3.
5 HOURS
Continuing Education
By Kathleen M. Z. Peiffer, BSN, RN, CCRN
Brain Death and
Organ Procurement
Nursing management of adults with brain injury is crucial
to the viability of donor organs.
Overview: Patients with severe brain injuries (as can result from
trauma, 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 of
determining 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 upon
brain death, as well as essential nursing interventions.
T
he need for donor organs far outstrips
their availability. More than 94,000
people nationwide are on waiting lists
for organs, yet from January through
September 2006, just 22,014 transplan-
tations were performed, according to the United
Network for Organ Sharing (UNOS).1 Until recently,
the donation rate among potential donors was less
than 50%: of 14,000 potential donors identified in
2002, fewer than half (46%) donated organs.2 In an
effort to improve that rate, the U.S. Department
Kathleen M. Z. Peiffer is a student in the master’s program in
nurse anesthesia in the College of Nursing and Health
Professions at Drexel University, Philadelphia, and a per diem
nurse in the surgical ICU at Holy Spirit Hospital, Camp Hill,
PA. Contact author: kzpeiffer@msn.com. The author of this
article has no significant ties, financial or otherwise, to any
company that might have an interest in the publication of this
educational activity.
58 AJN ▼ March 2007 ▼ Vol. 107, No. 3
of Health and Human Services and hospital and
transplantation leaders recently formed the Organ
Donation Breakthrough Collaborative. Between
2003 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 aggressive
and timely, the body’s tissues and organs cannot be
used for transplantation. Indeed, when a patient is a
potential or designated organ donor, the nursing
care required may be even more rigorous after brain
death than before. (At my facility, the nurse–patient
ratio for brain-dead organ donors may be as high as
3:1.) Consider this: one organ donor can provide as
many 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 donor
management is considered “one of the most neglected
areas of transplantation.”5
The transition from caring for the living to caring
for the brain dead (as potential organ donors) can
be difficult for nurses. How does your role change
when you begin working with a brain-dead patient
and an organ-procurement coordinator?
IDENTIFYING ORGAN DONORS: THE NURSE’S JOB
Patients with severe brain injuries (as can result
from trauma, subarachnoid hemorrhage, or brain
tumor) are monitored closely by nursing staff. It’s
therefore often the nurse who first recognizes signs
of decompensation (such as a lack of eye, verbal,
and motor responses according to the Glasgow
Coma Scale and the absence of ventilatory
attempts) and begins the process of determining
whether the patient is a potential organ donor.
Indeed, frequent neurologic assessments to evaluate
for signs of decompensation should be made before
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 a
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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
a diagnosis of brain death, in order to protect tissue
and organ viability. (See Determining Brain Death,
page 60.)
Typically, the nurse first informs the attending
physician, the neurologist, or the neurosurgeon of
the patient’s decompensation. Depending on the
facility’s protocol, either the nurse or another clini-
cian may then contact the local organ-procurement
organization (OPO) to say that there is a case that
may soon involve them. Ideally, the local OPO
should 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 is
done 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 of
the patient’s condition, and nurses will provide addi-
tional support and information, as will clergy and
social workers. Either the physician or the OPO coor-
dinator may bring up the subject of organ donation;
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A
this can happen either when brain death is immi-
nent or after it has been declared. (If the patient has
just been declared brain dead, it’s important to give
the family time to understand the diagnosis and to
absorb their loss before the prospect of organ dona-
tion is discussed. The length of time needed will
vary from case to case.)
Once the attending physician has declared the
time 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. The
OPO coordinator will direct the nursing staff to
maintain hemodynamic stability of the body while
the 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 designated
recipients’ facilities.
The OPO coordinator typically leads the discus-
sion about organ donation with a potential donor’s
family, with staff nurses providing emotional sup-
AJN ▼ March 2007 ▼ Vol. 107, No. 3 59
 Determining Brain Death
I n 1968, recognizing that advances in cardiopulmonary
resuscitation and life support were keeping hearts beat-
ing even when catastrophic brain damage had occurred,
the Ad Hoc Committee of the Harvard Medical School set
forth a new definition of death: irreversible coma.6 The
three primary criteria for diagnosis were total “unreceptiv-
ity and unresponsivity” to external stimuli, a complete lack
of spontaneous muscular movement or respiration, and
“the absence of elicitable reflexes.” A fourth, confirmatory
criterion—an isoelectric (flat) electroencephalogram
(EEG)—was also named. With some refinements, these
criteria have remained the standard.
