References for this Review were identified through searches of PubMed with the search terms “subarachnoid hemorrhage”, “treatment”, “management”, “cerebral aneurysm”, and “vasospasm” from 1970 to February, 2010. Articles were also identified through searches of the Cochrane library and searches of the authors' own files. Only papers published in English were reviewed.
ReviewMultidisciplinary management and emerging therapeutic strategies in aneurysmal subarachnoid haemorrhage
Introduction
The rupture of an intracranial aneurysm is a neurological emergency. The urgency of the situation might not seem intuitively obvious because many patients present only with a headache and initially have a nearly normal neurological examination. In the first 24 h, rebleeding is a major risk and can lead to early morbidity or even brain death. After the aneurysm is secured (ie, excluded from the circulation), the patient enters a new phase punctuated by cerebral vasospasm and decreased cerebral perfusion. Avoiding secondary damage then becomes the primary goal of care. Some patients present in a much worse clinical condition, requiring complex management of pulmonary oedema, cardiac failure, and arrhythmias. Other patients need emergency evacuation of a cerebral haematoma or decompressive craniectomy to control mass effect.
There has been a notable change in the management of aneurysmal subarachnoid haemorrhage (aSAH) over the past decade. In this era of neurointervention and neurointensive care, a multidisciplinary team is required to respond to the needs of the patient. Mortality from aSAH is decreasing1 and we are making progress in the understanding of its complex pathophysiology. Furthermore, new management strategies have emerged and their use might enable more patients to return to a good or even a full level of functioning.
In this Review, we first provide a practical overview of the care of patients with aSAH from the time of their first hospital assessment. Second, we highlight recent diagnostic and therapeutic advances and discuss promising new treatment options. This Review is not intended to be a guideline or to represent practice recommendations and we do not strictly follow the rules of evidence-based medicine. When evidence is available, we present a critical assessment of its strengths and weaknesses; when there is no evidence available, we offer recommendations based on our experience.
Section snippets
In the emergency department
The acute physiological abnormalities caused by the rupture of an intracranial aneurysm can be devastating. Probably no other acute neurological illness provokes the extent of sudden increase in intracranial pressure and sympathetic outflow as that produced by aSAH. Sudden death occurs in 10–15% of individuals at the time of rupture.2, 3 Coma from intracranial hypertension and cardiopulmonary complications caused by neurocardiogenic injury are common among survivors with extensive haemorrhage.
Surgical clipping versus endovascular coiling
Surgical clipping and endovascular coiling are both effective methods to exclude the ruptured aneurysm from the circulation. There has been much debate on the relative merits of these interventions, with some neurointerventionalists firmly preferring one technique over the other. These techniques should not be seen to be in competition with each other but rather as complementary. Certain aneurysms are best approached with open surgery (eg, those with a very wide neck or that incorporate
Management of patients with poor clinical grade
Management of poor-grade patients is particularly challenging because these patients are most often intubated and sedated. Thus, physical examination cannot be reliably used to recognise signs of delayed ischaemia. Invasive and non-invasive brain monitoring techniques can be used for these patients. Measurements and techniques include venous oximetry (by jugular bulb catheters), brain tissue oxygen tension (by probes such as the Licox catheter, GMS, Kiel-Mielkendorf, Germany), cerebral
Diagnosis of vasospasm
The risk of vasospasm increases between 3 and 7 days after aSAH, although earlier vasospasm can occur and might be associated with poor outcome.6 Fewer than 4% of deficits occur after day 13. More than 60% of patients with aSAH develop cerebral vasospasm during the hospital course, but only about 30% will become symptomatic. Cerebral vasospasm tends to be more severe in younger patients with poor neurological grade, thick subarachnoid clot, intraventricular haemorrhage, and history of smoking.7
New therapies for prevention of cerebral ischaemia and neuroprotection
Substantial progress is being made in the understanding of the pathophysiology of cerebral vasospasm, which is increasingly regarded as a disorder that predominantly affects the endothelial function and microcirculation.133 Robust theoretical rationale and strong experimental data have led to the design of clinical trials that investigate novel therapies for vasospasm and protection against delayed ischaemic damage. Panel 2 summarises the current state of the evidence for various therapeutic
Conclusions and future directions
The care of patients with aSAH is undergoing changes that hold great promise for improving patient outcomes. Over the past few years, we have learned about the value of endovascular coil occlusion and embraced its use, enhanced our understanding of the mechanisms leading to secondary brain ischaemia, and found new ways to identify brain tissue at risk of ischaemic damage through perfusion scans. We are now learning how to optimise the use of these new diagnostic modalities and how to evaluate
Search strategy and selection criteria
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