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Gastroesophageal
     Reflux
Esophageal Structure and Function


The esophagus is a hollow muscular tube coursing
through the posterior mediastinum joining the
hypopharynx to the stomach with a sphincter at
each end. It functions to transport food and fluid
between these ends, otherwise remaining empty.
Gastroesophageal Reflux
2 conditions for Reflux Episode to occur:

       1. Gastro-intestinal contents must be “ready”
       to reflux

       2. The anhireflux mechanism at the lower end of
       the esophagus must be compromised.

      Gastro-intestinal contents are most
      likely to reflux
1. When gastric volume is increased

       . after meals
       . in the presence of pyloric obstruction
       or gastric stasis syndrome
       . in acid hypersecretory states
2. When gastric contents are located near the
gastroesophageal due to:

       . Recumbence
       . bending down
       . Presence of hiatus hernia

3. When gastric pressure is increased

       . Obesity
       . Pregnancy
       . Ascitis
       . Tight binders/ girdles

 Normal antireflux mechanism

 Consist of LES and the anatomic configuration of
 gastroesophageal junction.
Situations that predisposes to
gastroesophageal reflux:

   1.   Reflux occur when the gradient of pressure
        between LES and the stomach is lost.

   2. It can be caused by increased intragastric
      pressure or by transient or sustained decrease
      in LES tone.

   3.   Decrease in sphincter tone maybe due to
        muscle weakness.

   4.   Inappropriate sphincter relaxation mediated by
        inhibitory nerves.
5. Secondary causes of

. LESIncompetence include

      5.1 Scleroderma- like diseases

      5.2 Myopathic type of chronic intestinal
      pseudoobstrution syndrome

      5.3 pregnancy

      5.4 smoking

      5.5 smooth muscle relaxant
      Ex.    Beta-adrenergenic agents
             Aminoplylline
             Nitrates
             Calcium channel blockers
6. Destruction of Sphinter by

       6.1 Surgical Resection

       6.2 Myotomy

       6.3 Baloon dilatation

       6.4 Esophagitis

7. Abnormal activity of the diaphragmatic crural muscles
which surrounds the esophageal hiatus in the diaphragm.

8. Changes in hiatal hernia.
Complications of Reflux:


1.   Esophagitis- develops when mucosal defenses that
     normally counteract the effect of the injurious agents on
     esophageal mucosa succumb to the onslaught of refluxed
     acid pepsin or bile.


Causing:       . Erosive esophagitis
               . Peptic stricture
               . Replacement of Squamous epithelium of
               esophagus by columnar epithelium ( Barret’s
               esophagus)
Major Esophageal Symtoms are:

1. Heartburn (pyrosis)- a discomfort or burning sensation behind
the sternum that arises the epigastrium and may radiate toward
the neck. Heartburn is an intermittent symptoms, most commonly
experienced after eating, during exercise, and while lying
recumbent.


2. Regurgitation- effortless return of food or fluid into the
pharynx without nausea or retching. Patients report a sour or
burning fluid in the
Throat or mouth that may also contain undigested food
particles. Bending, belching, or maneuvers that increase
intraabdominal pressure can provoke regulation.
3. Chest pain- is a common esophageal symptoms with
characteristics similar to cardiac pain, which closely mimics angina
pectoris. Features suggesting esophageal pain include pain that is
nonexertional, prolonged, interrupts sleep, is meal-related, is
relieved with antacids, and is accompanied by heartburn,
dysphagia, or regurgitation.


4. Esophageal dysphagia- a feeling of food “sticking” or even logging
in the chest.


5. Odynophagia- is pain either caused by or exacerbated by
swallowing. Odynophagia is more common with pill or infectious
esophagitis than with reflux esophagitis and should prompt a
search for these entities. When odynophagia does occur in GERD,
it is likely related in an esophageal ulcer or deep erosion.
Diagnostic Test

Endoscopy- also known as esophagogastroduodenoscopy EGD is
the best for the evaluation of the proximal gastrointestinal tract.


