Colorectal Flashcards
(117 cards)
1
Q
What is the aetiology of pilonidal disease?
A
Acquired/modern hypothesis
- Hairs fall down into the natal cleft.
- Friction from the buttocks causes the hairs to burrow in and create these tracts.
- Dilatation of the hair follicles around puberty provide entry points for hair.
This results in a foreign body reaction which generates the cysts.
2
Q
What are the risk factors for pilonidal disease?
A
-Modifiable – smoking, diabetes, prolonged sitting.
Non-modifiable - age, ethnicity (Mediterranean), hirsutism, male gender, excessive perspiration, deep natal cleft
3
Q
What are some non-operative treatments of pilonidal disease?
A
- Weight loss, hygiene, smoking cessation can help.
Lazer hair removal may help – although the evidence isn’t concrete.
4
Q
What is the PITSTOP study?
A
Study looking at quality of life outcomes for minimally invasive treatments of pilonidal disease vs surgery
Minimally invasive procedures had better QOL, fewer days of work, but higher recurrence rates.
5
Q
What are the factors which contribute to a rectal prolapse?
A
Weak pelvic floor muscles.
Redundant sigmoid colon.
Sphincter dysfunction/weakness/and low anal resting tone.
Chronic straining causing rectal intussusception
Slowed intestinal transit.
6
Q
What are the risk factors for rectal prolapse?
A
- Multiparity
- Pelvic floor dysfunction
- Prior pelvic floor surgery
- Pelvic floor anatomical defects such as an enterocoele, recto-coele, cystocoele.
- Pelvic floor anatomical disorders such as weakness of levator ani
- Collagen disorders such as scleroderma
- Deep pouch of Douglas
- obesity
7
Q
How is rectal prolapse graded?
A
Grade 1 - prolapse to proximal extent of rectocoele.
Grade 2 - prolapse to level of rectocoele but not into anal canal.
Grade 3 - prolapse to top of anal canal.
Grade 4 - prolapse into anal canal
Grade 5 - external prolapse.
8
Q
What factors help determine if the patient should have a Delormes or Altmeiers?
A
Length of prolapse
- >5cm should do Altmeiers.
Rectal ischaemia
- if evident may need to be resected (i.e. Altmeiers)
Medical co-morbidities
- Altmeiers has higher risk of anastomotic leak and pelvic sepsis
- Altmeiers has better longevity with lower recurrence rates (10% vs 30%)
9
Q
What are the causes of obstructive defecation?
A
Structural
- Rectocoele
- Intussusception
- Enterocoele.
- Perineal descent
- Rectal prolapse
Functional
- Pelvic floor dyssynergy
- Poor propulsion
10
Q
What is pelvic dyssynergy?
A
In normal evacuation, rectal pressure rises and anal pressure falls - allowing the passage of a stool. Pelvic dyssynergy is a functional cause of obstructive defecation where this is impaired.
11
Q
What is obstructive defection?
A
Obstructive defecation is a syndrome characterised by frequent passage of hard stool, straining, tenesmus, with self digitation.
12
Q
What does defecating protography assess?
A
Dynamic investigation of rectal empyting
Allows visualisation of:
- anatomical abnormalities - namely rectocoele, intussusception, rectal prolapse, enterocoele, sigmoidocoele, and perineal descent.
- Functional problems - changes in ano-rectal angle, the extent and duration or rectal emptying, “trapping” of stool within a rectocole, assessment of perineal descent
13
Q
What are the causes of a rectocoele?
A
Muscular or nerve damage sustained during vaginal delivery
Hormonal changes
Paradoxical contraction of the puborectalis.
Previous vaginal tear/repair.
14
Q
What is the pathogenesis of solitary rectal ulcer?
A
Secondary to disordered evacuation associated with straining
Associated with paradoxical contraction of pubo-rectalis upon straining.
Persistent and prolonged straining pushes the prolapsing rectum against the closed pelvic floor, resulting in ischaemia, trauma, and ulceration.
15
Q
What is the treatment of solitary rectal ulcer?
A
Non-surgical
- stool-bulking agents.
- avoidance of straining
- pelvic floor retraining
Surgical options
- rarely indicated
- usually only given for concomitant problems such as prolapse
16
Q
Explain how stool bulking agents, osmotic laxatives, stimulant laxatives, and stool softeners work - and give an example of each.
A
Stool bulking agents
- contains indigestible polysaccharides
- thus stool absorbs water and becomes bulky
- colonic wall stretches and triggers peristalsis
- psyllium husk
Osmotic laxatives
- osmotically active substances triggers fluid influx by osmosis - triggers peristalsis.
- lactulose, sorbitol, phosphate enemas, molaxol
Stimulant laxatives
- directly stimulate myenteric nervous system
- senna, bisocodyl
Stool softeners
- anionic surfactants reduce surface tension - allow water and lipids to mix into stool
- docusate sodium.
17
Q
What are the anatomical and mechanical factors which maintain continence?
A
Anal sphincter
- Internal anal sphincter – expansion of the circular layer of the bowel wall. Tone contributes 70-80% of the resting sphincter pressure.
- External anal sphincter – extension of the levator ani muscle (puborectalis). Contributes to the ability to voluntarily squeeze the anal sphincter complex.
- Thus, passive leakage is usually a problem with the internal sphincter, whereas’s frank incontinence and urge symptoms are due to the external sphincter.
