Download Inhalational Anesthesia for Organ Procurement: Potential Indications

Inhalational Anesthesia for Organ Procurement:
Potential Indications for Administering
Inhalational Anesthesia in the Brain-Dead
Organ Donor
Laurie J. Elkins, CRNA, MS, CCRN
2009 Student Writing Contest Winner
Organs needed for transplantation far outweigh their
availability. There is minimal research regarding perioperative care of the brain-dead organ donor during
the procurement procedure. Current research attributes a great deal of organ damage to autonomic or
sympathetic storm that occurs during brain death.
Literature searches were performed with the terms
brain death, organ donor, organ procurement, anesthesia and organ donor, anesthesia and brain death,
anesthesia and organ procurement, inhalational anesthetics and organ procurement, and inhalational anesthetics and brain dead. Additional resources were
obtained from reference lists of published articles.
The literature review showed there is a lack of published studies researching the use of inhalational anesthetics in organ procurement. No studies have been
published evaluating the effect of preconditioning with
n 2005, approximately 89,000 patients were on waiting lists for various organs. Even when potential
donors are stabilized and consent is obtained for transplant, 17% to 25% of those donors become medically
unsuitable.1 It is therefore desirable to improve the viability of transplanted organs. Research has afforded clinicians with growing knowledge to better support these
potential donors and increase the viability of the organs
procured. This benefits the recipients by providing less
acute and chronic rejection, better functioning organs, and
ultimately a longer lifespan with a better quality of life.
Evidence-based practice has led to meticulous care
being provided to potential organ donors.2-5 While in intensive care units, these brain-dead individuals receive
vigorous hormonal and fluid resuscitation to achieve hemodynamic stability and the maintenance or improvement of organ function. A current problem is that there is
a minimal amount of research concerning perioperative
care of the brain-dead organ donor during the procurement procedure.
The purpose of this article is to generate interest in researching and measuring the effect of administering inhalational anesthetic agents during the perioperative phase
I
www.aana.com/aanajournalonline.aspx
inhalational agents (administering 1.3 minimal alveolar concentration of an inhalational agent for the 20
minutes before periods of ischemia) in the brain-dead
organ donor population.
Further studies are required to determine if administration of inhalational anesthetics reduces catecholamine release occurring with surgical stimulation during
the organ procurement procedure and whether this technique increases viability of transplanted organs. Anesthetic preconditioning before the ischemic period may
reduce ischemia-reperfusion injury in transplanted
organs, further increasing viability of transplanted
organs.
Keywords: Brain-dead organ donor, inhalational anesthesia, organ procurement.
of organ procurement. Current research attributes a great
deal of organ damage to the autonomic or sympathetic
storm that occurs during brain death. The sympathetic
insult leads to a cascade of other metabolic and inflammatory irregularities. This cascade greatly increases the likelihood of acute rejection or delayed graft function in the recipient and increases the potential for ischemia reperfusion
injury in the grafted organ itself.1,3,6-12 Current guidelines
for maintenance of potential organ donors are increasing
the number of acceptable organs and improving the organ
function in the recipients.1,6,7,13-15
There are no clear recommendations regarding perioperative management of the brain-dead organ donor
outside of administering neuromuscular blocking agents
to prevent spinal reflexes or movements in response to
surgical stimulation, fluid resuscitation, and maintenance
of certain hemodynamic values.16-18 The same intact
spinal cord that exhibits spinal reflexes to noxious
stimuli is also capable of inducing the release of catecholamines through the adrenergic loop.2,8,19-22 Many researchers compare this sympathetic catecholamine surge
in organ donors to that which occurs in autonomic hyperreflexia in the living patient with a previous spinal
AANA Journal ß August 2010 ß Vol. 78, No. 4
293
cord injury. This is a well-documented phenomenon that
can occur with noxious stimuli of any type. The uncontrolled sympathetic outflow can cause deleterious effects
to body systems if it is not treated.23
When the potential donor is managed appropriately in
the intensive care unit, sympathetic discharge during the
autonomic storm can be attenuated or eliminated, resulting in less organ damage. Healthcare researchers should
determine if the sympathetic discharge that occurs with
surgical stimulation in the brain-dead organ donor results
in the same degree of damage. If this discharge does lead
to further organ damage, determination of treatments to
attenuate or eliminate this response would contribute to
a greater number of successful transplantations with less
acute graft rejection, delayed organ function, and ischemia reperfusion injury in the organ recipients.
