PROGRESSION Fulminant hepatitis Chronic hepatitis Carrier state
Diagnosis of Acute H epatitis To diagnose hepatitis Biochemistry Serum Bilirubin (Total & Conjugated) AST / ALT / ALP To determine etiology Serology (Initial testing) HBsAg , IgM Anti- HBc , Anti-HCV Ab , Anti-HAV Ab HBeAg , Anti-HEV Ab Molecular biology (Usually not required) HCV RNA HBV DNA
Diagnosis of Chronic H epatitis To diagnose chronic hepatitis Biochemistry AST / ALT (persistent elevation 6 months apart) To determine etiology Serology HBsAg , HBeAg , Anti-HCV Ab Molecular biology (for quantification, guided by serology) HBV DNA HCV RNA
Acute / Chronic Hepatitis co-infections HDV occurs only along with HBV infection Co-infection of HBV and HCV may occur HBV or HCV may coexist with HIV infection
LIVER ABSCESS
Pyogenic abscess , which is most often polymicrobial , accounts for 80% of hepatic abscess cases in the United States. Amebic abscess due to Entamoeba histolytica accounts for 10% of cases. Fungal abscess , most often due to Candida species, accounts for less than 10% of cases
PYOGENIC ABSCESS
AMOEBIC LIVER ABSCESS Protozoan parasite: Entamoeba histolytica Exposure via fecal-oral route Humans are the principal host Source of infection is the cyst-passing chronic patient or asymptomatic carrier It results from spread of the organisms from the intestinal submucosa to the liver via the portal system
Clinical Features History The most frequent symptoms of hepatic abscess include the following: a) Fever (either continuous or spiking) b) Chills c) Right upper quadrant pain d) Anorexia e) Malaise - Referred pain to the right shoulder may be present. - Fever of unknown origin (FUO) frequently can be an initial diagnosis in indolent cases. Multiple abscesses usually result in more acute presentations, with symptoms and signs of systemic toxicity. - Afebrile presentations have been documented!
Physical Findings Fever and tender hepatomegaly are the most common signs. A palpable mass need not be present. Mid epigastric tenderness, with or without a palpable mass, is suggestive of left hepatic lobe involvement. Decreased breath sounds in the right basilar lung zones, with signs of atelectasis and effusion on examination or radiologically , may be present. A pleural or hepatic friction rub can be associated with diaphragmatic irritation or inflammation of Glisson capsule. Jaundice may be present in as many as 25% of cases and usually is associated with biliary tract disease or the presence of multiple abscesses.
Current indications for the surgical treatment of amoebic liver abscess are- Surgical intervention :- perforated amebic colitis, massive GI bleeding, or toxic megacolon . Amebic liver abscess generally responds to medical therapy alone and drainage is seldom necessary. When necessary, imaging-guided percutaneous treatment (needle aspiration or catheter drainage) has replaced surgical intervention as the procedure of choice for reducing the size of an abscess. Indications for drainage : - Presence of left-lobe abscess (>10 cm in diameter) Rupture and abscess that does not respond to medical therapy within 3-5 days
C omplications metastatic complications e.g., CNS infection or endophthalmitis ( usually with K pneumoniae infection. sepsis abscess rupture – presents as perotinitis or pneumoperitoneum . subphrenic abscess - Patients may have symptoms of diaphragmatic irritation. pleuropulmonary or hepatobronchial fistula - Patients may present with a cough, productive of purulent sputum. Metallic-tasting sputum has been reported hepatic artery pseudoaneurysm abdominal or hepatic venous thrombosis liver failure - More common in people with pre-existing liver disease, or large abscesses acute pancreatitis - rare complication. Presents with acute epigastric pain and vomiting. fistula to adjacent organs - such as to the stomach, colon, small bowel, or kidney
HYDATID CYST
Life cycle of E.granulosus
The right lobe is the most frequently involved portion of the liver. Once in the human liver, cysts grow to 1 cm during the first 6 months and 2–3 cm annually thereafter, depending on host tissue resistance.