Anal mucosal folds and vascular cushions
- Help to create a seal and contribute about 10% of the resting tone
Puborectalis muscle
- Forms a sling around the rectum which leads to the anal-rectal angle which acts like a flap valve (similar to the GOJ)
17
Q
What are the two types of incontinence?
A
Passive incontinence
- characterised by lack of awareness of need to pass stool.
Urge incontinence
- has desire and incontinence occurs despite efforts to retain stool
17
Q
What are the 4 broad factors which maintain continence?
A
Mechanical and anatomical factors
Rectal and anal sensation
Rectal compliance.
Stool consistency
18
Q
How does rectal and anal sensation contribute to continence?
A
The anorectal inhibitory reflex pathway is when the rectum is full, the internal anal sphincter relaxes, which leads to a reflexive contraction of the external anal sphincter. This provides a sensation of urgency, and leads to relaxation of the puborectalis muscle which decreases the angulation of the rectum and allows defecation.
19
Q
What is the nerve supply of the rectum and anal canal?
A
Above the dentate line
- Receives visceral sensory innervation
* Pelvic splanchnic nerves - S2-S4
○ Transmits sensation of rectal distension and fullness, triggering the urge to defecate
* Superior hypogastric plexus (T11 - L2)
○ Modulates visceral sensation and regulates internal sphincter tone
Below the dentate line
- Receives visceral sensory innervation
* Pudendal nerve provides sensation (S2-S4)
○ Via inferior rectal nerve
* The pudendal nerve also supplies motor fibers to the external anal sphincter (which is under voluntary control)
- Via inferior rectal nerve
20
Q
What does ano-rectal manometry allow assessment of?
A
Anal sphincter tone and strength
Can test rectal tone or sensation.
Can assess resting tone of anal canal (IAS) and squeeze pressures (EAS)
Can fill up a balloon and assess the recto-anal reflex of the IES as the rectum is distended
21
Q
What are the non-operative treatments for constipation?
A
- Dietary modification
- Psyllium husk - can improve stool consisteny
- Loperamide for diarrhoea.
- Laxatives for constipation.
- Pads
- Pelvic floor physiotherapy – for period of biofeedback and retraining.
- Enemas - to allow complete evacuation.
There is actually no good evidence for any of these treatments but is still the mainstay of non-operative treatment.
22
Q
How does sacral nerve stimulation work for patients with incontinence?
A
- Thought to be a multifaceted process
- The sacral nerves are involved in rectal sensation, and function of the internal and external sphincters.
- Sacral nerve stimulators deliver electrical pulses which result in improved function of these nerves.
- What the outcome is:
- Turns off faecal urgency/reduces the overactivity of the rectum - thus good for urge incontinence.
- Slows down the waves of peristalsis
- Increases the sphincter tone.
- Improves rectal compliance and colonic motility.
- Patients need to have an intact sphincter mechanism
- Involves electrodes being placed on S2-S4 sacral nerve roots at the back
23
What is anal Pagets disease? What is it associated with?
Adenocarcinoma in-situ arising from apocrine glands of the perineum.
Is associated with an underlying colorectal cancer in about 50% of cases
Also associated with urothelial cancer and gastric cancer
24
What is the treatment of Perianal Pagets?
Includes excision or topical treatments (retinoids)
Tehre is no ev
25
Where abouts does HPV infection occur in the anal canal?
The dentate line is the macroscopic marker of the junction of the embryological ectoderm and embryonic hindgut at about 1/3 along the length of the anal canal.
Between the top of the anal canal, and the dentate line, is a transitional zone where epithelium is changing from columnar to squamous
- This zone is particularly vulnerable to HPV infection and dysplasia.
26
What is the treatment of anal warts?
Cryotherapy
5% imiquimod
Topical ablation.
Trichloroacetic acid.
Surgical excision.
Electrocautery
27
What are the risk factors for anal SCC?
Receptive anal intercourse
HIV
HPV 16 18
Smoking
Previous cervical or vulval cancer
Organ transplant recipients
28
How does HPV cause squamous neoplasia?
HPV infects the basal epithelial cells and has a prediliction for the anal transformation zone.
Oncoprotein E6 switches off p53 which is a tumour suppressor gene.
Oncoprotein E7 switches of retinoblastoma - again this is a tumour suppressor gene.
The above results in increased gene dysregulation - thus cellular proliferation increases - resulting in dysplasia and then cancer.
29
How is HSIL/LSIL diagnosed?
Acetic acid (stains the abnormal tissues) and then Lugols iodine (stains the normal tissues) is applied
Dysplastic lesions appear acetowhite
30
What is the risk of progression to cancer for HSIL?
10% at 10 years.
30% at 10 years if patient has HIV
If patients have risk factors for anal cancer - this can also elevate risk
- i.e. MSM, immunosuppression, HPV
31
What is the management of LSIL
Surveillance
In north shore
- EUA
- if EUA negative for HSIL or cancer then
- yearly clinical follow up.
32
What is the management of HSIL?
Ablation - uses electrocautery to destroy the tissue.
Excision - can be used for small areas which aren't going to cause anal stenosis.
Topical agents - such as topical 5FU or imiquimod.
ANCHOR 2022 (NEJM) was stopped early because of the significant benefit for preventing anal cancer in patients with HSIL
33
How would you workup a patient with anal cancer?
- Examination under anaesthetic.
* Can assess tumour, size, involvement of adjacent structures and nodal involvement.
