Colorectal Flashcards
What are the macroscopic and microscopic features of Crohn’s disease?
Macroscopic
Laparotomy
- stiff and thick walled segments of bowel
- fat wrapping
- fibrinous exudate, hyperaemia, adhesions
- mesenteric inflammation/lymphadenopathy
- complications (strictures, fistulas, sinuses, abscesses).
Colonoscopy
- aphthous ulcers
- cobblestones
- serpinginous linear ulcers
- inflammatory pseudo polyps
Microscopic
- deep non caseating granulomas
- focal ulceration
- transmural inflammation
- intra lymphatic granulomas
- granulomatous vasculitis
What is ulcerative colitis?
Type of inflammatory bowel disease charaterised by continuous inflammation of the colonic mucosa extending proximally from the rectum.
What is the cause and risk factors associated with UC?
Cause
- Not known but thought to be an interplay between environmental and genetic factors. Genetically susceptible individuals have a dysregulated immune response incited by unknown luminal antigens leading to colonic mucosal inflammation.
Risk factors
- Genetics - 10-20% have a first degree relatvie. Likely an aggregate mutations. Extra intestinal manifestations associated with HLA-B27, HLA-B8 and HLA-DR2
- NSAIDs
- Infective proctocolitis
- Smoking is protective
What are the microscopic features associated with UC?
- Mucosal thickening with infiltration by inflammatory cells
- Degree if neutrophilic infiltration
- Mucosal ulceration (regeneration of this leads to pseudopoplyps)
- Crypt abscesses - branching of crypts following regeneration
- Goblet cell depletion
- Epithelial dysplasia (metaplasia)
What are the extra intestinal manifestations associated with UC?
Musculoskeletal:
Peripheral - gets better with colectomy
Axial - ankylosing spondylitis and sacroileitis - stays the same despite colectomy
Eyes
Uveitis and scleritis
Episcleritis
Skin
Erythema nodosum
Pyoderma gangrenosum
Hepatic
Primary sclerosing cholangitis (risk of cholangiocarcinoma) (patients with PSC and UC are at a 5x increased risk of colonic cancer)
DVT
What histological features found on colonoscopy for UC warrant colonic resection?
Flat multifocal low grade dysplasia and high grade dysplasia after confirmation by a second pathologist and discussion in MDT.
What are the risks associated with CRC in UC patients?
Disease duration:
2% by 10 years
8% by 20 years
18% by 30 years
Disease extent and duration
PSC
Family history of CRC
Presence of dysplasia
When does surveillance of CRC start in patients with UC?
8 years after diagnosis OR straight away if PSC/family hx
Annual colonoscopy:
- Active disease
- PSC
- Family hx of CRC in 1st degree < 50 yo
- Colonic stricture
- Previous dysplasia
What technique is used for colonoscopy for UC?
- Chromoendoscopy and dye spraying (methylene blue to enhance mucosal irregularities)
- Targeted biopsies from visibly abnormal tissue and random biopsies every 5-10cm
What are the principles of stoma formation?
1) Within rectus
2) Patient to visualise and access
3) 5cm from all folds, creases, incisions, belt line, umbilicus, bony prominence (measure sitting and standing position)
4) Consider occupation and physical limitations
What are the complications associated with stomas?
Early
- Dehydration, skin irritation/ulceration/breakdown, stoma ischaemia, poor position, bowel obstruction, mucocutaneous separation, fistula
Late
- Stoma retraction, prolapse, stenosis
- Parastomal hernia, fistula, bleeding, skin irritation/ulceration, bowel obstruction, dehydration
What is mucocutaneous separation and possible causes?
Separation of the bowel from the surrounding dermis. This can lead to leakage and skin irritation and if circumferential, stomal stenosis as heals by secondary intention.
Causes -> inadequate or improper approximation, excessive tension, infection or poor wound healing
Management:
Minor -> observation with area filled with alginate/skin barrier powder
Complete -> Revision
What are the management options for stoma prolapse?
