It is the spontaneous haemorrhage into the subarachnoid space, 5% to 10% cases of strokes are due to subarachnoid haemorrhage.
When the cause of haemorrhage is located in the circle of Willis.
When the site of haemorrhage is inside the cerebral hemisphere primarily and then blood enters the subarachnoid space.
1. Rupture of congenital berry aneurysm (commonest, 80%).
Common sites of such aneurysm are-
(a) Posterior communicating artery.
(b) Anterior communicating artery
(c) Middle cerebral angioma.
2. Rupture of cerebral angioma.
3. Rupture of atherosclerotic artery.
4. Head injury.
5. Rupture of mycotic aneurysm from infective endocarditis.
6. Rupture of syphilitic aneurysm.
7. Leaking from arterio-venous malformation (5%) or angioblastic meningioma or glioma.
8. Blood dyscrasias including anticoagulant therapy.
9. Idiopathic (10%)
Includes all causes of cerebral haemorrhage.
Onset is sudden, may be precipitated by physical strain. Age: Common in younger age group. This is why subarachnoid haemorrhage is called “apoplexy of the young”. In older age group subarachnoid haemorrhage is due to rupture of atherosclerotic aneurysm.
1. Headache is extremely severe, not experienced by the patient previously and located in the occipital region and upper cervical region. It is splitting and thunderclap in character. There may be radiation of pain from the cervical region to both sides of the body to arms. Patient feels as if he is struck by a blow.
2. Vomiting occurs at the onset and is due to sudden increase of intracranial tension. Therefore, it is usually not preceded by nausea.
3. Rapid loss of consciousness.
4. Convulsive seizure may be seen.
5. Symptoms may be altogether absent.
Signs of meningeal irritation
Neck rigidity and Kernig’s sign are usually present. Blood in the subarachnoid space after lysis liberate bilirubin which irritates the meninges and hence these signs develop. Late development of fever, leucocytosis, delirium and mental changes may indicate chemical meningitis.
These indicate that aneurysm has caused local pressure effect or vascular spasm or obstruction or leak has occurred through a buried intracerebral aneurysm. There may be third nerve Palsy which indicates aneurysm of the posterior communicating artery. Due to compression of optic nerve there may be visual field defect as a result of affection of the visual pathway. Secondary vasospasm may give rise to hemiplegia, but it is rare. Monoplegia and quadriplegia may rarely develop.
Signs of increased intracranial tension
(a) Patient is in coma or in drowsy state. Persistent coma bears a bad prognosis and may indicate transtentorial herniation.
(b) Pulse is slow and bounding.
(c) Respiration is of Cheyne-Stoke’s or Biot’s type.
(d) Planter reflexes are extensor on both sides.
(e) Deep reflexes are diminished, so also are the abdominal reflexes.
(f) Fundoscopic examination reveals papilloedema with marked venous congestion and retinal haemorrhage. Boat (canoe) shaped subhyaloid haemorrhage may also be present.
(g) Albuminuria and glycosuria may develop
Due to severe headache and autonomic disturbance there is liberation of increased catecholamines which may cause diffuse micronecrosis of the myocardium resulting in ST-T changes in the ECG, fever, leucocytosis, hyperglycaemia and glycosuria.
Inappropriate ADH secretion
It may result in changes in electrolytes and urine volume.
It may develop and produce persistent coma, delirium, UMN signs.
This is commonest. Here the signs indicate meningeal irritation as mentioned above. In fact meningeal irritation of sudden onset without fever is an important clue to the diagnosis.
Here patient manifests signs of unilateral pyramidal lesion in presence of signs of meningeal irritation.
Lumbago sciatica syndrome
In some cases, the haemorrhagic blood gradually settles downwards to the lumbosacral region and irritates the emerging nerve roots, giving rise to manifestations of lumbago and sciatica. Sometimes subarachnoid haemorrhage may start in the region of lower spinal cord which starts with low back pain and pain in the lower limbs, flaccidity of muscles and sphincter disturbances. When blood goes to cerebral sub- arachnoid space patient develops headache and nuchal rigidity.
1. Blood may show leucocytosis, high sugar.
2. Urine may show albumin and sugar.
3. CSF-Tension is raised. Colour-Red, frank blood, RBC may be present for 72 hours. Centrifugalised supernatant fluid may show xanthochromia which is due to oxyhaemoglobin in early stages but later on due to bilirubin. White cell count may be increased due to meningeal irritation containing monocytes and lymphocytes mainly and few polymorphs. Protein is usually raised. LP is not routinely done now-a-days but just once for diagnosis.
4. Cerebral angiography may show not only the cause but also the site of bleeding. Bilateral carotid and vertebral angiography may be done in patients below 50 years when operative treatment may be apprehended.
5. X-ray of skull is usually normal; but may show calcification of the vascular wall or evidences of angioma.
6. CT scan is the most promising investigation in subarachnoid haemorrhage. It should be performed immediately so as to confirm haemorrhage and its source. It is superior to MRI because CT scan can be done fast and it is very sensitive for detecting blood in first 24 hours. Of course sometimes the CT findings are normal and then we have to depend on CSF findings.
Mortality rate is about 45%, about 30% of the patients will die in the first episode of bleeding, a further 20% will die in the first week of treatment in the hospital due to further bleeding. Patients who are having persistent coma or severe neurologic deficits will have a poor prognosis.
Onset is not so sudden, fever is constantly present, BP is normal, CSF shows no blood but other characteristic findings of meningitis. It occurs in children mostly.
Onset is sudden, BP is high, vomiting, bradycardia are present but neck rigidity and Kernig’s signs are usually minimal or absent, CSF shows no blood but increased tension.
Pyrexia, headache, convulsion and unconsciousness are present but nuchal rigidity and Kernig’s sign are not so much prominent. CSF may at times show few RBC but no frank blood as in cases of subarachnoid haemorrhage.
The disease occurs in higher age group, with hypertension. Hemiplegia and coma are constant. Most of the cases are usually fatal. Neck rigidity and Kernig’s signs are absent.
Other causes of Coma
Onset is not so sudden and in none excepting the above causes, signs of meningeal irritation will be present. Diabetic coma and uraemia may be confused due to the presence of albumin and sugar in the urine but other features and absence of signs of meningeal irritation are points for their exclusion.
All measures for a comatose patient should be taken.
If the BP is high it should be lowered which will prevent further bleeding.
Sedatives like Phenytoin, Phenobarbitone or Diazepam should be given particularly when convulsion is present or to prevent apprehension.
For headache, analgesics can be given but Aspirin should be avoided.
Nimodipine (30 mg/6 hourly) may be given for alleviating Symptoms of vasospasm which is usually seen between 4th and 14th day. To check bleeding, in some centres Aminocaproic acid 24 gm IV daily is being used for 2-3 weeks. Dexamethasone and antifibrinolytic agents are often prescribed but their value is doubtful. To prevent straining at stool mild purgatives or laxative may be given.
Electrolyte imbalance particularly hyponatraemia which develops few days after attack (cerebral salt depletion) should be corrected
LP should be done once for diagnostic purpose, as it may sometimes aggravate bleeding. Surgical treatment consists of ligation of common carotid artery or the bleeding artery after locating it by angiography or clipping the neck of the aneurysm. Angioplasty may be done to improve ischaemic symptoms when present in spite of medical treatment. Many authorities do not like to do surgery immediately because of postoperative complications but may prefer to do so after 10- 14 days from the attack.
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