Brain Death & Organ Procurement

58 AJN t March 2007 t Vol. 107, No. 3 http://www.nursingcenter.com

The need for donor organs far outstripstheir availability. More than 94,000people nationwide are on waiting listsfor organs, yet from January throughSeptember 2006, just 22,014 transplan-

tations were performed, according to the UnitedNetwork for Organ Sharing (UNOS).1 Until recently,the donation rate among potential donors was lessthan 50%: of 14,000 potential donors identified in2002, fewer than half (46%) donated organs.2 In aneffort to improve that rate, the U.S. Department

Brain Death and

Kathleen M. Z. Peiffer is a student in the master’s program innurse anesthesia in the College of Nursing and HealthProfessions at Drexel University, Philadelphia, and a per diemnurse in the surgical ICU at Holy Spirit Hospital, Camp Hill,PA. Contact author: [email protected]. The author of thisarticle has no significant ties, financial or otherwise, to anycompany that might have an interest in the publication of thiseducational activity.

Organ ProcurementNursing management of adults with brain injury is crucialto the viability of donor organs.

of Health and Human Services and hospital andtransplantation leaders recently formed the OrganDonation Breakthrough Collaborative. Between2003 and 2005, the organ donation rate rose 18%;but it’s still far short of what experts believe is possible.2

Clinicians bear part of the responsibility for this.If interventions after brain death are not aggressiveand timely, the body’s tissues and organs cannot beused for transplantation. Indeed, when a patient is apotential or designated organ donor, the nursingcare required may be even more rigorous after braindeath than before. (At my facility, the nurse–patientratio for brain-dead organ donors may be as high as3:1.) Consider this: one organ donor can provide asmany as 50 different organs and tissues to recipi-ents.3 Yet although essential to the successful recov-ery and long-term survival of viable organs,4 donormanagement is considered “one of the most neglectedareas of transplantation.”5

The transition from caring for the living to caringfor the brain dead (as potential organ donors) canbe difficult for nurses. How does your role changewhen you begin working with a brain-dead patientand an organ-procurement coordinator?

IDENTIFYING ORGAN DONORS: THE NURSE’S JOB Patients with severe brain injuries (as can resultfrom trauma, subarachnoid hemorrhage, or braintumor) are monitored closely by nursing staff. It’stherefore often the nurse who first recognizes signsof decompensation (such as a lack of eye, verbal,and motor responses according to the GlasgowComa Scale and the absence of ventilatoryattempts) and begins the process of determiningwhether the patient is a potential organ donor.Indeed, frequent neurologic assessments to evaluatefor signs of decompensation should be made before

By Kathleen M. Z. Peiffer, BSN, RN, CCRN

Overview: Patients with severe brain injuries (as can result fromtrauma, subarachnoid hemorrhage, or brain tumor) are moni-tored closely by nursing staff. It’s often the nurse who first recog-nizes clinical signs of decompensation and begins the process ofdetermining whether the patient is a potential organ donor.When a person is declared brain dead, it’s the nurse who main-tains hemodynamic stability so that donor organs remain viable.It’s therefore crucial for nurses to know how brain death is deter-mined in adults and how potential organ donors are identified,and to know the major physiologic changes that occur uponbrain death, as well as essential nursing interventions.

Continuing Education3.5HOURS

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a diagnosis of brain death, in order to protect tissueand organ viability. (See Determining Brain Death,page 60.)

Typically, the nurse first informs the attendingphysician, the neurologist, or the neurosurgeon ofthe patient’s decompensation. Depending on thefacility’s protocol, either the nurse or another clini-cian may then contact the local organ-procurementorganization (OPO) to say that there is a case thatmay soon involve them. Ideally, the local OPOshould be contacted when brain death is imminent,before a declaration of brain death has been made.25

However, if the OPO hasn’t been notified, that isdone once brain death is declared. (For more on the history and responsibilities of OPOs, see Organ-Procurement Organizations, page 63.)

When brain death appears imminent, if not sooner,the physician will inform the family of the severity ofthe patient’s condition, and nurses will provide addi-tional support and information, as will clergy andsocial workers. Either the physician or the OPO coor-dinator may bring up the subject of organ donation;

this can happen either when brain death is immi-nent or after it has been declared. (If the patient hasjust been declared brain dead, it’s important to givethe family time to understand the diagnosis and toabsorb their loss before the prospect of organ dona-tion is discussed. The length of time needed willvary from case to case.)

Once the attending physician has declared thetime of brain death, the local OPO coordinator—who is often a nurse or physician assistant19—assumes responsibility for the donor’s management,which includes directing clinical nursing care. TheOPO coordinator will direct the nursing staff tomaintain hemodynamic stability of the body whilethe family reaches a decision about organ donation.If the family opts for donation, the OPO coordina-tor continues to direct care until the organs and tis-sues are released to representatives of the designatedrecipients’ facilities.

