii:39-52. See: http://www.brit-thoracic.org.uk P.116
Deep venous thrombosis (DVT) Thrombotic occlusion of the deep veins of the leg can be difficult to diagnose and has received much media attention. Less than 25% of patients attending hospital with a suspected DVT have the diagnosis confirmed. The principal concern associated with DVT is the risk of morbidity and mortality from subsequent PE (p118). Risk factors

  • immobility
  • recent surgery (particularly orthopaedic)
  • malignancy
  • IV drug use
  • smoking
  • pregnancy/pelvic masses
  • combined OCP (risk ≈1-3 per million women per year)
  • obesity
  • previous DVT/PE
  • thrombophilia

Clinical features DVT classically produces leg pain with swelling, warmth, tenderness and dilated superficial veins on the affected leg. However, these signs are non-specific and are often not present. A small or partially occluding thrombus may be completely asymptomatic. History and clinical examination alone cannot safely exclude DVT: if a DVT is suspected, investigate further. The presence of respiratory symptoms and/or signs suggests PE—investigate this accordingly (p118). Differential diagnosis

  • muscular tear—typically acute onset
  • rupture of a Baker’s cyst—again, typically acute onset
  • cellulitis or other infection

Investigation and management Both investigation and management of patients with suspected DVT depend to a certain extent on local policy: many hospitals have developed local protocols. Investigation is usually guided by clinical risk stratification (for example, the modified Wells criteria shown below), together with D-dimer assay, compression USS (which can also detect ruptured Baker’s cyst or calf muscle tear) and contrast venography. Note that whilst a D-dimer may help to exclude DVT in low risk patients, all other patients require more definitive investigation. Having diagnosed a DVT, refer the patient to the medical team for anticoagulation and admission/follow-up. Some patients may be suitable for outpatient management after commencing LMWH (eg tinzaparin 175units/kg od SC)—follow local policy. If there is a family history of DVT/PE, consider a thrombophilia screen, but remember that some elements of this are difficult to interpret in the acute stage. Investigate and refer newly diagnosed intercurrent illness or malignancy as appropriate. P.117
Modified Wells criteria for clinical risk stratification in suspected DVT

Clinical feature Score
Active cancer (treatment ongoing, or within 6 months or palliative) 1
Paralysis, paresis or recent POP immobilization 1
Recently bedridden for >3days or major surgery <12wks 1
Localized tenderness along the distribution of the deep venous system 1
Entire leg swelling 1
Calf swelling >3cm compared with asymptomatic leg 1
Pitting oedema (greater in the symptomatic leg) 1
Collateral superficial veins (non-varicose) 1
Total score of 0 is ‘low’ risk, 1 or 2 is ‘moderate’ risk and 3 or more is ‘high’ risk.
(Note: IV drug use is an additional risk factor which does not feature in this list.)

Superficial thrombophlebitis Erythema, tenderness and induration are present along the course of the involved superficial vein, which may feel hard on palpation. Superficial thrombophlebitis may coexist with DVT and can propagate into deep veins. If there is any doubt as to the presence of a DVT, investigate. Otherwise, treat with NSAID. Pain usually improves over 1-2wks. P.118
Pulmonary embolus Pulmonary thromboembolism is a common life-threatening problem, responsible for many deaths each year. There may be no clinical evidence of DVT. History PE is notoriously difficult to diagnose. Suspect it in any patient with: pleuritic chest pain, dyspnoea, syncope, cough or haemoptysis. More than 80% have pre-disposing risk factors (see below and risk factors for DVT, p116). Examination In small PE, physical signs may be absent or subtle (mild fever, tachycardia, scattered crepitations or pleural rub). Search carefully for DVT (p116). In large PE, the patient is usually cyanosed, tachycardic, dyspnoeic and hypotensive. The JVP is ↑ (with prominent ‘a’ waves). Turbulent flow around the PE occasionally produces an audible murmur in the pulmonary area. Investigation If suspected, obtain the following:

  • SaO2 and ABG —ideally on air. This will allow detection of slightly low pO2 (<12kPa). The pCO2 may be ↓ (<4.5kPa), due to hyperventilation.
  • ECG—a number of changes may occur, although ‘S1, Q3, T3’ is rarely seen. Look for: sinus tachycardia, AF, RBBB, RAD (‘S1’), Q wave and inverted T in III (‘Q3, T3’), T inversion in V1-4.
  • CXR—this may show pulmonary oligaemia, an elevated hemidiaphragm, a small pleural effusion, linear opacities (the result of previous PEs).
  • FBC, ESR, U&E—there may be ↑ WCC

All of these investigations may be normal despite PE. D-dimer is usually ↑ in PE, but is non-specific. Local protocols may use it to effectively exclude PE in those identified as being at low risk. If the diagnosis is probable or possible, start treatment (see below) and refer for further investigations (V/Q lung scan and/or CT pulmonary angiography). In suspected massive PE, obtain expert help urgently and consider echocardiography. Treatment

  • Secure the airway and provide high flow O2 by face mask.
  • Obtain venous access.
  • Monitor respiration, SaO2, ECG, pulse, BP and urine output.
  • Assess the risk of PE (see below). Start anticoagulation pending further investigation in those patients judged to have an ‘intermediate’ or ‘high’ probability of PE: give LMWH (eg tinzaparin 175units/kg SC) in stable patients; in unstable patients give 10,000 units IV heparin as a bolus over 5mins, then start a continuous heparin IV infusion at 1000 units/h. Refer for further investigation.

Suspected massive PE

  • In patients with marked hypoxia and/or cardiovascular compromise, call for urgent CCU/ITU expert help: intra-arterial and CVP lines are likely to be required, together with inotropic support.
  • Give IV 0.9% saline/colloid according to CVP to maintain a high normal right ventricular filling pressure.
  • Insert a urinary catheter to monitor urine output.
  • Consider thrombolytic therapy under expert guidance: tPA (alteplase, eg starting dose 10mg IV over 1-2mins, then IVI 90mg over 2hrs) may be indicated before a definitive diagnosis has been made if cardiac arrest has occurred or is imminent.


Figure. ECG changes of major acute PE

Assessment of clinical risk of PE1 In patients with clinical features compatible with PE (breathlessness and/or tachypnoea, with or without chest pain), consider the following two statements:

  • Another diagnosis is unlikely
  • A major risk factor is present (any 1 of: major abdominal/pelvic surgery, postoperative intensive care, puerperium, lower limb fracture, metastatic/ advanced malignancy, hospitalization/institutional care, hip/knee replacement, Caesarian section, late pregnancy, varicose veins, abdominal/pelvic malignancy, previous proven PE)

If both are present, the patient has a ‘high’ probability of PE, if just 1 is present there is an ‘intermediate’ probability of PE and if neither is present, the probability of PE is ‘low’. Footnote 1 British Thoracic Guidelines. Thorax 2003; 58: 470-84. See: http://www.brit-thoracic.org.uk P.120
Upper GI bleeding Treatment demands a combined approach by physicians, surgeons and A&E staff. Adopt a low threshold for admission—hospital mortality is ≈10%. Factors associated with ↑ mortality include advanced age, shock on presentation, co-morbidity (hepatic or renal failure, cancer, ischaemic heart disease). Causes of upper GI bleeding Common

  • peptic ulceration
  • mucosal inflammation (oesophagitis, gastritis or duodenitis)
  • oesophageal varices
  • Mallory-Weiss tear
  • gastric carcinoma
  • coagulation disorders (thrombocytopenia, warfarin)


  • aorto-enteric fistula (especially after aortic surgery)
  • benign tumours (eg leiomyomas, carcinoid tumours, angiomas)
  • congenital (eg Ehlers-Danlos, Osler-Weber-Rendu, pseudoxanthoma elasticum)

History Take a detailed history, but remember that resuscitation takes priority. Upper GI bleeding usually presents with haematemesis and/or melaena; bleeding involving the lower GI tract with fresh PR bleeding. However, under certain circumstances, upper GI bleeding may present with fresh PR bleeding. Similarly, proximal colonic lesions may cause melaena. Enquire about the amount and duration of bleeding as well as any previous history of GI bleeding or liver problems. Ask about associated symptoms (abdominal pain, weight loss, anorexia). Syncope is a worrying feature as it usually infers a significant bleed. Take a full drug history (ask about aspirin, NSAIDs, warfarin, iron) and enquire about alcohol consumption. Examination Check ABCs. Rapidly assess for evidence of hypovolaemic shock (pulse and respiratory rates, BP, GCS, skin colour/temperature, capillary refill). Look at any available vomit or faeces. Check for abdominal masses, tenderness or surgical scars (including aortic grafting). Look for stigmata of liver disease. Perform a PR examination and check for FOB. Less typical presentations of GI haemorrhage are sometimes seen. These include coma and hepatic encephalopathy. Investigation and diagnosis Request old hospital notes and send blood for FBC, clotting screen, U&E, blood glucose, Group and Save or X-matching (according to clinical features). Urea may be ↑, but creatinine will be normal unless renal function is impaired. Check SaO2 (obtain ABG if <93%) and consider CXR and ECG. Endoscopy is the investigation of choice to identify the source of the bleeding (see below). P.121
Treatment of apparently mild haemorrhage Treat all patients with GI haemorrhage who are alert with no evidence of hypovolaemia as follows:

  • check airway/breathing and provide high flow O2 by face mask
  • insert 2 large (14G) IV cannulae, send FBC, U&E, clotting, Group and save
  • start IV fluids if regular monitoring suggests developing hypovolaemia (see below)
  • consider omeprazole (40mg diluted in 100mL saline as IVI over 30mins) if known peptic ulcer, otherwise avoid H2 antagonists or proton pump inhibitors acutely
  • keep fasted and refer to specialist team for admission and endoscopy

Treatment of moderate/severe haemorrhage If there is evidence of hypovolaemia, treat as described above, plus:

  • send an urgent X-match for 4-6 units of blood
  • start IVI 0.9% saline or Hartmann’s 1000mL, followed by blood asnecessary, aiming to maintain Hb ≈8-10g/dL
  • if the patient is anticoagulated, or has a clotting disorder (eg due to liver disease), discuss with a haematologist and give vitamin K/clotting factors/FFP accordingly
  • call the endoscopic and surgical teams and anaesthetist/ITU staff
  • insert a urinary catheter and monitor the urine output
  • once fluid replacement has commenced, consider inserting a central venous line (see p56), so that subsequent fluid replacement can be guided by the CVP.
  • ensure that patients with severe uncontrolled variceal bleeding, severe encephalopathy, hypoxia, acute agitation or evidence of aspiration have their airways secured, if necesaary by rapid sequence induction, tracheal intubation and IPPV

Managing severe haemorrhage possibly due to varices Some hypovolaemic patients may have clinical evidence suggesting that the bleeding has resulted from oesophageal varices (eg past history of varices, clinical features of hepatic failure). Arrange emergency endoscopy and endoscopic treatment (eg injection of varices) by an experienced practitioner. In the meantime:

  • Give vasopressin (20units IV over 15mins combined with a GTN infusion), or terlipressin (2mg IV repeated every 4-6hrs). Evidence suggests that each of these may ↓bleeding, but only terlipressin has been shown to ↓mortality.
  • If experienced in the technique, insert a 4 lumen Sengstaken/Minnesota tube. Inflate the gastric balloon then the oesophageal balloon to a pressure of ≈30-40mmHg to tamponade the bleeding varices. Regularly aspirate the oesophageal and gastric ports. This may stop bleeding in ≈90% of cases, but up to 50% re-bleed on deflation.
  • Consider prophylactic antibiotics (eg ciprofloxacin or second/third generation cephalosporin) which may ↓mortality in severe variceal haemorrhage.

