Brain Death and Organ Donation

Brain Death and Organ Donation


Brain death is defined as the permanent cessation of total brain function. The traditional criteria used to define brain death, which are an adaptation of the original Harvard Criteria established in 1968, are as follows:
1. Coma of an established and irreversible cause. All tests and reflexes listed should be performed after all possible reversible causes of coma have been ruled out.

a. Lack of spontaneous movement bearing in mind that spinal reflexes may remain intact.

b. Lack of all cranial nerve reflexes and function. This would include the failure of heart rate to increase by more than five beats per minute in response to intravenously, and preferably centrally, administered 0.04 mg/kg atropine, suggesting loss of vagal nuclear—and thus tonic vagal nerve function.

c. Positive apnea test indicating lack of function of the respiratory control nuclei in the brainstem. The test is performed by initially ensuring a PaCO2 of 40 ± 5 mm Hg and an arterial pH of 7.35 to 7.45. The patient is then ventilated with 100% oxygen for more than 10 minutes, and while monitoring vital signs and insufflating the trachea with 100%, mechanical ventilation is discontinued for 10 minutes. Arterial blood gases are obtained at 5 and 10 minutes following the cessation of mechanical ventilation and the patient is observed for signs of spontaneous respiration. Given that hypercarbia (where the PaCO2 > 60 mm Hg) is a potent stimulus for ventilation, if no respiratory activity is noted, the apnea test is deemed positive.

Other confirmatory tests include isoelectricity demonstrated with electroencephalography and absence of CBF as demonstrated by various techniques including transcranial Doppler ultrasonography, cerebral angiography, and magnetic resonance angiography.

Following the establishment of the diagnosis of brain death and discussions with family, legal guardian, or next of kin, the decision is made to either withdraw artificial means of support or proceed to organ harvesting if that was the wish of the patient, family, or legal guardian.

Management of Anesthesia

The major goal in patients presenting for multiorgan harvesting is to attempt to optimize oxygenation and perfusion of the organs to be harvested. It is important to be aware of the various physiologic sequelae of brain death because it is useful to direct management of physiologic parameters with the needs of the organ recipient, not the donor, in mind. Due to loss of central hemodynamic regulatory mechanisms (i.e., neurogenic shock), brain dead patients are often hypotensive. Hypovolemia due to diabetes insipidus, third space losses, or drugs (e.g., mannitol, contrast dyes) can contribute to hypotension. Aggressive fluid resuscitation should be considered, with efforts made to avoid hypervolemia, which could lead to pulmonary edema, cardiac distension, or hepatic congestion. Peripheral vasoconstrictive agents should be avoided when considering pharmacologic treatment of hypotension. Inotropic agents such as dopamine and dobutamine should be first-line agents for the treatment of hypotension in euvolemic patients, with low-dose epinephrine as a second-line agent. For those in whom the heart is to be harvested, catecholamine doses should be minimized because of a theoretical risk of catecholamine-induced cardiomyopathy. Electrocardiographic abnormalities such as ST- and T-wave changes, as well as arrhythmias, can occur. Possible causes include electrolyte abnormalities, loss of vagal nerve function, increased ICP, and cardiac contusion (if death was trauma related). Arrhythmias should be treated pharmacologically or by electrical pacing.



Hypoxemia can occur due to diminished cardiac output or multiple pulmonary factors such as aspiration, edema, contusion, and atelectasis. Inspired oxygen concentration and ventilatory parameters should be adjusted in an attempt to maintain normoxia and normocapnia. Excessive positive end-expiratory pressure should be avoided due to its effect on cardiac output as well as the risk of barotrauma in the setting of possible trauma-related lung injury. Oxygen delivery to tissues should be optimized by treating coagulopathy and anemia with blood products.



Diabetes insipidus frequently occurs in brain dead patients and, if not treated, can lead to hypovolemia, hyperosmolality, and electrolyte abnormalities that could contribute to hypotension and cardiac arrhythmias. Treatment should initially include volume replacement with hypotonic solutions titrated to volume status and electrolyte concentrations. In severe cases, patients may need inotropic support, and either vasopressin (0.04–0.1U/hr IV) or desmopressin (0.3 μg/kg IV) should be used. Due to its vasoconstrictive properties, vasopressin use should be minimized to avoid end-organ ischemia. Various vasodilators, such as nitroprusside, may be coadministered to avoid vasopressin-induced hypertension and excessive vasoconstriction to end organs.



Finally, due to loss of temperature regulatory mechanisms, brain dead patients tend to become poikilothermic and may require aggressive measures to avoid hypothermia. Despite mild hypothermia possibly providing some degree of organ protection, it can also result in cardiac arrhythmias, coagulopathy, and reduced oxygen delivery to tissue, thus causing harm to the organs to be harvested. A good rule of thumb for the management of patients for organ donation is the rule of 100s: systolic blood pressure greater than 100 mm Hg, urine output greater than 100 mL/hr, PaO2 greater than 100 mm Hg, and hemoglobin greater than 100 g/L.