Surgery

Dr.: Faruq Lec: -1-

3-Oct-06

Small & Large Intestine

General Consideration
Etiology-CIMETIDINE

Congenital
C
I Inflammatory
M Metabolic
E Endocrine
T Traumatic
I Infective
D Degenerative
I Iatrogenic
N Neoplastic
E Everything
Else

Congenital abnormalities:

1-Cong.atresia of small intestine→→→Acute intestinal obstruction in

neonate.

2-Volvolus neonatorum-→→→Acute intestinal obstruction in neonate.

3-Malrotation of colon→high caecum→ difficulty in Dx of Acute

Appendicitis

4-Megacolon.
N.B- Normal bowel motion:

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Constipation-

1-Megacolon-
a Cong. –(Hirschsprung’s disease)
b- Acquired (Non-hirschsprung’s megarectum &megacolon)

2-Normal colon (Non-megacolon):

a-Slow transit
b-Normal transit.

Hirschsprung’s disease(Aganglionic Megacolon):

Failure in the cephalocaudal migration of the parasympathetic myenteric

nerve cells into the distal bowel.

The absence of ganglion cells always begins at the anus & extends a varying
distance proximally.

Functional obstruction as the affected area fails to relax due to unopposed

sympathetic tone

Incidence:

1in 4500 live births

Familial tendency in 5-10 %
M.> F( 4:1 when the disease is limited to the rectosigmoid )
Down syndrome in 10-15%

Pathology

Basic abnormalities are-

1-Absence of ganglia in neural plexus of intestinal wall

2-Hypertrophy of nerve trunk

10% Short- segment aganglionosis in the terminal rectum

75% all rectum rextending to sigmoid
10%More proximal colocn involved
5% Entire colon with small bowel involvement

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 Presentations:

I- In Infants
Symptoms vary widely in severity, but almost always occur shortly after
birth
The infant passes no or little meconium within 24h
Chronic or intermittent constipation
Progressive abdominal extension, bilious vomiting, reluctance to feed,
diarrhea, irritability & poor growth
PR exam. In the infant may be followed by expulsion of the stool & flatus
with remarkable decompression of abd distension.
I.O --may be complicated by enterocolitis

II- In Children
1-chronic constipation & abd. Extension are characteristic

2-Passage of flatus & stool requires great effort& stools are small in caliber

3-No soiling of diapers or undergarments( Distinguishing this form of

constipation from idiopathic constipation.

4-These children are : sluggish, with wasted extremites& flared costal

margins.

5-Impacted stools in the greatly dilated & distended sigmoid colon can be
palpable across the lower abd.

6-PR Exam. In older children – a normal or contracted anus, & empty

rectum

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Dx

1-Radiology:

a- Plain XR of abdomen- Erect & supine:

If I.O present--- Air-fluid levels
If enterocolitis-- = -intramural gas
If perforation--- = free peritoneal gas
b-Water soluble contrast enema-+ Screening----length & site of involved
intestine:
Dilated prox.segment
cone –shaped Transitional zone
irregularity of mucosa & abnormal contractions

2-Manometric studies- Failure of relaxation of the internal following rectal

distension by a balloon( in older children)

3-Biopsy- Full thickness, 1-2 cm strip of mucosa & muscularis from post.
Rectum proximal to dentate line under G.A

DDx
I-Low I.O In neonate;1-rectal or colonic atresia
2-meconium plug syndrome
3- meconium ileus
4-Functional causes As; a-Hypermagnesemia
b-hypocalcemia
c-hypokalemia
d-hypothyroidism
2- Patients who develop enterocolitis & diarrhea may mimic other causes of
diarrhea.
3- In functional constipation; stool normal in caliber ,
soiling is frequent &
enterocolitis is not usually a problem
PR- Stool is palpable in lower rectum
Ba enema-shows uniformly dilated bowel to
the anus

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Treatment

Traditionally- surgery was staged: Colostomy several months later—

resection of aganglionic segment & pull-through procedure, later followed
by closure of colostomy.
Recently_ single-stage procedure( no colostomy) as follows;

1-bowel obstruction & enterocolitis ( if present) – relieved by

large(30F) rectal tube& repeated warmed saline irrigation(10mlL/ kg.).

