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G19 Gastroenterology Toronto Notes 2023

• Dukoral': oral vaccine that offers protection against V. cliolerac (efficacy -80%) and ETEC (efficacy

-50-67%)

two dosesshould be taken two weeks prior to traveling and the effect may last up to three months

» Public Health Agency of Canada recommends that it may be considered for the following

situations(not recommended for routine use in travellers):

increased risk of acquiring traveller’

s diarrhea (gastric hypochlorhydria or young children >2

y)

short-term travellers who are high-risk (e.g. chronic illness) and have an increased risk of

serious consequences of traveller'

s diarrhea (e.g. chronic renal failure,CHI'

,T1DM, IBD)

» immunosuppression

history of repeat traveller’s diarrhea

travellers to cholera endemic countries at increased risk of exposure

• two vaccines against Salmonella lyphi are available and their effectiveness is estimated to be 50-70%

Chronic Diarrhea K

Definition

• passage of frequent unformed stool for >4 wk (compared to persistent diarrhea lasting 14-30 d)

Etiology/Classification

• majority of cases are non-infectious

• see Differential Diagnosis of Common Complaints, G’

5

Investigations

• guided by history

• stool analysisfor:C.difficile toxin, C&S, O&P ± fecal fat, WBC,fecal calprotectin

• blood for:CBC, electrolytes, C-reactive protein (CRP) ,T

'

SH, celiac serology (IgA anti-tTG;ask for

serum protein electrophoresis or immunoglobulin quantitation to rule out IgA deficiency, which has

an increased frequency in celiac disease)

• colonoscopy and ileoscopy with biopsy

• upper G1 endoscopy with duodenal biopsy

• wireless small bowel endoscopy capsule (low yield)

• trial of lactose free diet

• caveat: may delay diagnosis of IBD and celiac disease

Treatment

• approach issimilar to that of acute diarrhea

Maldigestion and Malabsorption

Definition

• maldigestion:inability to break down large molecules in the lumen of the intestine into their

componentsmall molecules

• malabsorption:inability to transport molecules across the intestinal mucosa into circulation

Etiology

• maldigestion

• inadequate mixing of food with enzymes(e.g. post-gastrectomy)

• pancreatic exocrine deficiency

• primary diseases of the pancreas (e.g. cystic fibrosis(CF) (remember CF can result in pancreatic

exocrine insufficiency as well), pancreatitis, cancer)

bile salt deficiency

terminal ileal disease (impaired enterohepatic recycling in view of loss greater than

synthesis), bacterial overgrowth (deconjugation of bile salts),rarely liver disease (cholestatic,

e.g. PBC)

specific enzyme deficiencies (e.g. lactase)

• malabsorption

inadequate absorptive surface

infections/infestations (e.g. Whipple’s disease, (iiardia)

immunologic (e.g. celiac disease)

infiltration (e.g. lymphoma, amyloidosis)

fibrosis (e.g. systemic sclerosis, radiation enteritis): can lead to loss of surface area but also

areas ofstricture formation resulting in stasis with small bowel overgrowth

small bowel resection (length,site, location, presence/absence of ileocecal valve, and integrity

of colon are important)

congenital (e.g.short bowelsyndrome)

inflammatory':extensive ileal CD (pivotal number is 100 cm as <100 cm = bile salt or

choleretic diarrhea,>100 cm = fatty diarrhea orsteatorrhea) +

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G20 Gastroenterology Toronto Notes 2023

• drug-induced

cholestyramine,ethanol, neomycin, tetracycline, and other ABx

endocrine

DM (complex pathogenesis)

Clinical Features

• symptoms usually vague unless disease issevere

• weight loss, diarrhea,steatorrhea, weakness,fatigue

• manifestations of malabsorption/deficiency

Fat Soluble Vitamins:ADEK

vitamin A. vitamin D. vitamin E.vitamin

K

Table 12. Absorption of Nutrients and Fat Soluble Vitamins

Deficiency Absorption Clinical Disease and/or Features Investigations

Duodenum, upper jejunum Hypochromic, microcytic anemia,

glossitis, koilonychia (spoon nails), pica

Iron « Hb, serum Fe, a serum ferritin

Calcium Duodenum, upper jejunum (binds lo Cat'

binding-protein in cells:levels increased

by vitamin D)

Metabolic bone disease, may get tetany a Serum Cat', a serum Mg /

-, and

and paresthesias if serum calcium tails* t ALP

(see Endocrinology, E42) Evaluate for a bone mineralization

radiographically (dual energy x- ray

absorptiometry.OEXA)

Folic Acid Megaloblastic anemia, glossitis, a red

cell folate (may see t lolic acid with

bacterial overgrowth)

B12 ingested and bound to fi proteins mainly Subacute combined degeneration

Irom salivary glands:stomach secretesIF in of thespinal cord, peripheral/optic

acidic medium:in basic medium, proteases neuropathy, dementia,megaloblastic

Irom the pancreas cteave R protein and anemia, glossitis

EU- IF complex forms, protecting Bu Irom

further protease attack:B12 absorbed in

ileum and binds to Itanscobalamin (IC)

Complex polysaccharides hydrolyzed lo Generalized malnutrition, weight loss,

oligosaccharides and disaccharides by flatus, and diairhca

salivary and pancreatic enzymes

Monosaccharides absorbed in duodenum!

jejunum

Digestion at stomach, brush border, and

inside cell

Absorption occurs primarily in the jejunum

Lipase, colipase, phospholipase A

(pancreatic enzymes), and bile salts needed and diarrhea

lor digestion

Products ol lipolysis form micelles which

solubilize fatand aid in absorption

Absorption occurs primarily in the jejunum

Fatty acids diffuse into cell cytoplasm

Jejunum a Serum folic acid

Vitamin Biz Differentiate causes by nuclear

Schilling test (when available)

Positive anti-intrinsic factor

antibodies and atrophic gastritis

point toward perniciousanemia (see

Hematology.H25)

Carbohydrate Hydrogen breath test

trial of carbohydrate-restricted diet

0-xylose test

Protein General malnutrition and weight loss,

amenorrhea, and a libido it severe

a Serum albumin (lowsensitivity)

Fat Generalized malnutrition,weight loss. Small bowel biopsy

MRCP. ERCP, pancreatic function tests

(not routinely available)

Quantitative stool tat lest (72 h)

