Pediatric Dyspepsia & Gastro-esophageal

Reflux (GER):Acid – Related DisordersDiagnosis and Management

Wan Nedrawan.nedra@yarsi.ac.id

YARSI SCHOOL OF MEDICINE 2015

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1.Peptic ulcer disease (PUD)

2.GER

OBJECTIVE:

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Berupa kumpulan gejala yang non-spesifik berhubungan dengan saluran pencernaan

bagian atasyang terjadi berulang selama minimal 2

bulan

Chelimsky dan Czinn, 2001

MANIFESTASI KILINIK PUD: DYSPEPSIA

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Mayor: Nyeri perut di daerah epigastriumMuntah berulang ( minimal 3x/bulan)

Minor:Gejala yg berhubungan dg makan (Anoreksia, BB menurun)Nyeri perut yg dirasa pd malam hariHeartburnOral RegurgitasiNeusia kronikSendawa berulangNyeri perut disekitar umbilikalAda riwayat keluarga PUD. Dyspepsia

KRITERIA DIAGNOSTIK DYSPEPSIA

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Evaluasi: - 2

mayor atau

-1 mayor

+ 2 minor

-4 minor

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, NSAIDAlkohol, tembakau (rokok)Obat2 yang meransang pengeluaran asam lambung

ANAMNESIS

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Pemeriksaan awal: Hematologi dg differential count

LFT, ElektrolitFeses: Parasit

Urinalisis

Pemeriksaan lanjutan:USG hati dan saluran empedu

EndoskopiHydrogen breath test

PEMERIKSAAN LABORATORIUM

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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)

PENGOBATAN

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• forceful expulsion of gastrointestinal contents into the oesophagus

DEFINISI

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S.motorik somatik

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S.motorik somatik

Saraf otonomS. Simpatis

S. Parasimpatis

Saraf enterikN. Vagus

asetil kolinpleksus mienterikus

motilitas sal.cerna

pl. mienterikuspl. submukosa

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Impuls

Chemo-receptor Trigger Zone

Gastrointestinal tract, …

Vomiting center

endogen exogen

Impuls

vomiting

afferen N. Vagus

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Vomiting centre

Chemo-receptor Trigger Zone

Blood Brain Barrier

esophagus

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LES FundusCorpus

Tonus decrease

Antrum Peristaltic decrease

PylorusDuodenum

Tonus increase

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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Vomiting

•Age: neonates, infant, child•Gastrointestinal tract: obstruction & non obstruction• Extra-gastrointestinal tract

APPROACH

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NeonatesAtresia esophagus, pylorus stenosis, spitting up

GER, NEC, chalasia, Infection (UTI, OMA, sepsis)Infants

pylorus stenosis, intususeption, herniaRGE, gastroenteritis, infection, drugs, aerophagia

ChildrenIntusuception, stricture, gastritis, apendisitis

Infection, drugs

ETIOLOGY22/04/23

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~ etiologytreat acid and base inbalanced

Drugs: Domperidone

MetoclopramideCisapride

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Therapy

Gastroesophageal reflux

Just spitting up, or something more serious ?

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20% general infant population40% of children consulting a pediatrician70% of all 4 months old infants regurgitate at least 1 x/day25% is considered by the parents as ‘a problem’

RGE8% abnormal pH esophagus monitoring1/300 – 1/1000 ‘severe

(Chouchou, 92; Nelson et al, 1997)

REGURGITATION

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The involuntary passage of gastric contents into the esophagus

saliva, ingested food, drinks, gastric/pancreatic/ biliary secretions

normal phenomenon, +/- accompanying symptomsphysiologic or pathologic reflux

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

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GER

Physiologic refluxoccurs mainly after meal

does not normally cause symptomsshort duration of reflux episodes

Pathologic refluxfrequent reflux episodes of longer duration

reflux episodes occuring during the day/nightmay produce symptoms & inflamation/mucosal

injury

GER22/04/23

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MECHANISMS OF GER

attenuated swallows, dysfunctional peristalsis

Length of LES, Maturation of LESTLES relaxation

Inadequate gravitation

delayed gastric emptying, distension

Deficient or delayed esophageal

acid clearance

Incompetent LES

delayed gastric emptyingdistention

ILES: Lower essophageal sphinter

•Increased abdominal pressure (overweight, constipation)

•Increased respiratory effort related to exercise

(food) allergy, crying, cigarette smoking

•Hereditary predisposed

TRIGGER FACTORS FAVORING GER

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Emesis & regurgitation are the most common

‘primary’ GER disease‘secondary’ GER disease

infection, metabolic disorders, & food allergystimulation vomiting center in the dorsolateral

reticular formation by efferent & afferent impuls

CLINICAL MANIFESTATION GER

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Usual manifestationsSpecific manifestation

regurgitation, nausea, vomitingPossibly related to complications

~ anaemia (iron defiency anaemia)haematemesis & melena

dysphagia, weight loss, irritable infantsect ~ adult

SYMPTOMS OF GER

(- DISEASE)

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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

SYMPTOMS OF GER (- DISEASE)

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1. a. Parental reassurance b. Milk-thickening agents (?)2. Prokinetics3. Positional adjuvant therapy4. a. H2 receptor antagonist b. Proton pump inhibitors5. Surgery

TREATMENT RECOMMENDATIONS

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Frequent small feedingDecrease the number of transient LES relaxations

Reduced volume cause of distress to infantsRestriction volume in clearly overfed babies

Thickening infants formulaDecrease the frequency & volume of regurgitationtime crying, improves sleep, caloric retention ,

coughing (after feeding) (Vandenplas, 1994, Borelli,

1997)

REGURGITATION AND FEEDING

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Thickening formula should be considered as the first step

Can not be given to breastfed infants

Gastric emptying : Casein > Wheyhydrolysate

FORMULA AND MILK-

THICKENING

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Gastrokinetic action indirect release of acetylcholine in the myentericus plexus

Reduces regurgitationThe LES pressure and motility

Esophageal peristalsis, gastric emptying

Increased salivary secretionprotect esophagus via salivary component (bicarbonat

buffer)

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Prokinetics

Sleeping and crying decrease GERCrying increases abdominal pressure, but also

increases LES-P

300 prone anti-trendelenburg positionSIDS ?

Beyond the age of SIDS ( > 12 months)

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

POSITION, CRYING, AND

REFLUX

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THANK YOU

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