Gastroesophageal reflux disease ...

GUIDELINES IN FOCUS

Gastroesophageal reflux disease: nonpharmacological treatment ©2012 Elsevier Editora Ltda.

Este é um artigo Open Access sob a licença de CC BY-NC-ND

AUTHORS Federação Brasileira de Gastroenterologia, Sociedade Brasileira de Endoscopia Digestiva, Colégio Brasileiro de Cirurgia Digestiva, Sociedade Brasileira de Pneumologia, Associação Brasileira de Otorrinolaringologia e Cirurgia Cérvico-Facial

PARTICIPANTS Aloisio Carvalhaes, Angelo Paulo Ferrari Junior, Antonio Frederico Magalhães, Ary Nasy, Celso Mirra Paula e Silva, Claudio L. Hashimoto, Décio Chinzon, Edson Pedro da Silva, Eduardo G.H. Moura, Eponina Maria Oliveira Lemme, Farid Butros Iuan Nader, Fauze Maluf Filho, Gerson R. de Souza Domingues, Igelmar Barreto, Isac Jorge Filho, Ismael Maguilnik, Ivan CecconelloI, Jaime Natan Eisig, Joaquim Padro P. de Moraes-Filho, Joffre Rezende Filho, José Carlos Del Grande, José Luiz Pimenta Modena, José Roberto Almeida, Lilian R.O. Aprile, Luciana Camacho-Lobato, Luciana Dias Moretzohn, Marcelo de Souza Cury, Marcio Matheus Tolentino, Marco Aurélio Santo, Marcos Kleiner, Marcos Tulio Haddad, Maria do Carmo Friche Passos, Olavo Mion, Osvaldo Malafaia, Paulo Roberto Savassi Rocha, Rafael Stelmach, Ricardo Aires Correa, Ricardo Correa Barbuti, Richard Gursky, Rimon Sobhi Azzam, Roberto El Ibrahim, Rubens Antonio Aissar Sallum, Roberto Oliveira Dantas, Schilioma Zaterka, Sérgio Gabriel Silva de Barros, Tomas Navarro Rodriguez, Ulysses G. Meneghelli, Wilson Modesto Polara, Esophagus and Motility Group of the Discipline of Clinical Gastroenterology of the Department of Gastroenterology of FMUSP, Sociedade Brasileira de Motilidade Digestiva

FINAL

VERSION

May 20, 2009

CONFLICT

OF INTEREST

Chinzon D received reimbursement for attending conferences sponsored by Jansen and, also received speaker and consulting fees sponsored by Jansen, AstraZeneca and Medley. Lemme EMO received speaker fees sponsored by AstraZeneca and received grants for research sponsored by Nycomed. Moraes Filho JPP received reimbursement for attending a symposium sponsored by AstraZeneca, 18

Rev Assoc Med Bras 2012; 58(1):18-24

Nycomed, and Medley; received speaker fees sponsored by AstraZeneca and Nycomed; received financial support for organizing educational activities sponsored by Nycomed, Aché and AstraZeneca. Rezende Filho J received speaker fees sponsored by Nycomed. Mion O received speaker fees sponsored by AstraZeneca. Stelmach R received speaker fees; financial support to organize teaching activities and to perform research; and consulting fees sponsored by AstraZeneca, Aché, Bayer Shering Plough, BoerhingerInghelhein, Eurofarma, Glaxo-Smith Kline, Novartis and Mantercorpe. Barbut RC received speaker fees; financial support to organize teaching activities and to perform research; and consulting fees sponsored by AstraZeneca, Aché and Medley. Dantas RO received speaker fees sponsored by AstraZeneca. Zaterka S received financial support for teaching and consulting activities sponsored by Jansen-Cilag. Navarro T received speaker fees; financial support for teaching and consulting activities, and performed research sponsored by AstraZeneca.

