Currently, more than 110,000 Americans are on the waiting list for a life-saving organ transplant. Each year, more than 5,000 people die while still waiting. Between January and October 2010, only 23,960 transplants were performed, and there were 6,640 deceased donors. Clearly, there are not enough organs available. One way to combat these ever-increasing numbers is to ensure that we maximize the number of organs recovered from every consented donor.
The cessation of a heartbeat defined death until August 1968, when the Harvard Medical School ad hoc committee for irreversible coma published the Harvard criteria for brain death, which said irreversible coma is the end of life. The subsequent adoption of brain death legislation made it possible to recover organs from donors whose hearts are still beating after they have been pronounced dead. Over the years, various methods have been used to test for neurological death. The term “brain death” is a well-accepted term for “permanent loss of integrative function and consciousness without a chance of returning to meaningful life.”
The U.S. Department of Health and Human Services has recognized the need to increase the number of organs for transplantation. Many grants have been awarded to develop programs to maximize organ donations. Despite these efforts and programs, many organs go unused each year because of poor donor management strategies.
The time between brain death and organ procurement is often marked by significant instability. During this time, organs need timely monitoring to help ensure post-transplant graft survival. Some of the many conditions that challenge donor management are hemodynamic instability, endocrine dysfunction, coagulopathy, hypothermia, and electrolyte abnormalities.
In the normovolemic patient, hemodynamic instability develops first because of increased intracranial pressure (ICP). A transient increase in parasympathetic tone results in a widening pulse pressure and bradycardia. As the brainstem begins to herniate (this occurs when the increased ICP shifts the brain downward through the hole at the base of the skull called the foramen magnum) and cerebral ischemia increases, a resultant massive and uncontrolled release of catecholamines into the systemic circulation occurs. This condition is known as a catecholamine (or autonomic) storm, and it leads to tachycardia, hypertension, and peripheral vasoconstriction. The vasoconstriction is responsible for decreased perfusion to the organs; but the most notable changes occur in the myocardium, where massive vasoconstriction and the circulating catecholamines lead to increased myocardial oxygen consumption. As catecholamines are depleted following the autonomic storm, marked hypotension ensues and causes reduced cardiac output.
The goals of hemodynamic management are to maintain an adequate blood pressure, cardiac output, and vascular tone to preserve organ function. Hypotension is managed in different ways. The first treatment is aggressive and adequate fluid resuscitation. The type of fluid used is determined by hematocrit and electrolyte status. If hypotension persists after adequate volume resuscitation, then the use of vasoactive drugs must be considered, with Dopamine usually being the first-line agent. Salim used an aggressive approach to donor management that included insertion of a pulmonary artery catheter to facilitate tissue perfusion by monitoring specific hemodynamic and oxygenation parameters. The treatment included aggressively replacing fluids and using vasopressors to maintain a mean arterial pressure of at least 70 mmHg. This aggressive approach led to an 87% decrease in the number of donors lost as a result of hemodynamic fluctuations as well as a 71% increase in organs recovered.
Hypothalamus-pituitary dysfunction is thought to be the link to diabetes insipidus, which occurs in 70% of brain dead patients. Diabetes insipidus is characterized by polyuria (urine output greater than 300 ml per hour). It is diagnosed by serum sodium greater than or equal to 150 mEq/L, serum osmolarity greater than or equal to 300 mOsm, urine osmolarity less than or equal to 200 mOsm/L, and urine specific gravity less than or equal to 1.010. In addition, this same hypothalamic-pituitary dysfunction may be responsible for decreased circulating levels of thyroid stimulating hormone, thyroid hormone, and cortisol. This increases the need for inotropic support and can lead to deterioration of transplantable organs.
Management includes monitoring urine output, serum and urine electrolytes as well as fluid replacement and administration of desmopressin (DDAVP) or vasopressin (Pitressin). Both drugs promote reabsorption of water in the renal tubule. It is critical that diabetes insipidus be corrected as soon as possible because hypernatremia is associated with poor graft function after transplantation. Salim also added hormone replacement therapy in addition to early, aggressive fluid resuscitation. HRT decreases the need for inotropic support by increasing cardiac output, affecting cellular metabolism, and increasing the sensitivity of the adrenal receptors to catecholamines. Salim’s model for aggressive HRT includes one ampule Dextrose 50% (D50), 2 grams methylprednisolone (Solu-Medrol), 20 units regular insulin, and 20 micrograms of thyroid hormone, followed by continuous thyroid hormone infusion in patients unresponsive to vasopressors.
