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Colonic lesions
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Colonic lesions
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Colonic lesions
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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 -frombranches of the superior
mesenteric artery
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Colonic lesions
The hindgut -left one-
third to one-half of the
transverse colon,
the descending colon,
the sigmoid colon,
the rectum,
and the superiorportion of the anal
canal.
inferior mesentericarter
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Colonic lesions
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Colonic lesions
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Porto-systemic anastomosis
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Lymphatics of colon and rectum
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Para-aortic nodes
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Pelvic floor-diaphragm
The muscles
pubococcygeus,iliococcygeus,
puborectalis,
a group of muscles thattogether form the levator
ani.
The pelvic diaphragm
resides between thesacrum, obturator fascia,
ischial spines, and pubis.
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Physiology of the Colon
Right colon- fermentation chamber
Left colon- storage and dehydration of stool
Rectum- reservoir
Absorbs water, sodium, and chloride
Secretes mucus, potassium and bicarbonate
Sodium and chloride are absorbed actively in colon
Potassium secretion- passiveChloride and bicarbonate are exchanged in the lumen
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Physiology of the Colon
Approximately 1,500 mL of ileal effluent reachesthe 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 ofcarbohydrates that have not been absorbed in the
small intestine.
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Feature Right Colon Left Colon
Embryological origin Midgut Hindgut
Blood supply SMV IMVParasympathetic Vagus Pelvic nerves from
sacral S24 segments
Sympathetic Sup. mes. Ganglion. Inf.mes. ganglion
Function Mixing and storage Conduit
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Physiology of the ColonColonic Flora
The bacterial flora of the colon is established soonafter birth and depends in large part on dietary andenvironmental factors. Approximately 400 differentspecies of bacteria
Anaerobic bacteria ( Bacteroides ) B. fragilis,Lactobacillus bifidus, Clostridium species, andEubacterium species.
Aerobic bacteria are mainly coliforms andenterococci. Escherichia coli ,Klebsiella, Proteus,and Enterobacter.
The principal enterococcus is Streptococcus faecali.
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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)
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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
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Physiology of the Colon-Fns.of flora
Vitamin K -produced by many colonic bacteria.
The enterohepatic circulation of bilirubin and bileacids 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 ofpathogenic bacteria such as C. difficile in check.
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VOLVULUS
COLON
DEFINITION
Is the folding,twisting or axial rotation of aportion of GI Tract about its mesentery
It may be
1.Partial
2. Complete
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VOLVULUS
COLON
If complete, it forms a closed loop
obstruction with resultant ischemiadue to vascular occlusion.
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VOLVULUS
COLON
1.Primary-due to congenital
malrotaion of the
gut(v.neonatorum),
Congenital bands
2.Secondary-aquired bands(post-op)
3. spontaneous
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VOLVULUS
COLON
. Sites of vol.
Sigmoid-90%
Caecum
Tr.colon
Splenic flexure
Descending colon
Small bowel
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Volvulus of caecum
Occurs when the right half of colon is lax
and mobile.
Terminal ileum is also involved in the
rotation.
l l f
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Volvulus of caecum
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Volvulus caecum-
folding(bascule),twisting
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Bascule bridges
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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
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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.
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Volvulus of caecum
Treatment
If viable----caecopexy
If not-------right hemicolectomy with ileo-transverse anastomosis.
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Ileo-sigmoid knotting
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sigmoid volvulus Incidence
1.commonly seen in Russia,India,Pak,Africaand 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 thesigmoid&its mesentery elongate Cont.
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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 clock-
wise
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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.
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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
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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.
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sigmoid volvulus
Surgical management.
1.if the bowel is gangrenous.
resection without primary anastamosis-
Paul-Miculicz type of double barrel colostomywhich is closed after 4 weeks.
2.If,after untwisting,found viable
Fixation procedures.eg.sigmoidopexy to thetr.colon or parietes etc.
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Primary resection &
anastamosis
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Thank you
Congenital disorders of large bowel
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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 megacolon-
absence 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.
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Hi h di
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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
Hi h di
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Hirschsprungs disease Pathology
Aganglionosis leads to lack of propagation ofpropulsive waves and
Absence of relaxation of internal sphincter.
In the region of Internal anal sphincter-no ganglionsnormally
In HD, this segment extends proximally for varying
distance
Upto rectosigmoid-(80%) short segment disease
Beyond that-(15%) long segment
Entire colon- total colonic a an lionosis
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chagas disease, or South American trypanosomiasis, is similar in that the oesophagus and colon are aganglionic, but the
whole bowel is affected
Hi h di
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Hirschsprungs disease(In achalasia cardia-idiopathic or infectious
neurogenic degeneration)As the child grows-proximal ganglionic normal bowel
dialates, hypertrophies
Taenia disappears-Transition zone-funnel shaped
Distal aganglionic (abnormal) bowerlooks normal
and collapsed- this is the segment where pathologylies.
