06/01/2019

Pediatric Dyspepsia & Gastro-

esophageal Reflux (GER):
Acid – Related Disorders
Diagnosis and Management

Wan Nedra
wan.nedra@yarsi.ac.id
YARSI SCHOOL OF MEDICINE 2014
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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

Mayor:
Nyeri perut di daerah epigastrium
Muntah berulang ( minimal 3x/bulan)
Evaluasi:
Minor: - 2 mayor
Gejala yg berhubungan dg makan (Anoreksia, BB menurun)
atau
Nyeri perut yg dirasa pd malam hari
Heartburn -1 mayor
Oral Regurgitasi + 2 minor
Neusia kronik
Sendawa berulang -4 minor
Nyeri perut disekitar umbilikal
Ada riwayat keluarga PUD. Dyspepsia
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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
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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

Gastroesophageal reflux (GER)

• the involuntary passage of gastric contents into the
esophagus
Regurgitation:
• reflux dribbles effortlessly into or out of the mouth

Vomiting:
• forceful expulsion of gastrointestinal contents into the
oesophagus 8
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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

motilitas sal.cerna
S.motorik somatik
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Impuls

endogen exogen
afferen N. Vagus

Chemo-receptor
Vomiting center
Trigger Zone

Gastrointestinal tract, … vomiting

Impuls

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Vomiting centre

Blood Brain Barrier

Chemo-receptor Trigger Zone

esophagus

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LES
Fundus Tonus decrease
Corpus
Antrum Peristaltic decrease

Pylorus Tonus increase

Duodenum

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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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APPROACH

• 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
20 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
delayed gastric
gastric emptying
emptying,
distention
Incompetent distension
LES

Inadequate
ILES: Lower essophageal gravitation
sphinter

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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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