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Surgery_Schwartz. capabilities. It was initially described as a specific disease entity in the 1950s. Figure 31-12. Computed tomography (CT)–positron emission tomography (PET) scans before and after resection of liver metastasis from colorectal cancer in a 54-year-old patient. CT scan shows large 10-cm right lobe liver metastasis (left panel), and PET scan findings are strongly positive (middle panel). Two years after right hepatectomy, the patient has no evidence of recurrence and significant hypertrophy of the left lobe (right panel).Brunicardi_Ch31_p1345-p1392.indd 136020/02/19 2:36 PM 1361LIVERCHAPTER 31It also has been referred to as fulminant hepatic failure. ALF is a rare disorder affecting approximately 2000 patients annually in the United States. ALF is defined by the development of hepatic encephalopathy occurring within 26 weeks of severe liver injury in a patient without a history of previous liver dis-ease or portal hypertension.29 The manifestations of ALF may include cerebral edema,


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Surgery_Schwartz. occurring within 26 weeks of severe liver injury in a patient without a history of previous liver dis-ease or portal hypertension.29 The manifestations of ALF may include cerebral edema, hemodynamic instability, increased sus-ceptibility to bacterial and fungal infections, renal failure, coag-ulopathy, and metabolic disturbances. Even with current medical care, ALF can progress rapidly to hepatic coma and death. The most common cause of death is intracranial hypertension due to cerebral edema, followed by sepsis and multisystem organ failure. The causes of ALF, which are the most important variables in determining outcome, are numerous and can include viral infection as well as drug overdose, reaction, and toxicity. It has been determined that the etiologic factor leading to ALF varies according to geographic location.30 Before the introduc-tion of orthotopic liver transplantation (OLT), the chance for survival was <20%. Currently, most series report 5-year survival rates of >70% for


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Surgery_Schwartz. to geographic location.30 Before the introduc-tion of orthotopic liver transplantation (OLT), the chance for survival was <20%. Currently, most series report 5-year survival rates of >70% for affected patients.31EtiologyDifferences in etiology, management, and patient outcomes have been described for various regions of the globe. In the East and developing portions of the world, the most common causes of ALF are viral infections, primarily hepatitis B, A, and E.20 In these areas, there are a relatively small number of drug-induced cases. In contrast, 65% of cases of ALF in the West are thought to be due to drugs and toxins, with acetaminophen (paracetamol) being the most common etiologic agent in the United States, Australia, United Kingdom, and most of Europe. In France and Spain, where acetaminophen sales are restricted, the rate of acetaminophen-induced ALF is quite low.32 Acetaminophen-induced ALF is also uncommon in South America. The U.S. Acute Liver Failure Study Group


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Surgery_Schwartz. where acetaminophen sales are restricted, the rate of acetaminophen-induced ALF is quite low.32 Acetaminophen-induced ALF is also uncommon in South America. The U.S. Acute Liver Failure Study Group identified several other causes of ALF, including autoimmune hepatitis, hypoperfusion of the liver (in cardiomyopathy or cardiogenic shock), pregnancy-related conditions, and Wilson’s disease.33 Even with exhaustive efforts to identify a cause, approximately 20% of all cases of ALF remain indeterminate in origin.Clinical PresentationIn a multicenter study involving 17 tertiary care centers and 308 patients in the United States, 73% of all patients with ALF were female, with a median age of 38 years.34 The most common ethnic group affected was whites (74%), followed by Hispanics (9%) and African Americans (3%). Patients were ill for a median of 6 days before the onset of encephalopathy and had a median of 2 days between the onset of jaundice and the development of encephalopathy. Hepatic


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Surgery_Schwartz. Americans (3%). Patients were ill for a median of 6 days before the onset of encephalopathy and had a median of 2 days between the onset of jaundice and the development of encephalopathy. Hepatic coma grade at presentation was approximately equally distributed across grades I to IV. Eighty-four percent of the patients in the study were referred from outside hospitals, 40% had a serum creatinine level exceeding 2.0 mg/dL, and 14% had an arterial pH of <7.30. In addition, 44% of the patients acquired a culture-proven infection.Diagnosis and Clinical ManagementWhen the medical history is obtained, it is important to address the possibility of exposure to viral infections, medications, and other possible toxins. The possibility of previous liver disease needs to be explored. The physical examination must assess and document the patient’s mental status as well as attempt to identify findings of chronic liver disease. The initial laboratory examination must evaluate the severity of the ALF


Surgery_Schwartz

Surgery_Schwartz. must assess and document the patient’s mental status as well as attempt to identify findings of chronic liver disease. The initial laboratory examination must evaluate the severity of the ALF as well as attempt to identify the cause (Table 31-1). A liver biopsy should be performed if certain disease entities such as autoimmune hepatitis or lymphoma are a possibility. Because of the asso-ciated coagulopathy, if a liver biopsy is needed, it is usually safest to obtain the tissue via a transjugular approach. Patients with ALF should be admitted to the hospital and monitored fre-quently. Due to the rapidity with which this disease process may progress, a liver transplant center should be contacted, and the affected patient should be transferred to the center early in the evaluation period.If acetaminophen overdose is suspected to have occurred within a few hours of presentation, administration of activated charcoal may be useful to reduce the volume of acetamino-phen present in the


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Surgery_Schwartz. acetaminophen overdose is suspected to have occurred within a few hours of presentation, administration of activated charcoal may be useful to reduce the volume of acetamino-phen present in the gastrointestinal (GI) tract. N-acetylcysteine (NAC), the clinically effective antidote for acetaminophen over-dose, should be administered as early as possible to any patient with suspected acetaminophen-associated ALF.35 NAC also should be administered to patients with ALF of unclear etiol-ogy because replenishing glutathione may be beneficial in this patient population as well.36 NAC can be administered either orally (140 mg/kg initial dose, followed by 70 mg/kg every 4 hours × 17 doses) or via the intravenous route (loading dose of 150 mg/kg, followed by a maintenance dose of 50 mg/kg every 4 hours × 12 doses). For patients who are suspected of having drug-induced hepatotoxicity, it is important to obtain details regarding all prescription and nonprescription drugs, herbs, and dietary


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Surgery_Schwartz. 4 hours × 12 doses). For patients who are suspected of having drug-induced hepatotoxicity, it is important to obtain details regarding all prescription and nonprescription drugs, herbs, and dietary supplements that may have been taken in the previous year. Most instances of drug-induced hepatotoxicity occur in the first 6 months after drug initiation. Any suspected offending agent must be discontinued, and an attempt should be made to administer only essential medications.The majority of patients with ALF need to be monitored in the intensive care unit (ICU) setting, and specific attention needs to be given to fluid management, ulcer prophylaxis, hemody-namic monitoring, electrolyte management, and surveillance for and treatment of infection. Surveillance cultures should be performed to identify bacterial and fungal infections as early as possible. Serum phosphorus levels need to be monitored. 4Table 31-1Acute liver failure laboratory evaluationComplete blood countComplete metabolic


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Surgery_Schwartz. identify bacterial and fungal infections as early as possible. Serum phosphorus levels need to be monitored. 4Table 31-1Acute liver failure laboratory evaluationComplete blood countComplete metabolic panelAmylase and lipase levelsLiver function testsProthrombin time/international normalized ratioFactor V levelFactor VII levelArterial blood gas concentrationsArterial serum ammonia levelABO typingAcute hepatitis panelAutoimmune marker levelsCeruloplasmin levelToxicology screeningAcetaminophen levelHIV screeningPregnancy test (females)HIV = human immunodeficiency virus.Brunicardi_Ch31_p1345-p1392.indd 136120/02/19 2:36 PM 1362SPECIFIC CONSIDERATIONSPART IIHypophosphatemia, a sign of hepatic regeneration, may indi-cate a higher likelihood of spontaneous recovery and needs to be corrected via intravenous (IV) administration of phosphate. Sedation should be avoided, and the head of the bed should be elevated at least 30°. Neurologic examinations should be per-formed frequently.


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Surgery_Schwartz. via intravenous (IV) administration of phosphate. Sedation should be avoided, and the head of the bed should be elevated at least 30°. Neurologic examinations should be per-formed frequently. Intracranial pressure monitoring is reserved for patients in whom a neurologic examination is no longer reli-able. CT scans of the head should be performed to rule out mass lesion or hemorrhage, but they provide only limited informa-tion regarding increased intracranial pressure. The administra-tion of blood products for thrombocytopenia and prolonged PT is recommended only in the setting of hemorrhage or before invasive procedures. Acute renal failure is a frequent complica-tion in patients with ALF, and efforts should be made to protect renal function by maintaining sufficient perfusion and avoid-ing nephrotoxic medications. Should renal replacement therapy become necessary, continuous venovenous hemodialysis should be used rather than intermittent hemodialysis because continu-ous venovenous


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Surgery_Schwartz. nephrotoxic medications. Should renal replacement therapy become necessary, continuous venovenous hemodialysis should be used rather than intermittent hemodialysis because continu-ous venovenous hemodialysis provides better hemodynamic and intracranial pressure stability. The most severely affected patients have a poor prognosis with medical management alone and require liver transplantation. Identifying these patients early in the clinical course is important both to maximize the time available to obtain a donor liver allograft for those in need and to avoid transplant in those who will recover without it.PrognosisAccurate identification of ALF patients who will recover spon-taneously is important because of the severe shortage of donor liver allografts and the potential complications of lifelong non-specific immunosuppression. The most widely applied prognos-tic scoring system is the King’s College Hospital ALF criteria.37 This scoring system has separate criteria predicting a poor


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Surgery_Schwartz. lifelong non-specific immunosuppression. The most widely applied prognos-tic scoring system is the King’s College Hospital ALF criteria.37 This scoring system has separate criteria predicting a poor medical management outcome for acetaminophen-related and non–acetaminophen-related forms of ALF (Table 31-2). Many other prognostic models exist such as the Acute Physiology and Chronic Health Evaluation II (APACHE II) score, the Clichy criteria,38 and actin-free Gc-globulin serum concentration.39 Overall, prognostic scoring systems have proven to have acceptable specificity but low sensitivity in determining patient outcome and therefore should not replace the judgment of an experienced clinician.40Liver TransplantationDespite advances in medical management, OLT remains the only definitive therapy for patients unable to regenerate sufficient hepatocyte mass in a timely manner. The advent of OLT has coincided with a rise in overall ALF survival rates from approxi-mately 20% in the


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Surgery_Schwartz. therapy for patients unable to regenerate sufficient hepatocyte mass in a timely manner. The advent of OLT has coincided with a rise in overall ALF survival rates from approxi-mately 20% in the pretransplantation era to >70% at the pres-ent time. One-year posttransplantation survival for patients with ALF has been reported to be as high as 80% to 90%.31 Although these improvements in survival rates are impressive, it should be noted that 10% of patients still die while awaiting OLT, which confirms that the potential for improved patient outcome still has not been realized because of the ongoing liver allograft shortage.Emerging TechnologiesAs mentioned earlier, patient survival could be improved if additional time could be gained for the patient while awaiting liver replacement or hepatocyte regeneration. The development of a support device to replace the acutely failing liver has been a highly sought after (and elusive) goal. Several systems have been tested without definitive


