Enfermedad Por Reflujo gastroesofagico
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Enfermedad por reflujo gastroesofagico
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Enfermedad Por Reflujo gastroesofagico
- 1. ENFERMEDAD POR REFLUJO GASTROESOFAGICO Hospital Sergio E.Bernales Lima-Perú Dr. Freddy García Ortega
- 2. Relación entre reflujo gastrosofagico (RGE)y enfermedad por reflujo gastroesofagico (ERGE )
- 3. ESTOMAGO Nauseas Dispepsia BOCA Erosiones dentales Líquido en boca Hálitosis OTORRINOLARINGOLOGIA Enfermedad de cuerdas vocales Disfonía, Laringoespasmo Laringitis crónica, cáncer laringeo Secreción post nasal, Globus Otalgia, sinusítis, faringítis esófago Enfermedad por reflujo sin esofagitis Esofagitis Dolor toráxico inexplicado Estenosis , Hemorragia Barret - adenocarcinoma PULMON Asma, tos fibrosis pulmonar aspiración recurrente Apnea del sueño
- 4. PIROSIS REGURGITACION SÍNTOMAS EXTRAESOFAGICOS ODINOFAGIA DISFAGIA HEMORRAGIA ERGE SINTOMAS SUGESTIVOS
- 5. pirosis 7 a 10% cada día 15 a 30% cada semana o cada mes 45% cada año PREVALENCIA EN LA POBLACION Esta prevalencia de reflujo se basa solo en la presencia de los síntomas clásicos, por tanto hay una subestimacion de la prevalencia real de reflujo en la población
- 6. Una enfermedad fascinante, con múltiples presentaciones Afectaría a 30 a 40% de la población en algún momento de su vida. 20% de la población usa antiácidos o bloqueadores H2 o BB por síntomas sugestivos de ERGE >2 veces/ semana Un 60% de estos pacientes no presenta alteraciones endoscópicas (ERGE no erosiva). ENFERMEDAD POR REFLUJO
- 7. Se desconoce la proporción de pacientes con síntomas extra esofágicos Muchos de ellos pacientes no tiene pirosis dificultando el diagnóstico. 12 a18% tienen complicaciones entre ellas esófago de Barrett Una minoría de pacientes con ERGE presentan molestias con exposición normal o fisiológica al ácido ( esófago hipersensible.) ENFERMEDAD POR REFLUJO
- 8. La pirosis es generalmente percibida como síntoma trivial controlable con medicamentos Sin embargo la calidad de vida de un paciente con ERGE puede ser peor a la de un paciente con angina de pecho o ICC, úlcera péptica y menopausia PIROSIS
- 9. Características de la pirosis Disconfort subesternal Irradiación hacia la boca Aumenta con ingesta o decúbito Mejora con antiácido
- 10. Fisiopatologia y etiologia de la esofagitis por reflujo
- 11. Defensa tisular: estructural y funcional
- 13. Mecanismos de aclaramiento del acido de la luz esofágica Aclaramiento del Bolo Gravedad Peristalsis Aclaramiento del ácido Deglución de saliva rica en bicarbonato Secreción de bicarbonato por las glándulas esofágicas submucosas
- 14. Factores que alteran la defensa tisular
- 15. Condiciones asociadas con ERGE
- 16. Hernia hiatal
- 17. Concentración de sales biliares en esofagitis por reflujo
- 19. Debido a la gran variedad de manifestaciones clínicas, la evaluación diagnóstica puede ser difícil. La evaluación empieza con historia clínica adecuada Se pueden usar endoscopía y biopsia, monitorización de pH, radiología baritada, gammagrafía, manometría esofágica, pruebas de provocación, prueba terapéutica Todas las pruebas tienen sus ventajas y desventajas y no existe una prueba estándar o de oro para el diagnostico de ERGE, estas pruebas pueden complementarse . EVALUACION DIAGNOSTICA
- 20. Pruebas para evaluar ERGE * Principallmente en investigacion
- 21. Sistemas de clasificacion endoscopica de esofagitis por reflujo
- 23. Lesion en menos de 10% de esofago distal Savary Miller I Los Angeles B Hetzel II
- 24. Lesion en mas de 10 a 50% de esofago distal Savary Miller II Los Angeles C Hetzel -Dent III
