Résumé

Abstract

Rupture of intracranial saccular aneurysms is the most frequent cause of subarachnoid hemorrhage (SAH). If conservatively treated, 60 to 70% of the cases with ruptured aneurysms eventually die. Important factors (in the acute stage of SAH) influencing the mortality and morbidity of patients with aneurysmal SAH are listed in Table IX-1. When hemorrhage occurs in the subarachnoid space, intracranial pressure (ICP) inevitably rises dependent upon the amount and distribution of the subarachnoid blood. The increased ICP heralds a series of symptoms which may be termed direct effects of SAH or acute ischemic neurological deficits (AINDs). AINDs include transient global ischemia, impaired autoregulation, decrease in cerebral blood flow (CBF), systemic hypertensive response or Cushing response, vascular engorgement of the brain, brain swelling, microcirculatory disturbance, excessive release of excitatory neurotransmitters to cause neuronal hypermetabolism in decreased CBF, resulting in selective vulnerability of the brain, etc. AINDs affect the neurological conditions of the patient which can be expressed as grades. If the status of a patient with SAH is in a good grade, such as grade I of Hunt, it means the patient has minimal RIND. Grade III, IV, or V implies that AINDs are of a considerable or severe degree. When the subarachnoid clot is of a considerable amount, delayed cerebral vasospasm or arterial spasm will occur around a week or so after SAH, accompanied by neurological symptoms or delayed ischemic neurological deficits (DINDs).