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Surgery_Schwartz. regeneration. The development of a support device to replace the acutely failing liver has been a highly sought after (and elusive) goal. Several systems have been tested without definitive evidence of efficacy. Transient improvement in hepatic encephalopathy has been observed in several trials, but improvement in hepatocyte function and long-term benefit have not been realized.41 Liver support trials are dif-ficult to perform due to access to liver replacement, the rarity of affected patients, and the heterogeneous causes and varying levels of disease severity. Therefore, additional data are necessary, and liver support systems should be used only as part of an approved clinical trial. Focus has now shifted toward xenotransplantation,42 organ engineering, and cell transplantation.43 In the meantime, living donation and auxiliary liver transplantation can help over-come the organ shortage.44CIRRHOSIS AND PORTAL HYPERTENSIONCirrhosis, the final sequela of chronic hepatic insult, is


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Surgery_Schwartz. the meantime, living donation and auxiliary liver transplantation can help over-come the organ shortage.44CIRRHOSIS AND PORTAL HYPERTENSIONCirrhosis, the final sequela of chronic hepatic insult, is char-acterized by the presence of fibrous septa throughout the liver subdividing the parenchyma into hepatocellular nodules (Fig. 31-13).45 Cirrhosis is the consequence of sustained wound healing in response to chronic liver injury. Approximately 40% of cirrhotic patients are asymptomatic, but progressive deteriora-tion leading to the need for liver transplantation or death is typi-cal after the development of end-stage liver disease (ESLD). The complications of ESLD include progressive hyperbilirubinemia, malnutrition, decreased synthetic function of the liver, coagu-lopathy, portal hypertension (i.e., ascites and variceal bleeding), hepatic encephalopathy, and life-limiting fatigue. ESLD car-ries a 5-year mortality of 50%, with 70% of deaths due to liver failure.46 In the United States,


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Surgery_Schwartz. (i.e., ascites and variceal bleeding), hepatic encephalopathy, and life-limiting fatigue. ESLD car-ries a 5-year mortality of 50%, with 70% of deaths due to liver failure.46 In the United States, cirrhosis accounts for 30,000 deaths per year and is the most common nonneoplastic cause of death among patients with hepatobiliary and digestive diseases. An additional 10,000 to 12,000 deaths occur annually due to HCC, the most rapidly increasing neoplasm in the United States.46Morphologic Classification of CirrhosisMorphologically, cirrhosis can be described as micronodular, macronodular, or mixed. Micronodular cirrhosis is characterized Table 31-2King’s College selection criteria for liver transplantation in acute liver failureCAUSESELECTION CRITERIAAcetaminophenArterial pH < 7.30 irrespective of hepatic coma gradeOrProthrombin time >100 s + serum creatinine level >3.4 mg/dL + grade III or IV hepatic comaNot acetaminophenProthrombin time >100 s irrespective of hepatic coma gradeOrAny


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Surgery_Schwartz. of hepatic coma gradeOrProthrombin time >100 s + serum creatinine level >3.4 mg/dL + grade III or IV hepatic comaNot acetaminophenProthrombin time >100 s irrespective of hepatic coma gradeOrAny three of the following, irrespective of hepatic coma grade: Cryptogenic or drug-induced hepatitis Jaundice to coma interval >7 d Prothrombin time >50 s Serum bilirubin level >17.5 mg/dL Age < 10 y or > 40 yBrunicardi_Ch31_p1345-p1392.indd 136220/02/19 2:36 PM 1363LIVERCHAPTER 31by thick regular septa, small uniform regenerative nodules, and involvement of virtually every hepatic lobule. Macronodular cirrhosis frequently has septa and regenerative nodules of vary-ing sizes. The regenerative nodules consist of irregularly sized hepatocytes with large nuclei and cell plates of varying thick-ness. Mixed cirrhosis is present when regeneration is occurring in a micronodular liver and over time converts to a macronodu-lar pattern. This morphologic categorization is limited, and cir-rhosis is a


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Surgery_Schwartz. Mixed cirrhosis is present when regeneration is occurring in a micronodular liver and over time converts to a macronodu-lar pattern. This morphologic categorization is limited, and cir-rhosis is a dynamic process in which nodule size varies over time. The three patterns correlate poorly with etiology, and the same pattern can result from a variety of disease processes. Conversely, a single disease process can demonstrate several morphologic patterns. Irrespective of etiology and morphologic pattern, the cirrhotic liver frequently demonstrates right hepatic lobe atrophy, caudate lobe and left lateral segment hypertrophy, recanalization of the umbilical vein, a nodular surface contour, dilatation of the portal vein, gastroesophageal varices, and sple-nomegaly on radiographic evaluation.Etiology of CirrhosisCirrhosis can result from a wide range of disease processes, including viral, autoimmune, drug-induced, alcohol-induced, nonalcoholic fatty liver disease, and metabolic diseases


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Surgery_Schwartz. of CirrhosisCirrhosis can result from a wide range of disease processes, including viral, autoimmune, drug-induced, alcohol-induced, nonalcoholic fatty liver disease, and metabolic diseases (Table 31-3). In the diagnosis of alcoholic liver disease, docu-mentation of chronic alcohol abuse is imperative. Liver biopsy will reveal the typical findings of alcoholic hepatitis, including hepatocyte necrosis, Mallory bodies, neutrophil infiltration, and perivenular inflammation.Nonalcoholic fatty liver disease (NAFLD) covers a wide spectrum of disorders including simple fatty liver, nonalcoholic steatohepatitis (NASH), fibrosis/cirrhosis and NASH-associated hepatocellular carcinoma.47 NAFLD is now the most common chronic liver disease worldwide48 and NASH is a progressive form of NAFLD characterized by steatosis with hepatocellular injury and chronic inflammation.49 NASH affects 3% to 5% of the population, and approximately 1 in 10 NASH patients will progress to cirrhosis, thereby placing


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Surgery_Schwartz. by steatosis with hepatocellular injury and chronic inflammation.49 NASH affects 3% to 5% of the population, and approximately 1 in 10 NASH patients will progress to cirrhosis, thereby placing them at risk for the well-described consequences of cirrhosis, including hepatocellular carcinoma.50 Although hepatocellular carcinoma arises less fre-quently in patients with NASH compared to other liver diseases (e.g., hepatitis C viral infection), the overall higher prevalence and more rapidly increasing incidence of NASH relative to other chronic liver diseases mean that the majority of HCC will arise in the setting of NAFLD in the near future.51,52Patients with nonalcoholic steatohepatitis (NASH) often endorse a history of diabetes mellitus or metabolic syndrome. The diagnosis of NASH requires the demonstration of steato-hepatitis on biopsy, the lack of a history of significant alcohol consumption, and exclusion of other causes of hepatic steatosis. Although cryptogenic cirrhosis, or


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Surgery_Schwartz. the demonstration of steato-hepatitis on biopsy, the lack of a history of significant alcohol consumption, and exclusion of other causes of hepatic steatosis. Although cryptogenic cirrhosis, or cirrhosis without an apparent cause, accounted for a third of all cases in the past, this propor-tion has declined over time as it becomes increasingly appar-ent that many of such patients may actually have unrecognized NASH.Due to the high prevalence of fatty liver disease, many patients considered for hepatic surgery will have background hepatic steatosis or steatohepatitis. In addition, chemotherapy treatment (e.g., irinotecan) for colorectal cancer liver metasta-ses induces steatosis and steatohepatitis in the nontumor-bearing liver.53 This has important implications as fatty liver disease can increase morbidity after liver resection.54,55 Thus, under-standing the deleterious effects of steatosis and steatohepatitis Figure 31-13. Histology of cirrhotic liver with regenerating mac-ronodules.


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Surgery_Schwartz. morbidity after liver resection.54,55 Thus, under-standing the deleterious effects of steatosis and steatohepatitis Figure 31-13. Histology of cirrhotic liver with regenerating mac-ronodules. Upper panel: Grossly cirrhotic liver. Lower panel: Regenerative nodules and bridging fibrosis representative of cir-rhosis seen on standard light microscopy (hematoxylin and eosin stain).Table 31-3Etiology of cirrhosisViral hepatitis (hepatitis B, C, and D)CryptogenicAlcohol abuseMetabolic abnormalities Iron overload (hemochromatosis) Copper overload (Wilson’s disease) α1-Antitrypsin deficiency Glycogen storage disease (types IA, III, and IV) Tyrosinemia GalactosemiaNonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)Hepatic vein outflow abnormalities Budd-Chiari syndrome Cardiac failureAutoimmune hepatitisToxins and drugsBrunicardi_Ch31_p1345-p1392.indd 136320/02/19 2:36 PM 1364SPECIFIC CONSIDERATIONSPART IIis crucial for the multidisciplinary care of patients


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Surgery_Schwartz. failureAutoimmune hepatitisToxins and drugsBrunicardi_Ch31_p1345-p1392.indd 136320/02/19 2:36 PM 1364SPECIFIC CONSIDERATIONSPART IIis crucial for the multidisciplinary care of patients undergoing liver surgery.Chronic hepatitis C infection is the most common cause of chronic liver disease and the most frequent indication for liver transplantation in the United States. The identification of chronic hepatitis C infection is facilitated by serologic assays that detect antibody to hepatitis C and molecular assays that quantify hepatitis C viral RNA. Chronic hepatitis B, on the other hand, can be diagnosed based on the detection of hepatitis B surface antigen (HBsAg) more than 4 to 6 months after initial infection. Additional tests of hepatitis B viral replication, such as the hepatitis B e antigen (HBeAg) and hepatitis B viral DNA, can be used to confirm ongoing infection and to guide appropri-ate antiviral therapy.Autoimmune causes of cirrhosis include primary bili-ary cirrhosis,


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Surgery_Schwartz. B e antigen (HBeAg) and hepatitis B viral DNA, can be used to confirm ongoing infection and to guide appropri-ate antiviral therapy.Autoimmune causes of cirrhosis include primary bili-ary cirrhosis, primary sclerosing cholangitis, and autoimmune hepatitis. Patients with primary biliary cirrhosis may be asymp-tomatic or may present with a history of fatigue, pruritus, and skin hyperpigmentation that is not related to jaundice. Anti-mitochondrial antibodies will test positive in the vast majority of cases. Affected patients also may have marked elevations in serum cholesterol, while hyperbilirubinemia is seen late in the course of the disease. Primary sclerosing cholangitis is a chronic cholestatic disease of the liver associated with ulcer-ative colitis and Crohn’s disease. The clinical presentation can include pruritus, steatorrhea, fat-soluble vitamin deficiencies, and metabolic bone disease. The diagnosis is often established by imaging of the biliary tree, which reveals a


