Intracranial haemorrhage and stroke: initial management

Overview

Stroke is either ischaemic (about 85%) or haemorrhagic (intracerebral or subarachnoid). The first job is the same for all: resuscitate (ABC), check glucose, and get a CT scan to separate bleeding from infarction. The surgical role is to secure aneurysms, evacuate selected clots, drain hydrocephalus and decompress swollen brain.

This chapter covers subarachnoid haemorrhage, intracerebral haemorrhage, vascular malformations and the initial management of ischaemic stroke.

Spontaneous subarachnoid haemorrhage (SAH)

Causes

• Ruptured saccular ("berry") aneurysm: about 80%. Aneurysms form at branch points of the circle of Willis where flow is turbulent. Commonest sites: anterior communicating, posterior communicating and middle cerebral arteries; posterior circulation is less common.
• Arteriovenous malformation (AVM).
• Perimesencephalic SAH: blood confined to the cisterns in front of the midbrain and pons, angiogram normal; probably venous; excellent prognosis.
• Mycotic aneurysm: infected arterial wall in endocarditis or IV drug use.

Risk factors

Hypertension, smoking, female sex, age, cocaine, family history (two or more first-degree relatives), and inherited disorders: adult polycystic kidney disease, Ehlers-Danlos, Marfan's, neurofibromatosis type 1, fibromuscular dysplasia, coarctation of the aorta.

Clinical features

• Thunderclap headache: sudden, severe, "the worst ever", often during exertion. Some have a warning (sentinel) headache days before.
• Vomiting (common), brief loss of consciousness (about half), seizures (about 10%).
• Meningism (neck stiffness, photophobia, Kernig's sign) develops over hours, so it may be absent early.
• Focal signs; painful third nerve palsy with a dilated pupil = posterior communicating artery aneurysm.
• Subhyaloid (preretinal) haemorrhages; SAH with vitreous haemorrhage = Terson's syndrome (15–20%).
• About one-third are misdiagnosed at first presentation (as migraine or tension headache) and are then at risk of rebleeding.

Grading: World Federation of Neurological Surgeons (WFNS)

Graded after resuscitation, using GCS and motor deficit.

Investigations

1. Non-contrast CT: within 12 hours of onset it shows blood in over 98%; sensitivity falls to under 50% by 1 week. CT also shows hydrocephalus, haematoma and the likely aneurysm site.
2. Lumbar puncture if CT is negative but the story is suggestive: wait at least 6 hours, ideally 12 hours, then look for xanthochromia (bilirubin and oxyhaemoglobin) by spectrophotometry. This separates true SAH from a traumatic tap.
3. CT angiography: quick and sensitive for aneurysms and AVMs.
4. Digital subtraction (catheter) angiography: the gold standard; risks include stroke or arterial dissection (1–2%) and contrast reactions.

Initial (medical) management

• ABC; intubate if GCS low. Bed rest, hourly neuro-observations, strict fluid balance.
• IV normal saline to keep normal blood volume (around 2.5–3 L/day). Do not fluid restrict.
• Nimodipine 60 mg orally (or by NG tube) every 4 hours: reduces poor outcome from delayed ischaemia.
• Analgesia, anti-emetics, laxatives (avoid straining), gastric protection, compression stockings.
• Control severe hypertension carefully.
• Early transfer to a neurosurgical centre. Elderly patients in poor grade may receive supportive care only.

Securing the aneurysm

• Endovascular coiling: platinum coils (sometimes with a stent) fill the sac via a femoral catheter. Better outcomes for small anterior circulation aneurysms have made it the usual first choice; regrowth is commoner, so follow-up imaging is needed.
• Surgical clipping by craniotomy: still needed for some aneurysms (wide neck, MCA branch aneurysms, those with a large clot to evacuate).
• Done early, because rebleeding is most likely in the first days.

Complications

Prognosis

About half of all patients die, and about a third of survivors remain dependent. Treated aneurysms, especially coiled ones, need surveillance. Small, incidentally found anterior circulation aneurysms carry a low bleeding risk.

