Organ donation process and management of the organ donor


  • Successful organ recovery for transplantation requires perioperative donor management expertise to correct physiologic derangements associated with neurologic death.

  • A collaborative, multidisciplinary approach to end-of-life care and donation requires early referral to the organ procurement organization, allowing medical professionals to dialogue and improve authorization rates while supporting families with end-of-life care decisions.

  • Determination of neurologic death in children is based on clinical criteria that are consistent across the age spectrum.

  • Donation after circulatory death (DCD) permits donation from patients who have suffered a catastrophic brain injury but do not progress to neurologic death.

  • The sustained practice of pediatric DCD donation accounts for roughly 10% of all DCD donors nationally.

  • Patient and graft survival for organs, especially kidneys, transplanted from DCD donors is comparable to organ transplants from donation after neurologic death.

  • Neonatal donation provides another valuable opportunity to recover organs for transplantation.

A significant gap continues to exist between the numbers of organ transplants and transplant recipients on the national waiting list in the United States. Children less than 18 years of age account for approximately 1.5% of all patients waiting for a transplant. The majority of children and adults have end-stage renal failure and are waiting for a renal transplant, followed by those with hepatic disease waiting for a liver. Despite fewer pediatric donors following neurologic death, the total number of pediatric transplants is increasing. There is also a continued increase in children receiving organ transplants from pediatric donors. Unfortunately, children still die waiting for a life-saving transplant. The highest death rate observed occurs in those less than 1 year of age. At the same time, the proportion of children removed as a transplant candidate from the waitlist and die because their underlying illness progresses continues to increase. Taken in sum, there is a growing need for donated organs and improved therapies to preserve existing organ function for those awaiting transplantation. The global importance of organ donation is recognized and supported by the American Academy of Pediatrics (AAP) and other organizations. , The AAP emphasizes education, the need to shape public policy, and a system in which organ procurement, distribution, and costs are fair and equitable to children and adults.

Each state has laws and regulations for the determination of death that have been modeled after the Uniform Determination of Death Act (UDDA) in most cases. The UDDA provides a definition of death, stating that an individual who has sustained either (1) irreversible cessation of circulatory and respiratory functions or (2) irreversible cessation of all functions of the entire brain (including the brainstem) is dead. A determination of death must be made in accordance with accepted medical standards. Criteria for the determination of death have been established in national guidelines for adults and children. In accordance with the dead donor rule, donation can only occur after death has been declared. Donation cannot result in the death of the patient. An ethical discussion about defining and determining death and the dead donor rule are beyond the scope of this chapter (see Chapter 18 ).

Organ donation can occur following neurologic death (donation after brain death [DBD]), following circulatory death (donation after circulatory death [DCD]), or through living donation. The vast majority of organs are recovered following death established by neurologic criteria. Donor organs potentially recovered for transplantation are dependent on the type of donation. Organs recovered from DBD include the heart, lungs, liver, kidneys, pancreas, and intestines. Organs recovered following DCD include lung, liver, kidneys, and pancreas. Additionally, hearts have been recovered from DCD donors. , Tissues including skin, bone, cartilage, heart valves, and corneas can be recovered from both DBD and DCD donors.

Most pediatric deaths occur in intensive care units (ICUs) following the unplanned withdrawal of life-sustaining medical therapies, making opportunities for pediatric donation a rare event. Missed opportunities for organ donation occur for many reasons, but the majority can be accounted for when a family declines the option of donation. Families may not have been provided the opportunity for donation because the medical team did not recognize donor eligibility. Approaching families about donation at an inappropriate time, failing to develop a shared cognitive model for the concept of brain or circulatory death, unreliable or misleading educational resources, and racial barriers may also contribute to declined authorization rates. , Even after authorization, potential organs for transplantation may become unsuitable because of caregivers’ lack of familiarity with appropriate donor management, damage during recovery prior to transplantation, and medical examiner or coroner denials. Families who authorize donation are more likely to comprehend neurologic death and report a positive hospital experience compared with families that choose not to authorize donation. Unique aspects related to pediatric organ donation and transplantation are listed in eBox 20.1 .

• eBOX 20.1

Unique Issues With Pediatric Organ Donation and Transplantation

  • Parents and guardians must act as surrogate decision makers without benefit of being guided by the donor’s wishes, as is often possible with adults.

  • There is age-related variation in the timing associated with determination of brain death.

  • There are technical challenges related to surgical procedures in smaller children and infants.

  • Acquisition and use of organs recovered from children may be limited by size and weight constraints.

  • Specialized care required for the management of critically ill children and pediatric organ donors may be lacking at institutions without pediatric expertise.