In 1981 a group of medical consultants to the
President’s Commission for the Study of Ethical Problems in
Medicine and Biomedical and Behavioral Research pub-
lished Guidelines for the Determination of Death, which
clarified the need to confirm both the cessation of all brain
function and the irreversibility of that condition, and speci-
fied that drug intoxication, hypothermia, and shock must
be ruled out.7 (This was the basis for the Uniform
Determination of Death Act of 1981, a model statute
intended to lessen legal “confusion”8; brain death legisla-
tion has since been enacted in all 50 states.9) More
recently, in 1994 the American Academy of Neurology
(AAN) defined brain death as “the absence of clinical
brain function when the proximate cause is known and
demonstrably irreversible,” summarized practice parame-
ters for determining its occurrence in adults, and discussed
specific tools and confirmatory tests.10
When brain death occurs. Approximately 1% of all
deaths 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 and
subarachnoid hemorrhage, according to reviews12, 13; other
causes include infection such as meningitis or encephalitis
and brain tumor.
The initial trauma sets off a cascade of events. 14-19 Tissue
damage and fluid blockage or excessive fluid accumulation
result in increasing intracranial pressure, ischemia, and
brain cell death. When ischemia reaches the brain stem, it
triggers a massive release of catecholamines—an event
known as an autonomic or sympathetic “storm”—which
leads to an immediate, intense Cushing response (increased
systemic vascular resistance and hypertension) lasting about
15 minutes. Compression of the vasculature and worsening
ischemia cause infarction of brain tissue. Venous engorge-
ment and brain swelling cause the brain to herniate through
the foramen magnum, further inhibiting cerebral perfusion.
Inflammation and edema progress and intracranial pressure
rises even more, culminating in a complete loss of cerebral
blood flow.
As the sympathetic storm subsides, the initial Cushing
response is followed by a brief period of stability. Then a
second hemodynamic collapse occurs.17 This collapse is
characterized by a profound loss of vascular tone and a
subsequent loss of peripheral resistance, bradycardia,
hypotension, plummeting cardiac output, and systemic
60 AJN ▼ March 2007 ▼ Vol. 107, No. 3
1a
1b
organ hypoperfusion.17, 20 Although opinions vary as to the
cause, some studies attribute the second collapse to a sec-
ond catecholamine release.17, 21
Confirmatory findings on neurologic assessment. In
cases of imminent or suspected brain death, neurologic
assessment includes evaluating the level of coma or un-
responsiveness, testing brain stem reflexes, and assessing
for apnea.13, 22 The following findings, which are also out-
lined in Brain Death: Confirmatory Findings on
Neurologic Assessment, page 65, confirm brain death
except in cases of hypothermia, drug intoxication, or con-
founding conditions such as acute metabolic or endocrine
disturbances, all of which may be reversible.13, 22
Level of coma or unresponsiveness. Although not all
patients who are comatose progress to brain death, peo-
ple who are brain dead will be unresponsive to verbal
and painful stimuli. The Glasgow Coma Scale tests the lev-
els of verbal response to spoken stimuli (such as the
patient’s name) and eye and motor response to both spo-
ken and painful stimuli (such as pressure applied to the
supraorbital nerve [1a] or nail beds [1b]). Total scores
ranging from 3 (lowest) to 15 (highest) are possible. A
score of 3 indicates profound unresponsiveness.
Respiratory findings. Normal respiration occurs when
the respiratory center of the brain (an area within the
medulla oblongata and the pons) responds to rising serum
carbon dioxide levels. In a healthy brain, a partial pres-
sure of carbon dioxide (PaCO2) level above 60 mmHg
prompts respiration. In a patient who is brain dead, this
response is absent.
