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Table 2. Differential Diagnosis of Common Presenting Complaints

JAUNDICE

(UKCONJUGATED

BILIRUBIN)

Overproduction Decreased Hepatic Intake Decreased Conjugation

Ischemic Colitis

The splenic flexure and rectosigmoid

junction are watershed areas and are

susceptible toischemia. History and

symptoms include acute onset crampy

left abdominal pain,rectal bleeding,

In addition to possible abdominal

tenderness on exam. Risk factors

include atherosclerotic risk factors,

vasoconstricting medications,and

histocy of low flow state

Gilbert's syndrome

Drugs (e.g.rifampin)

Drug inhibition (e.g.chloramphenicol)

Crigler-Najjar syndromes typeIandII

Gilbert's syndrome

Neonatal jaundice

Hemolysis

Ineffective erythropoiesis

(e.g.megaloblastic anemias)

JAUNDICE

(CONJUGATED

BILIRUBIN)

Common Uncommon

Hepatocellular disease

Drugs

Cirrhosis (any cause)

Inflammation (hepatitis,any cause)

Infiltrative (e.g.hemochromatosis)

Familial disorders (e.g.Rotor syndrome,Dubin-Johnson syndrome. Sclerosing cholangitis

cholestasis of pregnancy)

Intraductal obstruction

Gallstones

Biliary stricture

Parasites

Malignancy (cholangiocarcinoma)

Dyspepsia - postprandial fullness,early

satiety,epigastric pain or burning Extiaductal obstruction

PBC Malignancy (e.g. pancreatic cancer,lymphoma)

Mctaslases in periportal nodes

Inflammation (e.g. pancreatitis)

PSC

Sepsis

Posloperativc/TPH Foods/Substances that May Aggravate

GERD Symptoms (but diet does not

change the underlying disease)

. EtOH

• Caffeine

• Tobacco

• Fatty/fried foods

• Chocolate

• Peppermint

• Spicy foods

• Citrus fruit juices

Esophagus

Gastroesophageal Reflux Disease

Definition

•a condition which develops when the reflux of gastric content causes troublesome symptoms or

complications

Etiology

•inappropriate transient relaxations of LES - most common cause

•low basal LES tone (especially in scleroderma)

•contributing factors include: delayed esophageal clearance, delayed gastric emptying, obesity,

pregnancy, acid hypersecretion (rare) from Zollinger-Ellison syndrome (gastrin-secreting tumour)

•hiatus hernia worsens reflux, does not cause it (see General Surgery and Thoracic Surgery. GS23)

Clinical Features

•“ heartburn" (pyrosis) and regurgitation (together are 80% sensitive and specific for reflux); less

sensitive and less specific: water brash,sensation of a lump in the throat (globussensation), and

frequent belching

non-esophageal symptoms are increasingly recognized as being poor predictors of reflux

GERD

Gastroscopy

T

Non-erosive reflux

disease (NERD)

Normal esophagus

Aim for symptom

relief only;

PPIPRN

Esophagitis

Esophageal

inflammation

Aim to heal

inflammation;

PPI indefinitely

or surgical

lundoplication

Figure 2. Classification and

gastroscopic findings of GERD

GERD signs/symptoms

1 Side Effects of Long-Term Use of PPIs

• Only some (C. difficile diarrhea,

hypomagnesemia,vitamin Bn

deficiency, small bowel bacterial

overgrowth) seem to be related to

suppressing gastric acid whereas

others (pneumonia,fractures,chronic

kidney disease,dementia) have

no apparent pathophysiological

relationship

• Stopping PPIs can increase gastric

acid above baseline by a "rebound

effect" causing heartburn even in

healthy volunteers

• May increase the risk of IBO with

prolonged regular use

• These associations do not preclude

long term use of PPIs In patients with

esophagitis or peptic ulcer,or those

needing gastric protection when

taking NSAIDs or anti-platelet drugs,

but do emphasize the importance

of being as definitive as possible

when making these diagnoses and

accurately assessing risk-benefit

ratios (as is true for all drugs)

I I

Non-esophageal Esophageal

! I

I 1

Respiratory

Chronic cough

Wheezing

Aspiration pneumonia

Noil-respiratory

Sore throat

Hoarseness

Dental erosions

Typical

Heartburn

Acid regurgitation

Atypical

Chest pain

Dysphagia (late)

Odynophagia (rare)

Figure 3. Signs and symptoms of GERD

Investigations

• usually, a clinical diagnosis issufficient based on symptom history and relief following a trial of

pharmacotherapy ( PPI:symptom relief 80% sensitive for rellux)

• however, response to anti-secretory agents such as PPI is not a requirement for GERD diagnosis

• gastroscopy indications

• absolute indications

heartburn accompanied by red-flags (bleeding, weight loss, dysphagia, persistent vomiting,

family history of G1cancer, etc.)

persistent reflux symptoms or prior severe erosive esophagitis after therapeutic trial of 4-8 wk

of PPI BID

history suggests esophageal stricture especially dysphagia

high-risk for BE (male, ages >50, obese, white, tobacco use, long history of symptoms)

• repeat endoscopy after 6-8 wk of PPI therapy indicated ifsevere esophagitis because it can mask BE or

symptoms

r T

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•esophageal manometry (study of esophageal motility):indicated in patients wh

chest pain and/or dysphagia with normal gastroscopy

• done to diagnose abnormalities of peristalsis and /or decreased LES tone, but cannot detect

presence of reflux; indicated before surgical fundoplication to ensure intact esophageal function;

exclude alternative diagnoses like scleroderma and achalasia

• surgical fundoplication (wrapping of gastric fundus around the lower end of the esophagus) more

likely to alleviate symptoms if lower esophageal pressure is diminished; less likely to be successful

if abnormal peristalsis

•24 h pH monitoring: most accurate test for reflux, but not required or performed in most cases

most useful if PPIs do not improve symptoms

Treatment

•PPIs are the most effective therapy and usually need to be continued as maintenance therapy

•empiric 8 wk trial of PP1 in patients with classic GERD symptoms; PPIs are the most effective therapy

and sometimes usually need to be continued as maintenance therapy

•discontinuation of PPIs after 8 wk in recovered patients without Barrett'

s esophagus or erosive

esophagitis;symptoms may recur if therapy is discontinued

•on-demand: antacids(Mg(OH) 2, Al(OH)j),alginate, H2-blockers, or PPIs can be used for non-erosive

esophagitis (NERD)

