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Critical care of the organ donor 

Critical care of the organ donor
Chapter:
Critical care of the organ donor
Author(s):

Matthew B. Bloom

, Ali Salim

, and Darren J. Malinoski

DOI:
10.1093/med/9780199651429.003.0008
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date: 22 October 2019

Marked physiological changes accompany the transition to neurological death as different portions of the brain become injured during the herniation process. These dramatic changes present a multifaceted challenge to the treating intensivist. Brainstem ischaemia causes a catecholamine surge as the medulla seeks to maintain cerebral perfusion pressure and improve local tissue oxygenation. This is followed by a loss of sympathetic activity causing profound vasodilatation, myocardial depression, and low levels of serum catecholamines. The SIRS seen in neurological death takes a toll upon the pulmonary system of potential donors, resulting in utilization rates of potential lungs of only around 20%. Sympathetic storm and subsequent cardiovascular collapse have a deleterious effect upon the renal system. Ischaemia of the hypothalamic–pituitary axis can lead to diminished circulating levels of adrenocorticotropic hormone, thyroid-stimulating hormone, and vasopressin, resulting in important endocrine derangements with marked systemic effects. Hypothermia and acidosis, along with the dilution of clotting factors, fibrinogen, and platelets, can contribute to a state of disseminated intravascular coagulation and uncontrollable bleeding. The development of donor management goals (DMGs) has created specific physiological targets for the organ procurement organization and intensivist to achieve, aimed at maximizing the total number of transplantable organs. The early and persistent attainment of DMGs is critical for maximizing the number of organs transplanted per donor.

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