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78 Hepatobiliary Surgery 5 Ascites Ascites manifests as a result of: 1) impaired albumin and protein synthesis, 2) increased hydrostatic pressure in hepatic sinusoids and splanchnic capillaries, 3) over-production, transudation and low reabsorption of lymph into the peritoneal space, 4) renal sodium retention and, 5) impaired renal water excretion, partially due to increased concentrations of antidiuretic hormone (ADH). Albumin infusion has no beneficial effect even in the presence of severe hypoalbuminemia. The treatment of ascites underscores bed rest and sodium restriction, to be followed by spirono- lactone if a spontaneous diuresis is not restored. If life threatening com- plications such as cardiac or respiratory compromise occur, these patients require hemodynamic monitoring. Paracentesis should be attempted in case ascites persists. Renal Failure Following hepatobiliary surgery, rapidly progressive renal failure may occur. The differential diagnosis includes acute tubular necrosis, prerenal azotemia and hepatorenal syndrome. Hepatorenal syndrome is the development of otherwise unexplained renal failure with urine sodium < 10 meq/l, hyperosmolar urine, olig- uria (< 400 ml/24hrs), fractional excretion of sodium (FeNa + ) < 1, and urine creati- nine to plasma creatinine ratio > 30:1 in patients with advanced liver disease. The pathophysiology of hepatorenal syndrome is based on the pooling of blood in the splanchnic bed and the resultant decrease in plasma volume. The kidney perceives a decreased glomerular filtration rate and causes a vasoconstriction that shunts blood away from the renal cortex. There is no specific treatment for hepatorenal syndrome. Dopamine (1-2.5 mcg/kg/min) may help maintain urine output. Although sponta- neous recovery has been reported, mortality is very high. These patients, generally cirrhotic, may benefit from liver transplant. Pulmonary Care Hepatopulmonary syndrome is defined by liver disease, increased alveolar arte- rial gradients, and evidence of reduced intrapulmonary vascular resistance. In cir- rhotic patients, an increased synthesis of nitric oxide has been demonstrated that may lead to arteriovenous shunts in the lungs. The resulting hypoxemia requires oxygen supplementation and may progress to respiratory failure. Glucose Metabolism We might expect the postoperative patient to be prone to hypoglycemia second- ary to diminished glycogen reserves, increased insulin levels, and impaired gluco- neogenesis. Yet, dangerous hypoglycemia is rare. Routine (5%) dextrose solutions should be infused while monitoring glucose serum levels. 79 Perioperative Care and Anesthesia Techniques 5 Coagulation Hypocoagulability derives from thrombocytopenia or reduced synthesis of vita- min K dependent factors; cholestasis also decreases vitamin K absorption and hepatic stores. Improvements in coagulation may be achieved with vitamin K 10 mg/day. Another cause of bleeding is fibrinogen deficiency; this situation may benefit from fresh frozen plasma transfusion. Decreased serum concentration of protein S, protein C and antithrombin III result in hypercoagulable states that can lead to disseminated intravascular coagulation (DIC). Sepsis Abdominal sepsis is the most common cause of mortality after hepatic resection. Preoperative biliary manipulation, infected bile, biliary stones, ascites, and blood loss may all predispose to abdominal sepsis. Other sources of sepsis include the respiratory and urinary systems. Wound infection and a central line catheter should also be considered as possible sources of infection. Gastrointestinal Bleeding The incidence of GI bleeding is 5%, with a mortality reaching 50%. The bleed- ing site can usually be identified by endoscopy. Treatment includes transfusions, antacids and H2 blockers. All postoperative hepatobiliary patients should be treated prophylactically. About 30% of cirrhotic