Neurological emergencies

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Chapter 24 Neurological emergencies

Donald S. Pryor, Adam C.F. Chan

COMA OR IMPAIRED CONSCIOUSNESS

Impaired consciousness is recognised and described by observation of response to sound, light, touch or painful stimulus. The Glasgow Coma Scale (GCS) gives a standard way of recording and monitoring the level of consciousness (see Chapter 15, ‘Neurosurgical emergencies’).

Coma signifies diffuse disturbance of brain function, e.g. trauma, epilepsy, drugs, hypoxia, hypoglycaemia or metabolic abnormality, or it can be due to a brainstem lesion or brainstem compression.

History

Available information may be limited. Sources to contact include family, workplace, police, ambulance officers, family doctor etc.

Examination

• Look for signs of:

• head injury
• meningitis, purpura
• raised intracranial pressure (hypertension, bradycardia with dilated and non-reactive pupil is classical, see Chapter 15)
• drug overdoses—narcotics (needle track marks, pinpoint pupils)
• psychostimulants (dilated pupils, tachycardia, hypertension)
• tricyclic antidepressants (tachycardia, hypotension ± seizures)
• metabolic causes—hypo/hyperglycaemia, hepatic or renal failure etc
• hypo/hyperthermia—measure temperature rectally; axillary or tympanic measurement is inaccurate in severe hypothermia or hyperthermia.

• Pupils: enlarged pupil with impaired response to light signifies a third nerve lesion. This can alert to transtentorial herniation. When bilateral, it suggests brainstem death. Small pupils occur with pontine lesions or opiate effect. Dilated pupils can be due to effect of psychostimulants.
• Eye movements: test by following a target or reflex with head turning (oculocephalic reflex). Failure of conjugate gaze to the side of the hemiplegia is common with a hemisphere lesion. When severe, the head and eyes stay deviated away from the hemiplegic side. Dysconjugate gaze is indicative of lesions of the 3rd, 4th and 6th cranial nerves or their nuclei or connections in the brain stem.
• Fundoscopy: look for papilloedema which usually indicates raised intracranial pressure. Preretinal haemorrhage, which may have a fluid level, suggests subarachnoid haemorrhage (SAH). Hypertensive or diabetic retinopathy may be present.
• Motor signs: look at posture and for absence of spontaneous movements.
• Brain or spinal cord lesions affect:

• tone—classically increased but, with acute CNS damage, decreased tone is usual
• tendon reflexes—classically increased but may be absent or reduced with an acute lesion
• plantar responses—classically extensor but may be absent with an acute lesion.

Notes:

1. Decerebrate posturing may be confused with purposive movements.
2. Drug effects and hypoglycaemia may mimic focal neurological lesions.

Investigations

• Blood count, blood sugar level (BSL), electrolytes, urea, creatinine (EUC), liver function tests (LFTs) and calcium
• Serum paracetamol and urine drug screen
• Arterial blood gases
• Cerebral CT scans
• Chest X-ray (CXR)
• If sepsis is suspected: blood and urine culture; lumbar puncture should only be performed if there are no contraindications (see ‘Lumbar puncture’, below)
• Urine analysis: catheterisation may be indicated to obtain urine for microscopy, drug screening, glucose and ketones; may be indicated for monitoring urinary output and nursing care reasons

Management

1. Ensure a patent airway and adequate oxygenation.
2. Establish venous access.
3. Treat hypo/hyperglycaemia.
4. Give naloxone 0.4 mg IV, up to 2 mg over 10 minutes for signs of narcotics.
5. Give thiamine 100 mg IV for unknown cause of coma or signs of alcoholism/neglect.
6. Treat underlying conditions.
7. Monitor neurological signs and GCS half hourly.
8. Maintain hydration, monitor urine output, temperature and pressure care.
9. Raised intracranial pressure is usually an indication for immediate neurosurgical consultation. Treatment to gain time for definitive surgery may include:

a. passive hyperventilation to a PCO2 of 30–35 mmHg
b. mannitol 20% (0.5–1.0 g/kg) by intravenous infusion over 20 minutes has an immediate effect which persists for hours
c. in proven cerebral tumours dexamethasone 12 mg IV—effect not apparent for hours, but has the potential for long-term use.

Specific investigations

Electroencephalography (EEG) for subclinical continuous seizures or metabolic coma, herpes simplex encephalitis and drug withdrawal

Lumbar puncture (LP) only after cerebral CT scans (see ‘Lumbar puncture’ below)

EPILEPSY

Fits are usually self-limiting and no urgent drug treatment is needed. During fits:

1. Immediate care should be directed to minimising injury from burns, cuts, falls or drowning.
2. Observe the features and duration of the fit: rigid (tonic) or jerking (clonic) or focal (arm, leg, face, eyes, lips etc), responsiveness, breathing, pallor, cyanosis, frothing, incontinence, eyes open or deviated, vocalisation etc. Classification as generalised or partial will influence management. Pseudoseizures are common and are often hard to recognise.
3. Turn patient semi-prone and clear airway as soon as tonic phase and clonic movements cease.
4. Do not put anything between the teeth during a fit. Damage to the patient’s teeth or the carer’s fingers is more likely than any benefit.
5. Exclude hypoglycaemia early using bedside blood sugar level testing.

After the fit, ask if there is a history of fits.

If YES:

• Is an antiepileptic drug being taken?
• Ask about compliance.
• Assay the drug to check dose/compliance.

If NO:

• Blood count and biochemistry including BSL and calcium. Consider drug screen.
• Cerebral CT scans.
• EEG: if recorded within 24 hours of a fit there is more chance of useful findings.
• Consider other tests for less common causes: HIV, syphilis.

