Abstract

For patients who survive the initial bleeding event of a ruptured brain aneurysm, delayed cerebral ischemia (DCI) is one of the most important causes of mortality and poor neurological outcome. New insights in the last decade have led to an important paradigm shift in the understanding of DCI pathogenesis. Large-vessel cerebral vasospasm has been challenged as the sole causal mechanism; new hypotheses now focus on the early brain injury, microcirculatory dysfunction, impaired autoregulation, and spreading depolarization. Prevention of DCI primarily relies on nimodipine administration and optimization of blood volume and cardiac performance. Neurological monitoring is essential for early DCI detection and intervention. Serial clinical examination combined with intermittent transcranial Doppler ultrasonography and CT angiography (with or without perfusion) is the most commonly used monitoring paradigm, and usually suffices in good grade patients. By contrast, poor grade patients (WFNS grades 4 and 5) require more advanced monitoring because stupor and coma reduce sensitivity to the effects of ischemia. Greater reliance on CT perfusion imaging, continuous electroencephalography, and invasive brain multimodality monitoring are potential strategies to improve situational awareness as it relates to detecting DCI. Pharmacologically-induced hypertension combined with volume is the established first-line therapy for DCI; a good clinical response with reversal of the presenting deficit occurs in 70 % of patients. Medically refractory DCI, defined as failure to respond adequately to these measures, should trigger step-wise escalation of rescue therapy. Level 1 rescue therapy consists of cardiac output optimization, hemoglobin optimization, and endovascular intervention, including angioplasty and intra-arterial vasodilator infusion. In highly refractory cases, level 2 rescue therapies are also considered, none of which have been validated. This review provides an overview of current state-of-the-art care for DCI management.

Highlights

  • Among subarachnoid hemorrhage (SAH) patients who survive the initial bleed of a ruptured aneurysm, delayed cerebral ischemia (DCI) is the most important preventable cause of mortality and poor neurological outcome

  • We have reported in poor grade patients that maintaining cerebral perfusion pressure (CPP) >70 mmHg is associated with a lower risk of brain metabolic crisis and tissue hypoxia [44], which may be a useful clinical guideline for minimizing the risk of secondary brain injury in unmonitored patients

  • DCI prevention, detection, and reversal are among the top priorities of clinicians caring for SAH patients

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Summary

Background

Among subarachnoid hemorrhage (SAH) patients who survive the initial bleed of a ruptured aneurysm, delayed cerebral ischemia (DCI) is the most important preventable cause of mortality and poor neurological outcome. In line with recent publications and guidelines [6,7,8], we reserve the terms vasospasm for narrowing of large cerebral arteries as evidenced by imaging, DCI for cerebral infarction or neurological deterioration, or both, when the cause is thought to be vasospasm, and cerebral infarction as an infarct from any cause demonstrated on CT or MRI within 6 weeks of aneurysm rupture (see Table 1). The latter is recognized as the primary determinant of long-term cognitive or motor deficits after SAH [9].

Delayed cerebral ischemia
Cerebral infarction
Prophylactic hypervolemia
Cerebral microdialysis
Findings
Conclusion
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