Ascites

Ascites: Excerpt from The 5-Minute Pediatric Consult

Ruben W. Cerri, MD

Ascites - BASICS

Ascites - description

• Ascites is defined as an abnormal amount of intraperitoneal fluid:
  • These may be transudates (thin, low protein count and low specific gravity) or exudates (high protein count and specific gravity)
• Peritoneal fluid formation is a dynamic process of production and absorption.
• See: (Table 1, Analysis of Ascitic Fluid)

Ascites - pathophysiology

• Development of ascitic fluid may be sudden or insidious, associated with nonhepatic etiologies, or secondary to acute reduction in hepatocellular function in a marginally compensated liver.
• Intra-abdominal factors (resulting in a net flow of fluid and protein out of the mesenteric capillary bed):
  • Decreased plasma colloid osmotic pressure
  • Increased capillary pressure
  • Increased ascitic colloid osmotic fluid pressure
  • Decreased ascitic fluid hydrostatic pressure
• Accumulation of fluid occurs with:
  • Inflammatory conditions (e.g., mesenteric adenitis, tuberculosis, pancreatitis, secondary to inflammation of visceral and/or parietal peritoneum)
  • Obstruction of portal vein flow and/or lymphatic flow by mass, tumor, or external pressure; tumors of abdominal viscera, retroperitoneum, thorax, or mediastinum (often characterized by chylous ascites)
  • Primary (congenital) abnormalities of the lymphatics (Milroy disease), congenital neonatal ascites, secondary to abdominal trauma (e.g. ureteral rupture), hematologic diseases (hydrops secondary to hemolysis), congestive heart disease; and lysosomal storage diseases including sialidosis (neuraminidase deficiency), Salla disease, GM1 gangliosidosis, Gaucher disease, and Niemann-Pick type C
  • Decreased plasma oncotic pressure secondary to hypoalbuminemia (increased losses: Renal, GI tract; decreased production: Hepatic failure)
  • Rupture of intra-abdominal viscus or peritoneal/mesenteric cyst

Ascites - etiology

• Hepatic: Liver cirrhosis, chronic liver failure, portal vein occlusion, Budd-Chiari syndrome, lysosomal storage disease
• Renal: Nephrotic syndrome, obstructive uropathy, perforated urinary tract, peritoneal dialysis
• Cardiac: CHF, constrictive pericarditis, inferior vena cava web
• Infectious: Abscess, tuberculosis, Chlamydia infection, schistosomiasis
• GI: Infarcted bowel, perforation
• Pancreatic: Pancreatitis, ruptured pancreatic duct
• Neoplastic: Lymphoma, neuroblastoma
• Gynecologic: Ovarian tumors, torsion, or rupture
• Miscellaneous: Systemic lupus erythematous, eosinophilic ascites, chylous ascites, hypothyroidism, ventriculoperitoneal shunt

Ascites - DIAGNOSIS

Ascites - signs & symptoms

Ascites - history

• The etiology for acute decompensation in hepatocellular function (e.g., massive bleeding, sepsis, superimposed infections) should be investigated.
• Use of umbilical catheters in newborn period
• Evidence of chronic liver disease
• Respiratory distress
• Exposure to hepatotoxins
• Mental retardation suggesting metabolic disease

Ascites - physical exam

• Vital signs
• Abdominal circumference
• Weight
• Auscultation of the pericardium
• Neurologic examination to evaluate for encephalopathy
• Skin changes suggestive of chronic liver disease
• Special attention should be directed toward identification of a distended abdomen, fullness in the flanks, inverted umbilicus, and development of hernias, scrotal edema, rectal prolapse, and a prominent anterior wall.
• Techniques to detect free intra-abdominal fluid include presence of a fluid wave, shifting dullness, and puddle sign (percuss abdomen with patient flexed at hip to detect dullness that may accurately detect fluid over 1 L).
• Other physical examination signs include splenomegaly and prominent abdominal veins (portal hypertension), cor pulmonale (congestive heart failure), pericardial friction rub (pericarditis), diffuse abdominal pain (peritonitis or visceral perforation), abdominal pain radiating to the back (pancreatitis), and lymphedema (lymphatic obstruction/trauma to the thoracic duct).

Ascites - tests

Ascites - lab

• Complete WBC count
• Electrolytes
• Liver function tests: Transaminases, prothrombin time/partial thromboplastin time:
  • Total protein, albumin
• Amylase and lipase (to exclude pancreatitis)
• Creatinine and blood urea nitrogen
• Blood cultures
• Urine for specific gravity
• Viral serologies, including hepatitis B and C viruses, coxsackievirus, enteroviruses

Ascites - imaging

• Abdominal radiography
• Ultrasound of the abdomen to differentiate between free and loculated fluid collection and the presence of intra-abdominal masses
• Abdominal computed axial tomography

Ascites - diag proced-surgery

• Abdominal paracentesis:
  • Safe procedure in the evaluation of etiologies of ascites. The 2 complications are perforation of the bowel and hemorrhage. With sterile conditions, a narrow-bore angiocatheter, usually 23-gauge, is inserted through the linea alba 2 cm below the umbilicus, using the Z-technique.
  • Done for: Routine studies, including WBC count, culture, LDH, total protein, albumin, glucose, Gram stain, amylase, cholesterol with triglycerides, and cytology
• Calculate serum–ascites albumin gradient (SAAG): Serum albumin–ascites albumin. SAAG ≥1.1 g/dL, portal hypertension very likely; SAAG <1.1 g/dL, suspect other causes. These tests require ~10–20 mL of fluid:
  • When glucose in the ascitic fluid is <30 mg/dL, tuberculous peritonitis must be excluded.
  • When ascitic amylase is greater than the normal serum amylase, pancreatitis is suggested.

