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CASE REPORT Table of Contents   
Year : 2011  |  Volume : 8  |  Issue : 2  |  Page : 232-234
Gastric serosal tear due to congenital pyloric atresia: A rare anomaly, a rare complication

Department of Paediatric Surgery, Ondokuz Mayis University, Samsun, Turkey

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Date of Web Publication14-Oct-2011


Congenital pyloric atresia (CPA) is a very rare malformation with unknown aetiology. It has has numerous complications including gastric perforation, aspiration pneumonia. Gastric perforations in newborns occur by three mechanisms: trauma, ischaemia, or spontaneous. Here, we report a newborn with CPA presenting with gastric serosal tearing without full-cut gastric perforation. The diagnosis was confirmed with the help of plain abdominal radiograph, ultrasound, contrast-study, and at operation. Treatment of CPA is surgery irrespective of the type of atresia. We performed serosa repair and then the solid, cord-like atretic pylorus was excised with accompanying gastroduodenostomy. Our patient had an uneventful course and was discharged at the end of the second postoperative week.

Keywords: Congenital abnormalities, Intestinal atresia

How to cite this article:
Gunaydin M, Rizalar R, Tuge Bozkurter A, Tander B, Ariturk E, Bernay F. Gastric serosal tear due to congenital pyloric atresia: A rare anomaly, a rare complication. Afr J Paediatr Surg 2011;8:232-4

How to cite this URL:
Gunaydin M, Rizalar R, Tuge Bozkurter A, Tander B, Ariturk E, Bernay F. Gastric serosal tear due to congenital pyloric atresia: A rare anomaly, a rare complication. Afr J Paediatr Surg [serial online] 2011 [cited 2021 Oct 28];8:232-4. Available from:

   Introduction Top

Congenital gastric outlet obstructions other than Infantile Hypertrophic Pyloric Stenosis (IHPS) are rather rare, with an incidence of 1 in every 100,000 live births and account for 1% of all intestinal obstructions. [1],[2] Among these, congenital pyloric atresia (CPA) is a very rare malformation with unknown aetiology. Most authors have approached it from an anatomic or embryologic point of view. Speculatively, it ay result from some developmental arrest between the 5 th and 12 th weeks of intrauterine life, resulting in the failure of recanalisation of the gut. [3],[4] Others suggested mechanical and vascular injury as causative factors, resulting in atresia of the affected portions of the gut. The anomaly is also thought to have an autosomal recessive inheritance.

The typical presentation of CPA is nonbilious vomiting immediately after birth, with upper abdominal distension. The diagnosis is easy with a single gas-filled bubble representing the dilated stomach on plain abdominal radiograph, which can further be confirmed by a barium contrast study. Isolated CPA has an excellent prognosis, while the overall mortality is high in the presence of associated anomalies, such as epidermolysis bullosa (EB) or intestinal atresias. [5],[6],[7],[8] CPA has many complications including gastric perforation and aspiration pneumonia.

   Case Report Top

Following hospitalisation of an otherwise healthy 27-year-old G3P1 woman for polyhydramnios and preterm labour, a male infant weighing 2120 g was born by caesarean section at 32+1/7 weeks of gestational age and transferred to the Newborn Intensive Care Unit. He passed meconium within the first 24 hours. He did not tolerate enteral feeding and had non-bilious vomiting. Upper left quadrant was distented. A nasogastric (N/G) drainage tube was placed. The plain abdominal radiograph demonstrated a huge dilated stomach and the remainder of the abdomen was gasless. The contrast material, introduced through the N/G tube, remained within the stomach and no passage to the intestine was observed on serial radiographs [Figure 1]. He was transferred to the paediatric surgery clinic with the diagnosis of gastric outlet obstruction. Abdominal ultrasound showed gas within the stomach with a 7.5-mm antral length, 5-mm transverse diameter, and 2-mm muscle thickness, but no gas within the remaining part of the intestine. Preoperative antibiotics and vitamin K were administered and an exploratory laparotomy was performed on day 4. Informed consent was obtained. At laparotomy, there was an obvious serosal defect at the anterior wall of the stomach extending from the gastroesophageal junction to the lesser curvature and antrum. Serosa was somewhat necrotic, with the mucosa bulging out [Figure 2].
Figure 1: Plain abdominal radiograph with contrast material (urographin), demonstrating a huge dilated "single bubble" stomach (thin arrow) with no air nor contast distally (thick arrow).

