CIRRHOSIS   28A

A 63-year-old man with a long history of alcohol use presents with a 6-month history of increasing abdominal girth, easy bruisability and worsening fatigue. He denies any history of gastrointestinal (GI) bleeding. He drinks three or four cocktails a night but says he is trying to cut down. Physical examination reveals a cachectic man who appears older than his stated age. His blood pressure is 108/70 mm Hg. His scleras are anicteric. His neck veins are flat, and chest examination demonstrates gynecomastia and multiple spider angiomas. There is a protuberant abdomen with detectable fluid wave, shifting dullness, and enlarged spleen. The liver edge is difficult to appreciate. He has trace pitting pedal edema. Laboratory studies show anemia, mild thrombocytopenia, and elevated prothrombin time. Abdominal ultrasonography confirms a shrunken, heterogeneous liver, ascites, and splenomegaly.

What are the salient features of this patient’s problem? How do you think through his problem?

Salient features: Chronic alcohol use; ascites; coagulopathy and thrombocytopenia; edema, gynecomastia; spider angiomas; splenomegaly; ultrasound showing a shrunken liver

How to think through: Portal hypertension, inadequate protein synthesis, and inadequate clearance of circulating estrogens explain most of this patient’s symptoms and signs. Which elements are caused by portal hypertension? (Ascites, edema, splenomegaly, and thrombocytopenia caused by splenic sequestration.) What other complications of portal hypertension is he at risk for? (Infection, e.g., bacterial peritonitis, hepatocellular carcinoma [HCC], hepatorenal syndrome, encephalopathy.) How would you determine if he has encephalopathy? What would you expect his liver enzymes to show? His liver biopsy? Besides chronic heavy alcohol intake, what are other major risk factors for cirrhosis? Is his cirrhosis currently compensated or decompensated? How should his ascites be treated? (Sodium restriction; loop diuretic; aldosterone receptor blocker; large-volume paracentesis). What data are needed to establish his prognosis? (Serum creatinine, albumin, bilirubin; imaging to evaluate for HCC and endoscopy for esophageal varices.) What scoring systems can help establish disease severity? Is he a candidate for liver transplantation? (Not while actively drinking alcohol.)

CIRRHOSIS   28B

What are the essentials of diagnosis and general considerations regarding cirrhosis?

Essentials of Diagnosis

End result of injury that leads to both fibrosis and nodular regeneration

May be reversible if the cause is removed

Symptoms from hepatic cell dysfunction, portosystemic shunting, and portal hypertension

General Considerations

Risk factors: chronic viral hepatitis, alcohol, drug toxicity, autoimmune and metabolic liver disease; may have multiple synergistic risk factors

Three clinical stages: compensated, compensated with varices, and decompensated (ascites, variceal bleeding, encephalopathy, or jaundice)

Patterns include micronodular, macronodular, and mixed cirrhosis

Micronodular cirrhosis: most common, with regenerating nodules smaller than 1 mm, typical of alcoholic liver disease (Laennec cirrhosis)

Macronodular cirrhosis: nodules are several centimeters large; may be posthepatic or follow episodes of massive necrosis and stromal collapse

Stay updated, free articles. Join our Telegram channel

Join