Benign lesions of the liver hepatobiliary lecture.pptx
XeniaPlaza
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53 slides
Mar 08, 2025
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About This Presentation
Benign lesions of the liver.pptx
Size: 4.14 MB
Language: en
Added: Mar 08, 2025
Slides: 53 pages
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DEPARTMENT OF SURGERY Eastern Visayas Medical Center Tacloban City BENIGN LESIONS OF THE LIVER Xenia C. Plaza, MD Level 1 General Surgery Resident
SIMPLE CYSTS contain serous fluid that do not communicate with the intrahepatic biliary tree <3cm in diameter usually asymptomatic Small cysts surrounded by normal hepatic tissue Large cysts produce atrophy with compensatory hypertrophy of the other lobe No septations Unilocular Clear cystic fluid bownish if there is intracystic bleeding
single layer of cuboidal or columnar epithelial cells uniform without atypia Small cysts - absent stroma Large cysts - thin layer of connective tissue SIMPLE CYSTS
uncommon before age 40 Larger in adults older than 40 years old female to male ratio 1.5:1 PREVALENCE SIMPLE CYSTS
Small cysts - asymptomatic Larger cysts - abdominal pain or discomfort, palpated as spherical tumors Liver function tests are normal High concentration of CA 19-9 and CEA in cyst fluid MANIFESTATIONS AND DIAGNOSIS SIMPLE CYSTS
Hypointense on T1 MRI SIMPLE CYSTS Hyperintense on T2
simple cysts - asymptomatic and remain silent Complications: Intracystic bleeding most frequent complication erosion of artery adjacent to cyst sudden severe pain, increase cyst size Spontaneous rupture Compression of nearby structures COURSE AND COMPLICATIONS SIMPLE CYSTS
asymptomatic cyst does not require treatment UTZ-guided aspiration of cyst Compression of hepatic vein 2 methods Sclerotherapy Cyst fenestration MANAGEMENT SIMPLE CYSTS
destro the epithelium lining the inner surface of the wall to stop intracystic fluid secretion Sclerosing agents: 95% ethanol - most frequently used Minocycline hydrochloride Ethanolamine oleate Hypertonic saline Bleomycin Contraindications Bile duct communication Leak to the peritoneal cavity Intracystic bleeding - delay sclerotherapy for 3 months MANAGEMENT - SCLEROTHERAPY SIMPLE CYSTS
excision of the roof of the cyst to establish a large communication between the cyst and the peritoneal cavity most often performed as laparoscopy - less invasive, quicker recovery Limitation: cyst located at segments VII or VIII limited access cyst recurent Injury to the diaphragm Complications: Bleeding - most severe Biliary leak May close periphery with running sutures or may use endovasclar staplers MANAGEMENT - FENESTRATION SIMPLE CYSTS
Epithelial focal nodular hyperplasia hepatocellular adenoma cholangiocellular tumors Mesenchymal hemangioma angiomyolipoma leiomyoma CLASSIFICATION BASED ON CELL OF ORIGIN BENIGN LIVER LESIONS
BENIGN LIVER LESIONS
most common of all solid liver tumors (70% of all benign liver lesions) 3-20% in general population F:M ratio of 5:1 mean age 50 y/o occur equally in left and right lobes usually less than 5cm Giant hemangiomas - >10cm; with fibrosis, thrombosis and calcification CAVERNOUS HEMANGIOMA
Well delineated, red-blue flat lesions that partially collapse on sectioning CAVERNOUS HEMANGIOMA Cavernous vascular spaces lined by flattened endothelium underlyign fibrous septa of various widths
asymptomatic and only an incidental finding pain is mostly due to other associated disorders Liver biologic tests are normal CLINICAL AND BIOLOGIC DATA CAVERNOUS HEMANGIOMA
INFLAMMATION consequence of hemangioma thrombosis Ssx: low grade fever, weight loss, abdominal pain, elevated ESR, anemia thrombocytosis and increased fibrinogen levels COAGULATION ABNORMALITIES (e.g. Kasabach-Merritt syndrome) intravascular coagulation, clotting and fibrinolysis within the hemangioma COMPRESSION OF ADJACENT STRUCTURES COMPLICATIONS CAVERNOUS HEMANGIOMA
homogenous hyperechoic sharp margins less than 3 cm in diameter with acoustic enhancement ULTRASONOGRAPHY CAVERNOUS HEMANGIOMA
Peripheral globular enhancement on arterial and portal venous phases and isoechoic pattern on late phase CONTRAST-ENHANCED ULTRASONOGRAPHY CAVERNOUS HEMANGIOMA
