The document provides an overview of rectal carcinoma and polyps, detailing the types, classification, spread, staging, clinical features, and treatment options for rectal cancer. It also discusses different types of polyps, their characteristics, risks of malignancy, and the significance of familial adenomatous polyposis and hereditary non-polyposis colorectal cancer. Effective treatment strategies and the importance of follow-up surveillance are highlighted to prevent colorectal cancer development.

1. Rectal Carcinoma & Polyps

2. Rectal Carcinoma
Colorectal cancer is most common GI cancer
The rectum is the most frequent site involved
Adenoma-carcinoma sequence: Arises from adenoma
in stepwise progression
Mostly present as an ulcer, also polypoid and
infiltrating types are common

3. Types of carcinoma spread
 Local spread
 Lymphatic spread
 Venous spread
 Peritoneal dissemination

4. Local spread
Occurs circumferentially rather than in a longitudinal
direction
Once muscular coat penetrated, growth spreads into
mesorectum
If penetration occurs it involves,
 Anteriorly: In female- vagina or uterus
In male- prostate, seminal vesicles or bladder
 Laterally : ureter
 Posteriorly : sacrum and sacral plexus

5. Lymphatic spread
 Above and below the peritoneal reflection- in an
upward direction
 But when neoplasm lies within the field of middle
rectal artery, primary lateral spread along lymphatics
occurs
 Lately metastasis is at higher level than main trunk of
the superior rectal artery
 Atypical and widspread lymphatic permeation
occurs in highly undifferentiated lesion

6. Venous Spread
 Principles sites – Liver -34%,
Lungs -22%
Adrenals 11%
Other areas(including brain) – 33%
Peritoneal Dissemination
May follow penetration of the peritoneal coat by a high –
lying rectal carcinoma

7. Staging
 Dukes’ Classification
 TNM staging

9. Modified Duke classification
Stage features Prognosis
A Growth limited to rectal wall Excellent
B Growth extended to extra rectal
tissues, but no metastasis to
regional lymph nodes
Reasonable
C Lymph nodes involved
C1= local pararectal lymph nodes
alone are involved,
C2 = nodes accompanying
supplying blood vessels are
implicated up to point of division
Poor
D Not described by this method,
signifies the presences of
widespread of metastases, usually

11. TNM classification
• Tumor stage
• T1 tumor invasion
through muscularis
mucosae but not into
muscularis propria;
• T2 tumor invasion into
muscularis propria but
not through it;
• T3 tumor invasion
through muscularis
propria but not through
serosa or mesorectal
fascia;
• T4 tumor invasion
through the serosa or
mesorectal fascia
• M metastases
• M0 No distant metastases;
• M1 distant metastases
N Nodal stage
• N0 No nodes involved;
• N1 One or three nodes involved;
• N2 four or more nodes involved

12. Clinical Features
 > 55 years of age
 Bleeding per rectum
 Earliest and most common symptom
 Slight in amount and occurs at the end of defecation
 Altered bowel habit
 has to get up early in order to defecate OR,
 one who passes blood and mucus in addition to faeces (‘early-
morning bloody diarrhoea’)
 annular carcinoma at the recto sigmoid junction
constipation

13. Contd…
 Sense of incomplete defecation (tenesmus)
 A distressing straining to empty the bowels without resultant
evacuation
 Presentation delayed or easily missed
 Initial rectal examination and a low threshold for investigating
persistent symptoms are essential to prevent this

14. Contd…
 Pain
 A late symptom
 A colicky character
 When a deep carcinomatous ulcer of the rectum erodes the
prostate or bladder severe pain
 Pain in the back, or sciatica cancer invading the sacral plexus
 Weight loss Suggestive of hepatic metastases

15. •ABDOMINAL EXAMINATION
Sign of obstruction when large tumor present
Liver metastasis may be palpable
•RECTAL EXAMINATION
Neoplasm can be felt
In female when neoplasm is situated in anterior
wall vaginal examination should be done
Investigation

