Colorectal Flashcards
Describe the grading system for haemorrhoids
Internal Hemorrhoids:
(Proximal to Dentate Line)
- Overlying Anoderm (Columnar Epithelium & Visceral Nerves)
Grading: Based on Prolapse Below Dentate Line
I (Primary): Prolapse Only with Strain
II (Secondary): Spontaneously Reduce
III (Tertiary): Manually Reduce
IV (Quaternary): Cannot Reduce
External Hemorrhoids:
Distal to Dentate Line
Overlying Skin (Squamous Epithelium & Somatic Nerves)
Mixed Hemorrhoids
Originate Both Above & Below the Dentate Line
List the non-excisional techniques available for management of haemorrhoids
- Avoidance of constipation or diarrhoea
- High fibre diet
- Adequate daily fluid intake
- Reduce time spent sitting on toilet advise don’t take phone or newspaper etc into loo with them
- sitz baths
- local anaesthetic gel analgesia
- haemorrhoidal banding risks of band misplacement below dentate line = immediate pain treat by removing it. delayed pain, urinary retention and sepsis could indicate pelvic sepsis.
- sclerotherapy by injecting small amount of 5% phenol in almond oil as irritatant that causes scarring and shrinking of haemorrhoidal tissue over time.
What are the surgical treatment options for haemorrhoids and what are their advantages/disadvantages?
HALRAR - Haemorrhoidal Artery Ligation and RectoAnal Repair - Where a proctoscope with doppler is used and guides suture placement to ligate the haemorrhoidal artery. Combined with mucopexy. Technically more challenging to learn, but equivalent results in terms of recurrence and less painful.
Closed Excision (Ferguson Technique)
Elliptical Excision of the Hemorrhoidal Bundle
Harmonic Shown to Have Decreased Pain and Bleeding than Monopolar
Deep Suture Ligation of the Vascular Pedicle at the Proximal Apex
Close with a Running-Locked Absorbable Suture
Consider Leaving the Distal End Open to Allow Drainage
Open Excision (Milligan-Morgan)
Elliptical Excision of the Hemorrhoidal Bundle
Do Not Close – Heals by Secondary Intention
No Difference in Results Between Open/Closed
Circumferential Stapled (Whitehead Hemorrhoidectomy)
By Transanal Circular Stapler
Only for Internal Hemorrhoids Proximal to the Dentate Line
Lower Pain & Recovery
Higher Recurrence & Incontinence Risk
How would you manage a patient with post-haemorrhoidectomy bleeding?
Simultaneously assess and resuscitate using CRISP algorithim.
Replace volume loss with blood if significant blood loss or haemodynamically unstable.
Ultimately patient needs to return to operating theatre to stop bleeding often requires suture if within the first 24 hours post surgery.
If >5 days down the track when eschar sloughs off, as long as patient stable will often settle without requirement for return to theatre.
What patients are at risk of post-haemorrhoidectomy bleeding and how can you mitigate some of these things?
Patient factors:
- On anticoagulants
- Haematological disorders
- Liver disease
(stop anticoagulants, don’t restart until >5 days post op, patient selection regarding the non-modifiable ones)
Disease factors:
- large grade 4 haemorrhoids
Technical factors:
- poor suture technique.
- Open haemorrhoidectomy higher risk of bleeding than closed.
What is pruritus ani and how is it worked up?
Itching/burning sensation around the anus.
Most common causes are:
Benign:
- Poor hygiene
- Idiopathic
- anorectal disease e.g haemorrhoids, fissures,
- Dietary e.g. caffeine, carbonated, spicy, dairy, tomatoes, citrus
- local irritation e.g. reaction to sanitary products or washing powder used on underwear
- infection
- lichen planus/ sclerosis
- dermatitis contact or radiation induced
- psoariasis
- diabetes
- CKD
Malignant:
SCC anus (bowens disease)
Pagets disease
Rectal cancer
Worked up with history and examination including proctoscopy. Skin biopsies may be required if any abnormality in skin appearance or concern for malignancy.
What is the rectosigmoid junction?
Junction where sigmoid becomes rectum denoted by the splaying of teniae coli, the sacral promontory, peritoneal reflection and is at level of S3.
What are Denovillier’s and Waldyers fascia?
Denovillier’s fascia is anterior to rectum (retrovesicular and restroprostatic in men, retrovaginal in women).
Waldyers fascia is posterior to rectum also called retrosacral
Describe the anatomy of the anus.
Anus extends from anorectal ring to anal margin and measures about 4cm. It is folded by 3 valves of Houston.
Anorectal ring corresponds to the levator ani muscle and is the superior margin of the surgical anal canal. (anatomical anal canal superior margin is dentate line)
The anus is divided by the dentate/pectinate line into upper 2/3 (columnar epithelium) and lower 1/3 (squamous epithelium). This is also where the crypts of Morgagni originate.
The introitus of the anal opening is called the anal verge and the anal margin extends radially 5cm out from the anal verge into the perianal skin.
The anus has an internal and external sphincter with intersphincteric groove indicated by white line landmark.
The internal sphincter is a continuation of muscularis propria and is smooth muscle and involuntary control by pelvic splanchnic nerves.
The external sphincter is striated muscle under voluntary control by internal pudendal nerve (inf rectal br) and S4 (perineal br.).
The blood supply by inferior rectal artery from internal iliacs via internal pudendal artery. The venous drainage follows artery into inferior rectal vein to internal iliac and inferior vena cava.
The lymphatic drainage anal canal to internal iliacs, anal verge to inguinal.
What is a HAL-RAR
Stands for Haemorrhoidal Artery Ligation and RectoAnal Repair.
It is a procedure used to treat grade 3/4 internal haemorrhoids.
It involves using an USS doppler to locate the haemorrhoidal artery and ligating around this with a suture (HAL) and a mucopexy or mucopexies are performed in a running suture (always culminating at least 5mm above dentate line) and then being pulled up with a slip knot to the origin to pexy the prolapsed mucosa back up into anal canal.
https://www.amisurgical.com/ami-hal-rar
What is the Cryptoglandular theory?
The anal glands/crypts of Morgagni at the dentate line become blocked by debris resulting in build up, nidus for infection to brew and then turns into an abscess.
What are the spaces where an anorectal abscess may arise? And how might these present?
- Perianal - subcutaneous around anal verge.
Submucosal - submucosal above dentate line
- Ischiorectal within fat of ischiorectal fossa, tender away from the anal verge, DRE not particuarly painful.
> post anal = posterior between levators and external anal sphincter. Can be superficial or deep to anococcygeal ligament.
> horseshoe = extends bilaterally - Intersphincteric between internal and external sphincters. Painful DRE but few external findings.
- Supralevator - Can really only evaluate on imaging e.g. CT or MRI.
How do you go about draining a perianal abscess, submucosal abscess, ischiorectal abscess, intersphincteric abscess and supralevator abscess?