Surgery_Schwartz

Surgery_Schwartz. presentation can include pruritus, steatorrhea, fat-soluble vitamin deficiencies, and metabolic bone disease. The diagnosis is often established by imaging of the biliary tree, which reveals a characteristic picture of diffuse, multifocal strictures with focal dilation of the bile ducts resulting in a beaded appearance. Complications are common and can include biliary strictures, cholangitis, choleli-thiasis, and cholangiocarcinoma. Autoimmune hepatitis is often accompanied by an elevation in serum globulins, particularly gamma globulins. Liver biopsy will show nonspecific changes such as a portal mononuclear cell infiltrate with the character-istic presence of plasma cells. Many patients with autoimmune hepatitis will respond to treatment with prednisone with or with-out azathioprine.Hereditary hemochromatosis is the most common meta-bolic disorder causing cirrhosis. This entity should be suspected if the patient’s clinical presentation includes skin hyperpigmen-tation, diabetes


Surgery_Schwartz

Surgery_Schwartz. hemochromatosis is the most common meta-bolic disorder causing cirrhosis. This entity should be suspected if the patient’s clinical presentation includes skin hyperpigmen-tation, diabetes mellitus, pseudogout, cardiomyopathy, or a fam-ily history of cirrhosis. Elevated plasma ferritin and increased iron saturation levels suggest the presence of iron overload, but these findings also can be seen in other diseases of the liver. Confirmatory testing can be achieved by means of genetic test-ing, liver biopsy, or by assessing the response to phlebotomy. Other uncommon metabolic disorders leading to cirrhosis include Wilson’s disease and α1-antitrypsin deficiency.Clinical Manifestations of CirrhosisThe clinical history associated with cirrhosis can include fatigue, anorexia, weight loss, jaundice, abdominal pain, peripheral edema, ascites, GI bleeding, and hepatic encephalopathy. On physical examination, a number of findings have been described in patients with cirrhosis. Spider angiomata


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Surgery_Schwartz. abdominal pain, peripheral edema, ascites, GI bleeding, and hepatic encephalopathy. On physical examination, a number of findings have been described in patients with cirrhosis. Spider angiomata and palmar ery-thema are believed to be caused by alterations in sex hormone metabolism. Finger clubbing may be a consequence of hypo-albuminemia, while the pathogenesis of white nail beds and Dupuytren’s contractures are less well understood. Males may develop features of feminization such as gynecomastia, loss of chest and axillary hair, and testicular atrophy. Splenomegaly is common, whereas the cirrhotic liver itself may be enlarged, nor-mal sized, or small. Ascites and pleural effusion can be seen with fluid accumulation. Portal hypertension can manifest as caput medusae and/or the presence of the Cruveilhier-Baumgarten murmur, a venous hum that can be auscultated in the epigas-trium resulting from collaterals between the portal system and the remnant of the umbilical vein. Jaundice


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Surgery_Schwartz. of the Cruveilhier-Baumgarten murmur, a venous hum that can be auscultated in the epigas-trium resulting from collaterals between the portal system and the remnant of the umbilical vein. Jaundice usually does not appear until the bilirubin rises above 2 to 3 mg/dL. Asterixis can be detected in patients with hepatic encephalopathy. Other manifestations include fetor hepaticus, as well as features sug-gestive of malnutrition such as weakness, weight loss, and tem-poral muscle wasting.Although fat stores and muscle mass are reduced, rest-ing energy expenditure is increased. Muscle cramps occur frequently in the cirrhotic patient and are felt to correlate with ascites, low mean arterial pressure, and plasma renin activity. Abdominal hernias are common with ascites and should be electively repaired only in patients with well-compensated cir-rhosis; otherwise, the hernia should be repaired at the time of or after hepatic transplantation. HCC can occur in all forms of cirrhosis, and every


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Surgery_Schwartz. only in patients with well-compensated cir-rhosis; otherwise, the hernia should be repaired at the time of or after hepatic transplantation. HCC can occur in all forms of cirrhosis, and every cirrhotic patient should undergo screening for the development of HCC every 6 months via imaging and measurement of a serum α-fetoprotein (AFP) level. Cirrhosis is associated with increased cardiac output and heart rate as well as decreased systemic vascular resistance and blood pres-sure. Patients with cirrhosis are more prone to infections due to impaired phagocytic activity of the reticuloendothelial system. Bacterial infections, often of intestinal origin, are common and must be suspected in a patient with unexplained pyrexia or clini-cal deterioration. Spontaneous bacterial peritonitis also is seen in cases of cirrhosis with ascites. Intrinsic drug metabolism is reduced in the cirrhotic liver, and this fact needs to be recog-nized when prescribing medications.Laboratory Findings Associated


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Surgery_Schwartz. seen in cases of cirrhosis with ascites. Intrinsic drug metabolism is reduced in the cirrhotic liver, and this fact needs to be recog-nized when prescribing medications.Laboratory Findings Associated With CirrhosisLaboratory findings vary in the cirrhotic patient depending on the degree of compensation; however, in general, a number of trends are seen. The cirrhotic patient usually has a mild normo-cytic normochromic anemia. The white blood cell and platelet counts are reduced, and the bone marrow is macronormoblastic. The PT is prolonged and does not respond to vitamin K therapy, and the serum albumin level is depressed. Urobilinogen is pres-ent and urinary sodium excretion is diminished in the presence of ascites. The serum levels of bilirubin, transaminases, and alkaline phosphatase may all be elevated. However, normal liver function test results do not eliminate the possibility of cirrhosis.Liver BiopsyThe diagnosis of cirrhosis can be made in many cases from a constellation of


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Surgery_Schwartz. may all be elevated. However, normal liver function test results do not eliminate the possibility of cirrhosis.Liver BiopsyThe diagnosis of cirrhosis can be made in many cases from a constellation of clinical features, laboratory values, and radio-graphic findings. Histopathologic examination of liver tissue is occasionally needed to confirm the diagnosis of cirrhosis and in determining disease etiology, activity, and progression. Liver biopsy can be performed via a percutaneous, transjugular, or laparoscopic approach. If needed, ultrasound or CT guidance can be helpful in obtaining an adequate sample and avoiding other viscera.Various serologic markers of hepatic fibrosis are currently being investigated to help predict the presence of cirrhosis with-out the need for liver biopsy. However, no currently available marker is sufficiently accurate for clinical use. Ultrasound elas-tography, which measures the stiffness of the liver by inducing Brunicardi_Ch31_p1345-p1392.indd


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Surgery_Schwartz. However, no currently available marker is sufficiently accurate for clinical use. Ultrasound elas-tography, which measures the stiffness of the liver by inducing Brunicardi_Ch31_p1345-p1392.indd 136420/02/19 2:36 PM 1365LIVERCHAPTER 31an elastic shear wave that propagates through the tissue, shows promise as a noninvasive test in identifying patients with advanced fibrosis and cirrhosis. (See earlier section, “Radio-logic Evaluation of the Liver.”)Hepatic Reserve and Assessment of Surgical Risk in the Cirrhotic PatientAssessing the hepatic reserve of the cirrhotic patient is impor-tant because cirrhosis and portal hypertension can have a negative impact on the outcome of nontransplant surgical pro-cedures. Patients with liver disease undergoing surgery are at increased risk for surgical and anesthesia-related complications. The actual risk depends on the type of anesthetic used, the spe-cific surgical procedure performed, and the severity of liver disease. Previous studies have


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Surgery_Schwartz. and anesthesia-related complications. The actual risk depends on the type of anesthetic used, the spe-cific surgical procedure performed, and the severity of liver disease. Previous studies have demonstrated that emergency operations, cardiac surgery, hepatic resections, and abdominal surgery, particularly cholecystectomy, gastric resection, and colectomy, generate the highest operative risk among cirrhotic patients. Additionally, preoperative patient characteristics such as anemia, ascites, encephalopathy, malnutrition, hypoalbumin-emia, hypoxemia, infection, jaundice, portal hypertension, and prolonged PT have also been associated with inferior outcomes after surgery. Nontransplant surgical procedures are contraindi-cated in patients with acute fulminant hepatitis and those with severe decompensated chronic hepatitis.A number of laboratory tests have been used to assess hepatic reserve in patients with cirrhosis. Tests of indocyanine green, sorbitol, and galactose elimination


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Surgery_Schwartz. decompensated chronic hepatitis.A number of laboratory tests have been used to assess hepatic reserve in patients with cirrhosis. Tests of indocyanine green, sorbitol, and galactose elimination capacity as well as the carbon-13 galactose breath test and carbon-13 aminopyrine breath test have all been disappointing clinically due to their dependence on flow to the liver as well as the unavailability and complexity of the tests. The monoethylglycinexylidide (MEGX) test, which measures MEGX formation after the administration of lidocaine, has been shown to be approximately 80% sensitive and specific in diagnosing cirrhosis. However, this test loses both sensitivity and specificity as the serum bilirubin level rises and interferes with the fluorescent readout system.Child-Turcotte-Pugh ScoreThe Child-Turcotte-Pugh (CTP) score was originally developed to evaluate the risk of portocaval shunt procedures performed for portal hypertension and subsequently has been shown to be useful in


Surgery_Schwartz

Surgery_Schwartz. ScoreThe Child-Turcotte-Pugh (CTP) score was originally developed to evaluate the risk of portocaval shunt procedures performed for portal hypertension and subsequently has been shown to be useful in predicting surgical risks of other intra-abdominal operations on cirrhotic patients (Table 31-4). Numerous studies have demonstrated overall surgical mortality rates of 10% for patients with class A cirrhosis, 30% for those with class B cir-rhosis, and 75% to 80% for those with class C cirrhosis.56 The CTP score is derived from five variables as shown in Table 31-4. The problems with the CTP score are the presence of subjective variables (encephalopathy and ascites), its narrow range (5 to 15 points), and the equal weighting given to each variable. Multiple retrospective studies have demonstrated that perioperative mor-tality and morbidity rates correlate well with the CTP score, and for over 30 years, this measure had been used as the principal predictor of operative risk.Model for


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Surgery_Schwartz. that perioperative mor-tality and morbidity rates correlate well with the CTP score, and for over 30 years, this measure had been used as the principal predictor of operative risk.Model for End-Stage Liver Disease Scoring SystemThe Model for End-Stage Liver Disease (MELD) is a linear regression model based on three objective laboratory values (INR, bilirubin level, and creatinine level). It was originally developed as a tool to predict mortality after transjugular intrahepatic portosystemic shunt (TIPS) but has been validated and used as the sole method of liver transplant allocation in the United States since 2002. The MELD formula is as follows:MELD Score = 9.57 Ln(SCr) + 3.78 Ln(Tbil) + 11.2 Ln(INR) + 6.43where Ln represents natural logarithm, SCr is serum creatinine level (in milligrams per deciliter), and Tbil is serum bilirubin level (in milligrams per deciliter).A number of studies have examined the relative values of MELD and CTP scores in predicting postoperative mortality


