Colorectal Flashcards
Diverticular dx pathophysiology
- Increased intraluminal pressure —> mucosa protrudes through natural weak points in colonic wall where vasa recta penetrate through muscularis propria
- Sigmoid narrow luminal diameter predisposes to high intraluminal pressure —> La Place law (pressure required to distend wall inversely proportional to radius)
- Low fibre intake —> reduced stool bulk —> higher pressure required to pass
Associations:
- Increasing age
- Low fibre
- Obesity
- Genetics (connective tissue disorder, polycystic kidney disease, genetic predisposition)
Diverticular morphology/histopath
- Thin wall composed of atrophic mucosa and compressed submucosa
- hypertrophy of circular layers of muscularis propria in affected segment —> shortening of taenia and luminal narrowing)
Distribution Diverticular dx
50% sigmoid only
40% descending
5-10% entire colon
Rt colon more commonly affected in Asians
Pathophysiology diverticulitis
Wall erosion secondary to increased pressure or inspissated food particles
—> inflammation and necrosis
—> extravasation of faeces abs bacteria
—> extraluminal pericolic inflammation
Diverticulitis risk factors
Smoking
NSAIDs/paracetamol use
Obesity
Low fibre diet
Hinchey classification
Stage 1a pericolic phlegmon and inflammation, no fluid collection
Stage 1b pericolonic abscess <4cm
Stage 2 pelvic/inter-loop abscess or abscess >4cm
Stage 3 purulent peritonitis
Stage 4 faecalent peritonitis
Mx uncomplicated diverticulitis
Abx
High fibre diet
F/U colonoscopy
<25% with have 2nd attack
5% will need emergency surgery
Colostomy risk highest in first attack
Sigmoidectomy if recurrent attacks (esp young and immunocompromised)
Mx complicated diverticulitis
Abscess
<2cm conservative (Abx)
2-5cm trial conservative (drain if not responding)
>5cm —> drain, percutaneous
Generalised peritonitis
Laparotomy and Hartmanns
- control infection
- resection sigmoid
- restore continuity
Fistula
Bladder/vagina/SB/skin
Trial non-operative (Abx, IDC) 50% close
Surgery
- take down fistula (blunt finger dissection)
- sigmoid colectomy
- close bladder defect, leave IDC
- consider ureteric stents to help identify and preserve ureters
Obstruction
Acute - phlegmon or abscess
Chronic - stricture
Diverticular bleed
How common, where, risk of rebleed
15%
1/3 massive
Diverticula at point vasa recta penetrated colonic muscle —> recurring injury, eccentric intimal thickening, thinning of media
This weakness predisposes to rupture
More common Rt colon
75% stop spontaneously
Rebleeding risk 15-40%
Reboeeding risk after 2nd episode 50%
Colonoscopy perforation: what are the mechanisms?
Perforation occurs by one of three mechanisms:
- Mechanical trauma from pressure by scope on wall of colon (often rectosigmoid) or at a stricture
- Barotrauma where colon pressure exceeds bursting pressure of colonic region (typically caecum)
- Electrocautery injury during polypectomy
Screening/ diagnostic perforation typically large as from mechanical/barotrauma
Therapeutic colonoscopy perf typically small
Colonoscopy perforation: what are the rates for different procedures?
Rate of perforation varies with procedure being performed:
- Screening colonoscopy – 0.001-0.1%
- Anastomotic stricture dilatation – 0-6%
Stent placement – 4% - Colonic decompression tube placement – 2%
- Colonic endoscopic mucosal resection - 0-5%
What is the life cycle of the sushi worm?
Ingestion of raw fish containing anisakis larvae, known as the “sushi worm”. Marine mammals are the natural host (whales, sea lions, seals, dolphins, walrus), humans are the incidental host.
- Marine mammals excrete unembryonated eggs
- Eggs become embryonated in water and L2 larvae from in eggs
- After the L2 larvae hatch from eggs they become free swimming
- Free swimming larvae ingested by crustaceans and mature into L3 eggs
- Infected crustaceans eaten by fish and squid, and on the hosts death the larvae migrate into muscle tissues, and through predation the larvae are transferred from fish to fish
- Fish and squid maintain L3 larvae that are infective ti humans and marine mammals
- When fish/squid containing L3 larvae are ingested by marine mammals the larvae molt twice and develop into adult worms. Adult worms produce eggs that are shed by marine mammals (back to step 1 of cycle)
- Humans become incidental host by ingesting infected raw or undercooked seafood
- After ingestion the larvae penetrate the gastric/intestinal mucosa —> maturation begins —> larvae dies as not natural host —> dying organism induces inflammatory reaction —> tissue abscess with eosinophil predominance.
- Anisakis larvae can penetrate into peritoneal cavity or other visceral organs and cause eosinophilic granuloma
Sx raw fish ingestion 5-7/7 before —> severe abdominal pain, abdominal distension, +/- palpable inflammatory mass that can cause intestinal obstruction. - Can develop diarrhoea and bloody mucous.
- May mimic appendicitis.
- May cause eosinophilic oesophagitis, gastroenteritis or enterocolitis.
What is the management of anasakis infection?
Diagnosis and treatment:
- Definitive diagnosis is through identifying the organism on histopathology associated with eosinophilic infiltration of intestinal wall, granulomatous reaction, and eosinophilic vasculitis.
- High eosinophils in blood raise suspicion in appendicitis
- Total and anisakis-specific IgE levels
- CT – oedematous wall thickening gastric/intestinal mucosa, dilated loops SB, perigastric stranding, ascites
Treatment – most self-limiting and only observation and supportive care required
Surgery may be necessary if symptoms of appendicitis
Physical removal of observed parasite at endoscopy is curative. Anasakis worms can only survive a few days in the human intestinal tract, however surgery may be necessary if worms penetrate intestine, omentum, liver or pancreas
Albendazole +/- prednisolone may be effective
Risk factors for colonoscopic perforation:
- advanced age
- multiple comorbidities
- diverticulosis
- obstruction
- resection of polyps >1cm on Rt side
- other therapeutic manoeuvres
- Anaesthesia/sedation
- Reduced mobility of colon
- existing weakness in colon wall
- previous incomplete attempt at endoscopic removal colonic lesion
- colonoscopy by non-gastroenterologist
- endoscopist experience
Quality indicators for colonoscopy
<1 in 1000 perforation at screening colonoscopy
<1 in 500 perforation for all colonoscopy
