Intestinal diseases by Dr.AmrithaAnilkumar

en love da Homoeopathy
INTESTINAL
DISEASES

It includes
Carcinoma colon
Diverticular Diseases of colon
Haematemesis
Intestinal obstruction
Intussception
Meckel’s Diverticulum
Paralytic Ileus
Crohns Diseases
Ulcerative colitis
Volvulus

CARCINOMA
COLON

CARCINOMACOLON
DEFINITION
• It is commonly
adenocarcinoma.
• Veryrarely adenosquamous,
squamous carcinoma can
occur.
• Adenocarcinoma
COMMONSITES
• Sigmoid colonis the most
commonsite of malignancy
after rectum
• In caecum

AETIOLOGY
• Diet
 Red meat and saturatedfat
(Cholesterol)
↓
increases the bile acid
concentration(acts as
cocarcinogen).
 High fibre diet & Calcium
protects the colonagainst
cancer.
↓
It directlyacts on the colonic
mucosal cells
↓
to reduce their proliferative
potential
 Diet withlack of fibre &
highfat increases the risk.
 Dietaryvitamins A,C, E and
zinc reduces the risk.
• Genetic:
 individuals with
adenoma colon
 familial adenomatous
polyposis (FAP)
 Gardner’s syndrome,
 Turcot’s syndrome.

• Long standing ulcerative
colitis & Crohn’s disease
• Alcohol and cigarette
smoking increases the risk.
• Hereditary nonpolyposis
coloniccancer (HNCC)
• After cholecystectomy and
ileal resectionthere is
increasedbile salts and so
more prone for carcinoma
colon.
• Radiationincreases the
risk(mucinous type).
• Ureterosigmoidostomy
• Acromegaly
PATHOGENESIS
• Adenoma—carcinoma
sequence
• Most of the colonic
carcinoma develops from
polyp/adenoma pathway.
Normal epithelium
→initiation by 5q loss APC
gene → dysplasia
(hyperproliferative) →
DNA methylation→ early
adenoma → 12p activation
K ras → intermediate
adenoma

→18q loss DCC→ late
adenoma → actionby 17p loss
p53 →carcinoma → spread .
• 80% of colorectal cancer
arises fromloss of
heterozygosity (LOH)
pathway.
• LOH pathway
↓
APC gene defects (inFAP)
↓
K ras mutation altering the
cell cycle
↓
K ras binds to GTP(guanosine
triphosphate)
↓
hydrolyse to GDP which
inactivates G proteinnormally
↓
K ras mutation blocks GTP
hydrolyse
↓
leading intopermanently active
formof G protein causing
carcinoma

↓
loss of DCCtumour suppressor
gene
↓
mutationof tumour suppressor
gene p53.
↓
LOH pathway is microsatellite
stable (MSS)and carries poor
prognosis compared with MSI.
• 20% of colorectal cancer
develops frommutation
fromRER (Replication Error
Repair) pathway
↓
whereinrepair mechanismof
DNA replication error is lost.
↓
It causes microsatellite regions of
genome to have repeated
sequences

↓
leading intoerror and is called
as microsatellite instability
(MSI)
↓
In colon, it is seenin right side
growths & is associated with
better prognosis
• Colonic cancer may be:
Nonhereditary colon
cancer
• It can be sporadiccolon
cancer—60%.
• It canbe familial colon
cancer. Commonin
Ashkenazi– Jewish
population.
• Hereditary colon cancer
• FAP
• HNCC.
• PeutzJeghers syndrome—
2–3%risk of cancer colon.
• Cronkite—Canada
syndrome.

• Juvenilepolyposis
syndrome—it differs
fromisolated juvenile
polyps discussedearlier. It
is an autosomal dominant
condition
TYPES
• Patient can have de novo
multiple primary
carcinomas in different parts
of the colon at the same time,
i.e. synchro nous (5–10%)
• can present with growthin
different partsof the colon
in different periods, i.e. meta
chronous (10–20%).
• Gross types:
• Annular,
• Tubular
• ulcerative
• cauliflower like.

Annular (stenosing) type:
• It is more common on left
side.
• Here the growthspreads
roundthe internal wall and
so it oftenpresents with
intestinal obstruction.
Ulcerative type:
• It is common on right side
Proliferative type
• Common in right side.
• It is fleshy, bulky and
polypoid. It is less
malignant.
Histology (WHO)
• Adenocarcinoma—90%.
• Mucinous
adenocarcinoma—5–10%.
• Signet ring cell carcinoma.
• Small cell/oat cell
carcinoma—rare—
extremely poor prognosis.
• Squamous cell carcinoma.
• Undifferentiated carcinoma

Duke’s histological grading of
carcinoma colon (nowmodified
Morson-Dawson)
• Grade I—low grade.
• Grade II—average grade.
• Grade III—highgrade.
• Grade IV—anaplastic.
Carcinoma confined to
muscularis mucosadoes not
metastasize.
Sessile MalignantPolyp
• InvasionSm 1: Submucosal
invasion into upper 1/3rd
(superficial/ inner)
• Sm 2: Submucosal invasion
into middle 1/3rd (inner
2/3rd)
• Sm3: Submucosal invasion
lower 1/3rd(deep).

SPREAD
• Direct spread:
• Locallyit can invade the
bladder, obstruct ureter
and so cause
hydronephrosis.
• Canperforate and cause
peritonitis/pericolic
abscess/faecal fistula.
• Growth may get
adherent to psoas
muscle posteriorly.
• Carcinoma sigmoid
colon caninfiltrateand
cause colovesical or
colovaginal fistula.
• It can infiltrate ureter,
ovary, uterus etc. It can
cause pericolicabscess
or abscess in lateral
abdominal wall.

• Lymphatic spread:
• Growththrough
lymphatics spreads to
pericolic, epicolic,
intermediate and
principal group of
lymph nodes. Groups of
lymph nodes draining
colon
• N1: Nodes immediately
adjacentto bowel wall.
• N2: Nodes along
ileocolic/right
colic/middle colic/ left
colic/ sigmoidarteries.
• N3: Nodes near the
originof SMA and IMA.
• Nodal spreadin
carcinoma colon is
sequential fromN1 →
N2 → N3

TNMCLASSIFICATION- Blood
spread
• 40%of carcinoma colon
spreads to liver via portal
veins.
• Secondaries may be either
solitaryor multiple, present
as liver with hard,
umbilicatednodules.
• Rarelyit spreads to bone,
lung, skin.
TNMstaging of colorectal cancer
Tumour—T
• Tx – Primary tumour
cannot be assessed
• T0 – No evidence of tumour
• Tis – Carcinoma in situ—
intraepithelial/invasioninto
lamina propria
• T1 – Invasion into
submucosa
muscularis propria
pericolorectal tissues/fat

• T4a – Invasionintosurface
of the visceral peritoneum
T4b – Direct Invasion or
adherent to adjacent
structures/organs
Regional nodes—N
• Nx – Nodes cannot be
assessed
• N0 – No nodal spread
• N1 – Regional nodes 1–3
involved –
• N1a – 1 regional node
• N1b – 2 to 3 regional
nodes
• N1c – Tumour deposits
in serosa/mesentery/
nonperitonealised
pericolic or perirectal
tissues without regional
nodes

• N2 – Regional nodes 4 or
more involved
• N2a – 4-6 regional nodes
• N2b – 7 or more regional
nodes .
Distant metastases—M
• M0 – No distantspread
• M1 – Distant spread present
• M1a – Spread confined
to one organ or site—
liver/lung/ovary/
nonregional nodes;
• M1b – Spread to more
than one organor
site/peritoneum.

