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Intestinal lesions

Intestinal lesions. Entercolitis - infective and non infective Appendicitis Hirschsprung’s disease Diverticulosis. Enterocolitis. DYSENTRY. Bacillary dysentry. Grossly, the lesions are mainly found in the colon and occasionally in the ileum.

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Intestinal lesions

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  1. Intestinal lesions

  2. Entercolitis- infective and non infective • Appendicitis • Hirschsprung’s disease • Diverticulosis

  3. Enterocolitis


  5. Bacillary dysentry Grossly, the lesions are mainly found in the colon and occasionally in the ileum. Superficial transverse ulcerations of mucosa of the bowel wall occur in the region of lymphoid follicles but perforation is seldom seen. The intervening intact mucosa is hyperaemic and oedematous. .

  6. Microscopically, the mucosa overlying the lymphoid follicles is necrosed. The surrounding mucosa shows congestion, oedema and infiltration by neutrophils and lymphocytes. The mucosa may be covered by greyishyellow ‘pseudomembrane’ composed of fibrinosuppurative exudate.

  7. Amoebic colitis Grossly, early intestinal lesions appear as small areas of elevation on the mucosal surface. In advanced cases, typical flask-shaped ulcers having narrow neck and broad base are seen. They are more conspicuous in the caecum, rectum and in the flexures .

  8. Microscopically, the ulcerated area shows chronic inflammatory reaction consisting of lymphocytes, plasma cells, macrophages and eosinophils. The trophozoites of Entamoeba are seen in the inflammatory exudateand are concentrated at the advancing margin of the lesion. Intestinal amoebae characteristically have ingested red cells in their cytoplasm. Oedema and vascular congestion are present in the area surrounding the ulcers

  9. Necrotisingenterocolitis Necrotizing enter colitis is an acute inflammation of the terminal ileum and ascending colon, occurring primarily in premature and low-birth-weight infants within the first week of life and less commonly in full-term infants.

  10. Variant of the spectrum of ischaemic bowel disease. Important factors in the etiology of this disorder, thus, are as follows: 1. Ischaemia 2. Hypoxia/anoxia of the bowel due to bypassing of blood from the affected area 3. Bacterial infection and endotoxins 4. Establishment of feeding 5. Infants fed on commercial formulae than breast-fed,implying the role of immunoprotective factors.

  11. MORPHOLOGIC FEATURES . Grossly, the affected segment of the bowel is dilated, necrotic, haemorrhagic and friable. Bowel wall may contain bubbles of air (pneumatosisintestinalis). .

  12. Microscopically, the changes are variable depending upon the stage. Initial changes are confined to mucosa and show oedema, haemorrhage and coagulative necrosis. A pseudomembrane composed of necrotic epithelium, fibrin and inflammatory cells may develop. As the ischaemic process extends to the subjacent layers, muscle layer is also involved and may lead to perforation and peritonitis

  13. Pseudomembranousenterocolitis • SYNONYM: antibiotic associated diarrhoea • SITE: colon, small intestine • ETIOLOGY: ANTIBIOTICS: Clindamycin, Ampicillin, Cephalosporin ORGANISMS: Clostridium difficile, Staphylococcal enterocolitis, Shigella Candida enterocolitis

  14. GROSS: Yellow-white plaques mucosal ulcers • MICROSCOPY: Pseudomembrane consisting of network of fibrin and mucous in which inflammatory cells [ neutrophils ] and mucosal epithelial cells are entangled

  15. Appendicitis

  16. Appendicitis • Acute inflammation of the appendix, acute appendicitis, is the most common acute abdominal condition confronting the surgeon. • The condition is seen more commonly in older children and young adults, and is uncommon at the extremes of age. • The disease is seen more frequently in the West and in affluent societies which may be due to variation in diet a diet with low bulk or cellulose and high protein intake more often causes appendicitis.

  17. Etiology Obstructive 1. Faecolith 2. Calculi 3. Foreign body 4. Tumour 5. Worms (especially Enterobiusvermicularis) 6. Diffuse lymphoid hyperplasia, especially in children. Non-obstructive 1. Haematogenous spread of generalised infection 2. Vascular occlusion 3. Inappropriate diet lacking roughage.

  18. MORPHOLOGIC FEATURES . Grossly, the appearance depends upon the stage at which the acutely-inflamed appendix is examined. • In early acute appendicitis, the organ is swollen and serosa shows hyperaemia. • In well developed acute inflammation called acute suppurative appendicitis, the serosa is coated with fibrinopurulentexudate and engorged vessels on the surface. • In advanced cases called acute gangrenous appendicitis, there is necrosis and ulcerations of mucosa which extend through the wall so that the appendix becomes soft and friable and the surface is coated with greenish-black gangrenous necrosis

  19. Fecoliths

  20. Microscopically, the most important diagnostic histological criterion is the neutrophilic infiltration of the muscularis. In early stage, the other changes besides acute inflammatory changes, are congestion and oedema of the appendiceal wall. In later stages, the mucosa is sloughed off, the wall becomes necrotic, the blood vessels may get thrombosed and there may be neutrophilic abscesses in the wall. In either case, an impacted foreign body, faecolith, or concretion may be seen in the lumen.