Perianal - Examine preop and confirm w patient where most tender and mark with permanent marker over most tender and fluctuant area. EUA, positioned lithotomy, good lighting. DRE +/- rigid sigmoidscopy. New gloves. Radial incision oriented over side closest to anal margin and drain cavity.
Submucosal abscess
Ischiorectal abscess similar to perianal except may need to puncture anococcygeal ligament if deep and may need bilateral incisions if horseshoe (see Hanley procedure)
Intersphincteric - requires transanal drainage through incision in internal sphincter.
Supralevator: Need to drain the source…
Intraabdominal source - transabdo surgery or perc drain
- Intersphincteric Fistula: Transanal Drainage (Divide IAS)
- Transsphincteric/Ischiorectal Source Through Levators: Ischiorectal I&D
What are the indications for antibiotics in anorectal abscess’?
Most do not require antibiotics post op. I would still tend to prescribe them pre-op while awaiting access to the acute theatre.
Those I would prescribe them for post-operatively would be those with cellulitis or systemic sepsis, diabetes or immunocompromised. Also those with metallic heart valves.
Describe Goodsall’s law
Anterior fistula tracts drain radially to their internal opening to the nearest crypt in a linear path unless >3cm away from anal verge in which case can drain like a posterior fistula via long curved path to posterior midline.
Posterior fistula tracts drain towards posterior midline and take a curved path.
Describe the different locations of anal fistula.
- Submucosal - Superficial between perianal skin and anal mucosa
- Intersphincteric between perianal skin, traverses internal sphincter but not external sphincter and terminates in anal mucosa
- Transphincteric between perianal skin, tranverses both internal and external sphincters and terminates in anal mucosa.
- Suprasphincteric between perianal skin, through levator ani and down into intersphincteric groove then traverses internal sphincter and into anal mucosa.
- Extrasphincteric between perianal skin, through levator ani and terminates in rectal mucosa more superiorly.
How does botox work for chronic anal fissures?
The pathogenesis of chronic anal fissures is hypertonia of the interal anal sphincter and resultant reduced blood flow to the anal skin and mucosa and leads to an ischaemic cycle and therefore reduced ability to heal.
The botullinum toxin works as a neuroblockade preventing release neurotransmitter acetylcholine from axon endings at neuromuscular junction and in doing so results in relaxation of the internal sphincter. In relaxing the sphincter it allows blood flow to resume to the skin and allow for better healing.
Describe a treatment ladder for anal fissure.
Starting with the least invasive/fewest side effects the patient would be advised to increase fluid intake, increase fibre in diet, avoiding constipation, avoiding straining or long periods sitting on the loo so stool softeners may be required. Sitz baths.
The next step I prescribe are topical treatments. For analgesia lidocaine gel. To try reverse the hypertonia of the internal sphincter I prescribe diltiazem 2% ointment that needs a compounding pharmacy to make it. This is a calcium channel blocker. I prefer this as less likely to give a headache over glyceryl trinitrate cream 0.2% which is an alternative. With both of these need to take care in patients with cardiac comorbidities.
Should these treatments fail then under anaesthesia injection of botox is recommended. I use a lateral sphincterotomy as last resort and am mindful of contraindications if any concerns for faceal incontinence already then these should not be attempted or if on use of botox the patient gets faecal incontinence then they should not proceed to sphincterotomy.
Lastly mucocutaneous advancement flaps can be used to cover over the fissure to facilitate healing.
Another relative contraindication to surgical procedures is in Crohns unless absolutely necessary.
What are the most common pathogens in perianal abscess’?
Most common gut microbiota found in perianal abscesses are Escherichia coli, Proteus vulgaris, Staphylococcus aureus, Streptococcus species, Bacteroides, and Peptostreptococcus species
Classify the different types of ano-rectal incontinence
Urge incontinence - sensate but unable to retain faecal material despite active attempts. Usually points to sphincter dysfunction or inability of rectum to hold on to stool.
Insensible incontinence - insensate passive incontinence indicates neurogenic cause, sphincter dysfunction or impaired anorectal reflexes
Faecal seepage - leakage post a bowel motion but retained continence.
What are the treatments for faecal incontinence?
Fecal incontinence is a complex issue that is not easy to manage. The vast number of methods used to manage the condition indicates that no method works reliably. It requires a multidisciplinary approach including mental health support.
Lifestyle:
- weight loss
- dietary changes to reduce caffeine
- high fibre diet
Medication
- fibre supplements
- stool softeners and laxatives for chronic constipation as underlying cause
- anti-diarrhoeal medication e.f loperamide, codeine for underlying diarrhoea as cause
- oestrogen relacement treatment may help post menopausal
- amitryptylline for faecal and urinary incontinence
Physio therapy:
- Exercises to strengthen pelvic floor
- electrode stimulation to contract pelvic floor in those that are unable to do so voluntarily due to pudendal nerve damage
- sacral nerve stimulation. Not publicly easily accessible in NZ.
Surgery
- those without intact sphincter or who have failed above management consider surgery.
Options include sphincteroplasty, post anal augmentation to recreate anorectal angle, reconstruction with a neosphincter e.g. using gracilis muscle
Repair of underlying cause e.g haemorrhoids, prolapse
- faecal diversion with stoma
https://www.ncbi.nlm.nih.gov/books/NBK459128/#:~:text=Urge%20Incontinence%3A%20Inability%20to%20retain,bowel%20movement%20with%20normal%20continence
What is demonstrated here and how would you treat it?
This is a defecating proctogram showing resting, squeezing, straining and defecating views. It is a fluoroscopy study to assess for ano-rectal function and to diagnose rectocoele and prolapse.
This one demonstrates a rectocoele. This would be treated with lifestyle modification with increased fluid and fibre, weight loss, physiotherapist and biofeedback and in those refractory to above then surgery can be considered via transanal or transvaginal approach.
What diagnostic tools are available for ano-rectal incontinence?
History and Examination:
- assess for anal tone
- anorectal descent
- sensation
- anal wink reflex (perianal skin with a cotton ball, which causes brisk contraction of the external anal sphincter. The absence of this reflex indicates a loss of spinal arc and possibly underlying neurological disease.)
Laboratory:
- Stool spec for diarrhoeal pathogens
- Faecal elastase to assess for Pancreatic insufficiency
Endoscopic:
- Colonoscopy to evaluate for IBD or malignancy
Imaging:
- Endoanal ultrasound - assess’ the thickness of IAS and EAS
- MRI
- Defecating proctogram (fluroscopic images obtained during defecation)
Other:
- anal manometry to assess the resting and squeeze rectal pressure; the technique can also be used to assess rectal capacity and compliance
- Measuring pudendal nerve latency: To assess the integrity of the pelvic floor neuromuscular integrity
How does biofeedback work for faecal incontinence?
It works on concept of cognitive retraining of the pelvic floor and abdominal musculature to overcome the defects. It is indicated for those that have shown on anal manometry to have impaired external sphincter tone and loss of sensation to rectal distension.
What is sacral nerve stimulation and how is it performed?
