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Brief Reports

Indian Pediatrics 2001; 38: 1277-1280  

Duodenal Atresia: Outcome Analysis From A Regional Neonatal Center


S.K. Chowdhary
S. Suri

K.L. Narasimhan
J.K. Mahajan

K.L.N. Rao

From the Department of Pediatric Surgery, Advanced Pediatric Center, Post Graduate Institute of Medical Education and Research, Chandigarh 160 012, India.

Correspondence to: Prof. K.L.N. Rao, Head, Department of Pediatric Surgery, Advanced Pediatric Center, Post Graduate Institute of Medical Education and Research, Chandigarh 160 012, India.

Manuscript received: July 5, 2000;
Initial review completed: July 21, 2000;
Revision accepted: March 29, 2001.

Duodenal atresia is a relatively common intestinal anomaly, with a cited incidence of 1:6,000-1:30,000(1). The presence of bile vomit without any abdominal distension in the newborn, occasional passage of green meconium and rarely, presence of distal gas in the bowel often misleads an unsuspecting clinician resulting in delayed diagnosis.

Western data report overall survival figures of over 90%(2). No Indian series is available for comparison. We undertook this study to gather preliminary data on the referral pattern, and evaluate the outcome in our unit on a fixed clinical protocol.

Patients and Methods

All consecutive neonates who were managed with the diagnosis of duodenal atresia between January 1998 to May 1999 were included in the study. Anatomical and physiological assessment was done by one consultant after upto 24 hours of resuscitation including fluids, ionotropers, antibiotics, blood products like platelets in septic babies and respiratory support. Surgery was done only in the elective theatre under the super-vision of consultant anesthetist and surgeon.

All babies underwent single layer inter-rupted diamond duodenoduodenal anastomo-sis by the Kimura’s technique(3). Electives ventilation was undertaken for every baby less than 2 kg wherever anesthesia time was more than 1 h, there was presence of an associated intestinal anomaly, baby was fasting for more than 5 days or in a septicemic state.

Similarly, every baby had a gastrostomy and a transanastomotic 6F feeding tube into the jejunum. Enteral feeded were started within 48 hours with expressed breast milk, unless there was distal bowel anastomosis. Ventilation was continued till next morning or later for sick neonates. Throughout the study, they were managed in the neonatal surgical intensive care by surgeons.

On discharge or death, the summaries were stored and the follow up data entered in the patient file separately maintained along with X-rays. This data was tabulated and analyzed.

Results

Fifteen consecutive babies were managed with the diagnosis of duodenal atresia by our unit during this period. Only one baby came to us with antenatal diagnosis from the city of Chandigarh in this period, all others were referred from the hinterland. Nine out of fifteen babies were born premature. The mean gestational age of the babies was 35 weeks with a range of 30-40 weeks. The birth weight varied from 1.2 kg to 3.2 kg with a mean of 2.2 kg. The referral diagnosis was duodenal atresia in four babies, intestinal obstruction in eight, esophageal atresia in two and septi-cemia in one. Polyhydramnios was present in 4 out of 15 and Downs’ syndrome was suspected in 4 babies and later confirmed.

Bile vomit within 24 hours was the presentation in all babies excepting the two babies with associated esophageal atresia. However, the babies were referred to the surgical unit between 48 hours to day 17 of life with a mean of 6.5 days. Only one baby was referred with an antenatal diagnosis on the day of delivery.

Only one baby arrived by a supervised transport, all others were brought by parents. Twelve came in public transport without any supportive measures like intravenous fluid or nasogastric tube. Six were critically ill with hypothermia, feeble pulses and low urine output. Two babies with associated tracheo esophageal fistula had to be ventilated preoperatively.

The correct diagnosis of duodenal atresia in 12, associated duodenal atresia with eso-phageal atresia in 2 was made preoperatively. In one baby associated multiple bowel atresia was diagnosed on the operating table. Diagnosis was confirmed in all babies by plain X-ray and use of contrast was necessary in only one baby with an atypical presentation of distal bowel gas.

Fifteen babies had duodenoduodeno-stomy, in addition two had ligation of tracheoesophageal fistula, gastrostomy and esophagostomy for long gap tracheoeso-phageal fistula with esophageal atreasia. One had bowel resection and bowel anastomosis at two sites in the distal bowel for associated bowel atresia. Two babies were operated by consultants and the rest were operated by surgical trainees. Nine babies were ventilated in the post operative period between(1-5 days). Enteral feeds were started in all babies by the first 48 hours. In three babies the transanastomtic tube could not be used for the entire period. In one it slipped back in the stomach, in another baby there was peritubal leak which settled, and in the third it fell out. The gastroduodenal ileus persisted between 7 days to 24 days (mean 10 days).