- 25. Ulceras circunferenciales Savary Miller III Los Angeles D Hetzel - Dent IV http://www.gastrosource.com/content/1384265/5994168/gastrointestinal-endoscopy-atlas/?layoutName=external_fullpage& Fuente de imágenes Hacer click en la dirección
- 26. Esofago de Barrett Savary Miller V
- 27. Alteraciones anatomo patologicas en ERGE Alteraciones no inflamatorias Hiperplasia de celulas basales Altura de las papilas incrementada Espacios intercelulares dilatados Cambios inflamatorios Agudos Congestión vascular c/s estasis Edema de mucosa Infiltrado por PMN (neutrófilos y eosinófilos) Crónicos Infiltrado mononuclear (macrófagos) Actividad aumentada de macrófagos Proliferación de fibroblastos Endotelio vascular aumenta Necrosis epitelial Erosión Ulceración Reparación de Epitelio Tejido de granulación Fibrosis (formación de estenosis) Regeneración del epitelio Replicación escamosa Metaplásia columnar (Esófago de Barrett)
- 28. Histopatologia en ERGE Hiperplasia basal y digitaciones elengadas
- 29. Histopatologia en ERGE Control ERGE erosiva ERGE No erosiva
- 31. Eliminación o alivio de síntomas En esofagitis erosiva: cicatrización y mantenerla En complicación con estenosis: control agresivo del ácido para evitar recurrencia de estenosis En esófago de Barrett: controlar síntomas, pero se desconoce si la eliminación del ácido previenen la progresión usual de epitelio de Barrett hacia displasia severa y carcinoma. Luego de controlar los síntomas y las alteraciones endoscópicas, debe mantenerse la mejoría METAS DEL TRATAMIENTO EN ERGE
- 32. Modificación de los estilos de vida en el tratamiento
- 33. BB bid con ARH2 al acostarse BB bid BB a.m y ARH2 al acostarse BB bid con gastrocinetico BB una vez al día EFICACIA RELATIVA DE TERAPIA ANTIREFLUJO ARH2 altas dosis ARH2 y gastrocinetico ARH2 o gastrocinetico ARH2 maximo minimo Minimo 8 semanas de tratamiento
- 34. Si no responde a tratamiento medico Cuando se requieren aumento de dosis con enfermedad progresiva, considerar cirugía temprana Si se requiere tratamiento medico agresivo prolongado, si son jóvenes considerar cirugía En Pacientes que no desean seguir terapia prolongada, por costoso, inconveniente y miedo a reacción adversa Si no cumplen con tratamiento medico En esofagitis grado I y II con déficit mecánico del esfínter por ser propensos a episodios persistentes de ERGE INDICACIONES PARA CIRUGIA
- 35. Pacientes con esofagitis grado III y IV por que requieren tratamiento prolongado y tienen riesgo de complicaciones Pacientes con hernia hiatal grande que frecuentemente son refractarios al tratamiento Pacientes con complicaciones severas ( estenosis, ulceración, esófago de Barrett y síntomas respiratorios severos) a pesar de tratamiento Pacientes con síntomas respiratorios como aspiración, neumonía recurrente, laringitis crónica INDICACIONES PARA CIRUGIA
- 37. Fundoplicacion parcial de Belsey
- 38. Fundoplicacion total de Nissen
- 39. Endocinch
- 41. Complicaciones de esofagitis por reflujo
- 42. El curso clínico de la ERGE es variada, la mayoría sigue un curso benigno con pirosis y regurgitación intermitente, pero puede ser severa. La secuela más frecuente de esofagitis severa prolongada es la estenosis esofágica péptica. Las molestias de estos pacientes son significativas sobre todo tomando en cuenta sus recidivas, mayor riesgo de impactación de alimentos, riesgo de aspiración pulmonar, coexistencia frecuente con esófago de Barrett y la necesidad de dilataciones con riesgo de perforación. ESTENOSIS
- 43. Casi 80 % de estenosis esofágica están relacionada a ERGE, estenosis postoperatorias 10%, estenosis por corrosivos son menos frecuentes. Ocurrirían en 7% a 23% de pacientes con esofagitis no tratadas, especialmente en ancianos, más por la duración de reflujo que por la edad en si . Son 10 veces más frecuentes en blancos que en descendientes de africanos o asiáticos Aunque generalmente esta presente en la endoscopía inicial, se reporta la aparición espontanea mientras recibe tratamiento ESTENOSIS PEPTICA