Histological grade—G
• Gx – Grade cannot be
assessed
• G1 – Well differentiated
• G2 – Moderately
differentiated
• G3 – Poorly differentiated
• G4 – Undifferentiated
CLINICALFEATURES
• Occurs usually after 50
years.
• Familial type can present in
younger age group.
• loss of appetite& weight
• Anaemia
• abdominal discomfort and
mass per abdomen.
• 20% - acuteintestinal
obstruction.
• 20% of colonic/colorectal
cancer has stageIV
disease at the time of first
presentation

• Right sided growth
commonly presents with
• Anaemia
• palpable mass in the
rightiliacfossa, which is
not moving
• with respiration
• Mobile
• Nontender
• hard, well-localised with
impairedresonant note.
• Carcinoma caecum
occasionallypresents
• Acuteappendicitis/
• intusscepion with
intestional
obstruction

• Left sided growth presents
• colicky pain
• alteredbowel habits
(alternating
constipationand
diarrhoea)
• palpable lump
• distensionof
abdomendue to sub
acute/chronic
obstruction.
• Later may presentlike
• complete colonic
obstruction
• Tenesmus, with passage
of blood and mucus
• with alternate
constipation&
diarrhoea, is common.
• Bladder symptoms may
warn colovesical fistula.
• Features of pericolic
abscess/obstruction
/perforation/ peritonitis
maybe the first
presentation

• Closedloop obstruction can
occur in transverse colon
growth(stricture type
causing block) with
competent ileocaecal valve.
• Enormouslydilated right
sided colonis prone for
• stercoral ulcer
• Perforation& faecal
peritonitis.
• Enlargedliver with multiple
umbilicatedhard
secondaries
• Ascites
• rectovesical secondaries
• palpable left supraclavicular
lymph nodes are other
presentations.
• Faecal strength of
Streptococcus bovisbacteria
increases many fold in
patients with coloniccancer
compared to individuals
without coloniccancer

INVESTIGATION
• Bariumenema
• Shows irregular filling
defect and ‘apple core’
lesion (inleft sided
carcinoma)
• It also helps in finding
colonicpolyps (air-
contrast barium
enema).
• Colonoscopy and biopsy
confirms the diagnosis.
Virtual colonoscopy (CT
colonography) is also useful to
visualize entirecolon

• CT scanabdomenand
pelvis—to see local spread,
invasion, size and extent,
stage, nodal status and liver
secondaries.
• Left supraclavicular lymph
nodeif palpable, its FNAC
may clinchthe histological
diagnosis.
• Hb%, PCV, haematocrit,
ESR. Look for occult blood in
stool is the initial test for
anaemia.
• LFT—mainlyenzyme
studies like alkaline phos
phatase
• SGPT.
• US
• secondaries in liver
• Peritoneum
• lymph nodestatus
• rectovesical secondaries.
• CEA(carcinoembryonic
antigen):
• It is a cell surface
glycoprotein
-- discovered by
Gold and Freedman

SURGERY
Right-sidedearly growth:
• Right radical hemicolec
tomy with ileo-transverse
anastomosis is done.
• Structures removedare
terminal 6 cm of ileum,
caecumand appendix,
ascending colon, 1/3 of
transversecolon, lymph
nodes (epicolic, paracolic,
intermediate).
• In inoperable rightsided
growth, ileotransverse
anastomosis is done as a by-
pass procedure.

Transverse colon growth:
• An extended right
hemicolectomyis the
procedure done for
transversecolon growth
Left-sided early growth:
• Left radical
hemicolectomyis done,
where in left ½ of
transversecolon and des
cending colon is removed
along withlymph nodes.
• Left-sided stenosing type
of growthcan present
with acuteintestinal
obstruction, in which case
initially colostomyis done

• Oftengrowthin the
transverseor left sided
colon, whichis stenosing or
obstructive type, can cause
closed loop obstruction
Multiple synchronous primaries
in the colon:
• Total abdominal colectomy
with ileorectal anastomosis
is done
• Surgical treatment of liver
secondaries:
• In solitaryliver secondary,
segmental hepaticresection
is useful
• Adjuvant Therapy
Chemotherapy

Indications for chemotherapy
• Positive nodes.
• T4 lesions.
• Venous (microscopic)
spread.
• Signet cell type.
• Poorlydifferentiated
tumour/aneuploidy.
• Changes in CEAlevel.
• Postoperative
chemotheraphy
• Radiotherapy (RT)
• Usually there is no role for
RT as tumour is
radioresistant.

• It is often usedin locally
advancedtumour,
infiltrating the psoas major
muscle or lateral abdominal
wall, left sided colonic
growth.
COMPLICATION
• Intestinal obstruction ™
• Closedloop obstruction ™
• Perforation& peritonitis ™
• Vesicocolicfistula ™
• Invasionof ureter ™
• Pericolic abscesss
PROGNOSIS
• Site—left sidedtumours
has got better prognosis as
theypresent early.
• Type—colloid carcinoma
has got poorer prognosis.
• Size of the tumour.
• Lymph nodes status:
Number of lymph nodes
involved decides the
prognosis.
• Liver secondaries has poor
prognosis.
• Age of the patient.

• Associateddiseases like HIV.
• Stage of the tumour.
• Presence of complications
• perforation
• peritonitis.
• On the whole, it is a
curable malignancy with
proper surgeryand
adjuvant therapy.
5 yearsurvival is:
• Stage I – 90%.
• Stage II – 75%.
• Stage III – 50%.
• Stage IV – less than 5%.
REFERENCE
1. SRB's Manual of Surgery
by SriramBhat M
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

DIVERTICUL
AR DISEASE
OF THE
COLON

DIVERTICULAR
DISEASE OF
THE COLON

DIVERTICULAR DISEASEOF
THECOLON
DEFINITION
• They are acquired
herniations of colonic
mucosathrough
circular muscles at
the points where
blood vessels
penetrate(points of
least resistance).

• It is more commonly
localised to sigmoid
colon (90%) but
occasionallyseenin full
lengthof the colon
• Rectumis not affected.
• Saint’s triad
• Diverticulitis
• hiatus hernia
• gallstones
• rare in Asian and African
countries - high fibre diet.
• commonin western
countries.
• Colonic diverticulosis is -
false type with only
mucosal herniation.
• more commonin females,
aged & non-vegetarian

AETIOLOGY
• Diet - it is the mainfactor.
• Low fibre diet
• ↑ stool transit time
• ↓the stool weight
• ↓bulkinessof stool
which
• ↑ intraluminal
pressure
• & muscle
hypertrophy.
• High fibre diet prevents
this.
• NSAIDintake by
inhibiting prostaglandin
synthesis may cause
diverticular disease
• Smoking and alcohol.
• Long-standing
constipation
• ↑stool transit time and
causes diverticulosis

.
TYPES
Diverticulosis
• false diverticula - occur
(where arterioleperforates
the muscular wall)
• occur on the mesenteric
side of the antimesenteric
taenia not on the
antimesentericborder.
• common- sigmoidcolon
(50%),
• descending colon (40%),
• rarely in other areas
• sigmoidcolon – muscular
wall thickening with
hypertrophy
↓
narrowed
↓
due to spasmwith mucosal false
diverticula adjacent to lateral
taenia

↓
raise in intraluminal pressure
90 mmHg or more.
↓
will be muscular
incoordination,
segmentation, causing
episodicspasmodic left iliac
fossa pain—painful
diverticular disease.

Diverticulitis
• is a misnomer
• it is perforation through the
diverticula with
peridiverticulitis;
TYPES
• if extraluminal
extraperitoneal perforation
with only pericolicinfection
it is calledas uncomplicated.
• peridiverticulitis with
extraluminal pericolic
infectioncausedby
luminal perforation into
pericolicarea without
formation of fistula are
abscessor
intraperitoneal
perforation.

• if there is pericolicabscess
or fistula or
intraperitoneal perforation
with peritonitis it is called
as complicated.
Presentations
• painin the left iliac fossa &
left groinpersistentor
recurrent
• Fever
• loose stool
• tender palpable thickened
colon
• urinary urgency
• Radiating paintowards back
and suprapubicregion.

Complicatedtype shows
• abscessor fistula into
urinary bladder
(commonly)or small
bowel (occasionally),
• intraluminal
perforation
• Peritonitis
• haemorrhage(close
proximityof diverticula
to perforating
arterioles).
PATHOLOGY
• Diverticula-associated
Colitis (DAC)
• It presents
tenesmus,
diarrhoea,
haematochezia&
segmental colitis.