Radiography       –       Contrast       radiography of    the
esophagus, stomach, and duodenum can demonstrate barium
reflux,             hiatal              hernia,         mucosal
granularity, erosions, ulceration, and strictures.
Endoscopic ultrasound (EUS) -        instrument combine an
endoscope with an ultrasound transducer to create a
transmural image of the tissue surrounding the endoscope tip.
The key advantage of EUS over alternative radiologic imaging
techniques is much greater solution attributable to the
proximity of the ultrasound transducer to the area being
examined

Esophageal manometry - or motility testing, entails
positioning a pressure sensing catheter within the esophagus
and then observing the contractility following test swallows.
The upper and lower esophageal sphincters appear as zones
of high pressure that relax on swallowing while the
intersphincteric esophagus exhibits peristaltic contractions.
Manometry is used to diagnose motility disorders (achalasia,
diffuse esophageal spasm) and to assess peristaltic integrity
prior to the surgery for reflux disease.
Reflux Testing
reflux testing can demonstrate excessive esophageal exposure to
refluxed gastric juice, the physiologic abnormality of GERD. This can
be done by ambulatory 24- to 48-hour esophageal pH recording using
either a wireless pH-sensitive transmitter that is anchored to the
esophageal mucosa or with a transnasally positioned wire electrode
with the tip stationed in the distal esophagus. Either way, the outcome
is expressed as the percentage of the day that the pH was less than 4
(indicative of recent acid reflux), with values exceeding 5% indicative
of GERD. Reflux testing is useful with atypical symptoms or an
inexplicably poor response to therapy. Intraluminal impedance
monitoring can be added to pH monitoring to detect reflux events
irrespective of whether or not they are acidic, potentially increasing
the sensitivity of the stud
Hiatal Hernia
Hiatus hernia is a herniation of viscera, most commonly the
stomach, into the mediastinum through the esophageal hiatus
of the diaphragm. Four types of hiatus hernia are
distinguished with type I, or sliding hiatal hernia comprising
at least 95% of the overall total. A sliding hiatal hernia is one
in which the gastroesophageal junction and gastric cardia
slide upward as a result of weakening of the
phrenoesophageal ligament attaching the gastroesophageal
junction to the diaphragm at the hiatus. True to its name,
sliding hernias enlarge with increased intraabdominal
pressure, swallowing, and respiration. The incidence of sliding
hernias increases with age and conceptually, results from
wear and tear: increased intraabdominal pressure from
abdominal obesity, pregnancy, etc., and hereditary factors
predisposing to the condition. The main significance of
sliding hernias is the propensity of affected individuals to
have GERD.
Types II, III, and IV hiatal hernias are all subtypes of
paraesophageal hernia in which the herniation into the
mediastinum includes a visceral structure other than the
gastric cardia. With type II and III paraesophageal hernias,
the gastric fundus also herniates with the distinction being
that in type II, the gastroesophageal junction remains fixed
at the hiatus, while type III is a mixed sliding/paraesophageal
hernia. With type IV hiatal hernias, viscera other than the
stomach herniate into the mediastinum, most commonly the
colon. With type II and III paraesophageal hernias, the
stomach inverts as it herniates and large paraesophageal
hernias can lead to an upside down stomach, gastric volvulus,
and even strangulation of the stomach. Because of this risk,
surgical repair is often advocated for large paraesophageal
hernias
GERD
With respect to the esophagus, the spectrum of injury
includes esophagitis, stricture, Barrett's esophagus, and
adenocarcinoma . Of particular concern is the rising incidence
of esophageal adenocarcinoma, an epidemiologic trend that
parallels the increasing incidence of GERD.
Pathophysiology


Esophagitis occurs when refluxed gastric acid and pepsin
cause necrosis of the esophageal mucosa causing erosions and
ulcers.

Three dominant mechanisms of esophagogastric junction
incompetence are recognized:

(1) transient LES relaxations (a vagovagal reflex in which LES
    relaxation is elicited by gastric distention),

(2) LES hypotension, or

(3) anatomic distortion of the esophagogastric junction
   inclusive of hiatus hernia.
Complications


1.   The complications of GERD are related to chronic
     esophagitis (bleeding and stricture) and the relationship
     between GERD and esophageal adenocarcinoma. However,
     both esophagitis and peptic strictures have become
     increasingly rare in the era of potent antisecretory
     medications.