The 2-step procedure involves initially placing temporary external electrodes into the sacral foramen. The stimulation decreases symptoms of fecal incontinence by enhancing the squeeze and resting anal pressures and colonic motility. Patients who respond then undergo permanent placement of an embedded neurostimulator. While good outcomes have been reported in several studies, the surgery can be associated with hematoma, seroma, and infection. In addition, lead migration and paresthesias are not uncommon. To counter these problems. sacral transcutaneous electrical nerve stimulation is now being evaluated.
Describe ways of classifying anal fistulas
Depth: High vs low (<30% transphincteric)
Complexity: Simple (single and low) vs complex (high or multiple)
By their anatomic location:(superficial, intersphincteric, transsphincteric, suprasphincteric, extrasphincteric)
Describe how you would place a seton.
In an appropriately worked up and consented patient I would position the patient in lithotomy with bright lighting. I would perform a digital rectal examination and proctoscopy. I would use a parks retractor with ample lubricant. I would use a Lockhart Mummery probe placing it into the external opening first so as not to inadvertently create false passages. Using Goodsall’s law I would look for the internal opening in the expected position. If the internal opening is not clear with these methods then using a syringe, an IVL catheter and hydrogen peroxide I can try locate the internal opening by flushing this in through external opening and observing for bubbles in anal mucosa. Once tract established I would feed a seton (vascular loop) on a mosquito clip through the external opening, retrieve it at internal opening and secure it with silk ties. I would apply this loose at skin. I would then leave this for minimum 6 weeks, often longer for tract to mature, dry
If setons fail or as part of a staged approach with setons what are the surgical options available for anorectal fistulas?
- Fistulotomy only if superficial enough.
- LIFT procedure
- Bio LIFT
- Mucosal or cutaneous advancement flap
- Fibrin glue
- Fistula collagen plug
What medical management options are available for anorectal fistulising Crohns disease?
- Immunomodulators e.g. 6-mercaptopurine and azathioprine
- Aminosalicylates e.g. sulfasalazine
- Methotrexate
- Inflixumab - anti TNFa chimeric monoclonal antibody. Other anti-TNFa therapies also available.
- Immunosuppresants e.g. cyclosporin, mycophenylate mofetil
Antibiotics - Ciprofloxacin and Metronidazole combo treatment, tacrolimus
Corticosteroids - not so much for fistulising Crohns.
https://www.gastrojournal.org/article/S0016-5085(00)80030-X/fulltext
What is Hirschsprungs disease?
Basics
Absence of Intramural Ganglion Cells of the Meissner (Submucosal) & Auerbach (Myenteric) Plexuses
From Defect in Craniocaudal Neuroblast Migration
Most Commonly Less Severe & Affects Only a Short Segment
Rare in Adults, 94% Diagnosed Before Age 5 Years
Associated with RET Mutation
Seen Especially with Long-Segment Disease – Consider MEN IIA Evaluation
More Common in Males
Presentation
Lifelong History of Chronic Constipation
Abdominal Pain
Abdominal Distention
Diagnosis
Dx: Full Thickness Rectal Bx with Aganglionosis
Radiology: Grossly Dilated Proximal Colon with Fecal Retention
Treatment
Treatment: Surgery
Short-Segment: Transanal Myomectomy
Long-Segment:
Swenson Procedure
Rectosigmoid Resection & Colorectal Anastomosis
Duhamel Procedure
Healthy Colon Lowered Posterior to Diseased Rectum Through the Avascular Plane
Diseased Rectum Left Intact
Soave Procedure
Resect Diseased Colon & Upper Rectum
Mucosa of Diseased Lower Rectum Resected
Colon Pulled Through the Lower Rectum
You see this on colonoscopy on anterior rectal wall. What are you differentials?
Benign:
Solitary rectal ulcer syndrome due to prolapse. Confirm with history, examination and biopsy.
Proctitis
Malignant:
Site of previously excised polyp/malignancy. Confirm with history, examination and biopsy.
What are the risk factors for pilonidal disease?
- Young (teens- 20s)
- Male > Female
- Hirsute (thick hairy)
- Obese
- Deep gluteal cleft
- Caucasian
- Sitting for long periods >6h
- Local trauma
Describe a classification system for pilonidal disease.
There are many out there!
I use Guner classification as easier to remember given this disease’s association with Jeep drivers in the world war ‘Gunner’.
Stage 1: single midline pit
Stage 2: Multiple pits in midline
Stage 3: Midline pits with lateral extension in one direction
Stage 4: Midline pits with lateral extension bilaterally
Stage R: Recurrent disease post operative intervention
Other classifications. include:
Tezel Classification looking at acuity of the disease
Chavoin Classification
Doll Classification
Irkorucu Classification
Karkas Classification
Lapsekili Classification
Awad Classification
How do you treat acute abscess associated with pilonidal disease?
Drain the pus through an incision lateral to the cleft. Heals better. Currettage or tract excision in acute disease is not successful. However simple drainage as above is successful final treatment for 60%.
Include antibiotics if systemically unwell, cellulitis, diabetic or immunocompromised.
What are the principles of elective surgery for pilonidal disease and describe some examples of how these priniciples are achieved.
Priniciples are predominantly to
- excise pits
- remove trapped hair
+ if performing flap surgery:
- flatten out gluteal cleft
- closure off midline
Examples are:
Minimally invasive options include:
- Pit picking - with punch biopsies of pits and removal of trapped hair with fine clamps
- video assisted sinus ablation
- midline pit excision
- marsupialisation
- excision plus flap reconstruction to flatten gluteal cleft
What are the differentials for causes of proctitis and how are they treated?
Infectious:
- most common in MSM
- gonnorhoea and chlaymida most common treated with ceftriaxone and doxycylcine respectively
- other causes HSV (acyclovir) and syphllis (penicillin)
Radiation induced
- acute usually within 6 weeks of treatment
- may require cessation of rtx
- hydration
- antidiarrhoeals
- butyrate enemas
- sucralfate enemas
chronic = obliterative arteritis (months-yrs)
- sucralfate enemas
- APC
- last resort surgery
Pouchitis after ileal ouch-anal anastomosis
Diversion proctitis
Neutropenic enterocolitis (Typhilitis) but rectal involvement v rare
Differentials go
- Anal warts secondary to HPV.
(Condyloma acuminata) - Anal SCC
- Pagets disease
Which HPV strains are high risk and which are low risk for malignancy?
High risk 16 & 18
Low risk 6, 11
Other high risks
31,33,35,39,45,51,52,56,58
Other low risks:
42,43,44
How do you treat anal condylloma acuminata?
Goal: Remove Macroscopic (Visible) Disease
At-Home Tx:
Topical Tx: Podofilox, Imiquimod or 5-Fluorouracil (5-FU)
40-60% Clearance Rate
Office-Based Tx:
Topical Tx: Podophyllin or Trichloroacetic Acid (TCA)
Liquid Nitrogen Cryotherapy
80-90% Clearance Rates
Surgical Tx: Electrocautery/Fulguration or Excision
Indications: Extensive External Disease or Lesions in Anal Canal
If Circumferential: Staged Surgery (Prevent Stricture)
If histology shows Dysplasia this does NOT require Wide Excision – Managed Similarly to Non-Dysplastic Condyloma.
