ANATOMY OF THE COLON & CROHN S DISEASE

FUNCTION OF LARGE INTESTINE

Water is absorbed from the indigestible residues of the liquid chyme, Faeces is stored temporarily and allowed to accumulate until defecation occurs.

ANATOMY
The large intestine consists of the cecum appendix ascending transverse descending sigmoid colon rectum.

The large intestine can be distinguished from the small intestine by: Omental appendices: small, fatty, omentum-like projections. Teniae coli: three distinct longitudinal bands: (1) mesocolic tenia, to which the transverse and sigmoid mesocolon attach; (2) omental tenia, to which the omental appendices attach (3) free tenia, to which neither mesocolon nor omental appendices are attached. Haustra: sacculations of the wall of the colon between the teniae A much greater caliber (internal diameter).

CAECUM
Blind intestinal pouch 7.5 cms Right illiac fossa Within 2.5 cm of the inguinal ligament Entirely enveloped by peritoneum No mesentery Attached to the lateral abdominal wall by one or more caecal folds of peritoneum. Terminal ileum enters the cecum obliquely and partly invaginates into it.

COLON

four parts
ascending Transverse Descending sigmoid

ASCENDING COLON
Second part Right lumbar region passes superiorly cecum to the right lobe of the liver, where it turns to the left at the right colic flexure hepatic flexure. Retroperitoneal fused to the posterior body wall Covered by peritoneum anteriorly and on its sides A deep vertical groove lined with parietal peritoneum, the right paracolic gutter.

HEPATIC FLEXURE
Location - under the 9th and 10th costal cartilages in the vicinity of the mid axillary line. Between the anterior surface of the lower half of the right kidney and the inferior surface of the right hepatic lobe. The gallbladder is located anteriorly, and the duodenum is located posteriorly. Cysto colic ligament - peritoneal fold between the hepatic flexure and the gallbladder Hepatogastric or Hepatoduodenal ligament - peritoneal fold which starts from the hepatogastric or hepatoduodenal ligament and ends at the right part of the hepatic flexure (hepatocolic ligament). A similar, but rare, peritoneal fold starts from the right lobe of the liver and extends over the entire hepatic flexure.

TRANSVERSE COLON
Third Longest Most mobile part of the large intestine Begins at the hepatic flexure, just beneath the inferior surface of the right lobe of the liver. Ends the splenic flexure related to the posterolateral surface of the spleen. Tail of the pancreas is above Anterior surface of the left kidney lies medially.

Mesentery fused secondarily with the posterior wall of the omental bursa. At the beginning of the mesentery, there may be additional bands of peritoneum, the hepatocolic and cystocolic ligaments. The splenic flexure, the colon is supported by the phrenocolic ligament, a part of the left side of the transverse mesocolon. Mesocolon is formed by a double peritoneal fold which extends upward and attaches to the anterior pancreatic border, suspending the transverse colon from the pancreas.

Contains the middle colic artery and vein, and lymph nodes as well as nerves. The transverse mesocolon and transverse colon provide the barrier between the supracolic and infracolic compartments of the peritoneal cavity; they are responsible for supracolic or infracolic collections of fluid.

SPLENIC FLEXURE
has an acute angle. located higher than the hepatic flexure, at the level of the 8th interspace in the midaxillary line. This high position is due not only to the small left hepatic lobe, but also to the multiple splenic ligaments and other ligaments in its vicinity. posteriorly to the left kidney anteriorly to the left costal arch and occasionally to the stomach.

DESCENDING COLON
Descending colon is related to
The quadratus lumborum muscle Left adrenal gland Left kidney and left ureter Left gonadal vessels The iliohypogastric and ilioinguinal nerves.

Covered anteriorly and on its medial and lateral sides by peritoneum no mesentery

SIGMOID COLON
At level of the iliac crest, the descending colon becomes the sigmoid colon and acquires a mesentery. Two portions:
(1) the iliac portion, which is fixed and located at the left iliac fossa (2) the pelvic portion, which is mobile. This entity is called "sigmoid" because of its "S" shape.

