Intestinal Duplication rare anomalies that consist of well-formed tubular or spherical structures firmly attached to the intestine with a common blood supply. Lining resembles that of the GIT Duplications: mesenteric border and may communicate with the intestinal lumen.
Classified to 3 categories: 1)Localized duplications may occur in any area of the GIT (commonly: ileum and jejunum) >usually cystic or tubular structures within the wall of the bowel >cause: unknown   : defects in recanalization of the intestinal lumen after the solid stage of embryologic development
2)Duplication of the intestine occurring with vertebral and spinal cord anomalies is thought to  arise from splitting of the notochord in the developing embryo 3)Duplication of the colon is associated with  anomalies of the urinary tract and genitals
Clinical Manifestations: bowel obstruction  lead point of an intussusception or site for a volvulus abdominal pain, vomiting, palpable mass, or acute GI hemorrhage.  May present as respiratory distress
constipation or diarrhea recurrent prolapse of the rectum
Diagnosis History physical examination Treatment: surgical resection management of associated defects.
 
Meckel Diverticulum Remnant of the embryonic yolk sac Referred as omphalomesenteric duct/ vitelline duct The omphalomesenteric duct connects the yolk sac to the gut in a developing embryo and provides nutrition until the placenta is established
5th and 7th wk AOG – duct attenuates and separates from the intestine Partial or complete failure of involution of the omphalomesenteric duct results in various residual structures.  Meckel diverticulum is the most frequent congenital GI anomaly, occurring in 2–3% of all infants.
A typical Meckel diverticulum: 3–6cm outpouching of the ileum along the antimesenteric border 50–75cm from the ileocecal valve
Clinical Manifestations: intermittent painless rectal bleeding  stool is brick colored or currant jelly colored Bleeding may cause significant anemia, usually self-limited Less often associated with partial or complete bowel obstruction
Diagnosis If an infant/child presents with significant painless rectal bleeding - Meckel diverticulum should be suspected.  Plain AXR: is of no value Meckel radionuclide scan  - most sensitive study performed after IV infusion of technetium-99m pertechnetate. The mucus-secreting cells of the ectopic gastric mucosa take up pertechnetate, permitting visualization of the Meckel diverticulum
 
Chronic Intestinal Pseudo-Obstruction group of disorders char by  signs/symptoms of intestinal obstruction in the absence of an anatomic lesion abnormal myoelectric activity to abnormalities of the nerves (intestinal neuropathy)
musculature (intestinal myopathy) of the gut.  The organs involved: entire GIT or may be limited to certain components (stomach or colon)
Clinical Manifestations >1/2 of children with congenital pseudo-obstruction experience symptoms within the first few months of life.  2/3 of infants presenting within the first few days of life are premature about 40% have malrotation of the intestine
abdominal distention and vomiting - present in 75%  Constipation, growth failure, and abdominal pain occur in approximately 60% of patients diarrhea occurs in 30–40%
The symptoms wax and wane in the majority of the patients poor nutrition and intercurrent illness tend to exacerbate symptoms Urinary tract involvement is common - recurrent urinary tract infection or mimic obstructive symptoms.
DX: presence of compatible symptoms in the absence of anatomic obstruction.  Plain abdominal XRAY- air-fluid levels in the small intestine Neonates with evidence of obstruction at birth have a microcolon.
Contrast studies demonstrate slow passage of barium Anorectal motility is normal and differentiates pseudo-obstruction from Hirschsprung disease Full-thickness intestinal biopsy: show involvement of the muscle layers or abnormalities of the intrinsic intestinal nervous system.