DESCRIPTION

OF THE EVIDENCE COLLECTION METHOD

A search was performed in the EMBASE, SciELO / LILACS, PubMed / Medline and Cochrane Library databases using the following words: gastroesophageal reflux, gerd, heartburn, nerd, gero, esophagus, esophagitis, extra-esophageal, asthma, atypical symptoms, chest pain, cough, globus sensations, hoarseness, otorhinolaryngology diseases, pain, respiratory tract diseases, laryngitis, anti-ulcer agents, enzyme inhibitors, proton pumps, lansoprazole, omeprazole, proton pump inhibitors, rabeprazole, continuous, on-demand, surgery, fundoplication, non acid*, alkaline, weakly acid*, gas, stomach diseases, stomach/pathology, Helicobacter, Helicobacter infections, burimamide, cimetidine, ebrotidine, etintidine, famotidine, lafutidine, loxtidine, metiamide, mifentidine, nizatidine, oxmetidine, ranitidine, ranitidine bismuth citrate, roxatidine acetate, tiotidine, zolantidine, histamine H2 antagonists, benzamides, dopamine antagonists, bromopride, domperidone metoclopramide, smoking, alcohol, obesity, weight loss, caffeine, coffee, citrus, chocolate, spicy food, head of bed elevation, late-evening meal, diet*, life style, body mass index, alcoholic, postprandial period, beer, wine, supine position, food*, eating, exercise, dietary fiber, dietary fats, beds*, bedding and linens*.

GASTROESOPHAGEAL REFLUX DISEASE: NONPHARMACOLOGICAL TREATMENT

A total of 5,000 publications were retrieved. Using the filters: humans, randomized controlled trial, randomized AND controlled AND trial, clinical AND trial, clinical trials, random*, random allocation, therapeutic use, epidemiologic methods, cohort studies, cohort AND stud*, prognos*, first AND episode, cohort, we selected 73 studies to support this Guideline.

DEGREE OF RECOMMENDATION AND STRENGTH OF EVIDENCE A: Experimental or observational studies of best consistency. B: Experimental or observational studies of lower consistency. C: Case reports (non-controlled studies). D: Opinion without critical evaluation, based on consensuses, physiological studies or animal models.

OBJECTIVE Due to high prevalence, variety of the clinical presentation forms and economic impact, consequences of loss of quality of life and clinical-laboratory research costs, the implementation of international consensus meetings has been encouraged. On the other hand, the diagnosis and therapeutic management of gastroesophageal reflux disease (GERD) has varied from center to center, which is an important factor in the search for scientific evidence on the issue, prompting the implementation of this Guideline, which seeks to answer four key clinical questions of the non-pharmacological treatment of GERD.

1. DOES

THE NONPHARMACOLOGICAL TREATMENT PRODUCE

RESULTS IN

GERD?

OBESITY Body mass index (BMI) > 25 is a risk factor for erosive GERD1 (B). There is an association between reflux symptoms and obesity (OR: 2.6)2 (B). BMI is associated with reflux (OR per 5 units: 1.9)3 (B). BMI > 25 is a risk factor (OR: 1.41) for GERD4 (B). Obesity is associated with GERD5 (B). Weight decrease does not reduce the manifestations of reflux6 (B). In patients with mean BMI of 42.5 kg/m2, there is no association with the prevalence of GERD7 (B). Obesity predisposes to gastroesophageal reflux, and weight loss improves postprandial reflux and reduces pH time < 48 (B). SMOKING Smoking is a risk factor for non-erosive GERD 1 (B) and for reflux symptoms2 (B). Smokers have more reflux episodes than nonsmokers, but a 24-hour abstinence does not reduce the pH time < 49 (B).

