Acute small bowel ischaemia
causes
1- An embolus from the heart or aorta to the superior mesenteric artery (40-50%) of cases
2- thrombosis of underlying atheromatous disease for approximately 25%
3- non-occlusive ischaemia due to hypotension complicating myocardial infarction, heart failure, arrhythmias or sudden blood loss (25%).
4- Vasculitis or venous occlusion is a rare cause.
pathophysiology
The pathological spectrum ranges from transient alteration of bowel function to transmural haemorrhagic necrosis and gangrene.
Clinical features
() Patients usually have evidence of cardiac disease and arrhythmia.
() Almost all develop abdominal pain
() In the early stages the physical signs may be a silent, later on distended abdomen or diminished bowel sounds, peritonitis.
management
() Leucocytosis, metabolic acidosis, hyperphosphataemia and hyperamylasaemia are typical.
() Plain abdominal X-rays show thumb-printing due to mucosal oedema.
()Mesenteric or CT angiography reveals an occluded or narrowed major artery with spasm of arterial arcades,
() Resuscitation, management of cardiac disease and intravenous antibiotic therapy, followed by laparotomy, are key steps.
()In patients at high surgical risk thrombolysis may sometimes be effective.
() Survivors often have nutritional failure from short bowel syndrome and require intensive nutritional support, sometimes including home parenteral nutrition, as well as anticoagulation.
() Small bowel transplantation is promising in selected patients.
Acute colonic ischaemia
() The splenic flexure and descending colon have little collateral circulation and lie in watershed areas of arterial supply.
() The spectrum of injury ranges from reversible transient colitis, colonic stricture, gangrene and fulminant pancolitis. () Arterial thromboembolism is usually responsible but colonic ischaemia can also follow severe hypotension, colonic volvulus, strangulated hernia, systemic vasculitis or hypercoagulable states.
() The patient is usually elderly and presents with sudden onset of cramping left-sided lower abdominal pain and rectal bleeding.
() Symptoms usually resolve spontaneously over 24-48 hours and healing occurs within 2 weeks.
() complicated by: a residual fibrous stricture or segment of colitis. A minority develop gangrene and peritonitis.
() The diagnosis is established by colonoscopy within 48 hours of presentation; otherwise, mucosal ulceration and oedema may have resolved.
() Resection is required for peritonitis
Chronic mesenteric ischaemia
This results from atherosclerotic stenosis affecting at least two of the coeliac axis, superior mesenteric and inferior mesenteric arteries.
Dull , severe mid- or upper abdominal pain develops about 30 minutes after eating. Patients lose weight because of reluctance to eat, and some experience diarrhoea.
Physical examination invariably shows evidence of generalised arterial disease.
Mesenteric angiography & Vascular reconstruction or percutaneous angioplasty is sometimes possible.
Colonic polyps
() neoplastic or non-neoplastic.
() single or multiple
() vary from a few millimetres to several centimetres in size.
Colorectal adenoma
()Theses include hamartomas, metaplastic ( hyperplastic ) polyps and inflammatory polyps.
()These have no malignant potential
() the prevalence rises with age; 50% of people over 60 years of age have adenomas, and in half of these the polyps are multiple.
() They are more common in the rectum and distal colon and are either pedunculated or sessile.
() Histologically, they are classified as either tubular, villous or tubulovillous, according to the glandular architecture.
() Villous adenomas sometimes secrete large amounts of mucus, causing diarrhoea and hypokalaemia.
() Risk factors for malignant change in colonic polyps:
Large size (> 2 cm)
Villous architecture
Multiple polyps
Dysplasia
() Colonoscopic polypectomy should be carried as this considerably reduces subsequent colorectal cancer risk.
() Very large or sessile polyps can sometimes be removed safely by endoscopic mucosal resection (EMR) but will otherwise require surgery.
() Once all polyps have been removed, patients should undergo surveillance colonoscopy at 3-5-year intervals, as new polyps develop in 50% of patients.
Familial adenomatous polyposis (FAP)
()uncommon autosomal dominant disorder affecting 1 in 13 000 of the population and accounting for 1% of all colorectal cancer.
() Around 20% of cases arise as new mutations and have no family history.
()Hundreds to thousands of adenomatous colonic polyps will develop in 80% of patients by age 15
() In those affected, cancer will develop within 10-15 years of the appearance of adenomas and 90% of patients will develop colorectal cancer by the age of 50 years.
Extraintestinal features of familial adenomatous polyposis
Congenital hypertrophy of the retinal pigment epithelium (CHRPE, 70-80%)
Epidermoid cysts (extremities, face, scalp) (50%)
Benign osteomas, especially skull and angle of mandible* (50-90%)
Dental abnormalities (15-25%)*
Desmoid tumours (10-15%)
Other malignancies (brain, thyroid, liver, 1-3%)
() In newly diagnosed cases with new mutations, genetic testing confirms the diagnosis, and all first-degree relatives should also undergo testing .
() In families with known FAP, at-risk family members should undergo direct mutation testing at 13-14 years of age. This is less invasive than regular sigmoidoscopy, which is reserved for those known to have the mutation.
() Affected individuals should undergo colectomy after school or college education has been completed.
() The operation of choice is total proctocolectomy with ileal pouch-anal anastomosis.
() Periodic upper gastrointestinal endoscopy is recommended to detect duodenal adenomas.
Colorectal cancer
() Although relatively rare in the developing world, colorectal cancer is the second most common internal malignancy and the second leading cause of cancer deaths in Western countries.