* Allows biopsy
- Flexi sig to investigate the rectum.
- PET-CT for systemic staging
* This is funded for staging in NZ
- MRI pelvis for locoregional staging
- Endo-anal can also be used for local staging.
FNA - for inguinal nodes if unclear clinically or radiologically.
34
T staging for anal cancer
N staging for anal cancer
T1 - tumour < 2cm.
T2 - 2-5cm
T3 - tumour > 5cm.
T4 - any size that invades adjacent organs.
N1a - inguinal, mesorectal, internal iliac, obturator nodes.
N1b - external iliac nodes.
N1c - both
NB: Common iliac nodes is M1
35
What is the treatment of anal SCC?
Modified Nigro protocol
- 50.4 Gy given in 28 daily fractions with mitomycin-c and 5-FU used as a radiosensitizer.
- Includes prophylactic low dose radiotherapy to the inguinal nodes.
- This achieves equivocal outcomes to APR
- Patients need re-assessment every 3 months
- If a patients tumour hasn’t completely regressed at 6-8 weeks, you can continue to monitor for up to 6 months before committing the patient to a salvage APR.
- Patients may have a response from treatment up to 6 months
- Approximately 30% of patients will have a local failure and require an APR.
36
When is surgery indicated for anal SCC?
Local excision
- Can only be considered in selected cases – T1 (less than 2cm) tumour at the anal margin. Which can be excised with clear margins (>5mm).
- Even in these cases, local recurrence is high – up to 50%.
- The companion series advises against local resection of T1 tumours
APR
- Is not first line.
- If offered for patients with tumour persistence or tumour recurrence after radiotherapy
- If occurs, usually requires are myocutaneous flap
- Sometimes patients will require an APR due to the complications of CRT i.e. incontinence, fistula’s.
Defunctioning stoma
- This may be required for patients to get them through there CRT.
- Indications include incontinence, obstruction, perianal sepsis, tenesmus and pain.
- If patients do need this treatment, only 50% will ever be reversed and if they are, they will have poor functional outcomes.
37
How are positive nodes managed in anal cancer?
- Higher dose of radiotherapy is given for patients with positive nodes.
- If patients have ongoing enlarged nodes after treatment
* Should FNA - as may be enlarged due to inflammation
- If persistent or recurrent nodal disease is confirmed - can proceed to radical groin dissection.
38
What are the causes of pruritis ani?
- Idiopathic
* Often related to over-washing or poor hygiene.
- Dermatological condition
* Contact dermatitis
* Psoriasis, lichen sclerosis, lichen planus.
- Infection
* Fungal
* Group A strep
* Parasitic.
- Anorectal disorders
* Haemorrhoids
* Anal fissures
* Fistula-in-ano
* Rectal prolapse
- Gastrointestinal disorders
* Faecal incontinence
* IBD
* Colorectal cancer
- Dietary
- Spicy foods, coffee, ETOH
39
What is the treatment of pruritis ani?
- Treat underlying pathology
- Hygiene – cleansing perineum with water and dabbing to dry.
- Any itch powder
- Systemic anti-histamine
- Short course of topical steroids.
- Loose underwear with non-allogenic material
40
How are perianal fistulas classified?
Parks classification
1. Inter-sphincteric - 45%
2. Trans-sphincteric - 30%
3. Supra-sphincteric - 20%
4. Extra-sphincteric - 5%
41
How much sphincter can you divide in anal fistula surgery?
Depends on
- pre-operative continence.
- previous surgery or trauma.
In general
- avoid dividing more than 1/3 of muscle (either internal or external sphincter)
42
What is the pathophysiology of a perianal fissure?
- Traumatic ulceration of the epithelium secondary to passing of a hard stool.
- This incites a secondary increased tone of the anal sphincter, resulting in reduced NO production, thus reduced blood supply/perfusion to the injured area.
6 and 12 o'clock are watershed areas (blood supply comes in from the side) - fissures occur here
43
What are the topical treatments of perianal fissure and how do they work?
- GTN cream – rectogesic cream. GTN results in release of NO binds which binds to cGMP leading to relaxation of the muscle and causes vasodilation to the smooth muscle stimulating healing. Can cause headaches which impacts on compliance.
- Nifedipine cream (0.3%) – CCB reduces intracellular calcium causing relaxation of the IES.
- Cream should be put on the tip of an ear bud and inserted into the anal canal – twice per day for 6 weeks.
This treatment is approximately 70% effective.
44
When performing a lateral sphincterotomy? How far can you extend the incision?
Do not extend more superiorly than the upper end of the fissure or the dentate line.
45
What is the location and venous drainage of internal and external haemorrhoids?
Internal
- above dentate line
- drain into middle rectal veins.
External
- below dentate line.
- drain into pudendal veins.
- have somatic pain fibers associated with them
46
What is the pathophysiology of haemorrhoids?
Internal haemorrhoids – fibromuscular ligaments supporting the anal cushions deteriorate, allowing them to slide down into the anal canal, which leads impaired venous drainage, stasis, transudation and venous thrombosis.
47
What are the risks of injecting haemorrhoids with phenol?
If injected anteriorly - can result in prostatitis
48
What are the 3 risk categories for colonoscopy surveillance for asymptomatic individuals with a family history?
Group 1
- Patients with first degree relative who had CRC > 55 years old.
- There is no specific surveillance recommendations for this group.
Group 2
- One first degree relative diagnosed with CRC < 55 years.
