Colorectal adenocarcinoma arising in the rectum (within 15 cm from the anal verge), presenting with bleeding per rectum, tenesmus, and altered bowel habits, often requiring multimodal treatment including neoadjuvant chemoradiation and surgical resection.

Exam domain	One-glance essentials
Definition / diagnosis	*Rectal carcinoma is usually adenocarcinoma within 15 cm of the anal verge; oncologically, the key rectum is below the peritoneal reflection* ^[3] Below the reflection there is no serosal barrier: radial spread and the circumferential resection margin (CRM) drive local control ^[3]
Epidemiology / risks	Major risks: age > 50, male sex and a first-degree family history ^[3]^[4] Think FAP/APC or Lynch/MMR with young onset, multiple polyps or a strong family history ^[3] Long-standing extensive IBD, smoking, obesity, alcohol and red/processed meat increase risk ^[3]^[4]
Core mechanism	Adenoma–carcinoma sequence: APC loss → KRAS activation → SMAD4/DCC loss → TP53 loss ^[3] dMMR/MSI-H tumours are immunogenic and may respond to checkpoint blockade ^[4] *Upper rectum drains portal-first; lower rectum can spread via systemic pelvic veins directly to lung* ^[2]
Clinical picture	*Rectal bleeding plus progressive change in bowel habit* is the core presentation ^[1] Tenesmus, mucus and narrow stools point to a distal/rectal lesion; obstruction is more typical of left-sided disease ^[1]^[3] An older patient with weight loss, pallor and a palpable rectal mass is a verified SAQ pattern ^[7]
Investigations	Start with DRE: record distance, surface, fixation, circumferential extent and sphincter involvement ^[1]^[3] *Colonoscopy of the whole colon + biopsy confirms diagnosis* and checks for synchronous lesions ^[1]^[3] *MRI pelvis is the standard local-staging test, assessing T/N stage, CRM/MRF, EMVI and sphincter relation; ERUS may help stage selected early T1 lesions ^[1]^[3] CT thorax/abdomen/pelvis* stages distant disease; obtain baseline CEA for prognosis/follow-up, not diagnosis ^[3]
Management	Plan in an MDT from pelvic MRI, distant staging, fitness and sphincter function ^[3]^[4] Early/favourable T1 may undergo local excision; mid–low rectal cancer usually undergoes oncological resection with TME ^[3] *Lecture trigger: mid–low T3/N+ disease or threatened CRM → pre-operative chemoradiotherapy; the MDT individualises the modern neoadjuvant sequence ^[1]^[6] Preserve sphincter with anterior resection when margins permit; APR requires a permanent colostomy* when safe preservation is impossible ^[3]
Complications	Tumour: large-bowel obstruction, perforation/faecal peritonitis and bleeding/IDA ^[3]^[4] Local/metastatic: rectovesical or rectovaginal fistula, sacral pain, ureteric obstruction, liver/lung/peritoneal spread ^[2]^[4] Treatment: anastomotic leak, LAR syndrome, pelvic autonomic dysfunction, stoma and radiation complications ^[3]^[4]
Prevention / follow-up	Use population FIT screening; a positive FIT requires diagnostic colonoscopy, not CEA ^[5] Strong family history, polyposis or suspected Lynch syndrome → genetic assessment and risk-adapted colonoscopic surveillance ^[3]^[4] Reduce modifiable risk: stop smoking, limit alcohol/processed meat, maintain activity and healthy weight ^[3]^[4]
Exam traps	CEA is neither a screening nor diagnostic test; tissue diagnosis is required ^[3] Haemorrhoids can coexist with cancer: do not stop at a benign anorectal finding when alarm features persist ^[4] A rectal lesion does not remove the need to examine the whole colon for synchronous disease ^[3] Distinguish rectal adenocarcinoma from anal squamous carcinoma because the treatment pathway differs ^[4]

References

^[1] Lecture slides: Clinical presentation, diagnosis and screening of colorectal cancer_rev1.pdf (p.6, p.9; “MRI pelvis for cancer of the rectum” slide) ^[2] Lecture slides: Molecular pathways, route of spread and staging.pdf (“Metastatic colorectal cancer” slide) ^[3] Senior notes: Maksim Surgery Notes.pdf (Colorectal cancer section, p.102–108) ^[4] Senior notes: Ryan Ho GI.pdf (Colorectal cancer and rectal-surgery sections, p.108–109, p.139, p.163, p.166, p.169, p.173, p.175–177) ^[5] Senior notes: Maksim Medicine Notes.pdf (Clinical oncology section, p.54) ^[6] Lecture slides: Professor Chiang Chi Leung - Role of Radiotherapy in Rectal Cancer_rev3.pdf (p.3, p.8) ^[7] Past paper: 2025 Fourth Summative SAQ.pdf (Question 12, p.15)

CA Rectum (Carcinoma of the Rectum)

Carcinoma of the rectum (CA Rectum) is a malignant neoplasm arising from the epithelial lining of the rectum. The rectum is defined differently depending on the context:

Endoscopic definition: up to 15 cm from the anal verge ^[1]^[2]
Oncological definition: bowel below the peritoneal reflection ^[1]^[2]

This distinction matters enormously because it dictates the surgical approach, the role of radiotherapy, and the patterns of local recurrence. The peritoneal reflection is the key landmark — below it, the rectum is surrounded by mesorectal fat rather than peritoneum, which means:

Radial spread into surrounding pelvic structures is a major concern (unlike colon cancer where peritoneum provides a serosal barrier)
Total mesorectal excision (TME) becomes the cornerstone of surgical technique
Neoadjuvant radiotherapy plays a role (unlike colon cancer)

Within the rectum, tumours are further sub-classified by distance from the anal verge:

Upper rectum: 10–15 cm from anal verge (above peritoneal reflection)
Mid rectum: 5–10 cm from anal verge
Low rectum: < 5 cm from anal verge (closest to anal sphincter complex)

This sub-classification is critical because low rectal tumours may threaten the anal sphincter, necessitating abdominoperineal resection (APR) with permanent colostomy, while higher tumours can undergo sphincter-preserving surgery (anterior resection).

Right-sided tumour: tumour before the splenic flexure. Left-sided tumour: tumour after the splenic flexure. ^[2] Rectal cancer is considered a left-sided/distal tumour.

Why does CA Rectum differ from CA Colon?

Although both are "colorectal cancers," CA Rectum is managed differently from CA Colon because: (1) the rectum lies deep in the bony pelvis making surgical access difficult, (2) it lacks a serosal covering below the peritoneal reflection facilitating local invasion, (3) the proximity to the anal sphincter complex raises continence issues, (4) the close relationship with pelvic structures (bladder, prostate/uterus, sacral nerves) raises concerns about functional morbidity, and (5) neoadjuvant chemoradiotherapy (nCRT) is a key component for locally advanced rectal cancer — a paradigm that does not exist for colon cancer.

2. Epidemiology

Colorectal cancer (CRC) is the 3rd most common cancer worldwide (after lung and breast) and the 2nd leading cause of cancer death globally ^[3].

Incidence is highest in developed/high-income countries — Australia/New Zealand, parts of Europe, North America
Incidence is rising in transitioning economies (e.g., Eastern Asia including China/Hong Kong) due to adoption of Western diets and lifestyles
Median age at diagnosis is 68 ^[3]

In Hong Kong, CRC is the most common cancer overall and in males (1st), and the 2nd most common cancer in females ^[4]^[3].

Incidence: 74.1 per 100,000 per year (one of the highest in Asia) ^[4]
Mortality: 28.5 per 100,000 per year (2nd cause of cancer death in both sexes) ^[4]
Male-to-female ratio ≈ 1.5–1.6 : 1 ^[3]^[4]
Stage at diagnosis: Stage I (10.6%), Stage II (22.5%), Stage III (25.5%), Stage IV (24.0%) — meaning nearly a quarter present with metastatic disease ^[4]

Rectal cancer specifically accounts for approximately 25–30% of all colorectal cancers. The rectosigmoid is the most common site ^[4], and approximately 70% of CRC are left-sided tumours ^[4].

Note: Right-sided tumours are becoming more common ^[4], a trend observed globally, possibly due to the increasing recognition of serrated polyp pathway lesions and microsatellite instability-high tumours.

Age > 50 — rare below 40 (unless hereditary syndrome); peak incidence 60–70 years ^[4]
Male predominance (M:F ≈ 1.6:1 in HK) ^[3]^[4]
10–15% have a positive family history ^[4]
25% show non-syndromal familial clustering ^[4]

High Yield – HK CRC Screening Programme

CRC screening in Hong Kong uses a 2-tier system ^[5]:

FIT (faecal immunochemical test) every 2 years starting from age 50
If FIT positive → colonoscopy (every 10 years) or flexible sigmoidoscopy (every 5 years)

This is part of the government's Colorectal Cancer Screening Programme launched in 2016.

3. Risk Factors

Risk Factor	Explanation
Age > 50 ^[3]^[6]	Accumulation of somatic mutations in colonic epithelium over time; adenoma-carcinoma sequence typically takes 10–15 years
Male sex ^[3]^[6]	Male-to-female ratio ~1.5:1 in HK; possibly related to hormonal protective effects of oestrogen in females (combined HRT is protective)
Family history ^[3]^[6]	First-degree relative with CRC increases risk ~2–3×; risk higher if relative diagnosed < 50 or if multiple relatives affected
Polyposis syndromes ^[4]	FAP (familial adenomatous polyposis — APC gene mutation, autosomal dominant, near 100% risk of CRC by age 40), MAP (MUTYH-associated polyposis), Peutz-Jeghers syndrome (PJS), Juvenile polyposis syndrome (JPS)
Non-polyposis syndromes ^[4]	HNPCC / Lynch syndrome (mutations in mismatch repair genes — MLH1, MSH2, MSH6, PMS2; autosomal dominant; 60–80% lifetime risk of CRC; also increased risk of endometrial, ovarian, gastric cancers)
History of colorectal polyps ^[3]^[4]	Especially large ( > 2.5 cm), villous, sessile, or dysplastic adenomatous polyps — these carry the highest malignant potential
History of CRC ^[4]	Metachronous tumours in 1.5–3% in post-op 5 years
IBD-related colitis ^[3]^[4]^[6]	5–15× risk; after 8–10 years in pancolitis, 15–20 years in left-sided colitis. UC > CD. The risk correlates with extent and duration of disease
Acromegaly ^[4]	2–14× risk — IGF-1 acts as a growth factor for colonic mucosal cells
Prior renal transplant ^[4]	Possibly related to immunosuppression
Prior cholecystectomy ^[4]	1.16× for right-sided CA — thought to be due to increased bile acid exposure to the right colon

Risk Factor	Explanation
Diet: red and processed meat, animal fat ^[4]^[6]	Heterocyclic amines and polycyclic aromatic hydrocarbons from cooking meat at high temperatures; haem iron generates free radicals and N-nitroso compounds that damage colonic DNA
Obesity, DM and insulin resistance ^[4]^[6]	1.15–1.23× risk — hyperinsulinaemia and elevated IGF-1 promote cell proliferation and inhibit apoptosis in colonic epithelium
Smoking ^[4]^[6]	1.18× risk, 1.25× mortality — carcinogens in tobacco smoke (e.g., aromatic amines, nitrosamines) reach the colonic mucosa via bloodstream
Alcohol ^[4]	1.21–1.52× risk depending on intake — acetaldehyde (alcohol metabolite) is a direct carcinogen; also impairs folate absorption (folate is needed for DNA repair)
Sedentary lifestyle ^[4]	Physical inactivity leads to prolonged colonic transit time → prolonged mucosal exposure to carcinogens
Androgen deprivation therapy ^[4]	Used in prostate cancer treatment

Protective Factor	Mechanism
High fibre diet ^[4]	Dilutes carcinogens, accelerates transit time, fermented by gut bacteria to produce butyrate (promotes apoptosis of neoplastic cells)
Aspirin and NSAIDs ^[2]^[4]	COX-2 inhibition → reduces prostaglandin E2 → decreases cell proliferation, increases apoptosis, inhibits angiogenesis. COX-2 is overexpressed in colorectal adenomas and carcinomas
Physical activity ^[4]	0.73–0.74× risk — reduces insulin resistance, decreases transit time
Calcium, vitamin D, dairy products ^[4]	Calcium binds bile acids and free fatty acids in the colonic lumen, reducing their proliferative effects
Dietary folate and B6 ^[4]	Essential for DNA methylation and synthesis; deficiency leads to uracil misincorporation and DNA strand breaks
Combined HRT ^[4]	Oestrogen may have anti-proliferative effects on colonic epithelium
Statins ^[4]	May inhibit Ras signalling pathway (KRAS is a key oncogene in CRC)

High Yield – Smoking and IBD/CRC Relationship

Smoking increases risk of Crohn's disease but appears to reduce the risk of ulcerative colitis ^[7]. However, smoking is a definite risk factor for CRC itself ^[6], regardless of IBD status. Don't confuse the UC-protective effect of smoking with an overall cancer-protective effect — it is not!

4. Anatomy and Function of the Rectum

The rectum is the terminal segment of the large intestine, approximately 12–15 cm in length, extending from the rectosigmoid junction (at the level of S3 vertebra) to the anal canal (at the anorectal junction/puborectalis sling).

Key anatomical relationships:

Anterior:
- Male: bladder, seminal vesicles, prostate, Denonvilliers' fascia
- Female: uterus, cervix, posterior vaginal wall, rectovaginal septum
Posterior: sacrum, coccyx, presacral fascia (Waldeyer's fascia), presacral venous plexus, middle sacral artery
Lateral: lateral ligaments of the rectum (containing middle rectal arteries), ureters, pelvic sidewall, obturator internus
Inferior: levator ani muscle (puborectalis, pubococcygeus, iliococcygeus), anal sphincter complex

The mesorectum is the fatty envelope surrounding the rectum, enclosed by the mesorectal fascia (a distinct fascial layer). It contains:

Perirectal lymph nodes (primary nodal drainage)
Branches of the superior rectal artery and vein
Perirectal fat

The concept of total mesorectal excision (TME) — removing the rectum along with its intact mesorectal envelope — revolutionised rectal cancer surgery. Before TME, local recurrence rates were 25–40%; with TME, local recurrence dropped to < 5–10%. This is because microscopic tumour deposits (satellite nodules) in the mesorectum are a major source of recurrence.

The circumferential resection margin (CRM) — the closest distance between the tumour and the mesorectal fascia — is one of the most important prognostic factors in rectal cancer ^[8]. A CRM ≤ 1 mm is considered involved/positive and predicts high local recurrence.

Artery	Origin	Area Supplied
Superior rectal artery	Inferior mesenteric artery (IMA)	Upper rectum (main blood supply)
Middle rectal artery	Internal iliac artery	Mid/lower rectum
Inferior rectal artery	Internal pudendal artery (branch of internal iliac)	Anal canal and lower rectum

Venous drainage follows a dual pathway:

Superior rectal vein → inferior mesenteric vein → portal system → liver (explains hepatic metastasis)
Middle and inferior rectal veins → internal iliac vein → IVC → lungs (explains why distal rectal tumours can metastasise directly to lungs bypassing the liver) ^[2]

Lymphatic spread follows the arterial supply ^[8]:

Upward (primary route): along superior rectal artery → inferior mesenteric lymph nodes → para-aortic nodes
Lateral: along middle rectal artery → internal iliac lymph nodes (especially relevant for tumours below the peritoneal reflection)
Downward (rare, only if proximal lymphatics blocked): to inguinal lymph nodes

This is why for low rectal tumours, lateral lymph node dissection may be considered (more practised in East Asian countries, e.g., Japan).

