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Gastroesophageal reflux
Dr. Adnan Hamawandi
Professor of pediatrics
GER
 This is a common disorder encountered in
pediatric practice. It is considered a
developmental variation in gastrointestinal
motility that resolves as the infant matures.
 When GER is unusually sever, persists
beyond 18 months of age or is associated
with complications it is considered pathologic
“GERD” and requires appropriate diagnostic
and therapeutic management.
GER- clinical features
 Vomiting may occur immediately or hours
after feeding which is usually effortless and
painless, consisting of small amount of
curdled formula. The vomiting is always
non-bilious and rarely contains blood.
In the older child a tendency to vomit easily,
heartburn, dysphagia, halitosis, and loss of
dental enamel may occur.
GER-Complications
 Persistent GER leads to a number of
complications:-
1.Blood loss and anemia. 2. Failure to thrive.
3.Peptic esophagitis. 4.Esophageal stricture.
5.Barrett’sesophagus.
6.Aspiration pneumonia and
bronchoconstriction.
GERD- Diagnosis
 History and physical examination.
 Barium swallow - anatomic abnormalities.
 Overnight PH monitoring for assessing and
quantitating GER.
 Esophageal manometry measures resting
lower end esophageal pressure in addition to
esophageal motility.
 Endoscopy visualizes mucosa + biopsy
GER-Therapy
 Conservative
1. Positioning
2. Dietary changes.
 Drugs, antacid, H2 receptors antagonist, and
proton pump inhibitors.
 Surgery
Peptic Ulcer disease
 In children less than 6 years of age ulcers
are found with equal frequencies in boys and
girls, a gastric location as common as
duodenal, and a precipitating factor is
common.
 In children older than 6 years ulcers are
more frequent in boys and more frequently
found in the duodenum.
Peptic ulcer- clinical features
 In neonates, bleeding and perforation are the
usual presentations in association with other
underlying problems like sepsis, asphyxia or
respiratory distress. Older infants and
toddlers frequently vomit and eat poorly.
Bleeding is also common with equal
frequency of primary and secondary ulcers.
 In older children pain becomes more
important feature, in addition to bleeding.
Peptic ulcer-Diagnosis
 Endoscopic evaluation of the upper
gastrointestinal tract is preferred because of
higher sensitivity in detecting pathology
compared with contrast radiology. In addition
endoscopy allows for tissue biopsy and
evaluation of pattern of inflammation and
possible infection ( H.pylori).
Peptic ulcer-Therapy
 If the ulcer is secondary to an underlying
disease, the predisposing factor must be
dealt with properly.
 The management of the ulcer itself is
directed against gastric acid either through
neutralization via antiacid or suppression of
secretion via H2 receptor antagonist or
proton pump inhibitors.
Peptic ulcer-Therapy
 Sucralfate can be of benefit by binding to the
ulcerated area and possible cytoprotective
properties.
 Documented H. pylori infection should be
treated.
Hypertrophic pyloric stenosis
 Occurs in about 1 in every 500 infant with
male to female ratio of 4:1.
 Symptoms begin between 2 and 4 weeks of
age as projectile non-bilious vomiting.
Constipation and poor weight gain may be
observed when the diagnosis is delayed.
After vomiting the infant is hungry and wants
to feed again.
Congenital pyloric stenosis
 As the vomiting continues a progressive loss
of fluid, hydrogen ion and chloride leads to
hypochloremic metabolic alkalosis. Serum
potassium levels are usually maintained but
there may be total body potassium depletion.
Congenital pyloric stenosis- diagnosis
 Can be established by palpation of the
pyloric mass, a firm, mobile, olive shaped
about 2cm in length best palpated from the
left side and located above and to the right of
the umbilicus in the midepigastrium beneath
the liver edge.
 If the mass cannot be palpated U/S confirms
the diagnosis in majority of cases.
Congenital pyloric stenosis- diagnosis
 Criteria for diagnosis include pyloric mass
thickness > 4mm or an overall pyloric length
greater than 14mm.
 Barium studies when performed show an
elongated pyloric channel, a bulge of pyloric
muscles in the antrum ( shoulder sign), and
parallel streaks of barium seen in the
narrowed channel “ double tract sign”
Congenital pyloric stenosis- treatment
 Correction of fluid, acid base and electrolyte
losses with 0.5-0.9% saline in 5-10% glucose
with 40meq/L Potassium chloride.
 Surgery “ Ramstedt’s” Pyloromyotomy.