High Recurrence Rates with Unknown Benefit in Prevention
Spot diagnosis go
Buschke-Lowenstein tumour/giant condyloma
- rare, large, slow growing anal wart with 50% risk of malignancy.
Needs wide local excision, high recurrrence rate and may need APR.
(think must be living in the bush (buschke) to present that late.
How do you diagnose a rectovaginal fistula?
History (esp take note of obstetric trauma, crohns, malignancy, surgery, diverticulitis, radiation), any gas or faeces from vagina, dyspareunia, recurrent UTIs
Examination - any faeces in vagina? any visible tract on speculum on proctoscopy.
EUA
Methylene blue tampon test, methylene blue enema in rectum, clean tampon in vagina, ambulate then assess tampon for any blue.
Endoscopy make sure to retroflex in rectum
Fluroscopic xray study or CT with rectal contrast
What is AIN and how is it managed?
Definition: Anal intraepithelial neoplasia is a dysplasia premalignant for anal SCC.
Incidence/risk factors:
- HPV + below
- HIV or immunocompromised incl solid organ transplant recipients
- MSM or anoreceptive sex
- smoking
- HPV‐related gynecological precancerous lesions or cancer (vulvar, cervical, or vaginal)
Pathogenesis:
HPV induced chronic inflammation induces dysplastic changes in epithelial cells that progress to squamous cell carcinoma if left unchecked.
Signs and symptoms:
Assymptomatic to perianal skin irritation or wetness or pruritis or bleeding.
Classification system:
LSIL: Low grade intrepithelial lesion = replacement of lower third of epithelium with abnormal cells
HSIL = replacemen of middle and upper thirds of epithelium with abnormal cells.
Investigations:
- EUA
- punch biopsies
use dilute acetic acid painted on to skin to identify areas to biopsy, if no areas visible then mapping biopsies in 4 quadrants.
- women also need cervical smears uptodate
Treatment: All should receive HPV quadrivalent vaccine as well.
LSIL: Observation
Surveillance Every 3-6 Months
Consider High Resolution Anoscopy (HRA) to Surveil
HSIL: Topical Therapy & Consider Ablation
Topical Tx: Imiquimod, 5-Fluorouracil (5-FU) or Trichloroacetic Acid (TCA)
Ablation Tx: Radiofrequency Ablation (RFA) or Electrocautery
What is the TNM staging of anal canal cancer?
T1 = <2cm
T2 = 2-5cm
T3 = >5cm
T4 = invading other organs
N1 = nodes involved
M1 = mets present
Stage 1 & 2 are all N0/M0
- stage 1 = T1
- stage 2a = T2
- stage 2b = T3
Stage 3a = T1/2, N1, M0
Stage 3b = T4, N0, M0
Stage 3c = T3/4, N1, M0
Stage 4 is any T any N M1
What is the treatment for anal SCC?
Nigro protocol
Chemoradiation with mitomycin and 5 flurouracil with reassessment at 8-12 weeks then again every 6-8 weeks until completion.
If fails after 6m, confirm with biopsy then APR unless if <2cm could consider WLE w 1cm margin.
Who should be considered for screening for anal cancer?
We don’t have a screening program in NZ but those that are at high risk should be aware of this and what to look out for. People at high risk include
- MSM
- prev precancer or cancer of vulva/vagina/cervix
- high risk HPV strain (16 &18)
- immunocompromised e.g. HIV or solid organ transplant recipients
What are the most common anal canal cancers?
SCC - most common ~85% Nigro
Adenocarcinoma ~10% WLE/APR
BCC
Melanoma (often mistaken for thrombosed haemorrhoid) NB no SNB required.
What is high resolution anoscopy?
Anal examination using proctoscope, colposcope and acetic acid. Allows for magnified look at anal epithelium to assess for SCC.
What is perianal Pagets disease?
Intraepithelial Adenocarcinoma of perianal skin.
usually presents as severe intractable pruritis ani and erythematous eczematous rash
Patients need colonoscopy as work up to look for synchronous colorectal malignancy (~50% pts have a synchronous visceral carcinoma) but can arise as primary pagets from apocrine glands without colorectal tumour.
What imaging is required in staging a rectal cancer and what are they each used for?
EUS - most useful for accurate T staging
MRI - best at assessing mesorectal fascia involvement and circumferential margin and nodes
CT - for distant mets.
What is the T staging for rectal cancer?
Follows that of colon cancer not anal cancer.
Stage 1-2 N0/M0
Stage 4 any T any N M1
What are the treatment options for low risk rectal cancer?
Low risk rectal cancer is defined as:
- T1/2
- <3cm
- <30% of circumference
- <8cm from anal verge
- mobile
- no lymphatic invasion
- no mucin production
These may be amenable to endoscopic or surgical resection.
If endoscopic required 10mm margin. Does not harvest any lymph nodes.
If resection options include low anterior resection or abdominoperineal resection. Need 5cm proximal margin, 1-2cm distal margin. Goal lymph node harvest 12+.
What are the treatment options for locally advanced rectal cancer?
Locally advanced rectal cancer includes those with:
- T3+ disease
- Nodal involvement
- Lymphovascular invasion
- >3cm
- >30% of circumference
- >8cm from anal verge
- tethered
- mucin production
Treatments are neoadjuvant chemoradiation therapy with 5 flurouracil or FOLFOX or CAPEOX followed by resection ~2-3months later.
Adjuvant therapy with 5FU, FOLFOX or CAPEOX in threatened CRM in T3 disease or for T4 or N+.
What are the layers of the colon wall?
- Mucosa (columnar epithelium, lamina propria, muscularis mucosa)
- Submucosa
- Mucularis propria (inner circular, outer longitudinal)
- Serosa
Describe the anatomy of the colon.
- Colon is ~155-165cm long.
- It is divided into caecum, asc, transverse, desc and sigmoid portions.
- It has 3 taenia coli (longitudinal strips of muscle that coalesce at the appendix and splay out over the rectum.
- the caecum, asc and desc portions are retroperitoneal, transverse and sigmoid are intrabdominal.
- the diameter of colon ranges from 3-9cm with caecum being the largest part at 9cm and is therefore place of highest risk for non-iatrogenic perforation (due to LaPlaces law (Largest radius will have highest surface tension)
- Wall is made up of mucosa, submucosa, muscularis propria (IC, OL) and serosa.
- it is folded into haustra by plicae semiluminares
- Its attached to the omentum along transverse colon.
- its relations include small bowel, kidneys and ureters, gonadal vessels, liver and spleen, stomach, pancreas and lesser sac.
Vascular supply:
- SMA > ileocolic, right colic & middle colic
- IMA > left colic, sigmoid and upper rectal arteries.