() The condition becomes increasingly common over the age of 50
Dietary risk factors for colorectal cancer development
()Increased risk
Red meat
Saturated animal fat:
()Decreased risk
Dietary fiber
Fruit and vegetables
Calcium
Folic acid
Omega-3 fatty acids
Non-dietary risk factors in colorectal cancer
1- Colorectal adenomas
2-Long-standing extensive ulcerative colitis or Crohn s colitis especially if associated with primary sclerosing cholangitis (PSC)
3-Ureterosigmoidostomy
4-Acromegaly
5-Pelvic radiotherapy
6- Obesity and sedentary lifestyle.
7- Smoking (relative risk 1.5-3.0)
8- Alcohol (weak association)
9- Cholecystectomy
10- Type 2 diabetes (hyperinsulinaemia)
11- Use of aspirin or NSAIDs (COX-2 inhibition) and perhaps statins associated with reduced risk
Clinical features
() In tumours of the left colon,
fresh rectal bleeding is common and obstruction occurs early.
() Tumours of the right colon present with anaemia from occult bleeding or with altered bowel habit, but obstruction is a late feature.
() Colicky lower abdominal pain is present in two-thirds of patients and rectal bleeding occurs in 50%.
() A minority present with features of either obstruction or perforation, leading to peritonitis, localised abscess or fistula formation.
() Carcinoma of the rectum usually causes early bleeding, mucus discharge or a feeling of incomplete emptying.
() Between 10 and 20% of patients present with iron deficiency anaemia or weight loss.
()On examination there may be a palpable mass, signs of anaemia or hepatomegaly from metastases. Low rectal tumours may be palpable on digital examination.
Investigations
() Colonoscopy : is the investigation of choice, lesions can be biopsied and polyps removed.
() CT colonography ( virtual colonoscopy ) is a sensitive non-invasive technique for diagnosing tumours and polyps greater than 1 cm that can be used if colonoscopy is incomplete or high-risk.
() CT is valuable for detecting hepatic metastases.
() A proportion of patients have raised serum carcinoembryonic antigen (CEA) concentrations but this is variable and so of little use in diagnosis. Measurements of CEA are valuable, however, during follow-up and can help to detect early recurrence.
Management
1- Surgery
The tumour is removed, along with adequate resection margins and pericolic lymph nodes.
Carcinomas within 2 cm of the anal verge may require abdominoperineal resection and formation of a colostomy.
Total mesorectal excision (TME) reduces recurrence rates and increases survival in rectal cancer.
Post-operatively, patients should undergo colonoscopy after 6-12 months and periodically thereafter to search for local recurrence or development of new metachronous lesions, which occur in 6% of cases.
Adjuvant therapy
Two-thirds of patients have lymph node or
distant spread (Dukes stage C) at presentation
, therefore, beyond cure with surgery alone.
Most recurrences are within 3 years of diagnosis.
Adjuvant chemotherapy with 5-fluorouracil and folinic acid (to reduce toxicity) for 6 months improves both disease-free and overall survival in patients with Dukes C colon cancer by around 4-13%.
Pre-operative radiotherapy can be given to patients with large, fixed rectal cancers to down-stage the tumour, making it resectable and reducing local recurrence.
In some countries, patients with metastatic disease are treated with monoclonal antibodies using bevacizumab or cetuximab either alone or with chemotherapeutic agents such as irinotecan.
Endoscopic laser therapy or insertion of an expandable metal stent can be used to relieve obstruction.
Prevention and screening
1- Widespread screening by regular faecal occult blood (FOB) testing reduces colorectal cancer mortality and increases the proportion of early cancers detected. FOB screening is recommended after the age of 50 years.
2- Colonoscopy remains the gold standard but is expensive and carries risks; many countries lack the resources to offer this form of screening.
3- Flexible sigmoidoscopy is an alternative option and has been shown to reduce overall colorectal cancer mortality by approximately 35%.
4- Screening for high-risk patients by molecular genetic analysis is an exciting prospect but is not yet available.
Diverticulosis
() Diverticula are acquired and are most common in the sigmoid and descending colon of middle-aged people.
() Asymptomatic diverticula (diverticulosis) are present in over 50% of people above the age of 70. Symptomatic diverticular disease supervenes in 10-25% of cases while complicated diverticulosis (acute diverticulitis, pericolic abscess, bleeding, perforation or stricture) is uncommon.
The colonic wall is weak between the taeniae.
The blood vessels that supply the colon pierce the circular muscle and weaken it further by forming tunnels.
Diverticula usually emerge through these points of least resistance.
Clinical features
Colicky pain is usually suprapubic or felt in the left iliac fossa. The sigmoid colon may be palpable and, in attacks of diverticulitis, there is local tenderness, guarding, rigidity ( left-sided appendicitis ) and sometimes a palpable mass.
During these episodes there may also be diarrhoea, rectal bleeding or fever.
Diverticular disease is complicated by perforation, pericolic abscess, fistula formation (usually colovesical) and acute rectal bleeding.
Management
Diverticulosis which is asymptomatic and discovered coincidentally requires no treatment.
Constipation can be relieved by a high-fibre diet with or without a bulking laxative (ispaghula husk, 1-2 sachets daily) taken with plenty of fluids.
Stimulants should be avoided.
Antispasmodics may sometimes help.
An acute attack of diverticulitis requires 7 days of metronidazole (400 mg 8-hourly orally), along with either a cephalosporin or ampicillin (500 mg 6-hourly orally). Severe cases require intravenous fluids, intravenous antibiotics, analgesia and nasogastric suction.
emergency surgery is reserved for severe haemorrhage or perforation.