PROGNOSIS

• Most patients with GERD do well with medications, although a relapse after cessation of medical therapy is common and indicates the need for long-term maintenance therapy [23].
• Identifying the subgroup of patients who may develop the most serious complications of the disease and treating them aggressively is important. Surgery at an early stage is most likely indicated in these patients [23].

• After a laparoscopic Nissen fundoplication, symptoms resolve in approximately 92% of patients.




COUNCELLING
• Avoid alcoholic beverages.
• Avoid carbonated beverages.
• Avoid chocolate.
• Avoid citrus products and juices.
• Avoid excessive physical activity.
• Avoid raw onions.
• Avoid voluminous meals
• Elevate the head of the bed.
• Favor decaffeinated coffee.
• Lose weight (if obese).
• Quit smoking.
• Reduce coffee intake.
• Reduce fat intake.
• Sleep in the left lateral decubitus position.
• Elevate the head of the bed
• Patients taking over the counter antacids should be aware of heir side effects as
Aluminum salts
• Constipation
• Accumulation in patients with renal impairment
• Hypophosphatemia
• Osteomalacia (rare)
Calcium salts

• Constipation
• Milk-alkali syndrome with high doses
• Rebound hyperacidity (depends on dosage)
Magnesium salts


• Diarrhea
• Accumulation in patients with renal impairment
Sodium bicarbonate

• Milk-alkali syndrome with high doses and should not be taken by hypertensives and patients of heart failure
Magnesium- aluminum combinations



