Pediatric Bowel Obstruction

1. Pediatric Bowel Obstruction

2. Pediatric Bowel Obstruction • Hypertrophic pyloric stenosis • Atresia and stenosis • Doudenal obstruction • Malrotation and Volvous neonatorum • Meconium Ileus • Intussusceptions • Hirsh sprung disease • Duplications of the gut • Neonatal necrotizing enter colitis • Anorectal malformation

3. Hypertrophic pyloric stenosis • It is not truly a congenital disorder and is often called infantile hypertrophic pyloric stenosis • 2nd common surgical problem in infancy after intussusception • Affects 3 per 1000 live births • Male: female 4:1 and most common in first born males

4. Hypertrophic pyloric stenosis(etiology) • In coordination between sympathetic and parasympathetic leading to continuous contraction of the circular muscle layer of pylorus leading to hypertrophy • High level of maternal and child gastrin • Variation in infant feeding

5. Hypertrophic pyloric stenosis(pathology) Hypertrophy of circular muscle layer Mucosa become compressed and folded Lumen narrow admit little finger

6. Hypertrophic pyloric stenosis (Clinically) • Males presenting at 2 to 8 weeks of age however late presentation up to 6 months can occur • Symptoms • Vomiting • Bile free, • projectile and • progressive in nature yet, • Child hungry and often feeds immediately after vomiting • Constipation • Loss of weight

7. Hypertrophic pyloric stenosis (Clinically) • Signs • General • Dehydration and alkalosis are prominent clinical features. • Wasting • Sunken eyes • Depressed fontanells • Dry woody tongue • Oligurea • Abdominal • Palpating an olive like tumor (pyloric tumor) • Peristalsis from left to right seen

8. Hypertrophic pyloric stenosis (investigations) • Upper GIT series (Barium) • Dilated stomach • Hypertrophic gastric rugae • Narrow elongated pyloric canal (string sign) • Beak sign (ant rum gave rise to pylorus) • Shoulder sign (pylorus bulge into ant rum) • Delayed gastric empting time • U/S • Laboratory • Repeated vomiting may lead to dehydration and • hypochloremic hypokalemic alakalosis;

9. Hypertrophic pyloric stenosis (Treatment) Pre-operative preparation • Correct deficits • dehydration • hypochloremic hypokalemic alakalosis should be corrected before surgery (no urgency in surgery 24 to 72 hours for correction) • Uses a nasogastric tube to decompress the stomach.

10. Hypertrophic pyloric stenosis (Treatment) • Operation is Frede- Ramstedt pyloromytomy • Incisions used, either trans lateral part of the rectus, or entirely muscle splitting • Traction on the omentum will bring out the stomach • Ramstedt pyloromyotomy is completed • Check out the integrity of the mucosa before closure

11. Hypertrophic pyloric stenosis

12. Hypertrophic pyloric stenosis (Treatment) Post operative • NG suction for 8-12 hour • Feeding re-established within 12-24 hours of surgery • Stating with dextrose 10 % every 2 hours • Increasing amount • Half formula • Full formula

13. Hypertrophic pyloric stenosis (Treatment) Post operative complications • Persistent vomiting • Wrong diagnosis • Gastritis • Inadequate surgery • perforation • Burst abdomen • Anesthetic complications

14. Intestinal Atresia and Stenosis

15. Intestinal Atresia and Stenosis Incidence • 95% Atretic 5% Stenotic • 1:330 infants in USA • Associated with Down’s syndrome Caused by • an intrauterine vascular occlusion

16. Small bowel atresiaPathology • Can be single or multiple • It can take different types • Membrane • atretic segment • typically missing segment with V shaped defect in mesentery • multiple segments (Chrismas tree)

17. Intestinal Atresia and Stenosis(clinically) Classical triad of • Bilious vomiting • Distention • Failure to pass meconium on first day of life.

18. Small bowel atresia • Diagnosis • Can be diagnosed during pregnancy by U/S • multiple fluid levels on X ray is diagnostic • Gastrographin full through detect site of obstruction • Treatment • Excision of the non-propulsive area of the dilated segment is better to be done with end-to-end anastomosis

19. Duodenal atresia

20. Duodenal atresia • It typically occurs at the second part of the duodenum • When there is a missing part of the duodenum the pancreas gives the impression of annular pancreas • The ampulla commonly drains into the proximal part (bile stained vomitus) • Down’s syndrome is present in 30% of cases (not usually associated with other intestinal atresia)

21. Duodenal atresiaCauses • Complete obstruction • Incomplete obstruction • Intrinsic stenos is by diaphragm • Extrinsic by • Annular pancrease • Band of Ladd

22. Duodenal atresiaClinical • Complete obstruction • Vomiting (persistent bile stained ) • Distention (sever) • No passage of meconium • May jaundice • Incomplete obstruction • Vomiting ( intermittent) • Distention (minimal) • Normal passage of meconium

23. Duodenal atresiaDiagnosis • Antenatal U/S at 16 -20 weeks can diagnose the case • Polyhydramnios may be present • 60% Features of Down’ syndrome • Plain X ray double bubble appearance • Upper GIT series

24. Atresia and Stenosis Doudenal atresia oesphageal atresia

25. Duodenal atresia Management • A nasogastric tube should be passed • Intravenous fluid resuscitation should be given • Major cardiac and other defects should be excluded • Duodenoduodenostomy should be performed when resuscitated • Duodenojujnostomy

