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Sameer D. Saini

, and Akbar K. Waljee

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date: 05 July 2022

  1. A. Introduction. Ascites is the accumulation of excess fluid within the peritoneal cavity. Sampling the fluid with a paracentesis can provide crucial diagnostic information about the cause of the ascites.

  2. B. Causes of Ascites. Ascites may occur as part of anasarca (generalized edema) or as isolated peritoneal fluid.

    1. a. Anasarca. The causes of a generalized edematous state can be remembered as the four “-osis”: nephrosis, cirrhosis, cardiosis, and hypothyroidosis.

    2. b. Isolated fluid collection. There are three primary mechanisms of ascites production. In addition, some disorders can cause ascites by other, miscellaneous mechanisms.

      1. i. Increased hydrostatic pressure in the splanchnic capillaries may result from diseases that produce elevated venous pressure. One way of thinking about the causes of increased hydrostatic pressure is to trace the venous blood from the heart down.

        1. 1. Cardiac

          • a. Right-sided heart failure and constrictive pericarditis both lead to elevated venous pressure, increased portal vein pressure, and ascites.

        2. 2. Hepatic

          • a. Postsinusoidal obstruction includes inferior vena cava obstruction, hepatic vein obstruction (i.e., Budd-Chiari syndrome), or hepatic venule obstruction (i.e., venoocclusive disease).

          • b. Sinusoidal obstruction is the most common cause of ascites and usually results from cirrhosis.

          • c. Presinusoidal obstruction may be caused by schistosomiasis or portal vein thrombosis. (Portal vein thrombosis may cause variceal bleeding but only rarely produces ascites.)

      2. ii. Decreased oncotic pressure may result from decreased protein intake (i.e., starvation), decreased albumin production (i.e., severe liver disease), or increased loss of albumin (e.g., nephrotic syndrome, protein-losing enteropathy).

      3. iii. Increased capillary permeability may occur with infection (e.g., tuberculosis) or malignancy.

      4. iv. Miscellaneous causes

        1. 1. Hypothyroidism. Myxedema usually produces anasarca, not isolated ascites.

        2. 2. Pancreatitis may cause pancreatic ascites.

        3. 3. Lymphatic obstruction from trauma, tumor, or infection (e.g., filariasis, tuberculosis) may cause chylous ascites.

  3. C. Approach to the Patient

    1. a. Patient history and physical examination. A complete history and physical examination (including rectal and pelvic examinations) are necessary. By remembering the underlying mechanisms, you can systematically pursue the diagnosis.

      1. i. Increased hydrostatic pressure

        1. 1. Right-sided heart failure or constrictive pericarditis. Ask about symptoms of left-sided heart failure (because this is the most common cause of right-sided heart failure). Perform a careful cardiac examination and evaluate the jugular venous pressure. Assess the patient for evidence of hepatojugular reflux. Patients with cirrhosis typically have low jugular venous pressure.

        2. 2. Budd-Chiari syndrome may be suggested by right upper quadrant pain and an enlarged liver in a patient with a myeloproliferative disorder, hypercoagulable state, or recent pregnancy.

        3. 3. Hepatic venoocclusive disease should be considered in patients with ascites and a history of chemotherapy or bone marrow transplantation.

        4. 4. Cirrhosis is the most common cause of ascites. Inquire about risk factors, including alcohol consumption, hepatitis exposures (e.g., intravenous drug use and family history). Look for signs of chronic liver disease (see Chapter 34).

      2. ii. Low oncotic pressure in the absence of severe liver disease may be suggested by a history of starvation or by the presence of nephrotic syndrome.

      3. iii. Increased capillary permeability may be suggested by a history of fevers or weight loss, which could suggest infection or malignancy.

      4. iv. Miscellaneous mechanisms

        1. 1. Pancreatic ascites should be considered whenever pancreatitis or pancreatic ductal disruption is a possibility.

        2. 2. Lymphatic obstruction should be suspected if there is a “milky” appearance to the ascites (so-called “chylous” ascites).

        3. 3. Myxedema. If myxedema is the etiology, the patient will usually have other symptoms of hypothyroidism (see Chapter 79).

    2. b. Laboratory tests. Routinely performed laboratory tests include a complete blood count (CBC) with differential, an electrolyte panel, blood urea nitrogen (BUN) and creatinine levels, prothrombin time (PT) and partial thromboplastin time (PTT), and liver function tests with serum albumin. A urine dipstick test for protein and thyroid function tests are also frequently performed, especially when anasarca is present.

    3. c. Diagnostic paracentesis is always needed to make a definitive diagnosis. Even when the diagnosis seems apparent, diagnostic paracentesis is still indicated to rule out secondary processes (e.g., spontaneous bacterial peritonitis [SBP]). For details on how to safely perform abdominal paracentesis, see chapter 98.

      1. i. Fluid analysis. A cell count with differential, bacterial Gram stain and cultures, albumin, and total protein level should be obtained on the fluid sample. Lactate dehydrogenase (LDH) and glucose levels may provide additional information. An amylase or triglyceride level should be ordered if there is a possibility of pancreatic or chylous ascites, respectively. In patients in whom malignancy is a concern, cytology can be performed on the fluid (the larger volume assessed, the higher the yield).

