Advances in Anesthesia 38 (2020) 251–267

ADVANCES IN ANESTHESIA

Anesthesia for the Patient with

Severe Liver Failure
Aidan Spring, LRCP&SI, MB BCh BAO, FCAIa,
Jagroop S. Saran, MDa,
Sinead McCarthy, MB BCh BAO, FCAIa,
Stuart A. McCluskey, MD, PhD, FRCPCb,*
a
Abdominal Organ Transplantation Anesthesia Fellowship Program, Department of Anesthesia
and Pain Management, Toronto General Hospital, University Health Network, University of
Toronto, 3 Eaton North, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada; bDepartment
of Anesthesia and Pain Management, Toronto General Hospital, University Health Network,
University of Toronto, 3 Eaton North, 200 Elizabeth Street, Toronto, Ontario M5G 2C4, Canada

Keywords

Anesthesia
End-stage liver disease
Liver failure
Anesthesia considerations
Key points

The incidence of liver failure continues to increase, and it is associated with
increased perioperative morbidity and mortality.

Liver failure is associated with multiorgan dysfunction, including central nervous,
cardiac, respiratory, gastrointestinal, renal, and hematological systems.

Preoperative identification, optimization, and tailored anesthetic management
are essential for optimum outcomes in patients with liver disease undergoing
surgery.

The coagulopathy of liver failure is a balanced coagulopathy better assessed by
thromboelastography than conventional testing, and it is not directly associated
with bleeding risk.

INTRODUCTION
Worldwide, liver disease is estimated to be responsible for 2 million deaths
each year, the vast majority owing to complications of cirrhosis, viral hepatitis,
and hepatocellular carcinoma.1 The incidence and prevalence of chronic liver

This article originally appeared in Anesthesiology Clinics, Volume 38, Issue 1, March 2020.
Financial Disclosures: None.
*Corresponding author. E-mail address: [email protected]

https://doi.org/10.1016/j.aan.2020.09.002
0737-6146/20/Crown Copyright ª 2020 Published by Elsevier Inc. All rights reserved.
252 SPRING, SARAN, MCCARTHY, ET AL

disease are not well established and are likely considerably higher best esti-
mates. The cause and burden of liver disease are also known to vary with
geographic region, ethnicity, and socioeconomic status.
The liver has many essential functions, including the production of bile, the
synthesis of plasma proteins (eg, clotting factors), drug metabolism, and the
storage of vitamins, minerals, and glucose, among many others. Historically,
the liver was divided into right and left lobes according to liver topography.
The functional and surgical anatomy of the liver is divided into 8 segments ac-
cording to vascular anatomy and biliary drainage.2 The vascular anatomy pro-
vides a unique blood supply, receiving blood from both the hepatic portal vein
and the hepatic arteries. The hepatic portal vein supplies approximately 75% of
hepatic blood flow and 50% of the liver’s oxygen.3 A novel flow relationship
exists between these 2 blood supplies in that the hepatic artery can produce
compensatory flow changes in response to changes in hepatic portal venous
inflow. This compensatory blood flow is known as the hepatic arterial buffer
response and maintains constant hepatic blood flow or oxygen supply.3
Liver disease is a multisystem disorder (Fig. 1) and is described as acute or
chronic according to time between symptom onset and the inciting event.

Fig. 1. Complications of advanced liver disease.

ANESTHESIA FOR SEVERE LIVER FAILURE 253

Acute liver failure is defined by the development of symptoms of severe liver

injury with encephalopathy, and impaired synthetic function in a patient
without preexisting liver disease, and an illness duration of less than 26 weeks.4
Anesthesia for patients with acute liver failure occurs mainly in the context of
orthotopic liver transplantation and will not be discussed further in this review.
Progressive chronic liver disease results in liver fibrosis, and cirrhosis is a term
used to describe advanced fibrosis. Cirrhosis is a histologic description charac-
terized by islands of hepatic regeneration surrounded by thin fibrous septa re-
sulting in parenchymal destruction and vascular distortion.5 Advanced chronic
liver disease may remain compensated for many years; the change to decom-
pensated cirrhosis occurs when features such as ascites, variceal bleeding, or en-
cephalopathy develop. Decompensated cirrhosis is associated with increased
mortality, and median survival decreases from 12 years to 2 years.6 Another
entity known as acute-on-chronic liver failure has more recently been
described.7 This syndrome is associated with increased short-term mortality
and is characterized by acute and severe hepatic disorder in patients with un-
derlying chronic liver disease.