The OPO coordinator typically leads the discus-sion about organ donation with a potential donor’sfamily, with staff nurses providing emotional sup-

Illustr

atio

nsby

Anne

lisa

Ochoa

A

B

A) Subdural hematoma in the frontal lobe (not a cross-section; only skull has been removed)B) Cross-section showing resulting brain swelling and herniation through the foramen magnum


Determining Brain Death

In 1968, recognizing that advances in cardiopulmonaryresuscitation and life support were keeping hearts beat-

ing even when catastrophic brain damage had occurred,the Ad Hoc Committee of the Harvard Medical School setforth a new definition of death: irreversible coma.6 Thethree primary criteria for diagnosis were total “unreceptiv-ity and unresponsivity” to external stimuli, a complete lackof spontaneous muscular movement or respiration, and“the absence of elicitable reflexes.” A fourth, confirmatorycriterion—an isoelectric (flat) electroencephalogram(EEG)—was also named. With some refinements, thesecriteria have remained the standard.

In 1981 a group of medical consultants to thePresident’s Commission for the Study of Ethical Problems inMedicine and Biomedical and Behavioral Research pub-lished Guidelines for the Determination of Death, whichclarified the need to confirm both the cessation of all brainfunction and the irreversibility of that condition, and speci-fied that drug intoxication, hypothermia, and shock mustbe ruled out.7 (This was the basis for the UniformDetermination of Death Act of 1981, a model statuteintended to lessen legal “confusion”8; brain death legisla-tion has since been enacted in all 50 states.9) Morerecently, in 1994 the American Academy of Neurology(AAN) defined brain death as “the absence of clinicalbrain function when the proximate cause is known anddemonstrably irreversible,” summarized practice parame-ters for determining its occurrence in adults, and discussedspecific tools and confirmatory tests.10

When brain death occurs. Approximately 1% of alldeaths occur first in the brain rather than in the cardiopul-monary system, according to one expert.11 The most com-mon causes of brain death in adults are trauma andsubarachnoid hemorrhage, according to reviews12, 13; othercauses include infection such as meningitis or encephalitisand brain tumor.

The initial trauma sets off a cascade of events.14-19 Tissuedamage and fluid blockage or excessive fluid accumulationresult in increasing intracranial pressure, ischemia, andbrain cell death. When ischemia reaches the brain stem, ittriggers a massive release of catecholamines—an eventknown as an autonomic or sympathetic “storm”—whichleads to an immediate, intense Cushing response (increasedsystemic vascular resistance and hypertension) lasting about15 minutes. Compression of the vasculature and worseningischemia cause infarction of brain tissue. Venous engorge-ment and brain swelling cause the brain to herniate throughthe foramen magnum, further inhibiting cerebral perfusion.Inflammation and edema progress and intracranial pressurerises even more, culminating in a complete loss of cerebralblood flow.

As the sympathetic storm subsides, the initial Cushingresponse is followed by a brief period of stability. Then asecond hemodynamic collapse occurs.17 This collapse ischaracterized by a profound loss of vascular tone and asubsequent loss of peripheral resistance, bradycardia,hypotension, plummeting cardiac output, and systemic

organ hypoperfusion.17, 20 Although opinions vary as to thecause, some studies attribute the second collapse to a sec-ond catecholamine release.17, 21

Confirmatory findings on neurologic assessment. Incases of imminent or suspected brain death, neurologicassessment includes evaluating the level of coma or un-responsiveness, testing brain stem reflexes, and assessingfor apnea.13, 22 The following findings, which are also out-lined in Brain Death: Confirmatory Findings onNeurologic Assessment, page 65, confirm brain deathexcept in cases of hypothermia, drug intoxication, or con-founding conditions such as acute metabolic or endocrinedisturbances, all of which may be reversible.13, 22

Level of coma or unresponsiveness. Although not allpatients who are comatose progress to brain death, peo-ple who are brain dead will be unresponsive to verbaland painful stimuli. The Glasgow Coma Scale tests the lev-els of verbal response to spoken stimuli (such as thepatient’s name) and eye and motor response to both spo-ken and painful stimuli (such as pressure applied to thesupraorbital nerve [1a] or nail beds [1b]). Total scoresranging from 3 (lowest) to 15 (highest) are possible. Ascore of 3 indicates profound unresponsiveness.

Respiratory findings. Normal respiration occurs whenthe respiratory center of the brain (an area within themedulla oblongata and the pons) responds to rising serumcarbon dioxide levels. In a healthy brain, a partial pres-sure of carbon dioxide (PaCO2) level above 60 mmHgprompts respiration. In a patient who is brain dead, thisresponse is absent.

To test for central apnea, the patient is taken offmechanical ventilation and 100% oxygen 6 L/min is deliv-ered by nasal cannula for as long as eight minutes whilethe patient is observed for signs of attempted breathing.22

An arterial blood gas sample is also obtained and thePaCO2 level measured to ensure that carbon dioxide lev-els are adequate to trigger respiration; if a PaCO2 levelgreater than 60 mmHg and no signs of attempted breath-ing are observed, the apnea test is confirmatory.

