Transcript H. pylori - Benton Franklin County Medical Society

CHRONIC ABDOMINAL PAIN IN
CHILDREN David Suskind M.D
.
Associate Professor of Pediatrics
Division of Gastroenterology Hepatology and Nutrition
University of Washington
Seattle Children’s Hospital
Talk outline
• General over view of chronic abdominal pain
• Disease specific entities
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Constipation
Lactose
Fructose intolerance
Celiac
GERD
H. pylori
• General work-up
Primary Causes of Chronic Abdominal pain
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Constipation
Lactose intolerance
Fructose intolerance
Functional abdominal
pain
• Celiac
• Food allergies
eosinophilic esophagitis
• Acid related disorders:
Gastroesophageal reflux
disease gastritis and
ulcers
• Infections:
Mononucleosis, intestinal
parasites, H. pylori
bacterial infection
• inflammatory bowel
disease: ulcerative colitis
and Crohn’s disease
A Physicians Aspiration
• ‘Our goal is to diagnose and treat our
patients’
• Unfortunately we only have a handful of
minutes to do so
• So we triage our patients based upon our
knowledge, our experience and the
medical literature
The History
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Timeframe and time of day
Location Apley’s Rule
Intensity and character
Aggravating or alleviating factors
Associated signs and symptoms
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Bowel habits
Vomiting
Gassiness
Weight loss
Dietary habits
Psychosocial stressors
• Diagnosis / Family history
“Red Flags” in Chronic Abdominal Pain
• Weight loss or growth
deceleration
• Vomiting
• Pain awakens patient
• Radiation pain
• Recurrent oral
ulcerations
• Rectal bleeding
• Constitutional symptoms
• Rash
• Arthralgia
• Temperature
• Pain well localized away
from umbilicus
• Positive family history
of celiac, H. pylori or
inflammatory bowel
disease, pancreatitis
Physical exam
• Rectal exam
Constipation: Recognition
3% of general pediatric outpatient visits and 25%
of pediatric gastroenterology
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TABLE 1. Normal frequency of bowel movements
Age
0-3 months
Breast-fed
Formula-fed
6-12 months
1-3 years
More than 3 years
Bowel movements
per weeka
Bowel movements
per dayb
5-40
5-28
5-28
4-21
3-14
2.9
2.0
1.8
1.4
1.0
Adapted from Fontana M. Bianch C, Cataldo F, et al. Bowel
frequency in healthy children. Acta Paediatr Scand 1987; 78:682-4.
a
Approximately mean ± 2 SD.
b
Mean.
Archives of disease, child 1983; 58:257 – 61.
Variable Symptoms
Constipation Treatment
• After two-month period - 37% remained constipated
• Specific fixed dose of laxative
• parents did not realize that they needed to adjust the dose
• failure to mention behavioral interventions and dietary
interventions
• Treatment success corresponded to how aggressively
treated
• colonic evacuation followed by daily laxative therapy
Borowitz, SM, et al treatment of childhood constipation by primary care
physicians: efficacy and predictors of outcome, Pediatrics 2005
April;115 (4):873-7.
The treatment plan
The four-step treatment plan
Step1 : Cleanout phase: emptying the colon
Step 2: Maintenance phase: keeping the colon empty
Step 3: Changing the behaviors and habits that increase the problem
Step 4: Recognizing and treating relapses early
The treatment plan
• Cleanout phase is to empty the old stool out of
the colon.
• Floppy colon can’t move firm stool
• Maintenance is to keep stools soft to let colon
empty itself easily.
• Exercise itself back into shape
• Can take a year or more to shrink
The treatment plan – cleanout
Step 1: The cleanout phase
Get old stool emptied out of the colon.
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Polyethylene Glycol
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Each cleanout lasts 2 days
• Usually needs to be repeated.
• May cause cramping as the stool moves
through the colon
• Stay near a bathroom during the cleanout
The treatment plan – cleanout
Cleanout, cont.
• Results during the first cleanout will vary from a slightly
noticeable increase to 4 to 6 large volume stools a day.
• Cleanout should be repeated every 2 weeks until
stools are daily, very soft and pain is gone.
• Symptoms will improve over time, not always
immediately.
The treatment plan – clean out
AND
• Stimulant laxatives
• Increase the strength of the colon’s contractions
and help move stool out.
• Examples: Senna, Little Tummy’s Laxative or
bisacodyl (Dulcolax)
The treatment plan – maintenance
Step 2: Maintenance phase
• Continue giving the stool softener once every day
at the maintenance dose
• Adjust maintenance to assure soft stool
• 1-3 soft mashed-potato-consistency stools per day.