The rectum and pelvic organs are innervated by autonomic nerves that run in close proximity to the mesorectum:

Sympathetic: superior hypogastric plexus (presacral nerves) and hypogastric nerves → injury causes retrograde ejaculation in males
Parasympathetic: pelvic splanchnic nerves (S2–S4, nervi erigentes) → injury causes erectile dysfunction and bladder dysfunction

These nerves form the inferior hypogastric (pelvic) plexus on the lateral pelvic sidewall. Damage during TME surgery leads to urogenital dysfunction.

The dentate (pectinate) line divides the upper 2/3 and lower 1/3 of the anal canal ^[9]:

Feature	Above Dentate Line	Below Dentate Line
Embryology	Endoderm	Ectoderm
Epithelium	Columnar (→ adenocarcinoma)	Stratified squamous (→ SCC)
Nerve supply	Autonomic (inf. hypogastric plexus)	Somatic (inf. rectal n. ← pudendal n.)
Venous drainage	Portal system (superior rectal vv.)	IVC (middle + inferior rectal vv.)
Lymphatic drainage	Internal iliac and inferior mesenteric LN	Superficial inguinal LN

This anatomy explains why very low rectal tumours extending to the anal canal may drain to inguinal lymph nodes and have different biological behaviour.

5. Aetiology and Pathophysiology

5.1 Molecular Pathways

Colorectal cancer develops through well-characterised molecular pathways:

This is the classic adenoma-carcinoma sequence (Vogelstein model):

APC gene (Adenomatous Polyposis Coli, chromosome 5q): tumour suppressor gene; loss of APC leads to constitutive activation of Wnt/β-catenin signalling → uncontrolled cell proliferation. This is the initiating event in most CRCs. In FAP, one allele of APC is inherited in a mutated state (germline mutation), and loss of the second allele (somatic "second hit") leads to adenoma formation — explaining why FAP patients develop hundreds to thousands of polyps.
KRAS oncogene (chromosome 12p): encodes a GTPase in the Ras-Raf-MEK-ERK signalling pathway. Activating mutations keep KRAS constitutively "on," promoting cell growth and survival.
SMAD4/DCC (chromosome 18q): tumour suppressor genes in the TGF-β signalling pathway; loss allows cells to escape growth inhibition.
TP53 (chromosome 17p): "guardian of the genome"; loss eliminates cell cycle arrest and apoptosis in response to DNA damage → allows malignant transformation.

Higher risk in large ( > 2.5 cm), villous, sessile adenomatous polyps ^[2].

The adenoma-carcinoma sequence typically takes 10–15 years, which forms the basis for screening intervals.

Caused by defective DNA mismatch repair (MMR) genes — MLH1, MSH2, MSH6, PMS2
Microsatellites are short tandem repeats of DNA. When MMR is defective, errors during DNA replication in these repeats accumulate → "microsatellite instability"
Hereditary: Lynch syndrome (HNPCC) — germline mutations in MMR genes
Sporadic: usually due to epigenetic silencing of MLH1 by promoter hypermethylation
MSI-high tumours tend to be:
- Right-sided, poorly differentiated, mucinous/signet ring histology
- Better prognosis stage-for-stage (more immunogenic — many tumour neoantigens attract immune cells)
- Responsive to immune checkpoint inhibitors (anti-PD-1: pembrolizumab, nivolumab)
- Do NOT benefit from 5-FU-based chemotherapy (important for stage II decision-making)

There is also the serrated pathway (CpG island methylator phenotype, CIMP) ^[8] — associated with BRAF V600E mutation, sessile serrated adenomas/polyps, right-sided location, and often overlaps with MSI-high phenotype in sporadic cases.

Syndrome	Gene	Inheritance	Features	CRC Risk
FAP	APC (5q21)	AD	> 100 adenomatous polyps; also duodenal polyps, desmoid tumours, osteomas, CHRPE	~100% by age 40
Attenuated FAP	APC	AD	10–100 polyps, right-sided	~70% lifetime
MAP	MUTYH	AR	10–100 polyps	~80% lifetime
Lynch syndrome (HNPCC)	MLH1, MSH2, MSH6, PMS2	AD	Fulfils Amsterdam/Bethesda criteria; increased risk of endometrial, ovarian, gastric, urothelial cancers	60–80% lifetime
Peutz-Jeghers	STK11/LKB1	AD	Hamartomatous polyps + mucocutaneous pigmentation	39% lifetime

Colorectal cancer spreads via four routes ^[2]^[8]:

Direct spread (local invasion):
- Radial/circumferential spread — implicated in resectability in rectal cancer ^[2]
- In rectal cancer, tumour can invade through the rectal wall into perirectal fat, mesorectal fascia, and adjacent pelvic structures (bladder, prostate, uterus, sacrum, pelvic sidewall)
- The CRM (circumferential resection margin) reflects the extent of radial spread
Lymphatic spread:
- Along the lymphatic channels following arterial supply
- Virchow's node (Troisier's sign) — left supraclavicular lymphadenopathy indicates advanced disease with spread via the thoracic duct ^[2]
Haematogenous spread:
- Liver (most common site of distant metastasis) — via portal venous drainage ^[2]
- Lung — upper rectal tumours drain via portal system → liver → lung; but distal rectal tumours can metastasise directly to lungs via middle/inferior rectal veins → IVC → lungs, bypassing the liver ^[2]
- Bone, brain (less common)
Transcoelomic spread (peritoneal seeding):
- Ovary (Krukenberg tumour) ^[2]
- Pouch of Douglas ^[2]
- Peritoneal carcinomatosis → ascites

Key biomarkers that affect management:

Biomarker	Significance
KRAS/NRAS	If mutant → anti-EGFR therapy (cetuximab, panitumumab) is ineffective. If wild-type → anti-EGFR can be added ^[5]
BRAF (V600E)	Poor prognosis; associated with MSI-H in sporadic cases; targeted by encorafenib + cetuximab
MSI/MMR status	MSI-H/dMMR → better prognosis, responsive to immunotherapy, do NOT benefit from 5-FU alone in stage II
HER2	Amplification in ~5% of CRC; potential target for trastuzumab/pertuzumab
VEGF	Angiogenesis target; anti-VEGF (bevacizumab, aflibercept, regorafenib) can be added regardless of RAS status ^[5]

6. Classification and Staging

Adenocarcinoma (> 90%) — the predominant type; arises from glandular epithelium
- Well, moderately, or poorly differentiated
- Mucinous adenocarcinoma (> 50% mucinous component) — tends to present at advanced stage, worse prognosis
- Signet ring cell carcinoma — very aggressive, poor prognosis
Squamous cell carcinoma (rare in rectum, more common in anal canal below dentate line)
Neuroendocrine tumours (carcinoid)
Gastrointestinal stromal tumour (GIST) — mesenchymal origin
Lymphoma — rare

Stage	T	N	M	Description
0	Tis	N0	M0	Carcinoma in situ (intramucosal)
I	T1–T2	N0	M0	Tumour invades submucosa (T1) or muscularis propria (T2)
IIA	T3	N0	M0	Tumour invades through muscularis propria into pericolorectal tissues
IIB	T4a	N0	M0	Tumour penetrates visceral peritoneum
IIC	T4b	N0	M0	Tumour directly invades other organs/structures
IIIA	T1–T2	N1	M0	1–3 regional lymph nodes positive
IIIB	T3–T4a	N1	M0	1–3 regional lymph nodes positive
IIIC	Any T	N2	M0	≥ 4 regional lymph nodes positive
IVA	Any T	Any N	M1a	Metastasis to 1 distant organ (e.g., liver)
IVB	Any T	Any N	M1b	Metastasis to > 1 distant organ
IVC	Any T	Any N	M1c	Peritoneal metastasis

T staging details:

T1: invades submucosa
T2: invades muscularis propria
T3: invades through muscularis propria into pericolorectal tissues (mesorectal fat)
T4a: penetrates visceral peritoneum (above peritoneal reflection)
T4b: directly invades or adherent to other organs/structures

N staging:

N1: 1–3 regional lymph nodes
- N1a: 1 node; N1b: 2–3 nodes; N1c: tumour deposits without identifiable LN
N2: ≥ 4 regional lymph nodes
- N2a: 4–6 nodes; N2b: ≥ 7 nodes

A minimum of 12 lymph nodes should be examined for adequate staging ^[5].

Dukes'	Equivalent	Description
A	Stage I	Confined to bowel wall
B	Stage II	Through bowel wall, no LN
C	Stage III	Lymph node involvement
D	Stage IV	Distant metastasis

Pelvic MRI is the gold standard for local staging of rectal cancer. Key features assessed:

T stage: depth of invasion through rectal wall layers
N stage: mesorectal and lateral pelvic lymph nodes
CRM (circumferential resection margin): predicted distance from tumour to mesorectal fascia
- CRM > 1 mm = clear
- CRM ≤ 1 mm = threatened/involved → indication for neoadjuvant chemoradiotherapy
Extramural vascular invasion (EMVI): tumour invasion into veins outside the muscularis propria — poor prognostic factor
Relationship to anal sphincter complex: determines sphincter-preserving surgery vs APR

7. Clinical Features

CA Rectum may present with ^[6]:

Rectal bleeding
Change in bowel habit
Anaemia
Abdominal mass
Rectal mass
Tenesmus
Mucus
Fistula
Obstruction
Perforation
Asymptomatic (detected on screening)

The most common presentation is rectal bleeding and change in bowel habit.

7.2 Symptoms with Pathophysiological Basis

Symptom	Pathophysiological Basis
Rectal bleeding (haematochezia) ^[6]	Tumour surface is friable and ulcerated → bleeds on contact with stool. Because the rectum is distal, blood is typically bright red/fresh and may be mixed with or coat the stool surface. Unlike upper GI bleeds which produce melaena (acid-haematin conversion), rectal tumours produce frank red blood because there is no time for bacterial/acid degradation
Change in bowel habit ^[2]^[6]	The growing tumour narrows the rectal lumen (annular/constricting growth pattern, especially left-sided/distal tumours where lumen is already smaller and stool is more formed). This produces: alternating constipation and diarrhoea (paradoxical diarrhoea — liquid stool passes around the obstruction while formed stool cannot), pencil-thin/ribbon stools (stool squeezed through narrow lumen), increased frequency of defaecation
Tenesmus ^[6]	Latin: "tenesmus" from Greek "teinesmos" = straining. The rectal tumour mass creates a sensation of incomplete evacuation by occupying the rectal ampulla and stimulating stretch receptors, giving a persistent urge to defaecate even after emptying. This is characteristic of rectal (not colon) tumours
Mucus per rectum ^[6]	Mucin-secreting adenocarcinoma or reactive mucus production from inflamed/ulcerated rectal mucosa. Villous adenomas classically produce copious mucus (can even cause hypokalaemia from mucus loss)
Rectal/pelvic pain	Dull aching perineal/sacral pain indicates locally advanced disease with invasion into perirectal tissues, sacral nerve plexus (S2–S4), or levator ani muscles. Intractable pain (sacral nerve invasion) is a sign of advanced disease ^[10]
Fistula ^[6]	Locally advanced rectal tumours can invade into adjacent organs creating abnormal communications: rectovesical fistula (→ pneumaturia, faecaluria, recurrent UTIs), rectovaginal fistula (→ passage of stool/gas per vagina)

Symptom	Pathophysiological Basis
Intestinal obstruction ^[6]	Left-sided/distal tumours tend to obstruct ^[2] because: (1) the lumen is narrower distally, (2) stool is more formed and solid in the left colon/rectum, (3) left-sided tumours tend to grow in an annular/constricting pattern ("napkin ring" appearance). Presents with colicky abdominal pain, distension, absolute constipation, vomiting (late)
Perforation ^[6]	Can occur at the tumour site (direct perforation through necrotic tumour) or proximal to the obstruction (closed-loop obstruction with caecal distension → caecal perforation when diameter > 12 cm — Laplace's law: wall tension = pressure × radius, so the caecum with the largest diameter is at highest risk of perforation)

Symptom	Pathophysiological Basis
Anaemia (iron deficiency) ^[6]	Chronic occult blood loss from the tumour surface → depletion of iron stores → microcytic hypochromic anaemia. Right-sided tumours are more likely to present with anaemia ^[2] because the bleeding is more occult (liquid stool mixes with blood, not noticed by the patient), while left-sided/rectal tumours tend to present with frank haematochezia
Weight loss, anorexia, malaise ^[10]	Cancer cachexia syndrome — tumour-derived cytokines (TNF-α, IL-6, IL-1) increase basal metabolic rate, promote muscle proteolysis, suppress appetite via hypothalamic signalling. Also reduced oral intake if obstructive symptoms
Fever	Tumour necrosis, secondary infection of obstructed segment, or abscess formation

Symptom	Site of Metastasis	Pathophysiology
Jaundice, RUQ discomfort ^[10]	Liver	Hepatic metastases compressing/obstructing bile ducts or replacing hepatic parenchyma
Dyspnoea, cough ^[10]	Lung	Pulmonary metastases; especially from distal rectal tumours that bypass the liver via IVC
Bone pain ^[10]	Bone	Skeletal metastases (less common in CRC than in breast/prostate/lung)
Ascites ^[10]	Peritoneum	Peritoneal carcinomatosis → exudative ascites
Abdominal distension	Peritoneum/liver	Massive hepatomegaly or malignant ascites
Irritative urinary symptoms ^[10]	Bladder invasion	Direct local extension of rectal tumour into bladder base

7.3 Signs with Pathophysiological Basis

Sign	Pathophysiological Basis
Pallor	Chronic iron deficiency anaemia from occult blood loss
Cachexia/wasting	Cancer cachexia — TNF-α/IL-6 mediated muscle wasting
Koilonychia	Severe iron deficiency anaemia (concave/spoon-shaped nails due to abnormal nail matrix growth from iron depletion)
Virchow's node (Troisier's sign) ^[2]	Left supraclavicular lymphadenopathy — represents end-stage lymphatic spread via the thoracic duct
Sister Mary Joseph nodule	Periumbilical nodule from peritoneal/transcoelomic spread
Hepatomegaly	Liver metastases — hard, irregular, nodular liver

Sign	Pathophysiological Basis
Abdominal mass ^[6]	Palpable mass is uncommon in rectal cancer (rectum is deep in pelvis) but may be felt if the tumour is large or if there is associated bulky mesenteric/omental disease
Abdominal distension	Intestinal obstruction (with tympanitic percussion) or ascites (with shifting dullness)
Hepatomegaly	Liver metastases — typically hard, irregular, non-tender
Ascites	Peritoneal carcinomatosis

DRE is the single most important examination in CA Rectum — low rectal tumours (within 8 cm of the anal verge, i.e., within finger reach) can be directly palpated.

Finding	Significance
Rectal mass ^[6]	Hard, irregular, ulcerated mass with rolled edges — characteristic of malignancy. Note position (anterior/posterior/lateral, distance from anal verge), size, circumferential involvement, mobility (fixed vs. mobile — fixity suggests T4 disease with invasion into surrounding structures)
Blood/mucus on glove	Confirms presence of bleeding/mucus-secreting lesion
Anal sphincter tone	Assess tone (may be reduced if tumour invades sphincter complex) — determines whether sphincter-preserving surgery is feasible
Rectovaginal septum / prostate	Assess for anterior invasion
Pouch of Douglas nodularity (Blumer's shelf)	Transcoelomic deposits in the Pouch of Douglas, palpable on DRE as a hard shelf anterior to the rectum — indicates peritoneal carcinomatosis

Never Forget the DRE!

Up to 70–80% of rectal tumours are palpable on DRE. A common exam mistake is to discuss investigations for rectal cancer without mentioning DRE first. DRE provides information on tumour location, size, fixity, sphincter involvement, and the presence of peritoneal deposits — all of which directly influence management. "If you don't put your finger in it, you'll put your foot in it." — A classic surgical teaching aphorism.