CAUSE OF LIVER DISEASE

The causes of liver disease include infection, toxins, metabolic abnormalities,
autoimmune conditions, and vascular abnormalities. In the United States,
infection with the hepatitis C virus, alcohol, and increasingly, nonalcoholic
fatty liver disease (NAFLD) are the leading causes of cirrhosis.1,8 The
obesity epidemic is strongly associated with the increase in NAFLD. Thera-
pies used to manage obesity and its associated metabolic syndrome are being
evaluated.9
The pathophysiology of cirrhosis is complex and involves inflammation, fi-
brogenesis, and angiogenesis. These processes result in hepatic microvascular
changes remodeling of hepatic sinusoids and the formation of intrahepatic
shunts.5 Increasing hepatic resistance to portal vein flow causes portal hyper-
tension, a hallmark of cirrhosis. Portal blood flow is enhanced further by
splanchnic vasodilation, and this ultimately leads to the development of portal
hypertension, ascites, and portosystemic shunts, such as gastric varices. Shunt-
ing of compounds such as ammonia directly into the systemic circulation are
thought to have a role in the development of hepatic encephalopathy. The
complex interaction of the failing liver with other organs can result in hepatore-
nal syndrome, portopulmonary hypertension, hepatopulmonary syndrome,
and cirrhotic cardiomyopathy.10
Patients with liver disease present for surgery as part of their liver disease
treatment or to manage complications. Surgical procedures may include hepatic
resection for hepatocellular carcinoma or the creation of transjugular intrahe-
patic portosystemic shunts (TIPS) to decompress the portal system in the
case of refractory variceal bleeds or massive ascites. However, more concern-
ing are the patients presenting for surgery with advanced liver disease who
are unaware of their health status.8
254 SPRING, SARAN, MCCARTHY, ET AL

RISK STRATIFICATION
A direct relationship between increased perioperative risk and the severity of
chronic liver disease has held for some time.11 Acute hepatitis, particularly alco-
holic hepatitis, is regarded as a contraindication to nonemergent surgery
because it is associated with unacceptably high mortality.12 However, assess-
ment of perioperative risk in other patients with liver disease is not straightfor-
ward. Certainly, the urgency and nature of the proposed surgery as well as
comorbid medical issues need to be considered, but the challenge is to deter-
mine whether it is feasible to proceed with a procedure as proposed, to post-
pone until optimization/liver transplantation, or to defer indefinitely. A
variety of clinical scoring systems are used to help make this determination.
The two most commonly used are the Child-Turcotte-Pugh (CTP) score
and the Model for End-Stage Liver Disease (MELD) score.
The CTP score was developed in the 1960s to predict operative mortality
associated with portocaval shunt surgery. It consists of 5 measures: serum al-
bumin, bilirubin, prothrombin time, and the presence of hepatic encephalopa-
thy and ascites. The patient is assigned to group A, B, or C in order of
increasing liver disease severity by adding the score for each parameter
(Table 1). A 2011 single-center retrospective analysis of patients undergoing
general surgery found that in-hospital mortality was 63% in CTP group C,
17% in group B, and 10% in group A.13
The MELD score was originally developed to predict mortality following
TIPS placement and is now used to prioritize patients on the liver transplant
list.14 It includes serum bilirubin, creatinine, and the international normalized
ratio (INR). Higher MELD scores have been shown to correlate with increased
mortality in nontransplant surgery with a MELD score greater than 15 associ-
ated with 54% in-hospital mortality.13 Another study found that the addition of
serum albumin less than 2.5 mg/dL (25 g/L) to a MELD score 15 identified a
subset of patients at particularly high perioperative risk, that is, greater than
60%.15 However, when considering retrospective analyses, it should be borne
in mind that patients with advanced liver disease (CTP group C or
MELD >15) are typically not considered for elective surgery and so dispropor-
tionately undergo emergent procedures. Emergent procedures are consistently

