Ascites occurs in the setting of cirrhosis as a result of the sequence of events detailed in Figure 91-1. The most recent theory of ascitic fluid formation, the “peripheral arterial vasodilation hypothesis,” proposes that both older hypotheses, the underfill and overflow theories, are correct, but that each is operative at a different stage.¹ The first abnormality that develops appears to be portal hypertension. Portal pressure increases above a critical threshold, and circulating nitric oxide levels increase. Nitric oxide leads to vasodilatation. As the state of vasodilatation worsens, plasma levels of vasoconstrictor, sodium-retentive hormones increase, renal function deteriorates, and ascitic fluid forms—that is, decompensation occurs.

Figure 91-1. Pathogenesis of ascites in the setting of cirrhosis. PHT, portal hypertension.

In the setting of volume overload in a patient with cirrhosis and ascites, the explanation for the neurohumoral excitation, which is characteristic of volume depletion, may relate to volume sensors. Animals have sophisticated systems for detecting and preserving vascular perfusion pressures and intravascular osmolality. An organism’s ability to detect changes in intravascular volume (especially volume overload) is limited, however, and is linked to pressure receptors. This observation may explain, in part, the paradox of dramatic volume overload in the face of sympathetic nervous traffic and hormone levels that are indicative of intravascular volume depletion.

NONCIRRHOTIC ASCITES

The mechanism of fluid retention in patients with malignancy-related ascites depends on the location of the tumor. Peritoneal carcinomatosis appears to cause ascites through the production of proteinaceous fluid by tumor cells lining the peritoneum. Extracellular fluid enters the peritoneal cavity to reestablish oncotic balance. Fluid accumulates in patients with massive liver metastases because of portal hypertension caused by stenosis or occlusion of portal veins by tumor nodules or tumor emboli.² In patients with hepatocellular carcinoma, ascites arises because of the underlying cirrhosis-related portal hypertension, tumor-induced portal vein thrombosis, or both. Chylous ascites in patients with malignant lymphoma appears to be caused by lymph node obstruction by tumor and rupture of chyle-containing lymphatics.

Ascites can complicate high-output or low-output heart failure or nephrotic syndrome. As in cirrhosis, effective arterial blood volume appears to be decreased, and the vasopressin, renin-aldosterone, and sympathetic nervous systems are activated.³ These changes lead to renal vasoconstriction and sodium and water retention. Fluid then “weeps” from the congested hepatic sinusoids as lymph, as in cirrhotic ascites. Tuberculosis, Chlamydia infection, and coccidioidomycosis probably cause ascites through the production of proteinaceous fluid, as in peritoneal carcinomatosis. Spontaneous bacterial peritonitis does not appear to cause fluid to accumulate; infection develops only in preexisting ascites.

In patients with pancreatic or biliary ascites, fluid accumulates by leakage of pancreatic juice or bile into the peritoneal cavity or forms secondary to a “chemical burn” of the peritoneum. After abdominal surgery, especially extensive retroperitoneal dissection, lymphatics may be transected and may leak lymph for varying amounts of time. The mechanism of development of ascites in this condition is similar to that for malignant chylous ascites, namely, lymphatic leak.

CLINICAL FEATURES

HISTORY

Most patients (approximately 85%) with ascites in the United States have cirrhosis. The three most common causes of cirrhosis are excess alcohol use, chronic hepatitis C, and nonalcoholic steatohepatitis (NASH) related in many cases to obesity. As the obesity epidemic evolves, NASH could become the most common cause of cirrhosis. Many patients have two of these conditions, and some have all three.⁴ In approximately 15% of patients with ascites, a nonhepatic cause of fluid retention is identified (Table 91-1).

Table 91-1 Causes of Ascites

CAUSE	%
Cirrhosis (with or without infection)	85
Miscellaneous portal hypertension-related disorder (including 5% with two causes)	8
Cardiac disease	3
Peritoneal carcinomatosis	2
Miscellaneous nonportal hypertension-related disorders	2

Data from Runyon BA, Montano AA, Akriviadis EA, et al. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med 1992; 117:215-20.

Ascites frequently develops during a patient’s first episode of decompensation of alcoholic liver disease. Ascites can develop early in alcoholic liver disease in the precirrhotic, alcoholic hepatitis stage. At this stage, portal hypertension and the resulting predisposition to sodium retention are reversible with abstinence from alcohol. Patients with precirrhotic alcoholic liver disease may lose their predisposition to fluid retention when they reduce or cease consumption of alcohol.

Evidence is accumulating that cirrhosis unrelated to alcohol use can also be reversible with effective therapy.⁵ Whether a decompensated cirrhotic liver can revert to a normal liver, however, remains to be seen. Many patients with cirrhosis and ascites will ultimately require liver transplantation.

Patients with ascites should be questioned about risk factors for liver disease other than alcohol, such as injection drug use, blood transfusions, sex with a same-gender partner, acupuncture, tattoos, ear piercing, and country of origin. Commonly, the cause of ascites in a middle-aged or elderly woman is viral hepatitis–induced cirrhosis resulting from a remote, often forgotten blood transfusion. Another cause of “cryptogenic” cirrhosis and ascites is NASH from long-standing obesity.⁶ Many patients who have been obese will spontaneously lose 50 or even 100 pounds after their liver disease decompensates. Unless the patient is questioned about lifetime maximum body weight and usual adult body weight, the possibility of NASH-related cirrhosis may not be considered. With careful history-taking and appropriate laboratory testing, the percentage of patients with cirrhosis who are now labeled cryptogenic is approaching zero.⁶

Patients with a long history of stable cirrhosis and the sudden development of ascites should be suspected of harboring a hepatocellular carcinoma that has precipitated the decompensation. Patients with ascites who have a history of cancer should be suspected of having malignancy-related ascites. Cancer in the past, however, does not guarantee a malignant cause of ascites. For example, patients with tobacco-related lung cancer and a history of alcohol abuse may have ascites due to cirrhosis. Breast, lung, colon, and pancreatic cancers are regularly complicated by ascites.² Abdominal pain is a helpful distinguishing feature. Malignancy-related ascites frequently is painful, whereas cirrhotic ascites usually is not, unless bacterial peritonitis or alcoholic hepatitis is superimposed.

A history of heart failure may raise the possibility of cardiac ascites. Alcoholic patients in whom ascites develops may have alcoholic cardiomyopathy or alcoholic liver disease, but usually not both.