The sigmoid colon begins at the iliac crest and ends at the 3rd sacral vertebra. The termination of the teniae coli, approximately 15 cm from the anus, indicates the rectosigmoid junction. It usually has a long mesenterythe sigmoid mesocolon and therefore has considerable freedom of movement, especially its middle part.

The mobile, omega-shaped ( ) pelvic colon begins at the medial border of the psoas major muscle. It has a mesentery (the pelvic mesocolon) that is fixed to the posterior pelvic wall, its fixation being like the capital Greek letter lambda ( ). The pelvic colon terminates at the rectosigmoid junction, which is located at the area of the 3rd sacral vertebra. (mesentery ceases) The middle of the base of the lambda is located at the point where the left ureter crosses the pelvic brim at the intersigmoid mesenteric recess just lateral and posterior to the fossa in which the left ovary rests. The left leg of the lambda is attached to the pelvic brim. The right leg travels medially and downward to the 3rd sacral vertebra. The superior rectal vessels are within the mesentery of the sigmoid colon.

BLOOD SUPPLY

VENOUS DRIANAGE

LYMPHATIC DRAINAGE

NERVE SUPPLY
The sympathetic supply to the right colon originates from the lower T1 T6 segments of the spinal cord. Preganglionic fibers pass through the sympathetic chain ganglia, then pass as thoracic splanchnic nerves to synapse in the celiac, aortic, and superior mesenteric plexuses. From the plexuses, postganglionic fibers pass with the arteries in the mesentery to the small intestine and the right colon. On the left, preganglionic fibers arise from the L1 , L2/L3 segments of the cord, then travel as lumbar splanchnic nerves to the aortic plexus and the inferior mesenteric plexus. From ganglia in this diffuse plexus, postganglionic fibers follow branches of the inferior mesenteric artery to the left colon and the upper rectum.

Parasympathetic Innervation Vagal fibers from the posterior trunk pass as the celiac division to and through the celiac ganglion without synapse. From the ganglion, preganglionic fibers pass on the superior mesenteric artery to the small intestine and the right colon, where they synapse with ganglion cells of the intramural plexuses. The left colon receives parasympathetic fibers from pelvic splanchnic nerves, which arise from the 2nd, 3rd, and 4th sacral nerves. These fibers follow the course of the presacral nerve to reach the inferior mesenteric plexus. From this plexus, the preganglionic fibers follow the branches of the inferior mesenteric artery to the left colon and the upper rectum.

CROHN S DISEASE
Crohn's disease is a chronic inflammatory condition of the gastrointestinal tract that can give rise to strictures, inflammatory masses, fistulas, abscesses, hemorrhage, and cancer. This disease commonly affects the small bowel, colon, rectum, or anus.

Definition - its is a granulomatous , noncaseating inflammatory condition of the ileum commonly and of the colon often.

Sites small intestine alone (35%) colon alone (20%) Both small bowel and colon (45%) mouth (6% to 9%) esophagus (<1%), stomach and duodenum (1% to 5%).

EPIDEMIOLOGY
Incidence is about 4-10/100000 annually Prevalence is 27-106/100000 More common in the West and Caucasians. Ashkenazi Jews M:F- 1:1.2 Occurs at a mean age of 26, although elderly are also at increased risk

ETIOLOGY
interplay of genetic and environmental factors are believed to cause Crohns disease.

Environmental Factors
INFECTIOUS AGENTS Two mycobacteria (Mycobacterium paratuberculosis and M. tuberculosis) have been considered possible etiologic agents because they cause granulomatous inflammation of the gut. Persistent measles virus and Yersinia enterocolitica have also been implicated

DIET

A dietary cause(s) has been suspected because of the finding of several antibodies against food antigens (e.g., milk, bakers yeast) in patients with Crohns disease.

SMOKING
twice as common in smokers than in nonsmokers.

GENETIC FACTORS
risk of developing CD is 30 times higher in siblings of patients with the disease than in normal subjects whose siblings do not have CD. weak correlation with some human leukocyte antigens (HLA) and an inverse correlation with others have been made. NOD2 mutations that are present only in patients with CD.

