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24/09/15

Pediatric Dyspepsia &


Gastro-esophageal
Reflux (GER):
Acid Related Disorders
Diagnosis and Management
Wan Nedra
wan.nedra@yarsi.ac.id
YARSI SCHOOL 1OF MEDICINE 2015

24/09/15

OBJECTIVE:

1.Peptic ulcer
disease (PUD)
2.GER
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MANIFESTASI KILINIK
PUD: DYSPEPSIA

Berupa kumpulan gejala yang non-spesifik


berhubungan dengan saluran pencernaan
bagian atas
yang terjadi berulang selama minimal 2
bulan
Chelimsky dan Czinn, 2001
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KRITERIA DIAGNOSTIK DYSPEPSIA

Evaluas
i:
-2
mayor
Minor:
Gejala yg berhubungan dg makan (Anoreksia, BB menurun)atau
-1
Nyeri perut yg dirasa pd malam hari
Heartburn
mayor
Oral Regurgitasi
+2
Neusia kronik
minor
Sendawa berulang
Mayor:
Nyeri perut di daerah epigastrium
Muntah berulang ( minimal 3x/bulan)

Nyeri perut disekitar umbilikal


Ada riwayat keluarga PUD. Dyspepsia
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-4
minor

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ANAMNESIS

Gejala: Nyeri perut di epigastrium, pada malam hari,


regurgitasi, hearburn, BB menurun, hematemesis dan
melena
Riwayan Makan:
Makanan berlemak, makanan pedas, caffein, laktose
Penggunaan Obat-obatan:
Kortikosteroid, NSAID
Alkohol, tembakau (rokok)
Obat2 yang meransang pengeluaran asam lambung
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PEMERIKSAAN
LABORATORIUM

Pemeriksaan awal:
Hematologi dg differential count
LFT, Elektrolit
Feses: Parasit
Urinalisis
Pemeriksaan lanjutan:
USG hati dan saluran empedu
Endoskopi
Hydrogen breath test
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PENGOBATAN

H2 reseptor antagonis:
Cimetidine 20 40 mg/ kg/ hari 2 kali / hari maks: 400
mb
Ranitidine 2- 4 mg/ kg/ hari, 2 kali sehari (mak: 150 mg)
Proton Pump Inhibitor
Lansoprazol 0,8 mg/kg/hari
Pmeprazol 0,8 mg/ kg/ hari
Cytoprotective Agents:
Sukralfat 40-80 mg/ kg/ hari, 4 kali sehari ( mak 1 g)
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DEFINISI

forceful expulsion of gastrointestinal contents into the


oesophagus
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S.motorik somatik

S. Simpatis
Saraf otonom

S. Parasimpatis
N. Vagus

Saraf enterik
pl. mienterikus
asetil kolin
pl. submukosa pleksus mienterikus
S.motorik somatik
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motilitas sal.cerna

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Impuls
endogen

exogen

afferen N. Vagus
Chemo-receptor
Trigger Zone

Vomiting center

vomiting

Gastrointestinal tract,

Impuls
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Vomiting centre

Blood Brain Barrier


Chemo-receptor Trigger Zone

esophagus

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LES
Fundus
Corpus

Tonus decrease

Antrum

Peristaltic decrease

Pylorus
Duodenum

Tonus increase

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Vomiting
Most common in children (> infant)
Confusing the parents
Life-threatening causes of vomiting

Three distinct phases


(1) nausea, (2) retching, (3) emesis
Not preceded in raised intracranial pressure or
mechanical obstruction
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APPROAC
H
Age: neonates, infant, child
Gastrointestinal tract:
obstruction & non obstruction
Extra-gastrointestinal tract

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ETIOLOGY
Neonates
Atresia esophagus, pylorus stenosis, spitting up
GER, NEC, chalasia, Infection (UTI, OMA, sepsis)
Infants
pylorus stenosis, intususeption, hernia
RGE, gastroenteritis, infection, drugs, aerophagia
Children
Intusuception, stricture, gastritis, apendisitis
Infection, drugs

