Colorectal Flashcards
What are the types of caecal volvulus and what is the treatment?
Type 1 – An axial cecal volvulus develops from clockwise axial torsion along its long axis; the volvulized cecum remains in the right lower quadrant.
Type II – A loop cecal volvulus develops from a torsion of the cecum and a portion of the terminal ileum, resulting in the cecum being relocated to an ectopic location (typically left upper quadrant) in an inverted orientation.
Type III – Cecal bascule involves the upward folding of the cecum rather than an axial twisting.
Types 1 and II account for 80% of caecal volvulus
Pathogenesis of melanosis coli
Develops due to abuse with anthraquinone based laxatives (Senna) - these have a direct toxic effect on colonic epithelium -> cell death -> lipofuscin deposition in the macrophage in the lamina propria gives the colour.
pigmentation may resolve after stopping laxatives.
What are desmoid tumors, how are they treated
Desmoids are benign soft tissue tumours arising from clonal proliferation of myofibroblasts.
They are associated with FAP, trauma, or oestrogens.
Have a mortality of 10%.
Can occur anywhere, but in the setting of FAP most commonly occurs intraabdominally or in abdo wall muscles.
Most desmoids exhibit cycles of growth and resolution.
Treatment -
Nonoperative - sulindac (NSAID - 200 mg BD) and Raloxifene (antioestrogen 120mg daily) have been reported anecdotally but high-quality data lacking.
surveillance - CT/ MR and renal tract US to look for and prevent renal obstruction.
Surgery - ideally in patients with consistently growing/ symptomatic desmoids
polyp surveillance protocol
- Low Risk = 5 yrs
- <2 small adenomas (<1cm)
- low grade dysplasia
- Intermediate = 3 yrs
- 3-4 small adenomas
- 1 adenoma >1cm
- villous adenoma
- High grade dysplasia
- High risk = 1 yr
- 5 or more small adenomas
- >3 adenomas with 1 >1cm
What are treatment options available for Pilonidal disease?
Acute presentation vs elective
Acute
I&D and reassess for elective surgery 3-4 months later
Elective
- Non-operative - Epilation and meticulous hygiene
-
Operative
- Laying open of fistula tract with marsupialization (can be done under local)
- Flap procedure - Bascom cleft lift / Karadakys
What chemotherapeutic agents used for colorectal cancer?
The options are
5 FU - this is IV form, oral form is capecitabine. This is main stay but not very effective in MSI patients (patients with MMR mutation).
Folinic acid (also called leucovorin) - potentiates 5FU
Oxaliplatin - further reduces recurrence when added to 5FU
Other agents used to potentiate 5FU particularly in metastatic disease - Irinotecan (IRI)
EGFR inhibitors (monoclonal antibodies) - e.g. bevacizumab (Avastin), Cetuximab - these bind to EGFR which are expressed in 60-80% of all colorectal cancers. These are not good in presence of KRAS mutation and have increased risk of perforation when used with stents in situ.
For rectal cancer there is lack of consensus for adjuvant chemo. But recommendations are extrapolated from colon cancer and are broadly the same. Adjuvant chemo is poorly tolerated in rectal cancer and many patients never finish the recommended course due to multiple factors like - treatment delay (longer convalescence after rectal surgery than colon surgery); presence of defunctioning stoma increases severity of diarrhoea.
How can you predict the risk of residual disease after resection of a malignant colorectal polyp?
A combination of Haggit, Kikuchi, resection margin and other high-risk features are used to predict the chance of residual malignancy after resection of a malignant colorectal polyp. Even when dealing with high-risk polyp, the final resection specimen will be devoid of malignancy in 80-90% of cases.
High risk:
Haggit 4 = 20%
Kikuchi SM3 = 20%
Sessile polyp = 20%
Resection margin <1mm = 20%
Poor differentiation = 15%
Moderate risk
Kikuchi SM2 = 10%
LVI = 10%
Low risk
Tumour budding = 5%
Resection margin 1-2 mm = 5%
What causes FAP?
