# 46 - 53 Abdominal Swelling and Ascites

### 53 Abdominal Swelling and Ascites

Jaundice with associated liver dysfunction can be seen in severe 
cases of Plasmodium falciparum malaria. The jaundice in these 
cases is due to a combination of indirect hyperbilirubinemia from 
hemolysis and both cholestatic and hepatocellular jaundice. Weil’s 
disease, a severe presentation of leptospirosis, is marked by jaundice 
with renal failure, fever, headache, and muscle pain.
Causes of extrahepatic cholestasis can be split into malignant 
and benign (Table 52-3). Malignant causes include pancreatic, 
gallbladder, and ampullary cancers as well as cholangiocarci­
noma. This last malignancy is most commonly associated with 
PSC and is exceptionally difficult to diagnose because its appear­
ance is often identical to that of PSC. Pancreatic and gallblad­
der tumors as well as cholangiocarcinoma are rarely resectable 
at the time of diagnosis and have poor prognoses. Ampullary 
carcinoma has the highest surgical cure rate of all the tumors 
that present as painless jaundice. Hilar lymphadenopathy due 
to metastases from other cancers may cause obstruction of the 
extrahepatic biliary tree.
PART 2
Cardinal Manifestations and Presentation of Diseases
Choledocholithiasis is the most common cause of extrahe­
patic cholestasis. The clinical presentation can range from mild 
right-upper-quadrant discomfort with only minimal elevations of 
enzyme test values to ascending cholangitis with jaundice, sepsis, 
and circulatory collapse. PSC may occur with clinically important 
strictures limited to the extrahepatic biliary tree. IgG4-associated 
cholangitis is marked by stricturing of the biliary tree. It is criti­
cal that the clinician differentiate this condition from PSC as it is 
responsive to glucocorticoid therapy. In rare instances, chronic 
pancreatitis causes strictures of the distal common bile duct, 
where it passes through the head of the pancreas. AIDS cholan­
giopathy is a condition that is usually due to infection of the bile 
duct epithelium with CMV or cryptosporidia and has a cholangio­
graphic appearance similar to that of PSC. The affected patients 
usually present with greatly elevated serum alkaline phosphatase 
levels (mean, 800 IU/L), but the bilirubin level is often near nor­
mal. These patients do not typically present with jaundice. Its inci­
dence has dropped dramatically since the introduction of potent 
antiretrovirals in the 1990s.
■
■GLOBAL CONSIDERATIONS
While extrahepatic biliary obstruction and drugs are common causes 
of new-onset jaundice in developed countries, infections remain the 
leading cause in developing countries. Liver involvement and jaundice 
are observed with numerous infections, particularly malaria, babesio­
sis, severe leptospirosis, infections due to Mycobacterium tuberculosis 
and the Mycobacterium avium complex, typhoid fever, infection with 
hepatitis viruses A–E, EBV, CMV, viral hemorrhagic fevers including 
Ebola virus, late phases of yellow fever, dengue fever, schistosomiasis, 
fascioliasis, clonorchiasis, opisthorchiasis, ascariasis, echinococcosis, 
hepatosplenic candidiasis, disseminated histoplasmosis, cryptococ­
cosis, coccidioidomycosis, ehrlichiosis, chronic Q fever, yersiniosis, 
brucellosis, syphilis, and leprosy. Bacterial infections that do not nec­
essarily involve the liver and bile ducts may also lead to jaundice, as 
in cholestasis of sepsis. The presence of fever or abdominal pain sug­
gests concurrent infection, sepsis, or complications from gallstones. 
The development of encephalopathy and coagulopathy in a jaundiced 
patient with no preexisting liver disease signifies acute liver failure, 
which warrants urgent liver transplant evaluation.
■
■FURTHER READING
Erlinger S et al: Inherited disorders of bilirubin transport and conju­
gation: New insights into molecular mechanisms and consequences. 
Gastroenterology 146:1625, 2014.