•diet helpssymptoms, not the disease; avoid EtOH, coffee,spices,tomatoes, and citrusjuices

•only beneficial lifestyle changes are weight loss (if obese) and elevating the head of bed (if nocturnal

symptoms)

•symptoms may recur if therapy is discontinued

Complications

•esophageal stricture disease -scarring can lead to dysphagia (solids)

•esophagitis (e.g. ulceration, bleeding)

•BE and esophageal adenocarcinoma - gastroscopy is recommended for patients with chronic GERD or

symptomssuggestive of complicated disease (e.g. anorexia, weight loss, bleeding, dysphagia)

o have non-cardiac

Up to 25% of patients with BE do not

report symptoms of GERD

Screening for Esophageal Adenocarcinoma in

Patients with Chronic Gastroesophageal Reflux

Disease

CMAJ 202O:192(27f:E768-E777

Though Barren'

s esophagus increasesthe

incidence of esophageal adenocarcinoma, the

Canadian lash Force on Preventive Health Core

currently does not recommend routine screening

lor esophageal adenocarcinom and precursor

conditions, including Barren's esophagus.In adults

vrrlh chronic GERD without red flag features(e.g.

dysphagia, odynophagia, weight loss, anemia,

gastrointestinal Weeding).In thissystematic review,

no clinically significant survival benefits were

identified in patients undergoing screening.This

systematic review repoited that patients receiving

screenng may he unnecessarily exposed to harm,

ranging from pre-procedural anxiety lo endoscopic

injury.Strikingly, the presence of risk factorsfor

esophageal adenocarcinoma , including age.male

sea.and family history,is notsuffidentto warrant

screening endoscopy in patients with chronic GERD.

On the othei hand, patientswith known Garrett's

esophagusshould be referred to a Gastroenterologist

for endoscopy.

Barrett’s Esophagus

Definition

• metaplasia of normal squamous esophageal epithelium to intestinal columnar epithelium

Etiology

• thought to be acquired via long-standing GERD and consequent damage to squamous epithelium

Clinical Features

• prominent GERD symptoms

Epidemiology

• in North America and Western Europe,0.5-20% of adults are thought to have BE

• up to 10% of GERD patients will have already developed BE by the time they seek medical attention

• more common in males, ages >50, White individuals,smokers, overweight, hiatus hernia, and long

history of reflux symptoms

Pathophysiology

• endoscopy shows salmon pink mucosa in distal esophagus;diagnosis of BE relies on biopsy

demonstrating the presence ofspecialized intestinal epithelium of any length within the esophagus

• BE predisposes the esophageal lining to premalignant changes characterized aslow or high-grade

dysplasia,which then progresses to adenocarcinoma

Significance

• rate of malignant transformation is approximately 0.12% per yr for all BE patients prior to dysplasia

• risk of malignant transformation in high-grade dysplasia issignificantly higher;studies have reported

a 32-59% transformation rate over 5-8 yr ofsurveillance

Treatment

• acid suppressive therapy with high-dose PPI indefinitely (or surgical fundoplication) may reduce the

transformation of BE to dysplasia

• surveillance gastroscopy every 3-5 yr if no dysplasia

• high grade dysplasia: regular and frequent surveillance with intensive biopsy, endoscopic ablation/

resection, or esophagectomy produce similar outcomes

however, evidence increasingly favouring endoscopic ablation with mucosal resection or

radiofrequency ablation

• if low grade dysplasia, both surveillance (every 6 mo for 1 yr then annually) and endoscopic ablation/

resection are satisfactory options

CllnicalGuidelinesUpdate onthe Diagnosisand

Management of Barrett's Esophagus

Fora report reviewing the US and International

guidelines on the diagnosisand management of 8E,

please refer to:Dig Dis So 2018:63:2122-2128

Randomized Trial of Medical vs. Surgical

Treatment lor Refractory Heartburn

NEJM 2019:381:1513 1523

Patients with PN-ielractory and icllun-related

heartburn (n*TB)wore randomly assigned to surgical

treatmenl(laparoscopic Nissen fundoplication).

octree medical treatment (omepraiole plus badolen,

and desipramlne pen), or control medical treatment

(omepraiole plus placebo). The Intrdenceol treatment

successin the surgical treatment group (67%) was

significantly greater than that in the active medical

treatment gioup (28%: P-0.007 ) or control medical

treatment group (12%;P«0.001). +

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G8 Gastroenterology Toronto Notes 2023

Dysphagia

Definition

• difficulty swallowing Remember

Dysphagia -Difficulty in swallowing

Odynophagia ~Pain on swallowing

Dysphagia

_

£

Oropharyngeal

(difficulty initialing swallowing,choking,

coughing,nasal regurgitation)

Esophageal

(inability to move food down esophagus)

I ; Key Questions in Dysphagia

• Abnormal features when initiating

the act of swallowing?

• Associated symptoms?(regurgitation,

chest pain,change in voice pitch,

weight loss)

• Solids,liquids,or both?

• Intermittent or progressive?

• History of heartburn?

• Change in eating habits/diet?

Structural

Muscular dystrophy Zenker'

s diverticulum

Polymyositis Thyromegaly

Cervical spur Mechanical obstruction

Neurological* Muscular Solid food only Solid foods and liquids

Cortical

Bulbar

Peripheral Myasthenia gravis

Cricopharyngeal

Y

MMM>I I MMM

I

Y

Progressive Intermittent Intermittent Prcg-essr.e

Y Y i i Y

Age >50 Heartburn

(weight loss)

Lower Diffuse Reflux

esophageal esophageal symptoms .

4 ^ IES I

Carcinoma* Peptic

stricture*

Scleroderma*

’

Most common

• Figure 4. Approach to dysphagia (eosinophilic esophagitis omitted)

Esophageal Motor Disorders

Clinical Features

• dysphagia with solids and liquids

• chest pain (in some disorders)

Diagnosis

• motility study (esophageal manometry)

• barium swallow sometimes helpful

Causes

• idiopathic

• achalasia

• scleroderma

• DM

• DKS: rare and can be difficult to diagnose due to intermittent presentation

Table 3. Esophageal Motor Disorders

Endoscopic or SurgicalMyotomy inPatients with

Idiopathic Achalasia

IDM2019;381:2219-2229

Purpose Tommpare peroralendoscopic myotpoiy

(POEM) to laparoscopic Heller's myotomy (LMH|inhe

treatment of achalasia.

