Subarachnoid Haemorrhage (SAH)
A subarachnoid haemorrhage is an uncommon type of stroke caused by bleeding on the surface of the brain. It's a very serious condition and can be fatal.
Subarachnoid haemorrhage accounts for 8% of all strokes.
Causes of SAH.
1. Ruptured berry aneurysm (> 50%).
2. Arteriovenous malformation (AVM).
3. Extension of ICH.
4. Haemorrhage into cerebral infarct.
5. Haemorrhage into the cerebral tumour.
6. Rupture of an atheromatous vessel.
7. Rupture of mycotic aneurysm.
8. Bleeding diathesis.
Common Sites of Aneurysm
1. Carotid system
a. Anterior communicating artery.
b. At the bifurcation of the middle cerebral artery from the internal carotid artery.
c. Origin of the posterior communicating artery from the internal carotid artery.
2. Vertebrobasilar system
a. At the apex of the basilar artery.
b. At the origin of posterior inferior cerebellar and superior cerebellar arteries from the basilar artery.
Aetiopathogenesis of Aneurysm Formation
1. Congenital defect in the media of the blood vessels at the point of bifurcation.
2. Hemodynamic stress at the point of bifurcation of the vessel.
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Conditions Associated with Aneurysm
1. Coarctation of the aorta
2. Polycystic kidneys
3. Moyamoya
4. Marfan’s syndrome
5. Hereditary haemorrhagic telangiectasia
6. Pseudoxanthoma elasticum
7. Ehlers-Danlos syndrome.
Clinical Features of SAH
a. Before rupture of aneurysm: The II, III, IV, VI and ophthalmic division of the V cranial nerves may be involved due to compression by the aneurysm of internal carotid artery within the cavernous sinus. Isolated III cranial nerve palsy may be seen with an aneurysm of the posterior communicating artery.
b. After rupture of aneurysm: SAH due to rupture of aneurysm often occurs during exertion, when there is a rise in blood pressure, as occurs during straining or during sexual intercourse.
Patients present with headache, vomiting, altered sensorium, meningeal irritation, seizures and rarely with focal neurological deficit. The focal neurological deficit, if present, may help to localize the site of aneurysm (e.g. aneurysm of anterior cerebral artery results in hemiplegia with lower limb involvement more than the upper limb involvement).
Neck stiffness takes six hours to develop but fundus shows retinal and sub-hyaloid haemorrhage.
Complications of SAH
1. Rebleed: This may occur maximally within 24 hours. In 90% of patients rebleed within 6 months. Rebleed is characterised by sudden deterioration of symptoms and signs, with onset of headache, meningeal irritation and loss of consciousness.
2. Vasospasm: Vasospasm of intracranial cerebral vessels leads to cerebral ischaemia. It is insidious in onset and multifocal. Twenty per cent of the patients experience this complication within the first 2 weeks of bleed.
This is characterised by fall in the level of consciousness and appearance of focal neurological deficit.
3. Hydrocephalus: This occurs due to blockage of normal CSF flow by Pacchionian granulation tissue. It is characterised by increase in severity of headache and progressive deterioration of sensorium.
4. Hyponatraemia.
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Causes of Thunderclap Headache
1. Sub-arachnoid haemorrhage (25%)
2. Meningitis
3. Migraine
4. Intra-cerebral bleeds
5. Cerebral venous thrombosis
6. Dissection of carotid or vertebral artery.
Investigations of SAH
1. CT Scan Brain: This may show
a. Blood in the subarachnoid space and associated parenchymal haematoma. Hyperdense areas are seen in anterior interhemispheric fissures, both sylvian fissures, in the ventricular system and basal cisterns.
b. Site of bleed.
c. Demonstration of presence of aneurysm (by contrast CT).
d. Presence of associated hydrocephalus.
2. Lumbar Puncture: This is done when CT is negative, and in presence of SAH, the following may be observed.
a. Homogenously blood-stained CSF (when LP is done early).
b. Xanthochromia (when LP is done later).
C. Rise in CSF pressure.
However, if there is strong clinical suspicion of SAH even after a normal CT, an urgent lumbar puncture has to be done 12 hours after the onset of headache to get blood-stained CSF. Xanthochromia of CSF takes 6-12 hours to develop.
3. Angiography: This helps in locating the site of aneurysm and for planning surgery. Do angiography as early as possible after ictus and selective 4 vessel angiography must be done. Multiple oblique views may show aneurysmal neck. Cross compression views delineate anterior communicating and posterior communicating arteries and cross-circulation. Subtraction images are preferred for posterior fossa aneurysms and Towne’s view for the carotid angiogram.
4. MRI Angiography: This is indicated in:
a. Angiography negative subarachnoid haemorrhage.
b. Complementary to angiography or DSA.
c. Renal failure or when contrast injection is contraindicated.
d. Screening in patients with the polycystic disease, coarctation, fibromuscular dysplasia, and family history of aneurysms.
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Treatment of SAH
1. In the acute phase, the patient is treated for signs and symptoms of raised intracranial tension.
2. General care of the patient (maintenance of fluid and electrolyte balance, care of the skin and adequate airway and ventilation).
3. Control of hypertension (diastolic BP to be maintained at about 110 mmHg).
4. SAH is usually associated with vasospasm of intracranial vessels which can lead to cerebral ischaemia and so must be managed as follows:
i. IV isoproterenol and nitroglycerine.
ii. Volume expansion.
iii. Slow calcium channel inhibitors have been proposed. Nimodipine 30–60 mg orally every 4 hours may be given for 3 weeks.
5. If SAH is found to be due to arterial aneurysm, then surgical clipping of the aneurysm is done after the patient has stabilised, to prevent rebleed. Aneurysms larger than 7 mm size, when detected before development of SAH, warrant prophylactic surgical obliteration.
Association
Intracranial saccular aneurysms may be associated with:
1. Polycystic kidneys
2. Cervical artery dissection
3. Fibromuscular dysplasia of arteries
4. Coarctation of the aorta.
5. Marfan’s syndrome
6. Ehlers-Danlos syndrome
7. Pseudoxanthoma elasticum
8. Hereditary haemorrhagic telangiectasia
9. Moyamoya disease
10. Klinefelter’s syndrome.
SAH Due to Other Causes
1. Bleeding diathesis
2. Rupture of small penetrating arterioles or venules
3. Bleeding from arteriovenous malformation.
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