- 44. Esofagitis erosiva distal, úlcera esofágica asociada con estenosis, y una hernia hiatal Larga estenosis irregular en sindrome de Zollinger Ellison con SNG prolongada post cirugía de cabeza y del cuello Larga estenosis
- 45. Imagen sugerente de estenosis pequeña Con maniobra de Valsalva se puede ver estenosis y hernia hiatal
- 46. Metaplasia intestinal por encima de la unión gastroesofágica e implica riesgo de adenocarcinoma de esófago, un cáncer que esta en aumento rápido en los EU. Se da en pacientes mayores y con mayor duración de sus síntomas, con alta proporción de blancos desconociéndose la causa de esta predominancia étnica. Tienen sensibilidad disminuida al ácido, y por ello tienen pirosis con menor frecuencia, a pesar de reflujo ácido mayor que otros pacientes con ERGE. ESÓFAGO DE BARRETT
- 47. Erosiones dentales en ERGE crónico
- 48. En hipofaringe debe buscarse cambios inflamatorios
- 49. No hay una relación clara entre ERGE e infección por H. pylori Datos epidemiológicos sugieren una relación inversa. No hay datos que indiquen que hay un efecto causal Hay pocos estudios y con muestras pequeñas que aclaren este asunto Hay un estudio de erradicación que sugiere que la infección por H. pylori puede tener efecto protector con respecto al ERGE ERGE Y HELICOBACTER PYLORI
- 51. El Helicobacter pylori protege contra esofagitis por reflujo
- 52. ERGE el desorden esofágico más frecuente y la causa más común de referencia hacia el gastroenterólogo pedíatra Prevalencia de 8% de reflujo anormal por monitorización de pH. Diferencias entre menores de 1 año y niños de 1 a 18 años Niños entre 1 a 18 años tienen manifestaciones similares a los adultos, preescolares tienen síntomas intermedios entre infantes y adultos Diferencias ocurren por que después de la infancia hay reducción en la ingesta calórica por disminución en el crecimiento, aumento en el tono dorsal y postura de pie ERGE EN NIÑOS
- 53. Se puede hacer terapia empírica en niños con ERGE por que hay pocos diagnósticos diferenciales La terapia conservadora es muy importante Fármacos pro cinéticos son muy importantes debido al rol de la motilidad comparados a la secreción acida en estos casos. ERGE EN NIÑOS
- 54. Reflujo Normal regurgitación sin esfuerzo Patológico Malnutrición Enfermedades respiratorias Esofagitis o sus complicaciones ERGE EN NIÑOS
- 55. Omeprazol 0.7 - 3.3 mg/kg/día 1 a 2 v/día antiácidos 1 ml/Kg/dosis 3-8 v/día Rantididina 3.5 mg/Kg/dosis bid -tid Lanzoprazol y pantoprazol dosis en niños aun no definidas MEDICAMENTOS EN ERGE DE NIÑOS
- 56. Invitacion al blog: www.hnsebgastro.blogspot.com
Notas del editor
- Figure 6-20. Characteristics of heartburn. Heartburn is a symptom complex characterized by substernal (burning) pain radiating toward the mouth, which is worsened by meals and recumbency and ameliorated by antacid ingestion. When typical, recurrent heartburn is adequate for the diagnosis of gastroesophageal reflux disease (GERD). Acid regurgitation, the spontaneous eructation of bitter material in the esophagus and mouth, and water brash, the spontaneous appearance of a bland or salty fluid in the mouth, are also common symptoms of GERD. Odynophagia, however, is very uncommon in those with GERD and usually reflects mucosal destruction from pills (doxycycline or tetracycline, nonsteroidal antiinflammatory agents, vitamin C, quinine) or infectious agents (Herpes simplex virus, cytomegalovirus, Candida albicans, HIV).
