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LOWER GI HEMORRHAGE COLORECTAL CARCINOMA Dr.B.SELVARAJ MS;Mch;FICS: PROFESSOR OF SURGERY MELAKA MANIPAL MEDICAL COLLEGE MELAKA 75150 MALAYSIA

Colorectal carcinoma - lower gi hemorrhage

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LOWER GI HEMORRHAGE

COLORECTAL

CARCINOMA

Dr.B.SELVARAJ MS;Mch;FICS:

PROFESSOR OF SURGERY

MELAKA MANIPAL MEDICAL COLLEGE

MELAKA 75150 MALAYSIA

COLORECTAL CARCINOMA

Causes of Lower GI Hemorrhage

Epidemiology

Etiology

Pathogenesis

Clinical Features

Investigations

Staging & Prognosis

Treatment

Followup

Mindmap

Diagnostic Algorithm

Management Algorithm

Causes for Lower GI Hemorrhage

Diverticular disease

Angiodysplasia- AV Malformation

Colorectal carcinoma

Hemorrhoids

Fissure-in-ano

Ischemic colitis

Inflammatory bowel disease

Meckel’s diverticulum

Upper GI hemorrhage

CLASSICAL CLINICAL VIGNETTE

A 57-year-old obese man is seen by his primary care physician for his yearly physical. He endorses a 20 Kgs weight loss in the past few months without changing his diet or exercise. He also reports pencil-thin stools and intermittent constipation

He feels that he cannot adequately evacuate his stool- tenesmus. He has smoked one pack per day for the past 20 years. He has a history of type 2 diabetes. He has never had a colonoscopy.

There was two episodes of bleeding per rectum

Family history is negative for any cancer.

CLASSICAL CLINICAL VIGNETTE

On exam, he is afebrile with a heart rate of 78/min and blood pressure of 132/74 mmHg. His abdomen is soft and non-tender. No abdominal masses are palpated and he is non-distended.

On rectal exam, he has no masses and no gross blood. Laboratory examination reveals a hematocrit of 37 % (normal 40–52 %).

Diagnosis: Left sided Colonic Cancer

Colonoscopy: This diagnosis should be confirmed by Colonoscopy

CRC- EPIDEMIOLOGY

Colorectal cancer is the second most common malignancy in the United States ,with more the 155,000 new cases diagnosed annually.

Incidence is highest in industrialized countries and is age specific, increasing steadily from the second to the ninth decades

Women: Third most lethal cancer after lung and breast

Men: Third most lethal cancer after lung and prostate

Site: More common in Recto sigmoid area. Incidence of cancers in the right colon as compared to the left has increased; therefore, screening should be of the entire colon and not just the recto sigmoid.

CRC- EPIDEMIOLOGY

CRC- ETIOLOGY

Genetics: Increased incidence in first-degree relatives of CRC patients, especially with age less than 50 years at diagnosis

A. Familial Adenomatous Polyposis (FAP): < 1% of CRC

- The gene responsible has been identified on the short arm of chromosome 5

- The condition is diagnosed when a patient has more than100 adenomatous polyps in the colon. It is autosomal dominant in character.

- Polyps are usually visible on endoscopy by the age of 15 years. Carcinomatous change occurs 10 to15 years after the onset of polyposis.

CRC- ETIOLOGY

B.HNPCC (Hereditary Non Polyposis Colonic Cancer):5 to10% of CRC

- Lynch syndrome: The genetic abnormality is usually on chromosome 17 or 18 and autosomal dominant in nature.

- Amsterdam criteria: a. Three or more relatives with CRC, spanning two generations, one of whom is a first-degree relative.

b. One or more CRC cases diagnosed before age 50 years

Premalignant Conditions: IBD- Crohn’s and Ulcerative Colitis

C.Environmental Factors: Diet Unsaturated fats induce progression from adenomas to carcinoma.

- Exposure to food additives, alcohol, lionizing radiation, bile acids promotes development of carcinoma.

