Published online before print December 8, 2005, doi: 10.1161/01.STR.0000195181.26935.8d
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(Stroke. 2006;37:8.)
© 2006 American Heart Association, Inc.
Editorial |
Does Hyperglycemia Contribute to Secondary Injury in Subarachnoid Hemorrhage?
From the Department of Neurology, Neurosciences Critical Care, Cerebrovascular Center, University Hospitals of Cleveland, Case Western Reserve University, Cleveland, Ohio.
Correspondence to Jose I Suarez, MD, Neurosciences Critical Care, Department of Neurology, University Hospitals of Cleveland, 11100 Euclid Ave, Hanna 5, Cleveland, OH 44106. E-mail jose.suarez@ uhhs.com
Key Words: acute stroke • brain infarction • hyperglycemia • intracranial hemorrhage • neuroprotection • outcomes • subarachnoid hemorrhage
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
See related article, pages 199–203
Central nervous system injury has been classified as primary and secondary. The most common primary injuries include trauma, ischemic stroke, intracranial hemorrhage, brain neoplasms, and subarachnoid hemorrhage (SAH). Secondary injuries may follow the primary injury very closely and in many instances may be viewed as its complication. Therefore, secondary injuries are potentially preventable. The final end result of secondary injuries is cerebral ischemia leading to neuronal death and worse clinical outcome. Examples of secondary injuries include hypotension, hypoxemia, elevated intracranial pressure, cerebral edema, and tissue herniation. In patients with SAH the most common insults are rebleeding, vasospasm, seizures, hyperthermia, and elevated intracranial pressure. In this issue of Stroke, Frontera et al,1 propose hyperglycemia as another secondary insult after SAH. The implications of this report may be important because hyperglycemia can be easily diagnosed at the patients’ bedside and potentially treated.
We have known for several years of a potential association between hyperglycemia and worsening outcome in animal models of cerebral ischemia.2–4 Such association was not initially evident in humans experiencing ischemic stroke. In fact, it was first believed that hyperglycemia represented a stress response to stroke without any impact on clinical outcome.5 Since then, several observational studies have reported on the independent association between persistent hyperglycemia and increased mortality or reduced functional recovery in patients with various primary injuries including ischemic stroke, intracerebral hemorrhage, and trauma.6–10 Possible mechanisms that have been proposed linking hyperglycemia with worse clinical outcome include the following: worsening of
Related Article:
Stroke 2006 37: 199-203.