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Surgery_Schwartz. per deciliter), and Tbil is serum bilirubin level (in milligrams per deciliter).A number of studies have examined the relative values of MELD and CTP scores in predicting postoperative mortality in cirrhotic patients undergoing nontransplant surgical procedures. Northup and colleagues demonstrated that MELD score was the only statistically significant predictor of 30-day mortality.57 In this study, mortality increased by approximately 1% for each MELD point up to a score of 20 and by 2% for each MELD point above 20. A comparison of the MELD model with the CTP classification showed good correlation between the two measures in predicting mortality, especially in the setting of emergency surgery.58 In these studies, the relative risk of mortal-ity increased by 14% for each 1-point increase in MELD score. As a result, it has been proposed that patients with a MELD score below 10 can safely undergo elective surgery, those with MELD between 10 and 15 may undergo surgery with caution, while


Surgery_Schwartz

Surgery_Schwartz. MELD score. As a result, it has been proposed that patients with a MELD score below 10 can safely undergo elective surgery, those with MELD between 10 and 15 may undergo surgery with caution, while those with MELD scores in excess of 15 should not be subjected to elective surgical procedures.59Portal HypertensionThe portal venous system contributes approximately 75% of the blood and 72% of the oxygen supplied to the liver. In the average adult, 1000 to 1500 mL/min of portal venous blood is supplied to the liver. However, this amount can be significantly increased in the cirrhotic patient. The portal venous system is without valves and drains blood from the spleen, pancreas, gallbladder, and abdominal portion of the alimentary tract into the liver. Tributaries of the portal vein communicate with veins draining directly into the systemic circulation. These collateral communications occur at the gastroesophageal junction, anal canal, falciform ligament, splenic venous bed and left renal


Surgery_Schwartz

Surgery_Schwartz. with veins draining directly into the systemic circulation. These collateral communications occur at the gastroesophageal junction, anal canal, falciform ligament, splenic venous bed and left renal vein, and retroperitoneum (Fig. 31-14). The normal portal venous pressure is 5 to 10 mmHg, and at this pressure, very little blood is shunted from the portal venous system into the systemic circulation. As portal venous pressure increases, however, the Table 31-4Child-Turcotte-Pugh (CTP) scoreVARIABLE1 POINT2 POINTS3 POINTSBilirubin level< 2 mg/dL2–3 mg/dL> 3 mg/dLAlbumin level> 3.5 g/dL2.8– 3.5 g/dL< 2.8 g/dLInternational normalized ratio< 1.71.7–2.2> 2.2EncephalopathyNoneControlledUncontrolledAscitesNoneControlledUncontrolledChild-Turcotte-Pugh class Class A = 5–6 points Class B = 7–9 points Class C = 10–15 pointsBrunicardi_Ch31_p1345-p1392.indd 136520/02/19 2:36 PM 1366SPECIFIC CONSIDERATIONSPART IIcollateral communications with the systemic circulation dilate, and a large amount of


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Surgery_Schwartz. C = 10–15 pointsBrunicardi_Ch31_p1345-p1392.indd 136520/02/19 2:36 PM 1366SPECIFIC CONSIDERATIONSPART IIcollateral communications with the systemic circulation dilate, and a large amount of blood may be shunted around the liver and into the systemic circulation.Imaging of the Portal Venous System and Measurement of Portal Venous PressureThe patency of the portal vein and the nature of the collateral circulation should be established. An understanding of portal vein patency and anatomy is crucial before undertaking porto-systemic shunts, hepatic resection, or hepatic transplantation. The simplest initial investigation is abdominal ultrasonography. A large portal vein suggests portal hypertension but is not diag-nostic. Doppler ultrasound is capable of outlining the anatomy of the portal vein, excluding the presence of thrombosis, and identifying the direction of portal venous blood flow. Doppler ultrasound also is useful in evaluating blood flow through sur-gical shunts and TIPS.


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Surgery_Schwartz. vein, excluding the presence of thrombosis, and identifying the direction of portal venous blood flow. Doppler ultrasound also is useful in evaluating blood flow through sur-gical shunts and TIPS. Abdominal CT and magnetic resonance angiography both are capable of revealing portal vein anatomy as well as patency. Visceral angiography and portal venography are reserved for cases that cannot be evaluated satisfactorily by noninvasive methods and require further clarification of portal patency or anatomy.The most accurate method of determining portal hyperten-sion is hepatic venography. The most commonly used procedure involves placing a balloon catheter directly into the hepatic vein and measuring the free hepatic venous pressure (FHVP) with the balloon deflated and the wedged hepatic venous pressure (WHVP) with the balloon inflated to occlude the hepatic vein. The hepatic venous pressure gradient (HVPG) is then calcu-lated by subtracting the free from the wedged venous pressure (HVPG =


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Surgery_Schwartz. pressure (WHVP) with the balloon inflated to occlude the hepatic vein. The hepatic venous pressure gradient (HVPG) is then calcu-lated by subtracting the free from the wedged venous pressure (HVPG = WHVP – FHVP). The HVPG represents the pressure in the hepatic sinusoids and portal vein and is a measure of por-tal venous pressure. Clinically significant portal hypertension is evident when HVPG exceeds 10 mmHg.Etiology and Clinical Features of Portal HypertensionThe causes of portal hypertension can be divided into three major groups: presinusoidal, sinusoidal, and postsinusoidal.60 Although multiple disease processes can result in portal hyper-tension (Table 31-5), in the United States, the most common cause of portal hypertension is usually an intrahepatic one, namely, cirrhosis. The most significant clinical finding asso-ciated with portal hypertension is the development of gastro-esophageal varices, which are mainly supplied by the anterior branch of the left gastric (coronary)


Surgery_Schwartz

Surgery_Schwartz. most significant clinical finding asso-ciated with portal hypertension is the development of gastro-esophageal varices, which are mainly supplied by the anterior branch of the left gastric (coronary) vein.a1aFGE1ABbD24cde 3C5Figure 31-14. Intra-abdominal venous flow pathways leading to engorged veins (varices) from portal hypertension. 1, Coro-nary vein; 2, superior hemorrhoidal veins; 3, paraumbilical veins; 4, Retzius’ veins; 5, veins of Sappey; A, portal vein; B, splenic vein; C, superior mesenteric vein; D, inferior mesenteric vein; E, inferior vena cava; F, superior vena cava; G, hepatic veins; a, esophageal veins; a1, azygos system; b, vasa brevia; c, middle and inferior hem-orrhoidal veins; d, intestinal; e, epigastric veins.Table 31-5Etiology of portal hypertensionPresinusoidal Sinistral/extrahepatic Splenic vein thrombosis Splenomegaly Splenic arteriovenous fistula Intrahepatic Schistosomiasis Congenital hepatic fibrosis Nodular regenerative hyperplasia Idiopathic


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Surgery_Schwartz. vein thrombosis Splenomegaly Splenic arteriovenous fistula Intrahepatic Schistosomiasis Congenital hepatic fibrosis Nodular regenerative hyperplasia Idiopathic portal fibrosis Myeloproliferative disorder Sarcoid Graft-versus-host diseaseSinusoidal Intrahepatic Cirrhosis Viral infection Alcohol abuse Primary biliary cirrhosis Autoimmune hepatitis Primary sclerosing cholangitis Metabolic abnormalityPostsinusoidal Intrahepatic Vascular occlusive disease Posthepatic Budd-Chiari syndrome Congestive heart failure Inferior vena caval web Constrictive pericarditisBrunicardi_Ch31_p1345-p1392.indd 136620/02/19 2:36 PM 1367LIVERCHAPTER 31Portal hypertension also results in splenomegaly with enlarged, tortuous, and even aneurysmal splenic vessels. Spleno-megaly is frequently associated with functional hypersplenism, causing leukopenia, thrombocytopenia, and anemia. Ascites occurs in the setting of severe portal hypertension in combina-tion with hepatocyte


Surgery_Schwartz

Surgery_Schwartz. is frequently associated with functional hypersplenism, causing leukopenia, thrombocytopenia, and anemia. Ascites occurs in the setting of severe portal hypertension in combina-tion with hepatocyte dysfunction. The umbilical vein may recan-nulate and dilate, leading to visible collaterals on the abdominal wall. Anorectal varices are present in approximately 45% of cirrhotic patients and must be distinguished from hemorrhoids, which do not communicate with the portal system and are not present at increased incidence in patients with portal hyperten-sion. Large spontaneous venous shunts may form between the portal venous system and the left renal vein or the IVC, but these shunts are ineffective in reducing portal venous pressures and preventing bleeding from gastroesophageal varices.Management of Gastroesophageal VaricesThe most significant manifestation and the leading cause of mor-bidity and mortality related to portal hypertension is variceal bleeding. Approximately 30% of patients


Surgery_Schwartz

Surgery_Schwartz. of Gastroesophageal VaricesThe most significant manifestation and the leading cause of mor-bidity and mortality related to portal hypertension is variceal bleeding. Approximately 30% of patients with compensated cir-rhosis and 60% of patients with decompensated cirrhosis have esophageal varices. One third of all patients with varices will experience variceal bleeding. Each episode of bleeding is associ-ated with a 20% to 30% risk of mortality. If left untreated, 70% of patients who survive the initial bleed will experience recurrent variceal hemorrhage within 2 years of the index hemorrhage.Prevention of Variceal BleedingCurrent measures aimed at preventing variceal bleeding include the administration of nonselective β-blockers and prophylac-tic endoscopic surveillance with variceal band ligation. Meta-analyses have demonstrated that nonselective β-blockers such as propranolol and nadolol reduce the index variceal bleed by approximately 45% and decrease bleeding mortality by 50%.61


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Surgery_Schwartz. ligation. Meta-analyses have demonstrated that nonselective β-blockers such as propranolol and nadolol reduce the index variceal bleed by approximately 45% and decrease bleeding mortality by 50%.61 However, approximately 20% of patients do not respond to β-blockade, and another 20% cannot tolerate β-blockade due to medication side effects. Endoscopic surveillance with prophy-lactic variceal band ligation has been associated with a lower incidence of a first variceal bleed.62 Variceal band ligation is rec-ommended for patients with medium to large varices, performed every 1 to 2 weeks until obliteration, followed by esophagogas-troduodenoscopy (EGD) 1 to 3 months later and surveillance EGD every 6 months to monitor for recurrence of varices.Management of Acute Variceal HemorrhagePatients with acute variceal hemorrhage should be admitted to an ICU for resuscitation and management. Blood resuscitation should be performed carefully to reach a hemoglobin level of approxi-mately 8 g/dL.