Treatment Nutritional support is the mainstay of treatment 30 to 50% require partial or complete parenteral nutrition Some patients can be treated with intermittent enteral supplementation, others on selective oral diets
Prokinetic drugs are generally not useful Isolated gastroparesis may follow episodes of viral gastroenteritis and spontaneously resolves usually within 6–24 mo Cisapride  (a 5-hydroxytryptamine receptor antagonist) &  erythromycin  (a motilin receptor agonist) may enhance gastric emptying and proximal small bowel motility
Ileus Is the failure of intestinal peristalsis without evidence of mechanical obstruction Lack of normal gut motility interferes with movement of intestinal contents  In children mostly associated with abdominal surgery or infection (pneumonia, gastroenteritis, peritonitis)
accompanies metabolic abnormalities (uremia, hypokalemia, or acidosis) occurs with admin of opiates and vincristine occurs with admin of antimotility drugs (loperamide)
Clinical Manifestations increasing abdominal distention  and initially minimal pain w/c increases with increasing distention Bowel sounds are minimal or absent , in contrast to early mechanical obstruction, when they are hyperactive Plain AXR: air-fluid levels throughout the abdomen.  Contrast radiographs - slow movement of the barium through a patent lumen.
Treatment: correction of the underlying abnormality Nasogastric decompression  if abdominal distention is asso with pain or to relieve recurrent vomiting Ileus after abdominal surgical procedures: return of normal motility within 24–72hr Prokinetic agents: metoclopramide/erythromycin may stimulate the return of normal bowel motility
 
Adhesions fibrous bands of tissue Cause: postoperative small bowel obstruction after abdominal surgery  The majority of obstructions: asso single adhesions and can occur at any time after the 2nd postoperative week.
Clinical Manifestations abdominal pain Nausea and vomiting quickly follow the development of pain Constipation Emesis a history of intraperitoneal surgery
Clinical manifestations: Bowel sounds initially are hyperactive, and the abdomen is flat The bowel subsequently dilates, producing abdominal distention in most patients, and bowel sounds disappear Fever and leukocytosis: suggestive of necrotic bowel and peritonitis.
Diagnosis Plain AXR: demonstrate obstructive features contrast studies may be needed to define the cause of obstruction.
Treatment NGT, IV resuscitation, and broad-spectrum antibiotics in anticipation of surgery. Nonoperative intervention is contraindicated unless a patient is stable with clear evidence of clinical improvement.
 
Intussusception Intussusception occurs when a portion of the alimentary tract is telescoped into an adjacent segment common cause of intestinal obstruction bet 3 mo and 6 yo 60 of patients are younger than 1 yr, and 80% of the cases occur before 24 mo; it is rare in neonates The incidence varies from 1–4 in 1,000 live births. The male:female ratio is 4:1.
A few intussusceptions reduce spontaneously, but if left untreated, most will lead to peritonitis, perforation, and death. cause: unknown.  Correlation with adenovirus infections has been noted, may complicate otitis media, gastroenteritis, Henoch-Schönlein purpura, or upper respiratory tract infections
Postulated : GIT infection/ introduction of new food proteins results in swollen Peyer patches in the terminal ileum The prominent mounds of tissue lead to mucosal prolapse of the ileum into the colon, thus causing an intussusception Postoperative intussusception is ileoileal, occurs within 5 days of an abdominal operation. Lead points are more common in children older than 2 yr of age.
Intussusceptions most often: ileocolic and ileoileocolic less commonly cecocolic rarely exclusively ileal
The upper portion of bowel,(intussusceptum), invaginates into the lower, (intussuscipiens), dragging its mesentery along with it into the enveloping loop Constriction of the mesentery obstructs venous return; engorgement of the intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody stool, sometimes containing mucus Most intussusceptions do not strangulate the bowel within the first 24hr but may later eventuate in intestinal gangrene and shock.