Process of organ donation

Organ donation should be viewed as a process. Like many other aspects in medicine, this process evolves over time and includes (1) identification of a potential donor, (2) determination of neurologic death in a timely manner, (3) authorization for organ donation, (4) perioperative management of the donor, and (5) recovery of organs for transplantation. The donation process begins when a critically ill or injured child is identified as a potential donor, with an early or timely referral to the organ procurement organization (OPO). A federal mandate requires notification of the designated OPO for any impending death. Early involvement and timely notification prior to the determination of death generates a greater amount of time for collaboration with the OPO. This best practice permits coordination of the donation process with the medical team. , , , Ensuring OPO engagement and the intensive care team’s understanding of the entire donation process is essential to eliminate confusion that may disrupt the donation process. Ensuring this best practice not only improves authorization rates but also assists families with understanding and coping with end-of-life care issues. A protective stance with parents or guardians of children because of preconceptions about donor eligibility may have the unintended consequence of denying families the opportunity to help or save the life of another person. Prior to approaching the family, the medical team and OPO should discuss potential donor suitability and coordinate the best way to approach a family about organ donation. , , , , Many national and international organizations have emphasized donation as a routine part of end-of-life care and have adopted this collaborative best practice to increase authorization and recovery of organs for transplantation. , , , , , Discussions about donation with parents or guardians may differ from spouse or relatives of adult donors. Contrary to the traditional approach of the OPO coordinator requesting donation and decoupling the death and authorization process, one study found that the timing of organ donation discussions did not appear to influence donation decisions. Parents want sufficient time to discuss end-of-life care issues, including donation, and may prefer discussions regarding donation with the pediatric intensivist or a member of the healthcare team they have come to trust. , Few families of either adults or children appear to suffer psychological harm by having the option of donation presented to them. In addition to collaboration with the OPO, successful authorization for pediatric donation may include the engagement of palliative care specialists. Palliative providers may act as an additional resource to assist the ICU team and provide family support during end-of-life care discussions and organ donation. ,

The benefits of organ donation extend beyond the transplant recipient. There are psychological and social benefits for the potential donor’s family. Organ donation may assist families in finding solace in the belief that their child’s death was not without meaning and helped or saved the life of other people. , Knowing that their child will be remembered after death is one important way that organ donation helps families heal.

Role of the pediatric intensivist and critical care team in the process of organ donation

Management of critically ill children and pediatric organ donors is best accomplished at a tertiary or quaternary pediatric facility that provides specialized pediatric critical care expertise required to manage this select group of patients. , Medical management of the potential pediatric organ donor requires knowledge of the physiologic derangements associated with this patient population. Hemodynamic instability, alterations in oxygenation and ventilation, metabolic and endocrine abnormalities, and coagulation disturbances are common. Support and care of the family provided by a team of physicians, nurses, social workers, chaplains, family service providers, organ donation specialists, and other support staff trained in the unique aspects of pediatric medicine are integral to the care of these children and their families. , , The pediatric intensivist is central in coordinating care to ensure the successful recovery of organs from pediatric donors.

The integral involvement of the pediatric intensivist and critical care team in the management of critically ill and injured children has been a foundation of clinical practice in many successful pediatric centers. Involvement of critical care specialists—especially in pediatric donation, in which there is a limited and decreasing number of donors—improves the quality and number of organs recovered. , Caring for the critically ill child and the child’s family through all phases of illness, including end-of-life issues, should be a seamless transition. The continuum of care for the dying patient who progresses to death and becomes a donor requires the expertise of the pediatric intensivist and critical care team to preserve the option of donation. Patient management to prevent deterioration of organ systems and subsequent loss of transplantable organs while helping family members deal with the death of their child is fundamental to facilitating the donation process and successful recovery of organs for transplantation. National and international best practices for deceased organ donation emphasize that patient management should preserve the option of donation for potential donors prior to and after declaration of death. , , , , ,

Preconceptions about eligibility for donation by the critical care team may not be current or accurate. Suitability of donor organs for transplantation is best assessed by the OPO. Thresholds for acceptable organ dysfunction can vary according to time of evaluation, transplant program comfort levels, and recipient urgency. For example, serial echocardiograms may demonstrate donor response to effective medical therapy, enabling cardiac recovery for transplantation: a positive blood culture or bacterial meningitis may not preclude organ donation if antibiotic therapy has been administered. In the United States health policy changes have impacted donor eligibility. The HIV Organ Policy Equity Act enacted in 2013 allows HIV-positive donors to donate organs for transplantation into HIV-positive recipients. Additionally, organs from hepatitis-positive donors are now being transplanted. Although these situations may be uncommon for pediatric patients, it emphasizes the need to be aware of the latest developments in public policy and use the expertise of the OPO as part of high-quality end-of-life care.

Collaboration with investigative teams, medical examiners, and coroners in cases of accidental or nonaccidental death is imperative to determine cause of death and allow the donation process to proceed. , Preservation of evidence and early consultation and discussions with the coroner, medical examiner, or forensic team may result in requests for additional noninvasive imaging needed to supplement the death investigation without precluding donation.

