Brain Death After Cardiac Arrest: Pathophysiology, Prevalence, and Potential for Organ Donation

Abstract

Hypoxic-ischemic brain injury is the major cause of death in patients resuscitated from cardiac arrest. While in the majority of patients this occurs because of withdrawal of life-sustaining treatment after prognostication of poor neurological outcome, in the remaining patients, hypoxic-ischemic brain injury directly causes extensive and irreversible brain injury resulting in death ascertained using neurological criteria. Mechanisms of brain death after cardiac arrest include massive cerebral edema, diffuse neuronal apoptosis, brain hypoperfusion, or direct neuronal injury from a neurological cause of arrest. Among adult patients who die after resuscitation from cardiac arrest the prevalence of brain death is around 13%, and it is higher in those who are resuscitated with extracorporeal cardiopulmonary resuscitation (ECPR) than in those resuscitated with conventional CPR. A high rate of brain death is also reported in children who die after cardiac arrest. The overall prevalence of brain death after cardiac arrest is probably underestimated, due to interference from early withdrawal of life-sustaining treatment in patients with severe hypoxic-ischemic brain injury and due to underreporting, because none of the recommended outcome measures of neurological outcome after cardiac arrest—cerebral performance categories (CPC) and modified Rankin Score (mRS)—includes brain death as a separate outcome. Patients who are brain dead after cardiac arrest represent an important source of organ donation. In comatose resuscitated patients, early identification of deterioration towards brain death is important, in order both to prevent its occurrence and to avoid missing potential organ donors once brain death has occurred.