Methods:PatientsnidiSymptomatic acialasa

i

“221|oarerandomly assigned to either POEM or

LMH.the p-nary endpoint was clinical success,

wh.le secondary endpo.nts included adverse evens,

esophageal.f nction.Gastro nrasdna. Ouality of Life

(GOoL) score.andgastroesopliagealrefkji|GEt).

Results 33.0% of patients in the POEM group and

81.7% of patens in Ce LNM group acnieied c -n cal

successat 2yr (P-0.007for nonmferionly].There

wasno difference in mjroemen!of esophageal

function or G Ool score between groups.Serious

adverse events were observed in 2.7% and 73% of

patents a tbePOEM and WM groups,respectively.St

12 oo.44% of patens m the POEM groupand 29% of

patens a tbeLHM group tadie9uiesophagitis.

Conclnsions POEMwasnonxifetoralHMinthe

treatsent of symptomatic achalasia. GER was more

common among patens who were treated wrtb POEM

Banttose heated with IHM.

Disorder Achalasia Scleroderma Diffuse Esophageal Spasm

Definition Failure of smooth muscle relaxation at IES

Increased LES pressure

Progressive loss of peristaltic function

See _BheL ___-_ato_:

_~ i.ItH14 Normal peristalsis interspersed with

Systemic disease charactered frequent,repetitive,spontaneous,

by vasculopathy and tissue fibrosis high pressure,non-peristaltic waves

(especially skin thickening) (tertiary peristalsis)

Etiology Usually idiopathic

2° or pseudo-achalasia e.g.malignancy.

Chagas disease (trypanosoma cruci)

Involves autoimmune,genetic. Idiopathic

hormonal,andenvironmental factors

Dysphagia:caused by reflux,

dysmotility.or both

Blood vessel damage «intramural

neuronal dysfunction distal

esophageal muscle weakening

apevistalsis and loss of IES tone-

- reflux »stnetute -*

dysphagia

Clinical features of scleroderma Barrum x-ray "Corkscrew pattern"

Manometry:decreased pressurein Manometry.>20% premature

LES.decreasedperistalsisnbody of contractions

esophagus

Pathophysiology Inflammatory degeneration of Auerbach'

s

plexus

*

increase in LES pressure,

incomplete relaxation ol LES with

swallowing,aperistalsis

Potential mechanismsinclude

impaired inhibitory innervation to

esophageal body,malfunctionin

endogenoos nitric oxide synthesis

Diagnosis CXR:no air in stomach,dilatedesophagus

Barium studies: esophagus terminates in

narrowing at IES ("bird's beak")

Endoscopy:normal mucosa

Manometry:definitive diagnosis Isigns listed

above)

Pneumatic dilation.5%risk of perforation

Injection of botulinum toxin into LES

(temporary)

Surgical myotomy

POEM (peroral endoscopic myotomy)

Endoscopy:normal mucosa r T

iJ

Treatment Medical:aggressive GERO therapy

(PPIs BID)

Beassuraxe that symptoms arenot

due tocardiac pain

Medical:nitrates,calciumchannel

blockers,anticholinergics have

variable benefit

Surgical:long esophageal myotomy

if unresponsive to above treatment

(rarely helpful),balloon dilatation

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Esophageal Diverticula

Definition

• outpouching*

of one or more layers of the esophageal tract

Clinical Features

• commonly associated with motility disorders

• dysphagia, regurgitation,retrosternal pain, intermittent vomiting, may be asymptomatic

Classification

• pharyngoesophageal (Zenker’s) diverticulum

most common form of esophageal diverticulum

posterior pharyngeal outpouching most often on the left side, above cricopharyngeal muscle and

below the inferior pharyngeal constrictor muscle

symptoms:dysphagia, regurgitation of undigested food, halitosis (bad breath)

treatment:small and asymptomatic: no treatment required,large and symptomatic: endoscopic

orsurgical myotomy of cricopharyngeal muscle ± surgical excision of sac

Peptic Stricture (from Esophagitis)

Definition

• a smooth, concentric narrowing most commonly seen in the lower esophagus

Clinical Features

• presents as dysphagia alongside a long history of reflux symptoms, but reflux symptoms may

disappear asstricture develops

Diagnosis

• diagnosed with endoscopy or barium study if endoscopy contraindicated or unavailable

Treatment

• endoscopic dilatation and indefinite PP1

Esophageal Carcinoma

• see General Surgery and Thoracic Surgery. GS21

Webs and Rings

Definition

• web = partial occlusion (upper esophagus)

• ring = circumferential narrowing (lower esophagus)

Clinical Features

• asymptomatic with lumen diameter >12 mm, provided peristalsisis normal

• dysphagia with large food boluses

• Schatzki ring

mucosal ring atsquamo-columnar junction

causesintermittent dysphagia with solids

treatment involves disrupting ring with endoscopic dilation

Plummer

-Vinson Syndrome Triad

• Iron deficiency anemia

• Dysphagia

. Esophageal webs

• Rare (prevalence <1in 1000000) but

good prognosis when treated with

iron and esophageal dilatation

Eosinophilic Esophagitis

• Eosinophils infiltrate the epithelium

of the esophagus

• Causes dysphagia, common cause of

bolusfood impaction

• Usually primary, but can be part

of the spectrum of eosinophilic

gastroenteritis,secondary to drugs,

parasites etc.

• Often associated with allergies

• Most characteristically occurs in

young men

• Diagnosis established by endoscopic

biopsy,suggested by mucosal rings

seen in the esophageal mucosa at

endoscopy

• Treatment:(a) diet (milk,soy.eggs,

wheat, peanuts/tree nuts, and

seafood), (b) PPI (c) swallowed

topical corticosteroid (fluticasone or

budesonide), (d) rarely prednisone

Infectious Esophagitis

Definition

• severe mucosal inflammation and ulceration as a result of a viral or fungal infection

Risk Factors

. DM

• chemotherapeutic agents

• immunocompromised states

Clinical Features

• characteristically odynophagia, less often dysphagia

Appearance

• Candida (most common): whitish-yellow plaques without visible ulceration or inflammation

• HSV (second most common),CM V:focal ulcers

Investigations

• diagnosis via endoscopic visualization and biopsy

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Treatment

• Candida: nystatin swish and swallow (forsimple Candida infection), ketoconazole,fluconazole