• Minor changes in bowel function





REFRENCES

1. DeVault, KR, Castell, DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol 2005; 100:190.
2. Dent, J, El-Serag, HB, Wallander, MA, Johansson, S. Epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut 2005; 54:710.
3. Camilleri, M, Dubois, D, Coulie, B, et al. Prevalence and socioeconomic impact of upper gastrointestinal disorders in the United States: results of the US upper gastrointestinal study. Clin Gastroenterol Hepatol 2005; 3:543.
4. Pan GZ, Xu GM, Ke MY, Han SM, Guo SP, Li ZS, et al. Epidemiological study of symptomatic gastroesophageal reflux disease in China: Beijing and Shanghai. Chin J Dig Dis 2000; 1:2-8.
5. Kang JY, Ho KY. Different prevalences of reflux oesophagitis and hiatus hernia among dyspeptic patients in England and Singapore. Eur J Gastroenterol Hepatol 1999; 11: 845-50.
6. Khek Yu Ho; Ting Kin Cheung; Benjamin Cy Wong. Gastroesophageal Reflux Disease in Asian Countries: Disorder of Nature or Nurture? J Gastroenterol Hepatol. 2006;21(9):1362-1365
7. Medical Advisory Panel for the Pharmacy Benefits Management Strategic Healthcare Group. VHA/DoD clinical practice guideline for the management of adults with gastroesophageal reflux disease in primary care practice. Washington (DC): Veterans Health Administration, Department of Defense; 2003 Mar
8. Kahrilas, PJ, Quigley, EM. Clinical esophageal pH recording: A technical review for practice guideline development. Gastroenterology 1996; 110:1982.
9. Pandolfino JE, Kahrilas PJ. American Gastroenterological Association medical position statement: clinical use of esophageal manometry. Gastroenterology 2005 Jan;128(1):207-8.
10. Howard, PJ, Maher, L, Pryde, A, et al. Symptomatic gastro-oesophageal reflux, abnormal oesophageal acid exposure, and mucosal acid sensitivity are three separate, though related, aspects of gastro-oesophageal reflux disease. Gut 1991; 32:128.
11. Levine, MS. Gastroesophageal reflux disease. In: Radiology of the Esophagus, Levine, MS, WB Saunders, Philadelphia 1989. p.1147.
12. Institute for Clinical Systems Improvement (ICSI). Initial management of dyspepsia and GERD. Bloomington (MN): Institute for Clinical Systems Improvement (ICSI); 2006 Jul. 53 p
13. van Pinxteren, B, Numans, ME, Bonis, PA, Lau, J. Short-term treatment with proton pump inhibitors, H2-receptor antagonists and prokinetics for gastro-oesophageal reflux disease-like symptoms and endoscopy negative reflux disease. Cochrane Database Syst Rev 2000; :CD002095.
14. Stein, HJ, DeMeester, TR. Who benefits from antireflux surgery? World J Surg 1992; 16:313.
15. Vigneri S, Termini R, Leandro G, Badalamenti S, Pantalena M, Savarino V, et al. A comparison of five maintenance therapies for reflux esophagitis. N Engl J Med 1995;333:1106-10.
16. University of Michigan Health System. Management of gastroesophageal reflux disease (GERD). Ann Arbor (MI): University of Michigan Health System; 2002 Mar.
17. ZerR F, des Varannes SB, Roman S, et al. Normal values and day-to-day variability of 24-h ambulatory oesophageal impedance-pH monitoring in a Belgian-French cohort of healthy subjects. Aliment Pharmacol Ther 2005; 22:1011-1021.
18. Eliakim R, Sharma VK, Yassin K, et al. A prospective study of the diagnostic accuracy of PillCam ESO esophageal capsule endoscopy versus conventional upper endoscopy in patients with chronic gastroesophageal reflux diseases. J Clin Gastroenterol 2005; 39:572-578.
19. Arts J, Tack J, Galmiche JP. Endoscopic antireflux procedures. Gut 2004; 53:1207-1214.
20. Emmanuel Coron; Jan G. Hatlebakk; Jean-Paul Galmiche. Novel Developments in Non-erosive and Erosive Gastro esophageal Reflux Disease. Curr Opin Gastroenterol. 2006;22(4):399-405.
21. Inadomi, JM, Sampliner, R, Lagergren, J, et al. Screening and surveillance for barrett esophagus in high-risk groups: A cost-utility analysis. Ann Intern Med 2003; 138:176.
22. Kahrilas PJ: Refractory heartburn. Gastroenterology 2003;124:1941
23. Spechler SJ, Lee E, Ahnen D, et al. Long-term outcome of medical and surgical therapies for gastroesophageal reflux disease: follow-up of a randomized controlled trial. JAMA. May 9 2001;285(18):2331-8.
24. Laine, L, Ahnen, D, McClain, C, et al. Review article: potential gastrointestinal effects of long-term acid suppression with proton pump inhibitors. Aliment Pharmacol Ther 2000; 14:651.
25. Kamel P, Kahrilas PJ, Hanson DG, McMahan J, Brenic S. Prospective trial of omeprazole in the treatment of "reflux laryngitis." Gastroenterology 1992;102:Suppl:A93-A93.
26. Katz, PO, Castell, DO. Gastroesophageal reflux disease during pregnancy. Gastroenterol Clin North Am 1998; 27:153.
27. Larson, JD, Patatanian, E, Miner, PB Jr, et al. Double-blind placebo-controlled study of ranitidine for gastroesophageal reflux symptoms during pregnancy. Obstet Gynecol 1997; 90:83.
28. Nikfar, S, Abdollahi, M, Moretti, ME, et al. Use of proton pump inhibitors during pregnancy and rates of major malformations: A meta-analysis. Dig Dis Sci 2002; 47:1526.

TREATMENT OF ACID LARYNGITIS

• If patient has acid laryngitis, with the present state of knowledge, it seems reasonable to try treatment with omeprazole for two months to suppress the output of acid, with monitoring of the clinical response and the appearance at laryngoscopy.

TREATMENT DURING PREGNANCY
• The smooth muscle relaxation that occurs during pregnancy predisposes to gastroesophageal reflux [26].
• Lifestyle modifications or antacids should be first-line therapy in symptomatic women [26].
• The greatest experience with pharmacologic acid-suppressive therapy in pregnant women has been with the H2 receptor antagonist ranitidine and cimetidine, which appear to be safe during pregnancy [27].
• There is less experience using proton pump inhibitors during pregnancy. However, they are probably safe [26, 28].





FOLLOW UP
• Following up at 8 weeks to see if there has been some improvement in symptoms may be done, once treatment has been started. If there is no improvement, the patient should be referred for endoscopy.