- Two first degree relatives on the same side of the family diagnosed with CRC at any age.
- Should have colonoscopy 5 yearly from aged 50 OR 10 years prior to earliest age at which CRC was diagnosed in family member. Once aged 60 – can join NBSB
Group 3
- Fhx of Lynch, FAP, or other CRC syndromes.
- 3 relatives on same side of family having CRC at any age with one being a first degree relative.
- There are quite a few other criteria but generally this looks Lynch syndrome risk factors and polyposis syndrome risk factors.
These patients should be referred to the NZFGCS
49
What genes are affected in the chromosomal instability pathway of bowel cancer?
APC
KRAS
SMAD4
TP53
50
What are the other manifestations of FAP?
Gastrointestinal
- Fundic gland polyps of the stomach (same as the ones patients on PPI’s get) – don’t have a malignant potential
- Duodenal polyps – 5-10% lifetime risk of duodenal cancers. Occur later in life.
- Hepatoblastomas
- Extra-hepatic biliary tree cancers
Non-GI
- Desmoid tumours (see below)
- Congenital hypertrophy of the retinal pigmented epithelium. If they have multiple and are bilateral this can be pathognomic of FAP.
- Multiple osteomas - often in mandible, skull or tibia.
- 4-5x risk of papillary thyroid cancers
- Adrenal tumours.
- Astrocytomas/glioblastomas.
51
What is the utility of the Spigelman classification? What are its components?
- Looks at number of polyps, polyp size, histology, and degree of dysplasia.
- Dictates how aggressively patient should be surveilled and when patient should undergo duodenectomy.
52
What is the Amsterdam criteria and what is its utility
Identifies who should be tested for Lynch syndrome amongst asymptomatic patients.
Can remember as the "3, 2, 1" rule.
- 3 family members with Lynch syndrome associated cancer
- across 2 generations.
- 1 cancer diagnosed before age of 50.
- FAP excluded
53
What is the pathological phenotype of lynch syndrome associated cancers?
- L - lymphocytes/lymphoid aggregates.
- A - associated cancers.
- M - mucinous/metachronous.
- P - poorly differentiated
- S - signet cell/synchronous.
54
What was the utility of the Bethesda criteria?
Was used to decide which tumours should be tested for MLH1, MSH2, MSH6 and PMS2
Is now obselete as all colon cancers in NZ get tested.
55
What is the immunohistochemical testing pathway for colon cancers in NZ?
1. All newly diagnosed cancers should be tested for MMR deficiency on initial biopsy.
- This is MLH1. MSH2, MSH6, PMS2
- If MSH2, MSH6 or PMS2 – need to refer to Genetics for Lynch testing
- If MLH1 is deficient – need to test BRAF which will help differentiate between a sporadic cancer and a Lynch syndrome associated cancer.
- If BRAF is positive in the context of a deficient MSH1 tumour, you can say this is a sporadic cancer.
- If BRAF is negative - test for MLH1 promotor hypermethylation - if negative - refer to genetic testing for lynch
2. Conduct BRAF mutation analysis in all newly diagnosed stage IV cancer
- MMR proficient stage IV tumours which a BRAF mutant have a significantly poorer prognosis.
- BRAF status will also determine what targeted therapy can be considered.
3. Conduct extended RAS mutation testing before considering EGFR targeted monoclonal antibodies.
of note: these treatments are not available in nz.
56
What are the other cancers associated with lynch syndrome?
Think "all epithelial linings of the abdominal cavity with endometrial being the highest risk"
Stomach
Small bowel
Pancreatic.
Biliary tree
Urothelial.
Endometrial - this is quite high.
57
What is the role of Aspirin in patients with lynch syndrome?
- There is good studies that aspirin from 25 years old reduces the risk of CRC in patients with lynch.
- NSAIDS block COX1/COX2
80% of CRC show COX-2 overexpression.
58
What is the surveillance and recommendations for patients with lynch syndrome?
Screening
- Yearly colonoscopies from 25 years old or 5 years before the earliest relative developed CRC.
- Prophylactic colectomy is usually not recommended
- Yearly transvaginal ultrasound until hysterectomy + BSO
Aspirin/chemoprevention
- There is good studies that aspirin from 25 years old reduces the risk of CRC in patients with lynch.
- NSAIDS block COX1/COX2
* 80% of CRC show COX-2 overexpression.
Prophylactic Surgery
- There is no evidence that subtotal colectomy reduces mortality over good surveillance.
- Some patients, however will elect for colectomy.
- Total abdominal hysterectomy
* Is recommended for patients once they have completed child-bearing .
Treatment of patients with a lynch syndrome associated colon cancer
- Subtotal colectomy versus segmental colectomy
* There is no clear cut recommendation
* The risk of developing a metachronous bowel cancer is about 16% in those who have had a cancer.
* Extended resection (ileorectal anastomosis)
○ is associated with poorer function - increased stool frequency
- Does reduce risk of metachronous colon cancer
59
What is Peutz-Jegher syndrome
- Autosomally dominant inherited mutation of the STK11 gene which encodes a tumour suppressor protein.
- Present with polyps in the SI, colon and rectum – non-neoplastic hamartomas.
- Polyps consist of non-neoplastic connective tissue covered by a hyperplastic epithelium.
- Typical presentation is small bowel intussusception in childhood or adolescents.
