Brain death and its implications for management of the potential organ donor

Abstract

The systemic physiologic changes that occur during and after brain death affect all organs suitable for transplantation. Major changes occur in the cardiovascular, pulmonary, endocrine, and immunological systems, and, if untreated may soon result in cardiovascular collapse and somatic death. Understanding these complex physiologic changes is mandatory for developing effective strategies for donor resuscitation and management in such a way that the functional integrity of potentially transplantable organs is maintained. This review elucidates these physiological changes and their consequences, and based on these consequences the rationale behind current medical management of brain-dead organ donors is discussed.

Clinical Outcomes and Genetic Expression Profile in Human Liver Graft Dysfunction During Ischemia/Reperfusion Injury

“…The data presented herein support these findings, demonstrating the importance of inflammasomes and IL-1b release in the process of IRI. Other known data, such as cold ischemia time, warm ischemia time, and other specific donor conditions, cannot be ignored and are described widely [24,25]. Nonetheless, the different clinical outcomes of IRI and the different clinical presentation, can be, at least partially, attributed to different gene expression of IL-1b in donor livers, leading to a more significant inflammatory process during IRI in OLT [26,27].…”

Manejo del potencial donante cadáver

“…La hiperglicemia es frecuente y multifactorial: secundaria al estrés, al aumento de los niveles de hormonas contrarreguladoras, al uso concomitante de esteroides, cambios en el metabolismo de carbohidratos, infusión de soluciones que contienen glucosa, y resistencia periférica a la insulina 1,6,71,72 . Algunos autores han mostrado una asociación entre hiperglicemia y disfunción renal post-trasplante 73 .…”

Brain Death: Assessment, Controversy, and Confounding Factors

“…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.…”

“…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.…”