Table 1
Child-Turcotte-Pugh score
Points Assigned
Variable 1 2 3
Serum bilirubin (lmol/L) <34 34–50 >50
Serum albumin (g/L) >35 23–35 <28
INR <1.7 1.7–2.3 >2.3
Ascites None Mild Severe
Encephalopathya None Grade I to II Grade III to IV
a
West Haven classification of hepatic encephalopathy.
ANESTHESIA FOR SEVERE LIVER FAILURE 255

associated with high mortality in those with advanced liver disease.13,15 Other
factors shown to be associated with adverse outcome include intraoperative
blood transfusion13,15,16 and high American Society of Anesthesiologists
(ASA) Physical Status classification score.11,13,15,17 Laparoscopic approaches
may be protective in abdominal surgery.18 A scoring system has been devel-
oped specifically to assess perioperative risk in patients with cirrhosis; essen-
tially age and ASA classification are added to the MELD score.17 This
prediction rule was derived from a Mayo Clinic surgical database and is avail-
able as an online calculator.19 This study also concluded that although ASA
classification was best at predicting 7-day mortality, MELD was superior at pre-
dicting later mortality. No scoring system provides a clear identification of
which elective surgery should proceed safely, and risk scores must be viewed
in their clinical context.

ASSESSMENT AND INVESTIGATIONS

As liver disease progresses to cirrhosis, the systemic effects of liver failure
become manifest (see Fig. 1). A thorough multimodal assessment is required
before undertaking elective surgery in these patients relying on history, exam-
ination, and focused investigation.
In brief, the history should determine the underlying cause and duration of
liver failure, the presence of complications, and treatments used. Knowing
whether a patient is currently active on a transplant list can also be very infor-
mative. In such cases, it is advisable to consult with the transplant center before
any elective procedure. The presence of other medical comorbidities should
also be actively sought because conditions such as coronary artery disease
and diabetes tend to occur at higher frequency in those with advanced liver
disease.20
Examination can reveal evidence of decompensated disease, including hepat-
ic encephalopathy and ascites. The presence of hepatic encephalopathy will
likely result in delayed emergence from anesthesia and increased susceptibility
to anesthetic drugs, such as benzodiazepines and delirium.21 Evidence of mus-
cle wasting (sarcopenia) often seen in advanced liver cirrhosis has important
prognostic implications.22 Assessment of frailty is a logical progression from
this, and measures of sarcopenia are included in many frailty scoring systems.
Frailty is an important topic in preoperative risk assessment, and early work
suggests that it can be similarly applied to cirrhosis.23
A minimum set of blood investigations should include a complete blood
count, coagulation profile, liver function tests as well as serum electrolytes
and creatinine. Coagulopathy, electrolyte disturbances, and renal dysfunction
are commonly encountered in cirrhotic patients and have obvious periopera-
tive implications. The differential diagnosis of deteriorating renal function in
cirrhosis is broad and can include sepsis, nephrotoxins, aggressive diuresis
causing hypovolemia, and hepatorenal syndrome. Reversible causes of renal
dysfunction should be explored and should prompt treatment. Hepatorenal
syndrome is a diagnosis of exclusion and is thought to be caused by renal
256 SPRING, SARAN, MCCARTHY, ET AL

