Chapter 108

108
CHAPTER
Liver Transplantation:
Anesthetic Considerations
Charles Lee
PREOPERATIVE ASSESSMENT
Increased mixed venous hemoglobin oxygen saturation and de -
ceased arteriovenous (AV) oxygen difference reflect AV shunting
Although the etiologies of end-stage liver disease in the pediatric
and decreased oxygen consumption.
patient are varied, liver failure culminates in a common patho -
7 Pulmonary blood flow is
increased, whereas hepatic and renal blood flow are diminished.
physiologic state. These pathophysiologic changes of liver disease
Although cardiomyopathy and portopulmonary hypertension
and their anesthetic implications dictate the anesthetic manage -
are rare in children, a thorough cardiac evaluation, including echo -
ment during orthotopic liver transplantation surgery.
cardiography, is warranted. Intracardiac shunts, particularly septal
Time permitting, comprehensive preoperative medical man -
defects, may predispose to paradoxical air embolism during revas -
agement in the intensive care unit may reduce perioperative
cularization. 7 Children presenting for retransplant subsequent to
morbidity and mortality in children with fulminant liver failure.
immunosuppressive therapy with tacrolimus may have hyper -
Infections should be treated, edema should be minimized or
trophic cardiomyopathy. 8–11 Children with Allagille syndrome,
corrected, renal and cardiopulmonary function should be opti -
which is associated with congenital cardiac abnormalities, may
mized, and irreversible brain injury secondary to cerebral edema
develop portopulmonary hypertension and right ventricular dys -
should be prevented.
function. These patients may require pulmonary artery pressure
measurement by cardiac catheterization as part of their preopera -
Central Nervous System
tive evaluation.
Hepatic encephalopathy is a multifactorial complication of endstage
liver disease. Factors that contribute to its development Pulmonary System
include hyponatremia, hypoglycemia, accumulation of ammonia Advanced liver disease in children is commonly accompanied by
and neuroactive peptides acting as false neurotransmitters, and impaired respiratory function and arterial hypoxemia. Pulmonary
cerebral hyperemia. 1 Sedative drugs should be used judiciously, dysfunction and increased work of breathing typically are mecha -
because they may have exaggerated effects in this group of nical in nature, resulting from reduced lung volumes asso ciated
patients. The use of hypertonic saline and moderate hypothermia,
in the treatment of raised intracranial pressure (ICP), has minemia may result in pulmonary edema, as well. Pulmonary
with ascites, hepatosplenomegaly, and pleural effusions. Hypoalbu -
shown therapeutic promise in adult patients with end-stage liver function is further adversely impacted by perioperative chest infec -
disease. 2,3 Pediatric patients in whom the cerebral perfusion tions, which are particularly common in children with encephalo
pathy, impaired gastric emptying, and those on mechan ical
pressure cannot be maintained at greater than 40 mmHg are likely
to have sustained irreversible brain damage and will not benefit ventilation. 1 Response to supplemental oxygen may help quantify
from orthotopic liver transplantation. 4 Although the use of ICP the degree of fixed shunting in patients with hypoxemia due to AV
monitoring has been advocated by some, in the management of shunting. 7
elevated ICP and to identify patients who are not candidates for Severe hypoxemia can also result from hepatopulmonary
transplantation, the risk of intracranial hemorrhage precludes syndrome (HPS). Hepatopulmonary syndrome is a clinical condi -
routine use of this monitor in this patient population. 1,5,6 Patients tion manifested by a triad of liver dysfunction, arterial hypoxemia,
with severe encephalopathy should undergo CT scanning or and intrapulmonary vascular dilatation. 12 The pathogenesis of HPS,
neuroultrasonography, as cerebral edema and intracranial hemor - although not clearly delineated, appears to be associated with portal
rhage may preclude transplantation.