See http://www.bsg.org.uk/guidelines/34362-15.html P.122
Lower GI bleeding The commonest cause of apparent lower GI bleeding is upper GI haemorrhage. ≈20% of acute GI haemorrhage is from the colon or rectum. Angiodysplasia and bleeding from diverticulae are the most frequent causes, but inflammatory bowel disease, or very rarely, aorto-enteric fistulae may be responsible. Lower GI haemorrhage often settles spontaneously: localisation of the bleeding source may be difficult. History Nature of bleeding Remember that melaena may occur following small bowel or proximal colon bleeding as well as upper GI haemorrhage. Conversely, large volumes of fresh or ‘plum-coloured’ rectal bleeding may actually follow upper GI haemorrhage. Bloody diarrhoea suggests inflammatory bowel disease or infective colitis. Associated symptoms Weight loss, anorexia or a change in bowel habit raise suspicion of colonic carcinoma. Abdominal pain may be a feature of ischaemic colitis, inflammatory bowel disease or carcinoma. Anal pain commonly occurs with anal fissure or complication of haemorrhoids. Syncope or postural dizziness May indicate significant haemorrhage. Past medical history Ask about inflammatory bowel disease, peptic ulceration or other illnesses. Previous aortic surgery with graft insertion can rarely result in formation of an aorto-enteric fistula (symptoms include sporadic or fulminant bleeding, often with syncope). Drug history Ask about salicylates, NSAIDs, corticosteroids and anticoagulants. Family and social history Note any family history of peptic ulcers, inflammatory bowel disease. Enquire about alcohol consumption. Examination First assess for signs of hypovolaemia and commence resuscitation if necessary. Document pulse, BP (comparing erect and supine may be useful, noting any postural drop), T° and SaO2. Examine the abdomen and rectum in all cases. Investigations Obtain blood for X-matching (ask for 4-6 units of type specific if urgent), FBC, U&E, glucose and coagulation studies. Perform an ECG on any patient >50yrs. Treatment Patients with signs of hypovolaemia require immediate resuscitation:

  • give high flow O2
  • attach monitoring (cardiac monitor, SaO2, BP monitoring)
  • insert two large bore IV cannulae
  • give 1 litre of 0.9% saline or Hartmann’s solution IV stat and give further fluids according to response
  • insert a NG tube
  • insert a urinary catheter
  • consider the need for a central venous line
  • contact the surgical team and the anaesthetist

Headache Headaches of non-traumatic origin account for ≈0.5% of A&E attendances, of which 10-15% have serious underlying pathology. Patients typically present in one of three ways:

  • Severe headache, unlike any previous one (‘first severe’ or ‘worst ever’).
  • Headache with associated worrying features (altered mental status, fever, focal neurology).
  • Chronic severe headache unresponsive to treatment.

Aetiology Differentiating between potentially life-threatening and relatively non-serious causes is difficult. Primary headaches

  • migraine
  • tension headaches
  • cluster headaches
  • miscellaneous (benign cough headache, benign exertional headache, headache associated with sexual activity)

Secondary headaches

  • head injury
  • vascular (stroke, intracranial haematoma, subarachnoid haemorrhage, unruptured arterio-venous malformation, venous thrombosis, hypertension)
  • non-vascular intracranial disorder (↑CSF pressure, post-LP, intracranial tumour)
  • substance misuse or withdrawal (including analgesia withdrawal or rebound)
  • infection (encephalitis or meningitis)
  • metabolic (hypoxia, hypercapnoea, hypoglycaemia, CO poisoning, dialysis)
  • craniofacial disorder (pathology of skull, neck, eyes, nose, ears, sinuses, teeth, mouth, temporomandibular joint dysfunction)
  • neuralgias (trigeminal, occipital and other cranial nerves)

Approach Use a detailed history and examination (including vital signs and neurological examination) to search for potentially serious causes. Look particularly for the following (some typical features in brackets):

  • subarachnoid haemorrhage (sudden and severe onset, syncope)—p126
  • meningitis or encephalitis (fever, neck rigidity)—p214
  • head injury (history or signs of trauma)—p342
  • ↑ICP (papilloedema, loss of retinal vein pulsation)—p342
  • stroke (focal neurological signs)—p142
  • acute glaucoma (painful red eye, ↓VA, irregular semi-dilated pupil)—p521
  • giant cell arteritis (jaw pain, temporal artery tenderness)—p518

History Features in the history suggesting possible serious pathology are:

  • sudden onset headache
  • worst headache ever
  • dramatic change in pattern of headache
  • known immunocompromise or malignancy
  • the presence of a ventriculo-peritoneal shunt
  • headache coming on during exertion
  • new onset headache in those aged >50yrs

Ask about drugs and the possibility of toxins (eg CO) P.125
Examination Assess vital signs, including GCS, pulse rate, respiratory rate, BP, T° and SaO2. Perform a thorough examination to include:

  • Feel the head for muscular tenderness, arterial tenderness, trigger points for neuralgia, and look for evidence of head injury.
  • Examine the eyes for VA, pupil reactions, eye movements and papilloedema.
  • Palpate the sinuses for tenderness.
  • Look in the ears for haemotympanum or infection.
  • Check the oral cavity for infection.
  • Look for evidence of purpura/rash of meningococcal infection.
  • Complete the neurological examination (include cranial nerves, limb power and reflexes).

Kernig’s sign may be useful: straightening the knee whilst the hip is flexed produces ↑discomfort in the presence of meningeal irritation. Management Investigation and emergency treatment will be tailored according to the presentation of the patient, based upon the likely diagnosis. In thosesituations where the diagnosis is unclear, but where there are features suggesting serious pathology, check FBC, ESR, U&E, blood glucose, blood cultures, ABG and consider CT scan. Arrange urgent CT scan for patients with altered mental status, focal signs and for any acute onset headache, particularly if associated with nausea and/or vomiting. Patients withsuspected meningitis need CT prior to LP if there are focal neurological signs or suspicion of ↑ICP (see p342). Admit and investigate patients with sudden severe headache suggestive of subarachnoid haemorrhage, even if physical signs are absent. P.126
Subarachnoid haemorrhage Consider subarachnoid haemorrhage in any ‘worst ever’ or sudden onset headache Atraumatic subarachnoid haemorrhage can occur at any age and is an important cause of sudden collapse and death. Most bleeds follow rupture of saccular (‘berry’) aneurysms in the circle of Willis. Other bleeds may be due to arterio-venous malformations, tumours or connective tissue disorders. History Up to 70% of patients with subarachnoid haemorrhage report rapid onset or ‘worst ever’ headache. This is classically described as ‘like a blow to the back of the head’, accompanied by neck pain, photophobia and vomiting. In 25%, exertional activities precede the event. The patient may present after syncope or fits. Drowsiness and confusion are common. ‘Warning headaches’ may precede subarachnoid haemorrhage. Unilateral eye pain may occur. Examination There may be focal motor and sensory signs due to intracerebral extension of the haemorrhage or vasospasm, subhyaloid haemorrhages (blotchy haemorrhages seen in the fundi) or cranial nerve palsies. Oculomotor nerve palsy is characteristic of a berry aneurysm involving the posterior communicating artery. Although neck stiffness is a ‘classical’ feature, it is often absent in A&E presentations, either because meningeal irritation has not yet occurred, or because the patient is deeply unconscious. Investigation This may need to proceed alongside resuscitation in seriously ill patients.

  • Obtain venous access and check BMG, FBC, clotting screen, U&E.
  • CXR may show changes of neurogenic pulmonary oedema.
  • ECG may demonstrate ischaemic changes.
  • Arrange urgent CT scan for all suspected cases (maximally sensitive within 12hrs). Admit patients with a history suggestive of subarachnoid haemorrhage for LP even if CT scan is normal.
  • Involve the neurosurgical team early.

Treatment Tailor this according to the presentation and the need for resuscitation:

  • Give O2 to all patients.
  • Provide adequate analgesia and antiemetic. Codeine (30-60mg PO), paracetamol (1g PO) and/or NSAID may suffice. Some patients require more potent analgesics (eg morphine titrated in 1mg increments IV according to response)—proceed slowly to avoid drowsiness.
  • If unconscious (GCS < 8), severely agitated or combative, tracheal intubation (with GA) will allow IPPV and control of pCO2 to within normal levels. Insert a urinary catheter and arterial line.

Contact neurosurgical team—further treatment options include:

  • Nimodipine (60mg PO every 4hrs or 1mg/hr IVI) to prevent and treat ischaemic neurological deficits secondary to vasospasm.
  • Mannitol IV (eg 200mL of 10%) if there is evidence of ↑ ICP.

Migraine Patients with recurrent migraine rarely attend A&E unless symptoms are different from usual—take care to avoid missing more serious conditions. The pathogenesis of migraine is not entirely clear, but there is initial vasoconstriction and subsequent vasodilatation of both intracranial and extracranial blood vessels. Presentation Precipitants include fatigue, alcohol, menstruation, OCP, hunger, chocolate, cheese, shellfish and red wine. A prodrome lasting 5-30mins occurs in a third of patients, with blurred vision, photophobia or scintillating scotomata (an area of ↓ or absent vision surrounded by moving zig-zag lines), malaise, anorexia and vomiting. A few experience hemiparaesthesiae, mild unilateral weakness, ataxia or dysphasia. The following headache may last 4-72h and is usually ‘throbbing’ and unilateral, but may be generalized. Photophobia, nausea or phonophobia is common. Rare forms of migraine Hemiplegic migraine Profound hemiplegia precedes the development of the headache by 30-60min. The weakness and other focal deficits usually resolve quickly. Occasionally, they may be slow or fail to resolve. Basilar migraine Brainstem disturbances, with impaired consciousness, vertigo, dysarthria, diplopia and limb weakness. Ophthalmoplegic migraine Transient unilateral ophthalmoplegia and ptosis which may last several days. Acephalgic migraine Very occasionally, neurological defects may be present without headache. Examination Look for evidence of other serious diagnoses. Treatment of acute attacks

  • Give simple analgesia (eg paracetamol 1g PO PRN qds or NSAID) in combination with an anti-emetic (eg metoclopramide 10mg PO, or if vomiting, IM).
  • Refer to the medical team for admission patients who have neurological signs, altered mental status or where there is diagnostic uncertainty (including change in severe headache pattern).
  • Acute attacks which fail to respond to simple measures may respond to other drugs, but these are associated with significant adverse effects. 5HT1 agonist sumatriptan (6mg SC or 50mg PO or 20mg intranasally) or ergotamine (1mg PO) are effective, but if patients have not been prescribed these previously, seek specialist advice first.

Sumatriptan causes vasoconstriction and is therefore contra-indicated in IHD, uncontrolled hypertension, basilar and hemiplegic migraine. Rebound headache may occur in up to 45%. Do not prescribe until ergotamine has been stopped for 24hrs. Similarly, do not prescribe ergotamine until sumatriptan has been stopped for 6hrs. Ergotamine is best avoided (see BNF). It causes nausea, vomiting, abdominal pain and muscular cramps. It is contra-indicated in peripheral vascular disease, IHD, pregnancy, breast feeding, hemiplegic migraine, Raynaud’s disease, liver and renal impairment and hypertension. P.129
Other causes of headache Cluster headache 90% occur in men. Often there is a family history. Headache usually occurs at night, waking the patient. Sometimes alcohol may act as a precipitant. Headaches are typically ‘clustered’ into up to eight attacks per day each lasting between 15 and 180 minutes. Pain is usually severe, unilateral and centred upon the eye. Associated symptoms include conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis. Treatment High flow O2 (12 litres/min via reservoir mask) for 15mins sometimes provides relief. Otherwise, use paracetamol/NSAID. Consult before contemplating starting ergotamine or sumatriptan. Trigeminal neuralgia Characterized by stabbing unilateral pain within the distribution of the trigeminal nerves. Stimulation of the ‘trigger area’ (eg by touching, hair brushing or even chewing) induces very severe pain. Treat with carbamezepine and oral analgesia, but consider admission if the pain is severe and unrelieved. Tension headache This is a common condition, but ensure that the diagnosis is only made after exclusion of more serious pathology. The history may be described in a dramatic manner. The headache is usually continuous, pressing or tight (‘band-like’) in nature. It is usually bitemporal, or occipital. Usual features of migraine are absent and the headache does not worsen with exertion. Examination often reveals pericranial muscle tenderness, but is otherwise normal. Treat with simple analgesia (eg paracetamol 1g PO qds PRN) and advise GP follow-up. Reassure the patient that a thorough history and examination have not revealed any worrying features. Temporal (‘cranial’ or ‘giant cell’) arteritis (see p518) Consider this in all patients >50yrs with recent onset of headache or change in headache pattern. There may be complaints of weight loss, night sweats, low grade fever, jaw claudication and ↓vision (up to 10% present with acute visual loss), shoulder girdle stiffness and muscular aches (polymyalgia). Involvement of the carotid or vertebral arteries may lead to TIAs or stroke. Examination may reveal the temporal arteries to be tender, reddened, pulseless, or thickened. Inital fundoscopy is usually normal, but papilloedema can occur later in the disease. Investigation: ↑ ESR >> 40mm/hr, often with a low grade anaemia and leucocytosis. A normal ESR does not exclude temporal arteritis. Treatment: in view of the serious risk of rapidly progressive visual loss, if temporal arteritis is suspected give 200mg IV hydrocortisone (or 40mg prednisolone PO) immediately. Refer to the neurologist as an emergency—the diagnosis may be confirmed by temporal artery biopsy. Space-occupying lesions If the headache is always located on the same side, consider spaceoccupying lesions and arterio-venous malformations. Headaches that are dull, aching and made worse by lying down or straining are typical of space occupying lesions. P.131
Malignant hypertension Hypertension is an unusual cause of headaches, but is seen in patients with malignant hypertension and diastolic BP > 130mmHg (p91). Ventricular shunts Assume that any patient who presents with headaches associated with a ventricular shunt has infection/blockage and refer as an emergency. Associated drowsiness is a particular pointer to blockage. Analgesic headache Chronic use of simple analgesics, sympathomimetics, ergotamine or cocaine is associated with headaches. Stopping or starting certain medications (eg OCP) can also cause headache, as can withdrawal from caffeine. Exclude serious causes and advise GP follow-up with advice on medication use. Cerebral venous thrombosis This is more common than was previously realized. It presents in similar fashion to subarachnoid haemorrhage: sudden onset headache with nausea and vomiting. It may be associated with sinus infections, pregnancy and the post-partum period. The diagnosis may be missed on CT, but a clue includes ↑ ICP at LP. Meningitis (see p214) Encephalitis Miscellaneous causes Headaches may also result from:

  • Hypoxia and hypercapnoea
  • Poisons eg CO and solvents (p202)
  • Drugs eg nitrates, sildenafil
  • Post-traumatic (p356)

The unconscious patient 1 Common causes of altered consciousness are:

  • hypoglycaemia
  • drug overdose
  • head injury
  • stroke
  • subarachnoid haemorrhage
  • convulsions
  • alcohol intoxication

Other causes to consider include:

  • respiratory failure
  • cardiac failure
  • arrhythmias
  • hypovolaemic shock
  • anaphylaxis
  • hepatic/renal failure
  • hypothermia/hyperthermia
  • meningitis/encephalitis
  • malaria
  • non-convulsive status epilepticus
  • Wernicke’s encephalopathy

Treatment may be needed before any diagnosis is made: remember

  • Airway
  • Breathing
  • Circulation

The ambulance crew and the patient’s relatives and friends may have important information: ensure that they stay to impart this. Initial resuscitation Airway and cervical spine Whatever the cause of coma, a patient may die or suffer brain damage due to airway obstruction, respiratory depression or circulatory failure. Clear and protect the airway immediately, and immobilize the cervical spine if trauma is suspected. Breathing If breathing appears inadequate ventilate with O2 using a self-inflating bag with an O2 reservoir. An uninjured patient who seems to be breathing adequately can be examined supine, but nurse him/her in the recovery position to ↓risk of airway obstruction. Record respiratory rate. Circulation Measure pulse and BP. Observe and feel the skin for colour, sweating and T°. Obtain reliable venous access. Monitor ECG. Replace IV fluid if indicated. Conscious level Assess level of consciousness using GCS (p349). Check the blood glucose (initially by BMG) and treat hypoglycaemia immediately (p147). Record pupil size. Give slow IV thiamine (i.e. 2 pairs of Pabrinex® ampoules in 100mL 5% dextrose over 15mins—see BNF) to patients with a history of alcoholism or who appear malnourished. P.133
History Investigate the following:

  • how was the patient found?
  • when was he/she last seen?
  • is there any suggestion of trauma?
  • is there any history of fits?
  • has there been recent foreign travel?
  • previous symptoms and medical history (including depression).
  • note any drugs available.
  • check previous A&E records and hospital notes.

The unconscious patient 2 Examination Examine the patient all over for signs of illness and injury. Check clothes and possessions for tablets and for cards or bracelets warning of pre-existing disease. If respiratory rate ↑ consider: airway obstruction, aspiration, pneumonia, DKA, hepatic/renal failure, poisoning by salicylates, methanol or ethylene glycol. Respiratory depression may be due to poisoning (eg opioids, barbiturates, tricyclic antidepressants) or ↑ICP. Brainstem compression or damage by a stroke may cause rapid, irregular or intermittent (Cheyne-Stokes) breathing. If bradycardic consider: hypoxia, complete heart block, ↑ ICP, digoxin or ß-blocker poisoning (p192). If tachycardic consider: airway obstruction, hypoxia, hypovolaemia, SVT, VT, or anticholinergic overdose. AF may be associated with cerebral emboli. Hypotension suggests hypoxia, shock (hypovolaemic, anaphylactic, septicaemic), or poisoning. Hypertension may be due to ↑ICP. Skin: look for pallor, cyanosis, jaundice, spider naevi, skin crease pigmentation (Addison’s disease), rashes (eg purpura in meningococcal infection or DIC), injection marks (drug addiction or medical treatment) and signs of trauma. Erythema or blistering over pressure points indicate the patient has been unconscious for some hrs. Measure rectal T° with a low-reading thermometer if the skin feels cold. Coma is common at <30°C (p256). Neurological examination should include GCS, limb strength, muscle tone and reflexes, optic fundi, ear drums, neck stiffness (except in neck injury) and palpation of the fontanelle in babies. Lateralizing signs, such as facial or limb weakness, may be caused by a stroke, intracranial bleeding or pre-existing problems (eg previous stroke or Bell’s palsy). Ocular nerve palsy or divergent squint with coma may indicate Wernicke’s encephalopathy, requiring IV thiamine. Look for subtle signs of seizure activity (eg twitching of ocular muscles or eyelids, unusual limb movements) which may indicate non-convulsive status epilepticus. Look at the fundi—spontaneous central retinal venous pulsations are rare with ↑ ICP. Subhyaloid haemorrhages (blotchy fundal haemorrhages) suggest subarachnoid haemorrhage. Hypoglycaemia can cause localised weakness and coma and mimic stroke (p146). Coma without lateralizing signs is usually due to poisoning, a post-ictal state, brainstem stroke or hepatic failure: extensor plantar reflexes are common in these conditions. Tricyclic antidepressants often cause coma with dilated pupils, a divergent squint, ↑muscle tone, jerky limb movements and extensor plantars. In severe poisoning there may be muscle flaccidity with respiratory depression and ↓reflexes (p188). Coma with small pupils and respiratory depression suggests opioid poisoning (p182). In unexplained coma, give a therapeutic trial of naloxone (0.8-2mg IV), observing for changes in conscious level, respiratory rate and pupil size. P.135

  • BMG and blood glucose (in every unconscious patient), but do not wait for the lab result to confirm this before starting treatment
  • ABG (record FiO2 and whether breathing spontaneously or IPPV)
  • FBC, prothrombin time, U&E
  • check paracetamol and salicylate levels if poisoning is suspected:paracetamol alone does not cause coma (except in late cases with liver failure), but a mixture of drugs may have been taken. Drug screening for sedatives/hypnotics is not needed, but in unexplained coma keep blood for later analysis
  • ECG may show arrhythmias or features of anticholinergic poisoning
  • CXR may show pneumonia, aspiration, trauma or tumour
  • CT scan may be needed to diagnose subarachnoid haemorrhage, stroke or head injury

Psychogenic coma Patients sometimes pretend to be unconscious. It can be difficult to be certain of this—exclude other causes first. Suspect psychogenic coma if serious pathology has been excluded and:

  • When the eyes are opened, only the sclera show as the eyes deviate upwards (Bell’s phenomenon).
  • When the patient’s hand is dropped onto his/her face, it does not hit the face.
  • Cold caloric testing results in nystagmus.

Collapse and syncope Syncope is a sudden, transient loss of consciousness, with spontanous recovery. The priorities are:

  • to identify serious or life-threatening problems and institute treatment
  • to decide which patients require admission
  • to decide which patients require follow-up

History of syncopal episode Was it a simple faint? Vasovagal or neurally mediated syncope is common. It is often a response to an overwarm environment or prolonged standing and can be precipitated by sudden fright or visual stimuli (eg sight of blood). Other contributors are large meals (or conversely, prolonged starvation) or alcohol. There are usually premonitory symptoms of feeling unwell, nauseated, dizzy or tired, with yawning, blurred or ‘tunnel’ vision or altered hearing. If the fainter cannot get supine (eg bystanders keeping them upright), seizure-like twitching may occur (convulsive syncope). Vomiting and incontinence may occur and so do not reliably discriminate seizures from faints. Was it a seizure? An eyewitness account is crucial if there is no past history of seizures. Ask what the witnesses actually saw (do not assume they know what a ‘fit’ looks like). There should typically be no prodrome, there is often a cry followed by tonic/clonic movements. Cyanosis, saliva frothing from the mouth, tongue biting, or incontinence suggest a generalized seizure. Post-ictal drowsiness or confusion is normal—very rapid recovery questions the diagnosis. Was it a cardiac event? Cardiac syncopal events are also abrupt in onset (eg collapse due to hypertrophic obstructive cardiomyopathy) and may be accompanied by pallor and sweating. Recovery may be rapid with flushing and deep/sighing respiration in some cases (eg Stokes-Adams attacks). Nausea and vomiting are not usually associated with syncope from arrhythmias. Ask about past episodes, chest pain, palpitations or history of cardiac disease. Syncope associated with exertion is worrying: possible causes include aortic or mitral stenosis, pulmonary hypertension, cardiomyopathy or coronary artery disease. Other causes Carotid sinus syncope is neurally mediated and often occurs with shaving or turning the head. Syncope may be due to medication effects (eg GTN, ß-blockers, anti-hypertensives). Syncope may be the presenting feature of subarachnoid haemorrhage, ruptured ectopic pregnancy, aortic or carotid dissection, PE or GI bleed. Assessment and treatment If a patient suddenly loses consciousness in A&E, assess responsiveness and check for a pulse. Keep the airway clear, give O2 and monitor pulse and ECG. Note any neurological signs during the episode and obtain BP, SaO2 and BMG. Patients seen following syncope Obtain a detailed account from the patient and witnesses. Look for signs of tongue biting, incontinence or other injuries, examine the heart for murmurs, arrhythmias or abnormalities. Do a neurological examination and look for focal signs. Do postural tests (supine and standing or sitting pulse and BP). A degree of postural hypotension is common, but postural symptoms (eg dizziness, weakness etc) are always significant (look for causes of hypovolaemia eg GI bleed, ectopic pregnancy). Do a BMG to exclude hypoglycaemia and an ECG looking for arrhythmias, LVH, ischaemia, previous or acute MI, and QT prolongation. Disposal It may be appropriate to discharge patients with full recovery, appropriate history for vasovagal syncope and a normal examination. Admit patients with continuing symptoms, abnormal examination or any worrying presenting features. P.137
Diagnoses not to be missed

  • GI bleed: syncope (± postural symptoms) indicate significant blood loss and hypovolaemia. Perform PR examination to check for blood/melaena.
  • Ectopic pregnancy: suspect this in women with syncope and abdominal pain or gynaecological symptoms. Do a pregnancy test in all these cases.
  • Ruptured abdominal aortic aneurysm.
  • PE (p118).