Tuberculous peritonitis usually manifests as fever and abdominal pain. Many affected patients are recent immigrants from an endemic area. In the United States, more than one half of the patients with tuberculous peritonitis have underlying alcoholic cirrhosis, which may contribute to the formation of ascitic fluid.

Ascites may occur in patients with acute pancreatitis with necrosis or a ruptured pancreatic duct from chronic pancreatitis or trauma. Often troublesome ascites also may develop in a small percentage of patients undergoing hemodialysis. Fitz-Hugh–Curtis syndrome caused by Chlamydia or gonorrhea may cause inflammatory ascites in a sexually active woman. Patients in whom ascites and anasarca develop in the setting of diabetes mellitus should be suspected of having nephrotic ascites. Ascites in a patient with symptoms and signs of myxedema should prompt assessment of thyroid function. Serositis in a patient with a connective tissue disease may be complicated by ascites.⁷

PHYSICAL EXAMINATION

On the basis of the history and the appearance of the abdomen, the diagnosis of ascites is readily suspected and usually confirmed easily on physical examination. The presence of a full, bulging abdomen should lead to percussion of the flanks. If the degree of flank dullness is greater than usual (i.e., if the percussed air-fluid level is higher than that normally found on the lateral aspect of the abdomen with the patient supine), the examiner should check for “shifting.” If flank dullness is absent, checking for shifting is unnecessary. Approximately 1500 mL of fluid must be present before dullness is detected.⁸ If flank dullness is not present, the chance that the patient has ascites is less than 10%.⁸ A fluid wave is not worth testing for.⁸

Gaseous distention of the bowel, a thick panniculus, and an ovarian mass can mimic ascites. Gaseous distention should be readily apparent on percussion. Ovarian masses usually cause tympanitic flanks with central dullness. Also, the speed of increase in abdominal girth can be helpful; ascites develops in days to weeks, whereas thickening of omentum and panniculus takes months to years. An obese abdomen may be diffusely dull to percussion, and abdominal ultrasonography may be required to determine if fluid is present. Ultrasonography can detect as little as 100 mL of fluid in the abdomen.⁹

The presence of palmar erythema, large pulsatile spider angiomata, large abdominal wall collateral veins, or fetor hepaticus is suggestive of parenchymal liver disease and portal hypertension. The presence of large veins on the patient’s back suggests inferior vena cava blockage. An immobile mass in the umbilicus, the Sister Mary Joseph nodule, is suggestive of peritoneal carcinomatosis.

The neck veins of patients with ascites should always be examined. Alcoholic cardiomyopathy with cardiac ascites can mimic cirrhosis with ascites; an elevated jugular venous pressure helps with this aspect of the differential diagnosis. Constrictive pericarditis is one of the few curable causes of ascites. Most patients with cardiac ascites have impressive jugular venous distention. Some have no visible jugular venous distention but such high central venous pressures that their bulging forehead veins rise to the top of their skulls. When present, peripheral edema in patients with liver disease is usually found in the lower extremities and occasionally may involve the abdominal wall. Patients with nephrotic syndrome or cardiac failure may have total body edema (anasarca).

DIAGNOSIS

Although the diagnosis of ascites may be suspected on the basis of the history and physical examination, final confirmation is based on successful abdominal paracentesis or detection of ascites on imaging. Determination of the cause of ascites is based on the results of the history, physical examination, and ascitic fluid analysis. In general, few other tests are required.

ABDOMINAL PARACENTESIS

Indications

Abdominal paracentesis with appropriate ascitic fluid analysis is probably the most rapid and cost-effective method of diagnosing the cause of ascites. Also, because of the possibility of ascitic fluid infection in a cirrhotic patient admitted to the hospital, a surveillance paracentesis performed on admission may detect unexpected infection.⁹ Not all patients with ascitic fluid infection are symptomatic; many have subtle symptoms, such as mild confusion noticed only by the family. Detection of infection at an early asymptomatic stage may reduce mortality. Therefore, ascitic fluid should be sampled in all inpatients and outpatients with new-onset ascites and in all patients with ascites who are admitted to the hospital. Paracentesis should be repeated in patients (whether hospitalized or not) in whom symptoms, signs, or laboratory abnormalities suggestive of infection develop (e.g., abdominal pain or tenderness, fever, encephalopathy, hypotension, renal failure, acidosis, peripheral leukocytosis).

Contraindications

Few contraindications to paracentesis have been recognized. Coagulopathy is a potential contraindication; however, most patients with cirrhotic ascites have coagulopathy, and if mild to moderate coagulopathy were viewed as a contraindication to paracentesis, few patients with cirrhosis would undergo this procedure.¹⁰ Coagulopathy should preclude paracentesis only when clinically evident fibrinolysis or disseminated intravascular coagulation is present.¹⁰ These conditions occur in fewer than 1 per 1000 paracenteses. No data are available to support cutoff values for coagulation parameters beyond which paracentesis should be avoided. Global coagulation is usually normal in the setting of cirrhosis despite abnormal tests of coagulation because there is a balanced deficiency of procoagulants and anticoagulants.¹¹ Even after multiple paracenteses, bloody ascites usually does not develop in patients with severe prolongation of the prothrombin time. Patients with cirrhosis and without clinically obvious coagulopathy simply do not bleed excessively from needlesticks unless a blood vessel is entered.¹⁰

Studies regarding complications of paracentesis in patients with ascites have documented no deaths or infections caused by paracentesis.⁹^,¹⁰ No episodes of hemoperitoneum or entry of the paracentesis needle into the bowel have been reported in these studies. Complications have included only abdominal wall hematomas in approximately 2% of paracenteses, even though 71% of the patients had an abnormal prothrombin time and 21% had a prothrombin time prolonged by more than five seconds.¹⁰ Complication rates may be higher when paracentesis is performed by an inexperienced operator.