May start with qualitative stool fat

test (Sudan stain of stool)

C-triolein breath test (not routinely

available)

Foul-smelling lcccs *gas

Steatorrhea

Vitamin A flight blindness

Dry skin

Keratomalacia

Skin (via UV light) or diet (e.g. eggs,fish oil. Osteomalacia in adults

fortified milk)

Dietary sources(e.g. vegetable oils. nuts. Retinopathy, neurological problems

leafy green vegetables)

Synthesized by intesbnal flora

t risk of deficiency after prolonged use of

broad spectrum ABx and /orstarvation

Dietary sources (e.g. milk, eggs, liver,

carrots,sweet potatoes)

Vitamin D

Rickets in children

Vitamin E

Vitamin K Prolonged INR may cause bleeding

'Calcium malabsorption more commonly causes decreased bone density rather than hypocalcemia because serum calcium levels are protected by

leaching calcium Iromlhe bone

Investigations

• tTG-lg/\ antibody serology/immunoglobulin A quantitation and abdominal imaging are most useful

because celiac disease and chronic pancreatitis are the two most common causes of steatorrhea

• 72 h stool collection (weight, fat content) documentssteatorrhea (gold standard)

• fecal elastase to screen for pancreatic insufficiency and/or consider empiric trial of pancreatic

enzymes based on clinical context

• serum carotene (precursor to vitamin A), folate, Ca J+,Mg 2 t, vitamin Bt 2, albumin, ferritin,serum

iron solution, international normalized ratio/partial thromboplastin time (1NR/PTT)

• stool fat globules on fecal smear stained with Sudan (used as an initial qualitative screening tool)

• other testsspecific for etiology (e.g.Cl'

scan/MRl to visualize pancreas)

Treatment

• dependent on underlying etiology

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Celiac Disease (Gluten Enteropathy/Sprue)

Definition

• abnormal small intestine mucosa due to intestinal reaction to gluten, a protein found in wheat, barley,

rye, and possibly oats (certified gluten-free oats may be acceptable in a subgroup of patients)

Etiology

• unique autoimmune disease because the genetics (HLA-DQ2/8), the auto-antigen (tTG), and the

environmental trigger (gluten) are all known

• associated with other autoimmune diseases, especially Sjogren’s,T1DM, thyroid disease

• gluten is broken down to gliadin, which is the toxic protein

• HLA-DQ2 (chromosome 6) found in 80-90% of patients compared to 20% of the general population;

celiac also associated with HLA-DQ8

• HLA-DQ2/Q8 are necessary permissive genes, but their presence docs not confer a diagnosis of celiac

disease (note: up to 40% of White individuals carry the HLA alleles, but will never develop celiac

disease)

Epidemiology

• more common in women

• prevalence:1 first degree relative: 10%; 2 first degree relatives:20%

• may present any time in life, with peak presentation in infancy (when cereals introduced)

Clinical Features

• classic presentation:diarrhea, weight loss, anemia,symptoms of vitamin/mineral deficiency, failure to

thrive; more common current presentation:bloating,gas, iron deficiency,or asymptomatic (patient at

risk)

• improves with gluten-free diet, deteriorates when gluten reintroduced

• disease is usually most severe in proximal bowel

iron, calcium, and folic acid deficiency (absorbed in proximalsmall bow'el) more common than

vitamin B 12 deficiency (absorbed in distalsmall bowel or ileum)

• gluten enteropathy may be associated with dermatitis herpetiformis skin eruption, epilepsy,

myopathy, depression, paranoia, infertility, bone fractures/metabolic bone disease

Investigations

• serological tests

• serum anti-tTG antibody, IgA, is 90-98% sensitive, 94-97% specific

• patients with selective IgA deficiency have false-negative anti-tTG

therefore, measure serum IgA concomitantly (via serum immunoglobulin quantitation)

• incorporate serum testing tTG and/or DGP IgG in IgA deficiencies

• small bowel mucosal biopsy (usually duodenum) is diagnostic:

• increased intraepithelial lymphocytes (earliest pathologic finding)

• crypt hyperplasia (next stage of pathophysiology)

villous atrophy (laststage of pathophysiology)

note:there is a wide differential diagnosisfor villous atrophy, including, but not limited to,small

bowel overgrowth, CD, lymphoma, Giardia, HIV

• improvement with a gluten-free diet, but should not be started in adults before serological tests and

biopsy

• considerCTenterography to visualize small bowel to rule out lymphoma

• evidence of malabsorption (localized or generalized)

• steatorrhea

low levels of ferritin/iron saturation, Ca 2

\ Fe,albumin, cholesterol, carotene, Bi:absorption

• quantitative fecal fat >7%

Treatment

• dietary counselling

• gluten free diet; avoid barley, rye,wheat (as these grains are related and have toxic proteins,

similar to gliadin)

oats allowed if not contaminated by other grains (grown in soil without cross-contamination)

• rice and corn flour are acceptable

• iron, folate supplementation (with supplementation of other vitamins as needed)

• if poor response to diet change, consider

• alternate diagnosis

» non-adherence to gluten-free diet (advertent or inadvertent)

concurrent disease (e.g. microscopic colitis, pancreatic insufficiency)

• development of intestinal (enteropathy-associated T-cell) lymphoma (abdominal pain, weight

loss, palpable mass)

development of diffuse intestinal ulceration,characterized by aberrant intraepithelial T-cell

population (precursor to lymphoma)

Early Gluten Introduction and Celiac Disease in

the MIStudy:A Prespecified Analysis of the MI

hodomited Clinical Trial

JAMA Pedralr 2020:114:1 ?

Purpose:Determine whether introdactlon of

high-dose gluten lowers celiac disease prevalence

at 3yr of age

Methods:l-fa

6allergenic foods In addition to breast milk from

age 4 mo (early introduction),or to avoid allergenic

foodsand followexclusive breastfeeding guidelines

(standard introduction). Evaluation of celiac

was an a priorisecondary outcoureoithe EAT

trial, tested at age 3with anh transglutaminase 2

antibodies.

Results:1.4% of infantsin thestandard introduction

group had a celiac disease diagnosisconfirmed.

versus 0% of infantsin theearly introduction group.

