Duodenal atresia overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2]
Overview
Historical Perspective
In 1900, J. Tandler reported duodenal stenosis due to failure of recanalization of duodenum during fetal development in pregnancy. In 1961, Thomas Santulli and William Blanc described the figure 8 formation of small bowel, which is described as apple-peel intestinal atresia. In 1936, William Ladd developed a surgical procedure to correct the duodenal malrotation.
Classification
Intestinal atresia, including duodenal atresia, may be classified into four subtypes: Type I, Type II, Type III, and Type IV. Type I is the most common subtype which involves the complete mucosal membrane, with muscularis and serosa remaining intact.
Pathophysiology
It is thought that duodenal atresia is the result of failure of neural cell migration during the 8th to 10th week of duodenal re-canalization. It is associated with down syndrome, vertebral defects, anal anomalies, esophageal atresia, annular pancreas, malrotation, renal abnormalities, cardiac causes, and mandibulofacial anomalies.
Causes
The cause of duodenal atresia has not been identified.
Differentiating ((Page name)) from Other Diseases
Epidemiology and Demographics
The prevalance of duodenal atresia is 0.1 to 0.4 per 100000. It commonly affects neonates and has a male to female ratio of 2 to 1.
Risk Factors
The most potent risk factor in the development of duodenal atresia is down syndrome. Other risk factors include annular pancreas, and VACTERL syndrome.
Screening
There is insufficient evidence to recommend routine screening for duodenal atresia.
Natural History, Complications, and Prognosis
The symptoms of duodenal atresia usually develop in the first 48 hours of life, and start with symptoms such as bilious vomiting in 80% of the cases. Prognosis is generally very good, and the survival rate of patients with duodenal atresia is approximately 90%.