2. Conversely, the most severe histologic consequence of
   GERD is Barrett's metaplasia with the associated risk of
   esophageal adenocarcinoma, and the incidence of these
   lesions has increased, not decreased in the era of potent
   acid suppression.
Treatment: Gastroesophageal Reflux Disease (GERD)

1. Lifestyle modifications are routinely advocated as GERD therapy.
   Broadly speaking, these fall into three categories:

(1) avoidance of foods that reduce lower esophageal sphincter pressure,
    making them "refluxogenic" (these commonly include fatty foods,
    alcohol, spearmint, peppermint, tomato-based foods, possibly coffee
    and tea);

(2) avoidance of acidic foods that are inherently irritating; and

(3) adoption of behaviors to minimize reflux and/or heartburn. In
    general, minimal evidence supports the efficacy of these measures.
    However, clinical experience dictates that subsets of patients are
    benefitted by specific recommendations, based on their unique
    history and symptom profile. A patient with sleep disturbance from
    nighttime heartburn is likely to benefit from elevation of the head of
    the bed and avoidance of eating before retiring,
but those recommendations are superfluous for a patient without
   nighttime symptoms. The most broadly applicable recommendation
   is for weight reduction. Even though the benefit with respect to
   reflux cannot be assured, the strong epidemiologic association
   between obesity and GERD and the secondary health gains of
   weight reduction are beyond dispute.



 2. The dominant pharmacologic approach to GERD management is
 with inhibitors of gastric acid secretion and abundant data support
 the effectiveness of this approach. Pharmacologically reducing the
 acidity of gastric juice does not prevent reflux, but it ameliorates
 reflux symptoms and allows esophagitis to heal. The hierarchy of
 effectiveness among pharmaceuticals parallels their antisecretory
 potency. Proton pump inhibitors (PPIs) are more efficacious than
 histamine2 receptor antagonists (H2RAs), and both are superior to
 placebo. No major differences exist among PPIs and only modest
 gain is achieved by increased dosage.
3. Reflux symptoms tend to be chronic, irrespective of esophagitis.
Thus, a common management strategy is indefinite treatment with
PPIs or H2RAs as necessary for symptom control. The side effects
of PPI therapy are generally minimal. Vitamin B12, calcium, and iron
absorption may be compromised and susceptibility to enteric
infections, particularly Clostridium difficile colitis increased with
treatment. Consequently, as with any medication, dosage should be
minimized to that necessary.