• HSV:often self-limiting; acyclovir, valacyclovir, famciclovir

• CM V:IV ganciclovir,famciclovir,or oral valganciclovir

Stomach and Duodenum

Dyspepsia

•

Definition

predominant epigastric pain/burning lasting at least 1 mo

O

• other symptoms under umbrella of dyspepsia; post-prandial fullness, early satiety

• although the most common cause is functional (investigations show no organic disease but pain

persists),sinister disease can present similarly (e.g. pancreatic cancer)

History and Physical Exam

• history:most important risk factors are age, associated symptoms (such as weight loss and vomiting),

and drugs (especially NSAlDs)

• physical exam:adenopathy, abdominal mass/organomegaly,Carnett’

ssign (if pain is due to abdominal

wall muscle problem then the pain will increase during muscle contraction,such as during a sit-up)

Investigations

• consider blood tests including CBC,liver enzymes, calcium, H. pylori serology, and U/S

• gastroscopy to investigate dyspepsia: most causes of dyspepsia are either functional or diagnosable

by either blood tests or PPI trial (for peptic disease); however, gastric cancer should not be missed.

Gastroscopy recommended if ages >60 (and if ages <60 and under special circumstances such as risk

factors for gastric cancer)

The most common cause of dyspepsia is

functional (idiopathic) dyspepsia

Red Flags of Dyspepsia

(raise suspicion of gastric malignancy):

Unintended weight loss

Persistent vomiting

Progressive dysphagia

Odynophagia

Unexplained anemia or iron

deficiency

Hematemesis

Jaundice

Palpable abdominal mass or

lymphadenopathy

Family history of upper Gl cancer

Previous gastric surgery

Stomach

Table 4. Cells of the Gastric Mucosa

Cell Type Secretory Product Important Notes

Parietal Cells Gastric acid (HCI) and IF

Pepsinogen

Somatostatin

Stimulated byhistamine, acetylcholine (ACh). gastrin

Stimulated by vagal input andlocal acid

Inhibits release of hormones including gastrin

Stimulates H+ production from parietal cells

Protect gastric mucosa

Chiel Cells

0-Cells

G-Cells

Superficial Epithelial Cells

Gastrin

Mucus. HC03 -

CO*

HrO -

*

l £0

Histamine (

J)

H .R antagonist

Gastrin

(

©

tin ZE syndrome)

Intrinsic

factor

receptor

0C3

ACh ® 1 T

— Anticholinergic

Protein

kinases

1

<

•

0 8

I— NSAlDs

PGE2/PGI2,

(CN

Misoprostol

^

PG

fcAMP receptor

K '

O L

Na‘

I

Gastric

lumen ©decrease acid secretion 1

©increase acid secretion

0inhibition Interstitial fluid

I +

Figure 5.Stimulation of H + secretion from the parietal cell

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Gastritis

Definition

• defined histologically:inflammation of the stomach mucosa

Etiology

• some causative agents may play a role in more than one type of gastritis and an individual patient may

have hlstopathological evidence of more than one type of gastritis

Table 5. Updated Sydney Classification of Gastritis

Type Common Etiology

Acute Gastritis

Hemorrhagicterosive gastritis

Helicobacter gastritis

Chronic Gastritis

Non - atrophic

Atrophic

Chemical

Radiation

lymphocytic

Eosinophilic

Non-infectious granulomatous

Other infectious gastritides

Eton.Aspirin

*

,

'NSAID.shock/physiological stress (seen inICI) patients)

H.pylori

H.pylori

H. pylori, dietary,environmental factors (multi-local),autoimmunity

USAID.Pile

Radiation injury

Celiac disease,drug

Food allergies

CD.sarcoidosis

Bacteria,viruses,tungi,parasite,IB.syphilis

Clinical Features

• non-erosive gastritis is asymptomatic (except with certain rare causeslike CD),does not cause pain;

difficult to diagnose clinically or endoscopically -requires biopsy for diagnosis

• erosive gastritis can cause bleeding (pain only if progresses to ulcers -rare); can be seen

endoscopically

Treatment

• determined by etiology (see H. pylori,G13, NSAID,GI 3and Stress-Induced Ulceration, ON )

• non-pharmacological: avoidance of mucosal irritantssuch as EtOH, NSAlDs, and foods that trigger

symptoms

Peptic Ulcer Disease EH

Definition

• focal defects in the mucosa that penetrate the muscularis mucosa layer

• PUD includes defects located in the stomach (gastric ulcers) and duodenum (duodenal ulcers)

Etiology

Table 6. Etiology of PUD

Duodenal Gastric

H.pylori Infection

NSAlDs

Physiologic Stress-Induced

Zollingcr-Elllson Syndrome

Idiopathic

90% 60%

7% 35%

«3% «5%

*1% «1%

15% 10%

•NSA1D negative, H. pylori negative ulcers becoming more commonly recognized as H.pylori

prevalence decreases

•others:CMV (especially immunocompromised patients), ischemic, idiopathic

•EtOH: damages gastric mucosa but rarely causes ulcers

•peptic ulcer associated with cigarette smoking, cirrhosis of liver,COPD, and chronic renal failure

Clinical Features

•dyspepsia: most common presenting symptom

• only 5% of patients with dyspepsia have ulcers, while most have functional disease

however, 70% of peptic ulcers are asymptomatic

•may present with complications

bleeding 10% (severe if from gastroduodenal artery), perforation 2% (usually anterior ulcers),

gastric outlet obstruction 2%

posterior inflammation (penetration) 2%;may also cause pancreatitis

Cigarette Smoking and PUD

. Increased risk ot ulcer

• Increased risk ot complications

• Increased chance of death from ulcer

• Impairedhealing

n

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•duodenal ulcers: 6 classical features, but history alone cannot distinguish from functional dyspepsia

• epigastric pain; may localize to tip of xiphoid

burning

develops 1-3 h after meals

relieved by eating and antacids

interrupts sleep

• periodicity (tends to occur in clusters of weeks with subsequent periods ofremission)

•gastric ulcers: more atypical symptoms; a biopsy is necessary to exclude malignancy

Investigations

•endoscopy (most accurate)

•upper G1 series

•H. pylori tests (see Table 7, G13 )

•fasting serum gastrin measurement if Zollinger-Hllison syndrome suspected (but most common cause

of elevated serum gastrin level is atrophic gastritis)

Treatment

•specific management depends on etiology; (see H. pylori, (i13, NSAID-Induced Ulceration, G13 and

Stress-Induced Ulceration, UN )

