Outcome after aneurysmal subarachnoid haemorrhage

Abstract

Aneurysmal subarachnoid haemorrhage (SAH) is a devastating disease. It accounts for approximately 5% of all strokes. Because it affects relatively young patients and often is fatal, the loss of productive life years is similar to that for cerebral infarction and intracerebral haemorrhage. Diagnostic and treatment strategies for SAH have advanced during the last decades. Whether these have led to a decrease in the case-fatality of SAH in the general population is not known. SAH used to be considered as once-in-a-lifetime disease, and patients surviving it to an independent state were considered to have a normal further life, but it has become clear that patients who survive an SAH have an increased risk of developing new intracranial aneurysms and new episodes of SAH. Some data also suggest an increased long-term mortality after SAH and increased risks of other vascular diseases. This thesis focuses on change in short-term outcome after SAH over time and on long-term outcome with special regard to new vascular diseases in the life after SAH. We found a decrease of worldwide case-fatality of 0.6% per study year, indicating an absolute decrease of 17% over the past thirty years. In more recent years in The Netherlands, a yearly decrease of the risk of death after admission for SAH of 1.6% was found. The reduction of case-fatality leads to increased numbers of patients who survive an episode of SAH. These patients were thought to have a normal life expectancy but evidence is emerging that this is not the case. We found a roughly twofold increased risk of death for SAH survivors compared with the general population. This is in part explained by an increased risk of other vascular diseases. The excess risk of vascular diseases and death was most pronounced in the older age groups, but the relative increase was most outspoken in younger patients. Our analysis with yearly standardised mortality ratios shows that the increased risk was stable over time up to 20 years after SAH and did not cluster in the first years after the SAH. The long-term risk of death in SAH patients did not differ from that in patients with TIA or minor ischaemic stroke. The high risk of other vascular diseases after SAH is probably explained by the shared risk factors smoking and hypertension. Our results underline the need of improving treatment of risk factors after SAH, not only because of the risk of developing new intracranial aneurysms or episodes of SAH, but also because of the observed increased risk of other vascular diseases. Treatment strategies could include lifestyle adaptations, cessation of smoking, stringent management of hypertension and secondary prevention with antihypertensives, statins and antiplatelet agents in SAH survivors. Although these treatments may seem intuitive with the current knowledge on long-term prognosis, the effects of these treatments in whole or part, are, however, unknown with regard to risk of rupture of aneurysms, new aneurysm formation and the risk of new vascular diseases and survival in general. They should be properly addressed in future studie