Gastroesophageal reflux disease (GERD):
Gastroesophageal reflux disease (GERD) is a chronic digestive disease. GERD occurs when stomach acid or, occasionally, stomach content, flows back into your food pipe (esophagus). The backwash (reflux) irritates the lining of your esophagus and causes GERD.
Physiology of Digestion:
|Gastroesophageal reflux disease (GERD)|
Digestion begins in the mouth as food is broken down by chewing into smaller pieces and by saliva releasing digestive enzymes such as α-amylase and Lingual lipase. When food is swallowed it enters the esophagus, a muscular tube that carries food from the mouth to the stomach for further digestion. Contractions call peristalsis push food down the esophagus.
At the bottom of the esophagus food passes through a muscular valve called the Lower Esophageal Sphincter or LES and into the stomach. The digestive juices secreted by the stomach are highly acidic. When the stomach contracts to move the food into the intestine the LES closes tightly in order to prevent these acidic juices from moving back into the esophagus where they can cause damage.
A breathing muscle called the diaphragm separates the chest from the abdomen. To reach the stomach the esophagus passes through the diaphragm at a point called the hiatal ring. If the patient has gastroesophageal reflux disease or GERD, their LES does not close properly allowing acidic stomach contents to flow backward into the esophagus.
Complications of Untreated GERD:
If GERD is not treated it can lead to variety of esophageal problems, including:
— Esophageal stricture or Schatzki rink, which is a well-known complication of GERD and is associated with Hiatal Hernia. It can cause osbructive dysphagia usually in the LOWER esophagus as the results of the healing process of ulcerative esophagitis.
— Barrett’s esophagus, in which the normal stratified squamous epithelium lining of the esophagus is replaced by simple columnar epithelium, which are usually found lower in the GI tract.
Factors That Can Contribute to GERD:
— Hiatal hernia,
— Zollinger-Ellison syndrome, which can present with increased gastric acidity due to gastrin production.
— Hypercalcemia, which can also increase gastrin production, leading to increased acidity.
— Scleroderma and systemic sclerosis, which can feature esophageal dysmotility.
Signs and Symptoms of GERD:
— Epigastric burning pain traveling up into the chest known as (heartburns), which can sometimes spread to the throat, along with a sour metallic taste in the mouth,
— Difficulty swallowing (dysphagia),
— Dry cough,
— Sore throat (due to acid reflux)
— Hoarseness, which is due to acid damaging the larynx or the voice box,
— Regurgitation of food or sour liquid (acid reflux),
— Sensation of a lump in the throat
Diagnosis of GERD (Dx):
GERD is most often diagnosed based on patient history and symptoms. In some patients in whom the diagnosis is not clear, 24-hour pH monitoring is done to confirm the etiology.
Upper endoscopy is not required in the presence of typical GERD symptoms of heartburn or regurgitation. Upper endoscopy is recommended if the diagnosis of GERD is unclear and in the following individuals:
— Patients with heartburn and alarm symptoms (dysphagia, bleeding, anemia, weight loss, and recurrent vomiting).
— Patients with severe erosive esophagitis after a two-month course of PPI therapy to assess healing and rule out Barrett’s esophagus. Repeat endoscopy after this follow-up examination is not indicated in the absence of Barrett’s esophagus unless patients have bleeding, dysphagia, or a significant change in symptoms while on effective therapy.
— Patients with typical GERD symptoms that persist despite a therapeutic trial of 4-8 of twice-daily PPI therapy.
— In men >50 years of age with chronic GERD symptoms (symptoms for > five years) and additional risk factors (nocturnal reflux symptoms, hiatal hernia, elevated body mass index, tobacco use, and intra-abdominal distribution of fat) to detect esophageal adenocarcinoma and Barrett’s esophagus.
— Patients with gastroesophageal reflux disease (GERD) may be managed with a step-up or step-down approach to therapy. The step-up approach involves incrementally increasing the potency of therapy until symptom control is achieved. The step-down approach starts with potent antisecretory agents and then involves incrementally decreasing the potency of therapy until breakthrough symptoms define the treatment necessary for symptom control.
Mild and intermittent symptoms:
Management approach to patients with GERD is based on the frequency and severity of symptoms and the presence of erosive esophagitis on upper endoscopy, if previously performed. Step-up therapy for GERD in patients with mild and intermittent symptoms (fewer than two episodes per week) who have no evidence of erosive esophagitis on upper endoscopy.