patients have esophageal varices. The emer- gent treatment should combine blood product transfusion to correct the coagulopathy, gastric endoscopy with variceal banding or sclerotherapy, and possibly, octreotide 25-100 mcg/min to control bleeding. Life saving procedures may include compres- sion of the varices via a Sengstaken-Blakemore tube. As rebleeding occurs in 50% of patients, a definitive surgical treatment should be pursued. Encephalopathy Hepatic encephalopathy may be precipitated by GI bleeding, infection, drugs, diet or dehydration. It manifests as a sudden change in a patient’s mental status or the onset of asterixis. The precise pathogenesis remains unknown. The historical postulate has been the accumulation of endogenous ammonia. Other etiologies have been suggested, including changes in the blood-brain barrier permeability, abnor- mal neurotransmitter balance, altered cerebral metabolism, impairment of neuronal Na + -K + ATPase activity, and increased endogenous benzodiazepines. Standard therapy is devised to reduce levels of ammonia and other potentially toxic metabolites. Flumazenil has been administered with some improvement; however, protein restriction and lactulose administration are still practiced. Suggested Reading 1. Belghiti J, Noun R, Zante E et al. Portal triad clamping or hepatic vascular exclu- sion for major liver resection—A controlled study. Ann Surg 1996; 224:155-61. 2. Brown BR. Postoperative jaundice. In: Brown BR, ed. Anesthesia in Hepatic and Biliary Tract Disease. Philadelphia: F.A. Davies 1988:265-273. 3. Delva E, Camus Y, Nordlinger B et al. Vascular occlusion for liver resections operative management and tolerance to hepatic ischemia in 142 cases. Ann Surg 1989; 209:211-8. 80 Hepatobiliary Surgery 5 4. Emre S, Schwartz ME, Katz E et al. Liver resection under total vascular isolation- variations on the theme. Ann Surg 1993; 217:15-9. 5. Emond J, Wachs ME, Renz JF et al. Total vascular occlusion for major hepatec- tomy in patients with abnormal liver parenchyma. Arch Surg 1995; 130:824-31. 6. Gelman S. Anesthesia and the liver. In: Barash P G, Cullen B F, Stoelting RK eds. Clinical Anesthesia, 2 nd edition. Philadelphia: JB Lippincott 1992: 1185-1214. 7. Gitlin N. Hepatic encephalopathy. In: Zakim D, Boyer TD, eds. Hepatology A Textbook of Liver Disease. 3rd.edition. Philadelphia: WB Saunders 1998; 605-17. 8. Goldman L, Caldera DL, Nussbaum SR et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. New Engl J Med 1997; 297:845-50. 9. Habib N, Zografos G, Dalla Serra G et al. Liver resection with total vascular exclu- sion for malignant tumors. Br J Surg 1994; 81:1181-4. 10. Hannoun L, Borie D, Delva E et al. Liver resection with normothermic ischemia exceeding 1 h. Br J Surg 1993; 80:1161-5. 11. Krowka MJ, Cortese DA. Hepatopulmonary syndrome. Current concepts in diag- nostic and therapeutic considerations. Chest 1994; 105:1528-1537. 12. Melendez JA, Arslan V, Fischer M et al. Peri-operative outcome of major hepatic resections under low central venous pressure anesthesia—blood loss, blood trans- fusion and the risk of postoperative renal dysfunction. J Am Coll Surg 1998; 178:620-25. CHAPTER 1 CHAPTER 6 Benign Tumors of the Liver: A Surgical Perspective Ronald S. Chamberlain Introduction Benign liver tumors are common and account for 83% of all hepatic tumors identified on diagnostic imaging or at the time of laparoscopy. Benign liver tumors may arise from either epithelial or mesenchymal cells. In rare instances, a variety of miscellaneous disorders may masquerade as liver tumors (Table 6.1). The frequency of different types of liver tumors is not well understood, but suffice it to say, far more than 50% of all hepatic lesions are either hemangiomas or benign cysts (Table 6.2). Focal nodular hyperplasia (FNH), metastatic tumors from an undiag- nosed primary cancer site, hepatic adenomas, focal fatty infiltration, and hepatocel- lular carcinomas are the