Acute physiological derangement is associated with early radiographic cerebral infarction after subarachnoid haemorrhage

Background

Cerebral infarction after aneurysmal subarachnoid haemorrhage (SAH) is presumed to be due to cerebral vasospasm, defined as arterial lumen narrowing from days 3 to 14.

Methods

We reviewed the computed tomography scans of 103 patients with aneurysmal SAH for radiographic cerebral infarction and controlled for other predictors of outcome. A blinded neuroradiologist reviewed the angiograms. Cerebral infarction from vasospasm was judged to be unlikely if it was visible on computed tomography within 2 calendar days of SAH or if angiography showed no vasospasm in a referable vessel, or both.

Results

Cerebral infarction occurred in 29 (28%) of 103 patients with SAH. 18 patients had cerebral infarction that was unlikely to be due to vasospasm because it was visible on computed tomography by day 2 (6 (33%)) or because angiography showed no vasospasm in a referable artery (7 (39%)), or both (5 (28%)). In a multivariate model, cerebral infarction was significantly related to World Federation of Neurologic Surgeons grade (odds ratio (OR) 1.5/grade, 95% confidence interval (CI) 1.1 to 2.01, p = 0.006) and SAH‐Physiologic Derangement Score (PDS) >2 (OR 3.7, 95% CI 1.4 to 9.8, p = 0.01) on admission. Global cerebral oedema (OR 4.3, 95% CI 1.5 to 12.5, p = 0.007) predicted cerebral infarction. Patients with cerebral infarction detectable by day 2 had a higher SAH‐PDS than patients with later cerebral infarction (p = 0.025).

Conclusions

: Many cerebral infarctions after SAH are unlikely to be caused by vasospasm because they occur too soon after SAH or because angiography shows no vasospasm in a referable artery, or both. Physiological derangement and cerebral oedema may be worthwhile targets for intervention to decrease the occurrence and clinical impact of cerebral infarction after SAH.Subarachnoid haemorrhage (SAH) is a common and serious disorder, affecting approximately 11 in every 100 000 people.¹ Cerebral infarction after SAH is a well‐described complication and is strongly associated with a poor outcome.² Strategies to improve outcome after SAH usually focus on preventing or treating vasospasm.Nimodipine reduces the risk of cerebral infarction after SAH due to vasospasm³; yet, cerebral infarction still occurs and remains a major predictor of poor outcome in multivariate models.⁴ Vasospasm is traditionally defined as arterial narrowing 3–14 days after SAH.⁵ Cerebral infarction after SAH is generally assumed to be due to vasospasm, but causality is difficult to prove in critically ill patients. Radiographic cerebral infarction allows different observers to independently review studies at leisure, but may not be symptomatic. Acute cerebral infarction may be due to the acute effects of haemorrhage and the spike in intracranial pressure, but there are few objectively defined risk factors. We sought to identify patients with cerebral infarction associated with SAH in whom the cerebral infarction was unlikely to be due to vasospasm and to describe novel risk factors for targeted intervention.