• Symptoms unchanged
If symptoms remain unchanged in a patient who has had a prior normal endoscopy, evidence for the need for repeat endoscopy is not known, but currently not recommended [16].
• Warning signs.
Patients with warning signs and symptoms suggesting complications from GERD should be referred to a GERD specialist [16]
• Risk for complications
Consider further diagnostic testing (e.g., esophagogastroduodenoscopy [EGD], pH monitoring) for those who do not respond to acid suppression therapy [16].
Further diagnostic testing should also occur in patients with a chronic history of GERD who are at risk for complications (e.g., Barrett’s esophagitis, adenocarcinoma, and stricture) [16]
• It is reasonable to assess vitamin B12 levels periodically in patients who are on long-term treatment with PPIs [24]


SURVEILLANCE

• Endoscopy to screen for Barrett’s esophagus is recommended in patients with a long duration of GERD symptoms (e.g., > 5 years), particularly white males who are 50 or more years of age [7].
• If patient has developed Barrett’s esophagus, the grade of dysplasia determines the endoscopy interval, and an abnormal epithelial surface such as a nodule or ulcer requires special sampling attention. Surveillance endoscopy intervals are lengthening in the absence of dysplasia on two consecutive endoscopies with biopsy—a 3-yr interval is appropriate [21].
• In patients without Barrett's esophagus on an initial examination, the cancer risk is too low to justify a follow-up endoscopy. Exceptions are patients who develop bleeding, dysphagia, or a significant change in symptoms while on effective therapy [21]
• In patients with low-grade dysplasia repeat endoscopic surveillance in 3-6 months to screen for coexisting high-grade dysplasia or cancer.
• If low-grade dysplasia persists (which occurs in < 25% of patients), endoscopic surveillance should be repeated yearly.
• If patient has high grade dysplasia, close endoscopic surveillance every 3-6 months with biopsy may also be considered, reserving surgery or alternative therapies for treatment of proven intramucosal or invasive adenocarcinoma.
•

Management for Refractory Reflux

• Approximately 10-20% of patients with gastroesophageal reflux symptoms do not respond to once-daily doses of proton pump inhibitors, and 5% do not respond to twice-daily doses [22].
• These patients undergo endoscopy prior to escalation of therapy. The presence of active erosive esophagitis usually is indicative of inadequate acid suppression and can almost always be treated successfully with higher proton pump inhibitor doses (eg, omeprazole 40 mg twice daily) [22] .
• Truly refractory esophagitis may be caused by gastrinoma with gastric acid hypersecretion (Zollinger-Ellison syndrome), pill-induced esophagitis, resistance to proton pump inhibitors, and medical noncompliance [22] .
• Patients without endoscopically visible esophagitis should undergo esophageal pH monitoring to determine the amount of esophageal acid reflux and to assess whether the symptoms are acid related.
• If the pH study shows a normal amount of acid reflux, treatment with a low-dose tricyclic antidepressant (eg, imipramine or nortriptyline 25 mg at bedtime) may be beneficial [22].
• As second-line therapy of refractory heartburn with or without esophagitis, standard-dose H2RA therapy for an additional 2 to 4 weeks produces a limited increase in the cumulative rate of heartburn resolution (range of increase, 2 to 8%).
• For refractory erosive reflux esophagitis, extending the duration of treatment by 4 to 12 weeks with standard-dose H2RA produces modest increases in cumulative healing rates (median increase, 14%; range, 13 to 21%).
• Patients with erosive esophagitis or worse should be treated with proton pump inhibitors (PPI) in a double therapeutic dose.
• If Esomeprazole (Nexium®) has not been used at this point, it would be reasonable to try a therapeutic trial.
• Patients intolerant of PPIs may receive a quadruple therapeutic dose of H2RA. Failure to respond should prompt doubling the dose of the antisecretory medication and referral to gastroenterology

• There are several indications for surgery in the patient with GERD [14]:

Persistent or recurrent symptoms despite medical therapy
Severe esophagitis by endoscopy
Benign stricture
Barrett's columnar-lined epithelium (without severe dysplasia or carcinoma)
Recurrent pulmonary symptoms (eg, aspiration, pneumonia) in association with GERD
• Different endoscopic techniques have been developed to treat chronic GERD on an outpatient basis since PPI therapy is expensive and not curative [19].
• In general these techniques use three different approaches to improve the function of the gastroesophageal barrier. The gastroesophageal junction can be tightened either by the delivery of radiofrequency-energy at the cardia with the Stretta procedure, by the creation of plications with the Full-Thickness Plicator or Endocinch, or by the injection/implantation of inert material into the wall with the Gatekeeper or Enteryx procedures [20].

Single Trial Step-Down Therapy
• All patients with GERD should have one attempt at discontinuation therapy.
• Step-down therapy gradually reduces the intensity of treatment as tolerated to maintain the patient in remission.
• Changes should be made at 2 – 4 weekly intervals
• Lifestyle modifications should be continued indefinitely. Patients whose initial symptoms were controlled by lifestyle measures initially may require only occasional PPIs.
MAINTENANCE THERAPY —
• Given the propensity of esophagitis to relapse, maintenance acid suppressive therapy is often necessary [15]
• After discontinuation of proton pump inhibitor therapy, relapse of symptoms occurs in 80% of patients within 1 year the majority of relapses occurring within the first 3 months. [1]
• The need for maintenance therapy depends largely on the severity of the disease and the persistence of symptoms after the withdrawal of initial pharmacologic therapy [15].
• If the symptoms relapse in < 3 months and endoscopy has not been done, advise endoscopy and H Pylori testing
• If no H Pylori infection and GERD proven on endoscopy, treat with previously effective treatment indefinitely.
• If symptoms relapse in > 3 months repeat course of previously effective acute treatment indefinitely [1]
• In most patients with mild symptoms, antacids or over-the-counter H2-receptor blockers can be used as needed to help control symptoms.
• The lowest effective scheduled dosage of an H2-receptor blocker or a prokinetic agent should be used in patients with nonerosive esophagitis and moderate to severe symptoms.
• Patients with erosive esophagitis or complicated disease should be given one of the proton pump inhibitors because of the higher rates of remission associated with these agents [15].
• The lowest effective dosage should be used to maintain remission
• Maintenance therapy should be continued for 3 – 6 months
DRUG SAFETY
With maintenance antisecretory therapy being the rule rather than the exception, drug safety becomes an important issue. Various problems that can arise due to long term acid suppression are [24]:
1. - Pneumonia
2. - Hypergastrinemia
3. - Atrophic gastritis
4. - Enteric infections
5. - Vitamin B12 malabsorption

PHARMACOLOGICAL TREATMENT

Initial Management (8 Weeks)
• Antacids were the standard treatment in the 1970s and are still effective in controlling mild symptoms of GERD. Antacids should be taken after each meal and at bedtime.
• Histamine H2 receptor antagonists are the first line agents for patients with mild-to-moderate symptoms and grades I-II esophagitis.
• Histamine H2 receptor antagonists are effective for healing only mild esophagitis in 70-80% of patients with GERD and for providing maintenance therapy to prevent relapse.
• Tachyphylaxis has been observed, suggesting that pharmacologic tolerance can reduce the long-term efficacy of these drugs.
• Additional H2 blocker therapy has been reported to be useful in patients with severe disease (particularly those with Barrett esophagus) who have nocturnal acid breakthrough.
• Proton pump inhibitors are the most powerful medications available.
• Patients whose symptoms persist despite 6 weeks of standard doses of H2-receptor antagonist therapy should be treated with a proton pump inhibitor (once daily omeprazole or rabeprazole 20 mg, lansoprazole 30 mg, esomeprazole or pantoprazole 40 mg). The decision to prescribe proton pump inhibitors is based on the presence of persistent symptoms, not endoscopic findings
• They should be used only when GERD has been objectively documented. Proton pump inhibitors work by blocking the final step in the H+ ion secretion by the parietal cell. They have few adverse effects and are well tolerated for long-term use.
• Initial treatment of GERD should consist of an eight-week trial of PPI therapy, more long-term behavioral modifications, and possibly endoscopy, designed to help reduce reflux both structurally and promoting proper function of the lower esophageal sphincter (LES), and also reducing acidity of gastric juices.
• Following up at 8 weeks to see if there has been some improvement in symptoms may be done. If there is no improvement, the patient should be referred for endoscopy
• If these modifications have already been tried by the patient and have been successful, then maintenance therapy would be appropriate.
• In patients who incompletely respond to a trial of either nonprescription or prescription H2RA, PPIs are preferred over continuing H2RA therapy because of their greater efficacy and faster symptom control, and the limited benefit gained from extending therapy with the same or higher dose of H2RA [7].
• Second-line therapy with H2RAs also takes longer to achieve a response rate similar to that with PPIs. Patients who had inadequate responses to at least 12 weeks of standard-dose H2RA may need to take an H2RA for 8 to 12 weeks more (even at double doses) to achieve a cumulative healing or heartburn resolution rate close to that seen with just 4 weeks of PPI therapy
• Switch to a PPI if there is an incomplete response to H2RA therapy
• The initial treatment approach may be either step-down therapy (PPI first) or step-up therapy (H2RA first)