Conelotion:Introduction of gluten from age 4 mo

was associated with a reduction in the prevalence of

celiacdrsease.

nts were random ued to consume

d scare

<§)

Gluten Founci in BROW

Barley

Rye

Oats (controversial)

Wheat

n ,

i

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G22 Gastroenterology Toronto Notes 2023

Prognosis

• associated with increased risk of lymphoma, carcinoma (e.g. small bowel and colon; slight increase

compared with general population),autoimmune diseases

• risk oflymphoma may be loweredby dietary gluten restriction

Inflammatory Bowel Disease

Definition

• group ofdisorders characterizedby inflammation, and potentially ulceration,ofthe gastrointestinal

tract;two main forms include CD and UC

Etiology

• complex,multifactorial etiology

• most likely a sustained response ofthe immune system,perhaps to enteric flora

• lack of appropriate down-regulation ofimmune responsiveness after an infection in a genetically

predisposed individual

Genetics

• increased risk ofboth UC and CD in relatives ofpatients with either disease, especially siblings;early

onset disease

• familial risk greater ifproband has CD rather than UC

• likely polygenomic pattern; 2001 associated gene loci

• CARD15/NOD2 gene mutation associated with CD (relative risk in heterozygote is 3,in homozvgote is

40), especially in Ashkenazi Jews,early onset disease,ileal involvement,and fistulizing, fibrostenotic,

or stricturing disease

• CARD15 gene product modulates Nl'

xp, which is required for the innate immune response to

microbial pathogens,best expressed in monocytes-macrophages

Clinical Features

Table 13. Clinical Differentiation of Ulcerative Colitis from Crohn’s Disease

Crohn's Disease Ulcerative Colitis

location Any part of Gl tract ("gum to bum")

Smallbowel coton:50%

Small bowel only;30%

Colon only;20%

Uncommon;possibin if colonic disease

Usually nonbloody (may be bloody,particularly if

distal colon isinvolved)

Post-prandial/colicky

Common

Uncommon (unless rectum involved)

Frequent (25%).#10

Common

Segmental inflammation, ulcers (aphthous, stellate,

linear),patchy lesions,pscudopolyps. cobblestoning

Isolated to large bowel

Always involves rectum,mayprogress proximally

Very common (90%)

Frequent,mucous,bloody, small volume stools

Rectal Bleeding

Diarrhea

Abdominal Pain

Fever

Urgency/Tenesmus

Palpable Mass

Recurrence After Surgery

Endoscopic Features

Predefecation/colicky

Uncommon

Common

Rare (if present,often related to cecum full of stool)

None post-colectomy (withpermanent ileostomy)

Continuous diffuse inflammation,erythema,

friability,loss of normal vascular pattern,

pseudopolyps

Mucosal distribution,continuousdisease (no skip

lesions)

Architectural distortion,gland disruption,crypt

abscess

Granulomas absent

Histologic Features Transmural distribution with skip lesions

Focal inflammation

t Noncaseating granulomas, deep

Assuring aphthous ulcerations,strictures

Glands Intact

RadiologicFeatures Cobblestone mucosa

Frequent strictures and fislulae

Abdominal x-ray;bowel wall thickening,‘string sign" complicating cancer

Strictures. Astulae,perianal disease

Increased if >30% of colon involved

lackofhaustra

Strictures rare;if present,need to rule out

Complications

Colon Cancer Risk

Toxic megacolon

Increased except inproctitis

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G23 Gastroenterology Toronto Notes 2023

Table 14. Extraintestinal Manifestations of IBD

System Crohn's Disease Ulcerative Colitis

Dermatologic

Erythema nodosum

Pyoderma gangrenosum

Perianalskin tags

Oral mucosal lesions,stomatitis Common

Psoriasis

15% 10%

10% Less common

75-80% Rare

Rare

Present in 5-10% ol those v/ith IBD but not an EIM

Rhcumatologic

Peripheral arthritis

Ankylosing spondylitis

Sacroiliitis

15-20% of those with IBD (CD>UC|

10% of those with IBD|CD»UC)

Occurs equally in CD and UC

Ocular|~10% ol IBD)

Uveitis (vision threatening)

Episcleritis (benign) 3- 4% of I80 patients(CD» UC )

Hepatobiliary

Cholelithiasis 15-35% of patients with ileal CD

1 PSC -5% of IBD cases with colonic involvement

Fatty liver

Gallstones Pigment stones in CO

Urologic

Calculi Most common in CD.especially following ileal resection or extensive terminal ileal disease (oxalate stones),

usually in context of an intact colon

Ureteric obstruction

Fistulas Characteristic Of CO

Others

Thromboembolism

Vasculitis

Osteoporosis

Vitamin deficiencies (Bij . ADEK )

Cardiopulmonary disorders

Pancreatitis (rare)

Phlebitis

Increased in CD with/without prior steroids, in UC only alter steroids usage

Crohn’s Disease

Definition

• chronic transmural inflammatory disorder potentially affecting the entire gut from mouth to perianal

region (“gum to bum")

Epidemiology

• worldwide incidence 3-15 to 10-20/100000; 135000Canadians living with CL)

• bimodal:onset before age 30,second smaller peak at age 60; M=l-

• incidence of CD increasing (relative to UC) especially in young females

• more common in White people, Ashkenazi lews

• risk in Asians increases with move to Western countries

• smoking incidence in CD patients is higher than general population

Pathology

• most common location; ileum + right colon

• linear ulcersleading to mucosal islands and “cobblestone"

appearance

• granulomas are found in 50% of surgical specimens, 15% of mucosal biopsies

Clinical Features

• natural history unpredictable; young age, perianal disease, and need for corticosteroids have been

associated with poor prognosis, but associations are not strong enough to guide clinical decisions

• commonly presents as recurrent episodes of abdominal cramps, diarrhea (with or without bleeding),

fatigue, and weight loss

• ileitis may present with post-prandial pain, vomiting, RLQ mass; mimics acute appendicitis

• ElMs are more common with colonic involvement

• fistulae, fissures, abscesses are common

• deep fissures with risk of perforation into contiguous viscera (leads to fistulae and abscesses)

• enteric fistulae may communicate with skin, bladder, vagina, and other parts of bowel

Effect of Tight Control Management on Crohn's

Disease (CAIM ):A Multi-Centre, Randomized

Gxitrollcd Phase 3 Trial

lancet 2017:390:2775-2789

Purpose fodefnethe m e ol incorporating

laboratory biomatkers in the management algorithm

ol active CD.