Ascites - pathological findings

Analysis of ascitic fluid:

• The fluid should be examined for its gross appearance; protein content, cell count, and differential cell count should be determined.
• Gram and acid-fast stains and culture should be performed. Cytologic and cell-block examination may disclose an otherwise unsuspected carcinoma or storage disorder.
• See details in Table 1

Ascites - differencial diagnosis

• Enlarged liver or spleen
• Mesenteric cyst: Does not have shifting dullness when position is changed
• Intestinal obstruction

Ascites - TREATMENT

Ascites - general measures

• The management of the ascites should be directed toward the underlying etiology. In a patient with cirrhosis, accumulation of ascites should be avoided by preventing complications such as sodium and fluid overload, esophageal hemorrhage, spontaneous bacterial peritonitis, hepatorenal syndrome, inferior vena cava obstruction, and renal and cardiac circulatory disturbances.
• Sodium intake should be restricted to 1–2 mEq/kg/d (low-salt diet).
• Water should be restricted to 50–75% of maintenance requirements in patients with significant water excess or profound hyponatremia.

  Table 1. Analysis of Ascitic Fluid

  Cell Count

  			Serum-Ascites
  			Albumin
  Condition	Gross Appearance	Protein, g/L	Gradient, g/dL	RBCs, >10,000/μL	Include WBC	Other Tests
  Cirrhosis	Straw-colored or bile-stained	<25 (95%)	>1.1	1%	<250 (90%); predominantly mesothelial
  Neoplasm	Straw-colored, hemorrhagic, mucinous, or chylous	>25 (75%)	<1.1	20%	>1000 (50%); variable cell types	Cytology, cell block, peritoneal biopsy
  Tuberculous peritonitis	Clear, turbid, hemorrhagic, chylous	>25 (50%)	<1.1	7%	>1000 (70%); usually >70% lymphocytes	Peritoneal biopsy, stain and culture for acid-fast bacilli
  Pyogenic peritonitis	Turbid or purulent	If purulent, >25	<1.1	Unusual	Predominantly polymorphonuclear leukocytes	Positive Gram’s stain, culture
  CHF	Straw-colored	Variable, 15–53	>1.1	10%	<1000 (90%); usually mesothelial, mononuclear
  Nephrosis	Straw-colored or chylous	<25 (100%)	<1.1	Unusual	<250; mesothelial, mononuclear	If chylous, ether extraction, Sudan staining
  Pancreatic ascites (pancreatitis, pseudocyst)	Turbid, hemorrhagic, or chylous	Variable, often >25	<1.1	Variable, may be blood-stained	Variable	Increased amylase in ascitic fluid and serum

• Diuretics may be used to promote negative sodium and water balance. Spironolactone (2–3 mg/kg/d). Furosemide may be added if no response to spironolactone. When diuretics are used, urine output and serum electrolytes should be closely monitored to prevent prerenal azotemia and decreased effective blood flow to the kidneys.
• Refractory ascites: Diuretic-refractory ascites derives from a lack of response to dietary sodium restriction and maximal diuretic therapy. Treatment options:
  • Therapeutic abdominal paracentesis (large-volume paracentesis) should be used only in resistant cases and for tense ascites, because ascitic fluid tends to reaccumulate. Paracentesis of volumes >1 L should be accompanied by IV infusion of 25% albumin during the procedure.
  • LeVeen shunt (peritoneal–venous shunting) connects the peritoneal cavity with the superior vena cava near its entrance into the right atrium. It is rarely used as a therapeutic option because of the high frequency of infection, obstruction, and other complications.
  • Transjugular intrahepatic portosystemic shunting (TIPS) consists of a metallic stent that bridges the branches of the portal and hepatic veins. May be valuable in cases where portal hypertension is felt to be the underlying etiology of ascitic accumulation. Variceal hemorrhage remains the main indication for transjugular intrahepatic portosystemic shunting.
  • Orthotopic liver transplantation (OLT) is the only curative therapy for refractory ascites from liver disease and the only definitive treatment that has been shown to improve survival.

Ascites - FOLLOW UP

Ascites - prognosis

Depends on the etiology:

• Nephrotic syndrome: Will regress as proteinuria clears
• Liver failure: Will depend on recovery of liver function
• Cirrhosis (complicated by ascites): Associated with significant morbidity and mortality, related in part to the severe underlying liver disease and in part to the ascites per se. Once ascites appears, the expected mortality rate is ~50% in just 2 years. With liver transplantation, survival is improved dramatically.

