Incidence, diagnosis, and outcomes of vocal fold immobility after esophageal atresia (EA) and/or tracheoesophageal fistula (TEF) repair.

BACKGROUND: The diagnosis of vocal fold paralysis in an infant is a devastating finding that may require a permanent tracheotomy. The incidence of congenital vocal fold paralysis is unknown, but it is thought to be more common in infants with anatomic anomalies in the aero-digestive system. Vocal fold paralysis after surgical repair of esophageal atresia and tracheoesophageal fistula is a rare finding often diagnosed after multiple failed extubations. Currently infants do not routinely undergo documentation of vocal fold motion prior to esophageal atresia repair. We report here on our experience with this rare complication. METHOD: A retrospective review was done of patients with esophageal atresia and/or tracheoesophageal fistula from 1985 to 2009. Patient demographics, operative techniques, and outcomes were collected. RESULTS: 150 patients were identified. Mean age at surgical intervention was 12 ± 33 days. Otolaryngology service was consulted for 13% of patients with postoperative failure. Awake fiberoptic laryngoscopy identified 3% of patients with vocal fold paralysis. Bilateral vocal fold paralysis was found in 3 patients, and 2 patients had unilateral vocal fold paralysis. Patients with bilateral paralysis were treated with tracheotomy; unilateral paralysis was treated expectantly. CONCLUSION: In this study, 3% of patients were diagnosed with vocal fold paralysis after esophageal atresia repair. The etiology of vocal fold paralysis in this study is difficult to assess. Pre-operative fiberoptic laryngoscopy is recommended to identify children with congenital vocal fold paralysis prior to surgical intervention, especially in those requiring revision surgery.

Age-related differences in cell-specific cytokine production by acutely ill Malawian patients.

Age-related changes in human cell-specific cytokine responses to acute illness have not been well examined. We therefore evaluated age-related differences in T, B and natural killer (NK) peripheral blood lymphocyte cytokine responses of 309 acutely ill hospitalized people in Malawi, Africa, < 1 month-61 years of age. We used four-colour flow cytometry and performed Wilcoxon rank sum and Kruskal-Wallis tests, Pearson (rp) and Spearman (rs) correlations, and linear and logistic regression analyses to control for human immunodeficiency virus infection (HIV) status, the percentages of lymphocytes expressing CD4, and the nature of the acute infection. The percentages of CD8- and CD8+ T cells producing induced IL-8 decreased with age (rs = -0.44 and -0.53). The percentages of T cells producing TNF-alpha were higher, and the percentages producing IL-10 were lower, in those > or =13 than those < 13 years old (medians: 17.7 versus 10.5 and 1.4 versus 3.0, respectively). The percentages of CD8- T cells producing IFN-gamma were higher and stable in those > or =1 year old compared to infants (medians: 23.5 versus 10.4); the percentages of NK producing IFN-gamma were higher post-infancy and then declined to relatively low levels with increasing age. The percentages of T cells producing IL-2 were highest in those 5- <31 years old (median 5.6) and lowest in those > or =31 years old (median 1.9). The ratios of the percentages of T cells producing IL-4 to those producing IL-8 and to those producing IL-10 both increased with age. These data suggest that innate immunity, represented by NK IFN-gamma production, dominates in early life. A number of shifts occur after infancy and before adolescence, including a proinflammatory shift from IL-8 to TNF-gamma and a type 2 shift from IL-10 to IL-4 dominance. These findings suggest distinct age-related differences in the human response to acute illness and may be useful in directing future efforts at immunomodulatory therapies.