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GASTRO-ESOPHAGEAL REFLUX DISEASE


(GERD)

 Introduction:
Stomach is divided into four areas: Cardia, Fundus, Body and Pylorus. It has two valve-
like sphincters
1. LES –Lower esophageal sphincter: High pressure zone-Length 3-6 cm & Pressure of
about 20 mmHg • Pressure < than 6 mmHg favors GER • 20% of all reflux episodes occur
in relation to a decreased basal low resting LES pressure
2. Pyloric sphincter

 Definition:
Gastroesophageal reflux (GER), defined as passage of gastric contents into the
esophagus or retrograde movements of gastric contents across the lower esophageal
sphincter (LES) into the esophagus. Itis normal physiological process that occurs
throughout the day in healthy infants, children and adults.
The terms: –
 Regurgitation is defined as passage of refluxed gastric contents into the oral
pharynx.
 Vomiting is defined as expulsion of the refluxed gastric contents from the mouth.
 Gastroesophageal reflux disease (GERD) occurs when gastric contents reflux into
the esophagus or oropharynx and produce symptoms.
Most infants occasionally spit up throughout the day, whenregurgitation causes other
problems or is associated with other symptoms, it may be due to Gastro-esophageal Reflux
Disease (GERD), which can also occur in older children.

 Epidemiology:
According to a research study in 2011,
The prevalence of GERD was 22.2% in southern India.
Worldwide: 18.1- 27.8% in north America, 8.8-25.9% in Euope, and 2.% to 7.8% in East
Asia, as estimated from 28 studies.
(http://www.ncbi.nih.gov/pmc/articles/PMC4791779/

 Predisposing factors:
 Neurologic impairement (absence of LES tone, delayed gastric emptying and
decreased anoduodenal motor function)
 Hiatal hernia (it may weakens the lower esophageal sphincture)
 Repaired esophageal atresia (the esophagus is permanently defective in EA/TEF
patients even when successful repair, sometimes under tension has been achieved.
Extrinsic and intrinsic innervations are abnormal and consequently, motor function
and sphincters are defective.)
 Morbid obesity (due to excess belly fat causing pressure on the stomach)
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 Premature infants (abundant milk intake, supine posture, immature oesophageal


motility and poor oesophageal clearance of refluxate.)
 Infants with broncho-pulmonary dysplasia
 Scoliosis (anatomic changes in diaphragm)
 Asthma (coughing leads to increase intra-abdominal pressure)
 Cystic fibrosis (chronic cough cause extra pressure, overinflated lungs can cause
pressure on diaphragm)
 Cerebral palsy (impaired oral motor control results in difficulty controlling the
muscles in their mouth and throat.)

 Causes of GERD:
 Increased pressure on the abdomen (over eating, obesity, straining with stool due to
constipation, etc.).
 Decreased gastric emptying and reduced acid clearance from esophagus.
 Supine position
 Medications: diazepam, theophylline, methylxanthines (decrease sphincter tone)
 Poor dietary habits: like overeating, eating late at night.
 Food allergies, certain foods like greasy highly acidic.
 Some beverages may also be implicated in facilitating such pathological reflux.
 Neurodevelopmental disabilities: like cerebral palsy, Down syndrome etc.
 Tracheo-esophageal fistula

 Pathophysiology of GERD:
Overfeeding, overweight,
Increased abdominal pressure

Gastric distension

Low basal LES tone,


Defective LES motility,
increased TLESRs

Increase in GER

Impaired pH neutralization,
Delayed acid clearance,
poor mucosal resistance
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GERD

 Clinical manifestations of GERD:


In infants:
 Spitting up, regurgitation, vomiting (may be forceful)
 Excessive crying, irritability
 Sandifer syndrome- is an uncommon condition, characterized by repetitive
stretching and arching of the head and the neck. It represents a physiologic
neuromuscular response attempting to prevent acid refluxate from reaching the
upper portion of the esophagus.

 May be silent (no clinical signs observed)


 Weight loss, failure to thrive
 Respiratory problems (cough, wheeze, stridor, gagging, choking with feedings)
 Hematemesis
 Apnea or Apparent life threatening event (ALTE)

In children:
 Heartburn
 Abdominal pain
 Noncardiac chest pain
 Chronic cough
 Dysphagia
 Nocturnal asthma
 Recurrent pneumonia
 Abdominal and/or chest pain

 Diagnostic Approaches:
 History and Physical Examination: The history may be facilitated by
questionnaires (e.g. the infant gastro-esophageal reflux questionnaires)such as
1. How often the baby usually spit up?
 1 to 3 times per day 1
 3 to 5 times per day 2
 >5 times/day 3
2. How much the baby does usually spits up?
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1 teaspoonful to 1 tablespoon 1
1 tablespoon to 1 ounce 2
>1 ounce 3
3. Does the spitting up seem to be uncomfortable for the baby? 2
4. Does the baby refuse feeding eve when hungry? 1