      2. ii. Interpretation.Table 32.1 summarizes common etiologies of ascites and their characteristic fluid findings. Remember that the findings given are only generalizations and will not apply in all cases. Furthermore, the presence of two or more disorders may skew the fluid analysis.

        Table 32.1 Characteristic Ascitic Fluid Findings


        Serum–Ascites Albumin Gradient

        Cell Count (Cells/μ‎L)

        Total Protein*

        Other Findings



        <250 (mesothelial)


        Abnormal liver function tests

        Spontaneous bacterial peritonitis (SBP)


        >250 (PMNs)


        Culture may be positive but typically is negative. A negative culture does not rule out SBP.

        Congestive heart failure


        <1000 (mesothelial)


        Elevated neck veins, gallops, abnormal EKG



        <250 (variable)


        Decreased free T4, increased TSH

        Liver malignancy (primary or secondary)




        Elevated serum AFP with primary malignancy

        Nephrotic syndrome


        <250 (mesothelial)


        Positive urine dipstick and 24-hour collection for protein

        Tuberculous ascites


        >1000 (variable)


        Ascitic acid-fast bacillus stain occasionally positive

        Secondary peritonitis


        >250 (PMNs)


        Very low ascitic glucose, polymicrobial growth on culture

        Pancreatic ascites


        >1000 (PMNs)


        Increased serum and fluid amylase

        Peritoneal malignancy


        >1000 (variable)


        Cytology, CT scan, peritoneal biopsy may be useful

        * Total protein is considered low if it is less than 1 g/dL, moderate if it is 1–3 g/dL, and high if it is >3 g/dL.

        AFP = α‎-fetoprotein; CT = computed tomography; EKG = electrocardiogram; PMNs = polymorphonuclear neutrophils; T4 = thyroxine; TSH = thyroid-stimulating hormone.

        1. 1. Cell count. The cell count can be used to assess the likelihood of SBP, tuberculosis, or malignancy.

          • a. SBP. Diagnosis of SBP is confirmed when the absolute neutrophil count exceeds 250 cells μ‎L. Counts greater than 500 cells/μ‎L are more specific, but less sensitive for SBP. Treatment is warranted if the neutrophil count exceeds 250 cells/μ‎L.

          • b. Tuberculosis or malignancy. A cell count that exceeds 250 cells/μ‎L and is lymphocyte predominant often implies tuberculous or malignant ascites (however, SBP can also occasionally have a lymphocyte predominant pattern).

        2. 2. Serum–ascites albumin gradient (SAAG). Subtract the ascitic fluid albumin value from the serum albumin value.

          • a. If the result is greater than or equal to 1.1, portal hypertension is implicated (i.e., a hydrostatic etiology is responsible).

          • b. If the value is less than 1.1, capillary permeability is probably abnormal (i.e., infection or malignancy may be implicated).

            Hot Key

            If portal hypertension is accompanied by another disorder that produces increased capillary permeability, the gradient will usually remain greater than or equal to 1.1. SBP usually occurs in patients with portal hypertension; therefore, the gradient is usually greater than or equal to 1.1 in these patients.

        3. 3. Gram stain and culture of ascitic fluid should be performed in all patients.

        4. 4. LDH and glucose levels. An elevated LDH or low glucose level may indicate tuberculosis or malignancy; however, these laboratory tests have limited value.

        5. 5. Amylase and triglyceride levels. Elevated amylase or triglyceride levels may indicate pancreatic or chylous ascites, respectively.

    4. d. Additional testing may be necessary when the ascitic fluid contains an elevated cell count with a lymphocyte predominance, increasing suspicion for tuberculous or malignant ascites.

      1. i. Purified protein derivative (PPD) test. A positive PPD skin test will increase suspicion for tuberculous peritonitis.

      2. ii. Acid-fast bacillus stain and culture of ascitic fluid. These are relatively insensitive tests, but a larger volume of fluid (e.g., 1 L) may increase the yield. Polymerase chain reaction (PCR) for mycobacteria can also be performed but may yield false-positive results.

      3. iii. Abdominal computed tomography may reveal an intra-abdominal malignancy.

      4. iv. Laparoscopy with peritoneal biopsy is often performed to make an expedient diagnosis.

  4. D. Treatment. The general management of ascites is discussed in Chapter 35; other specific therapies are tailored to the underlying etiology and will not be discussed here.

Suggested Further Readings

Abad CL, Moseley RH, Crnich CJ, Saint S, Safdar N. Clinical problem-solving. A gut instinct. N Engl J Med 2014;371:560–4.Find this resource:

Ge PS, Runyon BA. Treatment of patients with cirrhosis. N Engl J Med 2016;375:767–77.Find this resource:

Runyon BA. Management of adult patients with ascites caused by cirrhosis. Hepatology 1998;27:264–72. (Classic Article.)Find this resource:

Williams JW Jr., Simel DL. The rational clinical examination. Does this patient have ascites? How to divine fluid in the abdomen. JAMA 1992;267:2645–8. (Classic Article.)Find this resource: