Colonic lesions

Colonic lesions

Colonic lesions

Colonic lesions
Midgut derivatives 1.small intestine distal to the ampulla of Vater, 2.cecum and appendix, 3. ascending colon, right half to two-thirds of the transverse colon. Blood supply -from branches of the superior mesenteric artery

Colonic lesions
The hindgut -left onethird to one-half of the transverse colon, the descending colon, the sigmoid colon, the rectum, and the superior portion of the anal canal. inferior mesenteric

Colonic lesions

Colonic lesions

Venous drainage of colon and rectum

Porto-systemic anastomosis

Lymphatics of colon and rectum

Para-aortic nodes

Pelvic floor-diaphragm
The muscles pubococcygeus, iliococcygeus, puborectalis, a group of muscles that together form the levator ani. The pelvic diaphragm resides between the sacrum, obturator fascia, ischial spines, and pubis.

Physiology of the Colon

Right colonfermentation chamber Left colonstorage and dehydration of stool Rectumreservoir Absorbs water, sodium, and chloride Secretes mucus, potassium and bicarbonate Sodium and chloride are absorbed actively in colon Potassium secretion- passive Chloride and bicarbonate are exchanged in the lumen

Physiology of the Colon

Approximately 1,500 mL of ileal effluent reaches the cecum in a 24-hour period, of which 90% is water. Of this amount, only 100 to 150 mL of water remains in the stool Store intraluminal contents until elimination is socially convenient Salvage nutrients after bacterial metabolism of carbohydrates that have not been absorbed in the small intestine.

 Feature Right Colon Left Colon Embryological origin Midgut Hindgut Blood supply SMV IMV Parasympathetic Vagus Pelvic nerves from sacral S24 segments Sympathetic Sup. mes. Ganglion. Inf.mes. ganglion Function Mixing and storage Conduit

Physiology of the Colon

Colonic Flora The bacterial flora of the colon is established soon after birth and depends in large part on dietary and environmental factors. Approximately 400 different species of bacteria Anaerobic bacteria ( Bacteroides ) B. fragilis, Lactobacillus bifidus, Clostridium species, and Eubacterium species. Aerobic bacteria are mainly coliforms and enterococci. Escherichia coli ,Klebsiella, Proteus, and Enterobacter. The principal enterococcus is Streptococcus faecali.

Physiology of the Colon

Has a bacterial concentration of 10 to the power of 12 anerobes per gm of feces In colonic surgery- contamination and infection supervenes. To avoid this, colonic preparation is needed before surgery or on-table procedures- needed Bacterial load is reduced both mechanically and chemically. 3-days liquid low residue diet or 1-day administration of electrolyte solution of polyethylene glycol (Peglec or Golytely)

Physiology of the Colon

Neomycin,Erythromycin- broad spectrum and act intra luminally Metronidazole- for anerobes In emergency situations- on table Lavage is done with litres of saline

Physiology of the Colon-Fns.of flora

Vitamin K -produced by many colonic bacteria. The enterohepatic circulation of bilirubin and bile acids depends greatly on bacterial enzymes. Degradation of bile pigments by colonic bacteria gives stool its characteristic brown color. Influence colonic motility and absorption, Generate intestinal gases, Prevents infection by keeping the growth of pathogenic bacteria such as C. difficile in check.

VOLVULUS COLON
DEFINITION
Is the folding,twisting or axial rotation of a portion of GI Tract about its mesentery It may be 1.Partial 2. Complete

VOLVULUS COLON
If complete, it forms a closed loop obstruction with resultant ischemia due to vascular occlusion.

VOLVULUS COLON
1.Primary-due to congenital malrotaion of the gut(v.neonatorum), Congenital bands 2.Secondary-aquired bands(post-op) 3. spontaneous

VOLVULUS COLON
. Sites of vol.

Sigmoid-90% Caecum Tr.colon Splenic flexure Descending colon Small bowel

Volvulus of caecum
Occurs when the right half of colon is lax and mobile. Terminal ileum is also involved in the rotation.

Volvulus of caecum

Volvulus caecumfolding(bascule),twisting

Bascule bridges

Volvulus of caecum
Symptoms Features of distal small bowel obstr. Severe intermittent colicky pain in the right side abdomen. Vomiting

Bulging tympanic mass.

May be recurrent.-caecal bascule

Volvulus of caecum
Investigations X-ray abdomen erect

Hugely dilated caecum in the left epi and

hypo-gastrium with fluid level.

This may mimic distended stomach.

Volvulus of caecum
Treatment If viable----caecopexy If not-------right hemicolectomy with ileotransverse anastomosis.