 Barium Contrast Radiographic study of the esophagus and upper GI tract is


performed in children with vomiting and dysphagia to evaluate for achalasia,
esophageal strictures and stenosis, hiatal hernia and gastric outlet or intestinal
obstruction.
 Esophageal pH Monitoring: The 24-hours intra-esophageal pH monitoring is the
gold standard in the diagnosis of GER. The most important indications for
esophageal pH monitoring are for assessing efficacy of acid suppression during
treatment, evaluating apneic episodes in conjunction with a pneumogram and
perhaps impedance, and evaluating atypical GERD presentations such as chronic
cough, stridor and asthma.Probe inserted acc to length calculated by strobel’s
formula {length from nares to LES (cm)= 5+ 0.252 X (height)}. All medications
discontinued 72 hrs before test.
 Multichannel Intraluminal Impedanceis a cumbersome test, but with potential
applications both for diagnosing GERD and for understanding esophageal function
in term of bolus flow, and, volume clearance, and motor patterns associated with
GERD.
 Combined 24 hr multiple intraluminal impedance and pH monitoring detects
acid, weakly acid and nonacid reflux episodes. It is thus superior to pH monitoring
alone which detects only acid reflux episodes. Its main utility is to evaluate the
temporal relationship between symptoms and GER episodes.
 Endoscopy with biopsymay be helpful to assess the presence and severity of
esophagitis, strictures and barrett esophagus and to exclude other disorders such as
Crohn disease.Upper GI endoscopy may show erosions or mucosal breaks in the
distal esophageal mucosa, the most reliable evidence of reflux esophagitis. Mucosal
erythema and pallor are highly subjective and nonspecific findings. Complications
like stricture esophagus and Barrett's esophagus can be picked up at endoscopy.
Histological features like elongated rete pegs, basal cell layer hyperplasia and
dilated intercellular spaces, alone or in combination, are suggestive of reflux
esophagitis.
 Scintigraphy(gastroesophageal) detects radioactive substances in the esophagus
after a feeding of the compound and assess gastric emptying. It can differentiate
between aspiration of gastric contents from reflux vs. aspiration from poor
oropharyngeal muscle coordination.
 A modified barium swallow study with video fluoroscopy may also be used as a
diagnostic tool for this condition.
 Empiric trial of acid suppression: Using proton pump inhibitors for up to 4 weeks
is justified in older children or adolescents with typical symptoms suggesting GERD
(heart burn or chest pain). There is no evidence to support its use as a diagnostic test
in infants and young children where symptoms of GERD are less specific.
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 Management:
Treatment of GERD depends on patient's age and nature and severity of symptoms and
includes lifestyle changes, pharmacologic therapy and surgery.

Lifestyle changes
 Parental education, guidance and support are essential and usually sufficient to
manage healthy, thriving infants with symptoms due to physiologic GER.
 Infants should be placed in left lateral position with the head end elevated by 30°
in the postprandial period to reduce the frequency of reflux.
 Cow milk protein allergy is sometimes a cause of unexplained crying and
vomiting in infants. Therefore, formula-fed infants with recurrent vomiting may
benefit from a 2-4 weeks trial of an extensively hydrolyzed protein formula.
 Adding thickening agents such as rice cereal (one tablespoon, i.e. -10 gin 60 ml
milk) to formula does not decrease the time with pH <4 (reflux index) measured by
esophageal pH studies, but it does decrease the frequency of overt regurgitation.
Infants with inadequate weight gain because of losses by regurgitation may benefit
from increasing the energy density of formula. Careful followup with charting of
caloric intake and weight gain is essential.

 For children and adolescents with GERD, measures that are useful include: dietary
modification (to avoid caffeine, chocolate and spicy foods), weight loss if obese,
sleeping in the left lateral position with elevation of the head-end of the bed,
avoidance of alcohol and cessation of smoking.

Pharmacological therapies:
 Medications used for GERD include agents to buffer or suppress gastric acid
secretion.
 Proton Pump Inhibitors (PPis) Acts by blocking enzyme system
i.e.H+K+ATPase, which is found at acid secretory surface of parietal cells that
mediates final transport of H+ ions in exchange of K+ into gastric lumen. PPis are
the agent of choice for GERD. PPI maintain intragastric pH for long periods and
inhibit meal-induced acid secretion. PPis currently approved for use in children are
omeprazole (0.7-3.3 mg/ kg/day, max 80 mg), lansoprazole (0.6-1.6 mg/kg/day;
weight <30 kg: 15 mg, >30 kg: 30 mg; max 60 mg) and esomeprazole (<20 kg: 5-10
mg, >20 kg: 10-20 mg OD).