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Figure 2: Obvious serosal tear at the anterior wall of the stomach extending from the gastroesophageal junction to the lesser curvature and antrum (double arrow). Serosa was somewhat necrotic with the mucosa bulging out (thick arrow). Umbilicus (thin arrow)

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Following the repair of the serosa, stomach was inflated with air via the N/G tube, but air could not be passed through the pylorus indicating total obstruction. The solid, cord-like atretic pylorus was excised with accompanying gastroduodenostomy. Intravenous total parenteral nutrition was started. On postoperative day 7, the nasogastric tube was withdrawn and oral feeding was started with the amount being gradually increased. He had an uneventful course and was discharged at the end of second postoperative week.

   Discussion Top

There are three recognised anatomical variants of pyloric atresia. Type 1 pyloric atresia is mucosal membrane or pyloric membrane web occluding the lumen; type 2 is a longitudinal segmental atresia with a solid cord between the two ends; and type 3 is gap aplasia. [5],[6] Recurrent, projectile, non-bilious vomiting in the first month of life usually suggests IHPS, which may result with serious malnutrition, dehydratation, and acid-base imbalance. Gastroesophageal reflux, hiatal hernia, and duodenal obstruction should be differentiated from IHPS via radiologic evaluation. In contrast, definitive diagnosis of many other anomalies resembling IHPS in the newborn period such as pyloric atresia, pyloric duplication, prepyloric, or antral web/membrane, gastric duplication, and ectopic pancreatic tissue obstructing the pyloric channel, can mostly be made during surgery.

CPA may appear as an isolated entity but associated anomalies are frequently seen and epidermolysis bullosa (EB) is the most common. [5],[7],[8] Many studies have shown the association between pyloric atresia and EB where vesicobullous lesions appear on the skin with any trauma and lead to sepsis. The course of CPA with EB is generally fatal, where the cause of death is sepsis and fluid loss. CPA in association with other intestinal atresias may also be fatal and related to sepsis. Calsifications on plain radiographs indicate hereditary multiple intestinal atresias of the gastrointestinal tract. [9] Some authors reported associated anomalies with CPA, including Down's syndrome, Meckel's diverticulum, ureterovesical junction obstruction, pelviueretric junction obstruction, agenesis of the gallbladder and malrotation, high anorectal agenesis, congenital heart disease, cleft palate, and pylorocholedochal fistula. [10] In the CPA cases, prenatal ultrasonographic studies may show polyhidramnios, dilated stomach, and eosophagus. The gas bubble is larger than normal and there is no gas distally. Upper gastrointestinal contrast series or endoscopy enable diagnosis. Here, we present a CPA case with an extended serosal defect. Because the patient was not mask-ventilated previously, we failed to explain the reason and extend the serosal defect. It was thought to be due to any dissecting bleeding or haematoma. Further, it is unclear whether it was due to inadequate nasogastric drainage or forceful physical examination.

Gastric perforations in newborns occur by three mechanisms: trauma, ischaemia, or spontaneously. Iatrogenic perforations, mostly related to nasogastric tubes are more common and mostly observed at the greater curvature. Mask-ventilation during recussitation may result with overdistention of the stomach and perforation. Spontaneous perforations are seen in the first week of life in an otherwise healthy newborn and extremely rare. They are related with the sudden increase at intragastric pressure. In the amniotic fluid-filled stomach, the serosal layer is torn first and the mucosa bulges out like a diverticulum. More increase at the intragastric pressure due to vomiting, results in a whole-cut tear. Spontaneous gastric perforations occur at the greater curvature or ventral wall of the stomach where the wall is relatively thin.