Wolkoff AW et al: Bilirubin metabolism and jaundice, in Schiff’s 
Diseases of the Liver, 11th ed, Schiff ER et al (eds). Oxford, UK, John 
Wiley & Sons, Ltd, 2012, pp 120–150.

Lawrence S. Friedman

Abdominal Swelling 

and Ascites
ABDOMINAL SWELLING
Abdominal swelling is a manifestation of numerous diseases. Patients 
may complain of bloating or abdominal fullness and may note increas­
ing abdominal girth on the basis of increased clothing or belt size. 
Abdominal discomfort is often reported, but pain is less frequent. 
When abdominal pain does accompany swelling, it is frequently the 
result of an intraabdominal infection, peritonitis, or pancreatitis. 
Patients with abdominal distention from ascites (fluid in the abdomen) 
may report the new onset of an inguinal or umbilical hernia. Dyspnea 
may result from pressure against the diaphragm and the inability to 
expand the lungs fully.
■
■CAUSES
The causes of abdominal swelling can be remembered conveniently 
as the six Fs: flatus, fat, fluid, fetus, feces, or a “fatal growth” (often a 
neoplasm).
Flatus 
Abdominal swelling may be the result of increased intes­
tinal gas. The normal small intestine contains ~200 mL of gas made 
up of nitrogen, oxygen, carbon dioxide, hydrogen, and methane. 
Nitrogen and oxygen are consumed (swallowed), whereas carbon 
dioxide, hydrogen, and methane are produced intraluminally by bacte­
rial fermentation. Increased intestinal gas can occur in a number of 
conditions. Aerophagia, the swallowing of air, can result in increased 
amounts of oxygen and nitrogen in the small intestine and lead to 
abdominal swelling. Aerophagia typically results from gulping food; 
chewing gum; smoking; or as a response to anxiety, which can lead to 
repetitive belching. Celiac disease, or gluten-sensitive enteropathy, and 
gastroparesis may be associated with bloating and distention. In some 
cases, increased intestinal gas is the consequence of bacterial metabo­
lism of excess fermentable substances such as lactose, fructose, and 
other fermentable oligosaccharides, disaccharides, monosaccharides, 
and polyols (FODMAPs), which can lead to production of hydrogen, 
carbon dioxide, or methane, as occurs also in small intestinal bacterial 
overgrowth or intestinal methanogen overgrowth. In some persons, 
particularly those with irritable bowel syndrome and bloating, the 
subjective sense of abdominal pressure is attributable to impaired 
intestinal transit of gas (rather than increased gas volume) or to vis­
ceral hypersensitivity. Abdominal distention—an objective increase in 
girth—may result from a lack of coordination between diaphragmatic 
contraction and anterior abdominal wall relaxation (“abdomino­
phrenic dyssynergia”), a response in some cases to intraluminal bowel 
stimuli; dietary alterations, manipulation of the intestinal microbiota, 
or biofeedback may be effective therapy. Occasionally, increased lum­
bar lordosis accounts for apparent abdominal distention.
Fat 
Weight gain with an increase in abdominal fat can result in an 
increase in abdominal girth and can be perceived as abdominal swell­
ing. Abdominal fat may be caused by an imbalance between caloric 
intake and energy expenditure associated with a poor diet and seden­
tary lifestyle; it also can be a manifestation of certain diseases, such as 
Cushing’s syndrome. Excess abdominal fat has been associated with an 
increased risk of insulin resistance and cardiovascular disease.
Fluid 
The accumulation of fluid within the abdominal cavity (asci­
tes) often results in abdominal distention and is discussed in detail 
below. Grade 1 ascites is detectable only by ultrasonography; grade 2 
ascites is detectable by physical examination; and grade 3 ascites results 
in marked abdominal distention.
Fetus 
Pregnancy results in increased abdominal girth. Typically, an 
increase in abdominal size is first noted at 12–14 weeks of gestation,

when the uterus moves from the pelvis into the abdomen. Abdominal 
distention may be seen before this point as a result of fluid retention 
and relaxation of the abdominal muscles.
