Ascites The 5 Minute Pediatric Consult


	Ascites

Dror Wasserman

Database
Differential Diagnosis
Data Gathering
Physical Examination
Laboratory Aids
Therapy
Follow-Up
Common Questions and Answers
Bibliography

DATABASE

DEFINITION

Ascites is defined as effusion and accumulation of fluid in the abdominal cavity. Peritoneal fluid formation is a dynamic process of production and absorption. See table Analysis of Ascitic Fluid.

Analysis of Ascitic Fluid

PATHOPHYSIOLOGY

The development of ascitic fluid may be sudden or insidious associated with nonhepatic etiologies or an acute reduction in hepatocellular function in a marginally compensated liver (cirrhosis secondary to severe metabolic disturbances, i.e., tyrosinemia). Accumulation of fluid occurs with:

Inflammatory conditions, i.e., 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 obstruction; 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 GI tract trauma (ureteral rupture); hematologic (hydrops secondary to hemolysis from blood-type incompatibility); gastrointestinal or 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, gastrointestinal tract; decreased production: hepatic failure)
Rupture of intraabdominal viscus or peritoneal/mesenteric cyst

COMPLICATIONS

Spontaneous bacterial peritonitis is an infection of the peritoneal fluid of patients with ascites and may present with signs of peritoneal inflammation or more subtle findings. A high index of suspicion is necessary in order to make the diagnosis. Abdominal paracentesis is indicated, especially to establish the fluid’s white blood cell count and to obtain cultures. The blood culture bottle should be injected with peritoneal fluid at the bedside in order to increase the culture’s yield. Mortality is high.
- Treatment includes antibiotics, and paracentesis should be performed 48 hours after the introduction of treatment.
- An indication for therapeutic response will be 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.
Respiratory distress from decreased lung volume and diaphragmatic limitation

PROGNOSIS

Depends on the etiology. If from nephrotic syndrome, will regress as proteinuria clears. If from liver failure, will depend on recovery of liver function.

DIFFERENTIAL DIAGNOSIS

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

DATA GATHERING

HISTORY

The etiology for acute decompensation in hepatocellular function, i.e., massive bleeding, sepsis, superimposed infections, should be investigated.
Use of umbilical catheters in newborn period
Respiratory distress
Exposure to hepatotoxins

PHYSICAL EXAMINATION

Vital signs
Abdominal cavity 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 intraabdominal 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).

LABORATORY AIDS

TESTS

Laboratory Tests

Complete white blood cell count
Electrolytes
Liver-function tests: transaminases, PT/PTT
Amylase and lipase (to exclude pancreatitis)
Creatinine and blood urea nitrogen
Blood cultures
Urine for specific gravity
Viral serologies, including hepatitis B virus, coxsackievirus, enteroviruses

Imaging

Abdominal radiography
Ultrasound of the abdomen to differentiate between free and loculated fluid collection and the presence of intraabdominal masses
Abdominal computed axial tomography

Abdominal Paracentesis

Abdominal paracentesis is a safe procedure in the evaluation of etiologies of ascites. The two 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. Paracentesis is done for routine studies, including white blood cell count, culture, LDH, total protein, albumin, glucose, Gram stain, amylase, cholesterol with triglycerides, and cytology. These tests will require approximately 10 to 20 mL of fluid. Interpretation of these data are reflected in the table below.

When glucose in the ascitic fluid is below 30 mg/dL, tuberculous peritonitis must be excluded.
When ascitic amylase is greater than the normal serum amylase, pancreatitis is suggested.

THERAPY

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 esophageal hemorrhage, spontaneous bacterial peritonitis, hepatorenal syndrome, inferior vena cava obstruction, and renal and cardiac circulatory disturbances.

Sodium intake should be restricted to 1 to 2 mEq/kg/d (low-salt diet).
Water should be restricted to 75% of maintenance requirements.
Diuretics may be used to promote negative sodium and water balance. When diuretics are used, urine output and serum electrolytes should be monitored to prevent prerenal azotemia and decrease effective blood flow to the kidneys.
Therapeutic abdominal paracentesis should be used only in resistant cases, because ascitic fluid tends to reaccumulate. Paracentesis of volumes greater than 1 L should be accompanied by the IV infusion of salt-poor albumin during the procedure.
LeVeen shunt (peritoneal venous shunting) is rarely used as a therapeutic option because of the high frequency of infection, obstruction, and other complications.
Portosystemic shunting may be valuable in cases where portal hypertension is felt to be the underlying etiology of ascitic accumulation.

FOLLOW-UP

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 approximately 48 hours after the initiation of antibiotics for culture and white blood cell count.

PITFALLS

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.

COMMON QUESTIONS AND ANSWERS

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. Differentiation of a serous effusion versus exudate is thus achieved.

ICD-9-CM 789.5

BIBLIOGRAPHY

Clark, JH, Fitzgerald JF, Kleinman MB. Spontaneous bacterial peritonitis. J Pediatr 1984;104(4):495–500.

Fitzgerald JF. Ascites. In: Wyllie R, Hyams J, eds. Pediatric gastrointestinal diseases. Philadelphia: WB Saunders, 1993:151–160.

Gillan JE, Lowden JA, Gaskin K, et al. Congenital ascites as a presenting sign of lysosomal storage disease. J Pediatr 1984;104:225–231.

Hoefs JC, Runyon BA. Spontaneous bacterial peritonitis. Disease-A-Month 1985;31(9):1–48.

Machin GA. Diseases causing fetal and neonatal ascites. Pediatr Pathol 1985;4(3–4):195–211.

Wasserman D. Ascites. In: Altshuler S, Liacouras C, eds. Clinical pediatric gastroenterology. Philadelphia: Churchill Livingstone, 1997:323–325.

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