80 % are due to autosomal dominant germline mutation in adenomatous polyposis coli gene (APC gene), chromosome 5q
20% are due to de novo mutation of the same gene
Indications for surgery in Crohn’s and the main pre-op priorities
Emergency
- Perforation with peritonitis
- Toxic megacolon
- Massive bleeding
- Failure of medical therapy (typically after at least 7 days)
Elective
- Failure to wean off steroids
- Failure to thrive/ growth retardation
- Fistula
- Symptomatic stricture
- localised obstructive ileocecal disease with no inflammation
Pre-op prep
- Control sepsis (Perc drain collection >5cm)
- Optimize nutrition
- Assess disease with scope and cross-sectional imaging
- Plan procedure
What is the colorectal cancer risk in UC and what factors influence it?
Colorectal cancer risk is about 2% at 10 years after onset of disease and rises by 1% per year thereafter.
Risk is increased by
- continuous active disease
- severe disease
- diffuse involvement (pancolitis)
- prolonged disease
- PSC
- Dysplasia (LGD increases CRC risk by 9 times and can directly progress to cancer bypassing the high grade state - nearly 25% of patients with LGD harbour either HGD or invasive cancer elsewhere)
How would you classify Anal squamous intraepithelial lesion (SIL). What are the risk factors? What is the natural history? How would you follow up patients with SIL?
Classification:
SIL can be a pre-malignant lesion. It is graded LSIL/HSIL based on the proportion of epithelium above the basal layer that has been invaded by dysplastic cells and p16 staining. In LSIL <1/3rd of the epithelium is invaded (same as AIN 1). In HSIL >2/3rd of epithelium has been invaded or >1/3 invasion with positive p16 staining (same as AIN 3 and p16 positive AIN2).
Risk factors
- HPV (particularly type 16)
- Receptive anal intercourse
- Multiple sexual partners
- HIV
- genital warts
- smoking
- immunosuppression
Natural history
Natural history of SIL is not well understood. A proportion of SIL spontaneously regress. It is generally believed that LSIL does not progress to HSIL/anal cancer but is a marker of increased HSIL risk. 1% /year of HSIL patients will develop anal cancer, the rates are higher if the patient is immunosuppressed/immunodeficient.
Follow up
There are no agreed guidelines on surveillance, but HSIL are usually followed up 6-12 monthly intervals with high resolution anoscopy with anal mapping and acetic acid staining (HSIL appears white) and biopsy
What are the types of stricturoplasty for small bowel?
Conventional
- Heineke-Mikulicz stricturoplasty - <10 cm, open longitudinally and close transversely
- Finney - <15 cm - fold strictured segment as a U and perform enterotomy and anastomosis of the limbs
Non-conventional
- Michelassi isoperistaltic stricturoplasty - for more prolonged segments.
What is MAP (MYH associated polyposis)?
MAP is an inherited colorectal cancer due to mutation of MutY human homologue (MYH) gene of chromosome 1p. It is autosomal recessive.
CLINICAL FEATURES
- large bowel - behaves like FAP. 50% will have >100 polyps, others wil have <100. polyps are mostly right sided, average age 47yrs, risk of cancer 100% by 60 yrs
- upper GI - fundic gland polyp and doudenal adenomas 20-30 % but less problematic than FAP
- others- breast 18%
SUSPECT
- patients presenting with FAP/ attenuated FAP but negative for APC mutation
DIAGNOSIS
- genetic testing
SURVEILLANCE
- colonoscopy - annual from 25yrs
- gastroscopy - start at 25yrs
- breast screening - participate in population screenig
- Hetrozygotes - colrectal risk about 2% - national screening.