Feces 
In the setting of severe constipation or intestinal obstruction, 
increased stool in the colon leads to increased abdominal girth. These 
conditions are often accompanied by abdominal discomfort or pain, 
nausea, and vomiting and can be diagnosed by imaging studies.
Fatal Growth 
An abdominal mass can result in abdominal swelling. 
Neoplasms (including ovarian cancer in women), abscesses, or cysts 
can grow to sizes that lead to increased abdominal girth. Enlargement 
of the intraabdominal organs, specifically the liver (hepatomegaly) or 
spleen (splenomegaly), or an abdominal aortic aneurysm can result in 
abdominal distention. Bladder distention also may result in abdominal 
swelling.
APPROACH TO THE PATIENT
Abdominal Swelling 
HISTORY
Determining the etiology of abdominal swelling begins with 
history-taking and a physical examination. Patients should be 
questioned regarding the onset and timing of bloating and disten­
tion, the relationship to food or bowel movements, prior surgery, 
dietary habits, and medications, as well as symptoms suggestive 
of malignancy, including weight loss, night sweats, and anorexia. 
Inability to pass stool or flatus together with nausea or vomiting 
suggests bowel obstruction, severe constipation, or an ileus (lack of 
peristalsis). Increased eructation and flatus may point toward aero­
phagia or increased intestinal production of gas. Patients should 
be questioned about risk factors for or symptoms of chronic liver 
disease, including excessive alcohol use and jaundice, which sug­
gest ascites. Patients should also be asked about symptoms of other 
medical conditions, including heart failure and tuberculosis, which 
may cause ascites. 
PHYSICAL EXAMINATION
Physical examination should include an assessment for signs of sys­
temic disease. The presence of lymphadenopathy, especially supra­
clavicular lymphadenopathy (Virchow’s node), suggests metastatic 
abdominal malignancy. Care should be taken during the cardiac 
examination to evaluate for elevation of jugular venous pressure 
(JVP); Kussmaul’s sign (elevation of the JVP during inspiration); a 
pericardial knock, which may be seen in constrictive pericarditis 
and heart failure; or a murmur of tricuspid regurgitation. Spider 
angiomas, palmar erythema, dilated superficial veins around the 
umbilicus (caput medusae), and gynecomastia suggest liver disease.
The abdominal examination should begin with inspection for 
the presence of uneven distention or an obvious mass. Auscultation 
should follow. The absence of bowel sounds or the presence of highpitched localized bowel sounds points toward an intestinal obstruc­
tion or ileus. An umbilical venous hum may suggest the presence of 
portal hypertension, and a harsh bruit over the liver is heard rarely in 
patients with hepatocellular carcinoma or alcohol-associated hepatitis. 
Abdominal swelling caused by intestinal gas can be differentiated 
from swelling caused by fluid or a solid mass by percussion; an 
abdomen filled with gas is tympanic, whereas an abdomen contain­
ing a mass or fluid is dull to percussion. The absence of abdominal 
dullness, however, does not exclude ascites, because a minimum of 
1500 mL of ascitic fluid is required for detection on physical exami­
nation. The abdomen should be palpated to assess for tenderness, 
a mass, enlargement of the spleen or liver, or presence of a nodular 
liver suggesting cirrhosis or tumor. Light palpation of the liver may 
detect pulsations suggesting retrograde vascular flow from the heart 
in patients with right-sided heart failure, particularly tricuspid 
regurgitation. A rectal examination may help identify an evacuation 
disorder in patients with constipation.

Abdominal Swelling and Ascites 
CHAPTER 53
FIGURE 53-1  CT of a patient with a cirrhotic, nodular liver (white arrow), 
splenomegaly (yellow arrow), and ascites (arrowheads).
