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CROHN‘S DISEASE

Ulcerative colitis and Crohn’s disease are chronic inflammatory bowel diseases which pursue a protracted relapsing and remitting course, usually extending over years. The diseases have many similarities and it is sometimes impossible to differentiate between them. A crucial distinction is that ulcerative colitis only involves the colon, while Crohn’s disease can involve any part of the gastrointestinal tract from mouth to anus.

FACTORS ASSOCIATED WITH THE DEVELOPMENT OF INFLAMMATORYBOWEL DISEASE

Genetic

More common in Ashkenazi Jews have a first–degree relative or at least one close 10%.relative with IBDHigh concordance between identical twins

Environmental Crohn’s-most patients are smokersAssociated with low-residue, high refined sugar diet

PATHOLOGY

In Crohn’s- The intestinal wall is infiltrated with acute and chronic inflammatory cells. There are important differences in the distribution of disease and in histological features. The sites most commonly involved, in order of frequency, are terminal ileum and right side of colon, colon alone, terminal ileum alone, ileum and jejunum. Characteristically, the entire wall of the bowel is oedematous and thickened. There are deep ulcers which often appear as linear fissures; thus the mucosa between them is described as ‘cobblestone’. Deep ulcers may penetrate through the bowel wall to initiate abscesses or fistulae. Fistulae may develop between adjacent loops of bowel and the bladder, uterus or vagina, and may appear in the perineum.

CLINICAL FEATURES

The major symptoms are abdominal pain, diarrhea and weight loss.

Ileal Crohn’s disease causes abdominal pain, principally because of subacute intestinal obstruction, although an inflammatory mass, intra-abdominal abscess or acute obstruction may be responsible. Pain is often associated with diarrhea which is watery and does not contain blood or mucus. Almost all patients lose weight. This is usually because they avoid food since eating provokes pain. Weight loss may also be due to malabsorption, and some patients present with features of fat, protein or vitamin deficiencies.

Crohn’s colitis presents in an identical manner to ulcerative colitis, with bloody diarrhea, passage of mucus and constitutional symptoms including lethargy, malaise, anorexia and weight loss. Rectal sparing and the presence of perianal disease are features which favour a diagnosis of Chrohn’s disease rather than ulcerative colitis. Many patients present with symptoms of both small bowel and colonic disease. A few have isolated perianal disease, vomiting from jejuna strictures or severe oral ulceration.

Physical examination often reveals evidence of weight loss, anaemia with glossitis and angular stomatitis. There is abdominal tenderness, most marked over the inflamed area. An abdominal mass due to matted loops of thickened bowel or an intra-abdominal abscess may occur. Perianal skin tags, fissures or fistulae are found in at least 50% of patients.

COMPLICATIONS

Intestinal

Severe, life-threatening inflammation of the colon

This occurs in both ulcerative colitis and Crohn’s disease. In the most extreme cases the colon dilates (toxic megacolon) and bacterial toxins pass freely across the diseased mucosa into the portal then systemic circulation. This complication occurs most commonly during the first attack of colitis. An abdominal x-ray should be taken daily because when the transverse colon is dilated to more than 6cm, there is a high risk of colonic perforation.

Perforation of the small intestine or colon.This can occur without the development of toxic megacolon.Life-threatening acute hemorrhage.Hemorrhage due to erosion of a major artery is a rare

complication of both conditions.

Fistulae and perianal disease.

Fistulous connections between loops of affected bowel, or between bowel and bladder or vagina are specific complications of Crohn’s disease and do not occur in ulcerative colitis. Enteroenteric fistulae cause diarrhea and malabsorption due to blind loop syndrome. Enterovesical fistulation causes recurrent urinary infections and pneumaturia. An enterovaginal fistula causes a feculent vaginal discharge. Fistulation from the bowel may also cause perianal or ischiorectal abscesses, fissures and fistulae. These may sometimes be extremely severe and can be the source of great morbidity

SMALL BOWEL CROHN‘SDISEASEChrohn’s disease can usually be diagnosed with

confidence without histological confirmation in the appropriate clinical setting. Indium- or technetium-labelled white cell scanning may help identify inflamed intestinal segments. In atypical cases biopsy or surgical resection is necessary to exclude other diseases. This can often be done endoscopically by ileal intubation at colonoscopy, but sometimes laparatomy or laparoscopy with resection or full-thickness is necessary.

