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GASTRO ESOPHAGEAL REFLUX ( G E R )

( REFLUKS GASTRO ESOFAGIAL / R G E )

Bambang Mulyawan
FK-UMM

Pendahuluan / Definisi
RGE : disfungsi sfingter esofagus bawah
(SEB) regurgitasi isi lambung ke
esofagus
Makanan / minuman yg kembali dari
lambung ke esofagus : 1. masuk kembali ke
lambung 2. dikeluarkan mulut/muntah

Pendahuluan ..... (lanjutan)


Regurgitasi : kembalinya tanpa upaya
makanan yg sudah ditelan ke dalam mulut
Fisiologik: GER REGURGITASI PD
BAYI NORMAL
Patologik : GERD , episode sering /
persisten eosofagits, gejalan akibat
espiratori

Definition

Passive transfer of
gastric contents into
the esophagus due
to transient or
chronic relaxation
of the lower
esophageal
sphincter

QuickTime and a
TIFF (Uncompressed) decompressor
are needed to see this picture.

Definisi
GER : mengalirnya secara involunter isi
lambug ke dalam eosofagus
Regurgitasi : gejala paling umum dari GER
infantil
gumoh spitting up

Definitions
Gastroesophageal Reflux
Involuntary return of gastric
contents into the esophagus as a
result of a dysfunctional lower
esophageal sphincter

Physiologic vs Pathologic
Extraesophageal Reflux

Epidemiologi

Insidens RGE di Indonesia : ?


50% pada Bayi Baru Lahir : normal
Klinis : refluks / muntah ?
Refluks : pasif karena katup esofagus
lambung belum berfungsi baik.
Muntah:pengeluaran isi lambung mulut
dengan paksa

Epidemiology
First described as a clinical entity in pediatrics in the 1950s
incidence 1/4000 live births

Cherry and Margulies (1968) - contact ulcers of the larynx


Three-fold predominance in boys over girls
Increased incidence in certain clinical conditions

neurologic impairment
prematurity (70% preemies <1700 grams)
diaphragmatic hernia
esophageal atresia
feeding tubes
gastric/intestinal mobility disorders
various syndromes

Epidemiologi
Birth to 2 years
Physiologic, especially < 6 months
90% resolve by 12-18 months

2 years to adulthood
Vomiting is never physiologic
GERD is chronic relapsing disease

Epidemiologi
Gastroesophageal Reflux (GER)

Reflux of gastric contents into esophagus


Normal physiologic process
50% of infants 0-3 months of age
25% of infants 3-6 months of age
5% of infants 10-12 months of age
20% of pH probe reflux episodes are visible
reflux
Result of Transient LES relaxations

Pengertian / istilah
Possetting : pengeluaran isi lambung
sehabis makan, meleleh keluar dari mulut,
didahului sendawa/ glegeken
Rumination : keluarnya isi lambung ke
dalam mulut, mengunyah dan telan kembali
Istilah masyarakat : olab (Sunda), gumoh
(Jawa), menduga (Minang),meluah(Bali)

Pengertian / istilah . . .
Gastroesophageal reflux (GER) =
physiologic reflux
GERD = gastroesophageal reflux disease =
reflux with complications
Dysphagia = difficulty or problems with
swallowing

GER

GERD

Gastroesophageal reflux (GER), passage of


gastric materials into the esophagus, is a normal
physiologic process that can progress to
gastroesophageal reflux disease (GERD) when
the expelled gastric materials produce
undesirable symptoms and complications
It is therefore appropriate to think of GER as a
normal, benign physiologic process that
precedes GERD, a pathologic process

Anatomy and Physiology


Esophageal phase
Peristalsis moves food to stomach
Lower esophageal sphincter relaxes
Upper esophageal sphincter, Lower esophageal
sphincter constrict preventing reflux