Determination of neurologic death

Most organ donations occur following neurologic death; therefore, the determination of neurologic death must precede any efforts to recover organs. Timely and efficient determination of neurologic death is important for several reasons: it allows the family to begin the grieving process as they prepare for the loss of a loved one; if donation is planned, organ preservation and preparation for recovery can begin; and if donation is not planned, medical therapies can be stopped, permitting redistribution of scarce ICU resources to other critically ill and injured patients. Determination of neurologic death must never be rushed or take priority over the needs of the patient or the family. Appropriate emotional support for the family should be provided, including adequate time to grieve with their child after death has occurred. Determination of neurologic death in children is a clinical process based on specific criteria consistent across the age spectrum. Criteria for the determination of neurologic death in infants and children in the United States were revised in 2011. , These guidelines outline the minimum criteria to determine neurologic death for infants greater than 37 weeks estimated gestational age to 18 years of age. The guidelines do not challenge the definition but rather provide criteria for the determination of death. Although examination criteria for infants, children, and adults are similar, determination of irreversible injury and neurologic death can be more challenging in younger patients because of physiologic and anatomic differences, along with differences in the mechanism of injury in infants and children. Hypoxic-ischemic or traumatic brain injuries are the most common causes of neurologic death for infants and children. Two chronologically distinct, unbiased, independent neurologic examinations and age-based recommendations are a primary difference between adult and pediatric guidelines to determine neurologic death. eBox 20.2 lists the recommended observation periods based on the current pediatric guidelines for the determination of neurologic death. A clinical history, known cause of coma, and neurologic injury consistent with the clinical presentation are prerequisites to establish that an irreversible condition has occurred. Neurologic criteria to determine death in infants and children are listed in eBox 20.3 . Normal physiologic parameters must be established and maintained before a determination of neurologic death or neurodiagnostic testing can be meaningful. Coma and apnea must coexist. In addition, confounding variables must be corrected before an evaluation of neurologic death.

• eBOX 20.2

Data from Nakagawa TA, Ashwal S, Mathur M, et al. Guidelines for the determination of brain death in infants and children: an update of the 1987 Task Force recommendations. Crit Care Med. 2011;39(9):2139–2155; and Nakagawa TA, Ashwal S, Mathur M, et al. Clinical report—Guidelines for the determination of brain death in infants and children: an update of the 1987 task force recommendations. Pediatrics. 2011;128(3):e720–740.

Recommended Observation Periods to Determine Brain Death in Infants and Children

  • Term infants (37 weeks’ estimated gestational age) to 30 days of age: Two examinations and apnea tests separated by at least 24 hours a

  • More than 30 days to 18 years of age: Two examinations and apnea tests separated by at least 12 hours b

The observation period may be decreased if an approved ancillary study is used. A second clinical examination and apnea test must be performed following the ancillary study to declare death.

• eBOX 20.3

Data from Nakagawa TA, Ashwal S, Mathur M, et al. Guidelines for the determination of brain death in infants and children: an update of the 1987 Task Force recommendations. Crit Care Med. 2011;39(9):2139–2155; and Nakagawa TA, Ashwal S, Mathur M, et al. Clinical report—Guidelines for the determination of brain death in infants and children: an update of the 1987 task force recommendations. Pediatrics. 2011;128(3):e720–740.

Neurologic Examination Criteria for Brain Death Determination in Infants and Children

  • 1.

    Coma. Patient must lack all evidence of responsiveness. Noxious stimuli should not produce a motor response other than spinally mediated reflexes.

  • 2.

    Apnea. The patient must have the complete absence of documented respiratory effort (if feasible) by formal apnea testing demonstrating a Pa co 2 ≥ 60 mm Hg and >20 mm Hg increase above baseline Pa co 2 .

  • 3.

    Loss of all brainstem reflexes, including:

    • Midposition or fully dilated pupils that do not respond to light

    • Absence of movement of bulbar musculature, including facial and oropharyngeal muscles

    • Absent gag, cough, sucking, and rooting reflexes

    • Absent corneal reflexes

    • Absent oculovestibular reflexes

  • 4.

    Flaccid tone and absence of spontaneous or induced movements, excluding spinal cord events such as reflex withdrawal or spinal myoclonus.

  • 5.

    Reversible conditions or conditions that can interfere with the neurologic examination must be excluded prior to brain death testing.

Conditions that may interfere with the neurologic examination or factors capable of causing a comatose state imitating brain death should be considered, corrected, and ruled out. These include hypothermia, hypotension, severe hepatic or renal dysfunction, inborn errors of metabolism, metabolic disturbances including hypoglycemia, and toxic or iatrogenic ingestions. Toxins can interfere with the neurologic examination and should be considered in cases in which a definitive etiology of coma cannot be established. Longer-acting or continuous infusion of sedative agents and recent administration of neuromuscular blocking agents can interfere with the neurologic examination. When determining the appropriate timing of the clinical examination, the half-life of previously administered agents must be considered. End-organ dysfunction and the use of therapeutic hypothermia can delay pharmacologic clearance. Adequate time for clearance of sedatives and neuromuscular blocking agents must be provided. Testing for drug intoxication—including barbiturates, opiates, and alcohol—should be performed as indicated. Clearance of neuromuscular blocking agents can be confirmed by use of a nerve stimulator.