- Can also present with bleeding
- Other characteristic features are dark blueish buccal and mucosal pigmentation. Can also occur on hands, feet and anus.
- Also at risk of breast, ovary, cervical, fallopian tube, thyroid, lung, bile duct, pancreas, and testicular cancer.
***even though the polyps are hamartoma’s, adenocarcinomas can arise from these hamartomas. The lifetime risk of developing colon cancer for these patients is 40-60%***
60
What is Juveline polyposis syndrome?
- Another autosomally dominant inherited condition.
- Mutation of the SMAD4 gene – which encodes a tumour suppressor gene.
- Present with multiple juvenile or hamartomata polyps – similar to the Peutz-Jeghers polyps.
- Often present with childhood with intussusception or bleeding.
Diagnosis
- Any number of juvenile polyps in a patient with a family history.
OR
- Multiple juvenile polyps throughout the GI tract AND at least 5 juvenile polyps of the colon.
***unlike solitary juvenile polyps, patients with polyps who have familial juvenile polyposis syndrome, can develop adenocarcinoma from the polyps***
Other associated cancers
- Gastric, pancreatic, duodenal.
Other conditions associated with familial juvenile polyposis.
- Hereditary haemorrhagic telangiectasia – can cause bleeding from vascular malformation in the GI tract and lung.
- 20% of patients will have other genetic abnormalities such as malrotation, cardiac anomalies etc.
Treatment
- Patients should be colonoscopically surveilled
Prophylactic surgery is only recommended if there are too many polyps to endoscopically resect.
61
What is the WHO criteria for serrated polyposis syndrome?
Need one of the following
- At least 5 histologically confirmed serrated polyps, proximal to the rectum, with at least 2 > 1cm.
- At least 20 serrated polyps anywhere in the colon. Need 5 proximal to the rectum
- One serrated polyp in a patient with a first degree relative with SSP
62
What is the definition of the top of the rectum?
- Surgical - convergence of the teniae coli, at the sacral promontory
- Radiological - take-off of the sigmoid mesentery (level of S3)
- Distance - 12 to 15cm from the anal verge.
63
What are the predictors of local recurrence in rectal cancer?
- Size of primary
- Involvement of CRM
○ Main factor; which can also be modified by optimal treatment
○ Postive CRM defined as tumour within 1mm margin of specimen
- Distal location of tumour
- Extramural vascular invasion (n.b. also higher predictor of distant mets than nodal status; usually locoregional nodes will be removed by TME).
- Tumour differentiation
- Nodal status (N stage)
- Extent of extramural spread (T stage)
- Peritoneal involvement by tumour
64
What are the current indications for neoadjuvant treatment in rectal cancer ?
- Patients with an elevated of recurrence despite TME, should be identified, and offered neoadjuvant therapy.
- The indications is dependent on the location
Upper rectal
- Not indicated unless T4b
- These tumours are generally managed like a colon cancer
Mid rectal
- T3/T4 with or nodal positive
Low rectal
- T2+ tumours if close to sphincters
Other indications.
- Threated CRM
- LVI
65
When would you consider long course radiotherapy over short course radiotherapy for rectal cancer ?
- There is evidence that when the CRM is threatened, long course CRT is associated with a higher Ro resection rate.
- Thus for bigger tumours, where downstaging is important prior to surgery – it is likely better to give long course CRT – this is what is used more often in Australasia.
66
What are the indications for TEMS or TAMIS?
- Superficial T1 cancer - limited to the submucosa.
- Tumour < 3cm in diameter.
- Well differentiated histology - no LVI, no PNI
- Mobile, non-fixed.
- Involving <30% of the bowel lumen circumference
- Patient is able to comply with frequent post-operative surveillance
If tumour has adverse histology - should proceed to resection
67
How would I treat a splenic flexure cancer?
- Obstructed - do an extended right
- Not obstructed - segmental resection of the splenic flexure taking the left branch of the middle colic and left colic.
On the basis of
- study at NSH by Vasey et al showing most splenic flexure tumours drained to the left colic .
AND
- 2020 meta-analysis published in Diseases of the Colon and rectum showed no difference in overall complication rate or overall survival between extended right, segmental resection and left hemicolectomy.
68
What are the principles of ERAS
Pre-op principles
- Patient education and engagement.
* Informing patient about process, recovery milestones, active role in recovery
- Medical optimization
* Managing chronic diseases, smoking and ETOH cessation
- Pre-op nutritional support
* Screen for malnutrition and provide supplementation.
- Carbohydrate loading
* Carbohydrate drink 2 hours before to minimise fasting.
Intraoperative principles
- Minimally invasive surgery
- Multi-modal opioid-sparing analgesia.
- Goal directed fluid therapy
- Temperature control.
- Avoidance of unnecessary drains.
Post-op
- Early mobilisation
- Early oral intake.
- Early removal of catheters and IV lines
- Defined discharge criteria.
- MDT involvement.
69
What are the indications for adjuvant chemotherapy in colon cancer?
High risk stage II
- Poorly differentiated tumours
- Mucinous subtype
- LVI
- BD3 Tumour budding
- Bulking tumours – T3 or T4 or perforated cancer.
- <12 nodes in the specimen
Stage III
70
Write down the peritoneal cancer index
Look it up
71
What are the TWO principles of population screening
Important health problem
Suitable latent asymptomatic stage
Natural history of condition understood
Acceptable treatment
Facilities for diagnosis and treatment
Suitable test - high specificity and sensitivity
Safe and acceptable to population screened
Agreed policy on who to treat
Cost of finding is economically balanced with overall health
Case finding should be continuous proces
72
What endoscopic features suggest an adenoma may be malignant ?