Transfusion of blood products (fresh frozen plasma or platelets) routinely before paracentesis in cirrhotic patients with coagulopathy, presumably to prevent hemorrhagic complications, is not supported by data. Because a hematoma that necessitates blood transfusion develops in only approximately 1% of patients who undergo paracentesis without prophylactic transfusion of plasma or platelets, approximately 100 to 200 units of fresh frozen plasma or platelets would have to be given to prevent the transfusion of approximately 2 units of red blood cells. In a prospective study of 1100 therapeutic paracenteses, no blood products were given prior to the procedure nor were they needed after the procedure despite a platelet count as low as 19,000 cells/mm³ [0.25 × 10⁹/L]) and international normalized ratio (INR) as high as 8.7.¹²

Patient Position and Choice of Needle and Entry Site

The volume of fluid in the abdomen and the thickness of the abdominal wall determine, in part, how the patient should be positioned in preparation for paracentesis. Patients with a large volume of ascites and thin abdominal wall can be “tapped” successfully in the supine position, with the head of the bed or examining table elevated slightly. Patients with less fluid can be placed in the lateral decubitus position and tapped in the midline or in the right or left lower quadrant while supine (see later). Patients with small amounts of fluid may be tapped successfully only in the face-down position or with ultrasound guidance.¹³

The choice of the site for inserting the needle has changed over the years because of the increasing prevalence of obesity and frequency of therapeutic paracentesis. Paracentesis in obese patients poses special challenges. In obese patients, the abdominal wall usually is substantially thicker in the midline than in the lower quadrants on ultrasound examination.¹³ The abdominal wall may be even thicker than the length of a 3.5-inch paracentesis needle. Also, on physical examination, determining whether ascites is present or absent in the obese patient is frequently difficult. Ultrasound examination is helpful in confirming the presence of fluid and in guiding the paracentesis needle. Preferably, the needle is inserted into the left lower quadrant, rather than the right lower quadrant because the cecum may be distended with gas from lactulose therapy. Also, the right lower quadrant is more likely than the left to have a surgical scar (e.g., from an appendectomy). When therapeutic paracentesis is performed, more fluid can be obtained using a lower quadrant needle insertion site than a midline site.

The needle must be placed several centimeters from a surgical scar. The bowel may be adherent to the peritoneal surface of the abdomen near a scar, and a needle inserted there may enter the bowel.⁹ A long midline scar precludes midline paracentesis. An appendectomy scar precludes a right lower quadrant site, in general.

I usually choose a site in the left lower quadrant two fingerbreadths (3 cm) cephalad and two fingerbreadths medial to the anterior superior iliac spine.¹³ In a patient with multiple abdominal scars, ultrasound guidance may be required.

In a patient who is not overweight, I prefer to use a standard metal 1.5-inch, 22-gauge needle. Paracentesis in obese patients requires the use of a longer needle, for example, one that is 3.5 inches and 22 gauge. Steel needles are preferable to plastic-sheathed cannulas because plastic sheaths may shear off into the peritoneal cavity, with the potential to kink and obstruct the flow of fluid after the cannula is removed. Metal needles do not puncture the bowel unless the bowel is adherent to a scar or severe gaseous distention is present.

Technique

Diagnostic Paracentesis

Drapes, gown, hat, and mask are optional, but sterile gloves should be used when paracentesis is performed. The skin is disinfected with an iodine solution. The skin and subcutaneous tissue should be infiltrated with a local anesthetic. The sterile package insert enclosing the gloves can be used as a sterile field on which to place syringes, needles, gauze, and other supplies. When sterile gloves are not used, ascitic fluid cultures frequently grow skin contaminants; a single viable organism will grow to detectable levels in blood culture bottles.

To prevent leakage of fluid after the needle is withdrawn, a special technique is required. The previously used term “Z tract” led to confusion about the precise technique: It does not involve manipulating the needle up and down, as this could lead to tissue injury. This technique of needle insertion is accomplished by displacing (with one gloved hand) the skin approximately 2 cm downward and then slowly inserting the paracentesis needle mounted on the syringe held in the other hand. The hand holding the syringe stabilizes the syringe and retracts its plunger simultaneously. A steady hand and experience are needed. The skin is released only after the needle has penetrated the peritoneum and fluid flows. When the needle is ultimately removed, the skin resumes its original position and seals the needle pathway. (If the needle were inserted straight into the peritoneum from the skin surface, the fluid would leak out easily because the pathway would be straight.)

The needle should be advanced slowly through the abdominal wall in approximately 5-mm increments. Slow insertion allows the operator to see blood if a vessel is entered, so that the needle can be withdrawn immediately before further damage is done. Slow insertion also allows the bowel to move away from the needle, thereby avoiding bowel puncture. The syringe that is attached to the needle should be aspirated intermittently during insertion. If continuous suction is applied, bowel or omentum may be drawn to the end of the needle as soon as the needle enters the peritoneal cavity, thereby occluding flow and resulting in an apparently unsuccessful tap. Slow insertion also allows time for the elastic peritoneum to “tent” over the end of the needle and be pierced by it. The most common causes of an unsuccessful paracentesis are continuous aspiration during insertion of the needle and rapid insertion and withdrawal of the needle before the peritoneum is pierced. If the operator is certain that the needle tip is inserted far enough but no fluid is apparent, the syringe and needle can be twisted 90 degrees to pierce the peritoneum, thereby permitting flow of fluid.

Approximately 30 mL of fluid is obtained using one or more syringes. I prefer to use a 5- or 10-mL syringe for the initial portion of a diagnostic tap and then twist this syringe off the needle and replace it with a 20- or 30-mL syringe to obtain the remainder of the sample. The initial use of a small syringe allows the operator to have better control and to see fluid more easily as it enters the hub of the syringe. The syringe and attached needle are then pulled out of the abdomen, and the needle is removed and discarded. A sterile needle is then placed on the larger syringe, and an appropriate amount of fluid is inoculated into each of a pair of prepared blood culture bottles (see later). Usually, 5 to 10 mL is inoculated into 50-mL bottles, and 10 to 20 mL into 100-mL bottles. The next aliquot is placed into a “purple-top” ethylenediaminetetraacetic acid tube for a cell count, and the final aliquot is placed into a “red-top” tube for chemistries. Inoculating the culture bottles first with a sterile needle minimizes contamination. The fluid must be placed promptly into the anticoagulant-containing tube to avoid clotting; clotted fluid cannot be analyzed for cell count.

Therapeutic Paracentesis

Therapeutic paracentesis is similar to diagnostic paracentesis except that a larger-bore needle is used and additional equipment is required. In the patient who is not overweight, I prefer to use a standard metal 1.5-inch, 16- to 18-gauge needle. Obese patients may require a longer needle, for example, one that is 3.5 inches and 18 gauge. A set of 15-gauge five-hole needles has been produced specifically for therapeutic abdominal paracentesis; these needles may replace the spinal needles used currently for paracentesis in obese patients. The 15-gauge needles have a removable sharp inner component and a blunt outer cannula; they range in length from 3.25 to 5.9 inches. A tiny scalpel nick is required to permit the large needle to enter the skin.