Study:RCT

Population : 224adult patients|22 countnes at 74

hospitals)with activeCD wem random red to intensify

treatment based on either laboratory bomaikets

(serum CRP,fecai calpioietto) plus clinical evaluation

(CD activity inderand prednisone use) or treatment

based art clinical evaluation alone.

Outcomes: Mucosal healing via the absence ol

deep ulcers.

Results: At 2 yr.more patents receuir gtreatment

ciitena that me uded laboratory tests had complete

mucosal healing ( Le.ro ulcers) than the group treated

on the basisolsymptoms alone (46% vs.30%).

Admittedly,the endpoint ol mucosal healing is not

a strong dmiceSy relevant result, but other studies

hare shown that the gieater the mucosal ulceration ,

the higher the rate of complications(Le.strictores,

fistulae. abscesses,hospitalizations, and surgery).

Conclusions ISisrs not debalive data but adds

to other evidence showing that the traditional

management paradigm reeds renting,soia most

patients it is worthwhile aiming for endoscopic

healing of CO irrespective of symptoms.

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Investigations

• colonoscopy with biopsy to visualize (less often gastroscopy)

• CT/MR enterographv to visualize small bowel

• CRH elevated in most new cases, useful to monitor treatment response (especially acutely in UC)

• bacterial cultures, O&P, C. difficile toxin to exclude other causes of inflammatory diarrhea

Management (see Figure 8)

Traditional Medical Management of

Crohn's Disease

Induction of Maintenance

Remission

5 ASA* 1 ?

Table 15. Management of Crohn’s Disease Steroids

Imiminomodulators

Management Notes

Lifestyle/Dict Smoking cessation

Fluids only during acute exacerbation

Enteral diets may aid inremission only for Crohn's ileitis,not colitis

No evrdence for any non- enteral dietchanging tire natural history of CD. but may affect symptoms

Those with eitensive small bowel involvement or extensive resection require electrolyte,mineral,and vitamin

supplements (vitamin D, Ca2-. Mg2-.Zn.Fe, Bit)

Loperamide (Imodium -

) >diphenoxylate (Lomotil!

|> codeine (cheap but addictive)

All work by decreasing small bowel motility,used only for symptom relief

CAUTION:if colitis is severe frisk olprecipitating toxic megacolon), therefore avoid during flare- ups

Sulfasalazine (Salazopyrin 3 ): 5 ASA bound to sulfapyridme

Hydrolysis by intestinal bacteria releases 5-ASA (active component)

Dose-dependent efficacy

Mesalamine IPentasa -

. Salofalk - . Mezavant , Olsalazine :

):used for the treatment of mild ileitis (CO) and mild

UC, when inflammation is mild

E.g. metronidazole (20 mg/kg/d. 8ID or TID dosing) or ciprofloxacin

Best described for perianal CO,although characteristically relapse when discontinued

Prednisone:starting dose 40 mg once daily for acute exacerbations:IV methylprednisolone if severe

No proven role for steroids in maintaining remission;masks intra-abdominal sepsis

6-mcrcaptopurine (6 MP). azathioprine (Imuran '

); MIX (used less often)

More often used to maintain remission than to treat active inflammation

Most commonlyused as steroid sparing agents

i.e. to lower risk of relapse as corticosteroids are withdrawn

May require »3 mo to have beneficial effect:usually continued for several years

May help to heal frstulae, decrease disease activity

Increases efficacy of biologies plus lowerschances of biologic dosing efficacy (tolerance) so often given in

combination with biologies

Side effects: vomiting,pancreatitis, bone marrow suppression, increased risk of malignancy (i.e. lymphoma)

Infliximab IV (Remicade '

) or adalimumab SC (Humira '

):both - antibody to INF a

Proven effective for treatment of fistulae and medically refractor y CD

First- line immunosuppressive therapy with infliximab *azathioprine (dual therapy) more effective than using

either alone (monotherapy)

Ustekinumab. monoclonal antibody against P40 subunit of interleukin 12 and 23

Vedolizumab.monoclonal antibody directed against inlcgrin a4(17 thereby reducing lymphocyte traffic lo gutnow indicated for UC and CD

JAK (Janus Kinase) inhibitors (e.g.tofacitinib). Efficacy demonstrated in UC

(e.g.

azathioprine.

methotrexate

(MIX))

Antibiotics

Antidiarrheal Agents Biologies '

'Vxmlnosallcytlt add(VUi|in

*

In CO is

untromfvial.Ilowuvvi.maultrial lot mildivlthDitty

nwarranted(Induction and matnlcnamrIt dinkal

response)

5 ASA"

Antibiotics

Nutrition

Symptomatic tlierapv

(e.g.loperamide,acetaminophen)

Corticosteroids

I

Immunosuppressives

5-ASA (mesalamine)

Antibiotics (Flagyl

'”

Cipro )

I

Corticosteroids

(e.g.budesonide,prednisone)

I

Biologies Immunosuppression

(e.g.azathioprine.6-MP.methotrexate)

I

Immunomodulators

(e.g. TNF-antagonisls: infliximab,

adalimumab)

I

Immunotherapy (Small

molecules)

Surgical/ Experimental

Experimental therapy or surgery

Surgical treatment (see General and Thoracic Surgery.GS3G)

Surgery generally reserved for complications such as fistulae.obstruction, abscess,perforation,bleeding, and

for medically refractory disease

If <50% or <200 cm of functional small intestine,risk of short bowel syndrome

At least 50% clinical recurrence within 5 yr;85% within 15 yr;endoscopic recurrence rate even higher

40% likelihood of second bowel resection,30% likelihood of third bovrel resection

Complications of ileal resection

Figure 8. Traditional graded

approach to induction therapy in

Crohn's disease

Note:immunosuppresianb and

immunomodulators are increasingly used initially

(“top-down management strategy").5-ASA drugs

have limited role in Crohn's disease

<100 cm resected » watery diarrhea or cholorrhea (impaired bile salt absorption)

Treatment:cholestyramine or antidiarrheals. e.g. loperamide

>100 cm resected »steatorrhea (reduced mucosal surface area,bile salt deficiency)

Treatment:fat restriction, medium chain triglycerides

’Cholestyramine:a bile-salt binding resin;for watery diarrhea with <100 cm ol terminalileum diseased or resected:however,non-specific

antidiarrheals are more convenient and often morepotent

"5-ASA use inCD is controversial;however,initial trial tor mild ileitis only is warranted (induction and maintenance if clinicalresponse)

