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37 The Pediatric Patient Cared for in the Adult ICU
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28. Katayama Y, Horigome H, Murakami T, Takahashi-Igari M, Miyata D, Tanaka K. Evaluation of blood rheology in patients with cya­notic congenital heart disease using a microchannel array fl ow ana­lyzer. Clin Hemorheol Microcirc. 2006;35(4):499–508.
29. Kelly T, Buxbaum J. Gastrointestinal manifestations of cystic fi bro­sis. Dig Dis Sci. 2015;60(7):1903–13.
30. Khine HH, Corddry DH, Kettrick RG, Martin TM, McCloskey JJ, Rose JB, et al. Comparison of cuffed and uncuffed endotracheal tubes in young children during general anesthesia. Anesthesiology. 1997;86(3):627–31. discussion 27A.
31. King BR, Baker MD, Braitman LE, Seidl-Friedman J, Schreiner MS. Endotracheal tube selection in children: a comparison of four methods. Ann Emerg Med. 1993;22(3):530–4.
32. Kochanek PM, Carney N, Adelson PD, Ashwal S, Bell MJ, Bratton S, et al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents – second edition. Pediatr Crit Care Med. 2012;13 Suppl 1:S1–82.
33. Koyak Z, Harris L, de Groot JR, Silversides CK, Oechslin EN, Bouma BJ, et al. Sudden cardiac death in adult congenital heart dis­ease. Circulation. 2012;126(16):1944–54.
34. Kulvatunyou N, Erickson L, Vijayasekaran A, Gries L, Joseph B, Friese RF, et al. Randomized clinical trial of pigtail catheter versus chest tube in injured patients with uncomplicated traumatic pneu­mothorax. Br J Surg. 2014;101(2):17–22.
35. Lambert RL, Boker JR, Maffei FA. National survey of bedside ultrasound use in pediatric critical care. Pediatr Crit Care Med. 2011;12(6):655–9.
36. Liesching T, Kwok H, Hill NS. Acute applications of noninvasive positive pressure ventilation. Chest. 2003;124(2):699–713.
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38. Milling Jr TJ, Rose J, Briggs WM, Birkhahn R, Gaeta TJ, Bove JJ, et al. Randomized, controlled clinical trial of point-of-care limited ultrasonography assistance of central venous cannulation: the Third Sonography Outcomes Assessment Program (SOAP-3) Trial. Crit Care Med. 2005;33(8):1764–9.
39. Mitchell MH, Lynch MB. Should relatives be allowed in the resuscitation room? J Accid Emerg Med. 1997;14(6):366, 9, dis­cussion 370.
40. Moynihan RJ, Brock-Utne JG, Archer JH, Feld LH, Kreitzman TR. The effect of cricoid pressure on preventing gastric insuffl ation in infants and children. Anesthesiology. 1993;78(4):652–6.
41. Neuhaus D. Intraosseous infusion in elective and emergency pedi­atric anesthesia: when should we use it? Curr Opin Anaesthesiol. 2014;27(3):282–7.
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43. Patel B, Bingham R. Laryngeal mask airway and other supraglottic airway devices in paediatric practice. Contin Educ Anaesth Crit Care Pain. 2009;9(1):6,7–9.
44. Petel D, Li P, Emil S. Percutaneous pigtail catheter versus tube tho­racostomy for pediatric empyema: a comparison of outcomes. Surgery. 2013;154(4):655–60. discussion 660–1.
45. Philip S, Chaiwat O, Udomphorn Y, Moore A, Zimmerman JJ, Armstead W, et al. Variation in cerebral blood fl ow velocity with cerebral perfusion pressure >40 mm Hg in 42 children with severe traumatic brain injury. Crit Care Med. 2009;37(11): 2973–8.
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47. Pigula FA, Wald SL, Shackford SR, Vane DW. The effect of hypo­tension and hypoxia on children with severe head injuries. J Pediatr Surg. 1993;28(3):310–4. discussion 315–6.
48. Price S, Jaggar SI, Jordan S, Trenfi eld S, Khan M, Sethia B, et al. Adult congenital heart disease: intensive care management and out­come prediction. Intensive Care Med. 2007;33(4):652–9.
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51. Roy N. Critical care management of the adult patient with congeni­tal heart disease: focus on postoperative management and out­comes. Curr Treat Options Cardiovasc Med. 2015;17(2):362.
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2007.

