Mgmt of Crohn's Disease in Adults (2018) Flashcards
what are the hallmark/cardinal symptoms of Crohn’s?
abdominal pain chronic diarrhea (MC - most common) fatigue (likely 2/2 chronic inflammation, anemia, vitamin/mineral deficiencies) weight loss fever growth failure anemia recurrent fistulas extra intestinal manifestations
Is Crohn’s a pathologic, radiographic, clinical, or other type of dx?
clinical
there are no truly pathognomonic features
in general, it’s the presence of chronic intestinal inflammation that solidifies a dx of Crohn’s.
what features help distinguish Crohn’s from UC?
Crohn's: discontinuous involvement w/ skip areas sparing of the rectum deep/linear/serpiginous ulcers of the colon strictures fistulas granulomatous inflammation
what is backwash ileitis
presence of ileitis in pt w/ extensive colitis. w/ this feature, difficult to determine IBD subtype
What are the extra intestinal manifestations of Crohn’s?
classic ones: arthropathy (both axial and peripheral) term findings (pyoderma gangrenous, EN) ocular (uveitis, scleritis, episcleritis) hepatobiliary (PSC)
less common: thromboembolic (both venous and arterial) metabolic bone dz osteonecrosis cholelithiasis nephrolithiasis
what is the natural course of Crohn’s?
in most cases, chronic, progressive, destructive.
over time, the chronic intestinal inflammation leads to strictures, fistulas, abscesses.
what is the Lemann index?
quantifies degree of bowel damage from intestinal complications and subsequent surgery
in one study from Olmsted County, MN what was the median level of bowel resected?
64cm
what is the intestinal distribution of Crohn’s? Does the distribution usually change w/ time? are its constantly symptomatic?
approx 1/3 in:
- ileal
- ileocolonic
- colonic
only 6-14% of its will have change in disease location over time
symptoms of Crohn’s usually occur as chronic, intermittent course
What percentage of pts will develop intestinal complications (e.g. stricture, abscess, fistula, phlegm) w/n 20 yrs of dx?
about 50%
involvement of what part of the GI tract in Crohn’s disease is associated more w/ intestinal complications?
involvement of ideal, ileocolonic, and proximal GI tract
what percentage of Crohn’s pts will be lucky to have non progressing, indolent disease course over the long term?
only 20-30% of pts
everyone else will need to be actively monitored to achieve inflammation control
do pt’s symptoms correlate w/ level of active inflammation?
no
therefore, symptoms should not be the sole guide for therapy.
objective evals by endoscopy and imaging must be done periodically to avoid errors of under-or-over treatment.
what would happen to Crohn’s disease pts if there were no biologic or immunomodulating tx?
up to half of its would develop dependency and/or resistance to steroids
what risk factors increase Crohn’s pt risk of colorectal CA?
duration of disease extent of colonic involvement PSC fam h/o CRC severity of ongoing colonic inflammation
what other GI malignancy are Crohn’s its at increased risk of getting?
if small bowel involvement of Crohn’s, small bowel adenoma (18 fold increase risk; but the absolute risk remains low; approx 0.3 cases per 1,000 pt years)
how do you dx Crohn’s?
a combo of findings - clinical presentation, endoscopic findings, radiologic, histologic, and pathologic findings that demonstrate some degree of:
focal
asymmetric
transmural granulomatous inflammation
what labs do you order for initial eval for pt w/ symptoms for active Crohn’s?
depends on presentation
stool testing, including for fecal pathogens, C diff. also fecal calprotectin
fecal calprotectin helps distinguish b/w IBD and IBS (strong rec; mod ev)
what are common lab findings for active Crohn’s?
e/o inflammation - anemia nad thrombocytosis are most common
CRP (acute phase reactant made by liver) goes up for some pts as well
what makes CRP a useful marker for monitoring inflammation?
it has a short half life (19 hrs)
does ESR help distinguish b/w Crohn’s pts w/ IBS and healthy controls?
no
what is fecal calprotectin?
calcium binding protein derived from neutrophils; plays a role in regulation of inflammation
what is fecal lactoferrin?
iron-binding protein found in secondary granules of neutrophils
these serve as noninvasive markers of intestinal inflammation
may be useful in differentiating pts w/ BID vs pts w/ IBS
overall, fecal markers may also be useful in monitoring dz activity and response to tx
at this time, there is no role for genetic testing in the dx of Crohn’s. However, what are some better-known genetic loci associated w/ Crohn’s and how do they work?