• Wait 3 days between dose changes
• Continue treatment for 4 to 6 months
• Even if things seem much better
• Improves colonic tone
Treatment plan – changing behaviors
Step 3: Changing old behaviors and habits
• Constipation gets worse with certain habits
• Waiting too long to go
• Not drinking enough liquid
• Too much dairy
• Not eating enough fiber
• Eating too many constipating
foods like bananas and cheese
Treatment plan – changing behaviors
New behaviors to adopt
Have your child:
Drink enough liquid throughout the day so their urine
stays clear or pale yellow.
Treatment plan – changing behaviors
Get enough fiber every day
• General rule:
Your child’s age plus 5 = grams of fiber per day.
Teens over 15 years old need 20-30 grams
per day, just like adults.
Treatment plan – changing behaviors
Get enough fiber every day
• fruits and vegetables, legumes
and whole grains
• Eat most grains as whole
grains
• Include 5 servings of fruit or
vegetables every day.
(Serving size: 1 serving = 1/4-1/2 cup brown rice, ½ c or 5 broccoli
flowers, 1 handful raisins)
Treatment plan – changing behaviors
Know how to read food labels
for fiber
Treatment plan – changing behaviors
Regular, relaxed toilet time.
• After meals, sit on the toilet for about 5 minutes.
• Use a foot stool so their feet don’t dangle when sitting.
• Reward your child for cooperation in sitting on toilet. They
don’t need to stool to be rewarded.
• Star charts and point systems
• Make it fun and avoid getting into arguments.
• Continue this at least 2 times a day, consistently for at
least the next year.
Treatment plan – respond to relapses
Step 4: Recognize and respond to relapses
quickly
• The children with the least frequent relapses are the
ones who make the needed diet and behavior
changes.
• Restart stool softeners at the first sign of a relapse.
• Cleanout whenever needed, as often as every 2
weeks.
Lactose intolerance
• Symptoms caused by
maldigestion of
lactose
• Lactose is the
carbohydrate (sugar)
of milk
• Lactase splits lactose
in the intestine
Disaccharidase Activities in Children: Normal Values and Comparison Based
on Symptoms and Histologic Changes
Gupta, Sandeep K.; Chong, Sonny K. F.; Fitzgerald, Joseph F. Journal of
Pediatric Gastroenterology & Nutrition 28(3), March 1999, pp 246-251
Diagnostic tests
• H2 Breath Test
• bacteria in the bowel digest lactose
• generating hydrogen (H2) →
detection of H2 in the exhaled air
• Biopsy for lactase deficiency
• Removal of lactose from diet
Celiac disease
• Immune-mediated enteropathy caused by a
permanent sensitivity to gluten in genetically
susceptible individuals
• Healthy population:
1:133
• 1st degree relatives:
1:18 to 1:22
• 2nd degree relatives:
1:24 to 1:39
• Symptomatic and asymptomatic individuals
• including subjects affected by:
•Type 1 diabetes
•Williams/Downs/Turner syndrome
•Selective IgA deficiency
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The Celiac Iceberg
Symptomatic
Celiac Disease
Manifest
mucosal lesion
Silent Celiac
Disease
Latent Celiac Disease
Normal
Mucosa
Genetic susceptibility: - DQ2, DQ8
Positive serology
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Celiac: Epidemiological Study in USA
Population screened
13145
Healthy Individuals
4126
Risk Groups
9019
Symptomatic subjects
3236
Positive
31
Negative
4095
Prevalence
1:133
Positive
81
Negative
3155
1st degree relatives
4508
Positive
205
Prevalence
1:40
Negative
4303
Prevalence
1:22
2nd degree relatives
1275
Positive
33
Negative
1242
Prevalence
1:39
Projected number of celiacs in the U.S.A.: 2,115,954
Actual number of known celiacs in the U.S.A.: 40,000
For each known celiac there are 53 undiagnosed patients.
A. Fasano et al., Arch Int Med 2003;163:286-292.
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Celiac Disease Prevalence Data
Geographic Area
Prevalence on clinical
diagnosis*
Prevalence on screening
data
Brasil
?
1:400
Denmark
1:10,000
1:500
Finland
1:1,000
1:130
Germany
1:2,300
1:500
Italy
1:1,000
1:184
Netherlands
1:4,500
1:198
Norway
1:675
1:250
Sahara
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1:70
Slovenia
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1:550
Sweden
1:330
1:190
United Kingdom
1:300
1:112
USA
1:10,000
1:133
Worldwide (average)
1:3,345
1:266
*based on classical, clinical presentation
Fasano & Catassi, Gastroenterology 2001; 120:636-651.