• There is hypertrophy and
thickening of the muscle
layer
↓
along withprogressive colonic
narrowing & segmentationwith
raised intraluminal pressure
↓
causing pulsationdiverticula of
only mucosaadjacent to taenia in
antimesentericregion.
• commonin sigmoidcolon
CLINICALFEATURES
Features of diverticulosis
• fullnessof abdomen,
• bloating,
• flatulence,
• vague discomfort.

Features of diverticulitis
• painin left iliacfossa
whichis constant
radiates to back and
groin, tenderness
• bloodystool
• often massive
haemorrhage
• Fever
• rigidity & mass in left
iliac fossa.
• Mass is usually tender,
firm, resonant, non-
mobile.
Features of fistula
• colovesical is the
commonest type of
fistula
• causes passageof gas in
the urine
(pneumaturia)
commonly and
occasionallyfaeces.

COMPLICATION
• Abscess
• Stenosis
• & fistula.
• Abscesscan be
commonly pericolicand
pelvic, rarely in buttock
and ischiorectal fossa
• Perforationwith
pericolicabscessor
peritonitis ™
• Progressive stenosis
and intestinal
obstruction ™
• Profuse colonic
haemorrhage(17–
20%) ™
• Fistula formation
(5%)
• Vesicocolic
• Vaginocolic
• Enterocolic
• colocutaneous

INVESTGATION
• Bariumenema (best
methodto diagnose)
shows ’sawteeth’
appearance.
• Champagne glass
sign—partial filling of
diverticula by barium
with stercolithinside—
seenin sigmoid
diverticula.
• Sigmoidoscopyis useful
not be done in acute
stage.
SAW TEETH APPEARANCE

• Once acutestage
subsides, bariumenema,
sigmoidoscopy,
colonoscopycan be done
• CT scanin acute phase to
see pericolicabscess.
• Cystoscopy & colonoscopy
in case of fistula.
• Ureteric stenting is
needed to make eventual
surgery easier
Champagne glass sign

DIFF. DIAGNOSIS
• Carcinoma sigmoid
colon ™
• Amoebiccolitis
• Ulcerative colitis
• Ischaemiccolitis &
Crohn’s disease™
• Tuberculosis
Coexistence of
carcinoma
• & Diverticulitis can
occur in 12%of cases
TREATMENT
• In acute stages,
• conservative
treatmentlike
• bowel rest
• Antispasmodics
• antibiotics are
advised.
• aspirationof the
abscess(if small)

• Resectionof sigmoid
colonand
anastomosis
(colorectal) is done.
Indications for surgery ™
• Recurrent
diverticulitis ™
• Diverticulitis with
complications
REFERENCE
by SriramBhat M
Surgeryby Das
Surgeryby Das

HAEMATEMESIS

HAEMATEMESIS
- Means BLOODVOMITING
CAUSES
• Chronic peptic ulcer
(duodenal + gastric)
• Acute pepticulcer.
• Acute erosive gastritis
(Steroids, NSAIDs).
• Oesophageal varices.
• Mallory-Weisssyndrome
• Carcinoma stomach
• Gastric polyps, lymphomas,
leiomyomas
• gastropathy.

• Bleeding disorders.
• Pernicious anaemia.
• Thrombocytopenia
• Gastric antral vascular
ectasia
• It is a rare endoscopically
confirmedcondition which
shows segmenteddilated
vessel meshes in the antral
mucosa(watermelon/tiger
stripe stomach).
• It is oftenassociated with
achlorhydria &
hypergastrinaemia.
• It is common in middle aged
females; common in liver
diseases (25%) and
autoimmune connective tissue
disorders.
• Pathologically it shows
mucosal fibromuscular
hyperplasia and hyalinisation.
• Dieulafoy’s disease
• A gastricarteriovenous
malfor mation whichis
covered by apparently
normal mucosa.

• It occurs in proximal
stomachnear OG junction
(within 6 cm) along lesser
curve
• Bleeding often may be
severe and torrential
• Vasculitis or atheroma are
absent in the vessel.
• It is 5%of nonvariceal
upper GI bleed.
• A large 1–3 mm tortuous
abnormal submucosal
artery(AVM) is the cause,
whichdue to its pulsation
erodes themucosa to expose
itself to acidwhich further
erodes the artery causing
bleeding

INVESTIGATION
• Endoscopy and
endoscopictherapy or
excision of the lesionis
required.
• Angiography can be
done to confirmthe
diseaseand to do
therapeutic embolisation
using gel foam.
.
• Failure of endoscopic or
angiographic therapy needs
gastrotomy& excisionof
the entire lesion—gastric
wedge resection.
• It canbe done by
open/laparoscopic
approach.
• Prior endoscopictattooing is
mandatory to identify the
lesion during resection

TREATMENT
• Evaluation of patient by
measuring BP
• Pulse, respirationlooking for
features of shock
• Oxygensaturation,
• investigatingfor Hb%, blood
grouping
• Blood urea, serumcreatinine
• LFT
• Prothrombintime
• Plateletcount
• Arterial blood gas analysis,
• Gastroscopy.
• Initial treatment is
central line insertion,
fluid and blood
replacement;
catheterisation
• critical care (ICU)
• Antibiotics
• Treatment of
complications like sepsis,
DIC, ARDS.
• Specific treatment—
opensurgeryfor
uncontrolled bleeding
• Ligation of
gastroduodenal artery

• Underrunning of ulcer bed
with pyloroplasty
• Gastrectomy
• ligation of varices with
devascularisation.
• Definitive surgeryfor
underlying cause—shunt
surgery; vagotomy and GJ;
• Gastrectomy; splenectomy,
etc.
REFERENCE
by SriramBhat M
Surgeryby Das
Surgeryby Das

INTESTINAL
OBSTRUCTION

INTESTINALOBSTRUCTION
TYPES
ClassificationI: Depending on
Aetiopathology
A. Dynamic.
B. Adynamic
Dynamic
Outside the wall
• Hernia—25%
• Adhesions—40%
• Volvulus
• Intussusception
In the wall
• Tuberculous stricture
• Crohn’s disease
• Malignancy
In the lumen
• Gallstones
• Roundworm
• Inspissatedfaeces
• Meconiumileus.
Adynamic
• Cessation of peristalsis
• Postoperative period
• Electrolyte imbalance
• Spinal injuries

• Uraemia
• Diabetes mellitus
• Retroperitoneal—
haematomas and surgeries
• Renal surgeries
• Mesentericischaemia
• Pseudo-obstruction
ClassificationII: Depending on
Type of Obstruction
1. Acute: Commonin small
bowel.
2. Chronic.
3. Acute on chronic:
Common in large bowel.
4. Closedloop obstruction.
ClassificationIII: Depending on
Site of Obstruction
1. Proximal Small bowel.
• Duodenumand Jejunum-
Proximal Small bowel.
• Causes
• Congenital
• Lipomas
• Leiomyomas
• Malignancy, Bands and
adhesions.
• Clinical Features
• Severe Vomitting
• Dehydration

• NO or Less Distention
• ColickyPain.
• SPECIAL FEATURES
• XRAY- Valvulae
conniventes.
2.Distal Small bowel;
• Ileum.
• Causes
• Tuberculosis Strictures,
• Maliganancy,
• Crohns
• Gallstones
• Hernias
• Round worms
• congenital.
• Central Distension,
• Vomiting
• Dehydration
• Central Abdominal
Pain.
• SPECIAL FEATURES
• XRAY- Central Fluid
level.
3. Large Bowel;
• Any where Large Intestine.
• Causes
• Malignancy
• TB Strictures

• Anorectal Malformation
• Volvulus
• Congenital
Malformation.
• Constipation
• Distension
• Late vomitting
• less pain
• SPECIALFEATURES
• XRAY-Dilatation,
Haustration.
ClassificationIV
A. Congenital.
B. Acquired.
Congenital
• Anorectal malformations
• Congenital megacolon
• Duodenal atresia
• Intestinal atresia (ileal)
• Bands and adhesions
Malrotation
• Volvulus neonatorum.

Acquired
• Hernia
• Postoperative
• Intussusception
• Roundworms
• Gallstones
• Tuberculosis
• Maliganancy
• Internal Hernias.
DYNAMICOBTRUCTION
DEFINITION
• It is mechanical blockage of
normal propulsion and
passage of intestinal
contents.

