1. Neonatal Intestinal Obstruction(N.I.O)
Dr.Osama Esmaeel Hudder
MRCS(England)
Iraqi Board Pediatric Surgery

2. Presentation of neonatal intestinal obstruction(N.I.O)
Bilious vomiting(Always N.I.O until prove otherwise)
Abdominal distention (Depend on the level of I.O)
Failure to pass meconuim

3. COMMON CAUSES OF NEWBORN BOWEL OBSTRUCTION:
1-Mechanical:
Intestinal atresia
Malrotation with midgut volvulus
Meconium ileus (mostly due to cystic fibrosis)
Meconium plug
Small left colon syndrome (diabetic mothers)
Segmental volvulus (without malrotation)
Meconium peritonitis (with perforation, adhesions, and pseudocyst formation)
Incarcerated hernia (inguinal, diaphragmatic, internal)
Necrotizing enterocolitis
Duplication
Anorectal malformation

4. 2-Functional: Hirschsprung's disease (congenital megacolon)
Paralytic ileus (usually secondary to sepsis,Peritonitis, Hypokalemia and uremia)
Maternal drugs - magnesium, Valium, heroin

5. Doudenal Atresia Etiology: Associated anomalies: Symptoms:
Due to failure of recanalization .
Associated anomalies:
Low birth weight - (50%)
Down's syndrome - (30%)
Malrotation - (50%)
Symptoms:
Maternal polyhydramnios, Bilious vomiting, noabdominal distention

6. X-rays?

7. X-ray show double bubble appearance Differential diagnosis:- 1-Doudenal atresia 2-Malrotation with volvulus

8. Management Pre-op: 1) NG decompression 2) IV hydration 3) Antibiotic
Surgery: transverse supraumbilical incision, duodenoduodenostomy Diamond shape anastomosis

9. SMALL BOWEL ATRESIAS Etiology
Vascular occlusion of the vessel which supply this involved part of the bowel with aseptic necrosis and resorption.
This occlusion probably due to defect in mesenteric arcade or due to intrauterine volvulus.

10. Associated Anomalies:
    SMALL BOWEL ATRESIAS
Associated Anomalies:
Low incidence of other anomalies
Low birth weight
Meconium ileus
Symptoms
Maternal polyhydramnios, bilious vomiting, abdominal distension

11. X-rays Management Multiple dilated loops, air-fluid levels
Barium enema: microcolon
Management
Pre-op:
1) IV hydration (fluid bolus)
2) NG decompression
3) Antibiotics
Surgery: Transverse supraumbilical incision, resection with reanastomosis.

12. MALROTATION AND MIDGUT VOLVULUS
 Lack of retroperitoneal fixation of bowel and presence of Ladd’s bands
partial or complete duodenal obstruction
bowel may twist around SMA axis = volvulus

13. Week 6 Physiological Umbilical Herniation
As a result of rapid growth and expansion of the liver, the abdominal cavity temporarily becomes too small to contain all the intestinal loops.
The intestinal loops enter the extraembyronic cavity within the umbilical cord during the sixth week of development.
As herniation occurs, the loop undergoes a 90 degree counterclockwise rotation around the superior mesenteric artery.

14. Week 10 Return to Abdominal Cavity
During 10th week of development, herniated intestinal loops begin to return to the abdominal cavity.
Undergoes additional 180 degree counterclockwise rotation about the superior mesenteric artery. .

15. Symptoms Acute: bilious vomiting often with a scaphoid abdomen
75% onset symptoms in first week of life (usually first three days),
volvulus present in 85%
Chronic: (due to Ladd's bands or intermittent volvulus) cyclic abdominal pain,
bilious vomiting, malabsorption

16. Radiography
Abdominal X-ray: duodenal obstruction - dilated stomach, gasless abdomen or paucity of gas beyond duodenum
Ba.meal and follow through shows duodenojejunal junction to the Right of midline, more cephalic
Barium enema - cecum in left iliac fossa (helps confirm, but not diagnostic)

17. Malrotation

18. Management Pre-op: 1) IV hydration; 120-150 ml/kg per day
2) NG decompression
3) Antibiotics
Surgery:
Emergency laparotomy when unable to rule out volvulus
Principles of the operation:-
1-Do derotation ,counterclockwise.
2-Straightening of the doudenum
3-Excision of ladds band.
4-Widining of the mesentery.
5-Appendescectomy.

19. MECONIUM ILEUS
Neonatal intestinal obstruction due to inspisated abnormal thick meconium in terminal ileum.

20. MECONIUM ILEUS Types: Etiology:
Occurs in 10-15% of patients with cystic fibrosis. Very rarely occurs in the absence of cystic fibrosis (pancreatic enzyme deficiency).
Types:
1-50% simple or "uncomplicated"
2-50% are complicated and associated with volvulus, atresia, Intestinal perforation causing meconium peritonitis,

21. MECONIUM ILEUS Symptoms: ,
1-Abdominal distension with bilious aspirates through the NGT.
2-Abdominal palpation shows doughy feeling with palpable intestinal loops
3-PR. no meconium in rectum.