hypoperfusion. Splanchnic vasodilation leads to a state of relative hypovole-

mia, which is compounded by increased renal vascular resistance owing to acti-
vation of the renin angiotensin and sympathetic nervous systems. The reader is
directed to a detailed review of the condition, but it suffices to say that the onset
of hepatorenal syndrome (particularly type 1) portends a poor prognosis.24
Liver function tests commonly include serum aminotransferases, gamma glu-
tamyl transferase, and bilirubin. Despite the name, these tests are poor assays
of liver function and can be elevated for other reasons. Nonetheless, they are
useful because the serum aminotransferases are markers of hepatocellular dam-
age, and patterns of elevation are suggestive of particular causes of liver
injury.25 Serum albumin is regarded as a marker of hepatic synthetic function,
but may have a more complicated cause related to chronic inflammation.26
Given the prevalence of electrolyte disturbances and comorbid cardiac is-
sues, a recent electrocardiogram is a minimum requirement, but more
focused cardiac assessment may be indicated. A transthoracic echocardio-
gram (TTE) can evaluate ventricular function and cirrhotic cardiomyopathy,
screen for portopulmonary hypertension, and diagnose hepatopulmonary
syndrome. Cirrhotic cardiomyopathy is defined as chronic cardiac dysfunc-
tion characterized by impaired systolic and diastolic dysfunction with electro-
physiologic abnormalities in the absence of known cardiac disease.27
Worryingly, this condition is typically silent at rest and only manifests
with stress. TIPS used to decompress the portal system as a treatment of as-
cites and variceal bleeding may precipitate heart failure in patients with
cirrhotic cardiomyopathy. Chronotropic incompetence is an electrophysio-
logical feature of cirrhotic cardiomyopathy and is defined as the failure of
the heart rate to increase in response to metabolic demand.28 For this reason
cardiac stress testing in patients with advanced cirrhosis is typically nondiag-
nostic for ischemia.
Pulmonary hypertension is defined as an elevation of the mean pulmonary
artery pressure 25 mm Hg. In the presence of portal hypertension, it is
known as portopulmonary hypertension, but it is not correlated with cause
or severity of cirrhosis. Estimated right ventricular systolic pressures greater
than 45 mm Hg or signs of right heart dysfunction should prompt right heart
catheterization to establish a formal diagnosis. The presence of portopulmo-
nary hypertension is an indication for liver transplantation, but severe cases
are considered exceptionally high risk and are deferred until pulmonary pres-
sures are reduced.29 Undertaking anesthesia in these patients outside of liver
transplantation should not be considered lightly.
Hepatopulmonary syndrome is another pulmonary manifestation of
cirrhosis, and the diagnosis is suspected in the presence of shortness of breath
relieved by sitting up (platypnea) and desaturation in the lying position (ortho-
deoxia). It is the result of intrapulmonary shunting of deoxygenated blood, and
the diagnosis is established by TTE contrast echocardiography. It is a relatively
common condition (up to 20%) in those with cirrhosis, and liver transplanta-
tion is the only known treatment. Perioperative hypoxemia should be
ANESTHESIA FOR SEVERE LIVER FAILURE 257

anticipated, and prolonged mechanical ventilation with the need for rescue
therapies should be considered and avoided if possible by accepting reasonable
criteria for arterial oxygenation.30
The anesthesiologist routinely managing patients with advanced liver failure
should be able to appreciate the significance of more focused liver investiga-
tions, particularly when contemplating procedures on the hepatobiliary system,
such as hepatic resection or TIPS. Liver ultrasound, triphasic computed tomog-
raphy, and MRI liver may point to the cause of liver failure and likely anes-
thetic and operative difficulties. For example, a significant hepatic
hydrothorax may require thoracentesis before an elective procedure. The pres-
ence of portal vein thrombus can make TIPS a more complicated and involved
procedure.31 Similarly, the presence of ectopic biliary varices may make for a
more challenging hepatic dissection. Portal vein pressure measurements are
more esoteric and probably less clinically useful, although successful lowering
of portal pressure during TIPS is crucial, especially if performed emergently for
variceal hemorrhage. Anesthesiologists working in interventional radiology
suites in liver centers will often hear portal pressure measurements discussed.
Portal pressure measurement may be performed directly through the portal
vein puncture during TIPS, although more commonly it is determined indi-
rectly by measuring the hepatic venous pressure gradient (HPVG). The
HVPG is the difference between balloon wedged hepatic vein pressure and
free hepatic vein pressure. A gradient of greater than 10 mm Hg predicts the
likelihood of developing decompensation. It may also predict the likelihood
of decompensation after liver resection.32