There may be situations in which these conditions cannot be corrected and an ancillary study may be required to assist with the determination of neurologic death. For instance, the use of barbiturate coma in traumatic brain injury may require a prolonged observation period to ensure that measured levels are in the low- to mid-therapeutic range before a clinical determination of neurologic death can occur. Barbiturates reduce cerebral blood flow (CBF); however, there is no evidence that high-dose barbiturate therapy completely arrests CBF. Radionuclide CBF study or cerebral arteriography can be used in patients receiving high-dose barbiturate therapy to demonstrate the absence of CBF. ,

Patients receiving targeted temperature management and hypothermia protocols require adequate time for drug clearance following rewarming prior to initiating testing for neurologic death. Current adult and pediatric guidelines in the United States and Canada recommend a minimum core body temperature of >35°C (95°F). , The United States pediatric guidelines suggest waiting at least 24 hours following rewarming before instituting testing for neurologic death. , A period greater than 24 hours following targeted temperature management may be required to determine neurologic prognostication and ensure that diagnostic error does not occur when determining neurologic death.

Testing for apnea

Apnea testing is a critical and essential component of the clinical examination to determine neurologic death. Testing for apnea will result in respiratory acidosis and potential hypoxemia. Therefore testing must be performed safely with special attention to maintaining ideal oxygenation and hemodynamics. Apnea testing should be performed only after the patient has met the clinical criteria for neurologic death. , Apnea testing must allow adequate time for the partial pressure of carbon dioxide (Pa co 2 ) to increase to levels that would normally stimulate respiration. Baseline Pa co 2 should be measured and allowed to rise to 60 mm Hg or greater and 20 mm Hg above the baseline to account for infants and children with chronic respiratory disease or insufficiency who may breathe only in response to supranormal Pa co 2 levels. , The patient should be continually observed for any spontaneous respiratory movements over a 5- to 10-minute period or longer, with documentation of arterial blood gas(es) reaching the targeted threshold. During apnea, the Pa co 2 rises approximately 3 to 5 mm Hg/min. , Venous blood gas measurements have not been sufficiently studied to document elevated CO 2 during apnea testing.

Apnea testing requires preoxygenation with 100% oxygen to prevent hypoxia and enhance the chances of successful completion of the apnea test. Mechanical ventilatory support should be adjusted to normalize Pa co 2 initially. Mechanical ventilation is removed, permitting Pa co 2 to rise while observing the patient for spontaneous respiratory effort. During apnea testing, oxygenation can be maintained by using a T-piece circuit connected to the endotracheal tube (ETT) or attaching a self-inflating bag valve system with titration of positive end-expiratory pressure (PEEP). Tracheal insufflation of oxygen using a catheter inserted through the ETT has also been used to provide supplemental oxygen. This technique is not recommended in children, as high gas flow rates may promote CO 2 washout preventing adequate Pa co 2 rise, and catheter insertion too distally can potentiate barotrauma if gas outflow is not optimal or catheter size is too big relative to the ETT. , False reports of spontaneous ventilation have been reported with patients maintained on continuous positive airway pressure for apnea testing despite having the sensitivity of the mechanical ventilator reduced to minimum levels. ,

Apnea testing is consistent with neurologic death if no respiratory effort is observed during the testing period. The patient is placed back on mechanical ventilator support following apnea testing until death is confirmed with a second clinical examination and apnea test. Apnea testing should be aborted if hemodynamic instability occurs or oxygen saturation decreases to 85% or less. An ancillary study should be pursued to assist with the determination of neurologic death if targeted thresholds for apnea testing cannot be achieved or there is any concern regarding the validity of the apnea test. If an ancillary study is used, a second clinical examination and—if possible—a second apnea test must be performed. Any respiratory effort is inconsistent with neurologic death.

Ancillary studies

Ancillary studies are not necessary or mandatory if a determination of neurologic death can be made based on clinical examination criteria and apnea testing. , Ancillary studies can provide additional supportive information to assist in neurologic death. Importantly, ancillary studies are not a substitute for a complete physical examination. If the clinical examination and apnea test cannot be safely completed, an ancillary study should be used to assist in the determination of death. The need for an ancillary study will be determined by the physician caring for the child based on history, the ability to complete the clinical examination and apnea testing, and state and local requirements. , , A second neurologic examination and apnea test is required even if an ancillary study is performed to determine neurologic death. , Neurologic examination results must remain consistent with neurologic death throughout the observation and testing period. In circumstances in which an ancillary study is equivocal, the observation period can actually be increased until another study or clinical examination and apnea test are performed to determine neurologic death. A waiting period of 24 hours is recommended before performing another neurologic examination or follow-up ancillary study in situations in which the study is equivocal. , eBox 20.4 lists clinical situations in which ancillary studies may be useful.