■
■IMAGING AND LABORATORY EVALUATION
Abdominal x-rays can be used to detect dilated loops of bowel suggest­
ing intestinal obstruction or ileus. Motility studies may be considered 
in patients with severe constipation. Abdominal ultrasonography can 
detect as little as 100 mL of ascitic fluid, hepatosplenomegaly, a nodular 
liver, or a mass. Ultrasonography is often inadequate to detect retro­
peritoneal lymphadenopathy or a pancreatic lesion because of overly­
ing bowel gas. If malignancy or pancreatic disease is suspected, CT can 
be performed. CT may also detect changes associated with advanced 
cirrhosis and portal hypertension (Fig. 53-1).
Laboratory evaluation should include liver biochemical testing, 
serum albumin level measurement, and prothrombin time determina­
tion (international normalized ratio) to assess hepatic function as well 
as a complete blood count to evaluate for the presence of cytopenias 
that may result from portal hypertension or of leukocytosis, anemia, 
and thrombocytosis that may result from systemic infection. Serum 
amylase and lipase levels should be checked to evaluate the patient 
for acute pancreatitis. Urinary protein quantitation is indicated when 
nephrotic syndrome, which may cause ascites, is suspected. Hydrogen 
and methane absorbed from the intestine are not metabolized by 
the host and are excreted in expired air, and detection of increased 
amounts of these gases in expired breath is the basis for tests used to 
diagnose carbohydrate (e.g., lactose) malabsorption and small intes­
tinal bacterial overgrowth, although the reliability of the test results 
for the diagnosis of small intestinal bacterial overgrowth has been 
questioned.
In selected cases, the hepatic venous pressure gradient (pressure 
across the liver between the portal and hepatic veins) can be measured 
via cannulation of the hepatic vein to confirm that ascites is caused by 
cirrhosis. In some cases, noninvasive tests for liver fibrosis, including 
liver stiffness measurement by elastography, or a liver biopsy may be 
necessary to confirm cirrhosis (Chap. 355).
ASCITES
■
■PATHOGENESIS IN THE PRESENCE OF CIRRHOSIS
Ascites in patients with cirrhosis is the result of portal hypertension 
and renal salt and water retention. Similar mechanisms contribute to 
ascites formation in heart failure. Portal hypertension signifies eleva­
tion of the pressure within the portal vein. According to Ohm’s law,

pressure is the product of resistance and flow. Increased hepatic resis­
tance occurs by several mechanisms. First, the development of hepatic 
fibrosis, which defines cirrhosis, disrupts the normal architecture of 
the hepatic sinusoids and impedes normal blood flow through the liver. 
Second, activation of hepatic stellate cells, which mediate fibrogenesis, 
leads to smooth-muscle contraction and fibrosis. Finally, cirrhosis 
is associated with a decrease in endothelial nitric oxide synthetase 
(eNOS) production, which results in decreased nitric oxide production 
and increased intrahepatic vasoconstriction.

The development of cirrhosis is also associated with increased 
systemic circulating levels of nitric oxide (in contrast to the decrease 
seen intrahepatically), as well as increased levels of vascular endothe­
lial growth factor and tumor necrosis factor, that result in splanchnic 
arterial vasodilation. Vasodilation of the splanchnic circulation results 
in pooling of blood and a decrease in the effective circulating volume, 
which is perceived by the kidneys as hypovolemia. Compensatory 
vasoconstriction via release of antidiuretic hormone ensues; the con­
sequences are free water retention and activation of the sympathetic 
nervous system and the renin-angiotensin-aldosterone system, which 
lead in turn to renal sodium and water retention.
PART 2
Cardinal Manifestations and Presentation of Diseases
■
■PATHOGENESIS IN THE ABSENCE OF CIRRHOSIS
Ascites in the absence of cirrhosis generally results from peritoneal 
carcinomatosis, peritoneal infection, pancreatic disease, or marked 
hypoalbuminemia. Peritoneal carcinomatosis can result from primary 
peritoneal malignancies such as mesothelioma or sarcoma, abdominal 
malignancies such as gastric or colonic adenocarcinoma, or metastatic 
disease from breast or lung carcinoma or melanoma (Fig. 53-2). The 
tumor cells lining the peritoneum produce a protein-rich fluid that 
contributes to the development of ascites. Fluid from the extracellular 
space is drawn into the peritoneum, further contributing to the devel­
opment of ascites. Tuberculous peritonitis causes ascites via a similar 
mechanism; tubercles deposited on the peritoneum exude a protein­
aceous fluid. Pancreatic ascites results from leakage of pancreatic 
enzymes into the peritoneum. Marked hypoalbuminemia may result 
from nephrotic syndrome, protein-losing enteropathy, or malnutrition.
