Objectives: Refluxed gastric material aspirated into the lungs is an important cause of acute and chronic pulmonary disease. Currently, the presence of fat-laden macrophages (FLM) in tracheobronchial secretions of children is a conventional marker for reflux aspiration. However, this assay is limited by its apparent lack of specificity. The aim of this study was to reevaluate the role of this assay in diagnosing reflux aspiration.
Methods: The tracheal aspirates of sixty-four consecutive children with clinically significant gastroesophageal reflux undergoing upper gastrointestinal endoscopy under general anesthesia, and 34 other children from the routine operative schedule were evaluated. Both groups were further subdivided on the basis of presence or absence of associated respiratory symptoms. After intubation, tracheal aspirates were collected, fixed, and stained for FLM. By grading the amount of intracellular fat present, a semiquantitative lipid index was computed. Tracheal aspirates with a lipid index of 100 or greater were considered positive.
Results: Twenty-four of the 64 children with reflux symptoms and 14 of 34 children without reflux symptoms were positive for FLM. Sixteen of 37 children with both gastroesophageal reflux and respiratory symptoms and 10 of 26 children negative for both tested positive for FLM. The mean lipid index of the subgroup of children with both reflux and respiratory symptoms was not significantly different from that of the subgroup that was negative for both conditions. Despite computing a semiquantitative lipid index, an index of 100 or greater only had a sensitivity of 38% and specificity of 59%.
Conclusion: Assay of FLM in the tracheal aspirates of children considered at risk of reflux aspiration is not a sensitive or specific as a marker for reflux aspiration.
*Department of Pediatric Gastroenterology, Sydney Children's Hospital, New South Wales, Australia; †Retired, previously Sydney Children's Hospital and University of New South Wales, Australia; ‡Department of Anatomical Pathology, Sydney Children's Hospital, New South Wales, Australia; §School of Women's and Children's Health, University of New South Wales.
Received August 20, 2001; accepted May 9, 2002.
Supported by the Sydney Children's Hospital Research Foundation.
Address correspondence and reprint requests to Dr. Usha Krishnan, Department of Pediatric Gastroenterology, Sydney Children's Hospital, High Street, Randwick, New South Wales, Australia 2031 (e-mail: email@example.com).