Acute generalized weakness The complaint of weakness may be a feature of common neurological problems (eg TIA/stroke), or accompany many of the causes of collapse (see p136). Remember also that, less commonly, generalized muscle weakness may be the presentation of a number of other diseases, including:

  • Guillain-Barré syndrome
  • myasthenia gravis
  • tetanus
  • multiple sclerosis
  • spinal cord compression
  • acute periodic paralysis
  • polymyositis
  • alcoholic myopathy
  • botulism
  • diphtheria
  • lead poisoning

Guillain-Barré syndrome This is characterized by progressive symmetrical weakness, spreading from distal muscles to involve proximal muscles. There may be muscle tenderness, loss of muscle reflexes, sensory symptoms (paraesthesiae of fingers and toes) and disturbance of the autonomic nervous system (hyper- or hypotension, tachy- or bradycardia, bladder atony). Beware respiratory failure, which may rapidly progress to respiratory arrest. If suspected, refer to the medical team/ITU. Myasthenia gravis Results in painless weakness in which the muscles are fatiguable, but tendon reflexes and pupil responses are normal. Ptosis, diplopia and blurred vision are the commonest presentations. Usually, cranial nerves are involved to a greater extent than limb muscles and the distribution is asymmetrical. Crises may present with severe muscle weakness in which the major concern relates to respiratory compromise—the patient may require emergency temporary ventilatory support. If the diagnosis is suspected in a patient not known to have myasthenia gravis, refer to a specialist who may wish to perform an edrophonium test. Patients with known myasthenia gravis may present with weakness due to under-treatment, over-treatment (cholinergic crisis) or other causes. Refer to the medical team for investigation. P.139
Transient ischaemic attacks A TIA is an episode of transient focal neurological deficit lasting <24h. A TIA gives major warning for the development of stroke (5% within 48hrs, up to 50% in 5yrs). Even in patients with resolution of symptoms/signs, most have evidence of infarction on CT/MRI. Presentation Carotid territory involvement produces unilateral weakness or sensory changes, dysphasia, homonymous hemianopia or amaurosis fugax. Vertebrobasilar territory involvement produces blackouts, bilateral motor or sensory changes, vertigo and ataxia. Causes Most TIAs result from thrombo-embolic disease involving either the heart (AF, mitral stenosis, artificial valves, post-MI) or extracranial vessels (carotid artery stenosis). Other causes include:

  • hypertension
  • polycythaemia/anaemia
  • vasculitis (temporal arteritis, polyarteritis nodosa, SLE)
  • sickle cell disease
  • hypoglycaemia
  • any cause of hypoperfusion (eg arrhythmia, hypovolaemia)
  • syphilis

Assessment Document vital signs and perform a thorough neurological examination. Look for possible sources of emboli eg arrhythmias (especially AF), heart murmurs, carotid bruits, MI (mural thrombus). Investigations

  • Check BMG.
  • Send blood for FBC, ESR, U&E, blood glucose (and INR if on anticoagulants).
  • Record an ECG to search for MI, arrhythmia or evidence of a period of hypoperfusion (eg trifascicular block).
  • Obtain a CXR.

Management Refer all patients for investigation and follow-up. It is difficult to identify those patients who are most at risk, but usually patients with the following presentations are admitted:

  • continuing symptoms or residual deficit (by definition, not a TIA!)
  • ↑ frequency of TIAs, or more than 4 TIAs within the previous 2 weeks
  • known severe stenosis in a vascular territory corresponding to the TIA symptoms
  • those already taking anti-platelet therapy
  • suspected cardiac source of emboli (eg valvular disease or replacement, AF, MI)
  • those with TIAs who had severe symptoms/signs, even if fullyrecovered
  • diagnostic uncertainty

See http://www.clinicalevidence.com P.141
Stroke A stroke is an acute onset of focal neurological deficit of vascular origin which lasts >24hrs. Pathogenesis 70% of strokes occur in those aged >70yrs, but they can occur at any age. Cerebral infarction (80%) results from:

  • thrombosis secondary to atherosclerosis, hypertension and rarely arteritis
  • cerebral embolism from AF, valve disease/replacement, post-MI, ventricular aneurysm, myxoma, endocarditis or cardiomyopathy
  • an episode of hypoperfusion

Cerebral haemorrhage (20%) is associated with:

  • hypertension (rupture of small damaged arteries in the brain parenchyma)
  • subarachnoid haemorrhage (see p126)
  • bleeding disorders (including anticoagulants) and intracranial tumours

Presentation Stroke preceded by neck pain may indicate carotid/vertebral artery dissection or subarachnoid haemorrhage. Headache is an unusual presenting feature of stroke and may indicate a cerebral haemorrhage. Be alert to the possibility of different pathology requiring urgent treatment (eg hypoglycaemia, Todd’s paresis, hemiplegic migraine, meningitis, encephalitis, brain abscess, head injury, Bell’s palsy, ‘Saturday night palsy’, tumours). Undertake a thorough general and neurological examination including:

  • assessment of mental status and GCS
  • signs of meningeal irritation
  • evidence of head or neck injury
  • examination of pupils and cranial nerves
  • assessment of motor function (power and reflexes)
  • assessment of sensory function (including speech and comprehension)
  • examination for cerebellar signs
  • check for sources of embolism (AF, murmurs, carotid bruits)

Localisation on clinical grounds alone can be difficult, and differentiation between infarction and haemorrhage requires CT/MRI. Hemisphere stroke Common, often following infarction in the internal capsule. It may present in a variety of ways, with some or all of the following: contralateral limb weakness, flaccidity, ↓reflexes, sensory loss, receptive or expressive dysphasia, homonymous hemianopia. Aphasia usually suggests left hemisphere stroke; neglect or hemi-attention usually a right hemisphere stroke. The patient may be unable to gaze to the contra- lateral side from the stroke. Pontine stroke Sudden occlusion of the basilar circulation may cause quadriplegia and the ‘locked-in’ syndrome, in which the patient is able to understand his surroundings, but is unable to respond. Other features are pinpoint pupils and pyrexia. Midbrain stroke May produce coma, oculomotor nerve palsy, dilated pupils, hemi- or quadriparesis. Cerebellar stroke May cause headache, vertigo, vomiting, nystagmus and ataxia. Lateral medullary syndrome Sudden occlusion of the posterior inferior cerebellar artery results in characteristic features: vertigo and vomiting. Ipsilaterally there may be: palatal paralysis, Horner’s syndrome, cerebellar signs, sensory loss in the face. Contralaterally there may be sensory loss in the body. P.143
Investigation Examine and investigate firstly to exclude the conditions listed opposite as possible differential diagnoses and secondly to confirm the diagnosis of stroke. Search in particular for treatable underlying disease. The following investigations are a minimum requirement: BMG, FBC, ESR, U&E, blood glucose, ECG, CXR. Monitor with pulse oximeter (if SaO2<93% obtain ABG) and cardiac monitor. Many patients presenting with a stroke will have an extensive past medical history—therefore request old hospital records at an early stage. Emergency CT Arrange emergency CT scan where there is any doubt about the diagnosis or if there is a possibility of benefit from neurosurgery (eg possible head injury, subarachnoid haemorrhage, cerebellar haematoma, patients on anticoagulants or with known bleeding tendencies). Management

  • If the patient is unconscious, assess and resuscitate along standard lines. Clear the airway with appropriate manoeuvres and suction. Provide O2 and if tolerated, insert an oropharyngeal airway. If the gag reflex is absent, tracheal intubation and IPPV may be required. Prepare for RSI and get senior expert help.
  • Immediately correct hypoglycaemia if present (see p147).
  • Hypertension and labile BP is common in the early post-stroke period. ↓ BP may ↑ the penumbral area of ischaemia—do not attempt to do this except under specialist advice.
  • Keep nil by mouth until swallowing has been thoroughly assessed.
  • Ensure nursing care to keep the patient comfortable and preventpressure sores.
  • Insert a urinary catheter if there is urinary retention or coma.
  • Aspirin ↓ morbidity and mortality following acute ischaemic stroke, but do not start aspirin until haemorrhage has been excluded by a scan. LMWH and systemic anticoagulation have not been shown to be of benefit in the management of acute stroke.
  • Ensure that relatives are kept informed and aware of the prognosis. Advise them that the patient may be quite capable of understanding them even if unable to speak.

Stroke units Wherever possible, admit patients directly to units where they can be cared for by staff specializing in stroke treatment and rehabilitation. The evidence shows that this improves outcome. Thrombolysis To date, in the UK, thrombolysis is not routinely performed. Only a small minority of patients with stroke fit within the narrow time window and other required criteria, and prior CT/MRI scanning is mandatory. Follow local protocols. See: http://www.clinicalevidence.com P.144
Seizures and status epilepticus First fit A first fit has enormous consequences—do not diagnose without good evidence Pending a definitive specialist diagnosis, use the term ‘seizure’ to avoid the emotive label of epilepsy. A detailed history from both the patient and any witnesses is crucial to the diagnosis. The presence of jerking movements or incontinence does not necessarily reflect epilepsy. Carefully document what was seen to avoid confusion with vasovagal syncope or other types of collapse. Full rapid recovery suggests a syncopal event. Always consider alcohol/drug use, withdrawal states, hypoglycaemia, arrhythmia, head injury, subarachnoid haemorrhage, stroke/TIA, infection (including meningitis), metabolic disturbance. As part of the general examination, carefully examine the CNS, documenting: GCS, confusion, focal abnormalities, findings on fundoscopy. Todd’s paresis may follow seizures—focal deficit or hemiparesis may persist for up to 24hrs and indicates a high chance of structural lesion. Investigations Check BMG, glucose, FBC, U&E, blood cultures if pyrexial. Record an ECG. All patients with new onset seizures require brain imaging at some stage as there is a significant incidence of structural CNS abnormalities. MRI is more sensitive, but CT is more widely available. Arrange emergency CT scan for patients with focal signs, head injury, known HIV, suspected intracranial infection, bleeding disorder (including anticoagulants) or where conscious level fails to improve as expected. Disposal Refer to the medical team. It may be appropriate to subsequently discharge some patients to the care of a responsible adult, but only those who are fully recovered with no residual symptoms/signs and no suspicion of significant pathology. Ensure clear documentation of follow-up arrangements, including booked clinic appointment and CT scan (if not performed as an emergency) and provide the patient with written information explaining this. Meantime, advise the patient not to drive or use machinery and to take sensible precautions with supervision when performing activities such as swimming/bathing until reviewed. Document this advice in the notes. Seizures in known epileptics Ask about any change from the patient’s normal seizure pattern. Possible causes of ↓ seizure control include: poor compliance with medication, intercurrent illness/infection, alcohol or drug ingestion. Examine to exclude any injury occurring from the fit, especially to the head. Occult dislocations (eg shoulder) may occur. Check vital signs, BMG and anticonvulsant levels if toxicity or poor compliance is suspected. Refer patients with a significant change in seizure pattern to the medical team. Discharge to the care of a responsible adult those patients who are fully recovered with no injuries, symptoms or other concerns. Status epilepticus This is continuous generalised seizures lasting >30mins or without intervening recovery. Cerebral damage ↑ with duration. Precipitants include cerebral infection, trauma, cerebrovascular disease, toxic/metabolicdisturbances, childhood febrile seizures. Mortality is ≈10% (due to underlying pathology). Although seizures typically start as generalized, tonic/clonic, these features may gradually diminish, making diagnosis difficult (coma with virtually no motor evidence of seizure, eg minimal twitching of ocular muscles only). Complications include hypoglycaemia, pulmonary hypertension, pulmonary oedema and precipitous ↑ ICP can also occur. P.145
Treatment of status epilepticus1

  • Secure the airway (a nasopharyngeal airway may help).
  • Give high flow O2.
  • Monitor ECG, SaO2, T°, pulse rate and BP.
  • Obtain IV access, check BMG and correct hypoglycaemia if present (50mL of 50% dextrose IV).
  • Consider the possibility of pregnancy-related fits (eclampsia) in women of childbearing age and treat accordingly (with IV magnesium sulphate—as outlined on p566).
  • Give IV lorazepam 4mg slowly (diazepam 10mg is an alternative if lorazepam is not available).
  • Repeat IV lorazepam 4mg slowly after a maximum of 10mins if seizures continue.
  • If alcohol abuse or malnutrition is suspected, give slow IVI thiamine in the form of Pabrinex® 2 pairs of ampoules in 50mL of 0.9% saline (note that this occasionally causes anaphylaxis and be prepared to treat this—see BNF).
  • Check ABG and save blood for cultures, FBC, U&E, glucose, calcium, LFTs, clotting, drug levels (and toxicology screen if poisoning/overdose is suspected).
  • Search for features of injury (especially head injury) and infection (look for a rash).
  • If seizures continue despite above therapy, get senior help and consider the use of fosphenytoin (15mg/kg phenytoin equivalent IV, up to 150mg/min) or phenytoin (15mg/kg IV, 50mg/min) with ECG monitoring. Continuing seizures may require further specialist drugs, GA and admission to ITU.