Hence watershed areas are splenic flexure and between upper and middle rectum.
Drains to IMV which joins SMV and becomes portal vein behind the pancreas.
Lymphatics follow arteries > SMA/IMA > preaortic > cisternia chyli.
Innervation:
- Meissners submucosa plexus
- Auerbachs myenteric plexus, outer muscularis propria
- Pelvic splanchnic nerves parasympathetic
Functions to secrete K and resorb NaCl/H2O with largest H2O capacity in the asc colon.
What is the Paris classification of colonic polyps?
Describes their appearance.
Polypoid:
Type 1p - pedunculated (on a stalk)
Type 1s - sessile (base same diameter as top)
Non-polypoid:
Type 2a - slightly elevated
Type2b - flat (height <1/2 diameter(
Type2c - depressed
Excavated:
Type 3:Cratered
What are the histological subtypes of colonic polyps?
Hyperplastic - normal cellular components with proliferative characteristics but no dysplasia.
- classic saw tooth pattern
Adenomas -
-tubular adenoma = >75% tubular features with network of branching adenomatous epithelium. most common neoplastic polyp. usually pedunculated.
- villous adenoma = >75% villous features with long glands extending from the surface straight down. most likely to produce symptoms. 50% have cancer.
- tubulovillous >25% both tubular and villous features.
Hamartomas = disorganised growth of normal tissue elements. Benign but can degenerate to adenomatous.
What are the depth of invasion classification systems for colonic malignant polyps?
Level 0 - does not invade muscularis mucosa (in situ)
Level 1 - invades hed
Level 2 - invades neck
Level 3 - invades stalk
Level 4 - invades base or involved ina sessile polyp i.e. all sessile polyps with invasive cancer are level 4.
Risk of lymph node metastasis =
<1% for Levels 0-3
30% for Level 4
SM1 - Superficial third
SM2 - Middle third
SM3 - Deep third
Risk of lymph node metastasis =
SM1 <2%, SM2/3 22-33%
What are some genetic syndromes associated with increased risk of colorectal cancer?
- Familial Adenomatous Polyposis (FAP) mutation in APC gene close to 100% chance of developing ca.
- MUTYH-Associated Polyposis (MAP) mutation in MUTYH gene~85%
- Lynch syndrome also known as Hereditary Non-Polyposis Colon Cancer (HNPCC) (MLH1, MSH2, MSH6, PMS2, EpCAM mutations) 20-80%
- Serrated Polyposis Syndrome (genetic mutation largely unknown but closest link is with RNF43) 25-75%
- Juvenille Polyposis Syndrome (SMAD4, BMPR1A mutations) 68%
- Peutz-Jeghers (STK11 mutation) 39%
- PTEN Hamartomas syndrome (PTEN mutation) 9%
NB: FAP is only one where prophylactic colectomy is advised.
All are autosomal dominant inheritance except MAP (AR) and SPS where no clear consistent genetic mutation isolated.
What is the diagnosis? Tell me about this syndrome.
Familial Adenomatous Polyposis Syndrome (FAP)
Hallmark is 100-1000s of sessile polyps.
Incidence ~1/8300 births
Lifetime risk of developing colorectal ca 100%
Onset of polyps ~50% developed by 15yo, 95% by 35yo. Av age of ca dx 35-40yo. Most of these are left sided.
Each individual polyp not at an increased risk of developing ca but the sheer abundance is why such an increased risk.
Extracolonic manifestations:
- Duodenum polyps (graded with Spiegelmans staging system looking at number of polyps, size, histological subtype & dysplasia). 2nd most common site of polyps for FAP, 2nd most common cause of death for FAP pt w predilection for periampullary region.
- Stomach polyps usually benign fundic gland polyps.
- Desmoids locally advanced 3rd most common cause of death in FAP
- Osteomas
- Brain tumours e.g. medulloblastoma
- Congenital Hypertrophy of Retinal Pigment Epithelium (dark spots on retina). Most common and earliest extracolonic manifestation of FAP. Benign.
- Dental problems e.g. missing teeth, extra teeth, impacted teeth etc.
- less common include thyroid ca, hepatoblastoma, adrenal tumours, pancreatic ca…
Genetic counselling and screening recommendations:
- Those with family hx of FAP should undergo genetic counselling and screening by age 10-12yo
- yearly colonoscopy from age 10-15yo
- upper endoscopy age 20-25 or sooner once any colonic polyps are seen. Use Spigelman stage to define frequency of screening ranging from Stage 4 every 3-6m to Stage 0 every 3-5 years.
- May also consider USS thyroid screening from late teens.
Colectomy indicated in almost all patients as treatment or prophylaxis but exact timing is debatable. Most are around age 15-25yo. Nuances of selection see another flash card.
What are the surgical options and indications for FAP patients?
2015 ACG Guidelines
Therapeutic colectomy:
———————————-
Absolute indications:
- Documented colorectal cancer
- significant symptoms
Relative indications:
- multiple adenomas >6mm
- significant increase in adenoma numbers on serial exams
- adenoma with HGD
- inability to adequately survey colon due to multiple diminuitive polyps
If otherwise not indicated above but exact timing is debatable. Most will be age 15-25yo.
The options include:
Total Abdominal Colectomy with Ileal-rectal anastomosis (i.e. spares rectum)
Adv: technically easier, lower risk of complications, no risk of sexual and bladder dysfunction, no permanent stoma.
Disadv: risk of metachronous ca in rectum 5-25%. Generally contraindicated for severe rectal disease or if patient not reliable for follow up surveillance. Requires flexible proctoscopy every 6-12m.
Total proctocolectomy and Ileal pouch-anal anastomosis.
Adv: lower risk of metachronous ca, no permanent stoma
Disadv: technically more challenging, higher risk of complications, risk of sexual or bladder dysfunction. Requires flexible pouchoscopy every 6-12m.
Total proctocolectomy with end ileostomy.
Adv: Lowest risk of metachronous ca.
Disadv: Requires permanent stoma. Risks sexual and bladder dysfunction. Requires flexible endoscopy in ostomy every year.
What is the most common cause of hereditary colorectal cancer? Tell me about the syndrome.
Lynch syndrome otherwise known as Hereditary Nonpolyposis Colon Cancer (HNPCC).
Mutations:
Most common mutations are inherited in autosomal dominant pattern with mutations in Mismatch repair (MMR) genes: MLH1- MSH2, MSH6, PMS2 or in epCAM a mutation in which causes epigenetic silencing of MSH2.
Leads to microsatellite instability.
Incidence:
Accounts for 3-5% of all colorectal ca patients. Younger onset than sporadic cancers av age 45-60.
1/279 births. 20% are sporadic mutations.
Location:
- Most commonly ca on right colon (c.f. sporadic ca’s most commonly on left)
- Propensity of synchronous and metachronous cancers.
