Dear Viewers, Greetings from " Surgical Educator" Today in this video I am going to talk on one more cause for Lower GI hemorrhage- Colorectal Carcinoma. I talk on the various causes for Lower GI hemorrhage, Etiopathogenesis, clinical features, investigations, staging, treatment and followup of Colorectal carcinoma. I have also included a mindmap, a diagnostic algorithm and a treatment algorithm. Hope you will enjoy the video. You can watch the video in the following links: surgicaleducator.blogspot.com youtube.com/c/surgicaleducator Thank you for watching the video.

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

2. COLORECTAL
CARCINOMA
Causes of Lower GI
Hemorrhage
Epidemiology
Etiology
Pathogenesis
Clinical Features
Investigations
Staging & Prognosis
Treatment
Followup
Mindmap
Diagnostic Algorithm
Management Algorithm

3. 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

4. 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.

5. 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

6. 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.

7. CRC- EPIDEMIOLOGY

8. 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.

9. 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.

10. 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 atypia
and glandular disorganization
The adenoma-to-carcinoma sequence is always associated with genetic
changes, even in sporadic colon cancers

11. CRC- PATHOGENESIS

12. 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.

13. 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.

14. 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%

15. 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

16. CRC- INVESTIGATIONS
Apple Core
Appearance
MULTIPLE LIVER
SECONDARIES

17. CRC- INVESTIGATIONS

18. CRC- STAGING

19. CRC- STAGING &
PROGNOSIS

20. CRC-TREATMENT
Carcinoma 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

21. TREATMENT
COLON RESECTIONS LOW ANTERIOR RESECTION PERINEAL PART OF APR

22. 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.

23. MINDMAP

24. Diagnostic Algorithm

25. Treatment Algorithm

26. Treatment Algorithm

27. THANK YOU
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