next most common diagnoses in descending order of frequency. Additional benign tumors have also been described; however, most if not all, are sufficiently rare as to be labeled medical “fascinomas.” The infrequency of symptoms associated with most benign and many malignant liver tumors complicates the process of establishing a firm diagnosis when hepatic tumors are identified incidentally. Despite significant advances in a variety of diag- nostic imaging modalities, the appearance of these lesions is often not clear-cut and biopsy or resection is indicated as diagnosis is mandatory. Indeed, the most com- mon indication for surgical management of “benign” liver tumors is the inability to exclude a possible malignancy. Table 6.3 reviews an MSKCC experience in treating 152 patients with “presumably” benign liver tumors between 1995 and 1998. Fifty- four percent of patients underwent operation, in part or solely to exclude a potential malignant diagnosis. Less common indications for surgical management included: 1. Relief of debilitating symptoms 2. To reduce the risk of rupture (a rare event), or potential for malignant transformation. 3. To treat life-threatening complications of rupture or hemorrhage. Evaluation The most “appropriate” work-up for an asymptomatic patient with a newly iden- tified solid liver tumor is unclear and it is difficult to recommend precise algo- rithms. In general, the workup should be individualized based upon patient age, sex, personal medical and social history, as well as the stage and suspected histology of the tumor in question. Physical examination is typically unrevealing unless the tumor is expansive, and in this setting, pain or abdominal discomfort is normally Hepatobiliary Surgery, edited by Ronald S. Chamberlain and Leslie H. Blumgart. ©2003 Landes Bioscience. 82 Heptobiliary Surgery 6 Table 6.1. Benign solid tumors of liver Cell of origin Tumor Epithelial Hepatocellular Focal nodular hyperplasia (FNH) Hepatocellular adenoma (HA) Regenerative nodule Cholangiocellular Biliary adenoma Biliary cystadenoma Other Epitheliod leiomyoma Mesenchymal Endothelial Hemangioma Hemangioendothelioma Adult Infantile Mesothelial Solitary fibrous tumor Other names: benign mesothelioma or fibroma Adipocyte Lipoma Myelolipoma Angiomyelipoma Miscellaneous Tumors Biliary hamartoma Pseudotumors Focal fatty infiltration Adrenal neoplasm Inflammatory pseudotumor Chronic abscess Table 6.2. Incidental solid liver tumors: Diagnostic frequency for various histologies 3 Tumor Relative frequency Hemangioma 52% Focal nodular hyperplasia 11% Metastatic tumor (T x N x M1) 11% Hepatocellular adenoma 8% Focal fatty infiltration 8% Hepatocellular carcinoma 6% Extrahepatic process 3% (e.g., abscess, adrenal tumor) Other benign hepatic process 1% 83 Benign Tumors of the Liver 6 Table 6.3. MSKCC experience in managing 152 patients with benign solid liver tumors between 1995 and 1998. Diagnosis Total Age Resected Operated on Symptoms (Mean) (%) to exclude a (%) malignancy (%) Hemangioma 75 55 35 14 23 (47) (40) (66) FNH 33 42 16 9 8 (48) (56) (50) Adenoma 10 39 8 6 6 (80) (75) (75) Cyst 26 56 15 5 8 (58) (33) (53) Polycystic liver 4 46 4 0 4 (100) (100) Hydatid cyst 4 48 4 0 4 (100) (100) Total 152 49 82 34 53 (54) (41) (65) present. Hepatomegaly may develop in the setting of a large hepatic cyst, cavernous hemangioma, parenchymal bleed into a hepatocellular adenoma, or polycystic liver disease, but is not diagnostic. Laboratory tests, including liver function tests, are invariably normal in asymptomatic patients with liver tumors and are, therefore, not helpful. In rare instances, serum transaminase levels may be elevated in patients experiencing an acute hemorrhage, thrombosis, or necrosis of tumor, but it is not pathognomonic for a particular liver pathology. Elevated serum tumor markers, such as alpha fetoprotein (AFP), carcinoembryonic antigen (CEA), and CA-19-9, are rarely elevated in benign