24-hour smoking abstinence reduces the number of reflux episodes, but does not affect the total acid exposure10 (B). Individuals abstaining from smoking for 48 hours have increased esophageal acid exposure11 (B). Smoking is associated with GERD5,12 (B). ALCOHOL Alcohol intake is a risk factor for erosive GERD1 (B). Frequent consumption of alcohol is a risk factor for reflux symptoms2 (B). The habits of drinking wine or beer increase the risk of reflux (NNH 7 to 9)13 (B). Alcohol consumption is a risk factor for erosive GERD (OR: 2.42 to 2.85)4,5 (B). COFFEE Coffee consumption is associated with GERD (OR: 1.23)5(B). DIET The consumption of sweets and white bread is associated with symptoms of reflux2 (B). Fruit consumption has a protective effect on reflux symptoms2 (B). Protein intake is associated with erosive GERD, and fiber, with a lower risk of GERD14 (B). Excessive consumption of food and sweet food is associated with GERD5 (B). High-fat diet does not increase the number of reflux episodes, or acid esophageal exposure15 (B). POSTURE Working in an inclined position is a risk factor for nonerosive GERD1 (B). GERD episodes are triggered by posture5 (B). INCLINED HEAD OF THE BED Sleeping with a wedge-shaped support is associated with less acid exposure than in the horizontal position16 (B). Raising the head of the bed (28 cm) reduces the number of reflux episodes and pH time < 517 (B). NIGHT MEALS The later the night the meal is, the higher the rate of reflux episodes, especially in obese individuals and in those with erosive GERD18 (B). Going to bed immediately after dinner is associated with increased risk of GERD, especially within a time period of less than 3 hours19 (B). PHYSICAL EXERCISE Physical activity seems to have a protective effect against GERD2 (B). STRESS AND FATIGUE GERD episodes are triggered by stress and fatigue11 (B). Stress is among the risk factors for GERD12 (B). Rev Assoc Med Bras 2012; 58(1):18-24

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GUIDELINES IN FOCUS

RECOMMENDATION Although obesity (BMI > 25), smoking, alcohol consumption, coffee, sweets, proteins, excess food, inclined posture, stress and fatigue are associated with GERD, there is no consistent information to define that the resolution of these factors is followed by resolution or improvement of GERD. However, the elevation of the head of the bed and going to bed only after a minimum of three hours after the night meal are measures that reduce esophageal acid exposure.

2. WHAT ARE OF GERD?

THE INDICATIONS OF SURGICAL TREATMENT

HIATAL HERNIA PARAESOPHAGEAL The laparoscopic Nissen fundoplication is equally effective in patients with GERD and paraesophageal hernia20 (B). There is improvement in abdominal pain, reflux, digestion score and quality of life score in patients with large paraesophageal hernias submitted to laparoscopic surgery21 (B). At the average follow-up period of 72 months, 93% of patients are free of GERD-related symptoms22 (B). RISK FACTOR Hiatal hernia is a risk factor for erosive GERD1 (B). A hiatal hernia < 3 cm is a risk factor for non-erosive GERD, and a hiatal hernia > 3 cm, for erosive GERD and Barrett’s esophagus23 (B). The size of hiatal hernia, low pressures in the lower esophageal sphincter, esophageal acid exposure and number of reflux episodes are associated with esophagitis severity24 (B). Hiatal hernias > 2 cm are associated with Barrett’s esophagus and erosive GERD25 (B). The presence of hiatal hernia is associated with more severe esophagitis and predisposes patients with non-erosive GERD to more severe histological alterations26 (B). Patients with hiatal hernias have a high incidence of pathological reflux, regardless of the low pressure in the lower esophageal sphincter. Patients with pathologic reflux have esophageal propulsion failure and/or mechanical defects of the cardia associated with hiatal hernia27 (B). PROGNOSIS Recurrence after fundoplication (Nissen or Toupet) is higher in large hernias (grades 3 and 4)28 (B). The permanent migration of the esophagogastric junction has more relevance in GERD prognosis than in sliding hiatal hernia, with reduction of the junction. Hiatal insufficiency and concentric hiatal hernia are determinant factors of irreversible cardia incontinence29 (B). In patients with GERD and hiatal hernia (31% erosive GERD and 75% lower sphincter dysfunction), reduction, crural closure, and Nissen fundoplication result in symptom improvement, at a 20

