Organ and Tissue Donation and Recovery
Identification of the Potential Organ Donor
 

The ideal organ donor candidate is an individual who has suffered a fatal injury to the brain (with impending or actual brain death), yet has intact cardiovascular function. Severe traumatic head injury is the cause of death in the majority of cases. Other causes include primary brain tumors, cerebrovascular accidents, cardiac arrest, and drug overdose. By virtue of the nature of their injuries, these individuals are most often cared for in ICUs. However, suitable donors may also be identified in the emergency department and occasionally on a general care floor. Patients who can be considered as potential donors must: (1) meet age and brain death criteria, (2) be free of infection, (3) have no history of carcinoma with the exception of low-grade skin or brain tumors, (4) be free of severe systemic disease and have relatively normal organ function, and (5) be hemodynamically salvageable.

The critical care nurse is a key player in successful organ donation, beginning with early identification of potential donors and referral to an OPO, through understanding and supporting family dynamics during the organ recovery process. The family needs to be assured that every effort has been made to save the life of their loved one. If the sensitive and emotional nature of organ donation is understood, these issues can be addressed in a timely and compassionate manner, thus increasing the likelihood of the family giving consent for donation
.

Brain death
 

Brain death has been the subject of ethical debate for more than 3 decades. An understanding of brain death by all involved parties is essential to the successful recovery of organs. Brain death in the context of the historical perspective and clinical organ donation is described and discussed in detail in Chapter 5 of this book Policy and Practice in Organ Transplantation and in another Medscape program, Donation and Transplantation: into the New Millennium.

Although the determination and pronouncement of brain death are the responsibility of the physician, the critical care nurse has several important responsibilities including early recognition of impending brain death, open communication with the physician regarding the patient's status, peer support of nurses caring for brain-dead patients, assisting in the testing for brain death criteria, and care of the patient's family. In this last role, the critical care nurse has the opportunity to provide the family with and reinforce factual information about brain death. Only if the family understands and accepts that brain death is death will they consent to donation.

The Clinical Heurologic Examination
 

The clinical neurologic examination is the standard method for the determination of brain death. This examination can proceed only if: (1) complicated medical conditions that may confound the clinical assessment, particularly severe electrolyte, acid-base, or endocrine disturbances, have been ruled out; (2) severe hypothermia, defined as a core body temperature d" 32C, is absent; (3) the patient is not hypotensive; and (4) there is no evidence of drug intoxication, poisoning, or presence of neuromuscular blocking agents in the patient's system.

  Neurologic examination criteria for determining brain death include coma and an absence of

 

Motor response to painful stimuli; spinal cord reflexes may still be present
 

Pupillary reflex (response to light and pupils at mid position with respect to dilation)
 

Corneal reflexes
 

Oculovestibular reflex
 

Gag reflex
 

Coughing in response to tracheal suctioning
 

Respiratory drive at a PaCO2 of 60 mm Hg or 20 mm Hg above baseline level
 

Sucking and rooting reflex (in infant).

More than 1 consecutive neurologic examination may be necessary to determine brain death. Depending on the patient's age, the time intervals between neurologic examinations are as follows

 

48 hours for newborn term infant to 2 months
 

24 hours for > 2 months to 1 year,
 

12 hours for > 1 year to < 18 years
 

Optional for e" 18 years.

In some cases, confirmatory tests such as cerebral angiography, electroencephalogram, transcranial Doppler ultrasonography, or cerebral scintigraphy may be necessary to make the determination of brain death. Guidelines for the use of confirmatory tests to declare brain death are also based on the patient's age

 

2 confirmatory tests are necessary for newborn term infant to 2 months
 

1 confirmatory test is necessary for > 2 months to 1 year
 

Use of confirmatory tests is optional for > 1 year to < 18 years
 

Use of confirmatory tests is optional for e" 18 years
When brain death is imminent, the patient is considered to be a potential organ donor until determined otherwise, usually by the medical director of an OPO or a transplant physician or surgeon.
Determining suitability of Cadaveric Organ Donor
 

The next step after a potential organ donor has been identified is to determine his/her suitability for donation. All patients who are brain dead or whose brain death is imminent must be evaluated as a potential organ donor. The challenge facing donation and transplantation professionals is not to define ideal donors, but rather to definesuitable donors. A suitable donor is an individual who has at least 1 organ that has a reasonable likelihood of functioning well posttransplantation.
 
Knowledge of the potential donor's reason for admission to the hospital and their current hospital course is crucial to successful multi-organ recovery. The assessment begins with a review of the emergency department admission and prehospital events, if applicable. A review of the physicians' and nurses' progress notes, the admission history and physical, as well as conversations with caregivers generally provide an overview of the patient's hospital course.

