section name header

Basics ⬇

Basics

Definition

The escape of fluid, either transudate or exudate, into the abdominal cavity between the parietal and visceral peritoneum.

Pathophysiology

  • Ascites can be caused by the following:
    • CHF and associated interference in venous return
    • Depletion of plasma proteins associated with inappropriate loss of protein from renal or gastrointestinal disease-protein-losing nephropathy or enteropathy, respectively
    • Obstruction of the vena cava or portal vein, or lymphatic drainage due to neoplastic occlusion
    • Overt neoplastic effusion
    • Peritonitis-infective or inflammatory
    • Electrolyte imbalance, especially hypernatremia
    • Liver cirrhosis.

Systems Affected

  • Cardiovascular
  • Gastrointestinal
  • Hemic/Lymph/Immune
  • Renal/Urologic

Signalment

  • Dogs and cats
  • No species or breed predisposition

Signs

  • Episodic weakness
  • Lethargy
  • Abdominal fullness
  • Abdominal discomfort when palpated
  • Dyspnea from abdominal distension or associated pleural effusion
  • Anorexia
  • Vomiting
  • Weight gain
  • Scrotal or penile edema
  • Groaning when lying down

Causes

  • Nephrotic syndrome
  • Cirrhosis of liver
  • Right-sided CHF
  • Hypoproteinemia
  • Ruptured bladder
  • Peritonitis
  • Abdominal neoplasia
  • Abdominal hemorrhage

Risk Factors

N/A

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

Differentiating Abdominal Distension without Effusion

  • Organomegaly-hepatomegaly, splenomegaly, renomegaly, and hydrometra.
  • Abdominal neoplasia.
  • Pregnancy.
  • Bladder distension.
  • Obesity.
  • Gastric dilatation.

Differentiating Diseases

  • Transudate-nephrotic syndrome, cirrhosis of liver, right-sided CHF, hypoproteinemia, and ruptured bladder.
  • Exudate-peritonitis, abdominal neoplasia, and hemorrhage.

CBC/Biochemistry/Urinalysis

  • Neutrophilic leukocytosis occurs in patients with systemic infection.
  • Albumin is low in patients with impaired liver synthesis, gastrointestinal loss, or renal loss.
  • Cholesterol is low in patients with impaired liver synthesis.

Liver Enzymes

  • Low to normal in patients with impaired liver synthesis.
  • High in patients with liver inflammation, hyperadrenocorticism, gallbladder obstruction, and chronic passive congestion.

Total and Direct Bilirubin

  • Low to normal in patients with impaired liver synthesis.
  • High in patients with biliary obstruction caused by tumor, gallbladder distension, or obstruction.

BUN and Creatinine

  • High in patients with renal failure.
  • BUN low in patients with impaired liver synthesis or hyperadrenocorticism.

Glucose

Low in patients with impaired liver synthesis.

Other Laboratory Tests

  • To detect hypoproteinemia-protein electrophoresis and immune profile.
  • To detect proteinuria-urinary protein:creatinine ratio (normal <0.5:1).
  • To detect liver ascites-analysis of serum ascites albumin gradient.

Imaging

  • Thoracic and abdominal radiography is sometimes helpful.
  • Ultrasonography of the liver, spleen, pancreas, kidney, bladder, and abdomen can often determine cause.
  • Stages of ascites:
    • Stage I: minimal ascites. Detected by ultrasound only.
    • Stage II: moderate ascites. Abdominal distention visible and/or noted on ballottement.
    • Stage III: significant ascites. Marked abdominal distention. Patient uncomfortable, possibly with labored breathing.

Diagnostic Procedures

Ascitic Fluid Evaluation

Exfoliative cytologic examination and bacterial culture and antibiotic sensitivity-remove approximately 3–5 mL of abdominal fluid via aseptic technique.

Transudate

  • Clear and colorless.
  • Protein <2.5 g/dL.
  • Specific gravity <1.018.
  • Cells <1,000/mm3-neutrophils and mesothelial cells.

Modified Transudate

  • Red or pink; may be slightly cloudy.
  • Protein 2.5–5 g/dL.
  • Specific gravity >1.018.
  • Cells <5,000/mm3-neutrophils, mesothelial cells, erythrocytes, and lymphocytes.

Exudate (Non-septic)

  • Pink or white; cloudy.
  • Protein 2.5–5 g/dL.
  • Specific gravity >1.018.
  • Cells 5,000–50,000/mm3-neutrophils, mesothelial cells, macrophages, erythrocytes, and lymphocytes.

Exudate (Septic)

  • Red, white, or yellow; cloudy.
  • Protein >4.0 g/dL.
  • Specific gravity >1.018.
  • Cells 5,000–100,000/mm3-neutrophils, mesothelial cells, macrophages, erythrocytes, lymphocytes, and bacteria.

Hemorrhage

  • Red; spun supernatant clear and sediment red.
  • Protein >5.5 g/dL.
  • Specific gravity 1.007–1.027.
  • Cells consistent with peripheral blood.
  • Does not clot.

