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
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
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
35.40— Fig. 35.42).
AVMs
are treated by either removing the lesion surgically, endovascular embolisation
of the nidus, stereotactic radio-surgery or a combination of treatments.