PREOPTIMIZATION
Every effort should be made to optimize patients with advanced liver disease
when coming to the operating room. Hepatologists can be invaluable in this
and should be consulted early. In particular, reversible causes for deterioration
in cognition, pulmonary function, and cardiac and renal status should be
sought, and prompt treatment should be instituted. Treatment may involve
the addition of laxatives and rifaximin to treat hepatic encephalopathy33 or
treating alcohol withdrawal syndrome. It is also important to remember that
cirrhosis is a state of relative immunosuppression,34 and a high index of suspi-
cion for infection should be maintained. Infections such as spontaneous bacte-
rial peritonitis can precipitate deterioration in cognition and organ function.
Current medications should also be reviewed in the context of upcoming sur-
gery. Diuretics, sedatives, and anticoagulants may need to be adjusted
perioperatively.
Uncontrolled ascites is a contraindication to elective abdominal surgery
because it can compromise wound healing culminating in postoperative ascitic
leaks35 and later incisional hernias. Ascites may be controlled using a low-
sodium diet and diuresis. Preemptive TIPS before surgery has been described
to control refractory ascites and decompress portosystemic shunts to reduce
bleeding, but it cannot be recommended as standard of care.36
258 SPRING, SARAN, MCCARTHY, ET AL

Malnutrition is very common among patients with advanced liver disease.

The likely cause is multifactorial, including reduced intake owing to anorexia
and ascites, impaired absorption, and increased catabolism. Malnutrition is
an independent risk factor for mortality in these patients, and early specialist
input to optimize nutrition appears to be beneficial.37 As mentioned previously,
serum albumin is a marker of hepatic synthetic function, and hypoalbuminemia
is a predictor of mortality in cirrhotics undergoing surgery. Importantly, the
administration of intravenous albumin replacement does not modify this
risk.38 Restriction of dietary protein intake in those at risk of hepatic encepha-
lopathy is not evidence-based practice and may have adverse effects.39
Prehabilitation of patients with advanced liver failure, particularly in those
awaiting liver transplantation, is being considered.40 Prehabilitation has been
shown to be feasible in this population with 1 study showing improved cardio-
vascular fitness and reduced insulin resistance.41 Over the next few years, pre-
habilitation may become recognized as critical to securing better outcomes for
patients with advanced liver disease.

INTRAOPERATIVE MANAGEMENT
Monitoring
Standard anesthesia monitors should be placed as per society guidelines. In pa-
tients with severe liver disease, there should be a low threshold to place an
invasive arterial catheter to monitor blood pressure and to allow frequent blood
sampling to monitor respiratory and acid-base status. Central venous catheter
(CVC) placement should be considered when additional venous access is
needed or when vasopressor administration anticipated. Type and duration
of surgery, anticipated blood loss, hemodynamic swings, and extent of liver dis-
ease should also be considered when determining invasive monitoring. CVC
placement solely for central venous pressure monitoring is controversial.42
Intraoperative transesophageal echocardiography (TEE) may be considered
in decompensated liver disease and where significant intraoperative fluid shifts
are anticipated. The presence of esophageal varices should be taken into
consideration; however, the risk of complications appears to be low. Single-
center, retrospective studies from TEE use during liver transplantation place
the risk at less than 1%.43,44
Anesthetic Medications
Liver disease alters the drug pharmacokinetics by altering protein binding,
drug metabolism, and volume of distribution. Drug choice and dose adjust-
ments should be considered for patients with advanced disease as evidenced
by portal hypertension, renal dysfunction, or encephalopathy, but anesthetic
requirements are generally lower in patients with liver disease.45,46
Sedative-Hypnotics
Patients with liver disease have similar clearance rates of induction doses used
in routine clinical practice, such as propofol, etomidate, and methohexital,
when compared with healthy patients.47–49 Elimination half-time and free
ANESTHESIA FOR SEVERE LIVER FAILURE 259