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Pediatrics 5th year, 6th lecture (Dr. Adnan)

  • 1. Gastroesophageal reflux Dr. Adnan Hamawandi Professor of pediatrics
  • 2. GER  This is a common disorder encountered in pediatric practice. It is considered a developmental variation in gastrointestinal motility that resolves as the infant matures.  When GER is unusually sever, persists beyond 18 months of age or is associated with complications it is considered pathologic “GERD” and requires appropriate diagnostic and therapeutic management.
  • 3. GER- clinical features  Vomiting may occur immediately or hours after feeding which is usually effortless and painless, consisting of small amount of curdled formula. The vomiting is always non-bilious and rarely contains blood. In the older child a tendency to vomit easily, heartburn, dysphagia, halitosis, and loss of dental enamel may occur.
  • 4. GER-Complications  Persistent GER leads to a number of complications:- 1.Blood loss and anemia. 2. Failure to thrive. 3.Peptic esophagitis. 4.Esophageal stricture. 5.Barrett’sesophagus. 6.Aspiration pneumonia and bronchoconstriction.
  • 5. GERD- Diagnosis  History and physical examination.  Barium swallow - anatomic abnormalities.  Overnight PH monitoring for assessing and quantitating GER.  Esophageal manometry measures resting lower end esophageal pressure in addition to esophageal motility.  Endoscopy visualizes mucosa + biopsy
  • 6. GER-Therapy  Conservative 1. Positioning 2. Dietary changes.  Drugs, antacid, H2 receptors antagonist, and proton pump inhibitors.  Surgery
  • 7. Peptic Ulcer disease  In children less than 6 years of age ulcers are found with equal frequencies in boys and girls, a gastric location as common as duodenal, and a precipitating factor is common.  In children older than 6 years ulcers are more frequent in boys and more frequently found in the duodenum.
  • 8. Peptic ulcer- clinical features  In neonates, bleeding and perforation are the usual presentations in association with other underlying problems like sepsis, asphyxia or respiratory distress. Older infants and toddlers frequently vomit and eat poorly. Bleeding is also common with equal frequency of primary and secondary ulcers.  In older children pain becomes more important feature, in addition to bleeding.
  • 9. Peptic ulcer-Diagnosis  Endoscopic evaluation of the upper gastrointestinal tract is preferred because of higher sensitivity in detecting pathology compared with contrast radiology. In addition endoscopy allows for tissue biopsy and evaluation of pattern of inflammation and possible infection ( H.pylori).
  • 10. Peptic ulcer-Therapy  If the ulcer is secondary to an underlying disease, the predisposing factor must be dealt with properly.  The management of the ulcer itself is directed against gastric acid either through neutralization via antiacid or suppression of secretion via H2 receptor antagonist or proton pump inhibitors.
  • 11. Peptic ulcer-Therapy  Sucralfate can be of benefit by binding to the ulcerated area and possible cytoprotective properties.  Documented H. pylori infection should be treated.
  • 12. Hypertrophic pyloric stenosis  Occurs in about 1 in every 500 infant with male to female ratio of 4:1.  Symptoms begin between 2 and 4 weeks of age as projectile non-bilious vomiting. Constipation and poor weight gain may be observed when the diagnosis is delayed. After vomiting the infant is hungry and wants to feed again.
  • 13. Congenital pyloric stenosis  As the vomiting continues a progressive loss of fluid, hydrogen ion and chloride leads to hypochloremic metabolic alkalosis. Serum potassium levels are usually maintained but there may be total body potassium depletion.
  • 14. Congenital pyloric stenosis- diagnosis  Can be established by palpation of the pyloric mass, a firm, mobile, olive shaped about 2cm in length best palpated from the left side and located above and to the right of the umbilicus in the midepigastrium beneath the liver edge.  If the mass cannot be palpated U/S confirms the diagnosis in majority of cases.
  • 15. Congenital pyloric stenosis- diagnosis  Criteria for diagnosis include pyloric mass thickness > 4mm or an overall pyloric length greater than 14mm.  Barium studies when performed show an elongated pyloric channel, a bulge of pyloric muscles in the antrum ( shoulder sign), and parallel streaks of barium seen in the narrowed channel “ double tract sign”
  • 16. Congenital pyloric stenosis- treatment  Correction of fluid, acid base and electrolyte losses with 0.5-0.9% saline in 5-10% glucose with 40meq/L Potassium chloride.  Surgery “ Ramstedt’s” Pyloromyotomy.