■
■CAUSES
Cirrhosis accounts for 84% of cases of ascites. Cardiac ascites, perito­
neal carcinomatosis, and “mixed” ascites resulting from cirrhosis and 
a second disease account for 10–15% of cases. Less common causes 
of ascites include massive hepatic metastasis, infection (tuberculo­
sis, Chlamydia infection), pancreatitis, and renal disease (nephrotic 
FIGURE 53-2  CT of a patient with peritoneal carcinomatosis (white arrow) and 
ascites (yellow arrow).

syndrome). Rare causes of ascites include hypothyroidism and familial 
Mediterranean fever.
■
■EVALUATION
Once the presence of ascites has been confirmed, the etiology of the 
ascites is best determined by paracentesis, a bedside procedure in which 
a needle or small catheter is passed transcutaneously to extract ascitic 
fluid from the peritoneum. The lower quadrants are the most frequent 
sites for paracentesis. The left lower quadrant is preferred because of 
the greater depth of ascites and the thinner abdominal wall. Paracen­
tesis is a safe procedure even in patients with coagulopathy; complica­
tions, including abdominal wall hematomas, hypotension, hepatorenal 
syndrome, and infection, are infrequent.
Once ascitic fluid has been extracted, its gross appearance should 
be examined. Turbid fluid can result from the presence of infection or 
tumor cells. White, milky fluid indicates a triglyceride level >200 mg/
dL (and often >1000 mg/dL), which is the hallmark of chylous ascites. 
Chylous ascites results from lymphatic disruption that may occur with 
trauma, cirrhosis, tumor, tuberculosis, or certain congenital abnor­
malities. Dark brown fluid can reflect a high bilirubin concentration 
and indicates biliary tract perforation. Black fluid may indicate the 
presence of pancreatic necrosis or metastatic melanoma.
The ascitic fluid should be sent for measurement of albumin and 
total protein levels, cell and differential counts, and, if infection is sus­
pected, Gram’s stain and culture, with inoculation into blood culture 
bottles at the patient’s bedside to maximize the yield. A serum albumin 
level should be measured simultaneously to permit calculation of the 
serum-ascites albumin gradient (SAAG).
The SAAG is useful for distinguishing ascites caused by portal 
hypertension from nonportal hypertensive ascites (Fig. 53-3). The 
SAAG reflects the pressure within the hepatic sinusoids and correlates 
with the hepatic venous pressure gradient. The SAAG is calculated by 
subtracting the ascitic albumin concentration from the serum albumin 
level and does not change with diuresis. A SAAG ≥1.1 g/dL reflects the 
presence of portal hypertension and indicates that the ascites is due 
to increased pressure in the hepatic sinusoids. According to Starling’s 
law, a high SAAG reflects the oncotic pressure that counterbalances 
the portal pressure. Possible causes include cirrhosis, cardiac ascites, 
hepatic vein thrombosis (Budd-Chiari syndrome), sinusoidal obstruc­
tion syndrome (veno-occlusive disease), or massive liver metastases. 
A SAAG <1.1 g/dL indicates that the ascites is not related to portal 
hypertension, as in tuberculous peritonitis, peritoneal carcinomatosis, 
pancreatic ascites, or nephrotic syndrome.
For high-SAAG (≥1.1) ascites, the ascitic protein level can provide 
further clues to the etiology (Fig. 53-3). An ascitic protein level 
of ≥2.5 g/dL indicates that the hepatic sinusoids are normal and are 
allowing passage of protein into the ascites, as occurs in cardiac ascites, 
early Budd-Chiari syndrome, or sinusoidal obstruction syndrome. 
