Growths of colon

A PRESENTATION FROM DEPARTMENT OF SURGERY, RGKMC

EDITED BY PRITHWIRAJ MAITI FINAL YEAR MBBS

R.G.KAR MEDICAL COLLEGE

Tumours of colon

• Polyp/ tumour/ swelling arises from mucosal surface with a stalk/ pedicle- a mass projecting into the bowel lumen beyond the surface epithelium.

Classification • Inflammatory -

– Ulcerative colitis

– Segmental colitis

– Dysenteric colitis

– Crohn’s disease

– Diverticulitis

• Metaplastic - Hyperplastic polyps

• Harmartomatous -

• Peutz–Jeghers polyp

• Juvenile polyp

• Cronkhite-Canada syndrome

• Neoplastic -

– Adenoma

• Tubular

• Tubulovillous

• Villous

– Adenocarcinoma

– Carcinoid tumour

• Others -

– Lipoma

– Haemangioma

– Leiomyoma

• Metaplastic polyp- Not premalignant

• Hamartomatous polyp

– Peutz-Jegher’s polyp-

• Autosomal dominant, familial

• Multiple

• Premalignant

• Melanosis of oral mucosa, lips, and digits

– Juvenile polyp-

• Commonest in infant and children

• Cause intussusception, prolapse, bleeding PR

• Colonoscopic polypectomy

• Not premalignant

Colonic Adenoma

• Neoplastic – Adenoma

• Tubular-70% • Tubulovillous-25% • Villous-5%

– Solitary/ multiple – Sessile/ pedunculated – Premalignant

• Size • Sessile • Villous • Dysplasia

Clinical features

• Asymptomatic

• Anaemia

• Bleeding P/R

• Prolapse

• Diarrhoea, spurious diarrhoea

• Colicky abdominal pain

• Tenesmus

Investigation and treatment

Investigations:

• Hb

• Serum electrolyte

• Colonoscopy-

– Size

– Texture

– Colour

– ulceration

Treatment:

• Colonoscopic polypectomy

• Per anal polypectomy

• Resection anastomosis

• Total polypectomy if FAP

Familial adenomatous polyposis (FAP) • Autosomal dominant.

• Younger age group- 15-20 years.

• 80 % with a positive family

history. The remainder arise as a

result of new mutations in the

adenomatous polyposis coli (APC)

gene.

• This has been identified on the

short arm of chromosome 5.

• Clinical features-

• Pain abdomen,

• Loose stool with blood and

mucous,

• Weight loss.

Extracolonic manifestations of FAP

• Endodermal derivatives:

– Adenomas and carcinomas of the duodenum, stomach, small intestine, thyroid and biliary tree.

– Fundic gland polyps.

– Hepatoblastoma.

• Ectodermal derivatives:

– Epidermoid cysts.

– Pilomatrixoma.

– Congenital hypertrophy of the retinal pigment epithelium (CHRPE).

– Brain tumours.

• Mesodermal derivatives:

– Desmoid tumours.

– Osteomas.

– Dental problems.

SPECIAL NOTE

FAP + Benign mesodermal tumours (such as desmoid tumours)+ Osteomas+ Epidermoid cysts can also occur= Gardner’s syndrome.

• FAP+ Brain tumor= Turcot’s syndrome.

Investigations and treatment

Investigations:

– Double contrast barium enema

– Colonoscopy

Treatment:

– Proctocolectomy with ileo-anal anastomosis

Screening policy

• At-risk family members are offered – Genetic testing in early teens.

– Should be examined at the age of 10–12 years, repeated every year.

• Who are going to get polyps will have them at 20 years, require operation.

• If there are no polyps at 20 years, 5 yearly colonoscopy upto 50 years.

• If still no polyps, there is probably no inherited gene.

• Carcinomatous change may exceptionally occur before the age of 20 years

Hereditary non-polyposis colorectal cancer

(HNPCC: Lynch syndrome)

• Increased risk of colorectal cancer and also cancers of the endometrium, ovary, stomach and small intestines.

• Autosomal dominant condition.

• Cause-a mutation in one of the DNA mismatch repair genes. ( MLH1 and MSH2).

• The lifetime risk of developing colorectal cancer 80%.

• Mean age of diagnosis is 45 years.

• Most cancers develop in the proximal colon.

• Females with HNPCC have a 30–50% lifetime risk of developing endometrial cancer.

COLORECTAL CARCINOMA (CRC)

• One of the most common cancers in the world.

• US: 4th most common cancer (after lung, prostate, and breast cancers).

2nd most common cause of cancer death (after lung cancer).

• 2001 130,000 new cases of CRC 56,500 deaths caused by CRC

AETIOLOGY

Older age, Male gender, High intake of fat, alcohol, red meat; Obesity, Sedentary life style, Smoking, Inflammatory bowel disease, HNPCC, FAP, Family history of colorectal cancer.

Development of CRC

• Result of interplay between environmental and

genetic factors.

• Central environmental factors.

• Diet and lifestyle.

• 35% of all cancers are attributable to diet.

• 50%-75% of CRC in the US may be preventable through dietary modifications.

Colon cancers result from a series of pathologic changes that transform normal colonic epithelium into invasive carcinoma. Specific genetic events, shown by vertical arrows, accompany this multistep process. The various chemopreventive agents exert their effects at different steps in this pathway, and this is depicted on the basis of the available epidemiologic evidence.

Types of colon CA

• Synchrous- Multiple primary ca in different parts of colon at the same time.

• Metachronus- Growth in different parts of colon in different time.

