Key messages

• Suspect intracranial hemorrhage in any patient who presents with an acute change in conscious level.

• Intracranial hemorrhage causes over 30 per cent of all strokes, and the younger the patient the greater its probability. Mortality and morbidity remain high.

• Primary brain damage from the hemorrhage will be complete at time of presentation. Secondary brain damage can be prevented or ameliorated by prompt assessment and optimal management.

• Correction of hypoxia and hypotension and identification and treatment of raised intracranial pressure are absolutely mandatory in the prevention of secondary brain damage.

• Do not treat reactive hypertension as low blood pressure may reduce cerebral perfusion pressure. Etiology and pathology

Non-traumatic intracranial hemorrhage may occur within the subarachnoid space (subarachnoid hemorrhage), within the brain parenchyma (intracerebral hemorrhage), or into the ventricular system itself (intraventricular hemorrhage). Often a subarachnoid hemorrhage may present with an associated intracerebral hematoma. Likewise an intracerebral hematoma, depending upon its anatomical position, may burst into the subarachnoid space. Intraventricular hemorrhage is commonly associated with either of the former. Rarely, spontaneous hemorrhage can occur into the subdural or epidural spaces. Intracranial hemorrhage may be supratentorial or originate in the posterior fossa.

Beyond the third decade subarachnoid hemorrhage is most commonly due to rupture of a cerebral aneurysm, usually situated at the origin of the branches of the major cerebral arteries. A further 10 to 20 per cent of cases of subarachnoid hemorrhage are due to arteriovenous malformations and tend to occur in the younger patient. However, in 20 per cent of all subarachnoid hemorrhage no cause is detected. Intracerebral hemorrhage is more common in the older patient (60 years and above), in whom it is secondary to hypertension and located in the basal ganglia. Lobar hemorrhages constitute a further 40 per cent and are often related to underlying amyloid angiopathy. Coagulation abnormalities, intracranial tumors, and drug abuse make up some of the rare causes of bleeding.

The final outcome of these patients is related to the amount and location of neuronal loss that occurs both at the time of the hemorrhage (primary brain damage) and in the subsequent minutes, hours, and days (secondary brain damage). Primary brain damage is caused by the hemorrhagic destruction of brain tissue itself and is unalterable at the time of presentation. Further neuronal death secondary to cerebral ischemia around the hematoma is the final common cause of secondary brain damage (.M„en.d.,elow..,.e?...a.l: 1984). This is potentially preventable and forms the basis of patient management. Despite the differing etiologies and locations of intracranial hemorrhage, these patients tend to present with a similar spectrum of symptoms and signs, varying from headache only to deep coma, with or without a lateralizing neurological deficit. Assessment of these patients occurs in two parts: first a rapid appraisal of the vital signs and conscious level of the patient, with simultaneous correction of any reversible factors that may be contributing to the processes of secondary brain damage, and second, after stabilization, a more detailed examination to aid in the differential diagnosis and prognosis. A schematic approach to assessment is described.

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