Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) is an important cause of further morbidity and mortality after an already devastating condition. Though traditionally attributed to vasospasm of large capacitance arteries and the resulting down-stream disruption of cerebral blood flow, the pathogenesis of DCI has proven to be more complex with early brain injury, blood-brain barrier disruption, microthrombosis, cortical spreading depolarizations, and the failure of cerebral autoregulation as newly elucidated factors. Vasospasm is a known consequence of SAH. The standard of care includes close monitoring for neurological deterioration, most often with serial clinical examinations, transcranial Doppler ultrasonography, and vascular imaging (crucial for early detection of DCI and allows for prompt intervention). Nimodipine continues to remain an important pharmacological strategy to improve functional outcomes in patients with SAH at risk for developing vasospasm. The paradigm for first line therapy in patients with vasospasm of induced hypertension, hypervolemia, and hemodilution has recently been challenged. Current American Heart Association guidelines recommend targeting euvolemia and judicious use of the pharmacologically induced hypertension component. Symptomatic vasospasm patients who do not improve with this first line therapy require rescue intervention with mechanical or chemical angioplasty and optimization of cardiac output and hemoglobin levels. This can be escalated in a step-wise fashion to include adjunct treatments such as intrathecal administration of vasodilators and sympatholytic or thrombolytic therapies. This review provides a general overview of the treatment modalities for DCI with a focus on novel management strategies that show promising results for treating vasospasm to prevent DCI.
Keywords: Aneurysmal subarachnoid hemorrhage; Delayed cerebral neurological deficits; Medically refractory vasospasm.
Copyright © 2018. Published by Elsevier B.V.