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
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