TYPES
• Obstructionmay be
• external/internal
• partial (incompleteor
subacute)/complete
• acute/acute on chronic/or
chronic
• simple/closed
loop/strangulation
• congenital/acquired
• proximal/distal.
CAUSES
• hernia
• adhesions
• Adhesions commonly cause
small bowel obstruction
thanlargebowel.
• 80% intestinal obstruction
occurs in small bowel; 20%
in colon. 70% of colonic
obstruction is due to
malignancy.
• Other 30%is due to
volvulus
• Diverticulitis

• inflammatorycauselike
tuberculosis, etc.
• Mortality is 3% in
obstruction without
strangulation
• 30% in obstructionwith
strangulation.
• Recurrent obstruction is
more commonin
adhesions
PATHOLOGY
• Changes proximal to the
bowel obstruction
↓
Intestinal obstruction
↓
Increasedperistalsis
↓
Becomes vigorous
↓
Obstructionnot relieved
↓
Peristalsis ceases - Flaccid,
paralysed, dilated bowel

↓
Fluid collects just proximal to
the obstructionwhichis
derivedfromsaliva, stomach,
pancreasand intestine
↓
Because of oedema and
inflammationabsorption
decreases
↓
sequestrationof fluidfromthe
circulation intothe lumen
occurs and bacteria
↓
(E. coli, Klebsiella, anaerobes,
bacteroides and other
organisms)
↓
multiply, toxins are released—
toxaemiaoccurs.
↓
This leads to severe dehydration,
electrolyte imbalance.
↓
Proximal to the collected
fluid, air accumulates

↓
(derived fromswallowedair
(70%),
↓
Diffusion fromblood intothe
lumen(20%)
↓
Fromdigested product and
bacterial action (10%))
↓
in which, maincomponentis
nitrogen (90%) and also
hydrogensulphide.
↓
During vigorous peristalsis, air
enters the distal fluid
↓
results in churning, is the reason
to cause multiple air-fluidlevels
in plainX-ray abdomen
↓
Defective absorption, decreased
fluid intake, loss of fluidby
vomiting, sequestrationof fluid
intothebowel lumen

↓
leads into severe dehydration,
fluid and electrolyte imbalance
• Inflammatory response in
thebowel wall (intramural
inflammation)
↓
causes accumulation of activated
neutrophils and macrophages in
the muscle wall
↓
whichrelease reactive enzymes
and cytokines
↓
Thesesubstances damage
secretory and motor processof
muscle
↓
leading into dilatationof the
bowel.
↓
Increasedrelease of nitric oxide
in muscle wall and
↓
production of intramural
reactive oxygen metabolites alter
gut motilityand
permeability.

• Intestinal wall hypoxia is
also the cause for dilatation.
↓
In first 12 hours of obstruction
↓
there is only decreased
absorption
↓
whichcauses accumulation of
fluid and electrolytes in the
lumen.
↓
After 12 hours, there is also
increasedintestinal secretion
↓
causing further accumulation
of the fluid.
↓
Accumulationof bacterial
toxins, bile salts,
prostaglandins, and mucosa-
derivedfree radicals, VIP
↓
all increase theluminal
secretion of fluidin obstructed
bowel.
• Dilatation of bowel wall

↓
increases intraluminal pressure
↓
whichexceeds the bowel wall
venous pressure
↓
causing ischaemia
↓
whichcauses further dilatation
and ischaemic injury
↓
This leads intoeventual blockage
of arterial perfusion causing
bowel wall necrosis/gangrene.
↓
Increasedbacterial colony in the
bowel (Normal flora is less than
106 colonies/ml in jejunumand
108 colonies /ml in the ileum)
↓
due to alteredluminal content
and environment
↓
multiplication
↓
toxins
↓
further mucosadamage

↓
disrupted mucosal
defense/barrier/integrity
↓
translocation of bacteria across
mucosainto submucosaand
also absorptionof bacterial and
other toxins into the circulation
↓
bacteraemia/toxaemia/
septicaemia/SIRS/MODS.
FACTORScausing systemic
problems in intestinal
obstruction™
• Dilatation of the bowel ™
• Decreasedabsorptionacross
mucosa ™
• Increasedsecretion into the
lumen ™
• Intramural inflammation
and hypoxia ™
• Increasedintraluminal
pressure ™
Venous congestion
• increasedvenous
pressure ™

• Disruptedmucosal barrier
→ bacterial translocation
PATHOLOGYCHANGESIN
THE SITE OF OBSTRUCTION
Initially venous return is
impaired
↓
Congestion, oedema of bowel
wall occurs which turns purple.
↓
Laterthis jeopardizes the arterial
supply.
↓
Loss of shineness, blackish
discolouration, loss of peristalsis.
↓
Gangrene.
↓
Perforationoccurs.
↓
Bacteria and toxins migrateinto
the peritoneum.
↓
Peritonitis.

• Closedloop obstruction:
↓
Whenthere is obstruction in the
large bowel, with ileocaecal valve
competence (40%)
↓
pressure increases in the
caecum.
↓
Stercoral ulcer in the caecum.
↓
Gangrene.
↓
Perforation.
↓
Peritonitis (Faecal).
↓
Perforationalso can occur at
the site of obstructiondue to
the malignant growth
↓
Closedloop obstruction also
can occur whenbowel get
obstructed
↓
at both proximal and distal
parts of the loop of the bowel.

↓
It can occur in external or
internal hernias, volvulus, etc.
↓
Necrosis and perforationare
bothcommonat obstructedsite
↓
and over the convex summit of
the bowel content.
↓
Bowel distal to the obstructionis
inactive and collapsed.
CLINICALFEATURES
• Abdominal pain:
Initially colicky and
intermittent: later
continuous and severe.
• painsuggests
strangulation.
• Painbegins usually
aroundumbilicus in
small bowel obstruction

• In small bowel obstruction,
• it is crampy,
• recurrent paroxysms
occurring as short
crescendo/decrescendo
episodes (of 30 seconds)
• In large bowel obstruction,
• it is of longer episodes of
minutes (In
paralytic/adynamic
ileus, painis diffuse and
mild).
• Vomiting:
• In jejunal obstruction, it
is earlyand persistent.
• In ileal obstruction, it is
recurrent occurring at
an interval
• initially bilious later
faeculent.
• In large bowel
obstruction, vomiting is
a late feature.

• Distension
• It is absent or minimal
in case of jejunal
obstruction
• Obvious withvisible
intestinal peristalsis (VIP)
and borborygmi sounds in
case of ileal obstruction—
Step ladder peristalsis. It is
enormous in case of large
bowel obstruction.
• Features of toxaemia and
septicaemia:
• Tachycardia, tachypnoea,
fever, sunken eyes, cold
periphery.
• Constipation:
• It is absolute, i.e. neither
faeces nor flatus is
passed.
• Dehydration: Leads to
oliguria → renal failure

• Abdominal tenderness:
• It is initially localisedbut
later becomes diffuse—is
a feature of intestinal
obstruction.
• Reboundtenderness
• and guarding will not
be present in simple
obstructions which are
features of
strangulation
Features of strangulation:
• Continuous severe pain
• Shock
• Tenderness
• rebound tenderness
(Blumberg’s sign)
• Guarding and rigidity
• absence of bowel sounds.

• In case of strangulated
hernia, a swelling which is
tense, tender, rigid,
irreducible, no expansile
impulse on coughing and
history of recent increasein
size is seen.
• Temperature:
• Fever signifies
inflammationin the
bowel wall/
ischaemia/perforation.
• Hypothermia can occur
when septicaemia
develops due to lack of
pyrogenicresponse.
• It suggests poor
prognosis.
• Bowel sounds:
• They are increased—
high-pitched metallic
(rushes and groans)
sounds followed by
metallic tinkling sounds
of dilatedbowel.