Because our case had only serosal tear but no mucosal perforation, abdomen was clean, which further had a positive effect on the course of treatment.

Treatment of CPA is surgery irrespetive of the type of atresia. The surgical options include excision alone for membranous-type CPA or excision with  Heineke-Mikulicz pyloroplasty More Details, Finney, or Heineke-Mikulicz pyloroplasty if the solid pyloric atresia is short; or excision of the atretic segment with gastroduodenostomy if the solid core is long or in atresias with a gap. [6],[7] The use of high-resolution ultrasonography, particularly followed by fetal MRI, provides an excellent option for antenatal diagnosis of CPA, as noted in some recent reports. [11],[12]

In conclusion, gastric perforation due to CPA is extremely rare. In our case, there was only serosal defect at the anterior wall of stomach extending from the gastroesophageal junction to lesser curvature and antrum. Prognosis is related to the type of pyloric atresia and accompanied by an anomaly.

   References Top

1.Gester BC, Aberdeen SD. Prepyloric diaphragm, an unusual abnormality. Arch Surg 1965;90:472-5.  Back to cited text no. 1
2.Muller M, Morger R, Engert J. Pyloric atresia: Report of two cases and review of literature. Pediatr Surg Int 1990;5:276-9.  Back to cited text no. 2
3.Bar-Maor JA, Nissan S, Nevo S. Pyloric atresia: A hereditary congenital anomaly with autosomal recessive transmission. J Med Genet 1972;9:70-2.  Back to cited text no. 3
4.Bronsther B, Nadeau MR, Abrams MW. Congenital Pyloric atresia: A report of three cases and a review of the literature. Surgery 1971;69:130-6.  Back to cited text no. 4
5.Ilce Z, Erdogan E, Kara C, Celayir S, Sarimurat N, Senyüz OF, et al. Pyloric atresia: 15-year-review from a single institution. J Pediatr Surg 2003;38:1581-4.  Back to cited text no. 5
6.Moore CC. Congenital gastric outlet obstruction. J Pediatr Surg 1989;24:1241-6.   Back to cited text no. 6
7.Al-Salem AH. Congenital pyloric atresia and associated anomalies. Pediatr Surg Int 2007;23:559-63.   Back to cited text no. 7
8.Shaw DW, Fine JD, Piacquadio DJ, Greenberg MJ, Wang-Rodriguez J, Eichenfield LF. et al. Gastric outlet obstruction and epidermolysis bullosa. J Am Acad Dermatol 1997;36:304-10.  Back to cited text no. 8
9.Lambrecht W, Kluth D. Hereditary multiple intestinal atresias of the gastrointestinal tract: Report of a case and review of literature. J Pediatr Surg 1998;33:794-7.  Back to cited text no. 9
10.Okoye BO, Parikh DH, Buick RG, Lander AD. Pyloric atresia: Five new cases, a new association and a review of literature with guidelines. J Pediatr Surg 2000;35:1242-9.  Back to cited text no. 10
11.Yu DC, Voss SD, Javid PJ, Jennings RW, Weldon CB. In utero diagnosis of congenital pyloric atresia in a single twin using MRI and ultrasound. J Pediatr Surg 2009;44:21-4.   Back to cited text no. 11
12.Maheshwari P, Abograra A, Shamam O. Sonographic evaluation of gastrointestinal obstruction in infants: A pictorial essay. J Pediatr Surg 2009;44:2037-42.  Back to cited text no. 12

Correspondence Address:
Mithat Gunaydin
Department of Paediatric Surgery, Ondokuz Mayis University, Samsun
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0189-6725.86071

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