drug levels of benzodiazepines are increased in severe liver disease with the
exception of oxazepam and temazepam.
Analgesics
For the most part, analgesics are metabolized in the liver with renal elimination.
In liver disease, decreased doses of opioids with increased intervals should be
used to prevent drug accumulation. Long-acting opioids, such as morphine and
meperidine, should be avoided, but shorter-acting opioids, such as fentanyl and
hydromorphone, are well tolerated when used in lower doses and titrated to
effect. Acetaminophen is usually well tolerated, but caution should be used
in patients with advanced cirrhosis, especially malnourished patients. Nonste-
roidal anti-inflammatories should be used, bearing in mind risk of gastrointes-
tinal bleeding and renal function.
Neuromuscular Blockade
The aminosteroid neuromuscular agents, rocuronium and vecuronium, are
metabolized in part by the liver, and their duration of action may be prolonged
in liver failure. These drugs should be titrated to effect using peripheral nerve
stimulators. Benzylisoquinolinium neuromuscular agents, atracurium and cis-
atracurium, are not affected in liver disease. Succinylcholine is metabolized
by plasma cholinesterase, an enzyme produced by the liver; although the dura-
tion of action of succinylcholine is prolonged, it is not clinically significant.
Volatile Anesthetics
Modern halogenated volatile anesthetics are safe to use in cirrhotic patients.
Isoflurane and desflurane, but not sevoflurane, are metabolized to trifluoroace-
tyl chloride, the compound implicated in halothane hepatitis, to a much lesser
extent than halothane.
Coagulation
Liver disease affects both procoagulant and anticoagulant components of he-
mostasis leading to a new ‘‘balanced’’ steady state.50 As such, conventional tests
of coagulation, including INR, prothrombin time, and activated partial throm-
boplastin time, do not reflect the risks of bleeding and thrombosis. The assump-
tion that patients with liver disease are autoanticoagulated is incorrect.
Viscoelastic testing, such as rotational thromboelastometry (ROTEM) or
thromboelastography (TEG), reflects dynamic changes in clot formation and
lysis. These tests are superior and potentially provide a clinically relevant pic-
ture in patients with liver disease. These tests can also be used to guide specific
blood product transfusion (ie, cryoprecipitate, and fresh frozen plasma).51
Postoperative Analgesia
Providing effective perioperative analgesia to the patients with advanced liver
disease is challenging, balancing the risks of oversedation and uncontrolled
bleeding with optimal pain control. A potential coagulopathy made worse
with surgery is rightly regarded as a contraindication to neuraxial procedures
given the devastating consequences of epidural hematoma.52 However,
260 SPRING, SARAN, MCCARTHY, ET AL

neuraxial blockade has been used successfully in patients with cirrhosis as part
of enhanced recovery protocols in abdominal surgery.53 The best available
evidence suggests that epidural use is superior in terms of pain control to
patient-controlled opioid analgesia, and it is associated with reduced incidence
of postoperative respiratory failure.52
Other regional anesthetic techniques offer significant benefit without the
bleeding risk and should be considered, including subcostal transversus ab-
dominis plane (TAP), erector spinae, and quadratus lumborum blocks.54
They are performed using real-time ultrasound guidance, and catheters can
be placed if required for a more durable effect. Studies have shown that these
blocks achieve better pain control and reduce postoperative opioid require-
ments compared with intravenous opioids alone. The erector spinae and
quadratus lumborum blocks are more recently described. They are
ultrasound-guided blocks, and unlike TAP blocks, may offer visceral anal-
gesia in addition to somatic analgesia.55