Prognosis

• highly variable course

• 10% disabled by the disease eventually,spontaneous remission also described

• increased mortality, especially with more proximal disease, greatest in the first 4-5 yr

• complications include

intestinal obstruction/perforation

• fistula formation

malignancy (lower risk compared to UC)

• surveillance colonoscopy same as UC (see Ulcerative Colitis, G25) if more than 1/3 of colon involved

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Ulcerative Colitis SH

Definition

• inflammatory disease affecting colonic mucosa anywhere from rectum (always involved) to cecum

Epidemiology

• worldwide incidence 3-15 to 10-20/100000; 120000 Canadiansliving with UC (less common than CD)

• 2/3onset by age 30 (with second peak after 50 yr);M=l

;

• small hereditary contribution (15% of cases have 1st degree relative with disease)

• reduced risk in smokers

• inflammation limited to rectum orleft colon is more common than pancolitis

Pathology

• disease can involve any portion of lower bowel ranging from rectum only (proctitis) to entire colon

(pancolitis)

• inflammation is diffuse, continuous,and confined to mucosa

In UC. non-bloody diarrhea isfrequently

the Initial presentation:eventually

progressing to bloody diarrhea

Medical Management of Ukerative

Induction of

Clinical Features

• rectal bleeding is the hallmark feature;diarrhea present if more than the rectum isinvolved

can also have abdominal cramps/pain, especially with defecation

• severity of colonic inflammation correlates with symptoms(stool volume, amount of blood in stool)

• tenesmus, urgency, incontinence

• systemic symptoms; fever, anorexia, weight loss, fatigue in severe cases

• ElMs(see Table 14,023)

• characteristic exacerbations and remissions; 5% of cases are fulminant

5-ASA

Steroids

Immunosuppressive

i

Investigations

• sigmoidoscopy with mucosal biopsy (to exclude self-limited colitis) without bowel prep

sufficient for diagnosis

• colonoscopy helpful to determine extent of disease; contraindicated in severe exacerbation

• CT colonography (formerly barium enema) if colonoscopy cannot be done; contraindicated in severe

disease

• stool culture, microscopy, C. difficile toxin assay necessary to exclude infection

• no single confirmatory test

aration often

Treatment

• mainstaysof treatment:5-ASA derivatives (only in mild to moderate disease) and corticosteroids,with

azathioprine used in steroid-dependent or resistant cases

• diet oflittle value in decreasing inflammation but may alleviate symptoms

• antidiarrheal medications generally not indicated in UC

. 5-ASA

• topical (suppository or enema): effective for distal disease (rectum to splenic flexure) if inflammation is

mild, preferable to corticosteroids

» oral:effective for mild to moderate,but not severe colitis(e.g. sulfasalazine 3-4 g/d,mesalamine 4 g/d)

» commonly used in maintaining remission (decreases yearly relapse rate from60% to 15%)

» may decrease rate of colorectal cancer

• corticosteroids

to remit acute disease, especially if severe or first attack;may need maximum dose IV steroids initially

(e.g. methylprednisolone 30 mg IV ql2 h)

• limited role as maintenance therapy for mild to moderate disease

use suppositories(predominantly available in compound pharmacies) for proctitis

use enemas and topicalsteroids (e.g.hydrocortisone foam,budesonide enemas) for inflammation

distal to splenic flexure

• immunosuppressants(steroid-sparing)

» in hospitalized patients with severe UC- add IV'infliximab if no response to IV methylprednisolone

within 3d; then consider colectomy if inadequate response

• biologies (infliximab, adalimumab, golimumah, vedolizumab) and small molecules (tofacitinib)

can also be used for outpatients with moderate-severe disease, particularly those that are steroidunresponsive or steroid-dependent,some evidence that they are best used early in course of disease

• azathioprine and 6-MP: too slow to rapidly resolve acute relapse

most commonly used to maintain remission as corticosteroids withdrawn

given with biologies:increase efficacy of infliximab and decrease likelihood of developing

tolerance to infliximab (

-10% chance/yr)

• Ozanimod

an oralsphinogosine-l-phosphate receptor modulator used for treating moderate-to severe UC

does not require previous failure of immunosuppressants, glucocorticoids, biologies,or othersmall

molecules

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increases clinical remission rates compared to placebo

• surgical treatment (restorative)

aim for cure with colectomy;bowel continuity can be restored with ileal pouch-anal anastomosis

(IPAA)

indications:failure of adequate medical therapy, toxic megacolon, uncontrollable bleeding, precancerous changes detected either by endoscopy or endoscopic biopsies (dysplasia),inability to taper

corticosteroids, overt malignancy

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G26 Gastroenterology Toronto Notes 2023

Complications

• similar to CD, except:

more liver problems (especially PSC in men)

• greater risk of colorectal cancer

risk increases with duration and extent of disease (5% at 10 vr, 15% at 20 yr for pancolitis;

overall relative risk is 8%)

risk also increases with active mucosal inflammation and sclerosing cholangitis

thus, regular colonoscopy and biopsy in pancolitis of l>8 yr is indicated

• toxic megacolon (transverse colon diameter >6 cm on abdominal x-ray) with immediate danger of

perforation (see General Surgery and Ihoracic Surgery. GS45)

When Considering Complications of

ISO. Think:

ULCERATIVE COLITIS

Urinary calculi

Liver problems

Cholelithiasis

Epithelial problems

Retardation of growth/sexual

maturation

Arthralgias

Thrombophlebitis

Iatrogenic complications

Vitamin deficiencies

Eyes

Colorectal cancer

Obstruction

Leakage (perforation)

Iron deficiency

Toxic megacolon

Inanition (wasting)

Strictures

Prognosis

• chronic relapsing pattern in most patients

• 10-15% chronic continuous pattern

• >1 attack in almost all patients

- more colonic involvement in the 1st yr correlates with increased severity of attacks and increased

colectomy rate

• colectomy rate = 1% for all patients after the 1st yr; 20-25% eventually undergo colectomy

• normal life expectancy

• if proctitis only, usually benign course,lifetime risk of extension is 15%

• fecal calprotectin increasingly recognized as a marker of bowel mucosal inflammation, reported to be

especially useful in monitoring the activity of 1BD, but accuracy is still controversial