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2
1
2b
2a
8
8
Cytokines (IL2, IL15)
Tk
6b
7
P
6a
AGA, EMA,
atTG
B
3
TTG
4
APC
T
5
Submucosa
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Gastrointestinal Manifestations
6-24 months
Older Children and Adults
• Chronic or recurrent
diarrhea
• Abdominal distension
• Anorexia
• Failure to thrive or weight
loss
• Vomiting
• Constipation
• Irritability
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Dermatitis Herpetiformis
Dental enamel hypoplasia
Osteopenia/Osteoporosis
Short Stature
Delayed Puberty
Iron-deficient anemia
Resistant to oral Fe
Hepatitis
Arthritis
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Typical Celiac Disease
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Asymptomatic Celiac
• Silent - No or minimal symptoms
• Damaged mucosa and positive serology
• Asymptomatic individuals from groups at risk such:
• First degree relatives
• Down syndrome patients
• Type 1 diabetes patients
• Latent - No symptoms, normal mucosa
• May show positive serology.
• Identified by following in time asymptomatic individuals
previously identified at screening from groups at risk
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Major Complications of Celiac Disease
• Short stature
• Dermatitis
herpetiformis
• Dental enamel
hypoplasia
• Recurrent stomatitis
• Fertility problems
• Osteoporosis
• Gluten ataxia and
other neurological
disturbances
• Refractory celiac
disease and related
disorders
• Intestinal lymphoma
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Celiac Diagnosis
Diagnostic principles
• Confirm diagnosis before treating
• Diagnosis of Celiac Disease mandates a
strict gluten-free diet for life
• following the diet is not easy
• QOL implications
• Failure to treat has potential long term
adverse health consequences
• increased morbidity and mortality
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SerologicTesting for Celiac
Role of serological tests:
• Identify symptomatic individuals who need a
biopsy
• Screening of asymptomatic “at risk”
individuals
• Supportive evidence for the diagnosis
• Monitoring dietary compliance
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Serological Tests for Celiac
• Antigliadin antibodies (AGA)
• Antiendomysial antibodies (EMA)
• Anti tissue transglutaminase antibodies (TTG)
–first generation (guinea pig protein)
–second generation (human recombinant)
• HLA typing
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Serological Test Comparison
AGA-IgG
AGA-IgA
EMA (IgA)
TTG (IgA)
Sensitivity %
Specificity %
69 – 85
75 – 90
85 – 98
90 – 98
73 – 90
82 – 95
97 – 100
94 – 97
Farrell RJ, and Kelly CP. Am J Gastroenterol 2001;96:3237-46.
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Histological Features
Normal 0
Infiltrative 1
Hyperplastic 2
Partial atrophy 3a
Subtotal atrophy 3b
Total atrophy 3c
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Horvath K. Recent Advances in Pediatrics, 2002.
Treatment
• Only treatment for
celiac disease is a
gluten-free diet (GFD)
• Strict, lifelong diet
• Avoid:
• Wheat
• Spelt
• Rye
• Barley
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Gastroesophageal Reflux Disease
GER
GERD
Gastroesophageal reflux;
reflux of the stomach and
duodenal contents into the
esophagus
Any condition noted clinically
or histologically that results
from GER
Regurgitation - Gastric contents pass the lower and upper
esophageal sphincter
Vomiting - Ejection of gastric contents through the mouth.
Pathophysiology
• Lower Esophageal
Sphincter (LES)
• Cardioesophageal angle
of His
• Size Matters
Pathophysiology cont.
• Intragastric pressure
• gastric compliance
• meal size/volume relation
• gastric emptying
• body position
Diagnostic tests
• Upper GI x-ray
• Rules out structural causes of reflux
• congenital and acquired
• webs, rings, slings, strictures, or malrotation
• DOES NOT DIAGNOSE REFLUX
Diagnostic tests
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Upper GI contrast study
Esophageal pH probe monitoring
Impedance monitoring
Upper endoscopy and biopsy
Nuclear scintigraphy study
Hiatal hernia
diaphragm
stomach
Diagnostic test
• Esophageal pH monitoring
• regarded as the “gold standard” ( 24 Hr)
• Performed more often as inpatients.
• Placement determined by regression equations. And
check with x-ray
• Scored based on population criteria
• Age dependent
Ph Probe Criteria
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Number of reflux episodes in 24º
Longest reflux episode
Reflux index- % time the esophageal pH < 4
Symptom correlation
Diagnostic test
• Scintigraphy - Usually with technetium.
• Image is less sharp than barium
• Monitor reflux up to 1-1.5 Hr. after a meal, or even
overnight
• Aspiration and gastric emptying.
• Radiation several fold less than barium.
• Sensitivity: 60%-93%
Diagnostic test
• Endoscopy and biopsy
• Differentiate reflux from other GI disease with
similar symptoms.