During this initial review, special emphasis should be placed on gathering information on periods of hemodynamic instability and other vital sign trends, use of vasoactive drugs, periods of hypoxia, oliguria, and trends in laboratory test values. If the potential donor has been hospitalized for several days, a comprehensive review can take several hours to complete. Next, a thorough physical examination is performed following the same guidelines as for any other patient in an ICU. The presence of tattoos, body piercing jewelry, or suspected prehospital needle track marks should be further investigated.

Obtaining a thorough and accurate medical and social history is one of the most important aspects of determining donor suitability. The OPO coordinator conducts a medical and social history interview designed to elicit information from family members and/or significant others about general health and lifestyle information (including risk factors for the transmission of HIV) pertinent to the potential donor. The person or persons responding to the questionnaire are first asked if they knew the deceased well enough to answer questions regarding their medical and social history.

Answers to these questions from the most knowledgeable historian can make the difference between acceptance or refusal of a particular organ or tissue for transplantation. Although the donor's family and/or significant other will usually be able to provide this information,medical records must also be reviewed and discussions with physicians, nurses, friends and other healthcare agencies may be necessary to answer social and past medical history questions.

UNOS requires each OPO and transplant center to have guidelines for donor acceptance criteria. Regardless of what organs are to be donated, determining donor suitability must be performed in a systematic and comprehensive manner in order to recover as many organs as possible from each and every donor. Medical suitability of the organ donor is determined by an assessment of the following donor parameters:

 

Detailed medical and social history
 

Complete physical examination
 

Review of current hospital course
 

Organ-specific function
 

Age
 

Infectious disease status
 

Screen for malignancy (actual and history of)
Age Criteria
 

The age range of the potential donor is from term newborn to over 65 years, depending on the organ(s) being considered for donation, recipient needs, and quality of organ function in the potential donor. As the transplantable population ages, the upper limit for age of the organ donor has become more liberal and donor age is evaluated relative to organ function rather than in absolute chronologic terms. This practice is reflected in the significant change in donor age over the last decade. While the overall number of cadaveric donors has increased 30%, the number of donors older than 65 years of age has increased 535%.

In spite of this trend, however, the ideal donor age is still considered to be 10 to 50 years, as grafts from older donors generally do not function as well as grafts from younger donors. According to UNOS data, the 3-year graft survival rates for kidney and liver transplants from donors older than 65 years of age are 65.1% and 58.5% respectively, compared with 84.3% and 75.6% respectively, from donors 18-34 years of age. The use of grafts from older donors however, is justified by some on the basis of the greater number of patients who will survive if transplanted compared with the number who will die on the waiting list if older donors are not utilized

Evaluation for Infection:
 

In today's environment, few medical contraindications to organ donation are absolute, with the exception of infectious and malignant diseases that are associated with poor transplant outcomes. All potential donors undergo a comprehensive evaluation for the presence of malignant tumors, sepsis, and other infectious diseases. The organ donor must be free of active infection as well. Donors with a recent history of infection documented by a positive blood, sputum, or urine culture must receive appropriate antibiotic coverage and have negative culture results to be considered for donation.

A primary concern is the presence of sexually transmitted disease. Serologic screening includes tests for syphilis, HIV, HTLV, and viral hepatitis. Absolute contraindications to organ donation include a donor who has:

 

a transmissible infectious disease that will adversely affect the recipient (i.e., HIV, active hepatitis B virus (HBV) infection, West Nile virus, encephalitis of unknown cause, Jakob-Creutzfeldt's disease, malaria, or disseminated tuberculosis)

 

active visceral or hematologic neoplasm
 

Clinical signs that indicate the organ is unlikely to function
Bacterial infection:
 

If the donor has been hospitalized for more than 72 hours, blood and urine cultures are done. An active systemic bacterial infection at the time of the donor's death introduces the risk of transmitting infectious disease from donor organs to the recipient. In spite of the risks, however, donor infection must be evaluated on an individual basis in order to avoid excluding suitable organs. For example, donors with meningococcal or pneumococcal sepsis who have had 24-48 hours of appropriate antibiotic coverage should be considered for organ recovery. An infectious process localized outside the abdominal cavity does not preclude abdominal organ recovery, and lung recovery may be possible when the donor has a unilateral pneumonia.