4. Laparoscopic Nissen fundoplication, wherein the proximal stomach
is wrapped around the distal esophagus to create an antireflux
barrier, is a surgical alternative to the management of chronic GERD.
Just as with PPI therapy, evidence on the utility of fundoplication is
strongest for treating esophagitis and controlled trials suggest similar
efficacy to PPI therapy. However, the benefits of fundoplication
must be weighed against potential deleterious effects, including
surgical morbidity and mortality, postoperative dysphagia, failure or
breakdown requiring reoperation, an inability to belch, and increased
bloating, flatulence, and bowel symptoms after surgery.
Au med
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  • 2. Esophageal Structure and Function The esophagus is a hollow muscular tube coursing through the posterior mediastinum joining the hypopharynx to the stomach with a sphincter at each end. It functions to transport food and fluid between these ends, otherwise remaining empty.
  • 3. Gastroesophageal Reflux 2 conditions for Reflux Episode to occur: 1. Gastro-intestinal contents must be “ready” to reflux 2. The anhireflux mechanism at the lower end of the esophagus must be compromised. Gastro-intestinal contents are most likely to reflux 1. When gastric volume is increased . after meals . in the presence of pyloric obstruction or gastric stasis syndrome . in acid hypersecretory states
  • 4. 2. When gastric contents are located near the gastroesophageal due to: . Recumbence . bending down . Presence of hiatus hernia 3. When gastric pressure is increased . Obesity . Pregnancy . Ascitis . Tight binders/ girdles Normal antireflux mechanism Consist of LES and the anatomic configuration of gastroesophageal junction.
  • 5. Situations that predisposes to gastroesophageal reflux: 1. Reflux occur when the gradient of pressure between LES and the stomach is lost. 2. It can be caused by increased intragastric pressure or by transient or sustained decrease in LES tone. 3. Decrease in sphincter tone maybe due to muscle weakness. 4. Inappropriate sphincter relaxation mediated by inhibitory nerves.
  • 6. 5. Secondary causes of . LESIncompetence include 5.1 Scleroderma- like diseases 5.2 Myopathic type of chronic intestinal pseudoobstrution syndrome 5.3 pregnancy 5.4 smoking 5.5 smooth muscle relaxant Ex. Beta-adrenergenic agents Aminoplylline Nitrates Calcium channel blockers
  • 7. 6. Destruction of Sphinter by 6.1 Surgical Resection 6.2 Myotomy 6.3 Baloon dilatation 6.4 Esophagitis 7. Abnormal activity of the diaphragmatic crural muscles which surrounds the esophageal hiatus in the diaphragm. 8. Changes in hiatal hernia.
  • 8. Complications of Reflux: 1. Esophagitis- develops when mucosal defenses that normally counteract the effect of the injurious agents on esophageal mucosa succumb to the onslaught of refluxed acid pepsin or bile. Causing: . Erosive esophagitis . Peptic stricture . Replacement of Squamous epithelium of esophagus by columnar epithelium ( Barret’s esophagus)
  • 9. Major Esophageal Symtoms are: 1. Heartburn (pyrosis)- a discomfort or burning sensation behind the sternum that arises the epigastrium and may radiate toward the neck. Heartburn is an intermittent symptoms, most commonly experienced after eating, during exercise, and while lying recumbent. 2. Regurgitation- effortless return of food or fluid into the pharynx without nausea or retching. Patients report a sour or burning fluid in the Throat or mouth that may also contain undigested food particles. Bending, belching, or maneuvers that increase intraabdominal pressure can provoke regulation.
  • 10. 3. Chest pain- is a common esophageal symptoms with characteristics similar to cardiac pain, which closely mimics angina pectoris. Features suggesting esophageal pain include pain that is nonexertional, prolonged, interrupts sleep, is meal-related, is relieved with antacids, and is accompanied by heartburn, dysphagia, or regurgitation. 4. Esophageal dysphagia- a feeling of food “sticking” or even logging in the chest. 5. Odynophagia- is pain either caused by or exacerbated by swallowing. Odynophagia is more common with pill or infectious esophagitis than with reflux esophagitis and should prompt a search for these entities. When odynophagia does occur in GERD, it is likely related in an esophageal ulcer or deep erosion.
  • 11. Diagnostic Test Endoscopy- also known as esophagogastroduodenoscopy EGD is the best for the evaluation of the proximal gastrointestinal tract. Radiography – Contrast radiography of the esophagus, stomach, and duodenum can demonstrate barium reflux, hiatal hernia, mucosal granularity, erosions, ulceration, and strictures.
  • 12. Endoscopic ultrasound (EUS) - instrument combine an endoscope with an ultrasound transducer to create a transmural image of the tissue surrounding the endoscope tip. The key advantage of EUS over alternative radiologic imaging techniques is much greater solution attributable to the proximity of the ultrasound transducer to the area being examined Esophageal manometry - or motility testing, entails positioning a pressure sensing catheter within the esophagus and then observing the contractility following test swallows. The upper and lower esophageal sphincters appear as zones of high pressure that relax on swallowing while the intersphincteric esophagus exhibits peristaltic contractions. Manometry is used to diagnose motility disorders (achalasia, diffuse esophageal spasm) and to assess peristaltic integrity prior to the surgery for reflux disease.
  • 13. Reflux Testing reflux testing can demonstrate excessive esophageal exposure to refluxed gastric juice, the physiologic abnormality of GERD. This can be done by ambulatory 24- to 48-hour esophageal pH recording using either a wireless pH-sensitive transmitter that is anchored to the esophageal mucosa or with a transnasally positioned wire electrode with the tip stationed in the distal esophagus. Either way, the outcome is expressed as the percentage of the day that the pH was less than 4 (indicative of recent acid reflux), with values exceeding 5% indicative of GERD. Reflux testing is useful with atypical symptoms or an inexplicably poor response to therapy. Intraluminal impedance monitoring can be added to pH monitoring to detect reflux events irrespective of whether or not they are acidic, potentially increasing the sensitivity of the stud
