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

• 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.

Transient ischaemic attack (TIA)

This is a neurological dysfunction resulting from focal brain or retinal ischaemia lasting about 20 minutes. It is often resolved by the time of emergency department presentation.

Overall risk of stroke following TIA is around 8–10% at 1 week.

The diagnosis of TIA is intended to identify patients with platelet or cholesterol microemboli arising in neck vessel atheroma. Transient monocular visual loss is very suggestive of carotid artery stenosis.

The initial emergency department investigations for TIA should be the same as for stroke as listed above.

Hospital admission should be considered for TIA to avoid any delay in stroke prevention.

Intracerebral haemorrhage

• Haemorrhage accounts for 10–15% of all strokes.

• Associated with high mortality—a 12-month survival rate of 30%.

• Majority of haemorrhages are due to rupture of small vessels damaged by chronic hypertension.

• With older age amyloid angiopathy is common.

• Minority of cases are caused by bleeding from arteriovenous malformations or aneurysm.

• Severe headache, marked hypertension or existing anticoagulant therapy may suggest haemorrhage but the clinical signs do not distinguish from ischaemic stroke.

• Initial assessment and management are similar to ischaemic stroke as listed above.

• Acute haemorrhage is easily recognised as a radiodense area in CT scans.

• Hypertensive intracerebral haemorrhage will usually be in the internal capsule/striatum or pons. Intracerebral haematoma from a berry aneurysm will arise from near the circle of Willis and peripheral haematomas suggest amyloid angiopathy.

• MRI and contrast cerebral angiography may be needed to define suspected aneurysm or arteriovenous malformation (AVM).

Treatment

Treatment is as per stroke management check list with the following modifications:

1. Cease all antiplatelet or warfarin therapy. Consider fresh frozen plasma (FFP) and/or vitamin K if international normalisation ratio (INR, prothrombin) > 1.3.

2. Institute antihypertensive treatment if SBP > 180 mmHg or DBP > 110 mmHg on two consecutive readings and after adequate analgesia. Lowering blood pressure acutely may compromise cerebral perfusion and must be done with caution.

3. Hydration: fluid restriction may be needed as syndrome of inappropriate antidiuretic hormone secretion (SIADH) is common.

4. Consult neurosurgeon for possible surgical interventions. Surgical drainage may be life-saving for cerebellar haematoma.

5. Surgery may also be considered for presence of hydrocephalus, marked mass effect or haematoma associated with AVM or aneurysm.

HEADACHE

The vast majority of headaches are benign and self-limiting. The goal of managing patients presenting to emergency department with headache is to exclude potentially serious conditions and to relieve pain.

Important diagnoses to be considered:

• subarachnoid haemorrhage

• meningitis/encephalitis

• space-occupying lesions

• giant cell (temporal) arteritis

• acute narrow-angle glaucoma

• hypertensive encephalopathy.

Meningitis

Clinical features

• Headache with fever suggests meningitis and there may be vomiting, photophobia, neck pain or stiffness, confusion, coma, irritability or fitting.

• Examine for neck stiffness and also purpura or hypotension in meningococcaemia; sources of infection, e.g. middle ear, sinusitis, cerebrospinal fluid (CSF) leak; or viral infection like mumps or mononucleosis.

• Immune deficiency states will totally change the bacteria likely to be responsible.

Investigations

• FBC, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), electrolytes, creatinine, blood glucose and CXR.

• Blood cultures.

• Nose, throat and ear swabs.

• Viral cultures, viral antibody titres.

• Cerebral CT scans must be obtained before a lumbar puncture (LP) is performed. Focal neurological signs, altered conscious state or features of raised intracranial pressure are all contraindications to LP if CT scans are not obtainable.

• An LP is needed to confirm the diagnosis and to identify and culture the organism.

Treatment

1. Give IV antibiotics as soon as the possibility of bacterial meningitis is realised. Do not wait for CT scans or LP. (Blood cultures or CSF bacterial antigen tests may assist when antibiotic treatment has rendered the CSF negative to Gram stain and culture.)