hypertension and the production of vasoactive mediators including
nitric oxide in the lungs. 13–16 The resulting pulmonary vasodilation
may occur as diffuse precapillary and capillary dilation or discrete
Cardiovascular System
arteriovenous communications. 17 Arterial hypoxemia and right-toleft
shunting due to vasodilation of the pulmonary vasculature
Chronic liver failure is typically associated with a hyperdynamic
circulatory state with low systemic vascular resistance (SVR) and causes V˙/Q˙ mismatch and true anatomic shunts that bypass gas
increased cardiac output. Multiple factors including excessive exchange units. 17,18
sympathetic nervous system activity, fluid retention secondary to Hepatopulmonary syndrome is diagnosed clinically by a fall in
portal hypertension, and impaired clearance of vasoactive com - arterial oxygen levels upon standing from a supine position
pounds are thought to contribute to these physiologic changes. 1 (orthodeoxia), clubbing, and dyspnea. HPS may also be diagnosed

CHAPTER 108 ■ Liver Transplantation: Anesthetic Considerations 1817
by technetium 99 radio-labeled microalbumin scan or contrastenhanced
echocardiography. Although 95% of the microaggre -
gated albumin is taken up in the lungs of a normal individual,
intrapulmonary shunting in HPS causes the radio-labeled micro -
albumin spheres to be taken up in the systemic capillary beds. 1,19
Agitated saline contrast echocardiography can give a quick
diagnosis if bubbles appear in the left atrium in the absence of a
direct intracardiac communication. 13
Gastrointestinal System
Portal hypertension and chronic malnutrition may predispose
patients to spontaneous bacterial peritonitis and other infections
due to impaired immune function. Children who have undergone
Kasai portoenterostomy may also be at increased risk for devel -
oping cholangitits. Hypersplenism and associated thrombocy -
topenia resulting from portal hypertension can lead to catastrophic
hemorrhage, especially in the presence of esophagogastric varices
and coagulopathy. 7 Aspiration of blood during an acute variceal
bleed may cause pulmonary decompensation.
Hepatic System
Impaired hepatic synthetic function may affect drug metabolism,
glucose homeostasis, intravascular volume, and coagulation. De -
creased glycogen stores and impaired gluconeogenesis may pre -
dispose to hypoglycemia if supplemental glucose is not provided.
Coagulation defects result from reduced hepatic synthesis of
clotting factors as well as malabsorption of vitamin K secondary
to decreased bile acid secretion and antibiotic therapy. A
deficiency of vitamin K–dependent clotting factors may lead
to severe bleeding. Portal hypertension results in the development
of gastrointestinal varices as well as ascites. Anemia and
thrombocytopenia which are commonplace in end stage liver
disease, are exacerbated by dilutional effects from increased
plasma volume. 7 Anemia may result from bleeding, malnutrition,
and splenic sequestration of red blood cells. Thrombocytopenia
is commonly secondary to splenic sequestration, but it may also
occur as a result of sepsis. 7
Impaired metabolism of drugs, including anesthetic agents,
may result in prolongation of their duration of action. Impaired
protein synthesis, in addition to increased blood volume and
volume of distribution, results in decreased plasma concentrations
of coagulation proteins, plasma cholinesterase, and albumin. High
serum levels and prolonged elimination half-lives of anesthetic
drugs that are highly protein-bound and have small volumes of
distribution, can occur. However, drug protein binding does not
correlate well with albumin concentrations or the degree of liver
dysfunction. 20 Serum albumin concentrations are also influenced
by malnutrition and degradation. Because albumin has a half-life
of approximately 21 days, serum levels may not reflect current
albumin production. 7 Hypoalbuminemia results in low serum
oncotic pressure which leads to intravascular hypovolemia and
hypotension, interstitial edema, ascites, and pleural effusions. 7,21
Renal System
The majority of children presenting for liver transplantation have
adequate renal function. Hepatorenal syndrome is characterized
by decreased renal blood flow, glomerular filtration rate and urine
output, as well as elevated serum creatinine, low urine sodium (

1818 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations
arterial and venous catheters, particularly in the presence of
coagulopathy.
Pulmonary artery catheters may provide useful hemodynamic
information, but are not usually employed in pediatric liver trans -
plantation due to potential complications and size incom patibility.
Transesophageal echocardiography (TEE) can provide real time
monitoring of ventricular filling and contractile function, which
may help with fluid and inotropic drug management. 7 TEE can
also help to detect septal defects or a patent foramen ovale which
can predispose to paradoxical air emboli, as well as detect intra -
cardiac air or microthrombi during hepatic reperfusion.
