Clinical Management of the Organ Donor

Abstract

There is a critical mismatch between available organs for transplant and acutely or critically ill patients with end-stage organ disease. Patients who may benefit from organ transplantation far outnumber available organs. The causes for this imbalance are multiple. One cause is family refusal to donate. A second cause is nonrecognition or delay in determination of brain death. A third cause is donor loss due to profound cardiopulmonary and metabolic instability consequent to brain-stem herniation and brain death. Family refusal may be addressed by education, public awareness, as well as close attention to social, cultural and ethical issues, and optimal communication with donor families. Brain death may be consequent to traumatic brain injury, ischemic versus hemorrhagic stroke, as well as massive cerebral anoxia/ischemic following cardiac arrest. Nonrecognition or delay in brain death determination may be addressed by clinician education and frequent clinical assessment to detect early stages of brain-stem herniation refractory to aggressive measures for control of intracranial pressure. Donor loss due to profound cardiopulmonary and metabolic instability may be addressed by aggressive, mechanism-based treatment for clinical instability based on affected body system, as well as measures to support metabolic activity at the cellular and tissue level in the brain-dead organ donor. This article explores cerebral physiology related to impending brain death and catastrophic intracranial pressure elevations. In addition, physiologic consequences of brain death are correlated with affected body systems and mechanism-based therapies to support organ function pending transplantation. Ethical/legal issues are explored as related to patient autonomy and optimal family outcomes. Effective family communication, astute clinical assessment, and optimal clinical management of the organ donor are illustrated using a case study approach, highlighting the role of the advanced practice nurse in donor management.

Brain Death: Assessment, Controversy, and Confounding Factors

“…Anoxic or ischemic injury after cardiopulmonary arrest can initiate neuronal death and lead to terminal brain stem dysfunction. [13][14][15][16] Progression of injury and neurological decline after nonsurvivable traumatic brain injury or catastrophic brain hemorrhage generally follows a rostral to caudal path over various intervals but has the same final destination. In patients with rapid progression of brain edema and corresponding elevations in intracranial pressure (ICP), the cerebral cortex is compressed against the inner surface of the skull.…”

“…Continued increases in pressure then may lead to transtentorial (central) herniation syndromes with distortion of the posterior fossa and brain stem displacement through the foramen magnum. 13,[17][18][19][20] The Cushing response, due to pressure or ischemia on the pons, is considered a reflex response to maintain brain perfusion in patients with elevated ICPs and is characterized by hypertension, bradycardia, and widened pulse pressure. 20 Progression of ischemia or distortion of the medulla oblongata and hypothalamus results in additional sympathetic outflow as endogenous catecholamine stores are released, causing hypertension, tachycardia, and vasoconstriction in an effort to maintain cerebral perfusion pressure.…”

“…20 Progression of ischemia or distortion of the medulla oblongata and hypothalamus results in additional sympathetic outflow as endogenous catecholamine stores are released, causing hypertension, tachycardia, and vasoconstriction in an effort to maintain cerebral perfusion pressure. 13,14,17,18,20,21 Initially brain stem distortion results in a hypertensive state as a reflex response, an attempt to maintain brain perfusion. Final brain stem dysfunction or herniation, with total loss of catecholamine regulation, causes total loss of sympathetic control and typically occurs in 2 phases.…”

“…The cardiovascular state associated with terminal brain stem dysfunction can produce a high cardiac output and stroke volume and potentially cause movements of the chest or abdominal wall in phase with the cardiac cycle; this condition is termed hyperdynamic precordium. 5,13,42 Any members of the health care team involved in apnea testing should be aware of how quickly a patient's cardiovascular status can become unstable. Blood pressure may decrease from baseline to critically low levels within seconds ( Figure 3).…”

“…[26][27][28][36][37][38] Patients' movements in brain death may also be confounding factors in clinical evaluation. Possible confounding factors include spinal cord injury, movements in brain death (complex spinal reflexes, muscle fasciculations, ventilator autotriggering), therapeutic hypothermia, and transient brain stem depression after cardiopulmonary arrest 5,13,32,34,38,42,45, (Table 6). …”