1) Incarceration/strangulation -> urgent revision
2) Minimal prolapse/asymptomatic -> converservative management wiyth cool compresses, osmotic agent (sugar) and manual reduction/application of binder
3) Significant and symptomatic
Local repair -> ileostomy (division at mucocutaneous junction with delivery and excision of redundant bowel)
Laparotomy -> relocation or consider colectomy and end ileostomy
Reverse stoma
What are the risk factors for a parastomal hernia?
Patient
- Age
- Obesity
- Poor wound healing (malnutrition, immunosuppression, post operative wound infection, radiotherapy)
- Raised IAP (COPD, cough)
- Weak abdominal musculature
Surgical
- Emergnecy surgery
- Large trephine
- Loop stoma
- Stoma through laparotomy incision
- Stoma lateral to rectus muscle
What is the classification of parastomal hernia?
1) Subcutaneous - hernia protrudes alongside bowel into subcutaneous fat
2) Interstitial - hernia protrudes into intermuscular plane
3) Peristomal - hernia is prolapsed and loops of bowel and/or omentum enters hernia space between layers of prolapsed bowel
4) Intrastomal - protrudes into plane between emerging and everted part of bowel
What are the indications for surgery for a parastomial hernia?
Acute - incarceration/strangulation or obstruction or perforation
Elective - Symptomatic with pain, bulge, obstructive symptoms affecting QoL
What are the options for repair of a parastomal hernia?
Revision/mesh repair
Relocation - high rate of recurrence and complications
What are the indications for stents in laignant large bowel obstruction?
Disease
- Metastatic - definitive palliative mgmt (short life expectancy or not operative candidates) OR bridge to neoadjuvant chemotherapy /surgery (convert emergency surgery into an elective operation)
Patient
- not fit for surgical resection
- pts wishes
What are the complications associated with colonic stents?
Early
- Bleeding
- Perforation
- Malpositioning
- Failure
- Pain/tenesmus
Late
- Migration
- Perforation
- Recurrent obstruction
What is the proposed mechanism for pseudo obstruction?
Exact mechanism is unclear but thought to be an impairment of the ANS with SNS > PNS -> inhibitory effect on colonic motility
What are the causes of acute pseudo obstruction?
Trauma
Infection (pneumonia sepsis)
Neurological disease (Parkinsons, stroke, alzheimers, MS)
Cardiac disease (MI, heart failure)
Orthopaedic, pelvic, obstetric and spine surgery
Medications (narcotics, anticholinergics, TCAs, CCBs, epidural)
Metabolic imbalances (hypokalaemia, Ca, Mg, hypoT4)
What are the management options for pseudoobstruction?
1) Supportive care and removal of precipitants
- providing no signs of complications
- Treat underlying reversible disease (sepsis)
- Discontinue inciting medications
- Correct electrolytes
- Bowel rest and IVF
- NGT if vomiting (rectal tube/enema if distal)
- Serial PE and AXR to assess colonic dilation
2) Medical
- Neostigmine (caecum >10-12cm and failed 48h of supportive care). Acts as a acetylcholinesterase inhibitor, using 2mg IV dose with cardiovascular monitoring. Median time to respond is 4 min and decompression acheived in 80%.
- Erythromycin - stimulates smooth msucle contraction
3) Endoscopic
- Gas aspirated from colon and rectal tube left in situ
- Percutanous caecostomy if endoscopic treatment fails
4) Surgical
- rarely required - reserved for those that fail medical or endoscopic mgmt OR have signs of peritonism/perforation
- Resection, ileostomy, and mucous fistula for ischaemia/perforation
- Loop colostomy for no perforation
What are the causes of large bowel obstruction?