Hirschsprungs disease
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Hirschsprung s 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, chronicabdominal distention, and constipation
Enterocolitis -common cause of death - diarrhea
alternating with periods of obstipation, abdominaldistention, fever, hematochezia, and peritonitis.
Hirschsprungs disease
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Hirschsprung s disease
Diagnosis
Barium enema-normal -rectum is wider than thesigmoid colon.
In HD -spasm of the distal rectum -smaller caliber
when compared with sigmoid colon.Identification of a transition zone may be quite
helpful
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Hirschsprungs disease
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Anorectal manometry - failure of the internal
sphincter to relax when the rectum is distended witha 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.
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Hirschsprungs disease
Enzyme histochemistry
showing aberrant
acetylcholine esterase
(ACHE)-positive fibres
(brown) in the lamina
propria mucosae
Surgical management
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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
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Intestinal Atresia or Stenosis
The midgut -a tubular structure that progressively
undergoes several predictable, developmentalstages:
(a) elongation;
(b) herniation from and reduction into thecoelomic cavity;
(c) rotation; and
(d) fixation of the mesentery to the posterior bodywall.
Any aberration at these stages results in intestinal
atresia
Intestinal Atresia or Stenosis
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Intestinal Atresia or Stenosis
Atresia is a congenital interruption or
discontinuity of the luminal organresulting in its obstruction due to failure
of vacuolization or failure of
channelization from its solid state.
Intestinal Atresia or Stenosis
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Intestinal Atresia or Stenosis
Type I, muscular
continuity with a
complete web.
Type II, mesenteryintact, fibrous cord.
Type IIIa, muscular
and mesentericdiscontinuous.
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Intestinal Atresia or Stenosis
Type IIIb, apple-peeldeformity.
Type IV, multiple
atresias. (After
Grosfeld JL.Jejunoileal atresia
and stenosis.
Clinical Presentation
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Clinical Presentation
Detection of maternal polyhydramnios on routine
prenatal ultrasound screening can be an indication ofproximal 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
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Intestinal Atresia or Stenosis
1.Plain xray abd.-marked gaseous distention of the
proximal intestine with gasless distal small bowel andcolon
2. A contrast enema -. A diminutive, unused but
otherwise normal microcolon is typical of proximalintestinal obstruction.
The inability to reflux contrast into the proximal,
dilated small bowel segment is diagnostic forcongenital intestinal obstruction.
Intestinal Atresia or Stenosis
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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
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Meconium Ileus
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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
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Meconium Ileus
Meconium Ileus
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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 orsoap bubble appearance.
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Meconium Ileus
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contrast enema
-unused butfunctionally normal
microcolon
Reflux of contrastinto the terminal
ileum may confirm
the presence ofinspissated
meconium pellets
Treatment-Nonoperative
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p Useful in 60% to 70% of newborns
retrograde irrigation of the terminal ileum withnormal 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 evacuatemeconium from the intestine while preserving
maximal intestinal length
Meconium Ileus
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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
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A distal chimney
enterostomy,( Bishop
and Koop) involves
resection with
anastomosis between
the end of the proximalsegment and the side of
the distal segment of
bowel, approximately 4
cm from the opening ofthe distal segment. The
open end is brought out
as the ileostomy
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Thankyou
Colon-polyps
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Colon polyps
The term polyp (from the Greek polypous, morbid
excrescence) refers to a macroscopic protrusion ofthe 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 directlyfrom the colonic wall, or
pedunculated, extending from the mucosa
through a fibrovascular stalk.
Colo-rectal polyps-classification
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Colo rectal polyps classification
MUCOSAL
NEOPLASTIC
Benign
Adenomatous polyps
Tubular adenomaTubulovillous adenoma
Villous adenoma
Serrated polyp
MalignantCarcinoma in situ
Invasive carcinoma
Polypoid carcinoma
NONNEOPLASTIC
Hyperplastic polyps
Juvenile polyps
Peutz-Jeghers polypsInflammatory polyps
Normal epithelium
Colo-rectal polyps-classification
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p yp
SUB-MUCOSAL
LipomasLeiomyomas
Colitis cystica profunda
Pneumatosis cystoides intestinalisLymphoid aggregates
Lymphoma (primary or secondary)
Carcinoids
Metastatic neoplasms
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Neoplastic Mucosal Polyps
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p yp
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-to-
carcinoma sequence
Histopathology and Malignant
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PotentialAdenomatous 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
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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
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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
Management -polyps
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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.
Familial adenomatous polyposis
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p yp
(FAP)
Gardner's syndrome is distinguished by
osteomas, fibromas, in addition to the
intestinal polyps..
Total proctocolectomy with an ileostomy or ananal sphincter-saving procedure is indicated if
the diagnosis of FAP is made
Familial adenomatous polyposis
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