An ascitic protein level <2.5 g/dL indicates that the hepatic sinusoids 
have been damaged and scarred and no longer allow passage of protein, 
as occurs with cirrhosis, late Budd-Chiari syndrome, or massive liver 
metastases. Pro-brain-type natriuretic peptide (BNP) is a natriuretic 
hormone released by the heart as a result of increased volume and 
ventricular wall stretch. High levels of BNP in serum occur in heart 
failure and may be useful in identifying heart failure as the cause of 
high-SAAG ascites.
Further tests are indicated only in specific clinical circumstances. 
When secondary peritonitis resulting from a perforated hollow viscus 
is suspected, ascitic glucose and lactate dehydrogenase (LDH) levels 
can be measured. In contrast to “spontaneous” bacterial peritonitis, 
which may complicate cirrhotic ascites (see “Complications,” below), 
secondary peritonitis is suggested by an ascitic glucose level <50 mg/
dL, an ascitic LDH level higher than the serum LDH level, and the 
detection of multiple pathogens on ascitic fluid culture. When pancre­
atic ascites is suspected, the ascitic amylase level should be measured 
and is typically >1000 mg/dL. Cytology can be useful in the diagnosis 
of peritoneal carcinomatosis. At least 50 mL of fluid should be obtained 
and sent for immediate processing. Tuberculous peritonitis is typi­
cally associated with ascitic fluid lymphocytosis but can be difficult to

≥1.1 g/dL
Ascitic protein <2.5 g/dL
Heart failure/constrictive
pericarditis
Cirrhosis
Late Budd-Chiari syndrome
Early Budd-Chiari syndrome
Massive liver metastases
IVC obstruction
Sinusoidal obstruction
syndrome
FIGURE 53-3  Algorithm for the diagnosis of ascites according to the serum-ascites albumin gradient (SAAG). IVC, inferior vena cava.
diagnose by paracentesis. A smear for acid-fast bacilli has a diagnostic 
sensitivity of only 0–3%; a culture increases the sensitivity to 35–50%. 
In patients without cirrhosis, an elevated ascitic adenosine deaminase 
level has a sensitivity of >90% for tuberculous ascites when a cut-off 
value of 30–45 U/L is used. When the cause of ascites remains uncer­
tain, laparotomy or laparoscopy with peritoneal biopsies for histology 
and culture remains the gold standard.
TREATMENT
Ascites
The initial treatment for cirrhotic ascites is moderate restriction 
of sodium intake to 2 g/d. When sodium restriction alone is inad­
equate to control ascites, oral diuretics—typically the combination 
of spironolactone and furosemide—are used to increase urinary 
sodium excretion. Spironolactone is an aldosterone antagonist 
that inhibits sodium resorption in the distal convoluted tubule 
of the kidney. Use of spironolactone may be limited by hypona­
tremia, hyperkalemia, and painful gynecomastia. If the gyneco­
mastia is distressing, amiloride (5–40 mg/d) may be substituted 
for spironolactone. Furosemide is a loop diuretic that is generally 
combined with spironolactone in a ratio of 40:100; maximal daily 
doses of spironolactone and furosemide are generally 400 mg and 
160 mg, respectively. Fluid intake may be restricted in patients 
with hyponatremia (serum sodium <125 mEq/L). Nonsteroidal 
anti-inflammatory drugs, angiotensin-converting enzyme inhibi­
tors, and angiotensin receptor blockers should be avoided in 
patients with cirrhosis and ascites.
Refractory cirrhotic ascites is defined by the persistence of asci­
tes despite sodium restriction and maximum diuretic use (diuretic 
resistant) or the development of side effects of diuretics that 
preclude the use of maximum doses (diuretic intractable). Phar­
macologic therapy for refractory ascites includes the addition of 
midodrine, an α1-adrenergic agonist, or clonidine, an α2-adrenergic 
agonist, to diuretic therapy. These agents act as vasoconstrictors, 
counteracting splanchnic vasodilation. Midodrine alone or in com­
bination with clonidine improves systemic hemodynamics and 
control of ascites over that obtained with diuretics alone. Although 
β-adrenergic blocking agents (beta blockers) are often prescribed 
to prevent variceal hemorrhage in patients with cirrhosis, the use of 
beta blockers in patients with refractory ascites may be associated 
with decreased survival rates.
