PEDIATRIC INTESTINAL

OBSTRUCTION

DENNIS S. FLORES, MD, DPPS, DPSN, DPNSP

SCOPE

• An overview of the generalities in pediatric intestinal obstruction

• Specific causes of intestinal obstruction in pediatrics:• Hirschsprung’s disease• Incarcerated inguinal hernia• Intussusception• Gastric volvulus• Ileus• Adhesions• Superior mesenteric artery syndrome• Foreign bodies• Bezoars

INTESTINAL OBSTRUCTION

• Is the cessation, partial or complete, of the antegrade flow of the intestinal contents due to abnormalities in function and/or organic lesions along the wall in the vicinity of the intestinal tract

INTESTINAL OBSTRUCTION

FUNCTIONAL MECHANICAL

CLASSIFICATION

INTESTINAL OBSTRUCTION

• FUNCTIONAL CAUSES are usually due to electrolyte derangements

A maternal history of diabetes, systemic infection, complicated labor and delivery, maternal drug intake, or toxemia of pregnancyNeonatal sepsisRespiratory distress in the newborn

INTESTINAL OBSTRUCTION• MECHANICAL CAUSES • Involvement of the upper GI tract,

• distention is confined to the upper half of the abdomen• Persistent vomiting even when feeding has been

stopped

• Lower GI obstruction • Diffuse abdominal enlargement• Vomiting may be a late manifestation

INTESTINAL OBSTRUCTION

• MECHANICAL CAUSES

History of consanguinity and presence of anatomic defects in the familyMaternal polyhydramniosNon-passage or poor evacuation of meconium within the first 24 hours of lifeAccumulation of excessive mucus in the mouthBilious vomiting

INTESTINAL OBSTRUCTION

• MECHANICAL OBSTRUCTION• CAUSES• Atresias• Stenosis• Intussusception• Duodenal bands• Malrotation of the intestines• Volvulus• Postoperative adhesions• Meckel’s diverticulum• Inguinal hernia

INTESTINAL OBSTRUCTION

• The outstanding change is progressive fluid loss brought about by:• Vomiting• Intraluminal accumulation• Intramural trapping• Intraperitoneal extravasation

CLINICAL MANIFESTATIONS

• VOMITING – most frequent presenting manifestation

• More significant if it is bile stained, projectile, persistent, or even bloody

• Accompanied by ABDOMINAL PAIN characterized by incessant crying

• Followed by progressive ABDOMINAL ENLARGEMENT and ABNORMAL STOOLING (failure to pass both flatus and feces)

INTESTINAL OBSTRUCTION

• PHYSICAL EXAMINATION• SCAPHOID ABDOMEN

• Possibility of esophageal atresia or a diaphragmatic hernia

• RAPID & PROGRESSIVE DISTENTION OF THE ABDOMEN

• Mechanical nature of obstruction

• MILD & INTERMITTENT DISTENTION OF THE ABDOMEN

• Functional type of obstruction or a partial gut obstruction

MANAGEMENT

• Determine the cause or clinical impression• Aggressive fluid resuscitation to restore

adequate circulation• Recommended parental fluid: NSS or LRS• Antibiotic coverage for Gram positive and

Gram negative microorganisms are administered prophylactically

MANAGEMENT

• CBC• Urinalysis• Electrolyte levels• Plain radiographs

• very important is the determination of presence of air in the rectum located in the space before the sacrum

• free air in the peritoneum should also be searched and correlated clinically.

• contrast studies like Barium enema may be of help diagnostically

PROGNOSIS

• Invariably good• More critical factors affecting the outcome

• Prompt and adequate resuscitation• Early surgical intervention• Close post-operative monitoring

PROGNOSIS

• Most frequent complication is obstructive postoperative adhesions, but these are relatively infrequent, are entirely unpredictable, and no available measures for prevention

INTESTINAL OBSTRUCTION

• RETROSPECTIVE STUDY (PGH) 1975-1983, (PCMC) 1990-1993

• CAUSES (in decreasing order)

1. Hirschsprung’s disease

2. Incarcerated inguinal hernia

3. Intussusception

4. Congenital bands and intestinal atresia

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• Cause by abnormal innervation of the bowel

• Most common cause of lower intestinal obstruction in neonates

• Males are affected more often than females (4:1)

• Prematurity is uncommon

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• May be associated with other congenital defects like Down, Smith-Lemli Ortiz, Waardenburg, cartilage-hair hypoplasia, and congenital hypoventilation (Ondine curse) syndromes and urogenital or cardiovascular abnormalities

• Seen in association with microcephaly, mental retardation, and abnormal facies, with autism, or with cleft palate, hydrocephalus, and micrognathia