Ileo-sigmoid knotting

 Incidence 1.commonly seen in Russia,India,Pak,Africa and eastern Europe. 2.Age.-common in 60-70 yrs. 3.sex-Male preponderance 4.Economic condn.-rural poor strata 5.Diet-consumption of course grains in bulk quantity and with poor quality makes the sigmoid&its mesentery elongate
Cont.

sigmoid volvulus

sigmoid volvulus
Factors that facilitate formation

of volvulus.
1.long loop 2.narrow base of mesentery 3.loaded colon 4.adhesion at the summit of the loop Volvulus is mostly counter clockwise

sigmoid volvulus
Clinical features. 1.acute onset of int.obstrn 2.occasionally preceded by milder attcks with spontaneous recovery 3.absolute constipation with tenesmus due to traction of rectum 4.extreme distension of abd. 5.at late stage-faecal peritonitis.

sigmoid volvulus
Investigation Plain x-ray abdomen erect view. --huge dilated gas filled large bowel without haustra mainly on the left side. Inverted U shape,bent inner tube,omega loop, Frimann-Dahl sign.all may be seen Barium enema- bird beak appearance

sigmoid volvulus
Treatment 1.In the early stage.ie when no strangulation or perforation.pass a flexible fibroptic colonoscope gently-untwisting may occur 2.On suspecion of strang.,perf.,int.obstn. only surgical treatment.

sigmoid volvulus
Surgical management. 1.if the bowel is gangrenous. resection without primary anastamosisPaul-Miculicz type of double barrel colostomy which is closed after 4 weeks. 2.If,after untwisting,found viable Fixation procedures.eg.sigmoidopexy to the tr.colon or parietes etc.

Primary resection & anastamosis

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Congenital disorders of large bowel

Megacolon-is an abnormally large or dilated colon Primary- Hirschprungs disease Acquired- follows faulty bowel training Hirschprungs disease or congenital megacolonabsence of ganglion cells in both the submucosal (Meisseners plexus) and the intermuscular (Auerbachs plexus) layers with a marked increase in nerve fibers in the submucosa. This neurogenic abnormality is associated with muscular spasm of the distal colon and internal anal sphincter resulting in a functional obstruction.

Hirschsprungs disease
Etiology Unknown Seen in 1 out of 5000 newborns 70% to 80% -boys Familial-10% Sporadic-90% Associated anomalies- bowel atresia, Anorectal-urogenital-cardiac malformations

Hirschsprungs disease
Pathology Aganglionosis leads to lack of propagation of propulsive waves and Absence of relaxation of internal sphincter. In the region of Internal anal sphincter-no ganglions normally In HD, this segment extends proximally for varying distance Upto rectosigmoid-(80%) short segment disease Beyond that-(15%) long segment Entire colon- total colonic aganglionosis

chagas disease, or South American trypanosomiasis, is similar in that the oesophagus and colon are aganglionic, but the whole bowel is affected

Hirschsprungs disease
(In achalasia cardia-idiopathic or infectious neurogenic degeneration) As the child grows-proximal ganglionic normal bowel dialates, hypertrophies Taenia disappearsTransition zone-funnel shaped Distal aganglionic (abnormal) bower looks normal and collapsed- this is the segment where pathology lies.

Hirschsprungs disease
progressive abdominal distention and bilious emesis. Failure to pass meconium in the first 24 hours cardinal feature . diarrhea -enterocolitis. The diagnosis - overlooked - poor feeding, chronic abdominal distention, and constipation Enterocolitis -common cause of death - diarrhea alternating with periods of obstipation, abdominal distention, fever, hematochezia, and peritonitis.

Hirschsprungs disease
Diagnosis Barium enema-normal -rectum is wider than the sigmoid colon. In HD -spasm of the distal rectum -smaller caliber when compared with sigmoid colon. Identification of a transition zone may be quite helpful

Hirschsprungs disease

Anorectal manometry - failure of the internal sphincter to relax when the rectum is distended with a balloon. A rectal biopsy is the gold standard Absent ganglia, hypertrophied nerve trunks, and robust immunostaining for acetylcholinesterase are the pathologic criteria to make the diagnosis.

Hirschsprungs disease
Enzyme histochemistry showing aberrant acetylcholine esterase (ACHE)-positive fibres (brown) in the lamina propria mucosae

Surgical management
Laparotomy ,Biopsy- diverting colostomy in the region of normal ganglionated bowel. A definitive procedure is then performed later. 1. Swensons pullthrough 2. Duhamels pullthrough 3. Soaves pullthrough

Intestinal Atresia or Stenosis

The midgut -a tubular structure that progressively undergoes several predictable, developmental stages: (a) elongation; (b) herniation from and reduction into the coelomic cavity; (c) rotation; and (d) fixation of the mesentery to the posterior body wall. Any aberration at these stages results in intestinal atresia

Intestinal Atresia or Stenosis

Atresia is a congenital interruption or discontinuity of the luminal organ resulting in its obstruction due to failure of vacuolization or failure of channelization from its solid state.

Intestinal Atresia or Stenosis

Type I, muscular continuity with a complete web. Type II, mesentery intact, fibrous cord. Type IIIa, muscular and mesenteric discontinuous.

Intestinal Atresia or Stenosis

Type IIIb, apple-peel deformity.

Type IV, multiple atresias. (After Grosfeld JL. Jejunoileal atresia and stenosis.

