Ascites

Ascites is the abnormal accumulation of fluid in the peritoneal cavity and a common complication of diseases presenting with portal hypertension (e.g., liver cirrhosis, acute liver failure) and/or hypoalbuminemia (e.g., nephrotic syndrome). Other conditions resulting in ascites include chronic heart failure, visceral inflammation (e.g., pancreatitis), and malignant tumors. Clinical features include progressive abdominal distension, shifting dullness, and a positive fluid wave test. Ascites may be associated with abdominal pain in rare cases. An adequate clinical assessment should be followed by imaging (e.g., ultrasound), which helps to identify even very small quantities of ascitic fluid in the peritoneal cavity. If the onset of ascites is spontaneous or the origin is unclear, an abdominal paracentesis and ascitic fluid assessment may be performed (i.e., to determine the appearance, composition). Management involves treating the underlying condition in addition to sodium restriction and diuretic therapy. Severe or refractory ascites may require therapeutic abdominal paracentesis. A severe complication is spontaneous bacterial peritonitis.

• The etiology can be determined using the serum-ascites albumin gradient (SAAG) based on Starling's law.
• Calculation: SAAG = (albumin levels in serum) - (albumin levels in ascitic fluid)

		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 ↓ intravascular 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

References:^{[1][2][3][4][5][6][7]}

• Progressive abdominal distension
• 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.
• Abdominal pain may be present
• Abdominal wall hernias (e.g., umbilical, inguinal, or incisional hernias)
• Peripheral or generalized edema
• Symptoms associated with increased abdominal distension
  • Early satiety
  • Weight gain
  • Dyspnea
  • Features of malnutrition; diarrhea
• Signs of underlying disease
  • Enlarged liver, jaundice, spider angioma, palmar erythema: chronic liver disease
  • Elevated jugular venous pressure: heart failure
  • Virchow's node; and weight loss: upper abdominal malignancy

References:^[3][8][9]

• Clinical chemistry
  • Dilutional hyponatremia as a result of overhydration despite normal or increased sodium concentration (see electrolyte imbalance of sodium)
  • Hypoalbuminemia
• Imaging
  • Ultrasound (best initial test): Reliable detection even of smaller quantities of ascitic fluid: lower limit of detection approx. 30 mL
  • CT scan
    • Isodense areas of fluid in the lower region of the abdomen
    • Fluid can also be found around the liver , spleen, and flanks (e.g., perihepatic, posterior subhepatic, rectouterine pouch)

• Ultrasound-guided diagnostic paracentesis
  • Indications: first diagnosed ascites, worsening ascites or suspected complication.
• Ascitic fluid analysis
  • Appearance and color
  • Cell count and differentiation
  • Albumin and total protein
  • LDH
  • Gram stain and microbial culture
  • Acid-fast bacilli smear, mycobacterial culture, NAAT, and adenosine deaminase level if tuberculosis is suspected
  • Cytopathology

Criteria for analyzing ascitic fluid	Ascites due to portal hypertension (SAAG ≥ 1.1 g/dL) (Previously referred to as transudate)	Ascites due to other causes (SAAG < 1.1 g/dL) (Previously referred to as exudate)
Color	Clear, sometimes opalescent	Cloudy Bloody Milky Dark brown
Cell count and differentiation	↓ Cell count	↑ Cell count Neutrophil count > 250/μL
Protein concentration	↑ Protein levels (> 2.5 g/dL) Right heart failure ↓ Protein levels (< 2.5 g/dL) Hepatic cirrhosis	↑ Protein levels (> 2.5 g/dL) Hepatic malignancy Peritoneal carcinomatosis Pancreatitis Chylous ascites Tuberculosis ↓ Protein levels (< 2.5 g/dL) Nephrotic syndrome

Remember, eggs, like“EGGsudates” (exudates) are high in protein.

References:^[1][2]

General measures

• Treatment of the underlying disease (e.g., using anticoagulation in case of a thrombosis or tuberculostatics in case of a tubercular peritonitis)
• Sodium restriction
• Regular weight control
• Water restriction or avoiding overhydration

Diuretic therapy

• Indications
  • Portal hypertensive ascites: usually responsive; may be treated in the same way as ascites caused by liver cirrhosis (see treatment of cirrhosis).
  • Non-portal hypertensive ascites (exudate): usually not effective; therefore it is essential to focus on treating the underlying disease!
• Approach
  • Spironolactone
  • Additionally, or in the case of massive ascites: loop diuretics
• Regular control of potassium and creatinine during diuretic therapy

Diuretics should be used with precaution in cases of severe hyponatremia, hepatic encephalopathy, or deterioration of renal function!

Treatment of refractory ascites

• Indication: inadequate response to diuretics, frequent recurrence, or when diuretic therapy is contraindicated
• Procedures
  • Therapeutic large-volume paracentesis
  • Transjugular intrahepatic portosystemic shunt (TIPS)

References:^[1][2]

• Spontaneous bacterial peritonitis (ascitic fluid infection): abdominal tenderness, fever, altered mental status

We list the most important complications. The selection is not exhaustive.