•treat H. pylori infection if present;eradication of infection prevents recurrence of PUD

•stop NSA1Ds if possible

•start PPI:inhibits parietal cell H t /K i -AT'

Pase pump which secretes acid

heals most ulcers, even if NSAlDs are continued

•other medications (e.g. histamine H2-antagonists) less effective

•discontinue cigarette smoking

•no diet modifications required but some people have fewer symptoms if they avoid caffeine, EtOH, and

spices

Management of Bleeding Peptic Ulcers

•Gastroscopy (OGD) to explore upper Gl tract

•IV pantoprazole

•establish risk ofrebleeding/continuous bleed (since most ulcers stop bleeding spontaneously)

• clinical risk factors: increased ages >60, bleeding diathesis,history of PUD, comorbid disease,

hemodynamically unstable

endoscopic signs of recurrent bleeding (active bleeding, visible vessel, clot, red spot) more

predictive than clinical risk factors

if ulcer possesses high-risk stigmata, then endoscopic therapy (e.g. clip) should be performed,

consider 1CU admission

Gastric vs.Duodenal Ulcers

Most gastric ulcers are biopsied to rule

out malignancies:duodenal ulcers are

rarely malignant

Approach to PUD

. Stop NSAlDs

• Acid neutralization

• H.pylori eradication

• Quit smoking

Bleeding Peptic Ulcers

• Risk Factors tor Increased Mortality

• Co-existent illness

• Hemodynamic instability

• Ages >60yr

. Transfusion required

Suspected BleedingPeptic Ulcer

ABCs: assess vitals (BP and HR, orthostatic changes)

CBC. electrolytes, BUN, Cr, INR.blood type,cross and type

Resuscitate: crystalloids and blood products it indicated

I

Consider

NG placement + aspiration: confirm upper Gl source

IV pantoprazole:80 mg starting dose+8mg/h continuous infusion

Erythromycin 250 mg 30 min before endoscopy

1

Endoscopy

Flat,pigmented spot

oi clean base

Active bleeding

or visible vessel

High Risk:

Hemostasis: clips,thermal

coagulation± epinephrine inie

Continue (or start) IV PPI

Monitor for re-bleeding in hospital

If adherent clot consider removal

Low Risk:

No hemostasis necessary

Continue (or start) oral PPI

Decreased need for

in-hospital monitoring

ction

J

Post-Endoscopy

Resume clear fluids 6 h post

-endoscopy

Test (or H. pylori

Counselre: most likely causes (NSAlDs,anti

-platelet agents)

It re-bleeding: repeat endoscopy with aim of hemostasis

Consult interventional radiology or surgery ilneeded L J

i

Figure 6. Approach to management of suspected bleeding peptic ulcer

Adapted from: GralnekI,Barkun A.Bardou M.Management of acute bleeding from a peptic ulcer.NEJM 2008;359:928-937

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H. pylori-lnduced Peptic Ulceration

Pathophysiology

• H. pylori: Gram-negative flagellated rod that resides within the gastric mucosa, causing persistent

infection and inflammation

• acid secreted by parietal cells (stimulated by vagal ACh,gastrin, histamine) necessary for most ulcers

• etiology of PUD secondary to H . pylori is not well understood; however, the pattern of colonization

correlates with outcome

• gastritis only in antrum (15% of patients), high gastric acid, associated with duodenal ulcer, may

progress to gastric metaplasia of duodenum where ulcer forms

• gastritis throughout stomach (“pangastritis"

- 85% of patients), low gastric acid, associated with

stomach ulcer and cancer

Epidemiology

• H . pylori is found in about 20% of all Canadians, with increased prevalence in Indigenous populations

and immigrantsfrom high prevalence countries

• highest prevalence in those raised during 1930s

• infection most commonly acquired in childhood, presumably by fecal-oral route

• high prevalence in developing countries,low socioeconomic status(poor sanitation and

overcrowding)

Outcome

• gastritis (non-erosive) occurs in 100% of patients but is asymptomatic

• peptic ulcer in 15% of patients

• gastric carcinoma and mucosal associated lymphomatous tissue (MALT) lymphoma in 0.5% of

patients

• most are asymptomatic but still worthwhile eradicating to lower future risk of peptic ulcer/gastric

malignancy and prevent spread to others (mostly children ages <5)

Diagnosis

Helicobacter pylori Therapy forthe Prevention of

MetadiroaoasGastric Cancer

NEJM 2018:378:1085-1095

Purpose:Toeiafriatethe role of H. pylori eradication

in the prevention of metachronous gastric cancer.

J , .

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Population: 470 patents with a subtotal gastrectomy

lor gastric a ncet and H.pylori infection with or

w ittio.t ABv treatment.

Outcome:Incidence ol metachionous gastric cancer.

Result!: liter almost( yi. 1.2\of the Mu-treated

group developed anotter cancer in the gastric

remnant vs.13.4% ia the placebo control group.

Conclusions:Ibis provides definitive evidence

that H. pylori is worthwhile treating no matter how

advanced the gastric carcinogenic process.

Serology for H. pylorishould not be used

to check for eradication

Table 7. Diagnosis of H. pylori Infection

Test Sensitivity Specificity Comments

Non-invasive Tests

Urea breath test

Serology

Can remain positive after

treatment

Fecal antigen

90-100%

88- 99%

89-100%

89-95%

Affected by PPI therapy (false negatives)

Does not distinguish active vs.past infection

Only rarely usedin clinical practice

Invasive Tests (requireendoscopy)

Histology

Rapid urease test (on biopsy) 89-98%

Microbiology culture

93-99% 95-99%

93-100%

95-100%

Gold standard:affected by PPI therapy (false negatives)

Rapid

Hot widely available but can be used to determine ABi susceptibility.

