Over half of non-traumatic intracranial hemorrhage is secondary to the rupture of an intracranial aneurysm. About 20 per cent will have an associated intracerebral hematoma as illustrated in Fig 1. Aneurysmal rebleeding carries a high mortality and morbidity, with the peak incidence in the first 24 to 48 h, but with a continuing risk reaching 50 per cent over a month.
Fig. 1 (a) CT brain scan showing hemorrhage into the left temporal lobe. (b) This was later confirmed, after cerebral angiography, to be secondary to rupture of a left middle cerebral artery aneurysm: 1, left internal carotid artery; 2, left middle cerebral artery; 3, left middle cerebral artery aneurysm.
The best method of prevention of rebleeding, despite many attempts in the past to control 'transmural pressure' and the use of antifibrinolytic agents, remains obliterating the aneurysm from the intracranial circulation. This can be done surgically with a clip at craniotomy, as illustrated in Fig 2, or by the endovascular route, filling the aneurysm sac with coils (embolization). Endovascular techniques, although much less invasive, have not been evaluated in the long term and do not have the advantages of open operation, i.e. drainage of cerebrospinal fluid, removal of intracerebral hematoma or cisternal clot (believed to be helpful in the prevention of vasospasm), and control of proximal vessels in the event of an intraoperative aneurysmal rupture.
Fig. 2 (a) Left lateral carotid angiogram performed after subarachnoid hemorrhage revealing a large posterior communicating artery aneurysm and distal narrowing of cerebral vessels secondary to vasospasm: 1, left internal carotid artery; 2, left posterior communicating artery aneurysm. (b) A repeat postoperative angiogram shows successful surgical clipping of the aneurysm.
The timing of surgical clipping or embolization remains another neurosurgical controversy, but there is a growing trend to perform this in the first few days after hemorrhage to prevent rebleeding and allow the maximal treatment of vasospasm, particularly in the patient with a good grade. In patients with WFNS (World Federation Neurological Surgeons) grades 3 to 5, treatment of the aneurysm is usually delayed pending neurological improvement.
Preoperative preparation of such patients should follow on from their medical management at ictus. An assessment and any necessary treatment of general medical problems should be carried out, with particular attention to the respiratory system. All patients should receive adequate hydration (2-3 l/24 h), and the calcium-channel blocker nimodipine should be given to prevent deterioration secondary to vasospasm. If nimodipine cannot be adminstered orally (60 mg every 4 h), it should be given via the nasogastric or intravenous route. The dose should be decreased if it is thought to have a deleterious effect on systemic blood pressure. A recent full blood count, urea, electrolytes, and clotting profile should be available, and four units of blood should be cross-matched. Hyponatremia is common secondary to cerebral salt wasting and hemodilution, and may require correction. Fluid restriction should be avoided because of the adverse effect on cerebral perfusion pressure.
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