Hormonal Therapy In The Braindead Organ Donors

Based on the animal experimental work and evidence obtained from human brain-dead organ donors, the brain-dead undergo metabolic abnormalities such as reduction of plasma FT3, elevation of rT3, development of metabolic lactic acidosis, and elevation of plasma free fatty acids (FFA) necessitating progressive increases of the inotropic demand and bicarbonate replacement. Hormonal replacement was initially carried out in 21 circulatory unstable patients who were on high inotropic support, exhibiting high plasma lactic acidosis and FFA and compared with 26 donors managed in a standard fashion.20 Once the brain-dead organ donor was referred to the transplant program and hormonal therapy was initiated, triiodothyronine 2 mcg/h, cortisol 100 mg/h and insulin 10-20 IU/h was administered for four hours. The hemodynamic parameters rapidly normalized, inotropic requirements were significantly reduced as was the need of bicarbonate replacement. In six patients, the cardiac output improved over 100% within minutes after T3 replacement. All organs, including the heart, were successfully harvested and transplanted with excellent function in the recipient. However, in the control group during the same time interval, the hemodynamics continued deteriorating despite further inotropic increment and bicarbonate replacement. Four donors developed ventricular fibrillation and were excluded from the donor pool (p < 0.04).

The advantages of hormonal therapy was further explored by other transplant groups confirming again the value of the hormonal therapy in stabilizing the hemodynamic parameters. This was clearly shown in a prospective randomized study done in potential brain-dead humans.21 Vasopressin was added and sequential cardiac catheterization was done for hemodynamic assessment. In the control group, hemodynamic deterioration progressively took place and half of the brain-dead patients suffered a cardiac arrest. The hormonally treated group during the entire time maintained excellent hemodynamics.

The need of larger and more frequent T3 doses became evident in the hemody-namically unstable organ donors, allowing the use of hearts from donors dependent up to 40 mcg/kg/min of dopamine.22 In these particular patients, T3 therapy increased to 4-6 mcg bolus at 15 min intervals until the desired hemodynamic effect could be obtained and the dopamine requirements were reduced. The need for K+ replacement is markedly increased, as well as intravascular volume expansion as T3 is a potent vasodilator. The use of DDAVP or vasopressin will control the excessive diuresis and the need for crystalloid replacement.23,24

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