2-Infants with moderate to severe enterocolitis –diverting

colostomy.

Prognosis
M.R in untreated cases in infancy may be 80%. The main cause;
enterocolitis
Patients who are properly treated for Hirschsprung’s disease do well

Inflammatory Bowel disease

Crohn’s disease & ulcerative colitis – chronic inflam. Disorders of the gut of
unknown etiology.
U/colitis affects only the large bowel, whereas Crohn’s dis can affect any
part of GIT, from the mouth to the anus.
Occ.the two forms can be difficult or even impossible to distinguish.

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Epidemiology:

Crohn’s disease
U/Colitis
Incidence(UK) 5/ 100,000( 5/
constant) 100,000(increasing)
Age of onset Peak 20- Peak late teens
39years
Age of Dx Soon after 20-39years
onset of
symptoms
Sex 1:1 1;1.5
distribution(
M:F)
Geographical More More common in
distribution common in Anglo-Saxon &
Anglo-Saxon European races
& European
races
Associated HLA-B27 Smoking
factors
Implicated Autoimmune Measles virus
theories dis. Against Hypersensitivity
mucosal reaction(H.S)
cytoplasmic Pseudotuberculosis
Ag organism inf.
Milk protein H.S.
Toxic eff. Of small
bowel chyme
contents(>0.22μ
mdiameter)

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Pathology

U/Colitis:

A-Gross appearance

1-Changes confined to the rectum & colon, except when total colitis causes
incompetence of ileocaecal valve & back-wash ileitis.

2-the involvement is continuous & always includes the rectum, often the L.
colon & sometimes the whole colon.

3- the extend varies between patients & may do in a single patient over time.

4-Early changes ; Mucosal erythema & haziness of the submucosal vascular

pattern

5- in more severe dis., diffuse small ulcers appear on the red granular
mucosa with contact bleeding & loss of vascular pattern. The mucosa bet the
ulcers are abnormal.

6- Eventually the appearance is of small islands of congested mucosa on a

sea of smooth, inflamed submucosal base.

7- In quiescent disease , the appearance may be normal or show some

atrophy or loss of mucosal folds

B-Microscopic:

1- in active disease, mucosa-acute & ch inflam. cell infiltrate.polymorph

invade epith., resulting in distinctive crypt abscesses, that rupture into the
submucosa causing sloughing & ulceration

2-undermining &raising ofsurrounding areas---inflam.polyps.

3-Granulomas occur in relation to F.B or ruptured crypts.

4-Resolving dis. With re-epitheliaization & regeneration may be confused

with dysplasia.

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Clinical Features & Dx:

General features

1-The hallmark-increased stool freq. with blood&mucus per

rectum.(Bloodymucoid diarrhea)

2-The symptoms depend on the extent & severity of the dis.

3- there may be systemic features , either associated with more severe dis ,
or as extra-intestinal manifestation.

Site-Specific features:

Proctitis-or proctosigmoiditis:
Gradual onset of rectal bleeding
Tenesmus
Urgency
Are usually well systemically
Dx- by rigid sigmoidoscopy &biopsy
The proximal extent can be established at colonoscopy.
The disease may extend proximally over time

Left-sided disease:
more symptoms of colonic inflammation with bloody mucoid diarrhea.
Abdominal pain may be a feature.
Systemic features of malaise & feeling unwell are more likely.
Infective causes of diarrhea need to be distinguished from recent onset
U/colitis wit stool culture & microscopy.

Total colitis:
the systemic features are more pronounced, with fatigue, anorexia weight
loss.
Symptoms of distal involvement.
Dx by Colonoscopy& biopsy –extent & severity of the disease.

