Neonatal Intestinal Obstruction(N.I.O) - muhadharaty.com · 1 Fifth stage Surgery Lec-3 ةماسأ...

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1 Fifth stage Surgery Lec-3 د. أسامة13/12/2015 Neonatal Intestinal Obstruction(N.I.O) 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 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 2-Functional: Hirschsprung's disease (congenital megacolon) Paralytic ileus (usually secondary to sepsis,Peritonitis, Hypokalemia and uremia) Maternal drugs - magnesium, Valium, heroin . Doudenal Atresia : Etiology: Due to failure of recanalization . Associated anomalies: Low birth weight - (50%) Down's syndrome - (30%) Malrotation - (50%) Symptoms:

Transcript of Neonatal Intestinal Obstruction(N.I.O) - muhadharaty.com · 1 Fifth stage Surgery Lec-3 ةماسأ...

Page 1: Neonatal Intestinal Obstruction(N.I.O) - muhadharaty.com · 1 Fifth stage Surgery Lec-3 ةماسأ .د 13/12/2015 Neonatal Intestinal Obstruction(N.I.O) Presentation of neonatal intestinal

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Fifth stage Surgery

Lec-3

13/12/2015 د. أسامة

Neonatal Intestinal Obstruction(N.I.O)

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

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

2-Functional:

Hirschsprung's disease (congenital megacolon)

Paralytic ileus (usually secondary to sepsis,Peritonitis, Hypokalemia and uremia)

Maternal drugs - magnesium, Valium, heroin .

Doudenal Atresia : Etiology:

Due to failure of recanalization .

Associated anomalies:

Low birth weight - (50%)

Down's syndrome - (30%)

Malrotation - (50%)

Symptoms:

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Maternal polyhydramnios, Bilious vomiting, noabdominal distention .

X-rays :

X-ray show double bubble appearance

Differential diagnosis:-

1-Doudenal atresia

2-Malrotation with volvulus

Management

— Pre-op:

— 1) NG decompression

— 2) IV hydration

— 3) Antibiotic

— Surgery: transverse supraumbilical incision, duodenoduodenostomy Diamond shape

anastomosis .

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.

Associated Anomalies:

Low incidence of other anomalies

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Low birth weight

Meconium ileus

Symptoms

Maternal polyhydramnios

bilious vomiting,

abdominal distension

X-rays

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.

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 .

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.

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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.

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

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)

Malrotation :

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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.

MECONIUM ILEUS :

Neonatal intestinal obstruction due to inspisated abnormal thick meconium in terminal

ileum.

— 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 .

— 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.

Diagnosis

X-rays:

Multiple dilated loops and coarse granular appearance (“ground glass”), no air fluid levels,

calcifications .

Barium Enema: Microcolon

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Positive sweat test:

— Na > 60 mEq

— Cl > 60 mEq

Genetic testing .

— 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 12-24 hours if necessary

5) N-acetyl-cysteine enema if gastrograffin unsuccessful in providing full Evacuation

6) begin oral feedings (Pregestimil)

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 .

Hirschprung’s Disease

Aim:-

What is Hirschprungs disease

How to diagnose Hirschprungs disease

What is hirschprubgs enterocolitis

Out line for surgical treatment

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 .

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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.

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.

Visible transitional zone :

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 .

Presentation : varies from patient to patient depending on the length of the involved segment.

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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.

“Neonatal bilious emesis is a surgical emergency until proven

otherwise” Diagnosis : Barium enema will reveal a transition zone with narrow segment and dilated proximal

portion . Late films will show retention of barium at 24- 48 hours .

Rectal biopsy is the most reliable diagnostic measure

Histopathology 1) Absence of ganglionic cells 2) Hypertrophic cholinergic nerve trunks 3) Limited number of adrenergic fiber

Anorectal manometry

1) Absent rectoanal inhibitory reflex

2) Lack of internal anal sphincter relaxation in response to rectal stretch

Complicatons :

intestinal perforation (particularly at the appendix)

enterocolitis, malnutrition, failure to thrive, and anemia.

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Water intoxication from frequent tape water enema .

Pathophysiology of enterocolitis : Colonic stasis overgrowth of bacteria(Clostridium deficile) Invasion of bacteria to the

epithelium(Translocation) inflammation (entercollitis) septiceamia .

PRESENTATION OF ENTEROCOLITIS : 1) Abdominal distension .

2) Explosive foul-smelling diarrhea . 3) Bilious vomiting . 4) Fever . 5) Lethargy . 6) Colonic perforation / shock .

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 .

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.

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