Susan L. Smith, MN, PhD

Disclosures

March 28, 2003

Preoperative Clinical Management of the Organ Donor

The outcome of transplantation depends to a large extent on preoperative clinical management of the potential donor. In addition to continuing measures to treat the donor's primary condition, there is a shift away from cerebral resuscitation and intravascular volume contraction to safeguarding cellular oxygenation and perfusion, and anticipating the normal physiologic sequelae of brain death. Common problems in the care of the organ donor include cardiovascular and respiratory system changes, as well as alterations in metabolic and electrolyte homeostasis. The most common cardiovascular system changes encountered during the clinical management of the organ donor are hypertension, dysrhythmias, and hypotension.

Hypertension (mean arterial pressure [MAP] > 90 mm Hg) is rare following brain death but occurs in about 50% of patients during the final stages of brain herniation. The hypertension in this situation results from the intense catecholamine storm seen during herniation and is usually self-limiting and requires no treatment. If hypertension persists after declaration of brain death, vasopressor infusions, if present, should be titrated downward. If treatment is considered necessary, a quick-acting agent with a short half-life, such as nitroprusside, is preferred.

Atrial or ventricular dysrhythmias and various degrees of conduction block occur with varying frequency in the organ donor. The use of high-dose vasopressors, acid-base abnormalities, electrolyte disorders, hypothermia, and myocardial injury will increase the incidence of dysrhythmias in the organ donor, and timely therapeutic intervention must be implemented as dysrhythmias may be difficult to treat in the organ donor.

By far the most common cardiovascular system anomaly in the organ donor is hypotension (MAP < 60 mm Hg). Hypotension regularly occurs before or soon after brain death occurs, and its etiology is multifactorial. Hypovolemia, left ventricular dysfunction, loss of vasomotor control, and endocrine changes either alone or in combination with each other contribute to the hypotension seen in the organ donor. Hypovolemia is the most common cause of hypotension in the organ donor. The hypovolemia may be absolute due to a true reduction in intravascular volume from:

 

  • Therapeutic volume depletion to avoid central nervous system edema

  • Inadequate replacement of essential and third-space fluid losses

  • Polyuria from diabetes insipidus, osmotic diuresis, or the residual effects of diuretic drugs.

 

Or the hypovolemia may be relative -- that is, the vascular space is abnormally dilated, from the loss of central vasomotor control. Often the hypotension is a combination of absolute and relative hypovolemia. Additionally, the hypotension may be further compounded by left ventricular dysfunction from myocardial contusion, electrolyte disturbances, injury to the heart during the progression of brain death, or acute pulmonary hypertension.

Regardless of the cause of the hypotension, the goal is to stabilize and improve the donor's hemodynamic status in order to ensure optimal end organ perfusion. Aggressive therapy aimed at restoring and maintaining intravascular volume will usually improve the hemodynamic status of many donors. The choice of fluids used for volume expansion is based on the type of fluid lost, the hemoglobin levels, and the serum electrolytes. Crystalloids, colloids, and blood products should be used as required. Inadequate fluid resuscitation as well as overly aggressive fluid resuscitation can lead to a complete loss of organs and/or a reduction in the quality of organs transplanted. Despite the evidence of adequate rehydration or during the initial stages of fluid resuscitation, potential organ donors may require vasopressor support to maintain an adequate blood pressure. On the basis of its pharmacology, dopamine is the vasopressor of choice. Additional vasopressors may also be necessary to support the blood pressure of the unstable organ donor. Regardless of the type and rate of the vasopressor(s) infusions, every effort should be made to keep them at the lowest rate possible while still maintaining an adequate blood pressure and, if possible, titrated off all together. Coupled with the treatment of a potential donor's fluid volume deficit is the treatment of electrolyte, hormones, and glucose abnormalities. These abnormalities are usually a result of the treatment given during patient care prior to brain death or from the effects of brain death.

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