Clinical paperRisk factors for development of cerebral edema following cardiac arrest
Introduction
Over 600,000 individuals in the United States suffer cardiac arrest (CA) annually.1, 2 Most patients resuscitated from CA are initially comatose from neuronal injury, of whom some develop cerebral edema.3 Cerebral edema is observed as early as 1 h following CA, may become prominent 24 h following return of spontaneous circulation (ROSC) and is a predictor of poor neurological outcomes.4, 5, 6, 7 Severe cerebral edema may result in death by neurological criteria, withdrawal of life-sustaining therapies (WLST) for perceived poor neurological prognosis, and/or contribute to secondary brain injury.8, 9, 10, 11, 12 We identified factors associated with the development of moderate-to-severe cerebral edema after resuscitation from CA and secondarily quantified the association of edema with outcomes at hospital discharge.
Section snippets
Study design and participants
We performed a retrospective cohort study including patients resuscitated from in-and out-of-hospital CA between January 2015 and March 2020 at a single academic medical center. Our Institutional Review Board approved this study. We included all patients who survived to hospital care and underwent computed tomographic (CT) imaging of the head at any point after ROSC. We excluded those with other neurological conditions that could potentially cause cerebral edema, such as ischemic stroke,
Results
Of 1354 patients screened, 727 (54 %) had confirmed CA with at least one head CT acquired and were included in analysis. Of these, 102 (14 %) had moderate-to-severe cerebral edema. Demographic and clinical features are described in Table 1. Median time from collapse to CT used in analysis did not differ between groups (median 36 [IQR 10–72] vs 22 [IQR 6–72] hours, p = 0.5735), but GWR from a random subset of patients (12 %) differed between both groups (median 0.97 [IQR 0.90–1.02] vs median
Discussion
Cerebral edema is a well-known consequence of CA and is associated with poor outcome. Edema is observed in 2–34 % of patients following OHCA, with great variability based on the inclusion criteria, timing of imaging in relation to CA and the duration of CPR.4, 14 The clinical pathophysiology of hypoxic-ischemic brain injury involves a cascade of events leading to neuronal cell death, with primary injury from cessation of blood flow during CA and secondary injury from reperfusion.15 Cerebral
Conclusion
In our study, moderate-to-severe cerebral edema was more common in those who were younger, had PEA/asystole, prolonged arrest duration, unwitnessed CA, hyperglycemic and had a lower GCS score. There was a high rate of withdrawal of life-sustaining therapies in patients with moderate-to-severe cerebral edema. Although, more research needs to be done to identify if improved resuscitation algorithms could reduce or prevent the development of cerebral edema, our study provides insights on high-risk
CRediT authorship contribution statement
Archana Hinduja: Conceptualization, Investigation, Writing – review & editing. Yevgeniya Gokun: Writing – review & editing. Elochukwu Ibekwe: . Blake Senay: Writing – review & editing. Jonathan Elmer: Writing – review & editing, Supervision.
Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal relationship that could have appeared to influence the work reported in this paper.
Acknowledgements
None.
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