Literature Search Strategy
The terms brain death, organ donor, organ procurement,
anesthesia and organ donor, anesthesia and brain death,
anesthesia and organ procurement, inhalational anesthetics
and organ procurement, and inhalational anesthetics and
brain dead were entered in the search engines Ovid,
Medscape, MEDLINE, and Cumulative Index to Nursing
& Allied Health Literature (CINAHL). Searches were performed separately to comprehensively search for any
studies concerning the use of inhalational anesthetics
with organ procurement procedures. Additional resources were obtained from reference lists of published
articles, and all relevant literature was reviewed.
Published articles reviewed dated from 1985 to present.
vides a model or guideline that most of the states have
adopted.16
In the early 1980s, South African physicians hypothesized that with aggressive hormone therapy for hemodynamic instability in brain-dead organ donors, approximately 20% of hearts that were initially deemed
unsuitable for transplant secondary to decreasing function of the myocardium could be salvaged for transplantation. Today, the United Network for Organ Sharing
(UNOS) lists “hormone resuscitation” (HR) as the recommended treatment for comprehensive donor management6,25 (Figure 1). The effectiveness of HR was solidified after UNOS performed a retrospective analysis of
10,292 brain-dead donors from January 1, 2000, to
September 30, 2001. It was determined that significantly
more organs (22.5% greater) were successfully retrieved
from the 701 donors who received HR with the drugs
methylprednisolone, arginine vasopressin, triiodothyronine (T3 ), and thyroxine (T4 ) when compared with organ
donors who did not receive the treatment.6
Hormone resuscitation with these 3 drugs also increased the number of transplantable organs in donors
older than 40 years. After transplantation, patients who
received hearts from donors managed with the 3-drug HR
had significantly better 1-month survival and significantly less 1-month graft loss and early graft dysfunction.6
Multivariate analyses showed a 46% reduced odds of
death within 30 days and a 48% reduced odds of early
graft dysfunction when 3-drug HR was used.6 In addition
to increasing viability of organ grafts, treatment with HR
has been shown to decrease or eliminate requirements for
exogenous catecholamine infusions.6,13,15
History
Brain death, referred to as coma dépassé, was described as
early as 1959 by Mollaret and Goulon,24 who spoke of a
state “beyond coma” in which neurologic function and
reflexes were lost and patients were apneic. The authors
witnessed many of the derangements we see in braindead patients today, such as the inability to maintain adequate blood pressure, fluid volume, and temperature.2,16
The first human heart was transplanted in South
Africa in 1967. Shortly thereafter, a Harvard Medical
School committee issued a paper titled “A definition of irreversible coma, report … to examine the definition of
brain death.”16 This report established the term of brain
death, defined it as a “permanently non-functioning
brain,” gave diagnostic criteria for determining brain
death, and redefined brain death as a legally equivalent to
death. In 1970, Kansas legally recognized brain death as
a form of legal death and set precedence for the rest of the
United States. Over the next 11 years, half of the remaining states adopted nearly identical criteria. The guidelines for determining brain death in the 1981 President’s
Commission eventually led to the issuing of the Uniform
Determination of Death Act, a legislative act that pro-
294
AANA Journal ß August 2010 ß Vol. 78, No. 4
Donor Management During and After
Autonomic Storm
Autonomic or sympathetic storm (AS) is a phenomenon
that develops when the brain stem becomes ischemic.