• Gross type- – Annular (left side)

– Tubular (left side)

– Ulcerative (right side)

– Cauliflower type (right side).

Histology (WHO)

• Adencarcinoma- 90%

• Mucinous adenocarcinoma- 5-10%

• Signet ring cell carcinoma

• Small cell carcinoma

• Squamous cell carcinoma

• Undifferentiated carcinoma

Spread

Liver

(40% via

portal vein;

Hard

umbilicated)

Lung

Brain

Bones

Via blood

Lymph nodes

(Pericolic,

Epicolic

Intermediate

Principal)

Abdominal wall

Nerves

Vessels

Ureter, Bladder

Via lymphatics Direct

Staging of CRC

A Mucosa

B invade Into (B1)/ through (B2) Muscularis propria

C1 B1 + LN Involvement

C2 B2 + LN Involvement

D Distant metastatic spread

Dukes staging system

TNM system

Primary tumor (T)

Regional lymph nodes (N)

Distant metastasis (M)

Staging of CRC

TNM classification for colonic cancer

T-Tumour stage T1: Into submucosa T2: Into muscularis propria T3: Into pericolic fat or sub-serosa but not breaching serosa T4: Breaches serosa or directly involving another organ

N- Nodal stage N0: No nodes involved N1: 1–3 nodes involved N2: ≥4 nodes involved

M- Metastases M0: No metastases M1: Metastases

Typical sites and incidence of colon cancer

Clinical feature

• After 50 years • M:F- 3:2

• Weight loss

• Loss of appetite

• Night sweats, Fever

• Abdominal pain & mass

• Acute intestinal obstruction- 20%

• Rt sided growth- anaemia, palpable mass in RIF.

• LT sided growth- colicky pain, rectal bleeding, change in bowel habits, sub acute obstruction.

Typical sites and incidence of colon cancer

Investigation

• BARIUM ENEMA

• COLONOSCOPY AND BIOPSY

• VIRTUAL COLONOSCOPY

• USG W/A

• CEA

• Hb, PCV, ESR, FOBT

• CT

• LFT

• The barium enema of

colon-

• In this case, the

classic "apple core”

lesion is present,

representing an

encircling

adenocarcinoma that

constricts the lumen.

Therapy

Surgical resection the only curative treatment.

Likelihood of cure is greater when disease is

detected at early stage.

Early detection and screening is of pivotal

Importance.

SURGERY

• Rt sided early growth-

• Rt radical hemicolectomy-

– Terminal 6 cm of ileum

– Caecum

– Appendix

– Ascending colon

– 1/3rd of transverse colon

– Lymph node

• Transverse colon growth

• Extended Rt hemicolectomy- Rt. hemicolectomy+ transverse colon

• Lt sided growth- Left hemicolectomy

• Sigmoid growth- Sigmoidectomy

• Elective setting-prepared colon

• Emergency setting

• Type of anastomosis

• colostomy

Adjuvant therapy

• Adjuvant chemotherapy

• Indication

• Node+

• Venous spread

• Poorly differentiated CA

• Change in CEA

– Regime

• 5FU + Folinic acid- 6 month.

• Preoperative neoadjuvant therapy.

• No role of radiotherapy as colonic tumour is radioresistant.

Follow up

• For 3 years regular interval once in 3-6 month

• By

– Regular CEA

– USG

– Barium enema

– Colonoscopy

– Serum Alkaline phosphatase (ALP)

Prognosis

• Site

• Type

• Size

• Lymph node status

• Liver secondaries

• Age

• Stage

• Complication

Screening

What is screening?

A public health service in which members

of a defined population are examined to

identify those individuals who would benefit

from treatment to reduce the risk of a disease or

its complications.

Fecal occult blood test (FOBT)

Chemical test for blood in a stool sample.

Annual screening by FOBT reduces colorectal cancer

deaths by 33%.

Flexible sigmoidoscopy can detect about 65%–75% of

polyps and 40%–65% of colorectal cancers.

Rectum and sigmoid colon are visually inspected.

Types of Screening

Regular screening for all adults aged 50 years or

older is recommended

FOBT every year

Flexible sigmoidoscopy every 5 years

Total colon examination by colonoscopy

every 10 years or by barium enema every

5–10 years

Current Screening Guidelines

OGILVIE’S SYNDROME • Colonic pseudoobstruction.

• Clinical features:

– Distention,

– Tympanic,

– Nontender.

• Cause:

– Scleroderma,

– Myotonic dystrophy,

– Hypothyroidism, DM,

– CRF,

– Poisoning,

– Retroperitoneal irritation by blood fluid,

– Idiopathic.

• Investigation:

– X Ray –Dilated colon

– Barium- Normal

– CT

• Treatment:

– Conservative.

– Neostigmine,

– Tube cecostomy.

Colostomy

• A colostomy is a surgical procedure in which a stoma is formed by drawing the healthy end of the large intestine or colon through an incision in the anterior abdominal wall and suturing it into place. This opening, in conjunction with the attached stoma appliance, provides an alternative channel for feces to leave the body.

Types

• Loop

• End

• Double barrel

Temporary-

Loop colostomy, Devine’s double barrel

For diversion to facilitate distal healing

Permanent-

End

APR

• Diversion

• Decompression

– Blow hole

– Tube caecostomy

– Loop transverse colostomy

• Irrigation

Complication

• Prolapse • Retraction • Necrosis • Stenosis • Herniation • Bleeding • Diarrhoea • Enteritis • Skin excoriation

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