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Abdominal Problems In Children


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Powerpoint presentation of abdominal problem in children, including occlusion of GI, morility disorders and external compressions. Dieaseases discussed are following: Occlusions: Atresias: Esophageal, Duodenal, small bowel, anorectal, meconium ileus, hypertrophic pyloric stenosis. Motility Disorders: Esophageal sphincter immaturity, Necrotizing enterocolitis, Left Colon Syndrome, Hirsprung Disease.
Extrinsinc Compression- Malrotation.

Published in: Technology, Health & Medicine

Abdominal Problems In Children

  1. 1. Abdominal problems in the neonate Robert Shirinov MD
  2. 2. Pathophysiology <ul><li>Luminal occlusion </li></ul><ul><li>Motility dysfunction </li></ul><ul><li>External compression. </li></ul>
  3. 3. Luminal occlusion <ul><li>atresias </li></ul><ul><li>hypertrophic pyloric stenosis </li></ul><ul><li>meconium ileus </li></ul>
  4. 4. Atresias <ul><li>can affect different sites in the GI tract. </li></ul><ul><li>oesophageal </li></ul><ul><li>duodenal </li></ul><ul><li>small bowel </li></ul><ul><li>colonic </li></ul><ul><li>anorectal. </li></ul>
  5. 5. Esophageal Artesia. <ul><li>Failure of in-growth of the lateral plates which cause separation of the esophagus from the trachea. A history of maternal polyhydramnios is usually present. </li></ul><ul><li>87%         7%          4%         0.8%        0.7% </li></ul>
  6. 6. Duodenal atresia. <ul><li>Duodenal atresia, duodenal stenosis and duodenal web all produce gastric and duodenal dilatation resulting in a ‘double bubble’ appearance on X-ray of the abdomen </li></ul><ul><li>Downs syndrome accounts for 30% of cases of duodenal atresias. </li></ul><ul><li>Duodenal atresia is present in 10% of Downs children. </li></ul><ul><li>The atresia or stenosis is usually post ampullary and vomit will contain bile. In pre-ampullary stenosis fluid will be bile free. </li></ul>
  7. 7. Bowel Atresias <ul><li>Infants with small bowel atresia may pass a small amount of meconium since the ingested lanugo hair etc, may be in the amniotic fluid prior to the development of the atresia. </li></ul><ul><li>Colonic atresia is very rare. </li></ul><ul><li>Anorectal atresia is one of the commonest causes of intestinal obstruction in the neonate, occurring in one in 3000 live births. It is divided into two types, high or low, as defined by a line drawn from the coccyx to the pubis on a lateral X-ray taken with the baby inverted (invertogram). A fistula into the urinary tract is present in 80% of high anomalies in males and 20% in females </li></ul>
  8. 8. Treatment of Atresias <ul><li>Esophageal: If a fistula is present, ligation of this takes priority in surgical management. Restoration of oesophageal continuity may be, and is usually, undertaken if the condition of the baby is acceptable. The oesophagus is normally approached through a right thoracotomy using an extra- pleural technique. </li></ul><ul><li>Duodenal atresia and stenosis best treated by duodeno-duodenostomy which maintains the biochemical environment of the duodenal loop as close to normal as possible. This removes the potential problem, if gastroenterostomy is performed, of diverting acid into the jejunum. </li></ul><ul><li>Small bowel atresia : The restoration of intestinal continuity is carried out by end to back anastomosis. This is necessitated by the gross discrepancy in the calibre of the involved bowel. Intrauterine perforation releases meconium into the peritoneal cavity. Although sterile, this produces an intense chemical peritonitis which may obliterate the peritoneal cavity. </li></ul>
  9. 9. Treatment of Anorectal atresia <ul><li>Formation of a transverse colostomy and distal mucous fistula is performed after birth. </li></ul><ul><li>When the child is 1 year old, a posterior sagittal ano-rectoplasty is carried out with division of the fistula between rectum and urinary tract. This allows a tube of ‘neorectum’ to be tapered and brought through the perineal muscle group. </li></ul><ul><li>The muscles in the perineal group are identified using an electrical muscle stimulator </li></ul>
  10. 10. Hypertrophic pyloric stenosis <ul><li>Hypertrophy of the pyloric antrum results in occlusion of the gastric outlet. </li></ul><ul><li>The global incidence of this condition varies. The condition is less common in breast fed babies. </li></ul><ul><li>The child is typically a first-born male of 4-6 weeks of age, who presents with a history of projectile, non-bilious vomiting in the first, second or, less commonly, third month of life in previously normal babies. </li></ul><ul><li>Diagnosis rests on history and palpation of the pyloric lump during a test feed, when gastric peristalsis may also be present on inspection. </li></ul><ul><li>Although this is a self-limiting condition, the time taken for resolution is such that surgery is indicated to allow early restoration of a feeding regime and discharge from hospital. </li></ul><ul><li>... This selective loss of gastric juice with the preservation of duodenal and pancreatic secretions will result in a metabolic alkalosis. Several biochemical indices will be deranged.???? </li></ul>
  11. 11. Meconium ileus <ul><li>This condition results from failure of the pancreas to produce protease. It occurs in babies with cystic fibrosis or other causes of pancreatic insufficiency. </li></ul><ul><li>Dense pellets of protein impact in the terminal ileum causing hold up with gross proximal dilatation, distension of the bowel with inspissated meconium and distal microcolon as demonstrated by the X-rays. </li></ul>
  12. 12. Treatment of Meconium ileus <ul><li>Bishop-Koop anastomosis </li></ul><ul><li>If water-soluble contrast enema and other measures to ‘digest’ the pellets are unsuccessful, laparotomy and resection of the impacted ileum is required. </li></ul><ul><li>Increasingly primary anastomosis is performed, but the traditional treatment, first described by Bishop and Koop, was formation of a stoma. </li></ul>
