definition and pathophysiology

  • Pathologic accumulation of fluid within peritoneal cavity.
  • Results from increased hydrostatic and osmotic pressures within hepatic and mesenteric capillaries.
  • Fluid transfer from blood vessels to lymphatics overcomes drainage capacity.
  • Peripheral arterial vasodilation hypothesis: Portal hypertension causes splanchnic vasodilation, leading to decreased effective intravascular volume.
  • Baroreceptors trigger renin-angiotensin-aldosterone (RAA) system and antidiuretic hormone release, driving renal sodium and water retention.
  • Decreased plasma colloid osmotic pressure (hypoalbuminemia) further exacerbates fluid shift.

etiological classification

CategorySpecific etiologies
hepatic/portal hypertensionCirrhosis, portal vein thrombosis, Budd-Chiari syndrome, congenital hepatic fibrosis, veno-occlusive disease.
hypoalbuminemiaNephrotic syndrome, protein-losing enteropathy, severe malnutrition.
cardiacCongestive heart failure, constrictive pericarditis.
fetal/neonatalMeconium peritonitis (bowel perforation), parvovirus, urinary tract obstruction (uroascites), hydrops fetalis, biliary ascites.
chylousLymphatic malformations, trauma, thoracic duct injury, post-surgical.
infectious/inflammatoryTuberculous peritonitis, pancreatitis, systemic lupus erythematosus.

clinical evaluation

history

  • Rapid weight gain, increasing abdominal girth, ankle edema.
  • Neonatal umbilical catheterization (risk factor for portal vein thrombosis).
  • History of gastrointestinal bleeding or unexplained splenomegaly.

physical examination

  • Abdominal distension, bulging flanks, shifting dullness.
  • Fluid thrill, puddle sign (dullness over umbilicus in prone position).
  • Tense ascites associated with umbilical herniation.
  • Liver disease stigmata: Jaundice, palmar erythema, spider angiomata, caput medusae (dilated abdominal collaterals).
  • Cardiac evaluation: Markedly elevated jugular venous pressure indicates cardiac origin.

diagnostic investigations

imaging

  • Abdominal ultrasound: Most sensitive modality for ascites detection.
  • Differentiates ascites from obesity or pseudoascites (omental/ovarian cysts).
  • Identifies portal hypertension signs: Splenomegaly, enlarged portal vein.
  • Doppler evaluates hepatic vasculature flow and direction.

diagnostic paracentesis

  • Indicated upon initial detection, hospitalization, or clinical deterioration (fever, pain).
  • Ultrasound-guided tap recommended for loculated ascites.
  • No contraindication for prolonged prothrombin time unless disseminated intravascular coagulation present.

ascitic fluid analysis

TestFindingsInterpretation
serum-ascites albumin gradient (SAAG) 1.1 g/dLPortal hypertension (cirrhosis, fulminant failure, Budd-Chiari).
SAAG< 1.1 g/dLNon-portal hypertensive (tuberculous peritonitis, nephrotic syndrome).
polymorphonuclear (PMN) count 250 cells/mm3Spontaneous bacterial peritonitis (SBP).
lymphocyte countPredominant lymphocytesTuberculous infection.
triglycerides> 200 mg/dL, milky appearanceChylous ascites.
amylaseElevated ( > 5x serum level)Pancreatitis or intestinal perforation.
bilirubin> 6 mg/dL (greater than serum)Biliary or proximal small intestinal perforation.
urea/creatinineHigher than serum levelsUroascites.

management protocol

dietary modifications

  • Sodium restriction: Mainstay of therapy. Limit to 1-2 mEq/kg/day for infants/children or “no salt added” diet.
  • Fluid restriction: Rarely indicated unless severe hyponatremia (<125-130 mEq/L) present.
  • High-protein, high-calorie diet improves serum albumin and oncotic pressure.

pharmacologic therapy

  • Target optimal weight loss without intravascular volume depletion.
  • Spironolactone: Aldosterone antagonist, first-line agent. Dose 2-5 mg/kg/day.
  • Furosemide: Added for resistant ascites or to counteract spironolactone-induced hyperkalemia. Dose 0.5-2 mg/kg/day.
  • Optimal diuretic ratio: 5 (spironolactone) to 2 (furosemide).

refractory ascites interventions

  • Defined as ascites unresponsive to sodium restriction and maximal diuretic therapy.
  • Large volume paracentesis: Performed for tense ascites causing respiratory distress or severe pain.
  • Requires concurrent 20% albumin infusion (5 ml/kg) to prevent post-paracentesis circulatory dysfunction and rapid reaccumulation.
  • Transjugular intrahepatic portosystemic shunting (TIPS): Diverts portal blood flow, decreases portal pressure. Used as bridge to transplant.
  • Liver transplantation: Definitive treatment for ascites associated with end-stage liver disease, hypoalbuminemia, or recurrent SBP.

complications

spontaneous bacterial peritonitis (SBP)

  • Spontaneous infection of ascitic fluid without intra-abdominal source.
  • Pathogenesis: Bacterial translocation from gut to mesenteric lymph nodes, impaired immune clearance.
  • Presentation: Fever, abdominal pain, unexplained clinical deterioration, encephalopathy.
  • Diagnosis: Ascitic fluid PMN 250 cells/mm3.
  • Treatment: Intravenous third-generation cephalosporins (e.g., cefotaxime, ceftriaxone) for 5-7 days.
  • Prophylaxis: Long-term oral norfloxacin recommended after prior SBP episode.