Chyle

  • Pink, straw, or white.
  • Protein 2.5–7 g/dL.
  • Specific gravity 1.007–>1.040.
  • Cells <10,000/mm3-neutrophils, mesothelial cells, and large population of small lymphocytes.
  • Other-fluid in tube separates into cream-like layer when refrigerated; fat droplets stain with Sudan III.

Pseudochyle

  • White.
  • Protein >2.5 g/dL.
  • Specific gravity 1.007–1.040.
  • Cells <10,000/mm3-neutrophils, mesothelial cells, and small lymphocytes.
  • Other-fluid in tube does not separate into cream-like layer when refrigerated; does not stain with Sudan III.

Urine

  • Clear to pale yellow.
  • Protein >2.5 g/dL.
  • Specific gravity 1–>1.040.
  • Cells 5,000–50,000/mm3-neutrophils, erythrocytes, lymphocytes, and macrophages.
  • Other-if the urinary bladder ruptured <12 hours before, urinary glucose and protein could be negative; if bladder ruptured >12 hours before, urine becomes a dialysis medium with ultrafiltrate of plasma, and urine contains glucose and protein.

Bile

  • Slightly cloudy and yellow.
  • Protein >2.5 g/dL.
  • Specific gravity >1.018.
  • Cells 5,000–750,000/mm3-neutrophils, erythrocytes, macrophages, and lymphocytes.
  • Other-bilirubin confirmed by urine dipstick; non-icteric patient may have gallbladder rupture, biliary tree leakage, or rupture in the proximal bowel.

Treatment ⬆ ⬇

Treatment

Large-Volume Paracentesis

  • Stage III treatment.
  • Pretreat patient with hetastarch (6%) &commat 1–2 mL/kg for 2 hours.
  • Abdominal tap (paracentesis), until drainage slows.
  • Post-treat patient with hetastarch (6%) &commat 1–2 mL/kg for 4 hours.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

  • Patients with liver insufficiency or CHF-restrict sodium and give a diuretic combination of hydrochlorothiazide (2–4 mg/kg q12h PO) and spironolactone (1–2 mg/kg q12h PO); if control is inadequate, furosemide (1–2 mg/kg q8h PO) can be substituted for the thiazide with spironolactone continued; must monitor serum potassium concentration to prevent potassium imbalances.
  • Patients with hypoproteinemia, nephrotic syndrome, and associated ascitic fluid accumulation-can treat as above with the addition of hetastarch (6% hetastarch in 0.9% NaCl); administer an IV bolus (dogs, 20 mL/kg; cats, 10–15 mL/kg) slowly over ∼ 1 hour; hetastarch increases plasma oncotic pressure and pulls fluid into the intravascular space for up to 24–48 hours.
  • Systemic antibiotic therapy is dictated by bacterial identification and sensitivity testing in patients with septic exudate ascites.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Varies with the underlying cause.
  • Check sodium, potassium, BUN, creatinine, and weight fluctuations periodically if the patient is maintained on a diuretic.

Possible Complications

Aggressive diuretic administration may cause hypokalemia, which could predispose to metabolic alkalosis and exacerbation of hepatic encephalopathy in patients with underlying liver disease; alkalosis causes a shift from NH4 to NH3.

Miscellaneous ⬆

Miscellaneous

Age-Related Factors

N/A

Pregnancy/Fertility/Breeding

N/A

Synonyms

Abdominal effusion

Abbreviations

CHF = congestive heart failure

Suggested Reading

Kramer RE, Sokol RJ, Yerushalmi B, Liu E, MacKenzie T, Hoffenberg EJ, Narkewicz MR. Large-volume paracentesis in the management of ascites in children. J Ped Gastro Nutr 2001; 33:245–249.

Lewis LD, Morris MLJr, Hand MS. Small Animal Clinical Nutrition, 3rd ed. Topeka, KS: Mark Morris Associates, 1987.

Li MK. Management of ascites. Hong Kong Med Di 2009, 14:27–29.

Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatol 2004, 39:1–16.

Gompf RE. The history and physical examination. In: Smith FWK, Tilley LP, Oyama MA, Sleeper MM, eds., Manual of Canine and Feline Cardiology, 5th ed. St. Louis, MO: Saunders Elsevier, 2015 (in press).

Kumar KS, Srikala D. Ascites with right heart failure in a dog: diagnosis and management. J Adv Vet Anim Res 2014, 1(3):140–144.

Pradham , MS, Dakshinkar , NP, Waghaye UG, Bodkhe AM. Successful treatment of ascites of hepatic origin in dog. Vet World 2008, 1(1):23.

Saravanan M, Sharma K, Kumar M, Vijaykumar H, Mondai DB. Analysis of serum ascites albumin gradient test in ascitic dogs. Vet World 2012, 5(5):285–287.

Author Jerry A. Thornhill

Consulting Editors Larry P. Tilley and Francis W.K. Smith, Jr.

Client Education Handout Available Online