Duration of cardiopulmonary resuscitation and phenotype of post-cardiac arrest brain injury.

BACKGROUND: Patients resuscitated from cardiac arrest have variable severity of primary hypoxic ischemic brain injury (HIBI). Signatures of primary HIBI on brain imaging and electroencephalography (EEG) include diffuse cerebral edema and burst suppression with identical bursts (BSIB). We hypothesize distinct phenotypes of primary HIBI are associated with increasing cardiopulmonary resuscitation (CPR) duration. METHODS: We identified from our prospective registry of both in-and out-of-hospital CA patients treated between January 2010 to January 2020 for this cohort study. We abstracted CPR duration, neurological examination, initial brain computed tomography gray to white ratio (GWR), and initial EEG pattern. We considered four phenotypes on presentation: awake; comatose with neither BSIB nor cerebral edema (non-malignant coma); BSIB; and cerebral edema (GWR ≤ 1.20). BSIB and cerebral edema were considered as non-mutually exclusive outcomes. We generated predicted probabilities of brain injury phenotype using localized regression. RESULTS: We included 2,440 patients, of whom 545 (23%) were awake, 1,065 (44%) had non-malignant coma, 548 (23%) had BSIB and 438 (18%) had cerebral edema. Only 92 (4%) had both BSIB and edema. Median CPR duration was 16 [IQR 8-28] minutes. Median CPR duration increased in a stepwise manner across groups: awake 6 [3-13] minutes; non-malignant coma 15 [8-25] minutes; BSIB 21 [13-31] minutes; cerebral edema 32 [22-46] minutes. Predicted probability of phenotype changes over time. CONCLUSIONS: Brain injury phenotype is related to CPR duration, which is a surrogate for severity of HIBI. The sequence of most likely primary HIBI phenotype with progressively longer CPR duration is awake, coma without BSIB or edema, BSIB, and finally cerebral edema.

Malignant EEG patterns in cardiac arrest patients treated with targeted temperature management who survive to hospital discharge.

BACKGROUND AND PURPOSE: Cardiac arrest patients treated with targeted temperature management (TTM) have improved neurological outcomes, however mortality remains high. EEG monitoring improves detection of malignant EEG patterns (MEPs), however their prevalence in patients surviving to hospital discharge is unknown. DESIGN/METHODS: We examined consecutive cardiac arrest subjects who received TTM and continuous EEG monitoring at one academic center. Only subjects surviving to hospital discharge were included in the analysis. MEPs were defined as seizures, status epilepticus, myoclonic status epilepticus, or generalized periodic discharges. Subjects with suppression-burst (SB) without concomitant MEPs were categorized as having a "pure" SB pattern. Demographic, survival, hospital discharge disposition, and neurological function data were recorded retrospectively. Outcomes were assessed using the Glasgow-Pittsburgh Cerebral Performance Category (CPC). A CPC score of 1-2 was considered "good" neurological function, and a CPC of 3-4 "poor". RESULTS: Of 364 admissions due to cardiac arrest screened, 120 (29.9%) survived to hospital discharge and met inclusion criteria. MEPs and pure SB were observed in 19 (15.8%) and 22 (18.3%) survivors respectively. Two subjects with MEP and eight subjects with pure SB had good neurological function at discharge, however all SB cases were confounded by the use of anesthetic agents. Presence of MEPs was not an independent predictor of poor neurological function (p=0.1). CONCLUSIONS: MEPs are common among cardiac arrest patients treated with induced hypothermia who survive to hospital discharge. Poor neurological function at discharge was not associated with MEPs. Prospective studies assessing the role of EEG monitoring in cardiac arrest prognostication are warranted.