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This document discusses several gastrointestinal conditions: 1. Esophageal atresia, which is when the esophagus is not connected to the stomach, causing regurgitation in newborns. 2. Imperforate anus, which is when the anus is not fully open, causing issues passing stool. 3. Meckel's diverticulum, a common intestinal anomaly caused by incomplete involution of the vitelline duct that can cause pain, bleeding, or inflammation. 4. Congenital hypertrophic pyloric stenosis, a condition in infants where the pyloric sphincter muscle is thickened, causing projectile vomiting after feeding. 5. Hirsch
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Git 1-csbrp
- 2. Painful ulcers – what is your Dx?
- 3. What is your diagnosis?
- 4. What is your diagnosis?
- 6. Case • New born with regurgitation during feeding or • New born with cough and regurgitation during feeding • Happens every time when the mother tries to feed the child
- 7. Diagnosis • Congenital esophageal atresia
- 8. • Absence or agenesis of esophagus is very rare • Atresia is more common • There are different types
- 11. Case • New born baby - not passed meconium since two days • Bloating of the abdomen
- 13. Imperforate anus
- 15. Imperforate anus • Most common form of congential intestinal atresia • Due to failure of cloacal diaphragm to involute
- 17. Case • 4yo male child with complains of on/off pain abdomen since 2years • Pain located around the umbilicus • Not associated with vomiting / diarrhea • No tenderness at Mc Burney’s point • Diagnosed as appendicitis and was operated without much relief
- 19. Meckel's Diverticulum • Due to failed involution of vitelline duct, which connects the lumen of the developing gut to the yolk sac • Number: Solitary • Location: Antimesenteric border of the ielum • Ectopic tissue: Gastric mucosa / Pancreatic tissue • Have all the layers of the small intestine – may resemble small intestine histologically • May be the site for peptic ulceration and bleeding
- 21. Rule of ‘2s’ • 2% of population • 2 inches in length • With in 2 feet from the ileocecal valve • 2x more common in males • Symptomatic by the age of 2 years
- 22. Same Case – with a twist • 4yo male child with complains of on/off pain abdomen since 2years • Pain located around the umbilicus • Not associated with vomiting / diarrhea • Food intake precipitates pain • Lost weight because of anticipation of pain • No tenderness at Mc Burney’s point • Diagnosed as appendicitis and was operated without much relief Meckel’s diverticulum peptic ulcer due to ectopic gastric mucosa
- 23. Another Case • 25yo male patient complains of passing fresh blood in stool (Hematochezia) • H/O on / off pain abdomen since 5years • Not associated with vomiting / diarrhea • Food intake precipitates pain • He has no hemorrhoides / no h/o constipation Meckel’s diverticulum with bleeding peptic ulcer due to ectopic gastric mucosa
- 24. What are the causes for hematochezia? • Zollinger-Ellison syndrome (Ulcers in jejunum, ileum) • Angiodysplasia of colon • Hemorrhoides • Anal fissure / Constipation • Meckel’s divericulum
- 25. Case • 3 week old Child with history of vomitings • Child was well for two weeks • Vomiting – Projectile • Mother noticed moving swelling in the upper abdomen which passes from right to left • Loss of weight
- 29. • 300-900 live births • Genetic basis: – High concordance in monozygotic twins – Turner’s syndrome – Trisomy 18 • Presents 2-3week of life • Persistant projectile / nonbilious vomting • O/E freely mobile ovoid abdominal mass
- 30. Pathophysiology • Progressive hypertrophy of the circular muscles in the pyloric sphincter • Duodenum is normal • Not present at birth but occurs over 3 to 5 weeks
- 32. Causes for pyloric stenosis in adults? • Antral gastritis • Peptic ulcer close to pylorus • Carcinoma of distal stomach • Carcinoma of head of pancreas • Rarely annular pancreas (encircling the duodenum)
- 33. Ventral wall defects • Omphalocele • Gastroschisis
- 34. Omphalocele
- 35. Omphalocele • Abdominal musculature is incomplete • Abdominal viscera herniate into ventral membranous sac
- 36. Gastroschisis
- 37. Gastroschisis • Similar to omphalocele except that it involves all the layers of the abdominal wall – from the peritoneum to the skin
- 38. Case • Home delivered baby with a h/o passage of meconium on the third day • Mother noticed progressive distension of the abdomen and • Baby recently started vomiting
- 41. Air fluid levels
- 42. What is your diagnosis? • Hirschsprung’s disease
- 43. • Occasionally presents with chronic constipation in infancy • Accounts for 10% of neonatal intestinal obstruction • Child is at increased risk of enterocolitis and perforation