TREATMENT
similar to FAP
Why are UC patients more prone to DVT
Reason not clearly understood, but postulated to be due to:
- corticosteroid use
- Up-regulation of acute phase reactant
- pro-inflammatory state
How is a diagnosis of Lynch made
Family history - Amsterdam criteria
Tumour analysis (if tissue available)
- MMR immunohistochemistry
- MSI testing (gene testing)
Genetic testing
- Positive - discuss surveillance vs surgery
- Negative - no surveillance
- Mutation not detected - surveillance
NICE recommendation - all CRC tissue to be tested for MMR or MSI
Differentials for colonic polypoid lesion
colonic polyp
- adenoma
- tubular
- tubulo-villous
- villous
- Hyperplastic
- Inflammatory
- harartomatous
GIST
submucosal lipoma
Leiyomyoma
Mets
submucosal lymphoid hyperplasia
What are the indications of adjuvant chemotherapy for colon cancer?
Adjuvant chemo is recommended for patients with stage III (lymph node + / Dukes’c) and above disease.
Usual regime is FOLFOX (Folinic acid, 5 FU, Oxaliplatin).
Use of chemotherapy for stage II disease is more controversial but there is evidence that it may be beneficial in patients with high-risk features like: large Stage 4 cancer Perforated cancer LVI Mucinous differentiation (high grade) <12 nodes harvested
Outline the treatment options for pseudomyxoma peritoneii
2 varieties of pseudomyxoma with different prognosis are recognised
- DPAM - diffuse peritoneal adenomucinosis. this results from rupture of noncancerous mucinous tumour e.g. appendiceal mucinous neoplasm. Better prognosis than the other variant. Here the patients have acellular mucin.
- PMCA - peritoneal mucinous adenocarcinomatosis. This results from rupture of mucinous adenocarcinoma e.g. appendiceal mucinous adenoCa. Here the mucin contains abundant malignant cells.
Treatment options for both are similar, however given the poor prognosis of PMCA, it is debatable whether PMCA patients should be put through extensive surgical procedures. Options should be discussed and finalised in conjunction with an expert who performs cytoreductive surgery, MDM and the patient.
Options:
- Observation and best medical treatment
- Multiple debulking procedures
- Cytoreductive surgery with HIPEC
- cytoreductive surgery involves resection of all tumour deposits >2.5mm and may need removal of stomach, gallbladder, pancreas, rectosigmoid, uterus.
- HIPEC - instillation of Mitomycin and 5FU at 44C for 90 mins
How do you assess severity of IBD?
CROHNS
- Chron’s disease activity index
- Harvey Bradshaw Index
- AGA stratification
- ulcers, stricture, disease extent
- CRP, calprotectin
- Upper GI manifestations
- Upper GI disease, stricture, fistulation, perianal disease, smoking, extra intestinal signs and age <30 are bad severity indicators
UC
- Truelove and Witts
- stool frequency <4; 4-6; >6
- blood in stool (small vol, moderate, visible)
- Temp >38
- Pulse >90
- Hb <10
- ESR>30
- steroid responsive, steroid dependant, steroid resistant
- Mayo endoscopic score
Why is PSC in UC patients significant
Because it increases the risk of-
- colonic neoplasia (approx. 5 times more likely)
- cholangitis
- cholangiocarcinoma
- Pouchitis after RPC
- cirrhosis
Discuss the investigation and management of appendiceal NET
INVESTIGATIONS
- Serum Chromogranin A for diagnosis
- Urinary 5HIAA for diagnosis
- CT abdomen - to assess size and obvious mets
- Dotate PET - for mets
- colonoscopy
TREATMENT - depends on size and high-risk features
resectable
- <1cm - appendicectomy
- 1-2cm right hemi if high risk features
- involved margin
- >3mm mesoappendix involvement
- angioinvasion
- high grade