To test for central apnea, the patient is taken off
mechanical ventilation and 100% oxygen 6 L/min is deliv-
ered by nasal cannula for as long as eight minutes while
the patient is observed for signs of attempted breathing.22
An arterial blood gas sample is also obtained and the
PaCO2 level measured to ensure that carbon dioxide lev-
els are adequate to trigger respiration; if a PaCO2 level
greater 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 by
shining a light into the patient’s eyes (2); normally the pupils
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 2 3
5 6
constrict. If the pupils remain fixed and dilated at a size
greater than 4 mm, this is confirmatory of brain death
(except in cases of preexisting pupillary abnormalities).22 The
oculovestibular test involves injecting about 10 mL of ice
water or saline into the ear canal (3). Ordinarily the patient’s
eyes will turn toward the stimulated ear. If no eye movement
occurs, this test is confirmatory. In the oculocephalic test (also
known as the “doll’s eyes” test), the clinician moves the
patient’s head from midline to each side in turn (4). Normally
the patient’s gaze remains on a specific point, with the eyes
moving away from the direction of the head turn in order to
maintain that gaze. In patients without this reflex, the eyes
remain fixed at midline despite head movement.
Other reflexes. The corneal reflex is tested by gently
touching a sterile, cotton-tipped swab to the patient’s
cornea 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 be
absent in correlation with other assessment findings in
someone who is brain dead. The cough reflex may be
tested by performing deep bronchial suctioning through
the patient’s endotracheal tube; a lack of response is
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confirmatory (6). The gag reflex can be assessed either by
manually 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 difficult
to evaluate in orally intubated patients.”22
Confirmatory laboratory tests are optional in diagnos-
ing brain death in adults. However, the AAN recommends
such 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 the
AAN, the most sensitive test is cerebral angiography, but
the contrast dye used can render organs useless for trans-
plantation. With patients who are potential or designated
organ donors, electroencephalography or cerebral scintig-
raphy is preferred. If the patient is brain dead, an EEG will
reveal an isoelectric pattern. Cerebral scintigraphy may be
performed to verify the absence of cerebral blood flow23, 24;
its advantages are that it can be performed at bedside and
does not pose a threat to organs.23 Other confirmatory tests
may include transcranial Doppler ultrasonography and
somatosensory evoked potentials (responses evoked by
electrical stimulation of peripheral nerves).
AJN ▼ March 2007 ▼ Vol. 107, No. 3 61
 port. Many people identify themselves as organ
donors on their driver’s license. Because that infor-
mation can be useful in discussing the patient’s
wishes, the coordinator often contacts the state’s
department of motor vehicles before approaching
the family, to determine whether the patient has des-
ignated herself or himself a donor. However, in most
states 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 designated
recipients’ facilities, and scheduling the operating
room 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 the
patient’s chart and from staff nurses and physicians
and possibly family members). Previous laboratory
results will be evaluated, and several additional
studies (such as liver and kidney function studies
and blood tests to assess pancreatic enzyme and thy-
roid hormone levels) are often ordered to guide
treatment. A central line or pulmonary artery
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.
catheter may be inserted for hemodynamic monitor-
ing.5 The additional testing is labor intensive; often
the donor’s condition deteriorates so rapidly that
additional nurses are needed to perform stabilizing
tasks such as the monitoring of fluids and vital signs
and the administration of drugs and fluids.
The staff nurse reports all aberrancies in the
donor’s condition to the OPO coordinator, who, in
turn, provides orders for their correction. If the coor-
dinator isn’t available, the nurse may make treatment
decisions based on a critical pathway designated by
the coordinator. (One such pathway is UNOS’s
Critical Pathway for the Organ Donor [www.
unos.org/resources/pdfs/CriticalPathwayPoster.pdf].)
The coordinator reviews the laboratory test results
for the donor’s blood type and other serum markers
62 AJN ▼ March 2007 ▼ Vol. 107, No. 3
Brain Death Criteria
1. 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 the
Definition of Brain Death. JAMA 1968;205(6):337-40; The Quality
Standards Subcommittee of the American Academy of Neurology.
Neurology 1995;45(5):1012-4.
and compares this information with a national data-
base of patients in need of organs that is maintained
by UNOS’s Organ Center. Patients awaiting an
organ are compared with the donor in areas such as
blood and tissue type, weight, age, and urgency of
medical need, as well as the length of time the patient
has been on the waiting list. Proximity to the donor
is a major factor as well.
