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19 Brain death
The Case
A 35-year-old patient is comatose following a drowning. The treating neurologist has found the patient to be irreversibly unconscious with absent brainstem reflexes and no respiratory effort during an apnea test. Because of persistent limb movements thought to be most likely spinal in origin, the primary team elects to get a confirmatory EEG that indicates no brain activity. At the conclusion of EEG testing, the attending neurologist writes in the chart, “3/15/09 20:00. The patient is now deceased.” The next of kin decide the following morning not to donate the organs, and respiratory support is promptly removed with an accompanying chart note saying, “3/16/09: The patient has died. Time of death 0700.” Two weeks following this incident, the state medical examiner contacts the care team and inquires as to the proper time of death.
The historical development of a neurological standard of death
While the determination of death among many traditions has for thousands of years relied on the cessation of the pulse or respirations, twentieth-century medical care brought about both new possibilities and incentives for redefining death in terms of a neurological standard. The possibility of brain death in the presence of continued cardiovascular function emerged during the 1950s, largely as a consequence of new developments in the medical care of the critically ill. Shortly thereafter, the incentives for a new definition of brain death expanded and took on new practical urgency with the advent of deceased-donor organ transplantation.
Among the medical developments that led to the possibility of a new concept of brain death was the improvement in techniques of pulmonary support via mechanical ventilation during the polio epidemics of the 1940s and 1950s.1 Other techniques of cardiovascular support soon followed, including the development of cardiopulmonary bypass in the 1950s and the formalization of cardiopulmonary resuscitation in the late 1950s and early 1960s. As society was confronted with the possibility of an apparently alive body in an irreversibly brain dead patient, medicine was ripe for a neurologically based definition of death that could guide the ethical discontinuation of cardiopulmonary support in such patients. In 1959, the concept of irreversible coma was introduced by Mollaret and Goulon in France. However, it may have been the subsequent development of organ transplantation, and the accompanying increase in the practical import for determining brain death, that led 10 years later to the creation of the first widely accepted standard of brain death.
In 1968, 1 year after the first successful heart transplant, a well-publicized effort in the United States to reexamine the definition of death in terms of a neurological standard was conducted by a committee at Harvard Medical School.2 This committee, lead by the chairman of Anesthesiology at Harvard Medical School, Henry Beecher, MD, published what subsequently became known as the Harvard Criteria for determination of brain death which included: (1) unreceptivity and unresponsivity; (2) no movements or breathing; and (3) no reflexes (including deep tendon reflexes). The criteria also suggested checking an electroencephalogram (EEG) when available for its “great confirmatory value.”2 An isoelectric EEG should demonstrate no brain activity, and there should be no muscle movement. The Harvard Criteria mandated these tests be done twice separated by 24-hours. In addition, it was necessary to confirm that the patient was neither sedated nor hypothermic. While the Harvard criteria would be modified by various authorities over the subsequent four decades as described below, these guidelines represented the inaugural moment for a neurological standard of death into medical practice.
Current international neurological standards for determination of death
The whole brain death standard
While the concept of brain death is now well established, the specific criteria for its determination vary among different countries. The legal brain death standard that has been adopted in the majority of the United States is based on the advice of the National Conference of Commissioners on Uniform State Laws3 which formed a model of brain death legislation in 1980 that was subsequently adopted by both the American Medical Association and the American Bar Association as well as a large majority of state legislatures. This standard requires the determination of “irreversible cessation of all functions of the entire brain, including the brain stem.” Similar so-called “whole brain death” standards have also been adopted in Canada, Australia, and South America, as well as most European countries with the notable exception of the United Kingdom (see below).
East Asian countries have seen more recent acceptance of a neurological standard, with brain death criteria analogous to the US standards having been adopted in Japan in 19971 and in South Korea in 2000. A major meeting of Chinese officials to discuss the establishment of neurological standards of brain death occurred in 2008, but no English language summary of their findings was located by the present authors.
The determination of whole brain death, when made on clinical grounds, requires the demonstration of three things: (1) an irreversible comatose state; (2) the loss of brainstem reflexes; and (3) brainstem inactivity leading to apnea. After reversible causes of apparent coma, such as hypothermia, intoxication, severe metabolic derangement, or residual neuromuscular blockade have been ruled out or otherwise corrected, a patient meets the standard by demonstrating the absence of responses to painful stimuli including to cranial nerve territories (coma), the lack of all cranial nerve reflexes (brainstem areflexia), and the absence of respiratory efforts in the face of a hypercarbic challenge (brainstem inactivity). Of note, the whole brain death standard differs from the Harvard criteria in making no mention of spinal cord function or the total absence of muscle movements. This standard also requires no documentation of hypothalamic failure. Although hypothalamic dysfunction including diabetes insipidus is often seen in patients diagnosed as brain dead, both hypothalamic and pituitary function as well as spinal reflexes are commonly found to continue in patients who meet the current whole brain death criteria.
Protocols for the clinical determination of brain death vary among institutions but must generally be made by more than one doctor in one of several relevant specialties (usually some combination of neurology, neurosurgery, trauma, or anesthesiology). In some institutions, most commonly in reference to pediatric patients, clinical assessment must be repeated over various intervals of time before the declaration of death can be properly made.
Sufficiency of the clinical diagnosis of brain death versus neurophysiologic testing
The majority of the US as well as most European Union countries have followed the lead of the Harvard committee in specifying that the clinical diagnosis of brain death in adults is sufficient in itself for the determination of death, without the need for confirmatory neurophysiologic testing. In these jurisdictions, neurophysiologic assessment is reserved for young pediatric patients as well as for circumstances in which there is an inability to perform any of the required clinical tests of brain death or where, for whatever reason, some doubt exists about the clinical diagnosis of brain death. For example, a patient too unstable to tolerate an apnea test, may instead undergo alternative neurophysiologic testing. Exceptions to the sufficiency of the clinical standard in adults include France, Italy, Luxembourg, and the Netherlands, each of which requires some type of confirmatory neurophysiologic testing even in the presence of clinical brain death.4
Neurophysiologic testing generally falls into two categories that serve either “to confirm the loss of bioelectrical activity of the brain” or to “demonstrate cerebral circulatory arrest.”4 Confirmation of brain death via examination of bioelectrical activity can itself be conclusive via the finding of an isoelectric EEG in the absence of other causes for central neurological depression. The absence of brainstem auditory evoked potentials or somatosensory-evoked potentials can also be useful in certain circumstances. These tests have the advantage of being less susceptible than EEG to distortion by sedative drugs, but evoked potential monitoring, while suggestive, cannot in isolation conclusively determine whole brain death.
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