Abdominal Swelling And Ascites

ABDOMINAL SWELLING AND ASCITES ABDOMINAL SWELLING Abdominal swelling or distention is a common problem in clinical medicine and may be the initial manifestation of a systemic disease or of otherwise unsuspected abdominal disease. Subjective abdominal enlargement, often described as a sensation of fullness or bloating, is usually transient and is often related to a functional gastrointestinal disorder when it is not accompanied by objective physical findings of increased abdominal girth or local swelling. Obesity and lumbar lordosis, which may be associated with prominence of the abdomen, may usually be distinguished from true increases in the volume of the peritoneal cavity by history and careful physical examination. Clinical History Abdominal swelling may first be noticed by the patient because of a progressive increase in belt or clothing size, the appearance of abdominal or inguinal hernias, or the development of a localized swelling. Often, considerable abdominal enlargement has gone unnoticed for weeks or months, either because of coexistent obesity or because the ascites formation has been insidious, without pain or localizing symptoms. Progressive abdominal distention may be associated with a sensation of "pulling" or "stretching" of the flanks or groins and vague low back pain. Localized pain usually results from involvement of an abdominal organ (e.g., a passively congested liver, large spleen, or colonic tumor). Pain is uncommon in cirrhosis with ascites, and when it is present, pancreatitis, hepatocellular carcinoma, or peritonitis should be considered. Tense ascites or abdominal tumors may produce increased intraabdominal pressure, resulting in indigestion and heartburn due to gastroesophageal reflux or dyspnea, orthopnea, and tachypnea from elevation of the diaphragm. A coexistent pleural effusion, more commonly on the right, presumably due to leakage of ascitic fluid through lymphatic channels in the diaphragm, also may contribute to respiratory embarrassment. The patient with diffuse abdominal swelling should be questioned about increased alcohol intake, a prior episode of jaundice or hematuria, or a change in bowel habits. Such historical information may provide the clues that will lead one to suspect an occult cirrhosis, a colonic tumor with peritoneal seeding, congestive heart failure, or nephrosis. Physical Examination A carefully executed general physical examination can yield valuable clues concerning the etiology of abdominal swelling. Thus palmar erythema and spider angiomas suggest an underlying cirrhosis, while supraclavicular adenopathy (Virchow's node) should raise the question of an underlying gastrointestinal malignancy.

Inspection of the abdomen is important. By noting the abdominal contour, one may be able to distinguish localized from generalized swelling. The tensely distended abdomen with tightly stretched skin, bulging flanks, and everted umbilicus is characteristic of ascites. A prominent abdominal venous pattern with the direction of flow away from the umbilicus often is a reflection of portal hypertension; venous collaterals with flow from the lower part of the abdomen toward the umbilicus suggest obstruction of the inferior vena cava; flow downward toward the umbilicus suggests superior vena cava obstruction. "Doming" of the abdomen with visible ridges from underlying intestinal loops is usually due to intestinal obstruction or distention. An epigastric mass, with evident peristalsis proceeding from left to right, usually indicates underlying pyloric obstruction. A liver with metastatic deposits may be visible as a nodular right upper quadrant mass moving with respiration. Auscultation may reveal the high-pitched, rushing sounds of early intestinal obstruction or a succussion sound due to increased fluid and gas in a dilated hollow viscus. Careful auscultation over an enlarged liver occasionally reveals the harsh bruit of a vascular tumor, especially a hepatocellular carcinoma, or the

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leathery friction rub of a surface nodule. A venous hum at the umbilicus may signify portal hypertension and an increased collateral blood flow around the liver. A fluid wave and flank dullness that shifts with change in position of the patient are important signs that indicate the presence of peritoneal fluid. In obese patients, small amounts of fluid may be difficult to demonstrate; on occasion, the fluid may be detected by abdominal percussion with patients on their hands and knees. Small amounts of ascites often can only be detected by ultrasound examination of the abdomen. Careful percussion should serve to distinguish generalized abdominal enlargement from localized swelling due to an enlarged uterus, ovarian cyst, or distended bladder. Percussion also can outline an abnormally small or large liver. Loss of normal liver dullness may result from massive hepatic necrosis; it also may be a clue to free gas in the peritoneal cavity, as from perforation of a hollow viscus.

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. Computed tomography (CT) scanning provides similar information. CT scanning 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. ASCITES The evaluation of a patient with ascites requires that the cause of the ascites be established. In most cases ascites will appear as a 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