Organ Donor Management

Olubode Ademola Olufajo and Ali Salim
3 8

History of Organ Donation

The processes of organ donation and transplantation have developed considerably over the past decades. As early as the beginning of the twentieth century, there were successful reports of transplantation of human skin and cornea [ However, it was not until 1954 that the fi rst successful solid organ transplant between identical twins was reported at the Peter Bent Brigham Hospital, Boston [ 3 ]. The advancement of immunosuppressive therapy over the years and the improvement in life-sustaining therapy have increased the potentials for cadaveric organ donation.
In 1968, the Harvard Commission outlined the fi rst stan­dard set of criteria for brain death [ 4 ]. The Uniform Anatomic Gift Act was also passed into law during this time, legalizing cadaveric organ donation for transplantation. Because of the widening gap between organ demand and supply in the 1990s, the concept of donation after cardiac death (DCD) was introduced for patients with irreversible conditions whose hearts ceased to beat after withdrawal of life­sustaining therapy [ 3 ]. By 2000, the US Department of Health and Human Services introduced the “Final Rule” for organ procurement and transplantation to ensure broader and fair allocation of available organs to the patients with the most urgent medical conditions [ 5 ].
Other advances have been made in recent years to improve the quality and quantity of organs available for the transplan­tation to meet the demands of the ever-growing population of recipients. Organ donation is rapidly becoming a common and culturally accepted practice, while transplantation has
1 , 2 ].
become the preferred treatment for end-stage solid organ failure. The rest of this chapter will highlight the important parts of the organ donation process and recommendations for improved donation outcomes.

Identifying Potential Donors

There are three major sources of organs used for transplants. These are from cadaveric “brain-dead” donors (donors after neurologic determination of death, DNDD), cadaveric “car­diac death” donors (donors after circulatory determination of death, DCDD), and living (related and unrelated) donors. Currently, the majority of transplanted organs come from donors after neurologic determination of death. In 2014, there were 23,715 (80 %) deceased donor transplants, while there were only 5,817 (20 %) living donor transplants [ 6 ].
The vast majority of cadaveric “brain-dead” donors die from cerebrovascular accidents (CVA), head trauma, and anoxia [ 7 ]. Since nearly 50,000 US residents die from TBI and nearly 142,000 citizens die from CVA per year, these two causes of death are likely going to make large contribu­tions to the organ pool in the coming years [ 8 ].
In the course of patient care, it is important to be expect­ant and proactive in identifying individuals that may poten­tially donate organs and taking the next necessary steps toward organ recovery.

Referral of Potential Donors

Once the potential donors have been identifi ed, organ pro-
O. A. Olufajo , MD, MPH Department of Surgery , Brigham and Women’s Hospital , Boston , MA 02115 , USA
oao777@mail.harvard.edu; oolufajo@partners.org
e-mail: A. Salim , MD (
Division of Trauma, Burn, and Surgical Critical Care , Brigham and Women’s Hospital , Boston , MA 02115 , USA e-mail:
© Springer International Publishing Switzerland 2016 N.D. Martin, L.J. Kaplan (eds.), Principles of Adult Surgical Critical Care, DOI 10.1007/978-3-319-33341-0_38
*)
asalim@partners.org
curement organizations (OPOs) must be involved in the management of the donation process. This referral step should be taken as early as possible because early referral is associated with better outcomes including higher consent rates and conversion rates [ 9 ]. Early referral gives the OPOs the opportunity to form relationships with the caregivers, educate them on the details of the process, and attend to the
443
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O.A. Olufajo and A. Salim
unique ethical and social needs of each situation. In a study of families that denied donation, it was found that 53 % of them did not receive adequate education, and the next of kins that decided against donation usually had less understanding of brain death than those that agreed to donation [
Of note, the task of obtaining consent to donate should not be carried out by the physician but should be left to the staff of the OPOs since they have the necessary training and experience.
10 ].