ROLE IN INNATE IMMUNITY AND REGULATION OF EPITHELIAL BARRIER:
- NOD2 (predicts more complicated disease behavior, incl ideal involvement, stenosis, and penetrating disease, and need for surgery)
- IL-23R
- ATG16L1 (autophagy-related 16-like 1)
- IL12B (a/w need for early surgery)
what is goal of endoscopy for dx of Crohn’s? why?
get a sense of disease distribution and severity via biopsies
colonoscopy w/ intubation of TI + biopsy
severity and extent of disease is important as it has implications for CRC screening, disease prognosis, and therapeutic decisionmaking
what are mucosal changes suggestive of CD?
mucosal modularity, edema, ulcerations, friability, stenosis
what percentage of Crohn’s pts will have the classic granulomatous inflammation?
only 33% of pts have this. tf, this is not req’d for dx
What are some of the endoscopic scoring systems for CD?
Crohn’s Disease Endoscopic Index of Severity (CDEIS)
Simplee Endoscopic Score for Crohn’s Disease (SES-CD)
The SES-CD is the laeast cumbersome to use
Which pts should you also do EGD?
only perform EGD in pts w/ upper GI s/sx
overall, the prevalence of upper GI dz in Crohn’s is underestimated (5% vs the 16% in prospective studies)
In studies of Crohn’s pts w/ EGD findings c/w Crohn’s, what percentage of these pts were symptomatic?
What is the clinical implication?
Approx 37% of pts were symptomatic. There appear to be no clinical significant related to the mild changes seen on asymptomatic Crohn’s
what are some EGD findings (endoscopic, histologic) for Crohn’s?
endoscopic features:
mucosal modularity, ulceration (aphthous, linear), antral thickening, duodenal strictures
histologic changes:
granulomatous inflammation, focal cryptitis of duodenum, focally enhanced gastritis
who should get video endoscopy?
pts w/ strong suspicion of small bowel Crohn’s (e.g. obstructive symptoms)
may consider starting w/ potency capsule before VCE to decrease risk of capsule retention
what percentage of CD pts may have isolated small bowel involvement?
what’s the best way to dx small bowel CD?
up to 30% of pts w/ CD may have isolated small bowel dz
capsule endoscopy is superior to small bowel barium studies, CTE, and ileocolonoscopy
what is the lack of consensus re capsule endoscopy re small bowel CD?
no consensus as to which capsule findings constitute a dx of CD
What is the Lewis score?
scoring system based on 3 endoscopic parameters:
- villous appearance
- ulcers
- strictures
developed to standardize the description of lesions on endoscopy reports and increase inter-observer reliability
What is CECDAI?
Capsule Endoscopy Crohn’s Disease Activity Index (CECDAI) is another validated index for measuring small bowel CD activity on capsule endoscopy, just like the Lewis score.
(conditional rec; low level ev) what is recommended to increase diagnostic yield for detection of colorectal dysplasia for pts at high risk for colorectal neoplasia?
chromoendoscopy during colonoscopy.
pts considered particularly high risk for colorectal neoplasia (e.g. personal h/o dysplasia, PSC)
at what time interval is surveillance solo recommended for CD pts?
pts who’ve had a minimum of 8 yrs of disease and who have 30% or more colon involvement
risk of neoplasia in Crohn’s colitis increases w/ duration and extent of dz
at what time interval should pts w/ Crohn’s colitis _ PSC start surveillance colonoscopy?
pts w/ PSC and Crohn’s colitis should start surveillance colo immediately, regardless of disease distribution
Is there any difference in detection of neoplasia between chromoendoscopy and high-def white light colonoscopy?
no difference.
tf, as long as endoscopist has high-def white light colonoscopy, no need to do chromoendoscopy (which also takes about 9 min longer). also, no direct evidence of reduce all-case or cancer-specific mortality or time to interval cancer.
however, chromoendoscopy is superior to standard-def white light colonoscopy
what is the rate of dysplasia detection for random surveillance biopsies in pts w/ CD?
rate of dysplasia detection from random non targeted biopsies is very low - 0.1-0.2%
In some studies, what is the rate of dysplasia detection from targeted biopsies?
80-90%
in the 2018 ACG Crohn’s dz guideline, what is a rec re random vs targeted biopsies? what is the level of evidence?
endoscopists sufficiently trained and comfortable w/ chromoendoscopy may consider forgoing random surveillance biopsies and instead do targeted biopsies alone (conditional rec; very low ev)
since small bowel is one of the most common areas affected by CD, and up to 50% of pts w/ active small bowel disease may have lesions which skip the TI or are intramural (can’t be detected by ileocolonoscopy), what should be part of of every initial diagnostic workup of pts w/ suspected CD?
small bowel imaging
What are the options and considerations when choosing small bowel imaging for initial workup of CD?