• Erythema, erosions and ulcerations, to strictures
and Barrett’s esophagus, allergic esophagitis and
H. pylori.
Management of Pediatric GERD
• Antireflux measures and pharmacotherapy,
should be used in a stepwise and progressive
manner
• Begin with conservative measures
Multicenter, double-blind, randomized, placebocontrolled trial assessing the efficacy and safety of
proton pump inhibitor lansoprazole in infants with
symptoms of gastroesophageal reflux disease
Lansoprazole doubleblind (≤4 weeks, n =
81)
Placebo double-blind
(≤4 weeks, n =81)
P value
Primary efficacy:
Responder rate, n (%)
44 (54%)
44 (54%)
NS
Discontinued due to non
efficacy, n (%)
28 (35%)
29 (36%)
NS
Cry, % of feeds/week
-20
-20
NS
Regurgitate, % of
feeds/week
−14
−11
NS
Feed refusal, % of
days/week
−14
−10
NS
Arching back, % of
days/week
−20
−18
NS
Physician: Improved at
week 4
44 (55%)
40 (49%)
NS
Orenstein SR, et al J Pediatr 2009 April; 154(4):514-520
Efficacy of conservative therapy
• Feeding modifications,
positioning, and tobacco
smoke avoidance
• Infant Gastroesophageal
Reflux QuestionnaireRevised (I-GERQ-R; n =
40)
• 78% of infants improved
with 24% having normal IGERQ-R scores
Orenstein, et al. J Pediatr 2008 Mar; 152(3):310-4
Maternal Child Health J 2012 Aug; 16(6):1319-31
• “Milk protein allergy”
• Dietary elimination in
mother diet /
hypoallergenic formula
trial
Nonpharmacologic management
• Diet changes
• Infants: thickened feeds
• Children: limiting caffeinated foods, spicy foods, acidic
foods and fatty foods
• Positioning
• Left-side positioning and head elevation during sleep.
• Lifestyle changes
• Fast prior to bedtime
• Avoid large meals/tight fitting cloth
• Avoid alcohol and smoking
(An
H2 Receptor
H2Ranitidine
Receptor
Antagonist
Mechanism
Antagonist) Mechanism
of Action of Action
K+ H+
® (An
Ranitidine
H2 Receptor
PREVACID
(lansoprazole)
Mechanism of
Proton
Pump
Inhibitor
Antagonist)
Mechanism of Action
Action
Mechanism of Action
K+ H+
Rebound Acid Hypersecretion
Temporal changes in the proportion of subjects with heartburn, acid
regurgitation or dyspepsia.
Christina R., Gastroenterology 2009, 137(1) :80 – 87.
So what do you do?
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Make sure of diagnosis
Emphasize diet and exercise
If trialing acid suppression, do short course
Explain down side of medications
Helicobacter Pylori
• Infects >50% of the world’s human population
• Incidence in industrialized countries is ~0.5% of
the population/year
• Incidence in developing countries is 3-10%/year
• In North America, the prevalence among AsianAmericans, African-Americans and Hispanics are
similar to those of residents of developing
countries.
Risk factors
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residence in a developing country
poor socioeconomic conditions
family overcrowding
possibly an ethnic or genetic predisposition
When to suspect H. pylori infection
• Upper gastrointestinal hemorrhage
• Severe epigastric abdominal pain
• Protracted vomiting
But not in classic recurrent abdominal
pain syndrome.
Who not to test?
• Recurrent abdominal pain
• 6 studies performed in N Am, Europe, and Australia
• 2715 children evaluated by EGD, serology, or UBT
• 5-17% of children with abdominal pain infected
• 5-29% of children without abdominal pain also
infected
• Treating did not affect symptoms of chronic
abdominal pain
• Asymptomatic w/ increased risk
• Family history alone
Diagnosis
• Non-invasive tests
• Serum and whole
blood antibody
• Saliva antibody
• Urine antibody
• Stool antigen
• Urea breath testing
• Invasive tests
requiring endoscopy
• Biopsies and
histology
• Rapid urease testing
• Bacterial culture
• Polymerase chain
reaction of bacterial
DNA
Indications for treatment of H. pylori
Treatment indicated?
Diagnosis
No
No evidence of infection
No
Gastritis caused by H. pylori, no
symptoms
No  Yes
Gastritis caused by H. pylori, nonulcer dyspepsia
Gastritis caused by H. pylori, gastric
Yes
ulcer
Gastritis caused by H. pylori, duodenal
Yes
ulcer
Gastritis caused by H. pylori, MALT
Yes
lymphoma
H. pylori treatment:14-day regimen
• Omeprazole or Lansoprazole.
• Clarithromycin 30mg/kg/day.
• Amoxicillin 60mg/kg/day.
How to treat?
Summary
• Think Constipation, Lactose/fructose intolerance,
Functional abdominal pain
• Always do a rectal
• Don’t hesitate to screen for Celiac disease
• Hesitate to screen for H. pylori for Chronic
abdominal pain
• And beware of chronic acid suppression