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Seminar
On
“APPROACH TO GERD IN CHILDREN”
Presented by
Vijay kr. Singh
DNB PGT (Pediatrics)
Under guidance of
Dr T K MAITY
MD(PEDIATRICS)
Consultant physician M R Bangur Hospital
Date 23rd march 2013
Venue
DNB Seminar hall M R Bangur hospital Kolkata-33
APPROACH TO
GERD IN
CHILDREN
ANATOMY AND PHYSIOLOGY
 Esophagus begins at lower border of cricoids
cartilage.
 It develops from foregut and is recognizable by
third week of gestation.
 Food or fluid delivered from the esophagus to the
stomach, swallowing must be accompanied by a
coordinated wave of peristaltic contractions
It is lined by four layers
Mucosa- stratified squamous non
keratinized epithelium
Sub mucosa- mucous glands and
lymphoid tissue
Muscularis externa
Adventitia
Lower esophageal sphincter
 It is not a true anatomical sphincter.
 The lower 3-4 cm smooth circular muscle
fibers form LES.
 Its remain tonic activity prevent reflux of
gastric contain into stomach.
 The tone of LES is under control of
parasympathetic neural control.
 The tone of LES is also under influenced of
gastric hormone
Mechanism which prevent gastro
esophageal reflux
 Tonic activity of LES
 Valve like mechanism of short portion of
esophagus that extend into the diaphragm
 Fibres of crural portion of diaphragm surround
esophagus at the lower end which prevent
reflux
Introduction
 Gasrtroesophageal reflux disease is the most common
esophageal disorder in children.
 Gastroesophageal reflux signified the retrograde
movement of gastric contents across the lower
esophageal sphincter .
 The regurgitation is normal in infant,
 The phenomenon becomes pathological GERD in children
who have more frequent and persistent.
 It produce esophageal symptoms or have respiratory
symptoms.
Prevalence
 Infant reflux becomes evident in the 1st few months
of life.
 Peaks at 4months, at 12 months it resolves upto
88% and nearly all up to 24 months.
 Prevalence of GERD in the infant range from 1 to
8%.
 85% of premature infant have GERD, with upto 10%
of them having extra intestinal manifestations like
bradicardia and apnea.
Path physiology of reflux
 A well- coordinated relaxation of the lower
esophageal sphincter is essential for the
transport of food into stomach.
 Basal LES pressure is maintained above
4mmHg to prevent reflux.
 Pressure theory is disproved by many pressure
studies.
 Reflux is primarily due to Transient LES relaxation.
 TLESR occur independent of swallowing, reduce LES
pressure to 0-2mm Hg and last for>10 seconds, and
they appears by 26 wks of gestation.
 A vaso vagal reflex, composed of afferent
mechanoreceptors in the proximal stomach, a brain
stem pattern generated, and efferent in the LES,
regulates TLESRs.
 Gastric distention the main stimulus for TLESRs.
 The pathogenesis of reflux in premature infant is not
well understood.
Symptoms and manifestation
In Infant
 Vomiting
 Poor weight gain
 Irritability
 Feeding refusal
 Recurrent pneumonia
 Asthma or any upper respiratory tracts symptoms
 Apnea
children
Heartburn and retrosternal chest pain.
Dysphasia.
Regurgitation.
Asthma and chronic cough.
Recurrent pneumonia.
Anemia and haemetemesis.
Sandifer’s syndrome.
Conditions predisposing to severe
GERD
Obesity
 Neurological impairment
Rep. aired trachea- esophageal fistula
Congenital diaphragmatic hernia
 Chronic lung disease
Significant prematurity
Diagnostic approach to GERD
 History and physical examination suffice the
diagnosis.
 Evaluation aims to identify the positive
support of the diagnosis.
 The history standardized by ORENSTIEN’S
questionnaireI-GERQ and its derivatives I-
GERQ-R
Esophageal pH monitoring
 Ph monitoring help to establish the presence
of acid reflux Ph <4.
 It assess the efficacy of treatment.
 It is non-invasive and done in any age group.
 It does not measure the non –acid and weakly
acidic reflux.
Multichannel intraluminal -
impedance measurement
It detect the change in the electrical
resistance that occur during the passage
of a bolus of gas or liquid .
This study detects both acid and non acid
reflux and direction of reflux.
The limitation of the procedure is – high
cost, limited availability
Endoscopy
Upper GI endoscopy is the best method
of detecting esophagitis.
 Normal endoscopy does not rule out
GERD.
This type of GERD is called non-erosive
reflux.
Advantages of endoscopy
 It gives direct information about the presence of
esophagitis.
 Detects complications like ulcer, stricture, Barrett’s
esophagitis.
