Anoxic brain injury overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Anoxic brain injury or post-cardiac arrest is defined as absence of pulses requiring chest compressions, regardless of location or presenting rhythm. Post-cardiac arrest syndrome is characterized by resumption of spontaneous systemic circulation after prolonged ischemia of whole body.^[1] Anoxic or hypoxic brain injury is often seen after cardiac arrest as part of the post-cardiac arrest syndrome. Major efforts are underway to improve “The Chain of Survival” based upon early access to medical care, early defibrillation, early CPR and early hospital care. Therapeutic hypothermia may improve outcomes. Steroids, mannitol, diuresis and hyperventilation have not been documented to meaningfully improve clinical outcomes.

There are a variety of factors that contribute to anoxic brain injury. The primary mechanism for injury is a result of a lack of oxygen to the brain, therefore any condition which causes this, such as cardiac arrest or airway obstruction, can cause anoxic brain injury.

Persons with anoxic brain injury are at a high risk of death due to factors such as cardiac arrest, congestive heart failure, pneumonia, and sepsis. There are predictors of survival that have been studied. For example, persons with in-hospital cardiac arrest have a better chance of survival than out-of-hospital arrest, rapid defibrillation improves survival, and VT and VF have a better prognosis than asystole or PEA.

Physical examination involves a thorough neurologic evaluation, with a focus on the extent of involvement of the brainstem.

A number of laboratory tests are obtained in order to evaluate the underlying cause of the anoxic brain injury. Common laboratory tests include complete blood count, ABG, electrolytes, cardiac enzymes and serum lactate.

In the early hours and days after anoxic brain injury, there is often diffuse cerebral edema and blurring of the border between the grey and white matter. In some patients there may be discrete infarcts after a few days.

Most often the EEGs of patients in coma after cardiac arrest shows diffuse slowing of both the theta and delta waves, and periodic epileptiform firing. Severe slowing or a flat line appearance is associated with a poor prognosis.

Other pertinent diagnostic studies in anoxic brain injury, include evoked-response testing, and the steps in diagnosing brain death.

Medical therapy for anoxic brain injury, includes the use of therapeutic hypothermia. This has been associated with a reduction in ischemic brain injury, particularly in animal models. There are specific guidelines associated with the use of therapeutic hypothermia, as there can be significant complications and side effects from using this method of treatment.

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