• Prokinetic drugs (bethanechol, metoclopramide, cisapride, and tegaserod) have the potential to be useful adjuncts in the treatment of GERD by counteracting some physiologic abnormalities that are present[13]
• These agents are somewhat effective but only in patients with mild symptoms; other patients usually require additional acid-suppressing medications such as proton pump inhibitors [13].
• Long-term use of prokinetic agents may have serious, even potentially fatal, complications and should be discouraged [13].

Inadequate Response to PPI Therapy
• If there is an inadequate response to a course of standard-dose PPI, extend treatment with either the same or double dose of PPI
• The patient who does not respond to a course of standard-dose PPI should be referred for further diagnostic testing
• If Esomeprazole has not been used at this point, it would be reasonable to try a therapeutic trial

DIFFRENTIAL DIAGNOSIS

GERD needs to be distinguished from [7]
• Infectious esophagitis (cytomegalovirus, herpes and candida)
• Pill esophagitis
• Eosinophilic esophagitis
• Peptic ulcer disease
• Non-ulcer dyspepsia
• Biliary tract disease
• Coronary artery disease
• Esophageal motor disorders
INVESTIGATIONS

It is neither necessary nor practical to initiate a diagnostic evaluation in every patient with heartburn [1].
• No routine laboratory tests are required.
• Hemoglobin and hematocrit would be helpful to detect anemia, particularly in patients with hematemesis, other signs of gastrointestinal bleeding, or severe, unremitting symptoms.
• Empiric therapy for GERD is reasonable without diagnostic testing. Patients who present with typical symptoms of GERD in the absence of longstanding, frequently recurring, progressive, or alarm symptoms or complicated disease may be started on empiric treatment and rarely need a confirmatory diagnostic test since symptom resolution is the primary clinical end point
• Indications for Further Diagnostic Testing
o Lack of response to therapy
o Need for continuous chronic therapy
o Chronic symptoms in a patient at risk for Barrett’s esophagus
o Alarm symptoms suggesting complicated GERD:
 bleeding
 chest pain
 choking (acid causing coughing, shortness of breath, or hoarseness)
 dysphagia
 weight loss
• If alarm features are present, endoscopy should be performed urgently and time limit for refferal for endoscopy is:
• Anemia (7-10 days)
• Acute onset of total dysphagia (within 1 day)
• Hematemesis (within 1 day if ill)
• Melena (within 1 day if ill)
• Persistent vomiting (7-10 days)
• Weight loss greater than 5% (involuntary) (7-10 days)
• If endoscopy is done and patient has erosions, ulcerations, strictures or intestinal metaplasia (Barrett's esophagus) , they have a positive endoscopy. Patients who have either a normal esophageal examination or only distal esophageal erythema are considered to have a negative endoscopy.
• If patient has acid laryngitis, endoscopy shows erythema or white plaques on the posterior larynx (posterior laryngitis). Some patients have a normal-appearing larynx, just as some patients with serious symptoms of reflux have a normal-appearing esophageal mucosa, viewed endoscopically. In severe cases of acid laryngitis, ulceration or polyp formation is seen on the vocal cords.
• If endoscopy is done biopsy should be taken. Even though the esophagus may appear endoscopically normal, it is not necessarily histologically normal.
• Esophageal capsule endoscopy might be an accurate, safe, and well-tolerated method to screen patients for significant esophageal disorders. Preliminary data seem promising. Recently, Eliakim et al. conducted a multicenter trial at seven sites involving 106 patients (93 GERD, 13 Barrett) undergoing esophageal capsule endoscopy followed by conventional endoscopy. Sixty-six of 106 patients had positive esophageal findings. Esophageal capsule endoscopy identified esophageal abnormalities in 61 (sensitivity, 92%; specificity, 95%) [18].