16.  Proctosigmoidoscopy
 will always show a carcinoma, if present, provided that the rectum is
emptied of feces beforehand
 Biopsy
 Using biopsy forceps via a sigmoidoscope, a portion from edge and from
center of the mass
 Colonoscopy
 is required if possible in all patients to exclude a synchronous tumor
 CT colonography
 Barium enema

17. Treatment
 Before starting treatment:
 Assess the fitness of the patient
 Assess the extent of spread of the tumor
 Assessment of the extent of spread
 CT of the chest and abdomen to exclude distant metastases
 Positron emission tomography (PET) scanning
 Endoluminal ultrasound
 MRI

18. Principles of surgical treatment
 Aim: radical excision of the rectum, together with the
mesorectum and associated lymph nodes
 Locally advanced tumor: neoadjuvant chemo
radiotherapy(5-FU and Leucovorin) over
approximately 6 weeks may reduce its size and make
curative surgery possible
 Even in the presence of widespread metastases, a
rectal excision is often the best means of palliation

19. Contd…
 ‘Short-course’ (5 days) neoadjuvant radiotherapy (in
resectable rectal cancer) significantly reduces the
incidence of local recurrence, but increased
complications
 For unfit patients or having very early tumors or
who have widespread metastases:
 Transanal excision
 Laser destruction or
 Interstitial radiation should be considered

20. Contd…
 When a rectal excision is possible, the aim should be to
restore gastrointestinal continuity and continence
 A sphincter-saving operation (anterior resection) is
usually possible for tumors whose lower margin is 2 cm
above the anal canal
 Total mesorectal excision (TME): For tumors in the
middle and lower thirds of the rectum
 High anterior resection : for rectosigmoid tumors and
those in the upper third of the rectum

21. Preoperative Preparation
 Mechanical bowel preparation(Diet , purgative, enema)
 Counselling
 Correction of anaemia and electrolyte disturbance
 Cross-matching of blood
 Prophylactic antibiotics (Cefuroxime
750mg+Metronidazole 500 mg on induction of
anaesthia)
 Deep vein thrombosis prophylaxis
 Insertion of urethral catheter

22. Surgical Modalities
 Local operations
 For low-grade T1 tumours, curative;
 This is usually done via the anus
 however do not allow full histopathological staging or deal with the
mesorectal or lymphatic spread of the tumour
 local recurrence rate of 20 % after local excision of T2 tumours

23.  Anterior resection
 Sphincter saving operations to treat most tumours of the middle
third of the rectum, and indeed many in the lower third.
 Open or laparoscopic
 Abdominoperineal excision
 tumours of the lower third of the rectum, which are unsuitable for a
sphincter-saving procedure
 Abdominal procedure is laparoscopic or midline

25.  Hartman’s operation
 in old and frail patient in whom there is concern about
anal sphincter function or the viability of anastomosis
 Palliative colostomy
 In intestinal obstruction, or where there is gross
infiltration of the neoplasm
 Pelvic exenteration (Brunschwig’s operation)
 The aim is to remove all the pelvic organs, together
with the internal iliac and the obturator groups of
lymph nodes

26.  Liver resection
 well-localised liver metastases can now be resected
 Radiography
 Preoperative radiotherapy can reduce local recurrence
 Chemotherapy
 The most frequently used drug is 5-fluorouracil
 infused into the portal vein during and immediately after the
primary operation have shown a small benefit.

28. Results of surgery for rectal cancer
 Resectability rate is up to 95 %, with an operative
mortality of less than 5 %
 Overall, the five-year survival rate is about 50 %
 Survival rates are influenced by TNM/Dukes’ stage,
histological grade
 The lower the tumour is in the rectum, the worse the
outlook
 Local recurrence rates 2-25 %.
 The most common cause is inadequate removal of the
whole tumour at the initial operation.

