Chapter 044. Abdominal Swelling and Ascites (Part 2)

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Palpation is often difficult with massive ascites, and ballottement of overlying fluid may be the only method of palpating the liver or spleen. A slightly enlarged spleen in association with ascites may be the only evidence of an occult cirrhosis. When there is evidence of portal hypertension, a soft liver suggests that obstruction to portal flow is extrahepatic; a firm liver suggests cirrhosis as the likely cause of the portal hypertension. A very hard or nodular liver is a clue that the liver is infiltrated with tumor, and when accompanied by ascites, it suggests that the latter is due...

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Chapter 044. Abdominal Swelling and Ascites (Part 2) Palpation is often difficult with massive ascites, and ballottement of overlying fluid may be the only method of palpating the liver or spleen. A slightly enlarged spleen in association with ascites may be the only evidence of an occult cirrhosis. When there is evidence of portal hypertension, a soft liver suggests that obstruction to portal flow is extrahepatic; a firm liver suggests cirrhosis as the likely cause of the portal hypertension. A very hard or nodular liver is a clue that the liver is infiltrated with tumor, and when accompanied by ascites, it suggests that the latter is due to peritoneal seeding. The presence of a hard periumbilical nodule (Sister Mary Joseph's nodule) suggests metastatic disease from a pelvic or gastrointestinal primary tumor. A pulsatile liver and ascites may be found in tricuspid insufficiency.
An attempt should be made to determine whether a mass is solid or cystic, smooth or irregular, and whether it moves with respiration. The liver, spleen, and gallbladder should descend with respiration unless they are fixed by adhesions or extension of tumor beyond the organ. A fixed mass not descending with respiration may indicate that it is retroperitoneal. Tenderness, especially if localized, may indicate an inflammatory process such as an abscess; it also may be due to stretching of the visceral peritoneum or tumor necrosis. Rectal and pelvic examinations are mandatory; they may reveal otherwise undetected masses due to tumor or infection. Radiographic and laboratory examinations are essential for confirming or extending the impressions gained on physical examination. Upright and recumbent films of the abdomen may demonstrate the dilated loops of intestine with fluid levels characteristic of intestinal obstruction or the diffuse abdominal haziness and loss of psoas margins suggestive of ascites. Ultrasonography is often of value in detecting ascites, determining the presence of a mass, or evaluating the size of the liver and spleen. CT scanning provides similar information and is often necessary to visualize the retroperitoneum, pancreas, and lymph nodes. A plain film of the abdomen may reveal the distended colon of otherwise unsuspected ulcerative colitis and give valuable information as to the size of the liver and spleen. An irregular and elevated right side of the diaphragm may be a clue to a liver abscess
or hepatocellular carcinoma. Studies of the gastrointestinal tract with barium or other contrast media are usually necessary in the search for a primary tumor. Laboratory abnormalities that are highly suggestive of cirrhosis as the cause of ascites include unexplained thrombocytopenia, decreased albumin, and a prolonged prothrombin time. Ascites The evaluation of a patient with ascites requires that the cause of the ascites be established. In most cases ascites appears as part of a well-recognized illness, i.e., cirrhosis, congestive heart failure, nephrosis, or disseminated carcinomatosis. In these situations, the physician should determine that the development of ascites is indeed a consequence of the basic underlying disease and not due to the presence of a separate or related disease process. This distinction is necessary even when the cause of ascites seems obvious. For example, when the patient with compensated cirrhosis and minimal ascites develops progressive ascites that is increasingly difficult to control with sodium restriction or diuretics, the temptation is to attribute the worsening of the clinical picture to progressive liver disease. However, an occult hepatocellular carcinoma, portal vein thrombosis, spontaneous bacterial peritonitis, alcoholic hepatitis, viral infection, or even tuberculosis may be responsible for the decompensation. The disappointingly low success in diagnosing tuberculous peritonitis or hepatocullar carcinoma in the patient with
cirrhosis and ascites reflects the too-low index of suspicion for the development of such superimposed conditions. Similarly, the patient with congestive heart failure may develop ascites from a disseminated carcinoma with peritoneal seeding. It is important to note, however, that while there are many different causes of ascites, in the United States >80% of cases are due to cirrhosis. Risk factors for the development of cirrhosis include alcoholism, viral hepatitis, nonalcoholic steatohepatitis, and a family history of liver disease. Diagnostic paracentesis (50–100 mL) should be part of the routine evaluation of the patient with ascites, and does not routinely require the prior administration of platelets or fresh-frozen plasma unless disseminated intravascular coagulation is suspected. The fluid should be examined for its gross appearance; protein content, albumin level, cell count, and differential cell count should be determined; and Gram's and acid-fast stains and culture should be performed. Cytologic and cell-block examination may disclose an otherwise unsuspected carcinoma. A serum ascites–albumin gradient (SAAG) should be calculated to determine if the fluid has the features of a transudate or an exudate. The gradient correlates directly with portal pressure. A gradient >1.1 g/dL (high gradient) is characteristic of uncomplicated cirrhotic ascites and differentiates ascites due to portal hypertension from ascites not due to portal hypertension >97% of the time. Other etiologies of high-gradient ascites include alcoholic
hepatitis, congestive heart failure, hepatic metastases, constrictive pericarditis, and Budd-Chiari syndrome.