Footnote 1 See also: http://www.sign.ac.uk and http://www.nice.org.uk P.146
Hypoglycaemia Hypoglycaemia can mimic any neurological presentation including coma, seizures, acute confusion or isolated hemiparesis. Always exclude hypoglycaemia in any patient with coma, altered behaviour, neurological symptoms or signs. Plasma glucose is normally maintained at 3.6-5.8mmol/litre. Cognitive function deteriorates at levels <3.0mmol/litre, but symptoms are uncommon >2.5mmol/litre. In diabetics, however, the threshold for symptoms can be very variable. Hypoglycaemia is potentially fatal, and accounts for 2.4% of deaths in diabetics on insulin. Even mild episodes aggravate pre-existing microvascular complications and lead to cumulative brain damage. Causes In diabetics, the commonest cause is a relative imbalance of administered versus required insulin or oral hypoglycaemic drug. This may result from undue or unforeseen exertion, insufficient or delayed food intake, excessive insulin administration (due to time, dose or type of insulin). Other causes are:

  • alcohol (but beware, in addition to alcohol directly causing hypoglycaemia, the features of hypoglycaemia may be mistaken for alcohol intoxication or withdrawal)
  • Addison’s disease
  • pituitary insufficiency
  • post-gastric surgery
  • liver failure
  • malaria
  • insulinomas
  • extra-pancreatic tumours
  • attempted suicide or homicide with large doses of insulin or oral hypoglycaemic drug

Symptoms and signs Hypoglycaemia can present in various ways. Common features are: sweating, pallor, tachycardia, hunger, trembling, altered or loss of consciousness, irritability, irrational or violent behaviour, fitting, focal neurological deficit (eg hemiplegia). Look for Medic-Alert bracelet/chain. Diagnosis Check venous or capillary blood with glucose oxidase strip (BMG). If <3.0mmol/litre, take a venous sample for a formal blood glucose level, but give treatment without waiting for the result. Take appropriate samples if overdose of insulin, oral hypoglycaemic agent or other drugs is suspected. P.147
Treatment This depends upon the conscious state and degree of cooperation of the patient. Choose the appropriate option from the following:

  • Give 5-15g of fast-acting oral carbohydrate (eg Lucozade®, sugar lumps, Dextrosol®, followed by biscuits and milk).
  • Glucagon 1mg: can be given SC, IM or IV. Can be administered by relatives, ambulance crew and when venous access is difficult. Glucagon is not suitable for treatment of hypoglycaemia due to sulphonylurea drugs, liver failure or in chronic alcoholism (as there may be little glycogen available for mobilization).
  • Administer dextrose 25-50mL of 50% solution IV. Follow by a saline flush as the solution is hypertonic and causes thrombophlebitis. The time taken for return of consciousness and the incidence of nausea, vomiting and other adverse effects are nearly identical for IV glucagon or dextrose.

90% of patients fully recover in 20mins. Provided that the cause for the episode has been identified and fully corrected, it is reasonable to discharge the patient with appropriate follow-up. The persistence of an altered conscious level suggests another underlying pathology (eg CVA), or may reflect the development of cerebral oedema due to hypoglycaemia, which has a high mortality. Maintain plasma glucose at 7-11mmol/L and contact ITU. Arrange urgent investigation (eg CT scan) and search for other causes of altered consciousness. Contact ITU and consider mannitol and/or dexamethasone. Overdose Glucose infusions may be needed for 24h or longer after poisoning with insulin or oral hypoglycaemic drug, depending upon exactly what and how much has been taken. Hypokalaemia may be a problem. Block excision of the injection site has been used as successful treatment for insulin overdose. Octreotide may be helpful in recurrent hypoglycaemia due to overdose of a sulphonylurea urea drug (p191). Follow-up Arrange this having considered three questions:

  • Why did this episode occur?
  • Has there been a recent change of regimen, other drugs, alcohol etc?
  • Is the patient developing hypoglycaemic unawareness/autonomic dysfunction?

Hyperglycaemic crises Diabetic keto-acidosis (DKA) and hyperosmolar non-ketotic hyperglycaemia (HONK) are caused by absolute or relative ↓insulin levels. Plasma glucose levels rise causing an osmotic diuresis, with Na+ and water loss (up to 8-10 litres), hypotension, hypoperfusion and shock. Normal compensatory hormonal mechanisms are overwhelmed and lead to ↑lipolysis. In the absence of insulin this results in the production of non-esterified fatty acids, which are oxidised in the liver to ketones. Younger undiagnosed diabetics frequently present with DKA developing over 1-3days. Plasma glucose levels may not be grossly ↑, and euglycaemic ketoacidosis can occur. HONK develops over days or wks, is more common in the elderly, and glucose levels are often >30mmol/litre. In known diabetics both conditions often occur with intercurrent illness, especially infection. Mortality is ≈5-10%, but may be even higher in the elderly. Causes Think of the four ‘I’s separately or (often) in combination:

  • Infection: common primary foci are urinary tract, respiratory tract, skin
  • Infarction: myocardial, CVA, GI tract, peripheral vasculature
  • Insufficient Insulin
  • Intercurrent Illness: many underlying conditions precipitate or aggravate DKA and HONK

Clinical features Hyperglycaemic crisis may present in a variety of ways, depending upon associated or precipitating conditions. Some of the following are usually present: thirst, polydipsia, polyuria, signs of Na+/H2O depletion with dry tongue, ↓skin turgor, hypotension and tachycardia. GI symptoms are common (especially in the young) with nausea, vomiting and abdominal pain. This can be severe and misdiagnosed as an ‘acute surgical abdomen’. Hyperventilation (respiratory compensation for the metabolic acidosis) with deep rapid breathing (Küssmaul respiration) and the smell of acetone on the breath, is pathognomonic of DKA. True coma is uncommon, but altered conscious states and/or focal neurological deficits (which may correct with treatment) are seen particularly in older patients with HONK. Diagnosis and investigations Aim to both confirm the diagnosis and search for possible underlying cause(s):

  • check BMG and test the urine for glucose and ketones
  • send blood for U&E, blood glucose, creatinine, osmolality {or calculate it: mOsm/litre = 2 × [Na+ + K+] + glucose (mmol/litre) + urea (mmol/litre)}
  • calculate the anion gap (Na+ + K+ – HCO3- – Cl-) normal should be 14-18mmol/L. A normal anion gap makes DKA unlikely.
  • check ABG (look for metabolic acidosis ± respiratory compenstaion)
  • FBC
  • CXR (to search for pneumonia)
  • ECG and cardiac monitoring (look for evidence of hyper-/hypokalaemia)
  • blood cultures and if appropriate, throat or wound swabs
  • urine/sputum microscopy and culture


  • If altered consciousness/coma is present, provide and maintain a patent airway.
  • Give high FiO2 by mask and consider the possible need for GA and IPPV for coma ± severe shock.
  • Commence IV infusion with 0.9% saline (if the lab result subsequently shows initial plasma Na+ to be >150mmol/litre, give 0.45% saline). Give 1000mL of 0.9% saline over 0.5-1h, then 500mL/h for next 2-3h. Persistent hypotension may require ↑ in infusion rate and/or colloid administration. Avoid over-rapid infusion with the risks of pulmonary oedema and ARDS, especially in the elderly and patients with IHD.
  • Insulin: start an infusion of soluble insulin using an IV pump or paediatric burette at 6U/h. No loading dose is required. Alternatively, give 20U IM then 6U/h IM. Check plasma glucose levels every hr initially. When plasma glucose <14mmol/L, ↓insulin infusion rate to 4U/h and replace the saline solution with 10% dextrose to help ketone clearance and acid-base state.
  • Electrolyte balance: although total body K+ is low, plasma K+ may be normal, ↑or ↓. With treatment, K+ enters cells and plasma levels↓: therefore unless initial K+ levels are >5.5mmol/L, give 20mmol/h of KCl, monitor ECG and check levels regularly. Despite the presence of metabolic acidosis, there is no role for the routine use of sodium bicarbonate. Other electrolytes such as Ca2+, Mg2+ and PO42- are commonly disturbed, but rarely need emergency correction.
  • Consider a NG tube to ↓risk of gastric dilation and aspiration.
  • Insert a urinary catheter and closely monitor urine output.
  • Consider a central venous catheter to monitor CVP to guide treatment in the elderly or severe illness.
  • Arrange admission to ITU, HDU or acute medical admissions unit.

Other aspects of treatment Signs of infection are often masked. T° is rarely↑, and ↑WCC may only reflect ketonaemia. If in doubt, treat with a broad-spectrum antibiotic. Over-rapid fluid replacement can cause cardiac failure, cerebral oedema and ARDS, especially in patients with underlying cardiac disease or the elderly. CVP monitoring may be needed. Clotting: hyperglycaemia causes a hypercoagulable state: DVT ± PE may occur. After admission, prophylactic anticoagulation with LMWH is usually given in DKA or hyperosmolar states. P.150
Addisonian crisis Adrenal crisis and acute adrenal cortical insufficiency are rare, but do sometimes present to A&E. The most common cause is sudden withdrawal of chronic steroid therapy (deliberately or accidentally). An Addisonian crisis may also be precipitated in these patients by intercurrent injury, infection or stress – increasing steroid requirement. 80% of Addison’s disease in the UK is idiopathic (autoimmune), which may be associated with Graves’ disease, Hashimoto’s thyroiditis, IDDM, pernicious anaemia, hypoparathyroidism and ovarian failure. Other causes include TB, fungal infections, metastatic disease, congenital adrenal hyperplasia, drugs (eg metapyrone or cytotoxic agents), haemorrhage into the adrenal glands occurring as a complication of anticoagulation or meningococcal septicaemia (Waterhouse-Friderichsen syndrome). Look for a Medic-Alert bracelet indicating that the patient is taking steroids. Precipitating factors Infection, trauma, myocardial or cerebral infarction, asthma, hypothermia, alcohol, exogenous steroid withdrawal or reduction. Clinical features Addison’s disease frequently has an insidious onset with weakness, apathy, anorexia, weight loss, abdominal pain (which may be severe enough to mimic an acute abdomen) and oligomenorrhoea. In crisis, the main features may be shock (tachycardia, peripheral vasoconstriction, severe postural hypotension occasionally with syncope, oliguria, profound muscle weakness, confusion, altered consciousness leading to coma) and hypoglycaemia. Chronic features of Addison’s disease are: areas of vitiligo and hyperpigmentation in the palmar creases, buccal mucosa, areolae, scars and in the axillae Investigations Hyperkalaemia, hyponatraemia, uraemia, mild acidosis, hypercalcaemia and eosinophilia may be present. If Addisonian crisis is suspected, take appropriate blood samples but commence treatment without waiting for the results. Management

  • Obtain IV access.
  • Take blood for cortisol (10mL in a heparinized tube) and ACTH ifpossible. Contact the biochemistry lab to warn them that these tests will be required.
  • If features of haemodynamic compromise are present, commence volume replacement with IV 0.9% saline. Consider a gelatin solution in shocked patients.
  • Give hydrocortisone sodium succinate 100mg IV stat.
  • Take blood cultures, urine cultures and sputum for culture andsensitivity.
  • Check BMG and blood glucose, and treat hypoglycaemia with 50mL of 50% dextrose IV.
  • If infection is suspected as a precipitating cause, consider giving broad spectrum antibiotics.
  • Refer for admission.