• Eventually oncefatigue
occurs or gangrene develops,
bowel sounds are not
heard—silentabdomen of
peritonitis develops (in
paralyticileus, there are only
continuous metallic sounds
of dilatedbowel).
• Per-rectal examination
• Shows empty, dilated
rectum, often with
tenderness. If rectal growth
is the causefor obstruction,
it may be palpable.
CARDINALFEATURES
• Colickyabdominal pain
• Vomiting
• Distension
• constipationlater.
• In high jejunn—no
distension(scaphoid
abdomen),

• severeal obstruction
• bilious vomiting, no
peristalsis, without
constipation
• In ileal obstruction
• central moderate
distension
• bilious and faeculent
vomiting
• intermittent crescendo
colicky pain
• step ladder peristalsis
• constipationat a later
period.
• In low/colonic obstruction
• variable colickypain
• rightto left peristalsis
• markedenormous
distension
• constipationto begin with,
late feculent vomiting.
INVESTIGATION
PlainX-rayabdomen:
• (initially supine abdominal
X-rayis taken; later if
needed, X-rayin erect
posture is takenif
perforationis suspected).

• Multiple air-fluidlevels.
Proximal the obstruction→
Lesser the air fluid level.
Distal the obstruction→
More the air fluid level
• Normally, three fluidlevels
can be seenin plain X-ray
film—at fundus of
stomach, at duodenumand
often at caecum
• Jejunumshows concertina
effectdue to valvulae
conniventes (Herring bone
pattern)—by the valves of
Kerckring.

• Ileumis smoothand
characterless(by Wangen
steen). Large bowel shows
haustration.
• Pneumobilia (gasin biliary
tree)may be due to gall-
stone ileus. Distended
caecumis shownas round
gas shadowin the right iliac
fossa. Dilatedcaecum
signifies large bowel
obstruction.
• CT scan
• Barium(micro bar solution)
enema or gastrografin
contrast enema X-ray is
useful in intussusception.
[Bariummeal is usually
contraindicatedin acute
intestinal obstruction
• Haematocrit, blood urea
and serumcreatinine;
arterial blood gas analysis
(acidosis is common), LFT,
plateletcount (insevere
sepsis, there will be altered
LFT withthrombocytopenia).

• Serumelectrolytes
estimation.
• Hypokalaemia is common
• Total countis increased. But
can be significantly low in
severestage of sepsis
• US abdomen is useful to see
dilatedbowel and fluidin
the peritoneal cavity. It is
better than X-ray but not as
good as CT scan.
COMPLICATION
• Peritonitis
• Hypovolaemicand septic
shock
• Renal failure
• ARDS
• Intra-abdominal abscess
formation
• Moribundstatus
DIFFERENTIAL DIAGNOSIS
• Paralyticobstruction
• Pseudo-obstruction
• Ascites

TREATMENT
• Nasogastricaspiration: To
reduce toxic effects, to
reduce bowel distension
whichindirectlyimproves
pulmonary ventilationand
to reduce possibilityof
aspirationpneumonia.
• Replacement of fluid and
electrolytes.
• Antibiotics: Ampicillin,
gentamicin, metronidazole,
cephalosporins.
• Blood transfusion:
• ICUcritical care: Systemic
management of
complications like ARDS,
DIC, SIRS are important.
• If there is hypotension,
dopamine/dobutamine are
also needed.
• CVP for fluid and
monitoring

SURGERY
• Surgery: Immediate
laparotomy is done and the
site
• Warm-saline soakedmop is
placed over the doubtful area
with 100%oxygeninhalation
for 20 minutes; if colour
becomes normal with
peristalsis thenbowel is
viable. On table Doppler
studymay be useful.
• Small bowel can be
decompressedusing Savage’s
decompressor.
• In case of right-sidedcolonic
obstruction, right
hemicolectomywithileocolic
anastomosis is done
• In case of left-sidedcolonic
obstruction, left hemicolec
tomy (resection) and colo-
colic anastomosis is done
witha defunctioning
colostomy(right-sided
transverse) which is closed
after 6 weeks.

• Obstructiondue to
rectosigmoid growthwith
patient being severely ill—
Hartmann’s operationcan
be done .
REFERENCE
by SriramBhat M
Surgeryby Das
Surgeryby Das

INTUSSUSCEPTION

INTUSSUSCEPTION(ISS)
DEFINITION
• It is telescoping or
invagination of one
portion(segment) of
bowel intothe adjacent
segment.
TYPES
• 1. Antegrade: Most
common.
• 2. Retrograde: Rare
(jejunogastric in
gastrojejunostomy
stoma).

TYPES
• It can be ileo-colic - 75%
• Colocolic
• It is common in weaning
period of a child(common
in male), between the
period of 6–9months.
• It is the commonest cause
of intestinal obstructionin
childrenof 6–18 months
age.
• In elderly intussusception:
• Colocolic is most common
type.
• Apex is formedusually by
growth
• No role of hydrostatic
reduction
• It canbe singleor multiple
(rare).

AETIOLOGY
• Change in diet during
weaning
• Upper respiratorytract viral
infection
• Intestinal polyps
• Submucous lipoma
• Leiomyoma of intestine
• Meckel’s diverticulum
• Carcinoma
• Purpuric submucosal
haemorrhages
• IdiopathicISS
• is commonin children,
occurs in terminal 50
cm of ileum
• During weaning, change
in diet causes
inflammationand
oedema of Peyer’s
patches—may
stimulate ISS
• Upper respiratorytract viral
infectionwhichcauses
oedema of Peyer’s patches –
children

• Other causes in adolescents
and adults are sub mucous
lipoma, leiomyoma, polyps
in jejunum(Peutz-Jegher
syndrome), other polyps and
carcinomas with papillary
projections.
PATHOLOGY
• Apex is the one which
advances
• Intussuscipiensis the one
whichreceives (outer sheath)
• Intussusceptumare the
tubes whichadvance
(middle and inner
sheath).
↓
Apex and inner tubes will
havecompromisedblood
supply
↓
whichleads to gangrene.
↓
Because of ischaemia, apex
sloughs off and bleeds

↓
whichmixes withthe mucus to
produce the classicred-currant
jelly
↓
that is passed per anum.
↓
Gangrene whichsets in leads to
perforationand peritonitis.
↓
Red currant jellyis not
commonly observedin ISS in
adult, but it can occur.
COMMON
• Common in males (3:2).
• Common in 6–9months.
But canalso occur at later
age groupedchildren.
• Common in spring and
winter, coinciding with the
gastroenteritis and
respiratory infections in
respective periods.

CLINICALFEATURES
• Commonest causeof
intestinal obstruction in
infancy.
• Initial colicky abdominal
pain(75%) which
eventually becomes
severe and persistent.
• Suddenonset of pain in
a male child
• with progressive
distensionof the
abdomen
• Vomiting
• with passage of “redcurrant-
jelly” stool. - It is usually not
found in adult ISS.
• OftenISSis recurrent, when
it gets reduced, child
automatically becomes
asymptomatic(It means
child cries during an episode
and sleeps peacefully once it
gets reduced).

ON EXAMINATION
• On examination, a mass is
felt either on the left or right
of the umbilicus
• whichis sausage shaped
• with concavitytowards
umbilicus, smooth, firm,
resonant,
• not moving withrespiration,
mobile, contracts under the
palpating fingers.
• Oftenmass appears and
disappears
• Right iliac fossa is empty
(Signof Dance).
• After 24–48 hours,
abdominal distension
appears and increases
progressively with features
of intestinal obstruction.
• Features of intestinal
obstruction with step-ladder
peristalsis.
• Blood-stained stool is often
obvious on digital
examination
of the rectum.

• Occasionally ISS can be seen
per anally and felt with a
long mesentery.
• Eventually, gangrene and
perforationoccurs with
features of the peritonitis
COMPLICATION
• Intestinal obstruction
• Perforation
• Peritonitis
INVESTIGATION
• Bariumenema shows typical
claw signor coiled spring
sign(Pincer end).

• Ultrasoundshows target sign
or pseudokidney sign or
bull’s eye sign, whichis
diagnostic.
• Doppler may show mass with
doughnut signand is useful
to checkblood supplyof
bowel.

• PlainX-rayabdomenshows
multiple air fluidlevels.
• CT abdomenis needed.
TREATMENT
• Initial management
• Ryle’s tube aspiration
• IV fluids
• Antibiotics
• Catheterisation.
Later management-
Nonoperative management
• Reductionby hydrostatic
pressure using either warm
saline or microbarium
sulphate solution or air
(popular in China).