Clinical Manifestations. sudden onset of severe paroxysmal colicky pain in a previously well child recurs at frequent intervals, accompanied by straining efforts with legs and knees flexed and loud cries infant may initially be comfortable and play normally between the paroxysms of pain; but if the intussusception is not reduced, the infant becomes progressively weaker and lethargic
lethargy is out of proportion to the abdominal signs Eventually a shocklike state may develop with fever The pulse becomes weak and thready respirations become shallow and grunting  pain may be manifested only by moaning sounds Vomiting occurs in most cases and is usually more frequent early
In the later phase, the vomitus becomes bile stained Stools of normal appearance may be evacuated during the first few hours of symptoms After this time, fecal excretions are small or more often do not occur and little or no flatus is passed Blood generally is passed in the first 12hr but at times not for 1–2 days and infrequently not at all 60% pass a stool containing red blood and mucus, the currant jelly stool
Palpation: slightly tender sausage-shaped mass, sometimes ill defined, which may increase in size and firmness during a paroxysm of pain and mostly in the right upper abdomen About 30% of patients do not have a palpable mass The presence of bloody mucus on the finger as it is withdrawn after rectal examination supports the diagnosis of intussusception. Abdominal distention and tenderness develop as intestinal obstruction becomes more acute
Diagnosis Clinical history and physical findings Plain AXR: density in the area of the intussusception barium enema  shows a filling defect or cupping in the head of barium where its advance is obstructed by the intussusceptum.  A central linear column of barium may be visible in the compressed lumen of the intussusceptum, and a thin rim of barium may be seen trapped around the invaginating intestine in the folds of mucosa within the intussuscipiens ( coiled-spring sign ), especially after evacuation.
UTZ : The diagnostic findings of intussusception include a tubular mass in longitudinal views and a doughnut or target appearance in transverse images.  UTZ is also useful in demonstrating reduction of the intussusception by hydrostatic or air techniques.
Treatment Reduction of an acute intussusception  is an emergency procedure and performed immediately after diagnosis in preparation for possible surgery.  In patients with prolonged intussusception with signs of shock, peritoneal irritation, intestinal perforation, or pneumatosis intestinalis,  reduction should not be attempted.
 
Closed-Loop Obstructions defects in the mesentery (“internal hernias”) through which loops of small bowel may pass and become trapped Vascular engorgement of the trapped bowel results in intestinal ischemia and gangrene unless promptly relieved.
Clinical Manifestations bilious vomiting abdominal distention abdominal pain Peritoneal signs suggest ischemic bowel.
Plain AXR : signs of small bowel obstruction or free air if perforated Supportive management:  intravenous fluids Antibiotics nasogastric decompression Prompt surgical relief of the obstruction is indicated if intestinal gangrene is to be prevented
 
Foreign Bodies in the Stomach and Intestine 80% of all foreign body ingestions occur in children, peak: 6 mos to 3 yr.  Coins  are the most common foreign body ingested by  young children .  In older children, teenagers, and adults,  fish or chicken bones  are the most common objects accidentally ingested.  The risk of ingestion increases after alcohol consumption or cold liquids because of a decrease in oral sensory acuity.
Of the foreign bodies that come to medical attention, 80–90% pass through the gastrointestinal tract without difficulty.  Ten to 20% require endoscopic removal or other conservative management, whereas 1% or less require surgical intervention.  Once in the stomach, 95% of all ingested objects pass without difficulty through the remainder of the gastrointestinal tract.  Perforation after ingestion of a foreign body is estimated to be less than 1% of all objects ingested. Perforation tends to occur in areas of physiologic sphincters (pylorus and ileocecal valve), acute angulation (such as the duodenal sweep), congenital gut malformations (webs, diaphragms, or diverticula), or areas of previous bowel surgery.
bezoar is an accumulation of exogenous matter in the stomach or intestine  Most bezoars have been found in females with underlying personality problems or in neurologically impaired individuals.  The peak age at onset: 2nd decade of life.
Trichobezoars are composed of the patient's own hair Phytobezoars are composed of a combination of plant and animal material Lactobezoars: found in premature infants, may be attributed to the high casein or calcium content of premature formulas Swallowed chewing gum may occasionally lead to a bezoar.
 

Gastrointestinal Problems In Children

  • 1.
    Intestinal Duplication rareanomalies that consist of well-formed tubular or spherical structures firmly attached to the intestine with a common blood supply. Lining resembles that of the GIT Duplications: mesenteric border and may communicate with the intestinal lumen.
  • 2.
    Classified to 3categories: 1)Localized duplications may occur in any area of the GIT (commonly: ileum and jejunum) >usually cystic or tubular structures within the wall of the bowel >cause: unknown : defects in recanalization of the intestinal lumen after the solid stage of embryologic development
  • 3.