An old method of using a 60-mL syringe, stopcock, and collection bag is tedious; use of vacuum bottles (1 or 2 L) connected to the needle with noncollapsible tubing is much faster. Use of a pump is even faster than vacuum bottles. Unless the needle is allowed to drift subcutaneously, the needle (or blunt steel cannula) can be left in the abdomen during a therapeutic paracentesis without injury. Larger-bore needles or cannulas permit more rapid removal of fluid but leave larger defects if they enter vessels or the bowel inadvertently.

Once fluid is flowing, the needle should be stabilized to ensure steady flow. Not unusually, flow ceases intermittently. With respiratory movement, the needle may gradually work its way out of the peritoneal cavity and into the soft tissue, and some serosanguineous fluid may appear in the needle hub or tubing. When this happens, the pump should be turned off or a clamp placed on the tubing connected to the vacuum bottle. The tubing is removed from the needle, and the needle is twisted a few degrees. If flow does not resume, the needle is twisted a bit more. If flow still does not resume, the needle is inserted in 1- to 2-mm increments until brisk dripping of fluid from the needle hub is seen. The tubing is then reattached, and more fluid is removed. Occasionally, fluid cannot be aspirated but drips from the needle hub. In this situation, fluid is allowed to drip into a sterile container for collection, as in a lumbar puncture.

As the fluid is removed, the bowel and omentum draw closer to the needle and eventually block the flow of ascitic fluid. The patient must then be repositioned so that gravity causes the fluid to pool near the needle. It is useful to reposition the patient a few times during a total paracentesis to maximize the amount of fluid removed. Excessive manipulation of the needle is avoided, to minimize the risk of trauma to the bowel or blood vessels.

After samples of fluid are obtained for testing, 2 to 4 L of fluid is removed to relieve the pressure of tense ascites in patients with new or diuretic-sensitive ascites. A sodium-restricted diet and diuretics are prescribed to reduce the fluid further (see later). If a patient is known to be diuretic-resistant, a “total tap” is performed—that is, all of the fluid that is accessible is removed. If less is removed, the tap will need to be repeated soon (see later—“Refractory Ascites”).

ASCITIC FLUID ANALYSIS

Gross Appearance

Non-neutrocytic (i.e., ascitic fluid polymorphonuclear neutrophil [PMN] count less than 250/mm³ [0.25 × 10⁹/L]) ascitic fluid is transparent and usually slightly yellow (Fig. 91-2). Ascitic fluid with a very low protein concentration may have no pigment and look like water. The opacity of many cloudy ascitic fluid specimens is caused by neutrophils. The presence of neutrophils leads to a shimmering effect when a glass tube containing the fluid is rocked back and forth in front of a light. Fluid with an absolute neutrophil count less than 1000/mm³ (1.0 × 10⁹/L) may be nearly clear. Fluid with a count greater than 5000/mm³ (5.0 × 10⁹/L) is quite cloudy, and fluid with a count greater than 50,000/mm³ (50.0 × 10⁹/L) resembles mayonnaise.

Figure 91-2. Algorithm for the approach to the differential diagnosis of ascites. GI, gastrointestinal; LDH, lactate dehydrogenase; PMN, polymorphonuclear neutrophil; RBC, red blood cell; SBP, spontaneous bacterial peritonitis; TP, total protein.

Ascitic fluid specimens frequently are blood-tinged or frankly bloody. A red blood cell count of 10,000/mm³ (10.0 × 10⁹/L) is the threshold for a pink appearance; lower concentrations result in clear or turbid fluid. Ascitic fluid with a red blood cell count greater than 20,000/mm³ (20.0 × 10⁹/L) is distinctly red. Many ascitic fluid specimens are bloody because of a traumatic tap; these specimens are blood-streaked and frequently clot unless the fluid is transferred immediately to the anticoagulant-containing tube for the cell count. By contrast, nontraumatic or remotely traumatic blood-tinged ascitic fluid is homogeneous and does not clot because it has already clotted and the clot has lysed. Some patients with portal hypertension have bloody hepatic lymph, resulting in bloody ascitic fluid—perhaps because of rupture of lymphatics that are under high pressure. Samples from patients with hepatocellular carcinoma are regularly bloody, but only about 10% of samples from patients with peritoneal carcinomatosis are red.² Although many physicians have the impression that tuberculosis results in bloody ascitic fluid, less than 5% of tuberculous samples are hemorrhagic in my experience.

Ascitic fluid frequently is lipid-laden. Lipid opacifies the fluid. The degree of opalescence of ascitic fluid ranges from slightly cloudy to completely opaque and chylous. Most opaque, milky fluid samples have a triglyceride concentration greater than 200 mg/dL (2.26 mmol/L) and usually greater than 1000 mg/dL (11.30 mmol/L). Fluid that has the appearance of dilute skim milk has a triglyceride concentration between 100 mg/dL (1.13 mmol/L) and 200 mg/dL (2.26 mmol/L). A substantial minority of cirrhotic ascitic fluid samples are neither transparent nor frankly milky. These opalescent samples have slightly elevated triglyceride concentrations ranging from 50 mg/dL (0.56 mmol/L) to 200 mg/dL (2.26 mmol/L).¹⁴ The opacity of these fluids does not have the shimmering characteristics of ascitic fluid with an elevated white blood cell count. The lipid usually layers out when a tube of ascitic fluid is placed in the refrigerator for 48 to 72 hours. In contrast with findings in older published reports, most patients with chylous or opalescent ascites have cirrhosis.¹⁴^,¹⁵

Dark-brown fluid with a bilirubin concentration greater than that of serum usually indicates biliary perforation.¹⁶ Deeply jaundiced patients have bile-stained ascitic fluid, but the bilirubin level and the degree of pigmentation are visually less than those of the corresponding serum. Pancreatic ascites may be pigmented because of the effect of pancreatic enzymes on red blood cells. The red blood cells may have to be centrifuged before the discolored supernatant is revealed. The degree of pigmentation ranges from tea-colored to jet black, as in pancreatic necrosis (formerly hemorrhagic pancreatitis). Black ascitic fluid also may be found in patients with malignant melanoma.

Tests

The practice of ordering every available body fluid test on every ascitic fluid specimen is expensive and can be more confusing than helpful, especially when unexpectedly abnormal results are encountered. An algorithm for the analysis of ascitic fluid is shown in Figure 91-2. The basic concept is that screening tests are performed on the initial specimen; additional testing is performed only when necessary as indicated by the results of the screening tests. Further testing may require another paracentesis, but because most specimens consist of ascitic fluid resulting from uncomplicated cirrhosis, no further testing is needed in a majority of cases. Also, because laboratories frequently store the fluid for a few days, additional testing can often be ordered on the stored fluid.

