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PEDIATRIC INTESTINAL OBSTRUCTION DENNIS S. FLORES, MD, DPPS, DPSN, DPNSP.

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Presentation on theme: "PEDIATRIC INTESTINAL OBSTRUCTION DENNIS S. FLORES, MD, DPPS, DPSN, DPNSP."— Presentation transcript:

1 PEDIATRIC INTESTINAL OBSTRUCTION DENNIS S. FLORES, MD, DPPS, DPSN, DPNSP

2 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

3 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

4 INTESTINAL OBSTRUCTION FUNCTIONALMECHANICAL CLASSIFICATION

5 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 pregnancy Neonatal sepsis Respiratory distress in the newborn

6 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

7 INTESTINAL OBSTRUCTION MECHANICAL CAUSES History of consanguinity and presence of anatomic defects in the family Maternal polyhydramnios Non-passage or poor evacuation of meconium within the first 24 hours of life Accumulation of excessive mucus in the mouth Bilious vomiting

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

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

10 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)

11 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

12 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

13 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

14 PROGNOSIS Invariably good More critical factors affecting the outcome Prompt and adequate resuscitation Early surgical intervention Close post-operative monitoring

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

16 INTESTINAL OBSTRUCTION RETROSPECTIVE STUDY (PGH) , (PCMC) CAUSES (in decreasing order) 1.Hirschsprung’s disease 2.Incarcerated inguinal hernia 3.Intussusception 4.Congenital bands and intestinal atresia

17 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

18 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

19 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

20 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

21 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

22 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

23 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

24 Failure to pass stools Dilatation 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

25 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

26 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

27 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

28 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

29 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

30 VARIABLEFUNCTIONAL CONSTIPATION HIRSCHSPRUNG’S DISEASE HISTORY Onset of symptomsAfter 2 years of ageAt birth EncopresisCommonVery rare Failure to thriveUncommonPossible EnterocolitisNonePossible Forced bowel trainingUsualNone EXAMINATION Abdominal distentionUncommonCommon Poor weight gainRareCommon Anal toneNormal Rectal examinationStool in ampullaAmpulla empty MalnutritionNonePossible LABORATORY Anorectal manometryDistention of the rectum causes relaxation of the internal sphincter No sphincter relaxation or paradoxical increase in pressure Rectal biopsyNormalNo ganglion cells, increased acetylcholinesterase staining Barium enemaMassive amounts of stool, no transition zone Transition zone, delayed evacuation (>24 hr)

31 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

32 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

33 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

34 HIRSCHSPRUNG’S DISEASE PROGNOSIS Satisfactory Majority achieve fecal continence

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36 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

37 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

38 INCARCERATED HERNIA Symptomatology Irritability Pain in the groin and abdomen Abdominal distention Vomiting

39 INCARCERATED HERNIA Symptomatology Mass – tensed, nonfluctuant Pain, tenderness Does not reduce

40 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

41 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

42 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

43 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)

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

45 INTUSSUSCEPTION Epidemiology 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

46 INTUSSUSCEPTION Clinical 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

47 INTUSSUSCEPTION Clinical Manifestations Vomiting is common especially in the early phase. Later, the vomitus becomes bile stained Blood in the stools seen in the 1 st 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

48 INTUSSUSCEPTION Clinical 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

49 INTUSSUSCEPTION Treatment Reduction is an emergency procedure If manual operative reduction is impossible, resection of the intussusception is necessary with end to end anastomosis

50 INTUSSUSCEPTION Prognosis 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

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54 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

55 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

56 GASTRIC VOLVULUS In most children, other associated defects are present, including intestinal malrotation, diaphragmatic defects, or asplenia

57 GASTRIC VOLVULUS Clinical Manifestations Nonspecific Suggests high intestinal obstruction In infancy, is usually associated with nonbilious vomiting May advance rapidly to strangulation and perforation

58 GASTRIC VOLVULUS Diagnosis 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.

59 GASTRIC VOLVULUS Treatment Emergent surgery In selected cases of chronic volvulus, endoscopic correction has been successful

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61 ILEUS Failure of intestinal peristalsis without evidence of mechanical obstruction In children, is most often associated with abdominal surgery or infection (pneumonia, gastroenteritis, peritonitis)

62 ILEUS Also accompanies metabolic abnormalities, such as uremia, hypokalemia, hypercalcemia, hypermagnesemia, or acidosis After administration of certain drugs, opiates and vincristine, loperamide

63 ILEUS Clinical Manifestations Abdominal distention Emesis Pain initially minimal, increases with increasing distention Bowel sounds are minimal or absent, in contrast to early mechanical obstruction (hyperactive)

64 ILEUS Serial radiographs do not show progressive distention as they do in mechanical obstruction Treatment: correction of the underlying abnormality Nasogastric decompression

65 ILEUS Ileus after abdominal surgery usually results in return of normal intestinal motility in hours Prokinetic agents, such as metoclopramide or erythromycin can stimulate the return of normal bowel motility

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67 ADHESIONS Are fibrous bands of tissue that are a common cause of postoperative small bowel obstruction after abdominal surgery 2-3% of patients

68 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

69 ADHESIONS Fever and leukocytosis are suggestive of necrotic bowel and peritonitis Plain radiographs: obstructive features Abdominal CT: cause of obstruction

70 ADHESIONS Treatment Nasogastric decompression IV fluid resuscitation Broad spectrum antibiotics Surgery

71 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

72 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

73 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

74 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

75 FOREIGN BODIES Management Conservative Most objects pass through the intestine in 4- 6 days, although some may take as long as 3-4 weeks

76 FOREIGN BODIES Management 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

77 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: 2 nd decade of life

78 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

79 BEZOARS Diagnosis Plain abdominal film US or CT scan – confirmatory

80 BEZOARS Treatment Endoscopic removal Surgery Lactobezoars usually resolve when feedings are withheld for hours

81 SUGGESTED READINGS NELSON’S TEXTBOOK OF PEDIATRICS 18 TH EDITION Pages , 1557,


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