Types:
Type 1 - no extracolonic manifestations
Type 2 - colonic + extracolonic manifestations
Extracolonic manifestations:
- Endometrial ca
- Ovarian ca
- Cancers of KUB
- Stomach
- Pancreatic
- HPB
- Breast
- Brain
- Skin
Clinical diagnosis criteria:
Amsterdam II (remember 3,2,1 rule)
- ≥ 3 Relatives with Histologically Verified Lynch Syndrome-Associated Cancer, One of whom is a first-degree relative of the other two
- ≥ 2 Generations involved
- ≥ 1Cancer case was dx before age 50
- FAP excluded.
Sensitivity 78% and Specificity 61%
Screening recommendations:
- Colonoscopy age 20-25yo
- Repeat every 1-2 years
- Upper endoscopy age 30-40 every 2-4 years
- Consider endometrial biopsy froma age 35 every 1-2 years but no proven benefit
Therapeutic Colectomy
Indications: Colorectal Cancer or Unresectable Adenomas
Colon Cancer: Total Abdominal Colectomy with Ileorectal Anastomosis (TAC/IRA) is Generally Preferred but may consider segmental colectomy in select circumstances.
Requires surveillance with Flexible Proctoscopy or Repeat Colonoscopy annually respectively.
Rectal Cancer: Consider Total Proctocolectomy (w end colostomy or ileal pouch anal anastomosis) vs Segmental Resection (low anterior resection or APR)
Prophylactic Colectomy
- generally not performed.
some indications:
- Colon technically difficult to navigate
- Unable to comply with screening
- Severe psychological distress due to fear of developing CRC
- Families with early onset or severe penetrance of CRC
- Females already undergoing Hysterectomy for Endometrial ca or a Prophylactic Total Hysterectomy and Bilateral Salpingo-Oophorectomy (TH-BSO) in females after age 40 or once child bearing completed.
Tell me about Juvenile Polyposis syndrome.
Mutation in SMAD4 or BMPR1A genes with Autosomal dominant inheritance.
Juvenile refers to appearance of the polyp not the age of onset though most present symptomatic with GI bleeding and anaemia by age 20.
Polyps are Hamartmatous and found mostly through colon (98%) but also stomach, duodenum and rest of small intestine.
Most hamartomas are benign but malignant transformation can occur.
Extraintestinal manifestations include:
Hereditary Haemorrhagic telengectasia, epistaxis and pulmonary AVMs. Skeletal stigmata include macrocephalus, hydrocephalus, cleft palate, polydactyly and hypertelorism
Which colorectal cancer syndrome has autosomal recessive inheritance? Tell me about that syndrome.
MUTYH associated polyposis (MAP)
Develop 10s-100s of adenomatous polyps, predominantly right sided. Can also have increased number of hyperplastic and mixed polyps.
Increased risk of colorectal ca.
- ~60% by age 60
- 80-90% lifetime risk without surveillance.
Extracolonic manifestations:
Other GI tract polyps and cancers
-Duodenal Polyps (17-34%)
-Duodenal Cancer (4%)
-Gastric Polyps (11%)
-Gastric Cancer (1% – Not Significantly -Higher Than the General Population)
-Bladder Cancer
-6-8% in Females
-6-25% in Males
-Ovarian Cancer (6-14%)
-Endometrial Cancer (3%)
-Breast Cancer (12-25%)
Screening recommendations:
- Annual Colonoscopy age 25-30
- Upper endoscopy every 3m-2y age 30
Colectomy indications as per FAP except differ for prophylactic colectomy.
2015 ACG Guidelines
Therapeutic colectomy:
———————————-
Absolute indications:
- Documented colorectal cancer
- significant symptoms
Relative indications:
- multiple adenomas >6mm
- significant increase in adenoma numbers on serial exams
- adenoma with HGD
- inability to adequately survey colon due to multiple diminuitive polyps
Not generally recommended
How do you diagnose Serrated Polyposis syndrome?
Unlike other inherited CRC syndromes there is no clearly associated mutation to test for on genetic testing (RNF43 is closest association).
WHO 2019 criteria need either of:
- ≥5 serrated polyps/lesions proximal to rectum with ≥5mm in size or 2 ≥10mm in size
OR - 20+ serrated polyps/lesions in entire colon with ≥5 proximal to the rectum.
The polyp count is applied cumulatively and unfortunately it is not systematically applied and diagnosis is often missed especially due to different providers and may not have access to previous results.
What is the Hinchey classification?
Grading system for severity of diverticulitis to guide clinical management. Originally an intraoperative scoring system but modified to CT findings.
1 = pericolonic abscess <4cm treat w abx alone
2 = pelvic abscess or interloop abscess or abscess >4cm. Typically treat w drain percutaneous if amenable anatomically
3 = purrelent peritonitis and most likely need theatre
4 = faeculant peritonitis need theatre.
What constitutes complicated diverticulitis?
- Perf, abscess, fistula, obstruction or stricture
- In acute or chronic setting
Nb Phlegmon or extraluminal gas alone do not constitute complicated.
When is an elective segmental colectomy indicated for diverticular disease?
- symptomatic affecting quality of life, multiple episodes per year, same or limited area of colon affected each time
- stricture or partial obstruction
Generally however first episode is usually worse so if dealt with that ok may not need much intervention in future.
What is the recommended screening for those with serrated polyposis syndrome?
- Colonoscopies every 1-3 years
- Starting age not clearly defined.
- No extracolonic manifestations to screen for.
This patient presents with dark red PR bleeding in your emergency department. Aside from the resuscitation and management of the bleeding. What do they likely have and what are the other manifestations/risks?
This is a classic hyperpigmented spots of the buccal mucosa and around the nose associated with Peutz-Jegher syndrome or a mutation in STK11/LKB1 genes. These spots are rarely present at birth but are pronounced by age 5 and can fade during puberty. They can also be around perianal skin and fingers.
These patients have high numbers of Hamartomatous polyps which are generally benign but can have a malignant transformation so at risk of colonic, stomach and small bowel cancers and they are also at risk of many other malignancies including breast, endometrial and cervical and benign ovarian tumours in women and sertoli cell testicular tumours in men. Also risk of pancreatic and lung ca.
Polyps arise in small bowel, colon, stomach and rectum in order of most frequent to less.
What do you recommend for screening for patients diagnosed with Peutz-Jegher syndrome?
Triple endoscopy (upper, lower and pill cam)
- start w baseline aged 8
- repeat every 1-3years.
- if no polyps found at index next repeat at 18yo and every 2-3y thereafter.
Breast MRI/USS/mamms starting age 30 w breast clinical exams from age 18
Pelvic exams
- testicular from age 10 +/- test USS
- pelvic exam and speculum age 18 annually
MRCP or EUS
- every 1-2y from age 30
Chest radiographs in smokers
During colonoscopy you remove 3 adenomatous polyps, 1 of them is 11mm the others are 3 and 4mm. What do you recommend for when they should have their next surveillance colonoscopy?
The adenoma >10mm means recommendation for next colonoscopy in 3 years according to the 2020 NZ MOH guidelines.