Sign	Complication
Peritonism (guarding, rigidity, rebound)	Perforation → faecal peritonitis
Empty rectum on DRE with distended abdomen	Large bowel obstruction
Pneumaturia / faecaluria	Rectovesical fistula
Passage of stool/flatus PV	Rectovaginal fistula

Right-sided (proximal) and left-sided (distal) tumours present differently ^[2]:

Feature	Right-Sided (Proximal): present later	Left-Sided (Distal): present earlier
Growth pattern	Polypoid, exophytic	Annular, constricting ("napkin ring")
Luminal calibre	Larger	Smaller
Stool consistency	More liquid	More formed
Predominant presentation	Tend to bleed (occult) → iron deficiency anaemia, dull vague abdominal pain, right-sided abdominal mass	Tend to obstruct → change in bowel habits (tenesmus, reduced stool calibre, mucoid stool), hematochezia, intestinal obstruction
Change in bowel habits	Not common (stool is more liquid and colon more spacious)	Common

Rectal cancer specifically shares left-sided features but with additional features of tenesmus (tumour in the rectal ampulla) and sphincter-related symptoms.

High Yield Summary

CA Rectum — Definition, Epidemiology, Risk Factors, Anatomy, Aetiology, Pathophysiology, Classification, and Clinical Features

Definition: Malignant neoplasm of the rectum; endoscopically defined as up to 15 cm from anal verge; oncologically defined as bowel below peritoneal reflection
Epidemiology: CRC is the most common cancer in HK (1st in males, 2nd in females); incidence 74.1/100k/yr; M:F = 1.5–1.6:1; peak 60–70y; median age 68; ~24% present as stage IV
Key risk factors: Age > 50, male, FHx, FAP, Lynch syndrome, IBD (UC > CD after 8–10 years), obesity, red/processed meat, smoking, alcohol; protective: aspirin/NSAIDs, fibre, physical activity
Pathways: CIN pathway (85%) = adenoma-carcinoma sequence (APC→KRAS→SMAD4→TP53); MSI pathway (15%) = defective MMR genes → better prognosis, responsive to immunotherapy
Anatomy: Mesorectum is key — TME reduced local recurrence from 25–40% to < 5–10%; CRM is the most important prognostic factor; distal rectal tumours can metastasise to lungs bypassing liver via IVC
Spread: Direct (radial — critical in rectal CA), lymphatic (Virchow's node), haematogenous (liver MC, then lungs), transcoelomic (Krukenberg tumour, Pouch of Douglas)
Clinical features: Rectal bleeding, change in bowel habit, tenesmus, mucus, anaemia are the cardinal symptoms; DRE is essential — most rectal tumours are palpable; left-sided tumours tend to obstruct while right-sided tend to bleed
Staging: TNM (AJCC 8th ed); minimum 12 LN for adequate staging; MRI pelvis is the gold standard for local staging of rectal CA

Active Recall - CA Rectum (Part 1: Definition to Clinical Features)

^[1] Senior notes: Maksim Surgery Notes.pdf (Colorectal cancer section, p.102) ^[2] Senior notes: Maksim Surgery Notes.pdf (Colorectal cancer section, p.103) ^[3] Lecture slides: 2024-2025 Clin Epi colorectal cancer.pdf (p.2, p.7) ^[4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6.1, p.163) ^[5] Senior notes: Maksim Medicine Notes.pdf (Clinical oncology section, p.54) ^[6] Lecture slides: Clinical presentation, diagnosis and screening of colorectal cancer_rev1.pdf (p.6, p.9) ^[7] Senior notes: Block A - Chronic diarrhoea_ irritable bowel syndrome and inflammatory bowel disease.pdf (p.32) ^[8] Lecture slides: Molecular pathways, route of spread and staging.pdf ^[9] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.747 — Anal canal anatomy) ^[10] Senior notes: Ryan Ho Fundamentals.pdf (p.283) and Ryan Ho GI.pdf (p.108–109)

Differential Diagnosis of CA Rectum

When a patient presents with symptoms suggestive of rectal cancer — rectal bleeding, change in bowel habit, tenesmus, a rectal mass on DRE, or iron deficiency anaemia — the task is to systematically work through the differential. The clinical presentation overlaps significantly with many benign and malignant conditions, and the key is to determine which diagnoses you cannot afford to miss and which clues point towards one diagnosis over another.

A useful framework (from Murtagh's safe diagnostic model, taught in GC CFB lectures) is ^[11]:

Be systematic in problem solving:

What is the probability diagnosis?

What serious disorders cannot be missed (red flags)?

What conditions are often missed (pitfalls)?

Could this patient have a "masquerade"?

Is this patient trying to tell me something else (hidden agenda)?

For a patient presenting with rectal bleeding + change in bowel habit + tenesmus in someone > 50 years old, the probability diagnosis is CA rectum until proven otherwise. But the formal differential is broad.

The differential depends on the presenting complaint. CA Rectum can masquerade as — or be mimicked by — conditions presenting with:

Rectal bleeding (haematochezia / PR bleeding)
Change in bowel habit
Rectal mass
Iron deficiency anaemia
Large bowel obstruction

We will organise the DDx by presenting symptom cluster, then synthesise.

Hematochezia refers to passage of bright red blood or blood clots per rectum ^[12]^[13]. The colour, pattern, and associated symptoms help localise the source:

Bright red blood → from left colon or distal ^[12]
Dark/maroon blood mixed with stool → right colon ^[12]
Blood on surface of stools → anus/rectum ^[10]
Blood after defecation → anus (e.g., haemorrhoids) ^[10]
Blood mixed with faeces → above sigmoid ^[10]

Differential	Key Distinguishing Features	Why it mimics CA Rectum
Haemorrhoids	Blood coating stools or bleeding following defecation ^[10]; perianal prolapsing mass, pruritus (mucus), ± pain if thrombosed; at 3, 7, 11 o'clock positions in lithotomy ^[9]. No weight loss, no change in bowel habit, no mass on DRE (internal haemorrhoids are soft, compressible, not hard/irregular)	Fresh PR bleeding, commonest cause of rectal bleeding; can coexist with CA rectum — so finding haemorrhoids does NOT exclude cancer
Anal fissure	History of constipation; severe sharp pain upon defecation ^[10]; visible tear at anal margin (90% posterior midline); sentinel skin tag; sphincter spasm	Fresh blood on wiping, pain with defecation
Diverticular disease	Painless, usually profuse haematochezia (not chronic) ^[10]^[12]; right-sided diverticula are common in Asians and have higher haemorrhage risk ^[12]; bleeding occurs in the absence of diverticulitis	Acute PR bleeding, but typically sudden/profuse and self-limiting, NOT chronic like CA rectum
Angiodysplasia	Usually in elderly; may be associated with vascular malformations (e.g., HHT) and aortic stenosis (Heyde syndrome) ^[10]; painless, less severe than diverticular but tends to be intermittent ^[10]	Intermittent PR bleeding in elderly; but no mass, no change in bowel habit
Inflammatory bowel disease (UC/CD)	Usually bloody diarrhoea ^[10]; extra-intestinal manifestations: arthritis, episcleritis/uveitis, erythema nodosum ^[10]^[14]; younger age group (peak 20–40); UC: continuous rectal involvement with mucosal inflammation; CD: skip lesions, perianal disease	Bloody diarrhoea, tenesmus, rectal mass (inflammatory pseudopolyps); long-standing UC (8–10 years) is itself a risk factor for CA rectum ^[4]^[7]
Infective colitis	Fever, chills, rigors, nausea/vomiting, diarrhoea, pain ^[10]; TOCC, immunosuppression (CMV colitis) ^[10]; previous TB exposure ^[10]; acute onset, self-limiting	Bloody diarrhoea; TB colitis can mimic Crohn's and even carcinoma (stricturing, mass) — crucial to rule out in HK ^[7]
Ischaemic colitis	CVS risk factors, acute MI, stroke ^[10]; rapid onset abdominal pain + haematochezia/bloody diarrhoea; "watershed" areas (splenic flexure, rectosigmoid junction)	Bloody diarrhoea in elderly with vascular risk factors
Radiation proctitis	History of abdominal/pelvic irradiation ^[10]; e.g., prior RT for CA cervix, CA prostate; telangiectatic mucosa on sigmoidoscopy	PR bleeding, tenesmus; occurs months to years after pelvic RT
Rectal varices	Portal hypertension (cirrhosis); distinct from haemorrhoids — rectal varices are dilated portosystemic collaterals in the rectal submucosa above the dentate line	PR bleeding, but in the context of known liver disease
Solitary rectal ulcer syndrome	Young patients; straining, incomplete evacuation; mucosal prolapse; characteristic histology (fibromuscular obliteration of lamina propria)	PR bleeding, tenesmus, mucus
Upper GI bleed (massive)	Haematochezia can occur in patients with massive upper GI bleeding ^[12]; haematemesis, coffee ground vomitus, melaena; should be considered especially in severe haematochezia (10–15% from UGI) ^[10]	Profuse fresh PR bleeding in a haemodynamically unstable patient — don't forget UGI source

High Yield – GC Lecture Slide Point

Worrying signs of colorectal CA: alternating diarrhoea and constipation, passage of mucus, tenesmus, pencil-thin stools ^[10]. These should be sought in ANY patient presenting with rectal bleeding to distinguish malignancy from benign causes. The presence of constitutional symptoms (loss of appetite, loss of weight, malaise) ^[10] and signs of spread (intractable pain from sacral nerve invasion, irritative urinary symptoms from bladder invasion, ascites, jaundice/RUQ discomfort, bone pain, SOB) ^[10] dramatically raises the suspicion for CA rectum.

When a patient complains of altered bowel habit — especially alternating constipation and diarrhoea — the DDx includes:

Differential	Key Distinguishing Features	Why it mimics CA Rectum
Irritable Bowel Syndrome (IBS)	Diagnosis of exclusion; features that should NOT be found in IBS: weight loss, rectal bleeding, onset in older patients, family history of CA colon or IBD, positive FOBT, anaemia, raised ESR/WBC ^[15]; Rome IV criteria: recurrent abdominal pain ≥ 1 day/week for ≥ 3 months, related to defaecation; IBS-D is most common subtype ^[15]	Alternating bowel habit, abdominal pain, bloating. But IBS is a functional disorder — NO alarm features. In an older patient with new-onset symptoms, IBS should be a diagnosis of exclusion
IBD (UC/CD)	See above. Chronic relapsing-remitting course; extraintestinal manifestations; younger age group; endoscopic/histological findings	Chronic diarrhoea, PR bleeding, tenesmus
Diverticular disease	Altered bowel habit (constipation predominant), LLQ pain, episodes of acute diverticulitis; CRC can only be excluded with colonoscopy after resolution of acute inflammation ^[16]	LLQ pain, altered bowel habit; CT may show bowel wall thickening mimicking tumour. Features suggesting diverticulitis over CRC: pericolonic/mesenteric inflammation, involvement > 10 cm of colon, absence of enlarged pericolonic lymph nodes ^[16]
Thyroid disease	Hypothyroidism → constipation; hyperthyroidism → diarrhoea	Change in bowel habit but with endocrine features
Drugs	CCBs, opioids → constipation; metformin, colchicine, antibiotics → diarrhoea ^[17]	Altered bowel habit; always take a thorough drug history

A mass palpable on DRE or found on imaging/endoscopy:

Differential	Key Features
CA Rectum	Hard, irregular, ulcerated, fixed; rolled edges; may be circumferential
Rectal polyp (adenomatous)	Soft, pedunculated or sessile; may bleed; pre-malignant (adenoma-carcinoma sequence)
Rectal carcinoid (neuroendocrine tumour)	Smooth, firm, submucosal nodule; usually < 1 cm; most are benign; found incidentally
Rectal GIST	Submucosal mass; smooth overlying mucosa; diagnosed by biopsy (CD117/c-KIT positive)
Rectal lymphoma	Rare; may be part of systemic lymphoma; submucosal mass
Endometriosis (females)	Cyclical rectal bleeding coinciding with menstruation; tender nodule in rectovaginal septum
Presacral tumours	Extrinsic compression; smooth, palpable posteriorly; includes teratoma, chordoma, schwannoma
Inflammatory mass (Crohn's, TB, diverticular abscess)	Tender, ill-defined; associated with systemic inflammation; TB colitis can form a mass mimicking carcinoma ^[7]
Peridiverticular abscess	Mass or tenderness on DRE; presence of distal sigmoid abscess ^[16]
Rectal prolapse	Complete: protrusion of all layers of rectum through anus; partial: mucosa only ^[18]; circumferential folds visible; elder women
Thrombosed haemorrhoids	Acute onset, very tender, perianal mass; below dentate line
Pelvic mass (non-GI)	Don't forget pregnancy, ovarian cyst/tumour, uterine fibroid, bladder tumour, prostatic mass ^[19]

IDA in an older patient (especially > 50 years) should be considered GI malignancy until proven otherwise. The DDx:

Upper GI malignancy: gastric cancer, oesophageal cancer
Lower GI malignancy: CA colon (especially right-sided — occult bleeding), CA rectum
Peptic ulcer disease: chronic blood loss
Coeliac disease: malabsorption of iron in the duodenum
Angiodysplasia: occult intermittent bleeding
Menstrual blood loss: premenopausal women
Hookworm: endemic areas
Dietary deficiency: rare as a sole cause in developed settings

In HKUMed exams, the key teaching point is: In any patient > 50 with unexplained IDA, both upper and lower GI endoscopy are indicated to exclude malignancy.

CA Rectum is the most common cause of large bowel obstruction in adults. The DDx of LBO:

Cause	Key Features
Colorectal carcinoma	Most common cause (~60% of LBO); annular constricting lesion, especially left-sided
Sigmoid volvulus	Rotation of sigmoid around its mesentery; massive distension; "coffee bean sign" on AXR; elderly, institutionalised, psychiatric patients, chronic constipation
Diverticular stricture	History of recurrent diverticulitis; narrowing at sigmoid
Hernias (obstructed/strangulated)	Inguinal, femoral, incisional; palpable irreducible lump
Adhesions	Much less common cause of LBO than SBO; history of prior surgery
Pseudo-obstruction (Ogilvie syndrome)	Massive colonic dilatation without mechanical obstruction; in critically ill, post-operative, or hospitalised patients
Faecal impaction	Elderly, immobile, opioid use; hard stool palpable on DRE

Feature	CA Rectum	Haemorrhoids	Diverticular Disease	IBD (UC)	IBS
Age	> 50	Any	> 50	20–40 (peak)	Any
PR bleeding	Mixed with stool; dark or bright	After defaecation, on paper/surface	Profuse, painless, acute	Bloody diarrhoea, mucus	No bleeding
Pain	Late; pelvic/sacral if advanced	Only if thrombosed	LLQ, acute episodes	Cramping with defaecation	Abdominal pain related to defaecation
Change in bowel habit	Progressive; alternating	No	Constipation predominant	Diarrhoea ± urgency	Alternating but chronic, no progression
Weight loss	Yes	No	No	Possible (malabsorption in CD)	Not typical
DRE findings	Hard, irregular mass, fixed	Soft, non-tender (internal); tender swelling (external/thrombosed)	Tenderness	Mucosal tenderness, blood	Normal
Colonoscopy	Mass, ulcerated, biopsy → adenocarcinoma	Cushions at 3/7/11	Diverticula	Continuous mucosal inflammation (UC), skip lesions (CD)	Normal

Critical Pitfall

Haemorrhoids and CA Rectum can coexist. Finding haemorrhoids on examination does NOT exclude colorectal cancer. Any patient over 50 with rectal bleeding, or any patient with alarm features (weight loss, change in bowel habit, anaemia, family history), MUST have a colonoscopy even if haemorrhoids are found. "Treat the haemorrhoids, but scope the colon."