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Surgery_Schwartz. with acute variceal hemorrhage should be admitted to an ICU for resuscitation and management. Blood resuscitation should be performed carefully to reach a hemoglobin level of approxi-mately 8 g/dL. Overzealous replacement of blood products and administration of saline can lead to both rebleeding and increased mortality. Administration of fresh frozen plasma and platelets can be considered in patients with severe coagulopathy. Use of recom-binant factor VIIa has not been shown to be more beneficial than standard therapy and therefore is not recommended at this time. Cirrhotic patients with variceal bleeding have a high risk of devel-oping bacterial infections, which are associated with increased risks of rebleeding and mortality. Spontaneous bacterial peritoni-tis accounts for approximately half of these infections, with uri-nary tract infections and pneumonias comprising the remainder. The use of short-term prophylactic antibiotics (e.g., ceftriaxone 1 g/d intravenously) has been


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Surgery_Schwartz. half of these infections, with uri-nary tract infections and pneumonias comprising the remainder. The use of short-term prophylactic antibiotics (e.g., ceftriaxone 1 g/d intravenously) has been shown both to decrease the rate of bacterial infections and to increase survival.Vasoactive medications decrease blood flow to the gastro-esophageal varices and can be initiated as soon as the diagnosis of variceal bleeding is made. Although vasopressin is the most potent available vasoconstrictor, its use is limited by its systemic vasoconstrictive effects that can produce hypertension, myocar-dial ischemia, arrhythmias, ischemic abdominal pain, and limb gangrene. Octreotide, a somatostatin analog, has the advantage that it can be administered for 5 days or longer, and it is currently the preferred pharmacologic agent for initial management of acute variceal bleeding. In addition to pharmacologic therapy, endos-copy with variceal band ligation should be carried out as soon as possible. This


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Surgery_Schwartz. pharmacologic agent for initial management of acute variceal bleeding. In addition to pharmacologic therapy, endos-copy with variceal band ligation should be carried out as soon as possible. This combination of pharmacologic and endoscopic therapy has been shown both to improve the initial control of bleeding and to increase the 5-day hemostasis rate.62Luminal TamponadeWhen medical and endoscopic measures fail to control variceal hemorrhage, balloon tamponade using a Sengstaken-Blakemore tube will control refractory bleeding in up to 90% of patients. However, its application is limited due to the potential for com-plications, which include aspiration, airway obstruction, and esophageal perforation due to overinflation or pressure necro-sis. Therefore, the use of a Sengstaken-Blakemore tube should not exceed 36 hours to avoid tissue necrosis, and this treatment modality should only be considered a temporary bridge to more definitive measures of variceal hemorrhage control.Transjugular


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Surgery_Schwartz. should not exceed 36 hours to avoid tissue necrosis, and this treatment modality should only be considered a temporary bridge to more definitive measures of variceal hemorrhage control.Transjugular Intrahepatic Portosystemic ShuntThe TIPS procedure involves implantation of a metallic stent between an intrahepatic branch of the portal vein and a hepatic vein radicle. The needle track is dilated until a portal pressure gradient of ≤12 mmHg is achieved. TIPS can be performed in 95% of patients by an experienced interventional radiolo-gist, controls variceal bleeding in >90% of cases refractory to medical treatment, and should not affect subsequent hepatic transplantation. Possible complications include bleeding either intra-abdominally or via the biliary tree, infections, renal failure, decreased hepatic function, and hepatic encephalopathy, which occur in 25% to 30% of patients after the TIPS procedure. A high rate of thrombosis is seen and can be attributed to inti-mal hyperplasia of


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Surgery_Schwartz. hepatic function, and hepatic encephalopathy, which occur in 25% to 30% of patients after the TIPS procedure. A high rate of thrombosis is seen and can be attributed to inti-mal hyperplasia of the metallic stent. Frequent follow-up with repeated interventions such as dilation or restenting often are needed to maintain TIPS patency.Balloon-Occluded Retrograde Transvenous ObliterationThe balloon-occluded retrograde transvenous obliteration (BRTO) procedure has been used for the specific manage-ment of bleeding gastric varices in patients with spontaneous gastrorenal or splenorenal shunts shown on contrast-enhanced cross-sectional imaging. Using a transjugular or transfemoral approach, a balloon-occlusion catheter is directed through the left renal vein into the spontaneous shunt, which is then obliter-ated with the use of a sclerosing agent. BRTO effectively con-trols hemorrhage from gastric varices and preserves portal flow to the liver, thereby reducing the risk of hepatic


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Surgery_Schwartz. which is then obliter-ated with the use of a sclerosing agent. BRTO effectively con-trols hemorrhage from gastric varices and preserves portal flow to the liver, thereby reducing the risk of hepatic encephalopathy relative to TIPS. The occlusion of spontaneous shunts, how-ever, can theoretically exacerbate portal hypertension, precipi-tate hemorrhage from esophageal varices, and exacerbate the accumulation of ascites.Surgical ShuntingThe need for surgical shunts has been reduced since the intro-duction of the TIPS procedure and hepatic transplantation. At this time, the recommendation is that surgical shunts be consid-ered only in patients who have MELD scores of <15, who are 5Brunicardi_Ch31_p1345-p1392.indd 136720/02/19 2:36 PM 1368SPECIFIC CONSIDERATIONSPART IInot candidates for hepatic transplantation, or who have limited access to TIPS therapy and the necessary follow-up. The aim of the surgical shunt is to reduce portal venous pressure, maintain total hepatic and portal


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Surgery_Schwartz. hepatic transplantation, or who have limited access to TIPS therapy and the necessary follow-up. The aim of the surgical shunt is to reduce portal venous pressure, maintain total hepatic and portal blood flow, and avoid the high inci-dence of complicating hepatic encephalopathy. Patient survival is determined by hepatic reserve.The portacaval shunt, as first described by Eck in 1877, either joins the portal vein to the IVC in an end-to-side fashion and completely disrupts portal vein flow to the liver, or joins it in a side-to-side fashion and thereby maintains partial por-tal venous flow to the liver. Currently this shunt is rarely per-formed due to the high incidence of hepatic encephalopathy and decreased liver function resulting from the reduction of portal perfusion. The Eck fistula also makes subsequent hepatic trans-plantation much more technically difficult.The mesocaval shunt uses an 8or 10-mm polytetrafluo-roethylene (PTFE) graft to connect the superior mesenteric vein to


Surgery_Schwartz

Surgery_Schwartz. also makes subsequent hepatic trans-plantation much more technically difficult.The mesocaval shunt uses an 8or 10-mm polytetrafluo-roethylene (PTFE) graft to connect the superior mesenteric vein to the IVC. The mesocaval shunt is technically easier to perform and can be easily ligated during subsequent hepatic transplan-tation. The smaller caliber of the shunt avoids the deleterious effects of portal blood flow deprivation on hepatic function. Small-diameter portosystemic shunts have been reported to reduce the incidence of encephalopathy but at the expense of increased risks of shunt thrombosis and rebleeding.The surgical shunt currently used most often is the distal splenorenal or Warren shunt (Fig. 31-15). This shunt is techni-cally the most difficult to perform. It requires division of the gastroesophageal collaterals and allows venous drainage of the stomach and lower esophagus through the short gastrosplenic veins into the spleen, and ultimately decompresses the left upper


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Surgery_Schwartz. of the gastroesophageal collaterals and allows venous drainage of the stomach and lower esophagus through the short gastrosplenic veins into the spleen, and ultimately decompresses the left upper quadrant by allowing the splenic vein to drain directly into the left renal vein via an end-to-side splenic to left renal vein anas-tomosis. This shunt has the advantages of being associated with a lower rate of hepatic encephalopathy and decompensation and not interfering with subsequent liver transplantation.Nonshunt Surgical Management of Refractory Variceal BleedingIn the patient with extrahepatic portal vein thrombosis and refractory variceal bleeding, the Sugiura procedure may be considered. The Sugiura procedure consists of extensive devas-cularization of the stomach and distal esophagus along with tran-section of the esophagus, splenectomy, truncal vagotomy, and pyloroplasty. As with performance of surgical shunts, patient survival is dependent on hepatic reserve at the time of the


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Surgery_Schwartz. along with tran-section of the esophagus, splenectomy, truncal vagotomy, and pyloroplasty. As with performance of surgical shunts, patient survival is dependent on hepatic reserve at the time of the sur-gical procedure. Experience in Western countries is somewhat limited, and a number of modifications have been made to the original Sugiura procedure over time.Hepatic TransplantationPatients with cirrhosis, portal hypertension, and variceal bleed-ing usually die as a result of hepatic failure and not acute blood loss. Therefore, hepatic transplantation must be considered in the patient with ESLD because it represents the patient’s only chance for definitive therapy and long-term survival. Hepatic transplantation also can be considered for the patient with vari-ceal bleeding refractory to all other forms of management. Sur-vival after hepatic transplantation is not affected adversely by the previous performance of endoscopic variceal band ligation, TIPS, or splenorenal or mesocaval


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Surgery_Schwartz. to all other forms of management. Sur-vival after hepatic transplantation is not affected adversely by the previous performance of endoscopic variceal band ligation, TIPS, or splenorenal or mesocaval shunts. Previous creation of an Eck fistula, however, does make hepatic transplantation much more technically difficult, and therefore this procedure should be avoided in the transplant candidate. In addition to sav-ing the patient’s life, hepatic transplantation reverses most of the hemodynamic and humoral changes associated with cirrhosis.Budd-Chiari SyndromeBudd-Chiari syndrome (BCS) is an uncommon congestive hepatopathy characterized by the obstruction of hepatic venous outflow. The incidence of BCS is 1 in 100,000 of the general population worldwide.63 Patients may present with acute signs and symptoms of abdominal pain, ascites, and hepatomegaly or more chronic symptoms related to long-standing portal hyper-tension. BCS is defined as primary when the obstructive process involves an


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Surgery_Schwartz. and symptoms of abdominal pain, ascites, and hepatomegaly or more chronic symptoms related to long-standing portal hyper-tension. BCS is defined as primary when the obstructive process involves an endoluminal venous thrombosis. BCS is consid-ered as a secondary process when the veins are compressed or invaded by a neighboring lesion originating outside the vein.A thorough evaluation demonstrates one or more throm-botic risk factors in approximately 75% to 90% of patients with primary BCS.63 Primary myeloproliferative disorders, such as Figure 31-15. Surgical shunts for portal hyper-tension. Types of portacaval anastomoses. A. Nor-mal anatomy. B. Side-to-side portacaval shunt. C. End-to-side portacaval shunt. D. Mesocaval shunt. E. Distal splenorenal (Warren) shunt. (Reproduced with permission from Doherty GM, Way LW: Current Surgical Diagnosis and Treatment, 12th ed. New York, NY: McGraw-Hill Education; 2006.)ABCDEBrunicardi_Ch31_p1345-p1392.indd 136820/02/19 2:36 PM


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Surgery_Schwartz. with permission from Doherty GM, Way LW: Current Surgical Diagnosis and Treatment, 12th ed. New York, NY: McGraw-Hill Education; 2006.)ABCDEBrunicardi_Ch31_p1345-p1392.indd 136820/02/19 2:36 PM 1369LIVERCHAPTER 31essential thrombocythemia or polycythemia rubra, account for approximately 35% to 50% of the primary cases of BCS. All known inherited thrombophilias also have been implicated in the development of BCS. Activated protein C resistance, generally related to factor V Leiden mutation, is present in approximately 25% of patients. Anticardiolipin antibodies, hyperhomocystein-emia, and oral contraceptive use all have been shown to be risk factors for BCS.63Clinically significant BCS is usually the result of obstruc-tion of two or more of the major hepatic veins. The obstruction results in hepatomegaly, liver congestion, and right upper quad-rant pain. In addition, liver perfusion via the portal vein may be decreased, and 70% of affected patients have noninflammatory