On the basis of cost analysis, tests can be classified as routine, optional, unusual, and unhelpful (Table 91-2).⁹ The cell count is the single most helpful ascitic fluid test. Only approximately 10 µL of fluid is required for a standard manual hemocytometer count. Therefore, if only one drop of fluid can be obtained, it should be sent for cell count. More fluid is almost always obtainable, however. The fluid should be submitted in an anticoagulant-containing tube (i.e., ethylenediaminetetraacetic acid) to prevent clotting. Because the decision to begin empirical antibiotic treatment of suspected ascitic fluid infection is based largely on the absolute neutrophil count (which should have a turnaround time of a few minutes), rather than the culture (which takes 12 to 48 hours to demonstrate growth), the cell count is more important than the culture in the early detection and treatment of ascitic fluid infection. Even samples from asymptomatic outpatients undergoing therapeutic paracentesis should be sent for a cell and differential count; the information obtained can lead to early, life-saving treatment of bacterial infection.

Table 91-2 Ascitic Fluid Laboratory Tests

Cell Count

Surprisingly, ascitic fluid cell counts have not been standardized. Some laboratories count mesothelial cells in addition to white blood cells (WBCs) and label the sum as “nucleated cells.” The usefulness of mesothelial cell counts is not clear. The WBC count in uncomplicated cirrhotic ascites is usually less than 500 cells/mm³ (0.5 × 10⁹/L) (see Fig. 91-2).⁹^,¹⁷ During diuresis in patients with cirrhotic ascites, the WBC count can concentrate to more than 1000 cells/mm³ (1.0 × 10⁹/L).¹⁷ A diagnosis of diuresis-related elevation of the ascitic fluid WBC count, however, requires that a prediuresis count be available, that normal lymphocytes predominate in the fluid, and that unexplained clinical symptoms or signs (e.g., fever or abdominal pain) be absent.

The upper limit of normal for the absolute PMN count in uncomplicated cirrhotic ascitic fluid is usually stated to be lower than 250/mm³ (0.25 × 10⁹/L).⁹^,¹⁷ The short survival of PMNs results in relative stability of the absolute PMN count during diuresis.¹⁷ Therefore, the 250 cells/mm³ (0.25 × 10⁹/L) cutoff value remains reliable even after diuresis.

New methods have been developed to estimate the number of ascitic fluid cells.¹⁸ Dipsticks can detect an ascitic fluid PMN count greater than 250/mm³ (0.25 × 10⁹/L) in 90 to 120 seconds. Urine-specific dipsticks have been used to date and are not very sensitive.¹⁹ What is now needed is an ascitic fluid–specific dipstick.

Any inflammatory process can result in an elevated ascitic fluid WBC count. Spontaneous bacterial peritonitis is the most common cause of inflammation of ascitic fluid and the most common cause of an elevated ascitic WBC count (see later). The total WBC count, as well as the absolute PMN count, is elevated in spontaneous bacterial peritonitis, and PMNs usually account for more than 70% of the total WBC count. Also, in tuberculous peritonitis and peritoneal carcinomatosis, the total ascitic WBC count is frequently elevated, but usually with a predominance of lymphocytes.²

In most instances, bloody ascitic fluid is the result of a slightly traumatic tap. Leakage of blood into the peritoneal cavity leads to an elevated ascitic fluid WBC count. Because neutrophils predominate in blood, the ascitic fluid differential count may be altered by contamination of ascitic fluid with blood. To correct for this, 1 PMN is subtracted from the absolute ascitic fluid PMN count for every 250 red blood cells ¹⁷ (see Fig. 91-2). If the leakage of blood occurred at a remote time, the PMNs will have lysed, and the corrected PMN count will be a negative number. If the corrected PMN count in a bloody specimen is greater than or equal to 250 cells/mm³ (0.25 × 10⁹/L), the patient must be assumed to be infected.

Exudate/Transudate Classification

Before the 1980s, the ascitic fluid total protein concentration was used to classify ascites as either exudative (greater than 2.5 g/dL [25 g/L]) or transudative (less than 2.5 g/dL [25 g/L]). Unfortunately, this classification does not work well in ascitic fluid, and these terms as applied to ascitic fluid were never carefully defined or validated. Attempts at using combinations of lactate dehydrogenase (LDH) and serum-to–ascitic fluid ratios of LDH and protein also have not been shown to classify ascitic fluid accurately into exudates and transudates.²⁰

Serum-Ascites Albumin Gradient

The serum-ascites albumin gradient (SAAG) has been proved to categorize ascites better than the total protein concentration or other parameters ²¹ (Table 91-3). The SAAG is based on oncotic-hydrostatic balance. Portal hypertension results in an abnormally high hydrostatic pressure gradient between the portal bed and ascitic fluid. A similarly large difference must exist between ascitic fluid and intravascular oncotic forces. Albumin exerts greater oncotic force per gram than that exerted by other proteins. Therefore, the difference between the serum and ascitic fluid albumin concentrations correlates directly with portal pressure.

Table 91-3 Classification of Ascites by Serum-Ascites Albumin Gradient

HIGH GRADIENT ≥1.1 g/dL (11 g/L)	LOW GRADIENT <1.1 g/dL (11 g/L)
Alcoholic hepatitis	Biliary ascites
Budd-Chiari syndrome	Bowel obstruction or infarction
Cardiac ascites	Nephrotic syndrome
Cirrhosis	Pancreatic ascites
Fatty liver of pregnancy	Peritoneal carcinomatosis
Fulminant hepatic failure	Postoperative lymphatic leak
Massive liver metastases “Mixed” ascites Myxedema	Serositis in connective tissue diseases
Massive liver metastases “Mixed” ascites Myxedema	Tuberculous peritonitis
Portal vein thrombosis
Sinusoidal obstruction syndrome