Ocular reflex findings. The pupillary reflex is tested byshining a light into the patient’s eyes (2); normally the pupils

1a

1b


constrict. If the pupils remain fixed and dilated at a sizegreater than 4 mm, this is confirmatory of brain death(except in cases of preexisting pupillary abnormalities).22 Theoculovestibular test involves injecting about 10 mL of icewater or saline into the ear canal (3). Ordinarily the patient’seyes will turn toward the stimulated ear. If no eye movementoccurs, this test is confirmatory. In the oculocephalic test (alsoknown as the “doll’s eyes” test), the clinician moves thepatient’s head from midline to each side in turn (4). Normallythe patient’s gaze remains on a specific point, with the eyesmoving away from the direction of the head turn in order tomaintain that gaze. In patients without this reflex, the eyesremain fixed at midline despite head movement.

Other reflexes. The corneal reflex is tested by gentlytouching a sterile, cotton-tipped swab to the patient’scornea and observing for a reaction (blinking or eye move-ment [5]). Although the corneal reflex may be blunted nor-mally (for example, in contact-lens wearers), it will beabsent in correlation with other assessment findings insomeone who is brain dead. The cough reflex may betested by performing deep bronchial suctioning through the patient’s endotracheal tube; a lack of response is

confirmatory (6). The gag reflex can be assessed either bymanually manipulating the endotracheal tube or by touch-ing a cotton-tipped applicator to the posterior pharynx,although as one article states, “the results can be difficultto evaluate in orally intubated patients.”22

Confirmatory laboratory tests are optional in diagnos-ing brain death in adults. However, the AAN recommendssuch tests “in patients in whom specific components of clini-cal testing cannot be reliably performed or evaluated,”such as those with severe facial trauma.10 According to theAAN, the most sensitive test is cerebral angiography, butthe contrast dye used can render organs useless for trans-plantation. With patients who are potential or designatedorgan donors, electroencephalography or cerebral scintig-raphy is preferred. If the patient is brain dead, an EEG willreveal an isoelectric pattern. Cerebral scintigraphy may beperformed to verify the absence of cerebral blood flow23, 24;its advantages are that it can be performed at bedside anddoes not pose a threat to organs.23 Other confirmatory testsmay include transcranial Doppler ultrasonography andsomatosensory evoked potentials (responses evoked byelectrical stimulation of peripheral nerves).

2 3

4

5 6

and compares this information with a national data-base of patients in need of organs that is maintainedby UNOS’s Organ Center. Patients awaiting anorgan are compared with the donor in areas such asblood and tissue type, weight, age, and urgency ofmedical need, as well as the length of time the patienthas been on the waiting list. Proximity to the donoris a major factor as well.

NURSING IMPLICATIONS OF BRAIN DEATH The brain is in charge of the proper functioning ofall body systems. In a patient who is brain dead,therefore, keeping the donor organs viable involves,in a sense, fooling the body into thinking the brainis still functioning. The nurse’s goals in this regardare determined by the following changes as theytake place in various organ systems. (It should benoted that because there is scant research in the lit-erature pertaining to humans, most of the researchcited in this article was conducted in animals.)

The brain. Normal responses to any sympatheticstimulation include increases in blood pressure,heart rate, cardiac contractility, minute ventilation(the volume of air per minute that moves in and outof the lungs), and peripheral vasomotor tone.Catecholamines also “promote platelet aggregation,accompanied by serotonin release.”26 Serotonin hasvasospastic effects on coronary arteries. Bothplatelet aggregation and vasospasticity reduce coro-nary artery blood flow.

Almost immediately after brain death, activationof the sympathoadrenal axis causes a great increasein the levels of circulating catecholamines.15, 17, 18

During this sympathetic storm, circulating dopa-mine levels have been shown to increase by as muchas 800%, epinephrine levels by as much as 700%,and norepinephrine levels by up to 100%.17, 18 Theeffects can be catastrophic to human tissue.Hypercapnia resulting from the cerebral hypoperfu-sion that follows brain death also stimulates cate-cholamine release.15

Declining ADH. Infarction of the tissue of thehypothalamus eventually results in a decline in cir-

port. Many people identify themselves as organdonors on their driver’s license. Because that infor-mation can be useful in discussing the patient’swishes, the coordinator often contacts the state’sdepartment of motor vehicles before approachingthe family, to determine whether the patient has des-ignated herself or himself a donor. However, in moststates it’s the family that makes the final determi-nation. (For more on state regulations, see www.donatelife.net.)

The OPO coordinator is responsible for docu-menting and communicating orders aimed at main-taining organ viability, coordinating organ allocation,contacting organ recovery teams from the designatedrecipients’ facilities, and scheduling the operatingroom for the recovery of organs. From this point on,all orders are written by the coordinator; the attend-ing and consulting physicians are no longer involved.

The OPO coordinator will take a complete his-tory of the donor (both from the information in thepatient’s chart and from staff nurses and physiciansand possibly family members). Previous laboratoryresults will be evaluated, and several additionalstudies (such as liver and kidney function studiesand blood tests to assess pancreatic enzyme and thy-roid hormone levels) are often ordered to guidetreatment. A central line or pulmonary artery

catheter may be inserted for hemodynamic monitor-ing.5 The additional testing is labor intensive; oftenthe donor’s condition deteriorates so rapidly thatadditional nurses are needed to perform stabilizingtasks such as the monitoring of fluids and vital signsand the administration of drugs and fluids.