Friability
Ulceration
Induration.
Adherence to underlying tissue.
Demarcated depressed area.
Stalk of base swelling.
Chicken skin appearance
73
What is the definition of a malignant polyp?
Dysplasia which invades through the muscularis mucosa into the submucosa.
74
What is the risk of lymph node metastasis by depth of invasion for Haggit and Kikuchi?
Haggit 1-3
- very low risk (head, neck and stalk)
- don't need to offer resection.
Haggit 4
- equivalent to SM2 or SM3 (23%)
Kikuchi
- SM1 - 2%
- SM2 - 8%
- SM3 - 23%
75
Apart from invasion depth, what are other factors which increase the risk of a malignant polyp having lymph node metastasis?
- Villous architecture
- Poorly differentiated tumour
- Margin or resection < 1mm. This margin can be difficult to determine if there has been a hot snare removal.
- LVI
- Tumour budding
- Piecemeal resection
Piecemeal removal of a polyp
Invasion > 1mm is associated with a significantly increased risk of lymph node metastasis.
76
What is the treatment of microscopic colitis?
· Avoid culprit medication (statins, PPIS, NSAIDS, SSRIs)
· Anti-diarrhoeal medications.
· Budesonide course - 6-8 weeks
○ If not responding add cholestyrami
- Infliximab is third line treatment.
77
What toxins does C-diff cause?
Cytotoxin A (enterotoxin) and cytotoxin B (cytotoxin)
78
What is pseudomembranous colitis?
C-diff is one of the causes of pseudomembranous colitis.
Is a non-specific patter of injury resulting from decreased oxygenation, endothelial damage, and impaired blood flow to the mucosa, which can be triggered by a number of disease states.
These include:
- Medications - cisplatin, cyclosporin, Docetaxel.
- Infections
- CMV, E coli 0157
- Inflammatory disease
- Bechet's disease
- IBD
79
What are pseudomembranes composed of in pseudomembranous colitis?
Pseudomembranes are composed of bacteria, fibrin, neutrophils, from crypt erosions.
80
Talk about
- campylobacter
- E coli 0157:57
- Salmonella
Campylobacter
- Campylocater jejuni or campylobacter coli
- Inhabits intestinal tracts of poultry - foodborne and waterborne disease
- Sometimes a/w bloody diarrhoea.
- Associations and complications
* Pseudoappendicitis
○ Pain is caused by acute ileocaecitis.
* Reactive arthritis
* Guillain Barre syndrome
- Treatment
* Supportive
* If severe disease - azithyromycin
E coli 0157:H7
- Shiga toxin-producing E coli - Enterohaemorrhagic
- Bloody diarrhoea
- Is associated with haemolytic uraemic syndrome
- Treatment is typically supportive treatment as antibiotics may worsen the disease and is associated with HUS
Salmonella
- Enteric fever is caused by salmonella typhi and salmonella paratyphi
- Nontyphoidal salmonellae is most common infection.
- Non-typhoidal
- Causes
* Gastroenteritis.
* Enteric fever
* Osteomyelitis.
* Endovascular infection
- Enteric fever
* Classically get bradycardia, pulse-temperature dissociation, "rose spots"
* Hepatosplenomegaly, intestinal bleeding and perforation may occur.
* Requires treatment with antibiotics.
81
Talk about
- Shigella
- Yersinia
Shigella
- Gram negative rod.
- Is very contagious.
- Humas are only natural reservoir for disease
- Causes direct damage to the colon through toxin effects
- Inection is usually self-limiting.
- Antibiotics usually reserved
* Immunosuppressed
* Hospitalization
* Severe disease
Yersinia
- Zoonotic infections of domestic and wild animals
- Includes yersinia pestis, yersinia enterocolitica, yersinia pseudotuberculosis.
- Also associated with
* Pharyngitis.
* Pseudoappendicitis
* Can cause erythema nodosum and reactive arthritis
82
What is the pathophysiology of ischaemic colitis?
- Vascular insufficiency, inadequate collateral circulation, mucosal hypoxia, and reperfusion injury all contribute to ischaemic colitis.
- Vascular insufficiency
* Reduced perfusion due to hypotension, atherosclerosis, embolism/thrombosis, hypercoagulable states.
- Inadequate collateralization
- Mucosal hypoxia and reperfusion injury
* Initial hypoxia results in mucosal sloughing and loss of epithelial barrier integrity.
* Reperfusion results in oxidative stress which can drive inflammation.
83
What is the pathophysiology of acute and chronic radiation proctitis.
Acute - direct toxic effects to mucosa - mucosal cells break down resulting in inflammatory reaction
Chronic
- Mucosal atrophy and fibrosis occurs.
- sclerosis of blood vessels occurs - obliterative endarteritis - results in mucosal ischaemia.
84
What is the endoscopic findings of radiation proctitis
Vascular ectasia - hallmark finding
Pallor
Friability
Oedema
Ulceration
85
What is the treatment of radiation proctitis?
APC
RFA
Hyperbaric oxygen
86
What are the macroscopic features of Crohns disease?
- Stiff and thick walled
- Fat creeping
- Cobblestone appearance
- Deep linear ulcers that can lead to fistulation.