• 24-hour pH monitoring has been adopted as the diagnostic standard. 24-hour pH monitoring measures longer periods, captures transient pH changes not associated with symptoms, and can be coded into a scientific scoring system yielding acceptable sensitivities [12]
• Esophageal pH recording is indicated to document abnormal esophageal acid exposure in an endoscopy-negative patient being considered for surgical antireflux repair (pH study done after withholding antisecretory drug regimen for one week) [8]
• Esophageal pH recording is indicated to evaluate patients after antireflux surgery who are suspected to have ongoing abnormal reflux (pH study done after withholding antisecretory drug regimen for one week) [8]
• Esophageal pH recording is indicated to evaluate patients with either normal or equivocal endoscopic findings and reflux symptoms that are refractory to proton pump inhibitor therapy (pH study done after withholding antisecretory drug regimen for one week if the study is done to confirm excessive acid exposure or while taking the antisecretory drug regimen if symptom reflux correlation is to be scored) [8]
• Esophageal pH recording is possibly indicated to detect refractory reflux in patients with chest pain after cardiac evaluation using a symptom reflux association scheme, preferably the symptom association probability calculation (pH study done after a trial of proton pump inhibitor therapy for at least four weeks) [8]
• Esophageal pH recording is possibly indicated to evaluate a patient with suspected otolaryngologic manifestations (laryngitis, pharyngitis, chronic cough) of gastroesophageal reflux disease after symptoms have failed to respond to at least four weeks of proton pump inhibitor therapy (pH study done while the patient continues taking the antisecretory drug regimen to document the adequacy of therapy).
• Esophageal pH recording is possibly indicated to document concomitant gastroesophageal reflux disease in an adult onset, nonallergic asthmatic suspected of having reflux-induced asthma (pH study done after withholding antisecretory drugs for one week) [8]
• Impedance-pH monitoring is the most sensitive method for detection and characterization of gastroesophageal reflux episodes but normal values have been lacking.
• Zerbib et al conducted 24-h ambulatory impedance-pH studies in 72 healthy subjects to build a database of gastroesophageal reflux patterns. Most (59%) gastroesophageal reflux episodes were acid, while 28% and 10% were weakly acidic and weakly alkaline, respectively. In addition, the authors showed that 24-h ambulatory impedance-pH monitoring is reproducible [17]
• If patient has acid laryngitis, studies using pH probes just above and just below the upper esophageal sphincter have shown that during some episodes of reflux, gastric acid reaches the level of the larynx [25]
• Esophageal manometry is of minimal use in the diagnosis of GERD. It should not be used for making or confirming a suspected diagnosis of gastroesophageal reflux disease [9]
• Manometry should not be routinely used as the initial test for chest pain or other esophageal symptoms because of the low specificity of the findings and the low likelihood of detecting a clinically significant motility disorder [9]
• The Bernstein test is useful to determine symptom correlation with esophageal acidification in patients without endoscopic evidence of esophagitis [10].
• The test is done by alternately infusing saline or 0.1N HCl at a rate of 6 to 8 mL/min into the mid-esophagus via a nasogastric tube or manometric assembly [10].
• A positive test is defined as reproduction of the patient's symptoms with acid perfusion but not with saline. This test is ideal for determining acid sensitivity [10].
• Double contrast barium swallow examinations can identify early stages of reflux esophagitis by a granular or nodular appearance of the mucosa of the distal third of the esophagus with numerous ill-defined, 1 to 3 mm lucencies (show radiograph 1) [11]. A variety of other changes may also be seen [11]: Thickening of the longitudinally oriented esophageal folds may occur, with folds wider than 3 mm categorized as abnormal. These folds may be quite tortuous, mimicking varices. Shallow ulcers and erosions are recognized on double contrast radiographs as tiny collections of barium in the distal esophagus near the gastroesophageal junction, sometimes surrounded by a radiolucent halo of edematous mucosa
• The water siphon test (sipping water in supine position during a barium esophagram) has a sensitivity of only 60% and a false positive rate of 30% [12]