    2)Duplication of theintestine occurring with vertebral and spinal cord anomalies is thought to arise from splitting of the notochord in the developing embryo 3)Duplication of the colon is associated with anomalies of the urinary tract and genitals
  • 4.
    Clinical Manifestations: bowelobstruction lead point of an intussusception or site for a volvulus abdominal pain, vomiting, palpable mass, or acute GI hemorrhage. May present as respiratory distress
  • 5.
    constipation or diarrhearecurrent prolapse of the rectum
  • 6.
    Diagnosis History physicalexamination Treatment: surgical resection management of associated defects.
  • 7.
  • 8.
    Meckel Diverticulum Remnantof the embryonic yolk sac Referred as omphalomesenteric duct/ vitelline duct The omphalomesenteric duct connects the yolk sac to the gut in a developing embryo and provides nutrition until the placenta is established
  • 9.
    5th and 7thwk AOG – duct attenuates and separates from the intestine Partial or complete failure of involution of the omphalomesenteric duct results in various residual structures. Meckel diverticulum is the most frequent congenital GI anomaly, occurring in 2–3% of all infants.
  • 10.
    A typical Meckeldiverticulum: 3–6cm outpouching of the ileum along the antimesenteric border 50–75cm from the ileocecal valve
  • 11.
    Clinical Manifestations: intermittentpainless rectal bleeding stool is brick colored or currant jelly colored Bleeding may cause significant anemia, usually self-limited Less often associated with partial or complete bowel obstruction
  • 12.
    Diagnosis If aninfant/child presents with significant painless rectal bleeding - Meckel diverticulum should be suspected. Plain AXR: is of no value Meckel radionuclide scan - most sensitive study performed after IV infusion of technetium-99m pertechnetate. The mucus-secreting cells of the ectopic gastric mucosa take up pertechnetate, permitting visualization of the Meckel diverticulum
  • 13.
  • 14.
    Chronic Intestinal Pseudo-Obstructiongroup of disorders char by signs/symptoms of intestinal obstruction in the absence of an anatomic lesion abnormal myoelectric activity to abnormalities of the nerves (intestinal neuropathy)
  • 15.
    musculature (intestinal myopathy)of the gut. The organs involved: entire GIT or may be limited to certain components (stomach or colon)
  • 16.
    Clinical Manifestations >1/2of children with congenital pseudo-obstruction experience symptoms within the first few months of life. 2/3 of infants presenting within the first few days of life are premature about 40% have malrotation of the intestine
  • 17.
    abdominal distention andvomiting - present in 75% Constipation, growth failure, and abdominal pain occur in approximately 60% of patients diarrhea occurs in 30–40%
  • 18.
    The symptoms waxand wane in the majority of the patients poor nutrition and intercurrent illness tend to exacerbate symptoms Urinary tract involvement is common - recurrent urinary tract infection or mimic obstructive symptoms.
  • 19.
    DX: presence ofcompatible symptoms in the absence of anatomic obstruction. Plain abdominal XRAY- air-fluid levels in the small intestine Neonates with evidence of obstruction at birth have a microcolon.
  • 20.
    Contrast studies demonstrateslow passage of barium Anorectal motility is normal and differentiates pseudo-obstruction from Hirschsprung disease Full-thickness intestinal biopsy: show involvement of the muscle layers or abnormalities of the intrinsic intestinal nervous system.
  • 21.
    Treatment Nutritional supportis the mainstay of treatment 30 to 50% require partial or complete parenteral nutrition Some patients can be treated with intermittent enteral supplementation, others on selective oral diets
  • 22.
    Prokinetic drugs aregenerally not useful Isolated gastroparesis may follow episodes of viral gastroenteritis and spontaneously resolves usually within 6–24 mo Cisapride (a 5-hydroxytryptamine receptor antagonist) & erythromycin (a motilin receptor agonist) may enhance gastric emptying and proximal small bowel motility
  • 23.