- Figure 6-4. Pathophysiology and etiology. The initial cause of reflux esophagitis is unknown. However, the key pathogenetic mechanisms involve the ability of noxious gastric contents, especially hydrochloric acid (HCl) and pepsin, to access the esophagus and remain within the lumen long enough to produce damage to the epithelial lining. Because gastric acid and pepsin secretion are normal in patients with gastroesophageal reflux disease (GERD) and bile salts are present in noncytotoxic amounts in gastric juice, the likely cause of GERD involves one or more defects in the esophageal defense against refluxed acid-pepsin. This may include defects in the antireflux barrier (lower esophageal sphincter [LES], diaphragm), which controls the frequency of gastric contents entering the esophagus; the luminal clearance mechanisms (esophageal peristalsis, salivary and esophageal submucosal gland bicarbonate secretion), which control the duration of contact between gastric contents and esophageal epithelium; and the esophageal epithelium, which determines whether the time of contact between epithelium and gastric contents results in injury. (Adapted from Orlando [1].) References: [1]. Orlando RC, Reflux esophagitis. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Laine L. et al. Philadelphia: Lippincott Williams and Wilkins; 1999 1235-1263
- Figure 6-15. Tissue resistance. Tissue resistance can be envisioned as comprising structural and functional defenses. Structural barriers limit the rate of diffusion of luminal acid (H+) into and between the esophageal epithelial cells; these include the cell membrane and intercellular junctional complex, respectively. Functional defenses include both intracellular and extracellular buffers and processes for the extrusion of H+ from the cytosol (eg, basolateral membrane NaH+/H+ exchanger and Na+-dependent Cl-/HCO3- exchanger). CA—carbonic anhydrease; ICS—intercellular space. (Adapted from Orlando [1].) References: [1]. Orlando RC, Reflux esophagitis. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Laine L. et al. Philadelphia: Lippincott Williams and Wilkins; 1999 1235-1263
- Figure 6-14. Potential components of tissue resistance against acid injury in the esophagus. Tissue resistance is a multifaceted process that is designed to protect the esophageal epithelium from injury by noxious luminal elements. Those designed to protect against luminal acidity are depicted here and in Figure 6-11. (Adapted from Orlando [14].) References: [14]. Orlando RC, Esophageal epithelial resistance. In Gastroesophageal Reflux Disease. Pathogenesis, Diagnosis, Therapy. Edited by Castell DO, Wu WC, Ott DJ. Mt. Kisco, NY: Futura; 1985
- Figure 6-8. Esophageal luminal acid clearance mechanisms. Esophageal luminal acid clearance mechanisms act to minimize the time that refluxed gastric acid remains in contact with the esophageal epithelium. It consists of the four processes listed here. Two of the processes—esophageal peristalsis (both primary caused by swallowing and secondary caused by distension) and gravity—act to clear the refluxed bolus from the lumen. The other two processes—swallowed saliva and secretions from esophageal submucosal glands (both rich in bicarbonate)—act to dilute and neutralize residual acid within the lumen and unstirred water layer adjacent to the epithelium surface. On average, it takes a healthy subject about 3 to 5 minutes to clear acid from the esophagus after a single bout of reflux.
- Figure 6-16. Tissue resistance. A number of factors that can alter the ability of the esophageal epithelium to defend itself against refluxed gastric acid are depicted here. Among the most common factors are smoking; alcohol; hot (temperature) beverages; foods such as pizza; salt and spices that produce hypertonic luminal environments; and medications that produce topical irritation, including tetracycline or doxycycline, potassium chloride, vitamin C, quinine, and nonsteroidal anti-inflammatory drugs.
- Figure 6-17. Conditions and activities reported to be associated with gastroesophageal reflux disease.
- Figure 6-12. Hiatal hernia. An example of a moderate-sized sliding hiatal hernia (arrows) is demonstrated on this barium esophagogram. This figure illustrates the distorted anatomy of the gastroesophageal junction in the presence of the hernia. (From Eisenberg [12]; with permission.) References: [12]. Diaphragmatic hernias In Gastrointestinal Radiology. Edited by Eisenberg RL. Philadelphia: Lippincott Raven; 1996 161-177