CRITERIA FOR DIAGNOSIS low attenuation on noncontrast peripheral and globular enhancement of the lesion followed by central enhancement on contrast CT contrast ehancement on delayed phase CT SCAN CAVERNOUS HEMANGIOMA
Hypointense on T1 MRI CAVERNOUS HEMANGIOMA Hyperintense on T2
no treatment for asymptomatic hemangioma Indications for treatment: severe symptoms,complications, inability to exclude malignancy Arterial embolization - temporary control of hemorrhage Arterial ligation - manual decompression of large hemangioma Radiofrequency ablation - alternative treament for 5-10cm lesions Resection - deeply located lesions Enucleation - peripheral liver area Liver transplantation - unresectable complicated giant hemagiomas MANAGEMENT CAVERNOUS HEMANGIOMA
benign, tumor-like, in women 30 to 50 years of age second most frequent solid benign lesion - 1% prevalence F:M ratio 9:1 hyperplastic reaction resulting from arterial malformation increase in the angiopoietinin 1 : angiopoietinin 2 (which acts as an antagonist of angiopoietinin 1) ratio Main Diagnostic Feature: presence of large and dystrophic arteries in the fibrous septa FOCAL NODULAR HYPERPLASIA
well-circumscribed, unencapsulated, and usually solitary mass, and it is characterized by a central fibrous scar that radiates into the liver parenchyma FOCAL NODULAR HYPERPLASIA benign-appearing hepatocytes arranged in nodules that are partially delineated by fibrous septa originating from the central scar
NO TREATMENT FOR ASYMPTOMATIC FNH FNH has no risk of malignant transformation, and there is no risk of complications. Surgical resection is restricted to: large symptomatic FNH located in the left liver pedunculated lesion liver resection with a surgical margin is preferred over enucleation. MANAGEMENT FOCAL NODULAR HYPERPLASIA
rare (<0.5%) female:male ratio 9:1 potential complications: hemorrhage and malignant transformation risk factors: estrogen, androgen, obesity HEPATOCELLULAR ADENOMA
well-delineated, sometimes encapsulated, fleshy with heterogeneous areas of necrosis and/or hemorrhage. HEPATOCELLULAR ADENOMA proliferation of benign hepatocytes arranged in a trabecular pattern without the normal liver architecture.
HISTOLOGIC SUBTYPES HEPATOCELLULAR ADENOMA HNF1A HCAs Inflammatory HCAs B-catenin HCA Unclassified narked steatosis clusters of small arteries surrounded by extracellular matrix and inflammatory infiltrates associated with sinusoidal dilation or congestion pseudoglandular formation and cellular atypias, such as enlarged, irregular and hyperchromatic nuclei No specific histologic features Obese patients NASH Risk for hemorrhage Risk of malignant transformation (>5cm)
HISTOLOGIC SUBTYPES HEPATOCELLULAR ADENOMA H NF1A HCAs Inflammatory HCAs B-catenin HCA Unclassified homogenous on MRI T2 - variable T2-weighted fat suppressed - isointense or hypointense T1 - diffuse and homogenous signal dropout (most striking finding) T2 - strong hyperintense signal which may be diffused or appear as rim-like band in the periphery of the lesion (atoll sign) T1 - isointense or hyperintense similar findings with other hepatocellular tumors arterial enhancement and portal delayed washout
Bleeding most frequent complication of HCA (25%) risk factors: large tumors (>5cm), visualization of arteries within the lesion, location of the tumor in the left lateral liver and exophytic growth Malignant transformation second most common complication of HCA most important risk factors for malignancy: male sex and tumor size mainly observed in HCAs greater than 5 cm and has been found in large HCAs (8 cm) COMPLICATIONS HEPATOCELLULAR ADENOMA
Surgical management based on: patient’s sex size of the largest tumor, HCA subtype Men - resected regardless of size Women HCAs <5 cm: cessation of hormonal therapy, MRI surveillance large HCAs (>5 cm) should be resected Preoperative Percutaneous biopsy: suspicious steaotic lesion >5cm detected in MRI in a female patient MANAGEMENT HEPATOCELLULAR ADENOMA
