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William Durston is credited with providing the earliest description of esophageal atresia (EA) when he observed its occurrence in one of conjoined twins in 1670. In 1888, Charles Steele was the first to attempt surgical correction of EA. Although the child died, it gave an indication that the abnormality was potentially treatable. It was not until 1939 that Ladd and Leven independently obtained the first long-term survivors with EA. Two years later Cameron Haight successfully achieved a primary esophageal anastomosis.
Before 1939, esophageal atresia was considered a uniformly fatal condition. Nowadays, all patients with EA are expected to survive irrespective of their gestation, provided there are no major concomitant congenital abnormalities. There has been a steady decline in the overall mortality from EA in most institutions, but there remains a significant group of patients who will die as a result of their associated abnormalities: the prognosis for many of these infants is considered so poor that no active treatment to correct the atresia is justified.
The eventual quality of life is good in the majority of survivors. Despite this, many have ongoing minor but troublesome symptoms, many of which relate to esophageal function (Table 15a.1). In particular, there are concerns about the ultimate risk of malignancy in the esophagus exposed to persisting gastroesophageal reflux. This chapters outlines how the early management of esophageal atresia influences long term outcome, and identifies some of the persistent difficulties that adults with repaired EA may suffer.
To identify the timing, pattern, and determinants of colonization of neonates by Malassezia.
Prospective observational study.
A neonatal medical and surgical unit consisting of 10 special care, 10 high-dependency, 10 intensive care, and 10 surgical cots.
All neonates (≤ 28 days of age) or infants (> 28 days of age) admitted to the unit during the 20-week period from October 1995 to March 1996.
All infants or neonates were swabbed on the day of admission and every third day thereafter and risk factors were collected for every day on the unit.
During the study period, 245 neonates and 42 infants were sampled for their entire duration of stay on the unit. Of these, 41 infants (97.6%) were colonized with Malassezia on admission to the unit and thereafter, as assessed by subsequent samples. Within the neonate population, 78 (31.8%) became colonized, but none were colonized immediately after birth. Univariate analysis showed that many factors appeared to be significantly associated with colonization in the neonates, including use of ventilation, presence of central venous catheters, use of parenteral nutrition, and use of antibacterial or antifungal drugs. However, when the data were analyzed by multivariate logistic regression to control for confounding variables, only gestational age and length of stay on the unit were found to be significantly associated with colonization.
Colonization of infants is not as unusual as previously thought and many infants have established a cutaneous Malassezia commensal flora by the age of 3 to 6 months. Factors that predispose to colonization in neonates may not be the same as those that predispose to infection.
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