• eBOX 20.4

Clinical Situations for Which Ancillary Studies May Be Useful

  • When the clinical examination or apnea testing cannot be safely completed due to the underlying medical condition of the patient

  • When there is uncertainty about the findings of the neurologic examination

  • If a confounding medication effect may be present

  • To expedite the determination of neurologic death by reducing the clinical observation period

  • Social, medical, and legal reasons

The most widely available and commonly performed ancillary studies validated in children to assist with the determination of neurologic death are radionuclide CBF study and electroencephalography (EEG). , Evaluation of anterior and posterior cerebral circulation with four-vessel cerebral angiography is now rarely, if ever, used to evaluate blood flow in the determination of neurologic death in children. This test is difficult to perform in small infants and children, requires transporting a potentially unstable patient to the angiography suite, and necessitates technical expertise that may not be available in every facility. EEG and radionuclide CBF studies are more easily accomplished without the need for extraordinary technical expertise. EEG and radionuclide CBF studies evaluate different aspects of central nervous system (CNS) activity. EEG testing evaluates cortical and cellular function while radionuclide CBF testing evaluates blood flow and uptake into cerebral tissue. Each of these tests requires the expertise of appropriately trained and qualified individuals who understand the limitations of these studies to avoid misinterpretation. Specific criteria for these studies must be met to determine neurologic death. , , , EEG may be more specific, although less sensitive, than the radionuclide CBF study. , Radionuclide CBF studies have been used extensively with good results. The use of a portable gamma camera for radionuclide angiography has made CBF studies more accessible, allowing for the study to be undertaken at the bedside. This study has become a standard in many institutions, replacing EEG as an ancillary study to assist with the determination of neurologic death in infants and children. , , Transcranial Doppler sonography and brainstem audio-evoked potentials have not been studied extensively or validated in children. , , , As a result, these studies—along with CT angiography, perfusion MRI, magnetic resonance angiography-MRI, (MRA-MRI), and Doppler ultrasonography of the central retinal vessels are not currently acceptable ancillary studies to assist with the determination of neurologic death in infants and children. ,

The sensitivity of EEG and CBF studies are weaker in the neonatal age group. , , , Limited experience with ancillary studies performed in newborns younger than 30 days of age indicates that EEG is less sensitive than CBF in confirming the diagnosis of brain death. The younger the child, particularly neonates less than 30 days of age, the more cautious one should be in determining neurologic death. If there is any uncertainty about the examination, apnea testing, or the ancillary study, continued observation is warranted. Additional clinical evaluations and apnea testing or a repeat ancillary study followed by a second clinical examination and apnea test should be performed to make the determination of neurologic death.

Technologic advances continue to impact our ability to determine circulatory and neurologic death. In certain circumstances, determination of neurologic death may be complicated by open cerebral trauma or decompressive craniectomy, mechanical support with extracorporeal membrane oxygenation (ECMO), or use of advanced ventilation modalities. Performing apnea testing for a patient supported with ECMO has been safely accomplished. , The patient is transitioned to a flow-inflating bag valve system with titration of PEEP and hypercapnia induced by reducing the sweep gas or adding exogenous CO 2 to the circuit, thus permitting CO 2 to rise to an appropriate level to stimulate respiration. The rate of CO 2 rise will be variable depending on how much the sweep gas is reduced. Adding exogenous CO 2 may reduce the duration of the apnea test. Patients supported on advanced mechanical ventilation modes (e.g., airway pressure release ventilation, high-frequency oscillation ventilation) may not tolerate apnea testing due to impairment of oxygenation, ventilation, or hemodynamics. Additionally, apnea testing may be altered by sedation and use of neuromuscular blockade commonly employed with advanced modes of ventilation. Apnea testing should be aborted if the patient becomes hemodynamically unstable or oxygen saturations fall to less than 85 mm Hg. , The updated guidelines make no provisions for determining an oxygen saturation threshold for aborting apnea testing in patients with cyanotic heart disease. Patients with open craniocerebral trauma or decompressive craniectomy may not exhibit the increased intracranial pressure that commonly occurs in a closed skull or may retain limited regional circulation. In any situation in which the clinical examination and apnea test cannot be completed, an ancillary study is recommended to assist with the determination of neurologic death. The clinician should be aware that neurologic death cannot be determined if the required clinical examination or ancillary study cannot be completed.

Determining neurologic death has great implications with profound consequences. The clinical diagnosis of neurologic death is highly reliable when made by experienced examiners using established criteria. , Appropriate documentation of clinical examination, apnea testing, and any ancillary studies should be recorded when death has been determined. The updated guidelines for the determination of neurologic death in infants and children encourage the use of the incorporated guidelines checklist to assist with standardizing the process and documentation of neurologic death in children. , For detailed information about determining neurologic death, the reader is encouraged to become familiar with the current pediatric guidelines , and supplemental institutional or regional requirements.