Thyrotoxic crisis A rare condition, occurring in ≈1-2% of patients with establishedhyperthyroidism (usually toxic diffuse goitre ‘Graves’ disease’). Mortality is significant (≈10%). Causes It is often precipitated by a physiological stressor:

  • premature or inappropriate cessation of anti-thyroid therapy
  • recent surgery or radio-iodine treatment
  • intercurrent infection (especially chest infection)
  • trauma
  • emotional stress
  • DKA, hyperosmolar diabetic crisis, insulin-induced hypoglycaemia
  • thyroid hormone overdose
  • pre-eclampsia

Clinical features Onset may be sudden with features of severe hyperthyroidism and adrenergic overactivity. Fever, cardiovascular and neurological symptoms are common. Weight loss, appetite↑, tremor, irritability, emotional lability, heat intolerance, sweating, itch, oligomenorrhoea, agitation, anxiety, confusion, coma, palpitations, tachycardia, AF (or very rarely complete heart block). It may mimic an ‘acute abdomen’, with abdominal pain, diarrhoea and vomiting. Differential diagnosis Includes acute pulmonary oedema, neuroleptic malignant syndrome, septic shock, anticholinergic or sympathomimetic overdose, withdrawal or acute anxiety states. Investigations

  • U&E, BMG and blood glucose, Ca2+ (hypercalcaemia occurs in ≈10%)
  • FBC, differential WCC, coagulation screen
  • screen for infection: MSU, blood cultures, sputum
  • T4 and T3 (for later analysis), TSH
  • CXR (searching for pulmonary infection or congestive heart failure)
  • ECG (looking for arrhythmias)


  • manage the airway and give O2 if indicated
  • obtain IV access and commence IVI 0.9% saline (initially 500mL 4hrly)
  • pass NG tube if vomiting
  • if sedation is required, give small titrated amounts of benzodiazepine (eg diazepam 5-20mg PO/IV) or haloperidol
  • commence dexamethasone 4mg 6hrly PO or give hydrocortisone 100mg IV
  • give broad spectrum antibiotic if infection is suspected
  • refer for admission (consider admission to ITU)
  • once admitted, propranalol (or esmolol) and carbimazole will normally be given together with iodine
  • do not give aspirin (this can exacerbate the clinical problem bydisplacing thyroxine from thyroid binding globulin)

Ureteric colic New onset flank/back pain in the elderly may represent a leaking aortic aneurysm (even if haematuria is present) Causes Calculi or blood clots may cause ureteric (or ‘renal’) colic. Colicky pain is produced by ureteric obstruction, ↑intraluminal pressure, and muscle spasm. Calculi most commonly consist of calcium oxalate and/or calcium phosphate. Less common are magnesium ammonium phosphate (associated with UTIs and urea-splitting organisms such as Proteus), urate and cystine stones. Male: female ratio for renal calculi is 2:1. Calculi may be associated with hypercalcaemia, hyperoxaluria and hyperuricaemia. ‘Staghorn’ calculi may form in the collecting system and predispose to infections. Calculi may form at any point throughout the renal tract and vary in size from tiny particles to large ‘stones’ in the bladder. They cause symptoms from local obstruction, infection and rarely may ulcerate through the wall of the structure in which they are present. Clinical features The most common presenting symptoms are pain from obstruction or UTI and/or haematuria. Constant dull, severe, loin discomfort is associated with excruciating colicky pain, spreading to the respective iliac fossa, testis, tip of penis or labia. The patient may wish to move or walk about. Nausea, vomiting, pallor, sweating are common. There is frequently a previous history of stone disease—ask about this and whether there is any past history of renal disease. Enquire also about urinary and GI symptoms. Apart from loin tenderness, abdominal examination is usually normal, but check haemodynamic status, pulses, bruits and the abdominal aorta, as a ruptured aortic aneurysm can present similarly (p506). Pyrexia or rigors suggest associated infection. Microscopic (or sometimes, frank) haematuria is almost invariable. Symptoms are usually relieved when the stone passes into the bladder, but larger calculi may then obstruct at the bladder neck or urethra producing acute retention. Bladder calculi may present with symptoms of UTI and/or bladder irritation (frequency, dysuria, strangury and haematuria). Investigations

  • Urinalysis and MSU: blood on stix testing is present in >80% of patients with proven stones. A pH >7.6 implies associated infection with urea splitting organisms.
  • U&E, creatinine, glucose, Ca2+, PO42-, urate levels.
  • ‘KUB’ X-ray: 90% of urinary calculi are radio-opaque. X-ray is ≈50% sensitive and ≈70% specific for the diagnosis of ureteric calculi and is a very useful follow-up of patients with known stones. Common sites for calculi include the pelvi-ureteric and vesico-ureteric junctions. Remember that the ureters lie adjacent to the tips of the spinal transverse processes.
  • Use USS/Doppler instead in pregnant patients or those with renal disease.
  • CT without contrast is ≈95% sensitive and ≈95% specific and has the advantage of assisting diagnosis of other causes of abdominal and/or loin pain.
  • IVU is the most accurate investigation when CT is not available or where endoscopic or surgical treatment is contemplated. A delayed nephrogram on the affected side at 5mins is common. As contrast enters the collecting system, the site and degree of the obstruction can be assessed.

Treatment Give IV opioid titrated to effect, together with an antiemetic. Parenteral/ rectal NSAIDs may be useful later, but are slower to act, and the patient will not relish the additional delay in achieving analgesia. Antispasmodics, anticholinergics and ‘pushing fluids’ are of no benefit.

  • Aim to discharge patients (with arrangements for appropriate outpatient investigation) when symptoms have completely resolved, and in whom the IVU shows no obstruction. Note that in some patients the process of becoming pain-free merely represents complete obstruction.
  • Admit (for further investigation and treatment) patients whose pain persists, or in whom investigation confirms continued obstruction, infection, sepsis or renal impairment.

Urinary tract infection (UTI) The urinary tract is normally bacteriologically sterile. Urine infection is present if >105 colony-forming units are present per mL of urine. Except at the extremes of age, UTIs are much more common in females due to the shorter urethral length. Most UTIs occur because of organisms invading the bladder via the urethra. Proximal invasion via the ureter may result in acute or chronic pyelonephritis, particularly if anatomical derangement exists with impaired ureteric or bladder emptying. In both sexes, underlying structural abnormality ↑risk of UTI. Blood-borne spread of infection to the urinary tract can occur, (eg in bacterial endocarditis or systemic Gram -ve infection). UTI is usually caused by a single organism. The commonest organism (90%) at all ages is E. coli Proteus, Klebsiella and saprophytic staphylococci account for most of the remainder in adults. Other organisms (eg Pseudomonas) more commonly cause UTI in hospitalized patients or following instrumentation. UTIs usually presents to A&E in one of two ways: Lower UTI (Cystitis) Dysuria, frequency, haematuria, suprapubic discomfort, urgency, burning, cloudy urine with an offensive smell. Patients with acute urethral syndrome have identical symptoms, but -ve urine culture. Upper UTI (Acute pyelonephritis) Often systemically unwell withmalaise, fever, loin/back pain, vomiting, rigors and occasionally Gram -vesepticaemia. Investigations Reagent strip (dipstix) urinalysis may show haematuria, proteinuria, +ve nitrite and leucocyte esterase tests. A patient with clear urine, -ve on dipstix testing, is extremely unlikely to have a UTI. False +ve results may occur (eg haematuria secondary to urinary tract tumours, excessive exercise). A false -ve nitrite test may reflect pathogens which do not convert dietary nitrates to nitrites. Urine microscopy may show leucocytes (>100/mL correlates well with infection, but may be due to contamination or other urinary tract pathology). RBCs are commonly seen on microscopy but, in isolation have a low degree of sensitivity or specificity for UTI. Underlying renal pathology may be suggested by urinary crystals, RBC or granular casts. Obtain an MSU for culture and sensitivity. Transport the sample to the lab without delay to ensure that overgrowth does not artificially ↑ the count. Dipslides dipped into freshly passed urine and transported in a plastic container to the lab are an alternative. Treatment It is usually reasonable to discharge female patients with uncomplicated lower UTIs with antibiotics: commence a 3-5day course of (trimethoprim 200mg PO bd) or amoxicillin. Provide advice regarding fluid intake, no ‘holding on’, double-voiding and voiding after intercourse. Drinking barley water is as effective as attempts at urinary alkalinization with sodium bicarbonate. Advise the patient to see her GP for review, MSU result and repeat MSU. Refer for investigation and treatment all male patients and females with recurrent infections, pregnancy, GU malformation, immunosuppression or renal impairment. Patients with acute pyelonephritis usually require admission for parenteral antibiotics, fluid replacement and analgesia. P.155
Patients with chronic renal failure (CRF) Those patients with established CRF who present to A&E are likely to be very well known to the hospital: obtain old notes and recent blood results and liaise early with inpatient specialist teams. Established CRF (not on dialysis) Patients with mild CRF (GFR >40mL/min—normal 100mL/min) are unlikely to have specific problems related to their underlying renal failure. Once GFR falls <40mL/min, and especially if CRF is severe (<10mL/min), complications may influence presentation and treatment. These patients are prone to bony injury. Secondary hyperparathyroidism and osteomalacia (lack of active vitamin D) occur in moderate CRF. In severe CRF, aluminium bone disease and ß2-microglobulin related amyloidosis may be associated with pathological fractures. ‘Pseudo-gout’ due to high Ca2+/PO4- product and twitching/tetany due to hypocalcaemia may occur. Other problems include: Defective regulation of extra-cellular fluid volume There is an ↑risk of fluid depletion in moderate CRF and fluid retention in severe CRF. High dose diuretics may be required in severe disease: the combination of frusemide and metolazone may be effective even with very low GFRs. Hyperkalaemia Most patients preserve potassium balance, but cannot deal with sudden K+ loads (eg dietary, tissue damage/catabolism, GI bleed). Associated ↓Ca2+ compounds the cardiac effects. Plasma K+ may ↑ very quickly, so monitor ECG and check K+ frequently. Hypertension Often severe and resistant, with an ↑incidence of accelerated phase. Cyclosporin and erythropoietin ↑BP, and can precipitate hypertensive encephalopathy. Drug effects Drugs may accumulate (eg opioids, some antibiotics), worsen renal failure (eg NSAIDs, ACE inhibitors which ↓renal perfusion), cause hyperkalaemia (eg K+sparing diuretics, ACE inhibitors, NSAIDs). Infections Impaired WBC function, with ↑risk of severe infection and features of infection (eg pain, fever) may be masked by the relative immuno-compromised state. Bleeding Platelet function is impaired. Pericarditis A sign of severe CRF, indicating the need for dialysis. Neurological dysfunction Usually a sign of severe uraemia: convulsions and/or altered conscious state indicate a global metabolic disturbance. P.157
Haemodialysis patients Common emergency presentations include: Pulmonary oedema Usually occurs shortly before the next dialysis session and may reflect fluid overload due to non-compliance with diet and fluid restriction. Most are virtually anuric, so diuretics are ineffective. Get the patient on dialysis without delay. While this is being arranged give high flow O2 and SL, buccal or IV nitrates. Pre-dialysis hyperkalaemia May present with neuromuscular symptoms (eg muscle spasms, weakness, paralysis, paraesthesiae) or arrhythmias including cardiac arrest. Standard treatment (p158) can buy time while emergency dialysis is arranged. When giving dextrose/insulin, omit or give 6units of insulin at most (there is a risk of late hypoglycaemia, since insulin half-life will be ↑). Complications of vascular access Arterio-venous fistulae are a dialysis patient’s lifeline: never occlude the limb with BP cuffs or tourniquets and do not use for vascular access, except in life-threatening emergencies. Acute shunt thrombosis (loss of palpable thrill, often local pain and redness) is a vascular emergency. Arterio-venous fistulae and temporary central vein catheters are a common source of infection (usually staphylococcal), often with no overt external abnormality, simply presenting with acute ‘viral illness type’ symptoms. Continuous ambulatory peritoneal dialysis Bacterial peritonitis Occurs every 12-18 patient-months. Features are: cloudy drained dialysate bags, abdominal pain and peritonism. Systemic sepsis is usually absent or minimal. Staphylococci are most common organisms. Suspect an underlying surgical cause (most often diverticular abscess) if Gram -ve organisms or anaerobes are present in drainage fluid, and particularly if >1 type of organism is found on microscopy or culture. Diabetic patients on continuous ambulatory peritoneal dialysis can develop acute severe (usually non-ketotic) hyperglycaemia, related to high dialysate glucose concentrations (80-140mmol/L). Hernias of all types, leakage of dialysate into the abdominal wall or the pleural cavity, and scrotal swelling due to opening of the processus vaginalis may occur. Transplant patients Contact the transplant team whenever any transplant patient presents to A&E. They will know the patient well and will advise about drug therapy, intercurrent problems and help with follow-up. Acute rejection Signs include pain, tenderness, and swelling over graft, ↓urine output, fever, systemic upset, biochemical deterioration. Often indistinguishable from acute bacterial infection: if in doubt treat for both, pending results of further testing by specialists (renal biopsy, blood and urine cultures). Infections May be opportunist, whilst ‘conventional’ infections are unduly severe, with response modulated by steroids. Poor wound healing, avascular necrosis and pathological fractures May be caused by steroids. P.158
Hyperkalaemia Hyperkalaemia is classified as mild (K+ 5.5-6.0mmol/litre), moderate (K+ 6.1-6.9mmol/litre) or severe (K+ > 7.0mmol/litre). Causes Spurious Sample haemolysed, or taken from limb infused with IV fluids containing K+. ↑ renal excretion Acute renal failure, patients with chronic renal failure or on dialysis with K+ load, K+ sparing diuretics (eg spironolactone, amiloride). Cell injury Crush injury and other causes of rhabdomyolysis, burns, tumour cell necrosis, massive or incompatible blood transfusion. K+ cellular shifts Acidosis from any cause (eg DKA), drugs (suxamethonium, ß-blockers) Hyperaldosteronism Addison’s disease, drug-induced (NSAIDs, ACE inhibitors). Clinical features There may be muscle weakness/cramps, paraesthesiae, hypotonia, focal neurological deficits. Dangerous hyperkalaemia may be present without signs. ECG changes ECG changes typically progress as hyperkalaemia worsens as follows:

  • peaked T waves
  • small, broad or absent P waves
  • widening QRS complex
  • sinusoidal (‘sine wave’ pattern) QRST
  • AV dissociation or VT/VF

Management Provided that the result is not spurious, a K+ > 6.5mmol/L and/or where there are ECG changes requires urgent intervention, whilst at the same time trying to identify the cause:

  • Obtain venous access and monitor ECG.
  • Give 10-20mL of 10% calcium gluconate slowly IV. This does not lower K+, but antagonises cardiac membrane excitability. Hypercalcaemia will potentiate toxicity in patients on digoxin, so give as an IVI over 30mins in these patients.
  • Give 10units of short-acting human soluble insulin (eg Actrapid®) with 50mL of 50% dextrose IV. This helps cellular uptake of K+, lowering serum levels by up to 1mmol/litre within ≈15mins.
  • Give 5mg nebulised salbutamol, repeated once as necessary. This will lower K+ in most patients, acting in ≈30mins.
  • Correct volume deficits/acidosis with IV fluids and isotonic (1.26%) sodium bicarbonate or aliquots (25-50mL) of 8.4%. Beware fluidoverload/osmolar effects, especially in dialysis patients. Consider CVP monitoring in the elderly or in those with severe illness.
  • Correct the underlying cause if possible (eg steroid therapy for Addison’s disease).
  • Contact the nephrology team urgently for patients with acute or chronic renal failure as emergency dialysis may be needed.