liver tumors and should suggest the likelihood of an under- lying malignancy. In most instances, radiologic studies can provide a precise diagnosis based on the characteristic appearance of the tumor; however multiple studies yielding comple- mentary data are required (Table 6.4). In Chapter 4, Decorato and Schwartz pro- vide a detailed discussion of the advantages and disadvantages of various hepatobiliary imaging techniques. In brief, ultrasonography is the most common initial study since it can effec- tively differentiate between cystic and solid neoplasms. Contrast-enhanced com- puted tomography (CT) with delayed imaging, a so-called “triple phase CT scan”, can provide precise diagnostic information while also determining the number, size, and location of these tumor(s). Magnetic resonance imaging (MRI) is the most useful imaging modality with regard to differentiating between “indeterminate” and 84 Heptobiliary Surgery 6 Table 6.4. The radiographic appearance of common benign liver tumors Tumor Ultrasound CT MRI Tc 99 RBC scan Tc 99 SC scan Hemangioma Hyperechoic Very sensitive Very sensitive Highly specific Not indicated Well-demarcated Isodense on noncontrast scan Isodense on T1 Very sensitive Increased vascular flow Contrast: Irregular peripheral Hyperdense on T2 Blood pooling of Central venous pooling enhancement Gadolinium enhanced radionucleotide Delayed central filling scan shows similar findings to contrast CT Focal Nodular Nonspecific Isodense on noncontrast CT Isodense of T1 & T2 Not indicated Takes up Tc 99 SC Hyperplasia ?Hyperechoic may be well-demarcated on Early hyperdense Contains bile (FNH) contrast CT with central scar appearance after ducts and — often isodense gadolinium Kupffer cells Nonspecific Hepatic Nonspecific Nonspecific Nonspecific Nonspecific Generally does Adenoma ?Hyperechoic Hyperechoic Hyperechoic Not indicated not take up Tc 99 Increased blood flow SC because of the on duplex scanning lack of bile ducts and Kupffer cells Nonspecific * Tc 99 RBC scan—Technetium–labeled red blood cell scan; HIDA—Hepatic aminodiacetic acid scan; Tc 99 SC—Technetium sulfur colloid scan 85 Benign Tumors of the Liver 6 malignant tumors. Although many liver tumors have a characteristic angiographic appearance, the information it provides can currently be obtained by noninvasive imaging modalities in most situations. Laparoscopy can be used as a diagnostic tool in some patients by allowing the surgeon to obtain a reliable tissue biopsy using minimally invasive techniques. In rare cases, the surgical management may be car- ried out laparoscopically as well. Benign Liver Tumors Hemangioma Hemangiomas are the most common benign solid tumors of the liver and occur in two variants, capillary hemangiomas and cavernous hemangiomas. Capillary he- mangiomas are the most common, but are clinically insignificant. They are typically small, hypervascular lesions (< 2 cm) encountered at the time of laparotomy and may be the source of considerable diagnostic uncertainty. Establishing the diagnosis and excluding a malignancy is all that is required. Cavernous hemangiomas are clinically more relevant because of the potential for complications and associated symptoms. Cavernous hemangiomas have been reported in up to 7% of patients at autopsy and occur more commonly in adults than in children. The etiology of cavernous hemangiomas remains uncertain; however, they most likely represent benign congenital hamartomas. Although the incidence of cavernous hemangioma has been reported as 1.3-6 times higher in women than in men, the higher incidence of hemangioma in females is likely a reflection of referral bias rather than a true difference in incidence. Sex hormones have not been linked etiologically to the development of hemangiomas. Cavernous hemangiomas may vary in size from less than 1 cm, to “giant hemangiomas” which may be greater than 30-40 cm. The size of a hemangioma correlates with symptoms, as