small and large intestine

The small & large intestines

Dr. Basim Ghaib Al-Mukhtar

anatomy

Small intestines: it starts at the pylorus & extends to the ileocaecal valve. It is approx. 7m in length. It is divided into the duodenum, jejunum & ileum. Relations. The duodenum: is about 25 cm in length. It has no mesentery. The jejunum makes up the proximal two fifths of the small bowel & is wider, thicker & more vascular than the ileum. Valvulae conniventes. The ileum contains larger lymph node aggregates(Peyer s patches).

Large Intestine: it extends from the ileum to the anus. It is approxim. 1.5m in length. It is more fixed than the small bowel. It also differs in that it possesses appendices epiploicae on its surface & the presence of taenia. It can be divided into the caecal, ascending, transverse, descending & sigmoid colonic segments.

- Arterial supply. - Venous drainage . - Nerve supply.

Angiodysplasia
Is a vascular malformation associated with ageing. Incidence 5-25% over the age of 60 years. It occurs particularly in the ascending colon & caecum of elderly patients. The malformations consist of dilated tortuous submucosal veins. Clinical features: anaemia. Melaena or significant per rectal bleeding.

Investigations

Colonoscopy. Selective superior & inferior mesenteric angiography. Technetium-99m labelled red cells. Treatment Stabilise an unstable circulation. Localise bleeding by colonoscopy & cauterization. Radical surgery.

Diverticular disease

2 varieties:1 Congenital. All three coats of the bowel are present in the wall of the diverticulum, e.g. Meckel’s diverticulum.2 Acquired. The wall of the diverticulum lacks a proper muscular coat. Most alimentary diverticula are thought to be acquired.


Duodenal diverticula: 1 Primary. Mostly occurring in older patients on the inner of the second & third parts. Are usually asymptomatic. 2 Secondary. result from longstanding duodenal ulceration. Jejunal diverticula: Are usually of variable size & multiple. clinically may be 1 symptomless, 2 abdominal pain, 3 malabsorption syndrome, 4 acute abdomen.

Meckel’s diverticulum It represents the patent intestinal end of the vitellointestinal duct. Is present in 2% of the population. It is situated on the antimesentric border of the small intestine, commonly 2 feet from the ileocaecal valve. Is usually 2 inches long.


It should be sought when a normal appendix is found at surgery for suspected appendicitis.Manifestations:1 Severe haemorrhage.2 Intussusceptions.3 Meckel’s diverticulitis.4 Chronic peptic ulceration.5 Intestinal obstruction.

Imaging.Silent Meckel’s diverticulum.Meckel’s diverticulectomy

Colonic diverticula
Is found in the sigmoid colon in 90% of cases. The caecum can also be involved. The rectum is not affected. It is thought to be related to reduced fibre in the western diet. Diverticula of the colon are acquired herniations of colonic mucosa protruding through the circular muscle. On histological examination, the diverticulum consists of a protrusion of mucous membranes covered with peritoneum.

Complications

- diverticulitis. - Pericolic abscess. - peritonitis. - Intestinal obstruction. - hemorrhage. - Fistula formation.

Clinical features

Elective: distension, flatulence, & a sensation of heaviness in the lower abdomen. Emergency: persistent lower abdominal pain, usually in the left iliac fossa, with or without peritonitis. Fever, malaise, & leucocytosis.



diagnosis
CT scan: identify bowel wall thickening, abscess formation, & extraluminal disease.Barium enema & sigmoidoscopy.Water soluble enemas may be helpful in large bowel obstruction.Colonoscopy & biopsy. managementDiverticulosis ‘d be managed with a high residue diet. antispasmodics. Diverticulitis: Bed rest & i.v. antibiotics.

Surgical M.

Indications: general peritonitis & failure to resolve on conservative treatment.

Ulcerative colitis

Aetiology: real cause is unknown. 15% have first degree relative with IBD. UC is more common in Cauc. Than blacks or Asians. Relapse of colitis has been associated with bacterial dysenteries. Smoking seems to have a protective effects. Stress. UC is thought to be an immune disorder.

epidemiology

Higher in people of Jewish origin. 10-15% new cases per 100 000 population a year in the UK. Prevalence is 160 per 100 000 population. It has been rare in eastern population. The sex ratio is equal in the first four decades of life. It is uncommon before the age of 10 years & most patients are between the ages of 20 & 40 years at diagnosis.

pathology

In 95% of cases, the disease starts in the rectum & spreads proximally. It is a diffuse inflammatory disease. It is primarily affects the mucosa & submucosa. Multiple minute ulcers. Pseudopolyps in 20% of cases. Toxic megacolon. Crypt abscesses. Depletion of goblet cell mucin. Severe dysplasia or carcinoma in situ.