Cytomegalovirus (CMV) Infection:
 

The CMV serologic status of the donor is also tested, but not as an exclusionary criterion. Positive CMV serology in the donor does not appear to have adverse effects on patient and graft survival.[12] Although historically, studies demonstrated decreased patient and graft survival when a CMV-positive graft was transplanted into a CMV-negative recipient, many of these studies predated the development of effective antiviral agents for prevention and control of CMV infection. An additional factor in favor of transplanting organs from CMV-positive donors is the high prevalence of CMV-positive individuals (potential recipients) in the general population. The incidence of CMV among donors and recipients ranges from 40% to 80%.

Syphilis: 
 

Serologic tests for syphilis include the venereal disease research laboratory (VDRL) and rapid plasma reagin circle card test (RPR). The detection of the antibody to syphilis via either test is not a contraindication to organ donation, however, because there is no documented evidence of transmission of syphilis from a donor to a recipient. This test is performed so that the recipient of an organ from a donor positive for the antibody to syphilis can be prophylactically treated with an appropriate course of antibiotics.

HIV infection:
 

Serologic tests for HIV I and II antibody and HTLV I antibody are performed on all potential donors. According to UNOS policy, detection of the HIV I and II or HTLV I antibody is an absolute contraindication to donation unless subsequent confirmatory testing indicates that the original test results were falsely positive. Due to the risk of transmitting HIV to blood, tissue, and organ recipients, the Centers for Disease Control (CDC) developed guidelines for prevention of spreading HIV to recipients.[13] Regardless of potential donors' HIV antibody status, donors who meet the CDC criteria listed in Table 1 should be excluded from donation of organs and tissues unless the risk to the recipient of not performing the transplant is deemed to be greater than the risk of HIV transmission and disease. In such cases, organs may be recovered without restrictions, but the transplant center is required to inform the recipients of the potential risk of transmission of HIV infection from the donor.[14]

Even though HTLV I has been transmitted via blood transfusions, the transmission of HTLV I by solid organ transplantation has not been clearly demonstrated and, therefore, some OPOs and transplant programs do not reject donors who are HTLV I antibody-positive. Thus, depending on a potential recipient's severity status, he/she may have little alternative but to accept an organ from such a donor.[14]

Hepatitis B virus (HBV) infection.
 

The debate continues regarding the transplantation of organs from donors who test positive for HBV infection. The implications vary depending on the specific marker(s) present in the donor and the recipient. The hepatitis screen for HBV includes the following markers: HBV surface antigen (HbsAg), HBV core antibody (anti-HBc), and HBV surface antibody (anti-HBs). Table 2 summarizes HBV serologic markers and associated risks of HBV transmission to recipients.

Hepatitis C virus (HCV) infection.
 

As with HBV infection, there is lack of consensus within the transplant community about transplanting organs from HCV-positive donors. Fifty percent of such recipients become HCV-antibody positive, 24% become HCV-PCR positive, and up to 35% develop liver disease.
 
All potential donors are tested for HCV antibody (anti-HCV) either to rule out donation or to establish a basis for initiation of treatment in the recipient at centers where positive HCV serology is not a contraindication to donation. Several programs advocate that HCV-positive donors be used in recipients with a history of HCV-positive antibody. A liver graft from an HCV-positive donor to an HCV-positive recipient does not appear to be associated with increased morbidity or mortality compared with HCV-positive recipients of HCV-negative donor livers. Additional recommendations include that HCV-positive organs be reserved for cases with urgent need and patients who have a limited chance of being transplanted (ie, the highly sensitized patient waiting for a kidney transplant).

Evaluation for malignancy:
  Given the impact of donor-transmitted malignancy on the outcome of organ transplantation, detection of malignancy is an important measure of donor suitability. Not all malignancies, however, constitute an absolute contraindication to donation. Low-grade skin cancers, low-grade solid organ tumors with a greater than 5-year documented tumor-free interval, and primary brain tumors that have not undergone previous surgery usually do not preclude organ donation. As with other donor selection criteria, the acceptance of organs from donors at risk of transferring a malignancy to recipients must be weighed against the urgency of the transplant, and the recipient and/or the recipient's family must be informed of the potential risks.
Evaluation for Severe Systemic Disease
  The ideal organ donor is relatively young, and is free of and with no history of end-organ disease. Each organ system is evaluated separately. Other than carcinoma (except primary brain tumor), no disease by itself should be considered a contraindication to organ donation
Expansion of the Organ Donor Pool
  We live in an era of chronic diseases, and their related problems are the most common reasons that Americans and others seek healthcare. Transplantation has changed the natural history and prognoses associated with some chronic diseases of the kidney, liver, pancreas, intestine, heart, and lung, diseases that are no longer necessarily terminal. Thus, efforts to expand the pool of organ donors have been a high priority in the transplant community for some time.
The Marginal Donor
  As the organ shortage became more severe, it was realized that ideal requirements for selection of organ donors were far from feasible. Over the last decade, selection criteria for solid organ donors have eased. Organs that not long ago would have been considered unsuitable for transplantation are currently being used, ushering in a new class of organ donor termed the "marginal" donor, also referred to as the "expanded" donor and "extended criteria" donor. Although the marginal donor has not been precisely defined, marginal donors consist of donors who are older and who have diabetes mellitus, hypertension, renal insufficiency, or, in selected cases, infectious diseases such as hepatitis and HIV.