it is usually large pedunculated tumors that are encountered at surgery. These tumors are often sharply demarcated from surrounding liver tissue, have a spongy appearance, and may be partly necrotic or fibrotic. Occasionally, infarct of the hemangioma may cause it to be completely fibrosed and, in rare cases, calcified. When this occurs, these tumors can be extremely difficult to distinguish from other benign and malignant tumors. The acute nature of some symptoms related to hemangioma may, in fact, not be related to increase in size, but rather thrombosis and infarct that lead to focal fibrosis and obliteration of vascular channels in part or whole. Clinical Presentation Symptoms from hemangiomas of the liver are generally attributed to rapid expansion in the size of the lesion or to thrombosis and infarct that lead to stretch- ing or inflammation of Glisson’s capsule. Occasionally, a large hemangioma may present as a nontender mass in the right upper quadrant, but more often the physi- cal examination reveals only vague upper abdominal tenderness with no mass. It may be possible to auscultate a bruit over a large hemangioma, but this is not pathog- nomonic. Rarely, a hemangioma may rupture resulting in a hemoperitoneum and shock requiring emergency surgical care. Severe thrombocytopenia and the development of a consumptive coagulopathy have been associated with cavernous hemangiomas of the liver. Although the 86 Heptobiliary Surgery 6 Kasabach–Merritt syndrome was initially used to describe thrombocytopenia and afibrinogenemia associated with hemangiomas of the skin and spleen in infants, this term is often used to describe similar coagulopathies in children and adults (rare) with hemangiomas of the liver. Pathology Historically, hemangiomas are typically well demarcated and distinct from the surrounding hepatic parenchyma. The sharp interface between hemangioma and normal liver parenchyma permits surgical enucleation in most cases. However, not all hemangiomas are enucleable, and the histologic features of the tumor-liver inter- face define how easily a parenchymal-sparing technique may be utilized (Figs. 6.1A,B). Four variants of the interface between the hemangioma and liver have been described. A “fibrolamellar interface”, characterized by a capsule-like fibrous ring of variable thickness, is most common. The normal hepatic parenchyma is often atro- phic, and a plane between the hemangioma and the normal liver tissue can be well defined. A second variant, the “interdigiting” pattern, is marked by the lack of a fibrous lamella surrounding the hemangioma which is replaced by an ill-defined plane between normal liver tissue and the vascular channels of the hemangioma. These tumors can be quite hazardous to remove without a formal resection. Two additional histologic variants have been identified, including a “compression” inter- face, in which the periphery of the tumor is well demarcated in the absence of a fibrous lamella and an “irregular or spongy” variant which appears to intercalate into the surrounding liver parenchyma making complete excision hazardous and unnecessary. Note, despite the invasive appearance of this histologic variant, hemangiomas are not premalignant lesions and do not invade or metastasize. The diagnosis of a cavernous hemangioma is generally clear-cut on both macro- scopic and microscopic examination. In rare instances, an atypical hemangioma may be confused for other liver conditions including peliosis hepatis, hemorrhagic telangiectasia (Osler–Rendu–Weber), hemangioendothelioma and other malignant vascular tumors. As a rule, percutaneous biopsy of a suspected hemangioma should be avoided as this may result in unnecessary and uncontrollable hemorrhage. Symp- tomatic lesions, large lesions, or indeterminate lesions should be managed surgically. Radiologic Evaluation The initial radiologic evaluation of a suspected hemangioma is often dictated by the clinical