Authors:Dr.Ratan Vaish

In modern era, people are very busy with so many things, that they are getting less time for their health. Due to stress, fast food, junk food, cold drinks the situation are going worse. Approximately 15-30% of general population is suffering with GERD. There were approximately 8,000 patients suffering from esophageal adeno-carcinoma in United States in 2010. It is estimated that this disease burden has increased two to six fold in the last 20 years.

Clinical features: Heartburn and regurgitation are the typical symptoms of GERD, which is often provoked by bending, straining or lying down. Dysphagia and chest pain are less common symptoms.

Extra esophageal syndromes with an established association to GERD include chronic cough, laryngitis, asthma and dental erosions. A multitude of other conditions including pharyngitis, chronic bronchitis, pulmonary fibrosis, chronic sinusitis, cardiac arrhythmias, sleep apnea and recurrent aspiration pneumonia have proposed association with GERD. Some patients are wake up at night by choking as refluxed fluid irritates the larynx. A typical chest pain, which may be severe, can mimic angina and may be due to refluxed induced oesphageal spasm.

Figure 1: Factors associated with the development of gastro esophageal reflux disease


Some degree of gastro esophageal reflux is normal, but esophagitis results from excessive reflux, often accompanied by impaired clearance of the refluxed gastric juice. Restricting reflux to that which is physiologically intended depends on the anatomic and physiologically intended depends on the anatomic and physiologic integrity of the esophageal junction, a complex sphincter comprised of both the LES (lower esophageal sphincter) and the surrounding crural diaphragm. Three dominant mechanisms of esophago-gastric junction incompetence are recognized.

1) Transient LES relaxation (a vasovagal reflex in which LES relaxation is elicited by gastric distension)

2) LES hypotension

3) Anatomic distortion of the oesophago-gastric junction

Factors tending to exacerbate reflux regardless of mechanism are abdominal obesity, pregnancy, gastric hyper-secretory state, delayed gastric emptying, disruption of esophageal peristalsis and gluttony.

After acid reflux, peristalsis returns the refluxed fluid to the stomach and acid clearance is completed by titration of the residual acid by bicarbonate contained in swallowed saliva. Consequently, two causes of prolonged acid clearance are impaired peristalsis and reduced salivation. Impaired peristaltic emptying can be attributable to disrupted peristalsis or super imposed reflux associated with hiatus hernia.

Pepsin, bile and pancreatic enzymes within gastric secretion can also injure the esophageal epithelium, but there noxious properties are lessened in either an acidic environment or dependent on acidity for activation. Bile warrants attention because it persists in refluxate despite acid suppressing medications. Bile can transverse the cell membrane, impairing severe cellular injury in a weakly acidic environment, and has also been invoked as a cofactor in the pathogenesis of Barrett’s metaplasia and adenocarcinoma hence, the causticity of gastric refluxate extend beyond hydrochloride acid.

Figure 2: Histopathology of Barrett’s metaplasia and Barrett’s with high grade dysplasia. H & E, Hematoxylin and Eosin

Figure 3: Histopathology of eosinophillic esophagitis (EoE) showing dense infiltration of esophageal squamous epithelium with eosinophils.

Differential diagnosis
  1. Peptic ulcer disease
  2. Dyspepsia
  3. Biliary colic
  4. Coronary artery disease
  5. Symptoms related to injections , pills or eosinophilic esophagitis
  6. Esophageal motility disorder

Diagnosis is mainly based on clinical features. Upper GI Endoscopy is very much helpful for making diagnosis.


1. Upper GI Endoscopy
2. 24 hours ph monitoring.


Life style modification is mainstay for treatment.
  1. Avoidance of foods (fatty foods, alcohol, spearmint that reduce lower esophageal sphincter pressure, making them refluxogenic.
  2. Avoidance of acidic foods that are inherently irritating
  3. Adoption of behavior to minimize reflux
  4. A patient with sleep disturbance from nighttime heartburn is likely to benefit from elevation f the head of bad avoidance of eating before retiring.
  5. o
  6. The most broadly applicable recommendation is for weight reduction
  7. The dominant pharmacological approach to GERD managed is with inhibitors of gastric acid secretion and abundant data support the effectiveness of this approach.
  8. Pharmacologically reducing the acidity of gastric juice does not prevent reflux, but it ameliorates reflux symptoms and allows esophagitis to heal.
  9. Proper pump inhibitors (PPI) are more efficacious than H2 receptor antagonist.

Reflux symptoms tend to be chronic, irrespective of esophagitis. Thus a common management strategy is indefinite treatment with PPIs or H2 receptor antagonist as necessary for symptoms control.
Figure 4: Types of hiatus hernia.

There are numerous linear streaks of superficial ulceration extending up to the gullet.


The complications of GERD are related to chronic esophagitis (bleeding and stricture) and the relationship between GERD and esophageal adenocarcinoma.

Barrett’s esophagitis

It is most sever histologic consequence of GERD with associated risk of esophageal adenocarcinoma and the incidence of these lesions has increased not decreased in the era of potent acid suppression.

Figure 6: Barrett’s esophagus. Pink columnar mucosa is seen extending upwards above the esophago-gastric junction.

Barrett’s esophagus is a pre-malignant condition in which the normal sequence lining of the lower esophagus is replaced by columnar mucosa containing area of intestinal metaplasia. It occurs as on adaptive response to chronic gastro esophageal reflux and is found in 10% of patients undergoing gastroscopy for reflux symptoms.

Barrett’s metaplasia endoscopy recognized by tongues of reddish mucosa extending proximally from the gastro esophageal junction or histopathologically by the finding of specialized columnar metaplasia , is associated with at least a 20 fold increased risk for development of esophageal adenocarcinoma .

Barrett’s metaplasia can progress to adenocarcinoma through the intermediate stage of low and high-grade dysplasia. The rate of cancer development is estimated at 0.5% per year. The group at greatest risk is obese white males in their sixth decade of life.


A range of endoscopic findings, from mild reddened to severe, bleeding ulceration with stricture formation.

Figure 6: Barrett’s esophagus. Pink columnar mucosa is seen extending upwards above the esophago-gastric junction.


Iron deficiency anemia occurs as a consequence of chronic, insidious blood loss from long standing esophagitis.

Benign esophageal stricture Fibrous stricture develops as a consequence of long standing esophagitis most patients are elderly and have esophageal peristaltic activity.

Gastric volvulus Occasionally a massive intra-thoracic hiatus hernia may twist upon itself in either the organo-axial or the lateral axis, leading to a gastric volvulus.


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