- >2cm = right hemi (30% LN involvement)
- follow up - 6–12-month with CT/MRI, chromogranin A and HIAA
metastatic
- somatostatin analogue
- Liver - resect/embolize
- Everolimus
- Radioligand therapy with Lutentium Dotate
Describe risk stratification for colorectal cancers
CATEGORY 1 - no specific surveillance
- 1st degree x 1 >55yrs
CAT 2 - 5 yearly cols from 50 or 10 yrs earlier than earliset cancer
- 1st deg x 1 <55
- 1st deg x 2 any age
CAT 3
- familial CRC
- 2 x 1st deg with one <55yrs
- 3 rels with 1 st degree
- personal history or rel with CRC and multiple bowel polyps
Duke’s and TNM staging for colorectal cancer
Dukes A = muscularis propria
Duke’s B = through muscle laer but No nodes
Duke’s C = node positive (Same as Stage 3 cancer)
T1 = submucosal invasion
T2 = muscularis propria
T3 = subserosa
T4 = perforates serosa
N0 = no nodes
N1 = <3 nodes
N2 = 4 or more nodes
What are the extracolonic manifestations of FAP
ECTODERMAL
- Epidermoid cyst
- Pilomatrixoma
- CNS tumour
- CHRPE (congenital hypertrophy of retinal pigment epithelium)
MESODERM
- desmoid tumours, excessive adhesions
- Bone - osteoma, exostosis
- dental - unerupted/extra teeth, odontoma
Endodermal
- adenoma and carcinoma - stomach, duo, SB, Biliary tree, thyroid, adrenal cortex
- fundic gland polyp
- hepatoblastoma
What are your surgical options for caecal volvulus
The options are Right hemicolectomy/ ileocolic resection/caecectomy with primary anastomosis/end ileostomy or loop ileostomy depending on viability of caecum and patient stability.
Which extra intestinal manifestation of UC responds to colectomy?
RESPONDS
- Peripheral arthropathy
- Erythema nodosum
- Iritis
MAY RESPOND
- Pyoderma Gangrenosum
DOES NOT RESPOND
- Axial arthropathy
- Uveitis, episcleritis
- PSC
What is Peuts Jeghers syndrome?
Autosomal dominant condition characterised by muco-cutaneous pigmentation and multiple harmartomatous polyp of GI tract. Gene responsible is STK11 in chromosome 19p.
Risk of cancer: not well defined but appears to be significant.
Extra intestinal sites - Breast (refer for screening), ovaries, panc
Clinical features - dominated by bowel obstructions. Repeated laparotomies lead to difficult access and loss of length.
Surveillance protocols vary
- annual physical exam and Hb check
- 2-3 yrly upper, lower endoscopy and MR enterography/ pill cam
- Breast screening -? annual mam
Treatment
- Endoscopic polypectomy (large polyp intermittently obstructing/ bleeding/ low Hb)
- Double balloon enteroscopy or Laparotomy with enteroscopy for inaccessible SB polyps
Classify anal fistula
Parks classification (attached image)
- submucosal
- intersphincteric
- trans-sphincteric
- supra-sphincteric
- Extra-sphincteric
SIMPLE FISTULA
- Submucosal
- intersphincteric
- trans <30% ext sphincter involvement
COMPLEX
- LOCATION
- Transsphincteric >30% involvement
- suprasphincteric
- extrasphincteric
- colovaginal
- Horse shoe
- pathology
- Crohns
- cancer
- radiation
- recurrent
- multiple fistula tract
Causes of perianal fistula.
cryptoglandular infection
Crohn’s
Malignancy
TB
Iatrogenic - forceps delivery, tears
Radiation
Foreign body
OUTLINE THE MANMAGEMENT options for PERIANAL FISTULAS
Simple fistula -> fistulotomy (>90% healing, low incontinence in well selected patients)
Complex fistula -> seton + sphincter preserving procedure
- Cutting seton (80% success, 30% incont)
- LIFT (90% success, rare incon)
- Advancement flap (70% heal, 12% incont, 0-40% recur)
- Modified Hanley procedure (90% heal, no incon)
- Diversion
- Proctectomy
- Fibrin glue (up to 70% recur, useful adjunct to flap)
- Fistula plug (up to 70% recur)
