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Abdominal defect
Sanjeev Kumar Digra1, Niraj Kumar1, Pankaj Kumar Gupta2, Varun Kaul1.
1Department of Pediatrics, Government Medical College, Jammu, India,
2Department of Anesthesia, Government Medical College, Jammu, India.
ADDRESS FOR CORRESPONDENCE
Sanjeev Kumar Digra, Aayu Shree Child Care Centre, Pragati Nagar, Upper Barnai, Jammu, {JandK} 181124, India.
Email: sanjeevahsaas@yahoo.co.in
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What is the diagnosis?
Gastroschisis. This is a low birth weight neonate with gastrochisis who was born with herniation of small intestine from a small defect on the right side of umbilical cord with no covering membrane. Gastroschisis is a Greek term which stands for belly cleft. It is the herniation of abdominal contents through an abdominal wall defect, usually occurring on the right side of a normally positioned umbilical cord {1}. The defect is most often less than 4cm and as with the other abdominal wall defects, the rectus muscles are normally formed {2}. The prevalence of gastroschisis is about 1, 7000 total births and both sexes are equally involved {3,4}. Young maternal age {median age 21 years} is consistently associated with this condition and the neonates are typically of low birth weight {median weight 2.3kg} {3,4}. This defect is commonly believed to be a result of a vascular accident that leads to intrauterine interruption of omphalomesenteric artery {1}. This anomaly occurs early in gestation and bowel is left in contact with the amniotic fluid, which produces an intense inflammatory response or “Peel” causing poor intestinal motility {1,5}. Unlike exomphalos, there is no covering membrane and the extent of evisceration is variable which may include stomach, small bowel, colon, and ovary and fallopian tubes or testes. Liver is rarely involved. The incidence of associated anomalies in patients with gastroschisis is relatively infrequent. Intestinal atresia may occur in 10-15 percent of cases {1,4}. Maternal serum alpha- fetoprotein {AFP} is used as screening test although there is a 40 percent rate of false positive results. It is elevated in case of neural tube defects, abdominal wall defects, or atresia of duodenum or oesophagus. Analysis of amniotic AFP and acetylcholinestrase-pseudocholinesterase can be sensitive in detecting abdominal wall defects, especially Gastroschisis. The ultrasonography is helpful beyond 14 weeks {because midgut normally is herniated in 1st trimester} {1}. Unlike with Omphalocele, primary closure is possible in 90 percent patients, but larger defects may require staged repair. Mortality rates have decreased to 5 percent to 10 percent. Enteral feedings may not be established until 2 months after operation {1}.
REFERENCES:
1. Berseth CL, Poenaru D. Abdominal wall problems. In : Taeusch HW, Ballard RA, Gleason CA {eds}. Avery’s Diseases of the Newborn. 8th Edn. Elsevier, Saunders, Philadelphia, 2005: 1113-1117.
2. Klein MD. Congenital Abdominal wall Defects. In: Ashcraft KW, Holcomb GW, Murphy JP {eds}. Pediatric Surgery. 4th Edn. Elsevier, Saunders, Philadelphia, 2005: 665-669.
3. Curry JI, McKinney P, Thornton JG, Stringer MD. The aetiology of gastroschisis. BJOG. 2000` 107: 1339-1346.
4. Stringer MD, Sugarman I, Smyth AG. Congenital Defects And Surgical Problems. In: Rennie MJ {editor}. Roberton’s Text Book of Neonatology. 4th Edn. Elsevier, Churchill Livingstone, 2005: 733-737.
E-published: May 2010 Vol 7 Issue 5 Art No. 31 |