Brain death physiology

Progression to neurologic death results in neuroendocrine dysfunction requiring specific interventions to preserve organ function. Efforts to control cerebral perfusion pressure, hemodynamic manifestations of herniation, and loss of CNS function contribute to the instability that commonly occurs during and after progression to neurologic death. These physiologic changes clearly affect end-organ viability in the prospective organ donor. Understanding the physiologic changes and anticipating associated complications with neurologic death is therefore critical for organ function and recovery.

Loss of CNS function causes diffuse vascular regulatory and cellular metabolic injury. Neurologic death resulting from cerebral ischemia increases circulating cytokines, reduces cortisol production, and precipitates massive catecholamine release. The combination of these factors may result in physiologic deterioration and, ultimately, end-organ failure if left untreated.

Cerebral blood flow is approximately 50 mL/100 g per minute and accounts for 15% of the cardiac output. Without substrate consumption by the brain, glucose needs are reduced and the patient is prone to hyperglycemia. As neurologic death occurs, cerebral metabolism is further decreased and CO 2 production falls, resulting in a reduction in Pa co 2 . Hypothermia should be anticipated as a result of hypothalamic failure and loss of thermoregulation. Additionally, impaired adrenergic stimulation results in loss of vascular tone with systemic vasodilation and amplified heat losses. Ischemia of the anterior and posterior pituitary results in neuroendocrine dysfunction and pituitary hormone depletion. If left untreated, this leads to inhibition or loss of hormonal stimulation from the hypothalamus with subsequent fluid and electrolyte disturbances and, eventually, cardiovascular collapse.

Hemodynamic deterioration associated with neurologic death is initiated by a massive release of catecholamines, commonly referred to as sympathetic, catecholamine, or autonomic storm. This phenomenon is associated with cerebral ischemia and intracranial hypertension. Clinical manifestations include systemic hypertension and tachycardia. , Autonomic storm exposes organs to extreme sympathetic stimulation from increases in endogenous catecholamines. The local effects of elevated sympathetic stimulation include increased vascular tone, effectively reducing blood flow and potentially causing ischemia to donor organs. Autonomic storm also has direct effects on the myocardium as the surge of catecholamines increases systemic vascular resistance (SVR), myocardial work, and oxygen consumption. Ischemic changes occur as a result of an imbalance between myocardial oxygen supply and demand, resulting in subendocardial ischemia. , Myocardial ischemia impairs cardiac output, leading to dysfunction of donor organs. Myocardial dysfunction leads to elevated left ventricular end diastolic pressure and consequent pulmonary edema. This condition may be exacerbated by the displacement of systemic arterial blood into venous and pulmonary circulations due to catecholamine-mediated systemic vasoconstriction. Increased pulmonary vascular resistance and right heart volume overload may displace the ventricular septum into the left ventricle, further impairing cardiac output by impeding left ventricular filling. Progression to neurologic death results in a cascade of inflammatory mediator release, causing vasodilation as loss of sympathetic tone and catecholamine depletion occurs. Additionally, a shift from aerobic to anaerobic metabolism transpires as a result of ischemia and depletion of pituitary hormones, affecting cardiac performance and end-organ function.

Pediatric donor management

Perimortem management of the donor is a continuum of care extending from admission of a critically ill child to the recovery of organs for transplantation. Treatment of the DBD donor and the DCD donor differ and are discussed separately.

Following the determination of neurologic death and the decision to proceed with organ donation, efforts to reduce intracranial pressure are abandoned and care shifts toward providing adequate circulation and oxygen delivery to preserve vital organ function for transplantation. Subsequent care will differ from management prior to death. Families and staff must be prepared for the paradigm shift in the goals of therapy from lifesaving to organ-preserving. The critical care team should actively manage the potential donor and correct existing physiologic derangements that follow neurologic death to preserve the option of organ donation for the family. For example, decreased intravascular volume secondary to efforts aimed at reducing CBF and controlling intracranial hypertension (e.g., volume restriction and diuretic agents) must be repleted. Metabolic derangements should be corrected, such as iatrogenic hypernatremia from hyperosmolar therapy and hyperglycemia associated with catecholamine release and reduced cerebral metabolism. Volume loss from osmotic diuresis associated with hyperglycemia and diabetes insipidus (DI) following neurologic death must be anticipated and addressed to prevent cardiovascular collapse. Hemodynamic management goals are directed at maintaining normal peripheral perfusion and blood pressure for age. Additional donor management goals include preserving lung function, normalization of Pa co 2 , temperature regulation, and metabolic disturbances. Infections present prior to authorization must continue to be treated until organ procurement occurs. Even if no infectious disease concerns exist, prophylactic antibiotics are routinely administered by many OPOs prior to organ recovery. Progression from neurologic death to somatic death and loss of transplantable organs can result if prompt goal-directed care is not implemented. , , Donor management goals are listed in Table 20.1 .

