Subarachnoid Hemorrhage: Who Dies, and Why?

Hector Lantigua; Santiago Ortega-Gutierrez; J. Michael Schmidt; Kiwon Lee; Neeraj Badjatia; Sachin Agarwal; Jan Claassen; E. Sander Connolly; Stephan A. Mayer

Disclosures

Crit Care. 2015;19(309) 

In This Article

Abstract and Introduction

Abstract

Introduction: Subarachnoid hemorrhage (SAH) is a devastating form of stroke. Causes and mechanisms of in-hospital death after SAH in the modern era of neurocritical care remain incompletely understood.

Methods: We studied 1200 consecutive SAH patients prospectively enrolled in the Columbia University SAH Outcomes Project between July 1996 and January 2009. Analysis was performed to identify predictors of in-hospital mortality.

Results: In-hospital mortality was 18 % (216/1200): 3 % for Hunt-Hess grade 1 or 2, 9 % for grade 3, 24 % for grade 4, and 71 % for grade 5. The most common adjudicated primary causes of death or neurological devastation leading to withdrawal of support were direct effects of the primary hemorrhage (55 %), aneurysm rebleeding (17 %), and medical complications (15 %). Among those who died, brain death was declared in 42 %, 50 % were do-not-resuscitate at the time of cardiac death (86 % of whom had life support actively withdrawn), and 8 % died despite full support. Admission predictors of mortality were age, loss of consciousness at ictus, admission Glasgow Coma Scale score, large aneurysm size, Acute Physiology and Chronic Health Evaluation II (APACHE II) physiologic subscore, and Modified Fisher Scale score. Hospital complications that further increased the risk of dying in multivariable analysis included rebleeding, global cerebral edema, hypernatremia, clinical signs of brain stem herniation, hypotension of less than 90 mm Hg treated with pressors, pulmonary edema, myocardial ischemia, and hepatic failure. Delayed cerebral ischemia, defined as deterioration or infarction from vasospasm, did not predict mortality.

Conclusion: Strategies directed toward minimizing early brain injury and aneurysm rebleeding, along with prevention and treatment of medical complication, hold the best promise for further reducing mortality after SAH.

Introduction

Subarachnoid hemorrhage (SAH) is devastating acute neurological disease that affects over 30,000 people every year in the United States.[1–4] Despite advances in medical and surgical management, SAH remains a major cause of premature mortality, accounting for 27 % of all stroke-related potential years of life lost before the age of 65.[5] In a 1985 study, it was reported that SAH carried a 43 % risk of death immediately after ictus and a 57 % mortality rate at 6 months.[6] A systematic review in 1997 evaluated cases-fatality rates from 1960 to 1992 and found a 0.9 % decrease per year.[7]

Well-established risk factors for mortality included poor clinical grade at presentation, older age, aneurysm rebleeding, large aneurysm size, and cerebral infarction from vasospasm.[8] The International Cooperative Aneurysm Study, conducted in the 1980s, pointed to vasospasm, direct effects of the primary hemorrhage, and rebleeding as the most frequent causes of mortality after SAH.[9] More recently, global cerebral edema, intraventricular hemorrhage, and medical complications have been identified as contributors to poor outcome after SAH.[10–13] In this study, our goal was to re-evaluate the causes and mechanisms of in-hospital mortality after SAH in a large contemporary single-center cohort.

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