Generally AS results in the massive systemic release of
catecholamines. The catecholamine release triggers a
cascade of derangements that leads to inflammatory responses and ischemia in all organs of the body.1,3,23 Some
of the end products resulting from this insult are interleukins, cytokines, altered gene expression, coagulopathies, and infiltration of neutrophils and monocytes.
These end products increase the odds of nonviable organs
and acute rejection of transplanted organs in the recipient.1,3,6,7,9-13,15,17,26,27
During AS, circulating norepinephrine levels can rise
100%, epinephrine levels can rise 700%, and dopamine
levels can rise 800%.17 In 2006, researchers documented
improved myocardial function and increased probability
of successful transplant in brain-dead organ donors after
treating AS with the antihypertensive medications
esmolol, urapidil, or nicardipine.4 Arbour1 recommended
treatment of AS with esmolol and nitroprusside because
www.aana.com/aanajournalonline.aspx
1. Early echocardiogram for all donors—Insert pulmonary artery catheter (PAC) to monitor patient management (placement of the
PAC is particularly relevant in patients with an EF <45% or on high dose inotropes.)
• Use aggressive donor resuscitation as outlined below
2. Electrolytes
• Maintain Na < 150 meq/dl
• Maintain K+ > 4.0
• Correct acidosis with Na Bicarbonate and mild to moderate hyperventilation (pCO2 30 - 35 mm Hg)
3. Ventilation—Maintain tidal volume 10-15 ml/kg
• Keep peak airway pressures < 30 mm Hg
• Maintain a mild respiratory alkalosis (pCO2 30 - 35 mm Hg)
4. Recommend use of hormonal resuscitation as part of a comprehensive donor management protocol—key elements
• Tri-iodothyronine (T3): 4 mcg bolus: 3 mcg/hr continuous infusion
• Arginine Vasopressin: 1 unit bolus: 0.5—4.0 unit/hour drip (titrate SVR 800 - 1200 using a PA catheter)
• Methylprednisolone: 15 mg/kg bolus (Repeat q 24° PRN)
• Insulin: drip at a minimum rate of 1 unit/hour (titrate blood glucose to 120 - 180 mg/dl)
• Ventilator: (see above)
• Volume Resuscitation: Use of colloid and avoidance of anemia are important in preventing pulmonary edema
o Albumin if PT and PTT are normal
o Fresh frozen plasma if PT and PTT abnormal (value ≥ 1.5 X control)
o Packed red blood cells to maintain a PCWP of 8 -12 mm Hg and Hgb>10.0 mg/dl
5. When patient is stabilized/optimized repeat echocardiogram. (An unstable donor has not met 2 or more of the following
criteria.)
• Mean Arterial Pressure ≥ 60
• CVP ≤ 12 mm Hg
• PCWP ≤ 12 mm Hg
• SVR 800 - 1200 dyn/sec/cm5
• Cardiac Index ≥ 2.5 l/min/M2
• Left ventricular stroke work index > 15
• Dopamine dosage < 10 mcg/kg/min
Figure 1. Cardiothoracic Donor Management
Na indicates sodium; K+, potassium ion; pCO2, partial pressure of carbon dioxide; PA, pulmonary artery; SVR, systemic vascular
resistance; q 24° PRN, every 24 hours as needed; PT, prothrombin time; PTT, partial thromboplastin time; CVP, central venous pressure;
and PCWP, pulmonary capillary wedge pressure.