TABLE 20.1

Pediatric Donor Management Goals

Modified from Nakagawa TA. North American Transplant Coordinators (NATCO) Updated Donor Management and Dosing Guidelines. Lenexa, KS: 2008.

Hemodynamic Support

  • Normalization of blood pressure

  • Systolic blood pressure appropriate for age (lower systolic blood pressures may be acceptable if biomarkers such as lactate and SVO 2 are normal)

  • CVP <12 mm Hg (if measured)

  • Dopamine <10 µg/kg/min or use of a single inotropic agent

    • Normal serum lactate

Blood Pressure Age Systolic (mm Hg) Diastolic (mm Hg)
Neonate 60–90 35–60
Infant (6 mo) 80–95 50–65
Toddler (2 y) 85–100 50–65
School Age (7 y) 90–115 60–70
Adolescent (15 y) 110–130 65–80
Oxygenation and Ventilation

  • Maintain Pa o 2 >100 mm Hg

  • F io 2 0.40

  • Normalize Pa co 2 35–45 mm Hg

  • Arterial pH 7.30–7.45

  • Tidal volumes 8–10 mL/kg and PEEP of 5 cm H 2 O or tidal volumes 6–8 mL/kg and PEEP of 8–10 cm H 2 O

Fluids and Electrolytes Measurement Range
Serum Na + 130–150 (mEq/L)
Serum K + 3.0–5.0 (mEq/L)
Serum glucose 60–200 (mg/dL)
Ionized Ca ++ 0.8–1.2 (mmol/L)
Thermal Regulation
Core body temperature 36–38°C

In addition to targeting restoration of normal organ physiology, ideal donor management includes ongoing evaluation for organ suitability, serial assessment of organ function, immunologic testing, infectious disease screening, donor organ size matching, organ allocation, and coordination of surgical teams for organ retrieval. The goal of donor management therapy is to restore and maintain adequate oxygenation, ventilation, and perfusion to vital organs, thus preserving their function for successful transplantation. This can ultimately result in a higher yield of transplantable organs and improved graft function that may translate to a reduction in hospital length of stay and decreasing acquired morbidity and mortality in the transplant recipient. ,

Treatment of hemodynamic instability

Cardiac instability is the greatest limiting factor to successful organ recovery. Of all physiologic abnormalities encountered in the prospective organ donor, the cardiovascular system is fraught with the most complexity and variation. Hemodynamic instability and organ dysfunction account for a loss of up to 25% of potential donors when donor management is not optimized. Furthermore, initiation of hormonal replacement therapy (HRT) early in the donation process may assist with stabilization of the donor, improve the quality of organs recovered, and enhance posttransplant graft function. , The tremendous physiologic derangements associated with neuroendocrine dysfunction require specific interventions to restore normal physiology. These derangements are detailed later in this chapter and in Chapters 28 , 31 , and 34 .

The sympathetic storm associated with cerebral ischemia and intracranial hypertension results in intense but transient hypertension. If hypertension is severe and sustained, a cautious approach to treatment can be considered using a single IV dose or continuous infusion of a short-acting antihypertensive agent, such as hydralazine, sodium nitroprusside, esmolol, labetalol, or nicardipine titrated to effect. Profound vasodilation and hypotension following neurologic death occur due to cessation of sympathetic outflow. This should be anticipated and treated to restore normal circulation and perfusion.

Profound and abrupt hypotension with release of proinflammatory mediators initiates a cascade of molecular and cellular events with resultant ischemia and reperfusion injury in vital organs. Management during this phase should target aggressive restoration of circulating volume, optimizing cardiac output and oxygen delivery to the tissues, and maintaining normal blood pressure for age (see Table 20.1 ) using catecholamine infusions as necessary. , Isotonic crystalloid solutions—such as normal saline, colloid solutions (e.g., 5% albumin), or blood products (packed red blood cells for the anemic patient or plasma for the patient with a coagulopathy)—can be used for volume replacement. The use of artificial plasma expanders, such as hespan or dextran for volume resuscitation, should be avoided since large volumes of these agents can promote coagulation disturbances and impair renal function. , , Commonly used inotropic agents—such as dopamine, dobutamine, and epinephrine—can be titrated to effect. Catecholamines and dopamine appear to have immunomodulating effects that may help blunt the inflammatory response associated with brain death and improve kidney graft function. , Vasopressors such as norepinephrine, vasopressin, and phenylephrine can be used in situations in which there is profound vasodilation and low SVR, though high doses can reduce perfusion to donor organs, potentially jeopardizing their viability prior to recovery and transplantation. Many OPOs routinely use a combination of inotropic support, volume resuscitation, and hormonal replacement therapy (HRT) to reduce vasoactive infusions that may impair perfusion to potential donor organs. Agents such as thyroid hormone, corticosteroids, vasopressin, and insulin are commonly employed during donor management. , , HRT can reduce circulatory instability associated with thyroid and cortisol depletion, especially in situations in which significant inotropic support is required. , Acidosis, hypoxia, hypercarbia, and electrolyte disturbances can alter myocardial performance and must be corrected. Blood pressure, central venous pressure (CVP), mixed venous oxygen saturation, and serum lactate levels can guide adequate cardiac performance and tissue oxygen delivery. Echocardiography can provide useful information about filling pressures, wall motion abnormalities, and ventricular shortening or ejection fractions. Serial echocardiograms are routinely employed in donor management and performed to assess cardiac function as treatment of the donor progresses. In many instances, cardiac performance improves with aggressive resuscitation and institution of HRT following neurologic death. An initial echocardiogram showing poor myocardial function should not be used to preclude donation. ,