INVESTIGATIONS

Full blood count may show anaemia resulting from bleeding or malabsorption of iron, folic acid or vitamin B12. Serum albumin concentration falls as a consequence of protein-losing enteropathy, The ESR is raised in exacerbations or because of abscess. Elevation of CRP concentration is helpful in monitoring Crohn’s disease activity.

Bacteriology

Stool cultures are performed to exclude superimposed enteric infection in patients who present with exacerbations of IBD. Blood cultures are advisable in patients with known colitis or Crohn’s disease activity.

Sigmoidoscopy with biopsies is a simple but essential investigation in all patients who present with diarrhea. In crohn’s disease patchy inflammation with discrete, deep ulcer, perianal disease (fissures, fistulae & skin tags) or rectal sparing occurs.

Colonoscopy may show active inflammation with pseudopolyps or a complicating carcinoma. Biopsies are taken to define disease extent, as this is underestimated by endoscopic appearances alone, and to seek dysplasia in patients with long-standing colitis. In ulcerative colitis the macroscopic and histological abnormalities are confluent and most severe in the distal colon and rectum. Stricture formation does not occur in the absence of carcinoma. In Crohn’s colitis the endoscopic abnormalities are patchy, with normal mucosa between the areas of abnormalities. Aphthoid or deeper ulcers and strictures are common.

Barium Studies

Barium enema is a less sensitive investigation than colonoscopy. In Crohn’s colitis a range of abnormalities occur. The appearances may be identical to those of ulcerative colitis but skip lesions, strictures and deeper ulcers are characteristics. Reflux into the terminal ileum may show stricture and ulcers.

Contrast studies of the small bowel in ulcerative colitis, but in Crohn’s disease affected areas are narrowed and ulcerated; multiple strictures are common.

Other Investigations

A straight abdominal X-ray is essential in the management of patients who present with severe active disease. Dilation of the colon, mucosal oedema (‘thumb-printing’) or evidence of perforation may be found. In small bowel Chrohn’s disease there may be evidence of intestinal obstruction or displacement of bowel loops by a mass. Ultrasound may identify thickened small bowel loops and abscess development in Crohn’s disease.

Radio-labelled white cell scans show areas of active inflammation. They are less accurate than other imaging modalities with poor specificity but may be useful in severely ill patients in whom invasive tests are best avoided. MRI scans are very accurate in delineating pelvic or perineal involvement by Crohn’s disease.

MANAGEMENT

The key aims are to: Treat acute attacks Prevent relapses Detect carcinoma at an early stage Select patients for surgery

MEDICAL TREATMENT OF CROHNS DISEASE

Patients with active colitis or ileocolitis are initially treated Aminosalicylates and corticosteroids In severe disease intravenous prednisolone is indicated, but abscess or fistulating disease should be excluded before instituting therapy with corticosteroids. nutritional therapy using polymeric or elemental diets induces remission.

Patients with isolated ileal disease are treated with corticosteroids. Poorly respond patients should, at an early stage, be considered for surgical resection since this is associated with prolonged remission in most cases.

Infliximab given as an intravenous infusion 4-8 weekly on three occasions induces remission in patients with active Chrohn’s disease at any site within the gastrointestinal tract, Infliximab is contraindicated in the presence of infection, including TB.

FISTULATING AND PERIANAL DISEASE

Fistulae usually develop in association with active Crohn’s disease and are often associated with sepsis. The first step in management is to define the site of fistulation; this may involve barium radiology, CT and MRI. Surgical intervention is then required, although treatment of underlying active disease with corticosteroids and nutritional support, usually by TPN, are required in many cases. For simple perianal disease metronidazole and/or ciprofloxacin are first-line therapies.

MAINTENANCE OF REMISSIONThe most effective step and one greater than any

pharmacological intervention is smoking cessation. Aminosalicylates.

SURGICAL TREATMENTOperations are often necessary to deal with fistulae,

abscesses and perianal disease.Obstructing or fistulating small bowel disease may

require resection of affected tissue. Patients who have localized segments of Chrohn’s colitis may be managed by segmental resection and/or multiple stricturoplasties.

Patients who have perianal Chrohn’s disease are managed as conservatively as possible.

PROGNOSISLife expectancy in patients with IBD is now similar to

that of the general population.Around 80% of Crohn’s patients undergo surgery at

some stage, and 70% of these require more than one operation during their lifetime. Clinical recurrence following resectional surgery is present in 50% of all cases at 10 years.