29. Polyps
 Polyp is a non specific clinical term that
describes any projection form the surface
of the intestinal mucosa regardless of the
histologic nature.
 Polyps can occur singly, synchronously in
small numbers or as in small numbers or
as part of polyposis syndrome

30. Polyps of large intestine

31. Classification of polyps of large intestine
Class Variety
Inflammatory Inflammatory Polyps
Metaplastic Metaplastic or hyperplastic
polyps
Harmartomatous Peutz–Jeghers polyp
Juvenile polyp
Neoplastic Adenoma
– Tubular
– Tubulovillous
– Villous
Adenocarcinoma
Carcinoid tumour

32. Adenomatous polyps
 Vary from tubular adenoma (berry on a
stalk) to villous adenoma (flat spreading
lesion)
 Villous tumors give symptoms of:
Diarrhea
Mucus discharge
 Occasionally hypokalaemia
Hypoalbuminaemia

33. Fig: Pedunculated adenomatous polyp of the large intestine, lngitudinal
section
Tubular adenoma

34.  Risk of developing malignancy increase with
increasing size
• 1cm diameter Tubular adenoma = 10%
risk
• Villous adenoma >2cm = 15% risk
 Adenomas >5mm diameter are treated
because of their malignant potential

35. Familial adenomatous polyposis
 Presence of more than 100 colorectal adenomas
 but also characterized by duodenal adenomas
and multiple extraintestinal manifestations
 Autosomal dominant
 +ve family history80%
 20% from mutation in the adenomatous
polyposis coli (APC) gene on the short arm of
chromosome 5
 Accounts for <1% of colorectal cancer

36. Familial adenomatous polyposis

38.  Large bowel is mainly affected but can occur in the
stomach, duodenum, and small intestine
 It is inherited as a Mendelian dominant condition,
i.e. risk of colorectal cancer in patients with FAP is
100%
 Can be associated with benign mesodermal tumors
 Desmoid tumors
 Osteomas
 Polyps are seen on sigmoidoscopy and if
asymptomatic are shown in a double contrast
barium enema

39. Clinical features
Symptomatic
 Are patients in whom a new mutation has occurred or
those from an affected family who have not been
screened
 Loose stools
 Lower abdominal pain
 weight loss
 Diarrhoea
 passage of blood and mucous

40. Asymptomatic
 Direct genetic testing reveals mutations in 80% of cases.
 If there is identified mutation in the family with FAP, any
resulting negative tests for this can be interpreted as
individual does not carry mutation.
 If there is no adenoma by the age of 30 FAP is unlikely.
 If diagnosis is made during adolescence
• Operation is deferred to the age of 17 or 18
• Or when symptoms develop
• Or when multiple polyps develop

41. Screening policy
1. At-risk family members are offered genetic testing in their early teens
2. At-risk members of the family should be examined at the age of 10-12
years, repeated every year
3. Most of those who are going to get polyps will have them at 20 years, and
these require operations
4. If there are no polyps at the age of 20 years, continue five yearly
examination until age of 50 years: if there are still no polyps, there is
probably no inherited gene. Carcinomatous changes may exceptionally
occur before the age of 20 years.
Examination of blood relatives is essential and family tree should be
constructed and a register of affected family members maintained.

42. Treatment
 The aim of treatment is to prevent the
development of colorectal cancer
 Colectomy with Ileorectal anastomosis (IRA)
 Alternative is Restorative proctocolectomy
(RPC) with an ileal pouch-anal anastomosis
 Total proctectomy and end ileostomy (normally
reserved for patients with a low rectal cancer)

43. • Avoids an ileostomy in
young patient
• Avoids risks of pelvic
dissection to nerve
function
• Requires regular
surveillance
• Still, the risk of developing
carcinoma is 10% over a
period of 30 years.
• Higher complication rate
• Indication
• Serious rectal
involvement with polyps
• Poor attending for
followup
• Established cancer of
rectum and sigmoid
• Small cuff of rectal
mucosa left behind with
the stapled anastomosis
Restorative
proctocolectomy (RPC)
Ileorectal
anastomosis (IRA)

44. Postoperative surveillance:
 Because of risk of tumor formation, follow
up is important
 Takes the form of rectal/pouch surveillence
 Gastroscopies to detect upper GI tumors

45. Hereditary non-polyposis colorectal
cancer (Lynch’s syndrome)
 Characterized by:
increased risk of colo-rectal cancer
Cancers of endometrium, ovary, stomach,
and small intestines
 Autosomal dominant
 Caused by mutation in one of the DNA
mismatch repair genes
MLH1, MSH2, MSH6, PMS and PMS2
People with MLH1, MSH2 show
syndrome.