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Therapy
~ etiology
treat acid and base inbalanced
Drugs:
Domperidone
Metoclopramide
Cisapride
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Gastroesophageal reflux
Just spitting up, or
something more serious ?
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REGURGITATION

20% general infant population


40% of children consulting a pediatrician
70% of all 4 months old infants
regurgitate at least 1 x/day
25% is considered by the parents as a problem
RGE
8% abnormal pH esophagus monitoring
1/300 1/1000 severe
(Chouchou, 92; Nelson et al, 1997)
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GER
The involuntary passage of gastric contents
into the esophagus
saliva, ingested food, drinks, gastric/pancreatic/
biliary secretions
normal phenomenon, +/- accompanying symptoms
physiologic or pathologic reflux

(Carre 1983; Vandenplas, 1992; Orenstein, 1994; Vandenplas, 1993)

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GER
Physiologic reflux

occurs mainly after meal


does not normally cause symptoms
short duration of reflux episodes
Pathologic reflux

frequent reflux episodes of longer duration


reflux episodes occuring during the day/night
may produce symptoms & inflamation/mucosal injury

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MECHANISMS OF GER
Deficient or delayed
esophageal
acid clearance
attenuated swallows,
dysfunctional peristalsis
Length of LES,
Maturation of LES
TLES relaxation
delayed
gastric
emptying
delayed
gastric
emptying,
distention
distension

Incompetent
LES

ILES: Lower essophageal


sphinter

Inadequate
gravitation

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TRIGGER FACTORS
FAVORING GER
Increased abdominal pressure
(overweight, constipation)
Increased respiratory effort related to
exercise
(food) allergy, crying, cigarette smoking
Hereditary predisposed
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CLINICAL MANIFESTATION
GER

Emesis & regurgitation are the most common


primary GER disease
secondary GER disease
infection, metabolic disorders, & food allergy
stimulation vomiting center in the dorsolateral
reticular formation by efferent & afferent impuls
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SYMPTOMS OF
GER
(- DISEASE)
Usual manifestations
Specific manifestation
regurgitation, nausea, vomiting
Possibly related to complications
~ anaemia (iron defiency anaemia)
haematemesis & melena
dysphagia, weight loss, irritable infants
ect ~ adult
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SYMPTOMS OF GER
(- DISEASE)
Unusual presentations
~ chronic respiratory disease
apnea, apparent life threatening, SIDS

~ to congenital and/or CNS


abnormalities
cerebral palsy, psychomotory retardation
A careful history, observation of feeding, &
physical examination are mandatory
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TREATMENT
RECOMMENDATIONS

1. a. Parental reassurance
b. Milk-thickening agents (?)
2. Prokinetics
3. Positional adjuvant therapy
4. a. H2 receptor antagonist
b. Proton pump inhibitors
5. Surgery
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REGURGITATION AND
FEEDING
Frequent small feeding
Decrease the number of transient LES relaxations
Reduced volume cause of distress to infants
Restriction volume in clearly overfed babies
Thickening infants formula
Decrease the frequency & volume of regurgitation
time crying, improves sleep, caloric retention ,
coughing (after feeding)
(Vandenplas, 1994, Borelli, 1997)
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FORMULA AND
MILK-THICKENING
Thickening formula should be considered
as the first step
Can not be given to breastfed infants
Gastric emptying : Casein >
Wheyhydrolysate

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Prokinetics
Gastrokinetic action indirect release of acetylcholine
in the myentericus plexus

Reduces regurgitation
The LES pressure and motility
Esophageal peristalsis, gastric emptying

Increased salivary secretion


protect esophagus via salivary component (bicarbonat
buffer)
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POSITION,
CRYING, AND
REFLUX
Sleeping and crying decrease GER
Crying increases abdominal pressure, but also
increases LES-P

300 prone anti-trendelenburg position


SIDS ?
Beyond the age of SIDS ( > 12 months)

(Orenstein, 1990; Orenstein, 1997; Tobin, 1997)


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THANK YOU

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