• Bariumor salineis infused
into the rectumthrougha
catheter (Foley’s catheter).
• Under fluoroscopy,
reduction can be observed
• ISS more than 48 hours
FEATURESOF PERFORATION
• Strangulation
• peritonitis
• Recurrent ISS
• In adult commonly,
resection is required
SURGERY
Cope’s method:
• If reductiondoes not occur,
laparotomy is done under
G/A.
• By gentlymilking out the
intussusception withwarm
packs,it is reduced.
• After reduction, viability of
the bowel is checked
carefully.
• If manual reduction is not
possible, it is understood
that the bowel is likelyto be
gangrenous

• whichrequires resectionand
anastomosis.
• In case of viable bowel, often
terminal ileumis anchored
to the ascending colonand
Jackson veil band is cut.
• Patient also requires
nasogastric tube aspiration,
IV fluids, antibiotics.
• Appendicectomy shouldbe
done afterreduction of the
intussusception.
In children:
• Acute gastroenteritis.
• Purpurawithintestinal
symptoms.
In adults
• Carcinoma colon.
• Mesentericmass.
REFERENCE
by SriramBhatM
Surgeryby Das
Surgeryby Das

MECKEL’S
DIVERTICULUM

MECKEL’S DIVERTICULUM
DEFINITION
• It is congenital,
results from
incomplete closure
of vitellointestinal
duct..
• It is the most
commoncongenital
anomaly of small
intestine.

• Arises fromthe
antimesentericborder of
the ileum, containing all
three layersof the bowel
withindependent blood
supply.
• In 20% of cases mucosa
contains heterotopic
epitheliumlikegastric
(commonest—50%),
colonicand pancreatic
tissues (5%).
CLINICALFEATURES
• It may be connectedto
or communicatedwith
theumbilicus through
a band or fistula.
• oesophageal atresia,
• Exomphalos
• anorectal
malformations
• Presentations in
Meckel’sDiverticulum
• Severe haemorrhage
(Maroon-coloured
blood).

due to
bands/adhesions/
intussusception.
• Perforation.
• Intussusception
• Volvulus of small
bowel.
• Peptic ulceration.
• Diverticulitis features
mimicacute
appendicitis.
• Littre‘s hernia—it is
presence of Meckel’s
diverticulumin hernial
sac
• It is observedin
inguinal/femoral
hernia.

INVESTIGATION
• Silent Meckel’s
diverticulumfound
during
• laparotomy
• laparoscopy
• radioisotope
study.
• Carcinoid or GIST can
occur in Meckel’s
diverticulum
• Technetium(Tc99)
radioisotope scanis very
useful
• X-rayabdomento see
complications like
• Obstruction
• perforation.
• Laparoscopyis very
useful.
• Enteroclysis/small bowel
enema under fluoroscopy

TREATMENT
• AsymptomaticMeckel’s
diverticulumcan be left alone
whenidentifiedduring
laparotomy.
• Resectionof a short segment
of ileumcontaining Meckel’s
diverticulumand end-to-end
anastomosis is done.
• Meckelian diverticulectomy
with closure of enterotomy
also can be done
• But chances of retaining
heterotopictissues and
stenosis are higher.
REFERENCE
by SriramBhatM
Surgeryby Das
Surgeryby Das

PARALYTIC
ILEUS
(Adynamic
Intestinal
Obstruction)

PARALYTICILEUS (Adynamic
Intestinal Obstruction)
DEFINITION
• It is a state in which
intestines fail to transmit
peristalsis due to failure of
neuromuscular mechanism,
• i.e. Auerbach’s and
Meissner’s plexus.
• It may be localisedor
generalised

CAUSES
• Postoperative ™
Infective
• Pus
• Blood
• Bile
• Toxins
• enteritis ™
• Uraemia ™
• Hypokalaemia ™
• Spinal injury
• Retroperitoneal
haemorrhage ™
• Spinal surgery ™
• Plaster jacket
CLINICALFEATURES
• No passageof
flatus.
• No bowel sounds.
• Marked
abdominal
distension.
• Vomiting of large
volume of fluid.
• Tachycardia.

• Respiratorydistressdue to
pressure over the
diaphragm.
• High-pitched tinkling note
‘like bells at evening
pealing’.
• Dull abdominal pain(not
colicky).
• Features of
fluid/protein/electrolyte
imbalance
.
INVESTIGATION
• Serumelectrolyte
estimation- Especially
serumpotassium.
• ECG.
• X-rayabdomen.
• Ultrasound abdomen
to findout the possible
cause of ileus, e.g.
sepsis.
• Nasogastricaspiration.

• The primarycauseis
treated.
• IV fluids.
• Electrolyte management.
• Catheterisationand urine
output measurement.
TREATMENT
• Antibiotics and analgesics.
• Do not stimulate the
peristalsis (“Don’t flog a
tired horse”).
• Measurement of
abdominal girth is
necessaryto see whether
patient is recovering or
not.

• Decompressionof the large
bowel can be triedby
inserting a flatus tube per
anally intothe rectumand
keeping in place for few
hours.
• Drainage of terminal pulp
space by an oblique deep
incision.
• If there is osteomyelitis of
the terminal phalanx, it
has to be amputated.
REFERENCE
by SriramBhat M
Surgeryby Das
Surgeryby Das

REGIONAL
ENTERITIS
(Crohn’s
Disease)

REGIONALENTERITIS(Crohn’s
Disease)
DEFINITION
• It is a granulomatous, non-
caseating (transmural)
inflammatorycondition of
the ileumcommonly and of
the colon often.
• It is independent of age, sex,
socioeconomic status and
geographicareas.

• Rarely other parts of the
GIT likecolon, jejunum,
stomach, duodenum,
oesophagus can get
involved.
• Small bowel alone is
involved in 30%cases; in
50% cases bothsmall and
large bowels are involved.
• Terminal ileumis most
commonly
INCIDENCE
• Incidenceis 5/1,00,000;
prevalence is 50/1,00,000.
• It is common in North
America and north
Europe.
• Common in females

AETIOLOGY
• Unknown, but a familial
and infective nature is
thought of.
• Increasedautoantibodies.
• Dietand food allergy.
• It is slightly more common
in females.
• DNA of Mycobacterium
para tuberculosis
• Focal ischaemia as a
vasculitis
• monozygotictwins
• Genes NOD2/CARD15
in chromosome 16q12
has got strong
associationwith
Crohn‘s disease.
• CARD15 is expressed
in Paneth cells of the
ileum.
• Smoking is related to
Crohn‘s diseaseas
aetiology, as for
relapseand for
exacerbations

.
PATHOLOGY
• Transmural inflammation
↓
Granulomaformationwith
linear snake likeulcers -
Cicatrisation
↓
Thickening of the bowel wall
(Hose pipe pattern)
↓
Adhesions - Fistulaformation.
• There is increased mucous
membrane permeability
↓
antigen inducedcell-mediated
inflammatoryresponse
↓
release of cytokines like TNF,
interleukin 2
↓
defect in suppressor T cell
↓
granuloma and other
pathology

• Fibrosis, stricture formation,
deep ulcers, oedema of mucosa
betweenulcer areas
↓
whichlooks like ‘cobble stone’,
↓
skipped normal areas in between,
serosal opacity, mesenteric fat
stranding,
↓
enlargedmesentericlymph nodes
↓
abscesses in the mesentery
↓
fistula are the pathology

• Mesenteryis thickened,
oedematous, with enlarged
lymph glands
• whichwill neither break
nor calcify
• Rarely jejunum, stomach
and other parts of GIT like
oral cavity, oesophagus are
involved.
• In colon (30%), it is
commonly observedin
caecumand ascending
colon.
• Toxic megacolon with
acutecolitis eventhough
rare, can occur in Crohn‘s
disease.

GROSSFEATURES
• Small mucosalaphthous
ulcers are earliest gross
feature.
• Disease may be
inflammatory, stricturing or
perforating types
• Noncaseating giant cell
granuloma with chronic
inflammationof all layers

MICROSCOPICFEATURES
• focal arterial blocks in
muscularis propriaare
the microscopicfeatures.
• Extensive fat wrapping
aroundbowel
• whichis been thickened,
firm, rubbery,
incompressible,
segmental is typical.

