Lumbar puncture is the test required to exclude SAH when CT imaging is unhelpful.2,14 It is best performed more than 12 hours after SAH.15
The results of lumbar puncture can be confounded by ‘traumatic taps’, where the cerebrospinal fluid (CSF) is stained by blood contamination during puncture.16,17 Traditionally there should be clearing of the blood staining if it is traumatic, and consistency over tube collection if SAH is present.16,17 Other methods to differentiate SAH and contaminated collection are examination on spectrophotometry of the supernatant from centrifuged CSF samples (presence of xanthocromia indicating SAH) and laboratory assessment of CSF samples for extracellular blood products such as bilirubin (detection of bilirubin indicating SAH).15,16
The majority of patients with suspected SAH appear to have ‘traumatic taps’.17 Needless to say a clear result is comforting and as definitive as possible in the acute period after possible haemorrhage.16 CSF samples that are heavily contaminated with blood will often be problematic despite the above considerations.
CT angiography (CTA) is often used as an adjunct to CT and lumbar puncture, and can be a powerful tool for the noninvasive assessment of anomalies in the larger vessels of the circle of Willis.18,19 However, this assessment of vascular anatomy does not exclude that there has been haemorrhage.
The sensitivity of CTA is less than that of digital subtraction angiography.18,19
MRI and magnetic resonance angiography
MRI is less sensitive than CT at finding acute haemorrhage and therefore is not recommended as a primary screening modality patients with suspected SAH.20,21 Magnetic resonance angiography (MRA) also, in general, has somewhat less anatomical resolution than CTA, although new techniques for optimising images and defining pathology are promising.22
Digital subtraction angiography
Digital subtraction angiography (DSA) is the gold standard to assess vascular anatomy but has restricted availability and an attendant risk as it is an invasive test.2 It is uncommonly used to investigate patients with SAH, unless haemorrhage or vessel anomaly is seen on noninvasive tests.
Nonhaemorrhagic presentation of cerebral aneurysms
Most aneurysms are discovered incidentally in an outpatient setting. Increased access to noninvasive, relatively accurate imaging such as CTA and MRA has meant that the volume of incidental findings of cerebral aneurysm, which has a community prevalence of about 2%, is significant.23,24
Several multicentre and prospective trials have attempted to determine the natural history of cerebral aneurysms and the morbidity of therapy.8,25-29 Unfortunately, the heterogeneity of aneurysms in terms of size, morphology and site, along with the moving target of microsurgical and endovascular morbidity, conspires to cloud risk–benefit analysis for repair.30
In general terms, the larger the aneurysm, the greater the risk of haemorrhage.8,27 Certain sites, such as the posterior circulation and the posterior communicating artery (which is part of the circle of Willis), appear to have increased haemorrhage risk independent of the size of the aneurysm.8,27 Aneurysms with unfavourable morphology, such as daughter sacs, are also thought to be higher risk.27 It is generally agreed that the haemorrhage rate for small (less than 7 mm) aneurysms with no unfavourable features is less than 1% annually.8,27 Giant aneurysms (greater than 25 mm) have an adverse event rate of more than 2% annually.8,27,31
Mass effect generally relates to large aneurysms or those in specific sites.32 Large or giant aneurysms may have a mass effect on neural structures, causing focal or global neurological deficits or seizures.32,33 Standard imaging will usually make this diagnosis, although other lesions may be mimicked – for example, thrombosis of an aneurysm can lead to acute swelling and embolus that may mimic a brain tumour on imaging.34
Sites notorious for nerve deficit even with small or medium aneurysms are the posterior communicating artery, affecting the third cranial nerve (oculomotor nerve), and the anterior communicating artery, affecting the second cranial nerve (optic nerve) or chiasm.35 Compression of these or other nerves can cause acute or chronic deficit.
Acute cranial neuropathies related to aneurysms are an emergency in that they indicate a change in the aneurysm, which signals an increase in risk of haemorrhage.36 Differentiation of aneurysmal compression and diabetic mononeuropathy can be problematic (e.g. pupil involvement in aneurysmal compression), and is a classic pitfall.37
Therapy and outcome
Outcome following SAH due to a ruptured cerebral aneurysm remains concerning despite advances in therapy.2 A rough guide is that after SAH, one-third of patients will be treated and recover ‘back to normal’, one-third will survive and be disabled, and one-third will not survive.2 Prehospital mortality is up to 15%, which is probably an underestimation as many causes of sudden death in the elderly may go uninvestigated.38
The immediate treatment of patients presenting with haemorrhage involves basic resuscitation in poor grade patients (i.e. patients with a global or focal neurological deficit).39 A significant cause of ongoing coma following a SAH is hydrocephalus relating to the blood in the subarachnoid space. A patient with a decreased level of consciousness following a haemorrhage is not considered optimised until this pressure is relieved with external ventricular drainage. As an extension of this, no patient should be considered unsalvageable on the grounds of clinical condition without CSF diversion.40,41 Careful control of the patient’s blood pressure (by medication) is vital initially to decrease the risk of rebleeding.39
Securing of the aneurysm by the most appropriate means should be achieved at the earliest opportunity, when the multidisciplinary team required can be assembled.42 The patient’s current use of anticoagulant and antiplatelet medication has to be dealt with as effectively as possible with the administration of procoagulants, blood products and platelets as appropriate. The presence of irreversible or significant bleeding diathesis may be a relative indication for endovascular treatment (i.e. coiling) rather than microvascular treatment (i.e. clipping).
Vasospasm is a significant complication of SAH and typically has onset five to 10 days after the bleeding event.43 Treatment of vasospasm includes pharmacotherapy with nimodipine and induction of hypertension and hypervolaemia, to increase cerebral blood flow.44,45 Endovascular angioplasty (chemical and balloon) is being used increasingly to manage this problem, with great benefit.45,46 A typical stay in an intensive care or high dependency unit of a patient with vasospasm can be more than two weeks due to the intensity of this therapy.
Patients with unruptured aneurysms that are being repaired microsurgically require the same presurgical assessment and management of antiplatelet or anticoagulant therapy as those undergoing any other major craniotomy. In those undergoing elective coiling, there is often no need to stop antiplatelet medication, and in those requiring complex repairs and/or stents, preloading with significant antiplatelet medication prior to the procedure is often appropriate.47