There was three deaths. Their clinical data has been outlined in Table I. None of the parents agreed for autopsy.

The twelve surviving babies were discharged without any morbidity. All of them have been seen in the outpatient till 3 months of age. One baby with associated esophageal atresia is now 7 months old and awaits esophageal replacement.

Discussion

Contrary to the common symtoms and signs of neonatal intestinal obstruction, abdominal distension is not a feature in the early stages. In 5 babies who presented in the first 48 hours, none had abdominal distension. In the presence of bile vomiting, a significant number of them are known to pass green meconium(4). The baby who presented to us on the 17th day had gas in distal bowel and had passed meconium several times. A contrast study confirmed the diagnosis of duodenal atresia. The anatomical basis of such a clinical presentation is a membrane with central hole or bifid terminal end of bile duct opening in the upper and lower pouches(5).

Associated gastrointestinal malformations were seen in three of our babies. Two of them did not survive. The presence of features of Downs’ syndrome in only four babies (26%), is much less than that reported in some other series. This may be related to the practice of non consanguinous marriage and relatively younger maternal age in our country. The failure to detect a duodenal atresia in a baby with esophageal atresia is bound to create problems with the esophageal anastomosis, as has been reported in the past(6).

The mean time for referal in a study spread over 1980-1989 from Ireland was 3.6 days. This is 50% less than our mean time for referral, a decade later! In the same, study the reported mortality was 6.12%. All deaths were in babies with serious associated malformations(2). Our mortality figure for isolated duodenal atresia is similar.

An internal audit within our department of a similar time period previous to the beginning of this study, demonstrated an overall survival of 50% babies with duodenal atresia. The clinical protocol laid out for the management of these babies was followed for each of these babies, except one baby where ventilatory support could not be provided.

Table I__Outline of Non Survivors
 
Age/Wt
Anomalies associated
Days
Clincial status (at presentation)
Probable cause of death
1.       Premature 32 wks 1.6 kg   Isolated duodenal atresia   6 Aspiration pneumonia, Shock     Septicemia, Ventilatory support not available
2.     Term 36 wks 2.4 kg Associated multiple intestinal atresia 4     Aspiration pneumonia Septicemia Anastomotic leak
3.       Term 38 wks 2.2 kg   Associated TEF, Esophageal atresia 3     Aspiration pneumonia Preop ventilation   Septicemia, Cardiaac anomaly?

 

Conclusion

In conclusion, the referral pattern of duodenal atresia from our region is fairly representative of the developing world. The outcome for isolated duodenal atresia in this series is comparable to result previously published from western centers.

Contributors: SKC, KLN and KLNR designed and conducted the study. SS and JKM wrote the manuscript and SKC revised it. SKC will act as the guarantor for the study.

Funding: None.

Competing interests: None stated.

Key Messages

• Unlike other causes of neonatal intestinal obstruction, duodenal atresia often presents with occasional bile vomit without abdominal distension and passage of meconium.

• Adequate critical care support will lead to considerable improvement in the outcome of surgery.


 References

 

1. Rickham PP, Lister J, Irving IM. Duodenal atresia and stenosis, annular pancreas. In: Neonatal Surgery, 2nd edn. Eds. Lister J, Irving IM, Butterworth 1978; pp 359-361.

2. Akhtar J, Guiney EJ. Congenital duodenal obstruction. Br J Surg 1992; 79: 133-135.

3. Kimura K, Tsugawa C, Ogawa K. Diamond shaped anastomosis for congenital duodenal obstruction. Arch Surg 1977; 112: 1261-1263.

4. Al Salem AH, Khawaja S, Grant C, Dawodu A. Congenital intrinsic duodenal obstruction: Problems in the diagnosis and management. J Pediatr Surg 1989; 24: 1247-1249.

5. Gourevitch A. Duodenal atresia in the newborn. Ann R Coll Surg Eng 1971; 48: 141-158.

6. Moore TC. Congenital intrinsic duodenal obstruction: Report of 32 cases. Ann Surg 1951; 144: 159-164.

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