Prolonged fitting or frequent fitting (status epilepticus)

Partial seizures may be prolonged or frequently recurrent without major hazard.

Major generalised seizures lasting more than 5–10 minutes or recurring rapidly are life-threatening. This situation demands prompt and adequate IV drug therapy, monitoring and support.

Treatment

1. Arrange transfer to a resuscitation area while commencing drug treatment. Establish IV access.
2. Give midazolam 2.5 mg IV with repeated bolus doses up to 15 mg (0.2 mg/kg for a child). Buccal or intranasal administration can be used if venous access is delayed. May have been given by carers before reaching the emergency department. Alternatives to midazolam are:

• diazepam 10–20 mg by slow IV aliquots of 5 mg, repeated if necessary (child 0.1–0.25 mg/kg)
• clonazepam 1–2 mg bolus IV (child 0.25–0.5 mg bolus).

3. Add phenytoin 17 mg/kg IV at no more than 50 mg/minute (if not already taking phenytoin). For a child, administer 20 mg/kg IV at no more than 25 mg/minute.
4. Clonazepam 0.5 mg 8-hourly (oral or parenteral) for the next 24–48 hours may permit initiation of long-term oral anticonvulsant medication.
5. If seizures persist despite treatment, anaesthetise with thiopentone and muscle relaxant, provide ventilatory support and admit to intensive care unit. Prolonged seizures can result in damage to the brain and other organs with significant increase in mortality.
6. Monitor temperature, oxygenation, acidosis, hydration, urine output, serum electrolytes and EEG.
7. Review possible causes for the fits.
8. Re-establish or adjust long-term anticonvulsant medication.

Intravenous preparations of other long-term antiepileptic drugs may become available.

CEREBROVASCULAR DISEASE

Stroke is either cerebral infarction or haemorrhage. Infarction accounts for 80% of strokes. CT scans show haemorrhage immediately but the signs of infarction are usually delayed for several hours. Transient ischaemic attack (TIA) is a focal ischaemic neurological deficit which usually lasts about 20 minutes.

Initial assessment and management of stroke

Focus on:

• ensuring a clear airway, adequate oxygenation and circulation
• excluding stroke mimics, e.g. seizure, hypoglycaemia, sepsis, syncope, drug overdose, hypoxia, hyponatraemia and hemiplegic migraine
• documenting neurological deficits and level of consciousness
• identifying any cardiovascular abnormalities, e.g. atrial fibrillation (AF), signs of endocarditis, carotid bruit/dissection
• urgent cerebral CT scans to exclude haemorrhage or space-occupying lesions
• intravenous thrombolysis if possible within 3 hours of onset of symptoms.

Common patterns of neurological impairment

• Hemisphere—hemiplegia with dysphasia, sensory inattention—embolism likely
• Internal capsule—pure motor hemiplegia—hypertensive lacunar infarction likely
• Brainstem—bilateral motor signs, sensory loss, vertigo/nystagmus, coma, ataxia, cranial nerve signs—vertebrobasilar system disease

Clinical diagnosis of pathophysiology

• Is it intracranial arterial occlusion due to atheroma, hypertension, and diabetes? or
• Neck vessel disease with embolism—carotid bruit? or
• Embolism from the heart—e.g. atrial fibrillation, prosthetic valve, infective endocarditis, recent myocardial infarction?

Investigations

• Perform non-contrast CT scans, full blood count (FBC), electrolytes, creatinine, blood glucose level, coagulation studies, urinalysis, ECG and chest X-ray.
• Initial CT scans can be normal for ischaemic stroke as infarction is best shown a few days after the onset. Early CT is used to exclude haemorrhage or brain tumour to allow the commencement of antiplatelet or thrombolytic agents.
• Magnetic resonance imaging (MRI) and magnetic resonance angiography can replace CT scans and carotid ultrasound when available. MRI shows infarction immediately after a stroke and can distinguish a new from an old infarct. Small lesions and brainstem lesions invisible in CT scans can be seen with MRI.
• Perform transthoracic echocardiography and carotid Doppler ultrasound studies. Transoesophageal echocardiography may be needed to exclude cardiac embolism.

Stroke management checklist

• Oxygenation: maintain oxygen saturation at > 95%.
• Neurological status: hourly GCS and neurological observation for first 4 hours or until stabilised.
• Body temperature: control fever at < 37.5°C with paracetamol orally or rectally. Septic work-up if fever > 38°C.
• Blood glucose: aim for 5–11 mmol/L. If BSL < 3 mmol/L, give 50% dextrose. If BSL > 11 mmol/L, start SC or IV insulin.
• Blood pressure: established drug treatment for hypertension should be continued. Avoid new antihypertensive drug therapy during the first 24 hours as it may worsen the ischaemia. However, treatment is indicated by systolic blood pressure (SBP) > 220 mmHg or diastolic blood pressure (DBP) > 120 mmHg or hypertensive encephalopathy, acute myocardial infarction (AMI) or acute left ventricular failure (LVF).
• Swallowing status/hydration: until it is established that swallowing is safe a ‘nil by mouth’ order is applied. IV fluids without glucose are given to correct dehydration at presentation and provide maintenance fluid and electrolytes. Planning of oral intake or IV or nasogastric fluids and feeding needs daily review.
• Urine output: bladder catheterisation may be needed to monitor urine output and assist nursing care of pressure areas.
• Deep vein thrombosis (DVT) prophylaxis: compression stockings and subcutaneous low-molecular-weight heparin (LMWH) if not contraindicated
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