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Surgery_Schwartz. results in hepatomegaly, liver congestion, and right upper quad-rant pain. In addition, liver perfusion via the portal vein may be decreased, and 70% of affected patients have noninflammatory centrilobular necrosis on biopsy. Although ALF is rare, most patients will go on to develop chronic portal hypertension and ascites. Caudate lobe hypertrophy occurs in approximately 50% of cases and is due to the fact that the caudate lobe has direct venous drainage into the IVC. This caudate lobe hypertrophy, in turn, can result in further obstruction of the IVC.Abdominal ultrasonography is the initial investigation of choice and can demonstrate the absence of hepatic vein flow, spider web hepatic veins, and collateral hepatic veins.64 CT or MRI of the abdomen also is capable of demonstrating hepatic vein thrombosis and evaluating the IVC but is limited in that it cannot show direction of blood flow. The definitive radio-graphic study to evaluate BCS is hepatic venography to deter-mine the


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Surgery_Schwartz. vein thrombosis and evaluating the IVC but is limited in that it cannot show direction of blood flow. The definitive radio-graphic study to evaluate BCS is hepatic venography to deter-mine the presence and extent of hepatic vein thrombus as well as measure IVC pressures.Initial treatment consists of diagnosing and medically managing the underlying disease process and preventing exten-sion of the hepatic vein thrombosis through systemic anticoagu-lation. The BCS-associated portal hypertension and ascites can be medically managed in a manner similar to that in most cir-rhotic patients. Radiologic and surgical intervention should be reserved for patients whose condition is nonresponsive to medi-cal therapy. Percutaneous angioplasty and TIPS, in combination with thrombolytic therapy, are the preferred strategies to restore the outflow of blood from the liver. Thrombolytic therapy alone may be attempted for acute thrombosis. Surgical shunting, namely with the side-to-side portacaval shunt,


Surgery_Schwartz

Surgery_Schwartz. strategies to restore the outflow of blood from the liver. Thrombolytic therapy alone may be attempted for acute thrombosis. Surgical shunting, namely with the side-to-side portacaval shunt, essentially turns the portal vein into a hepatic outflow tract. Most patients with a portacaval shunt show improvement in hepatic function and fibrosis at 1 year without significant hepatic encephalopathy.64 However, the enthusiasm for this procedure has been curbed due to the relatively high rate of operative mortality and shunt dysfunction. Patients with progressive BCS and manifestations of ESLD will ultimately require hepatic transplantation.INFECTIONS OF THE LIVERThe liver contains the largest portion of the reticuloendothelial system in the human body and is therefore able to handle the continuous low-level exposure to enteric bacteria that it receives through the portal venous system. Due to the high level of retic-uloendothelial cells in the liver, nonviral infections are unusual.Pyogenic


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Surgery_Schwartz. low-level exposure to enteric bacteria that it receives through the portal venous system. Due to the high level of retic-uloendothelial cells in the liver, nonviral infections are unusual.Pyogenic Liver AbscessesPyogenic liver abscesses are the most common liver abscesses seen in the United States. They may be single or multiple and are more frequently found in the right lobe of the liver.65 The abscess cavities are variable in size and, when multiple, may coalesce to give a honeycomb appearance. Approximately 40% of abscesses are monomicrobial, an additional 40% are polymicrobial, and 20% are culture-negative. The most com-mon infecting agents are gram-negative bacteria. Escherichia coli is found in two thirds of cases, and other common organ-isms include Streptococcus faecalis, Klebsiella, and Proteus vulgaris. Anaerobic organisms such as Bacteroides fragilis also are seen frequently. In patients with endocarditis and infected indwelling catheters, Staphylococcus and Streptococcus


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Surgery_Schwartz. and Proteus vulgaris. Anaerobic organisms such as Bacteroides fragilis also are seen frequently. In patients with endocarditis and infected indwelling catheters, Staphylococcus and Streptococcus species are more commonly found.In the past, pyogenic liver abscesses often resulted from infections of the intestinal tract such as acute appendicitis and diverticulitis, which then spread to the liver via the portal circu-lation. With improved imaging modalities and earlier diagnosis of these intra-abdominal infections, this particular etiology of pyogenic liver abscesses has become less common. Pyogenic liver abscesses also occur as a result of impaired biliary drain-age, subacute bacterial endocarditis, infected indwelling cath-eters, dental work, or the direct extension of infections such as diverticulitis or Crohn’s disease into the liver. There appears to be an increasing incidence due to infection by opportunis-tic organisms among immunosuppressed patients, including transplant and


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Surgery_Schwartz. as diverticulitis or Crohn’s disease into the liver. There appears to be an increasing incidence due to infection by opportunis-tic organisms among immunosuppressed patients, including transplant and chemotherapy recipients as well as patients with acquired immunodeficiency syndrome (AIDS).Patients commonly present with right upper quadrant pain and fever. Jaundice occurs in up to one-third of affected patients. A thorough history and physical examination are usually helpful in identifying the underlying cause of the liver abscess. Leuko-cytosis, an elevated sedimentation rate, and an elevated AP level are the most common laboratory findings. Significant abnor-malities in the results of the remaining liver function tests are unusual. Blood cultures will only reveal the causative organism in approximately 50% of cases. Ultrasound examination of the liver reveals pyogenic abscesses as round or oval hypoechoic lesions with well-defined borders and a variable number of internal echoes. CT


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Surgery_Schwartz. approximately 50% of cases. Ultrasound examination of the liver reveals pyogenic abscesses as round or oval hypoechoic lesions with well-defined borders and a variable number of internal echoes. CT scan is highly sensitive in the localization of pyogenic liver abscesses, which appear hypodense with periph-eral enhancement and may contain air-fluid levels indicating a gas-producing infectious organism (Fig. 31-16). MRI of the abdomen can also detect pyogenic abscesses with a high level of sensitivity but plays a limited role because of its inability to be used for image-guided diagnosis and therapy.The current cornerstones of treatment include correction of the underlying cause and IV antibiotic therapy. Empiric antibiotic therapy should cover gram-negative and anaerobic organisms; percutaneous needle aspiration and culture of the aspirate may be useful in guiding subsequent antibiotic therapy. IV antibiotic therapy should be continued for at least 8 weeks and can be expected to be


Surgery_Schwartz

Surgery_Schwartz. needle aspiration and culture of the aspirate may be useful in guiding subsequent antibiotic therapy. IV antibiotic therapy should be continued for at least 8 weeks and can be expected to be effective in 80% to 90% of patients. Placement of a percutaneous drainage catheter is beneficial only for a minority of patients, as most pyogenic abscesses are quite viscous and catheter drainage is often ineffective.Surgical drainage either via the laparoscopic or open approach may become necessary if initial therapies fail. Ana-tomic surgical resection can be performed in patients with recalcitrant abscesses. It must be kept in mind throughout the evaluation and treatment of the presumed pyogenic abscess that a necrotic hepatic malignancy must not be mistaken for a hepatic abscess. Therefore, early diagnosis and progression to surgical resection should be advocated for patients who do not respond to initial antibiotic therapy.Amebic AbscessesEntamoeba histolytica is a parasite that is endemic


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Surgery_Schwartz. diagnosis and progression to surgical resection should be advocated for patients who do not respond to initial antibiotic therapy.Amebic AbscessesEntamoeba histolytica is a parasite that is endemic world-wide, infecting approximately 10% of the world’s population. Brunicardi_Ch31_p1345-p1392.indd 136920/02/19 2:36 PM 1370SPECIFIC CONSIDERATIONSPART IIAmebiasis is most common in subtropical climates, especially in areas with poor sanitation. E histolytica exists as cysts in a vegetative form that are capable of surviving outside the human body. The cystic form passes through the stomach and small bowel unharmed and then transforms into a trophozoite in the colon. Here it invades the colonic mucosa forming typical flask-shaped ulcers, enters the portal venous system, and is carried to the liver. Occasionally, the trophozoite will pass through the hepatic sinusoid and into the systemic circulation, which results in lung and brain abscesses.Amebae multiply and block small intrahepatic


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Surgery_Schwartz. liver. Occasionally, the trophozoite will pass through the hepatic sinusoid and into the systemic circulation, which results in lung and brain abscesses.Amebae multiply and block small intrahepatic portal radi-cles with consequent focal infarction of hepatocytes. They con-tain a proteolytic enzyme that also destroys liver parenchyma. The abscesses formed are variable in size and can be single or multiple. The amebic abscess is most commonly located in the superior-anterior aspect of the right lobe of the liver near the diaphragm and has a necrotic central portion that contains a thick, reddish brown, pus-like material. This material has been likened to anchovy paste or chocolate sauce. Amebic abscesses are the most common type of liver abscesses worldwide.Amebiasis should be considered in patients who have trav-eled to an endemic area and present with right upper quadrant pain, fever, hepatomegaly, and hepatic abscess.46 Leukocytosis is common, whereas elevated transaminase levels and


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Surgery_Schwartz. patients who have trav-eled to an endemic area and present with right upper quadrant pain, fever, hepatomegaly, and hepatic abscess.46 Leukocytosis is common, whereas elevated transaminase levels and jaundice are unusual. The most common biochemical abnormality is a mildly elevated AP level. Even though this disease process is secondary to a colonic infection, the presence of diarrhea is unusual. Most patients have a positive fluorescent antibody test for E histo-lytica, and test results can remain positive for some time after a clinical cure. This serologic test has a high sensitivity, and therefore amebiasis is unlikely if the test results are negative.Ultrasound and CT scanning of the abdomen are both very sensitive but nonspecific for the detection of amebic abscesses.65 Amebic abscesses usually appear on CT as well-defined low-density round lesions that have enhancement of the wall, some-what ragged in appearance with a peripheral zone of edema. The central cavity may have


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Surgery_Schwartz. abscesses usually appear on CT as well-defined low-density round lesions that have enhancement of the wall, some-what ragged in appearance with a peripheral zone of edema. The central cavity may have septations as well as fluid levels. CT scanning is also useful in the detection of extrahepatic involvement.Metronidazole 750 mg three times a day for 7 to 10 days is the treatment of choice and is successful in 95% of cases. Defervescence usually occurs in 3 to 5 days, but the time nec-essary for the abscess to resolve depends on the initial size at presentation and varies from 30 to 300 days.65 Both ultrasound and CT of the liver can be used as follow-up after the initiation of medical therapy. Aspiration of the abscess rarely is needed and should be reserved for patients with large abscesses, those who do not respond to medical therapy, or those who appear to be superinfected. Furthermore, abscesses of the left lobe of the liver at risk for rupture into the pericardium should be