CROHN‘S DISEASE

Patient Name: Mr. Mir Mohd AliFile Number: A-187710Date of Birth: 01-01-1971Gender: MaleNationality: IndianThis 38 yrs old Indian male who was on treatment for suspected

T.B. abdomen with obstruction was admitted on 12-2-09 as 2010 hours under the care of Dr. Rizwan Khan with severe pain abdomen and vomiting and fever of one week duration, in surgical ward. Admission care rendered. On admission his weight was 69kg and height 164 cms. Vital Signs: Temp: 38.5 C, Pulse: 92bpm, RR: 20bpm. Tab Panadol 2 stat was given as ordered by Dr. Rizwan Khan for fever after one hour of Tab Panadol Temp: 37.5 C.

Investigations on admission:

CBC, ESR, U/A, LFT, Total Protein Albumin, globulin, BUN, S. Creatinine, Electrolytes, Chest X-Ray of abdomen supine and Chest were requested and done. WBC: 17.6, Hb: 11.7mg/dl, ESR: 65m in 1st Hr, LFT: Alt: 133 /mmol/L. Diet as tolerated was advised. IV fluids 5% Dextrose Saline 500cc x 4 Hr started and continued. In Buscopan 1 gm IV, Inj Primperam 10mg IV, Inj Zantac 50mg IV stat was administered.

On 14/02/09 case transferred under the care of Dr. Siddiqui. Anti tubercular drugs were kept hold. Ultrasound of abdomen and pelvis CT abdomen and pelvis requested and done. Kept NPO CT report was suspected Crohn’s disease complicated by abscess and intestinal fistula. Potassium Chloride was added to the infusion 10mmol in 500cc of DNS.

On 14-2-09 blood for PCR (Polymerase Chain Reaction) ASCA(Antisacchymes Cytoplasmic Antibody) sent to laboratory. Inj. Cefizox 1 gm IV 8 hrs, Inj. Flagyl 500mg IV 8 Hr were started and continued.

On 15-2-09 PT, PTT, INR were done. TPN 2000 Cal/24Hr started. Patient was posted for possible Ultrasound guided aspiration of abscess on 17th of February at 2pm in Saad Hospital.

On 17th of February CT guided percutaneous drainage of abscess and biopsy done in Saad Hospital. A contrast X-ray through the drainage tube revealed a fistula. With small bowel colonoscopy was done on 21-2-09 by Dr. Moataz, revealed linear deep ulcer with cobble stone mucosa. Patient was kept NPO and TPN continued. Intake and output was maintained all the time with daily weight.

On 20-2-09 RBS: 177mg/dl. Inj. Humulin R 5 units given as ordered by Dr. Sheela. Sliding scale was followed for elevated blood sugar by the order of Dr. Moataz every 6 hourly. On 22nd of February 10% Dextrose with Inj. Humulin R 25 units with KCL 25 meq. was given LFT, S. Albumin, Calcium, Phosphorus, Magnesium were checked every 3rd day.

Cap Rifinah 600 daily P.O. started on 22-2-09. He was started on IV steroids and given first dose on Tumor necrosis factor antibody Inj. Remicade, 2nd dose was given after 15 days 1st of dose.

On 28-2-09 started with 30cc water PO hourly and increased to 60cc-90cc and tolerated by evening on same day mixed fluids was taken and well tolerated. Inj. Flagyl and Inj. Cefizox were discontinued. Steroid Inj. Solucortef shifted to oral Tab Prednisolone 40 mg.

On 1st March 2009 started with diabetic light diet as tolerated. Drain no output on 2nd of March 2009 IVF discontinued including Total Parenteral Nutrition. Vital Signs were normal. Abdomen was soft. Not passed stool.

On 3-3-09 central line was removed. Tolerated diet, passed stool. No complaints noted. He was discharged in a fair condition with drainage tube. Weight on discharge was 66.9kg. On 8th March drain was removed by Dr. Siddiqui in clinic.

Patient was instructed to take high protein diabetic diet with no restriction of activities and medication and regular follow up. His weight on 8-3-09 was 69kg.

On 1st March 2009 started with diabetic light diet as tolerated. Drain no output on 2nd of March 2009 IVF discontinued including Total Parenteral Nutrition. Vital Signs were normal. Abdomen was soft. Not passed stool.

On 3-3-09 central line was removed. Tolerated diet, passed stool. No complaints noted. He was discharged in a fair condition with drainage tube. Weight on discharge was 66.9kg. On 8th March drain was removed by Dr. Siddiqui in clinic.

Patient was instructed to take high protein diabetic diet with no restriction of activities and medication and regular follow up. His weight on 8-3-09 was 69kg.