Team Management Approaches to Donation

Like any successful process, the organ donation process requires teamwork. Aside from the primary physician, other members of the healthcare team play critical roles in guiding the families and supporting them in their grief. A senior phy­sician should interact with the families early in the process and be identifi ed as a ready source of support.
The presence of OPO staff housed within the hospital is also crucial for optimal donation outcomes. These in-house coordinators are usually nurses trained in organ procurement, and they form strong bonds with donor families, providing support, ensuring the timings of discussions are appropriate, and adapting the approaches to the cultural backgrounds of the families. They also ensure timely donor referral via donor sur­veillance, organize regular staff education sessions, and daily monitor the donation activities of the hospital. Implementation of in-house coordinators has been shown to increase consent and conversion rates signifi cantly [ 11 ]. Hospitals that operate this system have been shown to have up to 28 % greater con­sent rates and 48 % greater conversion rates when compared to other hospitals with similar resources but without in-house coordinators. Other improvements in outcomes shown after the implementation of in- house coordinators include higher referral rates, lower family decline rates, and increased organs transplanted per donor [ 12 ]. This effect is more marked in cen- ters with minority populations [ rates of up to 88 % have been shown in blacks after the imple­mentation of in- house coordinators in Level I trauma centers. The reasons for the better outcomes in hospitals with in-house coordinators can be linked to the better access they have to the patients and the ease of relationship building with the clinical and management staff of the hospital [
11 – 13 ]. Increases in consent
13 ].

Neurological Criteria for Determination of Death

Since the criteria for brain death were fi rst outlined by the Harvard Commission in 1968, there have been several modi­fi cations to adapt to the evolving clinical and ethical cli­mates. The recent 2010 evidence-based recommendations
for the determination of brain death among adult patients published by the Quality Standards Subcommittee of the American Academy of Neurology state that the apnea test is a safe method for determining neurological death [ 14 ]. Other important aspects of the evaluation for neurological death include response to pain, pupillary response, oculocephalic refl ex, corneal refl ex, and the cold caloric refl ex test.
Although there are several variations of the apnea test, the commonly accepted method is recommended by the American Academy of Neurology. This involves pre­oxygenating the patient with 100 % oxygen for 10 min and ensuring arterial pCO
36.5 °C (97 °F), and systolic blood pressure above 90 mmHg. Arterial blood gas (ABG) should be drawn at the beginning of the test. A cut nasal cannula is slid to approximately the level of the carina to deliver 100 % oxygen at 8 L/min. Once the pulse oximeter is confi rmed to be working, the ventilator is disconnected. The presence of spontaneous respiratory movements is then assessed. A fall of the pulse oximeter readings below 90 % or systolic blood pressure below 90 mmHg indicates completion of the test. Ventilatory sup­port should be resumed and ABG drawn. If the patient toler­ates the test for 10 min, then the test is also ended and the patient is placed back on the ventilator and an ABG is drawn. For both scenarios, if the ABG measures a pCO 2 above 60 mmHg or 20 mmHg above the pCO 2 measured on the ini­tial ABG, the apnea test result is considered positive, and the diagnosis of brain death is made.
Once the assessment of neurological death is made, family members should ideally be informed. On religious grounds, however, some families would prefer not to be informed about brain death. In several states such as New York and New Jersey, it is illegal to make the declaration of death by neuro­logic criteria if the family or individual previously objected to the concept of brain death based on religious beliefs [ 15 ]. Under these circumstances, the physician is required to con­tinue medical support. In addition, the number of physicians required to diagnose brain death, as well as the type and need for confi rmatory tests, varies among and within countries.
of 35–45 mmHg, core temperature of
2

Donation After Circulatory Determination of Death

Historically, because the “Dead Donor Rule” stipulates that patients be declared dead before the removal of life­sustaining organs, operations for donation were performed with organs from donors who had recently died of cardiopul­monary arrest. As the idea of death evolved to include the concept of a neurologic determination of death, patients with catastrophic brain injuries became a substantial source of organs for transplantation once declared dead by neurologic criteria. Because their hearts were still beating, their organs
38 Organ Donor Management
445
were better preserved than the previous donors who had been declared by cardiopulmonary criteria. In the last two decades, however, the scarcity of organs available for transplantation has renewed the interest in “non-heart-beating donors” or donation after cardiac death (DCD).
Based on recommendations of the Institute of Medicine, there are increasing numbers of organs being obtained from patients that were declared dead following the cessation of circulatory function, rather than neurological death [ Donation after circulatory determination of death (DCDD) has increased the supply of organs available for transplanta­tion and now accounts for about 12 % of deceased organ donors in the USA [ 17 , 18 ]. This option has been used when a patient or the patient’s surrogate desires to withdraw life support but would like to donate organs. Following the with­drawal of life support and resuscitative interventions, the patient is declared dead after permanent circulatory arrest has occurred [ 16 , 19 ]. Importantly, long-term graft survival of DCDD organs, particularly kidneys, appears to be similar to that of donation after neurological determination of death (DNDD) organs [ 20 – 24 ].
16 ].