2. Ceftriaxone 2 g IV every 12 hours (children 50 mg/kg/day).

3. Appropriate antibiotic for known organism/sensitivity, e.g. benzylpenicillin 1.2–1.8 g every 4 hours (children 350 mg/kg/day) IV for meningococcus or pneumococcus.

4. Steroid therapy (IV dexamethasone 10 mg 6 hourly or 0.15 mg/kg) reduces neurological sequelae and mortality in bacterial meningitis. Initial dose should be given prior to antibiotic therapy.

5. Treat disseminated intravascular coagulation, adrenal failure, SIADH and other complications.

6. Prophylaxis: it is recommended that household contacts of confirmed meningococcal and H. influenza type b meningitis be given prophylactic antibiotics. Healthcare workers are not at increased risk for the disease and do not require prophylaxis unless they have had direct mucosal contact with the patient’s secretions, as might occur during mouth-to-mouth resuscitation, endotracheal intubation or nasotracheal suctioning. The choices of prophylaxis can be rifampicin, ciprofloxacin or ceftriaxone.

Lumbar puncture (LP)

Indications

The major role for LP in the emergency department is the diagnosis of infection or bleeding within the central nervous system (refer to Chapter 3, ‘Resuscitation and emergency procedures’).

Preparation

• Discuss the reasons, procedure and possible complications of the procedure with the patient or carer.

• Obtain verbal or written consent.

Complications

The most common complication is post-LP headache. It is caused by gravity-dependent traction on pain sensitive intracranial structures due to low CSF pressure. The incidence of headache can be reduced by using a small size LP needle (22-gauge) or pencil-point tip with a side hole (Sprotte needle). Bed rest for 4 hours is recommended after LP.

Other complications include:

• bleeding into spinal canal

• local trauma to spinal cord or nerve roots

• infection such as discitis or epidural abscess.

Interpretation of CSF findings

• Normal CSF pressure is 5–20 cmH₂O when the patient is horizontal. High pressure may indicate the presence of space-occupying lesions or CSF outflow obstruction. Low pressure is associated with severe dehydration or CSF leak.

• Macroscopic appearance:

• normal—clear and colourless

• infection—cloudy

• blood—pink or frank blood

• old blood—yellow (xanthochromia)

• Laboratory testing:

• urgent microscopy for cell count, differential and Gram stain

• biochemistry: glucose and protein

• xanthochromia if SAH is suspected

• acid-fast bacillus and India ink stains if tuberculosis or Cryptococcus is suspected

• cultures

• antigen and polymerase chain reaction (PCR) testing if antibiotic therapy was given prior to LP.

Table 24.1 Laboratory findings for CSF in meningitis

Additional considerations

Pretreatment with antibiotics will diminish the yield of Gram stains and cultures but will not affect the CSF cell count.

The initial CSF cell counts may show lymphocytosis in bacterial meningitis and CSF may possibly be normal in culture-proven meningitis if LP is done in the early phase of the disease.

Presence of a clot in one of the tubes or the clearing of the CSF blood staining from tubes 1 to 3 suggests traumatic LP. If traumatic tap is suspected, subtract 1 white cell for every 1000 red blood cells.

Encephalitis

Clinical features

Headache and fever with neurological signs or fits suggests encephalitis. Impaired level of consciousness and delirium are common.

There is overlap between meningitis and encephalitis.

Encephalitis is mostly viral. Sometimes the specific virus can be identified from associated clinical features (e.g. mumps, rabies) or from laboratory tests, cultures and antibody titres, or from the epidemiology (e.g. Murray Valley encephalitis).

Herpes simplex encephalitis demands early diagnosis as treatment is life-saving.

Immunocompromised patients can present with parasitic or fungal as well as viral infections, e.g. toxoplasmosis, cytomegalovirus, progressive multifocal leuco-encephalopathy.

Investigations

• FBC, ESR, CRP, EUC, BSL and CXR

• Viral cultures and antibody titres

• Cerebral CT scans often show subtle changes, hypoattenuation in a temporal lobe and mass effect may be present

• EEG—abnormal in 80% of herpes simplex virus (HSV) encephalitis

• Lumbar puncture—WCC 50–500/mL, mild elevation in protein, normal glucose; CSF sent for viral cultures, antibody titres and PCR for HSV and other viruses

• MRI is more sensitive and more specific than CT scans

Treatment

Specific treatment is not available except for herpes simplex encephalitis which responds to acyclovir 10 mg/kg in IV infusions every 8 hours for 10 days. Each dose must be infused over not less than 1 hour. This drug should be commenced urgently on suspicion of herpes simplex encephalitis: i.e. clinical encephalitis with cells in the CSF—do not wait for characteristic CT, MRI or EEG features to develop.