Clinical features

In most cases the disease is chronic & characterised by remissions & relapses. Watery or bloody diarrhea. Proctitis : tenesmus & urgency. 10-15% spread to involve the rest of the colon. Colitis: diarrhea, systemic upset ,weight loss, extra-alimentary manifestations & cancer. Anemia & hypoproteinemia are common. Disease severity: mild moderate severe

Complications of UC

Toxic dilatation. Perforation. Hemorrhage. Cancer. Extra-alimentary manifestations: skin lesions, eye problems, liver disease.

investigations

Plain abdominal film. Barium enema. Sigmoidoscopy. Colonoscopy & biopsy.

Treatment.

Medical treatment: local or systemic corticosteroids. Topical & systemic 5-ASA derivatives to maintain remission Azathioprine or cyclosporine also used to induce remission Indications for surgery: Severe disease failing to respond to medical therapy. Chronic disease with anemia, frequent stool, urgency & tenesmus. Steroid dependent disease. Risk of neoplasia. Extraintestinal manifestations. Severe hemorrhage or stenosis causing obstruction.

operations

The first aid procedure is a total abdominal colectomy & ileostomy. Proctocolectomy & ileostomy. Restorative proctocolectomy with an ileoanal pouch. Colectomy & ileorectal anastomosis.

Crohn’s disease it can affect any part of the GIT from the lips to the anal margin, but ileocolonic disease is the most common presentation. Epidemiology: it is most common in North America & northern Europe. Incidence 5 per 100 000. Prevalence rates 56 per 100 000 in the UK. It is slightly more common in women than men. It is commonly diagnosed in young patients between the ages of 25 & 40 years. A second peak of incidence around the age of 70 years.

Aetiology

Focal ischemia originating from vasculitis. Smoking increases the risk threefold. Genetic factors. There is an association with ankylosing spondylitis. CD can predispose to cancer. Pathology: Ileal disease is the most common (60%). Large intestine (30%) Anal lesions are common. Strictures.

Deep mucosal ulceration & oedema between ulcers (cobblestone appearance). Transmural inflammation. The condition discontinuous (skip lesions). Discrete aphthous ulcer. Focal areas of chronic inflammation involving all layers of the intestinal wall. Non-caseating giant cell granuloma.

Clinical features

Acute CD: occur in only 5% of cases. symptoms & signs are those of acute appendicitis, but usually diarrhea preceding the attack. Free perforation may lead to local or diffuse peritonitis. Acute colitis less common than in UC. Chronic CD: mild diarrhea over many months accompanied by intestinal colic. Pain in the right iliac fossa & a tender mass may be palpable Fever, anaemia & weight loss are common. Perianal abscess or fissure. Obstructive symptoms. Children may have retarded growth.


Adhesions , intra-abdominal abscesses & fistulae . Anal disease: Painless superficial ulcers. Secondary abscesses & perianal fistulae.

Investigation

Full blood count to exclude anaemia. Fall in albumin, magnesium, zinc & selenium. Elevated C-reactive protein. Endoscopy: sigmoidoscopy & colonoscopy. Imaging: barium enema small bowel enema (string sign of Kantor). CT scan: fistulae, intra-abdominal abscesses. MRI : assessing perianal disease.

treatment

Medical therapy: Steroids inducing remission. Antibiotics, like metronidazole especially in perianal disease. Azathioprine is used for its additive & steroid sparing effect. Ciclosporin use is associated with 80% remission. Monoclonal antibody: infliximab used in patients with active disease who are refractory to conventional treatment. Nutritional support: it has been shown that parenteral nutrition can induce remission in up to 80% of patients.

Indications for surgery

Surgery focused on the complications of the disease. complications Recurrent intestinal obstruction. Bleeding. Perforation. Failure of medical therapy. Intestinal fistula. Fulminant colitis. Malignant change. Perianal disease.

surgery

The main aim is to preserve functional gut length & maintain gut function. Resection is kept to a minimum. Ileocaecal resection. Segmental resection as in stricture. Colectomy & ileorectal anastomosis. Emergency colectomy. Temporary loop ileostomy. Proctocolectomy. Strictureplasty.