Calculating the SAAG involves measuring the albumin concentration of serum and ascitic fluid specimens and simply subtracting the ascitic fluid value from the serum value. Unless a laboratory error has been made, the serum albumin concentration is always the larger value. The gradient is calculated by subtraction and is not a ratio. If the SAAG is 1.1 g/dL (11 g/L) or greater, the patient can be considered to have portal hypertension with an accuracy of approximately 97%.²¹ Also, if the serum albumin minus ascitic fluid total protein gradient is 1.1 g/dL (11 g/L) or greater, the patient has portal hypertension because the ascitic fluid albumin concentration cannot be greater than the ascitic fluid total protein concentration. Conversely, if the SAAG is less than 1.1 g/dL (11 g/L), the patient is unlikely to have portal hypertension. The SAAG does not explain the pathogenesis of ascites formation, nor does it explain where the albumin came from—that is, liver or bowel. It simply gives the physician an indirect but accurate index of portal pressure. The accuracy of the test is excellent, even with ascitic fluid infection, diuresis, therapeutic paracentesis, intravenous infusions of albumin, and various causes of liver disease.²¹

Measurement of the ascitic fluid albumin concentration has been routine in some laboratories since the 1980s. Nevertheless, before sending ascitic fluid for the first time to a laboratory to measure the albumin concentration, a physician should discuss the test with the laboratory chemist. The accuracy of the albumin assay at low albumin concentrations (e.g., less than 1 g/dL [10 g/L]) should be confirmed because many patients with ascites have a serum albumin concentration in the range of 2.0 g/dL (20 g/L) and an ascitic fluid albumin concentration in the range of 0 to 1.0 g/dL (0 to 10 g/L). If a patient with cirrhosis has a serum albumin level of less than 1.1 g/dL (11 g/L), as occurs in less than 1% of patients with cirrhotic ascites, the SAAG will be falsely low.

The accuracy of the SAAG is also reduced when specimens of serum and ascites are not obtained nearly simultaneously. The specimens should be obtained on the same day, preferably within the same hour. Both serum and ascitic fluid albumin concentrations change over time; however, these values change in parallel, so the difference is stable. Arterial hypotension may result in a decrease in the portal pressure and a narrowing of the SAAG. Lipid interferes with the assay for albumin, and chylous ascites may result in a falsely high SAAG.

Serum hyperglobulinemia (serum globulin level greater than 5 g/dL [50 g/L]) leads to a high ascitic fluid globulin concentration and can narrow the albumin gradient by contributing to the oncotic forces. A narrowed gradient caused by high serum globulin levels occurs in only approximately 1% of ascitic fluid specimens. To correct the SAAG in the setting of a high serum globulin level, the following formula is used ²²:

Approximately 5% of patients with ascites have “mixed” ascites (that is, two causes of ascites) (see Table 91-1). Most of these patients have portal hypertension from cirrhosis as well as another cause of ascites, such as tuberculous peritonitis or peritoneal carcinomatosis.²¹ The albumin gradient is high (1.1 g/dL [11 g/L] or greater) in mixed ascites, as a reflection of the underlying portal hypertension.²¹

The presence of a high SAAG does not confirm a diagnosis of cirrhosis; it simply indicates the presence of portal hypertension. Many causes of portal hypertension other than cirrhosis are recognized (see Tables 91-1 and 91-3 and Chapter 90). A low SAAG does not confirm a diagnosis of peritoneal carcinomatosis. Although peritoneal carcinomatosis is the most common cause of a low SAAG, other causes exist (see Table 91-3). The SAAG needs to be determined only on the first paracentesis specimen in a given patient; it does not need to be repeated on subsequent specimens, if the first value is definitive. If the first result is borderline (e.g., 1.0 or 1.1 g/dL [10 or 11 g/L]), repeating the paracentesis and analysis usually provides a definitive result. High-albumin-gradient and low-albumin-gradient should replace the modifiers “transudative” and “exudative” in the classification of ascites.²¹

Culture

In the past, culture methodology for ascitic fluid was based on the notion that most episodes of ascitic fluid infection were polymicrobial with high colony counts, as in surgical peritonitis. The most common bacterial infection of ascitic fluid, spontaneous bacterial peritonitis, is monomicrobial, however, with a low bacterial concentration (median colony count of only 1 organism/mL).²³ The older method of culture consisted of inoculation (in the microbiology laboratory) of each of three agar plates and some broth with a few drops of fluid. This method of culturing ascitic fluid, as is used for urine or stool, is predictably insensitive for detecting monomicrobial infections with a low colony count. Spontaneous bacterial peritonitis is more like bacteremia in terms of the number of bacteria present; culturing ascitic fluid as if it were blood has a high yield.²³ In fact, the sensitivity of culture in detecting bacterial growth in neutrocytic ascites (i.e., ascitic fluid with a PMN count of 250 cells/mm³ [0.25 × 10⁹/L] or greater) depends on the method of culture used. The older method of culture has been found to detect bacterial growth in approximately 50% of neutrocytic samples, whereas bedside inoculation of blood culture bottles with ascitic fluid detects growth in approximately 80%.⁹ Multiple prospective studies have demonstrated the superiority of the blood culture bottle method.⁹ Also, bedside inoculation is superior to delayed laboratory inoculation of blood culture bottles in the laboratory.²⁴ Gene probes are now commercially available for the detection of bacteremia; hopefully, they will also lead to rapid (30-minute) and accurate detection of organisms in ascitic fluid. Culture will continue to be required, however, for assessment of the susceptibility of the organism to antibiotics.

Total Protein

Therefore, the exudate/transudate method of classification of ascites places many patients with cirrhosis and ascites and all patients with cardiac ascites in the exudate category and many patients with malignant ascites and essentially all patients with spontaneously infected ascites in the transudate category. Clearly, this method of classification is not useful. By contrast, the SAAG classifies fluid by the presence or absence of portal hypertension and is much more physiologic and intuitive in nature.²¹ The albumin gradient classifies cardiac ascites in the high-SAAG category, similar to cirrhotic ascites. The high SAAG of cardiac ascites is presumably the result of high right-sided cardiac pressures. In patients with cardiac ascites, the SAAG may narrow with diuresis; such narrowing does not happen in patients with cirrhosis.