  21. CLINICAL COURSE. The patient presents with features of acute abdomen as under: 1. Colicky pain, initially around umbilicus but later localised to right iliac fossa 2. Nausea and vomiting 3. Pyrexia of mild grade 4. Abdominal tenderness 5. Increased pulse rate 6. Neutrophilicleucocytosis

  22. COMPLICATIONS. If the condition is not adequately managed, the following complications may occur: 1. Peritonitis. A perforated appendix as occurs in gangrenous appendicitis may cause localised or generalised peritonitis. 2. Appendix abscess. This is due to rupture of an appendix giving rise to localised abscess in the right iliac fossa. This abscess may spread to other sites such as between the liver and diaphragm (subphrenic abscess), into the pelvis between the urinary bladder and rectum, and in the females may involve uterus and fallopian tubes.

  23. 3.Adhesions. Late complications of acute appendicitis are fibrous adhesions to the greater omentum, small intestine and other abdominal structures. 4. Portal pylephlebitis. Spread of infection into mesenteric veins may produce septic phlebitis and liver abscess. 5. Mucocele. Distension of distal appendix by mucus following recovery from an attack of acute appendicitis is referred to as mucocele. It occurs generally due to proximal obstruction but sometimes may be due to a benign or malignant neoplasm in the appendix. An infected mucocele may result in formation of empyema of the appendix.

  24. Hirschsprung’s diseases

  25. Hirschsprungs disease The term ‘megacolon’ is used for any form of marked dilatation of the entire colon or its segment and may occur as a congenital or acquired disorder. Congenital form characterized by congenital absence of ganglion cells in the bowel wall (enteric neurons) is called Hirschsprung’s disease. As a result, the aganglionic segment remains contracted.

  26. Genetically, Hirschsprung’s disease is a heterogeneous disorder . 1. Autosomal dominant inheritance with mutation in RETproto-oncogene in some cases. 2. Autosomal recessive form with mutation in endothelin-B receptor gene in many other cases.

  27. Clinical features • The condition manifests shortly after birth with constipation, gaseous distension and sometimes with acute intestinal obstruction. • Its frequency is 1 in 5,000 live-births, • familial tendency in about 4% of cases • development in Down’s syndrome. • Pathogenesis lies in the failure of neuroblasts to migrate to the rectum which normally occurs at about 12 weeks of gestation.

  28. MORPHOLOGIC FEATURES . Two types of biopsies may be done on infants suspected of having Hirschsprung’sdisease— • full-thickness rectal biopsy • suction biopsy that includes mucosa and submucosa

  29. Grossly, typical case of Hirschsprung’s disease shows 2 segments—a distal narrow segment that is aganglionic and a dilated proximal segment that contains normal number of ganglion cells

  30. Microscopically, the distal narrow segment shows total absence of ganglion cells of all the three plexuses (Auerbach’s or myenteric plexus present between the two layers of muscularis, deep submucosal or Henle’s plexus, and superficial mucosal or Meissner’s plexus) and prominence of non-myelinated nerve fibres. Histochemical staining for acetylcholine esterase activity provides confirmation for identifying ganglion cells and nerve trunks.

  31. Types Depending upon the length of the segment affected by aganglionosis in Hirschsprung’s disease, following patterns are recognised: 1. Classic form: Aganglionosis from distal colorectal region to proximal dilated colon. 2. Short segment (rectal and recto-sigmoid) form: Aganglionosisinvolving a few centimeters of the rectum and rectosigmoid only. 3. Ultra-short form: Aganglionosis is in a very small segment which can be missed in a biopsy.

  32. 4. Long segment (subtotal colonic) form: Aganglionosis involves most of the colon from rectosigmoid to the ileocaecal valve, and sometimes may even extend into small bowel. 5. Zonal colonic aganglionosis: A short segment is involved in aganglionosis in which the ganglia cells are absent both above and below the aganglionic segment.

  33. Acquired causes of megacolon i. Obstructive e.g. due to tumour, post-inflammatory strictures. ii. Endocrine e.g. in myxoedema, cretinism. iii. CNS disorders e.g. spina bifida, paraplegia, parkinsonism. iv. Psychogenic e.g. emotional disturbances, psychiatric disorders. v. Chagas’ disease due to infection with Trypanosomacruzi is the only example resulting in acquired loss of ganglion cells. In all other acquired causes listed above, the bowel innervation is normal

  34. Diverticular disease, • Diverticula are the outpouchings or herniations of the mucosa and submucosa of the colon through the muscle wall. • Diverticular disease, as it is commonly known, is rare under 30 years of age and is seen more commonly as the age advances. • Multiple diverticula of the colon are very common in the Western societies, probably due to ingestion of lowfibre diet but is seen much less frequently in tropical countries and in Japan.

  35. Clinical features • Diverticulosis is often asymptomatic and may be detected as an incidental finding at autopsy. • low abdominal pain, distension, constipation and sometimes intermittent bleeding.

  36. Pathogenesis 1. Increased intraluminal pressure such as due to low fibre content of the diet causing hyperactive peristalsis and thereby sequestration, of mucosa and submucosa. 2. Muscular weakness of the colonic wall at the junction of the muscularis with submucosa

  37. MORPHOLOGIC FEATURES . Grossly, diverticulosis is seen most commonly in the sigmoid colon (95%) but any other part of the entire colon may be involved. They may vary in number from a few to several hundred. They appear as small, spherical or flask-shaped outpouchings,usually less than 1 cm in diameter, commonly extend into appendices epiploicae and may contain inspissatedfaeces. They are connected to the intestinal lumen by a narrow neck.

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