Ascites

C. Randall Clinch

Ascites, the accumulation of fluid within the abdominal cavity, is the most common major complication of cirrhosis; it is present in 50% of patients with cirrhosis of 10 years’duration (1). Ascites has important prognostic implications, carrying a 50% 2-year mortality rate (1). Once identified, an investigation should follow to determine its cause and plan appropriate management.

In the United States, most (80%) adult patients with ascites have cirrhosis caused by alcoholic hepatitis (Laennec’s cirrhosis), hemochromatosis, Wilson’s disease, autoimmune cirrhosis, or an idiopathic cause (1). Heart failure, constrictive pericarditis, peritoneal infection and inflammation (e.g., tuberculosis, viral hepatitis, chlamydia), nephrotic syndrome, malignancy, pancreatitis, marked hypoalbuminemia (<2 g/dl), trauma, or fulminant hepatic failure are the cause of ascites in approximately 20% of patients. Of patients, 5% have “mixed ascites,” or ascites from two causes (e.g., hemochromatosis and heart failure; Laennec’s cirrhosis and pancreatitis).

Approach

 A. Urgent need for diagnosis. An urgent approach to diagnosis may arise in patients with an extremely distended abdomen and respiratory compromise. Patients with a large umbilical herniation, which can rupture, or patients with encephalopathy, fever, and decreased urine output also warrant immediate diagnosis.

 B. Nonurgent need for diagnosis. Nonurgent scenarios are more common. The approach to diagnosis is the same, based on a thorough history, physical examination, and ascitic fluid analysis.

History

 A. Does the patient use alcohol or drugs? Alcoholic hepatitis is the most common cause of cirrhosis and ascites. Intravenous drug use places the patient at risk for ascites from either acute or chronic viral hepatitis (hepatitis B and C).

 B. Is the patient at risk for sexually transmitted diseases? Hepatitis B is commonly acquired sexually, therefore a complete sexual history is mandatory.

 C. Is the patient otherwise at risk for acquiring hepatitis? Other individuals at risk include hemodialysis patients, recipients of organ transplantations, close contacts of persons with hepatitis, members of high-risk populations (Asia, the South Pacific, sub-Saharan Africa), recipients of blood or blood products, individuals with tattoos, prior acupuncture or ear piercing, and needlestick victims.

 D. Does the patient have signs of fluid retention? Ask about increased abdominal girth, weight gain, leg edema, penile or scrotal edema, and umbilical herniation (Chapter 2.3).

 E. Are there any secondary symptoms to suggest fluid retention? Increased abdominal fluid leads to vague complaints of nausea, anorexia, early satiety, heartburn, abdominal pain, shortness of breath, or orthopnea.

F. Is there a suspicion of infection? Of patients admitted with ascites, 10% to 27% have spontaneous bacterial peritonitis (SBP); 48% to 57% of these patients will die (4). Ask about fever, abdominal pain, or mental status changes (encephalopathy) (Chapters 2.6, 3.2, and 9.1).

G. Is there a past history of heart failure, cancer, or tuberculosis? These are included in the 20% of nonhepatic causes of ascites.

Physical examination

Obtain vital signs (temperature, respiratory rate, blood pressure, and weight). Ascites is rarely the sole physical finding. Examine for evidence of liver disease (jaundice, spider angiomata, Dupuytren’s contracture, caput medusae); hepatomegaly may be absent if chronic cirrhosis exists. Examine the skin for evidence of intravenous (IV) drug use, tattoos, and pigment changes (hemochromatosis). Jugular venous distention, a third heart sound, pulmonary crackles, and peripheral edema suggest heart failure. Abdominal tenderness can reflect pancreatitis or infection. Tests for ascites include shifting dullness, bulging flanks, flank dullness, fluid wave, and the “puddle” sign (i.e., percussing the abdomen with the patient on hands and knees). The reliability of these tests are unpredictable (2). These techniques are not helpful when a small volume ( <1,000 ml) of ascites exists; 1,500 ml of fluid must be present before shifting dullness is detected. The “puddle” sign is no longer considered valuable because of its low sensitivity and patient discomfort (2,5).

Testing

A. Diagnostic paracentesis should be performed to determine the nature of the ascitic fluid and to evaluate for the presence of SBP.

B. An ascitic fluid polymorphonuclear leukocyte count of more than 250 cells/mm³ indicates infection (SBP) and the patient should be empirically treated as such.

C. If a culture is obtained, 10 ml of ascitic fluid should be injected into blood culture bottles at the bedside to increase sensitivity (1,4).

 D. The serum-ascites albumin gradient (SAAG) is the difference between the serum albumin concentration and the ascitic fluid albumin concentration. This gradient is 97% accurate in determining the underlying mechanism of ascites and replaces the former classification of ascitic fluid as either a transudate or an exudate (1). An SAAG of more than 1.1 g/dl indicates the patient has portal hypertension (seen with diagnoses such as cirrhosis, heart failure, alcoholic hepatitis, massive metastatic liver disease, or Budd-Chiari syndrome) (4). An SAAG of less than 1.1 g/dl indicates the patient does not have portal hypertension and a process such as peritoneal carcinomatosis, tuberculous peritonitis, pancreatic ascites, serositis from connective tissue diseases, nephrotic syndrome, or biliary ascites may be present (1,4).

 E. Cytology, smear, and culture for mycobacteria are expensive and have very low yields. They should only be ordered if there is a very high pretest probability.

 F. Other tests that can be ordered include amylase (pancreatic ascites), triglycerides (chylous ascites), and lactate dehydrogenase and glucose (secondary peritonitis) (4).

 G. Ultrasonography can detect as little as 100 ml of fluid in the abdomen (3). It is useful both for confirming the presence of ascites and in guiding diagnostic paracentesis.

Diagnostic assessment

If ascites is suspected on history and physical examination, a diagnostic paracentesis should be performed. Basic orders include a cell count and differential and albumin concentration (ascitic and serum). The SAAG should be calculated. Culture and other optional tests should be performed, based on clinical suspicion. If the diagnosis is uncertain because of a low volume of ascites, an ultrasound should be performed to guide a diagnostic paracentesis. If the patient is having significant symptoms or tense ascites, a therapeutic large-volume paracentesis should be performed and the fluid analyzed as above. Complications of paracentesis have been reported in approximately 1% of patients (i.e., abdominal wall hematomas), including those with an underlying coagulopathy (1).

A. Indications for hospitalization (5) or referral include:

1. Worsening ascites despite initial management attempts

2. Tense ascites

 3. Systemic signs or symptoms (liver failure, renal failure, encephalopathy, pancreatitis, gastrointestinal bleeding)

 4. Suspicion of infection (SBP)

5. Patient noncompliant with medical management

References

1. Runyon BA. Management of adult patients with ascites caused by cirrhosis. AASLD practice guidelines. Hepatology 1998;27(1):264–272.

2. Cattau EL, Benjamin SB, Knuff TE, Castell DO. The accuracy of the physical examination in the diagnosis of suspected ascites. JAMA 1982;247:1164.

3. Goldberg BB, Goodman GA, Clearfield HR. Evaluation of ascites by ultrasound. Radiology 1970;96:15–22.

4. Habeeb KS, Herrera JL. Management of ascites. Paracentesis as a guide. Postgrad Med 1997;101(1):191–200.

5. Lipsky MS, Sternbach MR. Evaluation and initial management of patients with ascites. Am Fam Physician 1996;54(4):1327–1333.>>

Book Source Details

• Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
• Author(s): Robert B. Taylor (editor)
• Year of Publication: 2000
• Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.

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