Urgent considerations

See Differentials for more details

Posterior circulation stroke

Posterior circulation stroke (ischaemic or haemorrhagic) may present in a similar fashion to vestibular neuritis, with sudden-onset intense vertigo, nausea, and vomiting.

Other presenting symptoms include unilateral limb weakness, dysarthria, headache, and diplopia.[8][38] Vertigo is continuous and prolonged. Patients may have at least one vascular risk factor (age >60 years, hypertension, diabetes, smoking, obesity).[8]

Signs include nystagmus, unilateral limb weakness, gait ataxia, unilateral limb ataxia, dysarthria, facial numbness, Horner’s syndrome, and diplopia.[8][38] Patients usually cannot stand without support, even with the eyes open, whereas patients with acute vestibular neuritis or labyrinthitis are usually able to do so.

The head impulse, nystagmus, test of skew (HINTS) assessment identifies stroke with a high degree of sensitivity and specificity in patients with acute vestibular symptoms when administered by a health professional with training and experience in its use. In this setting, it may rule out stroke more effectively than early diffusion-weighted magnetic resonance imaging (MRI).[35][89][90][91]​​​​​​​​ However, HINTS assessment alone does not reliably rule out stroke when used by emergency physicians.[92]

Based on the HINTS model, one algorithm suggests that stroke should be considered in patients presenting with acute-onset dizziness if:[93]

  • there is a central pattern of nystagmus

  • there is skew deviation

  • there is a negative head impulse test (in patients with nystagmus)

  • there are any central nervous system signs on focused neurological examination, or

  • the patient is unable to sit or walk unaided.

The US and UK guidelines recommend immediate brain imaging for patients admitted to hospital with suspected acute stroke.[94][95]​​ While MRI is more sensitive than computed tomography (CT) for the detection of acute infarct, non-contrast CT can reliably exclude intracerebral haemorrhage.[94][96][97]​ MRI (without contrast) is usually appropriate following initial CT screen.[96][97]

In patients who awake with stroke or who have unclear time of onset (>4.5 hours from known well), specific MRI sequences (diffusion-weighted imaging and FLAIR) can help to determine when the ischaemic infarct occurred and, therefore, patient eligibility for thrombolysis.[94]

​​Blood glucose must be checked in all patients with a suspected stroke.[94]

Vertebral artery dissection

Vertebral artery dissection may cause stroke in children and young adults. May be traumatic or spontaneous. Symptoms are sudden-onset vertigo, headache (often unilateral), tinnitus, and neck pain.[42][98]​​​ Neurological signs may be absent but, if present, include ataxia and dysarthria.[41]

CT imaging and angiography (CT/CTA), and MRI and angiography (MRI/MRA), can identify cervical artery dissection. MRI/MRA better identifies small intramural haematomas; however, CT is usually easier to access in the emergency setting.[99]​ Ultrasound may be considered as a follow-up investigation to assess arterial remodelling.[42]​ Digital subtraction angiography may be considered as a second-line imaging technique in patients with clinical symptoms and negative MRA and CTA.[42]

Anticoagulation or antiplatelet treatment should be started after confirming the diagnosis.[100][101]​ Intravascular therapy may be considered for urgent or complex cases.[102][103]​​ A combination of techniques including thrombolysis, thrombectomy, stenting, and angioplasty is used.[104]

Acute coronary syndrome

Patients with acute coronary syndrome (ACS) commonly report feeling dizzy/lightheaded; this is due to cerebral hypoperfusion as a result of hypotension and/or symptomatic bradycardia. Typically presents with intermittent or persistent retrosternal pain, pressure, or heaviness, radiating to the left arm, both arms, right arm, neck, or jaw. Immediate investigations include a 12-lead ECG, chest x-ray, cardiac biomarkers (high-sensitivity cardiac troponins), full blood count, and renal profile.

  • Unstable angina (UA): characterised by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency, longer in duration, or lower in threshold; or angina that occurs after a recent episode of myocardial infarction.[105]​ The ECG may be normal or may show ST-segment depression, transient ST-segment elevation, or T-wave inversion.[105]​ Cardiac biomarkers should be measured on presentation to rule out acute myocardial infarction; subsequent/serial measurements may be needed.[105][106]​​ The early management of patients with suspected UA is focused on initial interventions (e.g., single loading dose of aspirin and pain relief with glyceryl trinitrate) and triage according to the presumptive diagnosis. See Unstable angina.