presentation. In most instances, hemangiomas are discovered inciden- tally on a study performed for other reasons and the degree of diagnostic certainty provided by this study may obviate the need for additional imaging. If a patient presents with dull, nonspecific right upper quadrant complaints, ultrasonography is typically the first study performed. On ultrasound (US), a hemangioma appears as a hyperechoic mass well demarcated from the surrounding liver. The number and location of the lesion(s) can be precisely defined on B-mode ultrasound, and the addition of duplex ultrasonography can provide information with regard to peripheral blood flow and central pooling of venous blood. On a noncontrast CT scan, hemangiomas appear as a hypodense mass which exhibits a characteristic pattern of irregular peripheral nodular enhancement after initial injection of contrast material. Delayed CT scanning, several minutes after contrast injection, demonstrates central 87 Benign Tumors of the Liver 6 Fig. 6.1A, B. Cavernous hemangioma. A, The gross appearance of a cavernous hemangioma on cut section is shown. B, A sponge-like architecture with venous lakes is characteristic of these lesions . filling of the hypoechoic lesion which persists for some time and is felt to be diag- nostic of hemangioma (Figs. 6.2 and 6.3). MRI is the most sensitive and specific means to detect hepatic hemangiomas. The T-2 weighted image demonstrates a characteristic hyperechoic pattern. The administration of gadolinium results in similar peripheral enhancement with delayed central filling as was described with CT scan- ning. Although a technetium-99 labeled red blood cell scintigram (Tc99 RBC scan) has historically been considered the “gold standard” diagnostic evaluation for hemangiomas (Fig. 6.4). Technologic advances in axial imaging diagnostic tech- niques, such as MRI and CT, combined with the additional staging information these studies provide, have led to less reliance upon RBC scintigrams. Selective hepatic angiography demonstrates a characteristic neovascularity to these lesions often described as “corkscrewing.” Rapid filling of the central portion of hemangiomas from the neovascular periphery yields a “cottonwool” appearance to these lesions. Despite this characteristic finding, the diagnostic yield of less invasive studies is such that arteriography is unnecessary in the evaluation of most patients. As a rule, biopsies, by whatever means, are unnecessary unless a histologic diagnosis will alter planned therapy. Tr eatment Observation is the most appropriate treatment for nearly all asymptomatic hemangiomas. To date, there are no documented instances in which a hemangioma has spontaneously ruptured while being observed. Trastek et al followed 36 patients with a cavernous hemangioma for up to 15 years (mean 5.5). Among this group were two infants who were treated with steroids; one child responded. One adult patient was also treated with external beam radiation and showed marked reduction in the size of the lesion. The other 33 patients were observed with no other treat- ment. There were no spontaneous ruptures and, most importantly, no changes in [...]... Ascites Encephalopathy (grade) Grade 1 3.5 1-3 None None Points 2 2. 0-3 .0 2. 8-3 .5 4- 6 Slight 1-2 3 >3.0 6 Moderate 3 -4 A 5-6 points B 7-9 points C 1 0-1 5 points Imaging The goals of imaging are multiple and include: 1 identification of lesions, 2 as an aid in determining whether a lesion is cancerous, 3 to assess potential resectability, 4 as a guide in planning the extent of resection,... present Stage 1 Stage 2 Stage 3 Stage 4A Stage 4B T-Stage T1 T2 T3 T 1-3 T4 T-Any N-Stage N0 N0 N0 N1 N 0-1 N-Any M-Stage M0 M0 M0 M0 M0 M1 Table 7.3 Okuda staging of hepatocellular cancer Adverse Factor Tumor Size Ascites Serum Albumin Serum Bilirubin >50% hepatic involvement Present 3mg/dl Stage I Stage II Stage III No adverse factors 1-2 adverse factors 3 -4 adverse factors