26. Malrotation and volvulus neonatoum

27. Non-fixation and Malrotation of the bowel • Around the 10th week bowel commences its return from the physiological hernia in the umbilical cord to the abdomen • It rotates 270 counterclockwise • This will lead to the formation of the C duodenal loop, which passes beneath the superior mesenteric vein. • In a similar fashion the colon passes over the vessels bringing the cecum to the right iliac fossa

28. Anomalies of the bowel Rotation • Non rotation • Incomplete rotation • Midgut volvulus • Band of Ladd causing duodenal obstruction • Reversed rotation • Anomalies mesenteric fixation • Mobile caecum • Paradoudenal hernia • Internal mesenteric hernia

29. Non-fixation and Malrotation of the bowel • Failure of rotation may occur giving an • S shaped duodenum • absence of duodenojujenal junction • presence of small bowel in the right side of the abdomen . • The cecum lies in the left hypochondrium

30. Malrotation absence of duodenojujenal junction The cecum lies in the left hypochondrium presence of small bowel in the right side

31. Non-fixation and Malrotation of the bowel • The incomplete or arrested rotation with the previous description will lead to either • To midgut volvulus, due to the narrow attachment of the mesenteric base, and very long bowel loop • Or will lead to the presence of a fibrous tissue band (Band of Ladd) that cross the duodenum, from the right hypochondrium to the cecum, causing duodenal obstruction

32. Presentations Two principal clinical presentations • Presents late with intermittent bile stained vomiting and distension (duodenal obstruction) • Presents early with collapse and acidosis due to intestinal infarction Radiological investigations are often unhelpful • Double bubble sign • Multiple air fluid level • Gastrographin detect site of obstruction

33. Management • After resuscitation, early laparotomy may be required • Any volvulus should be reduced • Resection may be required if there has been small bowel infarction • Any Ladd's bands should be divided • Colon should be placed on the left of the abdomen • Small bowel should be placed on the right • Inversion appendicectomy should be performed to prevent future diagnostic uncertainty

34. Malrotation and volvulus

35. Meconium ileus

36. Meconium ileus • Commonest cause of neonatal intraluminal intestinal obstruction • 80% cases are associated with cystic fibrosis • on the other hand 15 % of patients with cystic fibrosis presents with meconium ileus • Cystic fibrosis is an autosomal recessive trait • Antenatal diagnosis is possible with U/S, showing dilated loops of bowel and abdominal distension

37. Meconium ileus • Due to loss of pancreatic enzymes (cystic fibrosis) • Abnormal mucous thick and tacky meconium obstructs the lower ileum, • The affected loops become heavy and dilated and thickened and become prone to volvulus . • The colon is atrophic, microcolon with pellets of desquamated epithelium due to non use.

38. obstructs the lower ileum Proximal bowel dilated and thickened prone to volvulus The colon is atrophic, microcolon

39. Meconium ileus • At birth, the baby is noted to have a markedly distended abdomen with • The presence of large visible and palpable dilated loops of bowel filled with pultaceous rubbery meconium • Then neoborn starts to vomit green. • With delayed muconium passage.

40. Meconium ileus • Abnormal radiographs show a granular appearance in dilated small bowel loops of variable diameter, with no fluid levels. • Eventually full blown picture of intestinal obstruction in the upper loops develop • Contrast enema reveals micro colon with pellets. • 40% are associated with complications, either volvulus neonatorum, atresia or meconium peritonitis, giving physical signs of acute intra-abdominal process

41. Meconium Ileus

42. Treatment • In 50% of non complicated cases the gastrografin enema (highly osmolar wetting agent) rapidly passing through the microcolon, can dislodge the meconium sufficiently to overcome the obstruction • Two indications of laparatomy • Residual obstruction • The presence of complications

43. Meconium Ileus

44. Laparotomy • An attempt is made to liquefy the meconium by intraluminal injection of • Gastrographin • Saline • Plus bowel massage • More frequently it is necessary to resect the dilated meconium filled loops back to bowel of a normal diameter then • Either end to end anastomosis +wash out the distal bowel or • Bishop Koop operation

45. Mikulicz Swenson Distal Chimney Proximal Chimney

46. Intussusception

47. Intussusception • The term describes telescopic invagination of bowel within itself . • As it advances more bowel is dragged through giving more bulky and tight mass. • The mesentery invaginated will be compressed leading to congestion and strangulation.

48. Intussusception • It is the commonest abdominal emergency between 3 months and 2 years • Peak incidence is between 6 and 9 months • Commonest site involved is the ileocaecal junction

49. IntussusceptionEtiology • Most cases are idiopathic • Weaning • Gastrorentritis in 50% of cases • with the lead point due to enlarged Peyer's patches usually due to a viral infection • Mobile ileocacecal junction • Long bloodless fold of trves • 5% are due to polyp, Meckel's diverticulum, duplication cyst or tumor

50. Intussusception • Obstruction is complete from beginning • 95% begin at ileocecal valve • 2-8% have a lead point • (polyp, Meckel’s, lymphoid patch) • Edema produces lymph node enlargement • Fluid, blood and mucus into the lumen • Current Jelly Stool