Hyperglycemia, often seen with the brain dead patient, may be due to stress, IV fluids that contain dextrose, and the catecholamine storm causing reduced insulin levels. The goal is to keep glucose levels within normal limits by the administration of insulin.
Disseminated intravascular coagulation (DIC) is common with brain dead patients—especially those with penetrating head wounds. DIC occurs secondary to the release of tissue thromboplastin by the dead brain tissue. This process causes blood to coagulate throughout the body, which in turn, decreases the amount of platelets and other coagulation factors. This results in an increased risk of hemorrhage. DIC can cause necrosis in the organs, especially the liver and kidneys. Management is aimed at correcting the coagulopathy with blood products.
The brain dead patient loses the ability to thermoregulate due to hypothalamus damage. The patient becomes poikilothermic, meaning the body takes on the temperature of the environment. Problems caused by hypothermia include cardiac dysfunction, coagulopathy, and arrhythmias. Treatment includes using warming devices for IV fluids and within the ventilator circuit. A warming blanket should be applied directly to the patient, and special care should be taken to keep the head completely covered.
There are several causes of electrolyte abnormalities. Not only can pre-hospital events and medical management before brain death contribute to imbalances, but the body’s inability to maintain homeostasis as a result of brain death itself plays a major role. Electrolyte abnormalities alter cellular activities, compromise cardiovascular stability, and contribute to post-transplant graft survival.
Some of the more common abnormalities include hypernatremia, hypocalcemia, hypophosphatemia, and hypomagnesemia. It is important to monitor for these abnormalities and treat accordingly as soon as possible.
Nurses’ role with organ donation
Critical care nurses play a key role in organ donation. They have the unique opportunity to care for both the dying patient and the patient’s family. This experience gives them the chance to impact up to eight other lives through the gift of organ donation and as many as 100 tissue and eye recipients.
The first and most important job of the critical care nurse is to care for the patient and his or her family. Communication is important; the family must have a firm understanding of what is happening to their loved one. But there are several other responsibilities.
Critical care nurses must learn to recognize and identify potential organ donors as early in the course of treatment as possible. To assist in this recognition, hospitals should have a set of specific criteria (known as clinical triggers) for referral. Once the patient meets these established triggers, the nurse makes the referral to the organ procurement organization (OPO). This allows for careful and strategic coordination between the various healthcare disciplines to ensure that optimal organ function is protected while also addressing the special needs of the family.
Through careful assessment, the nurse monitors for signs of brain death, which include the loss of brain stem reflexes. Testing to confirm neurological death should be done as soon as it appears the patient meets brain death criteria. During this period, communication with the potential donor family is extremely critical. The nurse caring for the patient bonds with the family and is often the most appropriate member of the healthcare team to approach the family about organ donation. Once the family has made the decision to donate, nursing care shifts from cerebral protective strategies to aggressive donor management along with continued family support.
The nurse works closely with the OPO during donor management. The nurse also assists the physician with line insertion, draws blood work, administers medications, monitors vital signs, and records intake and output. It is important that the nurse stay in constant communication with the OPO during this time. The nurse’s time and commitment to the donor management process are key in determining the successful outcome of this process, and they can dramatically influence the number of organs that are suitable for transplantation.
Care of the organ donor involves complex management from all members of the healthcare team. It is important to stay on top of the changing needs of these patients. Organ donation saves thousands of lives each year, but more work needs to be done to save thousands more. This can be accomplished by increasing the supply of transplantable organs through education, recognition of potential donors, and excellent nursing and medical management.
Kelly Walton Tanner is a Liver Transplant Coordinator at the Carolinas Medical Center in Charlotte, North Carolina.
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I am a family doctor in Fayetteville, WV. This article was forwarded to me by an family member of the author. I read it. I learned a lot of pathophysiology reading this article. It is well written with good explanations of unusual terms e.g. poikilothermia. Thanks for this effort.