    Ileus Is thefailure of intestinal peristalsis without evidence of mechanical obstruction Lack of normal gut motility interferes with movement of intestinal contents In children mostly associated with abdominal surgery or infection (pneumonia, gastroenteritis, peritonitis)
  • 24.
    accompanies metabolic abnormalities(uremia, hypokalemia, or acidosis) occurs with admin of opiates and vincristine occurs with admin of antimotility drugs (loperamide)
  • 25.
    Clinical Manifestations increasingabdominal distention and initially minimal pain w/c increases with increasing distention Bowel sounds are minimal or absent , in contrast to early mechanical obstruction, when they are hyperactive Plain AXR: air-fluid levels throughout the abdomen. Contrast radiographs - slow movement of the barium through a patent lumen.
  • 26.
    Treatment: correction ofthe underlying abnormality Nasogastric decompression if abdominal distention is asso with pain or to relieve recurrent vomiting Ileus after abdominal surgical procedures: return of normal motility within 24–72hr Prokinetic agents: metoclopramide/erythromycin may stimulate the return of normal bowel motility
  • 27.
  • 28.
    Adhesions fibrous bandsof tissue Cause: postoperative small bowel obstruction after abdominal surgery The majority of obstructions: asso single adhesions and can occur at any time after the 2nd postoperative week.
  • 29.
    Clinical Manifestations abdominalpain Nausea and vomiting quickly follow the development of pain Constipation Emesis a history of intraperitoneal surgery
  • 30.
    Clinical manifestations: Bowelsounds initially are hyperactive, and the abdomen is flat The bowel subsequently dilates, producing abdominal distention in most patients, and bowel sounds disappear Fever and leukocytosis: suggestive of necrotic bowel and peritonitis.
  • 31.
    Diagnosis Plain AXR:demonstrate obstructive features contrast studies may be needed to define the cause of obstruction.
  • 32.
    Treatment NGT, IVresuscitation, and broad-spectrum antibiotics in anticipation of surgery. Nonoperative intervention is contraindicated unless a patient is stable with clear evidence of clinical improvement.
  • 33.
  • 34.
    Intussusception Intussusception occurswhen a portion of the alimentary tract is telescoped into an adjacent segment common cause of intestinal obstruction bet 3 mo and 6 yo 60 of patients are younger than 1 yr, and 80% of the cases occur before 24 mo; it is rare in neonates The incidence varies from 1–4 in 1,000 live births. The male:female ratio is 4:1.
  • 35.
    A few intussusceptionsreduce spontaneously, but if left untreated, most will lead to peritonitis, perforation, and death. cause: unknown. Correlation with adenovirus infections has been noted, may complicate otitis media, gastroenteritis, Henoch-Schönlein purpura, or upper respiratory tract infections
  • 36.
    Postulated : GITinfection/ introduction of new food proteins results in swollen Peyer patches in the terminal ileum The prominent mounds of tissue lead to mucosal prolapse of the ileum into the colon, thus causing an intussusception Postoperative intussusception is ileoileal, occurs within 5 days of an abdominal operation. Lead points are more common in children older than 2 yr of age.
  • 37.
    Intussusceptions most often:ileocolic and ileoileocolic less commonly cecocolic rarely exclusively ileal
  • 38.
    The upper portionof bowel,(intussusceptum), invaginates into the lower, (intussuscipiens), dragging its mesentery along with it into the enveloping loop Constriction of the mesentery obstructs venous return; engorgement of the intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody stool, sometimes containing mucus Most intussusceptions do not strangulate the bowel within the first 24hr but may later eventuate in intestinal gangrene and shock.
  • 39.
    Clinical Manifestations. suddenonset of severe paroxysmal colicky pain in a previously well child recurs at frequent intervals, accompanied by straining efforts with legs and knees flexed and loud cries infant may initially be comfortable and play normally between the paroxysms of pain; but if the intussusception is not reduced, the infant becomes progressively weaker and lethargic
  • 40.
    lethargy is outof proportion to the abdominal signs Eventually a shocklike state may develop with fever The pulse becomes weak and thready respirations become shallow and grunting pain may be manifested only by moaning sounds Vomiting occurs in most cases and is usually more frequent early
  • 41.