Anesthesia is maintained with a balance of inhalational agent,
opioid, and nondepolarizing muscle relaxant. Isoflurane does not
undergo significant metabolism and it has not been associated
with renal or hepatic toxicity. 7 Midazolam may be useful in pro -
viding hypnosis and amnesia when use of inhalational anesthetic
agents is limited by hypotension. Administering an FiO 2
of 1.0
during hypotensive episodes may maximize oxygen delivery
to tissues.
Liver transplantation surgery is divided into three phases.
The preanhepatic or dissection phase begins with skin incision
and terminates with occlusion of the hepatic artery and portal
vein. This is followed by the anhepatic phase which begins with
devascularization of the liver or hepatectomy and is completed
when the I.V. and portal vein clamps are removed and the newly
transplanted liver is perfused, with or without unclamping of the
hepatic artery. The final phase, the postanhepatic or postreperfusion
phase, begins immediately after the new liver graft is reperfused
and ends with completion of surgery. Each phase presents specific
anesthetic challenges and management goals.
Dissection (Preanhepatic) Phase
In this first phase of surgery, there is potential for significant blood
loss during dissection of the diseased liver in the presence of
coagulopathy. Patients who have had previous upper abdominal
surgeries such as a Kasai procedure or previous liver trans planta -
tion are more likely to experience significant blood loss associated
with adhesions and prolonged dissection. 1,27 In fact, the greatest
blood loss typically occurs during this stage and during the
beginning of the anhepatic stage.
Anesthetic management is aimed at maintaining hemodynamic
stability and glucose homeostasis. Arterial blood gases should be
assessed hourly. Fluid and blood product administration, and
judicious correction of coagulation abnormalities can be guided by
serial hematocrit measurements, prothrombin time, and throm -
boelastography (TEG). Overcorrection of coagulopathy must be
avoided. Fresh frozen plasma may be administered to achieve an
INR near 1.5, and platelets may be administered to maintain
platelet counts greater than 50,000/mm 3 or when there is evidence
of thrombocytopenia by TEG. 1,7 However, it should be noted that
the TEG has lengthy endpoints, such that the coagulation profile
may have changed significantly by the time TEG results become
available. It is therefore necessary to communicate with the
surgeons and correlate test results with the clinical picture.
Correction of coagulopathy should be directed by coagulation
studies that differentiate particular clotting defects, and clinical
correlation. Overly aggressive correction of coagulation abnor -
malities may contribute to hepatic artery and/or portal vein
thrombosis, especially during the reperfusion phase. If the pro -
thrombin time (PT) and partial thromboplastin time (PTT) are
markedly prolonged, and the surgeon observes diffuse bleeding,
10 mL/kg of fresh frozen plasma should be administered. Further
transfusion therapy should be guided by close monitoring of
coagulopathy. Fresh frozen plasma transfusions at rates exceed ing
1 mL/kg/min will depress the ionized calcium concentration,
causing hypotension and, in extreme cases, electromechanical
dissociation. Calcium levels should be monitored closely during
massive blood loss necessitating rapid transfusion of blood
products. Ionized calcium should be maintained at greater than
1 mmol/L. A calcium chloride infusion may be initiated to main -
tain ionized calcium at a target level of 1.2 mmol/L. 1 The higher
concentration of citrate in FFP significantly chelates elemental
calcium and magnesium ions in blood. Citrate intoxication is the
most common complication of massive transfusion of blood
products, especially during the anhepatic phase when citrate
cannot be metabolized.
Thrombocytopenia may be secondary to preoperative hyper -
splenism, platelet consumption, or intraoperative dilution. Platelet
therapy is reserved for treating platelet counts less than 50,000
mm 3 in the presence of excessive surgical bleeding. Fibrinogen
depletion as a result of fulminant hepatic failure leads to pro -
longation of both PT and PTT. Excessive surgical bleeding
with associated fibrinogen depletion should be corrected with
cryoprecipitate 0.2 units/kg. The treatment of coagulopathy,
especially with cryoprecipitate and platelets, should be discussed
with the surgeon, who will be able to assess coagulation
abnormalities in the surgical field.