(Reprinted with permission from UNOS, Richmond, Virginia. The Critical Pathway for the Organ Donor can be accessed at:
http://www.unos.org/resources/pdfs/CriticalPathwayPoster.pdf.25)
they are effective, titrated easily, and have short durations
of action. Usually AS will be followed by a short period of
hemodynamic stability, then dramatic hypotension.1
Autonomic storm leads to extensive endothelial cell
injury, resulting from ischemia-reperfusion injury and
shearing stress. Studies in canines using intravenous Larginine supplements (an essential amino acid), have
demonstrated a reversal of the endothelial dysfunction,
converting a formerly unusable donor heart to one that
can be transplanted. L-arginine enhances the supply of
endogenous nitric oxide, a local vasodilator. Through the
actions of nitric oxide, the endothelial dysfunction is repaired and the myocardial function is improved.10
When circulating levels of antidiuretic hormone or vasopressin are decreased, diabetes insipidus develops,
which if not corrected leads to catastrophic imbalances in
www.aana.com/aanajournalonline.aspx
electrolytes, cellular dehydration, and hypovolemia.13,5,8,13,17,28
Treatment with desmopressin (DDAVP) or
arginine vasopressin can correct this phenomenon.
Because of a longer half-life, DDAVP is a better choice for
hemodynamically stable patients.28 For the hypotensive
patient, vasopressin is the agent of choice. Vasopressin
has also been demonstrated to reduce the need for exogenous catecholamines.1,13-15,17 Vasodilatory shock
causing ischemia results in increased levels of hydrogen
ion (H+) and lactate. This leads to adenosine triphosphate-sensitive potassium (KATP) channels opening and
potassium diffusing out, causing an inhibition of muscle
contraction by hyperpolarizing smooth muscles.
Vasopressin may allow the weaning of catecholamines
and helps restore vascular tone by facilitating the closure of
the KATP channels.15 By decreasing the need for inotropic
AANA Journal ß August 2010 ß Vol. 78, No. 4
295
drugs, myocardial oxygen consumption is decreased and
myocardial energy stores are preserved.13 It has been
shown that vasopressin decreases pulmonary edema and
pulmonary capillary leak, reduces the levels of chemokines
and cytokines (factors that contribute to the systemic
immune and inflammatory responses and cell death), and
reduces the expression of certain genes and neutrophils
that are known to infiltrate organs in acute rejection.15
Thyroid hormones exercise control over the cardiovascular system by maintaining a high cardiac output
(CO) and a low systemic vascular resistance (SVR). With
brain death, CO decreases and SVR increases, leading to
diffuse hypoperfusion of the tissues and organs and
anaerobic metabolism. By administration of thyroid supplementation (T4 or T3), CO and SVR are improved, rendering better tissue perfusion and oxygenation and reducing lactic acidosis.1,3,4,13,14,17 Triiodothyronine is
primarily responsible for the physiologic effects of
thyroid hormones; approximately 80% of T3 is formed in
the peripheral tissues via the deiodination of the T4 outer
ring.14 Owing to the expense of T3, T4 is used in many
centers, but the brain-dead organ donor’s ability to
convert T4 to T3 is unreliable, so T4 may not be as effective in supporting the donor.13,14 A theory explaining this
phenomenon is that the conversion of T4 to T3 in the
brain-dead organ donor is inhibited by cytokines released
during AS.13 Also, once brain death has occurred, there is
an increased conversion of T4 to an inactive reverse T3,
which is called sick euthyroid syndrome.13,14
For prevention of further osmotic diuresis and cellular
dehydration, serum glucose concentrations should be
maintained between 120 and 180 mg/dL. After brain
death there are decreased levels of circulating insulin;
thus, insulin resistance develops, leading to hyperglycemia from catecholamine surges.1-3,13,17
The intense release of inflammatory mediators that
follows brain death leads to more circulating cytokines
in the donor organs. This can cause an additional
immune response in the donor organs when they are
transplanted. Serum cortisol levels are decreased in the
brain-dead organ donor and should be replaced with intravenous methylprednisolone. This replacement supplements the deficit of cortisol, decreases the inflammatory response, and decreases production of cytokines in
the donor. Lung function and oxygenation are improved
in the donor, and the immune response in the recipient
is attenuated.1,3,6,13,17
The brain-dead donor cannot maintain normal body
temperature. Without treatment, the donor’s temperature