The staff nurse reports all aberrancies in thedonor’s condition to the OPO coordinator, who, inturn, provides orders for their correction. If the coor-dinator isn’t available, the nurse may make treatmentdecisions based on a critical pathway designated bythe coordinator. (One such pathway is UNOS’sCritical Pathway for the Organ Donor [www.unos.org/resources/pdfs/CriticalPathwayPoster.pdf].)The coordinator reviews the laboratory test resultsfor the donor’s blood type and other serum markers


Brain Death Criteria1. Condition has a known cause.2. Condition is irreversible.3. Neuromuscular blocking agents and central

nervous system depressants are absent.4. Temperature is higher than 35°C (95°F).5. Patient is apneic.6. Patient is areflexic.

Ad Hoc Committee of the Harvard Medical School to Examine theDefinition of Brain Death. JAMA 1968;205(6):337-40; The QualityStandards Subcommittee of the American Academy of Neurology.Neurology 1995;45(5):1012-4.

When a patient is a potential or

designated organ donor, the nursing

care required may be even more

rigorous after brain death than

before such death occurs.

culating antidiuretic hormone (ADH; also calledarginine vasopressin); this in turn affects the kid-neys’ ability to concentrate urine and leads to dia-betes insipidus.18, 20 The result is severe diuresis withaccompanying hypernatremia, hyperosmolarity,and dehydration in up to 80% of cases of braindeath.16

Declining T3 and T4. Ordinarily, the hypothala-mus stimulates the pituitary to secrete thyroid-stimulating hormone (TSH), which prompts thethyroid to release triiodothyronine (T3) and its part-ner hormone, thyroxine (T4). After brain death, T3levels drop as a result of infarction in the tissues ofthe hypothalamus and pituitary.17 T4 levels appearto decline as well; Chen and colleagues found in astudy in dogs that levels of both T3 and T4 declinedsignificantly after brain death (although remainingwithin normal limits) and suggested that suchdecreases “could have contributed to post–braindeath cardiac dysfunction.”18 Other effects are not aswell established. The decrease in T3 has been associ-ated with inhibited mitochondrial function, resultingin poor cardiac contractility, anaerobic metabolism,and lactic acidosis following brain death.16 However,Chen and colleagues stated that although anaerobicmetabolism and metabolic acidosis were observedimmediately after brain death in their canine study,these were not associated with declining thyroid hor-mone levels.18

Loss of thermoregulation. The hypothalamusregulates body temperature through a homeostaticfeedback mechanism. In a healthy person, if thebody becomes too hot, the hypothalamus promptsvasodilation, resulting in sweating. If the bodybecomes too cool, the hypothalamus prompts vaso-constriction in the skin, shivering, and piloerection,resulting in heat retention.

Systemic hypothermia—heat loss secondary tomassive peripheral vasodilation and loss of ther-moregulatory control by the hypothalamus—isoften seen after brain death.16 Without intervention,the donor’s body eventually assumes ambient tem-perature; therefore, thermoregulation is a priority.20

Nursing implications. Treatment of diabetesinsipidus involves fluid replacement to offset hourlyurine output and often includes an IV vasopressin(Pitressin) infusion as well. The nurse should be dili-gent in observing urine output (at a minimum, 0.5mL/kg/h) to determine whether the patient needsfluid resuscitation, a vasopressin infusion, or both.

According to UNOS’s Critical Pathway for theOrgan Donor, the following are essential to hor-monal management in potential donors: T34 microgram IV bolus followed by an infusion of 3 micrograms per hour; vasopressin 1 unit IV bolusfollowed by an infusion of 0.5 to 4 units per hour,adjusted to 800 to 1200 dyne/sec/cm5 for systemicvascular resistance; methylprednisolone (Solu-

Medrol) 15 mg/kg IV bolus, which may be repeatedin 24 hours if needed; and an insulin drip of 1 unitper hour adjusted to maintain blood glucose atbetween 120 and 180 mg/dL.25 Blood glucoseshould be measured hourly to determine the needfor coverage with regular insulin or the initiation ofan insulin drip.