  • Non-ST-elevation myocardial infarction (NSTEMI): initial ECG may show ischaemic changes such as ST depression, T-wave changes, or transient ST elevation; however, ECG may also be normal or show non-specific changes.[105]​ High-sensitivity cardiac troponins are elevated (>99th percentile of normal) at presentation or after several hours.[107]​ Treatment is directed towards relief of ischaemia, prevention of further thrombosis or embolism, and stabilisation of haemodynamic status, followed by early risk stratification for further treatment. See Non-ST-elevation myocardial infarction.

  • ST-elevation myocardial infarction (STEMI): suspected when a patient presents with persistent ST-segment elevation in two or more anatomically contiguous ECG leads in the context of a consistent clinical history.[108]​ Cardiac biomarkers are elevated. Treatment should, however, be started immediately in patients with a typical history and ECG changes, without waiting for laboratory results. Immediate and prompt reperfusion can prevent or minimise myocardial damage and improve the chances of survival and recovery.[109] See ST-elevation myocardial infarction.

Guidelines recommend that oxygen should not be routinely administered in normoxic patients with suspected or confirmed ACS.[107][110]

Arrhythmias

  • Atrial fibrillation with a rapid ventricular rate causing ongoing chest pain, hypotension, shortness of breath, dizziness, or syncope requires immediate direct current (DC) cardioversion. To prevent thromboembolism, anticoagulation should be started before cardioversion and continued for at least 4 weeks afterwards without interruption.[111]

  • Bradycardia associated with haemodynamic compromise (i.e., systemic hypotension, signs of cerebral hypoperfusion, progressive heart failure or angina) should be treated immediately, regardless of the cause. Intravenous atropine and adrenaline (epinephrine) are commonly used to increase ventricular rate. Medical therapy should be continued until temporary cardiac pacing is initiated.[112]

Pulmonary embolus

Typically presents with pleuritic chest pain, dyspnoea, and tachycardia. Six percent of patients with pulmonary embolus (PE) present with syncope or pre-syncope.[113]​ CT pulmonary angiography (CTPA) is the preferred investigation for diagnosing and excluding PE in a patient with suspected PE with a positive D-dimer; V/Q scan is an alternative if CTPA is contraindicated.[113]​ In patients with suspected PE who are haemodynamically unstable and/or hypoxic, thrombolysis (unless contraindicated) should be started without delay.[113]​ Give high-concentration oxygen if oxygen saturations are <90%.[113]​ Titrate oxygen to achieve saturations of 94% to 98% (or 88% to 92% in patients at risk of hypercapnic respiratory failure).[114] See Pulmonary embolism.

Carbon monoxide poisoning

Accidental poisoning can occur as a result of exposure to carbon monoxide (CO), a colourless, odourless gas generated from burning fuel. Sources include boilers, central heating systems, cookers, fireplaces, and chimneys. CO levels may rise if the outlet for these systems becomes blocked or if they are operated in an unventilated environment.[115]

Diagnosis of CO poisoning rests on a high index of clinical suspicion as symptoms vary and are mostly non-specific.[116]​ Symptoms include dizziness, vertigo, headache, nausea and vomiting, confusion, fatigue, chest pain, and shortness of breath.[117]

Physical examination may be normal. Signs are usually a consequence of hypoxia, and patients may present with tachycardia, hypotension, cardiac ischaemia, arrhythmias, cutaneous blisters, and pulmonary oedema. ​See Carbon monoxide poisoning.

Elevated carboxyhaemoglobin, measured by laboratory blood gas CO oximetry (drawn from venous or arterial blood), confirms the diagnosis. Normal levels are 1% to 3% in non-smokers and up to 10% in smokers.[117]

High-flow oxygen therapy should be initiated as soon as the diagnosis is considered, and should not be discontinued until the diagnosis is ruled out.​[116][117]

Use of this content is subject to our disclaimer