What is acid reflux?

Gastroesophageal reflux disease (GERD) is defined as symptoms or tissue damage resulting from reflux of gastric acid into the esophagus and more proximal structures.
The predominant symptoms of GERD are heartburn and regurgitation.
Atypical symptoms include cough, asthma, hoarseness, chest pain, hiccups, and dental erosions.
Symptom response to a therapeutic trial of PPIs can be diagnostic.
Endoscopic evaluation is recommended for patients with warning symptoms of dysphagia, odynophagia, early satiety, weight loss, or bleeding, and atypical symptoms (cough, asthma, hoarseness, chest pain, aphthous ulcers, hiccups, dental erosions).
Patients with symptoms refractory to empiric acid suppression or requiring continuous medication for prolonged periods should also undergo endoscopy.
Ambulatory pH monitoring is used to establish elevated esophageal acid exposure and symptom-reflux correlation in patients with ongoing symptoms despite acid suppression (especially if endoscopy is negative) or those with atypical symptoms. It is also used to determine adequacy of acid suppression in patients with established GERD and ongoing symptoms.
Lifestyle Modification
The basics of lifestyle modification include eating small meals; refraining from eating for 2-3 hours before lying down; elevating the head of the bed 4-6 in.; decreasing intake of fatty foods, chocolate, coffee, cola, and alcohol; and smoking cessation.
Lifestyle modification also includes avoiding medications such as calcium channel blockers, theophylline, sedatives/tranquilizers, and anticholinergics, as they may potentiate reflux.
Lifestyle modifications alone are unlikely to resolve symptoms in the majority of GERD patients, but should be recommended in conjunction with medications.
Medications
In patients with mild or intermittent symptoms, over-the-counter antacids and H2RAs can be used intermittently or prophylactically if necessary.
PPIs have been demonstrated to be more effective than placebo or standard-dose H2RA in symptomatic relief as well as endoscopic healing of GERD. Higher doses (omeprazole, 20–40 mg PO bid or equivalent) may be required in severe esophagitis or persistent symptoms. Continuous long-term PPI therapy is safe and effective in maintaining remission of GERD symptoms, and is recommended for patients with erosive esophagitis, Barrett's esophagus, and severe symptoms.
Standard doses of H2RAs can result in symptomatic benefit in up to 60% of patients and endoscopic healing in 50%. Higher doses of H2RAs (equivalent to ranitidine, 600 mg daily) improve the healing rate to 75% at a higher cost. Dosage adjustments are required in renal insufficiency.
Surgery
Indications for fundoplication include the need for continuous or increasing doses of medication in patients who are good surgical candidates. Patients who require aggressive long-term medical therapy should be offered the surgical option. Other indications include patient preference for surgery and noncompliance with medical therapy.
The success rate of laparoscopic fundoplication in controlling GERD symptoms exceeds 90%, with fewer complications compared to the open technique. Elevated esophageal acid exposure and correlation of symptoms to reflux events on ambulatory pH monitoring predict a higher likelihood of a successful outcome.
Patients with medical treatment failures need careful evaluation to determine whether symptoms are indeed related to acid reflux before surgical options are considered; these patients often have other diagnoses including visceral hypersensitivity and functional heartburn.
Complications
Esophageal ulceration and stricture formation can occur in patients with GERD. Iron-deficiency anemia is less common.
GERD can contribute to laryngitis, laryngeal ulcers, asthma, and dental caries.
Barrett's esophagus is a change in the esophageal mucosa from normal squamous epithelium to specialized intestinal metaplastic epithelium due to longstanding acid related injury. It carries a small risk of progression to esophageal adenocarcinoma. Endoscopic surveillance for Barrett's esophagus should be considered in patients with a symptom history that exceeds 5 years.

REFLUX ESOPHAGITIS
Reflux of stomach contents into the lower esophagus is the first and foremost cause of esophagitis. Many causative factors are involved, less well characterized than the name implies:

Decreased efficacy of esophageal antireflux mechanisms, particularly LES tone. Central nervous system depressants, hypothyroidism, pregnancy, systemic sclerosing disorders, alcohol or tobacco exposure, or the presence of a nasogastric tube may be contributing causes. In most instances, no antecedent cause is identified.

Presence of a sliding hiatal hernia.

Inadequate or slowed esophageal clearance of refluxed material.

Delayed stomach emptying and increased stomach volume, contributing to the volume of refluxed material.

Reduction in the reparative capacity of the esophageal mucosa by protracted exposure to stomach juices.
Any one of the aforementioned influences may assume primacy in an individual case, but more than one is likely to be involved in most instances. The acid-peptic action of stomach juices is critical to the development of esophageal mucosal injury; in severe cases, refluxed bile from the duodenum also may contribute to the mucosal disruption.