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Acute severe (toxic) colitis:

1-occurs in3-10% & in about 9% of patients coming to emergency op.

stool frequency of at least 6 actions /day is characteristic.
Severe constitutional upset (severely ill;toxic)
May be the flare-up of established disease or the 1st presentation, in which it
may be impossible to distinguish the disease from other form of colitis.
Usually have One or more of the following contributory factors ;
Inflammation involving the muscular coat.
Hypokalemia
Opioid use
Anticholinergic use
Ba enema exam.

Suspect Toxic colitis in the following cases :

a-Worsening general condition of the patient

b-failure to improve with Rx
c-abdominal distension
d- local peritonism
e-sudden cessation of frequent loose bowel actions
f- worsening blood test parameters

6-Dx-plain abdominal XR or Ba enema; thickened bowel wall & dilatation

of the transverse colon › 6cm

7-CT is useful to Dx sealed perforation

8-Nuclear WBC scanning can judge the extent of the disease, avoiding bthe
risk of colonoscopy in the acute setting.

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Investigations:

sigmoidoscopy-is essential-Lumen-blood mixed with mucopus present.

Rectal mucosa is:granular,dull, hyperemic &
friable
Submucosa-loss of vascular pattern
The lesion is diffuse- uniform in the affected
bowel &
patches of normal mucosa are not seen.
If the mucosa is not grossly diseased , biopsy
may be
helpful to confirm Dx

Lab.

HB↓. WBC↑. ESR↑

Severe disease—depletion of water & electrolytes, hypoalbuminemia

Radiological:

Plain XR-megacolon
Ba enema-should not be preceded by catharsis in acute cases & should not
be performed at all in severely ill patients because it may precipitate acute
colonic dilatation.
It show; mucosal irregularity from fine serrations to rough, ragged
undermined ulcers .
Loss of hautration, narrowing & shortening of colon,(lead-pipe appearance)
Widening of the space between rectum & sacrum(due to periproctitis or
shorteningof bowel)
Stricture( although majority benign, but suspect malignant changes)
Indium 111-labelled leukocyte scan-if the presence of inflammation in the
colon is in question.
Colonoscopy-done if sigmoidoscopy & radiographic findings are not
diagnostic.
Contraindicated in the presence of toxic colon & with great care if the
disease is active

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Complications:

Extra-colonic manifestations:a-lesions of the skin & MM-

erythema nodosum,erythema multiforme,
pyoderma gangrenosum, pustular
dermatitis, &
aphthus stomatitis.
b-uveitis
c- bone & joint lesions
e.g.arthralgia,arthritis,&
ankylosing
spondylitis
d-hepato-biliary & possibly pancreatic
lesions e.g;
fatty infiltration,pericholangitis,cirrhosis,
sclerosing
cholangitis,cholangiocarcinoma,
gallstones,& pancreatic insufficiency
e-Anemia, usually iron deficiency
f-Malnutrition & growth retardation
h-pericarditis
i- Anal complication- fissures(12%),
anorectal
abscesses &
fistulas(5%)

2-Perforation of the colon

3-Acute colonic dilatation( Toxic megacolon)
4-Massive haemorrhage
5-Stricture
6-Carcinoma of the colon or rectum.

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DDx-

Malignant neoplasms of the colon including lymphomas

Diverticular disease of the colon
Salmonellosis & other bacillary dysenteries – Dx by repeated stool cultures
Shigellosis may be suspected on the basis of a positive methylene blue stain
for fecal leukocytes
Campylobacter jejuni is a common cause of bloody diarrhea. The M.O can
be cultured from the stool & serum antibody titers rise during the illness.

6-E . Coli O157:H7—hemorrhagic colitis; a syndrome of bloody diarrhea &

abdominal cramps but no fever.

7-Legionella infection mimic U/colitis

8-G.C. proctitis-culture of rectal swab Dx

9-Herpes simplex proctitis-the most common cause of non-gonococcal

proctitis in homosexual men

10-Chlamydia trachomatis infection also common in homosexual men.

11-Amebiasis- Dx by microscopic exam. Of stool, rectal swabs or rectal

biopsies .Serological tests confirm that clinical infection has occurred.