NURSING IMPLICATIONS OF BRAIN DEATH
The brain is in charge of the proper functioning of
all 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 brain
is still functioning. The nurse’s goals in this regard
are determined by the following changes as they
take place in various organ systems. (It should be
noted that because there is scant research in the lit-
erature pertaining to humans, most of the research
cited in this article was conducted in animals.)
The brain. Normal responses to any sympathetic
stimulation include increases in blood pressure,
heart rate, cardiac contractility, minute ventilation
(the volume of air per minute that moves in and out
of the lungs), and peripheral vasomotor tone.
Catecholamines also “promote platelet aggregation,
accompanied by serotonin release.”26 Serotonin has
vasospastic effects on coronary arteries. Both
platelet aggregation and vasospasticity reduce coro-
nary artery blood flow.
Almost immediately after brain death, activation
of the sympathoadrenal axis causes a great increase
in the levels of circulating catecholamines.15, 17, 18
During this sympathetic storm, circulating dopa-
mine levels have been shown to increase by as much
as 800%, epinephrine levels by as much as 700%,
and norepinephrine levels by up to 100%.17, 18 The
effects 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 the
hypothalamus eventually results in a decline in cir-
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culating antidiuretic hormone (ADH; also called
arginine 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 with
accompanying hypernatremia, hyperosmolarity,
and dehydration in up to 80% of cases of brain
death.16
Declining T3 and T4. Ordinarily, the hypothala-
mus stimulates the pituitary to secrete thyroid-
stimulating hormone (TSH), which prompts the
thyroid to release triiodothyronine (T3) and its part-
ner hormone, thyroxine (T4). After brain death, T3
levels drop as a result of infarction in the tissues of
the hypothalamus and pituitary.17 T4 levels appear
to decline as well; Chen and colleagues found in a
study in dogs that levels of both T3 and T4 declined
significantly after brain death (although remaining
within normal limits) and suggested that such
decreases “could have contributed to post–brain
death cardiac dysfunction.”18 Other effects are not as
well established. The decrease in T3 has been associ-
ated with inhibited mitochondrial function, resulting
in poor cardiac contractility, anaerobic metabolism,
and lactic acidosis following brain death.16 However,
Chen and colleagues stated that although anaerobic
metabolism and metabolic acidosis were observed
immediately after brain death in their canine study,
these were not associated with declining thyroid hor-
mone levels.18
Loss of thermoregulation. The hypothalamus
regulates body temperature through a homeostatic
feedback mechanism. In a healthy person, if the
body becomes too hot, the hypothalamus prompts
vasodilation, resulting in sweating. If the body
becomes too cool, the hypothalamus prompts vaso-
constriction in the skin, shivering, and piloerection,
resulting in heat retention.
Systemic hypothermia—heat loss secondary to
massive peripheral vasodilation and loss of ther-
moregulatory control by the hypothalamus—is
often 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 diabetes
insipidus involves fluid replacement to offset hourly
urine output and often includes an IV vasopressin
(Pitressin) infusion as well. The nurse should be dili-
gent in observing urine output (at a minimum, 0.5
mL/kg/h) to determine whether the patient needs
fluid resuscitation, a vasopressin infusion, or both.
According to UNOS’s Critical Pathway for the
Organ Donor, the following are essential to hor-
monal management in potential donors: T3
4 microgram IV bolus followed by an infusion of
3 micrograms per hour; vasopressin 1 unit IV bolus
followed by an infusion of 0.5 to 4 units per hour,
adjusted to 800 to 1200 dyne/sec/cm5 for systemic
vascular resistance; methylprednisolone (Solu-
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Organ-Procurement
Organizations
T he National Organ Transplantation Act of 1984 cre-
ated a multidisciplinary task force to study organ
donation, procurement, and transplantation. It also
established a national organ sharing system, the Organ
Procurement and Transplantation Network (OPTN),
which has been administered since its inception by the
United Network for Organ Sharing (www.unos.org), a
national nonprofit organization. The Omnibus
Reconciliation Act of 1986 implemented many of the
task force’s recommendations, including that organ-
procurement organizations (OPOs) be members of the
OPTN. And in 1998, the Department of Health and
Human Services’ Health Care Financing Administration
issued Hospital Conditions of Participation for Organ
Donation, which delineated criteria for reimbursement
under Medicare and Medicaid. To be in compliance,
hospitals must “have an agreement with an OPO,”
“notify OPOs in a timely manner about patients who
have died or whose death is imminent,” and collaborate
with the OPO “to ensure every family is offered the
option of donation.”9
Most OPOs are independent, although a few are hospi-
tal based. An OPO team doesn’t recover organs itself; that
is handled by organ recovery teams from the designated
recipients’ facilities. An OPO team’s responsibilities typi-
cally include9:
• providing public and professional education on the
donation process.