- Figure 6-13. Bile salt concentrations in various forms of reflux esophagitis. There is uniform acceptance of the fact that gastric acid and pepsin, although secreted in normal amounts, play the primary role for the development of reflux esophagitis (data not shown). There continues, however, to be debate about the role that refluxed bile salts play in esophageal injury and its complications. The data in this figure illustrate that the concentration of bile salts present in stomach and refluxed into the esophagus increases with increasing severity of disease. The predominant bile acids detected were the primary bile acids—cholic, taurocholic, and glycocholic acid—with significantly greater proportions of secondary bile acids—deoxycholic and taurodeoxycholic acid—present in patients with erosive esophagitis, Barrett's esophagus, and stricture. It should be noted, however, that the maximum concentrations of the bile salts reported fall well below the 5 mM concentrations shown to be cytotoxic to esophageal epithelium. (Adapted from Nehra et al. [13].) References: [13]. Nehra D, Howell P, Williams J, et al. Toxic bile acids in gastroesophageal reflux disease: influence of gastric acidity. Gut 1999 44 598-602
- Figure 6-35. Tests for diagnostic assessment of gastroesophageal reflux disease (GERD), its mechanisms, and its consequences. Testing falls into four categories, depending on the information desired. For example, there are tests that can document reflux, assess symptoms, assess esophageal damage, or the assess the pathophysiology of GERD. GI—gastrointestinal; PPI—proton pump inhibitor [1]. (Adapted from Orlando [1].) References: [1]. Orlando RC, Reflux esophagitis. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Laine L. et al. Philadelphia: Lippincott Williams and Wilkins; 1999 1235-1263
- Figure 6-26. Endoscopic grading systems for reflux esophagitis. The grading system lacks standardization. The table lists the criteria used for three of the most commonly cited classifications in the literature. The Savary-Miller is the oldest and most widely used classification in the United States [24]; it grades erosions as single (I), multiple (II), and circumferential (III) and then uses more advanced grades for complications, with IV for ulcer and stricture and V for Barrett's esophagus. The Los Angeles and Hetzel classifications also grade erosions but, unlike the Savary-Miller classification, they do not have grades for complications of esophagitis.The Los Angeles classification grades erosion length and extent more importantly than number. Erosions with maximum length of less than 5 mm are denoted as grade A; erosions with at least one whose length is greater than 5 mm denoted as grade B; erosions that form a lesion that connects the tops of two folds denoted as grade C; and erosions that are completely circumferential denoted as grade D [25]. The Hetzel (or Hetzel-Dent) classification is the only classification that gives a grade (other than 0) for more subtle (and subjective) endoscopic findings, mucosal edema, friability, and hyperemia being reported as grade I; erosions whose area covers less than 10% of the distal (5 cm) esophagus reported as grade II; erosions that cover 10% to 50% of the distal esophagus are reported as grade III; and erosions that cover more than 50% of the distal esophagus or deep ulceration are reported as grade IV [26]. References: [24]. Ollyo JB, Lang F, Fontollet CH, et al. Savary's new endoscopic grading of reflux-esophagitis: a simple, reproducible, logical, complete and useful classification. Gastroenterology 1990 89(suppl A) 100 [25]. Armstrong D, Bennett JR, Blum AL, et al. The endoscopic assessment of esophagitis; a progress report on observe agreement. Gastroenterology 1996 111 85-92 [26]. Miller LS, Endoscopy of the esophagus. In The Esophagus. Edited by Castell DO. Boston: Little Brown & Co; 1995 93-132
- Figure 6-52. Endoscopic views of gastroesophageal reflux disease. A, Grade 1: normal squamocolumnar junction and esophageal mucosa. B, Grade 2: esophageal erosions in less than 10% of the mucosa. C, Grade 3: esophageal erosions in 10% to 50% of the mucosa. D, Grade 4: esophageal ulcers and ulcerations without stricture. See also Color Plate.
- Figure 6-52. Endoscopic views of gastroesophageal reflux disease. A, Grade 1: normal squamocolumnar junction and esophageal mucosa. B, Grade 2: esophageal erosions in less than 10% of the mucosa. C, Grade 3: esophageal erosions in 10% to 50% of the mucosa. D, Grade 4: esophageal ulcers and ulcerations without stricture. See also Color Plate.
- Figure 6-52. Endoscopic views of gastroesophageal reflux disease. A, Grade 1: normal squamocolumnar junction and esophageal mucosa. B, Grade 2: esophageal erosions in less than 10% of the mucosa. C, Grade 3: esophageal erosions in 10% to 50% of the mucosa. D, Grade 4: esophageal ulcers and ulcerations without stricture. See also Color Plate.
- Figure 6-52. Endoscopic views of gastroesophageal reflux disease. A, Grade 1: normal squamocolumnar junction and esophageal mucosa. B, Grade 2: esophageal erosions in less than 10% of the mucosa. C, Grade 3: esophageal erosions in 10% to 50% of the mucosa. D, Grade 4: esophageal ulcers and ulcerations without stricture. See also Color Plate.
