SC2: Special Considerations

Xenobiotics can cause brain death due to the unique vulnerabilities of the central nervous system. With supportive care, however, such patients may be suitable candidates for organ donation.^9,10,31,38 Early identification of potential donors is critical because the viability of transplantable tissue diminishes as duration from the time of brain or cardiac death prolongs.^26,38 Timely identification may be further complicated by the presence of xenobiotics that mimic brain death.^4,10,36

A variety of protocols to establish brain death are reviewed elsewhere.^4,10,36 Once brain death is established, organ procurement personnel assist in obtaining familial consent, deciding which organs are most suitable for transplant, and maximizing physiological support and perfusion until organ procurement occurs.³⁸ The protocols following controlled or uncontrolled donation after cardiac arrest are socially complicated and practiced extensively in Europe.³⁵

Successful transplantation of organs is reported from poisoned donors associated with a variety of xenobiotics^{1,2,5,7,9,10,12,16,25,29,30,31,32,33, and 34, 37} (Tables SC2–1 and SC2–2). Although some xenobiotics are highly toxic, such as cyanide and carbon monoxide (CO), transfer of clinical poisoning to the organ recipient is not reported. This is likely caused by several factors, including xenobiotic metabolism, tissue redistribution or binding prior to procurement, as well as the means of handling organs during the transplantation process. For example, some xenobiotic clearance may occur in the myocardium during organ rinsing and cardiopulmonary bypass.²⁹ Furthermore, individual organs may not uniformly manifest toxicity in response to xenobiotic insults. For example, the heart of a CO poisoned donor was examined after a transplantation failed for technical reasons. The myocardium did not demonstrate histological signs of CO poisoning.³⁴ A comprehensive review with organ-specific procurement recommendations post–carbon monoxide poisoning is presented elsewhere.³

Probably more critical to transplantation success is adequate tissue perfusion and well-maintained cellular morphology. For example, patients suffering brain death from acetaminophen poisoning are not suitable liver donors given the hepatoxicity. Alternatively, xenobiotics considered toxic to organ function by impairing enzymes have resulted in successful transplantation if the cellular structure is otherwise maintained. For example, a death from cardioactive steroid poisoning did not preclude successful heart transplantation even when the donor had a bradydysrhythmia, an elevated serum digoxin concentration, and required cardiopulmonary resuscitation.³⁴ Similarly, the liver of a patient poisoned with brodifacoum was transplanted after administration of fresh frozen plasma and vitamin K₁. The recipient’s international normalized ratio (INR) post-transplant was 2 and corrected rapidly with supportive care. Recipient concentrations of brodifacoum were not reported and not clearly causative of the elevated INR.²⁹ In both examples, the target of toxicity was enzymatic and the tissue morphology was otherwise minimally affected. Organs from a patient who suffered hypoxic brain death after malathion poisoning were procured 2 weeks after the exposure at which time no further evidence of acute cholinergic toxicity was present and successfully transplanted.⁵ Most transplant failures from poisoned donors are due to rejection, sepsis, or technical reasons. The one year survival in recipients from poisoned donors approximates that from nonpoisoned donors; one series reported at 75% survival.¹² In another review, 5-year survival rates were between 33% and 100%, with heart transplant recipients the lowest.⁹

Ideally, a comprehensive international registry of transplants from ­poisoned donors will be established to improve understanding of transplants from such patients. It appears that patients who suffer brain death from poisoning are potentially suitable donors when cellular infrastructure is preserved.^22,24,26,38 Consideration for organ procurement should not be limited by the xenobiotic.

• Organ procurement from poisoned donors may reach success rates similar to non-poisoned donors when carefully selected.

• Clinically significant xenobiotic concentrations have not been reported in organ recipients.

• Adequate tissue perfusion is important for the viability of a transplanted organ, regardless of the primary toxicological insult.

References