Pathophysiology of Brain Death

Neurologic death is caused by the herniation of cerebral con­tents due to supranormal intracranial pressures. Early pon­tine ischemia results in a catecholamine surge with hypertension, known commonly as the fi rst stage of the Cushing’s refl ex. As ischemia progresses caudally to the vagal nucleus in the medulla oblongata, the loss of barore­fl ector refl exes and unopposed sympathetic activity results in a profound hyperdynamic state [ 25 ]. This sympathetic vaso- constriction causes compromise of end-organ perfusion.
As the brain continues to herniate, a sudden cardiovascu­lar collapse can develop, in part due to direct catecholamine­induced myocardial injury and subsequent cardiac dysfunction, as well as destruction of pontine and medullary vasomotor centers [ 26 , 27 ]. The effects of this hemodynamic instability can cause marked damage to potentially donatable end organs. Profound hypotension develops due to loss of sympathetic tone, amplifi ed by the development of diabetes insipidus (DI) due to an infarcted posterior pituitary.
The physiologic changes that manifest as different por­tions of the brain become injured during the herniation pro­cess present a multifaceted challenge to the treating intensivist. These physiologic alterations result in diffuse vascular regulatory disturbances and widespread cellular injury [ 28 ]. Major swings in hormone levels are seen. Severe alterations also occur in metabolism, immunology, and coag­ulopathy [ 29 – 31 ]. Understanding these physiological responses is important for the optimal care of the injured patient and maximal utility of donated organs.

Systemic Sequelae of Brain Death

Cardiovascular System

Two distinct, and in many ways, opposite, profi les of hemo­dynamic activity are seen during the process of neurologic death. Brain stem ischemia causes a catecholamine surge as the medulla endeavors to maintain cerebral perfusion pres­sure and improve local tissue oxygenation. This response manifests as increases in heart rate, blood pressure, cardiac output, and systemic vascular resistance. This surge of cate­cholamines can challenge the balance between myocardial supply and demand. Several autopsy studies have demon­strated left ventricular subendocardial necrosis [ 32 , 33 ]. ECG changes and cardiac arrhythmias are common and are thought to be due to both metabolic and electrolyte abnormalities, as well as infarction of the conduction system. The use of stan­dard antiarrhythmic therapy is appropriate. An important caveat to remember is that vagus nerve disruption in the brain stem may result in a bradyarrhythmia which is resistant to the effects of atropine, and a beta-adrenergic agonist such as iso­proterenol or epinephrine may be required [ 34 ]. Untreated arrhythmias may become completely refractory to manage­ment if not treated early and aggressively.
The second phase of cardiovascular activity, character­ized by hemodynamic collapse, coincides with brain stem herniation and results in the loss of sympathetic activity causing profound vasodilatation, myocardial depression, and low levels of serum catecholamines. The hemodynamic effects can be amplifi ed by hypovolemia due to diabetes insipidus which is often present concurrently. Additional myocardial depression may be due to a concurrent reduction in triiodothyronine (T3) production as well as direct mito­chondrial inhibition.
Cardiac catheterization may be more selectively employed for donors >55 years of age and younger patients with a his­tory of cocaine use, or three or more risk factors for coronary artery disease such as hypertension, diabetes, dyslipidemia, prolonged smoking history, or family history of premature coronary artery disease [ 35 ]. In the setting of left ventricular dysfunction, pulmonary artery catheter-directed manage­ment can maximize donor recovery. Knowledge of the patient’s cardiac output and left ventricular fi lling pressures allows for optimal management of vasopressors and fl uids. The role of adjunctive hormone therapy to improve cardiac function is discussed below.