CLINICALFEATURES
• It is common in young age
group.
• Abdominal pain& diarrhoea
is the initial slow insidious
presentation. Thereis also
asymptomaticperiod in
between.
• Diarrhoea is usually less
severewithout blood, pus or
mucous.
• Mild fever, weight loss,
lethargy.
• Crohn’s diseasemay
present as tender, firm,
resonantmass in right iliac
fossa
• Obstruction, fistula
formation, often
perforation
• Bleeding whichis usually
chronic but occasionally
massivecan occur.
• Perianal diseasewith
fissure, fistula, and abscess
• Extra- intestinal
manifestations

PRESENTATION
a. Acute presentations :
• It mimics acuteappen
dicitis withsevere
diarrhoea.
• Oftenthere will be
localised or diffuse
peritonitis.
• b. ChronicCrohn’s:
First stage
• Mild diarrhoea,
• colicky pain,
• fever,
• anaemia,
• mass in right iliac fossa
whichis tender, firm,
nonmobile along with
recurrent perianal
abscess.

Secondstage
• acuteor chronic intestinal
obstruction due to
cicatrisation with narrowing.
Thirdstage
• Fistula formation—
enterocolic, enteroenteric,
enterovesical,
enterocutaneous, etc.
• It is precancerous condition
but not as muchas ulcerative
collitis.
OTHER FEATURES
Extraintestinal manifestations of
Crohn’s disease™
• Skin: Erythema nodosum,
pyoderma gangre nosum
• mostcommon ™
Eyes: Iritis,
uveitis ™
• Joints: Arthritis, ankylosing
spondylitis, sacroiliitis ™
Sclerosing cholangitis,
• gallstones ™

• Nephrotic syndrome
• renal stones ™
• Pancreatitis,
• Chronicactive hepatitis ™
• Amyloidosis
• Aphthousulcers ™
• Blood: Anaemia,
thrombocytosis, DVT,
arterial thrombosis.
INVESTIGATION
• PlainX-rayabdomen
• ultrasoundabdomen.
• Bariummeal followthrough
or small bowel enema shows:
Straightening of valvulae
conniventes.
• Multipledefects (cobblestone
appearance).
• Cicatrisation of ileum(string
signof Kantor).

• Rose-thorn appearance of
thebowel wall.
• Radiologically Crohn’s
diseaseis classified as
nonstenosing type or
stenosing type.
• CT scanand CTfistulogram
is useful method.
• Colonoscopy usually shows
normal rectum; withcolon
showing aphthoidlike ulcers
and reddenedmucosal
margin.
• Deep ulcers, stricture and
fistula will be evident in late
cases.
• Colonoscopy also shows
segmental, deep, cobblestone
look.
• Blood tests for anaemia,
proteinloss, mineral and
trace element loss like
magnesium, zinc, and
selenium.

• There will be raised C
reactive protein and
orosomucoid in active
• Capsule endoscopyis useful
investigation, but when
stricture is present capsule
may get stuckin the narrow
part.
• MRI to diagnoseanal
disease. MR enteroclysis is
very useful to demonstrate
fistula.
• Serummarkers: 90% of
patients with Crohn’s
disease
COMPLICATION
• Intestinal obstruction ™
• Stricture ™
Bleeding ™
• Fistula formation™
• Carcinoma small and large
bowel ™
• Perianal abscess™
• Peritonitis ™
• Pericolicabscess

DIFF. DIAGNOSIS
• Radiation enteritis and
Yersinia enteritis.
• Ulcerative colitis, acute
appendicitis.
• Intestinal tuberculosis,
Salmonella, Shigella, CMV
• Carcinoma ileumor
caecum.
• Differential diagnosis for
mass in the right iliac fossa
• carcinoma caecum
• actinomycosis,
• appendicular
mass
• ileocaecal TB
• ectopickidney
• mesenteric
lymphadenitis

TREATMENT
• Medical
• Cessationof smoking
• Bed rest, protein and
vitaminsupplementations.
• Oftennasogastrictube
nutrition or TPnis required.
• Steroids are mainlyused to
induce remissionof the
diseasein initial phase.
• It is less useful for
maintenance.
• Dose is 20–40 mg
SURGERY - INDICATION
• Failure of medical
treatment.
• If patient cannot be
weaned off systemicsteroid
after 6 months.
• Fistula formation, bleeding,
malignant change.
• Perforation
• fulminant colitis.
• Perianal problems.
• Crohn’s diseasechildren
with growthretardation

• Ileocaecal resection (common
procedure done because
commonly ileocaecal region
is involved).
• Segmental resection—
conservative resectionis
better.
• Total colectomy and
ileorectal anastomosis
• Stricturoplasty.
• Temporary ileostomy.
• Right hemicolectomyis
done occasionally.
• Emergency colectomy
• Laparoscopic resectionis
good alternative

REFERENCE
by SriramBhat M
Surgeryby Das
Surgeryby Das

ULCERATIVE
COLITIS

ULCERATIVECOLITIS
DEFINITION
• It is an inflammatory
conditionof rectum& colon
of unknownaetiology
perhaps related to stress,
westernized diet,
autoimmune factor, familial
tendency, allergic factor.
• commonly starts in the
rectum, spreads proximally
to thecolon& oftenintothe
ileumas back wash ileitis
(5%).

AETIOLOGY
• Westernized diet
• red meat
• Defective mucinproduction
in the colonic mucosaand
mucosal immunological
reaction.
• Autoimmune factors—
cytotoxicT lymphocytes
against colonicepithelial
cells& presence of anti-
colon antibodies.
• Association with HLA DR2
is observedin ulcerative
colitis.
• DR 1501 is associated with
less severe type’
• DR 1502 is associated with
more severe form.
• Appendicectomy &
smoking protects ulcerative
colitis especially from
extraintestinal features
and frompostoperative
complications.

• Allergy to milk(cow milk)
and other dietaryfactors.
• Excessreactive oxidative
metabolismin ulcerative
colitis.
• Psychological aspects
• Stress
• Lifestyle
• Personality disorders
PATHOLOGY
To begin with, multiple minute
ulcers (pinpoint ulcers) occur
with proctitis and colitis
↓
Theseulcers extendintothe
deeper layer
↓
Spasmof the bowel
↓
Stricture of the colon↓
Permanently contractedcolon
(pipe stemcolon)

↓
In between ulcers, epithelial
thickening occurs which
appears likepolyps –
Pseudo polyposis
↓
It is confined to mucosaand
submucosa.
↓
no bowel wall thickening
and no granuloma
formation& no skiplesions.
↓
Rectumis alwaysinvolved,
thenspreads proximally.
↓
Entire colonincluding
caecumand appendix may be
involved.
↓
Proctitis occurs in 25%cases.
↓
5%risk of developing rectal
cancer
↓
In 15% left sided ulcerative
colitis presenting withsevere
recurrent diarrhoea.

↓
In 25%patients, total
proctocolitis is the presentation.
↓
Bloody diarrhoea,
Malnutrition.
↓
complications like toxic
megacolon, perforation (steroid
may maskthe features) and
carcinoma are common here.
↓
Pseudo polyps are of
inflammatoryin nature.
↓
Absence of normal mucosa
betweenthesepseudo
polyps is importantto
differentiate it from
neoplastic polyps.
↓
Multiple crypt abscesses
↓
Sparing of the deeper
layersof the colonicwall
↓
Inflammatory
pseudopolyps
↓

Multiple pinpointulcers
Increase in substance p
containing nerve fibres
↓
Lymphoidhyperplasia in
mucosaand submucosa
↓
Presence of anti neutrophil
cytoplasmic antibodies with
a perinuclear staining
pattern
↓
Decreasedgoblet cell
mucin
↓
Only in toxic megacolon-
there is acuteinflammation
extending to entire thickness
of the colonicwall including
the serosa.
↓
It is precipitatedby non
specificcauses, during
bariumenema study, due to
drugs like opiates,
antidiarrhoeal drugs and
anticholinergics.
↓

Toxic megacolon commonly
affects the transversecolonwhich
will be more than6 cm in
diameter.
↓
Left colon or entire colon also may
be involved.
↓
Caecumwhenrarely involved;
becomes more than10 cm in
diameter.
↓
Colonwill be likewet
blotting paper
↓
Carcinoma in ulcerative
colitis is more prevalent than
in Crohn‘s disease.