Research only

98%

Treatment:H. pylori Eradication

• bismuth quadruple therapy recommended for 14 d: PPI (e.g.lansoprazole 30 mg BID) + bismuth 525

mg QID + metronidazole 500 mg Q1D + tetracycline 500 mg

• alternatively, concomitant non-bismuth quadruple therapy fc

metronidazole i clarithromycin

QID

'

or 14 d: PPI t amoxicillin t

NSAID-Induced Ulceration

Pathophysiology

• NSA1D use causes gastric mucosal petechiae in virtually all, erosions in most, ulcers in some (25%)

• direct: erosions/petechiae - are due to local (direct) effect of drugon gastric mucosa

• indirect:systemic NSA1D effect (IV NSA1D causes ulcers,but not erosions)

NSAlDs also inhibit mucosal cyclooxygenase,leading to decreased prostaglandin synthesis

this resultsin ulcers from reduced secretion of protective bicarbonate and mucous,and decreased

mucosal blood flow

Risk Factors for NSAID-induced Peptic Ulcer

• previous peptic ulcers/UGIB

• age (S65 yr)

• high dose of NSAI D/multiple NSAlDs being taken

• concomitant corticosteroid use

• concomitant cardiovascular disease/other significant diseases

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Clinical Features

• erosions bleed, but usually only ulcers cause significant clinical problems

• most NSAlD-induced ulcers are clinically asymptomatic: dyspepsia is as common in patients

with ulcers as in patients without ulcers; NSAlD-induced ulcers characteristically present with

complications (bleeding, perforation, obstruction)

• NSAlDs more commonly cause gastric ulcers than duodenal ulcers

• may exacerbate underlying duodenal ulcer disease

Treatment

• prophylactic cytoprotective therapy with a PPI is recommended if any of the above risk factors exist

concomitantly with ASA/NSA1D use

• lower NSAID dose or stop all together and replace with acetaminophen

• combine NSAID with PHI or misoprostol (less effective) in one tablet

• enteric coating of Aspirin* (ECASA) provides minor benefit since this decreases incidence of erosion,

not incidence of ulceration

If at high-risk for development of ulcers,

prophylaxis with PPI indicated

Stress-Induced Ulceration

Definition

• ulceration or erosion in the upper Gl tract of ill patients, usually in 1CU (stress is physiological, not

psychiatric)

• lesions most commonly in fundus ofstomach

Pathophysiology

• unclear:likely involves ischemia; may be caused by CNS disease, acid hypersecretion,Cushing'

s ulcers

• mechanical ventilation is the most important risk factor

Risk Factors

• mechanical ventilation

• anti-coagulation

• multi-organ failure

• septicemia

• severe surgery/trauma

• CNS injury (“Cushing’s ulcers”)

• burns involving more than 35% of body surface

Curling's and Cushing's Ulcers

• Curling's Ulcer:acute peptic ulcer

of the duodenum resulting as a

complication from severe burns

when reduced plasma volume

leadsto ischemia and cell necrosis

(sloughing) of the gastric mucosa

(think BURN from a CURLING iron)

• Cushing's Ulcer: peptic ulcer

produced by elevated ICP (may be

due to stimulation of vagal nuclei

secondary to elevated ICP which

leadsto increased secretion of

gastric add)

Clinical Features

• UG1B (see Upper Gastrointestinal Bleeding, G2&)

• painless

Treatment

• prophylaxis with gastric acid suppressants decreases risk of UGIB; PPI most potent but may increase

risk of pneumonia; H2 blockers less potent but lesslikely to cause pneumonia

• treatment same as for bleeding peptic ulcer but often lesssuccessful

Gastric Carcinoma

• see General Surgery' and Ihoracic Surgery. GS26

Small and Large Bowel

Classification of Diarrhea

Definition

• clinically:diarrhea defined as stools that are looser and/or more frequent than normal (i.c. S3x/d);

physiologically: 24 h stool weight >200 g (less useful clinically)

Classification

• acute vs.chronic

• small volume (tablespoons ofstool;typical of colonic diseases) vs.large volume (>l/2 cup stool;typical

ofsmall bowel diseases)

• watery:secretory (diarrhea persists with fasting) vs. osmotic (diarrhea stops with fasting)

• steatorrhea

• inflammatory

• transit or functional

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Acute Diarrhea

• see Paediatrics, P43

Definition

• passage of >3 loose or liquid stools/d OR >200 g stool/d for >2 d but <14 d

Epidemiology

• one of the leading causes of death worldwide (about 88% of diarrhea associated deaths are caused by

unsafe water, inadequate sanitation, and insufficient hygiene)

• significant morbidity in developed countries (over 900000 hospitalizations in the United States each

year)

Etiology

• most commonly due to infections

• most infections are self-limiting and resolve within 7 d

Risk Factors

• food (raw or undercooked meat and seafood, unpasteurized dairy products)

• medications: ABx,laxatives

• others: high-risk sexual activity, infectious outbreaks, occupational exposures (daycare workers),

family history (IBD)

Approach to Acute Diarrhea

• the most common cause of acute diarrhea is infectious

• in most cases, acute diarrheal illness is viral and/or self-limited, and lasts <3d

• investigations are costly and are necessary only in certain circumstances

therefore, evaluation of acute diarrhea involves identifying characteristics of the patient or illness

that warrant further investigation and assessing volume status to determine the most appropriate

method of rehydration

Physical Exam

• volume status:appearance, level of alertness, pulse, BP, orthostatic vitals, J VP, mucous membranes,

skin turgor, capillary refill

• abdominal exam: pain, guarding, peritoneal signs

Useful Questions in Acute Diarrhea

Those Fads Wilt

Travel

High-risk sexual activity (increased risk

of fecal-oral exposure)

Outbreaks

Seafood

Extra intestinal signs of IBD

Family history

ABx

Diet

Steatorrhea

Weight loss

Immunosuppression

Laxatives

Tumour history

Infectious Causes of Inflammatory

Diarrhea

Your Stool Smells Extremely Crappy

Yersinia

Shigella

Salmonella

£. coli (EHEC 0157:H7), E. histolytica

Campylobacter.C. difficile

Table 8. Classification of Acute Diarrhea

Inflammatory Non-lnflammatory An Update on the Bole for Bacteriotherapy

SER -109, an OralMicrobiome Therapy for

Recurrent Clostridiodes difficile Infection

NiJM 2022:386220 229

Building on the soccess of prior work demonstrating

the efficacy of donor fecal transplant in patients

with recurrent C.dfficite infections, this randomized

controlled trialshowsthat oral microhxxne therapy

(SER-109) effectnrefy reduces the recurrence of C.

d fllcile infection to 12% compared to 40% in cohorts

receiving placebo.This trial along with similar

prospective and retiospective work may standardize

the use of medxal piobiotic therapy in patients with

gastrointestinal disorders, including recurrent C.

difficile infection.