MORPHOLOGY.
The anatomic changes depend on the causative agent and on the duration and severity of the exposure. Simple hyperemia ( redness) may be the only alteration. In uncomplicated reflux esophagitis, three histologic features are characteristic
1. The presence of inflammatory cells, including eosinophils, neutrophils, and excessive numbers of lymphocytes, in the epithelial layer

2. Basal zone hyperplasia exceeding 20% of the epithelial thickness

3. Elongation of lamina propria papillae with congestion, extending into the top third of the epithelial layer
Infiltrates of intraepithelial eosinophils are believed to be an early histologic abnormality, since they occur even in the absence of basal zone hyperplasia. Intraepithelial neutrophils are markers of more severe injury, such as ulceration, rather than reflux esophagitis per se.

Clinical Features.
Although largely limited to adults over age 40, reflux esophagitis is occasionally seen in infants and children. The clinical manifestations consist principally of dysphagia; heartburn; and sometimes regurgitation of a sour brash, hematemesis, or melena. The severity of symptoms is not related closely to the presence or degree of histologic esophagitis; most people experience reflux symptoms without damage to the distal esophageal mucosa, owing to the short duration of the reflux. Anatomic damage appears best correlated with prolonged exposure of the lower esophagus to refluxed material. Rarely, chronic symptoms are punctuated by attacks of severe chest pain that may be mistaken for a heart attack. The potential consequences of severe reflux esophagitis are bleeding, development of stricture, and a tendency to develop Barrett esophagus, with its attendant risks.

The clinical course of reflux esophagitis depends to a great extent on whether the patient has erosive or nonerosive GERD on initial presentation. Furthermore, patients tend not to cross over from one group to another unless they are treated medically or surgically: in follow-up ranging from 6 months to more than 5 years, only 15% of patients with nonerosive disease evolved over time to having esophagitis or complications of GERD.

Nonerosive Acid Reflux Disease

Although early studies from tertiary referral centers suggested that nearly half of patients with GERD had esophagitis, studies carried out in community practices reveal that up to 70% of the patients with GERD had a normal endoscopic examination. Furthermore, another community-based study of antacid users found that 53% of patients with GERD had nonerosive disease, and two thirds of the remaining had only minimal erosive changes at endoscopy. Endoscopy-negative patients with GERD are more likely to be female, younger, thin, and without hiatal hernia. Despite their mild mucosal damage, these patients demonstrate a chronic pattern of symptoms with periods of exacerbation and remission.

Nonerosive GERD is suspected by the presence of typical reflux symptoms with a normal endoscopic examination and is confirmed by the patient’s response to antisecretory therapy. When performed, 24-hour esophageal pH monitoring identifies three distinct subset of patients with nonerosive disease. First, there are the patients with abnormal acid exposure time who are usually responsive to antisecretory therapy. Second are the patients with normal reflux parameters but a good relationship between acid reflux episodes and symptoms. This group represents 30% to 50% of patients with nonerosive GERD and has “functional heartburn.” These patients probably have heightened esophageal sensitivity to acid and are less likely to respond to antireflux therapy. The third group is characterized by normal acid exposure times and poor symptom correlation. Despite sometimes having classical reflux symptoms, other diseases such as achalasia, gastroparesis, bile reflux, or functional dyspepsia are the cause of their symptoms. Overall, patients with nonerosive GERD do not respond to antireflux treatments as well as do patients with erosive GERD, probably because these three subsets are not carefully defined before treatment.

Erosive Acid Reflux Disease

The clinical course of patients with erosive esophagitis is more predictable and is associated with complications of GERD. Controlled studies have shown that in the absence of ongoing maintenance therapy, up to 85% of patients with erosive GERD will have a relapse within 6 months, and the relapse rate is highest in those with the more severe grades of esophagitis. This observation, however, should not prevent at least one attempt to withdraw medication, because 20% of patients remain in remission for up to 1 year, especially those with milder esophagitis grades. Although the natural history of untreated erosive GERD is well studied, two European studies suggest that these patients are more prone to reflux complications. In a Finnish study, 20 patients with erosive GERD treated with lifestyle changes, antacids, and prokinetic drugs were followed up for a median of 19 years. Fourteen patients continued to have erosions, and 6 new cases of Barrett esophagus were detected. Likewise, a large retrospective European study with 6.5 years of follow-up found a high rate of complications (21%) including 13 esophageal ulcers, 15 with strictures, and 45 patients with Barrett epithelium. However, these data must be contrasted with other studies in which no patients with erosive esophagitis developed Barrett esophagus in a 2-year trial in the United States, and over a 12-year period, in 3800 French patients, development of stricture was reported in only 0.26%.