22. Diagnosis
X-rays:
Multiple dilated loops and coarse granular appearance (“ground
glass”), no air fluid levels, calcifications
Barium Enema:
Microcolon
Positive sweat test:
Na > 60 mEq
Cl > 60 mEq
Genetic testing:

23. Management: Simple Meconium Ileus
40-60% can be handled non-operatively therapy
1) IV hydration (fluid bolus prior to enema)
2) antibiotics
3) NG decompression
4) Gastrografin enema (hyperosmolar)
- monitor urine output and hemodynamics since the hyperosmolar enema can lead to severe hypovolemia.
must reflux back into dilated loops to be successful repeat in hours if necessary
5) N-acetyl-cysteine enema if gastrograffin unsuccessful in providing full Evacuation
6) begin oral feedings (Pregestimil)

24. Surgery: if enema fails, proceed to surgery
1) Supraumbilical transverse incision
2) Enterotomy with evacuation of meconium and pellets
3) Irrigate intestine with 1% N-acetyl cysteine
4) Primary closure of enterotomy if bowel healthy or consider ileostomy if health of bowel questionable

25. Hirschprung’s Disease
Aim:-
What is Hirschprungs disease
How to diagnose Hirschprungs disease
What is hirschprubgs enterocolitis
Out line for surgical treatment

26. Hirschprung’s Disease
More than 50 years old since the discovery of the cause and the treatment for Hirschprung disease.
Incidence : 1 in 5000 live birth
Male to Female is 4-1

27. Hirschsprung Disease
The primary defect is the absence of the intramural ganglion cells of the submucosal and myenteric plexuses as the result of a defective migration of ganglion cell precursors of the neural crest into the hind gut.

28. Hirschsprung Disease
This absence of normal parasympathatic innervation prevents gut peristalsis, leading to functional constipation.
The proximal colon hypertrophied by trying to overcome functional obstruction.
Transitional zone exists between normal and abnormal aganglionic intestine.

30. Visible transitional zone

31. Hirschsprung’s disease
To rectosigmoid in 75%
Short segment (rectum)
Ultra short (part of the rectum)
Long segment
Total aganglionosis (large intestine, sometimes a part of small intestine) up to 10%
Segmental

32. Presentation
varies from patient to patient depending on the length of the involved segment.
Infant:-
95% - failure to pass meconium in first 24 hours life
Chronic contipation and abdominal distention
Older children :– Chronic constipation, failure to thrive
Hirschsprung’s enterocolitis:-10-15% will have severe diarrhea and billious vomiting alternating with constipation.

33. “Neonatal bilious emesis is a surgical emergency until proven otherwise”

34. Diagnosis
Barium enema will reveal a transition zone with narrow segment and dilated proximal portion. Late films will show retention of barium at hours. .

35. Diagnosis
Transition zone

36. Hirschsprung’s disease
Rectal biopsy is the most reliable diagnostic measure
-:Histopathology
Absence of ganglionic cells
Hypertrophic cholinergic nerve trunks
Limited number of adrenergic fiber

37. Anorectal manometry Absent rectoanal inhibitory reflex
Lack of internal anal sphincter relaxation in response to rectal stretch

38. Complicatons Complications of Hirschsprung`s disease include
intestinal perforation (particularly at the appendix)
enterocolitis,
, malnutrition, failure to thrive, and anemia.
Water intoxication from frequent tape water enema

39. Pathophysiology of enterocolitis
Colonic stasis…….overgrowth of bacteria(Clostridium deficile)…………..Invasion of bacteria to the epithelium(Translocation)………….inflammation (entercollitis)……….septiceamia

40. PRESENTATION OF ENTEROCOLITIS
Abdominal distension
Explosive foul-smelling diarrhea -
Bilious vomiting -
Fever -
Lethargy -
Colonic perforation / shock -

41. DIAGNOSIS OF HD ENTEROCOLITIS
Diffusely tender, distended abdomen
Digital rectal exam results in explosive gas and stool
Errect abdominal x-ray :-Air fluid levels
Contrast enemas is contraindicated due to the risk of perforation

42. TREATMENT OF HD ENTEROCOLITIS
Prompt recognition ESSENTIAL
**Rectal tube decompression
Aggressive IV fluid resuscitation
Broad spectrum antibiotics
Vancomycine and metronidazole.
Occasional emergent colostomy.
Can be life-threatening if unrecognized

43. congenital megacolon (Hirschprungs disease).
diagnosis
surgical approaches A
colostomy
after
pull through
few months
after
2 months
closure colostomy

45. B C Laparascopic assisted pullthrough
Resent approach is the transanal one stage pull-through without colostomy & without laparatory. the advantages of this new procedure are less risk of damage to the pelvic structures , lower incidence of intraabdominal bleeding and adhesion formation, lower cost and absence of abdominal incisions.