Definition Disruption of intestinal mucosa

Usually colon

Organisms and cytotoxinsinvade mucosa, resulting in the

destruction of mucosal cells,and perpetuation of the diarrhea

Usually abnormal mucosa seen

Bloody (not always)

Small volume, high frequency

Often lower abdominal cramping with urgency t tenesmus

May have (evenshock

Fecal WBC and BBC positive

See DifferentialDiagnosis ol CommonComplaints. 64

Acute presentation of idiopathic IBD

Intestinal mucosa intact

Usually small inleslinc

Stimulation of inlestinat water secrebon and inhibition

of water absorption (i.e. netsecretion)

Usually normal mucosa seen

Watery, litile or no blood

large volume,low frequency

Upper/periumbilical pain/cramping tshock

Site

Mechanism

Sigmoidoscopy

Symptoms

Investigations

Etiology

Diffcrcnlial

Diagnosis

Significance

fecal WBC negative

See Dilletenhol Diagnosis olCommonComplaints. 64

Acute presentation of noninflammatory chronic

diarrhea (e.g. celiac disease)

Lower yield with stool CBS

Chief life-threatening problem is electrolyte

disturbances/ fluid depletion

ABx unlikely lobe helpful

Higheryield with stool CBS

Can progresslo life - threatening megacolon, perforation.

hemorrhage

ABx may be helpful

Investigations

• stool cultures/microscopy (C&S/O&P) are required only if diarrhea is inflammatory,severe,or

for epidemiological purposes (daycare worker, nursing home resident, community outbreaks, e.g.

Walkerton, etc.)

• O&P takes up to three weeks to obtain the results

C&S only tests Campylobacter, Salmonella, Shigella, E. coli, Yersinia

other organisms must be ordered separately

• flexible sigmoidoscopy (without bowel preparation ): useful if inflammatory diarrhea suspected

• histology (i.e. biopsies of mucosa) helps to distinguish idiopathic IBD (CD and UC) from

infectious colitis or acute self-limited colitis

• C. difficile toxin:indicated in cases with recent/remote antibiotic use, hospitalization, nursing home

living, or recent chemotherapy

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Treatment

• fluid and electrolyte replacement orally in most cases, intravenously if severe extremes of age/coma

> antidiarrheals

antimotility agents: diphenoxylate, loperamide (Imodium* ) should be used with caution;

contraindicated in patients with mucosal inflammation, bloody diarrhea

side effects:abdominal cramps, toxic megacolon

modifiers of fluid transport: bismuth subsalicylate (Pepto-Bismol*) may be helpful (butshould

not be used in the presence of bloody diarrhea or fever)

• ABx: rarely indicated

• risks

Causes of Acute Bloody Diarrhea

CHESS

Campylobacter

Hemorrhagic C. coli(e.g. 0157:H7)

Entamoeba histolytica

Salmonella

Shigella

prolonged excretion of enteric pathogen (especially Salmonella )

drug side effects (including C. difficile infection)

development of resistant strains

renal failure/hemolysis (enterohemorrhagic E. coli 0157:H7)

indications for antimicrobial agents in acute diarrhea

septicemia

prolonged fever with fecal blood (bloody diarrhea ) or VVBCs seen on O&P

clearly indicated: Shigella, V. cholerae, difficile,traveller's diarrhea ( E. coli (ET EC)),

Giardia, Entamoeba histolytica,Cyclospora

situational:Salmonella,Campylobacter, Yersinia, non-enterotoxigenic E.coli

Salmonella: always treat Salmonella typhi (typhoid or enteric fever); treat other Salmonella

only if there is underlying immunodeficiency, hemolytic anemia, extremes of age, aneurysms,

prosthetic valve grafts/joints,sickle cell disease

• report diarrheal illness to public health if appropriate

Initial Assessment

Any of:

• fever

• blood in stool

• severe abdominal pain i peritoneal signs

• profuse diarrhea with signs of hypovolemia

• hospitalized or recent use of ABx

• age >£5 yr with comorbidities

• immunocompromised (chemotherapy,HIV)

• diarrhea >7 d in duration

• exposure to suspicious foods or untreated water

• sexual contacts: men who have sex with men (MSMI

YES NO

Treat Symptoms

Rehydration

Antidiarrheal agents

• bismuth subsalicylate

• loperamide

Investigations

Roubne Tests:

Stool for fecal leukocytes

Stool C&Sfor Campylobacter,Salmonella, andShigella

Special Tests

Stool C&S for EHEC,stool

lor Shiga toxin

Stool for C. <Wffe//e toxins

A and B

Indication

Blood in stool

4 f

Illness persists ] ( Illness resolves Recent use of ABx or

hospitalized

Age>65 yrwith comorbidities

Immunocompromised

Diarrhea >7 d

Exposure tountreated watei

Indications lor Antimicrobial Therapy

Absolute Indications:

•infection with S. typhi,Shigella, C. difficile,

Cryptosporidium, t. histolytica

•immunocompromised patients

Relative Indications:

•infection with V. cholerae. non-typhoid Salmonella,

Campylobacter, Yersinia,Giardia,ETEC

•decision to treat is determined by severity of illness

(see Tables 9,10, and 11 for information on

common pathogens)

Stool O&P for Giardia,

Cryptosporidium,

£. histolytica HIV

MSM

Figure 7. Approach to acute diarrhea

Note: S. typhi has a rose spot rash (transient moculopapular rash on anterior thorax, upper abdomen),and a prodrome ol high fover,bradycardia,

headache,andabdominal pain.Diarrhea Is not theInitial presentation

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Table 9. Bacteria in Infectious Diarrhea

Source or Mode Incubation

ot Transmission

Pathogen Clinical Features Duration Antimicrobial Therapy Notes

Fever Bloody Abdo Nausea/

Stool Pain Vomiting

B. cereus -TypeA Ricedishes

(emetic)

B.cereus -TypeB Meats,vegetables,

(diarrheal)

Campylobacter

jejuni

1-6 h <12 h None Preformed exotoxin

8-16 h <24 h None Secondary endotoxin

dried beans,cereals

Uncooked meat,

especially poultry

2-10 d Macrolide or fluoroquinolone if

diarrhea >1wk.bloody diarrhea,or

immunocompromised

Most common bacterial cause of

diarrhea in Canada

Associated withGuillain-Barre

syndrome

± t <1wk

Clostridium difficile Can be normally

present in colon

in small numbers

(primary risk

laclorfor disease

is exposure to

antimicrobials)

Slop culprit anlibiolic therapy if possible Usually follows antibiotic

Supportive therapy (IV fluids) treatment (especially

Empiric Ireatmenlwrlh either clindamycin,fluoroquinolones,

vancomycin or fidaxomlcin penicillins,cephalosporins)