Irritable Bowel Syndrome s

Definition

• a form of functional bowel disease, now also known as disorder of gut-brain interaction;more than

just a label for G1 symptoms unexplained after normal investigations

Epidemiology

• 11% worldwide prevalence

• onset of symptoms usually in young adulthood

• F>M

Clinical Features

• Rome IV Criteria are used for diagnosis

• diagnosis is based chiefly on history; no specific diagnostic test available

Pathophysiology

• associated with either abnormal perception of intestinal activity or abnormal intestinal motility

• abnormal motility; multiple abnormalities described; unclear if associated or causative

• psychological:stress may increase IBS symptoms but probably does not cause IBS

• 4 main types of IBS

1BS-D: IBS with predominant diarrhea

• IBS-C:IBS with predominant constipation

• IBS-M: IBS-mixed with both diarrhea and constipation (each >25% of all abnormal bowel

movements)

IBS untyped:insufficient abnormalities to be IBS-C, D, or M

Diagnosis

Emerging Biologic Treatments for

Ulcerative Colitis

Generic

Name

Brand Name Major Study

Ustekinumab Stelara ' NEJM 2019;

381:1201

1214

Vedolirumab Entyvio ' HUM 2019;

381:1215-

1226

HUM 2019;

381:1215-

Adalimumab Humira '

1226

Table 16. Rome IV Criteria for Diagnosing Irritable Bowel Syndrome

IBS Rome IV Criteria

Recurrent abdominal pain lor more than 6 mo, at least1d /wk in the last 3mo.associated with 2 or more of the following:

1.Related to defecation

2.Associated vrlth a change In frequency ol stool

3.Associated with a change in form (appearance) of stool

Symptom onset at least 6 mo before diagnosis and criteria present during the last 3 mo

Ihe Mowing are supportive, but not essential to the diagnosis:

Abnormal stool frequency (>3/d or «3/wk)

Abnormal stool lorm flumpy/hard/loose/watery) >114 of defecations

Abnormal stool passage (straining,urgency, feeling of incomplete evacuation) >1/4 of defecations

Passage of mucus »1/4 of defecations

8loating r ~t

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Diagnosis ol IBS lesslikely in Presence of "Red Flag"

Features

Weight loss

Fever

Hodurnal defecation

Anemia

Blood or

Abnorm,

i pus in stool

al gross findings on flexible sigmoidoscopy

Hormal Physical fxam +

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G27 Gastroenterology Toronto Notes 2023

Investigations

• if history consistent with Rome IV criteria, no alarm symptoms, and no family history'of 1BD or

colorectal cancer,limited investigations required

• aim is to rule out diseases which mimic IBS, particularly celiac disease and 1BD

• investigations can be limited to CBC and celiac serology

• if available, fecal calprotectin is likely more reliable test to rule out IBD

• consider1SH,stool cultures depending on clinical circumstances

• consider colonoscopy (e.g. if alarm features present, family history of IBD, or ages >50)

IBS Mimickers

• Enteric infections e.g. Giardia

• Lactose Intolcranco/other

dlsaccharidase deficiency

. CO

• Celiac sprue

• Drug-induced diarrhea

• Diet-induced (excess tea, coffee,

colas)

Treatment

• education:reassurance, explanation,support, aim for realistic goals

• relaxation therapy,biofeedback, hypnosis,stress reduction, cognitive behavioural therapy, probably

exercise

• dietary: low l

:

01)MAH ( fermentable Qllgo-, Pi-, Monosaccharides And Polyols) diet for pain, bloating,

gas, irregular bowel movements (BMs)

• no therapeutic agent consistently effective, pain most difficult to control, no drug changes natural

history so the drug should be “wanted,since it is not needed”

• symptom-guided treatment

pain predominant

antispasmodic medication before meals (e.g. hyoscine, pinaverium, trimebutine - low level of

evidence)

• tricyclic antidepressants(TCA),selective serotonin reuptake inhibitors(SSKI) • moderate

level of evidence

Rilaxiniin therapy for Patients with Irritable

Bowel Syndrome withont Constipation

NEJM 2011:364:22-32

Purpose:Previous evidencesuggeststhat gut flora

may play an important role in the pathophysiology

of ISS.Ihisstudy evaluated nfatimin, a minimally

absorbed antibiotic,in beating IBS without

constipation.

Methods: two phase 3.double -blind, placebocontrolled trials( IMMI1and IMCil |2.12(0

patients who had I8S without constipation were

randomly assigned to rifanmin (5(0 mg dose) or

placebo,110 for 2 wk.with a follow-up of 10 wk.The

primary endpoint wasadequate self-reported relief of

global IBS symptoms.

Results:Significantly more patentsin the rifanmin

group had adequateself-reported relief of global

IBS symptoms compared to the placebo groupduring

the first 4 wk after treatment (40.831 vs. 31,2V

respectively!. Also,more patients In the rifaximln

group had adequate relief of bloating compared to the

placebogroup (39.5

*

vs.28.7V respectively).

Conclusions:Rifaiinnim therapy for 2 wk provided

significant relief ofsymptoms,bloating, abdominal

pain, and stool consistency associated with IBS

without constipation.

• 1BS-D

increase fibre (bran or psyllium) to increase stool consistency but may worsen abdominal gas

(controversial)

loperamide (Imodium*) (continuous use advised against)

diphenoxylate (Lomotil*)

cluxadoline

rifaximin

• IBS-C

increase fibre in diet

linaclotide, plecanatide, tenapanor

osmotic or otherlaxatives (help more with the constipation than the pain)

Prognosis

• 80% improve over time

• most have intermittent episodes

• normal life expectancy

Constipation s

Definition

• passage of infrequent/hard stools and/or difficult stool evacuation (e.g.straining,sensation of

anorectal blockage)

Epidemiology

• increasing prevalence with age; F>M

• rare in Africa and India where stool weight is 3-4x greater than in Western countries

Etiology

• most common:functional, idiopathic attributed to colon dysmotility but thisis difficult to measure

• organic causes:likely only if there are symptoms other than constipation

• medication side effects (e.g. narcotics, antidepressants) are the most common

• intestinal obstruction, left sided colon cancer (consider in older patients), and fecal impaction

