Ascites Fluid Continues to Accumulate Because the Hepatic Portal Vessels Contain Blood With a

Ascites

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October 10, 2022

Summary

Ascites is the abnormal accumulation of fluid within the peritoneal cavity and is a common complication of portal hypertension (e.g., due to liver cirrhosis, acute liver failure) and/or hypoalbuminemia (e.g., due to nephrotic syndrome). Other conditions resulting in ascites include chronic heart failure, inflammation of abdominal viscera (e.g., pancreatitis), and malignancies. Clinical features include progressive abdominal distention, shifting dullness, and a positive fluid wave test. Abdominal pain may be present in ascites due to acute inflammation. Diagnostics are aimed at identifying the underlying etiology and determining whether the ascitic fluid is infected. They include imaging (e.g., with abdominal ultrasound or CT abdomen and pelvis), which is used to identify free intraperitoneal fluid and possibly the underlying cause, and diagnostic paracentesis with ascitic fluid analysis. The serum-ascites albumin gradient (SAAG), or the difference between albumin levels in serum and ascitic fluid, is essential to determine the underlying cause. A high SAAG indicates that the ascites is secondary to portal hypertension. An ascitic fluid neutrophil count ≥ 250 cells/mm³ indicates spontaneous bacterial peritonitis (SBP), which should be urgently managed with empiric antibiotic therapy. Management of ascites involves identifying and managing the underlying cause as well as dietary sodium restriction and diuretic therapy. Additionally, tense ascites and refractory ascites require therapeutic paracentesis. Liver transplant is a treatment option for patients with cirrhosis who develop ascites. Transjugular intrahepatic portosystemic shunts (TIPS) and peritoneovenous shunts are advanced treatment options for refractory ascites, which carries a high risk of mortality.

Etiology

		Etiology	Pathophysiology
High SAAG ascites ≥ 1.1 g/dL (obsolete term: transudate)		Portal hypertension Presinusoidal Splenic or portal vein thrombosis Schistosomiasis Sinusoidal Hepatic (common) Cirrhosis Alcohol-related liver disease Liver metastases Postsinusoidal Cardiac Right heart failure Constrictive pericarditis Budd-Chiari syndrome	Arterial vasodilation hypothesis in cirrhosis : Portal hypertension → vasodilation → reduced systemic vascular resistance and reduced mean arterial blood pressure Activation of endogenous vasoconstrictors, renal sodium and water retention, and renal vasoconstriction → hyperdynamic circulation Right-sided heart failure: backflow of blood obstructing the venous outflow of the liver Budd-Chiari syndrome : congestion of the portal/hepatic collateral veins and hypertrophy of the caudate lobe of the liver → compression of the sinusoids and intrahepatic inferior vena cava		All result in ↑ pressure in portal vein → ↑ hydrostatic pressure in the hepatic vessels → pushing of fluid out from the intravascular space to the peritoneal cavity
Low SAAG ascites < 1.1 g/dL (obsolete term: exudate)		Hypoalbuminemia Nephrotic syndrome Severe malnutrition Protein-losing enteropathy	Nephrotic syndrome → primary renal sodium retention		All result in ↓ int ravascular osmotic gradient → secondary influx of water from the intravascular space to the peritoneal cavity
		Malignancy	Various mechanisms of malignant-related ascites exist: Peritoneal carcinomatosis → blockage of lymphatic channels and increased vascular permeability → accumulation of peritoneal fluid Lymph obstruction (by a lymphoma ) → chylous ascites If an underlying liver condition exists (typically hepatocellular carcinoma) → loss of synthetic liver function or portal vein thrombosis
		Infections (e.g., tuberculosis )	Production of protein-rich fluid from tubercles
		Pancreatitis	Accumulation of pancreatic fluid in the peritoneal cavity

Remember, exudative ascitic fluid is high in protein, like eggs.

References:^{[1] [2] [3]}

Clinical features

• Progressive abdominal distention ; symptoms associated with increased abdominal distention include
  • Early satiety
  • Weight gain
  • Dyspnea
  • Diarrhea, which, if chronic, may be associated with features of malnutrition
• Fluid wave test: wave produced by tapping one side of the abdomen in a patient in supine position; this wave will be transmitted to the other side via ascitic fluid.
• Shifting dullness : change of resonance from dull to tympanic resonance when patient changes from supine to lateral decubitus position .
• Flank dullness: typically elicited only if > 1.5 L of ascitic fluid is present ^[4]
• Abdominal pain may be present
• Abdominal wall hernias (e.g., umbilical, inguinal, or incisional hernias )
• Peripheral or generalized edema
• Signs of underlying disease
  • Enlarged liver, jaundice, spider angioma, palmar erythema: signs of chronic liver disease
  • Elevated jugular venous pressure: heart failure
  • Virchow node ; and weight loss: abdominal or pelvic malignancy

References:^[2]

Subtypes and variants

Diagnostics

Diagnostics are used to confirm the presence of ascites, assess its severity, determine the underlying etiology, and evaluate for complications. ^[5]

Abdominal ultrasound with Doppler (initial study of choice)

CT abdomen and pelvis ^[5]

Laboratory studies ^[6]

The choice of laboratory studies should be guided by the pretest probability of the suspected underlying etiology.

• CBC: abnormalities related to an underlying condition
• Coagulation panel: Thrombocytopenia and coagulopathy are signs of advanced liver disease.
• Liver chemistries
  • Elevated transaminases suggest liver disease.
  • Serum albumin (for SAAG calculation)
• BMP
  • Elevated creatinine and BUN: Acute kidney injury is common in patients with decompensated cirrhosis. ^[9]
  • Serum electrolytes: hypervolemic hypotonic hyponatremia (as a complication of cirrhosis) ^[10]
• Additional evaluation for the underlying condition: E.g., see "Diagnostics for cirrhosis."