• evaluating the “medical suitability” of potential
donors.
• with hospital staff, offering families the option of
donation.
• managing and coordinating organ procurement and
allocation.
• providing support to donor families.
• maintaining documentation.
Medrol) 15 mg/kg IV bolus, which may be repeated
in 24 hours if needed; and an insulin drip of 1 unit
per hour adjusted to maintain blood glucose at
between 120 and 180 mg/dL.25 Blood glucose
should be measured hourly to determine the need
for coverage with regular insulin or the initiation of
an insulin drip.
Following the loss of thermoregulation, an IV
fluid warmer, a forced-air room warming device,
and warming blankets should be used to maintain
the 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 by
both the sympathetic and parasympathetic branches
AJN ▼ March 2007 ▼ Vol. 107, No. 3 63
 of the autonomic nervous system. Sympathetic stim-
ulation of both the sinoatrial (SA) and the atrioven-
tricular (AV) nodes originates in the medulla
oblongata. The sympathetic fibers in the heart
release norepinephrine, increasing heart rate and
contractility. Parasympathetic stimulation of the SA
and AV nodes also originates in the medulla through
cranial nerve X (the vagus nerve). The parasympa-
thetic fibers release acetylcholine, decreasing heart
rate and contractility. Cranial nerve IX (the glos-
sopharyngeal nerve) is also responsible for stimula-
tion of cardiac events. These nerves are linked
through connections to baroreceptors in the carotid
arteries, controlling heart rate variability and arterial
pressure.
‘Uncoupling’ of the autonomic
and cardiovascular systems is
believed to be responsible for
the eventual cessation of cardiac
function after brain death.
After brain death, the cardiovascular system is no
longer under autonomic control.27 The arterial
baroreceptors that once allowed for automatic reg-
ulation of blood pressure and heart rate are no
longer functional.28 This “uncoupling” of the auto-
nomic and cardiovascular systems is believed to be
responsible for the eventual cessation of cardiac
function after brain death.27 During the first
Cushing response, “exaggerated uneven peripheral
vasoconstriction” causes areas of hypoperfusion in
organ vasculature.15 However, the loss of autonomic
control soon causes “a decline in the sympathetic
outflow to the blood vessels,”28 leading to vasodila-
tion. A second hemodynamic collapse causes fur-
ther systemic vasodilation or vasoplegia, decreasing
preload, adversely affecting afterload, and further
compromising cardiac output.17, 29
Increased catecholamines. Even in an adequately
perfused heart, high catecholamine levels will
decrease the myocardial cells’ ability to pump effec-
tively.30 Commenting on earlier studies, Herijgers
and colleagues observed that “the severity of the
myocardial damage is correlated with the amount
of catecholamines released at the moment of brain
death.”26 Catecholamines also are associated with
platelet aggregation and the release of serotonin;
this study suggests that brain death may cause
myocardial damage through vasospasm caused by
the effects of serotonin release.26
64 AJN ▼ March 2007 ▼ Vol. 107, No. 3
Another study found evidence to suggest that the
myocardial damage that occurs during brain death
“may be related to endogenous catecholamine
release (possibly resulting in increased calcium
uptake by the myocardial cells), inducing various
forms of myocyte necrosis.”31 The calcium ion Ca++
is responsible for the normal excitation and contrac-
tion of myocardial tissue that results in the pumping
action of the myocardium. After brain death, the
increased calcium uptake desensitizes the cardiac
myofilaments to calcium, compromising cardiac con-
tractility and output.32
The sympathetic storm also results in increased
myocardial adenosine and lactate levels, which are
associated with myocardial dysfunction and
myocardial ischemia.16, 26, 33
Accumulation of neutrophils. In a canine study by
Chen and colleagues, they found that “irreversible
focal injuries and myocytolysis” occurred soon after
brain death.18 They also observed an “accumulation
and infiltration of neutrophils and subendocardial
hemorrhage,” as well as edema. Hemorrhage and
edema may adversely affect the ability of the organ
to function fully after transplantation.
Altered gene expression. Yeh and colleagues
speculated that after brain death, “fluctuations in
catecholamine levels might act as important signals
in the subsequent alterations” in the expression of
myocardial genes that regulate functions such as
contractility and growth.34 They hypothesized that
the 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 of
myocardial gene products” could be suppressed by
exogenous sympathetic blockade.34 Treatment with
b-adrenergic blockers such as metoprolol (Lopressor)
and labetalol (Normodyne, Trandate) is standard.
Nursing implications. Exogenous catechol-
amines, including epinephrine and dopamine, are
often used as inotropic agents to maintain blood
pressure and systemic perfusion. After brain death,
epinephrine is usually infused at a standard dose
range of 0.05 to 1 micrograms per kilogram per
minute; dopamine is infused at a standard dose
range of 5 to 10 micrograms per kilogram per
minute. It’s imperative that the potential donor’s
actual, not estimated, weight be used in determining
the infusion dosage. Some OPO coordinators may
want to estimate current weight by averaging the
patient’s weight on admission and her or his last
known weight. Patients often become severely edem-
atous during an ICU stay, with consequent and
sometimes marked increases in body weight. This
edema may dramatically change the effect of vaso-
pressors from therapeutic to toxic.
The OPO coordinator should be notified of heart
rate, blood pressure, or central venous pressure lev-
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els that vary from limits established in the critical
pathway being used. Diagnostic evaluation of the
potential donor’s heart may be necessary to deter-
mine its viability for transplantation. Tests such as
echocardiography, transesophageal echocardiogra-
phy, or cardiac catheterization may be necessary
in older donors or those with concurrent illnesses in
order to visualize valves, heart wall motion, and
overall function. (Although older age or a history of
illness does not necessarily preclude donation, each
case 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 the
medulla oblongata and pons. In cases of traumatic
brain injury, cerebral inflammation and edema
cause infarction of the tissues of the respiratory cen-
ter.15, 16, 35 Central apnea results.6
The sympathetic storm following brain death has
direct, detrimental effects on lung tissue. Increasing
systemic hypertension and left atrial pressure result
in elevated pulmonary capillary pressures and sub-
sequent endothelial damage to these capillaries.16
Their permeability increases and fluid leaks into the
alveoli 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 of
95% or greater on 100% oxygen cannot be
achieved or maintained, or those in whom lung tis-
sue viability is questionable, may undergo bron-
choscopy so that lung tissue can be visualized to
determine its viability for transplantation.
According to UNOS’s critical pathway, a state of
mild respiratory alkalosis (partial pressure of car-
bon dioxide between 30 and 35 mmHg) is prefer-
able for potential donors.25
Nursing implications. Peak airway pressures
should be maintained at less than 30 cm H2O.25
Accordingly, although ventilatory settings will be
controlled by the OPO coordinator and the respira-
tory therapist, the nurse will monitor tidal volumes
delivered to the patient, the inspiratory flow rate,
and the fraction of inspired oxygen.
The liver. Blood flow to the liver has been found
to decrease after brain death, but the implications of
this are unclear. One study found that “morpho-
logic change in the liver was slight” and that “the
liver remained viable for as long as six hours follow-
ing brain death,”36 while another study found that
liver functions were impaired.37 The hyperosmolar-
ity associated with diabetes insipidus has been cor-
related with hepatocyte destruction and altered
hepatocyte mitochondria.38
The shift to anaerobic metabolism leads to a
depletion of liver glycogen.20 Organs must delve into
their own glycogen stores for the energy necessary
to carry out normal cell functions; once these are
ajn@wolterskluwer.com
Brain Death: Confirmatory
Findings on Neurologic Assessment
Glasgow Coma Scale score: 3 (no eye, verbal, or
motor responses to auditory or painful stimuli)
Apnea: a partial pressure of carbon dioxide > 60
mmHg off ventilator, no spontaneous breathing
Absent pupillary reflex: pupils remain fixed and
dilated, size > 4 mm, upon exposure to light
Absent oculovestibular reflex: eyes remain midline
when ear canal is irrigated with ice water 10 mL
Absent oculocephalic (“doll’s eyes”) reflex: eyes
remain fixed in position when head is turned from
side to side
Absent corneal reflex: no blinking upon corneal stimu-
lation with cotton-tipped applicator
Absent gag reflex: no gag reflex upon manual manip-
ulation of patient’s trachea or upon deep endotra-
cheal suctioning
Absent cough reflex: no cough reflex upon deep
endotracheal 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.