Ideally, the hematocrit should be maintained in the range of
26% to 30% to minimize risk of thrombotic complications asso -
ciated with increased viscosity. 1,28 Massive transfusion of banked
red blood cells to infants can result in severe hyperkalemia. Irra -
diation of blood products is not necessary in liver trans plantation
as graft versus host disease in liver recipients is almost always due
to the donor organ. 29,30 Irradiated blood should not be used routi -
nely for infants undergoing liver transplantation because irradia -
tion of packed red blood cells can increase the potassium
concentration in the supernatant by two- to threefold. Nonirra -
diated blood that is as fresh as possible should be requested
from the blood bank when infants are undergoing liver trans -
plantation as massive transfusions of blood greater than 2 weeks
of age has been associated with severe intraoperative hyperkalemia
and cardiac arrest in infants. 31,32 Massive blood transfusions are
also associated with dilutional coagulopathies, acidosis, and hypo -
thermia.
Fluid administration and occasionally inotropic support may
be necessary to treat hypotension. Systemic vascular resistance
(SVR) is often unresponsive to -agonists in liver failure patients,
and may exacerbate peripheral and renal ischemia in high con -
centrations. Surgical manipulation of the liver may also contribute
to hypotension by impeding venous return. Sodium bicarbonate
should be administered to maintain a base deficit above negative
6 mEq/L. Intravenous dextrose (D5 NS) should be administered to
maintain serum glucose concentration greater than 100 mg/dL.
These patients are prone to hypoglycemia due to impaired glu -
coneogenesis and glycogen storage. Impaired hepatic degradation
of insulin may further exacerbate hypoglycemia.
There is no consensus on the optimal replacement fluid,
which tends to vary with institutional preference. Additional
fluid replacement is most often given as balanced salt and/or
colloid solution. Albumin solution may be used for intravascular

CHAPTER 108 ■ Liver Transplantation: Anesthetic Considerations 1819
ex pansion if serum albumin concentration is less than 2.5 g/dL.
Overzealous intravenous fluid transfusion must be avoided, as this
may lead to undesired edema of the abdominal viscera.
Anhepatic Phase
Progressive metabolic derangement and coagulopathy, as well as
decreased venous return to the heart, are prominent features of this
phase of surgery. Venous return to the heart will be decreased while
the I.V. clamp is cross-clamped. Judicious fluid adminis tration and
inotropes may be required to treat systemic hypo tension. Fluid
administration during this stage should be minimized and limited
to that volume necessary to preserve cardiac output for adequate
tissue perfusion. 7 A central venous pressure (CVP) of 2 to 4 cmH 2
O
during this phase may help decrease blood loss, but this goal may
be unattainable if tissue perfusion is compromised. Excessive
I.V. fluid administration during the anhepatic phase may lead
to intravascular hyper volemia following release of portal and
vena cava clamps upon reperfusion, resulting in increased right
atrial and hepatic venous pressures. This will cause congestion
of the liver graft. Intravenous nitroglycerin infusion may be used
to acutely ameliorate this predicament by increasing venous
capacitance.
Fibrinolysis usually starts in this period, but is not treated
unless severe. Fibrinogen depletion resulting in prolonged PT,
PTT, and excessive surgical bleeding may need to be corrected
with cryoprecipitate. Arterial blood gas and coagulation profile
should be checked 10 minutes after the anhepatic phase has begun
and every 30 minutes thereafter for the remainder of this phase.
Sodium bicarbonate should be administered as necessary to
neutralize serum pH. Calcium chloride in incremental doses to
10 to 20 mg/kg can be administered to maintain ionized calcium
concentration of 1.1 to 1.2 mmol/L. This will partially antagonize
the adverse cardiac effects of hyperkalemia and enhance cardiac
output. Potassium concentrations greater than 5 mEq/L should be
treated with hyperventilation and or administration of sodium
bicarbonate to alkalinize pH before reperfusion of the liver graft.