 Endoscopic biopsy help to exclude other cause of
esophagitis.
 Histology is more sensitive than endoscopy in the
early stage. Erosive esophagitis is the most definite
evidence of GERD on endoscopy.
Barium UGI series
This test is useful to detect anatomical
abnormalities but it is not useful in
diagnosis of GERD.
The sensitivity and specificity is less
than 50%.
Nuclear scintigraphy
Nuclear scintigraphy has poor sensibility and
specificity.
Used in recurrent aspiration pneumonia.
 Retention of radioactivity in lung beyond 24
hours suggests GERD .
Nuclear scintigraphyis not recommended for
the routine evaluation.
MANAGEMENT
GER in infant (Happy splitters)
Counseling and natural history of GER in infant
to be explained to the parents or care givers.
It is advised to give small and frequent
feeding .
 Thickening of feed.
GERD in children
Acid suppressants- GERD need acid
suppression therapy for 12weeks.
Proton pump inhibiter is more potent than H2
blocker.
Neutralizing agent- Useful in symptomatic
relief of heartburn.
Not for long term due to risk of side effects.
Prokinetics
There is insufficient evidence to justify the
role of prokinetics in management of GERD.
 It is only indicated in GERD associated with
gastro paresis.
Duration of therapy
PPI therapy is recommended for at least
12weeks .
Taper over 2 to 3 months to prevent rebound
hyperacidity .
 If there is no improvement in 4 weeks then
the dose of PPI need to be increased.
Surgery
Nissen fundoplication may be of
beneficial in children with confirmed
GERD who have failed optimal medical
therapy.
Bronchial asthma and GERD
The clinical association of bronchial
asthma and GERD is very strong.
 Causal relationship between these two
entities has no yet established.
Persistent asthma with
symptomatic GERD
It can be treated with a clear explanation given
to the parents.
 Reflux symptoms will improve but chance of
improvement of asthma is remote.
GERD in neurologically impaired
children
Prevalence of GERD in neurological impaired
children is 50% higher than normal child .
The prevalence of erosive esophagitis about
30 to 70%.
This group of children needs prolonged
treatment and often surgery.
Conclusion
 GER is common in infant.
 Most infant have physiological reflux and need
minimal intervention.
 Symptoms resolve by 18 months of age.
 No gold standard test for GERD diagnosis
 Medical therapy with PPI is very effective and safe.
 Surgical therapy is not recommended because of its
morbidity and often fails in those who need it most.
Gerd in children and its treatment

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Gerd in children and its treatment

  • 1. Seminar On “APPROACH TO GERD IN CHILDREN” Presented by Vijay kr. Singh DNB PGT (Pediatrics) Under guidance of Dr T K MAITY MD(PEDIATRICS) Consultant physician M R Bangur Hospital Date 23rd march 2013 Venue DNB Seminar hall M R Bangur hospital Kolkata-33
  • 3. ANATOMY AND PHYSIOLOGY  Esophagus begins at lower border of cricoids cartilage.  It develops from foregut and is recognizable by third week of gestation.  Food or fluid delivered from the esophagus to the stomach, swallowing must be accompanied by a coordinated wave of peristaltic contractions
  • 4.
  • 5. It is lined by four layers Mucosa- stratified squamous non keratinized epithelium Sub mucosa- mucous glands and lymphoid tissue Muscularis externa Adventitia
  • 6. Lower esophageal sphincter  It is not a true anatomical sphincter.  The lower 3-4 cm smooth circular muscle fibers form LES.  Its remain tonic activity prevent reflux of gastric contain into stomach.  The tone of LES is under control of parasympathetic neural control.  The tone of LES is also under influenced of gastric hormone
  • 7. Mechanism which prevent gastro esophageal reflux  Tonic activity of LES  Valve like mechanism of short portion of esophagus that extend into the diaphragm  Fibres of crural portion of diaphragm surround esophagus at the lower end which prevent reflux
  • 8.
  • 9. Introduction  Gasrtroesophageal reflux disease is the most common esophageal disorder in children.  Gastroesophageal reflux signified the retrograde movement of gastric contents across the lower esophageal sphincter .  The regurgitation is normal in infant,  The phenomenon becomes pathological GERD in children who have more frequent and persistent.  It produce esophageal symptoms or have respiratory symptoms.
  • 10. Prevalence  Infant reflux becomes evident in the 1st few months of life.  Peaks at 4months, at 12 months it resolves upto 88% and nearly all up to 24 months.  Prevalence of GERD in the infant range from 1 to 8%.  85% of premature infant have GERD, with upto 10% of them having extra intestinal manifestations like bradicardia and apnea.