 H2RA (H2 Receptor Antagonist): These block H2 receptors on parietal cells, and
antagonize normal stimulatory effect of histamine on acid secretion e.g. Ranitidine,
Famotidine. Inhibit acid production by reversibly competing with histamine for
binding to H2 receptors on the basolateral membrane of parietal cells. Inhibit basal
and stimulated acid secretion, which accounts for their efficacy in suppressing
nocturnal acid secretion. These are considered one of the best option for the
treatment of GERD and APD in children because of their excellent safety profile.
-
The duration was reduced by 90% for gastric pH <4
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- Suppress acid production > 90% within 45 minutes.

 Ranitidine 5 mg/kg per dose orally has been shown to increase gastric pH for 9 to
10 hours in infants, very useful for infants who need persistent acid suppression.

 Antacid therapy is not recommended for most patients with GERD. Currently, there
is insufficient evidence to justify the routine use of prokinetic or other agents such
as cisapride, metoclopramide, domperidone, bethanechol, erythromycin or baclofen
for GERD.

Surgical therapy:
Nissen fundoplication is the most common surgical procedure, which is performed
laparoscopically with outcomes of decreased time to feedings, better cosmetic results, less
pain and fewer complications. This surgery involves passage of the gastric fundus behind
the esophagus to encircle the distal esophagus. Long-term complications include
breakdown of the wrap, small bowel obstruction, gas-bloat syndrome, infection, retching
and dumping syndrome.

Nursing management:

Nursing Diagnosis for Gastro-esophageal Reflux Disease (GERD)

1. Deficient Fluid Volume related to input, nausea and vomiting / excessive spending.
2. Acute pain related to inflammation of the esophagus lining.
3. Imbalanced Nutrition: less than body requirements related to anorexia, nausea,
vomiting.
4. Risk for Impaired Gas Exchange
5. Risk for Impaired Home Maintenance
6. Risk for Aspiration related to barriers to swallow, decreased reflux larynx and
glottis to liquid reflux.
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7. Ineffective airway clearance related to fluid reflux into the larynx and throat.
8. Impaired swallowing related to narrowing / stricture of the esophagus due to
gastroesophageal reflux disease.
9. Anxiety related to the disease process.

Nursing care is directed at

Nursing Interventions for Gastroesophageal Reflux Disease (GERD)

1. Increase fluid intake and adequate nutrition.

 Keep head of bed at a position 60 degrees for 30 minutes to 40 minutes.


 Give food a little but often 2 to 3 hours.
 Thicken the milk with cereal.
 Give dinner.
 Measure weight each morning.
 Monitor intake and output.

2. Observe and report any signs of respiratory distress, assess for changes in respiratory
status.

3. Before the surgery is done to prepare the client and family for surgery.

4. Monitor the operating side to wholeness.

5. Prevent abdominal distension.

 Maintain patency of a nasogastric tube (NG) or gastrostomy, if installed.


 Check hose NG position.
 Auscultation bowel sounds.

6. Monitor for signs and symptoms of postoperative hemorrhage.

 Decreased blood pressure and increased pulse apex.


 Blood in NG drainage.
 Drainage like coffee grounds would exist in the first 24 hours.

7. Help the parents to express feelings or frustration because they feel responsible or not
enough help.

8. Give the stimulation activity.

 Discharge planning and home care.


 Encourage parents about drug administration.
 Encourage parents about feeding.
 Encourage parents to report any vomiting or presence of fresh blood

Complications:
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 Esophagitis
 Esophageal stricture (due to prolonged esophagitis)
 Laryngitis
 Recurrent pneumonia
 Anemia
 Barret esophagus (long-standing esophagitis predisposes to metaplastic
transformation of the normal esophageal squamous epithelium into intestinal
columnar epithelium)
 Adenocarcinoma (due to persistent barret esophagus)

Bibliography:

 Paul K Vinod, Bagga Arvind; Ghai Essential Pediatrics; Edition 8 th; published by
CBS Publishers and distributors Pvt. Ltd; page referred: 280-282.
 Kliegman et al; Nelson Textbook of Pediatrics; Edition 21 st; published by Elsevier;
page referred: 1934-1938.
 Wilson David, Hockenberry J. Marilyn; Wong’s Essentials of pediatric nursing, first
south asia edition, published by Elsevier, page referred: 668-670.
 https://www.slideshare.net/mobile/drtakvani/gastroesophageal-reflux-disease-in-
children

GER and Asthma:


GERD and Asthma Coexistence seem to be more frequent than would be expected for a
chance occurrence.
Does Asthma Trigger GERD?
Proposed Mechanisms
Coughing

Asthma
Medications
Increase Intra-
abdominal Pressure

Lower the
Increasing Pressure Gradient pressure of
across the LES LES

GERD

Does GERD Trigger Asthma?


Reflux Theory
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Direct contact between gastric refluxate and lung tissues

Inflammation of the airway

Bronchial smooth muscle reactivity

Reflex Theory

Esophagus and bronchial tree have


identical embryological derivation

Share common innervation (via vagus


nerve) and common reflexes

Stimulation of receptors in distal


esophagus by reflux

Leads to vagal reflux Producing bronchial


constriction and/or cough

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