within 6 weeks complete... hepatocellular carcinoma T-Staging T 1- No poor prognostic features (multiplicity, size >2 cm, vascular invasion) T 2- One poor prognostic feature T 3- Two or three of the poor prognostic features T 4- Bilobar disease, tumor involving major portal or hepatic venous branches N-Staging N 0- No nodal involvement N 1- Regional nodal involvement M-Staging M 0- No distant metastatic disease M 1- Distant metastatic disease... curative partial hepatectomy is associated with a 5-year survival of 4 0-5 0%, whereas in patients with cirrhosis most recent large studies report a 5-year survival of 2 0 -4 0% As 7 106 7 Heptobiliary Surgery Fig 7.1 Treatment algorithm for patients with hepatocellular carcinoma based upon resectability and liver function demonstrated in a large series recently published by the Memorial Sloan-Kettering... as CEA, α-fetoprotein and CA1 9-9 ), are not elevated Fig 6.7 Focal nodular hyperplasia (FNH) Pre- and postgadolinium MRI images of a FNH A, A noncontrast T1-weighted image shows an isodense lesion in Segment 4B Portal venous tributaries re nondisplaced and are seen to course through the lesion B and C, On T2-weighted image of the same lesion, no mass is visible D, E, and F, Postgadolinium T1-weighted... white-to-gray, lesions that may be well or ill-defined Histologically, most have a bland appearance with a classic short storiform (so-called patternless) pattern and absence of cellular atypia, mitoses and/or necrosis; however, in malignant cancer there may be marked cellular atypia and a high mitotic rate Immunohistochemically, all the SFTs show a strong positive reaction against antibodies for CD- 34. .. 6 3 4 5 6 7 8 9 10 11 12 13 14 Ishak KG, Rabin L Benign tumors of the liver Med Clin North Am 1975; 59:99 5-1 013 Ishak KG Mesenchymal tumors of the liver In: Okuda K, Peters RL eds Hepatocellular Carcinoma Wiley, New York, 1976 pp 24 7-3 07 Dehner L P, Ishak K G Vascular tumors of the liver in infants and children A study of 30 cases and review of the literature Archives of Pathology 1971; 92:10 1-1 11... 1977; 73:386–3 94 Scott LD, Katz AR, Duke JH, Cowan DF, Maklad NF Oral contraceptives, pregnancy, and focal nodular hyperplasia of the liver JAMA 19 84; 251: 146 1–3 Whelan Jr, Baugh JH, Chandon S Focal nodular hyperplasia of the liver Ann Surgery 1973; 177:150–8 Foster JH, Berman M Solid Liver Tumors W B Saunders, Philadelphia 1977 Leese T, Farges O, Bismuth H Liver cell adenomas: a 12-year surgical experience... figure is approximately 4 0-5 0% It is thought that cirrhosis arising in the setting of Hepatitis C carries a greater risk of developing HCC For patients with cirrhosis from Hepatitis B, the estimated risk is 0.5% per year In contrast, the risk of developing HCC over a 10-year period in patients with Hepatitis C has been reported to be nearly 50% In Western series, Hepatobiliary Surgery, edited by Ronald... Network for Organ Sharing) figures, 4, 413 cadaveric liver transplants were performed in 1998 Of these, only 87 (2.1%) were given to recipients with malignant neoplasms UNOS survival data on transplants performed from 1989 through 1998 demonstrate a 5-year survival of 41 % for patients with a primary malignant neoplasm of the liver compared to an overall survival of 74% for all patients undergoing cadaveric . 35 14 23 (47 ) (40 ) (66) FNH 33 42 16 9 8 (48 ) (56) (50) Adenoma 10 39 8 6 6 (80) (75) (75) Cyst 26 56 15 5 8 (58) (33) (53) Polycystic liver 4 46 4 0 4 (100) (100) Hydatid cyst 4 48 4 0 4 (100). Engl J Med 1997; 297: 84 5-5 0. 9. Habib N, Zografos G, Dalla Serra G et al. Liver resection with total vascular exclu- sion for malignant tumors. Br J Surg 19 94; 81:118 1 -4 . 10. Hannoun L, Borie. felt to be an FNH based on radio- logic features, particularly if it is small and centrally located, a trial of close observa- tion with repeat imaging every 3 -4 months is rational. 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