A 5-week-old previously healthy male presented to an ER with 2 days of fever. He was lethargic with a sunken fontanel. Labs revealed a WBC of 13.5 with 15% bands, c-reactive protein of 8, and negative rapid influenza and RSV. Lumbar puncture obtained only 1 ml of spinal fluid, which was sent for culture without other indices. He received ampicillin and ceftriaxone for presumed neonatal sepsis. During evaluation he had an episode of tachypnea and drop in oxygen saturation to 80%, so was intubated and transferred to a pediatric intensive care unit. Ultimately, blood, urine, and CSF cultures were negative and rhinovirus/enterovirus (from nasal swab PCR) was the only infectious organism identified. However, due to the severity of his initial presentation, he was empirically treated for meningitis with 14 days of hospitalization and IV antibiotics. Near the end of this course, he developed new fever and non-bloody non-mucousy diarrhea and received a second septic work up; stool studies identified rotavirus. At this time, he became remarkably “puffy” and edematous. Labs were significant for low albumin of 1.0 g/dL and a stool alpha 1 anti-trypsin (A1AT) of 12.5mg/g dry stool (normal range 0.3-3) which is consistent with Protein-Losing Enteropathy (PLE). He received 25% albumin intravenous infusion after which he clinically improved and the albumin stabilized. He was prescribed low-fat formula with increased medium-chain triglycerides (MCT).
PLE is a syndrome of protein loss via the gastrointestinal system that can complicate several disorders of the lymphatic tissue, heart, and intestinal tract. Although only rarely reported with rotavirus, it is postulated that certain infectious diarrheal pathogens cause PLE through direct protein leakage across damaged intestinal mucosa. If unrecognized, complications of PLE include ascites, pleural or cardiac effusion, and worsening of any underlying protein malnutrition. Diagnosis of PLE is clinical, although laboratory findings such as elevated fecal A1AT and low albumin are supportive. The prognosis of PLE depends upon the underlying condition responsible. A high-protein, low-fat diet (with MCT supplementation to off-set reduction in calories) may diminish lymphatic transport of fatty acids in the gut and lymph leakage of proteins; hence the recommendation for dietary change in our patient.
Hospitalists should be aware that PLE can be associated with certain diarrheal infections. Dietary modifications and albumin infusions are sometimes required to avoid malnutrition or complications. This patient is the youngest reported patient with PLE due to rotavirus. Nosocomial acquisition of rotavirus in our patient emphasizes the risks to unimmunized infants during prolonged hospitalizations. Further studies on the viral etiologies of neonatal fevers may reduce prolonged hospital stay by limiting extended courses of IV antibiotics for presumed bacterial infections.
To cite this abstract:DeSena J, Bhardwaj V, Lakhole A, Trost M. Mystery Edema in an Infant During Prolonged Hospitalization. Abstract published at Hospital Medicine 2015, March 29-April 1, National Harbor, Md. Abstract 419. Journal of Hospital Medicine. 2015; 10 (suppl 2). https://www.shmabstracts.com/abstract/mystery-edema-in-an-infant-during-prolonged-hospitalization/. Accessed November 17, 2019.