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Surgery_Schwartz. those who do not respond to medical therapy, or those who appear to be superinfected. Furthermore, abscesses of the left lobe of the liver at risk for rupture into the pericardium should be treated with aspiration and drainage.Hydatid DiseaseHydatid disease is due to infection by the tapeworm Echinococ-cus granulosus in its larval or cyst stage.66 The tapeworm lives in canids, which are infected by eating the viscera of sheep that contain hydatid cysts. Scolices, contained in the cysts, adhere to the small intestine of dogs and become adult taenia, which attach to the intestinal wall. Each worm sheds approximately 500 ova into the bowel. The infected ova-containing feces of dogs contaminate grass and farmland, and the ova are ingested by intermediate hosts such as sheep, cattle, pigs, and humans. The ova have chitinous envelopes that are dissolved by gastric juice. The liberated ovum then burrows through the intestinal mucosa and is carried by the portal vein to the liver, where it


Surgery_Schwartz

Surgery_Schwartz. humans. The ova have chitinous envelopes that are dissolved by gastric juice. The liberated ovum then burrows through the intestinal mucosa and is carried by the portal vein to the liver, where it develops into an adult cyst. Most cysts are caught in the hepatic sinusoids, and therefore 70% of hydatid cysts form in the liver. A few ova pass through the liver and are held up in the pul-monary capillary bed or enter the systemic circulation, forming cysts in the lung, spleen, brain, or bones.Hydatid disease is most common in sheep-raising areas, where dogs have access to infected offal. These include South Australia, New Zealand, Africa, Greece, Spain, and the Middle East. Hydatid cysts commonly involve the right lobe of the liver, usually the anterior-inferior or posterior-inferior segments. The uncomplicated cyst may be silent and found only incidentally or at autopsy. Occasionally, the affected patient presents with symptoms such as dull right upper quadrant pain or abdomi-nal


Surgery_Schwartz

Surgery_Schwartz. The uncomplicated cyst may be silent and found only incidentally or at autopsy. Occasionally, the affected patient presents with symptoms such as dull right upper quadrant pain or abdomi-nal distention. Cysts may become secondarily infected, involve other organs, or even rupture, which leads to an allergic or ana-phylactic reaction.The diagnosis of hydatid disease is based on the findings of an enzyme-linked immunosorbent assay (ELISA) for echino-coccal antigens, and results are positive in approximately 85% of infected patients.66 The ELISA results may be negative in an infected patient if the cyst has not leaked or does not contain scolices or if the parasite is no longer viable. Eosinophilia is seen in approximately 30% of infected patients. Ultrasonography and CT scanning of the abdomen are both quite sensitive for detecting hydatid cysts. The appearance of the cysts on images depends on the stage of cyst development. Typically, hydatid cysts are well-defined hypodense lesions


Surgery_Schwartz

Surgery_Schwartz. are both quite sensitive for detecting hydatid cysts. The appearance of the cysts on images depends on the stage of cyst development. Typically, hydatid cysts are well-defined hypodense lesions with a distinct wall. Ring-like cal-cifications of the pericysts are present in 20% to 30% of cases. As healing occurs, the entire cyst calcifies densely, and a lesion with this appearance is usually dead or inactive. Daughter cysts generally occur in a peripheral location within the main cyst and are typically slightly hypodense compared with the mother cyst. MRI of the abdomen may be useful to evaluate the pericyst, cyst matrix, and daughter cyst characteristics.Unless the cysts are small or the patient is not a suitable candidate for surgical resection, the treatment of hydatid disease Figure 31-16. Computed tomographic scan of pyogenic liver abscesses. Multiple hepatic abscesses are seen in a patient after an episode of diverticulitis. Note the loculated large central abscess as well as the


Surgery_Schwartz

Surgery_Schwartz. tomographic scan of pyogenic liver abscesses. Multiple hepatic abscesses are seen in a patient after an episode of diverticulitis. Note the loculated large central abscess as well as the left lateral segment abscess.Brunicardi_Ch31_p1345-p1392.indd 137020/02/19 2:36 PM 1371LIVERCHAPTER 31is surgically based because of the high risk of secondary infec-tion and rupture. Medical treatment with albendazole relies on drug diffusion through the cyst membrane. The concentration of drug achieved in the cyst is uncertain but is better than that of mebendazole, and albendazole can be used as initial treat-ment for small, asymptomatic cysts. For most cysts, surgical resection involving laparoscopic or open complete cyst removal with instillation of a scolicidal agent is preferred and usually is curative. If complete cystectomy is not possible, then formal anatomic liver resection can be undertaken. During surgical resection, caution must be exercised to avoid rupture of the cyst with release


Surgery_Schwartz

Surgery_Schwartz. If complete cystectomy is not possible, then formal anatomic liver resection can be undertaken. During surgical resection, caution must be exercised to avoid rupture of the cyst with release of protoscolices into the peritoneal cavity. Perito-neal contamination can result in an acute anaphylactic reaction or peritoneal implantation of scolices with daughter cyst forma-tion and inevitable recurrence.Echinococcus multilocularis occurs in the Northern Hemisphere and can infect the liver in a fashion similar to that described earlier, although the cysts are multilocular. Infection of the lung also is common (alveolar echinococcosis). Canine species such as wolves, foxes, and dogs ingest infected vis-cera of an intermediate host (e.g., rodents, moose) and become infected; humans become infected incidentally by ingesting contaminated food or water. Treatment consists of albendazole; however, infection in the lung produces a more generalized granulomatous reaction, can present in a manner


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Surgery_Schwartz. incidentally by ingesting contaminated food or water. Treatment consists of albendazole; however, infection in the lung produces a more generalized granulomatous reaction, can present in a manner similar to that of a malignancy, and often requires resection.AscariasisAscaris infection is particularly common in the Far East, India, and South Africa. Ova of the roundworm Ascaris lumbricoides arrive in the liver by retrograde locomotion in the bile ducts from the GI tract. The adult worm is 10 to 20 cm long and may lodge in the common bile duct, causing partial bile duct obstruction and secondary cholangitic abscesses. The Ascaris may serve as a nidus for the development of intrahepatic gallstones. The clini-cal presentation in an affected patient may include biliary colic, acute cholecystitis, acute pancreatitis, or hepatic abscesses.67 Plain abdominal radiographs, abdominal ultrasound, and ERCP can demonstrate the Ascaris as linear filling defects within the bile ducts. Occasionally,


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Surgery_Schwartz. acute pancreatitis, or hepatic abscesses.67 Plain abdominal radiographs, abdominal ultrasound, and ERCP can demonstrate the Ascaris as linear filling defects within the bile ducts. Occasionally, worms can be seen moving into and out of the biliary tree from the duodenum. Treatment consists of the administration of piperazine citrate, mebendazole, or alben-dazole in combination with endoscopic extraction of the worms. Surgical intervention may become necessary if the Ascaris can-not be removed via ERCP.SchistosomiasisSchistosomiasis affects >200 million people in 74 countries. Hepatic schistosomiasis occurs when emboli of the ova in the intestines reach the liver via the mesenteric venous system. Eggs excreted in the feces hatch in water to release free-swimming embryos, which enter snails and develop into fork-tailed cercar-iae. They then reenter human skin during contact with infected water. They burrow down to the capillary bed and enter the bloodstream, leading to widespread


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Surgery_Schwartz. snails and develop into fork-tailed cercar-iae. They then reenter human skin during contact with infected water. They burrow down to the capillary bed and enter the bloodstream, leading to widespread hematogenous dissemina-tion. Those entering the intrahepatic portal system grow rapidly, resulting in a granulomatous reaction. The degree of consequent portal fibrosis is related to the adult worm load.Schistosomiasis has three stages of clinical symptomatol-ogy: the first includes itching after the entry of cercariae through the skin; the second includes fever, urticaria, and eosinophilia; and the third involves hepatic fibrosis followed by presinusoidal portal hypertension. During this third phase, the liver shrinks, the spleen enlarges, and the patient may develop complications of portal hypertension while hepatic function is maintained. Active infection is detected by stool examination. Serologic tests indicate past exposure but do not provide information regarding the timing of


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Surgery_Schwartz. hypertension while hepatic function is maintained. Active infection is detected by stool examination. Serologic tests indicate past exposure but do not provide information regarding the timing of infection. A negative serologic test result excludes the presence of schistosomal infection. Serum levels of transaminases are usually normal, but the AP level may be mildly elevated. A decreased serum albumin level is usually the result of frequent GI bleeds and malnutrition.Medical treatment of schistosomiasis includes education on hygiene and the avoidance of infected water. Treatment with praziquantel 40 to 75 mg/kg as a single dose is the treatment of choice for all forms of schistosomiasis and produces few side effects. GI bleeding usually is controlled by endoscopic variceal ligation. However, in a patient with refractory GI portal hyper-tensive bleeding, distal splenorenal shunt or gastric devascular-ization and splenectomy may be considered.Viral HepatitisThe role of the surgeon in


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Surgery_Schwartz. in a patient with refractory GI portal hyper-tensive bleeding, distal splenorenal shunt or gastric devascular-ization and splenectomy may be considered.Viral HepatitisThe role of the surgeon in the management of viral hepatitis is somewhat limited. However, the disease entities of hepatitis A, B, and C need to be kept in mind during any evaluation for liver disease. Hepatitis A usually results in an acute self-limited ill-ness and only rarely leads to fulminant hepatic failure. Patients can present with fatigue, malaise, nausea, vomiting, anorexic fever, and right upper quadrant abdominal pain. The most com-mon physical findings are jaundice and hepatomegaly. Because the disease is self-limited, the treatment is usually supportive. Patients who develop fulminant infection require aggressive therapy and should be transferred to a center capable of per-forming liver transplantation.Hepatitis B and C, on the other hand, can both lead to chronic liver disease, cirrhosis, and HCC. The


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Surgery_Schwartz. therapy and should be transferred to a center capable of per-forming liver transplantation.Hepatitis B and C, on the other hand, can both lead to chronic liver disease, cirrhosis, and HCC. The prevalence of chronic hepatitis B infection in the U.S. population is estimated to be 0.27%, but hepatitis B remains a major burden in resource-limited countries, accounting for 30% of cirrhosis and 53% of HCC cases. The ultimate goal of treatment for chronic hepati-tis B is viral suppression, thereby preventing the development of clinical outcomes such as cirrhosis, liver failure, and HCC. The cornerstone of current antiviral therapy includes pegylated interferon and nucleoside analogs such as tenofovir or entecavir.68 These agents have been proven to reduce complications of cirrho-sis and HCC and perhaps reverse previous damage to the liver. Interferon therapy produces various side effects including fatigue, flu-like symptoms, mood changes, bone marrow suppression, and stimulation of


