Rotavirus is a common gastrointestinal pathogen in children younger than 3 years of age. Complications are rare in well-nourished infants, although death from dehydration is more frequently described in developing countries. With emergency department personnel's increasing use of ultrasound to evaluate abdominal pain, new insights about disease processes are being recognized (1). We describe ultrasound identification of portal vein gas in a child with severe dehydration, secondary to rotavirus gastroenteritis, that resolved rapidly following rehydration therapy.
A 5-month-old male infant was brought to the emergency department with a 4-day history of nausea, vomiting, and diarrhea. Before this episode, the infant had been well and no one else in the family was ill. The child had been born by spontaneous vaginal delivery without complications. At birth, the child weighed 2.4 kg. On examination, the infant was listless with sunken eyes and the oral mucosa and lips were dry. Body temperature was 39°C. Pulse rate was 152 beats/min and respiratory rate was 32 breaths/min. Abdominal discomfort was noted although no abdominal masses could be palpated. A clinical diagnosis of 10% dehydration secondary to gastroenteritis was made. The weight on admission was 9.2 kg and on discharge was 10.1 kg. Rehydration with an intravenous bolus injection of 200 ml normal saline (20 mL/kg) was initiated. Oral fluids were also encouraged. Following admission, the infant became more lethargic and somnolent. Serum electrolytes revealed acidosis and prerenal azotemia consistent with severe dehydration (Table 1).
In view of the infant's vomiting with persistent abdominal discomfort and striking lethargy, intussusception was suspected, and an ultrasound examination of the abdomen was obtained. Plain films of the abdomen had not revealed pneumatosis of the bowel wall, portal vein gas, or evidence of intestinal obstruction. Abdominal ultrasound examination showed multiple fluid-filled loops of bowel with normal bowel wall thickness. No free intraperitoneal fluid or intussusception was noted. Ultrasound did not detect pneumatosis within the bowel wall. The liver, which had not been the focus of clinical concern but which was examined as part of the complete abdominal ultrasonography, had a diffusely abnormal pattern of increased echogenicity (Fig. 1) related to hepatic intraparenchymal and portal vein gas. Trapped gas bubbles within the liver caused the increased echogenicity of the liver. Doppler examination of this patient demonstrated high-amplitude echoes consistent with portal vein gas streaming in a hepatopetal direction. Color flow Doppler ultrasound easily determined that the gas was within the perivascular spaces rather than in the biliary tract.
During the next 24 hours, the patient received further intravenous fluids (dextrose 5% in half normal saline) with rapid clinical improvement. Following intravenous rehydration, serum electrolytes and serum urea nitrogen returned to normal (Table 1). Repeat ultrasound examination 2 days later demonstrated a normal liver (Fig. 2) with complete resolution of portal vein gas. Following clinical improvement, oral feeding was encouraged and intravenous fluid therapy discontinued. The presence of rotavirus infection in this patient was confirmed by latex agglutination assay of rotavirus antigen in the stool. The patient was discharged with the diagnosis of severe viral gastroenteritis caused by rotavirus.
Rotavirus is a relatively large 70-n m nonenveloped double-stranded RNA virus. Initially named in 1973 because its electron microscopic appearance resembles a wheel (2), rotavirus consists of a triple-shell structure with the inner shell containing the viral protein and viral genome. Infection is common and most children experience infection by age 3 years. Deaths are usually associated with dehydration and electrolyte imbalance. Rare extraintestinal complications occur. Neurologic injury may be caused by severe electrolyte imbalance or may represent direct viral invasion of the central nervous system. Minor hepatic involvement is commonly seen during acute rotaviral infection, and elevations of serum transaminase values are common. More severe hepatic involvement may occur in patients with immune deficiency (3) and in patients with liver transplants.
The association of portal vein and intrahepatic pneumatosis with acute rotavirus infection has not been reported. Although ultrasound examination is of little value in investigating recurrent abdominal pain in children and adolescents (4), it is ordered frequently during the investigation of the acute abdomen in children. Ultrasound is an excellent imaging modality for investigating intussusception. It is sensitive and specific for this diagnosis (1).
Intussusception is not a recognized complication of community-acquired rotavirus infections, but the possibility of an association following immunization against rotavirus with the tetravalent rhesus-human vaccine has been suggested (5) and is the reason for withdrawal of the live attenuated rotavirus vaccine from clinical use. A causal association between this immunization and subsequent intussusception was noted along with a higher incidence of surgery and bowel resection than generally reported (6).
Ultrasound examination can detect gas in the portal vein and in the hepatic parenchyma (7). Ultrasound has been most commonly used in pediatrics for the recognition of portal vein gas complicating necrotizing enterocolitis in neonates (8). Ultrasound is superior to plain abdominal film for diagnosing portal venous gas. We postulate that in our patient, gas probably entered the portal vein and liver parenchyma as a result of severe mucosal damage from gastroenteritis associated with rotavirus infection. We suspect that gas within the bowel lumen was forced through the damaged bowel mucosa as a consequence of ileus accompanying infection and that it dissected along perivascular tissue into the liver. Pneumatosis intestinalis has been previously described in children with rotavirus gastroenteritis (9). The pneumatosis intestinalis in these cases was identified on plain abdominal radiographs with no ultrasound examination performed. As with our case, pneumatosis of the bowel wall in these reported cases was presumed to result from air dissecting through mucosal ulcers. In light of our patient's rapid recovery after simple intravenous hydration, we saw no evidence of bowel wall ischemia, the common explanation for pneumatosis in the neonate with necrotizing enterocolitis. Rapid resolution of clinical and radiologic abnormalities occurred. No sequelae of the portal venous gas could be demonstrated. With increased use of ultrasound examination to evaluate possible acute abdominal emergencies in infants and children, we predict that these may be recognized more frequently in the future.
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