Clinical Presentation
Detection of maternal polyhydramnios on routine prenatal ultrasound screening can be an indication of proximal bowel obstruction caused by the interruption of normal amniotic fluid absorption in the fetal gut. Bilious emesis, Abdominal distention, and Failure to pass meconium

Intestinal Atresia or Stenosis

1.Plain xray abd.-marked gaseous distention of the proximal intestine with gasless distal small bowel and colon 2. A contrast enema -. A diminutive, unused but otherwise normal microcolon is typical of proximal intestinal obstruction. The inability to reflux contrast into the proximal, dilated small bowel segment is diagnostic for congenital intestinal obstruction.

Intestinal Atresia or Stenosis

Surgical treatment-restore gastrointestinal tract continuity while preserving as much intestinal length as possible. an end-to-end or end-to-oblique anastomosis is typically performed . Short segmental bowel resection and excision of an intraluminal web or diaphragm are used when necessary

Meconium Ileus
Mi. -earliest clinical manifestation of CF inherited disease the terminal ileum is dilated and filled with thick, tarlike, inspissated meconium. Smaller pellets of meconium are found in the more distal ileum, leading into a relatively small colon.

Meconium Ileus

Meconium Ileus
Diagnosis X ray abd .-dilated, gas-filled loops of small bowel, absence of air-fluid levels, mass of meconium within the right side of the abdomen mixed with gas to give a ground-glass or soap bubble appearance.

Meconium Ileus
contrast enema

-unused but functionally normal microcolon Reflux of contrast into the terminal ileum may confirm the presence of inspissated meconium pellets

Treatment-Nonoperative
Useful in 60% to 70% of newborns retrograde irrigation of the terminal ileum with normal saline, hyperosmolar contrast agents, or dilute N-acetylcysteine designed to dissipate the obstructing meconium. operative management The goal of operative management in simple uncomplicated meconium ileus is to evacuate meconium from the intestine while preserving maximal intestinal length

Meconium Ileus
Indications for surgery Persistent or worsening abdominal distension Persistent bowel obstruction Enlarging abdominal mass Intestinal atresia Volvulus Perforation Meconium cyst formation with peritonitis Bowel necrosis

 A distal chimney enterostomy,( Bishop and Koop) involves resection with anastomosis between the end of the proximal segment and the side of the distal segment of bowel, approximately 4 cm from the opening of the distal segment. The open end is brought out as the ileostomy

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Colon-polyps
The term polyp (from the Greek polypous, morbid excrescence) refers to a macroscopic protrusion of the colonic mucosa into the bowel lumen. This can result from abnormal growth of the mucosa or from a submucosal process that causes the mucosa to protrude into the lumen. Mucosal polyps can be sessile, protruding directly from the colonic wall, or pedunculated, extending from the mucosa through a fibrovascular stalk.

Colo-rectal polyps-classification MUCOSAL

NEOPLASTIC Benign Adenomatous polyps Tubular adenoma Tubulovillous adenoma Villous adenoma Serrated polyp Malignant Carcinoma in situ Invasive carcinoma Polypoid carcinoma NONNEOPLASTIC Hyperplastic polyps Juvenile polyps Peutz-Jeghers polyps Inflammatory polyps Normal epithelium

Colo-rectal polyps-classification SUB-MUCOSAL

Lipomas Leiomyomas Colitis cystica profunda Pneumatosis cystoides intestinalis Lymphoid aggregates Lymphoma (primary or secondary) Carcinoids Metastatic neoplasms

Neoplastic Mucosal Polyps

colorectal cancers arise in preexisting adenomatous polyps. Neoplastic mucosal epithelium evolves through a series of progressive, cumulative molecular and cellular steps that lead to altered proliferation, cellular accumulation, and glandular disarray. invade and metastasize through the adenoma-tocarcinoma sequence

Histopathology and Malignant Potential

Adenomatous polyps are characterized according to physical features, -sessile or pedunculated size,-Malignant potential increases with polyp size glandular structure, - Tubular, villous,tubulo-villous degree of dysplasia,-ca.insitu or invasive -all have important implications for clinical management

Pathology of polyps
a left-sided predominance mucosa to polyp--5 to 10 years Polyp to invasive carcinoma 3 to 5 years Associated conditions-acromegaly elevated gastrin levels prior cholecystectomy, atherosclerosis, acrochordons (skin tags)

Clinical Features-polyps
Occult bleed, haematochezia Alteration of bowel habits Lower abdominal crampy pains Secretory diarrhoea (hypokalemia and hypochlorhydria ) Diagnosis Fecal Occult Blood Test Sigmoidoscopy air-contrast barium enema or colonoscopy Computed tomographic (CT) colography

 Excision of poylps to resectional surgery according to the histological report and other risk factors. Familial adenomatous polyposis (FAP) and Gardner's syndrome. autosomal dominant. hundreds of colorectal polyps in the first three decades of life. Seen in the stomach and small intestine.

Management -polyps

Familial adenomatous polyposis (FAP)

Gardner's syndrome is distinguished by osteomas, fibromas, in addition to the intestinal polyps.. Total proctocolectomy with an ileostomy or an anal sphincter-saving procedure is indicated if the diagnosis of FAP is made

Familial adenomatous polyposis