What are the NZ direct to colonoscopy referral criteria?
The NZ MOH referral criteria for direct access to outpatient colonoscopy are divided into 2 week category and 6 week category.
- known or suspected CRC based on imaging or DRE to plan surgery or look for synchronous tumours.
- IDA and PR bleeding unexplained by benign pathology.
- > 50yo w altered bowel habit >6w + unexplained PR bleeding .
- > 50yo w altered bowel habit >6w
- 40-50yo w altered bowel habit >6w + unexplained PR bleeding.
- > 50yo unexplained PR bleeding
- Unexplained IDA
- NZGuidelines Group (NZGG) Category 2 family hx + 1 or more of altered bowel habit >6w + unexplained PR bleeding and aged ≥40 years
- NZGG Category 3 family hx + 1 or more of altered bowel habit >6w + unexplained PR bleeding and aged ≥25 years
- imaging reveals >5mm polyp
- suspected IBD
https://www.health.govt.nz/system/files/2019-02/referral-criteria-direct-access-outpatient-colonoscopy-computed-tomography-colonography-feb19-v2.pdf
What is the Dukes classification for colorectal cancer?
Applied to rectal and colon adenocarcinomas. No longer used as TNM staging favoured.
Stage A - CRC as far as muscularis propria, no nodal involvement
Stage B - CRC through wall as far as serosa, no nodal involvement.
Stage C - CRC involves nodes
Stage D - CRC has metastasised.
What are the Faecal occult blood tests available and their limitations.
There is the FIT test (faecal immunohistochemical test) assessing for presence of haemoglobin in the faeces. This is the one used by NZ bowel screening program and offered every 2 years to those aged 60-74.(or 50yo for Maori/Pacific Is in some areas of country).
There is the FOBT using Guaiac which reacts to peroxidase activity of haeme. many false negatives and false positives. Also will test postive if patient has eaten beef recently, vit C, iron supplementation.
There is a multi-targeted stool DNA test (Cologuard) which tests for molecular markers of CRC and is more sensitive but still low and optimal set of markers still to be developed.
What is CTC and what is its sensitivity?
CT colonography is a CT abdo/pelvis with bowel prep administered prior and then air insufflation and oral contrast given prior to scanning.
It is >90% sensitivity and specificity for polyps >10mm but drops significantly for polyps <5mm.
What is/are the serum tumour marker(s) used for colorectal cancer?
Carcinoembryonic antigen (CEA) is the most common.
Can also be expressed by pancreatic, stomach, breast, ovarian, lung, bladder and thyroid cancers
Can also be raised in many non-malignant states too including:
- smokers
- gastritis
- COPD
- fatty liver, cirrhosis or gallstones
- diverticulitis
- autoimmune conditions
- IBD
Used as marker of size or spread of known malignancy or highly suspected malignancy. Not used as a screening/diagnostic marker as not specific enough. Routinely performed once cancer diagnosed as pre-resection baseline then again 3months post resection and 3monthly thereafter for 5 years to assess for trends.
What are some good or poor prognostic features for colon cancer that you might see on the synoptic report?
Good prognosis features:
- no lymph node involvement
- low T stage
- no mets
- deficient MMR
- Microsatelite instability
- Lymphovascular penetration/reaction
Poor prognosis features
- lymph node involvement
- high T stage
- mets
- proficient MMR
- Microsatelite stable
- Lymphvascular invasion
- KRAS, NRAS or BRAF mutations
What is the TNM staging for colon cancer?
Stage 1-2 N0/M0
Stage 4 any T any N M1
You’ve excised an adenocarcinoma endoscopically. When would you say the excision is regarded complete vs need for segmental colectomy still required.
It is important to note that these decisions will be made in an MDM setting and taking into account patient wishes and comorbidities. However for an endoscopic excision to be regarded as complete (i.e. no lymphadenectomy will be performed) it has to be a low risk tumour taken in one piece (not piecemeal) with clear margins i.e. T1 and margins >2mm. It also has to be a well differentiated tumour with no lymphovascular invasion.
When is adjuvant chemotherapy recommended in colon cancer?
For stage 1 or 2:
- T4 disease
- Perforated disease
- Indeterminate or positive margins
- Poorly differentiated or undifferentiated
- Lymphvascular or perineural invasion
- Non-oncologic resection (<12nodes)
Stage 3 disease
Stage 4:
- Resectable or potentially resectable (i.e. isolated lung or liver) may consider neoadjuvant chemo
- isolated peritoneal mets (controversial)
in unresectable disease palliative chemo.
When would you consider neoadjuvant chemo in colon cancer?
- T4b disease
- Bulky lymph nodes
- Potentially resectable tumour to downgrade to resectable
- Mets
What is meant by R0, R1 and R2 resection?
R0 resect for cure.
R1 resect to microscopic residual disease
R2 resect to macroscopic residual disease
What are the typical chemotherapy agents for colorectal cancer?
FOLFOX (Folinic acid, 5 Flurouracil and Oxaloplatin)
CAPEOX (Capcitabine and Oxaloplatin)
FOLFIRI (Folinic acid, 5 Flurouracil, Irinotecan)
What is meant by the term ‘complete mesocolic excision’?
Resection of the cancer with clear margins (5cm) en bloc with its mesocolon with resection back to the primary vessel origin and including minimum nodal harvest of 12 lymph nodes.
In which appendiceal cancers would you proceed to a completion right hemicolectomy?
- adenocarcinoma
- mucinous if ruptured, incomplete margins or mod-poor differentiation
- goblet cell
What curative resection options are available for caecal or ascending colon cancers?
Right hemicolectomy (lap or open)
- includes 7-10cm of TI
- Blood supply ligated ileocolic, right and middle colics.
What curative resection options are available for transverse colon cancers?
If very proximal transverse can treat with extended right.
Transverse colectomy (includes both hepatic and splenic flexures)
- middle colic ligated
If very distal transverse can treat with extended left.
What curative resection options are available for descending colon cancers?
Left hemicolectomy
- ligated left branch of middle and left colics.
What curative resection options are available for sigmoid colon cancers?
Sigmoid colectomy/ high anterior resection.
- Ligated portion of IMA
What is a diverticulum?
Diverticula are saclike mucosal pouches that protrude from a tubular structure.
True diverticulum is projection of all layers of the GI tract wall. e.g. Zenkers, and Meckels
Pseudodiverticulum is projection of mucosa and submucosa through the muscular wall of the bowel e.g. colonic diverticulosis.
Describe a way of classifying appendiceal neoplasms.
Mucinous and non-mucinois
Mucocoele
LAMNs
HAMNs
Mucinous adenocarcinomas
Epithelial tumours:
- Non-mucinous adenocarcinoma
- Goblet cell adenocarcicnoma
Neuroendocrine (NETs)
How are NETs of appendix classified?
