Subarachnoid hemorrhage

Dr Okanga
Introduction
• SAH is less common than ischemic/ hemorrhagic stroke
• Women affected > men.
• usually presents before the age of 65.
• The immediate mortality of aneurysmal SAH is about 30%; survivors have a
recurrence (or rebleed) rate of about 40% in the first 4 weeks and 3% annually
thereafter.
• 85% of cases of SAH are caused by saccular or ‘berry’aneurysms arising from the
bifurcation of cerebral arteries particularly in the region of the circle of Willis.
• Berry aneurysms are common in first degree relatives, polycystic kidney disease
and patients with congenital connective tissue defects such as Ehlers–Danlos
syndrome.
• 10% of SAHs are caused by non-aneurysmal haemorrhages (so-called
peri-mesencephalic haemorrhages) – these have a benign outcome in
terms of mortality and recurrence.
• Around 5% of SAHs are due to arteriovenous malformations and
vertebral artery dissection.
Clinical features
• Sudden, severe, ‘thunderclap’ headache (often occipital), which lasts for hours
or even days, often accompanied by vomiting, raised blood pressure and neck
stiffness or pain.
• It commonly occurs on physical exertion, straining and sexual excitement.
• There may be loss of consciousness at the onset, so SAH should be considered if
a patient is found comatose.
• About 1 patient in 8 with a sudden severe headache has SAH.
• O/E, - patient is usually distressed and irritable, with photophobia. There may
be neck stiffness due to subarachnoid blood but this may take some hours to
develop.
• Focal hemisphere signs, such as hemiparesis or aphasia, may be present.
Investigations
• CT scan – SAH appears as a high-attenuating, amorphous substance
that fills the normally dark, CSF-filled subarachnoid spaces around the
brain.
• LP - should be performed 12 hours after symptom onset if possible, to
allow detection of xanthochromia.
• CT angiography – If either of the above test is positive, then ct
angiography is done to identify the aneurysm
CT angiography
Management
• Nimodipine (30–60 mg IV for 5–14 days, followed by 360 mg orally for a
further 7 days) is usually given to prevent delayed ischaemia in the acute
phase.
• Insertion of platinum coils into an aneurysm (via an endovascular procedure)
or surgical clipping of the aneurysm neck reduces the risk of both early and
late recurrence.
• Coiling is associated with fewer perioperative complications and better
outcomes than surgery; where feasible, it is now the procedure of first choice,
• Arteriovenous malformations can be managed either by surgical removal, by
ligation of the blood vessels that feed or drain the lesion, or by injection of
material to occlude the fistula or draining veins
aneurysm coiling
aneurysm clipping
Management of complications of SAH
• Obstructive hydrocephalus – drainage via a shunt,
• delayed cerebral ischaemia due to vasospasm - vasodilators
• Hyponatraemia - best managed by fluid restriction
• Immobility – Compression stockings and physiotherapy
Cerebral venous thrombosis
• Presents with symptoms of raised intracranial pressure, seizures and
focal neurological symptoms.
• Clinical features vary according to the sinus involved
Predisposing systemic causes
1. Dehydration
2. Pregnancy
3. Behçet’s disease
4. Thrombophilia
5. Hypotension
6. Oral contraceptive use
Predisposing Local causes

1. Paranasal sinusitis
2. Meningitis, subdural empyema
3. Penetrating head and eye
4. wounds
5. Facial skin infection
6. Otitis media, mastoiditis
7. Skull fracture
Investigations and management
• MR venography demonstrates a filling defect in the affected vessel.
• Anticoagulation, initially with heparin followed by warfarin, is
beneficial, even in the presence of venous haemorrhage.
• In selected patients, endovascular thrombolysis has been advocated.
• Management of underlying causes is important.
• About 10% of cerebral venous sinus thrombosis, particularly
cavernous sinus thrombosis, is associated with infection (most
commonly Staphylococcus aureus), needing antibiotic treatment
Bp control in hemorrhagic stroke
• BP should be reduced gradually to 150/90mmHg, using beta-blockers
(labetalol, esmolol), ACE inhibitor (enalapril), calcium channel blocker
(nicardipine) or hydralazine.
• For patients presenting with SBP >220 mmHg, an aggressive reduction
of BP with a continuous intravenous infusion is needed.
Control of ICP in hemorrhagic stroke
• Elevating the head of the bed to 30 degrees
• Osmotic agents (mannitol, hypertonic saline). 20 % mannitol is given
at a dose of 1.0 to 1.5 g/kg.
• Hyperventilation after intubation and sedation, to a pCO of 28 to
32 mmHg will be necessary if ICP increases further
Hemostatic therapy intracerebral hemorrhage
• Thrombocytopenia – Administer platelet concentrates
• Patients on anticoagulants - Vitamin K, prothrombin complex
concentrates (PCCs), recombinant activated factor VII (rFVIIa), fresh
frozen plasma (FFP),
Anticonvulsant therapy for ICH
• Prophylactic anticonvulsant medication is not recommended.
• Those with clinical seizures or electrographic seizures should be
treated with antiepileptic drugs.
• Continuous EEG monitoring is indicated in patients with a decreased
level of consciousness
Surgery for ICH
• STICH trial showed that there is no overall benefit from early surgery for
supratentorial intracerebral hemorrhage when compared with initial conservative
treatment.
• lobar hemorrhages within 1cm of the surface of the brain and milder clinical
deficits (GCS>9) may benefit from early surgery.
• Emergency surgical evacuation is indicated in cerebellar hemorrhage with
hydrocephalus or brainstem compression.
• Patients with cerebellar hemorrhages of >3 cm in diameter will have better
outcomes with surgery.
• Decompressive hemicraniectomy with hematoma evacuation is performed in
patients with GCS scores of 8 or less and large hematomas with a volume greater
than 60 ml