Bleeding HCAs - transarterial embolization within the first 2-3 days discharge patient after cessation of hormonal therapy ff up CT scan 6 months after discharge Liver resection - resorption of peritumoral hematoma on follow up CT scan Indications for liver transplant multiple unresectable lesions in men large HCA associated with intrahepatic venous shunt glycogen storage disease unresponsive to medical treament MANAGEMENT HEPATOCELLULAR ADENOMA
INFECTIONS OF THE LIVER
most common abscess seen in the US 40% monomicrobial, 40% polymicrobial, 20% culture-negatic MC bacteria: E. coli (⅔ of cases) SSx: RUQpain, fever, jaundice PYOGENIC LIVER ABSCESS
PYOGENIC LIVER ABSCESS Ultrasound - round, oval, hypoechoic, with well-defined borders CT scan - hypodense with peripheral enhancement with or without air-fluid levels MRI - high sensitivity but limited role
cornerstone: treat the underlying case and IV antibiotics Antibiotic coverage: gram negative and anaerobes IV antibiotics should continue for at least 8 weeks Surgical drainage (laparoscopic or open) if initial therapies fail Anatomic surgical resection - recalcitrant abscesses PYOGENIC LIVER ABSCESS MANAGEMENT
common in subtropical climates most comon type of liver abscess worldwide common location: superior-anterior aspect of the right lobe near the diaphragm anchovy paste or chocolate sauce SSX: RUQ pain, hepatomegaly, fever, hepatic abscess MC biochemical abnormality: elevated AP levels AMOEBIC LIVER ABSCESS
AMOEBIC LIVER ABSCESS well defined, low density round lesions wall enhancement with ragged appearance peripheral zone of edema
Metronidazole 750mg three times daily for 7-10 days Aspiration: large abscess do not respond to medical therapy superinfected abscess of the left lobe AMOEBIC LIVER ABSCESS MANAGEMENT
Echinococcus granulosus most common in sheep raising areas common in right lobe of the liver: anterior inferior and posterior inferior segments Ssx: dull RUQ pain, abdominal distension Diagnosis: ELISA for echinococcal antigens HYDATID DISEASE
HYDATID DISEASE well defined, hypodense lesions with distinct wall healing: entire cyst calcifies densely
Albendazole Surgical resection (laparoscopic or open) with instillation of scolicidal agent Anatomic liver resection HYDATID DISEASE MANAGEMENT
OTHER BENIGN LESIONS OF THE LIVER
mesenchymal tumors formed from smooth muscle cells, adipose tissue, and proliferating blood vessels mainly affect women 30-50 years > 5cm in diameter Macroaneurysms are highly characteristic <5cm and asymptomatic: careful observation with serial imaging >5cm (high risk for malignant transformation): liver resection ANGIOMYOLIPOMA
markedly enhanced on the arterial phase without washout on portal and delayed phases ANGIOMYOLIPOMA
very rare liver tumor that can mimic angiomyolipoma CT - homogeneous, circumscribed, fat attenuation, do not enhance with IV injection of contrast material MRI imaging hyperintense on T1-weighted images moderately hyperintense on T2-weighted images. no drop in signal intensity on fat-suppressed MR sequences. No need for Resection LIPOMA
known as the Von Meyenburg complex multiple and small (<5 mm) nodules scattered throughout the liver frequent in patients with congenital hepatic fibrosis or polycystic liver disease T2-weighted MRI: multiple small lesions that are strongly hyperintense often mistaken for Caroli’s No treatment required BILIARY HAMARTOMA
benign cholagioma benign and asymptomatc <5mm, well-circumscribed and subcapsular confused with metastatic carcinoma during surgery BILE DUCT ADENOMA
inflammatory myofibrolastic tumors rare 0.2-0.7% caused by exaggerated inflammatory response more common in men, non-European,age 50-65years old 3 patterns on imaging: ill-defined, large, heterogeneous and hypervascular encapsulated, solitary necrotic nodule ill-defined with periportal infiltration, dilated bile ducts and elarged hepatic lymph nodes no malignant potential Management: surveillance, steroids and antibiotics INFLAMMATORY PSEUDOTUMORS
seen in patients with liver disease or liver vessel disease Associated with: Budd-Chiaari syndrome, hereditary hemorrhagic telangiectasia, congenital hepatic fibrosis hepatic response to arterial inflow MRI: hyperintense in T1 hypointense in T2 strongly enhanced on arterial pphase FOCAL NODULAR HYPERPLASIA-LIKE LESIONS