Pulmonary System

Increased systemic pressures and left atrial pressures during the catecholamine surge can result in elevated pulmonary artery pressures and subsequent endothelial damage, leading
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to direct pulmonary damage due to capillary leak. During cardiovascular collapse, intravenous fl uid administration needed to maintain systemic blood pressure can cause fur­ther pulmonary damage due to volume overload, pulmonary capillary leak, and resultant development of pulmonary edema. Increased pulmonary capillary permeability as well as decreased pulmonary resistance makes the lungs particu­larly sensitive to increases in volume loading [
Lung protective strategies commonly used in the intensive care unit should continue to be performed in the potential organ donor. In the brain-injured patient, hyperventilatory strategies are often employed, aimed at promoting hypocapnia and lower intracranial pressures through cerebral vasocon­striction. These same alkalinizing strategies can exasperate bronchospasm, airway edema, and pulmonary microvascular permeability [ 38 ]. High-minute ventilation strategies should be reversed after the declaration of neurologic death. Strategies to minimize atelectasis and promote alveolar recruitment should be employed. Protective modes of ventilation should be used to achieve a target PaO 2 /FiO 2 ratio of >300. The pro­tective strategies of the ARDSNET goals of low tidal volumes (6–8 mL/kg) and low plateau pressures (<30 cm H 2 O) serve to minimize alveolar shear injury, volutrauma, and barotrauma [ 39 ]. Appropriate pressure control modes or newer modes such as airway pressure release ventilation can minimize lung injury and improve PaO 2 /FiO 2 ratios [ 40 ].
Pulmonary toilet maneuvers such as chest percussion, postural drainage, recruitment maneuvers, and serial bron­choscopy can also improve lung function. Protocols with built-in lung recruitment maneuvers of brief periods of increased positive end-expiratory pressure to 30 cm H 2 O have been shown to improve gas exchange and increase the number of suitable lungs for transplantation [ 41 ]. Bronchoscopy and lavage for microbiology is a routine part of the donation workup. Bronchoscopy allows for evaluation of individual lungs, as one may be suitable for transplant and the other injured from a process such as contusion or aspira­tion pneumonitis. Bronchial colonization or infection with bacteria or yeast is seen in up to 80 % of organ donors and correlates with lung recipient survival [ 42 ]. High endotra- cheal cuff pressures can minimize aspiration into the lungs, an important risk in this patient population with likely earlier neurologic injury and loss of cough refl ex [ 40 ].
Other proposals for interventions to optimize organ function prior to potential donation include the use of high- frequency chest wall oscillation for pulmonary optimization and inhaled nitric oxide to support cardiopulmonary function [ 43 , 44 ].
36 , 37 ].
Hypoperfusion of the juxtaglomerular cells of the kidney activates the renin-angiotensin-aldosterone axis, causing salt and water retention as well as vasoconstriction, which in turn can lead to compromised renal blood fl ow, glomerular and tubular injury, and ultimately renal insuffi ciency. This directly compromises kidney viability and post­transplantation function and underscores the need for active hemodynamic management in donors.
While dopamine administration is no longer recom­mended as a fi rst-line vasopressor in the management of the DNDD because of its tachycardic and pro-arrhythmic effects, transplanted kidneys that come from donors treated with low-dose dopamine are better able to withstand ischemic damage during cold preservation and have better graft func­tion post transplantation [ output to a minimum of 0.5 cc/kg/h, while avoiding the mas­sive diuresis of diabetes insipidus, is the goal of reno­protective resuscitation.
45 , 46 ]. The maintenance of urine

Hepatic System

While the overall infl ammatory process of brain death takes its toll less on the liver, hypernatremia (sodium >155 mmol) has been associated with increased rates of transplanted liver allograft loss [ 47 , 48 ]. It is theorized that hypernatremia pro- motes the infl ux of osmotic molecules into hepatocytes which then promote water infl ux and cell lysis when trans­planted into a eunatremic recipient.

Coagulation and Thermoregulation Disorders

Disorders of coagulation are a direct consequence of the release of thromboplastin, cerebrogangliosides, and plasminogen- rich substrate from traumatized brain tissue [ 49 ]. Hypothermia and acidosis, along with the dilution of clotting factors, fi brinogen and platelets, can contribute to a state of disseminated intravascular coagulation and uncon­trollable bleeding [ 50 ]. Massive transfusion protocols includ- ing the use of fresh frozen plasma, platelets, and cryoprecipitate are often required. Transfusion of packed red blood cells to a hematocrit >30 % for organ donors is recommended to maxi­mize end-organ oxygen delivery [ 35 ]. Hypothermia should be proactively addressed with patient warming devices, includ­ing heated intravenous fl uids and ventilated gases.

Renal System

Sympathetic storm and the subsequent cardiovascular col­lapse have a deleterious effect upon the renal system.

