dyspepsia in children-ok
DESCRIPTION
dispepsia pada anakTRANSCRIPT
Pediatric Dyspepsia & Gastro-esophageal
Reflux (GER):Acid – Related DisordersDiagnosis and Management
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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