The combination of ascitic fluid total protein, glucose, and LDH is of value in distinguishing spontaneous bacterial peritonitis from intestinal perforation with leakage of gut contents into ascites ²⁸ (Fig. 91-3). Patients who have neutrocytic ascitic fluid, in whom the clinical picture suggests bacterial peritonitis (rather than peritoneal carcinomatosis or tuberculous peritonitis) and who meet two of the following three criteria, are likely to have surgical peritonitis and merit immediate radiologic evaluation to determine if intestinal perforation with leakage of intestinal contents into ascites has occurred: total protein greater than 1 g/dL (10 g/L), glucose less than 50 mg/dL (2.8 mmol/L), and LDH greater than the upper limit of normal for serum.²⁸

Figure 91-3. Algorithm for differentiating spontaneous from secondary bacterial peritonitis in patients with neutrocytic ascites (i.e., neutrophil count of 250 cells/mm³ [0.25 × 10⁹/L] or greater) in the absence of hemorrhage into ascitic fluid, tuberculosis, peritoneal carcinomatosis, or pancreatitis. Antibiotic therapy should be started at the time peritonitis (ascitic fluid PMN count ≥250 cells/mm³) is detected. CT, computed tomography; LDH, lactate dehydrogenase; PMN, polymorphonuclear neutrophil; US, ultrasound.

(Reproduced with permission from Akriviadis EA, Runyon BA. The value of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. Gastroenterology 1990; 98:127-33.

Glucose

The glucose molecule is small enough to diffuse readily into body fluid cavities. Therefore, the concentration of glucose in ascitic fluid is similar to that in serum, unless glucose is being consumed by ascitic fluid WBCs or bacteria.²⁸ In early spontaneous bacterial peritonitis, the ascitic fluid glucose concentration is similar to that of sterile fluid.²⁵ By contrast, in spontaneous bacterial peritonitis detected late in its course (as well as in the setting of intestinal perforation into ascitic fluid), the ascitic fluid glucose concentration usually drops to 0 mg/dL (0 mmol/L) because of large numbers of stimulated neutrophils and bacteria.²⁸

Lactate Dehydrogenase

The LDH molecule is too large to enter ascitic fluid readily from blood,²⁸ and the ascitic fluid concentration of LDH usually is less than one half of the serum level in uncomplicated cirrhotic ascites. In spontaneous bacterial peritonitis, the ascitic fluid LDH level rises because of the release of LDH from neutrophils, and the ascitic fluid concentration is greater than that of serum. In secondary peritonitis, the LDH level is even higher than that seen in spontaneous bacterial peritonitis and may be several-fold higher than the serum LDH level.²⁸

Amylase

In uncomplicated ascites in the setting of cirrhosis, the ascitic fluid amylase concentration usually is one half that of the serum value, approximately 50 U/L.²⁹ In patients with acute pancreatitis or intestinal perforation (with release of luminal amylase into the ascitic fluid), the fluid amylase concentration is elevated markedly, usually greater than 2000 U/L and approximately five-fold greater than simultaneous serum values.²⁸^–³⁰

Gram Stain

Gram stains of body fluids demonstrate bacteria only when more than 10,000 bacteria/mL are present. The median ascitic concentration of bacteria in spontaneous bacterial peritonitis is only 1 organism/mL, similar to the colony count in bacteremia.²³ Requesting an ascitic fluid Gram stain to detect bacteria in spontaneous bacterial peritonitis is analogous to requesting a Gram stain of blood to detect bacteremia. Bacteria are detected on Gram stain only with overwhelming infection, as in advanced spontaneous bacterial peritonitis or asplenic pneumococcal sepsis. Gram stain of ascitic fluid is most helpful in the diagnosis of free perforation of the intestine into ascitic fluid. In this setting, sheets of multiple different bacteria are found. Gram stain of the centrifuged sediment of 50 mL of ascites has a sensitivity rate of only 10% for visualizing bacteria in spontaneous bacterial peritonitis.²³

Smear and Culture for Tuberculosis

A direct smear of ascitic fluid to detect mycobacteria is almost never positive because of the rarity of tuberculous peritonitis and the low concentration of mycobacteria in ascitic fluid in tuberculous peritonitis.³¹ The older literature suggests that 1 L of fluid should be cultured. The largest centrifuge tube found in most laboratories, however, has a capacity of 50 mL. In general, only one 50-mL aliquot of fluid is centrifuged, and the pellet is cultured. In contrast to a sensitivity rate of approximately 50% for ascitic fluid mycobacterial culture with optimal processing, laparoscopy with histology and culture of peritoneal biopsies has a sensitivity approaching 100% for detecting tuberculous peritonitis.³¹ Tuberculous peritonitis can easily be confused with spontaneous bacterial peritonitis because both conditions are associated with abdominal pain and fever, and one half of the patients with tuberculous peritonitis have cirrhosis. A negative bacterial culture and predominance of mononuclear cells in the differential count, however, provide clues to the diagnosis of tuberculous peritonitis. DNA probes are now available to detect mycobacteria and probably will replace older methods of detection.³² Nevertheless, cultures still will be required to determine susceptibility to antimicrobial agents.

Cytologic Examination

In the past, ascites related to malignancy was assumed to be caused only by peritoneal carcinomatosis; massive liver metastases and hepatocellular carcinoma superimposed on cirrhosis were not recognized as causes of malignant ascites. These studies did not compare cytologic examination with a standard diagnostic test, such as autopsy, laparotomy, or laparoscopy, and cytologic study was reported to have a sensitivity of only about 60% in detecting malignant ascites.³³ Cytologic studies, however, can be expected to detect malignancy only when tumor cells line the peritoneal cavity and exfoliate into the ascitic fluid—that is, in peritoneal carcinomatosis. Such studies should not be expected to detect tumor when the peritoneum is uninvolved, as in ascites resulting from portal hypertension in patients with hepatocellular carcinoma or massive liver metastases or from lymph node obstruction in patients with malignant lymphoma.² In one study in which the location and type of tumor that caused ascites were confirmed by a standard test, only approximately two thirds of patients with malignancy-related ascites were found to have peritoneal carcinomatosis, but nearly 100% of patients with peritoneal carcinomatosis were reported to have positive findings on cytologic examination of ascitic fluid; the remaining one third of patients with massive liver metastases, chylous ascites caused by lymphoma, or hepatocellular carcinoma had negative cytologic findings.² Therefore, the sensitivity of cytology is approximately 100% for detecting peritoneal carcinomatosis but much lower for detecting malignancy-related ascites caused by conditions other than peritoneal carcinomatosis. Cytologic studies should not be falsely positive if performed carefully; I have never encountered a false-positive result.

