Organ donation management centers on understanding the pathophysiological cascade following brain death and maintaining organ perfusion until surgical recovery. Brain death — the irreversible cessation of all brain function including the brainstem — triggers a predictable sequence of physiological derangements. Initially, rostral-to-caudal brainstem herniation causes an autonomic storm (Cushing response): massive catecholamine surge producing severe hypertension, tachycardia, and myocardial injury. As herniation progresses through the medulla, sympathetic tone is lost entirely (neurogenic shock), resulting in vasodilation, hypotension, and loss of cardiac chronotropic drive. The posterior pituitary infarcts, abolishing antidiuretic hormone (ADH) secretion and causing central diabetes insipidus — manifesting as massive polyuria (>300 mL/hr), dilute urine (specific gravity <1.005), and rapidly rising serum sodium. Hypothalamic destruction eliminates thermoregulation, causing poikilothermia with progressive hypothermia. The release of tissue thromboplastin from necrotic brain tissue triggers disseminated intravascular coagulation (DIC). Brain death determination requires two clinical examinations demonstrating absent brainstem reflexes (pupillary, corneal, oculocephalic, oculovestibular, cough, gag) and no respiratory drive on apnea testing (PaCO2 >60 mmHg with no respiratory effort). Donor management goals focus on maintaining organ perfusion: vasopressin replaces absent ADH...