When medical therapy alone is insufficient, refractory cirrhotic 
ascites can be managed by repeated large-volume (>5 L) paracente­
sis (LVP) or a transjugular intrahepatic peritoneal shunt (TIPS)—a 
radiologically placed portosystemic shunt that decompresses the 
hepatic sinusoids. Intravenous (IV) infusion of albumin accom­
panying LVP decreases the risk of “postparacentesis circulatory 
dysfunction” and death. Patients undergoing LVP should receive IV 

SAAG
<1.1 g/dL
Ascitic protein ≥2.5 g/dL
Biliary leak
Abdominal Swelling and Ascites 
CHAPTER 53
Nephrotic syndrome
Pancreatitis
Peritoneal carcinomatosis
Tuberculosis
albumin infusions of 6–8 g/L of ascitic fluid removed. TIPS place­
ment is superior to LVP in reducing the reaccumulation of ascites 
but is associated with an increased frequency of hepatic encepha­
lopathy, with no difference in mortality rates. The Alfapump sys­
tem, which consists of an automated pump and tunneled peritoneal 
catheter that transports ascites from the peritoneal cavity to the 
urinary bladder, has shown promise in the management of refrac­
tory ascites but is associated with a high frequency of technical 
difficulties and renal dysfunction.
Malignant ascites does not respond to sodium restriction or 
diuretics. Patients must undergo serial LVPs, transcutaneous drain­
age catheter placement, or, rarely, creation of a peritoneovenous 
shunt (a shunt from the abdominal cavity to the vena cava) or place­
ment of the Alfapump system, if available.
Ascites caused by tuberculous peritonitis is treated with standard 
antituberculosis therapy. Noncirrhotic ascites of other causes is 
treated by correction of the precipitating condition.
■
■COMPLICATIONS
Spontaneous bacterial peritonitis (SBP; Chap. 137) is a common and 
potentially lethal complication of cirrhotic ascites. Occasionally, SBP 
also complicates ascites caused by nephrotic syndrome, heart failure, 
acute hepatitis, and acute liver failure but is rare in malignant asci­
tes. Patients with SBP generally note an increase in abdominal girth; 
however, abdominal tenderness is found in only 40% of patients, and 
rebound tenderness is uncommon. Patients may present with fever, 
nausea, vomiting, or the new onset or an exacerbation of preexisting 
hepatic encephalopathy.
In hospitalized patients with ascites, paracentesis within 12 hours 
of admission reduces mortality because of early detection of SBP. SBP 
is defined by a polymorphonuclear neutrophil (PMN) count of ≥250/
μL in the ascitic fluid. Cultures of ascitic fluid should be performed 
in blood culture bottles and typically reveal one bacterial pathogen. 
The presence of multiple pathogens in the setting of an elevated ascitic 
PMN count suggests secondary peritonitis from a ruptured viscus or 
abscess (Chap. 137). The presence of multiple pathogens without an 
elevated PMN count suggests bowel perforation from the paracentesis 
needle. SBP is generally the result of enteric bacteria that have translo­
cated across an edematous bowel wall. The most common pathogens 
are gram-negative rods, including Escherichia coli and Klebsiella, as well 
as streptococci and enterococci.
Treatment of SBP has traditionally been with a third-generation 
cephalosporin such as IV cefotaxime, 2 g every 12 hours, and is gen­
erally effective against gram-negative and gram-positive aerobes. A 
5-day course of treatment is sufficient if the patient improves clini­
cally. Repeat paracentesis is recommended after 48 hours of antibiotic 
therapy to confirm that the ascitic PMN count has decreased by at 
least 25% from baseline. Increasingly, SBP, particularly if nosocomial 
or health care–acquired, is caused by multidrug-resistant bacteria, and