1. CBC. Leukocytosis or left shift suggests infection; anemia may be associated with intra-abdominal bleeding.
2. Serum electrolytes, BUN, creatinine, liver function tests. Hypokalemia can cause an ileus. Elevated bilirubin and transaminases can identify hepatic disease. Elevated BUN and creatinine indicate renal failure.
3. ABGs. Respiratory acidosis implies hypoventilation from distention. Metabolic acidosis accompanies intestinal ischemia (eg, with severe necrotizing enterocolitis).
TABLE I-1. IDENTIFICATION OF ASCITIC FLUID
Transudate Clear yellow
Sp gr < 1.020, protein < 2.5 g/dL, serumiascltes albumen > 1.1
Sp gr > 1.020, protein > 3 g/dL serumiascltes albumen < 1.1, elevated leukocyte count Triglycerides < 1000 mg/dL, leukocytes 1000-5000 cells/mm3, 70-90% lymphocytes Creatinine 5-10 mg/dL Bilirubin 100-400 mg/mL
Many leukocytes, bacteria on Gram stain and culture
Clear yellow Green, golden yellow Purulent a Clear yellow In neonates who have never been fed.
4. Paracentesis. If ascites is present, insert butterfly needle in left lower quadrant and aspirate. Fluid is readily identified as serous, chyle, urine, bile, or pus (Table I-1). Serous fluid may be transudate (from increased hydrostatic pressure) or exudate (from inflammatory process).
5. p-HCG. Measure in any patient who may be pregnant. C. Radiographic and Other Studies
1. Chest and abdominal x-rays. Chest x-ray may show limited lung volumes from increased intra-abdominal pressure or pneumonia as a cause of ileus. Upright chest x-ray is the best view for detecting pneumoperitoneum. Abdominal x-rays will demonstrate intestinal obstruction, fecal retention, and adynamic ileus. A mass is suggested by a paucity of intestinal loops in a particular area; ascites is seen as generalized haziness.
2. GI contrast x-rays. May be indicated if there is evidence of obstruction.
3. Ultrasonography. Can characterize abdominal masses and is very sensitive in detecting fluid; can also differentiate free fluid, loculated fluid, and fluid in a cyst.
4. CT scan. Provides excellent anatomic detail of enlarged intraabdominal organs and other masses.
V. Plan. If respiration or perfusion is impaired, provide urgent resuscitation. Perform intubation with positive pressure ventilation and give IV fluid therapy if needed, even while diagnostic workup is carried out. Specific treatment depends on cause of distention.
A. Obstruction. Insert NG tube to suction, usually followed by surgery. Exceptions include meconium ileus, meconium plug, and intussusception, which may be treated successfully with contrast enemas. Hirschsprung disease may be managed with decompressive enemas until surgery is performed.
B. Adynamic ileus. Usually temporary; treat underlying cause.
C. Pneumoperitoneum. A surgical emergency with peritonitis; administer IV fluids and antibiotics while preparing patient for surgery.
D. Ascites. Aspirate only if there is respiratory compromise or pain, because this measure is only temporary (fluid will reaccumulate). If fluid is removed too rapidly, hypovolemia and hypotension may result.
1. Serous. Salt and fluid restriction, diuretics, and rarely, if intractable, peritoneovenous shunting. Definitive management of transudative and exudative ascites requires treatment of underlying condition (cirrhosis, constrictive pericarditis, peritonitis).
2. Biliary. Surgical drainage and alleviation of biliary obstruction.
3. Urinary. Decompression and drainage of obstruction.
4. Chylous. Reduce flow through obstructed or perforated lymphatic channels by withholding oral intake with TPN initially, then implement low-fat diet enhanced with medium-chain triglycerides. Surgery if no response.
E. Constipation. Rectal irrigations followed by comprehensive bowel management program. If Hirschsprung disease is suspected, order barium enema and rectal biopsy to confirm.
F. Masses. Enlarged intra-abdominal organs are treated by managing underlying condition. Urinary obstruction is decompressed. Abnormal masses are resected.
VI. Problem Case Diagnosis. The 8-month-old boy with abdominal distention had a history of delayed passage of meconium and infrequent bowel movements. He presented with respiratory distress and poor perfusion and had a massively distended, tympanitic abdomen. Rectal exam yielded an explosive output of stool and gas with decompression. Contrast enema and rectal biopsy confirmed Hirschsprung disease.
VII. Teaching Pearl: Question. Why do infants who are born with congenital obstruction of the intestine usually have no significant abdominal distention at the time of birth?
VIII. Teaching Pearl: Answer. Before birth, the GI tract does not contain air; thus, even with complete obstruction distention is rare. Over 24-48 hours, distention develops as air is swallowed, with the degree of distention being proportional to how far down in the intestine the obstruction is located. If an infant's abdomen is distended at birth, consider something other than simple mechanical obstruction (ie, meconium peritonitis or intra-abdominal fluid).
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