TB Colitis vs CA Rectum — Hong Kong Relevance

In Hong Kong, TB colitis is an important differential for Crohn's disease and can also mimic colorectal carcinoma ^[7]. TB can form strictures, masses, and fistulae indistinguishable from malignancy on imaging. It is crucial to rule out TB infection before starting biologics (anti-TNF-α) for IBD, as these can cause TB reactivation ^[7]. Always check for TB history, chest X-ray, IGRA/Mantoux, and send biopsies for AFB stain and culture.

High Yield Summary

Differential Diagnosis of CA Rectum — Key Points

Rectal bleeding DDx: Haemorrhoids (most common cause of PR bleeding but can coexist with CA), anal fissure, diverticular disease (acute, profuse, painless), angiodysplasia, IBD, infective/ischaemic/radiation colitis, solitary rectal ulcer syndrome; don't forget massive UGI bleed can present as haematochezia (10–15%)
Change in bowel habit DDx: IBS (diagnosis of exclusion — no alarm features), IBD, diverticular disease, thyroid disease, drugs
Rectal mass DDx: Adenomatous polyp, carcinoid, GIST, lymphoma, endometriosis, presacral tumour, inflammatory mass (TB, Crohn's, diverticular abscess), rectal prolapse; don't forget non-GI pelvic masses (ovarian, uterine, bladder, prostate)
IDA in > 50: Always scope both upper and lower GI to exclude malignancy
LBO: CA colon/rectum is the most common cause (~60%); DDx includes sigmoid volvulus, diverticular stricture, hernia, pseudo-obstruction
Critical pitfalls: Haemorrhoids + CA coexist → always scope; TB colitis mimics CA in HK → rule out before biologics; IBS is a diagnosis of exclusion requiring absence of alarm features

Active Recall - Differential Diagnosis of CA Rectum

References

^[4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6.1, p.163) ^[7] Senior notes: Block A - Chronic diarrhoea_ irritable bowel syndrome and inflammatory bowel disease.pdf (p.32, p.41) ^[9] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.747 — Anal canal anatomy) ^[10] Senior notes: Ryan Ho GI.pdf (p.108–109) and Ryan Ho Fundamentals.pdf (p.283) ^[11] Lecture slides: CFB (FM02) Introduction to common problems - Differentiating the normal from the abnormal.pdf (p.6) ^[12] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.345) and MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.651) ^[13] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.651) ^[14] Lecture slides: Inflammatory bowel disease.pdf (p.9–10) ^[15] Senior notes: Block A - Chronic diarrhoea_ irritable bowel syndrome and inflammatory bowel disease.pdf (p.22) ^[16] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.644) ^[17] Senior notes: Maksim Surgery Notes.pdf (p.88) and Maksim Medicine Notes.pdf (p.119) ^[18] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.763) ^[19] Lecture slides: Block C - Pelvic mass_ ovarian cancer and cysts; uterine fibroid; pelvic imaging.pdf (p.17)

Diagnostic Criteria, Algorithm and Investigations for CA Rectum

There is no single "diagnostic criterion" for rectal cancer in the way that, say, the Duke's criteria exist for infective endocarditis. Rather, the diagnosis is established through a combination of:

Clinical suspicion — symptoms, signs, and risk factors
Endoscopic visualisation — direct visualisation of the tumour
Histological confirmation via biopsy — this is the definitive diagnostic step ^[1]^[4]

The diagnosis of CA rectum is confirmed by colonoscopy with biopsy demonstrating adenocarcinoma (or other malignant histology). Everything else — blood tests, imaging, tumour markers — serves to support the clinical suspicion, stage the disease, or guide management.

Key Principle

Colonoscopy with biopsy is the gold standard for diagnosis of colorectal cancer ^[1]^[4]. No blood test or imaging study can replace tissue diagnosis. CEA is NOT a diagnostic test — it has low sensitivity and low specificity for CRC.

The approach follows a logical sequence: Clinical suspicion → Physical examination (including DRE) → Diagnostic endoscopy with biopsy → Staging investigations → Molecular biomarker testing.

3. Investigation Modalities

We organise investigations into: (A) Bedside/Clinical, (B) Blood tests, (C) Tumour markers, (D) Endoscopic investigations, (E) Imaging for staging, and (F) Molecular biomarker testing.

Investigation	Key Findings and Interpretation
Digital Rectal Examination (DRE)	The single most important bedside examination. Tumours within ~8 cm of the anal verge are palpable. Assess: position (anterior/posterior/lateral, clock face), distance from anal verge (determines surgical approach), size and circumferential involvement, mobility vs fixity (fixed = T4, invading surrounding structures), surface (hard, irregular, ulcerated = malignancy; smooth = benign), sphincter tone (invaded sphincter = may preclude sphincter-preserving surgery), blood/mucus on glove, Blumer's shelf (hard shelf of tumour deposits in Pouch of Douglas anteriorly = peritoneal carcinomatosis)
Rigid sigmoidoscopy	Allows precise measurement of tumour distance from anal verge (more accurate than flexible scope as the rigid scope does not loop). Also allows biopsy. Important for surgical planning — the exact distance determines whether anterior resection vs APR is appropriate

Investigation

Key Findings and Interpretation

Digital Rectal Examination (DRE)

The single most important bedside examination. Tumours within ~8 cm of the anal verge are palpable. Assess: position (anterior/posterior/lateral, clock face), distance from anal verge (determines surgical approach), size and circumferential involvement, mobility vs fixity (fixed = T4, invading surrounding structures), surface (hard, irregular, ulcerated = malignancy; smooth = benign), sphincter tone (invaded sphincter = may preclude sphincter-preserving surgery), blood/mucus on glove, Blumer's shelf (hard shelf of tumour deposits in Pouch of Douglas anteriorly = peritoneal carcinomatosis)

Rigid sigmoidoscopy

Allows precise measurement of tumour distance from anal verge (more accurate than flexible scope as the rigid scope does not loop). Also allows biopsy. Important for surgical planning — the exact distance determines whether anterior resection vs APR is appropriate

High Yield – GC Point

DRE assesses characteristics of stool ^[20] — this is also important in the context of rectal cancer to detect melaena, fresh blood, or mucus. Always perform DRE before endoscopy.

Test	Rationale and Key Findings
CBC with differential ^[1]	Anaemia — typically microcytic hypochromic (iron deficiency) from chronic blood loss. May also show normocytic anaemia of chronic disease in advanced cancer. Thrombocytosis can be reactive (inflammatory response to tumour)
Iron profile (serum iron, ferritin, transferrin saturation, TIBC) ^[1]	Confirms iron deficiency anaemia: low serum iron, low ferritin, low transferrin saturation, raised TIBC. Why? Chronic occult blood loss depletes iron stores
LFT ^[1]	Liver metastasis — elevated ALP (from bone or liver), elevated GGT, elevated bilirubin suggest hepatic involvement. Pattern of raised ALP + GGT (cholestatic pattern) suggests metastatic infiltration
RFT ^[1]	Baseline renal function — important for contrast CT planning (contrast nephropathy risk if eGFR < 30), and to assess for hydronephrosis from locally advanced pelvic disease obstructing ureters
Coagulation profile	Pre-operative assessment; also relevant if patient on anticoagulants

Serum carcinoembryonic antigen (CEA) ^[1]:

CEA is an oncofetal glycoprotein — normally produced during foetal development, minimal levels in healthy adults
Cut-off: < 4.7 ng/mL (varies by lab)
Low diagnostic ability: low sensitivity + low specificity for CRC ^[1]
- Elevated in only ~50% of CRC — may be first-pass metabolised by the liver (so portal-drained tumours may not elevate CEA as much) ^[1]
- False positives: pregnancy, smoking, TB, IBD, other carcinomas (GI tract, pancreas, breast) ^[1]

So why do we still measure CEA? Because its roles are:

Prognostication — very high pre-operative CEA ( > 5) correlates with worse prognosis

Treatment monitoring — declining CEA after surgery indicates successful resection; rising CEA during follow-up suggests recurrence

Detection of recurrence — even if pre-operative CEA was normal, post-operative CEA can pick up non-portovenous distant metastases (e.g., lung) ^[1]

Post-op: takes 4–6 weeks to return to normal ^[1]

CEA is NOT a Screening or Diagnostic Test

A common exam mistake is to list CEA as a "diagnostic test" for CRC. It is NOT. CEA has too many false positives and false negatives to be used for diagnosis or screening. Its value lies in prognostication, monitoring, and recurrence detection. Do not order CEA to "diagnose" CRC — order a colonoscopy.

D. Endoscopic Investigations

This is the most accurate and versatile investigation for CRC. It is both diagnostic (visualise + biopsy) and therapeutic (polypectomy, stenting).

Endoscopic findings in CA Rectum ^[4]:

Majority are endoluminal masses (exophytic or polypoid) but occasionally can be flat ^[4]
May have bleeding (oozing/frank bleeding) in friable, necrotic or ulcerative masses ^[4]
May be circumferential → may obstruct distal scoping ^[4]

Biopsy ^[4]:

Important to tattoo location in polypectomy for future resection if proven to be invasive carcinoma ^[4]
Especially important in distal rectal CA as anorectal SCC is treated by upfront chemo/RT instead of surgery ^[4] — histological confirmation determines the entire treatment pathway
Certain histological patterns, e.g., mucinous CA, poorly differentiated CA, are associated with poorer prognosis ^[4]

Performance ^[4]:

Missed CRC only in 2–6% ^[4]
Important to scope the entire colon ^[4] — because:
- Synchronous tumours occur in 3–5% of patients ^[1]^[4]
- Synchronous polyps in 30–50% ^[1]^[4]
- If malignant obstruction precludes complete colonoscopy, then should consider additional pre-op investigation (CT colonoscopy or flexible sigmoidoscopy) with mandatory post-op repeat colonoscopy or intra-operative colonoscopy ^[4]
- Colonoscopy is incomplete in 11–12% of cases ^[4]

High Yield – Why Scope the Entire Colon?

Even when a rectal tumour is found, you must visualise the proximal colon. Synchronous cancers are found in 3–5% and synchronous polyps in 30–50%. Missing a second cancer would be a catastrophic surgical error — you might do an anterior resection for the rectal tumour while a caecal cancer grows undetected.

Spiral CT with IV contrast, air insufflation, and intraluminal contrast — creates virtual fly-through images
Requires mechanical bowel preparation (stools can simulate polyps) ^[4]
Similar sensitivity to colonoscopy for tumours > 1 cm ^[1] but cannot detect polyps < 5 mm and sessile (flat) polyps ^[5]
Does not offer therapeutic procedures — still need colonoscopy if lesion found ^[4]
Provides extraluminal information (lymph nodes, liver, other organs) ^[1]
Lower risk of perforation than colonoscopy ^[1]
Used when: caecum cannot be reached by colonoscopy ^[1], patient unfit for colonoscopy, or as pre-operative assessment when complete colonoscopy is impossible due to obstructing tumour

Considered inadequate for diagnosis given gradual shift towards proximal tumours worldwide ^[4]
No sedation required (office procedure) ^[4]
Can visualise rectum and sigmoid — useful for rectal tumours specifically
No bowel prep required ^[5]
Misses approximately 25% right-sided cancers ^[5]
Still requires colonoscopy if positive finding ^[5]

Superseded by CT colonography ^[1]
Classical finding: "apple core" lesion — near-circumferential involvement of bowel walls ^[1] with shouldered edges and mucosal destruction
Risk of barium peritonitis ^[1] if there is an unsuspected perforation
Limited diagnostic value ^[4]; rarely used in modern practice

E. Imaging for Staging

Once the histological diagnosis is confirmed, staging determines the extent of disease and directly guides treatment (especially the decision for neoadjuvant therapy in rectal cancer).

MRI pelvis is the single most important staging investigation for rectal cancer. It provides exquisite soft tissue contrast in the pelvis, allowing assessment of:

MRI Feature	What It Tells You	Clinical Significance
T stage	Depth of tumour invasion through the rectal wall layers (mucosa → submucosa → muscularis propria → mesorectal fat → adjacent organs)	Determines whether neoadjuvant therapy is needed (T3/T4 lesions)
N stage	Mesorectal lymph nodes and lateral pelvic lymph nodes; criteria for malignancy include short-axis diameter > 5 mm, irregular border, mixed signal intensity	N+ disease generally warrants neoadjuvant chemoRT for rectal cancer
Circumferential resection margin (CRM)	Distance from the tumour to the mesorectal fascia	CRM ≤ 1 mm = threatened/involved → indication for neoadjuvant chemoRT. CRM is the single strongest predictor of local recurrence
Extramural vascular invasion (EMVI)	Tumour within veins outside the muscularis propria, seen as tumour signal within the vessel lumen	EMVI-positive tumours have higher risk of distant metastasis; may influence decision for neoadjuvant therapy
Relationship to sphincter complex	Distance of tumour's lower edge to the anorectal junction/puborectalis	Determines whether sphincter-preserving surgery (anterior resection) or APR with permanent colostomy is necessary
Relationship to peritoneal reflection	Tumour above vs below	Below = truly "rectal"; above = some centres treat more like sigmoid colon
Mucinous component	High T2 signal (mucin lakes)	Mucinous tumours respond less well to neoadjuvant CRT; important to flag

Why MRI and not CT for local staging? CT has poor soft tissue contrast in the pelvis — it cannot reliably differentiate the layers of the rectal wall or assess CRM. MRI's superior soft tissue resolution makes it indispensable for rectal cancer. However, CT is better for detecting distant metastases (lungs, liver) and is faster to perform.

Finding	Interpretation
Liver metastases	Most common site of distant metastasis. Appear as hypodense lesions on portal venous phase CT. Multiple lesions suggest widespread disease; isolated metastasis may be resectable
Lung metastases	Second most common. Round, well-defined soft tissue nodules. Remember: distal rectal tumours can metastasise directly to lungs via IVC ^[1]
Peritoneal carcinomatosis	Ascites, omental caking, peritoneal nodules
Retroperitoneal/para-aortic lymphadenopathy	Suggests extensive lymphatic spread
Bone metastases	Lytic or sclerotic lesions (less common in CRC)
Obstructing tumour	Proximal bowel dilatation, caecal distension (risk of perforation if diameter > 12 cm)

Principle: injection of 18FDG tracer → tissues with increased metabolic rate show increased glucose uptake → tracer retained because FDG cannot be incorporated into glycolysis → tissues with increased metabolic rate will "light up" (SUVmax > 2.5) ^[21]
High sensitivity for occult metastasis ^[21]
Indications in rectal cancer:
- Suspected recurrence (especially rising CEA with negative conventional imaging)
- Evaluation of oligometastatic disease (to determine resectability of metastases)
- Pre-operative assessment when considering metastasectomy
Limitations:
- False positives: inflammation, infection, physiological uptake (e.g., post-surgical changes)
- Not good for brain metastasis (high background brain metabolic activity) ^[21]
- Mucinous tumours may be FDG-avid but can also be falsely negative

Provides high-resolution imaging of the rectal wall layers
Accurate for early T staging (T1 vs T2) — important when considering local excision (transanal excision or transanal endoscopic microsurgery, TEM)
Less accurate for advanced T stage (T3/T4) — MRI is superior
Also assesses perirectal lymph nodes (but MRI is better for this)
Main role: when considering local excision for early rectal cancer, ERUS helps confirm the tumour is confined to the submucosa (T1) or muscularis propria (T2)

Investigation	Role
Chest X-ray	Baseline; may detect large pulmonary metastases, pleural effusion
Abdominal X-ray (AXR)	If presenting with obstruction: dilated loops of large bowel proximal to the obstruction; caecal diameter > 12 cm indicates imminent perforation
Liver MRI	If CT findings are indeterminate for liver metastases; MRI with liver-specific contrast (e.g., gadoxetic acid/Primovist) has superior sensitivity for small hepatic lesions
RBC scan	For GI bleeding localisation: labelled RBCs detect bleeding rate as low as 0.1–0.4 mL/min; delayed images up to 24h can detect intermittent bleeding ^[22]. Rarely needed for CA rectum diagnosis but may be used when the source of GI bleeding is unclear

Once adenocarcinoma is confirmed on biopsy, molecular profiling of the tumour is essential for guiding targeted therapy, especially in the advanced/metastatic setting:

Biomarker	Test Method	Clinical Significance
KRAS/NRAS ^[1]^[4]	PCR or NGS on tumour tissue	Mutated in ~45% → no response to anti-EGFR therapy (cetuximab/panitumumab) ^[1]. If wild-type → anti-EGFR monoclonal antibodies can be used ^[4]^[5]
BRAF (V600E) ^[1]	PCR or IHC	Poor prognosis; targetable with encorafenib + cetuximab in metastatic setting
MMR / MSI status ^[1]^[4]	IHC for MMR proteins (MLH1, MSH2, MSH6, PMS2) or PCR-based MSI testing	MMR-deficient/MSI-high → responsive to PD-1 pathway inhibitors (e.g., pembrolizumab) ^[1]^[4]; better prognosis; do NOT benefit from 5-FU alone in stage II ^[5]; also triggers germline testing for Lynch syndrome
HER2	IHC/FISH	Amplified in ~5% of CRC; potential target (trastuzumab/pertuzumab)

High Yield — Biomarkers Select the Treatment Pathway

Test MMR/MSI before neoadjuvant decisions, and RAS/BRAF plus other actionable markers in metastatic disease. MSI-H/dMMR may select checkpoint blockade; left-sided RAS/BRAF-wild-type pMMR disease often uses chemo–anti-EGFR. RAS-mutant/right-sided pMMR disease often uses chemo–bevacizumab. BRAF V600E and KRAS G12C have matched inhibitor–anti-EGFR combinations in defined settings. Aflibercept and regorafenib are not interchangeable first-line additions. See the current Mx pathway and its indication-specific sources.