Following the loss of thermoregulation, an IV

fluid warmer, a forced-air room warming device,and warming blankets should be used to maintainthe donor’s body temperature at 36.5°C to 37.5°C(97.7°F to 99.5°F).25

The heart. The normal heart is innervated byboth the sympathetic and parasympathetic branches


Organ-ProcurementOrganizationsThe National Organ Transplantation Act of 1984 cre-

ated a multidisciplinary task force to study organdonation, procurement, and transplantation. It alsoestablished a national organ sharing system, the OrganProcurement and Transplantation Network (OPTN),which has been administered since its inception by theUnited Network for Organ Sharing (www.unos.org), anational nonprofit organization. The OmnibusReconciliation Act of 1986 implemented many of thetask force’s recommendations, including that organ-procurement organizations (OPOs) be members of theOPTN. And in 1998, the Department of Health andHuman Services’ Health Care Financing Administrationissued Hospital Conditions of Participation for OrganDonation, which delineated criteria for reimbursementunder Medicare and Medicaid. To be in compliance,hospitals must “have an agreement with an OPO,”“notify OPOs in a timely manner about patients whohave died or whose death is imminent,” and collaboratewith the OPO “to ensure every family is offered theoption of donation.”9

Most OPOs are independent, although a few are hospi-tal based. An OPO team doesn’t recover organs itself; thatis handled by organ recovery teams from the designatedrecipients’ facilities. An OPO team’s responsibilities typi-cally include9:

• providing public and professional education on thedonation process.

• evaluating the “medical suitability” of potentialdonors.

• with hospital staff, offering families the option ofdonation.

• managing and coordinating organ procurement andallocation.

• providing support to donor families.• maintaining documentation.

Another study found evidence to suggest that themyocardial damage that occurs during brain death“may be related to endogenous catecholaminerelease (possibly resulting in increased calciumuptake by the myocardial cells), inducing variousforms of myocyte necrosis.”31 The calcium ion Ca++

is responsible for the normal excitation and contrac-tion of myocardial tissue that results in the pumpingaction of the myocardium. After brain death, theincreased calcium uptake desensitizes the cardiacmyofilaments to calcium, compromising cardiac con-tractility and output.32

The sympathetic storm also results in increasedmyocardial adenosine and lactate levels, which areassociated with myocardial dysfunction andmyocardial ischemia.16, 26, 33

Accumulation of neutrophils. In a canine study byChen and colleagues, they found that “irreversiblefocal injuries and myocytolysis” occurred soon afterbrain death.18 They also observed an “accumulationand infiltration of neutrophils and subendocardialhemorrhage,” as well as edema. Hemorrhage andedema may adversely affect the ability of the organto function fully after transplantation.

Altered gene expression. Yeh and colleaguesspeculated that after brain death, “fluctuations incatecholamine levels might act as important signalsin the subsequent alterations” in the expression ofmyocardial genes that regulate functions such ascontractility and growth.34 They hypothesized thatthe resulting malfunctions may be the cause of rejec-tion or dysfunction of the donor heart after trans-plantation. In a study with rabbits, they found that“brain death–associated increases in expression ofmyocardial gene products” could be suppressed byexogenous sympathetic blockade.34 Treatment withb-adrenergic blockers such as metoprolol (Lopressor)and labetalol (Normodyne, Trandate) is standard.

Nursing implications. Exogenous catechol-amines, including epinephrine and dopamine, areoften used as inotropic agents to maintain bloodpressure and systemic perfusion. After brain death,epinephrine is usually infused at a standard doserange of 0.05 to 1 micrograms per kilogram perminute; dopamine is infused at a standard doserange of 5 to 10 micrograms per kilogram perminute. It’s imperative that the potential donor’sactual, not estimated, weight be used in determiningthe infusion dosage. Some OPO coordinators maywant to estimate current weight by averaging thepatient’s weight on admission and her or his lastknown weight. Patients often become severely edem-atous during an ICU stay, with consequent andsometimes marked increases in body weight. Thisedema may dramatically change the effect of vaso-pressors from therapeutic to toxic.

The OPO coordinator should be notified of heartrate, blood pressure, or central venous pressure lev-

of the autonomic nervous system. Sympathetic stim-ulation of both the sinoatrial (SA) and the atrioven-tricular (AV) nodes originates in the medullaoblongata. The sympathetic fibers in the heartrelease norepinephrine, increasing heart rate andcontractility. Parasympathetic stimulation of the SAand AV nodes also originates in the medulla throughcranial nerve X (the vagus nerve). The parasympa-thetic fibers release acetylcholine, decreasing heartrate and contractility. Cranial nerve IX (the glos-sopharyngeal nerve) is also responsible for stimula-tion of cardiac events. These nerves are linkedthrough connections to baroreceptors in the carotidarteries, controlling heart rate variability and arterialpressure.

After brain death, the cardiovascular system is nolonger under autonomic control.27 The arterialbaroreceptors that once allowed for automatic reg-ulation of blood pressure and heart rate are nolonger functional.28 This “uncoupling” of the auto-nomic and cardiovascular systems is believed to beresponsible for the eventual cessation of cardiacfunction after brain death.27 During the firstCushing response, “exaggerated uneven peripheralvasoconstriction” causes areas of hypoperfusion inorgan vasculature.15 However, the loss of autonomiccontrol soon causes “a decline in the sympatheticoutflow to the blood vessels,”28 leading to vasodila-tion. A second hemodynamic collapse causes fur-ther systemic vasodilation or vasoplegia, decreasingpreload, adversely affecting afterload, and furthercompromising cardiac output.17, 29