Mouth: Foodstuffs broken down by chewing; saliva added


as lubricant
Oesophagus: Conduit between mouth and stomach
Stomach: Digestion of proteins; foodstuffs reduced to
liquid form; storage; sterilisation
Pancreas: Digestive enzymes for digestion of fats,
carbohydrates and proteins
Liver: Bile salts for digestion/absorption of fats in
small intestine
Gallbladder: Stores and concentrates bile
Small intestine: Final stages of chemical digestion and nutrient
absorption
Large intestine: Water absorption, bacterial
fermentation and formation of faeces

Pathophysiology

The primary barrier against GE


reflux is the lower esophageal
sphincter
sphincter lacks appropriate
tone or other incompetency
gastric volume or pressure
poor gastric emptying
altered neuromuscular
development
abnormal esophageal motility
acuity of the angle of His
other anatomic defects

Pathophysiology
1.
2.
3.
4.

A decrease in lower esophageal sphincter (LES)


tone -- the most important factors
Changes in the pressure gradients between the
esophagus and stomach
Stress maneuvers include straining, crying,
coughing, eating, or the valsalva maneuver
Other factors include gastric distention,
delayed esophageal clearance and gastric
emptying, neurologic disease, and hiatal hernia

Patogenesis
Neonatus : tonus otot SEB belum sempurna,
panjang belum maksimal
Para ahli : penyebab RGEketidak
mampuan SEB menahan kembalinya isi
lambung karena tekanan SEB yg rendah/
cenderung pada periode relaksasi otot SEB
Dapat terjadi pd > tekanan intra abdominal,
meteorismus, sepsis, tumor

Patogenesis
Jarang terjadi pd waktu tidur : pengosongan
lambung dan aktifitas menelan lebih lambat
Posisi tengkurap dg kepala lebih tinggi
menurunkan frekuensi RGE
Pengaruh pH esofagus : < 4 merangsang
peningkatan peristaltiknya > insidens RGE
RGE: menimbulkan ggn pertumbuhan, striktura,
esofagitis, hematemesis,infeksi sal nafas berulang,
kadang menimbulkan kematian mendadak
( Sudden Infant Death Syndrome )

Faktor Resiko

Genetic - autosomal dominant


Immaturity of the LES
Increased abdominal pressure
Gastric distention
Esophagus dysmotility
Prematurity
Neurologic problems
Chronic lung disorder
H.Pylori infection
Cows milk allergy

Gejala klinis
Muntah tidak proyektil/ ortu menganggap
normal, kecuali terus menerus
Infeksi paru berulang
Muntah saat bayi ditidurkan setelah makan
Bila pH isi lambung < 4 : esofagitis,
striktura, disfagia, perdarahan
Gagal tumbuh kembang (Failure to thrive)

GER Symptoms

Vomiting (72%)
Abdominal pain (36%)
Feeding problems (29%)
Failure to thrive (28%)
Irritability (19%)
Heartburn (1%)

Clinical Features
Regurgitationmild symptomsno treatment
Recurrent vomiting occurs in 50%of infants in the first
three months of life, in 67% of four month old infants,
and in 5% of 10 to 12 month old infants
Oesophagitis, failure to thrive or recurrent aspiration
pneumoniasevere and complicationsneed to
treat
Risk of severe GER premature infants,infants with
cerebral palsy,and infants with congenital
oesophageal anomalies

Clinical Presentation
Classic symptoms
vomiting, pain / irritability, failure to thrive
Hiccuping, yawning, and sneezing

Severe symptoms
Pulmonary compromise
apnea, pneumonia, wheezing, asthma, stridor
Epigastric bleeding, anemia, hematemesis
esophagitis
Sandifer syndrome

Silent reflux

Gejala klinis
Bila asam lambung ke faring : aspirasi pneumoni, obstruksi
dg gejala spt asma
Penyakit paru : serangan apnea, pneumoni berulang, batuk
malam hari /kronis, wheezing berulang, sering muntah malam
Sudden Infant Death Syndrome (SIDS) : imaturitas sal nafas /
rentan infeksi, Resapiratory Distress Syndrome , infeksi paru
berulang, spasme laring
Perdarahan mukosa esofagus distal karena erosi dan radang
kronis
Head cocking (gerakan seperti mengangguk), anemi besi
(Sindrom Sandifer )