For Lynch assessment, MLH1/PMS2 loss needs reflex MLH1 methylation/BRAF testing as appropriate for CRC; BRAF wild-type alone is not proof of Lynch syndrome. Unexplained MMR loss warrants genetics referral. NICE Lynch pathway.

Purpose	Investigation
Diagnosis	Colonoscopy + biopsy (gold standard) ^[1]^[4]; DRE; rigid sigmoidoscopy
Local staging (rectal cancer)	MRI pelvis (T, N, CRM, EMVI, sphincter relationship); ERUS (for early T staging)
Distant staging	CT thorax + abdomen + pelvis; PET-CT (for recurrence/oligometastatic assessment)
Bloods	CBC, Fe profile, LFT, RFT, CEA ^[1]
Molecular profiling	KRAS/NRAS, BRAF, MSI/MMR ^[1]^[4]
If colonoscopy incomplete	CT colonography ^[1]^[4]; flexible sigmoidoscopy + post-op repeat colonoscopy
Recurrence surveillance	Serial CEA (every 3–6 months for 5 years); CT (periodic); colonoscopy (at 1 year post-op then every 3–5 years)

Finding	Investigation	Significance
"Apple core" lesion ^[1]	Barium enema / CT	Near-circumferential involvement of bowel walls — annular constricting carcinoma with shouldered edges and mucosal destruction. Classic but rarely seen now as barium enema is superseded
Irregular rectal wall thickening with loss of fat planes	MRI pelvis	Suggests T3/T4 tumour invading through muscularis propria into mesorectal fat or adjacent structures
CRM ≤ 1 mm	MRI pelvis	Threatened/involved CRM → indication for neoadjuvant chemoRT
Hypodense hepatic lesions	CT abdomen (portal venous phase)	Liver metastases
"Target sign"	CT/MRI	Concentric rings of bowel wall — intussusception (may be lead point of colorectal tumour)
Large bowel dilatation with caecal diameter > 12 cm	AXR / CT	Impending caecal perforation due to closed-loop obstruction from obstructing tumour

High Yield Summary

Diagnostic Criteria, Algorithm and Investigations for CA Rectum

Colonoscopy + biopsy is the gold standard for diagnosis — tissue is needed; CEA is NOT diagnostic
DRE is the essential bedside examination — palpates ~70–80% of rectal tumours; assesses distance from anal verge, mobility, sphincter involvement, and Blumer's shelf
Staging paradigm for rectal cancer:
- MRI pelvis for local staging (T, N, CRM, EMVI, sphincter) — determines need for neoadjuvant therapy
- CT thorax + abdomen + pelvis for distant staging (liver, lung, peritoneum)
- Molecular profiling (KRAS/NRAS, BRAF, MSI/MMR) for targeted therapy decisions
CEA: low sensitivity/specificity for diagnosis; role is in prognostication, monitoring, and recurrence detection; post-op takes 4–6 weeks to normalise
Always scope entire colon: synchronous cancers in 3–5%, synchronous polyps in 30–50%
CRM ≤ 1 mm on MRI = threatened → neoadjuvant chemoRT indicated
Apple core lesion on barium enema is the classical radiological finding of annular constricting carcinoma

Active Recall - Diagnosis and Investigation of CA Rectum

References

^[1] Senior notes: Maksim Surgery Notes.pdf (Colorectal cancer section, p.103) ^[4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6, p.166) ^[5] Senior notes: Maksim Medicine Notes.pdf (Clinical oncology section, p.54) ^[20] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf (p.8) ^[21] Senior notes: Ryan Ho Respiratory.pdf (p.143–144) ^[22] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p.62)

Management Algorithm and Treatment Modalities for CA Rectum

Faculty surgical extension — peritoneal metastases: selected fit patients with limited peritoneal disease may be assessed for complete cytoreduction at an experienced centre; PCI, small-bowel involvement and the likelihood of complete resection matter. Do not equate cytoreduction with a proven benefit from adding HIPEC: PRODIGE 7 found no overall-survival advantage from its short-duration oxaliplatin HIPEC regimen and more late postoperative complications. PRODIGE 7, PMID 33476595.

Test MMR/MSI before neoadjuvant treatment. For dMMR/MSI-H locally advanced rectal cancer, immunotherapy is a recommended initial approach; specialist response assessment determines subsequent treatment. For pMMR/MSS disease, lower rectal location and high-risk MRI findings favour total neoadjuvant therapy (TNT). Selected lower-risk tumours can follow a chemotherapy-first pathway with selective radiation. ASCO rectal guideline.

TNT means planned systemic chemotherapy and pelvic radiation are delivered before surgery. Consolidation chemotherapy after CRT is an important organ-preservation sequence; induction chemotherapy is another option. Do not automatically add another full adjuvant course after completed TNT. Regimens such as PRODIGE-23 included postoperative treatment and should be described by their actual protocol.

Clinical complete response is not pathological proof of cure. After appropriate therapy, selected complete responders may choose watch-and-wait with expert DRE, endoscopic and MRI surveillance and access to salvage surgery. The 2025 dostarlimab study supports this approach in dMMR disease but does not justify omitting surgery after an incomplete response. Dostarlimab study.

Management of CA rectum is fundamentally different from CA colon because of three anatomical realities:

The rectum sits deep in the bony pelvis — surgical access is constrained, and achieving clear radial margins is technically challenging
Below the peritoneal reflection, there is no serosal covering — local recurrence is a major problem if the circumferential resection margin (CRM) is not clear
Proximity to the anal sphincter complex — the surgeon must balance oncological radicality against functional preservation (continence)

These factors mean that neoadjuvant chemoradiotherapy plays a central role in locally advanced rectal cancer ; colon cancer usually starts with surgery, with selected neoadjuvant systemic-treatment exceptions ^[1]^[4]^[23].

The management of rectal cancer is decided by a multidisciplinary team (MDT) comprising colorectal surgeons, clinical oncologists (radiotherapy), medical oncologists (chemotherapy), radiologists, pathologists, and specialist nurses. Every case should be discussed at an MDT meeting.

Management principles by stage ^[5]:

Stage	Management
Stage I	Surgery + analysis of ≥ 12 LN
Stage II	MRI/MMR-directed neoadjuvant treatment for higher-risk disease; surgery-first or selective radiation pathways for selected lower-risk tumours
Stage III	Usually neoadjuvant treatment, followed by response assessment and TME or selected watch-and-wait; MMR and MRI risk guide the pathway
Stage IV	Chemo ± surgery for isolated liver metastasis

For CA rectum specifically, the key decision point is whether the tumour is early, locally advanced, or metastatic, and this is determined primarily by MRI pelvis.

3. Surgical Treatment

Surgical principles for CRC (important!) ^[1]:

En-bloc resection of primary tumour and locoregional nodes (75% cure rate) ^[1]
Adequate resection margins: at least 5 cm proximally and distally — actual margin depends on blood supply ^[1]
- For rectal cancer specifically, a distal margin of ≥ 1 cm is generally accepted for tumours treated with neoadjuvant chemoRT (previously 2 cm was required, but studies show 1 cm is oncologically equivalent after downstaging)
Resect major vascular pedicles and lymphatic drainage basin ^[1]
- Excise colonic mesentery, ligate arterial supply at its origin, and excise all accompanying lymph nodes ^[1]
At least 12 nodes for proper N staging: inadequate LN harvest might require adjuvant chemo ^[1]^[5]
Restore bowel continuity whenever possible ^[1]

Total mesorectal excision (TME): precise dissection of the mesorectal envelope (containing tumour, surrounding mesorectal fat, lymph nodes and vessels), preserving pelvic autonomic nerves ^[1]:

Plane: "holy plane" — avascular areolar plane between presacral and mesorectal fascia ^[1]
Benefits: decreased local recurrence rate and decreased post-operative genitourinary dysfunction ^[1]
Approaches: transabdominal (open / laparoscopic / robotic), transanal (rarely) ^[1]

Why TME? Before TME was introduced by RJ Heald in 1982, rectal cancer surgery involved blunt dissection that often left mesorectal tissue behind — containing microscopic tumour deposits. This resulted in local recurrence rates of 25–40%. TME reduced this to < 5–10% by ensuring complete excision of the mesorectal envelope under direct vision, following a defined anatomical plane.

High Yield – TME and the 'Holy Plane'

The "holy plane" is the avascular areolar plane between the mesorectal fascia (surrounding the mesorectum) and the presacral fascia (covering the sacrum). Dissection in this plane ensures the mesorectal envelope is removed intact, autonomic nerves running on the presacral fascia are preserved, and blood loss is minimal. The quality of TME (graded as complete, nearly complete, or incomplete by the pathologist) is one of the strongest predictors of local recurrence.

Procedure	Indication	Description
Local Excision (Transanal excision / TEM)	Very early rectal cancer: T1 with favourable features (well/moderately differentiated, no lymphovascular invasion, sm1–2 invasion depth, < 3 cm, < 30% circumference)	Full-thickness excision of the tumour through the anus without abdominal incision. Avoids major surgery but NO lymph node assessment. Risk: if final pathology shows adverse features (sm3, LVI, poor differentiation), salvage radical surgery is needed
Anterior Resection (AR) with TME	Mid and upper rectal cancer where adequate distal margin can be achieved while preserving the sphincter complex	Resection of the rectum and mesorectum via abdominal approach. Bowel continuity is restored with a colorectal or colo-anal anastomosis. A temporary diverting loop ileostomy is usually created to protect the low anastomosis (reversed ~8–12 weeks later after confirming anastomotic integrity with contrast study)
Abdominoperineal Resection (APR) ^[1]	Indicated if ANY one of: poor pre-op sphincter function / failure to achieve negative distal margin / locally advanced or recurrent low-lying CA rectum ^[1]	Combined abdominal and perineal approach. En-bloc removal of sigmoid, rectum, and anus. Construction of permanent end colostomy ^[1]. This is the operation patients fear most because of the permanent stoma
Intersphincteric Resection (ISR)	Very low rectal tumours where the tumour is above the dentate line but close to the anorectal junction — selected cases to avoid APR	Dissection between the internal and external sphincter to achieve adequate distal margin while preserving the external sphincter. Technically demanding; functional outcomes (continence) can be suboptimal
Hartmann's Procedure	Emergency setting (obstruction, perforation) where primary anastomosis is unsafe	Resection of rectosigmoid with formation of end colostomy and closure of the rectal stump. Avoids the risk of anastomotic leak in an unprepared, inflamed, or contaminated abdomen

APR detailed steps ^[1]:

Insert catheter to protect membranous urethra in males
Abdominal part (open/laparoscopic): similar to anterior resection
Perineal dissection via circumanal incision for en-bloc resection of sigmoid, rectum, and anus
Construction of permanent end colostomy

Elective surgery: laparoscopic/robotic approach is preferred ^[1]:

Benefits of robotic surgery: high-quality 3D vision, restoration of eye-hand-target axis ^[1]
Better cosmesis, faster recovery, less adhesion formation

Emergency surgery ^[1]: Indicated if complicated (obstruction, perforation, haemorrhage):

Left-sided lesion: Hartmann's operation ^[1]
The key difference from elective surgery is that primary anastomosis is usually avoided in the emergency setting due to:
- Unprepared bowel (high bacterial load → risk of anastomotic breakdown)
- Peritoneal contamination (perforation)
- Haemodynamic instability

Endoscopic stenting for malignant obstruction ^[4]:

Indications: ^[4]
- As bridge to surgery — to avoid emergency surgery; definitive operation 1–2 weeks after initial stenting ^[4]
- As palliative treatment in unresectable, metastatic disease ^[4]
Procedure: self-expanding metallic stent (SEMS), inserted and deployed under endoscopic and/or fluoroscopic guidance ^[4]
Contraindications: perforated/strangulated, persistent coagulopathy, distal rectal lesion (≤ 5 cm of anal verge) — excruciating pain if stent migrates beyond the dentate line ^[4]
Advantages: avoid stoma for terminal patients; avoid emergency surgery (mortality > 10%); elective operation allows bowel prep → better outcome; more time to stage disease ^[4]
Outcome: 92% successful, median patency 106 days, 4.5% perforate, 12% re-obstruction ^[4]

4. Neoadjuvant Therapy for CA Rectum

This is one of the defining features that separates rectal cancer management from colon cancer management. Neoadjuvant treatment is selective in colon cancer, but it is central to locally advanced rectal cancer.

3 main indications (need to know!) ^[1]:

Resectable but locally advanced disease: sterilise tumour bed, decrease intra-operative tumour spillage and decrease local recurrence rate ^[1]
- T3/T4 disease — only definite indication proven by RCT ^[1]
- Nodal disease ^[1]
- Threatened CRM ( < 2 mm) ^[1]
Borderline resectable disease: downstage the tumour and increase resectability rate ^[1]
Low-lying tumour: downsize the tumour and increase sphincter preservation rate ^[1]

Why neoadjuvant and not adjuvant RT for rectal cancer? The landmark German Rectal Cancer Study Group trial (CAO/ARO/AIO-94) showed that pre-operative chemoRT compared to post-operative chemoRT resulted in: (1) lower local recurrence (6% vs 13%), (2) fewer acute and late toxicities, and (3) higher rate of sphincter preservation. Overall survival was similar, but the toxicity advantage firmly established neoadjuvant as the standard.