- Figure 6-29. Barrett's esophagus. The endoscopic appearance of a long segment (= 3 cm) of columnar-lined lower (Barrett's) esophagus is shown. The typical red coloration of the columnar epithelium is readly distinguished from the lighter pink or orange stratified squamous epithelium. Endoscopic biopsy, however, is essential for histologic confirmation. Barrett's esophagus is characterized by a specialized columnar epithelium with prominent goblet cells containing acidic mucin (see Figure 6-30). Esophageal segments of less than 3 cm but with similar histopathologic features have been designated as “short segment” Barrett's esophagus. Short segment Barrett's esophagus has been reported in approximately 18% of subjects undergoing endoscopy irrespective of complaints or evidence for reflux disease [28]. In many instances, it is difficult to distinguish short segment Barrett's esophagus from metaplasia of the gastric cardia, which also exhibits the same histopathology (ie, a lining containing specialized columnar epithelium). (From Tytgat [28]; with permission.) References: [28]. Tytgat GJJ, Upper gastrointestinal endoscopy. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Owyang C. et al. Philadelphia: JB Lippincott; 1991 435-436
- Figure 6-21. Esophageal pathology in gastroesophageal reflux disease. Reflux-induced damage to the esophageal epithelium exhibits a broad spectrum of pathology, ranging from noninflammatory to inflammatory changes and from normal epithelial (squamous) repair to aberrant repair in the form of Barrett's esophagus. The newest addition to these changes is the presence of dilated intercellular spaces, a lesion initially identified on electron microscopy but one that may also be appreciated on light microscopy (see Figure 6-23). (Adapted from Orlando [17].) References: [17]. Orlando RC, Pathology of reflux esophagitis and its complications. In Surgery of Oesophagus. Edited by Jamieson GG. Edinburgh: Churchill Livingstone; 1988 189-200
- Figure 6-22. Histopathology. The histopathologic changes of reflux damage to the esophageal epithelium most commonly noted on esophageal biopsy are basal cell hyperplasia and elongation of the rete pegs (arrows) [18]. These features have a high sensitivity but relatively low specificity for disease, the latter because of the presence of these features in 20% of healthy subjects in the lower 2.5 cm of esophagus [19]. (From Lewin [18]; with permission.) References: [18].Inflammatory disorders of the esophagus, reflux and nonreflux types. In Gastrointestinal Pathology and its Clinical Implications vol 381. Edited by Lewin KJ, Riddell RH, Weinstein WM. New York: Igaku-Shoin; 1992 418 [19]. Weinstein WM, Goboch ER, Bowes KL, The normal human esophageal mucosa: a histologic reappraisal. Gastroenterology 1975 68 40
- Figure 6-23. Histopathology of gastroesophageal reflux disease (GERD). Dilated intercellular spaces are another important feature of early reflux damage to the esophageal epithelium. This abnormality, which reflects an increase in paracellular permeability, has been noted in both patients with nonerosive and erosive esophagitis using transmission electron photomicroscopy. A, Control subject. B, Erosive GERD. C, Nonerosive GERD. Original magnification, × 3000. (From Tobey et al. [20]; with permission.) References: [20]. Tobey NA, Carson JL, Alkiek RA, Orlando RC, Dilated intercellular spaces: a morphological feature of acid reflux-damaged human esophageal epithelium. Gastroenterology 1996 111 1200-1205
- Figure 6-36. Modifications of lifestyle to lessen reflux esophagitis. Lifestyle modifications are indicated for all patients with reflux disease. Many of the recommended strategies do not only improve reflux disease but also reduce the risk of some other illnesses (eg, a low-fat diet reduces the risk of colon cancer and heart disease). Moreover, most of these strategies come at little or no cost. The benefit of reducing or stopping medications that may promote reflux needs to be balanced against the necessity for treatment of other conditions. Most of the medications, although they do lower esophageal sphincter (LES) pressure, do so only modestly and may not adversely influence LES relaxation. (Adapted from Orlando [35].) References: [35]. Orlando RC, Gastroesophageal reflux. In Current Therapy in Gastroenterology and Liver Disease, edn 3. Edited by Bayless TM. Philadelphia: BC Decker; 1990 7