Complications of
gastroesophageal reflux

Recurrent vomiting
Weight loss or poor weight gain
Irritability in infants
Regurgitation
Heartburn or chest pain
Hematemesis
Dysphagia or feeding refusal
Apnea
Wheezing or stridor
Hoarseness
Cough

Diagnosis

Fluroskopi dg kontras Barium


Memeriksa pH esofagus
Radionuclide Gastro Esofagosgrafi
Biopsi esofagus
Keterlambatan waktu pengosongan
lambung

Diagnosis Banding

Hiatus hernia
Akhalasia
Stenosis pilorus hipertrofi kongenital
Obstruksi/ atresia duodenum
Mekonium ileus

Penatalaksanaan
80% kasus dapat teratasi dg intervensi minimal, sebelum
dipertimbangkan pembedahan
Pemberian ASI/SF dan posisi bayi, formula hipoalergi, anti
regurgitasi
Penambahan sereal
Farmakoterapi : antasida dan pelindung mukosa
( sukralfat), prokinetik ( domperidone,metoclopramide),
antagonis reseptor histamin H2 ( cimetidine, ranitidin),
inhibitor pompa proton ( omeprasol, lansopresol)
Pembedahan anti refluks : pd RGE dg komplikasi berat

Summary

Very common during 1st year of life


Reduced LES pressure or greater LES relaxation
GERD = Aspiration (chronic cough or wheeze),
Esophagitis, failure to thrive
Dx: Clinical, Esophageal pH probe, UGI series (anatomy)
Medical tx: Thickened feeds, position, acid
suppression, pro-kinetic agent
Surgical tx: Nissen fundoplication

Anatomy and Physiology


Swallowing reflex begins at
16 weeks gestation
Can suckle by 2nd to 3rd
trimester
34 weeks, infant can suckle
and feed normally
Pharyngeal phase earlier
developed
Oral preparatory phase
maldeveloped in premature
infants

Anatomy and Physiology

Infant larynx at C2-C3


Adult larynx at C5-C7
At 4 months, enlargement of oropharynx,
descent of larynx causes dysphagia
Chewing begins at 6 months
40% efficacy of chewing at 6 years

Anatomy and Physiology


Swallow divided into 4 phases

Oral preparatory phase


Oral transport phase
Pharyngeal phase
Esophageal phase

Anatomy and Physiology


Oral preparatory phase
Suckle in infant, mastication in child and adult
Soft palate meets base of tongue and epiglottis
allowing breathing during suckle

Oral transport phase


Anterior tongue propels bolus back to
oropharynx

Anatomy and Physiology


Pharyngeal phase

Vocal folds close


Arytenoid cartilages tilt up and forward
Base of tongue moves posteriorly
Epiglottis moves posteriorly
Soft palate closes off nasopharynx
Larynx elevates, cricopharyngeal muscle
relaxes

Anatomy and Physiology


Cough reflex
Present in 25% of children less than 5 days old
Tactile receptors present at highest
concentrations at larynx and bifurcations of
airway
C-fiber receptors respond to chemical stimuli
Stretch receptors present in bronchioles

Normal Daily GE Reflux

Hassall E 2005

Nelson SP 1998

20 GER episodes/24 hours are normal!!

Pathophysiology
The pathogenesis of GERD is involving

The frequency of reflux


Gastric acidity and gastric emptying
Esophageal clearing mechanisms
The esophageal mucosal barrier
Visceral hypersensitivity
Airway responsiveness

1.

PH (<4) in the refluxate

Diagnosis
Upper GI Series
The upper gastrointestinal (GI) series is neither
sensitive nor specific for the diagnosis of GER, but is
useful for the evaluation of the presence of anatomic
abnormalities, such as pyloric stenosis, malrotation
and annular pancreas in the vomiting infant, as well
as hiatal hernia and esophageal stricture in theolder
child.

