Even though 80% total length and 90% of mucosal surface area of the GIT is small bowel, small bowel tumours are rare
Reasons why malignancy is uncommon in the small bowel
Rapid transit time, 30 minute to 2 hours
Alkaline mucus rich luminal content is protective
Cells of small bowel produce the enzyme benzopyrene hydroxylase which detoxifies the carcinogen—benzopyrone
High levels luminal IgA provides immunity
Plenty of lymphoid tissue in the wall provides immunity
Healthy small bowel has got less bacterial load and so their toxic metabolites (as compared to colon)
Risk factors for small bowel tumours
Bile acids and their metabolites
Post-cholecystectomy status
Familial adenomatous polyposis (FAP) especially with duodenal adenomas
Crohn's disease
Chronic immunosuppression
Von Recklinghausen's disease of neurofibromatosis
Smoking, red meat, alcohol, salt food
Presentations of small bowel tumours
Asymptomatic initially
Features of obstruction/intussusception/bleeding
Vague abdominal discomfort
Investigations for small bowel tumours
Small bowel enteroclysis
CT abdomen
CT enteroclysis
Video capsule endoscopy
CT angiography
Enteroscopes (push type or Sonde pull enteroscopes)
Intraoperative enteroscopes
Benign tumours of small bowel
Leiomyoma or GIST
Adenomas
Lipoma
Peutz-Jegher's Syndrome
Haemangioma
Malignant tumours of small bowel
Adenocarcinoma
Non-Hodgkin's lymphoma (NHL)
Carcinoid tumour
GIST
Liposarcoma and myxoliposarcoma
Adenocarcinoma
Most common primary malignant small bowel tumour, 40% of small bowel tumours
Adenocarcinoma
80% cases in the duodenum and jejunum
In Crohn's disease, occurs in younger age group and commonly in ileum (70%)
Nonspecific features, anorexia, crampy pain abdomen, bleeding and diarrhoea, obstruction or features of metastases (liver)
CT scan, capsule endoscopy are the investigations
RT and chemotherapy are less beneficial
It carries a poor prognosis
Non-Hodgkin's lymphoma (NHL)
25% of small bowel tumours, GI is the commonest extranodal site of NHL (20%), with small bowel (primary intestinal NHL) as second common site (30%) for extranodal site of NHL
Non-Hodgkin's lymphoma (NHL)
Lymphadenopathy/mediastinal lymph node enlargement are absent, Normal spleen, liver, blood peripheral smear are observed
B cell type is the commonest type 75%, common in ileum
Presentations are malabsorption, obstruction, perforation, haemorrhage or palpable mass
In children lymphomas are the most common intestinal neoplasm
25% of patients develop perforation
Fever when present suggests systemic spread
CT scan with CT guided biopsy or laparoscopic biopsy is needed
Surgical resection and chemotherapy are the treatment
Prognosis is poor
Carcinoid tumour
30% of small bowel tumours, commonly occurs in appendix (45%), ileum (25%) and rectum (15%), 10% of cases are associated with MEN syndrome type I
Carcinoid tumour
Most often asymptomatic—an incidental finding
May present with abdominal pain, features of intestinal obstruction, diarrhoea
Hindgut carcinoids present with constipation, bleeding per rectum, rectal tenesmus
Once secondaries develop in the liver Carcinoid syndrome develops
Surgical treatment for carcinoid tumours
Appendix: Tip/lesion less than 2 cm but not involving base—appendicectomy, Lesion more than 2 cm/involving base right hemicolectomy
Small bowel lesion: Less than 1 cm—segmental resection, More than 1 cm—radical resection with adjacent mesentery, Terminal ileum—right hemicolectomy
Rectal lesion: Less than 1 cm—endoscopic resection, 1 cm invasive—wide excision, More than 1 cm—anterior resection
GIST (gastrointestinal stomal tumour)
Rare but most common nonepithelial small bowel tumours, 25% of GIST occurs in small bowel
GIST
Palpable mass, compression, haemorrhage are the features, has less affinity for lymphatics
