Diverticulosis and Its Complications Flashcards
1
Q
epidemiology of diverticulosis
A
- True incidence difficult to measure as most patients asymptomatic
- No sex predilection generally
- “Disease of Western Civilization” – very much in America, Europe, Australia, etc. (Rare in rural Africa & Asia, Common in US, Europe, Australia, Japanese migrating to Hawaii have rate intermediate b/w native Japanese and mainland born, suggesting ‘westernization’ of colon)
2
Q
incidence of diverticulosis
A
increases with age
3
Q
pathologic anatomy of diverticulosis
A
- Typically arise in 2 or 4 parallel rows:
- Along the mesenteric sides of the anti-mesenteric taenia and along both sides of the mesenteric taenia (Happens where blood vessels go through the walls of the colon, Bands of muscle in the colon are tinea!, Where the blood vessels go through the wall is a weak spot – pouches that happen at very specific places (looks like little pock marks through the colon)
- Corresponds to sites of arterial penetration through smooth muscle
- Pseudo-diverticula in that mucosa and submucosa herniate through the muscle, but diverticulum does not include all layers of wall.
4
Q
western and asian individuals
A
- Western individuals: 90% left-sided, 15% right-sided
- Asian individuals: 25% left-sided, 75% right-sided
- WHY DO WE HAVE LEFT SIDED AND ASIANS HAVE RIGHT SIDED? Probably due to diet
- Vary in number from few to hundreds
- Typically 5-10mm in diameter, although ‘giant’ diverticula described
5
Q
Pathogenesis of diverticulosis
A
-colonic wall resistance, disordered mobility
6
Q
colonic wall resistance
A
- No evidence that atherosclerosis or venous changes predispose
- > 200% increase in elastin deposition, laid down in contracted form, with shortening of taenia and ‘concertina-like’ bunching of circular muscle
- If you have more proteins in your colon that are contracting, you have more contraction and then you have higher pressures which will make more pouches!
- Precocious diverticulosis occurs in patients with connective tissue disorders (Ehlers-Danlos, Marfan’s)
7
Q
Disordered mobility
A
- Increased resting, post-prandial, & neostigmine-induced luminal pressures demonstrated in patients with tics vs. controls without
- Symptomatic pts have higher motility indices than asymptomatic patients –> PRESSURE IS THE PROBLEM!!!
- Higher right-sided pressures seen in Asian patients with right-sided diverticula
- Wynne-Jones: westernized urban lifestyle “impermissive of flatus” -> air retention -> increased intraluminal pressures & tic formation (Impermissive of flatus = afraid to fart, When you fart, you are preventing diverticulitis)
- Diverticulosis (having diverticula), diverticulitis is inflammation, disease state
8
Q
Fiber Deficiency Hypothesis
A
- Evidence for: Worldwide striking geographic correlation with low dietary fiber intake, Developed in the west after the introduction of grain milling, Humans & animals on low-fiber diets: only species to get diverticula, Lower rates diverticular disease in vegetarians
- Burkitt and Painter: stool weights & transit times in Brits (low fiber diet) vs rural Ugandans (high fiber diet)
- Also supported by rodent data (lifelong low vs high fiber diet) –> Low-fiber diet: 45% developed diverticula (right sided), High-fiber diet: 9% developed diverticula
- Popular and logical thesis, but evidence supporting is actually poor, assumes uniform population diet and uncontrolled for lifespan etc
- There is no animal in the wild that has diverticulosis!!
- Vegetarians and vegans have a much lower rate of diverticulosis
9
Q
Can dietary fiber prevent complications?
A
- 2 large prospective cohort studies showing inverse relationship b/w fiber intake and diverticular complications
- HPFU, >43K men, US, 1988-1992, no prior colonic dz (RR for symptomatic disease in highest vs lowest fiber quintiles = 0.63 (.44-.91) (insoluble fiber, esp cellulose))
- EPIC-Oxford Study, 47K M & F, UK, 12 year follow up
- You can’t get rid of diverticulosis but you can reduce risk of diverticulitis
10
Q
Risk of seeds/nuts
A
-ACG Practice Guidelines 19991 (“Controlled studies that support this belief are lacking….no role for ‘elimination’ diet”)
o Not only ‘no association’ but may actually protect
11
Q
Genetic risk factors
A
- Swedish Twin Registry linked to Inpatient Registry1 (>100K twins; 2300 had dx of diverticular disease, OR for developing DD if monozygotic twin affected = 7.15 (4.8-10.6) (3.2 for same gender dizygotic twins), Estimate hereditability at 40%)
- Danish Registry2, >10K siblings, 900+ twins (RR for developing DD if monozygotic twin affected = 14.5 (8.9-23) (5.5 for dizygotic twins), Estimated hereditability at 53%)
12
Q
posture during defecation
A
-Conclusion: “Sitting during defecation (Western type toilet) seems to increase the risk of DD. To optimize the anorectal angle, placing a footstool during defecation may have a protective role against diverticula formation”.
13
Q
uncomplicated diverticulosis: the asymptomatic patient
A
- The majority of patients with diverticula (80%) will remain asymptomatic.
- There is no justification of any specific therapy or follow-up to be offered to such patients, other than a higher fiber diet.
- Incidentally discovered diverticulosis requires no intervention or treatment.
14
Q
Symptomatic Uncomplicated Diverticular Disease (SUDD)
A
- SUDD: lower abdominal symptoms in absence of overt inflammation (by vital signs, labs, CT)
- Now recognizing a continuum of inflammation, with evidence for a middle ground of subclinical inflammation in SUDD patients
- Possible mechanisms: Inflammatory damage to enteric nerves (and aberrant re-innervation leading to visceral hypersensitivity), Altered neuropeptides, Muscle hypertrophy with increased intraluminal pressure, Microbiota alterations
15
Q
emerging treatments for SUDD
A
- If there is indeed a symptomatic state of DD marked by low-grade inflammation, and/or visceral hypersensitivity or abnormal motor function or abnormal biome, can we intervene in such patients?
- Historically, we’ve prescribed fiber or anti-spasmodics, although data in support is weak
- ? Antibiotics, ? Probiotics ? Anti-inflammatories
- Cyclic Rifaximin in SUDD (400mg BID, 7 d/month)