Spontaneous intracerebral haemorrhage (ICH)

Facts

• About 10–15% of strokes; mortality about 40% at 1 year.
• Causes: chronic hypertension (deep bleeds: putamen/basal ganglia, thalamus, pons, cerebellum), cerebral amyloid angiopathy (lobar bleeds in the elderly), anticoagulants (warfarin), bleeding disorders, AVMs, aneurysms, tumours, haemorrhagic change in an infarct, drugs (cocaine, amphetamines).

Presentation

Sudden focal deficit with headache, vomiting and a reduced conscious level; signs of raised ICP.

Initial management

• ABC; CT confirms the bleed, its size and site, ventricular extension and hydrocephalus.
• Reverse anticoagulation urgently (vitamin K, prothrombin complex concentrate).
• Blood pressure: lower carefully. Long-standing hypertension resets autoregulation, so lower acutely only if very high (Bailey & Love gives MAP above 130 mmHg as an example).
• Hourly neuro-observations; treat seizures, fever and glucose.
• CT or catheter angiography if a vascular lesion is suspected (young patient, lobar bleed, no hypertension). Delayed MRI to look for a hidden tumour.

Who needs surgery?

Vascular malformations

Acute ischaemic stroke: initial management

1. ABC, oxygen if hypoxic, check blood glucose, monitor BP and rhythm.
2. Urgent non-contrast CT to exclude haemorrhage (early infarcts may not show; MRI diffusion imaging is more sensitive).
3. Thrombolysis with IV alteplase if eligible: start as soon as possible and within 4.5 hours of a clearly known onset.
   • Dose 0.9 mg/kg (maximum 90 mg): 10% as a bolus over 1 minute, the rest over 60 minutes.
   • Key contraindications: haemorrhage on CT, BP persistently above 185/110 mmHg, recent stroke or head injury (3 months), previous ICH, recent major surgery, active bleeding, low platelets, INR above 1.7, glucose very low or very high, symptoms suggesting SAH.
4. Mechanical thrombectomy for proximal anterior circulation (large vessel) occlusion in selected patients, usually after alteplase.
5. Aspirin 300 mg daily: start it a day after alteplase, or straight away once CT shows no bleed in those not thrombolysed; switch to long-term antiplatelet after about 2 weeks.
6. Admit to a stroke unit: swallow assessment before oral intake, DVT prevention, early mobilisation, therapy, secondary prevention (statin, BP control, anticoagulation for atrial fibrillation usually after about 2 weeks).
7. Blood pressure: do not lower routinely in the first days unless very high or the patient needs thrombolysis.

Surgical roles in ischaemic stroke

• Decompressive craniectomy for malignant middle cerebral artery infarction (swelling of more than half the MCA territory) in younger patients, ideally within 48 hours: prevents coning and improves survival.
• Posterior fossa (cerebellar) infarct with swelling: suboccipital decompression ± EVD for hydrocephalus.
• Carotid endarterectomy within 2 weeks for symptomatic 70–99% stenosis (non-disabling stroke or TIA). Carotid stenting is an alternative in some patients.

Quick revision

• Spontaneous SAH: aneurysm 80%; perimesencephalic SAH has an excellent outlook.
• CT first; if negative, LP at 12 hours for xanthochromia.
• Nimodipine 60 mg every 4 hours; normal saline; no fluid restriction.
• Rebleed: early (first 24 h); vasospasm: days 3–10; hydrocephalus: communicating.
• Coil or clip early.
• ICH: hypertension (deep) or amyloid (lobar); reverse anticoagulants; operate on cerebellar clots and deteriorating young lobar bleeds.
• AVM rebleed about 4%/year; cavernoma seen only on MRI.
• Ischaemic stroke: alteplase 0.9 mg/kg (max 90) within 4.5 h; thrombectomy for large vessel occlusion; aspirin 300 mg.
• Craniectomy for malignant MCA infarct within 48 h; endarterectomy for symptomatic 70–99% stenosis.

Written by The House Job from standard references (Bailey & Love; Kumar and Clark's Clinical Medicine).

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