D J Nieuwkamp

BACKGROUND: The number of elderly patients being admitted with aneurysmal subarachnoid haemorrhage (SAH) has been increasing. Treatment of the aneurysm may be offset by the higher rate of surgical or endovascular complications. AIM: To study the clinical condition at onset, complications during clinical course, treatment and outcome in a consecutive series of elderly patients. METHODS: Patients who were > or = 75 years at the onset of SAH were selected from the databases of two hospitals. Data on clinical condition at onset (poor condition defined as World Federation of Neurological Surgeons (WFNS) Scale IV and V), clinical course, treatment and outcome were extracted. Univariate and multivariate regression analyses were carried out to identify predictors for in-hospital death and poor outcome, defined as death or dependency. RESULTS: The data of 170 patients were retrieved, of whom 25 (15%) patients were independent at discharge; none of these patients had been admitted in a poor condition. Poor clinical condition on admission (odds ratio (OR) 7.9; 95% confidence interval (CI) 3.7 to 17) and recurrent haemorrhage (OR 7.5; 95% CI 2.5 to 23) were the strongest predictors for in-hospital death. Recurrent haemorrhage was the strongest predictor for poor outcome in the subset of patients who were admitted in good clinical condition. In all, 10 of 47 (21%) patients were independent at discharge after neurosurgical clipping (n = 34) or endovascular coiling (n = 13). CONCLUSION: Elderly patients with SAH have a poor prognosis. The effect of the initial haemorrhage is the most common reason for poor outcome. For patients who are admitted in good clinical condition, the most important complication leading to poor outcome is recurrent haemorrhage. Treatment of the aneurysm in patients > or = 75 years is feasible, may improve the outcome and should be strongly considered in patients who are admitted in a good condition.

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 studies