Brain Death: Assessment, Controversy, and Confounding Factors

Abstract

When brain injury is refractory to aggressive management and is considered nonsurvivable, with loss of consciousness and brain stem reflexes, a brain death protocol may be initiated to determine death according to neurological criteria. Clinical evaluation typically entails 2 consecutive formal neurological examinations to document total loss of consciousness and absence of brain stem reflexes and then apnea testing to evaluate carbon dioxide unresponsiveness within the brain stem. Confounding factors such as use of therapeutic hypothermia, high-dose metabolic suppression, and movements associated with complex spinal reflexes, fasciculations, or cardiogenic ventilator autotriggering may delay initiation or completion of brain death protocols. Neurodiagnostic studies such as 4-vessel cerebral angiography can rapidly document absence of blood flow to the brain and decrease intervals between onset of terminal brain stem herniation and formal declaration of death by neurological criteria. Intracranial pathophysiology leading to brain death must be considered along with clinical assessment, patterns of vital signs, and relevant diagnostic studies.

Performing the Brain Death Examination and the Declaration of Pediatric Brain Death

“…16 A Glasgow coma scale score of 3 (no eye opening, verbal response, or movement either spontaneous or in response to stimulation) is indicative of loss of consciousness. 17 Spinal cord events present as a wide range of movements that are reflexive, but can appear to be spontaneous and purposeful to caregivers and family members. In brain death literature, there have been several mechanisms suggested for the etiology of spinal reflexes; however, the exact pathophysiology is unknown.…”

“…In brain death, the pupils should be midsized or dilated, approximately 4 to 9 mm and nonreactive to light. 16,17 It also should be noted that in patients with severe facial trauma or ocular trauma and those with preexisting pupillary abnormalities, this test may be unreliable or inconclusive, and an ancillary test should be entertained. 16 The corneal reflex assesses CNs III, V, and VII (oculomotor, trigeminal, and facial nerves, respectively) and the pons.…”

“…This stimulation will not produce a response from the brain-dead patient. 4,[15][16][17] The cough reflex may be tested by advancing a suction catheter down the ETT to the level of the carina. One or two suction passes should be made.…”

“…4 This establishes a starting point for CO 2 measurement intervals; furthermore, if in a hypocarbic state, the patient is at increased risk for cardiovascular instability waiting for the PaCO 2 to increase. 17 Some children with chronic respiratory insufficiency may be hypercarbic at baseline and only respond to supranormal PaCO 2 levels. In this case, the PaCO 2 level should increase to 20 mm Hg above the baseline PaCO 2 .…”

“…The rationale for preoxygenation is to facilitate oxygenation, eliminate nitrogen stores, avoid desaturation, and prevent possible secondary cardiovascular effects. 16,17 Once the patient has a normal PaCO 2 and is hyperoxygenated, the apnea test may commence. The patient is disconnected from the ventilator, or place in a mode that stops intermittent mandatory mechanical ventilation.…”