I. Epidemiology
b/w sexes
age
geography
who get’s diverticulitis
asymptomatic roughly equal between sexes disease of western civilization incidence increases with age and there os a increasing prevalence over time
what % of population has diverticulosis
2/3 of elderly have diverticulitis
where does diverticulosis occur
Along the mesenteric sides of the anti-mesenteric taenia and along both sides of the mesenteric taenia
vascular penetration
in the colon the long muscles are designed how
three bands of muscle
that attach to the mesentery
sends and brings back
most of us get diverticulitis in our
sigmoid colon
but in asia most people have right sided diverticulitis
how does elastin create diverticulitis
proteins in colon that contract
increase pressures
and pooch
higher pressures AFTER you eat
which populations are prone to diverticulitis
people with connective tissues dz
Precocious diverticulosis occurs in patients with connective tissue disorders (Ehlers-Danlos, Marfan’s)
Pathogenesis I Colonic Wall Resistance
> 200% increase in elastin deposition, laid down in contracted form, with shortening of taenia and ‘concertina-like’ bunching of circular muscle
more elastin more squeeze
a. No evidence that atherosclerosis or venous changes predispose
mortality is higher fore this population with diverticulitis
b. Symptomatic pts have higher motility indices than asymptomatic patients
Wynne-Jones theory
thesis is that the reason is because the westernized life style is “impermissive of flatus”
diverticulosis
that state of having diverticula
what types of BM prevent diverticulitis
high volume low pressure
relationship between diverticulitis and starting a fiber diet
i. Those with higher fiber had less complicated disease
lower risk of complications by 30-40%
inherited risk
40%
poop stuck in diverticula
fecalith
SUDD
XII. Symptomatic Uncomplicated Diverticular Disease (SUDD)
lower abdominal symptoms in absence of overt inflammation (by vital signs, labs, CT)
c. Possible mechanisms SUDD
i. Inflammatory damage to enteric nerves (and aberrant re-innervation leading to visceral hypersensitivity)
ii. Altered neuropeptides
iii. Muscle hypertrophy with increased intraluminal pressure
iv. Microbiota alterations
Cyclic Rifaximin
antibiotic that is not absorbed
Significant improvement in SUDD Sxs and greater prevalence of Sx-free patients at 1 year WITH fiber plus rifaximin in comparison with fiber alone.
what type of probiotics should we use?
fermented food
Mesalamine
Mesalamine - 1st line tx for ulcerative colitis
(IBD )
(Chrons and choelitis tx for inflammation )
People felt better but diverticulitis symptoms were not decreased. Mesalamine doesn’t really help
Complicated diverticulosis - Diverticulitis
pathology
Inflammation and/or infection associated w/ diverticula
probably a perforation
Bacteria breach mucosa, through wall, and cause (often limited) perforation.
Affects <10% of patients with diverticula
CM of diverticulitis
Pain and tenderness, usually LLQ, but in Asians or those with redundant sigmoids, can be RLQ or suprapubic.
Altered bowel habits Anorexia, nausea, vomiting Hematochezia rare dysuria: sympathetic cystitis Fever common; shock or hypotension increase WBC common; no other labs routinely useful
dx test for diverticulitis
i. CT scanning - most accurate
1. Abd & Pelvic scans; oral / rectal / IV contrast
2. Findings: pericolic infiltration of fatty tissues, wall thickening, abscess
3. Sensitivity and Specificity: 85-95%
4. Severe disease predicts complications and poor prognosis.
you can diagnose without it w/ hx of diverticulosis and LLQ pain
TX for antibiotics
if you use anitbiotics
i. Antibiotics: cover gut organisms (eg GNRs & anaerobes, esp E. coli and bacteroides)
ii. Oral: consider T/S or cipro plus flagyl
1. Single agent: Augmentin
iii. IV: aminoglycoside/aztreonam/3rd gen ceph plus metronidazole or clindamycin.
1. Single agent: Unasyn
iv. Sxs should ß w/in 2-3 days, advance diet.
v. Continue Rx for 7-10 days
but you DON’T NEED TO