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 cell-
block 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, right-
sided 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.