Electroencephalography, Hospital Complications, and Longitudinal Outcomes After Subarachnoid Hemorrhage

Abstract

Background: Following non-traumatic subarachnoid hemorrhage (SAH), in-hospital delayed cerebral ischemia is predicted by two chief events on continuous EEG (cEEG): new or worsening epileptiform abnormalities (EAs) and deterioration of cEEG background frequencies. We evaluated the association between longitudinal outcomes and these cEEG biomarkers. We additionally evaluated the association between longitudinal outcomes and other in-hospital complications. Methods: Patients with nontraumatic SAH undergoing ≥ 3 days of cEEG monitoring were enrolled in a prospective study evaluating longitudinal outcomes. Modified Rankin Scale (mRS) was assessed at discharge, and at 3-and 6-month follow-up time points. Adjusting for baseline severity in a cumulative proportional odds model, we modeled the mRS ordinally and measured the association between mRS and two forms of in-hospital cEEG deterioration: (1) cEEG evidence of new or worsening epileptiform abnormalities and (2) cEEG evidence of new background deterioration. We compared the magnitude of these associations at each time point with the association between mRS and other in-hospital complications: (1) delayed cerebral ischemia (DCI), (2) hospital-acquired infections (HAI), and (3) hydrocephalus. In a secondary analysis, we employed a linear mixed effects model to examine the association of mRS over time (dichotomized as 0-3 vs. 4-6) with both biomarkers of cEEG deterioration and with other in-hospital complications. Results: In total, 175 mRS assessments were performed in 59 patients. New or worsening EAs developed in 23 (39%) patients, and new background deterioration developed in 24 (41%). Among cEEG biomarkers, new or worsening EAs were independently associated with mRS at discharge, 3, and 6 months, respectively (adjusted cumulative proportional odds 4.99, 95% CI 1.60-15.6; 3.28, 95% CI 1.14-9.5; and 2.71, 95% CI 0.95-7.76), but cEEG background deterioration lacked an association. Among hospital complications, DCI was associated with discharge, 3-, and 6-month outcomes (adjusted cumulative proportional odds 4.75, 95% CI 1.64-13.8; 3.4; 95% CI 1.24-9.01; and 2.45, 95% CI 0.94-6.6), but HAI and hydrocephalus lacked an association. The mixed effects model demonstrated that these associations were sustained over longitudinal assessments without an interaction with time.

Development and validation of an early predictive nomogram for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

“…The model had a high degree of differentiation and calibration as well as good clinical application value. It has been reported that DCI occurs in approximately 30% of patients surviving the initial hemorrhage (21,22). In the present study, the incidence of DCI was 23.16% in 285 consecutive patients with aSAH, which was consistent with previous studies and indicated that our data was representative.…”

Neurologic Outcome Prediction in the Intensive Care Unit

“…The most employed monitoring modality is transcranial Doppler; however, its prediction performance varies widely because of technical factors and limited temporal resolution. EEG has emerged as an attractive tool with high temporal and spatial resolution; however, no consensus exists on thresholds for predicting delayed cerebral ischemia and significant expertise is required for the interpretation of findings 36 . Laboratory abnormalities such as leukocytosis, 37 hypokalemia, and hyponatremia are also predictors of vasospasm 32 .…”

“…EEG has emerged as an attractive tool with high temporal and spatial resolution; however, no consensus exists on thresholds for predicting delayed cerebral ischemia and significant expertise is required for the interpretation of findings. 36 Laboratory abnormalities such as leukocytosis, 37 hypokalemia, and hyponatremia are also predictors of vasospasm. 32 Important prevalent systemic complications that carry prognostic meaning for poor outcome include paroxysmal sympathetic hyperactivity and stress-induced cardiomyopathy.…”

Neutrophil Extracellular Traps and Delayed Cerebral Ischemia in Aneurysmal Subarachnoid Hemorrhage

“…However, effective prediction and prevention measures of DCI are lacking (6). While DCI development might be preceded by clinical deterioration, angiographic vasospasm, increase in transcranial Doppler (TCD) flow velocities, or electroencephalographic changes, DCI often occurs silently and is mostly identified in retrospect (7)(8)(9)(10). Finding markers of impending DCI could lead to a paradigm shift in the diagnosis and possibly in the prevention and treatment of this severe complication of subarachnoid hemorrhage (SAH) (11).…”