The Role of Protocols in Organ Donation

Because of the complexities involved in the caring for the critically ill patient and the numerous considerations for opti­mizing donation, it is useful to have written guidelines to
38 Organ Donor Management
447
Table 38.1 Sample checklist of donor management goals
End points Donor management goals Mean arterial pressure 60–110 mmHg Central venous pressure 4–10 mmHg Ejection fraction ≥50 % Arterial blood gas pH 7.3–7.55
/FiO 2 >300
PaO
2
Vasopressors ≤1 at low dose Serum sodium 135–155 mEq/L Serum phosphate >1.5 mEq/L Blood glucose ≤150 mg/dL Urine output ≥0.5 cc/kg/h over 4 h
direct the steps taken during the organ donation process. Most organ donors donate after neurological determination of death and may have been earlier managed with the goal of optimiz­ing brain tissue outcome. Many intensive care units have catastrophic brain injury guidelines (CBIGs), which are use­ful in guiding patients with neurological injuries to recovery.
For the potential donor with severe irreversible neurologic injuries, however, care shifts from maximizing neurologic recovery to the maintenance of the remaining organ systems. Often, there are confl icts about which organ systems to priori­tize as attempts to optimize one system may be deleterious to another. Unless the intensivist knows a priori that a particular organ will not be suitable for transplantation, one is faced with a delicate balancing act between the competing needs of sev­eral different organ systems. Therefore, the use of a checklist of standardized critical care end points, or donor management goals (DMGs), or aggressive donor management (ADM) pro­tocols, will be benefi cial in guiding care providers to optimize the number of organs suitable for transplant from donors. DMGs have been shown to lead to resuscitation of 92 % of organs that initially did not meet transplant criteria, and meet­ing DMGs prior to organ recovery is an independent predictor for achieving ≥4 organs transplanted per donor (OTPD) [ 51 , 52 ]. In one center, adoption of a protocol of ADM was associ- ated with an 82 % increase in the number of actual donors, a 71 % increase in the number of organs recovered, and an 87 % decrease in the number of donors lost from hemodynamic instability [ 53 ]. Because decreasing the number of donors lost from cardiovascular collapse increases the number of organs available for transplantation, the DMGs have been shown to be effective in improving donation outcomes. A sample check­list of donor management goals is shown in Table 38.1 .

Aggressive Resuscitation of Potential Donors

Optimal and aggressive critical care of the potential donor begins long before the declaration of death. To ensure that the donor organs would be of utmost benefi t to the recipients,
efforts must be made to ensure optimal organ status through the process of referral, consent, and organ recovery. Because brain death is associated with profound physiologic altera­tions that result in diffuse regulatory disturbances and wide­spread cellular injury, severe alterations in metabolism, endocrine function, and coagulopathy are commonly observed in potential donors [ 54 ]. The following compo- nents of resuscitation would be useful in addressing some of these responses.

Hemodynamic Monitoring

In order to guide resuscitation and support, a recommended practice is to institute some sort of hemodynamic monitor­ing. Placement of a pulmonary catheter upon ICU admission has been recommended in the past and has been shown to improve donor outcomes including higher number of recov­ered organs [ 55 ]. This is attributable to the maintenance of optimal cardiac output through the donation process. Echocardiography is routinely used to assess the left ven­tricular function of a potential donor heart. In the setting of left ventricular dysfunction, pulmonary artery catheter­directed management can maximize donor recovery. It has been shown that properly managed younger hearts with left ventricular dysfunction can markedly recover function after transplantation [ 56 ].
Recently, the use of noninvasive methods that measure pulse pressure variations has been introduced to the care of organ donor [ 57 ]. The variations in pulse pressure have been used as a measure fl uid responsiveness. A variation in pulse pressure of up to 20 % has been shown to be a very sensitive measure of fl uid responders.

Aggressive Hemodynamic Management

Due to severe intracranial swelling, there is disruption of the function of the posterior pituitary leading to low or absent levels of vasopressin in up to 90 % of organ donors [ consequence of this is cardiovascular collapse and hypoten­sion with neurogenic diabetes insipidus (DI) occurring in nearly half of all DNDDs [ 31 , 59 ]. Without adequate inter- vention, this could result in a massive hypoosmolar diuresis and electrolyte abnormalities. The loss of intravascular vol­ume leads to profound hypotension. It is therefore a high pri­ority to maintain optimal fl uid status, through aggressive fl uid management, in order to preserve perfusion.
Aggressive fl uid resuscitation is recommended to main­tain a CVP of 8–12 mmHg and a systolic arterial pressure of between 90 and 140 mmHg [ 60 ]. Of note, however, in lung donors, it has been shown that maintenance of a CVP between 8 and 10 mmHg may result in an increased alveolar
58 ]. The
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O.A. Olufajo and A. Salim
arterial oxygen gradient when compared with potential donors maintained between 4 and 6 mmHg [
61 ]. The target
mean arterial pressure should be maintained above 70 mmHg throughout resuscitation.