Hyperkalaemia in children— see p654 P.159
Porphyria The porphyrias are haem biosynthesis disorders in which enzyme deficiencies cause accumulation of porphyrin and porphyrin precursors. Most cases are hereditary, but abnormal porphyrin metabolism may develop in iron deficiency, alcohol excess and lead poisoning. The acute porphyrias (acute intermittent porphyria, variegate porphyria and hereditary coproporphyria) affect ≈1 in 10,000 people in the UK. The non-acute porphyrias (eg porphyria cutanea tarda), do not produce acute attacks, but cause skin photosensitivity sometimes associated with liver disease. Precipitants of acute porphyria Attacks are often caused by drugs: barbiturates, oestrogens, progesterones, sulphonamides, methyldopa, danazol, phenytoin, carbamazepine, sulphonylureas, chloramphenicol, tetracyclines, some antihistamines. Other precipitants include: alcohol, smoking, sudden dieting, emotional and physical stress, infection, substance misuse, pregnancy. Clinical features of acute porphyria

  • Look for a Medic-Alert bracelet.
  • Abdominal pain occurs in most attacks and can be severe, with constipation, nausea or vomiting. Abdominal examination may be normal or there may be mild generalized tenderness.
  • Peripheral neuropathy is usually motor rather than sensory, and may progress to paralysis and respiratory failure.
  • Tachycardia, hypertension and postural hypotension.
  • Psychiatric manifestations: agitation, depression, mania and hallucinations.
  • Hyponatraemia due to inappropriate ADH secretion can cause fits or coma.

Investigation If an acute attack is suspected, send a fresh urine sample (protected from light) to test for amino laevulinic acid and porphobilinogen concentrations. In an attack, urine goes dark red or brown, especially if left exposed to light (due to polymerization of porphobilinogen). Obtain old medical notes. Management of acute attacks Treat acute attacks supportively (sometimes in ITU), maintaining carbohydrate intake (PO or IV). Control mild pain with paracetamol or aspirin; moderate pain with dihydrocodeine; severe pain with morphine or diamorphine (± cyclizine or prochlorperazine as antiemetic). Consider chlorpromazine for agitation; propranolol to control severe hypertension. Management of status epilepticus is difficult as many anticonvulsants are contraindicated: choose IV diazepam in the first instance. Haem arginate helps some patients with acute crises (take specialist advice). Prescribing for patients with porphyria Many drugs can precipitate attacks, so check with the patient and the BNF. Data is also available on the internet: http://www.uq.edu.au/porphyria However, the safety of many drugs is uncertain and effects vary between patients. If in doubt, obtain specialist advice. In addition to those mentioned above, safe drugs appear to be: ibuprofen, penicillin V, ciprofloxacin, bupivicaine. P.160
Bleeding disorders 1 Contact a haematologist whenever treating a patient with a known or suspected bleeding disorder Haemostasis requires co-ordination between the vascular system, platelets and coagulation pathways to limit blood loss from the circulation. Platelets interact with vascular subendothelium, forming a primary platelet plug which is strengthened by cross-linked fibrin strands formed via the coagulation cascade to allow restoration of vascular integrity (see below). The fibrinolytic systems prevent excess clot formation and inappropriate local or generalized thrombosis, by promoting lysis of fibrin. Recognition of bleeding Bleeding is to be expected after penetrating or blunt trauma, but suspect a bleeding disorder if spontaneous or excess haemorrhage occurs from multiple or uninjured sites, into deep tissues, joints or delayed bleeding occurs after hrs/days. Bleeding disorders may be congenital or acquired. Ask about previous bleeding after trauma, dentistry or surgery and the family history. Congenital disorders Most adults with a congenital disorder know the nature of it and carry a National Haemophilia card or Medic-Alert bracelet giving details and contact numbers. Many haemophiliacs know more about their required treatment than many doctors! They will be registered and known at a haemophilia centre. Acquired disorders May be due to liver disease, uraemia, drug use (ask specifically about aspirin, NSAIDs, warfarin/anticoagulants, alcohol), or unrecognized conditions such as haematological malignancy. Hypothermia (p256) from whatever cause (accidental, rapid infusion of cold fluid/blood products, etc) aggravates any bleeding tendency. The severity of this may not be recognized merely from standard tests as these are performed at 37°C. For example, an INR assay performed at 32°C will be prolonged to the same extent as would occur with a Factor IX level of 2.5% of normal. The site of bleeding can give a clue as to the abnormality. Platelet problems (usually thrombocytopenia) often present with mucocutaneous bleeding (eg epistaxis, GI, GU or heavy menstrual bleeding, bruising, purpura and petechial haemorrhages). Bleeding into joints or potential spaces (eg retroperitoneal) and delayed bleeding is more often due to coagulation factor deficiencies. Patients with mucocutaneous bleeding and haemorrhage into deep spaces may have a combined platelet and coagulation factor abnormality (eg DIC). Investigations FBC Remember that in acute bleeds, Hb and Hct values fail to demonstrate the severity of red cell loss as haemodilution takes time. Platelet counts <100 ×109/L indicate thrombocytopenia, and <20 x109/L are associated with a risk of spontaneous bleeding. However, bleeding because of platelet problems can occur with ‘normal’ counts if platelet function is abnormal (eg with aspirin). Prothrombin time (INR) Used to monitor anticoagulant control in patients on coumarin drugs and may be prolonged in patients with liver disease. Activated partial thromboplastin time (APTT) Tests components of the intrinsic and common coagulation pathways (essentially all factors except VII and XIII). Individual Factor levels Can be determined by specific assays together with inhibitor screening tests for antibodies that can prolong normal plasma clotting. P.161

Figure. Reactions involved in haemostasis

Bleeding disorders 2 General aspects of treatment

  • Routine wound management of patients with bleeding disorders with local pressure, appropriate wound closure, splintage/MUA of fractures, follow standard patterns, but may require prior or simultaneousadministration of factor concentrates/platelets under haematological guidance.
  • Spontaneous or traumatic bleeding into the neck or pharynx may cause rapid airway compromise.
  • Always consider the possibility of intracranial haemorrhage in any patient who complains of headache, neurological symptoms orfollowing even minor head trauma. Consult and consider the need for commencing treatment before specific investigation (eg CT scanning).
  • Never give IM injections.
  • Do not attempt central line placement except in extremis, since life-threatening, uncontrollable bleeding can result.
  • Before giving any drug, check whether it may aggravate the condition or interfere with intercurrent therapy.

Specific conditions Vascular lesions May rarely be inherited (Ehlers-Danlos syndrome, pseudo-xanthoma elasticum, osteogenesis imperfecta, haemorrhagic telangiectasia) or acquired (eg secondary to steroids, infection such as meningococcaemia, thrombotic thrombocytopenic purpura, some forms of snakebite, scurvy, vasculitis). Platelet disorders Capillary-related mucocutaneous bleeding is common and may occur immediately after injury or elective surgery (eg dental extractions). The platelet count may be normal or↓. Acquired thrombocytopenia may be due to drugs, toxins, infections, autoimmune conditions (eg ITP), DIC or secondary to massive blood transfusion. Abnormal platelet function occurs with uraemia, myeloproliferative disorders and drugs (eg aspirin). Coagulation pathway disorders Congenital coagulation pathway disorders predominate in males. They cause intramuscular or deep soft tissue haematomas. Onset of bleeding after injury or surgery may be delayed 2-3days. Von Willebrand’s Disease The commonest congenital bleeding disorder, with VW Factor and Factor VIII deficiency, and abnormal platelet function. Clinically, the condition is similar to a platelet disorder, but milder. Bleeding is commonly mucosal (eg epistaxis) and usually treated with Factor VIII concentrate (which includes VW Factor). Haemophilia A Caused by normal levels of variant form of Factor VIII which lack clot-promoting properties. Often presents with bleeding into deep muscles, large joints or urinary tract. Intracranial bleeding is a major cause of death at all ages. Anticipate bleeding up to three days after trauma. In the UK, haemophilia A associated with bleeding or potential bleeding complications is normally treated by Factor VIII concentrate (some patients have ‘home supplies’ and may bring them to hospital). The volume (dose) required depends upon the severity of the haemophilia of the individual patient and the purpose of treatment (ie prophylaxis or therapy for current bleeding). Haemophilia B (Christmas disease) Involves a deficiency of Factor IX activity and is genetically and clinically indistinguishable from haemophilia A, but much less common. It is normally treated with factor IX concentrate. P.163
Disseminated intravascular coagulation (DIC) Patients may present to A&E with DIC due to infection (especially Gram -ve sepsis), trauma, malignancy, pregnancy (amniotic fluid embolism, placental abruption, toxaemia, retained products), any cause of shock, incompatible blood transfusion or massive volume replacement. Following triggering of the coagulation process, consumption of platelets and coagulation factors (particularly fibrinogen, V, VIII and XIII) occurs with thrombin formation overwhelming the normal inhibition system, resulting in systemic fibrin deposition. Simultaneous activation of the fibrinolytic system results in dissolution of fibrin and release of fibrin degradation products and D-dimers. Investigations Platelet count is usually↓, INR↑ and APTT↑, fibrinogen level↓, fibrin degradation products↑. Treatment Is complex and requires control of the primary cause of the DIC to avoid total depletion of clotting factors. Obtain expert advice about replacement therapy with platelets, coagulation factors and blood (particularly required if the patient is actively bleeding).