By differentiation:
Well differentiated
G1 low grade
G2 mod grade
G3 high grade
Poorly differentiated = Neuroendocrine carcinomas (NECs)
small cell
large cell
Mixed neuroendocrine and non-neuroendocrine neoplasms (MiNENs)
What is this?
Angiodysplasia of colon
Abnormal ectatic, dilated and thin walled blood vessels.
Most common cause of obscure GI bleeding.
Most commonly found in right colon.
Causes venous bleeding.
Can be associated with aortic stenosis, ESRD,Von willebrands.
Can treat endoscopically w haemostatic measures e.g. clips or coagulation, if refractory then resection or angiography. Can also consider octreotide and thalidomide…
Describe the intraoperative and endoscopic findings and macroscopic and microscopic findings associated with Crohns disease
Crohns is an inflammatory bowel disease that can affect anywhere along GIT.
Intraoperative:
- Fat creeping
- Bowel oedema
- Obstruction
- Fistulas
- Strictures
Endoscopic:
- Fissures and deep ulcers create Cobblestone appearance
- Serpinginous ulcers
Macroscopic:
- Transmural disease
- Skip lesions (discontinuous)
Microscopic:
- Non caseating granulomas
What are the extraintestinal manifestations of Crohns?
- Arthritis typically large
joints e.g. SIJ - Skin - erythema nodosum and pyoderma gangrenosum
- Eyes - uveitis, iritis, episcleritis
- HPB - gallstone disease due to reduced resorption of bile salts in TI, and PSC although more typical of UC.
- Renal stones (Ca Oxalate stones due to stetorrhoea > increased luminal binding of calcium > increased oxalate absorption in colon.
- Haematological: Pernicious anaemia due to reduced B12 absorption in TI. Increased VTE risk.
Compare and contrast Crohns’ with UC.
What is the Montreal classification used for Crohns?
Montreal score looks at age, location and behaviour or phenotype of the disease.
What is the Truelove Witt classification system for Ulcerative Colitis?
Combines clinical values including HR, # of BMs/24, bloody stools and fever and laboratory values including Hb <105 and ESR >30 to assess the severity of the Ulcerative Colitis during an acute flare.
Easy to use, lab values easy to obtain except CRP in may institutions is preferred to ESR.
What is the Montreal score for UC?
A scoring system evaluating the extent (E) and severity (S). The Severity is based off Truelove Witt.
What is the UCEIS score for UC?
Endoscopic evaluation of severity. Looks at 3 factors: vascular pattern (0-2), bleeding (0-3), ulceration (0-3).
Interpretation
0-1 =Remission
2-4 = Mild
5-6 = Moderate
7-8 = Severe
What is the disease activity index used for Crohn’s?
Combines clinical values including weight loss, abdominal pain, abdo mass, # of soft stools, # of bloody stools and extraintestinal manifestations (above is essentailly the Harvery-Bradshaw index) with use of antidiarrhoeal medications and lab values Hct.
CDAI <150 is a marker of remission of Crohn’s disease.
CDAI >450 is a marker of severe Crohn’s disease.
Describe the pathogenesis of colorectal cancer.
Colorectal cancer develops through a multistep process involving the accumulation of genetic and epigenetic changes. Key mutations occur in oncogenes like KRAS and tumour suppressor genes like APC and TP53, leading to uncontrolled proliferation, evasion of apoptosis, induction of angiogenesis and loss of cell cohesion can lead to progression from benign polyps to malignant tumours, and potential metastasis.
Environmental factors, such as diet and inflammation, can also contribute to its pathogenesis likely through epigenetic influences.
Spot diagnosis and pathogenesis
This is showing pseudomembranous colitis.
It is most commonly driven by clostridium difficile (a gram positive bacillus, spore forming anaerobe) infection following antibiotics and imbalance in gut microflora.
Clostridium difficile produces Exotoxins A and B. Leads to damage of mucosa, drives inflammation cascade with oedema and extensive neutrophil infiltration in lamina propria. Pseudomembranes are comprised of bacteria, fibrin, mucous and neutrophils from intercrypt erosions.
Can lead to SIRS and sepsis.
How would you work up and manage this patient?
This is pseudomembranous colitis most commonly caused by C.diff.
Work up and management with simultaneous assessment and resuscitation using CRISP algorithm.
Investigations include:
Lab: FBC, U&E, Cr, Lactate and albumin
Stool spec: M/C/S, c.diff toxin
Imaging: AXR, CT Abdo/pelvis
Endoscopy: May have diagnosis on flexi sig but 1/3 cases limited to right colon so may need colonoscopy.
Management:
- Correct fluid and electrolyte imbalances
- Contact isolation
- Cease offending antibiotics
- Oral metronidazole 400mg TDS for 14 days
- monitor for complications
- avoid antiperistaltic agents
- consult ID to exclude resistant strains
- cholestyramine mya be useful in refractory cases to bind toxin.
Surgery reserved for:
- toxic megacolon
- fulminant disease (severe SIRS/sepsis)
- colonic perforation
- failure of medical therapy in 48-72h w continued sign of toxicity.
- once decision made to operate it must be performed in expeditious and aggressive manner with total colectomy with preservation of rectum and end ileostomy even if segmental colitis. *NB exterior may appear normal at time of surgery as is a mucosa disease.
If no improvement 2nd line is vancomycin oral +/- rectal if ileus or toxic megacolon.
- for refractory or recurrent disease consider faecal microbiome transplant in consultation with ID.
What is the pathogenesis of ischaemic colitis?
Can be acute or chronic and non occlusive/ low flow states or occlusive eitiology.
Non-occlusive states:
- sepsis
- haemorrhagic shock
- hypotension
- MI
- haemodialysis
- cardiopulmonary bypass
- medications e.g. opioids
vs occlusive:
thrombi
emboli
most common sites are watershed areas i.e. splenic flexure and upper rectum.
What is the modified Paris classification for endoscopic lesion appearance?
Divides lesions into polypoid and non-polypoid and invisible.
Polypoid includes peduculated and sessile
Non-polypoid includes flat-elevated, flat and flat-depressed.
Invisible is dysplastic lesion that is picked up on random biopsy from an area of normal appearing. mucosa.
What are the possible positions of the appendix relative to the caecum and ileum?
Retrocaecal (32-62%)
Paracolic/ precaecal
Post ileal
Pre ileal
Pelvic
Subcaecal
Who benefits from neoadjuvant radiation in rectal cancer?
DisTANCE
Distance - low/close to anus
T >3
Anal sphincter involvement
Nodal disease
CRM threatened or involved (w/n 1mm)
Extramural vascular invasion
What are the possible complications in radiation therapy in rectal cancer?
What is low anterior resection syndrome?
What are the familial CRC syndromes? How could you classify them?
What are the subtypes of FAP?
What are the extracolonic manifestations of FAP?
Causes of mortality in FAP are CRC, duodenal/periampullary adenocarcinomas, desmoids.
What are the surgical options for someone with an acutely obstructing distal colon cancer?
What are the types of caecal volvulus?
Axial
Loop
Caecal bascule
