Case 2: Edematous toddler with acute abdominal pain

A previously healthy three-year-old boy with a three-week history of intermittent abdominal pain presented with a sudden exacerbation of pain. The pain was diffuse but was most severe in the right lower quadrant. In addition, his parents noted some abdominal distension and fever starting on the day of presentation to the physician. There was no associated anorexia, vomiting, change in bowel habit or blood in the stools. On examination he had a temperature of 38.5°C, a pulse of 120 beats/min, a blood pressure of 94/56 mmHg and a respiratory rate of 35 breaths/min, and he appeared distressed. Examination of his abdomen confirmed a distended and diffusely tender abdomen that was most tender in the right lower quadrant with guarding and rebound tenderness. No organomegaly or masses were felt. The rest of the examination was unremarkable except for some mild periorbital edema and bilateral ankle edema. Laboratory investigations revealed a white blood cell count of 18.1×109/L (polymorphs 10×109/L, band cells 3×109/L and lymphocytes 3×109/L) with normal hemoglobin and platelet counts. The sodium level was slightly low at 132 mmol/L, and the other electrolyte levels were in the normal range. Blood urea nitrogen, creatinine, transaminases and alkaline phosphatase levels were all in the normal range. Blood cultures were drawn and the patient was started on intravenous gentamicin and metronidazole and transferred for urgent surgical consultation. The correct diagnosis was made with further investigation. The presentation of a child with an acute abdomen is a medical emergency. Perforated appendicitis is the most common cause of peritonitis in childhood, but the differential diagnosis of abdominal pain in children is both broad and challenging. Any previously healthy child presenting with edema should have his or her urine checked for protein, and children with fever and abdominal pain should also have their urine examined for evidence of infection. A dipstick of the present patient's urine was negative for nitrites, leukocytes and blood, but it was positive for protein at greater than 3.0 g/L, which was suggestive of nephrotic range proteinuria. With a low serum albumin of 14 g/L (normal 33 g/L to 58 g/L), elevated cholesterol of 5.9 mmol/L (normal 3.2 mmol/L to 4.4 mmol/L), history of generalized edema and nephrotic range proteinuria confirmed later on a 24 h urine collection, the patient was diagnosed with nephrotic syndrome. An abdominal ultrasound showed a large amount of ascites with a normal appendix. A peritoneal tap was performed revealing numerous white blood cells on microscopy and the fluid was sent for culture. Blood cultures from the referring hospital were positive for Streptococcus pneumoniae. The patient was diagnosed with pneumococcus sepsis/peritonitis as a complication of his nephrotic syndrome. The signs and symptoms of spontaneous bacterial peritonitis (SBP) include fever, abdominal pain, abdominal tenderness, altered mental status, and rebound tenderness. Vomiting and shallow respirations secondary to the discomfort associated with breathing are also seen. Note that fever and some physical findings may be masked in those patients already diagnosed with nephrotic syndrome and being managed on steroid therapy. The diagnosis of SBP is made when there is a positive culture with an elevated absolute polymorphonuclear cell count (greater than 0.25×109/L) in the ascitic fluid without evidence of an intra-abdominal, surgically treatable source of infection. Polymicrobial ascitic infections are more typically suggestive of surgical causes of peritonitis such as a perforated appendicitis. In the present case, white blood cells were seen in the fluid but the culture was negative. This can be attributed to the fact that the cultures were taken from this child after the initiation of antibiotic therapy. Risk factors for the development of SBP include nephrotic syndrome, gastrointestinal hemorrhage, contaminated paracentesis, urinary tract infection and liver cirrhosis. The humoral antibody abnormalities seen in nephrotic syndrome, with the loss of immunoglobulins in the urine, coupled with the loss of factors B and I, which culminate in deficits in the complement pathway, are thought to contribute to the pathophysiology of SBP. The ascitic fluid may act as a culture medium for organisms. Also, the hemodynamic changes seen in nephrotic syndrome, with third spacing of volume and intravascular depletion, are thought to decrease splachnic blood flow, causing hypoxia with a tendency to form thrombosis. This can then go on to cause microinfarction of the bowel wall, allowing for movement of bacteria from the gut into the peritoneal cavity. Classically, the pathogens most frequently responsible for SBP are S pneumoniae (25% to 50% of cases) and Escherichia coli (3% to 38%) but can include enterococcus, and other Gram-negative bacteria such as Klebsiella, Enterobacter and Acinetobacter species. The treatment of SBP, especially with regard to the duration of therapy and the choice of antibiotics is somewhat controversial. Initially, a combination of penicillin or a third-generation cephalosporin plus an aminoglycoside is recommended. Coverage can be narrowed once the culture and sensitivities of the organism are known. In the case of penicillin-resistant S pneumoniae, vancomycin is the antibiotic of choice. Opinions regarding duration of therapy vary between five and 14 days. Prevention of a recurrence of pneumococcal peritonitis in patients with relapsed nephrotic syndrome can be improved through prophylaxis with penicillin and pneumococcal vaccination. Children with periorbital and/or ankle edema should have their urine dipped for protein. Children with nephrotic syndrome are vulnerable to infections with SBP being the most frequent. Sepsis, pneumonia, cellulitis and urinary tract infections, may also be seen. Most common pathogens for SBP include S pneumoniae and E coli. Initial empiric therapy should cover these two pathogens.

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