Many commonly used clinical indicators of end-organ perfusion become less reliable once brain death has occurred. For example, urine output is traditionally used as a gauge of adequate intravascular volume and renal perfusion but becomes unreliable in the setting of brain death and DI. Similarly, heart rate may not be a reliable sign of intravascular volume status. After death of the brainstem, there is loss of beat-to-beat variation, lack of vagal tone, and, thus, a fixed heart rate is commonly observed. Perfusion may be affected by temperature instability and hypothermia, resulting in delayed capillary refill time. Biomarkers such as mixed venous oxygen saturation and serum lactate levels may be more useful to guide cardiovascular management to ensure optimal oxygen delivery to tissues. Elevations in serum lactate and the development of metabolic acidosis provide evidence of tissue ischemia and should prompt immediate attention. Importantly, elevated serum lactate may be present following CNS or multisystem trauma and may persist following neurologic death or in those with profound hepatic dysfunction.

Arrhythmias can occur during progression and following neurologic death. The catecholamine storm triggered by adrenergic stimulation results in myocardial ischemia and can cause necrosis of the conduction system, promoting tachydysrhythmias. Following neurologic death, bradyarrhythmias may not be responsive to atropine because of denervation of the heart; epinephrine then becomes the pharmacologic treatment of choice. Other factors contributing to arrhythmias include hypoxemia, hypothermia, cardiac trauma, and the proarrhythmic properties of inotropes. Hypotension from hypovolemia and vasodilation causes poor cardiac output and metabolic acidosis. Metabolic acidosis from inadequate cardiac output and electrolyte disturbances (specifically hypomagnesemia, hypocalcemia, and hypokalemia) that occur with DI may also promote rhythm disturbances. Identification and correction of the underlying cause of the arrhythmia are essential to address and treat rhythm disturbances.

Cardiac arrest may be treated as part of active donor management in a decedent following neurologic death. , Extracorporeal support for the hemodynamically unstable donor has been considered in extreme cases, including hemodialysis for correction of fluid overload and electrolyte disturbances. The use of extracorporeal support to limit warm ischemic time for DCD donors should be avoided because anterograde circulation may be reestablished and negate determination of death.

Hormonal replacement therapy

Significant volume resuscitation and inotropic support are routinely required to correct severe cardiovascular derangements following neurologic death. Anterior pituitary hormone deficits result in thyroid and cortisol depletion and may contribute to hemodynamic instability. HRT restores aerobic metabolism, replaces hormones derived from the hypothalamus and pituitary, augments blood volume, and minimizes the use of inotropic support while optimizing cardiac output.

HRT in adult donors is controversial, with correlations of hormone use, cardiac function, and variable clinical outcomes reported. , One adult study demonstrated a reduced need for vasoactive infusions in 100% of unstable donors and abolished the need in 53% of such donors. Decreased inotropic requirements have also been noted in children who received levothyroxine and vasopressin as part of donor management following neurologic death. Although studies are limited, HRT is a reasonable consideration when hemodynamic status does not improve with fluid and inotropic support. Based on a retrospective analysis of 40,124 organ donors over a 10-year period, the optimal HRT combination associated with multiple organ recovery appears to be thyroid hormone, a corticosteroid, vasopressin, and insulin. Existing literature supports improved outcomes with HRT and greater procurement rates may be seen with earlier administration of HRT. No published studies are available in children; however, one unpublished abstract retrospectively reviewed 1903 pediatric donors and showed that HRT was associated with increased odds of having the liver and at least one kidney and lung transplanted. The greatest benefit of HRT in donor management may, in fact, be improved graft function following transplantation. , , Given these observations, many OPOs have adopted the use of HRT as a routine part of donor management. Commonly used agents and doses for HRT in pediatric donors are listed in Table 20.2 .

Jun 26, 2021 | Posted by in CRITICAL CARE | Comments Off on Organ donation process and management of the organ donor
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