Options ^[1]^[4]:

	Long-course chemoRT (HK standard)	Short-course high-dose RT
Regimen	5-FU based chemotherapy × 2 cycles + concurrent RT (50.4 Gy = 1.8 Gy daily × 28 fractions) ^[1]	RT 25 Gy = 5 Gy × 5 days ^[1]
Interval to surgery	Wait 8–10 weeks before surgery ^[1]	Immediate surgery or delayed surgery/systemic chemotherapy, according to protocol
Post-surgery	Depends on systemic therapy already completed; not automatic after TNT	—
Advantages	Standard option; associated with better tumour shrinkage ^[4]; can downstage/downsize for sphincter preservation	Shorter treatment duration; less time off work
Disadvantages	Cumulative dose limits any later re-irradiation; delays surgery ^[1]	More side effects of high-dose RT ^[1]; Immediate surgery permits little interval shrinkage, but short-course RT followed by chemotherapy/delayed surgery can downstage disease. Long-course CRT is often preferred when maximal local regression is important; MRI risk and the full protocol guide selection

Total neoadjuvant therapy (TNT) — a standard option for lower rectal/high-risk locally advanced disease:

Chemotherapy and radiation before surgery, using induction or consolidation chemotherapy
Indications: locally advanced cases at increased risk of margin-positive resection (e.g., T4 or involved mesorectal fascia), node-positive disease, and low-lying tumour ^[4]
Advantages: increased chemo compliance (better tolerated pre-op), increased local control, option of watch and wait ^[4]
Selection: lower-risk cT3N0 tumours may avoid full TNT; cT3N0 alone does not determine treatment without tumour height, MRI risk, MMR and patient factors.

After neoadjuvant therapy, re-staging MRI is performed (usually ~2 months after completion to allow tumour shrinkage) ^[4].

Clinical complete response (cCR) ^[4]:

Definition: no rectal mass felt clinically + no tumour seen endoscopically + no tumour seen radiologically on MRI ^[4]
Basis: those with pathological complete response (pCR) after pre-op therapy have excellent prognosis → researchers question whether selected patients with cCR may avoid surgery altogether ^[4]
Option of watchful waiting increasingly popular ^[4]
- Must have intensive surveillance: PR examination, endoscopy, MRI every 3 months in the first 2 years ^[4]
- However, cCR ≠ pCR: post-neoadjuvant clinical staging is still somewhat inaccurate → ~20% will regrow and < 10% will have distant metastasis ^[4]

Watch and Wait — A Paradigm Shift

The "watch and wait" (organ preservation) strategy is one of the most exciting developments in rectal cancer management. In carefully selected patients who achieve a clinical complete response after neoadjuvant chemoRT, avoiding surgery means avoiding permanent stomas, urogenital dysfunction, and major surgical morbidity. However, it requires rigorous patient selection and intensive surveillance, and patients must understand the ~20% risk of local regrowth (which is usually salvageable with surgery).

5. Adjuvant Chemotherapy

Adjuvant chemotherapy: aims to eradicate micro-metastasis and reduce risk of recurrence ^[1].

After surgery-first or an incomplete preoperative systemic course, consider chemotherapy according to pathological stage, fitness and prior exposure; completed TNT does not mandate further routine chemotherapy
High-risk Stage II — consider adjuvant chemo if ^[23]^[24]:
- T4 tumour
- Lymphovascular invasion
- Perineural invasion
- Poorly differentiated histology
- Inadequate lymph node dissection ( < 12 LN)
- Positive resection margin
- Presentation with obstruction or perforation

Options ^[1]^[5]:

FOLFOX for 6 months: folinic acid (leucovorin) + 5-fluorouracil + oxaliplatin ^[1]
CAPOX (capecitabine + oxaliplatin): duration depends on the rectal treatment protocol and preoperative exposure; do not automatically import the colon IDEA duration rule

Drug mechanisms:

Oxaliplatin: alkylating agent — forms platinum-DNA adducts that crosslink DNA strands, preventing replication and transcription
5-Fluorouracil (5-FU): anti-metabolite (pyrimidine analogue) — inhibits thymidylate synthase, blocking DNA synthesis (thymidine production)
Capecitabine: oral prodrug of 5-FU — converted to 5-FU preferentially in tumour tissue by thymidine phosphorylase (which is overexpressed in tumours); more convenient than IV 5-FU
Irinotecan: topoisomerase I inhibitor — prevents religation of single-strand DNA breaks during replication, leading to cell death
Folinic acid (leucovorin): not cytotoxic itself; enhances the binding of 5-FU metabolite (FdUMP) to thymidylate synthase, making 5-FU more effective

Adverse effects of chemotherapy ^[24]:

Mucositis, nausea and vomiting, diarrhoea
Febrile neutropenia (myelosuppression)
Alopecia
Hand-foot syndrome (especially capecitabine) — painful erythema, swelling, and desquamation of palms and soles due to drug accumulation in sweat glands
Oxaliplatin-specific: peripheral neuropathy (dose-limiting; cumulative; cold-triggered paraesthesias)

6. Targeted Therapy and Immunotherapy (Stage IV / Metastatic Disease)

Non-surgical treatment for metastatic CRC ^[5]^[24]:

Upfront chemotherapy: dual therapy — oxaliplatin/irinotecan + fluorouracil/capecitabine ^[5]:

FOLFOX: folinic acid + 5-FU + oxaliplatin
FOLFIRI: folinic acid + 5-FU + irinotecan
XELOX: capecitabine + oxaliplatin

Biomarker Status	Targeted Agent	Mechanism	Key Points
RAS-mutant pMMR disease	Anti-VEGF: bevacizumab / aflibercept / regorafenib ^[5]^[24]	Bevacizumab: monoclonal antibody targeting VEGF-A ^[24] — blocks tumour angiogenesis (new blood vessel formation); tumours need blood supply to grow beyond ~2 mm	ONLY indicated in stage IV (metastatic) disease; no evidence to support use in the adjuvant setting ^[24]. Contraindications: haemorrhage, wound healing impairment, arterial thromboembolic diseases ^[24]
KRAS/NRAS/BRAF wild-type	Anti-EGFR: cetuximab / panitumumab ^[5]^[24]	Monoclonal antibody blocking the extracellular domain of EGFR → prevents ligand binding → inhibits Ras-Raf-MEK-ERK proliferation signalling	RAS mutations predict resistance to routine anti-EGFR use; matched KRAS G12C inhibitor–anti-EGFR combinations are a later-line exception. RAS and BRAF V600E mutations are usually mutually exclusive.
MSI-H / dMMR	Immune checkpoint inhibitors: pembrolizumab / nivolumab ^[1]^[5]	Anti-PD-1 monoclonal antibodies — block PD-1 on T cells, preventing tumour cells from evading immune detection via PD-L1	MSI-H tumours have high mutational burden → many neoantigens → more immunogenic → excellent response to immunotherapy. Also first-line option in dMMR metastatic CRC (KEYNOTE-177 trial)
BRAF V600E mutant	Encorafenib + cetuximab + fluorouracil-based chemotherapy	BRAF inhibitor + anti-EGFR (dual pathway blockade needed because BRAF inhibition alone causes feedback EGFR activation)	First-line BREAKWATER pathway; encorafenib–cetuximab without chemotherapy also has established later-line use. FDA
HER2 amplified (~5%)	Trastuzumab + pertuzumab	Anti-HER2 monoclonal antibodies	Emerging evidence; usually in RAS wild-type tumours

High Yield – Anti-EGFR vs Anti-VEGF Decision

The decision tree is simple:

Test KRAS/NRAS/BRAF first
For left-sided RAS/BRAF-wild-type pMMR disease, chemotherapy + anti-EGFR is an important option
RAS-mutant/right-sided pMMR disease often uses chemotherapy + bevacizumab; BRAF V600E has an encorafenib–cetuximab–chemotherapy pathway
If MSI-H/dMMR → consider immunotherapy (pembrolizumab) as first line

Anti-EGFR alone cannot reliably suppress constitutively activated downstream signalling. In BRAF V600E or KRAS G12C disease, however, pairing it with the matched inhibitor suppresses feedback reactivation; these combination indications are distinct from routine anti-EGFR monotherapy.

7. Radiotherapy in Rectal Cancer

Radiotherapy (RT) plays a much more important role in rectal cancer than in colon cancer ^[23].

The rectum is fixed in the pelvis → the radiation field can be precisely targeted with reproducible anatomy
Below the peritoneal reflection, there is no serosal barrier → radial spread is the dominant failure pattern → RT can sterilise the mesorectal/pelvic field
For colon cancer, the mobility of the colon in the abdomen makes it a poor target for RT, and the proximity to small bowel (radiosensitive) causes excessive toxicity

Neoadjuvant (pre-operative): Locally advanced disease (T3/T4, N+, threatened CRM) — discussed above
Adjuvant (post-operative): Considered if positive CRM or other adverse pathological features not identified pre-operatively (less common now with improved MRI staging)
Palliative: Symptomatic locally advanced/recurrent rectal cancer causing bleeding, pain, or obstruction
Definitive chemoRT: For anorectal SCC (squamous cell carcinoma) — this is treated by upfront chemo/RT instead of surgery ^[4]

Modern rectal cancer RT uses intensity-modulated radiation therapy (IMRT) or volumetric modulated arc therapy (VMAT) to:

Deliver a conformal dose to the tumour and pelvic lymph nodes
Minimise dose to organs at risk (small bowel, bladder, femoral heads, pelvic bones)
The faculty RT lecture (pp. 6, 13–15) links anatomy to planning: GTV is visible tumour, CTV adds areas at risk of microscopic disease, and PTV accounts for motion/setup uncertainty. Pelvic MRI, tumour height and nodal distribution guide target selection.
Positioning and bladder preparation aim to reduce irradiated small bowel; prone belly-board/full-bladder techniques are options, while modern IMRT protocols may use supine positioning. Follow the planning team's reproducible protocol.

8. Management of Specific Scenarios

~20–25% of patients with CRC liver metastases are candidates for hepatic resection
5-year survival after liver metastasectomy: 25–40% (compared to < 5% without surgery)
Criteria for resectability: technically feasible to resect all disease with clear margins while preserving adequate future liver remnant (≥ 20–30% of total liver volume)
Peri-operative chemotherapy (e.g., FOLFOX for 3 months pre- and post-hepatectomy) improves disease-free survival

Pulmonary metastasectomy considered if: isolated lung metastases, primary tumour controlled, all disease can be resected, adequate pulmonary reserve
Remember: distal rectal tumours can metastasise directly to lungs bypassing the liver via IVC ^[1]

Modality	Indication
Palliative chemotherapy	Extends survival and improves quality of life in metastatic disease; median OS ~24–30 months with modern regimens
Palliative stenting	Malignant obstruction in unresectable disease ^[4]
Palliative RT	Symptomatic bleeding, pain, pelvic recurrence
Diverting colostomy	Obstruction not amenable to stenting
Best supportive care	When further oncological treatment is inappropriate; includes symptom management, psychosocial support, end-of-life care

Patients undergoing major rectal surgery may require perioperative nutritional support:

Enteral feeding is always first choice if the GI tract can be used safely ^[25]
Indications for perioperative nutritional support: malnourished patients undergoing major surgery, major operations with prolonged fasting ( > 5–7 days) post-operatively, postoperative complications resulting in increased catabolism and nil food intake ^[25]
Enhanced Recovery After Surgery (ERAS) protocols encourage early oral feeding (within 24 hours of surgery), early mobilisation, and minimisation of perioperative fasting

Modality	Schedule	Rationale
Clinical review + DRE	Every 3–6 months for 2 years, then every 6 months to year 5	Detect local recurrence
CEA	Every 3–6 months for 5 years	Rising CEA may indicate recurrence before imaging becomes positive
CT thorax/abdomen/pelvis	Annually for 3–5 years	Detect distant metastases
Colonoscopy	At 1 year post-op, then every 3–5 years	Detect metachronous tumours and polyps
Pelvic MRI (for rectal cancer)	Every 6–12 months for 3 years if high risk	Detect pelvic recurrence

High Yield Summary

Management of CA Rectum — Key Points

Surgery with TME is the cornerstone — dissection along the "holy plane" between mesorectal and presacral fascia; decreases local recurrence and preserves autonomic nerves
Surgical options: Local excision (very early T1), Anterior Resection with TME (sphincter-preserving), APR with permanent colostomy (low tumours/poor sphincter/positive margins)
Neoadjuvant chemoRT is indicated for locally advanced rectal cancer (T3/T4, N+, threatened CRM) — 3 indications: resectable but locally advanced, borderline resectable, low-lying tumour for sphincter preservation
Long-course chemoRT (50.4 Gy + 5-FU) is the HK standard; short-course RT (25 Gy in 5 fractions) can be part of a delayed-surgery/TNT protocol; choose by MRI risk and regression needs
Watch and Wait: Clinical complete response after neoadjuvant → option of organ preservation with intensive surveillance; ~20% regrowth rate
Postoperative chemotherapy: depends on pathology and treatment already given; no automatic extra course after completed TNT
Metastatic CRC targeted therapy: Left-sided RAS/BRAF-wild-type → chemo + anti-EGFR; RAS-mutant/right-sided → often chemo + anti-VEGF; BRAF V600E → combined BRAF/EGFR targeting; MSI-H/dMMR → checkpoint blockade
CEA is NOT diagnostic — used for prognostication, monitoring, and recurrence detection

Active Recall - Management of CA Rectum

References

^[1] Senior notes: Maksim Surgery Notes.pdf (Colorectal cancer section, p.104–107) ^[4] Senior notes: Ryan Ho GI.pdf (Section 3.3.6, p.139, p.166, p.173) ^[5] Senior notes: Maksim Medicine Notes.pdf (Clinical oncology section, p.54) ^[23] Lecture slides: Professor Chiang Chi Leung - Role of Radiotherapy in Rectal Cancer_rev3.pdf (p.3, p.8) ^[24] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.693) and MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.896) ^[25] Senior notes: Ryan Ho Fluids and Nutrition.pdf (p.8–11)

Complications of CA Rectum

Complications of CA rectum can be divided into three broad categories:

Complications of the disease itself (untreated or advanced tumour)
Complications of treatment (surgery, radiotherapy, chemotherapy, targeted therapy)
Complications of recurrence

Understanding the pathophysiological basis of each complication is essential — it helps you anticipate, prevent, and manage them.

1. Complications of the Disease Itself

These arise from the natural history of an untreated or advanced rectal tumour.