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• PATHOLOGY• Result of the absence of ganglion cells in the

bowel wall, extending proximally and continuously from the anus for a variable distance

• The absence of neural innervation is a consequence of an arrest of neuroblast migration from the proximal to distal bowel

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• PATHOLOGY• Usually sporadic; dominant and recessive

patterns of inheritance have been demonstrated in family groups

• Genes identified: RET, GDNF, NTN, EDNRB, EDN3, EVE-1, L1CAM, SOX10, SIP1

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• The aganglionic segment is limited to the rectosigmoid in 75% of patients

• In 10%, the entire colon lacks ganglion cells• Total bowel aganglionosis is rare• Histologically: absence of Meissner and

Auerbach plexus and hypertrophied nerve bundles with high concentrations of acetylcholinesterase between the muscular levels and in the submucosa

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• CLINICAL MANIFESTATIONS• Begin at birth, with delayed passage of

meconium• In 99% of full-term infants, meconium is

passed within 48 hr of birth• It should be suspected in a full-term infant

(the disease is unusual in preterm infants) with delayed passage of stool

HIRSCHSPRUNG’S DISEASE(Congenital Aganglionic Megacolon)

• CLINICAL MANIFESTATIONS• Some infants pass meconium normally but

subsequently present with a history of constipation

• Failure to thrive, with hypoproteinemia from a protein losing enteropathy, is a less common presentation because Hisrschsprung’s disease is usually recognized early in the course of the illness

• Breastfed infants may not suffer as severe a disease as formula fed infants

Failure to pass stoolsDilatation of the proximal bowel

Abdominal distention

Intraluminal pressure increases

decreased blood flow deterioration of the mucosal barrier

Stasis allows proliferation of bacteria,

which can lead to enterocolitis (Clostridium difficile,

Staphylococcus aureus, anaerobes, coliforms)

with associated sepsis and signs of bowel obstruction

EARLY RECOGNITION

HIRSCHSPRUNG’S DISEASE

• Rectal suction biopsies are the procedure of choice and should be performed no closer than 2 cm to the dental line to avoid the normal area of hypoganglionosis at the anal verge

• Histology: large number of hypertrophied nerve bundles that stain positively for acetylcholinesterase with absence of ganglion cells

HIRSCHSPRUNG’S DISEASE

• ANORECTAL MANOMETRY• Measures the pressure of the internal anal

sphincter while a balloon is distended in the rectum

• In normal individuals, rectal distention initiates a reflex decline in internal sphincter pressure

• In patients with Hirschsprung’s disease, the pressure fails to drop or there is a paradoxical rise in pressure with rectal distention

HIRSCHSPRUNG’S DISEASE

• ANORECTAL MANOMETRY• Accuracy: >90%• Technically difficult to perform in young

infants• A normal response precludes the diagnosis• An equivocal or paradoxical response

requires a repeat motility or rectal biopsy

HIRSCHSPRUNG’S DISEASE

• RADIOGRAPHIC DIAGNOSIS:• Based on the presence of a transition zone

between normal dilated proximal colon and a smaller-caliber obstructed distal colon caused by the nonrelaxation of the aganglionic bowel

• Transition zone – funnel shaped area of intestine between the proximal dilated colon and the constricted distal bowel; not usually present before 1-2 wk of age

HIRSCHSPRUNG’S DISEASE

• RADIOGRAPHIC DIAGNOSIS:• 24-hour delayed films are helpful. If

significant barium is still present in the colon, it increases the suspicion of Hirschsprung’s disease even if a transition zone is not identified

VARIABLE FUNCTIONAL CONSTIPATION

HIRSCHSPRUNG’S DISEASE

HISTORY

Onset of symptoms After 2 years of age At birth

Encopresis Common Very rare

Failure to thrive Uncommon Possible

Enterocolitis None Possible

Forced bowel training Usual None

EXAMINATION

Abdominal distention Uncommon Common

Poor weight gain Rare Common

Anal tone Normal Normal

Rectal examination Stool in ampulla Ampulla empty

Malnutrition None Possible

LABORATORY

Anorectal manometry Distention of the rectum causes relaxation of the internal sphincter

No sphincter relaxation or paradoxical increase in pressure

Rectal biopsy Normal No ganglion cells, increased acetylcholinesterase staining

Barium enema Massive amounts of stool, no transition zone

Transition zone, delayed evacuation (>24 hr)

HIRSCHSPRUNG’S DISEASE

• DEFINITIVE TREATMENT• Surgery• Options:

• as soon as the diagnosis is established • perform a temporary colostomy and wait until

the infant is 6-12 mo old to perform definitive repair

HIRSCHSPRUNG’S DISEASE

• ULTRASHORT SEGMENTAL• Limited to the internal sphincter• Clinically similar to constipation• Ganglion cells are present on biopsy, but

the rectal motility is abnormal• Excision of a strip of rectal muscle leads to

a more regular pattern

HIRSCHSPRUNG’S DISEASE

• LONG SEGMENT• Involves the entire colon and part of the

small bowel• Radiologic studies show no colonic

transition• When the entire colon is aganglionic, ileal-

anal anastomosis is the treament of choice

HIRSCHSPRUNG’S DISEASE

• PROGNOSIS• Satisfactory• Majority achieve fecal continence

INCARCERATED HERNIA

• A hernia in which the contents of the hernia sac cannot be reduced into the abdominal cavity

• Contained structures: small bowel, appendix, omentum, colon, or rarely Meckel diverticulum

• In females, the ovary, fallopian tube, or both are commonly incarcerated

INCARCERATED HERNIA

• Unless treated, may rapidly progress to strangulation (tightly constricted in its passage through the inguinal canal), with potential infarction of the hernia contents

• The testis is also at risk for ischemia because of the compression of the spermatic cord by the strangulated hernia

INCARCERATED HERNIASymptomatology• Irritability• Pain in the groin and abdomen• Abdominal distention• Vomiting

INCARCERATED HERNIASymptomatology• Mass – tensed, nonfluctuant• Pain, tenderness• Does not reduce

INCARCERATED HERNIA

• Abdominal radiographs: features of partial or complete intestinal obstruction, and gas within the incarcerated bowel segment may be seen below the inguinal ligament or within the scrotum

INTUSSUSCEPTION

• Occurs when a portion of the alimentary tract is telescoped into an adjacent segment

• The most common cause of intestinal obstruction between 3 mo-6 years

• Male: female ratio 4:1• A few resolve spontaneously, but if left

untreated, most will lead to intestinal infarction, perforation, peritonitis, and death

INTUSSUSCEPTION

• Lymphoid aggregates in the submucosa of the intestine may enlarge and project into the lumen (e.g. viral infections and gastrointestinal allergy)

• Such projections can be entrapped in the persistalsis of the intestine and be propelled distally invaginating the bowel wall

• Anatomic causes such as Meckel’s diverticulum, intestinal polyp or tumor can serve as focal stimuli or lead points for intussusception

INTUSSUSCEPTION

• The most common type is at or near the ileocecal valve

• Few cases occur in the small intestines (enteroenteral)

• Least common is localized in the colon (colocolic)

INTUSSUSCEPTION

• Double intussusception was encountered in a 9 year old Filipino patient occurring at the ileocecal and the colosigmoid areas

INTUSSUSCEPTIONEpidemiology• Cause is unknown• Correlation with prior or concurrent

respiratory adenovirus (type C) infection has been noted

• May complicate otitis media, gastroenteritis, Henoch Schonlein purpura, or upper respiratory tract infection

INTUSSUSCEPTIONClinical Manifestations• Sudden onset of severe paroxysmal colicky

pain that recurs at frequent intervals and is accompanied by straining efforts with legs and knees flexed and loud cries in a previously well child

• Initially comfortable, but comes weaker and lethargic

• Shock-like state

INTUSSUSCEPTIONClinical Manifestations• Vomiting is common especially in the early

phase. Later, the vomitus becomes bile stained

• Blood in the stools seen in the 1st 12 hours but at times not for 1-2 days

• 60% of infants pass a stool containing red blood and mucus, the currant jelly stool

INTUSSUSCEPTIONClinical Manifestations• Palpation of the abdomen: sausage-shaped

mass, sometimes ill-defined, which may increase in size and firmness during a paroxysm of pain

• Abdominal distention and tenderness develop as intestinal obstruction becomes more acute

INTUSSUSCEPTIONTreatment• Reduction is an emergency procedure• If manual operative reduction is impossible,

resection of the intussusception is necessary with end to end anastomosis

INTUSSUSCEPTIONPrognosis• If untreated, may be fatal• The chances of recovery are directly related

to the duration of the intussusception before reduction

• Recurrence rate after reduction is 10%• Corticosteroids may reduce the frequency

of recurrent intussusception

GASTRIC VOLVULUS

• Presents as a triad of:• a sudden onset of severe epigastric pain• intractable retching with emesis• inability to pass a tube into the stomach

GASTRIC VOLVULUS

• The stomach is tethered longitudinally by the gastrohepatic, gastrosplenic, and gastrocolic ligaments

• In the transverse axis, it is tethered by the gastrophrenic ligament and the retroperitoneal attachment of the duodenum

• A volvulus occurs when one of these attachments is absent or stretched, allowing the stomach to rotate around itself

GASTRIC VOLVULUS

• In most children, other associated defects are present, including intestinal malrotation, diaphragmatic defects, or asplenia

GASTRIC VOLVULUSClinical Manifestations

• Nonspecific• Suggests high intestinal obstruction• In infancy, is usually associated with

nonbilious vomiting• May advance rapidly to strangulation and

perforation

GASTRIC VOLVULUSDiagnosis

• Plain abdominal radiographs by the presence of a dilated stomach

• Erect abdominal films demonstrate a double fluid level with a characteristic “beak” near the lower esophageal junction, in mesenteroaxial volvulus

• In organoaxial volvulus, a single air-fluid level is seen without the characteristic beak.

