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Gastro-Oesophageal Reflux Disease


Gastro-oesophageal reflux disease (GERD) refers to symptoms of oesophageal mucosal injury caused by the reflux of gastric contents into the oesophagus. Twenty-four hour pH studies have shown that all human beings have intermittent reflux, but in most cases the refluxate is rapidly cleared from the oesophagus and hence causes no injury. This is called 'physiological reflux'. On the other hand, patients with GERD have mucosal injury caused by increased frequency and duration of reflux episodes. It is well recognized that clinical symptoms, oesophageal pH monitoring and histological oesophagitis have poor correlation with each other.


Symptomatic GERD occurs when the balance between various aggressive factors (potency and frequency of reflux) and defensive factors (oesophageal acid clearance and mucosal resistance) tilts in favour of aggressive factors. The various pathogenetic mechanisms that have been postulated in the causation of GERD are:

1. Lower esophageal sphincter (LES) dysfunction

(a) Primary LES hypotonia.

(i) Physiological - pregnancy, infancy, drugs, food, belching, hiccups, smoking.

(ii) Pathological - Scleroderma, diabetes, amyloidosis, hypothyroidism, intestinal pseudo-
obstruction, gastric distension, hiatus hernia.

(b) Secondary LES hypotonia.

(c) Transient LES relaxation.

2. Abnormal esophageal clearance mechanisms.

(a) Primary peristaltic dysfunction.

(b) Secondary peristaltic dysfunction - hypothyroidism, amyloidosis, pseudo-obstruction, scleroderma.

3. Decreased esophageal epithelial resistance.

4. Gastric factors.


Inability to maintain an adequate LES tone is the best characterized abnormality in patients with GERD. The strongest evidence in its favour comes from patients of achalasia who have undergone Heller's myotomy. Certain physiological states which are associated with LES hypotonia cause increased gastro-esophageal reflux. These include pregnancy, infancy, belching and hiccups. The LES is also affected by specific neurogenic and myogenic disease such as scleroderma, hypothyroidism, diabetes mellitus and amyloidosis. However, a large majority of patients with GERD have normal basal pressures on manometry.


At present, it is believed that in patients with hiatus hernia there is progressive loss of action of the diaphragmatic sphincter, depending upon the extent of axial herniation, thus increasing the susceptibility to reflux.

Abnormal Oesophageal Clearance Mechanisms

1. The secondary peristalsis wave initiated by the acid bolus.
2. Swallowed saliva acting as a neutralizer for the acid that remains after peristaltic clearance.

Investigations using radiolabelled acid have shown that the secondary peristaltic wave reduces a 15 mL acid bolus to less than 1 mL within 15 seconds. However, it is now clear that secondary peristalsis plays only a minor role, particularly in the supine position and during sleep.

Primary peristalsis (initiated by swallowing) is the main mechanism by which the acid bolus is pushed into the stomach. Continued swallowing brings saliva rich in bicarbonate into the distal oesophagus to neutralize any remaining acid. The prevalence of peristaltic dysfunction is aggravated with increasing severity of esophagitis, from 25% (in patients with mild oesophagitis) to 48% (in patients with severe oesophagitis).

Decreased Oesophageal Epithelial Resistance

Damage to the oesophageal mucosa by refluxed acid depends on the contact time between the acid and the mucosa and tissue resistance. The resistance of the esophageal epithelium is determined by three sets of defences - pre-epithelial, epithelial and post-epithelial. These must be breached by the H+ ions present in gastric acid. The pre-epithelial defences include the mucus layer, the unstirred water layer and surface bicarbonate ion concentration. The epithelial defences include the cell membranes, intercellular junction complexes, epithelial transport systems and intracellular/extracellular buffers. The post-epithelial defences are mainly blood flow and tissue acid-base balance.

Gastric Factors

Symptomatic patients tend to have reflux of acid at lower intragastric volumes (140 mL) compared to asymptomatic patients (who have reflux at >308 mL). However, the majority of patients with GERD have normal or accelerated gastric emptying to both solids and liquids.

Epidemiology and Natural History

Those with moderate-to-severe disease tend to have chronic relapsing symptoms. The relapse occurs within 30 weeks of discontinuation of medical therapy. Among the serious complications of GERD, the prevalence of strictures is 1%-23%. The incidence of Barrett's esophagus is 8%-20% in symptomatic refluxers and as high as 30%-40% in those with strictures. Less than 2% of patients with oesophagitis develop significant bleeding and oesophageal perforation is rare.

Clinical spectrum

The clinical spectrum of GERD can be divided into three sets of symptoms - typical, atypical and complications.

The typical symptoms of GERD include heartburn and regurgitation. However, only one-third of patients with typical symptoms will have endoscopic evidence of esophagitis. About two-thirds of patients have intolerance to coffee, fruit juice, alcohol, chocolate and fat. Amongst the atypical symptoms of GERD are epigastric pain (in about 20% of patients), angina-like chest pain, reflux laryngitis, nocturnal asthma, protracted hiccups and loss of dental enamel. The major complications which may be the presenting symptoms are bleeding due to erosions or ulceration, dysphagia due to peptic stricture and metaplasia producing a columnar-epithelium lined oesophagus or 'Barrett's oesophagus'. Development of adenocarcinoma in Barrett's oesophagus is the most serious complication.