Complication	Pathophysiology	Clinical Features	Management
Intestinal obstruction	Left-sided/distal tumours tend to obstruct ^[1] — the annular constricting growth pattern narrows the lumen progressively. The rectum has a smaller calibre and stool is more formed, increasing the risk of complete obstruction	Colicky abdominal pain, abdominal distension, absolute constipation, late vomiting. AXR shows dilated large bowel proximal to the obstruction. Caecal diameter > 12 cm → imminent perforation (Laplace's law)	Initial resuscitation ("drip and suck"): NPO, NGT decompression, IV fluids ^[4]. Consider endoscopic SEMS as bridge to surgery ^[4] or emergency Hartmann's procedure ^[1]. Intestinal obstruction is a common surgical emergency; high mortality if complications occur ^[26]
Perforation	Can occur at the tumour site (necrotic tumour wall breaks down) or proximal to the obstruction (closed-loop obstruction → caecal perforation). Perforation leads to faecal peritonitis, which is the most lethal complication	Sudden severe abdominal pain, peritonism (guarding, rigidity, rebound tenderness), septic shock (fever, tachycardia, hypotension). Erect CXR: free gas under the diaphragm (pneumoperitoneum)	Emergency laparotomy — Hartmann's procedure (resection + end colostomy without anastomosis); peritoneal lavage; broad-spectrum IV antibiotics. Mortality is very high (15–30%)
Haemorrhage	Erosion of tumour surface into blood vessels. Usually chronic low-grade bleeding causing IDA, but occasionally massive acute PR bleeding	Chronic: progressive IDA, fatigue, pallor. Acute: profuse haematochezia, haemodynamic instability	Chronic: iron supplementation, definitive surgery. Acute: resuscitation, transfusion; if uncontrolled → emergency surgery or angiographic embolisation
Fistula formation	Locally advanced tumour (T4b) invades adjacent organs, creating abnormal communications. The tumour outgrows its blood supply → central necrosis → wall breaks down into adjacent hollow viscus	Rectovesical fistula: pneumaturia, faecaluria, recurrent UTIs. Rectovaginal fistula: passage of stool/flatus per vagina. Enterocutaneous fistula: faecal discharge from abdominal wall or perineum (rare)	Proximal faecal diversion (loop colostomy/ileostomy) to divert faecal stream away from the fistula, then definitive resection ± neoadjuvant chemoRT if feasible
Sacral nerve/plexus invasion	Locally advanced/recurrent tumour invading the sacral nerve plexus (S2–S4) in the presacral space	Intractable pelvic/perineal pain (neuropathic character — burning, lancinating, worse at night); sciatica-like radiation; bladder and bowel dysfunction	Palliative RT; neuropathic pain management (gabapentin/pregabalin, opioids); nerve block; consideration of pelvic exenteration in highly selected cases
Ureteric obstruction	Locally advanced pelvic tumour directly compressing or invading the ureters (more common on the left side due to the anatomy of the sigmoid-rectal junction)	Hydronephrosis → progressive renal impairment (raised creatinine); may be asymptomatic or cause flank pain; bilateral obstruction → post-renal AKI	Ureteric stenting (JJ stent) or percutaneous nephrostomy (PCN); definitive treatment of the tumour

Complication	Pathophysiology	Clinical Features
Hepatic metastases	Most common site of distant metastasis via portal venous drainage (superior rectal vein → IMV → portal vein → liver). Distal rectal tumours may bypass the liver and metastasise directly to the lungs via the IVC ^[1]	Hepatomegaly (hard, irregular, nodular), RUQ discomfort, jaundice (if mass effect on bile ducts or extensive parenchymal replacement), raised ALP/GGT, deranged LFTs
Pulmonary metastases	Haematogenous spread to lungs. Also transcoelomic seeding to pleura	Dyspnoea, cough, haemoptysis, pleural effusion
Peritoneal carcinomatosis	Transcoelomic spread — tumour cells shed from the serosal surface into the peritoneal cavity, implanting on peritoneal surfaces	Ascites (exudative), abdominal distension, early satiety, small bowel obstruction from omental caking, Blumer's shelf (pelvic nodularity on DRE), Krukenberg tumour (ovarian metastasis) ^[1]
Bone metastases	Haematogenous spread — less common in CRC than breast/prostate/lung	Bone pain (often sacral/pelvic due to anatomical proximity), pathological fractures, hypercalcaemia
Venous thromboembolism	Malignancy induces a hypercoagulable state through tissue factor expression, tumour-derived procoagulant factors, venous stasis (pelvic tumour compression), and immobility	DVT (leg swelling, calf tenderness, Homan's sign), PE (chest pain, dyspnoea, tachycardia, hypoxia). Malignancy is the most common condition associated with VTE in our locality — up to 10% of patients with unprovoked VTE have an underlying malignancy ^[27]

High Yield – VTE and Malignancy

Up to 10% of patients with "unprovoked" VTE have an underlying malignancy ^[27]. For every patient with unprovoked VTE, perform a thorough history (constitutional symptoms), physical examination, and appropriate investigations (CXR, AXR, abdominal ultrasound, tumour markers). Colorectal cancer is one of the common occult malignancies discovered in this scenario.

2. Complications of Treatment

A. Post-Operative Complications (After Rectal Surgery)

These are organised by timing: immediate (intra-operative) → early ( < 30 days) → late ( > 30 days) ^[1]^[4]^[24]^[28].

Complication	Pathophysiology	Key Points
Massive bleeding requiring conversion to laparotomy ( < 10%) ^[1]	Injury to presacral venous plexus (massive venous bleeding from sacral basal vertebral veins — these are valveless and communicate with the vertebral venous plexus, making haemostasis very difficult), or injury to major vessels (iliac artery/vein)	Presacral venous bleeding can be catastrophic and notoriously difficult to control. Surgical strategies include packing with haemostatic agents, thumbtack pins into the sacrum
Injury to neighbouring structures ^[1]^[4]^[28]	The deep pelvis is a tight space with many vital structures in close proximity	Left ureter and gonadal vessels, iliac artery ^[1]; GB, D2 (right hemicolectomy) ^[1]; seminal vesicles (LAR) ^[1]; spleen (splenic flexure mobilisation in TME) ^[1]; ureteral/bladder/urethral injury ^[28]
Autonomic nerve injury (especially in rectal surgery) ^[1]	The pelvic autonomic nerves (sympathetic hypogastric nerves and parasympathetic pelvic splanchnic nerves S2–S4) run in close proximity to the mesorectum	Sympathetic injury → urinary incontinence, impaired ejaculation ^[1]. Parasympathetic injury → urinary retention, erectile dysfunction ^[1]. TME with nerve-sparing technique minimises this risk. High tie vs low tie: high tie if reducing tension is desired; low tie (distal to left colic artery) avoids damage to the hypogastric nerve and thus lower risk of autonomic dysfunction ^[1]
GI organ injury ^[28]	Splenic/duodenal/pancreatic/gastric injury during mobilisation	Splenic injury during splenic flexure mobilisation may require splenectomy

Complication	Pathophysiology	Clinical Features and Management
Surgical site infection ^[28]	Contamination from bowel contents (colorectal surgery is clean-contaminated at minimum); risk factors: malnutrition, DM, immunosuppression, age > 60, ASA > 2, faecal contamination, extensive surgery, prolonged pre-op hospitalisation ^[4]	Incidence 5–15% ^[4]. Wound erythema, warmth, swelling, purulent discharge. Management: wound opening, drainage, antibiotics, dressing changes
Post-operative ileus ^[28]	Normal physiological response to bowel handling during surgery; exacerbated by opioid analgesia, electrolyte imbalance (hypokalaemia, hypomagnesaemia), intra-abdominal sepsis	Abdominal distension, absent bowel sounds, nausea/vomiting, inability to tolerate oral intake. Management: supportive (NGT decompression, IV fluids, correct electrolytes), consider prokinetics; prolonged ileus ( > 5 days) should prompt a search for complications (e.g., anastomotic leak, intra-abdominal collection)
Anastomotic leak — the most feared early complication ^[4]^[28]	Breakdown of the surgical anastomosis — ischaemia at the anastomotic site (inadequate blood supply), tension on the anastomosis, poor tissue quality (irradiated tissue, malnutrition, steroids), or technical error. Classically occurs on day 4–7 ^[4]	Incidence: 1–5% overall, but up to 10% in low anterior resection ^[4] (risk increases the lower the anastomosis — ileoileal < ileocolic < colocolic < ileoanal ^[4]). Risk factors: patient factors (liver/renal impairment, steroid use, suboptimal bowel condition in emergency surgery) and surgeon factors (experience and expertise) ^[4]
		Clinical signs: pain, fever, tachycardia, feculent or purulent drainage ^[28]. Radiological signs: fluid or gas containing collections ^[28]
		Management: fluid resuscitation + broad-spectrum IV antibiotics, bowel rest, image-guided percutaneous drainage of abscess, temporary faecal diversion, or drainage/resection of the anastomosis ^[28]. This is why a temporary diverting loop ileostomy is routinely fashioned after low anterior resection — if a leak occurs, faecal diversion is already in place, converting what could be a life-threatening faecal peritonitis into a contained and manageable pelvic collection
Anastomotic bleeding ^[28]	Bleeding from the staple/suture line	Management: blood transfusion and correction of underlying coagulopathy ^[28]. Most settle spontaneously; endoscopic haemostasis or re-operation if severe
Pelvic bleeding ^[4]	Oozing from the raw presacral surface after TME, especially if irradiated tissue	Monitor haemoglobin; transfuse as needed; re-operation if haemodynamically significant
Infections ^[4]	UTI, phlebitis, pneumonia, wound infection	Standard post-operative infection management
DVT/PE	Post-operative immobilisation + malignancy-associated hypercoagulability	Prophylaxis with LMWH, early mobilisation, pneumatic compression devices

Anastomotic Leak — Why is Low Anterior Resection Riskier?

The lower the rectal anastomosis, the higher the risk of leak (up to 10% in LAR). This is because: (1) the blood supply to the distal rectal stump relies on the middle and inferior rectal arteries after ligation of the superior rectal artery at the IMA; (2) the deep pelvis makes technical suturing/stapling difficult; (3) neoadjuvant radiotherapy impairs tissue healing by causing fibrosis and microvascular damage; (4) there is no serosal covering below the peritoneal reflection to seal micro-leaks. This is exactly why a diverting loop ileostomy is created — it does NOT prevent the leak, but it protects the patient from the catastrophic consequences of a free faecal leak into the pelvis.

Complication	Pathophysiology	Clinical Features and Management
Low Anterior Resection (LAR) Syndrome ^[1]^[4]	Signs/symptoms: change in bowel movement (ranging from constipation to faecal urgency, faecal incontinence) that persists ≥ 1 month after surgery ^[1]. Pathophysiology: colonic dysmotility, neorectal reservoir dysfunction, and anal sphincter dysfunction ^[1]	Affects up to 50–90% of patients after LAR to varying degrees. Prevention: post-op pelvic floor muscle exercise, anterograde colonic irrigation via stoma/enema, faecal diversion ^[1]. Management: antidiarrhoeal agents, transanal irrigation, pelvic floor rehabilitation, sacral nerve stimulation ^[1]. Patients must be counselled pre-operatively
Anastomotic stricture ^[1]^[28]	Fibrosis and scarring at the anastomotic site, exacerbated by prior radiotherapy, subclinical leak, or ischaemia	Progressive difficulty passing stool, narrow-calibre stools. Majority do not require intervention ^[28]. For those requiring treatment: finger dilatation for low anastomosis and endoscopic balloon dilatation for high anastomosis ^[1]^[28]
Fistula ^[1]^[28]	Late breakdown of the anastomosis or radiation-induced tissue necrosis creating abnormal communications	Enterocutaneous fistula: can be managed conservatively since most will close spontaneously ^[28]. Rectovaginal or rectourinary fistula: should be managed initially with proximal faecal diversion ^[1]^[28]
Impotence ^[4]	Damage to pelvic autonomic nerves during TME — parasympathetic nervi erigentes (S2–S4) control erectile function; injury causes neurogenic erectile dysfunction	Occurs in 15–50% of males ^[4]. Risk is higher with APR, very low tumours, and extensive lateral lymph node dissection. Can be mitigated by nerve-sparing TME technique
Urinary dysfunction	Sympathetic nerve injury → bladder neck incompetence → incontinence. Parasympathetic injury → detrusor underactivity → retention	Urinary retention requiring catheterisation, or stress/urge incontinence. May improve over 6–12 months as nerves recover
Perineal hernia ^[1]	Follows APR — the perineal wound creates a defect in the pelvic floor through which abdominal contents can herniate	Perineal bulge, discomfort, rarely obstruction. May require surgical repair
Adhesions / Adhesive small bowel obstruction ^[4]	Post-surgical adhesion formation — fibrous bands between loops of bowel and between bowel and abdominal wall/pelvis	Colicky abdominal pain, distension, vomiting. Management: initially conservative ("drip and suck"); surgery if signs of strangulation or failure to improve
Tumour recurrence ^[4]	Local recurrence in the pelvis (from residual microscopic disease, especially if CRM was positive/threatened) or distant metastasis (liver, lung)	Recurrence occurs in ~40% of CRC patients ^[1]. Follow-up to detect recurrence: CEA, rigid sigmoidoscopy, LFT, CT, colonoscopy ^[1]. Salvage resection can confer survival benefit if recurrence is detected early ^[4]

Stomas (colostomy or ileostomy) are commonly fashioned in rectal cancer surgery — either as temporary diverting loop ileostomy (to protect low anastomosis in AR) or permanent end colostomy (after APR). Each has its own complications ^[1]^[28]:

Timing	Complication	Pathophysiology
Early ( < 30 days)	Stomal bleeding ^[28]	From mucocutaneous junction or mesenteric vessels
	Stomal necrosis ^[28]	Ischaemia of the terminal bowel due to mesenteric vessel compromise or excessive tension — appears dark/dusky rather than healthy pink/red. Urgent revision if necrosis extends below fascial level
	Stomal retraction ^[28]	Insufficient bowel length mobilised, excessive tension, or ischaemia → stoma sinks below skin level → poor appliance fit → leakage
	Mucocutaneous separation ^[28]	Breakdown of the suture line between bowel and skin — risk of peritonitis if deep
	Skin irritation and dermatitis ^[28]	Most common in end and loop ileostomy due to high-output and high alkaline enzymatic effluent ^[28] — the ileal content contains active digestive enzymes that cause chemical burns to the peristomal skin
Late ( > 30 days)	Parastomal hernia ^[28]	Herniation of bowel through the fascial defect around the stoma — most common late stoma complication. Risk factors: obesity, coughing, wound infection. May require surgical repair with mesh
	Stomal prolapse ^[28]	Telescoping of bowel through the stoma — more common with loop colostomies. Usually reducible; surgical revision if recurrent or complicated
	Stomal stenosis ^[28]	Fibrosis and contracture at the skin/fascial level — difficulty with appliance function, obstruction. May require dilatation or revision

3. Complications of Neoadjuvant/Adjuvant Therapy

Timing	Complication	Pathophysiology
Acute (during/shortly after RT)	Radiation proctitis	Direct radiation damage to rapidly dividing mucosal cells → inflammation, oedema, ulceration. Symptoms: diarrhoea, tenesmus, urgency, mucoid/bloody PR discharge
	Radiation cystitis	Bladder mucosa is within the radiation field → irritative urinary symptoms (frequency, urgency, dysuria, haematuria)
	Radiation enteritis	Small bowel loops that fall into the pelvis receive radiation damage → watery diarrhoea, cramping, nausea
	Skin reaction	Erythema, desquamation of perineal/gluteal skin — painful but usually self-limiting
	Myelosuppression	Radiation to pelvic bone marrow → leucopenia, thrombocytopenia (usually mild with modern conformal techniques)
Late (months to years after RT)	Chronic radiation proctitis	Progressive vascular damage (radiation vasculopathy → endarteritis obliterans) → mucosal telangiectasia → chronic PR bleeding. Can present years after treatment. Management: endoscopic argon plasma coagulation, sucralfate enemas, formalin application
	Radiation fibrosis	Fibrosis of pelvic tissues → anastomotic stricture, ureteric stricture, bowel stricture
	Small bowel stricture/obstruction	Fibrosis and adhesion of irradiated small bowel → chronic SBO
	Secondary malignancy	Radiation-induced cancers (rare, latency > 10 years) — sarcoma within the radiation field
	Pelvic insufficiency fractures	Radiation damage to pelvic bones (sacrum, pubic rami) → stress fractures. Presents with pelvic pain; diagnosed on MRI
	Impaired wound healing	Irradiated tissue has reduced vascularity → poorer healing of the surgical anastomosis and perineal wound (in APR) — this is why pre-operative RT causes less long-term morbidity than post-operative RT, as the tissue has not yet been surgically disrupted ^[4]

This is why neoadjuvant RT is preferred over adjuvant RT: pre-op RT is associated with a risk of poor wound healing, but post-op RT is associated with increased fibrotic strictures ^[4] — and overall, pre-op RT has fewer acute and late toxicities because the tissue being irradiated has intact vascularity.