The use of reduced-quality organs has met with increasing rates of delayed graft function and PNFG. Donor risk factors associated with poorer outcomes include age, previous diseases with a systematic influence on the vascular system (ie, arterial hypertension, diabetes mellitus), cause of death (cardiovascular or cerebrovascular disease), and brain death (may represent an additional non-immunologic injury contributing to perioperative and postoperative alloantigen-independent and -dependent events).
The Nonbeating Heart Donor:
  One alternative source of donor organs is donors without a heartbeat, the NBHD. Death in donors without a heartbeat is defined as an irreversible cessation of circulatory and respiratory function. Thus, by definition, the NBHD has had a prolonged phase of hypotension followed by cardiac arrest before organ recovery. Historically, the use of NBHDs has been restricted to kidney donation, but limited experience in liver transplantation has begun to be reported. Weber and colleagues[20] recently reported findings from a single-center, matched-pair study of the use of NBHDs for kidney transplantation. In their study, the incidence of delayed graft function was approximately twice that in allografts from heartbeating donors, but both groups had low rates of PNFG and similar long-term outcomes.
Donor Management Physiologic Alterations of Brain Death
  After the diagnosis of brain death, the focus of patient care shifts from interventions aimed at saving the patient's (donor's) life to interventions aimed at maintaining viability of potentially transplantable organs. The main goal of organ donor management is the maintenance of optimal conditions that will ensure functional, intact, and infection-free organs. The quality of organs to be recovered is preserved by optimal management of hydration and perfusion, oxygenation, diuresis, temperature control, and prevention of infection.

A number of physiologic changes occur with brain death, including hemodynamic instability, endocrine abnormalities, hypothermia, coagulopathy, pulmonary dysfunction, and electrolyte imbalances. Therefore, medical management ideally begins as soon as brain death appears imminent, as the window of time for optimal recovery is narrow. Irreversible cardiac arrest usually occurs within 48 to 72 hours of brain death in adults. The reader is referred to a critical pathway developed for management of the organ donor.[25] This pathway provides a multidisciplinary approach to promote communication in the care of organ donors and incorporates key events, multidisciplinary processes, and corresponding timelines or phases that caregivers should anticipate in the care of an organ donor. The components of the pathway include collaborative practice guidelines, referral of potential donors, declaration of brain death, and acquisition of consent for donation, donor evaluation, donor management, and the surgical recovery of donor organs.
Hemodynamic Instability
  Hemodynamic changes begin to occur prior to the diagnosis of brain death. A decrease in blood pressure and heart rate is noted during the onset of brain death. As cerebral ischemia progresses and reaches the brainstem, a severe increase in systemic vascular resistance (SVR) and blood pressure occurs due to the release of endogenous catecholamines, commonly referred to as a "catecholamine storm." These changes reflect the body's attempt to maintain cerebral circulation and reverse brain ischemia.

However, at the peak of increased SVR, cardiac output decreases and perfusion to abdominal organs is decreased due to intense vasoconstriction. As ischemia continues, the catecholamine storm subsides with a decline in SVR. Blood pressure then drops to a hypotensive level, resulting in further hypoperfusion of vital organ systems unless treated. Hypotension is the most frequently encountered problem in the patient being managed as a potential organ donor.
 
