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Although the incidence is declining, subarachnoid hemorrhage (SAH) continues to exact a substantial toll on society, with an estimated 20,000 aneurysmal SAHs (aSAHs) a year in the United States.1 Outcomes have improved, but the mortality remains ≈35%, and half of the survivors cannot return to their previous level of functioning.2 The most important prognostic factors for outcome are the neurologic condition of the patient on admission to hospital, the patient’s age, and preexisting hypertension.3 aSAH has a unique biphasic course, with initial or early brain injury (reflected in the neurologic condition) and a delayed phase of brain injury called delayed cerebral ischemia (DCI). Subarachnoid blood and specifically the erythrocytes and their main content, hemoglobin, appear to mediate DCI in humans. Extravascular free hemoglobin and iron released from it, whether into the CSF or the brain, are highly inflammatory and cytotoxic oxidants.4 The body has developed ways to mitigate this, including synthesis of haptoglobin, which binds free hemoglobin, abrogating its toxicity. Therefore, clearing away the hemoglobin more quickly or preventing its deleterious effects by binding hemoglobin may decrease brain injury and improve patient outcomes from SAH.
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