TREATMENT
• Mild symptomatic GERD can usually be managed empirically; lifestyle and dietary modifications along with antacids and nonprescription histamine-2 (H2) receptor antagonists are usually sufficient.
• Patients with debilitating symptoms usually require more pharmacologic acid-suppressive therapy or antireflux surgery.
• Between these extremes, matching the potency of therapy with disease severity can be achieved either by a "step up" approach (beginning with lifestyle and dietary measures and incrementally increasing the therapeutic intervention over time until symptom control is achieved) or a "step down" approach (beginning with potent antisecretory agents to achieve rapid symptom control and then incrementally decreasing the intervention until break-through symptoms define the therapy necessary for continued symptom control)
NON PHARMACOLOGICAL TREATMENT


Lifestyle modifications are aimed at enhancing esophageal acid clearance, minimizing the incidence of reflux events, or both as with cessation of smoking and avoidance of late meals:
• Head of bed elevation, which can be achieved either by putting 6- to 8-inch blocks under the head end of bed or having more pillows to elevate head. Head of bed elevation is important for individuals with nocturnal or laryngeal symptoms; its necessity in other situations is questionable.
• Dietary modification may be helpful. It is practical to suggest avoidance of a core group of reflux-inducing foods (fatty foods, chocolate, peppermint, and excessive alcohol, which may reduce lower esophageal sphincter pressure) and then to suggest that the patient selectively avoid foods known to cause symptoms. As an example, a number of beverages have a very acidic pH and can exacerbate symptoms. These include colas, red wine, and orange juice (pH 2.5 to 3.9).
• Refraining from assuming a supine position after meals for 2- 3 hours and avoidance of meals before bedtime, both of which will minimize reflux.
• Avoidance of tight fitting garments, which reduces reflux by decreasing the stress on a weak sphincter.
• Obesity is a risk factor for GERD [1]. However, improvement in symptoms following weight loss is not uniform after weight loss. Nevertheless, because of a possible benefit, and because of its other salutary effects, weight loss should be recommended and BMI maintained between 19 – 24.9 kg/m2.
• Promotion of salivation by either chewing gum or use of oral lozenges may also be helpful in mild heartburn. Salivation neutralizes refluxed acid, thereby increasing the rate of esophageal acid clearance.
• Restriction of alcohol use is advised
• Elimination of smoking; smoking is deleterious in part because it diminishes salivation.
• Consider changing medications that can lower the LES pressure (i.e., Theophylline, calcium channel blockers, and barbiturates).

RISK FACTORS FOR GERD

The risk factors associated with GERD include the following [7]:
• Psychological stress,
• Psychiatric disease,
• Alcohol
• Smoking
• Obesity (body mass index >30 kg/m2)
• An immediate family history of heartburn or gastroesophageal disease
• Use of nonsteroidal anti-inflammatory drugs


