hepatic and biliary disorders
Cirrhosis
Diagnosis of Cirrhosis
Liver blood tests, coagulation tests, complete blood count (CBC), and serologic tests for viral causes Conventional liver imaging tests: Ultrasonography, CT, MRI Noninvasive imaging assessment of fibrosis: Transient elastography, acoustic radiation force impulse imaging, 2-dimensional shear wave elastography, magnetic resonance elastography +/- proton density fat fraction Identification of cause based on clinical evaluation, routine testing for common causes, and selective testing for less common causes Sometimes liver biopsy (eg, when clinical and noninvasive tests are inconclusive, or when biopsy results may change management) ), particularly portal hypertension or Ascites . Early cirrhosis should be considered in patients with nonspecific symptoms or characteristic laboratory abnormalities detected incidentally during laboratory testing, particularly in patients who have a disorder or take a medication that might cause fibrosis. Testing seeks to detect cirrhosis and any complications and to determine its cause. Diagnostic testing begins with Laboratory Tests of the Liver and Gallbladder , coagulation tests, CBC, and serologic tests for chronic viral hepatitis (see tables Test results may be normal or may indicate nonspecific abnormalities. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels are often modestly elevated, but they can be normal. Alkaline phosphatase and gamma-glutamyl transpeptidase (GGT) are often normal; elevated levels indicate cholestasis or biliary obstruction. Bilirubin is usually normal but increases when cirrhosis progresses, particularly in Primary Biliary Cholangitis (PBC) . Decreased serum Anemia is common and usually normocytic with a high red blood cell distribution width (RDW). Anemia is often multifactorial; contributing factors may include chronic Overview of Gastrointestinal Bleeding (usually causing microcytic anemia), Conventional imaging tests are not highly sensitive or specific for the diagnosis of cirrhosis by themselves, but they can often detect its complications. Noninvasive imaging studies (eg, transient elastography, acoustic radiation force impulse imaging, 2-dimensional shear wave elastography, and magnetic resonance elastography) are useful in detection of early cirrhosis when conventional imaging findings are equivocal and portal hypertension is not evident. In advanced cirrhosis, ultrasonography shows a small, nodular liver. Ultrasonography also detects Portal Hypertension and CT and MRI with and without contrast can detect a nodular texture, varices, portal/splenic vein thrombosis, and delineate a liver lesion suspect for hepatocellular carcinoma. Radionuclide liver scans using technetium-99m sulfur colloid may show irregular liver uptake and increased spleen and bone marrow uptake, but it has limited use in contemporary practice. Determining the specific cause of cirrhosis requires key clinical information from the history and examination, as well as selective testing. 2), elevated gamma-glutamyl transpeptidase (GGT), and Megaloblastic Macrocytic Anemias . Fever, tender hepatomegaly, and jaundice suggest the presence of acute Detecting serum antibody to hepatitis C (anti-HCV) and HCV-RNA indicates hepatitis C. Detecting hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (anti-HBcAb) confirms Hepatitis B, Chronic . Chronic hepatitis B with very low HBV viral load can occur in HBV/HDV co-infection. Most clinicians also routinely test for the following: Autoimmune hepatitis: Suggested by a high antinuclear antibody titer (a low titer is nonspecific and does not always mandate further evaluation) and confirmed by hypergammaglobulinemia (IgG) and the presence of other autoantibodies (eg, anti–smooth muscle or anti-liver/kidney microsomal type 1 antibodies) Hereditary Hemochromatosis : Suggested by increased serum iron and transferrin saturation and confirmed by homeostatic iron regulator (HFE) genetic testing Alpha-1 Antitrypsin Deficiency : Suggested by a low serum alpha-1 antitrypsin level and confirmed by genotyping/phenotyping If these causes are not confirmed, other causes are sought: Presence of antimitochondrial antibodies (in 95%) and elevated IgM suggest Primary Biliary Cholangitis (PBC) (PBC), which needs to be confirmed with biopsy. Strictures and dilations of the intrahepatic and extrahepatic bile ducts, seen on magnetic resonance cholangiopancreatography (MRCP), suggest primary sclerosing cholangitis (PSC). test results suggest Wilson Disease . The presence of obesity and a history of diabetes suggest Metabolic Dysfunction–Associated Liver Disease (MASLD) (MASH), a diagnosis of exclusion unless confirmed with liver biopsy. Liver biopsy is invasive and is subject to sampling error, but it remains the gold standard for the diagnosis of cirrhosis. Liver biopsy is required in the following situations: If clinical criteria and noninvasive testing are inconclusive for diagnosis of cirrhosis or its etiology (for example, if well-compensated cirrhosis is suspected clinically and imaging findings are inconclusive) To confirm certain causes of cirrhosis (eg, amyloidosis, PBC, or small duct PSC) To assess the severity and/or activity of some causes of cirrhosis (eg, autoimmune hepatitis) in order to direct the intensity of treatment. To confirm cirrhosis for certain disorders for which noninvasive imaging for fibrosis assessment has not been validated (eg, pregnancy, congestive hepatopathy, and rare liver disorders) In obvious cases of cirrhosis with marked coagulopathy, Portal Hypertension , All patients with cirrhosis, regardless of cause, should be screened regularly for Hepatocellular Carcinoma . Abdominal ultrasonography with or without serum alpha-fetoprotein (AFP) is recommended every 6 months. If abnormalities that are suspect for HCC are detected, contrast-enhanced MRI or triple-phase CT of the abdomen (pre-contrast, arterial phase, and venous phase) should be done. Certain features on contrast imaging (Liver Imaging Reporting and Data System 5 criteria, including early arterial enhancement, washout in portal phase, enhancing capsule) can confirm HCC, sparing the patient a biopsy. Contrast-enhanced ultrasonography appears promising as an alternative to CT or MRI but is still under study. The presence of clinically significant portal hypertension (defined as hepatic venous pressure gradient ≥ 10 mmHg) should be assessed in patients with compensated cirrhosis, in a manner consistent with the Baveno VII consensus guidelines ( Diagnosis references ). Proposed diagnostic criteria using noninvasive methods to diagnose clinically significant portal hypertension include the following ( Liver stiffness (LS) on transient elastography (TE) ≥ 25 kPa LS on TE 20 – 25 kPa and platelet count<150 k/mL LS on TE 15 – 20 kPa and platelet count<110 k/mL ) is recommended to prevent decompensation. (See Treatment .) Upper endoscopy is not required to screen for gastroesophageal varices in patients on nonselective beta-blockers with compensated cirrhosis. However, if the patient is not a candidate for a nonselective beta-blocker, an upper endoscopy should be done every 2 to 3 years to monitor for gastroesophageal varices, and endoscopic banding should be performed as needed. 1.de Franchis R, Bosch J, Garcia-Tsao G, Baveno VII Faculty.: Baveno VII - Renewing consensus in portal hypertension.J Hepatol76(4):959-974, 2022. doi: 10.1016/j.jhep.2021.12.022. Erratum in:J Hepatol. 2022 Apr 14 2.Podrug K, Trkulja V, Zelenika M, et al: Validation of the new diagnostic criteria for clinically significant portal hypertension by platelets and elastography.Dig Dis Sci67(7):3327-3332, 2022. doi: 10.1007/s10620-021-07277-8 