Are We Barking Up the Wrong Vessels? Cerebral Microcirculation After Subarachnoid Hemorrhage.

Abstract

Subarachnoid hemorrhage (SAH) is a severe subtype of hemorrhagic stroke with a particularly unfavorable outcome, limited therapeutic options, and not a well understood pathophysiology.1 It affects ≈6 to 10 patients per 100 000 thereby accounting for 3% to 4% of all strokes.2,3 The prevalence of SAH peaks at ≈55 years of age therefore SAH accounts for 25% of all productive life-years lost to all subtypes of stroke.4 Consequently, with yearly total costs of >5 billion Euro/5.5 billion US $ in the European Union and United States alone, SAH causes a significant socioeconomic burden which almost equals that of ischemic stroke, a condition which is >20× more frequent.5,6 In 85% of cases, SAH is caused by a spontaneous rupture of a cerebral aneurysm. Less common causes of SAH include arteriovenous malformations, traumatic brain injury, substance abuse, vasculitis, and spinal vessel abnormalities (Figure 1 for examples).7 Bleeding in the subarachnoid space causes excruciating headache because of contact of blood with the dural sheaths (Figure 2) and a rapid, large increase in intracranial pressure because of the connection between the intravascular and the intracranial space and the evolving hematoma. If significant intracranial hypertension persists, cerebral perfusion pressure (CPP) drops, patients become unconscious and may die within minutes because of global cerebral ischemia. In fact, ≤21% of patients with SAH die before receiving medical attention.8 Despite significant advances in emergency and neurocritical care, and improved surgical and minimally invasive techniques for the prevention of rebleeding, those patients reaching the hospital still have a 30-day mortality of about one third,9 a number which did not change significantly over the past 3 decades.10,11 Figure 1. Examples of subarachnoid hemorrhage (SAH). A , Patient presenting with decreased level of consciousness, headache, and vomiting (GCS 7; E2, …