CRC- PATHOGENESIS

Development of carcinoma is a multistep process

The mucosal epithelium progresses through a series of molecular and cellular events

Further genetic alteration results in higher degrees of cellular atypiaand glandular disorganization

The adenoma-to-carcinoma sequence is always associated with genetic changes, even in sporadic colon cancers

CRC- PATHOGENESIS

CRC- PATHOLOGY

Macroscopic Types:

A. Nonstenozing type

a. Proliferative or cauliflower type

b. Ulcerative type.

B. Stenozing type

a. Annular—The stenosed segment is short in length like a ring.

b. Tubular—The stenosed segment is rather long.

CRC- PATHOLOGY

Spread:

Local spread: By continuity along the bowel wall.

By contiguity to adjacent structures

Lymphatic spread: Lymph nodes draining the colon are arranged in three groups viz. paracolic nodes lying in the immediate vicinity of the bowel wall. Intermediate nodes along the ileo colic, right colic, middle colic and sigmoid arteries and the apical nodes around the origins of superior and inferior mesenteric arteries.

Bloodstream spread: Metastasis may occur, quite early in the liver via the portal system. Lower rectal ca spread to lungs.

Clinical Features

1. Mass or lump in the

right iliac fossa.

2. Anemia due to

protracted occult

blood loss.

3. Pyrexia of unknown

origin.

4. Appendicitis when

carcinoma occludes

the appendicular

orifice.

5. Weight loss.

1. Pain in the left iliac

fossa, which is referred

to the suprapubic area.

2. Alteration of bowel

habit (constipation/

Diarrhea) is the most

common symptoms.

3. Palpable lump in

the left iliac fossa.

4. Loss of weight.

5. Small caliber stool

1. Blood and mucus

per rectum - Most

common and earliest

symptoms

2. Tenesmus

3. Sacral or perineal

pain.

4. Weight loss

Rt COLON-10%Lt COLON-30% RECTUM-60%

CRC- INVESTIGATIONS

Laboratory studies: include hemoglobin/hematocrit, fecal occult blood, liver enzymes and Carcino Embryonic Antigen- CEA

Sigmoidoscopy: both rigid and flexible

Colonoscopy: necessary to confirm the diagnosis and exclude any synchronous lesions proximally

DCBE( Double Contrast Barium Enema): Apple core appearance-demonstrates the site and configuration of the lesion

Endorectal ultrasound: information of the depth of invasion into the bowel wall by a rectal tumor and involvement of lymph nodes

CT scan is used to evaluate the chest and abdomen for metastases

CRC- INVESTIGATIONS

Apple CoreAppearance

MULTIPLE LIVERSECONDARIES

CRC- INVESTIGATIONS

CRC- STAGING

CRC- STAGING & PROGNOSIS

CRC-TREATMENTCarcinoma right colon Radical Rt Hemicolectomy

Ca Hepatic fexure & Rt Transverse colon Radical Extended Rt

Hemicolectomy

Ca Transverse colon Radical Transverse Colectomy

Ca left colon Radical Lt Hemicolectomy

Ca sigmoid colon Radical Sigmoidectomy

Ca in upper1/3rd of Rectum High anterior resection- >15cms from

anal verge

Ca in lower 1/3rd of Rectum Low anterior resection if > 8cms from

anal verge or Abdomino Perineal Resection with Total Mesorectal

Excision if < 6cms from anal verge

Hartman’s procedure In emergency situation in an unprepared

large bowel

TREATMENT

COLON RESECTIONS LOW ANTERIOR RESECTION PERINEAL PART OF APR

CRC- FOLLOWUP

Most tumors recur in the first 2 years after curative resection.

Colonoscopy and Ba enema are done in the postoperative period to

establish a base line.

Colonoscopy is repeated annually for at least 4 years, then every 2 to

3 years.

CEA level is done every 2 months for 2 years, every 4 months for 2

years, then annually. CEA level is sign of recurrence.

CXR every 6 months for 3 years, then annually.

Complete blood count and liver function tests should be performed

every 3 months for 2 years, then every 6 months for 2 years, and then

annually.

MINDMAP

Diagnostic Algorithm

Treatment Algorithm

Treatment Algorithm

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