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 the
parameters established by the OPO coordinator.
The pancreas. Insulin is normally secreted by the
beta cells of the pancreas in response to blood glucose
levels. Cranial nerve X also stimulates the production
of pancreatic secretions. A study by Obermaier and
colleagues determined that brain death “causes sig-
nificant pathophysiological alterations in the pan-
creas,” including deterioration of pancreatic
microvasculature, inflammation, and histologic dam-
age.39 Each of these sequelae plays a role in disrupting
beta cell functioning, ultimately destroying the pan-
creas’s ability to secrete sufficient insulin.
That a hyperglycemic state results after brain
death is undisputed.16, 18, 40 Endocrine pancreatic
functions are normal after brain death, according to
Masson and colleagues, and hyperglycemia results
from tissue-insulin resistance,41 although further
study is needed to determine what causes the resis-
tance. Hyperglycemia may be complicated by the
large volume of glucose-containing fluids often used
for fluid resuscitation to correct hypernatremia.16
Although the mechanism underlying the disruption
of serum glucose regulation remains unclear, it is
well established that fluctuations occur.
AJN ▼ March 2007 ▼ Vol. 107, No. 3 65
 Nursing implications. Hyperglycemia can lead to
osmotic diuresis and cellular dehydration, resulting
in hypovolemia. Regular blood-glucose monitoring
with corrective interventions is crucial. Finger-stick
measurement is usually adequate. Insulin should
be administered at a minimum rate of 1 unit per
hour, adjusted to keep blood glucose between 120
and 180 mg/dL.25
The kidneys. One study with rats found that,
immediately after brain death, severe vasoconstric-
tion occurred, causing increased regional vascular
resistance.42 Renal vascular resistance was especially
high, rising to four times higher than normal. Such
markedly heightened vascular resistance can cause
ischemia. Perfusion to abdominal organs also
decreases as a result of vasoconstriction.19
Under normal conditions, hypoperfusion of the
kidneys activates the renin–angiotensin–aldosterone
system, resulting in vasoconstriction and salt and
water retention. The activation of the renin–
angiotensin–aldosterone system after brain death
further exacerbates vasoconstriction and compro-
mises renal blood flow. Eventually renal insuffi-
ciency results, possibly compromising kidney
viability and posttransplantation function.
Cardiovascular collapse following the sympa-
thetic storm and lack of ADH leading to diabetes
insipidus may also cause significant renal hypoper-
fusion. Significant, irreversible glomerular and
tubular injury will follow if renal perfusion is not
restored.
Nursing interventions that maintain hemody-
namic stability and replace volume best ensure
renal-tissue viability for transplantation. IV infu-
sions of diuretics for oliguria or antidiuretics for
diabetes insipidus, at levels set by the OPO coordi-
nator in accordance with the critical pathway being
used, may be warranted. Fluid intake and urine out-
put should be closely monitored, as well as the
patient’s overall state of hydration. Hydration can
be monitored noninvasively by frequent measure-
ment of urine output, heart rate, and blood pres-
sure, and invasively by using a central line to
monitor central venous pressure. ▼
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ajn@wolterskluwer.com
3.5 HOURS
Continuing Education
EARN CE CREDIT ONLINE
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GENERAL PURPOSE: To explain for registered professional
nurses how brain death is determined in adults and how
potential organ donors are identified, and to describe
essential nursing interventions.
LEARNING OBJECTIVES: After reading this article and taking
the 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.
TEST INSTRUCTIONS
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will fax your certificate within two business days of receiv-
ing your enrollment form. You will receive your CE certifi-
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your results. There is no minimum passing grade.
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TEST CODE: AJN0607
AJN ▼ March 2007 ▼ Vol. 107, No. 3 67