Subarachnoid haemorrhage and aneurysms

Introduction

The blood supply to the brain enters the cranium through the skull base via the paired internal carotid and vertebral arteries. Within the subatachnoid space these vessels com­municate to form the circle of Willis and then branch out over the surface of the brain before entering into and supplying the brain parenchyma. Subarachnoid haemorrhage (SAH) occurs when a vessel ruptures into this subarachnoid layer. Patients present with a typical sudden, unusual and severe headache. They may die apoplectically or present with a range of clinical conditions varying from being moribund, to a mild residual headache. The clinical status of these patients is graded according to the World Federation of Neurological Surgeons (WFNS) scale where the Glasgow Coma Scale (GCS) is used to measure consciousness (Table 35.6). This gives a measure of severity and prognosis of the haemorrhage.

Epidemiology

The incidence of SAH is 6—16 cases per 100000 per year representing 2—10 pet cent of all cerebrovascular events and can have various causes (Table 35.7). While in some countries SAH is predominantly traumatic in origin, in most, these bleeds arise from thin-walled sacculat dilatations or aneurysms situated at the bifurcation of intracranial vessels, particularly upon the circle of Willis (Fig. 35.34a and b). These are usually sacculat with a neck and fundus but may be fusiform. They are most likely to be caused by haemodynamic stresses, the result of turbulent blood flow, possibly acting on a weak point in a vessel wall. Such lesions ate found in about 7.8 per cent of individuals at post mortem examination. The total prevalence in the general population appears to be in the region of 1.5 per cent and aneurysmal SAH accounts for 0.1 per cent of deaths within the general population. The prevalence increases with each decade reaching a peak at 40—60 yeats.

Arteriovenous malformations (AVM) are vascular hamar­tornas. Several groups are recognised. The most common is the true arteriovenous malformation while the other types include cavernous angiornas, venous malformations or capillary telangiectasis. These latter types seldom bleed and ate usually incidental findings on MRI. AVMs present with either haernorrhage, epilepsy or a neurological deficit. They may also cause ischaemia by shunting blood away from cerebral tissue (‘steal phenomenon’) and are graded according to their size, situation and the direction of their venous drainage.

Clinical features

SAH is typically heralded by a severe, unusual headache of sudden onset, frequently associated with neurological symptoms and often accompanied by nausea and vomiting. This is a result of exttavasation of blood under pressure into the CSF space, ventricles or into the brain itself. The accom­panying acute rise in ICP causes compromise of the cerebral perfusion pressure and the cerebral blood flow, tamponading the bleed and allowing time for a clot to develop. The patient’s level of consciousness may as a consequence be depressed to varying degrees for varied periods of time and there might be concomitant photophobia and neck stiffness from meningeal irritation. Rarely, the patient may develop back and radicular pain as blood accumulates in the spinal canal. Physical examination reveals meningism and a positive

Kernig’s sign. Fundoscopy can sometimes show globular subhyloid haemorrhages, scattered retinal haemotrhages and occasionally papilloedema. A focal neurological deficit or seizures reveals concomitant parenchyrnal damage. Fever, leucocytosis and hypertension ate not unusual. Although the majority of aneurysms presents with rupture, they can present with symptoms of compression alone resulting in pain, dysfunction (classically a third nerve palsy) or epilepsy.

Investigations

Diagnosis is classically made by LP but all patients should be investigated with CT. This is the investigation of choice and

within the first 24 hours of the bleed has a 90 per cent sensitivity, falling to 50 per cent at 3 days. This is able to confirm the diagnosis noninvasively, detect the presence of intracerebral haematomas, exclude hydrocephalus and indicate the likely source of a bleed — directing cerebral angiography. If the CT is normal or equivocal, if the bleed is more than 72 hours old and if no contraindications to LP are present, then the patient should undergo a lumbar puncture looking for uniformly bloodstained CSF, xanthochtomia or bilirubin byproducts of haemoglobin breakdown on spectrophotometry (Fig. 35.35a and b). Acute bacterial meningitis can mimic SAH so microbiological analysis should

also be requested. Confirmation of haemorrhage should be investigated with cerebral angiography to determine the cause (Fig 35.36 and Fig 35.37). This should be considered with some urgency as the potential for a ruptured aneurysm to rebleed within the first 2 weeks is 25 per cent or 60 per cent within 6 months of the initial SAH with a mortality rate of greater than 60 per cent.

Fifteen per cent of aneurysms are multiple and 15 per cent of angiograms will be negative, indicative of an occult source such as a perimesencephalic bleed, a thrornbosed aneurysm or a spinal arteriovenous malformation. The first angiograrn describing intracranial aneurysms was performed by Moniz in 1933. Bilateral angiography including the internal carotids and vertebral arteries is the gold standard for delineating vascular lesions. With the advent of digitised angiography, it has been possible to reduce significantly the dosage of con­trast material given. The increasing sophistication of the noninvasive imaging techniques, magnetic resonance angio­graphic (MRA) and CT angiography, enables resolution of aneurysms 3 mm in size.

Management

The clinical course of patients with SAH is frequently unpre­dictable owing to the development of complications. The most severe are tebleeding and delayed ischaernic neurological deficit (DIND) — also known as vasospasrn. The risk of rebleeding is 4 per cent in the first 24 hours and 19 per cent in the first 2 weeks, and carries a mortality and morbidity of 60 per cent. Aneurysms are secured by the surgical appli­cation of a clip across the neck at craniotomy (Fig. 35.38), isolating it from the circulation. Recently, endovascular techniques have been developed enabling aneurysms to be secured by packing them with platinum coils (Fig 35.38 and Fig 35.39).

The cause of vasospasm remains unknown and is a signifi­cant cause of morbidity. Overall, 30 per cent of SAH patients will suffer DIND due to vasospasm, with the majority suffer­ing permanent neurological deficits. Treatment of vasospasm relies on maintaining an adequate blood pressure and intra­vascular volume with intravenous fluids (mixture of 3.5 litres per 24 hours of crystalloid and colloid) since cerebral per­fusion is related to arterial pressure and intracranial pressure. Cerebral blood flow is further optimised by decreasing the haematocrit and if necessary using inotropic agents to elevate the blood pressure above physiological levels. All SAH patients develop some degree of hydrocephalus. This usually resolves spontaneously but may requite temporary or per­manent CSF diversion. Cardiac arrhythrnias and hyponatrae­mia ate also frequent complications of this condition.

The potential for rebleeding from an AVM (2—4 per cent per annum) is lower than for an aneurysm and there is therefore less urgency with treatment (Fig 35.40Fig. 35.42).

AVMs are treated by either removing the lesion surgically, endovascular embolisation of the nidus, stereotactic radio-surgery or a combination of treatments.