Because hepatocellular carcinoma rarely metastasizes to the peritoneum, a positive ascitic fluid cytology in a patient with hepatocellular carcinoma is unusual enough to be the subject of a case report.³⁴ Measurement of the serum alpha fetoprotein concentration (which is always higher in serum than in ascitic fluid) may be of value in detecting hepatocellular carcinoma; serum alpha fetoprotein is much more sensitive than ascitic cytology for this purpose.² In malignancy-related ascites, the fluid may have an elevated PMN count, presumably because dying tumor cells attract neutrophils.² The elevated PMN count may cause confusion with spontaneous bacterial peritonitis; however, a predominance of lymphocytes in malignancy-related ascites is usual. Flow cytometry and magnetic enrichment of ascitic fluid as an adjunct to cytology may further increase diagnostic accuracy.³⁵

Triglyceride

A triglyceride level should be measured in opalescent or frankly milky ascitic fluid (see Fig. 91-2). By definition, chylous ascites has a triglyceride concentration greater than 200 mg/dL (2.26 mmol/L) and greater than the serum level; usually, the level is greater than 1000 mg/dL (11.30 mmol/L).³⁶ In sterile ascitic fluid specimens in the setting of cirrhosis that are slightly cloudy, without an elevated cell count (i.e., opalescent), the triglyceride concentration is elevated—64 ± 40 mg/dL (0.72 ± 0.45 mmol/L), compared with 18 ± 9 mg/dL (0.20 ± 0.10 mmol/L) for clear ascites in the setting of cirrhosis.¹⁴

Bilirubin

The bilirubin concentration should be measured in ascitic fluid that is dark brown. An ascitic fluid bilirubin level greater than 6 mg/dL (102 µmol/L) and greater than the serum level of bilirubin suggests biliary or proximal small intestinal perforation into ascitic fluid.¹⁶^,²⁸

Tests That Are Seldom Helpful

Tests that have been proposed to be helpful in the analysis of ascitic fluid but shown subsequently to be of no benefit include determination of pH, lactate, fibronectin, and cholesterol. The studies that attempted to validate the value of pH and lactate included small numbers of patients and used suboptimal culture techniques. In the two largest and most recent studies, which did not have some of the deficiencies of the earlier studies, the ascitic fluid pH and lactate were found not to be helpful.³⁷^,³⁸ The pH was found to have no impact on decision-making regarding the use of empirical antibiotic therapy.³⁷

Fibronectin and cholesterol have been proposed to be useful in detecting malignant ascites. The basic premise in studies of these markers was that ascitic fluid cytologic examination is insensitive. Unfortunately, the design of the studies was problematic, several subgroups of malignancy-related ascites (e.g., massive liver metastases, hepatocellular carcinoma with cirrhosis) were not considered, and appropriate control groups (e.g., patients with ascites caused by conditions other than cirrhosis or peritoneal carcinomatosis) were not included. Other studies have demonstrated that in patients with massive liver metastases, ascitic fluid fibronectin and cholesterol concentrations are not abnormally elevated.³⁹^,⁴⁰ Therefore, in patients with malignancy-related ascites and negative cytologic findings, these “humoral tests of malignancy” are usually negative. Additionally, patients with high-protein noncirrhotic ascites nearly always have ascitic fibronectin and cholesterol elevations despite the absence of malignancy.²^,³⁹^,⁴⁰

Carcinoembryonic antigen (CEA) in ascitic fluid has been proposed as a helpful marker for detecting malignant ascites.⁴¹ The study that attempted to validate this proposal, however, was flawed, and more studies, with various subgroups of patients, are required before testing for ascitic fluid CEA can be considered validated.

Measurement of adenosine deaminase has been proposed as a useful test for detecting peritoneal tuberculosis. In the United States, however, where greater than 50% of patients with tuberculous peritonitis have underlying cirrhosis, the adenosine deaminase level has been found to be too insensitive to be helpful.³¹

DIFFERENTIAL DIAGNOSIS OF ASCITES

Although cirrhosis is the cause of ascites in most patients with ascites evaluated by an internist, a cause other than liver disease is found in approximately 15% of patients (see Table 91-1). Approximately 5% of patients have two causes of ascites, that is, “mixed” ascites.²¹ Usually, these patients have cirrhosis plus one other cause, such as peritoneal carcinomatosis or tuberculous peritonitis (see Table 91-1). Because tuberculosis is potentially fatal but curable and frequently occurs in cirrhotic patients with preexisting ascites, the physician must not assume that liver disease is the only cause of ascites in a febrile alcoholic patient if the ascitic fluid analysis is atypical. For example, if the ascitic fluid lymphocyte count is unusually high, tuberculous peritonitis may be present. Interpretation of the results of ascitic fluid analysis is difficult in patients with mixed ascites but crucial to accurate diagnosis and treatment. Additionally, liver diseases other than cirrhosis (e.g., alcoholic hepatitis or fulminant hepatic failure) may cause ascites (see Table 91-1).

An algorithm for the differential diagnosis of ascites is shown in Figure 91-2. This proposed strategy is applicable to a majority of patients with ascites, including many with the causes listed in Table 91-1. Not every patient (including patients with rare causes of ascites) can be categorized readily with such an algorithm, however. Many patients with enigmatic ascites eventually are found to have two or even three causes of ascites (e.g., heart failure, cirrhosis caused by NASH, diabetic nephropathy). In these cases, the sum of predisposing factors leads to sodium and water retention, even though each factor alone may not be severe enough to cause fluid overload.

In most patients with ascites, cirrhosis is the cause. This form of ascites, especially when low in protein, is complicated frequently by spontaneous bacterial peritonitis (see later).²⁶ Other forms of ascites are complicated by spontaneous peritonitis so rarely that they are the subjects of case reports or small series.

The intestine can perforate with spillage of contents in patients with ascites of any cause, cirrhosis or otherwise. The ascitic fluid analysis in intestinal perforation is dramatically different from that in spontaneous bacterial peritonitis (see Fig. 91-3).²⁸ Distinguishing spontaneous bacterial peritonitis from surgical peritonitis in a patient with cirrhosis is critical to the patient’s survival; spontaneous bacterial peritonitis is treated with antibiotics alone, whereas surgical peritonitis is treated with antibiotics and emergency surgical intervention (see Chapter 37).

Cancer accounts for fewer than 10% of cases of ascites (see Table 91-1). Not all cases of malignancy-related ascites are caused by peritoneal carcinomatosis; the characteristics of the ascitic fluid and the treatments vary, depending on the pathophysiology of the ascites—for example, peritoneal carcinomatosis versus massive liver metastases² (Table 91-4; see also “Ascitic Fluid Analysis”).

Table 91-4 Classification of Malignancy-Related Ascites

Hepatocellular carcinoma

Malignant Budd-Chiari syndrome (tumor emboli in hepatic veins)

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