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Assessing surgical risk in patients with liver disease
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Mar 2012. | This topic last updated: Mar 14, 2011.

INTRODUCTION — Patients with liver disease who require surgery are at greater risk for surgical and anesthesia related complications than those with a healthy liver [1-4]. The magnitude of the risk depends upon the type of liver disease and its severity, the surgical procedure, and the type of anesthesia.

The assessment of surgical risk in patients with liver disease will be reviewed here. Patients with liver disease may have concomitant disorders (such as cardiovascular disease) that influence surgical outcomes; these issues are discussed separately. (See "Preoperative medical evaluation of the healthy patient" and "Estimation of cardiac risk prior to noncardiac surgery".)

SCREENING FOR LIVER DISEASE BEFORE SURGERY — Patients undergoing surgery should undergo a history and physical examination to exclude findings or risk factors for liver disease. This may include asking about prior blood transfusions, tattoos, illicit drug use, sexual promiscuity, a family history of jaundice or liver disease, a history of jaundice or fever following anesthesia, alcohol use (current, prior and quantity), and a complete review of current medications. Clinical features suggestive of liver disease (such as fatigue, pruritus, increased abdominal girth, jaundice, palmar erythema, spider telangiectasias, splenomegaly, and gynecomastia and testicular atrophy in men) should be evaluated.

Whether otherwise healthy surgical candidates should undergo biochemical screening for liver disease is controversial. The vast majority of patients found to have abnormal liver biochemical test results do not have advanced liver disease. Thus, it is unlikely that routinely obtaining a liver biochemical profile in otherwise healthy patients without risk factors for liver disease would lead to improved outcomes; thus, such testing is not recommended. (See "Preoperative medical evaluation of the healthy patient".)

EFFECTS OF ANESTHESIA AND SURGERY ON THE LIVER — The effects of anesthesia and surgery on the liver depend upon the type of anesthesia used, the specific surgical procedures, and the severity of liver disease. In addition, perioperative events, such as hypotension, sepsis, or the administration of hepatotoxic drugs, can compound injury to the liver occurring during the procedure. (See "Effects of anesthesia and surgery on the liver".)

ESTIMATING SURGICAL RISK — Assessment of surgical risk in patients with liver disease includes an appraisal of the severity of liver disease, the urgency of surgery (and alternatives to surgery), and coexisting medical illness. Surgical risk assessment is less relevant if immediate surgery is required to prevent death. On the other hand, the vast majority of decisions are made in the setting of semi-urgent or elective procedures for which there is time for risk assessment, optimization of the patient's medical status, and consideration of alternative approaches.

The majority of studies examining the risk of surgery in patients with liver disease have focused on patients with cirrhosis from which a number of risk factors have been identified (table 1) [5-17]. Much less information has been published on the risk of surgery in patients with milder forms of liver disease. The available evidence is derived mostly from small retrospective studies and clinical experience. Furthermore, many of the studies were published prior to the availability of a number of serologic tests for specific types of liver disease, and modern hepatobiliary imaging. Thus, there is relatively little information on the risk of surgery in patients with specific types of liver disease.

Patients in whom surgery is contraindicated — A number of settings have been identified that are associated with unacceptable surgical mortality. As a result, these conditions are usually considered to be contraindications to elective surgery (table 2).

Acute or fulminant hepatitis — Acute hepatitis is a contraindication to elective surgery. This recommendation is based upon older studies, in which operative mortality rates of 10 to 13 percent were reported among icteric patients who underwent laparotomy as part of a diagnostic evaluation that ultimately led to a diagnosis of acute viral hepatitis [18].

Similarly, patients with fulminant hepatitis are gravely ill and are unlikely to withstand surgery other than liver transplantation. (See "Acute liver failure: Definition and etiology".)

Alcoholic hepatitis — Elective surgery is contraindicated in patients with histologic evidence of alcoholic hepatitis. Mortality rates as high as 55 to 100 percent have been observed in such patients undergoing open liver biopsy [19], portosystemic shunt surgery [20-22], or exploratory laparotomy [23]. (See "Clinical manifestations and diagnosis of alcoholic liver disease".)

However, it is possible that advances in surgical technique and postoperative care may have improved the outcome in such patients compared to the above studies, some of which were conducted more than 20 to 30 years ago. This was illustrated in a report from 1984, in which operative liver biopsy findings were reviewed in 164 patients with alcoholic cirrhosis and bleeding varices who underwent emergency portacaval shunt surgery [24]. Of these patients, 49 (30 percent) had histologic evidence of alcoholic hepatitis, but had survival rates similar to those without alcoholic hepatitis. These results have not been duplicated.

We recommend that elective surgery should be delayed for at least 12 weeks, or that a repeat liver biopsy should be considered to confirm resolution. The severity of underlying liver disease should be reassessed prior to making a final recommendation.

Severe chronic hepatitis — Surgical risk in patients with chronic hepatitis correlates with the clinical, biochemical, and histologic severity of disease. Patients with symptomatic and histologically severe chronic hepatitis have increased surgical risk, particularly in those with impaired hepatic synthetic or excretory function, portal hypertension, or bridging or multilobular necrosis on liver biopsy [25,26].

Patients at variable increased risk — The risk of surgery in patients with cirrhosis depends upon the severity of disease, the clinical setting and type of surgical procedure. For over 30 years, the principal predictor of operative risk in patients with cirrhosis has been the Child's classification, but newer studies suggest that the Model for End-Stage Liver Disease (MELD) score may be superior [27].

Child's classification — A number of retrospective studies have demonstrated that perioperative mortality and morbidity in patients with cirrhosis correlate well with the Child-Turcotte (table 3) [28] or Child-Pugh [17,29] classification of cirrhosis (table 4). In one study in 1984, for example, perioperative mortality rates of 10, 31, and 76 percent were observed in 100 patients with predominantly alcoholic cirrhosis undergoing abdominal surgery who were Child-Pugh class A, B, and C, respectively [16]. On multivariate analysis, the Child-Pugh classification was the best predictor of surgical mortality and morbidity. Nearly identical results were observed in a similarly designed study published in 1997 of 92 patients with cirrhosis (approximately 50 percent alcoholic) undergoing abdominal surgery (mortality rates of 10, 30, and 82 percent in patients with Child-Pugh class A, B, and C, respectively) [30]. A study published in 2010, however, showed lower mortality rates of 2, 12, and 12 percent for patients with Child-Pugh class A, B, and C cirrhosis, respectively, undergoing abdominal surgery. A study of 138 patients undergoing intra-abdominal or abdominal wall surgery published in 2011 showed rates of 10, 17, and 63 percent, respectively [31]. Mortality rates have declined in the 2000s, presumably because of improvements in the overall care of critically ill patients [32].