Rev Assoc Med Bras 2012; 58(1):18-24

14-month follow-up30 (B). In patients with GERD (complicated or not), the presence of hiatal hernia determines significant increase in the PPI dose to achieve intraesophageal acid suppression31 (B). RECOMMENDATION Considering that: The presence of the permanent migration of esophagogastric junction and size of hiatal hernia (> 2 cm) are factors of worst prognosis for GERD; The presence of hiatal hernia requires higher doses of PPIs; The result of the laparoscopic fundoplication is adequate, including for paraesophageal hernia. Hiatal hernias associated with GERD, especially those > 2 cm and fixed, should be treated surgically. MOTILITY The Nissen fundoplication has good results in patients with normal esophageal motility, and the Toupet technique, in patients with esophageal dysmotility32 (B). There is no difference in postoperative symptoms in patients with or without esophageal dysmotility submitted to fundoplication (Nissen or Toupet)33 (A). The type of fundoplication should not be determined by the presence of dysmotility, as the postoperative dysphagia is not related to it34 (A). Preoperative dysmotility reflects a more severe disease, does not affect the postoperative outcomes, does not improve fundoplication and may occur after surgery35 (B). RECOMMENDATION Considering that: The preoperative dysmotility reflects a more severe disease, does not affect the postoperative outcomes, does not improve with fundoplication and may occur after surgery; no surgical treatment should be indicated using the parameter of esophageal dysmotility. COST From the perspective of the National Health System, laparoscopic fundoplication is more cost-effective over eight years than PPI36 (B). Over five years, the cost of PPI is lower than the open surgery for GERD37 (B). Apparently, the Nissen fundoplication is more cost-effective in the treatment of GERD than treatment with PPI38 (B). RECOMMENDATION Apparently, the laparoscopic Nissen fundoplication, from the perspective of the National Health System, is more cost effective than PPI therapy over eight years. However, this is not the case with open surgery.

GASTROESOPHAGEAL REFLUX DISEASE: NONPHARMACOLOGICAL TREATMENT

3. WHEN

SHOULD CLINICAL TREATMENT BE INDICATED

VERSUS SURGICAL TREATMENT?

In patients with GERD (erosive and non-erosive), antireflux surgery, compared to drug treatment with a PPI reduces the pH time < 4.0 and improves the VAS symptom score, the GERSS score, and scores of heartburn and regurgitation39 (A). In patients with chronic erosive GERD, the Nissen surgery, compared to the use of PPIs, improves symptom scores, including the digestive score, and reduces the pH time < 4.040 (A). In patients with chronic erosive reflux disease, Nissen surgery compared to PPI increases the degree of patient satisfaction (NNT 5)41 (A). In patients with erosive reflux disease, antireflux surgery (Nissen or Toupet) compared to omeprazole 20 mg daily reduces the risk of treatment failure over 5 years. There is a greater number of treatment failures over five years with clinical treatment of omeprazole 40 mg or 60 mg compared to surgery (Nissen or Toupet). Surgery reduces the risk of treatment failure by 11.6% (95% CI: 0.6-22.6) - NNT: 9. However, symptom scores (GSRS) and quality of life scores (PGWB) were similar in the two compared forms of treatment42 (A). In patients with chronic erosive reflux disease, antireflux surgery (Nissen or Toupet) in comparison to omeprazole 20 mg reduces treatment failure, and, maintained for seven years, reduces dysphagia (NNT 38) and hiatal hernia (NNT 2)43 (A). In patients with chronic GERD (reflux symptoms + esophagitis + previous treatment > 3 months), treatment with esomeprazole 20 mg or 40 mg is equivalent to laparoscopic surgery (Nissen), with 93% and 90% of patients remaining in symptom remission, respectively 44 (A). There is a greater number of therapeutic failures in three years with the clinical treatment of omeprazole 40 mg or 60 mg, when compared to surgery (Nissen or Toupet). Surgery reduces the risk of treatment failure by 12.9% (95% CI: 1.9-23.9) - NNT: 8. However, symptom scores (GSR) and quality of life (PGWB) were similar in the two forms of treatment45 (A). SYMPTOMS, ESOPHAGITIS AND PH In patients with GERD not submitted to surgery, at a follow-up of 17 to 22 years, symptoms improved in 70% and worsened in 20%. Of these patients, 66% developed erosive GERD and/or pH changes, and 10% Barrett’s esophagus46 (B). At 12 months of follow-up, GERD treatment with medication and surgery (Nissen) is effective. However, surgery offers additional benefit to patients who had partial improvement with medication at a mean follow-up of 6.9 years41 (A).