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Surgery_Schwartz. HCC and perhaps reverse previous damage to the liver. Interferon therapy produces various side effects including fatigue, flu-like symptoms, mood changes, bone marrow suppression, and stimulation of autoimmunity. On the other hand, the nucleoside analogs are generally well-tolerated by patients. Compared with lamivudine, the nucleoside analogs are less likely to produce resistance and are more likely to be clinically effective. Despite its high rate of viral resistance, lamivudine may be the preferred treatment in some countries because of its relatively low cost.Acute hepatitis C viral (HCV) infection typically devel-ops 2 to 26 weeks after exposure to the virus, and presenting symptoms can include jaundice, nausea, dark urine, and right upper quadrant abdominal pain. Diagnosis is confirmed by testing for the presence of HCV RNA and anti-HCV antibod-ies in the serum; viral RNA is first detectable in the serum by polymerase chain reaction (PCR) within days to weeks follow-ing the


Surgery_Schwartz

Surgery_Schwartz. by testing for the presence of HCV RNA and anti-HCV antibod-ies in the serum; viral RNA is first detectable in the serum by polymerase chain reaction (PCR) within days to weeks follow-ing the exposure, whereas antibodies will not appear until 2 to 6 months after. If the diagnosis of acute hepatitis is established and the virus is not spontaneously cleared within 12 weeks, patients should generally be treated with pegylated interferon Brunicardi_Ch31_p1345-p1392.indd 137120/02/19 2:36 PM 1372SPECIFIC CONSIDERATIONSPART IImonotherapy. High rates of sustained viral response, in excess of 80%, have been achieved with the early treatment of acute HCV infection.69 Unfortunately, patients with acute HCV infec-tion are typically asymptomatic, and the vast majority of cases go undetected. Untreated, most of these patients will eventually develop chronic infection.Chronic HCV infection often follows a progressive course over many years and can ultimately result in cirrhosis, HCC, and the


Surgery_Schwartz

Surgery_Schwartz. most of these patients will eventually develop chronic infection.Chronic HCV infection often follows a progressive course over many years and can ultimately result in cirrhosis, HCC, and the need for liver transplantation. Cirrhosis secondary to hepa-titis C remains the leading indication for liver transplantation in the United States, Europe, and Japan. The decision to treat a patient with chronic HCV infection is complex and involves consideration of multiple factors including the natural history of the disease, stage of fibrosis, and the efficacy and adverse effects related to the treatment regimen. Patients with genotype 1 are now treated with triple-agent therapy including pegylated interferon, ribavirin, and a protease inhibitor. The protease inhibitors telaprevir and boceprevir were recently approved for the treatment of chronic HCV genotype 1 infection, and their addition to the treatment regimen has been shown to increase the rate of sustained viral response from 40% to 70%.


Surgery_Schwartz

Surgery_Schwartz. recently approved for the treatment of chronic HCV genotype 1 infection, and their addition to the treatment regimen has been shown to increase the rate of sustained viral response from 40% to 70%. These prote-ase inhibitors do no exhibit significant antiviral activity against other HCV genotypes, and therefore genotypes 2, 3, and 4 are treated with interferon and ribavirin alone. Genotypes 2 and 3 are generally more responsive to treatment than genotypes 1 and 4, but the therapeutic response also is dependent on other factors such as baseline viral load, ethnicity, and the patient’s genetic background and compliance with the regimen.EVALUATION OF AN INCIDENTAL LIVER MASSA liver mass often is identified incidentally during a radio-logic imaging procedure performed for another indication. For example, a liver mass may be discovered during evaluation for gallbladder disease or kidney stones. In addition, with advances in imaging technology, previously undetected lesions not


Surgery_Schwartz

Surgery_Schwartz. indication. For example, a liver mass may be discovered during evaluation for gallbladder disease or kidney stones. In addition, with advances in imaging technology, previously undetected lesions not infre-quently are now identified. Although many of these lesions are benign and will require no further treatment, the concern for malignancy requires a thorough evaluation. Thus, an orderly approach should be taken to the workup of an incidental liver lesion to minimize unnecessary testing.70The evaluation of an incidental liver mass begins with a history and physical examination (Fig. 31-17). The patient should be asked about abdominal pain, weight loss, previous Figure 31-17. Algorithm for diagnostic workup of an incidental liver lesion. The evaluation includes history and physical examination, blood work, imaging studies, and liver biopsy (if needed). AFP = α-fetoprotein; BUN = blood urea nitrogen; CA 19-9 = cancer antigen 19-9; CBC = complete blood count; CEA = carcinoembryonic


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Surgery_Schwartz. blood work, imaging studies, and liver biopsy (if needed). AFP = α-fetoprotein; BUN = blood urea nitrogen; CA 19-9 = cancer antigen 19-9; CBC = complete blood count; CEA = carcinoembryonic antigen; creat = creatinine; CT = computed tomography; EGD = esophagogas-troduodenoscopy; glu = glucose; Gyn = gynecologic; HTN = hypertension; MRI = magnetic resonance imaging; OCP = oral contraceptive pill; PAP = Papanicolaou; US = ultrasound.DiagnosisAbdominal pain/weight lossLiver disease/cirrhosis/alcohol useHepatitis/blood transfusion/tattoosOCP/hormone use/cancer historyJaundice/scleral icterusPalpable mass/hepatomegalyStigmata of portal HTNCBC, platelet countLytes/BUN/creat/glu/albuminLiver function tests/ammoniaCoagulation studiesHepatitis screenTumor markers (CEA, AFP, CA 19-9)USCT or MRI scanNuclear med.AngiogramOccult primary eval.EGDColonoscopyMammogramGyn/PAP smear(Percutaneous or laparoscopic)Liver biopsy (if needed)Additional imaging studiesLaboratory testsHistory and physical


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Surgery_Schwartz. scanNuclear med.AngiogramOccult primary eval.EGDColonoscopyMammogramGyn/PAP smear(Percutaneous or laparoscopic)Liver biopsy (if needed)Additional imaging studiesLaboratory testsHistory and physical examMass identified incidentally by US or CTBrunicardi_Ch31_p1345-p1392.indd 137220/02/19 2:36 PM 1373LIVERCHAPTER 31liver disease, cirrhosis, alcohol use, viral hepatitis, blood trans-fusions, tattoos, oral contraceptive use (in women), and personal or family history of cancer. On physical examination, jaundice, scleral icterus, hepatomegaly, splenomegaly, palpable mass, or stigmata of portal hypertension should be noted. After comple-tion of the history and physical examination, blood work should be performed, including complete blood count; platelet count; measurement of levels of electrolytes, blood urea nitrogen, creatinine, glucose, and albumin; liver function tests; serum ammonia level; coagulation studies; hepatitis screen; and mea-surement of levels of the tumor markers


Surgery_Schwartz

Surgery_Schwartz. electrolytes, blood urea nitrogen, creatinine, glucose, and albumin; liver function tests; serum ammonia level; coagulation studies; hepatitis screen; and mea-surement of levels of the tumor markers carcinoembryonic anti-gen, AFP, and cancer antigen 19-9.The differential diagnosis for an incidental liver mass includes cysts, benign solid lesions, and primary or metastatic cancers (Table 31-6). Ultrasound or CT is commonly performed to evaluate respiratory or abdominal symptoms, and these imag-ing studies usually lead to the discovery of an incidental liver lesion. Further radiologic evaluation by dualor triple-phase CT scan or MRI is often necessary to fully characterize the extent and nature of the lesion. Different types of liver masses have distinct appearances and patterns of contrast enhancement on these studies, facilitating the clinician in the diagnosis and for-mulation of the treatment plan. The use of liver-specific contrast agents in MRI provides information on hepatocyte


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Surgery_Schwartz. enhancement on these studies, facilitating the clinician in the diagnosis and for-mulation of the treatment plan. The use of liver-specific contrast agents in MRI provides information on hepatocyte function in combination with the structural data obtained during a standard MRI, and yields improved detection and characterization of liver lesions. CT cholangiography or MRCP can be obtained, par-ticularly when visualization of the biliary tract is desired. These modalities may be useful in the depiction of benign or malignant strictures resulting in biliary obstruction. In the evaluation of metastases to the liver from a variety of primary cancers, FDG-PET/CT has emerged as an indispensable tool in disease staging and in the follow-up after treatment. The techniques available for imaging of liver lesions are described in detail earlier in the section “Radiologic Evaluation of the Liver.”Liver biopsy is indicated when biochemical analysis and diagnostic imaging fail to lead to a


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Surgery_Schwartz. of liver lesions are described in detail earlier in the section “Radiologic Evaluation of the Liver.”Liver biopsy is indicated when biochemical analysis and diagnostic imaging fail to lead to a definitive diagnosis. Percu-taneous liver biopsy with ultrasound or CT guidance is the sim-plest, fastest, and most commonly performed approach to obtain hepatic tissue for histologic examination. Absolute contraindi-cations to percutaneous liver biopsy include significant coagu-lopathy (as in patients with decompensated cirrhosis), biliary Table 31-6Classification of liver lesionsBenign Cyst Hemangioma Focal nodular hyperplasia Adenoma Biliary hamartoma AbscessMalignant Hepatocellular carcinoma Cholangiocarcinoma (bile duct cancer) Gallbladder cancer Metastatic colorectal cancer Metastatic neuroendocrine cancer (carcinoid) Other metastatic cancersdilatation, and suspicion for hemangioma or echinococcal cyst. Obesity and the presence of ascites are relative contraindica-tions that can present a


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Surgery_Schwartz. cancer (carcinoid) Other metastatic cancersdilatation, and suspicion for hemangioma or echinococcal cyst. Obesity and the presence of ascites are relative contraindica-tions that can present a challenge to the percutaneous approach. In these patients, laparoscopic liver biopsy can be considered. The laparoscopic technique is likely to have a higher diagnos-tic yield in cirrhotic patients with ascites and/or coagulopathy, in whom bleeding risk is excessive by the percutaneous route. Laparoscopy also offers the opportunity to stage the extent of disease in patients with various intra-abdominal malignancies.HEPATIC CYSTSCongenital CystsThe majority of hepatic cysts are asymptomatic. Hepatic cysts are usually identified incidentally and can occur at any time throughout life. The most common benign lesion found in the liver is the congenital or simple cyst. The exact prevalence of simple hepatic cysts in the U.S. population is not known, but the female to male ratio is approximately 4:1,


Surgery_Schwartz

Surgery_Schwartz. benign lesion found in the liver is the congenital or simple cyst. The exact prevalence of simple hepatic cysts in the U.S. population is not known, but the female to male ratio is approximately 4:1, and the prevalence is approximately 2.8% to 3.6%.71 Simple cysts are the result of excluded hyperplastic bile duct rests. Simple cysts usually are identified in hepatic imaging studies as thin-walled, homoge-neous, fluid-filled structures with few to no septations. The cyst epithelium is cuboidal and secretes a clear nonbilious serous fluid. With the exception of large cysts, simple cysts are usually asymptomatic. Large simple cysts may cause abdominal pain, epigastric fullness, and early satiety. Occasionally the affected patient presents with an abdominal mass.Asymptomatic simple cysts are best managed conserva-tively. The preferred treatment for symptomatic cysts is ultra-soundor CT-guided percutaneous cyst aspiration followed by sclerotherapy. This approach is approximately 90%