Increased catecholamines. Even in an adequatelyperfused heart, high catecholamine levels willdecrease the myocardial cells’ ability to pump effec-tively.30 Commenting on earlier studies, Herijgersand colleagues observed that “the severity of themyocardial damage is correlated with the amountof catecholamines released at the moment of braindeath.”26 Catecholamines also are associated withplatelet aggregation and the release of serotonin;this study suggests that brain death may causemyocardial damage through vasospasm caused bythe effects of serotonin release.26


‘Uncoupling’ of the autonomic

and cardiovascular systems is

believed to be responsible for

the eventual cessation of cardiac

function after brain death.

els that vary from limits established in the criticalpathway being used. Diagnostic evaluation of thepotential donor’s heart may be necessary to deter-mine its viability for transplantation. Tests such asechocardiography, transesophageal echocardiogra-phy, or cardiac catheterization may be necessary in older donors or those with concurrent illnesses inorder to visualize valves, heart wall motion, andoverall function. (Although older age or a history ofillness does not necessarily preclude donation, eachcase is evaluated on its own merits and at the coor-dinator’s discretion.)

The lungs. Breathing is controlled by the respira-tory center of the brain, an area located in themedulla oblongata and pons. In cases of traumaticbrain injury, cerebral inflammation and edemacause infarction of the tissues of the respiratory cen-ter.15, 16, 35 Central apnea results.6

The sympathetic storm following brain death hasdirect, detrimental effects on lung tissue. Increasingsystemic hypertension and left atrial pressure resultin elevated pulmonary capillary pressures and sub-sequent endothelial damage to these capillaries.16

Their permeability increases and fluid leaks into thealveoli and interstitium of the lungs. Fluid resuscita-tion of a patient who is hemodynamically compro-mised further exacerbates pulmonary edema.16

Potential donors in whom oxygen saturation of95% or greater on 100% oxygen cannot beachieved or maintained, or those in whom lung tis-sue viability is questionable, may undergo bron-choscopy so that lung tissue can be visualized todetermine its viability for transplantation.According to UNOS’s critical pathway, a state ofmild respiratory alkalosis (partial pressure of car-bon dioxide between 30 and 35 mmHg) is prefer-able for potential donors.25

Nursing implications. Peak airway pressuresshould be maintained at less than 30 cm H2O.25

Accordingly, although ventilatory settings will becontrolled by the OPO coordinator and the respira-tory therapist, the nurse will monitor tidal volumesdelivered to the patient, the inspiratory flow rate,and the fraction of inspired oxygen.

The liver. Blood flow to the liver has been foundto decrease after brain death, but the implications ofthis are unclear. One study found that “morpho-logic change in the liver was slight” and that “theliver remained viable for as long as six hours follow-ing brain death,”36 while another study found thatliver functions were impaired.37 The hyperosmolar-ity associated with diabetes insipidus has been cor-related with hepatocyte destruction and alteredhepatocyte mitochondria.38

The shift to anaerobic metabolism leads to adepletion of liver glycogen.20 Organs must delve intotheir own glycogen stores for the energy necessaryto carry out normal cell functions; once these are

depleted, the body begins breaking down fat, lead-ing to lactic acidosis.

Nursing interventions include frequent assess-ment for diabetes insipidus, with treatment accord-ing to status, and fluid replacement according to theparameters established by the OPO coordinator.

The pancreas. Insulin is normally secreted by thebeta cells of the pancreas in response to blood glucoselevels. Cranial nerve X also stimulates the productionof pancreatic secretions. A study by Obermaier andcolleagues determined that brain death “causes sig-nificant pathophysiological alterations in the pan-creas,” including deterioration of pancreaticmicrovasculature, inflammation, and histologic dam-age.39 Each of these sequelae plays a role in disruptingbeta cell functioning, ultimately destroying the pan-creas’s ability to secrete sufficient insulin.

That a hyperglycemic state results after braindeath is undisputed.16, 18, 40 Endocrine pancreaticfunctions are normal after brain death, according toMasson and colleagues, and hyperglycemia resultsfrom tissue-insulin resistance,41 although furtherstudy is needed to determine what causes the resis-tance. Hyperglycemia may be complicated by thelarge volume of glucose-containing fluids often usedfor fluid resuscitation to correct hypernatremia.16

Although the mechanism underlying the disruptionof serum glucose regulation remains unclear, it iswell established that fluctuations occur.


Brain Death: ConfirmatoryFindings on Neurologic AssessmentGlasgow Coma Scale score: 3 (no eye, verbal, ormotor responses to auditory or painful stimuli)Apnea: a partial pressure of carbon dioxide > 60mmHg off ventilator, no spontaneous breathingAbsent pupillary reflex: pupils remain fixed anddilated, size > 4 mm, upon exposure to lightAbsent oculovestibular reflex: eyes remain midlinewhen ear canal is irrigated with ice water 10 mL Absent oculocephalic (“doll’s eyes”) reflex: eyesremain fixed in position when head is turned fromside to side Absent corneal reflex: no blinking upon corneal stimu-lation with cotton-tipped applicatorAbsent gag reflex: no gag reflex upon manual manip-ulation of patient’s trachea or upon deep endotra-cheal suctioningAbsent cough reflex: no cough reflex upon deependotracheal suctioning Wijdicks EF. N Engl J Med 2001;344(16):1215-21; Sullivan J, et al.Crit Care Nurse 1999;19(2):37-9, 41-6.