FACTORS INVOLVEDARE
• Extent of involvement (more
in total colonic)
• Durationof the disease;
continuous active disease
thanintermittent disease.
• Dysplasia developing into
cancer is common.
• Ulcerative colitis with
primary sclerosing
cholangitis has still
increasedriskof
developing cancer.
• In ulcerative colitis,
dysplasia is very
importantfactor to
transforminto
carcinoma.

INCIDENCE
• Incidence of carcinoma is
equal in both sexes.
• Carcinoma in ulcerative
colitis is commonly
aggressive
• poorlydifferentiated
• Multicentric
• Synchronous
• infiltrative & scirrhous
• half the patients will
havecolloid carcinoma
(signet ring)
CLINICALFEATURES
• Disease usuallybegins in
rectumas proctitis later
becomes left sidedcolitis
and eventually causes
severetotal proctocolitis.
• Waterydiarrhoea, mucus
or blood staineddis
charge per rectum.
• Colickypain, spasms.
• Decreasedappetite and
loss of weight.
• Relapses and remissions
at regular intervals

TYPES
a. Fulminanttype
• 5%common
• It is a severe form, with
continuous diarrhoea
withpassage of blood,
mucus and pus.
• Mimics fulminant
amoebic colitis
• severe typhoid
• Dysentery
• Fever
• Hypokalaemia
• Acidosis
• Dehydration
• Shock
• Abdominal distension
occurs
• Acute toxic dilatation of
transversecolon may
occur wherethe diameter
of transversecolon >6 cm.
• requires surgery
• i.e. either colostomyor
resection withileostomy
and later illeo-anal
anastomosis.
• Here colon is likewet
blotting paper.

b. Chronictype
• 95%common
• Lasts for months to
years
• withdiarrhoea
• blood loss
• Anaemia
• Invalidism
• abdominal discomfort
• pain.
• Severe malnutrition
• hypoproteinaemia
INVESTIGATION
• Bariumenema shows loss of
haustrations
• Narrowcontracted
colon (hose pipe colon)
• Mucosal changes
• Pseudo-polyps.
• Sigmoidoscopy &
biopsy.
• Colonoscopy is also required.
• High incidence of malignant
transformation - multiple
biopsies should be taken

DIFF. DIAGNOSIS
• PlainX-rayabdomenis
useful in obstruction
• toxicmegacolon
• perforation.
• C-reactive proteinwill be
very highin acutephase.
• Crohn’s disease™
• Ischaemiccolitis ™
• Irritable bowel syndrome ™
• Amoebiccolitis™
• Bacillary dysentery ™
• Carcinoma colon™
• Collageous colitis in
females ™
• Infectious colitis by
Clostridiumdifficile,
Campylobacterjejuni

COMPLICATION
GIT ™
• Pseudopolyposis ™
-
Turning into malignancy ™
• Stricture formation
• Toxic megacolonin
transversecolon ™
• Massive haemorrhage
• Fistula in ano
• Perforation
Extraintestinal ™
• Severe malnutrition™
• Liver cirrhosis ™
• Skin lesions
• pyoderma,
• Erythema nodosum™
• Arthritis
• Iritis
• Ankylosing
spondylitis
• Sclerosing
cholangitis
• Carcinoma of bile
duct

TREATMENT
• Correctionof anaemia ™
• Fluid and electrolyte
supplimentation™
• Nutrition
• highprotein
• Carbohydrate
• Vitamin
• but low fat diet
• TPN™
Sedatives and
tranquillisers ™
• Psychological counselling
INDICATIONS OF SURGERY
• Intractability—
commonest indication™
• Toxic dilatation ™
• Perforation™
• Haemorrhage ™
• Risk of malignant
transformation
• Dysplasia (DALM) ™
• Onset at earlyage ™
• Chronicinvalidism™

• Progressive disease with
• Stricture
• Abscess
• Fistulae ™
• Steroiddependency,
• Persistent active disease™
• Malignancy ™
• Severe extraintestinal
manifestations ™
• Growth retardationin
children
SURGERY
• Total proctocolectomy with
ileo-anal anastomosis with
pouches as reservoir (“J’, ’S’,
or “W’ pouches). I
• It is called as restorative
proctocolectomy withileal
pouchanal anastomosis
(IPAA).
• It is ideal curative
procedurefor ulcerative
colitis.

• Total proctocolectomy
with ileostomy
(permanent, continent
Kock’s ileostomy, with one
way valve is done)
• Total proctocolectomy
with end non continent
ileostomy was the earliest
operation done for
ulcerative colitis.
REFERENCE
by SriramBhatM
Surgeryby Das
Surgeryby Das

VOLVULUS

VOLVULUS
FEATURES
• It is the twist (rotation) in
the axis of the loop of the
bowel either clockwise or
anticlockwise.
• 15%of large bowel
obstruction is due to
volvulus.
• Sigmoid colonis the
commonest site (anti
clock wise)

• Caecal volvulus Caecumis
the secondcommonsite
(clockwise)
• It is common in females,
present as intestinal
obstruction.
• Caecal bascule is the
presence of constricting
band acrossthe ascending
colon(Bascule—
French—see-sawand
balance).
• Caecumwill be markedly
distendedand found in the
centre of the abdomen.
• It is due to lack of fixation
of the caecum—mobile
caecum.
• malrotation.
• Caecal volvulus is the
commonest cause of large
bowel obstructionin
pregnancy.

COMMON
• It is common becauseof high
fibre diet.
• commoncauseof large bowel
obstruction in Peru and
Boliviadue to high altitude.
• More common in males and
old age.
• It is common in patients with
chronic constipation with
laxative abuse.
PREDISPOSINGFACTORS
• Ogilvie’s syndrome ™
• Mentally-retarded
individuals™
• Chaga’s disease™
• Hypothyroidism™
• Anticholinergicdrugs ™
• Multiplesclerosis ™
• Scleroderma ™
• Parkinson’s disease
• Adhesions ™
Peridiverticulitis ™
• mesocolon™
• Narrowattachment of
sigmoidmesocolon

PATHOLOGY
Alwaysrotation is
anticlockwise.
↓
It requires one and half turn
of rotationto causevascular
obstruction and gangrene
↓
whicheventuallyleads into
perforation
↓
either at the root or at the
summitof the sigmoid loop.
↓
Enormous distension of the
colon occurs.
↓
Some times ileumcomes to the
root of thesigmoidvolvulus and
encircles it .

TYPES
1. Acute.
2. Recurrent.
CLINICALFEATURES
• Pain in the
abdomen—initially
left sided
• Absolute
constipation
(obstipation—no
faeces, no flatus).
• Enormous distension
of abdomen, starting
fromleft iliac fossa
extending to the
whole of the
abdomen(Tympanic
abdomen).

• Late vomiting and
eventually dehydration.
• Features of peritonitis.
• Hiccoughand retching
can occur.
• Tyre likefeel of the
abdomenis diagnostic.
INVESTIGATION
1. PlainX-ray
Ω sign(omega sign)—
single, grossly distended
loop of colonarising out
of thepelvis and
extending towards the
diaphragm. Coffee-bean
signor Bent-inner tube
sign.

• Ogilvies’s syndrome
• It is acutecolonicpseudo
obstruction.
• It is due to malfunctioning
sacral parasympathetic
nerves.
• Splenic flexure is the junction
of collapsed and dilated large
bowel.
• Descending colonis atonic
causing acute functional
obstruction.
• It may be due to trauma
• retroperitoneal irritation
• antidepressants
• Uraemia
• Diabetes
• Myxoedema
• Hypokalaemia etc.
• Prokineticdrugs
• colonoscopic
decompression
• Faecal impaction. ™
• Carcinoma recto sigmoid
region. ™
• Idiopathicmegacolon.

A
Special Thanks
To A Very
Special Doctor

Intestinal diseases by Dr.AmrithaAnilkumar

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