Surgical Management Indications: 1-Large liver cysts with multiple daughter cysts; superficially located single liver cysts that may rupture (traumatically or spontaneously). 2-liver cysts with biliary tree communication or pressure effects on vital organs or structures. 3-infected cysts . 4-cysts in lungs, brain, kidneys, eyes, bones .
Medical therapy Indications: Chemotherapy is indicated in patients with primary liver or lung cysts that are inoperable (because of location or medical condition ), patients with cysts in 2 or more organs, and peritoneal cysts. Chemotherapeutic agents: Two benzimidazoles are used, albendazole and mebendazole . Albendazole is administered in several 1-month oral doses (10-15 mg/kg/d) separated by 14-day intervals. The optimal period of treatment ranges from 3-6 months, with no further increase in the incidence of adverse effects if this period is prolonged. Mebendazole is also administered for 3-6 months orally in dosages of 40-50 mg/kg/d.
PAIR This technique, performed using either ultrasound or CT guidance, involves aspiration of the contents via a special cannula , followed by injection of a scolicidal agent for at least 15 minutes, and then reaspiration of the cystic contents. The cyst is then filled with isotonic sodium chloride solution. Perioperative treatment with a benzimidazole is mandatory (4 d prior to the procedure and 1-3 mo after). The cysts should be larger than 5 cm in diameter and type I or II according to the Gharbi ultrasound classification of liver cysts
CIRRHOSIS
Normal Histology Hepatocytes : Radiate from central vein to portal tract Sinusoids lined by endothelial cells Space of Disse Bile canaliculus : between the hepatocytes Limiting plate: Cells adjacent to the portal tract
Cirrhosis Definition : It is an end stage of chronic liver disease characterized by : 1.Bridging fibrous septae : Scars extending between portal tracts; portal tract and central vein 2.Parenchymal nodules : Proliferating hepatocytes encircled by fibrosis 3.Disruption of the architecture of the entire liver
Pathogenesis
Gross -Normal
Cirrhosis
Microscopy NORMAL CIRRHOSIS
Classification Based on the size of the nodules Micronodular : ( < 3 mm size) : Alcoholic liver disease, hemochromatosis , Biliary cirrhosis. Macronodular : ( > 3 mm size) : Viral hepatitis, Wilson disease, Indian childhood cirrhosis Micro-macro nodular (Mixed) : alcoholic, drug induced
PORTAL HYPERTENSION
Elevation of portal venous pressure >5mm Hg Clinically significant - >10mm Hg Risk of variceal bleeding - >12mm Hg
Portosystemic Venous Shunts Sites : - Rectum – hemorrhoids. Cardioesophageal junction – Esophagogastric varices - in 65% of pts with advanced cirrhosis – life threatening hemetemesis . Retroperitoneum Falciparum ligament of liver – Periumbilical & abdominal wall collaterals – caput medusae ; important clinical hall mark of portal HT
Hepatic Failure
LIVER TUMOURS
Benign Adenoma Cavernous hemangiomas • Malignant Hepatocellular carcinoma Cholangiocarcinoma Hepatoblastoma Angiosarcoma • Metastatic: colon, lung, and breast • Tumour like conditions Cavernous hemangioma Focal nodular hyperplasia Nodular regenerative hyperplasia.
Solitary or multiple benign hepatocellular nodules Focal nodular hyperplasia : localized, well-demarcated but poorly encapsulated lesion - hyperplastic hepatocyte nodules with a central fibrous scar -appear in noncirrhotic livers and may reach up to many centimeters in diameter. - not a neoplasm but a nodular regeneration Macroregenerative nodules appear in cirrhotic livers - larger than surrounding cirrhotic nodules but do not display atypical features. Dysplastic nodules : larger than 1 mm in diameter -appear in cirrhotic livers. - Hepatocytes are highly proliferative and show atypical features such as crowding and pleomorphism
Hepatocellular Carcinoma Pathogenesis Repeated cycles of cell death & regeneration Genetic alterations : - Point mutations - Loss of heterozygosity in tumor suppressor genes - DNA Methylation changes - Increased expression of HGF, TGF-α Viral protein Hepatocyte replication Hepatocyte dysplasia Accumulation of mutations in repeat cell cycles - Damage DNA repair mechanism Transformation of the Hepatocyte