Diagnosis
Esophageal pH Monitoring
Esophageal pH monitoring is a valid and
reliable measure of acid reflux.
Esophageal pH monitoring is useful to establish
the presence of abnormal acid reflux, and to
assess the adequacy of therapy in patients.
Esophageal pH monitoring may be normal in
some patients with GERD, particularly those
with respiratory complications.

Diagnosis
Endoscopy and Biopsy
Endoscopy with biopsy can assess the presence and
severity of esophagitis, strictures and Barretts
esophagus.
Exclude other disorders, such as Crohns disease
and eosinophilic or infectious esophagitis.
A normal appearance of the esophagus during
endoscopy does not exclude histopathological
esophagitis; subtle mucosal changes such as
erythema.

Management
Diet Changes in the Infant
There is evidence to support a one to two-week trial
of a hypoallergenic formula in formula fed infants with
vomiting.
Milk-thickening agents do not improve reflux index
scores but do decrease the number of episodes of
vomiting.

Management
Positioning in the Infant
Esophageal pH monitoring has demonstrated
that infants have significantly less GER when
placed in the prone position than in the supine
position. However, prone positioning is
associated with a higher rate of the sudden
infant death syndrome (SIDS). In infants from
birth to 12 months of age with GERD, the risk of
SIDS generally outweighs the potential benefits
of prone sleeping. Therefore, non-prone
positioning during sleep is generally
recommended.

Management
Positioning in the Infant
Supine positioning confers the lowest risk for SIDS
and is preferred.
Prone positioning during sleep is only considered in
unusual cases.
When prone positioning is necessary, it is particularly
important that parents be advised not to use soft
bedding, which increases the risk of SIDS in infants
placed prone.

Management
Positioning in the Child & Adolescent
In children older than one year it is likely that there is
a benefit to left side positioning during sleep and
elevation of the head of the bed.

Lifestyle Changes in the Child &


Adolescent
children and adolescents with GERD avoid caffeine,
chocolate and spicy foods that provoke symptoms.

Management
Acid-suppressant Therapy
Histamine-2 receptor antagonists (H2RAs) produce
relief of symptoms and mucosal healing.
Proton pump inhibitors (PPIs), the most effective
acid suppressant medications, are superior to H2RAs
in relieving symptoms and healing esophagitis.
Chronic antacid therapy is generally not
recommended since more convenient and safe
alternatives (H2RAs and PPIs) are available.

Management
Surgical Therapy
Surgery is often considered for the child with GERD
who has persistence of symptoms following medical
management or who is unable to be weaned from
medical therapy.
The Nissen fundoplication is the most popular of the
many surgical procedures that have been used.
Recently experience with laparoscopic procedures
has been reported. Results and complication rates
do not appear to vary by procedure.

Management
Prokinetic Therapy
Cisapride reduces the frequency of symptoms, including
regurgitation and vomiting.
The potential for serious cardiac arrhythmias in patients
receiving cisapride, appropriate patient selection and
monitoring as well as proper use, including correct
dosage (0.2mg/kg/dose QID) and avoidance of coadministration of contraindicated medications, are
important.
Other prokinetic agents have not been shown to be
effective in the treatment of GERD in child.

Gastro-Esophageal Reflux

Aim and Claim


1. Familiar with the
normal features and
assessment of
digestive system.
2. Get hold of the
examination of
digestive system.

Key points
The common symptoms of gastrointestinal
disease in childhood, its pathogenesis and
management
The presentation of common infections of
the gastrointestinal tract
Assessment for dehydration in a child with
diarrhoea and how to carry out rehydration
Chronic gastrointestinal disorders that can
lead to malabsorption and failure to thrive
Infections that can affect the liver

Normal Features and Assessment

Mouth: Foodstuffs broken down by chewing; saliva added


as lubricant
Oesophagus: Conduit between mouth and stomach
Stomach: Digestion of proteins; foodstuffs reduced to
liquid form; storage; sterilisation
Pancreas: Digestive enzymes for digestion of fats,
carbohydrates and proteins
Liver: Bile salts for digestion/absorption of fats in
small intestine
Gallbladder: Stores and concentrates bile
Small intestine: Final stages of chemical digestion and nutrient
absorption
Large intestine: Water absorption, bacterial
fermentation and formation of faeces

Severe key points


1.
2.
3.
4.