CONSIDERATIONS FOR SPECIFIC PROCEDURES

Cardiac Surgery
With increasingly complex patients, a wider variety of surgical procedures be-
ing offered, and an increased prevalence of hepatic disease, there are an
increasing number of patients with liver cirrhosis presenting for cardiac sur-
gery.56 There is little doubt that liver disease or its perioperative management
has a negative impact on postoperative mortality57 and morbidity.58 Despite
this observation, the evaluation of liver function has not been included in
many of the most widely used cardiac surgery risk scoring systems, including
EuroSCORE II and Society of Thoracic Surgeons risk prediction model.59,60
Studies have identified CTP score as well as Na-MELD score as predictors of
early postoperative mortality following cardiac surgery.61,62 The mortalities in
these patients range from 9.88% for patients in CTP class A to 69.23% for pa-
tients with CTP class C.56 Using robust risk adjustments, outcome at 5 years
postoperatively was strongly associated with CTP: 82.4% for Child A, 47.6%
for Child B, and 33.3% for Child C (P ¼ .001).63 A Taiwanese population-
based study looking at 10-year survival demonstrated a similar pattern of
reduced long-term survival following cardiac surgery in cirrhotic patients.
Cirrhotic patients had a higher incidence of readmission primarily with liver
and heart failure, with most deaths being due to the progression of the primary
liver disease.64 Although cardiac surgery can be successfully carried out with
careful patient selection, mortality with redo procedures has been reported as
high as 50%.62
Cardiopulmonary bypass can exacerbate a preexisting coagulopathy by
inducing platelet dysfunction, fibrinolysis, and/or hypocalcemia.65 Dhoble
and colleagues66 looked at the outcomes in cirrhotic patients undergoing aortic
valve surgery with transcatheter aortic valve replacements (TAVR, n ¼ 156)
versus surgical aortic valve replacements (SAVR, n ¼ 189). Interestingly, after
propensity matching, there were no significant differences between in-hospital
ANESTHESIA FOR SEVERE LIVER FAILURE 261

mortality, readmissions, hospitalization costs, and discharges to home within

the TAVR and SAVR groups. Postprocedure length of stay (6.3 vs
10.2 days; P < .001) and blood transfusion rates (22% vs 58%; P < .001) were
significantly lower in TAVR patients.

TRAUMA
Multiple studies have identified that patients with cirrhosis and severe liver dis-
ease who present with traumatic injuries are at increased risk for morbidity and
mortality. Hepatic cirrhosis is a poor prognostic factor in trauma, with as high
as a 4-fold increase in mortality independent of their CTP classification.67 This
association appears to be consistent with the most common traumatic injuries,
for example, abdominal trauma and traumatic brain injury.68,69 Mortalities and
morbidities were increased even for patients considered to have relatively mi-
nor trauma.70 A 12-year study from Demetriades and colleagues70 looked at
outcomes following trauma laparotomy in cirrhotic patients versus control
matched noncirrhotic patients undergoing trauma laparotomy. The mortality
in the cirrhotic group was significantly higher than that in the matched noncir-
rhotic group, even in low Injury Severity Score (ISS) groups (29% vs 5%,
ISS <16) with an overall mortality of 45% versus 24% (P ¼ .021). Based on
this significant increase in mortality, they suggested, regardless of the severity
of the injury, these cirrhotic patients should be monitored in a level 1 or 2
intensive care environment in the postoperative period. A more recent system-
atic review focusing on trauma and orthopedic surgery in the cirrhotic patient
showed increased mortality in the cirrhotic versus the noncirrhotic group (12%
vs 6%). This association included an increased incidence of complications, such
as acute respiratory distress syndrome, trauma coagulopathy, and sepsis.71
Cirrhotic patients are significantly more likely to suffer severe morbidity
(10% vs 4%) and mortality (40%) compared with that of noncirrhotic at 15%.72
An analysis of the national trauma databank over an 8-year period from
2002 to 2010 of adult patients with blunt splenic injury revealed that cirrhotic
patients had a lower success rate (83% vs 90%, P ¼ .004) of nonoperative man-
agement of their injury73 with an increased rate of splenectomy.74 Cirrhotic pa-
tients were also discovered to have a higher rate of complications per patient,
increased length of intensive care and inpatient length of stay, and higher over-
all mortality (22% vs 6%, P<.0001), regardless of their treatment group. Factors
contributing to unsuccessful nonoperative management were preexisting coa-
gulopathy and grade 4 to 5 blunt splenic injury. Male sex, hypotension, preex-
isting coagulopathy, and a Glasgow Coma Score of less than 13 were predictors
of mortality.73
Traumatic brain injury as an isolated injury demonstrated much the same
pattern of increased mortality. An analysis of nearly nine thousand trauma pa-
tients showed that hepatic cirrhosis patients had an increased rate of mortality
compared to matched non-cirrhotic controls (31% vs 17%, P ¼ .03) and were
also less likely to proceed to urgent operative interventions (12% vs 25%,
P ¼ .03).69
262 SPRING, SARAN, MCCARTHY, ET AL