At 18 months, regression from dysplasia to Barrett’s esophagus obtained with Nissen fundoplication (93.8%) is higher than that obtained with PPI (63.2%)47 (B). The quality of life is higher in patients submitted to surgery compared to those undergoing medical treatment, at 12 months of follow-up48 (B). The laparoscopic Nissen fundoplication leads to lower esophageal acid exposure in three months and better quality of life after 12 months, when compared to clinical treatment40 (A). Patients with Barrett’s esophagus have a 33% regression after antireflux surgery. The regression is more significant the longer the time after surgery49 (B). PATIENT PREFERENCE Laparoscopic surgery improves the quality of life of patients whose symptoms are adequately controlled with PPIs50 (B). PROGNOSIS In patients with GERD submitted to surgery after a follow-up of 5.9 years, 37% were using medications (PPIs, H2 blockers or antacids), of which 17% had never stopped and 83% resumed after 2.5 years due to return of symptoms. The pH-metry was abnormal in 32%51 (B). Comparing the response to surgical treatment of GERD, after 43 months, 66% had symptom improvement, which was lower in patients with non-erosive GERD52 (B). After five years, there was no difference in symptom improvement, adverse effects, or quality of life scores among patients with erosive and non-erosive GERD who underwent laparoscopic Nissen fundoplication53 (B). There was no difference in response rates among patients undergoing surgery for GERD with open or laparoscopic techniques, and this was higher in patients undergoing clinical treatment54 (B). In two years, 14.5% of medically treated patients developed Barrett’s esophagus compared with no patients submitted to surgery55 (B). Heartburn and esophagitis are effectively treated by medical and surgical therapy. Only surgery improved regurgitation, dysphagia and esophageal motility56 (B). At 10.9 years of follow-up, the Nissen fundoplication produces 84% symptom resolution, 89% esophagitis resolution and 5% use of medication, while the clinical treatment produces, respectively, 53%, 45%, and 21%57 (B). Laparoscopic fundoplication produces the same results in patients with erosive or nonerosive GERD, with symptom improvement and reduction in PPI use58 (B). Patients with Barrett’s esophagus have a 33% regression after antireflux surgery. The regression is more significant the longer the time after surgery49 (B). Rev Assoc Med Bras 2012; 58(1):18-24

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GUIDELINES IN FOCUS

LOWER ESOPHAGEAL SPHINCTER PRESSURE In patients with erosive GERD treated with PPI, the rate of recurrence at 12 months was 7.7% when they had normal pressure of the lower esophageal sphincter (> 8 mmHg), 38.1% in those with sphincter dysfunction and preserved motility and 79.5% in those with sphincter dysfunction and dysmotility59 (B). In five years of follow-up, patients with inadequate response to PPIs can benefit from laparoscopic fundoplication, especially regarding the improvement of the quality of life60 (B). During one year of follow-up, antireflux surgery obtained better results than medical treatment in relation to the symptoms of heartburn (19% versus 43%), regurgitation (8% versus 30%), increase in the need for PPIs (19% versus 74%), quality of life score (4 ± 0.6 versus 21 ± 1.4); and patient satisfaction (21.6% versus 5.9%)61 (B). The success rate of Nissen fundoplication is 75.3%, and is associated with 77.1% of patients who responded to medical treatment and 56.0% who did not respond62 (B). STENOSIS In two years of follow-up of patients with erosive GERD and stenosis, antireflux surgery reduces the number of dilations by a factor of 10, reduces the dysphagia score in 50%, and 91.9% of patients were satisfied63 (B). In a 10-year follow-up of patients that underwent Nissen fundoplication, the persistence or presence of symptoms was 32%, and 68% were asymptomatic. The quality of life remained high, although 80% had to undergo a new fundoplication procedure64 (B). NON-ACID GERD In patients on acid suppression, episodes of acid reflux are not associated with symptoms, but with mixed reflux episodes (liquid-gas)65 (B). When compared to healthy patients, the number of reflux events in 24 hours after fundoplication is significantly lower. Most reflux episodes after surgery are nonacid66 (B). Most preoperative patients had a positive symptom index, and 14 months after surgery, these patients were asymptomatic or had improved greatly67 (B). Most patients undergoing prolonged PPI use, with persistent symptoms and a positive symptom index, have non-acid reflux, including patients with atypical symptoms68 (B). In patients with GERD refractory to medical therapy, where gastric acid production is small (< 1 mEq/hour), about 50% have esophageal pH < 4.0 for more than 1.7% of the time69 (B). 22