Figure. Coagulation cascade

Patients on anticoagulants The commonest oral anticoagulant is warfarin sodium, a vitamin K antagonist. This inhibits the production of Factors II (prothrombin), VII, IX and X and ↓plasma levels of these factors. Patients, or their relatives, who are able to give a history will usually know if they are taking warfarin and their most recent prothrombin time or INR test result, together with any changes in treatment. All patients should be carrying an anticoagulant booklet. If this history is not available, suspect patients with prosthetic heart valves, mitral valve disease, post-coronary artery bypass graft, AF, a past history of DVT/PE or TIAs to be on anticoagulants. Intercurrent illness, liver disease and changes in diet and/or alcohol consumption may affect anticoagulant control. Concurrent drug administration with unrecognized potential for interaction is probably the commonest cause for acute changes in anticoagulant control. These patients usually present to A&E with one of three problems: Acute haemorrhage Spontaneous bleeding in patients on warfarin therapy most commonly affects the GI tract, GU tract, joints or muscles. Following injury, expect excessive or continued haemorrhage. Anticipate the ↑risks of occult or unrecognized bleeding (eg intraperitoneally or intracranially) after even minor trauma and maintain a high index of suspicion as to these possibilities. Check INR and FBC in all patients. Other investigations (eg CT scan of head/abdomen, USS) will be dictated by the nature of the acute problem. Patients with life-threatening haemorrhage For patients with life-threatening haemorrhage, commence volume replacement and blood transfusion as appropriate (see p166). Give phytomenadione (vitamin K1) 5mg by slow IV injection and contact haematology/blood transfusion service for specific advice and provision of concentrate of Factors II, VII, IX and X. If Factor concentrate is not available, FFP may be an alternative under specialist direction. Patients with less severe haemorrhage Patients with muscle haematomas, haematuria or epistaxis also require hospital admission for observation and specific local treatment. Stop warfarin therapy for one or more days. Phytomenadione 0.5-2mg by slow IV injection may be considered appropriate by the haematologists, but anticoagulant control may be rendered difficult and close INR monitoring required. INR levels within the therapeutic range Patients who develop bleeding with INR levels within the therapeutic range require investigation of a possible underlying cause (eg GI or GU tract pathology). Check of control of anticoagulation The therapeutic range for the INR may vary according to the indicationfor anticoagulation. An INR of 2-2.5 is usually appropriate for DVTprophylaxis and 3-4.5 for patients with recurrent DVT/PE or mechanical prosthetic heart valves. For patients who have INR 4.5-7 without haemorrhage, withhold warfarin therapy for 1 or 2 days and arrange review by appropriate specialist team or GP. For patients with INR > 7 without haemorrhage, withhold warfarin and obtain specialist consultation before considering phytomenadione (vitamin K1) 500micrograms by slow IV injection. P.165
Interactions with other prescribed or proprietary medications Many drugs can interfere with anticoagulant control. Before giving or stopping any drug to a patient taking warfarin or other anticoagulant, check the potential for interaction—Appendix I in the BNF has a useful up-to-date list. Particular groups of drugs, likely to be prescribed in A&E, which may cause problems include analgesics (especially NSAIDs), antibacterials and antiepileptics. The safest policy is always to LOOK IT UP. P.166
Blood transfusion 1 It is better to stop bleeding than to have to replace blood loss General aspects Correctly documenting and labelling blood tubes and forms, combined with checking blood products prior to administration, is crucial for safe patient care. If a patient’s name(s), date of birth, clinical details and address are unknown or uncertain, identify them for transfusion purposes by a unique number (usually their unique A&E number) and inform the blood transfusion laboratory. To avoid confusion, the doctor taking the blood sample must label and sign the tube, complete the form and contact the transfusion service. Only take blood from one patient at a time. Label tubes immediately to minimize the risk of mislabelling. Blood banks may refuse to handle incorrectly labelled forms/tubes. If you knowingly give a blood product to a patient whom you know would not accept this (eg a Jehovah’s Witness) you are likely to face an indefensible medicolegal claim. What to send 10mL clotted blood is usually adequate for adults. Where it is obvious that massive transfusion may be required, send two 10mL samples. On the request form, indicate how much blood is needed, when and where the blood is to be sent. Date and sign the form. What to request The amount of blood to be delivered and to be kept available at the transfusion centre for immediate dispatch depends on the patient’s clinical state and assessment of future blood losses. Assessment of a patient with hypovolaemic shock is complex and includes a recognition of the clinical situation, the potential blood loss, together with a current assessment of the patient and investigations. Hb and Hct values may be misleading as it may take several hrs for their values to equilibrate to those indicating the degree of blood loss. Group and screen The patient’s ABO and Rhesus D group is determined and the serum tested for unexpected red cell antibodies. Subsequently, if required, blood can be provided within 10-15mins, assuming the antibody screen is clear. Request ‘Group and screen’ where a patient does not need transfusion in A&E, but may require it later. Cross-match Full blood compatibility testing may take up to 1hr. If blood is required more urgently, ABO and Rh compatible units can usually be provided within 15mins, including an ‘immediate spin cross-match’ as a final check on ABO compatibility. In exsanguinating haemorrhage, uncross-matched Group O Rhesus -ve blood can be issued immediately. P.167
Blood products Usually in the UK, blood component therapy is provided. There appears to be no specific advantage in using ‘whole’ blood as opposed to red cells plus a volume expander. Red cells (additive solution) Each pack (volume 300mL) is from a single donor and has a Hct of 0.65-0.75 (0.55-0.65 for RBCs in additive solution). A transfusion of 4mL/kg will ↑ circulating Hb by ≈1g/dL. Whole blood A ‘unit’ contains 530mL (470mL of blood from a single donor + 63mL preservative solution), with a Hct of 0.35-0.45. Platelet concentrate, FFP and Factor concentrates. P.168
Blood transfusion 2 Blood product administration Blood transfusion is not a universal panacea. Its limitations and potential hazards must be recognized. Even an improvement in O2 delivery cannot be assumed. RBC function deteriorates during storage and changes in O2 affinity occur with ↓2,3-diphosphoglycerate levels, while ↓ATP levels alter RBC membrane deformability causing ↑cell stiffness and micro-circulatory problems. UK donations are routinely screened for hepatitis B, C, HIV, syphilis and where necessary, CMV. However, blood cannot be sterilized: small but definite risks of infection transmission exist. Transfusion procedure

  • Ensure each pack is labelled with ABO and Rhesus (D) group, and that the individual component number is as recorded on the blood product document.
  • Check the patient’s identity on the blood product document against the patient’s wrist band and with the patient if conscious.
  • Prior to administration, record details of the blood component infusion in the patient’s notes, including the date, the time of issue, product pack number, the ordering medical officer’s name, who it was given by, who checked by, and the time started.
  • Infuse all blood components through a giving set with an integral filter to trap large aggregates. Microaggregate filters are not routinely required.
  • Never add any drug to a blood component infusion.
  • Do not use giving-sets which previously contained dextrose or gelatin solutions.
  • Red cell concentrates may be diluted with 0.9% saline using a Y giving-set to improve flow rates. Never add any other solution.
  • Use a blood warmer, especially for large and/or rapid transusions.

How much to transfuse The optimal Hct for a patient with acute blood loss requiring blood replacement is uncertain. Much depends on the nature of the indication and the previous clinical state of the patient. In a young, otherwise fit, individual with no previous cardiac or respiratory disease, a Hct of 0.25-0.30 is probably adequate, provided there is a normal circulating blood volume. In older patients with pre-existing disease, levels of 0.3-0.35 should theoretically improve O2 delivery, but may actually ↑myocardial and pulmonary problems by ↑viscosity. Circulatory overload/cardiac failure may develop. P.169
Transfusion complications Rapid infusion of blood products may lead to: Hypothermia Blood products are normally stored at 2-6°C. Rapid infusion can cause significant hypothermia. Use blood warmers routinely for rapid transfusions (eg >50mL/kg/h or 15mL/kg/h in children). Never warm a blood product by putting a pack into hot water, on a radiator or any other heat source. Electrolyte disturbances With massive transfusion, the citrate anticoagulant may cause significant toxicity, ↓plasma Ca2+ (impairing cardiac function) and acid-base balance disturbance. This is aggravated in patients with underlying liver disease, hypotension or hypothermia. Citrate may also bind Mg2+, causing arrhythmias. Prophylactic or routine administration of IV calcium salts is not recommended. Monitor the ECG and measure ionised plasma Ca2+ levels during massive transfusion. K+ levels↑ in stored blood and hyperkalaemia may follow massive infusion. Routinely monitor the ECG and check plasma K+levels. Transient hypokalaemia may follow 24h after large volume transfusion. Mismatched transfusion By far the commonest cause is a clerical error when labelling, ordering or administering blood. Transfusion of ABO incompatible blood causes acute severe haemolysis and circulatory collapse. In a hypovolaemic, shocked, or anaesthetized patient these features may be obscured and missed. Transfusion reactions Monitor the patient closely for the first 5-10mins of the infusion of each unit of blood to detect early clinical evidence of acute reactions. Treat allergic reactions include itching, urticaria, bronchospasm and fever conventionally (see p42). If a transfusion reaction is suspected:

  • stop the transfusion
  • keep the IV line open with 0.9% saline
  • double-check the blood unit label with the patient’s wrist identity band and other identifiers
  • send the unit of blood product and the giving set to the blood bank
  • take 40mL of blood. Send it as follows:
    • 5mL anticoagulated and 5mL clotted blood to blood bank
    • 10mL for U&E
    • 10mL for coagulation screening
    • 10mL for blood cultures
  • contact the blood bank directly by phone for further advice and if further transfusion is required.

Sickle cell disease Sickle cell disease occurs in African, Indian, Middle Eastern, Caribbean, US and Mediterranean populations. It is caused by a genetic mutation with a single amino acid substitution in one of the chains of the Hb molecule. The normal adult Hb genotype AA produces HbA. In heterozygotes (sickle cell trait) one gene is abnormal (HbAS) and about 40% of the patient’s Hb will be HbS. In homozygotes (sickle cell anaemia), both genes are abnormal (SS) and >80% of the Hb will be HbS. HbS molecules polymerize in deoxygenated or acidotic conditions, causing RBC sickling. Sickle cells are rigid and fragile. They may haemolyse, or block small vessels (vaso-occlusion) leading to tissue ischaemia, infarction and therefore further sickling (see figure below). Sickling also occurs with genes coding other analogous amino acid substitutions (eg HbSC and SD diseases). Clinical features Sickle cell trait causes no disability except during conditions of severe hypoxia (eg sudden depressurization in aircraft, or cardiac arrest). Patients with sickle cell anaemia have chronic anaemia (Hb 8-10g/dL) and alternating periods of good health and acute crises. Later, chronic ill health supervenes with renal failure, bone necrosis (evident in 50% of patients by age 35yrs), osteomyelitis, leg ulcers and iron overload as a consequence of transfusions. There is predisposition to infection, especially Staphylococcus, Pneumococcus and Haemophilus. Sickle cell crises can occur de novo or follow infection, cold, dehydration, or any situation where tissue hypoxia/ischaemia occurs. The crisis may involve thrombosis, haemolysis, marrow aplasia or acute splenic/liver sequestration (especially in children aged <5yrs). Any acute medical or surgical emergency may be mimicked (eg an acute abdomen, PE, CVA). Severe aching bony pain and low-grade fever (even in the absence of infection) is common. Cerebral sickling may present with bizarre behaviour, psychosis, fits, TIAs, stroke or other focal neurological signs. Priapism, jaundice and painful swelling of hands and feet may occur. Acute chest syndrome This is the leading cause of death in sickle cell anaemia. It presents as chest pain, hypoxia and pulmonary infiltrates. There may be cough, tachypnoea and wheezing. The cause is poorly understood, but infection may be a precipitating factor. Hypoxia may be severe. Acute splenic sequestration Sudden trapping of large numbers of RBCs in the spleen results in severe anaemia, an enlarging spleen, hypovolaemia and thrombocytopenia. It occurs most commonly in young children—those with sickle cell disease have a 30% chance of having acute splenic sequestration by the age of 5yrs. It may present with shock and splenomegaly, with a mortality of >15%. Osteomyelitis and septic arthritis Osteomyelitis and septic arthritis occur more commonly in sickle cell disease. Be suspicious if a patient presents with high fever, soft tissue swelling or pain in a different pattern to normal. Salmonella is implicated relatively frequently. P.171
Investigations No specific tests can detect a sickle cell crisis

  • All patients in the at-risk groups require a sickle test before anyanaesthetic procedure (including IVRA, Bier’s block, p282).
  • Sickle testing (using an oxidising agent) will detect sickling in homo- and heterozygote forms. Hb electrophoresis can then distinguish between HbSS, HbAS and other Hb variants.
  • FBC typically shows anaemia (Hb 6-8g/dL, but Hb may be much lower if acute haemolysis, sequestration or aplasia is present). Post-splenectomy features may be seen on blood film. WCC may be ↑ (20-60 x109/litre) in the absence of infection, and platelet count is also usually ↑.
  • Infection screen, including blood cultures, MSU and CXR.
  • Joint aspiration for culture if septic arthritis is suspected.
  • U&E, ABG, ECG.
  • Arrange CT brain scan if there are neurological symptoms or signs.

Management of crises Provide supportive therapy, directed to the patient’s symptoms:

  • Get expert help!
  • Keep the patient warm, rested and give O2 if any obvious symptoms or SaO2 < 94%.
  • Opioids (given IV and titrated to the response) are often required for pain. A morphine IVI or patient analgesia pump are often useful.
  • Commence rehydration with oral or IV fluids, but take care not to precipitate heart failure.
  • Transfusion may be required if severe anaemia from acute haemolysis, sequestration or aplasia occurs, or if there are CNS or lung complications.
  • Empirical antibiotic therapy may be required if infection is thought to be the trigger for the sickling crisis.
Figure. Sickling Cycle

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