• Clinical science

Ascites

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

High SAAG

≥ 1.1 g/dL (obsolete term: transudate)

Low SAAG

< 1.1 g/dL (obsolete term: exudate)

Etiology Pathophysiology Etiology Pathophysiology
  • Arterial vasodilation hypothesis in cirrhosis :
    • Portal hypertensionvasodilation → 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
  • All result in intravascular osmotic gradient → secondary influx of water from the intravascular space to the peritoneal cavity
  • Malignancy
  • 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
  • Signs of underlying disease

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
  • 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

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
  • 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: 3rd 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.