5. Wheeldon DR, et al. Transforming the “unacceptable”donor: outcomes from the adoption of a standardized donormanagement technique. J Heart Lung Transplant 1995;14(4):734-42.

6. A definition of irreversible coma. Report of the Ad HocCommittee of the Harvard Medical School to Examine theDefinition of Brain Death. JAMA 1968;205(6):337-40.

7. Guidelines for the determination of death. Report of themedical consultants on the diagnosis of death to thePresident’s Commission for the Study of Ethical Problems inMedicine and Biomedical and Behavioral Research. JAMA1981;246(19):2184-6.

8. Capron AM. Brain death—well settled yet still unresolved.N Engl J Med 2001;344(16):1244-6.

9. Chabalewski F, et al. Policy and practice in organ transplan-tation. In: Organ transplantation: concepts, issues, practice,and outcomes. Medscape; 2002. http://www.medscape.com/viewpublication/704_about.

10. Practice parameters for determining brain death in adults(summary statement). The Quality Standards Subcommitteeof the American Academy of Neurology. Neurology 1995;45(5):1012-4.

11. Lock M. Inventing a new death and making it believable.Anthropology and Medicine 2002;9(2):97-115.

12. Wijdicks EF. Determining brain death in adults. Neurology1995;45(5):1003-11.

13. Wijdicks EF. The diagnosis of brain death. N Engl J Med2001;344(16):1215-21.

14. Dominguez-Roldan JM, et al. Changes in the intracranialpulse pressure waveform associated with brain death.Transplant Proc 1999;31(6):2597-8.

15. Shoemaker WC, et al. Hemodynamic and oxygen metabolicpatterns in brain death after head trauma. RussianNeurosurgery 2002;3(8). http://www.neuro.neva.ru/English/Issues/Articles_3_2002/zelman.htm.

16. Smith M. Physiologic changes during brain stem death—lessons for management of the organ donor. J Heart LungTransplant 2004;23(9 Suppl):S217-22.

17. Chiari P, et al. Biphasic response after brain death induction:prominent part of catecholamines release in this phenome-non. J Heart Lung Transplant 2000;19(7):675-82.

18. Chen EP, et al. Hormonal and hemodynamic changes in avalidated animal model of brain death. Crit Care Med1996;24(8):1352-9.

19. Smith SL. Organ and tissue donation and recovery. In:Organ transplantation: concepts, issues, practice, and outcomes. Medscape; 2003. http://www.medscape.com/viewpublication/704_about.

20. Marshall VC. Pathophysiology of brain death: effects onallograft function. Transplant Proc 2001;33(1-2):845-6.

21. Bittner HB, et al. A valid experimental brain death organdonor model. J Heart Lung Transplant 1995;14(2):308-17.

22. Sullivan J, et al. Determining brain death. Crit Care Nurse1999;19(2):37-9, 41-6.

23. Huang AH. The hot nose sign. Radiology 2005;235(1):216-7. 24. Conrad GR, Sinha P. Scintigraphy as a confirmatory test of

brain death. Semin Nucl Med 2003;33(4):312-23. 25. United Network for Organ Sharing. Critical pathway for the

organ donor. The Network. 2002. http://www.unos.org/resources/pdfs/CriticalPathwayPoster.pdf.

26. Herijgers P, et al. Endothelial activation through braindeath? J Heart Lung Transplant 2004;23(9 Suppl):S234-9.

27. Goldstein B, et al. Uncoupling of the autonomic and cardio-vascular systems in acute brain injury. Am J Physiol1998;275(4 Pt 2):R1287-92.

28. Kuo TB, et al. Diminished vasomotor component of sys-temic arterial pressure signals and baroreflex in brain death.Am J Physiol 1997;273(3 Pt 2):H1291-8.

29. Szabo G. Physiologic changes after brain death. J HeartLung Transplant 2004;23(9 Suppl):S223-6.

30. Smith JM, Pilati CF. Effect of massive sympathetic nervoussystem activation on coronary blood flow and myocardialenergy pool. Exp Biol Med (Maywood) 2002;227(2):125-32.

Nursing implications. Hyperglycemia can lead toosmotic diuresis and cellular dehydration, resultingin hypovolemia. Regular blood-glucose monitoringwith corrective interventions is crucial. Finger-stickmeasurement is usually adequate. Insulin should be administered at a minimum rate of 1 unit perhour, adjusted to keep blood glucose between 120and 180 mg/dL.25

The kidneys. One study with rats found that,immediately after brain death, severe vasoconstric-tion occurred, causing increased regional vascularresistance.42 Renal vascular resistance was especiallyhigh, rising to four times higher than normal. Suchmarkedly heightened vascular resistance can causeischemia. Perfusion to abdominal organs alsodecreases as a result of vasoconstriction.19

Under normal conditions, hypoperfusion of thekidneys activates the renin–angiotensin–aldosteronesystem, resulting in vasoconstriction and salt andwater retention. The activation of the renin–angiotensin–aldosterone system after brain deathfurther exacerbates vasoconstriction and compro-mises renal blood flow. Eventually renal insuffi-ciency results, possibly compromising kidneyviability and posttransplantation function.