CARD15 mutated in 10-30% of patients DRB1*0103 severe, perianal & uveal disease DRB1*0701 is associated with ileal involvement

PATHOLOGY
Transmural inflammation

Granuloma formation with linear snake like ulcers

Cicatrisation

Thickening of the bowel wall (hose pipe pattern)

Adhesions

Fistula formation

PATHOLOGY: MACROSCOPIC
Involved small bowel is thickened and narrowed Colonic fistulaeenteroenteral, enterovesical, enterovaginal, or enterocutaneous Deep mucosal ulcers and fissures, with a cobblestone appearance

PATHOLOGY: MACROSCOPIC
Aphthoid ulceration- small round ulcers with circumscribed margins, erythematous haloes and grey or yellow floors

Abscesses Skip lesions

PATHOLOGY: MICROSCOPIC
Non-caseating granulomas Transmural inflammation

Neuromuscular

hyperplasia and thickening of bowel wall with stricture formation

PATHOLOGY: MICROSCOPIC
Lymphoid hyperplasia

Cryptitis and crypt abscesses (more common in UC)

CLINICAL FEATURES: VIENNA CLASSIFICATION

Inflammatory disease Stricturing disease- narrowing of bowel with obstruction or changes in faecal calibre Penetrating disease-abnormal passageways between bowel and other structures

CLINICAL FEATURES: SYMPTOMS OF CHRONIC BOWEL INFLAMMATION

Prolonged diarrhoea in 80% with (colonic involvement less common than UC) or without blood and mucous, often intermittent Low-grade fever Generalised fatigability Crampy or steady abdominal pain and tenderness often in RIF or periumbilical pattern relieved by defaecation.

ADDITIONAL SYSTEMIC FEATURES

Malabsorption with extensive small intestinal disease Weight loss Failure to grow in children and during puberty Signs of anaemia

PRESENTING WITH OBSTRUCTION

Vomiting and nausea Colicky abdominal pain Abdominal distension and bloating Constipation

ANAL AND PERIANAL COMPLICATIONS

Skin tags Fissure in ano Haemorrhoids Perianal abscess Ischiorectal abscess Fistula in ano/ vesicular Anorectal fistula

EXTRA-INTESTINAL MANIFESTATIONS
Eyes- Uveitis and conjunctivitis Joints-Seronegative arthropathies, arthralgia, ankylosing spondylitis and inflammatory back pain Skin- Erythema nodosum, pyoderma gangrenosum Hepatobiliary - Sclerosing cholangitis,fatty liver, hepatitis, sclerosis, gallstones Systemically- Increased risk of clotting, osteoporosis, autoimmune haemolytic anaemia

INVESTIGATIONS
Blood

FBC and peripheral blood film: Normocytic normochromic anaemia, Raised ESR and CRP Hypoalbuminaemia in severe disease Deranged LFTs Antibodies: Anti-Neutrophil Saccharomyces cerevisiae Stool cultures
Imaging

Cytoplasmic

Antibodies,

anti-

Barium follow-through- Deep ulceration and areas of narrowing and structuring Colonoscopy- Cobblestone appearance with patchy aphthoid and deeper ulcers Biopsy from colonoscopy granulomatous tissue Wireless capsule endoscopy CT Abdomen shows transmural inflammation and

MEDICAL MANAGEMENT
Inducing remission Oral glucocorticosteroids eg budenoside Enteral nutrition Azathioprine/mercaptopurine Maintenance Aminosalicylates Azathioprine, mycophenolate mofetil Biologicals eg infliximab Antibiotics: Ciprofloxacin and metronidazole
Infliximab

SURGICAL MANAGEMENT
Indicated with:
Failure of medical therapy Complications- toxic dilatation, obstruction, perforation, abscesses, fistulas Failure to thrive

80% of patients require an operation at some point In colonic CD, a subtotal colectomy + iliorectal anastomosis or panproctocolectomy+ end iliostomy are performed. Recurrence is common

PROGNOSIS
Follows a chronic relapsing course 6-10 times more likely to develop bowel cancer, but < UC Reduced fertility in women with active disease Mortality data is equivocal