Surgery

Dr. Faruq Lec: -2-

10-Oct-06

Crohn’s Disease

Definition
Chronic progressive granulomatous inflammatory disorder of GIT

Incidence

2-9 cases /100,000 population detected annually.

The prevalence ranges broadly from 20-90/ 100,000population.
Peak incidence bet.2nd&4th decades

Etiology

• Unknown.
• Favored hypothesis; interaction of genetic & environmental factors.
• Family Hy of IBD in 15-20%.
• Offsprings of couples , both of whom have IBD, have a high risk(36%)
• Tansmissible agents;including small viruses, cell wall-deficient pseudomonas
–like bacteria, mycobacteria,chlamydiae,& yersinia-isolated from tissues of
patients.

Pathology

• Affects any part of GIT,from lips to anus.

• May spill over into larynx,or extend beyond the gut to the skin.
• The distal ileum – the most freq. site of involvement, eventually becoming
diseased in ¾ of patients.
• The small bowel alone is involved in 15-30%.
• Both the distal ileum & colon in 40-60%.
• The large bowel alone in25-30%.
• Duodenal Crohn’s dis in 0.5-7% of patients.

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Pathology (continued)

• Granulomas –in the bowel wall in50-70% & in mesenteric L.nodes in 25%.
• Mucosal lesions: aphthus ulcer.
punched out ulcer .
Linear ulcers
Fissures-knife-like clefts.
*Fissures & linear ulcers surrounding islands of intact mucosa, overlying edematous
submucosa—give cobble-stone appearance to theluminal surface.
*Crohn’s dis—ultimately becomes a transmural inflam. Process,with thickening of the
bowel wall- & often progress to stricture formation.
*The bowel & its mesentry—foreshortened in advanced cases.
* Mesentric fat seems to have advanced over the surface of the bowel toward the
antimesentric border

Clinical features:
Modes of presentations

• 1-Diarrhea
• 2-Recurrent abdominal pain
• 3-Abdominal symptoms & constitutional effects.
• 4-Anorectal lesions.
• 5-Anemia
• 6-malnutrition.
• 7-acute onset.
• 8-systemic complications

Presentations-Diarrhea

• Continuous or episodic is noted in 90% of cases.

• Stools ; liquid or semisolid & no blood if small bowel alone is diseased.
• 1/3rd of patients with colonic dis.-pass blood & a few present with bloody
diarrhea similar to U/colitis

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Recurrent abdominal pain

• Mild colic –initiated by meals, centered in the lower abd.. & relieved by
defecation-is common( due to partial bowel obstruction.)
• Complete I.O—severe cramping, vomiting & abd. Distension

Presentations(Abd. Symptoms &constitutional effects)

• Episodic attacks of abd. Pain & diarrhea accompanied by: lassitude, malaise,
wt.loss,
fever & anemia are a common syndrome
A mass –often palpable in the right lower quadrant.
Occasionally- present with PUO alone

Presentations (Anorectal lesions)

• Chronic anal fissures

• Large ulcers.
• Complex anal fistulas.
• Pararectal abscesses.
• The above are seen in 15-25% of patients with dis. Limited to small bowel.&
in50-70% of those with colonic involvement.
• These problems may appear many years before the intestinal disease.
• Histological features of Crohn’s dis, including granulomas, are often found in
biopsies of anorectal lesions.

Presentations( Anemia)

• Iron deficiency anemia

• Macrocytic anemia-due to B12 or folate deficiency may occur in the absence
of abdominal symptoms

Presentations (Malnutrition)

• Protein-losing enteropathy
• Steatorrhea
• Chronic obstruction.
• Diminished dietary intake from chronic illness. All these ---malnutrition &
Wt.loss
• Mineral & vitamin def.( esp vit.D)
• Def. of water-sol & fat-soluble vitamins in small bowel dis
• Zinc def.
• Children- failure to thrive & severely retarded sexual maturation

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Presentations(Acute Onset)

• Acute abd.pain & R.lower quadrant tenderness- mimicking AA – at op—found

to have regional ileitis
• Only 15% of such cases evolve into chronic Crohn’s dis- suggesting that most
patients with acute ileitis have an infectious process unrelated to Crohn’s dis.

Presentations (Systemic complications)

• Hepato-biliary disease
• Uveitis
• Arthritis, ankylosing spondylitis
• Aphthus ulcers, erythema nodosum, amyloidosis,
• thromboembolism.
• Vascular disorders
• Urinary complications-cystitis, calculi & ureteric obstruction

Investigations-Laboratories:

• ESR- may not be elevated in small bowel dis.

• Low S. albumin
• Anemia
• Steatorrhea.

Investigations (Radiological )

Barium study:

1-Thickened bowel wall + stricture

(string sign).
2-Longitudinal ulceration- shallow at 1st then becomes deep & undermining.
3- deep transverse fissures resembling spicules.
4- Cobble-stone formation.
5-Deformityof caecum.
6-fistulas
7-abscesses.
8-skip lesions

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Radiology

• CT scan
• Ultrasound
• MRI.
• These have diagnostic value in some cases.

Radiological-Scintiscan

• Indium 111-tagged granulocytes accumulate in Crohn’s dis over 2-3 h.

• Tc-99 hexamethylpropyleneamineoxime(Tc-99 HMPAO)

Endoscopy

• Upper GIT endoscopy-Dx-esoph, gastric,& duod.lesions.