If serum concentration remains >5 mEq/L despite alkalinizing the
pH, furosemide 0.5 to 1 mg/kg (efficacy is reduced if vena cava is
cross-clamped) or glucose 0.5 g/kg and regular insulin 0.2 units/g
of glucose can be administered. 7
Steroids and other immunosuppressant drugs such as basilixi -
mab (Simulect) are administered at the beginning of the anhepatic
phase. As this phase of transplantation nears completion, prepara -
tion for the postreperfusion phase should be addressed (Box
108–1). Correcting acid-base and electrolyte abnormalities may
decrease the risk of significant hemodynamic instability at the time
of reperfusion of the donor liver.
Postreperfusion Phase
The period of greatest risk of hypotension is immediately
following reperfusion of the allograft. It is essential to maintain
communication with the surgeons during this period of time.
Hemodynamic instability is associated with rapid infusion of
effluent from the transplanted liver, which is high in potassium
and low in pH and temperature. 7 Potential circulatory distur -
bances include hypotension, bradycardia, supraventricular and
ventricular arrhythmias, decreased cardiac output and occa -
sionally, cardiac arrest. This postreperfusion syndrome is further
characterized by severely decreased SVR in the face of acutely
BOX 108-1. Preparation for Reperfusion of Liver Graft
Restore serum potassium, ionized calcium, and normal pH
Hyperventilation
Sodium bicarbonate
Calcium chloride
Increase body temperature to 36–37 C if possible
Raise room temperature
Lavage warm saline in peritoneal cavity if hypothermic
Convective warming device
Administer 100% FiO 2
Discontinue volatile anesthetic agent 5 minutes before reper -
fusion
Epinephrine and atropine readily available to treat hypotension
and bradycardia
Calcium chloride, sodium bicarbonate, and dextrose/insulin
readily available to rapidly treat acidemia and hyperkalemia
Blood available for transfusion
increased right-ventricular filling pressures associated with acute
pulmonary hypertension and left-ventricular dysfunction. 27
Air and microthrombi emboli may precipitate acute pulmonary
hypertension. Epinephrine boluses may be required to prevent
cardiovascular collapse immediately following reperfusion.
Hyperkalemia following reperfusion may be manifest by
electrocardiography changes including peaked T waves, prolonged
QT interval, and in severe cases, widened QRS complexes. Hyper -
kalemia and circulatory changes associated with reperfusion
usually subside within 10 minutes if appropriate therapeutic
measures are implemented. Blood must be immediately available
for transfusion in the event of hemorrhage following removal of
vascular clamps. However, excess I.V. fluid transfusion promotes
liver congestion, intestinal edema, increased intra-abdominal
pressure, and difficult surgical closure of the abdomen. A high
CVP can also result in excessive bleeding from the cut surface of
the liver if a segmental graft is transplanted. Hyperglycemia is
common following reperfusion, resulting from administration of
corticosteroid, blood products preserved with citrate, phosphate,
and dextrose, as well as decreased glucose utilization. 7
Vasopressors may be required to maintain adequate mean
arterial pressure for organ perfusion due to very low SVR. How -
ever, at the completion of surgery, arterial hypertension may occur
as anesthetic depth is decreased and sympathetic activation,
BOX 108-2. Goals of I.V. Fluid Therapy
Following Reperfusion
Maintain adequate cardiac output by administering the minimum
volume of I.V. fluid necessary to facilitate cardiac filling
Nitroglycerin infusion should be available to acutely alleviate liver
congestion
Furosemide 0.5–1 mg/kg may be administered if intravascular
hypervolemia results in liver congestion
Maintain hematocrit between 26–30% to reduce the risk of
hepatic artery thrombosis
Maintain adequate coagulation function (avoid overcorrection as
the incidence of hepatic artery thrombosis is greater in the pediatric
age group)
Administer dextrose-free I.V. solution unless serum glucose is
less than 100 mg/dL

1820 PART 5 ■ Anesthetic, Surgical, and Interventional Procedures: Considerations
corticosteroid administration, or intravascular hypervolemia exert
their effects. Incremental doses of parenteral opioids and vasoac -
tive drugs such as nicardipine and nitroglycerine can be titrated to
effect while transporting the patient to the intensive care unit.
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