- Figure 6-45. Surgical management. Patients who are successfully controlled with acid suppressant therapy but do not desire to remain on medications lifelong are candidates for antireflux surgery. The most commonly performed surgical procedures for gastroesophageal reflux disease are the Hill gastropexy (A), Belsey (partial) fundoplication (B), and Nissen (complete) fundoplication (C) [28]. The Nissen procedure is the most popular and can be performed either as an open procedure or using the laparoscopic approach. The laparoscopic Nissen procedure has an initial failure rate of approximately 10% and an approximate 1% breakdown of the wrap each year. The procedure itself carries little mortality risk, but morbidity rates, including esophageal perforations, wound infections, splenic tears, postoperative dysphagia, and gas bloat, occur in about 10% of patients. The cost of a successful Nissen procedure is estimated to be equivalent in cost to 10 years of chronic proton pump inhibitor (PPI) therapy, but this analysis will change in favor of PPI therapy after a generic version is available in 2002. (Adapted from Pope [43].) References: [28]. Tytgat GJJ, Upper gastrointestinal endoscopy. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Owyang C. et al. Philadelphia: JB Lippincott; 1991 435-436 [43]. Pope CE II, Gastroesophageal reflux disease (reflux esophagitis). In Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Edited by Sleisenger MH, Fordtran JS. Philadelphia: WB Saunders; 1983 449
- Figure 6-45. Surgical management. Patients who are successfully controlled with acid suppressant therapy but do not desire to remain on medications lifelong are candidates for antireflux surgery. The most commonly performed surgical procedures for gastroesophageal reflux disease are the Hill gastropexy (A), Belsey (partial) fundoplication (B), and Nissen (complete) fundoplication (C) [28]. The Nissen procedure is the most popular and can be performed either as an open procedure or using the laparoscopic approach. The laparoscopic Nissen procedure has an initial failure rate of approximately 10% and an approximate 1% breakdown of the wrap each year. The procedure itself carries little mortality risk, but morbidity rates, including esophageal perforations, wound infections, splenic tears, postoperative dysphagia, and gas bloat, occur in about 10% of patients. The cost of a successful Nissen procedure is estimated to be equivalent in cost to 10 years of chronic proton pump inhibitor (PPI) therapy, but this analysis will change in favor of PPI therapy after a generic version is available in 2002. (Adapted from Pope [43].) References: [28]. Tytgat GJJ, Upper gastrointestinal endoscopy. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Owyang C. et al. Philadelphia: JB Lippincott; 1991 435-436 [43]. Pope CE II, Gastroesophageal reflux disease (reflux esophagitis). In Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Edited by Sleisenger MH, Fordtran JS. Philadelphia: WB Saunders; 1983 449
- Figure 6-45. Surgical management. Patients who are successfully controlled with acid suppressant therapy but do not desire to remain on medications lifelong are candidates for antireflux surgery. The most commonly performed surgical procedures for gastroesophageal reflux disease are the Hill gastropexy (A), Belsey (partial) fundoplication (B), and Nissen (complete) fundoplication (C) [28]. The Nissen procedure is the most popular and can be performed either as an open procedure or using the laparoscopic approach. The laparoscopic Nissen procedure has an initial failure rate of approximately 10% and an approximate 1% breakdown of the wrap each year. The procedure itself carries little mortality risk, but morbidity rates, including esophageal perforations, wound infections, splenic tears, postoperative dysphagia, and gas bloat, occur in about 10% of patients. The cost of a successful Nissen procedure is estimated to be equivalent in cost to 10 years of chronic proton pump inhibitor (PPI) therapy, but this analysis will change in favor of PPI therapy after a generic version is available in 2002. (Adapted from Pope [43].) References: [28]. Tytgat GJJ, Upper gastrointestinal endoscopy. In Textbook of Gastroenterology. Edited by Yamada T, Alpers DH, Owyang C. et al. Philadelphia: JB Lippincott; 1991 435-436 [43]. Pope CE II, Gastroesophageal reflux disease (reflux esophagitis). In Gastrointestinal Disease: Pathophysiology, Diagnosis, Management. Edited by Sleisenger MH, Fordtran JS. Philadelphia: WB Saunders; 1983 449
- Figure 6-46. Endoscopic therapy of reflux disease. The Food and Drug Administration has approved two novel endoscopic techniques for the treatment of gastroesophageal reflux disease, the EndoCinch (A) procedure and the Stretta procedure (B). The EndoCinch procedure permits the endoscopist to create a gastroplication just below the esophagogastric junction using an overtube and sewing attachment, and this plication serves as a barrier to reflux [44], [45]. The Stretta procedure, through the use of thermocouples attached to a balloon and catheter system positioned at the esophagogastric junction, permits the delivery of high-frequency energy to the lower esophageal sphincter and cardia of the stomach. This injury within the sphincter region controls reflux by producing collagen deposition, remodeling, and reduced compliance of the esophagogastric junction [46], [47]. Although these procedures have been met with initial enthusiasm and some success in reducing the reliance on chronic acid suppressant medications, neither one is free of serious side effects, and their