Early identification and management of brain death-related complications such as disseminated intravascular coagulation (DIC), diabetes insipidus (DI), neurogenic pulmonary edema (NPE), hypothermia, and cardiac arrhythmias are required [DIC-related coagulopathy can be corrected with FFP, Factor VII, and Factor XI]. DI treatment is with desmopressin or vasopressin if vasopressors are otherwise required. NPE may require high-frequency percussive ventilation, or lung-protective pressure-controlled ventilator management. Salt replacement with hypertonic saline is helpful for SIADH. The complex hemodynamic, endocrine, and metabolic dysfunction associated with brain death is frequently associated with major complications in the potential donor. If inappropriately treated, these complications can progress to cardiovascular collapse with loss of valuable organs for transplantation.

In conclusion, identify potential donors early with the expectation that organ recovery will primarily occur in the CVA and TBI population. Optimize consent for donation by involving senior surgical staff (Fig. 84.1). Early admission of critically ill patients to the ICU with aggressive management even in cases of terminal injury will increase recovered organs. Brain death is associated with profound physiologic alterations that result in diffuse vascular regulatory disturbances and widespread cellular injury. As such, donor management with a pulmonary artery catheter leads to significantly greater recovered organs. Fluid resuscitation, vasopressors, and inotropes are utilized to maintain a MAP greater than 70 mmHg. With increased vasopressor requirements, start a “T4 protocol.” Aggressive management of brain death-related complications such as disseminated intravascular coagulation, diabetes insipidus, neurogenic pulmonary edema, hypothermia, and cardiac arrhythmias will increase recovered organs.