Diagnostic evaluation of a patient with GERD is necessary when the symptoms are chronic, refractory to treatment or accompanied by dysphagia, odynophagia or gastrointestinal bleeding. The two most important investigations are endoscopy and pH monitoring. All the other tests such as barium swallow, radionuclide assessment for reflux, Bernstein test, etc. are obsolete.


For assessing reflux-induced damage (oesophagitis) and the presence of columnar epithelium-lined oesophagus (Barrett's oesophagus). Most patients with GERD do not require an endoscopy. Also, most patients diagnosed as having GERD on endoscopy do not require endoscopic follow-up.

Endoscopy should be done to :

1. Differentiate GERD from infectious oesophagitis.
2. Assess the severity of oesophagitis.
3. Diagnose the complications of GERD such as stricture or Barrett's oesophagus.
4. Assess reflux disease refractory to medical therapy.

A number of grading systems have been developed to assess oesophagitis. The more popular ones are the modified Savary-Miller system (1990) and the Tytgat new system (1990).

Oesophageal pH Monitoring

1. Assessment of relationship between symptoms and reflux.
2. Typical reflux symptoms without endoscopic oesophagitis
3. Atypical symptoms with or without oesophagitis
4. When antireflux surgery is considered.
5. Evaluation of the effect of drug therapy if symptoms or endoscopic changes do not improve.

The criteria for reflux is a fall in intra-oesophageal pH to less than 4. Other reflux parameters used are :

1. Reflux time or acid exposure time, expressed in minutes or as a percentage of the total time for which the oesophageal pH remains below 4.
2. The acid clearance time which is the mean duration for which the oesophageal pH remains below 4 and is calculated by dividing the reflux time by the number of reflux episodes.
3. The number of reflux episodes longer than 5 minutes
4. The duration of the longest episode of reflux.

Medical Management

GERD is a chronic relapsing disorder with little or no tendency for spontaneous healing. Since the primary cause is unknown, cure is not available and the aim of treatment is to relieve symptoms and prevent complications. A step-wise approach to the management of GERD is as follows:

Phase 1 Diet modification
Weight loss
Elevation of head-end of bed
Avoiding recumbency for 3 hours after a meal
Restriction on smoking and drinking alcohol.
Antacids and alginic acid

Phase 2A Histamine receptor antagonists
Drugs to augment the pressure of the lower esophageal sphincter

Phase 2B Proton pump inhibitors

Phase 3 Antireflux surgery.


Modifiable factors associated with GERD

Change in body position produces physiological benefits - head elevation reduces the reflux episodes. Chocolates, carminatives and fatty foods reduce LES pressure. Avoiding these will prevent acid reflux. Alcohol and smoking decrease LES pressure and smoking also decreases salivary secretion and esophageal clearance.

Current Drug Therapy

A number of recent trials have convincingly shown that compared to standard dose and high dose H2 receptor antagonists, proton pump inhibitors provide faster relief from symptoms and healing of oesophagitis. Combination therapy with a proton pump inhibitor and a prokinetic is not recommended unless there is evidence of severely delayed gastric emptying. Also, eradication of Helicobacter pylori does not help as it may worsen the symptoms.

ANTIREFLUX SURGERY : Comparison With Medical Therapy

Indicated for
1. Persistent or recurrent symptoms or complications after 8-12 weeks of intensive acid suppression therapy, particularly in young patients.
2. Documentation of a mechanically defective LES on manometry.
3. Development of a stricture in a patient with a mechanically defective sphincter
4. Barrett's oesophagus.
The advent of laparoscopic fundoplication has increased the scope of surgical therapy as it is accompanied by significantly lower morbidity.


The complications of GERD include ulceration, hemorrhage or perforation, stricture formation, Barrett's metaplasia and consequent adenocarcinoma. Extra-oesophageal complications include reflux laryngitis, bronchial asthma and aspiration pneumonia. Barrett's oesophagus is a condition in which the normal stratified squamous epithelium of the distal oesophagus is replaced by columnar epithelium. This condition has traditionally being associated with severe gastro-oesophageal reflux disease and oesophageal adenocarcinoma. In patients with Barrett's oesophagus, the mean length of the oesophagus lined by columnar epithelium is 6-7 cm and the mean age at diagnosis around 60 years. Management of Barrett's oesophagus involves aggressive antireflux drug therapy, endoscopic surveillance for dysplasia, laser ablative therapy or surgical therapy for high-grade dysplasia and oesophagectomy for adenocarcinoma.


Gastro-oesophageal reflux disease is a common problem which is difficult to evaluate and manage. The potential complications of the disease are serious, leading to considerable morbidity. The pathogenesis of the disease is still unclear, although the role of decreased LES pressure, transient LES relaxation and impaired oesophageal acid clearance have been elucidated. Short term medical management seems to provide good results but the relapsing nature of the disease makes long term medical management frustrating. Surgery appears to be a good alternative, particularly in young patients. Among the important complications are peptic stricture and the development of Barrett's oesophagus which is a premalignant lesion, leading to adenocarcinoma. The quest for a definitive therapy for GERD, therefore, continues.