In patients who are naïve to treatment, lifestyle and dietary modification are recommended first along with low-dose histamine 2 receptor antagonists (H2RAs).
> Lifestyle and Dietary Modification:
— Weight loss if obese.
— Avoid alcohol, nicotine, spicy food, caffeine, chocolate and peppermint.
— They should also Avoid eating 3-4 hours before sleep.
— Elevate their head off the bed while sleeping.
— Avoidance of tight-fitting garments to prevent increasing intragastric pressure and the gastroesophageal pressure gradient.
— As antacids do not prevent GERD, their role is limited to intermittent (on-demand) use for relief of mild GERD symptoms that occur less than once a week. Antacids usually contain a combination of magnesium trisilicate, aluminum hydroxide, or calcium carbonate, which neutralize gastric pH, thereby decreasing the exposure of the esophageal mucosa to gastric acid during episodes of reflux. Antacids begin to provide relief of heartburn within five minutes, but have a short duration of effect of 30 to 60 minutes.
> Surface Agents and Alginates:
— Sucralfate (aluminum sucrose sulfate), a surface agent, adheres to the mucosal surface, promotes healing, and protects from peptic injury by mechanisms that are incompletely understood. It has a short duration of action and limited efficacy as compared with PPIs.
— Sodium alginate is a polysaccharide derived from seaweed that forms a viscous gum that floats within the stomach and reduces the postprandial acid pocket in the proximal stomach.
> H2 Receptor Antagonists (H2RA):
— H2RAs decrease the secretion of acid by inhibiting the histamine 2 receptor on the gastric parietal cell. In contrast to antacids, H2RAs have a slower onset of action, reaching peak concentrations 2.5 hours after dosing, but a significantly longer duration of action of 4 to 10 hours. H2RAs are also more effective in decreasing the frequency and severity of heartburn symptoms as compared with antacids and placebo. However, H2RAs have limited efficacy in patients with erosive esophagitis. While mucosal healing rates in patients with mild erosive esophagitis are 10 to 24 percent higher with H2RA therapy as compared with placebo, H2RAs are ineffective in patients with severe esophagitis.
Severe or frequent symptoms or erosive esophagitis:
Step-down therapy is recommended in patients with erosive esophagitis, frequent symptoms (two or more episodes per week), and/or severe symptoms that impair quality of life in order to optimize symptom relief. Begin with standard-dose PPI once daily for eight weeks in addition to lifestyle and dietary modification.
> Proton pump inhibitors (PPIs):
— PPI’s should be used in patients who fail twice-daily H2RA therapy and in patients with erosive esophagitis and/or frequent (two or more episodes per week) or severe symptoms of GERD that impair quality of life. PPIs are the most potent inhibitors of gastric acid secretion by irreversibly binding to and inhibiting the hydrogen-potassium (H-K) ATPase pump. Compared with H2RAs, PPIs provide faster symptom relief and are more effective in relieving symptoms of GERD. PPIs should be taken 30 minutes before a meal to maximize acid inhibition.
> Treatment of Helicobacter pylori infection:
— It is uncertain whether chronic acid suppression with PPIs increases the risk for atrophic gastritis in patients with H. pylori. Therefore, routine screening for H. pylori infection and empiric eradication of H. pylori are not recommended in patients with GERD. However, for H. pylori diagnosed in the setting of GERD, eradication of H. pylori has been associated with an improvement of symptoms in patients with antral-predominant gastritis.
— For those patients who do not respond to medical therapies surgery may be required. The standard surgical treatment for severe GERD is Nissen Fundoplication. In this procedure, the upper part of the stomach is wrapped around the lower esophageal sphincter to reinforce the sphincter and prevent acid reflux and to repair a hiatal hernia.
— The standard surgical treatment for severe GERD is Nissen Fundoplication. In this procedure, the upper part of the stomach is wrapped around the lower esophageal sphincter to reinforce the sphincter and prevent acid reflux and to repair a hiatal hernia.
— Endocinch can also be done which by using a scope a suture is placed around the LES to make it tighter.
References for Gastroesophageal reflux disease:
– www.uptodate.com 1
– www.uptodate.com 2