  • 11. Path physiology of reflux  A well- coordinated relaxation of the lower esophageal sphincter is essential for the transport of food into stomach.  Basal LES pressure is maintained above 4mmHg to prevent reflux.  Pressure theory is disproved by many pressure studies.
  • 12.  Reflux is primarily due to Transient LES relaxation.  TLESR occur independent of swallowing, reduce LES pressure to 0-2mm Hg and last for>10 seconds, and they appears by 26 wks of gestation.  A vaso vagal reflex, composed of afferent mechanoreceptors in the proximal stomach, a brain stem pattern generated, and efferent in the LES, regulates TLESRs.  Gastric distention the main stimulus for TLESRs.  The pathogenesis of reflux in premature infant is not well understood.
  • 13. Symptoms and manifestation In Infant  Vomiting  Poor weight gain  Irritability  Feeding refusal  Recurrent pneumonia  Asthma or any upper respiratory tracts symptoms  Apnea
  • 14. children Heartburn and retrosternal chest pain. Dysphasia. Regurgitation. Asthma and chronic cough. Recurrent pneumonia. Anemia and haemetemesis. Sandifer’s syndrome.
  • 15. Conditions predisposing to severe GERD Obesity  Neurological impairment Rep. aired trachea- esophageal fistula Congenital diaphragmatic hernia  Chronic lung disease Significant prematurity
  • 16. Diagnostic approach to GERD  History and physical examination suffice the diagnosis.  Evaluation aims to identify the positive support of the diagnosis.  The history standardized by ORENSTIEN’S questionnaireI-GERQ and its derivatives I- GERQ-R
  • 17. Esophageal pH monitoring  Ph monitoring help to establish the presence of acid reflux Ph <4.  It assess the efficacy of treatment.  It is non-invasive and done in any age group.  It does not measure the non –acid and weakly acidic reflux.
  • 18. Multichannel intraluminal - impedance measurement It detect the change in the electrical resistance that occur during the passage of a bolus of gas or liquid . This study detects both acid and non acid reflux and direction of reflux. The limitation of the procedure is – high cost, limited availability
  • 19. Endoscopy Upper GI endoscopy is the best method of detecting esophagitis.  Normal endoscopy does not rule out GERD. This type of GERD is called non-erosive reflux.
  • 20. Advantages of endoscopy  It gives direct information about the presence of esophagitis.  Detects complications like ulcer, stricture, Barrett’s esophagitis.  Endoscopic biopsy help to exclude other cause of esophagitis.  Histology is more sensitive than endoscopy in the early stage. Erosive esophagitis is the most definite evidence of GERD on endoscopy.
  • 21. Barium UGI series This test is useful to detect anatomical abnormalities but it is not useful in diagnosis of GERD. The sensitivity and specificity is less than 50%.
  • 22. Nuclear scintigraphy Nuclear scintigraphy has poor sensibility and specificity. Used in recurrent aspiration pneumonia.  Retention of radioactivity in lung beyond 24 hours suggests GERD . Nuclear scintigraphyis not recommended for the routine evaluation.
  • 24. GER in infant (Happy splitters) Counseling and natural history of GER in infant to be explained to the parents or care givers. It is advised to give small and frequent feeding .  Thickening of feed.
  • 25. GERD in children Acid suppressants- GERD need acid suppression therapy for 12weeks. Proton pump inhibiter is more potent than H2 blocker. Neutralizing agent- Useful in symptomatic relief of heartburn. Not for long term due to risk of side effects.
  • 26. Prokinetics There is insufficient evidence to justify the role of prokinetics in management of GERD.  It is only indicated in GERD associated with gastro paresis.
  • 27. Duration of therapy PPI therapy is recommended for at least 12weeks . Taper over 2 to 3 months to prevent rebound hyperacidity .  If there is no improvement in 4 weeks then the dose of PPI need to be increased.
  • 28. Surgery Nissen fundoplication may be of beneficial in children with confirmed GERD who have failed optimal medical therapy.
  • 29. Bronchial asthma and GERD The clinical association of bronchial asthma and GERD is very strong.  Causal relationship between these two entities has no yet established.
  • 30. Persistent asthma with symptomatic GERD It can be treated with a clear explanation given to the parents.  Reflux symptoms will improve but chance of improvement of asthma is remote.
  • 31. GERD in neurologically impaired children Prevalence of GERD in neurological impaired children is 50% higher than normal child . The prevalence of erosive esophagitis about 30 to 70%. This group of children needs prolonged treatment and often surgery.
  • 32. Conclusion  GER is common in infant.  Most infant have physiological reflux and need minimal intervention.  Symptoms resolve by 18 months of age.  No gold standard test for GERD diagnosis  Medical therapy with PPI is very effective and safe.  Surgical therapy is not recommended because of its morbidity and often fails in those who need it most.