Rev Assoc Med Bras 2012; 58(1):18-24

RECOMMENDATIONS Patients refractory to acid suppression, with typical or atypical symptoms, have non-acid reflux most of the time, and may benefit from surgical treatment. In a two-year follow-up of patients with erosive GERD and stenosis, antireflux surgery shows a 10-fold reduction in the number of dilations, reduces the score of dysphagia in 50%, and 91.9% of patients are satisfied. Considering that: Low pressures in the lower esophageal sphincter are related to the severity of esophagitis, and in patients with erosive GERD treated with PPIs for 12 months, the recurrence rate, when there is lower sphincter dysfunction with pressure < 8 mmHg, whether or not associated with dysmotility, is respectively 38.1% and 79.5%. Surgical treatment should be considered in these patients. There is evidence of estimated surgery benefit, with treatment failure reduction of 12% (NNT 8), when compared to medical treatment, and rates are maintained in the long term (7 years). But there is also evidence of equivalence for medical treatment with PPIs and laparoscopic surgery (Nissen), with 93% and 90% of patients remaining in symptom remission for 3 years, respectively. In the long term, surgery reduces the risk of esophagitis by 44% (NNT: 2), and of Barrett’s esophagus and dysplasia, when compared to PPI therapy. In seven years of followup, surgery may benefit patients with GERD (erosive or non-erosive) who had partial response to PPIs, especially in relation to quality of life. However, after 2.5 years, 37% of patients may be using PPIs, and, additionally, in 10 years, many (80%) may require reoperation. Laparoscopic surgery enhances patient’s quality of life, even in those whose symptoms are adequately controlled with PPIs.

4. AMONG

PATIENTS WITH SURGICAL INDICATION, WHICH

TECHNIQUE HAS THE BEST RESULT: TOTAL PARTIAL FUNDOPLICATION

(TOUPET)?

(NISSEN)

OR

There is no difference after one year regarding the presence of symptoms of heartburn, regurgitation or other symptoms related to reflux in patients who underwent Nissen versus Toupet surgeries. However, the Nissen surgery increases the risk of dysphagia of any degree by 18.7% (95% CI: 6.0-31.4) – NNH: 5, and chest pain at meals by 17.1% (95% CI: 5.7-28.5) – NNH: 6. There is no difference regarding postoperative symptoms related to esophageal motility33 (A). After two postoperative years, patient satisfaction is equivalent between those submitted to the Nissen or Toupet laparoscopic techniques. However, the Nissen surgery increases the risk of dysphagia by 11.0% (95% CI: 1.7-20.3) – NNH: 934 (A). There is no difference between Nissen and Toupet surgeries, regarding the severity of symptoms in the one-year postoperative period70 (A).

GASTROESOPHAGEAL REFLUX DISEASE: NONPHARMACOLOGICAL TREATMENT

In patients treated by Nissen surgery versus Toupet, there was no difference related to heartburn or acid regurgitation control. There was also no difference in the prevalence of dysphagia between the two surgical techniques71 (A). Patients who underwent the Nissen or Toupet techniques are equally satisfied and reflux control is equivalent. However, the Nissen surgery increases the risk of dysphagia, not correlated to differences in esophageal motility, in 19.0% (95% CI: 8.1-29.9) – NNH: 572 (A). There was no difference regarding symptom recurrence, dysphagia, or reflux control in the three-year postoperative period of Nissen versus Toupet techniques73 (A). RECOMMENDATION There is no difference between the Nissen and Toupet surgical techniques in relation to therapeutic response; however, the Nissen technique may produce more dysphagia, with NNH of 5 to 9, not correlated with motility.

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