46.  Life time risk of developing colorectal cancer
is 80%
 Mean age of diagnosis is 44 years
 Most cancers develop in proximal colon
 Females with HNPCC have 30-50% risk of
developing endometrial cancer.
 The average age of diagnosis is 46 years in
this group.

47. Diagnosis
By genetic testing or Amsterdam criteria II
or genetic testing :
 Three or more family members with an
HNPCC-related cancer one of whom is a
first-degree relative of the other two
 Two successive affected generations
 One or more HNPCC related cancer
diagnosed before the age of 50 years;
 FAP excluded;

49. Polyps of rectum

50. Polyps in the rectum
 Are either single or multiple
 Adenomas are the most frequent histological type
 Villous adenomas may be extensive and undergo
malignant change more commonly than tubular
adenomas
 All adenomas must be removed to avoid carcinomatous
change
 All patients must undergo colonoscopy to determine
whether further polyps are present
 Most polyps can be removed by endoscopic techniques,
but sometimes major surgery is required

51. Juvenile Polyp
 Is a bright red glistening pedunculated
sphere (‘cherry tumour’)
 Found in infants and children
 Occasionally persist into adult life
 Can cause:
Bleeding
Pain if it prolapses during defecation
 Often separates itself but, can be removed
easily with forceps or snare

52.  Solitary Juvenile polyp has no tendency to
malignant change
 Unique histological structure
Large mucous filled spaces covered by a smooth
surface of thin rectal cuboidal epithelium
 Juvenile polyposis syndrome
 Rare
 Autosomal dominant
 Characterized by
Multiple Juvenile Polyps and
Positive family history

53. Hyperplastic Polyps
 Small, pinkish, sessile Polyps
 2-4mm in diameter
 Frequently multiple
 Harmless

54. Inflammatory Pseudopolyps
 Are oedematous islands of mucosa
 Usually associated with colitis but most
inflamatory disease can cause them
 They are more likely to cause radiological
difficulty as the sigmoidoscopic appearances
are usually associated with obvious signs of
the inflammatory cause.

55. Villous Adenomas
 Have a characteristic frond-like appearance
 May be very large and occassionally fill the
entire rectum
 Enhanced tendency to become malignant
 Rarely, the profuse mucous discharge from
these tumors which is rich in potassium
Causes dangerous electrolyte and fluid
losses

56. Villous adenoma

57.  If cancerous change has been excluded, these tumors
can be removed by:
 Submucosal resection endoscopically
 Surgically per anum
 Or by sleeve resection from above
 Occasionally rectal excision required
 Transanal endoscopic microsurgery
Recent technique
Has improved the endoanal approach for the local
removal of villous adenomas
Requires the insertion of large sigmoidoscope

58. Familial Adenomatous Polyposis
 Autosomal dominant
 Characterised by development of multiple
rectal and colonic polyps around puberty
 Adenomatous polyposis coli(APC)
 Colonoscopy and biopsy will confirm the
diagnosis

59.  As this is pre-malignant condition:
 A total colectomy must be performed
 Rectum can be preserved
 But regular flexible endoscopy and removal of
polyps before they develop carcinoma is required
 Alternative:
 Restorative proctocolectomy with pouch-anus
anastomosis
 If patient follow up is poor
 A Pan-proctocolectomy with permanent ileostomy
is necessary

60. Treatment
 Colonoscopic polypectomy is satisfactory in
the case of most adenomas
 For large lesions, especially the sessile
variety, transanal excision or even
excision of the rectum may be the only
curative treatment
 Follow-up is required, the frequency
depending on the number, size and
histological type of adenomas

61. Fig : Transanal
endoscopic
microsurgery technique
a
.
c
b.

62. References
 Bailey and Love’s, short practice of surgery,
25th edition.
 Robins Basic Pathology, 9th edition.

63. THANK YOU