CT enterography (CTE):
- sensitive (90%) and comparable to MRE
- able to see mucosal enhancement, mesenteric hypervascularity, mesenteric fat stranding (all e/o active inflammation)
MR enterography (MRE)
- preferred for younger pts (<35y/o) b/c of lack of radiation
- preferred in pts in whom serial exams are likely
- able to see wall enhancement, mucosal lesions, T2 hypersensitivity (e/o intestinal inflammation)
What types of CD pts are likely to require serial imaging exams?
pts who are young, have penetrating dz, upper GI involvement, and pts requiring steroids, biologics, surgery.
what are imaging options for pelvic/peri-rectal complications of CD?
endoscopic ultrasound ->90% accuracy in dx of perianal fistulizing dz
MRI pelvic has comparable accuracy
what percentage of pts w/ CD develop perirectal complications?
approx 25% of pts w/ CD develop perirectal complications (fistula formation and/or perirectal abscess)
w/ medical therapy alone, there’s a high relapse rate of fistulous drainage
What should you do if you suspect intraabdominal abscess?
cross-sectional imaging - CTE or MRE (both have accuracy >90%)
What should you document in every visit w/ a IBD pt?
- age of onset
- disease distribution
- disease activity
- disease phenotype
What are the categories of disease activity and how do you determine it?
CDAI - Crohn’s Disease Activity Index
DISEASE ACTIVITY CATEGORIES:
- remission
- mild - ambulatory, normal PO, <10% wt loss, no complications (obstruction, fever, abd mass, dehydration), minimal impact on QoL, CDAI 150-220
- moderate
- severe - may be cachectic, + complications, symptoms despite aggressive tx, often hospitalized, CDAI >450
(determined by impact on QoL, complications of dz, complications of tx)
What are the phenotype categories of CD?
international standard of phenotype classification (2005 Montreal revision of Vienna classification)
- age of onset
* A1 - <= 16y/o
* A2 - 17-40y/o
* A3 - >40y/o
- location (generally stable)
* L1 (TI)
* L2 (colon)
* L3 (ileocolonic)
* L4 (upper GI)
- behavior (tends to progress)
* B1 (nonstricturing, non penetrating)
* B2 (stricturing)
* B3 (penetrating)
\++++ p modifier if there's perianal fistulizing dzHow do we monitor disease activity and what is the goal?
monitor by control of symptoms and trend of inflammation (fecal markers, serum markers, imaging, endoscopic findings).
At this time, unclear if such targeting will lead to long-term improvement of outcomes or modify the disease course.
What are some of the fecal markers we use for disease activity?
FECAL MARKERS:
- fecal calprotectin (levels > 100 ug/g indicate endoscopic recurrence)
- fecal lactoferrin
both markers are sensitive for dz activity and correlate w/ endoscopic activity indices (such as colonic SES-CD)
What are some serum markers we use for disease activity?
SERUM MARKERS:
- CRP (nonspecific; but serial monitoring useful esp in pts on infliximab)
high baseline level (>15mg/l) predict primary nonresponse to infliximab
normalization f CRP during infliximab tx at 14 weeks is a/w greater chance of continued response or remission
what subsets of CD pts would you consider using cross-sectional imaging to monitor disease activity?
small bowel CD pts
endoscopically, what are you looking for for disease monitoring?
what is the scoring system?
mucosal healing
mucosal healing is defined as an absence of ulceration.
mucosal healing predicts sustained clinical remission, decreased need for surgery and hospitalizations
SES-CD (simple endoscopic score - CD) reliably correlates w/ clinical remission. used to quantify degree of inflammation and ulceration in pts w/ CD w/n the reach of the colonoscope.
What effect do NSAIDs have on CD?
many case reports and observational studies suggesting NSAIDs associated w/ IBD flares - mucosal damage and increased mucosal permeability –> more exposure to luminal toxins and antigens.
avoid NSAIDs for IBD pts (strong rec; low ev)
What effect does smoking have on CD?
cigarette smoking worsens disease activity (higher rate of surgery, hospitalization, peripheral arthritis)
active smoking a/w penetrating phenotype of CD
active smoking increases risk of relapse after d/c of anti-TNF tx
active smoking cessation programs should be encouraged (strong rec; low ev)
thoughts on abx in pts w/ CD?
BLUF: abx use should not be restricted in CD (conditional rec; very low ev)
disruption of intestinal microbiome may be detrimental to pts w/ IBD.
Dysbiosis is a/w increased intestinal inflammation.
in pts w/ worsening diarrhea after abx, eval for C diff.
thoughts on C diff and IBD?
pts w/ IBD have a higher carriage rate of C diff
what is the impact of comorbid depression and/or anxiety on pts w/ CD?
BLUF: assess and manage stress, depression, anxiety as part of comprehensive care plan for pt w/ CD (strong rec; very low ev)
greater risk of surgery and higher degree of healthcare utilization
many pts associate stress leading to increase in IBD sx. Perceived stress includes issues related to control, dz mgmt, and impact on lifestyle
increased bowel symptoms for these pts aren’t always a/w increased inflammation
Broadly speaking, what are the diff stages of tx for pts w/ CD?
acute disease
induce clinical remission
maintain remission
how long from starting therapy do you expect a clinical response?
how long until you expect maximal improvement?
clinical improvement should be evident w/n 2-4 weeks
maximal improvement should occur w/n 12-16 weeks