12-Rare cases:histoplasmosis,T.B,CMV, Schistosomiasis,amyloidosis,&

Behcet disease.

13-AIDs-related GI infection

14-NSAIDS—can cause mucosal inflammation & even strictures in the

colon.

15-Antibiotic-associated colitis.

16-Collagenous colitis-may or may not be related to NSAIDS—watery

diarrhea.Dx biopsy- thickened-band of collagen just beneath the surface.

17-schemic colitis- segmental pattern of involvement

18-Functional diarrhea

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Rx-
Conservative measures:

Aims- i-to terminate the acute attack as rapidly as possible

ii-to prevent relapse

1-Mild Attack:
-reduced physical activity-even bed rest is advisable.
-diet- free of bovine milk products& any other food that exacerbates diarrhea
in the individual patient

-Medical therapy;
Sulfasalazine-2-8g/d orally—effective in controlling acute attack.
aminosalicylic acid agents(5-ASAs)- derivative of sulfasalazine, but have
fewer side –effects; oral preparation, topical-allergic to sulfonamide drugs
can obtain similar benefit with oral mesalamine, 2-5 g./d

-Patients
Maintenance doses –prevent in 50-80% of patients over 12months.
Bone marrow suppression is an occasional problem.
Corticosteroids-Topical –foam or suppository- for distal colitis.

2-Severe attack-
-hospitalization
-N/G suction in colonic dilatation.
-TPN & if the danger of colonic dilatation passed , oral (entral) nutrition is
effective.
-Corticosteroids- i.v. 100-300 mg./ d. or prednisolone 20-80 mg/d
-AB-metronidazole + gentamycin or cephalosporin
-Cyclosporine(immunosuppressive agent)- drug of choice for steroid-
resistant acute severe attack.
4mg./kg./d i.v.

3-Maintenance:
- For distal colitis;Nightly mesalamine suppositories or oral mesalamine-
- more severecolitis- oral mesalamine or 5-ASA- reduces relapse rates
-Immunosuppressive Rx in patients who cannot tolerate discontinuation of
steroid Rx

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B-Surgical Rx:

1-Indications:

A-acute disease;
i- Emergency op. for perforation of colon
ii- Urgent op. for an acute problems; toxic megacolon
haemorrhage
fulminating colitis
These are treated medically at 1st & then surgically if the response is
inadequate.
If toxic megacolon does not respond to Rx within a few hours, operation is
essential to avoid perforation.
Fulminating disease without megacolon should improve in 4-5 days or less;
otherwise, op. may be advisable.
Prolonged medical R may result in the need for a staged surgical approach,
whereas earlier intervention may require only one operation.

Chronic disease;

I-Intractable disease-difficult to define, Its elements are:

frequent exacerbation
chronic continuous symptoms.
malnutrition
Weakness
Inability to work
Incapacity to enjoy a full social & sexual life
II-Prevention or Rx of carcinoma.
III- severe extracolonic manifestation such as arthritis,pyoderma
gangrenosa
Or hepatobilary disease may respond to colectomy ( but ankylosing
spondylitis will not improve.

2-Surgical procedures:
1-Subtotal colectomy, end ileostomy
2-Proctocolectomy & end ileostomy
3-Total abdominal colectomy & ileorectal anastamosis
4-Proctocolectomy , ileal pouch & ileoanal anastamosis(restorative
proctocolectomy)

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Prognosis;

Emergency colectomy – required in 25 % of patients with severe 1st attacks;

60% respond rapidly to medical Rx.
15% improve slowly on medical Rx.

Overall colitis-related MR during the year after onset is about 1%

Emergency colectomy has a MR of 6% & most of these deaths are due to

perforation, a complication that has a fatal outcome in 40% of cases.

Op. MR for elective colectomy is less than 1 %

10% of cases develop chronic dis by 10 years.

The likelihood of op. during the 1st year is 25% & MR of 5%

Ca. colon- by 10% about 5% develop ca colorectal

The cumulative incidence is 20-25% after 20years & 30-40% by 30years

Written By:
Rand Aras Najeeb

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