GASTRIC VOLVULUSTreatment

• Emergent surgery• In selected cases of chronic volvulus,

endoscopic correction has been successful

ILEUS

• Failure of intestinal peristalsis without evidence of mechanical obstruction

• In children, is most often associated with abdominal surgery or infection (pneumonia, gastroenteritis, peritonitis)

ILEUS

• Also accompanies metabolic abnormalities, such as uremia, hypokalemia, hypercalcemia, hypermagnesemia, or acidosis

• After administration of certain drugs, opiates and vincristine, loperamide

ILEUSClinical Manifestations• Abdominal distention• Emesis• Pain initially minimal, increases with

increasing distention• Bowel sounds are minimal or absent, in

contrast to early mechanical obstruction (hyperactive)

ILEUS

• Serial radiographs do not show progressive distention as they do in mechanical obstruction

• Treatment: correction of the underlying abnormality

• Nasogastric decompression

ILEUS

• Ileus after abdominal surgery usually results in return of normal intestinal motility in 24-72 hours

• Prokinetic agents, such as metoclopramide or erythromycin can stimulate the return of normal bowel motility

ADHESIONS

• Are fibrous bands of tissue that are a common cause of postoperative small bowel obstruction after abdominal surgery

• 2-3% of patients

ADHESIONS

• Diagnosis is suspected in patients with abdominal pain, constipation, emesis, and a history of intraperitoneal surgery

• Bowel sounds are initially hyperactive, abdomen is flat

• The bowel subsequently dilates, producing abdominal distention. Bowel sounds disappear

ADHESIONS

• Fever and leukocytosis are suggestive of necrotic bowel and peritonitis

• Plain radiographs: obstructive features• Abdominal CT: cause of obstruction

ADHESIONSTreatment• Nasogastric decompression• IV fluid resuscitation• Broad spectrum antibiotics • Surgery

SUPERIOR MESENTERIC ARTERY SYNDROME• Extrinsic compression of the duodenum in

children after rapid weight loss and in supine position

• Compression occurs as the mesentery loses its fat and allows the SMA to collapse on the duodenum, compressing it between the SMA and the aorta posteriorly

SUPERIOR MESENTERIC ARTERY SYNDROME• Classic example is an adolescent who starts

vomiting after application of a body cast for orthopedic surgery

• Diagnosis: radiographic demonstration of a cutoff of the duodenum just to the right of the midline

SUPERIOR MESENTERIC ARTERY SYNDROME

Treatment: relief of the obstruction• Positioning in a lateral or prone position• Prokinetic drugs• Total parenteral nutrition to restore lost

body fat• Occasionally, surgical intervention

FOREIGN BODIES

• Once in the stomach, 95% of all ingested objects pass without difficulty through the remainder of the GI tract

• Radiologic examination: to determine the type, number, and location of the suspected objects

FOREIGN BODIESManagement • Conservative • Most objects pass through the intestine in 4-

6 days, although some may take as long as 3-4 weeks

FOREIGN BODIESManagement • Watch out for abdominal pain, vomiting,

persistent fever, hematemesis or melena• Failure of the object to progress within a 3-

4 weeks period seldom implies impending perforation but may be associated with a congenital malformation or acquired bowel abnormality

BEZOARS

• Is an accumulation of exogenous matter in the stomach or intestine

• In females with underlying personality problems or in neurologically impaired individuals

• Peak age at onset: 2nd decade of life

BEZOARS

• Classified on the basis of composition• TRICHOBEZOARS – patient’s own hair• PHYTOBEZOARS – combination of plant and

animal material• LACTOBEZOARS – high casein or calcium

content of some premature formulas• Swallowed chewing gum can occasionally lead to

a bezoar

BEZOARSDiagnosis • Plain abdominal film• US or CT scan – confirmatory

BEZOARSTreatment• Endoscopic removal• Surgery • Lactobezoars usually resolve when feedings

are withheld for 24-48 hours

SUGGESTED READINGS

• NELSON’S TEXTBOOK OF PEDIATRICS 18TH EDITION

• Pages 1646-1647, 1557, 1565-1571