Long-term Excess Mortality of 244 Familial and 1502 Sporadic One-Year Survivors of Aneurysmal Subarachnoid Hemorrhage Compared With a Matched Eastern Finnish Catchment Population.
Huttunen, Terhi BM *; von und zu Fraunberg, Mikael MD, PhD *; Koivisto, Timo MD, PhD *; Ronkainen, Antti MD, PhD *; Rinne, Jaakko MD, PhD *; Sankila, Risto MD, PhD +; Seppa, Karri MSc +; Jaaskelainen, Juha E MD, PhD *
68(1):20-27, January 2011.
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BACKGROUND: Saccular intracranial aneurysms (sIAs) develop in 2% of the population. Rupture of the sIA wall causes almost all cases of aneurysmal subarachnoid hemorrhage (aSAH).
OBJECTIVE: We analyzed the long-term excess mortality of 244 familial and 1502 sporadic 1-year survivors of aSAH from sIA compared with a matched Eastern Finnish catchment population.
METHODS: The Kuopio Neurosurgery Database contains 1746 one-year survivors of aSAH (1980-2007) from a defined population. The median follow-up time, until death (n = 494) or the end of 2008, was 12 years. Relative survival ratios were calculated compared with the matched (sex, age, calendar time) catchment population. Relative excess risk of death (RER) was estimated for variables known on admission for aSAH as well as Glasgow Outcome Scale score at 12 months.
RESULTS: There was 12% excess mortality at 15 years (cumulative relative survival ratio: 0.88; 95% confidence interval: 0.85-0.91). Independent risk factors were male sex (RER: 1.6), age older than 64 years (RER: 2.9), ruptured basilar tip sIA (RER: 4.5), severe hydrocephalus on admission (RER: 3.6), no occlusive therapy (RER: 6.0), and Glasgow Outcome Scale scores of 2, 3, or 4 at 12 months (RER: 23, 4.1, 2.1, respectively), but not familial sIA disease. There were lethal rebleeds from 13 of the 1440 clipped sIAs, 2 of the 265 coiled sIAs, and 2 from the 17 nonoccluded sIAs, and 14 new lethal bleeds from other sIAs.
CONCLUSION: The impact of both sporadic and familial aSAH and their sequelae in the central nervous and cardiovascular systems may cause long-term morbidity and mortality. The complex sIA disease may predispose to other vascular events later in life. The causes of the long-term excess mortality are heterogeneous, and more detailed analyses are required.
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