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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 obvious 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, 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. Diagnostic paracentesis (50 to 100 mL) should be part of the routine evaluation of the patient with ascites. The fluid should be examined for its gross appearance; protein content, cell count, and differential cell count should be determined, and Gram's and acid-fast stains and culture performed. Cytologic and cellblock examination may disclose an otherwise unsuspected carcinoma. Table 46-1 presents some of the features of ascitic fluid typically found in various disease states. In some disorders, such as cirrhosis, the fluid has the characteristics of a transudate (<25 g protein per liter and a specific gravity of <1.016); in others, such as peritonitis, the features are those of an exudate. Rather than the total protein content of ascites, some authors prefer the use of a serum-ascites albumin gradient (SAG) to characterize ascites. The gradient correlates directly with portal pressure. A gradient >1.1 g/dL is characteristic of uncomplicated cirrhotic ascites; a gradient <1.1 g/dL is seen in conditions characterized by exudative ascites. Although there is variability of the ascitic fluid in any given disease state, some features are sufficiently characteristic to suggest certain diagnostic possibilities. For example, blood-stained fluid with >25 g protein per liter is unusual in uncomplicated cirrhosis but is consistent with tuberculous peritonitis or neoplasm. Cloudy fluid with a predominance of polymorphonuclear cells and a positive Gram's stain are characteristic of bacterial peritonitis; if most cells are lymphocytes, tuberculosis should be suspected. The complete examination of each fluid is most important, for occasionally only one finding may be abnormal. For example, if the fluid is a typical transudate but contains more than 250 white blood cells per microliter, the finding should be recognized as atypical for cirrhosis and should warrant a search for tumor or infection. This is especially true in the evaluation of cirrhotic ascites where occult peritoneal infection may be present with only minor elevations in the white blood cell count of the peritoneal fluid (300 to 500 cells per microliter). Since Gram's stain of the fluid may be negative in a high proportion of such cases, careful culture of the peritoneal fluid is mandatory. Bedside innoculation of blood culture flasks with ascitic fluid results in a dramatically increased incidence of positive cultures when bacterial infection is present (90 versus 40 percent positivity with conventional cultures done by the laboratory). Direct visualization of the peritoneum (laparoscopy) may disclose peritoneal deposits of tumor, tuberculosis, or metastatic disease of the liver. Biopsies are taken under direct vision, often adding to the diagnostic accuracy of the procedure.

Chylous ascites refers to a turbid, milky, or creamy peritoneal fluid due to the presence of thoracic or intestinal lymph. Such a fluid shows Sudan-staining fat globules microscopically and an increased triglyceride content by chemical examination. Opaque milky fluid usually has a triglyceride concentration of >1000 mg/dL. A turbid fluid due to leukocytes or tumor cells may be confused with chylous fluid (pseudochylous), and it is often helpful to carry out alkalinization and ether extraction of the specimen. Alkali will tend to dissolve cellular proteins and thereby reduce turbidity; ether extraction will lead to clearing if the turbidity of the fluid is due to lipid. Chylous ascites is most often the result of lymphatic obstruction from trauma, tumor, tuberculosis, filariasis (see Chap. 223), or congenital abnormalities. It also may be seen in the nephrotic syndrome.

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Rarely, ascitic fluid may be mucinous in character, suggesting either pseudomyxoma peritonei (Chap. 288) or rarely a colloid carcinoma of the stomach or colon with peritoneal implants. On occasion, ascites may develop as a seemingly isolated finding in the absence of a clinically evident underlying disease. It is then that a careful analysis of ascitic fluid may indicate the direction the evaluation should take. A useful framework for the workup starts with an analysis of whether the fluid is an exudate or transudate. Transudative ascites of unclear etiology is most often due to occult cirrhosis, rightsided venous hypertension raising hepatic sinusoidal pressure, or hypoalbuminemic states such as nephrosis or protein-losing enteropathy. Cirrhosis with well-preserved liver function (normal albumin) resulting in ascites invariably is associated with significant portal hypertension (see Chap. 298). Evaluation should include liver function tests, liver-spleen scan, or other hepatic imaging procedure (i.e., CT or ultrasound) to detect nodular changes in the liver or a colloid shift of isotope to suggest portal hypertension. On occasion, a wedged hepatic venous pressure can be useful to document portal hypertension. Finally, if clinically indicated, a liver biopsy will confirm the diagnosis of cirrhosis and perhaps suggest its etiology. Other etiologies may result in hepatic venous congestion and resultant ascites. Right-sided cardiac valvular disease and particularly constrictive pericarditis should raise a high index of suspicion and may require cardiac imaging and cardiac catheterization for definitive diagnosis. Hepatic vein thrombosis is evaluated by visualizing the hepatic veins using imaging techniques (Doppler ultrasound, angiography, CT scans, magnetic resonance imaging) to demonstrate obliteration, thrombosis, or obstruction by tumor. Uncommonly, transudative ascites may be associated with benign tumors of the ovary, particularly fibroma (Meigs' syndrome) with ascites and hydrothorax.

Exudative ascites should initiate an evaluation for primary peritoneal processes, most importantly infection and tumor. Routine bacteriologic culture of ascitic fluid often will yield a specific organism causing infectious peritonitis. Tuberculous peritonitis (see Table 46-1) is best diagnosed by peritoneal biopsy, either percutaneously or via laparoscopy. Histologic examination invariably shows granulomata that may contain acid-fast bacilli. Since cultures of peritoneal fluid and biopsies for tuberculosis may require 6 weeks, characteristic histology with appropriate stains allows antituberculosis therapy to be started promptly. Similarly, the diagnosis of peritoneal seeding by tumor can usually be made by cytologic analysis of peritoneal fluid or by peritoneal biopsy if cytology is negative. Appropriate diagnostic studies can then be undertaken to determine the nature and site of the primary tumor. Pancreatic ascites (see Table 46-1) is invariably associated with an extravasation of pancreatic fluid from the pancreatic ductal system, most commonly from a leaking pseudocyst. Ultrasound or CT examination of the pancreas followed by visualization of the pancreatic duct by direct cannulation (viz., endoscopic retrograde cholangiopancreatography, ERCP) will usually disclose the site of leakage and permit resective surgery to be carried out. An analysis of the physiologic and metabolic factors involved in the production of ascites (see Chap. 298 for details), coupled with a complete evaluation of the nature of the ascitic fluid, will invariably disclose the etiology of the ascites and permit appropriate therapy to be instituted.

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