Tumours of the small intestine
Adenomas Submucous lipomas Benign GI stromal tumours Complications: intuss. intestinal bleeding. Peutz-Jeghers syndrome: Autosomal domin disease consists of : intestinal hamartomatosis is a polyposis affecting the whole small bowel & colon. melanosis of the oral mucous membrane & the lips. Complication: recurrent bowel ca.& wide range of cancers so it is necessary to keep these patients under surveillance by endoscopy.


Histology: the polyps can be likened to trees.Treatment: resection is necessary for serious bleeding or intuss. Large single polyps can be removed by enterotomy.Malignant:Lymphoma: western type lymphoma(non-hodgkin’ s B- cell) primary lymphoma associated with coeliac dis. mediterranean lymphoma. these conditions are usually treated with chemotherapy.Carcinoma can present with obstruction, bleeding or diarrhea. Complete resection offers the only hope of cure.

Carcinoid tumour: occur throughout the GIT most commonly in the appendix, ileum & rectum. They arise from neuroendocrine cells at the base of intestinal crypts. The tumours can produce a number of vasoactive peptides ,most commonly 5-HT (serotonin). The clinical syndrome itself consists of reddish-blue cyanosis, flushing attacks (induced by alcohol), diarrhea, asthmatic attacks & sometimes pulmonary & tricuspid stenosis. Treatment: surgical resection is usually sufficient. octreotide reduces flushing & diarrhea. multiple enucleations of hepatic metastases or partial hepatectomy.

GI stromal tumours

They can be benign or malignant. GIST is a type of sarcoma that develops from connective tissue cells. It is found most commonly in the stomach but can be found in other sites of the gut. It occurs most commonly in the 50-70 year age group. Symptoms: asymptomatic, lethargy, pain, nausea, haematemesis or melaena. Treatment: Glivec is effective in advanced cases. Surgery.

Tumours of the large intestine

Benign: adenomatous polyps- tubular adenoma (size) villous adenoma inflammatory polyps metaplastic polyps hamartomatous: peutz-jeghers. juvenile. FAP is defined by the presence of more than 100 colorectal adenomas. Over 80% of cases have a positive family history. 20% arise as a result of mutations in the APC gene on the short arm of ch. 5. The large bowel is mainly affected. The main risk is large bowel cancer. It is inherited as Mendelian dominant condition


FAP can be associated with benign mesodermal tumours such as desmoid tumours & osteomas. Surgery is the only means of preventing colonic cancer. Hereditary non-polyposis colorectal cancer: this syndrome is characterised by increased risk of colorectal cancer & ca of the endometrium, ovary, stomach & small intestines. it is an autosomal dominant condition. the lifetime risk of developing colorectal cancer is 80%. most cancers develop in the proximal colon.


Malignant: adenocarcinoma of the colon Risk factors: age: more than 90% of cases occur in people older than age of 50 years. hereditary:20% have a known family history. mutations in tumour suppressor genes APC, P53. environment & dietary factor: the incidence rises with diet high in animal fat & low in fibers; alcohol; obesity & sedentary lifestyle. IBD. Others: smoking; ureterosigmoidostomy;

Pathology

Microscopically the neoplasm is a columnar cell cancer. Macroscopically annular-obstructive symptoms. tubular ulcer- bleeding cauliflower- the least malignant. Adenoma-carcinoma sequence. Tumours are more common in the left colon & rectum-60% Of colorectal tumours.

Spread

It is slow growing neoplasm. Local spread: into the bladder- colovesical fistula. local perforation & abscess external faecal fistula. Lymphatic spread. Bloodstream spread: it accounts for a large proportion(30-40%) of late deaths.

Staging

Staging colon cancer is done by - Duke’s classification.- TNM classification.

Clinical features

Ca colon usually occurs in patients over 50 years of age.20% of patients present with I.O. or peritonitis.Complete investigation of the colon is required in any case of colonic bleeding in patients over the age of 40.Careful family history ‘d be taken.Ca of the left side of the colon. The main symptoms are those of increasing I.O. Pain rectal bleeding alteration of bowel habit tenesmus obstruction

ca of the caecum & ascending colon. anaemia abdominal mass intussusception. Metastatic disease: hepatomegaly ,ascites ,jaundice & metastases to the lung, bone, skin & brain.