- Aphthous ulcers - develop on surface of submucosal lymphoid nodules and are usually the first macroscopic appearance of CD
- Pseudopolyps
- Lymphadenopathy
- Strictures
87
What microscopic features are used to determine between Crohns and UC
Goblet cells
- UC - depleted
- CD - preserved
Glandular architecture
- UC - depleted
- CD - perserved
Lymphocytic infiltrate
- UC - dense
- CD - light
Muscularis propria.
- UC - thickened
- CD - normal
Submucosal inflammation
- UC - nil
- CD - heavy
Granulomas
- UC - nil
- CD - lots
88
What endoscopic findings are seen in Crohns?
Apthous ulcers.
Fissures
Cobblestone appearance.
Bleeding.
Oedema.
Hyperaemia
Ulcers
89
What is the Montreal classification used for?
Used to classify/phenotype Crohns
Divided into
- Age
- location
- ileal
- colonic
- ileocolonic
- upper
- Behavous
- non-stricturing, non-penetrating.
- stricturing
- penetrating
- perianal
90
What does the simple endoscopic score for CD look at?
5 regions
- TI, R colon, T colon, L colon, rectum.
- Looks for presence of ulcers, size of ulcers, extent of ulcerated surface, and narrowings.
91
Why does bile salt malabsorption occur in Crohn's disease and what is the sequalae?
- This is common in ileal Crohn’s. Due to the fact that bile salts are not being absorbed in the inflamed terminal ileum.
- Can get associated reduced absorption of Vitamins ADEK.
- Decreased bile salt absorption can lead to precipitation of cholesterol stones.
- Decreased bile salt absorption can lead to steatorrhoea. Steatorrhoea promotes the absorption of oxalate which can cause kidney stones.
- Bile salts in the colon precipitate diarrhoea.
92
What is the medical treatment of Crohns?
Inducing remission
- Mild to moderate
* First line
○ Steroids.
§ Budesonide 9mg
§ IV prednisone.
○ Aminosalicylates
§ Used for Crohns colitis
□ Mesalazine
□ Sulfasalazine
○ Anti-TNF
§ Can be used first line for perianal fistulas.
* Second line
○ Biologics and immunomodulators.
- Maintenance of remission
* Immunomodulators
○ Should be started and then steroid weaned.
○ Includes 6-MP, Azathioprine, methotrexate.
* Biologics
○ Often used second line OR upfront in severe disease.
Immunomodulators
- Azathioprine and 6-mercaptopurine are commonly used
* These inhibit cytotoxic T cells and NK cells
* Thiopurine methyltransferase needs to be tested (TPMT)
○ Low TPMT is associated with increased risk of myelotoxicity
○ High TPMT activity - often don't respond to treatment.
* Side effects
○ Bone marrow suppression, pancreatitis, hepatitis.
- Methotrexate
* Folic acid antagonist.
* Inhibits T cell activation
* Side effects
* Hepatic fibrosis, BM suppression, pulmonary fibrosis, kidney failure.
- Mycophenolate mofetil
* converted to mycophenolic acid which blocks purine synthesis and thus proliferation of new cells.
Biologics
- These are commonly used
- Includes TNFa inhibitors (infliximab and adalimumab), anti-integrin therapies (vedolizumab), and anti-interleukin therapy (Stelara)
- Very effective at inducing remission.
- Possible increased risk of malignancy long term.
- Increased risk of infective complications.
Antibiotics
- Metronidazole has been shown to reduce recurrence of disease after ileal resection and there are some small studies which show that they can induce remission.
EEN
- Patients are exclusively enterally fed which may induce remission.
- Is something which is generally used in children
- Patients are given a polymeric diet (who carbohydrates and proteins)
(as opposed to amino acids/elemental diet which is used in severe malnutrition)
93
What are the indications for surgery in CD?
Indications for surgery
- Failed medical management
- Disease associated complications (i.e. perforation, abscess, stricturing etc).
Failed medical management
- Ongoing symptoms despite medical therapy.
- Poor compliance with medications
- Adverse side-effects to medications.
Disease associated complications
- Can include acute and chronic complications.
Acute complications
- Development of an abscess/perforation
- Haemorrhage
- Obstruction
- Toxic megacolon.
Chronic complications
- Fistulas
- Growth retardation in children
- Cancers
- Obstruction due to fibrotic strictures.
94
What are the different types of stricturoplasty which can be performed for CD and UC?
look it up
95
Indications for surgery in UC
- Emergency
- Refractory disease not responsive to medical therapy
- Fulminant colitis
* Severe inflammation with toxic symptoms (fever, pain, tachycardia, hypotension, leucocytosis)
- Bleeding
- Perforation
- Toxic megacolon
* Colonic dilatation >6cm with toxicity.
- Elective
- Malignant transformation - dysplasia or carcinoma
- Side-effects of medical management.
- Chronic refractory disease.
Growth failure in paediatric patients.
96
What is the Mayo score?
- Has 4 categories
* No inflammation
* Mild disease
* Moderate
* Severe
- Looks at
* Erythema
* Vascular pattern (gets lost)
* Friability
* Contact bleeding
- Ulceration
97
What are the histological findings of UC?
- Mucosal inflammation, ulcers, atrophy
- Goblet cell depletion (doesn’t occur in Crohn’s)
- Distorted and atrophic glandular architecture
- Vascular congestion.