Adverse effects of cytotoxic chemotherapy ^[24]:

Mucositis — direct toxicity to rapidly dividing oral and GI mucosal cells → painful oral ulcers, dysphagia, diarrhoea
Nausea and vomiting — stimulation of CTZ (chemoreceptor trigger zone) in area postrema and peripheral 5-HT3 receptors on vagal afferents; managed with ondansetron (5-HT3 antagonist), dexamethasone, aprepitant (NK1 antagonist)
Diarrhoea — direct mucosal injury (especially irinotecan, which causes both early cholinergic diarrhoea and late secretory diarrhoea)
Febrile neutropenia — myelosuppression → profound neutropenia (ANC < 0.5 × 10⁹/L) + fever → medical emergency requiring urgent IV broad-spectrum antibiotics (e.g., piperacillin-tazobactam), blood cultures, and close monitoring. Neutrophils are the first-line phagocytic defence; their depletion leaves patients vulnerable to overwhelming bacterial sepsis
Alopecia — damage to rapidly dividing hair follicle cells
Hand-foot syndrome — especially capecitabine ^[24] — capecitabine is metabolised to 5-FU by thymidine phosphorylase, which is highly expressed in the palms and soles → localised drug accumulation → painful erythema, swelling, desquamation
Oxaliplatin-specific: peripheral neuropathy — dose-limiting; cumulative; presents as cold-triggered distal paraesthesias (tingling, numbness in fingers/toes); acute cold-induced laryngospasm. Mechanism: oxaliplatin chelates Na⁺ channels, causing hyperexcitability of peripheral nerves. May be irreversible at high cumulative doses

Agent	Key Side Effects	Pathophysiology
Bevacizumab (anti-VEGF) ^[24]	Haemorrhage, impaired wound healing, arterial thromboembolic events ^[24]; hypertension, proteinuria, GI perforation (1–2%)	VEGF is essential for normal vascular homeostasis, wound healing (angiogenesis), and endothelial integrity. Blocking VEGF → disrupted vascular repair → bleeding, poor wound healing, fragile tumour vasculature → perforation
Cetuximab/Panitumumab (anti-EGFR) ^[24]	Cutaneous reactions (rash, pruritus, nail changes), headache, diarrhoea, infection ^[24]	EGFR is highly expressed in skin (keratinocytes); blockade → impaired epidermal proliferation and differentiation → acneiform rash (paradoxically, severity of skin rash correlates with treatment response)
Pembrolizumab/Nivolumab (anti-PD-1)	Immune-related adverse events (irAEs): pneumonitis, colitis, hepatitis, thyroiditis, dermatitis, hypophysitis	Checkpoint inhibitors unleash T-cell activity, which can attack normal tissues → autoimmune-like inflammation in virtually any organ. Managed with corticosteroids and, if severe, immunosuppression

5-year survival by stage ^[4]:

Stage	Rectal CA 5-Year Survival
Stage I	74%
Stage IIA	65%
Stage IIB	52%
Stage IIC	32%
Stage IIIA	74%
Stage IIIB	45%
Stage IIIC	33%
Stage IV	6%

Note that Stage IIIA (T1–2, N1) paradoxically has a similar survival to Stage I — this is because the tumour is small and only 1–3 nodes are positive. In contrast, Stage IIC (T4b, N0) has worse survival despite being "Stage II" — because the tumour directly invades other organs.

Aim: detect recurrence (~40%) and metachronous tumours (new primary CA diagnosed > 6 months afterwards) ^[1].

Use a stage-, recurrence-risk- and treatment-specific plan for patients who could benefit from treatment of recurrence. Clinical review and CEA are commonly performed every 3–6 months initially, with CT chest/abdomen/pelvis at scheduled intervals during the first 3–5 years. Exact schedules vary by guideline; routine PET-CT is not recommended. New symptoms or an unexplained CEA rise need investigation. Five years without recurrence does not eliminate future second-primary risk.

Clear the colon perioperatively; if obstruction prevented complete colonoscopy, complete it within 3–6 months after surgery. Surveillance colonoscopy is generally at 1 year, then 3 years later, then 5 years later if normal; shorten for relevant polyp findings or hereditary syndromes. Rectal local excision and non-operative watch-and-wait require additional local surveillance and must not use the routine colectomy schedule alone.

NICE follow-up recommendations, ACS survivorship guideline, US Multi-Society Task Force colonoscopy guidance.

High Yield Summary

Complications of CA Rectum — Key Points

Disease complications: Obstruction (most common presentation leading to emergency surgery), perforation (caecal perforation via closed-loop mechanism — highest mortality), fistula formation (rectovesical, rectovaginal), sacral nerve invasion (intractable pain), VTE
Post-surgical complications: Classified as immediate/early/late
- Anastomotic leak is the most feared early complication — classically day 4–7; incidence up to 10% in LAR; diverting ileostomy protects the patient
- LAR syndrome is the most common late functional complication — faecal urgency, frequency, incontinence; multifactorial (colonic dysmotility, neorectal reservoir dysfunction, sphincter dysfunction)
- Autonomic nerve injury: sympathetic → ejaculatory dysfunction/incontinence; parasympathetic → erectile dysfunction/urinary retention
- Stoma complications: early (necrosis, retraction, skin irritation) and late (parastomal hernia, prolapse, stenosis)
Therapy complications: Pelvic RT causes radiation proctitis/cystitis/enteritis acutely and fibrosis/stricture/secondary malignancy late; chemo causes myelosuppression, mucositis, neuropathy (oxaliplatin), hand-foot syndrome (capecitabine); anti-VEGF causes bleeding/poor healing/perforation; anti-EGFR causes acneiform rash
Recurrence: ~40% overall; detected by serial CEA, CT, and colonoscopy; salvage resection can confer survival benefit if detected early

Active Recall - Complications of CA Rectum

References

^[1] Senior notes: Maksim Surgery Notes.pdf (Colorectal cancer section, p.107–108) ^[4] Senior notes: Ryan Ho GI.pdf (p.139, p.169, p.173, p.175–177) ^[24] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.699, p.708) and MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.902, p.911) ^[26] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (p.67) ^[27] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf (p.16) ^[28] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (p.708) and MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.911)

High Yield Summary

CA Rectum — Definition, Epidemiology, Risk Factors, Anatomy, Aetiology, Pathophysiology, Classification, and Clinical Features

Definition: Malignant neoplasm of the rectum; endoscopically defined as up to 15 cm from anal verge; oncologically defined as bowel below peritoneal reflection
Epidemiology: CRC is the most common cancer in HK (1st in males, 2nd in females); incidence 74.1/100k/yr; M:F = 1.5–1.6:1; peak 60–70y; median age 68; ~24% present as stage IV
Key risk factors: Age > 50, male, FHx, FAP, Lynch syndrome, IBD (UC > CD after 8–10 years), obesity, red/processed meat, smoking, alcohol; protective: aspirin/NSAIDs, fibre, physical activity
Pathways: CIN pathway (85%) = adenoma-carcinoma sequence (APC→KRAS→SMAD4→TP53); MSI pathway (15%) = defective MMR genes → better prognosis, responsive to immunotherapy
Anatomy: Mesorectum is key — TME reduced local recurrence from 25–40% to < 5–10%; CRM is the most important prognostic factor; distal rectal tumours can metastasise to lungs bypassing liver via IVC
Spread: Direct (radial — critical in rectal CA), lymphatic (Virchow's node), haematogenous (liver MC, then lungs), transcoelomic (Krukenberg tumour, Pouch of Douglas)
Clinical features: Rectal bleeding, change in bowel habit, tenesmus, mucus, anaemia are the cardinal symptoms; DRE is essential — most rectal tumours are palpable; left-sided tumours tend to obstruct while right-sided tend to bleed
Staging: TNM (AJCC 8th ed); minimum 12 LN for adequate staging; MRI pelvis is the gold standard for local staging of rectal CA

High Yield Summary

Differential Diagnosis of CA Rectum — Key Points

Rectal bleeding DDx: Haemorrhoids (most common cause of PR bleeding but can coexist with CA), anal fissure, diverticular disease (acute, profuse, painless), angiodysplasia, IBD, infective/ischaemic/radiation colitis, solitary rectal ulcer syndrome; don't forget massive UGI bleed can present as haematochezia (10–15%)
Change in bowel habit DDx: IBS (diagnosis of exclusion — no alarm features), IBD, diverticular disease, thyroid disease, drugs
Rectal mass DDx: Adenomatous polyp, carcinoid, GIST, lymphoma, endometriosis, presacral tumour, inflammatory mass (TB, Crohn's, diverticular abscess), rectal prolapse; don't forget non-GI pelvic masses (ovarian, uterine, bladder, prostate)
IDA in > 50: Always scope both upper and lower GI to exclude malignancy
LBO: CA colon/rectum is the most common cause (~60%); DDx includes sigmoid volvulus, diverticular stricture, hernia, pseudo-obstruction
Critical pitfalls: Haemorrhoids + CA coexist → always scope; TB colitis mimics CA in HK → rule out before biologics; IBS is a diagnosis of exclusion requiring absence of alarm features

High Yield Summary

Diagnostic Criteria, Algorithm and Investigations for CA Rectum

Colonoscopy + biopsy is the gold standard for diagnosis — tissue is needed; CEA is NOT diagnostic
DRE is the essential bedside examination — palpates ~70–80% of rectal tumours; assesses distance from anal verge, mobility, sphincter involvement, and Blumer's shelf
Staging paradigm for rectal cancer:
- MRI pelvis for local staging (T, N, CRM, EMVI, sphincter) — determines need for neoadjuvant therapy
- CT thorax + abdomen + pelvis for distant staging (liver, lung, peritoneum)
- Molecular profiling (KRAS/NRAS, BRAF, MSI/MMR) for targeted therapy decisions
CEA: low sensitivity/specificity for diagnosis; role is in prognostication, monitoring, and recurrence detection; post-op takes 4–6 weeks to normalise
Always scope entire colon: synchronous cancers in 3–5%, synchronous polyps in 30–50%
CRM ≤ 1 mm on MRI = threatened → neoadjuvant chemoRT indicated
Apple core lesion on barium enema is the classical radiological finding of annular constricting carcinoma

High Yield Summary

Management of CA Rectum — Key Points

Surgery with TME is the cornerstone — dissection along the "holy plane" between mesorectal and presacral fascia; decreases local recurrence and preserves autonomic nerves
Surgical options: Local excision (very early T1), Anterior Resection with TME (sphincter-preserving), APR with permanent colostomy (low tumours/poor sphincter/positive margins)
Neoadjuvant chemoRT is indicated for locally advanced rectal cancer (T3/T4, N+, threatened CRM) — 3 indications: resectable but locally advanced, borderline resectable, low-lying tumour for sphincter preservation
Long-course chemoRT (50.4 Gy + 5-FU) is the HK standard; short-course RT (25 Gy in 5 fractions) can be part of a delayed-surgery/TNT protocol; choose by MRI risk and regression needs
Watch and Wait: Clinical complete response after neoadjuvant → option of organ preservation with intensive surveillance; ~20% regrowth rate
Postoperative chemotherapy: depends on pathology and treatment already given; no automatic extra course after completed TNT
Metastatic CRC targeted therapy: Left-sided RAS/BRAF-wild-type → chemo + anti-EGFR; RAS-mutant/right-sided → often chemo + anti-VEGF; BRAF V600E → combined BRAF/EGFR targeting; MSI-H/dMMR → checkpoint blockade
CEA is NOT diagnostic — used for prognostication, monitoring, and recurrence detection

High Yield Summary

Complications of CA Rectum — Key Points

Disease complications: Obstruction (most common presentation leading to emergency surgery), perforation (caecal perforation via closed-loop mechanism — highest mortality), fistula formation (rectovesical, rectovaginal), sacral nerve invasion (intractable pain), VTE
Post-surgical complications: Classified as immediate/early/late
- Anastomotic leak is the most feared early complication — classically day 4–7; incidence up to 10% in LAR; diverting ileostomy protects the patient
- LAR syndrome is the most common late functional complication — faecal urgency, frequency, incontinence; multifactorial (colonic dysmotility, neorectal reservoir dysfunction, sphincter dysfunction)
- Autonomic nerve injury: sympathetic → ejaculatory dysfunction/incontinence; parasympathetic → erectile dysfunction/urinary retention
- Stoma complications: early (necrosis, retraction, skin irritation) and late (parastomal hernia, prolapse, stenosis)
Therapy complications: Pelvic RT causes radiation proctitis/cystitis/enteritis acutely and fibrosis/stricture/secondary malignancy late; chemo causes myelosuppression, mucositis, neuropathy (oxaliplatin), hand-foot syndrome (capecitabine); anti-VEGF causes bleeding/poor healing/perforation; anti-EGFR causes acneiform rash
Recurrence: ~40% overall; detected by serial CEA, CT, and colonoscopy; salvage resection can confer survival benefit if detected early

CA Rectum

1. Definition

2. Epidemiology

2.1 Global Burden

2.2 Hong Kong Epidemiology

2.3 Demographics

3. Risk Factors

3.1 Non-Modifiable Risk Factors

3.2 Modifiable Risk Factors

3.3 Protective Factors

4. Anatomy and Function of the Rectum

4.1 Gross Anatomy

4.2 The Mesorectum

4.3 Blood Supply

4.4 Lymphatic Drainage

4.5 Nerve Supply

4.6 Anal Sphincter Complex

5. Aetiology and Pathophysiology

5.1 Molecular Pathways

A. Chromosomal Instability (CIN) Pathway (85%) [2][8]

B. Microsatellite Instability (MSI) Pathway (15%) [2][8]

5.2 Hereditary Syndromes

5.3 Routes of Spread

5.4 Tumour Biology Relevant to Rectal Cancer

6. Classification and Staging

6.1 Histological Types

6.2 TNM Staging (AJCC 8th Edition, 2017)

6.3 Modified Dukes' Classification (Historical but still used)

6.4 MRI-based Staging for Rectal Cancer

7. Clinical Features

7.1 Overview

7.2 Symptoms with Pathophysiological Basis

A. Local Symptoms

B. Obstructive Symptoms

C. Constitutional/Systemic Symptoms

D. Symptoms of Metastatic Disease

7.3 Signs with Pathophysiological Basis

A. General Examination

B. Abdominal Examination

C. Digital Rectal Examination (DRE)

D. Signs of Complications

8. Summary of Right-sided vs Left-sided Clinical Presentations

Active Recall - CA Rectum (Part 1: Definition to Clinical Features)

References

Approach to Differential Diagnosis

Organising the Differential

A. Differential Diagnosis of Rectal Bleeding

B. Differential Diagnosis of Change in Bowel Habit

C. Differential Diagnosis of a Rectal Mass

D. Differential Diagnosis of Iron Deficiency Anaemia (IDA)

E. Differential Diagnosis of Large Bowel Obstruction (LBO)

Diagnostic Decision Flowchart

Key Differentiating Features — Summary Table

Active Recall - Differential Diagnosis of CA Rectum

1. Diagnostic Criteria

2. Diagnostic Algorithm

3. Investigation Modalities

A. Bedside and Clinical Examination

B. Blood Tests

C. Tumour Markers

D. Endoscopic Investigations

1. Colonoscopy + Biopsy — The Gold Standard [1][4]

2. CT Colonography (Virtual Colonoscopy) [1][4]

3. Flexible Sigmoidoscopy [4]

4. Double-Contrast Barium Enema (DCBE) [1]

E. Imaging for Staging

1. MRI Pelvis — The Gold Standard for Local Staging of Rectal Cancer

2. CT Thorax + Abdomen + Pelvis (with IV contrast) — Distant Staging

3. PET-CT (18F-FDG PET/CT)

4. Endorectal Ultrasound (ERUS)

5. Other Imaging

F. Molecular Biomarker Testing

4. Summary of Investigations by Purpose

5. Classical Radiology Findings Worth Knowing

Active Recall - Diagnosis and Investigation of CA Rectum

Treatment selection: MRI risk and MMR (reviewed September 2026)

1. Overarching Principles

2. Management Algorithm — Stage-by-Stage Overview

3. Surgical Treatment

3.1 Surgical Principles