Investigations

FOBT.Flexible sigmoidoscopyColonoscopy & biopsy. Picking up the primary synchronous polyp multiple ca.Radiology : double contrast barium enema “apple core appearance” US scan screening for liver metastases CT for large palpable abdominal masses determine local invasion used in assessment of rectal Ca



treatment
Preoperative preparation- purgation of the colon dietary restriction to fluids stoma site discussion antiembolus stockings. subcutaneous heparin i.v. antibiotics Test of operability presence of liver metas is not C.I. to resection. peritoneum. lymph node groups. mobility & operability.

operations

More than 95% of colon ca can be resected. Operations are designed to remove the primary tumour & its draining loco regional L.N. When the growth is inoperable: colostomy or bypass using ileocolic anastomosis. Hepatic metastases: hepatic resection. cytotoxic drugs. ablative treatments.

The Rectum

Surgical anatomy- It is approximately 12-18cm in length. - It begins where the taenia coli of the sigmoid colon join to form a continuous outer longitudinal layer at the level of the sacral promontry. - It is divided into three equal parts: the upper third is mobile & has a peritoneal coat. The middle third where the peritoneum covers only the anterior & part of the lateral surfaces. The lower third lies deep in the pelvis surrounded by fatty mesorectum & has important relations to fascial layers. - the lower third is separated by a fascial condensation-Denonvilliers’ fascia- from the prostate/vagina in front, & behind by Waldeyer’s fascia – from the coccyx & lower two sacral vertebrae.

The blood supply consists of inferior, middle & superior rectal vessels. The lymphatic drainage is upwards along the superior rectal vessels to the para-aortic nodes. Clinical features of rectal disease bleeding per rectum altered bowel habit mucus discharge tenesmus prolapse


Injuries: to the rectum are serious & invariably require surgery. A temporary colostomy is often necessary. Broad spectrum antibiotics are mandatory. Bladder or urethral injury may occur. Prolapse: it may be mucosal or full thickness. in children, the prolapse is usually mucosal & should be treated conservatively. in the adult, the prolapse is often full thickness & is frequently assoc. with incontin. Surgery is required for full thick. rectal prolap

Benign tumours

The rectum & sigmoid colon are the most frequent site of polyps(& cancers) in the GIT. No rectal polyp should be removed until the possibility of a proximal carcinoma has been ruled out. Polyps are either single or multiple. Adenomas are the most frequent histological type. Juvenile polyp is found in infants &children it can cause bleeding or pain. Villous adenomas have an enhanced tendency to become malignant.

Carcinomas

Colorectal ca arises from adenomas (the adenoma-ca seq) Spread: local- occurs circumferentially. Anter.,the prostate seminal vesicles or bladder in the male. In the female, the vagina or the uterus. Laterally the ureter, posteriorly the sacrum & the sacral plexus. lymphatic spread above the peritonel reflection occ. almost exclusively in an upward direction. venous spread. Liver, lungs & adrenals peritoneal dissemination.

Staging

Dukes’ staging A the growth is limited to the rectal wall. B the growth is extended to the extrarec. tissue. C there are secondary deposits in the reg lymph nodes. D distant (usually hepatic ) metastases.TNM stagingTumours are adenocarcinomas & are well, moderately or poorly differentiated.

Clinical features

Bleeding per rectum Tenesmus Early morning diarrhea Pain is a late symptom Weight loss is suggestive of hepatic metastases. Investigation Abdominal exam.is normal in early cases ; signs of large bowel obstruction; palpable liver; ascites. Rectal examination. Proctosigmoidoscopy & biopsy. Colonoscopy.

Differential diagnosis

Inflammatory stricture Amoebic granuloma Endometrioma Carcinoid tumor. Treatment Assess the fitness of the patient for operation. Assess the extent of spread of the tumor by CT of the chest & abdomen &MRI in local staging.

Radical excision of the rectum, together with the mesorectum & associated lymph nodes, should be the aim.Preoperative preparationCombined(abdominal & perineal) excision of the rectumAnterior resectionHartmann’s operation

Palliative colostomy Nd:YAG laser Intraluminal stents Preoperative radiotherapy can reduce local recurrence Adjuvant chemotherapy can improve survival in node positive disease.