Patients with Child's class A cirrhosis and portal hypertension are at increased risk of postoperative ascites, jaundice, and encephalopathy [33]. Limited observations suggest that postoperative morbidity may be reduced by preoperative placement of a transjugular intrahepatic portosystemic shunt [34].

Measures of hepatic function and the APACHE score — A number of measures of hepatic function have been proposed as predictors of perioperative morbidity and mortality in patients with cirrhosis. Examples include quantitative assessment of liver function with dynamic tests such as galactose elimination capacity, aminopyrine breath testing, indocyanine green clearance, and the rate of metabolism of lidocaine to monoethylglycinexylidide (MEGX). (See "Tests of the liver's biosynthetic capacity (eg, albumin, coagulation factors, prothrombin time)".) However, none has been shown convincingly to provide additional prognostic information compared to the Child-Pugh classification, and, as a result, they are not used widely [35].

The Acute Physiology, Age, and Chronic Health Evaluation System (APACHE III) score can predict survival in cirrhotic patients admitted to an intensive care unit [36]. However, it has not been studied specifically in cirrhotic patients undergoing surgery. (See "Predictive scoring systems in the intensive care unit".)

MELD score — The MELD score is a statistical model predicting survival in patients with cirrhosis (calculator 1 and calculator 2). It has been evaluated principally for selecting patients for liver transplantation. Use of this model for predicting surgical risk in the nontransplant setting has been promising and thus it may ultimately supplant the Child's classification as the principal method for determining surgical risk [37-42]. However, more studies involving diverse groups of surgical patients with a wide range of MELD scores are needed to understand its performance as a predictive model for surgery. The following summarizes representative studies. (See "Model for End-stage Liver Disease (MELD)".)

  • The MELD score, American Society of Anesthesiologists class, and age predicted mortality in a study of 772 patients with cirrhosis who underwent major digestive, orthopedic, or cardiovascular surgery [37]. The MELD score was the best predictor of 30 and 90 day mortality. Mortality at 30 days ranged from 6 percent (MELD score, <8) to more than 50 percent (MELD score, >20) and correlated linearly with the MELD score.
  • Another study compared the MELD score with the Child-Turcotte-Pugh classification in 40 cirrhotic patients who required either elective or emergency surgery with general anesthesia [39]. Emergency surgery was associated with significantly higher one- and three-month mortality rates. There was good correlation between the Child-Turcotte-Pugh classification and the MELD scores in predicting mortality, especially in the emergency surgery group.
  • In other reports in selected settings, a MELD score ≥8 was useful for predicting morbidity in 33 patients undergoing cholecystectomy [40], a MELD score >14 was a better predictor of poor outcomes than the Child-Pugh classification in a series of 53 cirrhotic patients undergoing abdominal surgery [41], a MELD score ≥15 with an albumin ≤2.5 mg/dL predicted significantly increased mortality in a series of 100 patients undergoing abdominal surgery (60 versus 14 percent) [32], and a MELD score ≥11 predicted a high risk for postoperative liver failure in 154 patients with cirrhosis undergoing hepatectomy for hepatocellular carcinoma [42].

It has been suggested that patients with a MELD score below 10 can undergo elective surgery, those with a MELD score of 10 to 15 may undergo elective surgery with caution, and those with a MELD score >15 should not undergo elective surgery [43]. A calculator is available (calculator 3)to calculate the estimated 7-day, 30-day, 90-day, 1-year, and 5-year mortality rates after surgery based on the patient's age, ASA class, INR, serum bilirubin and creatinine. The model is based on the original MELD score, not the one currently being used for organ transplantation.

Obstructive jaundice — Patients with obstructive jaundice are at increased risk for several perioperative complications including infections (which result in part from bacterial colonization of the biliary tree, impaired Kupffer cell function, defective neutrophil function, and a high rate of endotoxemia), stress ulceration, disseminated intravascular coagulation, wound dehiscence, and renal failure [44-47]. Perioperative mortality ranged from 8 to 28 percent in several reports [48-50]. As an example, an overall mortality rate of 9 percent was found in a large retrospective study that included 373 patients undergoing surgery for obstructive jaundice [49]. Multivariate analysis identified three predictors of postoperative mortality:

  • An initial hematocrit value <30 percent
  • An initial serum bilirubin level >11 mg/dL (200 micromoles/L)
  • A malignant cause of obstruction (eg, pancreatic carcinoma or cholangiocarcinoma)

When all three factors were present, mortality approached 60 percent; when none was present, mortality was only 5 percent. Several other preoperative predictors of poor surgical outcome have been observed in other studies including azotemia, hypoalbuminemia, and cholangitis (table 5) [48-53]. The presence of portal hypertension can also be presumed to increase the surgical risk.

A number of interventions have been attempted to reduce morbidity and mortality in these patients:

  • Perioperative administration of broad-spectrum intravenous antibiotics reduces the frequency of postoperative infections but does not influence mortality [54].
  • External biliary drainage via a transhepatic approach has not been proven to improve morbidity or mortality in controlled studies [55-58]. In one report, it increased overall and infectious postoperative complication rates when used before resection for hilar cholangiocarcinoma [59].
  • Endoscopic biliary drainage has the advantage of restoring enterohepatic circulation of bile acids while avoiding the complications of percutaneous puncture. However, as for external biliary drainage, it also has not been shown to improve surgical mortality in patients with a malignant cause of biliary obstruction [60,61], although preoperative biliary drainage has been recommended in patients undergoing extended hepatic resection [62] or with cholangitis or pruritus when surgery is delayed [63]. In patients with cholangitis and choledocholithiasis, broad spectrum intravenous antibiotics and endoscopic drainage have been associated with lower mortality and morbidity rates compared to surgical decompression [64-66]. Although endoscopic sphincterotomy is associated with an increased rate of complications in patients with cirrhosis [67], morbidity and mortality rates are low even in patients with Child's class C cirrhosis when biliary decompression can be achieved [68]. (See "Endoscopic management of bile duct stones: Standard techniques and mechanical lithotripsy".)
  • A major cause of morbidity in patients with obstructive jaundice is postoperative renal failure, which is usually due to acute tubular necrosis; the average frequency was approximately 8 percent in several reports [46,69,70]. The high incidence may be related to the absorption of endotoxin from the gut [71]. In normal subjects, endotoxin absorption is limited by the detergent effect of bile salts on the lipopolysaccharide endotoxin molecule; this protection is lost with obstructive jaundice, since bile salt secretion is minimal. As a result, patients may develop exaggerated renal vasoconstriction. (See "Pathogenesis and etiology of postischemic acute tubular necrosis".)

Limited evidence suggests that the administration of bile salts or lactulose to patients with obstructive jaundice can prevent both the endotoxemia and the exaggerated renal vasoconstriction [54,71-73]. In one report, for example, 102 patients with obstructive jaundice who had a serum bilirubin concentration >5.8 mg/dL (100 micromoles/liter) were randomly assigned to receive lactulose, sodium deoxycholate (a bile salt) or no specific treatment prior to surgery [72]. Postoperative deterioration in renal function in patients with normal preoperative function was significantly more common in patients who had received no specific treatment.

Another approach that has been attempted to reduce the incidence of renal failure is the postoperative administration of mannitol [54,74]. Despite its theoretical benefit, maintenance of intravascular volume, and the avoidance of nephrotoxic drugs, such as aminoglycosides, are probably more critical elements in management [75-77].

Prophylactic oral antibiotics, such as rifaximin, have also been proposed as a means to reduce adverse effects of endotoxemia but a benefit has not yet been demonstrated. Furthermore, it is possible that oral antibiotics could increase endotoxemia because they may lead to increased release of endotoxin caused by destruction gram-negative organisms. On the other hand, intravenous broad-spectrum antibiotics should generally be given perioperatively to reduce the incidence of postoperative infection, although a benefit on mortality has not been demonstrated [54].

Whether patients with cholestatic liver disease (such as primary biliary cirrhosis and primary sclerosing cholangitis) also have an increased risk of acute tubular necrosis following surgery has not been well studied. An interesting clinical observation is that patients with primary biliary cirrhosis appear to be at decreased risk for developing hepatorenal syndrome after surgery compared to patients with other forms of liver disease [78]. A possible explanation is the natriuretic and renal vasodilator actions of retained bile salts.

Cardiac surgery — Cardiac surgery is associated with increased mortality in patients with cirrhosis compared to other surgical procedures.

  • One of the largest series included 44 patients with cirrhosis of whom 12 developed hepatic decompensation and 7 died [38]. The Child's class was a significant predictor of decompensation and mortality. For mortality, a CPT score of >7 had sensitivity, specificity, positive, and negative predictive values of 86, 92, 67, and 97 percent, respectively. The authors concluded that cardiopulmonary bypass can be conducted safely in patients with a CPT score of <7. However, in other reports, major complications have been described in patients with lower scores [79].
  • Another series included 27 patients with cirrhosis (10 with Child class A, 11 with Child class B and 6 with Child class C, with an overall mean MELD score of 14.2) [80]. Operative mortality was 11, 18, and 67 percent for Child class A, B, and C, respectively (26 percent overall), and the Child classification was a better predictor or mortality than the MELD score (using an arbitrary MELD classification of 0-12 and ≥13).
  • A third report included 13 patients with predominantly alcoholic cirrhosis (eight with Child class A, and five with Child class B) who required coronary artery bypass grafting, valve replacement or both [81]. All patients who were Child class B experienced major complications and only one patient survived. All patients who were Child class A survived despite a complication rate of 25 percent. The high mortality rate in patients with Child class B was attributed to postoperative infections and bleeding, rather than cardiac dysfunction.

A number of risk factors for hepatic decompensation following cardiac surgery have been identified including the total time of cardiopulmonary bypass, use of nonpulsatile as opposed to pulsatile cardiopulmonary bypass, and need for perioperative pressor support [82]. Cardiopulmonary bypass can exacerbate underlying coagulopathy by inducing platelet dysfunction, fibrinolysis, and hypocalcemia [83].

Thus, the least invasive options, such as angioplasty, valvuloplasty, or minimally invasive revascularization techniques, should be considered in patients with advanced cirrhosis who require invasive intervention for cardiac disease [84]. (See "Minimally invasive coronary artery bypass graft surgery: Clinical efficacy of beating heart surgery".) Cardiac surgery followed by liver transplantation has been performed in rare instances [82,85,86]. Even more rarely, liver transplantation has been undertaken before cardiac surgery in patients with left ventricular dysfunction [83]. This approach is hazardous because of the risk of hemodynamic instability resulting from reduced venous return and reperfusion of the graft during liver transplantation [82].

Hepatic resection — Patients with cirrhosis undergoing resection for hepatocellular carcinoma or other liver tumors are at increased risk for hepatic decompensation compared to those undergoing other types of operations [87]. In addition to having severe underlying disease, a significant portion of functional hepatocellular mass may be removed in a setting in which patients already have severely compromised hepatic reserve. In the past, cirrhosis was considered to be a contraindication to resection of hepatic tumors since mortality rates exceeded 50 percent.

More recently, the perioperative mortality rate for hepatic resection has decreased to 3 to 16 percent, although postoperative morbidity rates are still as high as 60 percent [88-96]. The improvement in outcomes has been attributed to better patient selection (including earlier detection of tumors), meticulous preoperative preparation, intensive intra- and postoperative monitoring, and improved surgical techniques. Postresectional liver failure is defined as an INR >1.7 (prothrombin time index <50 percent) and serum bilirubin greater than 2.9 mg/dL (50 micromol/L), the so-called 50-50 criteria, and is associated with a mortality rate of about 60 percent compared with 1.2 percent when the criteria are not met [97]. Options for treating hepatocellular carcinoma, including surgical resection, are discussed elsewhere. (See "Surgical resection for hepatocellular carcinoma".)

