Elsevier

Resuscitation

Volume 162, May 2021, Pages 149-153
Resuscitation

Short paper
Recovery among post-arrest patients with mild-to-moderate cerebral edema

https://doi.org/10.1016/j.resuscitation.2021.02.033Get rights and content

Abstract

Background

Cerebral edema after cardiac arrest may be a modifiable cause of secondary brain injury. We aimed to identify processes of care associated with recovery in a cohort of patients with mild to moderate edema.

Methods

We conducted a retrospective cohort study of adults resuscitated from out-of-hospital arrest (OHCA) at a single center from 2010 to 2018. We included those with cerebral edema ranging from mild to moderate (gray to white matter attenuation ratio (GWR) 1.2 to 1.3 on initial brain computerized tomography (CT). We used Pittsburgh Cardiac Arrest Category (PCAC) to adjust for illness severity and considered the following values in the first 24 h of admission as additional predictors: GWR, lab values affecting serum osmolality (sodium, glucose, blood urea nitrogen (BUN)), total osmolality, change in osmolality from 0 to 24 h, cardiac etiology of arrest, targeted temperature to 33 °C (vs 36 °C), time-weighted mean arterial pressure (MAP), partial pressures of arterial oxygen and carbon dioxide and select medications. Our primary outcome was discharge with cerebral performance category 1–3. We used unadjusted and adjusted logistic regression for analysis.

Results

We included 214 patients for whom CT was performed median 3.8 [IQR 2.4–5.2] hours after collapse. Median age was 57 [IQR 48−67] years, 82 (38%) were female, and 68 (32%) arrested from ventricular tachycardia or fibrillation. In adjusted models, modifiable processes of care were not associated with outcome.

Conclusions

Illness severity, but not modifiable processes of care, were associated with recovery among post-arrest patients with mild-to-moderate cerebral edema.

Introduction

Early cerebral edema seen on computerized tomography (CT) imaging of the brain is an ominous sign after resuscitation from cardiac arrest.1, 2 Beyond marking injury severity, cerebral edema may contribute to preventable secondary brain injury by compromising capillary blood flow, increasing capillary-tissue oxygen gradients, or raising intracranial pressure.3, 4 These effects may decrease cerebral blood flow and oxygen delivery.3, 4 Edema severity can be approximated by the ratio of grey matter attenuation to white matter attenuation (GWR) on CT imaging. Previous studies have shown that severe edema (GWR <1.1) likely reflects irrecoverable brain injury.2, 5 These studies found variable recovery among patients with GWR 1.2–1.3.2, 5

Whether mild to moderate cerebral edema is a modifiable contributor to secondary brain injury is unknown. We analyzed a large cohort of subjects with potentially recoverable early cerebral edema, described their baseline clinical phenotypes, and sought to identify modifiable factors associated with survival without severe neurological impariment. Specifically, we hypothesized that higher sedation dose, temperature management to 33 °C and rising serum osmolality would be associated with improved outcome.

Section snippets

Setting and population

The University of Pittsburgh Human Research Protection Office approved this study. We performed a retrospective observational cohort study including consecutive patients admitted to a single academic medical center in Western Pennsylvania after resuscitation from out-of-hospital cardiac arrest (OHCA) with GWR 1.2–1.3 on initial brain CT. In a secondary analysis, we included patients with GWR 1.2−1.4. We excluded patients that were awake (following verbal commands) or died within 6 h of return

Results

We identified 1500 out-of-hospital cardiac arrest during our study period of which 214 met inclusion and exclusion criteria (Fig. 1). Median age was 57 [interquartile range (IQR) 48−67] years, 82 (38%) were female, and the most common presenting rhythm was ventricular tachycardia or fibrillation (32%) (Table 1). The large majority of CT scans (88%) were obtained within 6 h of collapse. CPC 1–3 was seen in 43 (21%) patients, with the median length of stay for survivors 15 [IQR 9–22] days.

In

Discussion

We did not identify modifiable processes of care associated with recovery among patients with mild-to-moderate cerebral edema. Both cytotoxic and vasogenic components contribute to edema formation in this population.3, 11 Disruption of the blood brain barrier (BBB) from oxidative stress or inflammation, for example, results in extravasation of large osmotically active molecules and fluid typically excluded from the extracellular space, although some data suggest that ionic shifts and active

Conflicts of interests

All authors declare no conflicts of interests

CRediT authorship contribution statement

Zachary L. Fuller: Conceptualization, Methodology, Formal analysis, Writing - original draft. John W. Faro: Data curation, Writing - review & editing. Clifton W. Callaway: Methodology, Supervision, Writing - review & editing. Patrick J. Coppler: Data curation, Writing - review & editing. Jonathan Elmer: Conceptualization, Methodology, Supervision, Writing - original draft.

Acknowledgement

Dr. Elmer’s research time is supported by the NIH through grant 5K23NS097629.

References (21)

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    Importantly, that authors concluded that neuroimaging interpretation discrepancies between radiology and neurointensivists were common and agreement on the severity of HIBI on early brain CT is poor. The Pittsburgh group has studied 214 comatose OHCA patients with a grey to white matter ratio (GWR) of 1.2–1.3 (deemed to indicate mild to moderate cerebral oedema) on initial brain CT (median 3.8 h after collapse).98 In adjusted analysis, none of the potentially modifiable processes of care predefined by the group (hypothermic temperature control, mean arterial pressure, PaO2, PaCO2, hypertonic medication) were independently associated with outcome.

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