  13. 13. Motility Disorders <ul><li>There are four different causes of motility disorder in the neonate . </li></ul><ul><li>immaturity of the gastroesophageal sphincter (with gastroesophageal reflux) </li></ul><ul><li>necrotising enterocolitis </li></ul><ul><li>left colon syndrome </li></ul><ul><li>Hirschsprung’s disease. </li></ul>
  14. 14. Immaturity of the gastroesophageal sphincter <ul><li>This condition will cause recurrent vomits and acid oesophagitis which will, in turn, cause pain and irritability during feeding. The resultant disordered sleep pattern will soon result in a very tired and anxious mother. It may be part of a more generalised upset of gut function seen in response to an allergy to the cows’ milk protein content of formula. </li></ul><ul><li>... If gastroesophageal reflux is suspected consider the following questions: Is there a history of atopy in the baby’s family? Do any first degree relatives have asthma, eczema or hay fever? </li></ul><ul><li>In the first year of life gastroesophageal reflux is treated medically in virtually all circumstances. Such treatment comprises: </li></ul><ul><li>1. nursing the baby at 45 degrees head elevation </li></ul><ul><li>2. thickening the feeds with a proprietary thickener </li></ul><ul><li>3. use of H2 antagonists and prokinetic agents for severe cases with oesophagitis. </li></ul>
  15. 15. Necrotising enterocolitis <ul><li>The motility of the small and large bowel can be affected by ischaemia. This may be segmental or diffuse and will disrupt gut motility. </li></ul><ul><li>Oedema and mucosal ulceration resulting in gastro-intestinal bleeding is the mildest presentation, but neonatal necrotising enterocolitis will often progress to infarction and perforation. </li></ul><ul><li>The causes are poorly understood but it is thought to result from a shutdown of mesenteric blood flow with consequent ischaemic damage. The global or focal reduction in mesenteric blood flow with subsequent reperfusion injury will result in patchy gangrene of the bowel wall. Multi-organ failure may follow from the associated sepsis. </li></ul>
  16. 16. Treatment of necrotising enterocolitis <ul><li>is supportive with: </li></ul><ul><li>antibiotics </li></ul><ul><li>ventilatory support </li></ul><ul><li>blood product replacement. </li></ul><ul><li>If perforation occurs (detected on clinical examination or X-ray) then laparotomy, resection of the affected bowel and stoma formation is usually carried out. </li></ul>
  17. 17. Left colon syndrome <ul><li>This is a term given to severe dysmotility of the hind gut. The proximal colon and small bowel are distended but the distal large bowel is collapsed. </li></ul><ul><li>Babies with this syndrome are invariably infants of diabetic mothers and this history should lead to a water-soluble contrast enema which will show the transition of calibre at the junction of mid gut ( from papilla of Water, 2 nd half of duodenum , small intestine and until 1/3 of transverse colon) and hind gut ( from distal 1/3 of transverse colon to rectum) </li></ul><ul><li>90% of cases occur in premature infants. </li></ul><ul><li>For reference, midgut supplied with SMA- superior mesenteric artery, and hindgut with IMA- inferior mesenteric artery. Foregut supplied with celiac artery. </li></ul>
  18. 18. Hirschsprung’s disease <ul><li>Presents with abdominal distension and passage of stool. </li></ul><ul><li>A newborn baby has significant abdominal distension, bile vomiting, and delayed passage of meconium which only occurred after digital examination. </li></ul><ul><li>Tasks to perform: </li></ul><ul><li>Antenatal history. </li></ul><ul><li>Maternal diabetes. </li></ul><ul><li>Family history. </li></ul><ul><li>Abdominal and rectal examination. </li></ul><ul><li>Consider contrast study. </li></ul><ul><li>Consider rectal biopsy. </li></ul><ul><li>X-ray examination to ensure distension is gaseous. </li></ul><ul><li>Abdominal ultrasound to exclude ascites or organomegaly. </li></ul>
  19. 19. Hirschsprung’s disease <ul><li>Diagnosis is made by histo-chemical examination of a ‘suction rectal biopsy’ of the mucosa and submucosa. The absence of ganglion cells in the myenteric plexus results in proliferation and ‘sprouting’ of the preganglionic fibres which migrate into the muscularis mucosa and lamina propria in an attempt to ‘locate’ the absent ganglia. These stain darkly with Acetylcholinesterase.Hirschsprung’s disease is characterised by an absence of ganglion cells in the myenteric plexuses of the bowel wall. The deficiency commences at the internal anal sphincter and extends proximally for varying distances. </li></ul><ul><li>The failure of the colon to relax as part of the initial component of peristalsis results in proximal distension of the bowel with meconium. The involved segment may not appear particularly narrow in the first instance, and contrast appearances may be misleading. </li></ul><ul><li>The major complication of this condition is enterocolitis which may affect the patient even after successful treatment. </li></ul><ul><li>Meconium follow rectal examination because the digital examination overcomes the ‘spasm’ of the aganglionic segment, with the high pressure in the distended, ganglionic segment causing forceful explosion of meconium </li></ul>
  20. 20. Treatment of Hirschsprung’s Disease <ul><li>Colostomy is usually performed in the sigmoid colon at a site identified intraoperatively (by frozen section pathology) as containing ganglion cells. </li></ul><ul><li>A variety of subsequent corrective operations are carried out at approximately 1 year of age, although the recent trend is to perform this as a one stage procedure in the neonatal period. </li></ul><ul><li>All procedures have in common the aim of bringing innervated bowel to, or close to the anal margin with minimal disruption of neural anatomy. </li></ul>
  21. 21. References: <ul><li>George G Youngson, </li></ul>