The Role of Vasopressin

After the achievement of adequate fl uid resuscitation, vaso­pressin should be considered as the fi rst choice hemody­namic therapy. Vasopressin (or antidiuretic hormone, ADH) acts upon its V1 subtype receptors found in vascular smooth muscle which are responsible for its vasopressor activity, as well as the V2 subtype found in renal collecting duct epithe­lia which increases water permeability and is responsible for its antidiuretic activity. 1-Desamino-8-D-arginine vasopres­sin (DDAVP) is highly selective for the V2 subtype alone and may be used as an adjunctive treatment for DI.
Administration of vasopressin acts to inhibit the diuresis of DI and the resultant hypotension due to its catecholamine­sparing effects and ability to counteract vasodilatation. Vasopressin is also usually seen to be defi cient in donors who require catecholamine support [ 59 ]. It has replaced dopamine as the fi rst-line of treatment in treating hypotensive patients and is associated with improved organ yield [ 62 ].

The Role of Thyroxine

The hemodynamic instability in DNDDs is partly due to low circulating levels of thyroxine. These low levels lead to diminished production of adenosine triphosphate, causing myocardial dysfunction, accumulation of lactate, and resul­tant circulatory collapse [ 29 , 33 , 54 ]. The etiology of this functional “hypothyroid state” is poorly understood, but may be a result of lower than normal thyroid-stimulating hormone levels caused by the irreversible damage to the hypothalamus and pituitary from ischemia. Another expla­nation is a decrease in the peripheral conversion of T4 to its more potent analog T3, similar to the euthyroid sick syndrome [ 63 , 64 ].
Therapeutic replacement with T3 has been associated with complete reversal of anaerobic metabolism and subse­quent stabilization of cardiac function when applied to DNDDs [ 48 , 65 ]. It has been demonstrated that hemodynam- ically unstable organ donors require a signifi cant decrease in, or complete lack of, vasopressor support after T4 administra­tion [ 66 ]. In addition, the use of thyroid hormone has been associated with signifi cant improvements in cardiovascular status, reductions in inotropic support, and decreases in donors lost from cardiac instability [ 33 , 66 ]. In a study of DNDDs, T4 administration was associated with signifi cantly more organs procured per donor group (3.9 ± 1.7 vs. 3.2 ± 1.7, P = 0.048) [ 67 ].
A “T4 protocol” is recommended in situations where there are increased vasopressor requirements. This protocol consists of one ampule 50 % dextrose, 2 g of Solu-Medrol, 20 units regular insulin, and 20 mcg of thyroid hormone (T followed by a continuous infusion of 10 mcg/h [
68 ].
),
4

The Role of Insulin

After the development of neurologic death, insulin levels have been measured to decrease to 50 % of baseline at 3 h, and even further to 20 % at 13 h [ 69 ]. The resulting hypergly- cemia has profound effect on allograft function. Hyperglycemia is well known to impact renal function. Protein glycosylation from uncontrolled glucose levels pro­motes tissue damage. In addition, osmotic diuresis resulting from glucose spillage may overtax renal medullary function and contribute to the diuresis seen in brain death.
Inadequate glucose control among potential donors is associated with declining renal function prior to organ recov­ery [ 70 ]. This may be attributable to the up-regulation of glu- cose transporter 1 and 2 expression, impaired autoregulation of glomerular capillary pressure, and increased production of multiple infl ammatory molecules [ 59 , 71 , 72 ].
Keeping glucose levels under 150 mg/dL using parenteral insulin yields renal allografts with lower creatinine levels [ 70 ]. Several studies have demonstrated concern for exceeding tight glucose control leading to hypoglycemic episodes, but in the setting of neurologic death, the concern for brain injury or stroke resulting from hypoglycemia no longer applies. Therefore, strict glucose control to attain levels from 80 to 110 mg/dL may lead to improved renal allograft function.

The Role of Steroids

The systemic responses known to follow brain death include a massive infl ammatory response characterized by elevations in plasma levels of infl ammatory mediators such as interleukin- 6 and tumor necrosis factor. This increase in cytokine levels can be detrimental to the function and survival of grafts from poten­tial organ donors [ 73 ]. Increased plasma levels of interleukin-6 have been shown to be associated with decreased graft survival [ 74 ]. Animal studies have demonstrated the effect of neuro- logic death upon ICAM-1 expression and leukocyte infi ltration into peripheral organs, as well as a time-dependent progression of immune-mediated organ dysfunction [ 75 ].
Steroids exert anti-infl ammatory effects by decreasing levels of serum cytokines [ 76 ]. Decreases in serum cyto- kines can lead to improved post-transplant organ viability [ 77 ]. Steroids also act to overcome a relative adrenal insuf- fi ciency as a result of the stress of traumatic brain injury
58 ]. The use of steroids has been shown to improve pul-
[ monary function and lead to the utilization of lungs which
38 Organ Donor Management
Fig. 38.1 Algorithm
for optimal donor management
449
Early identification of potential organ donor
ICU admission and management by dedicated ICU team
1. Advanced hemodynamic monitoring to optimize perfusion (Swan-Ganz catheterization, echo, stroke volume variation etc.)
2. Aggressive fluid resuscitation
T4 protocol
administration
Diabetes insipidus– Desmopressin; Vasopressin utilization if pressors reruired
MAP <70
MAP <70
Vasopressors
MAP ≥70
Supportive
care
Early identification and treatment of brain-
death related complications interventions
Neurogenic Pulmonary Edema – Aggressive optimization of pulmonary function; utilization of High Frequency Precussive ventilation as indicated
MAP ≥70
Supportive
care
Coagulopathy – Aggressive correction (FFP, Cryoprecipitate, Factor VII utilization)
SIADH – Salt replacement with hypertonic saline, fluid restriction when appropriate
may have been previously deemed unacceptable for trans­plantation [ 78 ].

Managing Potential Complications

Brain death is associated with numerous complications such as disseminated intravascular coagulation (DIC), diabetes insipidus (DI), neurogenic pulmonary edema (NPE), hypo­thermia, and cardiac arrhythmias [ 68 ]. There are major swings in various hormones such as cortisol, vasopressin, thyroxine, and insulin. The effects of these hormones are sometimes syn­ergistic and may cause dramatic changes in the physiological status of the potential donor. Understanding and anticipating
these complications is important for the managing physician. Early identifi cation of these complications coupled with ade­quate supplementation is necessary to maintain hormonal bal­ance, hemodynamic stability, and organ perfusion. Figure 38.1 shows the complex interplay of all the various complications and interventions to ensure optimization of organ recovery.

Considerations During Organ Recovery

Once the declaration of death has been made and all neces­sary interventions have been taken to optimize the donor organs, it is important to put certain things into consideration during organ recovery.
450
O.A. Olufajo and A. Salim
Although individuals could be brain dead, they may still have hemodynamic responses to certain stimuli mediated by the spinal refl exes or adrenal medulla stimulation [
79 , 80 ].
Also, the determination of brain death does not preclude the possibility of spinal refl exes due to painful stimuli [ 14 ]. Therefore, chemical neuromuscular paralysis is usually administered to block muscle twitching.
All operating staff are expected to understand the need for timeliness in their operations and they will need to work simultaneously and effi ciently. Except for cases of lung recov­ery where ventilatory support is needed, the anesthesiologist only needs to ensure aortic cross-clamping during the recov­ery process. Communication between all staff is necessary, and the leader of the operation should be well outlined in order to ensure smooth running of the procurement process.
Conclusion
Organ donation is an important process that ensures the
availability of organs for individuals whose only opportu-
nities for survival lie on receiving transplants. Efforts to
ensure the success of every step of the process are there-
fore of utmost importance. Recommendations for all
institutions that care for the critically ill patient include
incorporating skilled team-driven approaches to the con-
sent process, protocol- guided steps for the management
of potential donors, and adequate balance of the physio-
logical status of donors. Optimal hemodynamic manage-
ment, multidrug hormone replacement therapy, and
effi cient organ recovery are strategies to improve organ
yield and the viability of donor organs.

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