Normal function of the gastrointestinal tract


Oral feeding
Intestinal microflora
Stool :meconium, green-brown transition stool,
gold-like stool, orange-like stool
5. A palpable liver and a soft spleen tip
6. A protuberant abdomen in infant and toddlers

Examination Of The Gastrointestinal Tract

Examination of the gastrointestinal


tract 1
Systemic signs of dysfunction
Aneamia
Jaundice
Clubbing
Oedema
Distended vein
Dehydration

Examination of the gastrointestinal


tract 2
Exposure pelvic region dont miss
torsion of the testis or incarcerated hernia
Inspection of the abdomen
Palpation of the abdomen
Hernial orifices region
Scrotum and anal regions
Rectal examination





1 5

Abdominal Pain

Aim and Claim


Familiar with the causes acute abdominal
pain
Get hold of the causes of recurrent
abdominal pain

Acute Abdominal Pain


Trauma
Inflammation

Acute gastroenteritis
Appendicitis
Pancreatitis
Henoch-Schonlein Purpura

Anatomic

Bowel obstruction
Intussusception
Volvulus
Incarcerated hernia
Gallbladder disease

Extra-abdominal

Lower lobe pneumonia


Strep pharyngitis
DKA (diabetic ketoacidosis)
UTI/pyelonephritis
Renal stones

Gynecologic

PID (pelvic inflammatory disease)


Mittelschmerz
Dysmenorrhea
Ovarian cyst
Ectopic pregnancy

Acute Abdominal Pain


Evaluation

Careful history
- Quality/location/timing
- Relieving/aggravating
- Associated symptoms
Physical
Abdominal exams serial
Distention/BS
Rebound/rigidity/guardi
ng
Tenderness
Rectal exam
Pelvic exam

Abdominal X-ray
Flat:
Flatobstruction
perforation
Upright:
Upright
Specific imaging
CT scan
Ultrasound
Lab tests
CBC/diff, ESR, CRP
Urinalysis
Serum amylase/lipase

Recurrent Abdominal Pain


Inflammatory

Crohns Disease
Ulcerative Colitis
Celiac disease

Acid peptic disease

Esophagitis
Gastritis
Gastric/duodenal ulcer
GE Reflux

Anatomic
Intrabdominal tumor (Wilms,
neuroblastoma)
Meckels diverticulum
Malrotation

Bloating/gas/diarrhea
Lactose intolerance
Giardiasis

Functional 90%
Irritable Bowel Syndrome
FRAP

Vomiting
Aim and claim
Understand the causes of vomiting

Vomiting
Anatomic

Pyloric stenosis
Bowel obstruction
Malrotation
Intussusception
Ulcer
GE Reflux

Inflammatory

Gastroenteritis
Systemic infection
Appendicitis
Pancreatitis
Hepatitis
Milk protein allergy

Metabolic
Inborn errors
DKA

CNS
Increased ICP
Migraine

Post-tussive
Toxic ingestion
Chemotherapy
Pregnancy
Gastroparesis
Post-infectious
Neurologic impairment

Aim and claim

Familiar with the clinical features of


gastro-esophageal reflux
Get hold of the diagnosis of gastroesophageal reflux
Understanding management of gastroesophageal reflux

Vomiting
Evaluation
Bile-stained vomiting suggests obstruction distal
to ampulla of Vater
Abdominal plain film
Flat: look for dilated loops of bowel
Upright: look for free air under diaphragm

Contrast radiograph (UGI series, barium enema)


Electrolyte panel look for acidosis, disturbance
Other labs: UA, amylase/lipase, LFT
Appendicitis: CBC/diff, CT w/contrast

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