- 44. • 1 in 5000 live births • May occur: – In isolation or – In combination with: • Down’s syndrome (10% of all cases) • Other serious neurological abnormalities (5% of all cases) • Clinical presentations: – Failure to pass meconium in 48hours – Chronic constipation
- 45. Abdominal distension, one of the common clinical presentations of Hirschsprung's disease
- 46. Failure to pass meconium in the first 48 hours of life or chronic constipation is one of the common clinical presentations of Hirschsprung's disease
- 47. Pathogenesis: During normal development:During normal development: •Neural crest cells migrate in the intestine from ceacum to rectum •They form Aurbach (Myentric plexus) and Meissner’s plexus (Submocosal) In Hirschsprung’s disease:In Hirschsprung’s disease: •This migration gets arrested prematurely • This produces aganglionic segment distally • Coordinated peristaltic contractions are absent • Functional abstraction • Dilatation of proximal normal segment
- 48. Why this defect in migration: • Loss of heterozygosity in Receptor tyrosine kinase RET • Most of the familial cases • 15% of sporadic cases • Mutations of genes of the protein involved in enteric neurodevelopment: (30% of cases) • Neurotrophic factor derived from RET • Endothelin • Endothelin receptor • Modifying genes and other environmental factors • Sex: males are mostly affected, however, disease is more extensive in females
- 49. Diagnosis: • By demonstrating the absence of ganglion cells in the affected segment • Suction rectal biopsy to demonstrate absence of submucosal Meissner’s plexus • IHC for Acetylcholinestrase Site of biopsy: • Rectum is always affected (hence preferred and also easily accessible) • Length of involved segment varies widely • Intraoperative frozen section to identify the proximal uninvolved level
- 50. Transiti on zone
- 51. Barium enema showed contracted diseased segment (thick arrow), dilatation of normal bowel segment (thin arrow) and the transitional zone (TZ)
- 54. Complications: • Megacolon (upto 20cms in diameter) • Rupture (most common: ceacum) • Mucosal ulcers • Enterocolitis (Major threat to life) • Fluid and electrolyte disturbances
- 55. Toxic megacolon
- 56. Enterocolitis:
- 57. Acquired causes for megacolon: • Chaga’s disease (of all the following, only this disease is associated with loss of ganglion cells) • Obstruction by neoplasm • Inflammatory strictures • Toxic megacolon – Ulcerative colitis – Visceral myopathy – Psychosomatic disorders
- 58. END
Editor's Notes
- Atresia is a condition in which a body orifice or passage in the body is abnormally closed or absent.
- Esophageal atresia - contrast
- Imperforate Anus and Related Anomalies Immediate relief of the acute colonic obstruction is provided by colostomy, after which further repair can be planned. Remember that the first operation has the greatest chance for a successful outcome. The best procedure may be less than perfectly successful if it follows an earlier, inadequate attempt at repair. The procedures following colostomy vary with the specific anatomy of the defect to be treated. They are outside the field of general surgery.
- Diagram of stages in development of the anus and rectum from the fifth to tenth weeks of gestation. A, Closing plate (proctodeum separates the cloaca from the outside). Urorectal septum (arrow) grows downward to divide the cloaca. B, Cloaca almost separated into dorsal rectum and ventral urogenital sinus. Tailgut is vanishing. C, Fusion of urorectal septum with closing plate to form the perineal body. D, Closing plates rupture. E, Division into rectum and urogenital sinus by the perineal body is complete. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.) In the fifth week, the embryonic cloaca is an endodermal sac receiving the hindgut dorsally and the allantoic stalk ventrally. The cloaca (Fig. 18-2A, B) is separated from the outside by a thin cloacal membrane (proctodeum), which occupies the embryo's ventral surface between the tail and the body stalk. During the sixth week, a septum of mesoderm divides the cloaca into a ventral urogenital sinus and a dorsal rectum (Fig. 18-2C) . This mesodermic septum fuses with the cloacal membrane in the seventh week to form the perineal body. The cloacal membrane is divided into a larger, ventral urogenital membrane and a smaller, dorsal anal membrane. Externally, the anal membrane becomes slightly depressed, forming the anal dimple. By the eighth week, the anal membrane ruptures, leaving no trace of itself (Fig. 18-2D). The pectinate line in the adult is often considered to be at the level of the anal membrane, but little evidence exists to either support or contradict this view. Whatever the exact line of demarcation, the rectum and the upper anal canal are endodermal and are supplied by the inferior mesenteric artery, while the lower anal canal is ectodermal and is supplied by branches of the internal iliac artery.