Ascites - complications

• Infection:
  • Ascitic fluid infection can be classified into 3 categories based on ascitic culture results, polymorphonuclear leukocyte count, and presence or absence of a surgical source of infection
  • An abdominal paracentesis must be performed and ascitic fluid must be analyzed before a confident diagnosis of ascitic fluid infection can be made. The blood culture bottle should be injected with peritoneal fluid at the bedside in order to increase the culture’s yield.
  • Spontaneous ascitic fluid infection: Infection of the peritoneal fluid of patients with ascites in the absence of secondary causes, such as bowel perforation or intra-abdominal abscess
• Subtypes:
  • Spontaneous bacterial peritonitis (SBP) (65%)
  • Monomicrobial nonneutrocytic bacterascites (MNB)
  • Culture-negative neutrocytic ascites (CNNA)
• Secondary bacterial peritonitis: An identified intra-abdominal surgically treatable primary source of infection (e.g., perforated gut, perinephric abscess) that usually requires emergency surgical intervention
• Polymicrobial bacterascites: This diagnosis should be suspected when the paracentesis is traumatic or unusually difficult because of ileus, or when stool or air is aspirated into the paracentesis syringe (diagnostic of gut perforation by the paracentesis needle). Antibiotic therapy should be started if there is a high index of suspicion and:
  • Polymorphonuclear leukocytes <250/mm³: No treatment
  • Polymorphonuclear leukocytes >250 but <500 mm³: IV antibiotics if clinical suspicion high; or, wait and retap
  • Polymorphonuclear leukocytes >500 mm³: IV antibiotics (e.g., cefotaxime + ampicillin)
  • Polymorphonuclear leukocytes >500 mm³: Rule out secondary peritonitis.
  • An indication of therapeutic response is a decrease in the neutrophil count in the ascitic fluid by 50% from that detected on presentation. It is appropriate to treat according to sensitivities when cultures are available. The length of therapy depends on clinical response but should be a minimum of 10 days.
• Other complications:
  • Respiratory distress from decreased lung volume and diaphragmatic limitation: Hepatic hydrothorax (large symptomatic pleural effusion that occurs in a cirrhotic patient in the absence of primary cardiopulmonary disease); abdominal wall hernias with rupture; tense ascites with leakage (especially after paracentesis)
• Conservative management consists of appropriate initial therapy for most of these except hernia rupture, which requires surgical reduction.

Ascites - patient monitoring

• Weight and effects of diuretics should be assessed closely, with attention to preservation of renal function.
• Urine and serum electrolytes should be monitored.
• Abdominal girth should be measured frequently.
• In cases of infection or peritonitis, a repeat paracentesis should be performed ~48 hours after the initiation of antibiotics for culture and WBC count.

• With congenital ascites, evaluate for lysosomal storage diseases.
• When performing paracentesis, make certain that the fluid is ascitic and not intraluminal.
• Ultrasonography may be helpful to determine the location of this fluid.
• With new onset of ascites, make certain to evaluate for abdominal neoplasia.
• With marginally compensated liver disease, attempt to identify the source of the patient’s acute decompensation.

Ascites - bibliography

McDiarmid SV. Treatment of end-stage liver disease. In: Wyllie R, Hyams J, eds. Pediatric Gastrointestinal Diseases. Philadelphia: WB Saunders; 2002: 1250–1271.Reif S, Blendis L. Portal hypertension and ascites. In: Wyllie R, Hyams J, eds. Pediatric Gastrointestinal Diseases. Philadelphia: WB Saunders; 2002: 233–247.
1. Sabri M, Saps M, Peters JM. Pathophysiology and management of pediatric ascites. Curr Gastroenterol Rep. 2003;5(3):240–246.
2. Wongcharatrawee S, Garcia-Tsao G. Clinical management of ascites and its complications. Clin Liver Dis. 2001;5:833–850.
3. Wong F. The pathophysiologic basis for the treatment of cirrhotic ascites. Clin Liver Dis. 2001;5(3):819–832.
4. Yu AS, Hu KQ. Management of ascites. Clin Liver Dis. 2001;5(2):541–568.
5. Zervos EE. Management of medically refractory ascites. Amer J Surg. 2001;181(3):256–264.

Ascites - CODES

Ascites - icd9

789.5 Ascites

Ascites - FAQ

• Q: What is the common thought regarding neonatal ascites?
• A: Exclude lysosomal storage and/or other metabolic diseases.
• Q: What is the best test to discriminate the type of ascites?
• A: Analysis of the peritoneal fluid collected by abdominal paracentesis is required for this purpose.

Book Source Details

• Book Title: The 5-Minute Pediatric Consult
• Author(s): M. William Schwartz MD; et al.
• Year of Publication: 2008
• Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

More About Ascites

• Back to disease: Ascites: Introduction
• Next Book Extract About Ascites: Peritonitis (The 5-Minute Pediatric Consult)
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: The 5-Minute Pediatric Consult Authors: M. William Schwartz MD; et al. Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7577-9

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