Cardiovascular collapse following the sympa-thetic storm and lack of ADH leading to diabetesinsipidus may also cause significant renal hypoper-fusion. Significant, irreversible glomerular andtubular injury will follow if renal perfusion is notrestored.

Nursing interventions that maintain hemody-namic stability and replace volume best ensurerenal-tissue viability for transplantation. IV infu-sions of diuretics for oliguria or antidiuretics fordiabetes insipidus, at levels set by the OPO coordi-nator in accordance with the critical pathway beingused, may be warranted. Fluid intake and urine out-put should be closely monitored, as well as thepatient’s overall state of hydration. Hydration canbe monitored noninvasively by frequent measure-ment of urine output, heart rate, and blood pres-sure, and invasively by using a central line tomonitor central venous pressure. t

REFERENCES1. United Network for Organ Sharing. Data. The Network.

2006. http://www.unos.org/data. 2. Organ Donation Breakthrough Collaborative. About the col-

laborative: charter for the Organ Donation BreakthroughCollaborative. U.S. Department of Health and HumanServices. 2003. http://www.organdonationnow.org/index.cfm?fuseaction=Page.viewPage&pageId=471.

3. National Women’s Health Information Center. Frequentlyasked questions about women’s health: organ donation andtransplantation. Office on Women’s Health, U.S. Departmentof Health and Human Services. 2006. http://www.4woman.gov/faq/organ_donation.htm.

4. Lopez-Navidad A, et al. Organ shortage: viability of poten-tial organ donors and possible loss depend on health careworkers who are responsible for the organ procurement pro-gram. Transplant Proc 1997;29(8):3614-6.


31. Novitzky D, et al. Prevention of myocardial injury duringbrain death by total cardiac sympathectomy in the Chacmababoon. Ann Thorac Surg 1986;41(5):520-4.

32. Szabo G, et al. Role of neural and humoral factors in hyper-dynamic reaction and cardiac dysfunction following braindeath. J Heart Lung Transplant 2000;19(7):683-93.

33. Ryan JB, et al. Functional evidence of reversible ischemicinjury immediately after the sympathetic storm associatedwith experimental brain death. J Heart Lung Transplant2003;22(8):922-8.

34. Yeh T, Jr., et al. Central sympathetic blockade amelioratesbrain death-induced cardiotoxicity and associated changes inmyocardial gene expression. J Thorac Cardiovasc Surg2002;124(6):1087-98.

35. Takada M, et al. Effects of explosive brain death on cytokineactivation of peripheral organs in the rat. Transplantation1998;65(12):1533-42.

36. Imai K, et al. Experimental evaluation of hepatic circulation,energy metabolism, and morphologic changes in brain death.Transplant Proc 1998;30(7):3282-3.

37. Onumata O, et al. Effects of hypotension on hepatic circula-tion and function: comparison of brain death and exsan-guination models. Transplant Proc 2000;32(7):2293-6.

38. Florman SS, et al. Hyperosmolarity associated with diabetesinsipidus alters hepatocyte structure and function but notsurvival after orthotopic liver transplantation in rats.Transplantation 1998;65(1):36-41.

39. Obermaier R, et al. Brain death impairs pancreatic microcir-culation. Am J Transplant 2004;4(2):210-5.

40. Masson F, et al. Thyroid function in brain-dead donors.Transpl Int 1990;3(4):226-33.

41. Masson F, et al. The endocrine pancreas in brain-deaddonors. A prospective study in 25 patients. Transplantation1993;56(2):363-7.

42. Herijgers P, et al. Changes in organ perfusion after braindeath in the rat and its relation to circulating catechol-amines. Transplantation 1996;62(3):330-5.


GENERAL PURPOSE: To explain for registered professionalnurses how brain death is determined in adults and howpotential organ donors are identified, and to describeessential nursing interventions.

LEARNING OBJECTIVES: After reading this article and takingthe test on the next page, you will be able to• describe the process of managing potential organ

donors who have been declared brain dead.• outline the pathophysiologic changes that occur follow-

ing brain death.• review the criteria and diagnostic parameters that define

brain death.

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• complete the registration information and course evalua-tion. Mail the completed enrollment form and registrationfee of $27.95 to Lippincott Williams and Wilkins CEGroup, 2710 Yorktowne Blvd., Brick, NJ 08723, byMarch 31, 2009. You will receive your certificate in four tosix weeks. For faster service, include a fax number and wewill fax your certificate within two business days of receiv-ing your enrollment form. You will receive your CE certifi-cate of earned contact hours and an answer key to reviewyour results. There is no minimum passing grade.

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Brain Death & Organ Procurement