Several systems for risk stratification of patients undergoing hepatic resection have been proposed, although none has been validated extensively. A database study of 587 patients who underwent hepatic resection concluded that the Child-Pugh Score and American Society of Anesthesiologists (ASA) physical status classification were better predictors of morbidity and mortality than the MELD score [98]. The ASA score was the only significant predictor of 30-day mortality (area under the receiver operating curve {ROC} of 0.63) while the ASA and Charlson Index of Comorbidity were the only significant predictors of morbidity (ROC of 0.56 and 0.40, respectively). However, the low ROC areas indicate that none of these models was an accurate predictor of outcomes. Moderate to severe hepatic steatosis (>30 percent of liver volume) is a risk factor for postoperative complications after major hepatectomy [99].

Trauma — Trauma patients found to have cirrhosis at laparotomy are at increased risk for morbidity and mortality. In one study, the overall mortality rate was 45 percent, significantly higher than of a matched control population (24 percent) [100]. Mortality and morbidity rates were increased even for patients considered to have relatively minor trauma. The authors recommended that trauma patients found to have cirrhosis at laparotomy be admitted to the intensive care unit for close monitoring and aggressive management irrespective of the severity of their injuries.

Patients with minimally increased risk — Patients with mild to moderate chronic liver disease without cirrhosis usually tolerate surgery well. However, medical therapy should be optimized prior to surgery.

Mild chronic hepatitis — Asymptomatic patients with mild chronic hepatitis are at low risk for complications [101]. In one report, for example, no major complications were noted during 34 surgical procedures in 24 patients with mild to moderate chronic hepatitis [101]. Two patients developed sustained hyperbilirubinemia, both of whom had preoperative bilirubin levels of 2.5 mg/dL (35.91 micromoles/liter) or more.

Fatty liver and nonalcoholic steatohepatitis — Although the histologic appearance of nonalcoholic steatohepatitis (NASH) is similar to alcoholic hepatitis, patients with NASH do not appear to have excessive mortality following elective surgery. However, a trend toward increased mortality following hepatic resection has been observed in those with moderate to severe steatosis (>30 percent of hepatocytes containing fat) [102].

NASH is relatively common in patients with morbid obesity who undergo gastric bypass surgery. Cirrhosis, due presumably to NASH, has been found unexpectedly in up to 6 percent of such patients, in whom a perioperative mortality rate of 4 percent has been observed [15].

It may be difficult to distinguish NASH from alcoholic hepatitis since the histologic features can be identical, and patients do not always admit to alcohol ingestion. (See "Epidemiology, clinical features, and diagnosis of nonalcoholic steatohepatitis" and "Screening for unhealthy use of alcohol and other drugs".) Thus, recommending a period of abstinence from alcohol prior to surgery is advisable for all patients with the histologic appearance of steatohepatitis, or those who are suspected of excessive alcohol consumption, since alcoholics are at increased risk for perioperative complications, such as alcohol withdrawal and hepatotoxicity with therapeutic doses of acetaminophen (often used for analgesia in the postoperative period) [103], even if they do not have liver disease. Furthermore, alcohol may potentiate the toxicity of halothane [104,105].

Autoimmune hepatitis — Elective surgery is usually well-tolerated in patients with autoimmune hepatitis who have compensated liver disease. Perioperative "stress" doses of hydrocortisone should be given to patients taking prednisone.

Hemochromatosis — Patients with hemochromatosis should be evaluated for complications such as diabetes and cardiomyopathy, which could influence perioperative care. (See "Clinical manifestations of hereditary hemochromatosis".) In the past, a relatively poor outcome of liver transplantation in these patients compared to other types of liver disease was attributed to underlying cardiomyopathy [106], but outcomes have improved with careful patient selection.

Wilson disease — Patients with Wilson disease who have neuropsychiatric involvement may not be able to provide informed consent. Furthermore, surgery can precipitate or aggravate neurologic symptoms. (See "Diagnosis of Wilson disease".) D-penicillamine (a copper chelator commonly used for treatment), interferes with the crosslinking of collagen and may impair wound healing [107,108]. As a result, the dose should be decreased prior to surgery and during the first one to two postoperative weeks. (See "Treatment of Wilson disease".)

OPTIMIZING MEDICAL THERAPY — In addition to assessing surgical risk, all patients with known liver disease should be assessed for the presence of jaundice, coagulopathy, ascites, electrolyte abnormalities, renal dysfunction and encephalopathy, all of which may require specific treatment prior to surgery. The basic principles involved in the evaluation of patients with specific forms of liver disease are discussed in detail separately. (See "Diagnostic approach to the patient with cirrhosis".)

  • In patients with an elevated prothrombin time, a reasonable goal is to attempt correction with vitamin K and fresh frozen plasma to achieve a prothrombin time within three seconds of normal prior to surgery. Experience is also accumulating with recombinant factor VIIA, which can temporarily correct the prothrombin time, but its use is limited by its high cost, transient effect, an absence of data showing improved outcomes, and the associated risk of thromboembolism. (See "Endoscopic procedures in patients with disorders of hemostasis".)
  • A prolonged bleeding time can be treated with diamino-8-D-arginine vasopressin (DDAVP). (See "Treatment of von Willebrand disease", section on 'Desmopressin'.)
  • Optimal surgical technique and maintenance of low central venous pressure may reduce blood loss [109].
  • Ascites should be treated aggressively to reduce the chance of wound dehiscence and abdominal wall herniation. This can be achieved safely with diuretics in patients who also have peripheral edema. In patients without edema or those in whom there is not enough time for a course of diuretic therapy, ascites can be drained completely during laparotomy. (See "Initial therapy of ascites in patients with cirrhosis".)
  • Electrolyte abnormalities, particularly hypokalemia and metabolic alkalosis, should be corrected to reduce the chance of cardiac arrhythmias and hepatic encephalopathy.
  • Conditions known to exacerbate hepatic encephalopathy should be corrected. (See "Pathogenesis of hepatic encephalopathy".) However, there is no evidence that prophylactic therapy can prevent encephalopathy after surgery.
  • Renal function should be evaluated. For most patients, assessment of the blood urea nitrogen and creatinine is sufficient. However, these measures often overestimate renal function in patients with advanced liver disease because of the reduction in urea and creatinine synthesis. (See "Diagnosis and treatment of hepatorenal syndrome", section on 'Estimation of renal function'.)
  • Patients with known gastroesophageal varices should receive the appropriate prophylactic treatment. (See "Primary and pre-primary prophylaxis against variceal hemorrhage in patients with cirrhosis".) Although surgery has not been associated with an increased risk of variceal bleeding, fluid overload should be avoided postoperatively.
  • TIPS may be considered before surgery in patients with portal hypertension [110-113], but the role of preoperative TIPS has not been well-studied.
  • Patients with cirrhosis are often malnourished. Perioperative nutritional support can reduce the frequency of postoperative complications and short-term mortality; its benefit on long-term survival is uncertain [114-118]. A reasonable approach is to provide total calories equal to 1.2 times the estimated resting energy expenditure and a 1 g/kg per day of protein. Approximately 30 to 35 percent of total energy should be given as fat and the remainder (typically 50 to 55 percent) as carbohydrates. Supplementation of the fat soluble vitamins A, D, E, and K, may also be necessary [117].