CT is diagnostic, Histochemistry and tumour markers are needed
Surgical wide resection is the treatment
Other malignant tumours of small bowel
Liposarcoma and myxoliposarcoma
Secondaries in small bowel (very rare, if present, primary being commonly melanoma)
Autosomal dominant disease, common in small intestine (jejunum) but can also occur in large intestine, features are multiple, familial, hamartomatous intestinal polyps, associated with melanosis of the oral mucosa, lips
Adenoma of colon
Can be solitary or multiple, sessile or pedunculated, Tubular is commonly 1-2 mm sized and sessile is 3-4 mm sized, It has malignant potential
Factors increasing malignant potential of adenoma
Size (>2 cm—30-50% chances of developing carcinoma, 1-2 cm —10% chances of carcinoma, < 1 cm —1-5% chances of carcinoma)
Sessile nature
Villous architecture
Dysplasia
Grading of adenoma
Minimal hyperplasia, no cellular atypia
Mild hyperplasia, cellular atypia
Moderate hyperplasia, cellular atypia
Severe hyperplasia, cellular atypia
Carcinoma in situ
Features of adenoma
Can be asymptomatic
Bleeding per anus is usually chronic but rarely can be acute
Colonoscopy—biopsy is a must, Size should be noted, Texture—harder tumour more likely to be malignant, Colour of the lesion—pale is benign, pink, red and active—could be carcinoma, Ulceration on the surface if it has turned into malignancy
Treatment for adenoma
Colonoscopic polypectomy using snare, Any adenoma more than 5 mm in size should be removed colonoscopically
Diathermy excision/coagulation with sigmoidoscope
Per-anal polypectomy
Per-anal excision with clear margin of the rectal sessile adenoma
Open-abdominal colotomy and polypectomy in case of huge adenoma
Segmental resection of the colon if polyps/adenomas are limited to one segment of the colon confirmed by Colonoscopy
Total colectomy/proctocolectomy if multiple polyps present all over colorectum and if associated with FAP
Bloodtransfusions, correction of electrolytes, protein supplements
Problems in therapeutic colonoscopy
Perforation due to necrosis
Haemorrhage—secondary
Intracolonic explosions
Sepsis
Familial adenomatous polyposis (FAP)
Inherited disorder autosomal dominant (AD) characterized by cancer of the large intestine (colon) and rectum, People with the classic type may begin to develop multiple noncancerous (benign) growths (polyps) in the colon as early as their teenage years
Familial adenomatous polyposis (FAP)
Male >female
If left untreated, carcinoma develops in 100% of affected patients by the fifth decade
Gardner syndrome: desmoid tumour in the abdomen, osteomas (75%) and epidermoid cysts
Turcot"s syndrome [FAP + brain tumour (medulloblastoma or gliomas)]
Surgical treatment for colon polyps/adenomas
1. Limited to one segment of the colon - Partial colectomy
2. Multiple polyps present all over colorectum and associated with FAP - Total colectomy/proctocolectomy
Supportive treatment for colon polyps/adenomas
Blood transfusions
Correction of electrolytes
Protein supplements
Problems in therapeutic colonoscopy
Perforation due to necrosis
Haemorrhage—secondary
Intracolonic explosions
Sepsis
Familial adenomatous polyposis (FAP)
Inherited disorder autosomal dominant (AD) characterized by cancer of the large intestine (colon) and rectum
People with the classic type of familial adenomatous polyposis may begin to develop multiple noncancerous (benign) growths (polyps) in the colon as early as their teenage years
Male > female in FAP
If left untreated, carcinoma develops in 100% of affected FAP patients by the fifth decade
Gardner syndrome
Desmoid tumour in the abdomen, osteomas (75%) and epidermoid cysts
Turcot's syndrome
FAP + brain tumour (medulloblastoma or gliomas) or sarcoma of bone