Diagnostic paracentesis

For further information on this procedure, see "Paracentesis."

Indications

• All patients with new-onset ascites (to identify the underlying etiology) ^{[4] [5] [11]}
• To detect spontaneous bacterial peritonitis (SBP) or other peritoneal infections in the following situations:
  • Clinical features of SBP
  • Hospitalization for any cause in patients with cirrhosis and ascites (to identify occult SBP) ^{[4] [8] [12]}

Occult SBP is common in patients with ascites and cirrhosis and delays in diagnosis result in increased mortality. ^[13]

Ascitic fluid analysis ^{[5] [6] [11]}

Routine studies

• Gross appearance : can provide supportive evidence of the underlying cause or complications
• Cell count and differential : A neutrophil count ≥ 250 cells/mm³ indicates spontaneous bacterial peritonitis .
• Ascitic fluid albumin : for SAAG calculation (obtain same-day serum and ascitic fluid samples ) ^[6]
• Ascitic fluid total protein

Additional studies (based on the pretest probability of the underlying etiology)

• Suspected infection
  • Microbiology: ascitic fluid culture ; in blood culture bottles (aerobic and anaerobic) and G ram stain ^[8]
  • Studies to differentiate SBP from secondary spontaneous peritonitis: LDH , glucose, CEA, alkaline phosphatase (see "Spontaneous bacterial peritonitis" for details)
  • A cid-fast bacilli smear and mycobacterial cultures (low sensitivity): only if there is clinical suspicion or a high risk of tuberculous peritonitis
• Suspected malignancy (e.g., peritoneal carcinomatosis)
  • Ascitic fluid cytology
  • Ascitic fluid tumor markers: not routinely recommended for the assessment of malignancy-related ascites
    • Cancer antigen 125 (CA-125): elevated in most patients with ascites regardless of etiology
    • Carcinoembryonic antigen (CEA): potentially of diagnostic and prognostic value in patients with gastric and intestinal carcinoma ^[8]
• Suspected chylous ascites (milky ascitic fluid): Ascitic fluid triglyceride levels; levels > 200 mg/dL indicate chylous ascites ^[15]
• Suspected pancreatic ascites or bowel perforation: Ascitic fluid amylase levels; elevated levels provide supportive evidence of pancreatitis or bowel perforation ^[16]

Classification

The International Ascites Club classifies the severity classification of ascites as follows: ^[2]

• Mild ascites (grade 1): ascites only detectable by ultrasound
• Moderate ascites (grade 2): moderate abdominal distention
• Large ascites (grade 3): marked abdominal distention

Treatment

Approach ^{[5] [6] [11]}

• All patients
  • Identify and treat the underlying condition.
  • Therapeutic paracentesis for tense or large ascites
• Patients with cirrhotic ascites
  • Treatment of cirrhosis, including avoidance of certain medications such as NSAIDs and ACE inhibitors
  • Sodium restriction and diuretics are the mainstays of medical and supportive therapy. ^[8]
  • Consider advanced therapies for refractory ascites, e.g., liver transplant.
• Patients with noncirrhotic ascites: treatment of the underlying cause, e.g.
  • Surgery or radiochemotherapy for malignancy
  • Treatment of heart failure
  • Antituberculosis therapy

Obtain hepatology consult for patients with new-onset ascites and known or suspected liver disease.

Medical and supportive therapy ^{[6] [11] [17]}

This section details the management of ascites due to cirrhosis. Medical and/or supportive management of other causes of ascites (e.g., heart failure, nephrotic syndrome, peritoneal carcinomatosis, tuberculosis) are outlined in the respective articles for these conditions.

Salt and fluid restriction

• Dietary sodium restriction : 2 g/day or 88 mEq/d ( 2 g of sodium = 5 g of salt)
• Fluid restriction: 1 L/day (only if serum Na⁺ < 125 mEq/L)

Diuretics

• Monotherapy with spironolactone may be preferable for new-onset ascites, mild ascites , moderate ascites , and outpatients.
• Combination therapy with spironolactone ; PLUS furosemide in a 10:4 ratio may be preferable for recurrent gross ascites or when faster resolution of ascites is required (e.g., in hospitalized patients).
• Once ascites is under control, taper to the minimum effective dose to reduce side effects.

Combination diuretic therapy is associated with more rapid ascites reduction and a lower risk of potassium imbalance than monotherapy. ^{[8] [17]}

Diuretics should be used with caution in patients with severe hyponatremia, hepatic encephalopathy, and/or renal function deterioration.

Empiric antibiotic therapy ^{[6] [11]}

Antibiotic therapy for patients with cirrhosis and ascites is recommended in the following situations:

Monitoring ^{[6] [17]}

Therapeutic paracentesis may be performed for symptom relief. Paracentesis is also a diagnostic procedure (see "Diagnostic paracentesis").

Clotting factors (e.g., fresh frozen plasma) and/or platelets are not routinely recommended before paracentesis in patients with INR > 1.5 or platelets < 50 cells/mm³ , as procedure-related hemorrhage is uncommon. ^{[6] [17]}

Consider performing paracentesis under ultrasound guidance to reduce the risk of serious complications and improve success rates. See "FAST" for basic principles of abdominal ultrasound. ^[19]

Ascites is considered refractory if it does not respond to treatment or recurs after therapeutic paracentesis despite dietary sodium restriction and high-dose diuretic therapy. The following recommendations apply to refractory ascites in patients with cirrhosis.

Half of all patients with cirrhosis who develop refractory ascites die within a year. Do not delay referral for surgical management. ^[6]

Complications

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References

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