Percutaneous gastrostomy (PEG) is contraindicated in patients with ascites, and should usually be avoided in patients with portal hypertension due to the possibility of lacerating an abdominal wall varix during PEG insertion.

Following surgery, patients with liver disease should be observed closely for hepatic decompensation, which often presents with worsening jaundice, encephalopathy, and ascites. The best biochemical measures of liver function are probably the prothrombin time and serum bilirubin concentration. However, the serum bilirubin concentration usually rises, particularly after complicated surgery, multiple blood transfusions, excessive bleeding, hemodynamic instability, or systemic infection. Renal function, serum electrolytes, and glucose should also be monitored carefully.

SUMMARY AND RECOMMENDATIONS — Considering the above data and clinical experience, guidelines for assessing the risk of elective or semi-urgent surgery in patients with liver disease can be suggested:

  • Medical therapy should be optimized in all patients as described above. (See 'Optimizing medical therapy' above.)
  • Operative mortality can be estimated based upon the Child classification and the MELD score (calculator 3) taking into consideration other factors such as the patient's age, ASA score, and additional comorbidities.
  • We recommend elective or semi-urgent surgery not be performed in patients with acute or fulminant hepatitis, alcoholic hepatitis, severe chronic hepatitis, Child class C or MELD >15 cirrhosis, severe coagulopathy, or severe extrahepatic manifestations of liver disease (such as hypoxia, cardiomyopathy, or acute renal failure) (Grade 1B).

For other patients, the risk of surgery should be considered individually depending upon the clinical setting and the type of procedure:

  • It is well-tolerated in patients with Child's class A or MELD <10 cirrhosis and those with mild chronic liver disease without cirrhosis.
  • It is permissible in patients with Child's class B or MELD 10-15 cirrhosis (except those undergoing extensive hepatic resection or cardiac surgery) who have undergone thorough preoperative preparation.

Consideration should also be given as to whether surgery can be deferred until after liver transplantation (either orthotopic or live donor) in appropriate candidates.

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REFERENCES

  1. Friedman LS, Maddrey WC. Surgery in the patient with liver disease. Med Clin North Am 1987; 71:453.
  2. Friedman LS. The risk of surgery in patients with liver disease. Hepatology 1999; 29:1617.
  3. O'Leary JG, Yachimski PS, Friedman LS. Surgery in the patient with liver disease. Clin Liver Dis 2009; 13:211.
  4. Patel T. Surgery in the patient with liver disease. Mayo Clin Proc 1999; 74:593.
  5. Bloch RS, Allaben RD, Walt AJ. Cholecystectomy in patients with cirrhosis. A surgical challenge. Arch Surg 1985; 120:669.
  6. Aranha GV, Sontag SJ, Greenlee HB. Cholecystectomy in cirrhotic patients: a formidable operation. Am J Surg 1982; 143:55.
  7. Aranha GV, Kruss D, Greenlee HB. Therapeutic options for biliary tract disease in advanced cirrhosis. Am J Surg 1988; 155:374.
  8. Castaing D, Houssin D, Lemoine J, Bismuth H. Surgical management of gallstones in cirrhotic patients. Am J Surg 1983; 146:310.
  9. Schwartz SI. Biliary tract surgery and cirrhosis: a critical combination. Surgery 1981; 90:577.
  10. McSherry CK, Glenn F. The incidence and causes of death following surgery for nonmalignant biliary tract disease. Ann Surg 1980; 191:271.
  11. Pitt HA, Cameron JL, Postier RG, Gadacz TR. Factors affecting mortality in biliary tract surgery. Am J Surg 1981; 141:66.
  12. Lehnert T, Herfarth C. Peptic ulcer surgery in patients with liver cirrhosis. Ann Surg 1993; 217:338.
  13. Metcalf AM, Dozois RR, Wolff BG, Beart RW Jr. The surgical risk of colectomy in patients with cirrhosis. Dis Colon Rectum 1987; 30:529.
  14. Sleeman D, Namias N, Levi D, et al. Laparoscopic cholecystectomy in cirrhotic patients. J Am Coll Surg 1998; 187:400.
  15. Brolin RE, Bradley LJ, Taliwal RV. Unsuspected cirrhosis discovered during elective obesity operations. Arch Surg 1998; 133:84.
  16. Garrison RN, Cryer HM, Howard DA, Polk HC Jr. Clarification of risk factors for abdominal operations in patients with hepatic cirrhosis. Ann Surg 1984; 199:648.
  17. Ziser A, Plevak DJ, Wiesner RH, et al. Morbidity and mortality in cirrhotic patients undergoing anesthesia and surgery. Anesthesiology 1999; 90:42.
  18. HARVILLE DD, SUMMERSKILL WH. Surgery in acute hepatitis. Causes and effects. JAMA 1963; 184:257.
  19. Greenwood SM, Leffler CT, Minkowitz S. The increased mortality rate of open liver biopsy in alcoholic hepatitis. Surg Gynecol Obstet 1972; 134:600.
  20. Mikkelsen WP. Therapeutic portacaval shunt. Preliminary data on controlled trial and morbid effects of acute hyaline necrosis. Arch Surg 1974; 108:302.
  21. Mikkelsen WP, Kern WH. The influence of acute hyaline necrosis on survival after emergency and elective portacaval shunt. Major Probl Clin Surg 1974; 14:233.
  22. Mikkelsen WP, Turrill FL, Kern WH. Acute hyaline necrosis of the liver. A surgical trap. Am J Surg 1968; 116:266.
  23. Powell-Jackson P, Greenway B, Williams R. Adverse effects of exploratory laparotomy in patients with unsuspected liver disease. Br J Surg 1982; 69:449.
  24. Bell RH Jr, Miyai K, Orloff MJ. Outcome in cirrhotic patients with acute alcoholic hepatitis after emergency portacaval shunt for bleeding esophageal varices. Am J Surg 1984; 147:78.
  25. Hargrove MD Jr. Chronic active hepatitis: possible adverse effect of exploratory laparotomy. Surgery 1970; 68:771.
  26. Higashi H, Matsumata T, Adachi E, et al. Influence of viral hepatitis status on operative morbidity and mortality in patients with primary hepatocellular carcinoma. Br J Surg 1994; 81:1342.
  27. O'Leary JG, Friedman LS. Predicting surgical risk in patients with cirrhosis: from art to science. Gastroenterology 2007; 132:1609.
  28. Child, CG, Turcotte, JG. Surgery and portal hypertension. In: The Liver and Portal Hypertension, Child, CG (Eds), Saunders, Philadelphia 1964. p.50.
  29. Pugh RN, Murray-Lyon IM, Dawson JL, et al. Transection of the oesophagus for bleeding oesophageal varices. Br J Surg 1973; 60:646.
  30. Mansour A, Watson W, Shayani V, Pickleman J. Abdominal operations in patients with cirrhosis: still a major surgical challenge. Surgery 1997; 122:730.
  31. Neeff H, Mariaskin D, Spangenberg HC, et al. Perioperative mortality after non-hepatic general surgery in patients with liver cirrhosis: an analysis of 138 operations in the 2000s using Child and MELD scores. J Gastrointest Surg 2011; 15:1.
  32. Telem DA, Schiano T, Goldstone R, et al. Factors that predict outcome of abdominal operations in patients with advanced cirrhosis. Clin Gastroenterol Hepatol 2010; 8:451.
  33. Bruix J, Castells A, Bosch J, et al. Surgical resection of hepatocellular carcinoma in cirrhotic patients: prognostic value of preoperative portal pressure. Gastroenterology 1996; 111:1018.
  34. Azoulay D, Buabse F, Damiano I, et al. Neoadjuvant transjugular intrahepatic portosystemic shunt: a solution for extrahepatic abdominal operation in cirrhotic patients with severe portal hypertension. J Am Coll Surg 2001; 193:46.
  35. Friedman, LS, Martin, et al. Liver function tests and the objective evaluation of the patient with liver disease. In: Hepatology: A Textbook of Liver Disease, 4th, Zakim, D, Boyer TD (Eds), Saunders, Philadelphia 2003. p.661.
  36. Zimmerman JE, Wagner DP, Seneff MG, et al. Intensive care unit admissions with cirrhosis: risk-stratifying patient groups and predicting individual survival. Hepatology 1996; 23:1393.
  37. Teh SH, Nagorney DM, Stevens SR, et al. Risk factors for mortality after surgery in patients with cirrhosis. Gastroenterology 2007; 132:1261.
  38. Suman A, Barnes DS, Zein NN, et al. Predicting outcome after cardiac surgery in patients with cirrhosis: a comparison of Child-Pugh and MELD scores. Clin Gastroenterol Hepatol 2004; 2:719.
  39. Farnsworth N, Fagan SP, Berger DH, Awad SS. Child-Turcotte-Pugh versus MELD score as a predictor of outcome after elective and emergent surgery in cirrhotic patients. Am J Surg 2004; 188:580.
  40. Perkins L, Jeffries M, Patel T. Utility of preoperative scores for predicting morbidity after cholecystectomy in patients with cirrhosis. Clin Gastroenterol Hepatol 2004; 2:1123.