Subarachnoid haemorrhage (SAH)

(See also Chapter 15, ‘Neurosurgical emergencies’.)

Clinical features

SAH should be considered in any new headache as the diagnosis is often missed.

In particular, patients presenting with sudden onset of severe, ‘worst ever’ headache with or without neurological findings should be suspected of having a subarachnoid haemorrhage. Loss of consciousness and vomiting are common. Up to 50% of patients experience a ‘warning bleed’ associated with headache which settles spontaneously or with simple analgesia. Re-presentation with second bleed is usually catastrophic and associated with poor outcome. It is often due to a ruptured berry aneurysm and sometimes due to a vascular malformation.

Hypertension, polycystic disease and aortic coarctation are associated with berry aneurysms. Monoamine oxidase therapy or illicit drug use may result in acute hypertension with SAH.

On examination, look for meningism, altered level of consciousness, confusion or focal neurological signs (such as hemiparesis or dysphasia). Papilloedema may be present. Preretinal (subhyaloid) haemorrhage is virtually diagnostic. A cranial bruit may indicate an arteriovenous malformation. Absence of physical signs cannot exclude subarachnoid haemorrhage.

Note: Migraine is not a likely diagnosis in a first-time severe headache.

Investigations

• Non-contrast cerebral CT scans in the first 24 hours will demonstrate subarachnoid blood in 90–95% of cases. Sensitivity of CT scans decreases with time, 80% positive at 3 days and 50% at 1 week.

• Lumbar puncture (LP) is necessary if there is clinical suspicion of SAH and CT scans do not provide a diagnosis. The diagnosis of SAH is dependent upon the finding of red cells or xanthochromia in the CSF. Xanthochromia is due to breakdown products of haemoglobin in the CSF and is usually present within 6 hours of haemorrhage. Hence LP can be delayed for 6–12 hours from the onset of symptoms to minimise false negative findings.

• Angiography is the gold standard for confirming the presence of aneurysm and will be necessary if surgical treatment is contemplated. CT angiography has a sensitivity of over 90% and may evolve as the alternative imaging modality. Magnetic resonance angiography can be effective.

• Others: FBC, electrolytes, creatinine, blood glucose level, ECG and CXR are relevant.

• SIADH, temporary hyperglycaemia and cardiac tachyarrhythmias may complicate the bleed.

Migraine

Clinical features

The pathophysiology of migraine is complex and poorly understood. It is defined as idiopathic recurring headache disorder with attacks that last 4–72 hours. There is often presence of a family history and sometimes triggers such as food or menstruation. The headache may be preceded by a prodrome or aura of visual or other neurological symptoms. Typical characteristics include gradual onset, throbbing quality, unilateral location, nausea, vomiting, photophobia and prostration. Major but temporary neurological signs may result from migraine, causing diagnostic problems, e.g. aphasia, hemiplegia.

Investigations will be normal and should be directed towards excluding other serious diseases as suggested by the clinical features—subarachnoid haemorrhage, meningitis, etc.

Although not life-threatening, migraine causes great suffering. When the diagnosis is secure, the goal is to relieve pain and other associated symptoms.

Treatment

1. Soluble aspirin 600–900 mg or paracetamol 1–1.5 g 4-hourly, up to 4 g/day.

2. Metoclopramide (10 mg orally or IV) has both antiemetic and direct analgesic effect.

3. NSAIDS can be an alternative: ibuprofen 400–800 mg orally or indomethacin 100 mg rectally.

If previous experience with these measures has failed:

4. Chlorpromazine: very effective treatment in 80% of cases who are unresponsive to oral analgesics. Preload patient with 1 L of normal saline, followed by chlorpromazine 12.5 mg given as a slow IV push over a few minutes. Further 12.5 mg boluses can be administered every 15–20 minutes, up to 37.5 mg if headache persists. Hypotension should be treated with 500 mL boluses of normal saline and acute dystonia is treated with 2 mg of IV benztropine.

5. Sumatriptan is effective in 60–75% of cases. The recommended dose is 50–100 mg orally, 10–20 mg intranasally or 6 mg subcutaneously. Other triptans: naratriptan 2.5 mg orally or zolmitriptan 2.5–5 mg orally.

If treatment with the above measures has also failed, consider:

6. Dihydroergotamine, a potent vasoconstrictor. The recommended dose is 0.5–1 mg SC or IM or IV with metoclopramide to minimise the gastrointestinal side effects.

Notes:

1. Narcotics are not advised.

2. Repeated doses of ergotamine or concomitant use of a macrolide antibiotic or a triptan can cause serious vasospasm.

Giant cell arteritis (temporal arteritis)

This disorder needs urgent diagnosis and steroid treatment as delay may result in loss of vision. It occurs in older age (> 50 years), often female, and severe headache may be the only symptom. Jaw claudication and tenderness and swelling over the temporal artery may be present. The diagnosis is confirmed by a high ESR, temporal artery biopsy and response to steroids.

Treatment

If the clinical diagnosis is likely, commence steroid therapy immediately with prednisone 75 mg orally. Response within hours to the first dose of steroids can be diagnostic. Temporal artery biopsy and ESR help plan long-term treatment.

Acute narrow-angle glaucoma

May present with unilateral headache and vomiting. Refer to Chapter 36, ‘Ophthalmic emergencies’.

Other causes of head pain

Very many other diseases of ears, eyes, nose, sinuses, teeth and temporomandibular joints may cause head pain.

PARAPLEGIA

Acute paraparesis or paraplegia is an emergency as any delay in treatment may result in irreversible spinal cord damage. Mild or early cord lesions due to compression are most likely to benefit from prompt diagnosis and decompression and just such cases are more likely to be misdiagnosed.

Clinical features

Motor

Weakness in the legs presents as difficulty walking. There is a pyramidal pattern of weakness (flexors and abductors more than and before extensors). Spasticity may be present.

Tendon reflexes are increased with extensor plantar responses, but in an acute cord lesion upper motor neurone signs may be absent. There may be flaccid paralysis with absent reflexes (spinal shock).

Flexor spasms can be mistaken for voluntary movements.

Sensory

Numbness or paraesthesias start in the feet regardless of the level of the lesion. Only when the damage has progressed will a distinct sensory level clearly indicate the segment of cord involved.

In spinal cord disease, look for the highest abnormal signs. Minor abnormalities in the arms or a Horner’s syndrome indicate that the disease is in the neck, when most of the deficit may still be in the legs.

Autonomic

Careful interrogation is often necessary to reveal significant symptoms in early cord lesions.

Constipation—insidious changes in bowel habit occur in subacute or chronic lesions.

Urgency of micturition is often admitted only after leading questions. Retention of urine in severe lesions is revealed by a palpable bladder. The retained volume should be recorded if a catheter is passed. Retention with overflow (palpable bladder and large volume on catheterisation or ultrasound) should not be confused with simple incontinence.

Erectile impotence may be revealed only on specific enquiry.

Investigations

• FBC, CRP, ESR, electrolytes, creatinine, LFTs, CXR and plain X-rays of cervical and thoracic spine.

• Urgent MRI of the whole spinal cord if there is any possibility of cord compression.

• Myelography is appropriate if MRI is not available.

• CT scans can show the lesion, particularly if the exact level is known, but MRI or myelography is needed to exclude a compressive lesion.

Treatment

• Emergency surgery to decompress the cord is the important measure to consider.

• Bladder care is also an urgent matter. Failure to relieve retention by catheter will damage the bladder. Leave an indwelling catheter draining.

• Nursing and medical care is a specialised problem, and transfer to a special unit should be arranged without delay in acute or severe paraplegia.

CONFUSION

Clinical features

Document conscious state, behavioural and emotional disturbance, impairment of thought processes, disorientation, confabulation, delusions and hallucinations.

Differential diagnosis

Exclude focal cerebral disorder—e.g. dysphasia.

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