  • 14. Hiatal Hernia Hiatus hernia is a herniation of viscera, most commonly the stomach, into the mediastinum through the esophageal hiatus of the diaphragm. Four types of hiatus hernia are distinguished with type I, or sliding hiatal hernia comprising at least 95% of the overall total. A sliding hiatal hernia is one in which the gastroesophageal junction and gastric cardia slide upward as a result of weakening of the phrenoesophageal ligament attaching the gastroesophageal junction to the diaphragm at the hiatus. True to its name, sliding hernias enlarge with increased intraabdominal pressure, swallowing, and respiration. The incidence of sliding hernias increases with age and conceptually, results from wear and tear: increased intraabdominal pressure from abdominal obesity, pregnancy, etc., and hereditary factors predisposing to the condition. The main significance of sliding hernias is the propensity of affected individuals to have GERD.
  • 15. Types II, III, and IV hiatal hernias are all subtypes of paraesophageal hernia in which the herniation into the mediastinum includes a visceral structure other than the gastric cardia. With type II and III paraesophageal hernias, the gastric fundus also herniates with the distinction being that in type II, the gastroesophageal junction remains fixed at the hiatus, while type III is a mixed sliding/paraesophageal hernia. With type IV hiatal hernias, viscera other than the stomach herniate into the mediastinum, most commonly the colon. With type II and III paraesophageal hernias, the stomach inverts as it herniates and large paraesophageal hernias can lead to an upside down stomach, gastric volvulus, and even strangulation of the stomach. Because of this risk, surgical repair is often advocated for large paraesophageal hernias
  • 16. GERD With respect to the esophagus, the spectrum of injury includes esophagitis, stricture, Barrett's esophagus, and adenocarcinoma . Of particular concern is the rising incidence of esophageal adenocarcinoma, an epidemiologic trend that parallels the increasing incidence of GERD.
  • 17.
  • 18. Pathophysiology Esophagitis occurs when refluxed gastric acid and pepsin cause necrosis of the esophageal mucosa causing erosions and ulcers. Three dominant mechanisms of esophagogastric junction incompetence are recognized: (1) transient LES relaxations (a vagovagal reflex in which LES relaxation is elicited by gastric distention), (2) LES hypotension, or (3) anatomic distortion of the esophagogastric junction inclusive of hiatus hernia.
  • 19. Complications 1. The complications of GERD are related to chronic esophagitis (bleeding and stricture) and the relationship between GERD and esophageal adenocarcinoma. However, both esophagitis and peptic strictures have become increasingly rare in the era of potent antisecretory medications. 2. Conversely, the most severe histologic consequence of GERD is Barrett's metaplasia with the associated risk of esophageal adenocarcinoma, and the incidence of these lesions has increased, not decreased in the era of potent acid suppression.
  • 20. Treatment: Gastroesophageal Reflux Disease (GERD) 1. Lifestyle modifications are routinely advocated as GERD therapy. Broadly speaking, these fall into three categories: (1) avoidance of foods that reduce lower esophageal sphincter pressure, making them "refluxogenic" (these commonly include fatty foods, alcohol, spearmint, peppermint, tomato-based foods, possibly coffee and tea); (2) avoidance of acidic foods that are inherently irritating; and (3) adoption of behaviors to minimize reflux and/or heartburn. In general, minimal evidence supports the efficacy of these measures. However, clinical experience dictates that subsets of patients are benefitted by specific recommendations, based on their unique history and symptom profile. A patient with sleep disturbance from nighttime heartburn is likely to benefit from elevation of the head of the bed and avoidance of eating before retiring,
  • 21. but those recommendations are superfluous for a patient without nighttime symptoms. The most broadly applicable recommendation is for weight reduction. Even though the benefit with respect to reflux cannot be assured, the strong epidemiologic association between obesity and GERD and the secondary health gains of weight reduction are beyond dispute. 2. The dominant pharmacologic approach to GERD management is with inhibitors of gastric acid secretion and abundant data support the effectiveness of this approach. Pharmacologically reducing the acidity of gastric juice does not prevent reflux, but it ameliorates reflux symptoms and allows esophagitis to heal. The hierarchy of effectiveness among pharmaceuticals parallels their antisecretory potency. Proton pump inhibitors (PPIs) are more efficacious than histamine2 receptor antagonists (H2RAs), and both are superior to placebo. No major differences exist among PPIs and only modest gain is achieved by increased dosage.
  • 22. 3. Reflux symptoms tend to be chronic, irrespective of esophagitis. Thus, a common management strategy is indefinite treatment with PPIs or H2RAs as necessary for symptom control. The side effects of PPI therapy are generally minimal. Vitamin B12, calcium, and iron absorption may be compromised and susceptibility to enteric infections, particularly Clostridium difficile colitis increased with treatment. Consequently, as with any medication, dosage should be minimized to that necessary. 4. Laparoscopic Nissen fundoplication, wherein the proximal stomach is wrapped around the distal esophagus to create an antireflux barrier, is a surgical alternative to the management of chronic GERD. Just as with PPI therapy, evidence on the utility of fundoplication is strongest for treating esophagitis and controlled trials suggest similar efficacy to PPI therapy. However, the benefits of fundoplication must be weighed against potential deleterious effects, including surgical morbidity and mortality, postoperative dysphagia, failure or breakdown requiring reoperation, an inability to belch, and increased bloating, flatulence, and bowel symptoms after surgery.