• metabolic

DM

hypothyroidism

hypercalcemia, hypokalemia, uremia

• neurologic

intestinal pseudo-obstruction

Parkinson'

s disease

MS

collagen vascular disease (e.g.scleroderma )

painful anal conditions (e.g.fissures)

Clinical Features

• overlaps with IBS with constipation (IBS-C) but labeled as IBS-C when pain is a predominant feature

• stool firm, difficult to expel, passed with straining, abdominal pain relieved by defecation, flatulence,

overflow diarrhea, tenesmus, abdominal distension, infrequent BMs (<3/wk)

Causes of Constipation

DOPED

Drugs

Obstruction

Pain

Endocrine dysfunction

Depression

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G28Gastroenterology Toronto Notes 2023

Investigations

• underlying disease rarely found if constipation is the only presenting symptom

only test indicated in thissituation is a CBC (2013 recommendation of American

Gastroenterology Association),but also consider TSH,calcium, glucose, and abdominal x-ray

• colon visualization (colonoscopy,Cf colonography) if concomitant symptomssuch as rectal bleeding,

weight loss, anemia or ages >50

• if refractory to treatment, consider classification based on colon transit time; can measure colonic

transit time with radio-opaque (Sitz) markersthat are ingested and followed with a series of plain film

abdominal x-rays (normal:elimination of markers within 70 h)

1. normal = misperception of normal defecation (IBS)

2. prolonged throughout = “colonic inertia” (infrequent bowel movements with gas/bloating,tends

to occur in youth)

3. outlet obstruction inability to coordinate pelvic floor muscles to empty rectum,straining,stool

in rectum on digital exam, tends to occur in old age

• combination of 1 and 3 common

Treatment (in order of increasing potency)

• dietary fibre

useful if mild or moderate constipation, but not ifsevere

aim for 30 g daily, increase dose slowly

• surface-acting (soften and lubricate)

docusate salts(likely limited efficacy based on evidence), mineral oils

• osmotic agents (effective in 2-3d)

• polyethylene glycol 3350, lactulose,sorbitol, magnesium salts (e.g. magnesium hydroxide, i.e.

milk of magnesia), lactitol ((3-galactosido-sorhitol)

• cathartics/stimulants (effective in 24 h)

senna, bisacodyl

• enemas and suppositories(e.g.saline enema, phosphate enema, glycerin suppository, bisacodyl

suppository)

• prokinetic agents (e.g. prucalopride)

• secretagogues:linaclotide, plecanatide (increases water secretion into the intestinal lumen)

• NHE3 inhibitors: tenapanor

Always ask about NSAID/Aspirin '

or

anticoagulant therapy in Gl bleed

Upper Gastrointestinal Bleeding Aortoenteric Fistula is a rare and lethal

cause of Gl bleed,most common in

patients with a history ot aortic graft

surgery.Therefore,perform emergency

endoscopy if suspected,emergency

surgery if diagnosed

Note: The window of opportunity is

narrow. Suspect if history of aortic graft,

abdominal pain associated with bleeding

Definition

• bleeding proximal to the ligament of Treitz,see Overview of Gastrointestinal Tract,G2 (75% of Gl

bleeds)

ligament of Treitz:suspensory ligament where fourth portion of the duodenum transitions to

jejunum

Etiology

• above the GE junction

epistaxis

esophageal varices (10-30%)

esophagitis

• esophageal cancer

Mallory-Weisstear (10%)

stomach

gastric ulcer (20%) (see Peptic Ulcer Disease,Gl I )

* erosive gastritis (e.g. from EtOH or post-surgery) (20%)

gastric cancer

gastric antral vascular ectasia (rare, associated with cirrhosis and connective tissue disease)

Dieulafoy’slesion (very rare)

• duodenum

ulcer in bulb (25%)

aortoenteric fistula: usually only if previous aortic graft (see sidebar)

• coagulopathy (drugs, renal disease, liver disease)

• vascular malformation (Dieulafoy’slesion, arteriovenous malformation)

Clinical Features

• in order of decreasing severity of the bleed: hematochezia (brisk UG1B) > hematemesis > melena >

coffee ground emesis > occult blood in stool

Traasfusaon Strategies for Acute Upper

Gastrointestinal Bleeding

St JM 2013:368:11-21

Study:Prospective, unblmded. RCI,follow-up up

toASd.

Population: 921 patientswith hematemesis,bloody

nasogastric aspirate,melena.or both.Exclusion

criteria inebded massive Meed, acute coronary

syndrome,strohel transient ischemic attack or

transfusion within previous90 d:rece nt traumaf

surgery; lower Gl Weed.

Intervention: Patientsrandomized to restrictive («20

gl) or liberal|

«90 gfl)transfusion.

Outcome:Mortality,further bleeding,adverse

events.

lesults:fewer patients in the restrictive group

required transfusion (51% vs.15%; P *0.001). Ihe

hazard ratio loi death for restrictive compared to

tbera I transfusion was 0.55:05%Cl 0.33-0.92;

P^O.02.Further bleeding occurred in 10% vs.16%

(P-0.01) of patients,while adverseeffects occurred

in 40% vs. 48% (P-0.02) of patientsin the restrictive

and liberalstrategies,respectively.The restrictive

strategy had a better survival rate in patientswith

bleeding associated with cirrhosisChild-Pugh class A

or 6 (HR:0.30; 95% Cl 0.11-0.85), but not in cirrhosis

Child-Pugh class C (HR:1.04:05% Cl 0.45-2.37) or a

peptic ulcer (HR:0.70;05% 00.2(125).