ANESTHESIA FOR TRANSHEPATIC PORTOSYSTEMIC SHUNT

AND MINOR PROCEDURES
Transhepatic portosystemic shunt is a percutaneous procedure carried out un-
der sedation or general anesthesia to reduce portal pressure by creating a shunt
between the hepatic vein and the intrahepatic portal vein.75 Performance of a
TIPS procedure can be complex, requiring multiple attempts, and general anes-
thesia may be indicated for patients who cannot tolerate sedation or those who
cannot lie flat for several hours. In addition, preprocedural screening for
congestive heart failure and pulmonary hypertension is imperative because
an increased systemic flow can worsen both of these conditions.
Patients for minor procedures, such as liver biopsies, tunneled intravenous
lines, drain insertion, interventional radiology procedures, and paracentesis
that requires sedation, are often encephalopathic and require intubation for
risk of aspiration. In addition, many cannot tolerate lying flat secondary to
massive ascites and pleural effusions. Aside from the complexity of these
high-risk patients undergoing sedation or general anesthesia, the anesthesiolo-
gist must consider that these procedures mainly occur outside of the operating
room environment, primarily in radiology suites. Additional factors, such as
unfamiliar equipment, lack of trained help, hostile environmental factors,
such as a cold room with an inability to warm the patient, poor access to the
patient, and rotating workspace, all contribute to making these procedures
more difficult.76
Blood typing and screen should be performed in case of a need for blood
products. Goals should be a platelet count greater than 50  109/L and fibrin-
ogen greater than 150 to 200 mg/dL, without attempts to correct the INR.
Viscoelastic testing (ie, thromboelastography) may be used to guide therapy,
if available. Correction of INR is not recommended because multiple studies
have shown INR is a poor correlation for bleeding risk in the cirrhotic
patients.77–82

ABDOMINAL SURGERY
Gastrointestinal surgery, including both elective and emergency surgery,
comprises the bulk of the operations performed on cirrhotic patients. Laparo-
scopic and open approaches are associated with increased morbidity and
mortality. Cholecystectomy is the most frequently performed surgery in
cirrhotic patients.83 A prospective randomized trial demonstrated that an
open cholecystectomy was associated with increased morbidity (including
bleeding, length of hospital stay, and length of surgery) compared with lapa-
roscopic procedures (30% vs 13%) and a favorable benefit in mortality (0% vs
0%–7%)84; however, the difference in morbidity during elective hernia repair
was not statistically significant compared with noncirrhotic controls.85
Abdominal wall hernias develop in 20% of all cirrhotic patients, and elective
repair is associated with morbidity (7%–15%) and significant mortality (0%–
5%).85 However, multiple studies acknowledge significantly higher morbidity
and mortality in emergency hernia repair compared with elective repair.85–87
ANESTHESIA FOR SEVERE LIVER FAILURE 263

Mortality was 7-fold higher in emergencies (3.8% vs 0.5%; P<.0001), and

elective repair in these patients may be the optimal course to pursue to avoid
increased mortality.85
For hepatic resection secondary to hepatocellular carcinoma, preoperative
screening can identify those patients with an increased risk of mortality by de-
tecting an increased MELD score. Although previous studies have reported
mortality approaching as high as 25%, careful selection and screening have
led to improved outcomes and mortality.88 The MELD score is a strong pre-
dictor of both perioperative mortality and long-term survival in patients with
cirrhosis undergoing hepatic resection for hepatocellular cancer. In patients
with cirrhosis, hepatic resection with an MELD score less than 9 was associated
with no perioperative mortality versus 29% for patients with an MELD score
greater than 9 (P<.01).89

Conflicts of Interest
None.

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