  41. Befeler AS, Palmer DE, Hoffman M, et al. The safety of intra-abdominal surgery in patients with cirrhosis: model for end-stage liver disease score is superior to Child-Turcotte-Pugh classification in predicting outcome. Arch Surg 2005; 140:650.
  42. Cucchetti A, Ercolani G, Vivarelli M, et al. Impact of model for end-stage liver disease (MELD) score on prognosis after hepatectomy for hepatocellular carcinoma on cirrhosis. Liver Transpl 2006; 12:966.
  43. Hanje AJ, Patel T. Preoperative evaluation of patients with liver disease. Nat Clin Pract Gastroenterol Hepatol 2007; 4:266.
  44. Greve JW, Gouma DJ, Soeters PB, Buurman WA. Suppression of cellular immunity in obstructive jaundice is caused by endotoxins: a study with germ-free rats. Gastroenterology 1990; 98:478.
  45. Plusa S, Webster N, Primrose J. Obstructive jaundice causes reduced expression of polymorphonuclear leucocyte adhesion molecules and a depressed response to bacterial wall products in vitro. Gut 1996; 38:784.
  46. Wait RB, Kahng KU. Renal failure complicating obstructive jaundice. Am J Surg 1989; 157:256.
  47. Grande L, Garcia-Valdecasas JC, Fuster J, et al. Obstructive jaundice and wound healing. Br J Surg 1990; 77:440.
  48. Shirahatti RG, Alphonso N, Joshi RM, et al. Palliative surgery in malignant obstructive jaundice: prognostic indicators of early mortality. J R Coll Surg Edinb 1997; 42:238.
  49. Dixon JM, Armstrong CP, Duffy SW, Davies GC. Factors affecting morbidity and mortality after surgery for obstructive jaundice: a review of 373 patients. Gut 1983; 24:845.
  50. Greig JD, Krukowski ZH, Matheson NA. Surgical morbidity and mortality in one hundred and twenty-nine patients with obstructive jaundice. Br J Surg 1988; 75:216.
  51. Pain JA, Cahill CJ, Bailey ME. Perioperative complications in obstructive jaundice: therapeutic considerations. Br J Surg 1985; 72:942.
  52. Blamey SL, Fearon KC, Gilmour WH, et al. Prediction of risk in biliary surgery. Br J Surg 1983; 70:535.
  53. Lai EC, Chu KM, Lo CY, et al. Surgery for malignant obstructive jaundice: analysis of mortality. Surgery 1992; 112:891.
  54. Diamond T, Parks RW. Perioperative management of obstructive jaundice. Br J Surg 1997; 84:147.
  55. Hatfield AR, Tobias R, Terblanche J, et al. Preoperative external biliary drainage in obstructive jaundice. A prospective controlled clinical trial. Lancet 1982; 2:896.
  56. McPherson GA, Benjamin IS, Hodgson HJ, et al. Pre-operative percutaneous transhepatic biliary drainage: the results of a controlled trial. Br J Surg 1984; 71:371.
  57. Pitt HA, Gomes AS, Lois JF, et al. Does preoperative percutaneous biliary drainage reduce operative risk or increase hospital cost? Ann Surg 1985; 201:545.
  58. Clements WD, Diamond T, McCrory DC, Rowlands BJ. Biliary drainage in obstructive jaundice: experimental and clinical aspects. Br J Surg 1993; 80:834.
  59. Liu F, Li Y, Wei Y, Li B. Preoperative biliary drainage before resection for hilar cholangiocarcinoma: whether or not? A systematic review. Dig Dis Sci 2011; 56:663.
  60. Lai EC, Mok FP, Fan ST, et al. Preoperative endoscopic drainage for malignant obstructive jaundice. Br J Surg 1994; 81:1195.
  61. van der Gaag NA, Rauws EA, van Eijck CH, et al. Preoperative biliary drainage for cancer of the head of the pancreas. N Engl J Med 2010; 362:129.
  62. Khan AZ, Makuuchi M. Trends in the surgical management of Klatskin tumours. Br J Surg 2007; 94:393.
  63. Baron TH, Kozarek RA. Preoperative biliary stents in pancreatic cancer--proceed with caution. N Engl J Med 2010; 362:170.
  64. Lai EC, Mok FP, Tan ES, et al. Endoscopic biliary drainage for severe acute cholangitis. N Engl J Med 1992; 326:1582.
  65. Jacyna MR, Summerfield JA. Endoscopic management of biliary tract obstruction in the 1990s. J Hepatol 1992; 14:127.
  66. Chijiiwa K, Kozaki N, Naito T, et al. Treatment of choice for choledocholithiasis in patients with acute obstructive suppurative cholangitis and liver cirrhosis. Am J Surg 1995; 170:356.
  67. Freeman ML, Nelson DB, Sherman S, et al. Complications of endoscopic biliary sphincterotomy. N Engl J Med 1996; 335:909.
  68. Prat F, Tennenbaum R, Ponsot P, et al. Endoscopic sphincterotomy in patients with liver cirrhosis. Gastrointest Endosc 1996; 43:127.
  69. Fogarty BJ, Parks RW, Rowlands BJ, Diamond T. Renal dysfunction in obstructive jaundice. Br J Surg 1995; 82:877.
  70. Kimmings AN, van Deventer SJ, Obertop H, et al. Inflammatory and immunologic effects of obstructive jaundice: pathogenesis and treatment. J Am Coll Surg 1995; 181:567.
  71. Cahill CJ. Prevention of postoperative renal failure in patients with obstructive jaundice--the role of bile salts. Br J Surg 1983; 70:590.
  72. Pain JA, Cahill CJ, Gilbert JM, et al. Prevention of postoperative renal dysfunction in patients with obstructive jaundice: a multicentre study of bile salts and lactulose. Br J Surg 1991; 78:467.
  73. Greve JW, Gouma DJ, von Leeuwen PA, Buurman WA. Lactulose inhibits endotoxin induced tumour necrosis factor production by monocytes. An in vitro study. Gut 1990; 31:198.
  74. Gubern JM, Sancho JJ, Simó J, Sitges-Serra A. A randomized trial on the effect of mannitol on postoperative renal function in patients with obstructive jaundice. Surgery 1988; 103:39.
  75. Moore RD, Smith CR, Lietman PS. Increased risk of renal dysfunction due to interaction of liver disease and aminoglycosides. Am J Med 1986; 80:1093.
  76. Lucena MI, Andrade RJ, Cabello MR, et al. Aminoglycoside-associated nephrotoxicity in extrahepatic obstructive jaundice. J Hepatol 1995; 22:189.
  77. Gentilini P. Cirrhosis, renal function and NSAIDs. J Hepatol 1993; 19:200.
  78. Better OS. Renal and cardiovascular dysfunction in liver disease. Kidney Int 1986; 29:598.
  79. Bizouarn P, Ausseur A, Desseigne P, et al. Early and late outcome after elective cardiac surgery in patients with cirrhosis. Ann Thorac Surg 1999; 67:1334.
  80. Filsoufi F, Salzberg SP, Rahmanian PB, et al. Early and late outcome of cardiac surgery in patients with liver cirrhosis. Liver Transpl 2007; 13:990.
