Diagnostic tests

CT scanning of the brain is the procedure of choice for the diagnosis of SAH. The CT scan can demonstrate the magnitude and location of the SAH, give clues to probable aneurysm location, and assess ventricular size (Figure 8.1).

CT's success in detecting SAH is dependent upon the length of time between SAH and scan acquisition. Eighty-five per cent of patients scanned within 48 hours of SAH and 75% of patients scanned within five days will have detectable subarachnoid blood.38-41 The distribution of blood on the CT scan may suggest the probable aneurysm location. Acute blood within the interhemispheric and supratentorial ventricular system is often the consequence of a ruptured anterior communicating artery aneurysm. Focal blood within the fourth ventricle suggests a vertebral or posterior inferior cerebellar artery (PICA) aneurysm. Intracerebral haematomas are most frequently seen with ruptured middle cerebral, internal carotid bifurcation, or distal anterior cerebral artery aneurysms. Inferior frontal lobe and interhemispheric flame shaped haematomas commonly occur with ruptured anterior communicating artery aneurysms and are a highly accurate CT scan finding for localising the source of the SAH.42,43

In 1980, Fisher developed a grading scale for the CT scan appearance of SAH dependent upon the severity and location of subarachnoid blood.44 Grade I had no blood detectable, whereas grade II patients had a layer of blood less than 1 mm thick diffusely spread throughout the subarachnoid cisterns. Grade III patients had CT appearance of SAH greater than 1 mm thick and grade IV patients had intraventricular or intracerebral blood without significant subarachnoid blood. The Fisher grading system is used to relate the amount of subarachnoid blood on a CT scan to the probability of developing delayed ischaemia secondary to vasospasm. Grade I, II, and IV patients had no or minimal incidence of clinically significant vasospasm while grade III patients had a 958% incidence. These findings implicate blood breakdown products in the genesis of cerebral vasospasm. The greater the magnitude of subarachnoid clot, the higher the likelihood that delayed cerebral ischaemia from vasospasm will occur.

Visual examination of CSF obtained by lumbar puncture can confirm the diagnosis of SAH when the CT scan is negative. In 1901, Si card found that yellow discoloration of CSF after centrifugation was a reliable diagnostic sign of previous SAH.45 The term xanthochromia (xanthochromie) was first used in 1902 to describe the yellow colour of CSF in a case of pneumococcal meningitis and was later used in the 1920s to refer to the colour of CSF several hours after SAH.46-50 The CSF

supernatant does not demonstrate discoloration immediately following SAH, but only after red blood cells haemolyse and release oxyhaemoglobin. Xanthochromia can usually be detected four hours after SAH, becomes maximal one week after haemorrhage, and is usually undetected at three weeks.51 If xanthochromia is present in the CSF, SAH has probably occurred. If a traumatic lumbar puncture is suspected, partial or total clearing of the CSF may occur during collection. In addition, bloody CSF allowed to stand undisturbed in a test tube will form a clot while blood from SAH will generally not. Repeat lumbar puncture hours following a traumatic tap will be of little diagnostic value, since blood contaminating the CSF will produce xanthochromia.

Lumbar puncture after SAH is not without risk. Duffy found that 13% of patients undergoing post-SAH lumbar puncture had significant neurological deterioration.52 Whether or not these changes were directly related to the lumbar puncture is unknown, but because lumbar puncture carries the risk of brain herniation or aneurysm rebleeding, the procedure should only be performed if the diagnosis remains in question following the CT scan or when CT scanning is unavailable. Lumbar puncture is also useful in ruling out infectious meningitis, which may mimic SAH.

After making a diagnosis of SAH, four-vessel cerebral angiography should be performed as soon as possible. The angiographic investigation must visualise the full course of all intracranial vessels in at least two planes, including both posterior inferior cerebellar arteries. The angiographer's goal is to demonstrate the cause of the SAH, define the aneurysm's neck and projection, delineate the vessels arising adjacent to the aneurysm, determine whether multiple aneurysms are present (20% incidence), and assess the degree of any concomitant vasospasm. If no aneurysmal bleeding source is detected, common carotid injections must be performed to rule out the possibility of a dural arteriovenous fistula with retrograde cortical venous drainage as the aeteology of the haemorrhage. In 1977, Nibbelink reported a significant complication rate for cerebral angiography in acute SAH.53 Complications and their frequencies were: transient hemiparesis 2%; permanent neurological deficits 25%; death 2 6%; worsening of ischaemic deficit 3%; and aneurysmal rebleeding 15%. The present day complication rate for cerebral angiography should be less than 1%, with an experienced neuroradiologist,54-56 and is approximately 0 4% in our institution. Aneurysm rupture during angiography has been reported, but is fortunately an infrequent occurrence.57-61 With the advent of rapid scanning helical CT technology, three-dimensional CT angiography has become more widely used in the detection and investigation of cerebral aneurysms.62,63 We currently use CT angiography to augment the information provided by arterial angiography in the analysis of complicated aneurysms. The CT images help detect the position of afferent and efferent vessels and the relationship of the lesion to surrounding structures. CT angiography is also useful to investigate the possibility of arterial dissection when a patient presents with SAH and a negative or equivocal cerebral arteriogram.

MRI is not useful in the acute diagnosis of SAH because of the difficulty in imaging blood products immediately following SAH. MRI has proven valuable in the localisation of subarachnoid clot beyond the time the blood is detectable with CT scanning.64 We have found MRI invaluable in the evaluation of giant intracranial aneurysms. Because giant aneurysms are often partially thrombosed, they often opacify incompletely during angiography, and MRI can demonstrate the magnitude and location of these lesions. We have used MR angiography, and occasionally CT angiography, to follow the size of untreated giant aneurysms in which no treatment was performed due to medical issues.65-70

Serial CT scans are performed periodically for the first several days following SAH to detect hydrocephalus or rebleeding. Hydrocephalus may present with headache, drowsiness, confusion, or agitation. The incidence of acute hydrocephalus following SAH varies extensively among reported series. Bohn and Hugosson found that 1% of their patients operated on for ruptured cerebral aneurysms ultimately required shunting for hydrocephalus.71 Modesti and Binet found a 63% incidence of abnormal ventricular enlargement on CT scanning within 24 hours of SAH.72 In 1985, van Gijn reported a series of 174 patients who suffered SAH. Thirty-four (20%) developed acute hydrocephalus within 72 hours of the haemorrhage. Although intraventricular blood was closely associated with the development of hydrocephalus, the extent of cisternal haemorrhage was not. The mortality rate among those patients with acute hydrocephalus was significantly higher than in those without this complication.73 If hydrocephalus develops following SAH, clinical judgement should be used to assess its severity and the need for CSF diversion. We have found that some patients will exhibit transient, asymptomatic ventricular enlargement following SAH. If hydrocephalus causes clinical manifestations, continuous external ventricular or lumbar drainage is instituted until the ventricular size and intracranial pressure normalise. One exception to this strategy is the existence of an unsecured ruptured aneurysm. In these cases CSF drainage, if required, is carefully controlled so as not to reduce ventricular size or intracranial pressure to a point that the tamponade effect on the aneurysm is lost and re-rupture is promoted.74 Continuous external ventricular drainage can usually be performed with little additional morbidity or mortality.75 If the external ventriculostomy cannot be weaned without the recurrence of hydrocephalus, a permanent ventriculo-peritoneal shunt is placed.

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