• Colonoscopy- Crohn’s dis of colon.

DDx

• 1-U/colitis. Crohn,s dis of Colon,may be difficult to differentiate from

U/colitis.
• 2- Appendicitis- X- acute ileitis.
• 3-T.B.
• 4-Lymphoma
• 5-Other diseases-Ca., amebiasis, ischemia, enteropathy from NSAIDs.

Complications (A-Intestinal)

1-obstruction, abscess, fistula, & anorectal lesions –are so common, are regarded as
part of the characteristic clinical picture.
2-Free perforation & massive haemorrhage- are uncommon.
3- risk of cholelithiasis –increased
4-Oral manifestations-may cause disabiling pain
5-Ca. may occur in segment s of small or large bowel

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Complications (B-systemic)

• 1-eye- uveitis
• 2-Skin
• 3-Bone & J
• 4- Hepatobiliary
• 5-Amyloidosis
• 6-vascular, TEP.

Rx (Medical)

• Used in Rx of acute attack, bit its role in preventing relapse is not clear.
• 5ASAs- effectively control symtomatic attacks.
• Steroids- topical for colonic dis., & systemic Rx for small bowel dis.
• Immunosuppressives- in patients, unresponsive to steroids.
• Metronidazole-symtomatic improvement in some cases, for unknown reasons.
Stasis with bacterial overgrowth

Surgery-

• 1-incurable disease, so the aim of surgery is to treat symptomatic

complications.
• 2-multiple recurrent op.s are needed in a few patients.
• 3-During exploration, potential future lat. Stoma sites avoided.
• 4- If localized sepsis is encountered- drain it & anastamosis avoided.
• 5-incidental lesions –should be left alone & only symtomatic inflammatory
lesions that have failed medical Rx should be dealt with.
• 6-Acute complications are best treated by resection of the affected portion of
bowel.

Resection & Anastamosis

usually required for inflammatory dis.

• 1-In ileal & ileocaecal disease:only the macroscopically involved segment

resected, to preserve small bowel function
• 2- in colonic disease:The options are;segmental colectomy.total colectomy &
ileorectal anastamosis,proctocolectomy &ileostomy

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Strictureplasty

• Safe & reliable way of providing good symptomatic relief from fibrostenotic
lesions in the small bowel.

Perineal Surgery

• Drainage Should be conservative.

• Adequate drainage of sepsis.
• Fistulas are controlled with seton & only the most superficial fistulas are laid
open.
• Anal stenosis- treated medically initially;manual dilatation is reserved for
unresponsive stenosis

Prognosis

• 1- incurable & has a tendency to recur clinically.

• 2- Each major op. carries a 50/50 risk of future major surgery.
• 3- mortality is low.
• 4-the main causes of death are; colorectal CA & postop. Complications.
• 5- Quality of life scores &employment prospects are lower than those of the
general population.

Antibiotic-Associated colitis
(AAC)

1-Ab-associated diarrhea-diarrhea without gross mucosal abnormality.

2-gross inflammation of mucosa.
3-Pseudomembranous colitis- whitish – green or yellow plaques on the inflamed
mucosa

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AAC (continued)
Clostridium difficle

• Resident of the gut in 3% of general population & 10% of hospitalized

patients.It elaborates at least 4 toxins, includingtoxin A(an enterotoxin) &
toxin B( a cytotoxin)
• Major cause of nosocomial AA diarrhea & colitis.
• Clindamycin—watery diarrhea in 15-30% & true pseudomemb colitis in 1-
10%.
• Lincomycin, ampicillin,cephalosporins, & pencillin- are common inciting
Ab.s.
• Many others have been implicated including metronidazole.
• Parentral aminoglycosides seem to be exception.
• Colitis may develop as early as 2 days after beginning Ab, or as late as 3
weeks after they are discontinued

S&S

• Diarrhea ( usually watery, occasionally bloody).

• Abdominal cramps.
• Vomiting.
• Fever.
• Leukocytosis

Investigations- Sigmoidoscopy)

• In pseudomembranous – shows:elevated plaques or a confluent

pseudomembrane, & the mucosa is edematous & erythematous.
• Rectum is normal in 1/4of cases& colonoscopy may be necessary for Dx

Investigation- Biopsy; reveals

• Acute inflammation.
• The pseudomembrane is made up of WBC, necrotic epithelial cells, & fibrin

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Investigation(Bacteriology)

• Demonstration of C.difficle cytotoxin in stool is sensitive & specific.

• Stool culture is less efficient since some strains of C. difficle are
nontoxicogenic.

Rx

• 1- stop the inciting AB.

• 2-usually the condition subsides in 1-2 weeks.
• 3- severe symptoms or persistent diarrhea needs additional Rx
• 4-Vancomycin(125-500mg) orally qds for 7-10 days- expensive but effective
& the relapse rate is 15-20% after it is discontinued.
• 5-metronidazole(1.5-2gm/d) orally for 1-2 weeks –also effective.
Paradoxically ,however, it may cause AAC.
• 6-Bacitracin- is also effective .
• 7-Avoid antidiarrheal drugs, as they may prolong symptoms.

Prognosis

• The outcome of AAC –usually excellent if the dis is recognized & treated.
• Untreated pseudomembranous colitis-may lead to severe dehydration &
electrolyte imbalances, toxic megacolon or colonic perforation.
• Op.- required for perforation or toxic megaacolon.

Prepared by:
Rand Aras Najeeb