Mechanical
- Carcinoma 90%
- Volvulus 5%v
- Diverticular disease 3%
- Inflammatory bowel disease
- Anastomotic stricture
- Intussusception
- External compression
Adynamic
- Colonic pseudoobstruction
- Colonic dysmotility
Congenital
- Hirschprung’s disease
- Imperforate anus
What is volvulus and where does this occur?
This is when a portion of the colon twists around a fixed point in its mesentery causing strangulation of mesenteric vasculature and a closed intestinal loop.
Common sites
- sigmoid colon 75%
- caecum 20%
- transverse colon 5%
What are the risk factors for sigmoid volvulus?
- Elderly
- Institutionalised
- Redundant sigmoid colon with narrow mesenteric attachment
- Pregnancy
- Pelvic malignancy
- Parkinsons disease
- Megacolon
What is the pathophysiology of sigmoid volvulus?
- Axial rotation around inferior mesenteric vessels between fixed DC and rectum
- Counter clockwise direction more common
- Leads to closed loop obstruction (increased distension, impaired venous return, oedema, thrombosis, ischaemia) with compression/occlusion of mesenteric vessels.
What are the risk factors for caecal volvulus?
Main:
Failure of fusion of ascending colon mesentery to retroperitoneum with mobile ileo-caecum
Other:
Adhesions
Pregnancy
Malignancy
Colonic atony
Colonoscopy
Hirchspungs disease
Caecal distension
What are the types of caecal volvulus?
Type 1 - clockwise axial torsion along long axis with caecum remaining in RLQ
Type 2 - counterclockwise loop caecal volvulus from torsion of caecum and TI -> caecum in LUQ in an inverted orientation
Type 3 - Upward folding from inferior to superior caecum (CAECAL BASCULE)
What are the management principles of caecal volvulus?
Dont attempt endoscopic decompression as rarely succesful
Laparotomy - avoid detorsion if ischaemic as prevents reperfusion injury. Right hemicolectomy required if iscahemic.
Prevention of recurrence
- resection
- caecostomy tube (high rates of complications such as fistula, faecal peritonitis, wound infection
What is the genetic basis for Lynch syndrome?
AD germline mutation in one of the DNA mismatch repair genes including MLH1 and MSH2 (30-40% risk of CRC) and MSH6 (10-20%) and PMS2 (15-20%) .
MMR role is to correct errors in base pair matching during replication and to initiate apoptosis when damage beyond repair. With defective MMR, there is an accumulation of mutations in other genes.
Defective MMR -> microsatellite instability (microsatellites are tandem repeats of short sequences).
What are the clinical features of lynch syndrome?
Lymphocytic
Associated with endometrial ca (33%), ovary (9%), stomach (6%), urothelium and small bowel (<3%)
Mucinous & metachronous
Poorly differentiated and proximal
Signet cell and synchronous
What are the different modes of diagnosis for lynch syndrome?
1) Amsterdam criteria
- Aimed at identifying families at risk of Lynch and for consideration of genetic testing -> 50% of families fulfilling the criteria will have MMR mutation
- 3 relatives (one a 1st degree relative of the other2) affected by lynch associated cancer over **2 **generations with 1 < 50 years (FAP must be excluded)
2) Analysis of tumour tissue
- Microsatellite instability - panel of 5 microsatellite markers used to detect MSI (2 markers show instability, 1 marker is low, MS stable no markers)
- 15% of all CRC is MSI-H and only 5-10% due to HNPCC
- Bethesda criteria used to determine whether tumour tissue should be tested.
- Immunohistochemistry - use of antibodies to measure expression of MMR proteins in tumour tissue (can be first line test with MSI reserved for patients with family hx suugestive but IHC normal).
3) Genetic testing
- Patient with tumour testing indicative of MMR mutation
- Youngest affected family member in family fulfilling Amsterdam criteria
- BRAF V600E testing required as in sporadic mutations, MLH1 can be silenced by somatic methylation, loss of expression of MLH1 and PMS2 on IHC (typically older females without fam hx)