- Crypt abscesses
- Heavy mucosal (lamina propria) lymphocytic and neutrophil infiltration
* Minimal submucosal lymphocytic infiltration
- Pseudopolyps – granulation tissue over exposed muscularis propria.
98
What does the Montreal classificaiton in UC look at?
Disease extent and severity
E1 – proctitis only.
E2 – left side colitis distal to splenic flexure.
E3 – extensive colitis, proximal to the splenic flexure.
S0 – clinical remission.
S1 – mild disease. < 4 bowel motions per day, with or without blood with no features of systemic illness.
S2 – moderate disease, >4 stools per day with minimal signs of systemic toxicity.
S3 – severe disease - >6 bloody stools per day, HR > 90, temp > 37.5, Hb <105, ESR > 30.
99
What is True-love and Witts criteria?
- Either mild or severe
- Mild - < 4 stools per day with no macroscopic blood and no systemic toxicity.
- Severe > 6 stools bloody stools per day, HR > 90, temp > 37.5, anaemia, ESR > 30
100
How do aminosalicylic acids work?
Work by inhibiting the production of inflammatory mediators by the COX and lipoxygenase pathway.
101
How does Aziothioprine and 6-MP work?
- Azathioprine and 6-mercaptopurine.
- Take 2-3 months to start working thus not good for induction.
- Both purine analogues – inhibit cell proliferation and suppress the production of cytotoxic T cells and NK cells.
- Patients need to be tested for the enzyme thiopurine S-methyltransferase (TPMT) prior to starting these drugs.
If they do not have TPMT, they will not break down the drugs and they can get bone marrow suppression.
102
How does vedolizumab and Ustekinumab work?
Vedolizumab – prevents lymphocyte migration into intestinal tissue. Slower onset than other biologic treatments.
Ustekinumab (Stelara) - inhibits inflammatory mediators IL-12 and IL23
103
What is the pathophysiology of Toxic megacolon?
On histopathology there is inflammation which spreads to the smooth muscle layer – this causes paralysis of the SM and subsequent dilatation.
Increased production of NO by macrophages which inhibits smooth muscle tone which contributes to dilatation.
It is equivocal as to whether the myenteric plexus is affected.
104
What is the risk of colorectal cancer in patients with UC? With regards to time since UC diagnosis
Incidence increases with duration of time with UC. 2% after 10 years, 8% after 20 years, almost 20% by 30 years.
105
What is the diagnostic criteria for toxic megacolon?
Radiographic evidence (mandatory)
* Colonic dilatation >6cm (mandatory) affecting the transverse colon
Systemic toxicity (at least 3)
* Fever
* Tachycardia
* Leucocytosis
* Anaemia
Clinical (at least 1)
* Hypotension
* Altered mental status
* Electrolyte disturbance
- Hypotension
106
What is the role of laparoscopic lavage in diverticulitis
Laparoscopic lavage is probably feasible in selected patients – i.e. patients who a physiologically robust enough to tolerate a “lavage treatment failure” but not unwell enough where you want to commit them to a resection.
As per Siraj Rajaratnam, you could see peritoneal lavage as “an extension of non-operative management"
107
Hinchey classification
Stage I Pericolic abscess confined by the mesocolon
Stage II Pelvic abscess, distant from area of inflammation
Stage III Generalised peritonitis resulting from pericolic/pelvic abscess rupture into peritoneal cavity
Stage IV Faecal peritonitis resulting from free perforation of colonic diverticulum
108
What is the pathophysiology of colonic pseudoobstruction
Thought to result from autonomic imbalance, particularly:
↓ Parasympathetic activity (esp. sacral outflow)
↑ Sympathetic inhibition
Leads to suppression of colonic peristalsis → functional obstruction
109
What is the pathophysiology of neutropenic enterocolitis ?
Mucosal injury occurs either due to cytotoxic drugs OR impaired host defense to invasion by micro-organisms
110
What is the AAST grading system for rectal injuries?
- Grade 1
· Haematoma
· Contusion, without devascularisation
- Grade 2
· Laceration <50% of circumference.
- Grade 3
· Laceration >50% of circumference.
- Grade 4
· Laceration with extension into the perineum.
- Grade 5
- Devascularised segment.
111
What is the Rome IV criteria for IBS
Recurrent daily abdominal pain with two or more
- related to defecation.
- associated with change in frequency of stool
- associated with change in form of the stool
112
What is the Devlin classification for parastomal hernias?
1. Subcutaneous.
2. Interstitial
- hernia sac lies within the layers of the abdominal wall.
3. Intra-stomal
- sac penetrates the lumen of an ileostomy (as opposed to next to it)
4. Peristomal prolapse
- prolapsed stoma
113
What is the European hernia society classification of parastomal hernias?
1. Small <5cm parastomal hernia without incisional hernia.
2. Large >5cm parastomal hernia without incisional hernia.
3. Small < 5cm parastomal hernia with incisional hernia.
4. Large > 5cm parastomal hernia with incisional henria.
114
What are the advantages of an onlay or sublay mesh for a parastomal hernia repair?
Onlay
- straightforward technically
- no intra-abdominal dissection.
- higher risk of wound infection
Sublay
- Increased intra-abdominal dissection
- increased risk of intestinal obstruction
- associated with fewer recurrences.
115
What are the important considerations when marking someone for a stoma?
Posture
Shape of abdomen.
Skin folds.
Other stomas.
Pendulous breasts.
Vision.
Dexterity
Presence of a hernia.
