Severe hypoxic-ischemic encephalopathy may result in brain swelling of such severity that all blood flow into the cranium is blocked, thereby worsening the ischemia to a terminal stage. Brain death is a clinical diagnosis based on the absence of neurologic function in the context of a diagnosis that has resulted in irreversible coma. In the United States, it indicates death of the entire brain; in the United Kingdom, it refers to death of the brainstem. Coma and apnea must coexist. A complete neurologic examination that includes the elements outlined in Plates 6-4 and 6-9 is mandatory to determine brain death, with all components appropriately documented. The current recommendation in adults is that a single evaluation suffices for the diagnosis of brain death. In children, two assessments should be performed, with the duration of interval between tests varying with age.
the assessment for brain death, reversible conditions or conditions that can
interfere with the neurologic examination must be excluded. For example,
hypothermia, hypotension, and metabolic dis- turbance that could affect the
neurologic examination must be corrected. After cardiopulmonary resuscitation
or use of therapeutic hypothermia, evaluation for brain death should be
deferred for 24 to 48 hours, or longer if there are concerns or inconsistencies
in the examination. Sedatives, analgesics, neuromuscular blockers, and
anticonvulsant agents should be discontinued for a reasonable period, based on
the elimination half-life of the pharmacologic agent, to ensure that they do
not affect the examination; blood or plasma levels can be used to confirm that
the drug is in the low to midtherapeutic range.
of the clinical neurologic examination consistent with brain death include
presence of coma, loss of all brainstem reflexes, apnea (see Plate 6-9), and
absence of spontaneous or induced movements, but excluding spinal cord events
such as reflex withdrawal or spinal myoclonus.
Coma. The patient must exhibit complete loss of consciousness, vocalization, and
volitional activity. Noxious stimuli should produce no eye opening or eye
movement, and no motor response other than spinal-mediated reflexes.
Loss of All Brainstem Reflexes. The patient exhibits the following: midposition or fully dilated pupils that do not respond to light, either directly or consensually (assessment 1); absence of movement of bulbar musculature, including facial and oropharyngeal muscles, such as in response to deep pressure on the condyles at the level of the temporomandibular joints and over the supraorbital ridge (assessment 2); absent corneal reflexes so that touching the cornea with a sterile cotton swab does not elicit any eyelid movement (assessment 3); absent oculovestibular reflexes (assessment 4); and absence of gag and cough on stimulation of the posterior pharynx with a tongue blade or suction catheter (assessment 5). Assessment of these brainstem functions should be carried out sequentially and systematically because they relate to different levels of brainstem functioning (see Plate 6-9). The oculovestibular reflex is tested by irrigating each ear with ice water (caloric testing) after first checking that the external auditory canal is not occluded by wax and that the eardrum is intact. The head of the bed is elevated to 30 degrees, and the patient’s head is kept in the midline. Each ear is irrigated with 50 to 60 mL of ice water, and this should elicit no movement of the eyes during one minute of observation. The aim is to reduce local temperature at the tympanic membrane so that there is a gradient with core body temperature. Both sides are tested with an interval of several minutes. In normal individuals, nystagmus is induced in both eyes. The fast phase is toward the side opposite that which is being irrigated with cold water and is triggered by the cerebral cortex. The slow phase of nystagmus is caused by the oculovestibular reflex. In comatose patients with an intact response, cold water will turn both eyes slowly toward the side being irrigated. These movements are comparable with the slow phase of the nystagmus induced in normal individuals. Caloric-induced movements are absent when the midbrain or rostral pons is im aired and the oculovestibular path is no longer intact.