CLINICAL FEATURES

SYMPTOMS
• GERD is the probable diagnosis if the patient has heartburn (retrosternal pain) or acid regurgitation (a sour or bitter taste in mouth) as the dominant symptom.
• These symptoms are sought because their presence is associated with a probability of 89% and 95%, respectively, of GERD based on studies using esophageal pH monitoring as the reference standard [7]
• Symptoms of heartburn, regurgitation, or both, occuring after meals (particularly large or fatty meals) are highly specific
• Unusual symptoms include Hypersalivation (waterbrash), nausea and odynophagia (painful swallowing
• Extra intestinal symptoms include asthma, chest pain, noncardiac, chronic cough, dental disease, globus sensation, hoarseness, laryngitis and respiratory symptoms [7]
• Alarm Features include dysphagia, odynophagia, weight loss, hematemesis, black or bloody stools, chest pain, or choking (acid reflux causing coughing, hoarseness, or shortness of breath). Patients with alarm symptoms require immediate referral for further diagnostic testing [7]
• Complications include [7]:

• Barrett’s esophagus -- 10% to 15%
• Esophageal stricture -- 4% to 20%
• Esophageal ulceration -- 2% to 7%
• Esophageal hemorrhage -- < 2%
• Esophageal perforation -- < 0.2%
• Esophageal adenocarcinoma
• With Barrett’s esophagus -- 0.5%/y
• Without Barrett’s esophagus -- 0.07%/y


• Factors that may exacerbate or contribute to symptoms include the following:
o Gastric distension (e.g., voluminous meals)
o Supine position, particularly the right lateral decubitus position
o Bending over
o Certain foods or beverages (e.g., alcohol, caffeinated beverages, carbonated beverages, peppermint/spearmint, chocolate, citrus, high-fat foods, milk, onions, garlic, spicy foods, tomato juices)
o Excessive physical activity (e.g., running)
SIGNS
• Physical examination is not helpful [7]
• Look for any signs of extraesophageal disease, complications of advanced disease, or diseases that may present with GERD symptoms (e.g., gastric or esophageal carcinoma) [7].
HISTORY
A detailed history should be obtained from all patients regarding [7]:
• Symptom description
• Exacerbating factors
• Measures taken to relieve symptoms
• Response to previous treatments

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

DEFINITION
Symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus is known as gastro esophageal reflux disease [1]
Nonerosive gastro esophageal reflux disease
The majority of patients with typical symptoms of GERD do not have esophagitis; such patients have been referred to as having nonerosive reflux disease (NERD) [10]
DIAGNOSTIC CRITERIA

• The cardinal symptoms associated with GERD are heartburn and regurgitation. However, complications from GERD can arise even in patients who lack these typical symptoms [1].
• Heartburn may be exacerbated by meals, bending, or recumbency.
• Typical uncomplicated cases do not require diagnostic studies.
• Endoscopy demonstrates abnormalities in < 50% of patients [1].
• Barium esophagography is seldom helpful.

EPIDEMIOLOGY
An approximate prevalence of 10 to 20 percent is identified for GERD (as defined by at least weekly heartburn and/or acid regurgitation) in the Western world while the prevalence is lower (5 percent) in Asia. The incidence in the Western world was approximately 5 per 1000 person years [2, 3]. One study from Singapore [5] reported very low prevalence in the region at 2% while another from China reported the prevalence at 6% [4], but there is now evidence to suggest that its frequency is rapidly rising in Asia [6].
Race
• White males are at a greater risk for Barrett esophagus and adenocarcinoma than other populations.
Sex
• No sexual predilection exists. GERD is as common in men as in women [2].
• The male-to-female ratio for esophagitis is 2:1-3:1. The male-to-female ratio for Barrett esophagus is 10:1.
Age
• GERD occurs in all age groups [2].
• The prevalence of GERD increases in people older than 40 years [2].

Causal Mechanisms of GER [7]
o Transient relaxation of the lower esophageal sphincter
o Increased intra-abdominal pressure that overpowers a decrease in lower esophageal sphincter tone
o Impaired esophageal or gastric motility
o Certain medical conditions like scleroderma are associated with diminished peristalsis. Sjogren's syndrome, anticholinergic medications and oral radiation therapy may exacerbate GERD due to impaired salivation
o If hiatal hernia is present which is usually silent may be associated with higher amounts of acid reflux and delayed esophageal clearenceleading to more severe esophigitis especially Barret's esophagus