    In the laterphase, the vomitus becomes bile stained Stools of normal appearance may be evacuated during the first few hours of symptoms After this time, fecal excretions are small or more often do not occur and little or no flatus is passed Blood generally is passed in the first 12hr but at times not for 1–2 days and infrequently not at all 60% pass a stool containing red blood and mucus, the currant jelly stool
  • 42.
    Palpation: slightly tendersausage-shaped mass, sometimes ill defined, which may increase in size and firmness during a paroxysm of pain and mostly in the right upper abdomen About 30% of patients do not have a palpable mass The presence of bloody mucus on the finger as it is withdrawn after rectal examination supports the diagnosis of intussusception. Abdominal distention and tenderness develop as intestinal obstruction becomes more acute
  • 43.
    Diagnosis Clinical historyand physical findings Plain AXR: density in the area of the intussusception barium enema shows a filling defect or cupping in the head of barium where its advance is obstructed by the intussusceptum. A central linear column of barium may be visible in the compressed lumen of the intussusceptum, and a thin rim of barium may be seen trapped around the invaginating intestine in the folds of mucosa within the intussuscipiens ( coiled-spring sign ), especially after evacuation.
  • 44.
    UTZ : Thediagnostic findings of intussusception include a tubular mass in longitudinal views and a doughnut or target appearance in transverse images. UTZ is also useful in demonstrating reduction of the intussusception by hydrostatic or air techniques.
  • 45.
    Treatment Reduction ofan acute intussusception is an emergency procedure and performed immediately after diagnosis in preparation for possible surgery. In patients with prolonged intussusception with signs of shock, peritoneal irritation, intestinal perforation, or pneumatosis intestinalis, reduction should not be attempted.
  • 46.
  • 47.
    Closed-Loop Obstructions defectsin the mesentery (“internal hernias”) through which loops of small bowel may pass and become trapped Vascular engorgement of the trapped bowel results in intestinal ischemia and gangrene unless promptly relieved.
  • 48.
    Clinical Manifestations biliousvomiting abdominal distention abdominal pain Peritoneal signs suggest ischemic bowel.
  • 49.
    Plain AXR :signs of small bowel obstruction or free air if perforated Supportive management: intravenous fluids Antibiotics nasogastric decompression Prompt surgical relief of the obstruction is indicated if intestinal gangrene is to be prevented
  • 50.
  • 51.
    Foreign Bodies inthe Stomach and Intestine 80% of all foreign body ingestions occur in children, peak: 6 mos to 3 yr. Coins are the most common foreign body ingested by young children . In older children, teenagers, and adults, fish or chicken bones are the most common objects accidentally ingested. The risk of ingestion increases after alcohol consumption or cold liquids because of a decrease in oral sensory acuity.
  • 52.
    Of the foreignbodies that come to medical attention, 80–90% pass through the gastrointestinal tract without difficulty. Ten to 20% require endoscopic removal or other conservative management, whereas 1% or less require surgical intervention. Once in the stomach, 95% of all ingested objects pass without difficulty through the remainder of the gastrointestinal tract. Perforation after ingestion of a foreign body is estimated to be less than 1% of all objects ingested. Perforation tends to occur in areas of physiologic sphincters (pylorus and ileocecal valve), acute angulation (such as the duodenal sweep), congenital gut malformations (webs, diaphragms, or diverticula), or areas of previous bowel surgery.
  • 53.
    bezoar is anaccumulation of exogenous matter in the stomach or intestine Most bezoars have been found in females with underlying personality problems or in neurologically impaired individuals. The peak age at onset: 2nd decade of life.
  • 54.
    Trichobezoars are composedof the patient's own hair Phytobezoars are composed of a combination of plant and animal material Lactobezoars: found in premature infants, may be attributed to the high casein or calcium content of premature formulas Swallowed chewing gum may occasionally lead to a bezoar.
  • 55.