will quickly decrease to ambient temperature. Normothermia must be maintained with fluid warmers, warming
blankets, a higher room temperature, and heated or humidified ventilator circuits. Hypothermia affects clotting
times and platelet aggregation and can lead to disseminated intravascular coagulopathy.1,2,13,17,22
296
AANA Journal ß August 2010 ß Vol. 78, No. 4
Surgery for Organ Procurement
Common recommendations for the perioperative management of the brain-dead organ donor include the use
of neuromuscular blocking agents to prevent reflex
movements during surgical stimulation.16-18 Spinal reflexes include cardiovascular responses that commonly
occur during the organ procurement surgery.2,16,18
Importantly, some authors suggest that the administration of a volatile anesthetic agent prevents this from occurring.16 Cardiovascular stimulation is believed to
involve a reflex arc to the adrenal medulla and may be
exaggerated by the increased excitability of the spinal
cord distal to the lesion. In this case, the lesion is at or
below the brain stem, which potentially leads to excitability of the entire spinal cord.2,21
In 1985, Wetzel et al21 published a retrospective chart
review of 10 organ procurement surgeries. The authors
summarized that within minutes of surgical stimulation,
each of the donor’s systolic and diastolic blood pressures
and heart rates increased substantially (31 mm Hg, 16
mm Hg, and 23/min, respectively).21 These same responses have been observed and are mentioned throughout the available literature.
In 2003, Fitzgerald et al19 hypothesized that the administration of fentanyl could suppress this intraoperative release of catecholamines associated with the hemodynamic changes during the organ procurement surgery.
Although these authors were not successful in proving
their hypothesis, they published valuable data regarding
the intraoperative increases in circulating catecholamines.19 Measured serum epinephrine and norepinephrine levels were taken at baseline (before injection of fentanyl, 7 µg/kg, or placebo), 10 minutes after injection of
the bolus, 5 minutes after skin incision, and 5 minutes
after sternotomy. In addition to finding that fentanyl, 7
µg/kg, was not sufficient in blocking intraoperative
release of catecholamines with surgical incision or sternotomy, they found that serum levels of epinephrine increased with surgical incision in all cases and that these
changes were not consistent with changes in the donor’s
heart rates and mean arterial pressures. Many of the documented changes in heart rate and blood pressure seen in
this study exceeded those previously reported in conjunction with AS.19
Potential Indications for Use of Volatile
Anesthetics
Even in living animals, the spinal cord appears to be more
responsible for cardiovascular responses to noxious
stimuli than the brain. In 1995, Antognini and Berg29
published a study indicating that the brain has little to do
with the suppression of adrenergic responses when
isoflurane anesthesia was administered. The minimal
alveolar concentration blocking adrenergic response
(MAC-BAR) for isoflurane was determined in goats. In
www.aana.com/aanajournalonline.aspx
Anesthetic preconditioning
could reduce ischemiareperfusion injury and
resulting organ dysfunction
in heart, liver and kidneys
Preventing or reducing
adrenergic responses could
lead to less ischemiareperfusion injury and
infiltration of inflammatory
substances into
transplanted organs
Reducing the release of
TNF-α and other proinflammatory substances
reduces incidence of
infiltration into donor
organs that can increase
probability of acute
rejection
Better organ
function posttransplant and
less acute
rejection in the
recipient
Figure 2. Potential Benefits for Organ Recipients When Inhalational Anesthetic Agents are Administered During
Organ Procurement Surgery
TNF indicates tumor necrosis factor.
one group isoflurane was administered in the conventional fashion (whole body group). In the remaining 2
groups, circulation to the cranium and the torso were isolated and perfused by separate cardiopulmonary bypass
machines to determine if there were differences in MACBAR of the cranium (representing the brain) and MACBAR of the torso (representing the spinal cord).29 In each
bypass machine, blood was oxygenated and isoflurane
was delivered by a vaporizer and returned to the goat. In
the spinal cord group, the brain concentration of isoflurane was 0.2% to 0.3%, and spinal cord concentration of
isoflurane was titrated to achieve MAC-BAR. In the brain
group, spinal cord concentration of isoflurane was 0.2%
to 0.3%, and brain concentration of isoflurane was titrated to achieve MAC-BAR.