In addition to the loss of central vasomotor control, other factors contribute to hemodynamic instability in the organ donor. Hypovolemia is the most common cause of hemodynamic instability in the organ donor and may result from therapeutic dehydration to decrease cerebral edema, incomplete fluid resuscitation after hemorrhage, diabetes insipidus, or osmotic diuresis from hyperglycemia or mannitol administration. Ventricular dysfunction from a myocardial contusion, electrolyte imbalances, and acute pulmonary hypertension also contribute to hemodynamic instability in the potential organ donor.
Endocrine Abnormalities
  Brain death leads to rapid disturbances that affect the hypothalamus-pituitary axis. In most cases, vasopressin release is decreased, resulting in diabetes insipidus, which leads to polyuria, dehydration, hypernatremia, a hyperosmolar state, hypocalcemia, hypophosphatemia, hypokalemia, and hypomagnesemia. Brain death also affects the hypothalamus-pituitary-thyroid axis; however, it remains unclear how it is affected. It has been suggested that this endocrine abnormality is characteristic of the "euthyroid sick syndrome" (low T3, low T4, low TSH, or all 3), more commonly associated with acute major stress than actual hypothyroidism. The roles of other pituitary hormones, including adrenocorticotrophic hormone, prolactin, growth hormone, and gonadotropin, are less clear.
Hypothermia
  Many brain-dead patients become poikilothermic (core temperature drifts toward ambient temperature as a result of interruption of the temperature-regulating center in the hypothalamus) due to the lack of hypothalamic regulation of temperature and as a result become hypothermic. Hypothermia contributes to hemodynamic instability. As body temperature falls, myocardial depression occurs, leading to decreased cardiac output. At very low temperatures, the ventricles become irritable and refractory dysrhythmias often develop. Other harmful effects of hypothermia include reduced tissue oxygen delivery, impaired ability of the kidneys to maintain tubular concentration gradients, and coagulopathy.
Coagulopathy
  Coagulopathy is common in the brain-dead patient, but is usually not the primary problem; it generally occurs secondary to other disorders. Coagulopathy results from the continuous release into the systemic circulation of large amounts of tissue thromboplastin and plasminogen from ischemic or necrotic brain tissue. Hypothermia and catecholamines also affect clotting factors and contribute to coagulopathy, and fluid resuscitation may also cause a dilutional coagulopathy.
Pulmonary Injury
  Brain death is also associated with numerous pulmonary problems. The lungs are highly susceptible to injury resulting from the rapid changes that occur during the catecholamine storm. At the moment of peak vasoconstriction, left-sided heart pressures exceed pulmonary pressure, temporarily halting pulmonary blood flow. Exposed lung tissue is severely injured, resulting in interstitial edema and alveolar hemorrhage, a state commonly referred to as neurogenic pulmonary edema.

Hypoxia in the absence of pulmonary edema is often seen in the brain-dead patient, and a variety of factors are involved, including ventilation-perfusion mismatch, microatelectasis, and increased oxygen consumption. Pneumonia, aspiration, pneumothorax, pulmonary contusion, or other residual effects of the morbid event that caused brain death can also lead to hypoxia.
Electrolyte and Glucose Imbalances
  Abnormal serum concentrations of electrolytes and glucose are common in the brain-dead patient and may result from the events that led to hospital admission, from treatment given prior to brain death, or from the effects of brain death. The effects of individual abnormalities may alter cellular processes, potentially interfering with cardiovascular stability and organ viability in the recipient, but may not always be appreciated clinically.

Hypoglycemia is rarely encountered in the brain-dead patient; however, mild-to-severe hyperglycemia is often seen. Hyperglycemia results from a variety of factors such as the stress response to injury, reduced insulin levels due to catecholamine release or inotropic infusion, and resuscitation with glucose-containing fluids. The major consequences of hyperglycemia are a hyperosmolar state leading to dehydration and a shift in electrolytes from intracellular to extracellular fluids, osmotic diuresis with a subsequent loss of water and electrolytes, metabolic acidosis, and ketosis.

Sodium is primarily an extracellular electrolyte and is responsible for osmolality in the extracellular space. Hyponatremia is uncommon in the brain-dead patient and when it occurs is often secondary to hyperglycemia. Hypernatremia, on the other hand, is common in the brain-dead patient as a result of dehydration, sodium administration, and free water loss secondary to administration of diuretics or diabetes insipidus. The impact of hypernatremia on posttransplant organ function is not fully understood.

Potassium is primarily an intracellular electrolyte, and its regulation becomes impaired in the brain-dead patient. Hyperkalemia, although somewhat rare, is most often the result of situations that impair renal elimination of potassium (ie, kidney failure) or that cause potassium to move into the extracelluar fluid (ie, metabolic acidosis).Ninety percent of brain-dead patients develop hypokalemia. The most common causes are the use of diuretics, polyuria from any cause, and alkalosis.

Hypocalcemia, hypophosphatemia, and hypomagnesemia are common in the brain-dead patient and are most often related to the polyuria associated with osmotic diuresis, the use of diuretics, and diabetes insipidus. Hypocalcemia is often present when the brain-dead patient has been aggressively transfused with blood. Below-normal levels of magnesium may cause dysrhythmias and other electrocardiographic changes, and low levels of calcium and phosphorus may affect cardiac contractility and blood pressure, leading to an increased need for vasopressor support. Hypercalcemia, hyperphosphatemia, and hypermagnesemia as a consequence of brain death are rare.
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, and 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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