  81. Klemperer JD, Ko W, Krieger KH, et al. Cardiac operations in patients with cirrhosis. Ann Thorac Surg 1998; 65:85.
  82. Morris JJ, Hellman CL, Gawey BJ, et al. Case 3-1995. Three patients requiring both coronary artery bypass surgery and orthotopic liver transplantation. J Cardiothorac Vasc Anesth 1995; 9:322.
  83. Pollard RJ, Sidi A, Gibby GL, et al. Aortic stenosis with end-stage liver disease: prioritizing surgical and anesthetic therapies. J Clin Anesth 1998; 10:253.
  84. Gaudino M, Santarelli P, Bruno P, et al. Palliative coronary artery surgery in patients with severe noncardiac diseases. Am J Cardiol 1997; 80:1351.
  85. Eckhoff DE, Frenette L, Sellers MT, et al. Combined cardiac surgery and liver transplantation. Liver Transpl 2001; 7:60.
  86. Ehtisham J, Altieri M, Salamé E, et al. Coronary artery disease in orthotopic liver transplantation: pretransplant assessment and management. Liver Transpl 2010; 16:550.
  87. Clavien PA, Petrowsky H, DeOliveira ML, Graf R. Strategies for safer liver surgery and partial liver transplantation. N Engl J Med 2007; 356:1545.
  88. Di Bisceglie AM, Carithers RL Jr, Gores GJ. Hepatocellular carcinoma. Hepatology 1998; 28:1161.
  89. Mor E, Tur-Kaspa R, Sheiner P, Schwartz M. Treatment of hepatocellular carcinoma associated with cirrhosis in the era of liver transplantation. Ann Intern Med 1998; 129:643.
  90. MacIntosh EL, Minuk GY. Hepatic resection in patients with cirrhosis and hepatocellular carcinoma. Surg Gynecol Obstet 1992; 174:245.
  91. Wu CC, Ho WL, Yeh DC, et al. Hepatic resection of hepatocellular carcinoma in cirrhotic livers: is it unjustified in impaired liver function? Surgery 1996; 120:34.
  92. Bruix J. Treatment of hepatocellular carcinoma. Hepatology 1997; 25:259.
  93. Capussotti L, Polastri R. Operative risks of major hepatic resections. Hepatogastroenterology 1998; 45:184.
  94. Cohnert TU, Rau HG, Buttler E, et al. Preoperative risk assessment of hepatic resection for malignant disease. World J Surg 1997; 21:396.
  95. Grazi GL, Ercolani G, Pierangeli F, et al. Improved results of liver resection for hepatocellular carcinoma on cirrhosis give the procedure added value. Ann Surg 2001; 234:71.
  96. Wu CC, Yeh DC, Lin MC, et al. Improving operative safety for cirrhotic liver resection. Br J Surg 2001; 88:210.
  97. van den Broek MA, Olde Damink SW, Dejong CH, et al. Liver failure after partial hepatic resection: definition, pathophysiology, risk factors and treatment. Liver Int 2008; 28:767.
  98. Schroeder RA, Marroquin CE, Bute BP, et al. Predictive indices of morbidity and mortality after liver resection. Ann Surg 2006; 243:373.
  99. McCormack L, Petrowsky H, Jochum W, et al. Hepatic steatosis is a risk factor for postoperative complications after major hepatectomy: a matched case-control study. Ann Surg 2007; 245:923.
  100. Demetriades D, Constantinou C, Salim A, et al. Liver cirrhosis in patients undergoing laparotomy for trauma: effect on outcomes. J Am Coll Surg 2004; 199:538.
  101. Runyon BA. Surgical procedures are well tolerated by patients with asymptomatic chronic hepatitis. J Clin Gastroenterol 1986; 8:542.
  102. Behrns KE, Tsiotos GG, DeSouza NF, et al. Hepatic steatosis as a potential risk factor for major hepatic resection. J Gastrointest Surg 1998; 2:292.
  103. Zimmerman HJ, Maddrey WC. Acetaminophen (paracetamol) hepatotoxicity with regular intake of alcohol: analysis of instances of therapeutic misadventure. Hepatology 1995; 22:767.
  104. Takagi T, Ishii H, Takahashi H, et al. Potentiation of halothane hepatotoxicity by chronic ethanol administration in rat: an animal model of halothane hepatitis. Pharmacol Biochem Behav 1983; 18 Suppl 1:461.
  105. Zimmerman HJ. Effects of alcohol on other hepatotoxins. Alcohol Clin Exp Res 1986; 10:3.
  106. Farrell FJ, Nguyen M, Woodley S, et al. Outcome of liver transplantation in patients with hemochromatosis. Hepatology 1994; 20:404.
  107. Scheinberg, IH, Sternlieb, I. Wilson's disease. In: Major Problems in Internal Medicine, 23, Smith, LH (Eds), Saunders, Philadelphia 1984..
  108. Yarze JC, Martin P, Muñoz SJ, Friedman LS. Wilson's disease: current status. Am J Med 1992; 92:643.
  109. Alkozai EM, Lisman T, Porte RJ. Bleeding in liver surgery: prevention and treatment. Clin Liver Dis 2009; 13:145.
  110. Semiz-Oysu A, Moustafa T, Cho KJ. Transjugular intrahepatic portosystemic shunt prior to cardiac surgery with cardiopulmonary bypass in patients with cirrhosis and portal hypertension. Heart Lung Circ 2007; 16:465.
  111. Vinet E, Perreault P, Bouchard L, et al. Transjugular intrahepatic portosystemic shunt before abdominal surgery in cirrhotic patients: a retrospective, comparative study. Can J Gastroenterol 2006; 20:401.
  112. Saad WE, Saad NE, Davies MG, et al. Elective transjugular intrahepatic portosystemic shunt creation for portal decompression in the immediate pretransplantation period in adult living related liver transplant recipient candidates: preliminary results. J Vasc Interv Radiol 2006; 17:995.
  113. Norton SA, Vickers J, Callaway MP, Alderson D. The role of preoperative TIPSS to facilitate curative gastric surgery. Cardiovasc Intervent Radiol 2003; 26:398.
  114. Fan ST, Lo CM, Lai EC, et al. Perioperative nutritional support in patients undergoing hepatectomy for hepatocellular carcinoma. N Engl J Med 1994; 331:1547.
  115. Nompleggi DJ, Bonkovsky HL. Nutritional supplementation in chronic liver disease: an analytical review. Hepatology 1994; 19:518.
  116. Long-term oral administration of branched chain amino acids after curative resection of hepatocellular carcinoma: a prospective randomized trial. The San-in Group of Liver Surgery. Br J Surg 1997; 84:1525.
  117. Cabre E, Gonzalez-Huix F, Abad-Lacruz A, et al. Effect of total enteral nutrition on the short-term outcome of severely malnourished cirrhotics. A randomized controlled trial. Gastroenterology 1990; 98:715.
  118. Hirsch S, Bunout D, de la Maza P, et al. Controlled trial on nutrition supplementation in outpatients with symptomatic alcoholic cirrhosis. JPEN J Parenter Enteral Nutr 1993; 17:119.
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