Conclusions: Transfusing patients with anacute

UGIB at Hb of <70 g/l rather than 90g/lisassooated

with fewer transfusions, better survival,and fewer

adverse events.

n

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G29 Gastroenterology Toronto Notes 2023

Treatment

• stabilize patient (1-2 large bore IVs, IV fluids, monitor)

• send blood for CBC, cross and type, platelets, FT, PIT, electrolytes, BUN, Cr, LI-

"

Ts

• keep NPO

• consider nasogastric ( NG) tube to determine upper vs. lower G1 bleeding in some cases

• IV PP1:decrease risk of rebleed if endoscopic predictors of rebleeding seen (see prognosissection)

given to stabilize clot, not to accelerate ulcer healing

if given before endoscopy, decreases need for endoscopic therapeutic intervention

• for variceal bleeds,octreotide 50 pg loading dose followed by constant infusion of 50 pg/h and ABx for

those with cirrhosis (reduces risk of infections)

• consider IV erythromycin (or metoclopramide) to accelerate gastric emptying prior to gastroscopy to

remove clots from stomach

• H2-antagonists should not be used since they have minimal impact on rebleeding rates and need for

surgery

• endoscopy (OGD):establish bleeding site + treat lesion

if bleeding peptic ulcer:most commonly used method of controlling bleeding is injection of

epinephrine around bleeding point + thermal hemostasis ( bipolar electrocoagulation or heater

probe);less often thermal hemostasis may be used alone, but injection alone not recommended

endoclips

Hemospray "

dual therapy (more than one therapeutic intervention method ) is standard of care and has greater

efficacy than single therapy

Forrest Prognostic Classification of

Bleeding Peptic Ulcers

Forrest type of Lesion

Class

Risk of

Rebleed (%)

I Arterial bleeding 55-100

(oozing.'sp

-jrting)

Visible vessel

Sentinel clot

lla 43

lib 22

Ik Hematn covered 10

flatspot

No stigmata of

hemorrhage

5

Lancet1974:2:394-397

Prognosis

• 80% stop spontaneously

• peptic ulcer bleeding:low mortality (2%) unless rebleeding occurs (25% of patients, 10% mortality)

• endoscopic predictors of rebleeding (Forrest classification):spurt or ooze, visible vessel, fibrin clot

• can send home if clinically stable, bleed is minor, no comorbidities, endoscopy shows clean ulcer with

no high-risk predictors of rebleeding

• esophageal varices have a high rebleeding rate (55%) and mortality (29%)

Management ol Monvariceal Upper

Gastrointestinal Bleeding:Guideline

Recommendationsfrom tbelnternational

Consensus Group

Ann Intern Med 2019:171:805822

Pro Endoscopic Management In patients without

cardiovascular disease,the suggested Kb threshold

lor blood transfusion is <80 gIL The threshold is

higher for patients with cardiovascular disease.

Endoscopic Management Patients with acute

tIGIB should undergo endoscopy within 24 h of

presentation. In patents with high -risk stigmata,

thermocoagulation and sclerosant injection are

recommended. 1C 325. a hemostatic powder.can

be used as a tempoiiiing agent for actively bleeding

ulceis.

Ovort Gl blooding (homatochozia,molona)

4

m No

I

1

Upper and lower endoscopy I

Rule oul non-61 sources ol Has the anemia 1 ding (e.g. menorrhagia, resolved?

hemolysis)

blue

Source of bleeding found?

1

1 T

1 Yes: treat

No: proceed as if overt

Gl bleeding present

Yes: follow Pharmacologic Management High dosePPIsho.'d

be given lor 3 d to patientswith bleed ng ulcers with

high-risk stigmata who have undergone successful

endoscopic therapy.Continued oral PPI therapya

recommended twice daily for 14 d. then once daily

for a duration that depends on the nature of the

bleeding lesion.

No: wireless endoscopy capsule/

double balloon endoscopy*

•Wireless endoscopy capsule results help double balloon endoscopy localize source of bleeding

• Angiography il overt bleeding hemodynamically significant, estimated >0.5 cc/min

• CT enterography if wireless endoscopy capsule/double balloon endoscopy not available

Figure 9. Approach to iron deficiency anemia

Esophageal Varices

Etiology

• almost always due to portal hypertension

Clinical Features

• characteristically massive upper Gl bleeding

Prognosis

• risk of bleeding: 30% in 1st yr

• risk of rebleeding: 50-70% (20% mortality at 6 wk)

Investigations

• endoscopy r i

L J

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G30 Gastroenterology Toronto Notes 2023

Management

1. Assess hemodynamic stability and resuscitate*

1

2. IV octreotide

•Causes splanchnic vasoconstriction

* Decreases portal collateral circulation and pressure

If varices isolated to stomach,think of

splenic vein thrombosis I

3. Endoscopic therapy: variceal ligation (EVLI or sclerotherapy

I

j 1

'

PERSISTENT or RECURRENT

bleed-treatment options

• Transjugular intrahepatic

portosystemic shunt (TIPS)

• Balloon tamponade

• Liver transplant

Long-term treatment to decrease

risk of recurrentbleed

• Bblockerle.g. nadolol)

• Repeat EVUsclerotherapy

• Nitrates

• Follow-up

Gastric varices best treated by

endoscopic injection of cyanoacetate

(“crazy glud)

’

IV ceftriaxone lowers risk of sepsis, especially SBP

Figure 10. Management of bleeding esophageal varices

Mallory-Weiss Tear

Definition

• longitudinal laceration in gastric mucosa on lesser curvature near GH junction (20% straddle junction,

5% in distal esophagus)

Etiology

• due to rapid increases in gastric pressure from retching/vomiting against a closed glottis

• hiatus hernia often present

Clinical Features

• hematemesis ± melena, classically following an episode of retching without blood

• can lead to fatal hematemesis

Management

• 90% stop spontaneously

• if persistent:endoscopy with epinephrine injection ± clips orsurgical repair

Lower Gastrointestinal Bleeding

Definition

• bleeding distal to ligament of Treitz

Etiology

• diverticular

• vascular

angiodysplasia (small vascular malformations of the gut)

anorectal (hemorrhoids, fissures)

Lower Gl Bleed

CHAND

Colitis (radiation,infectious,ischemic.

IBD (UC>CD))

Hemorrhoids/fissure

Angiodysplasia

Neoplasm

Diverticular disease

Neoplasm

• cancer

• polyps

• inflammation

colitis (ulcerative, infectious, radiation, ischemic) (see Ulcerative Colitis, G25)

• post-polypectomy

Clinical Features

• hematochezia

• anemia

• occult blood in stool

• occasionally melena due to slow small bowel or right-colonic course

Treatment

• ifblood per rectum with hemodynamic instability,stabilize patient (1-2 large bore lVs, IV fluids,

monitor) and rule out upper G!source with endoscopy (OGD)

• send blood forCBC, cross and type, INR/PTT,electrolytes, BUN, Gr, LITs

• initial examination of choice is colonoscopy to determine source of the bleeding

• if bleeding is severe or ongoing, consider radionuclide imaging or angiography (see Medical Imaging,

M l16)

• treat underlying cause

majority of cases will stop bleeding spontaneously

c

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