IIaccess lo empiric treatment is limited. Can develop pseudomembranous

then metronidarole may be used

For fulminant C.dillicile inlcdlon

(previously called severe),oral

vancomycin is used.IV metronidarole

added loregimen If ileus present

None

Unclear s Variable

colitis

Clostridium

perfringens

Contaminated food, 8-12h

especially meat and

poultry

<24 h Clostridium spores are heal

resistant

Secondary enterotoxin

Enteroinvasive

Relatively uncommon

Enterotoxigenic

Most common cause of traveller’s

diarrhea

Heat-labile and heat-stable

toxins

*

E. coli (ElEC) Contaminated food/ 1-3 d

water

Contaminated food/ 1-3 d

water

+ ± + 7-10 d None

E.coli(ETEC) 3 d Fluoroquinolone or azithromycin for

moderate to severe symptoms

Enterohcmorrhagic Contamination of

E.coli (EHEC7STEC) hamburger,raw

i.c. 0157:H7

3 3 d 5-10 d None:ABx increase risk ol HUS Shiga toxin production

Monitor renal lunction:10%

develop HUS

Anlidiarrheals increase risk

of HUS

»

milk,drinking,and

recreational water

Salmonella Typhi

$.Paratyphi(i.c.

Enteric Fever.

Typhoid)

Fecal-oral

Contaminated food/

water

Travel to endemic

10 14 d <5- 7 d Empiric treatment withceftriaxone,

ciprofloxacin,or azithromycin

Fluoroquinolone resistance is increasing abdomen),fever,and abdominal

pain precedes diarrhea

Solmonello typin'. "Rose spot"

rash (on anterior thorax,upper

t l

area

Non-typhoidal

Salmonellosis

S.Typhimurium.

S.Enteritidis

Shigella dysenteriae

Contaminated animal 12-72 h

food products,

especially eggs,

poultry,meat,milk

Fecal-oral

Contaminated food/

water

3-7 d Ciprofloxacin only in severe illness,

extremes of age.joint prostheses,

valvular heart disease,severe

atherosclerosis,cancer,uremia

Fluoroquinolone

i

Very small inoculum needed for

infection

Complications include toxic

megacolon.HUS

Anlidiarrheals may increase risk

of toxic megacolon

Heal stable preformed exotoxin

1-4 d t <1wk

Staphylococcus

aureus

Unrelrlgcratcdmeat 2 4 h

and dairy products

(custard,pudding,

potato salad,mayo)

Contaminated food/ 1-3 d

water,especially

shellfish

Contaminated food 5 d

Unpasteurized milk

1-2 d None

Vibrio choterac 3 -7 d Tetracycline or fluoroquinolones

(ciprofloxacin)

Massive watery diarrhea (1- 3 L/d)

Mortality <1% with treatment

Yersinia Up to 3 wk Fluoroquinolone only for severe illness Majority of cases inchildren

1-4 yr

Mesenteric adenitis and terminal

ileitis can occurwithout diarrhea,

mimicking appendicitis

Can also mimicCD of terminal

ileum

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Table 10. Parasites in Infectious Diarrhea

Pathogen Source or Mode Incubation

of Transmission

Clinical Features Duration Antimicrobial Therapy Notes

Fever Bloody Abdo

Stool Pain

Nausea/

Vomiting

Cryptosporidium Fecal-oral 7 d 1-20 d Paromomycin +nilazoxanide Immune reconstitution if

immunosuppressed

i

Worldwide endemic 2-4 wk

areas

Fecal-oral

If untreated,potential for liver

abscess

Sigmoidoscopy may show flat ulcers

Only iodoquinol or paromomycin with yellow exudates

for asymptomatic cyst passage

Metronidazole or nilazoxanide

Treatments asymptomatic

carriers NOT recommended

Intamoeba

histolytica

Variable Metronidazole iodoquinol or

paromomycin if symptomatic

infection

T +

Giardia lamblia fecal- oral

Contaminated food.

1

water

Variable Higher risk in:daycare children,

intake of untreated water (

"

beaver

fever").MSN.immunodeficiency

(decreasedIgA)

May need duodenal biopsy

1-4 wk

Table 11. Viruses in Infectious Diarrhea

Pathogen Source or Mode Incubation Clinical Features Duration Antimicrobial Therapy

of Transmission

Notes

Fever Bloody Abdo Nausea/

Stool Pain Vomiting

Norovirus Fecal-oral 24h 24 h None Noroviruses includeNorwalk virus

Can causesevere dehydration

Virtually all children are infected

by 3 yr

Oral vaccine given at 2 and 4 mo

Rotavirus Fecal-oral 2-4d t t 3- 8 d None

Traveller’s Diarrhea

Epidemiology

• most common illnessto affect travellers

• up to 50°

b of travellersto developing countries affected in first 2 wk and 10-20% after returning home

Etiology

bacterial (80-90%);t.coli most common (ETEC),Campylobacter, Shigella, Salmonella, Vibrio (noncholera);wide regional variation (e.g.Campylobacter more common in Southeast Asia)

• viral: norovirus,rotavirus, and astrovirus account for 5-8%

• protozoal ( rarely):Giardia, Entamoeba histolytica,Cryptosporidium, and Cyclospora for ~10% in longterm travellers

• pathogen-negative traveller’

s diarrhea common despite exhaustive microbiological workup

Treatment

• rehydration is the mainstay of therapy

• rehydrate with sealed beverages

in severe fluid loss, use oral rehydration solutions ( I package in I L boiled or treated water)

• treat symptoms: antidiarrheal agents (e.g. rifamycin ABx, bismuth subsalicylate, loperamide)

• empiric ABx in moderate orsevere illness:ciprofloxacin,azithromycin, or rifaximin

note: there is increasing fluoroquinolone resistance in causative agents, especially in South and

Southeast Asia

Prevention

• proper hygiene practices

avoid consumption oft foods or beverages from establishments with unhygienic conditions(e.g.

street vendors), raw fruits or vegetables without a peel, raw or undercooked meat and seafood

avoid untreated water

• bismuth subsalicylate ( Pepto-Bismol’):60% effective (2 tablets Q1D)

• antibiotic prophylaxis not recommended

• increased risk of infection with resistant organisms

high-risk groups (e.g.immunocompromised individuals) likely to be infected with pathogen not

covered by standard antimicrobial agents

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