- A previously healthy 3-week-old baby is brought by his parents to your emergency department with a 1-day history of emesis. The parents describe the emesis as "forceful", non-bloody, and non-bilious. The baby is exclusively breastfed and continues to be hungry after each episode of vomiting. They deny any fevers. You notice an active baby boy with unremarkable vital signs. Physical examination is significant for a peristaltic wave on the abdomen and a 2x2 cm firm mass palpated in the midepigastric region. Laboratory studies show a bicarbonate level of 18 mEq/L. The most likely diagnosis isA. annular pancreasB. gastroesophageal refluxC. intussusceptionD. malrotation with volvulusE. pyloric stenosis (Answer)
- \ga-ˈsträs-kə-səs\
- Normally meconium is passed on the first day of life. Passing meconium on the third day is abnormal.
- It can present in neonates and also in older children.
- Note: Meissner’s and Aurbach plexus migrate simultaneously and equally. Therefore presence or absence of one reciprocates the other.
- 1-Operative finding of transitional zone in Hirschsprung's disease at upper rectum. 2-Operative finding of transitional zone in Hirschsprung's disease at splenic flexure.
- Modern Pathology: Utilization of peripherin and S-100 immunohistochemistry in the diagnosis of Hirschsprung disease Susan K Holland, Richard B Hessler, Michelle D Reid-Nicholson, Preetha Ramalingam and Jeffrey R Lee Modern Pathology (2010) 23, 1173–1179; doi:10.1038/modpathol.2010.104; published online 21 May 2010 (a) S-100 immunostaining highlights neural hypertrophy in a patient with Hirschsprung disease ( × 40). (b) Increased muscularis mucosae and lamina propria nerve fibrils in a patient with Hirschsprung disease on S-100 staining ( × 100). (c) Diff Quik staining reveals bright blue cytoplasm of ganglion cells ( × 40). (d) H&E control of frozen section ( × 20).
- Chagas disease (pron.: /ˈʃɑːɡəs/; Portuguese: doença de Chagas [duˈẽsɐ dʒi ˈʃagɐʃ], Spanish: enfermedad de Chagas [eɱfermeˈðað ðe ˈtʃaɣas], also known as mal de Chagas[-Mazza] in both languages; also called American trypanosomiasis) is a tropical parasitic disease caused by the flagellate protozoan Trypanosoma cruzi. T. cruzi is commonly transmitted to humans and other mammals by an insect vector, the blood-sucking "kissing bugs" of the subfamily Triatominae (family Reduviidae), most commonly from species belonging to the Triatoma, Rhodnius, and Panstrongylus genera.[1] The disease may also be spread through blood transfusion and organ transplantation, ingestion of food contaminated with parasites, and from a mother to her fetus.[2] The symptoms of Chagas disease vary over the course of an infection. In the early, acute stage, symptoms are mild and usually produce no more than local swelling at the site of infection. The initial acute phase is responsive to antiparasitic treatments, with 60–90% cure rates. After 4–8 weeks, individuals with active infections enter the chronic phase of Chagas disease that is asymptomatic for 60–80% of chronically infected individuals through their lifetime.[3][4][5] The antiparasitic treatments also appear to delay or prevent the development of disease symptoms during the chronic phase of the disease, but 20–40% of chronically infected individuals will still eventually develop life-threatening heart and digestive system disorders. The currently available antiparasitic treatments for Chagas disease are benznidazole and nifurtimox, which can cause temporary side effects in many patients including skin disorders, brain toxicity, and digestive system irritation.[3][4][5] Chagas disease is contracted primarily in the Americas, particularly in poor, rural areas of Mexico, Central America, and South America; very rarely, the disease has been found in the Southern United States. The insects that spread the disease are known by various local names, including vinchuca in Argentina, Bolivia, Chile and Paraguay, barbeiro (the barber) in Brazil, pito in Colombia, chinche in Central America, chipo in Venezuela, chupança, chinchorro, and "the kissing bug". It is estimated that as many as 11 million people in Mexico, Central America and South America have Chagas disease, most of whom do not know they are infected. Large-scale population movements from rural to urban areas of Latin America and to other regions of the world have increased the geographic distribution of Chagas disease, and cases have been noted in many countries, particularly in Europe.[4][6] Control strategies have mostly focused on eliminating the triatomine insect vector and preventing transmission from other sources.