Summary

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 are 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.

Etiology

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)

High SAAG ≥ 1.1 g/dL (obsolete term: transudate)			Low SAAG < 1.1 g/dL (obsolete term: exudate)
Etiology	Pathophysiology		Etiology	Pathophysiology
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	→ ↑ pressure in portal vein → ↑ hydrostatic pressure in the hepatic vessels → pushing of fluid out from the intravascular space to the peritoneal cavity	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
			Infectious (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]

Clinical features

Progressive abdominal distension
Fluid wave test; : a 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 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: liver disease
- Elevated jugular venous pressure: heart failure
- Virchow's node and weight loss: upper abdominal malignancy

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

Subtypes and variants

Chylous ascites
- Definition: collection of lymph in the abdominal cavity, which is characteristically triglyceride-rich and has a milky appearance
- Etiology: malignancy (e.g., lymphoma), hepatic cirrhosis, or other lymph disorders (e.g., lymphatic hyperplasia) which result in increased lymph production
Bloody ascites
- Definition: ascitic fluid with RBC > 50,000 mm³
- Etiology: : may be spontaneous (e.g, malignant mass eroding into vessels) or iatrogenic (e.g., following paracentesis or biopsy in patients with cirrhosis)

References:^[10]

Diagnostics

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 und total protein
- LDH
- Direct detection of pathogens
- Diagnostic (cyto‑)pathology

Criteria for analyzing ascitic fluid
	Portal hypertensive ascites (high albumin gradient)	Non-portal hypertensive ascites (low albumin gradient)
Color	Clear, sometimes opalescent	Cloudy Bloody
Cell count and differentiation	↓ Cell count	↑ Cell count
Protein concentration	↓ Protein levels (< 2.5 g/dL)	↑ Protein levels (> 2.5 g/dL)

Eggs (protein) → “EGGsudate”

References:^[1]^[2]

Treatment

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]

Complications

Spontaneous bacterial peritonitis (SBP)

Definition: bacterial infection of ascitic fluid in the absence of other intra-abdominal causes (which would otherwise lead to secondary bacterial peritonitis )
Etiology and risk factors
- Often seen in patients with progressed liver cirrhosis; or patients receiving peritoneal dialysis.
- Bacterial species: E. coli most common in ascites. Klebsiella spp. and streptococci are frequently involved in nosocomial cases of SBP.
Pathophysiology
- Migration of bacteria through the intestinal wall and colonization of mesenteric lymph nodes (bacterial translocation)
Clinical features
- Often asymptomatic
- Abdominal pain, tense abdominal wall, and fever is possible.
Diagnosis
- Gold standard: diagnostic paracentesis BEFORE application of antibiotics
- > 250 polymorphonuclear leukocytes/μL ascites: SBP per definition
- Determination of pathogens is rarely successful
Treatment:
- First-line: 3^rd generation cephalosporin IV broad spectrum therapy
- Follow-up after 48 h via repeated paracentesis
  - If granulocytes decrease to < 250 /μL, treatment can be terminated after five additional days
  - If granulocytes do not decrease by ≥ 25%: modify treatment according to resistogram
Prognosis: high recurrence and mortality rate

References:^[1]

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