The authors found that they were sometimes unable to
deliver sufficient concentrations of isoflurane to the brain
to achieve MAC-BAR, even when using an enflurane vaporizer that enabled them to deliver higher concentrations than the isoflurane vaporizer would allow.29 In this
study, whole body MAC-BAR averaged 3.7% ± 0.4%,
MAC-BAR of the brain averaged 5.6% ± 2.4%, and MACBAR of the spinal cord averaged 2.2% ± 0.7%. These
results demonstrated a significant decrease in MAC-BAR
requirements, and interestingly, minimal decreases in
mean arterial pressure in the spinal cord group compared
with the whole body and brain groups (12 ± 9 mm Hg, 31
± 22 mm Hg, and 21 ± 16 mm Hg, respectively).
In addition to preventing or reducing adrenergic re-
www.aana.com/aanajournalonline.aspx
sponses to noxious stimulation, isoflurane and other inhalational agents have been shown to reduce ischemiareperfusion injury and resulting organ dysfunction in the
heart, kidneys, liver, and brain (Figure 2).30 Ischemiareperfusion injury is defined as “a complex process involving the generation and release of inflammatory cytokines,
the accumulation and infiltration of neutrophils, and cell
death.”31 Studies on living animals have shown a significant decrease in ischemia-reperfusion injury and resulting
organ dysfunction when 1.5% isoflurane is administered
for the 20 minutes before periods of ischemia. This technique is referred to as anesthetic preconditioning. The
authors studied the differences between 2 groups that
were subjected to renal ischemia. One group received
isoflurane before ischemia and the other did not.31
The serum urea nitrogen and creatinine levels were
monitored at 0, 12, 24, and 48 hours after reperfusion. In
the group that did not receive isoflurane, serum creatinine levels were 2.4 ± 1.2 mg/dL and 2.9 ± 0.9 mg/dL at
24 and 48 hours after reperfusion, respectively, and
serum urea nitrogen levels were 99 ± 29 mg/dL and 187
± 31 mg/dL. The group that received isoflurane showed
significantly decreased levels. Serum creatinine levels
were 1.2 ± 0.7 mg/dL and 1.1 ± 0.2 mg/dL, and serum
urea nitrogen levels were 62 ± 19 mg/dL and 79 ± 20
mg/dL at 24 and 48 hours after reperfusion.31
Anesthetic preconditioning has also been shown to
protect the heart from damage during periods of ischemia. With preconditioning, areas of myocardial injury
AANA Journal ß August 2010 ß Vol. 78, No. 4
297
Actions of
inhalational
anesthetic agents in
live subjects
Prevent or reduce
adrenergic responses
to noxious
stimulation
Reduce ischemia/
reperfusion injury via
anesthetic
preconditioning
Suppress effects of
TNF-α and other proinflammatory
products
Figure 3. Documented Actions of Inhalational Anesthetic Agents in Live Subjects
TNF indicates tumor necrosis factor.
are decreased and myocardial contractility is better preserved. In addition to the effects on the myocardium
itself, the endothelium and vasculature are protected.
Preconditioning also attenuates the inflammatory responses occurring with ischemia/reperfusion.30
The increased release of tumor necrosis factor α
(TNF-α), a proinflammatory cytokine, worsens the
cascade of events occurring with ischemia-reperfusion
injury and its attack on endothelium (Figure 3).
Researchers have demonstrated the ability of isoflurane,
xenon, and nitrous oxide, all at 0.43% MAC, to suppress
the effects of TNF-α on certain gene and protein expressions that further damage the endothelium.32
Conclusions
These findings call into question the routine recommendations of the organ procurement agencies that the donors
require no anesthesia.16 It only seems reasonable to consider that it is not the organ donor who requires the anesthesia; instead, the administration of inhalational anesthesia to the brain-dead organ donor can potentially benefit
each of the recipients of that donor’s organs. Because the
literature suggests so strongly that AS in the donor causes
deterioration of body systems and ultimately of organs, it
makes sense that by preventing sympathetic surge of catecholamines during surgical stimulation, the likelihood of
successful transplantation will increase.
Ischemia-reperfusion injury is known to be a major
contributing factor in acute organ rejection. Although the
studies cited were performed on live subjects, reduction
in ischemia-reperfusion injury as a result of anesthetic
preconditioning is well documented in the heart and
kidneys. Further research would determine if anesthetic
preconditioning would prove to be beneficial for preserving the viability of transplanted organs.
Given the shortage of viable organs for transplantation, any treatment regimen that improves their viability
298
AANA Journal ß August 2010 ß Vol. 78, No. 4
would benefit the recipient population. Increasing the
number of adequately functioning organs will reduce the
need for repeated transplantations and will lead to better
quality of life in recipients.
REFERENCES
1. Arbour R. Clinical management of the organ donor. AACN Clin Issues.
2005;16(4):551-580.
2. Sarti A. Organ donation. Paediatr Anaesth. 1999(4);9:287-294.
3. Peiffer KM. Brain death and organ procurement. Am J Nurs. 2007;107
(3):58-67.
4. Audibert G, Charpentier C, Seguin-Devaux C, et al. Improvement of
donor myocardial function after treatment of autonomic storm during
brain death. Transplantation. 2006;82(8):1031-1036.
5. Kutsogiannis DJ, Pagliarello G, Doig C, Ross H, Shemie SD. Medical
management to optimize donor organ potential: review of the literature. Can J Anesth. 2006;53(8):820-830.
6. Novitzky D, Cooper DK, Rosendale JD, Kauffman HM. Hormonal
therapy of the brain-dead organ donor: experimental and clinical
studies. Transplantation. 2006;82(11):1396-1401.
7. Avlonitis VS, Fisher AJ, Kirby JA, Dark JH. Pulmonary transplantation: the role of brain death in donor lung injury. Transplantation.
2003;75(12):1928-1933.
8. Spiss CK, Metnitz PH, Schafer B, Steltzer H. Management of the
multi-organ donor. Acta Anaesthesiol Scand Suppl. 1997;111:77-78.
9. Nijboer WN, Schuurs TA, van der Hoeven JA,et al. Effect of brain
death on gene expression and tissue activation in human donor kidneys. Transplantation. 2004;78(7):978-986.
10. Szabó G, Soós P, Heger U, et al. L-Arginine improves endothelial and
myocardial function after brain death. Transplantation. 2006;82(1):
108-112.
11. Kaminska D, Tyran B, Mazanowska O, et al. Cytokine gene expression
in kidney allograft biopsies after donor brain death and ischemiareperfusion injury using in situ reverse-transcription polymerase
chain reaction analysis. Transplantation. 2007;84(9):1118-1124.
12. Sánchez-Fructuoso AI, Prats D, Marques M, et al. Does donor brain
death influence acute vascular rejection in the kidney transplant?
Transplantation. 2004;78(1):142-146.
13. Ullah S, Zabala L, Watkins B, Schmitz ML. Cardiac organ donor management. Perfusion. 2006;21(2):93-98.
14. Zuppa AF, Nadkarni V, Davis L, et al. The effect of a thyroid hormone
infusion on vasopressor support in critically ill children with cessation of neurologic function. Crit Care Med. 2004;32(11):2318-2322.
15. Rostron AJ, Avlonitis VS, Cork DM, Grenade DS, Kirby JA, Dark JH.
www.aana.com/aanajournalonline.aspx
16.
17.
18.
19.
20.
21.
22.
23.
24.
25.
Hemodynamic resuscitation with arginine vasopressin reduces lung
injury after brain death in the transplant donor. Transplantation.
2008;85(4):597-606.
Elliot JM. Brain death. Trauma. 2003;5:23-42.
Berry R. Brainstem death and the management of the organ donor.
Anaesth Intensive Care Med. 2006;7(6):212-214.
Munn J. Focus on: medico-legal issues in anaesthesia—part 1. Brainstem
death and organ donation. Curr Anaesth Crit Care. 1998;9(5):236-241.
Fitzgerald RD, Hieber C, Schweitzer E, Luo A, Oczenski W, Lackner
FX. Intraoperative catecholamine release in brain-dead organ donors
is not suppressed by administration of fentanyl. Eur J Anaesthesiol.
2003;20(12):952-956.
Young PJ, Matta BF. Anaesthesia for organ donation in the brainstem
dead—why bother? Anaesthesia. 2000;55(2):105-106.
Wetzel RC, Setzer N, Stiff JL, Rogers MC. Hemodynamic responses in
brain dead organ donor patients. Anesth Analg. 1985;64(2):125-128.
Otte JB, Squifflet JP, Carlier MC, et al. Organ procurement in children:
surgical, anaesthetic and logistic aspects. Intensive Care Med. 1989;15:
S67-S70.
Yoo KY, Jeong CW, Kim SJ, et al. Sevoflurane concentrations required
to block autonomic hyperreflexia during transurethral litholapaxy in
patients with complete spinal cord injury. Anesthesiology. 2008;108
(5):858-863.
Mollaret P, Goulon M. Le coma dépassé. Rev Neurol. 1959;101:3-15.
Cardio-thoracic donor management. In: Critical pathway for the
organ donor. United Network for Organ Sharing website. http://www.
unos.org/resources/pdfs/CriticalPathwayPoster.pdf. Published 2002.
Accessed November 15, 2008.
www.aana.com/aanajournalonline.aspx
26. Matuschak GM. Optimizing ventilatory support of the potential organ
donor during evolving brain death: maximizing lung availability for
transplantation. Crit Care Med. 2006;34(2):548-549.
27. Koudstaal LG, ¢t Hart NA, Ottens PJ, et al. Brain death induces inflammation in the donor intestine. Transplantation. 2008;86(1):148-154.
28. Gelb AW, Robertson KM. Anaesthetic management of the brain dead
for organ donation. Can J Anesth. 1990;37(7):806-812.
29. Antognini JF, Berg K. Cardiovascular responses to noxious stimuli
during isoflurane anesthesia are minimally affected by anesthetic
action in the brain. Anesth Analg. 1995;81(4):843-848.
30. De Hert SG, Turani F, Mathur S, Stowe DF. Cardioprotection with
volatile anesthetics: mechanisms and clinical implications. Anesth
Analg. 2005;100(6):1584-1593.
31. Hashiguchi H, Morooka H, Miyoshi H, Matsumoto M, Koji T,
Sumikawa K. Isoflurane protects renal function against ischemia and
reperfusion through inhibition of protein kinases, JNK and ERK.
Anesth Analg. 2005;101(6):1584-1589.
32. Weber NC, Kandler J, Schlack W, Grueber Y, Frädorf J, Preckel B.
Intermitted [sic] pharmacologic pretreatment by xenon, isoflurane,
nitrous oxide, and the opioid morphine prevents tumor necrosis factor α-induced adhesion molecule expression in human umbilical vein
endothelial cells. Anesthesiology. 2008;108(2):199-207.
AUTHOR
Laurie J. Elkins, CRNA, MS, CCRN, is a staff nurse anesthetist at Charleston
Area Medical Center, Charleston, West Virginia. At the time this article was
written, she was a student at Charleston Area Medical Center School of
Nurse Anesthesia, Charleston, West Virginia. Email: [email protected].
AANA Journal ß August 2010 ß Vol. 78, No. 4
299