data have not established their durability. These procedures are also not indicated in patients with hiatal hernias or erosive esophagitis, and they should currently be considered experimental. References: [44]. Swain P, Park PO, Kjellin T, et al. Endoscopic gastroplasty for gastroesophageal reflux disease. Gastrointest Endosc 2000 51(suppl A) 144 [45]. Filipi CJ, Edmundowicz SA, Gostout CJ, et al. Transoral endoscopic suturing for gastroesophageal reflux disease: a multicenter trial. Gastrointest Endosc 2000 51(suppl A) 143 [46]. Utley DS, Kim M, Vierra M, et al. Augmentation of lower esophageal sphincter pressure and gastric yield pressure after radiofrequency energy delivered to the gastroesophageal junction: a porcine model. Gastrointest Endosc 2000 52(suppl) 81-86 [47]. Triadafilopoulous G, Utley DS, DiBise J, et al. Radiofrequency energy delivery to the gastroesophageal junction for the treatment of GERD. Gastrointest Endosc 2001 53 407-415
- Figure 6-46. Endoscopic therapy of reflux disease. The Food and Drug Administration has approved two novel endoscopic techniques for the treatment of gastroesophageal reflux disease, the EndoCinch (A) procedure and the Stretta procedure (B). The EndoCinch procedure permits the endoscopist to create a gastroplication just below the esophagogastric junction using an overtube and sewing attachment, and this plication serves as a barrier to reflux [44], [45]. The Stretta procedure, through the use of thermocouples attached to a balloon and catheter system positioned at the esophagogastric junction, permits the delivery of high-frequency energy to the lower esophageal sphincter and cardia of the stomach. This injury within the sphincter region controls reflux by producing collagen deposition, remodeling, and reduced compliance of the esophagogastric junction [46], [47]. Although these procedures have been met with initial enthusiasm and some success in reducing the reliance on chronic acid suppressant medications, neither one is free of serious side effects, and their data have not established their durability. These procedures are also not indicated in patients with hiatal hernias or erosive esophagitis, and they should currently be considered experimental. References: [44]. Swain P, Park PO, Kjellin T, et al. Endoscopic gastroplasty for gastroesophageal reflux disease. Gastrointest Endosc 2000 51(suppl A) 144 [45]. Filipi CJ, Edmundowicz SA, Gostout CJ, et al. Transoral endoscopic suturing for gastroesophageal reflux disease: a multicenter trial. Gastrointest Endosc 2000 51(suppl A) 143 [46]. Utley DS, Kim M, Vierra M, et al. Augmentation of lower esophageal sphincter pressure and gastric yield pressure after radiofrequency energy delivered to the gastroesophageal junction: a porcine model. Gastrointest Endosc 2000 52(suppl) 81-86 [47]. Triadafilopoulous G, Utley DS, DiBise J, et al. Radiofrequency energy delivery to the gastroesophageal junction for the treatment of GERD. Gastrointest Endosc 2001 53 407-415
- Figure 6-27. Esophageal complications of reflux esophagitis. The prevalence of the major complications of reflux esophagitis are depicted here. (Adapted from Spechler [2].) References: [2]. Spechler SJ, Epidemiology and natural history of gastroesophageal reflux disease. Digestion 1992 51(suppl 1) 24-29
- Figure 6-53. Dental erosion from chronic acid reflux disease. Acid has eroded the white enamel, uncovering the yellow-appearing dentin.
- Figure 6-54. View of hypopharynx during upper gastrointestinal endoscopy in a patient with chronic cough and hoarseness. Erythema of the cricoarytenoid folds is present, and bilateral red streaks are visible posteriorly on the true vocal cords.
- Figure 6-18.Helicobacter pylori. One important pathogenetic factor in duodenal (and gastric) ulcer disease is chronic infection with H. pylori. This figure illustrates that unlike duodenal ulcer disease, the prevalence of H. pylori infection in reflux esophagitis is similar to that of healthy control subjects. This supports the lack of causality for H. pylori infection in patients with reflux disease. Also, patients with Barrett's esophagus, particularly when infected with CAG A+ strains (data not shown), generally have lower frequencies of infection with H. pylori than healthy subjects. The observation raises the question as to whether infection with H. pylori, by damaging gastric mucosa and raising gastric pH, may serve a protective role against reflux disease and its complications. (Adapted from Newton et al. [15].) References: [15]. Newton M, Bryan R, Burnham W, Kamn MA, Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett's oesophagus. Gut 1997 40 9-13
- Figure 6-19. The protective role of Helicobacter pylori. The possibility that infection with H. pylori may serve a protective role against the development of reflux esophagitis has support in the observation that the incidence of endoscopic esophagitis occurred twice as much over a 3-year period in patients with duodenal ulcer in whom H. pylori was successfully eradicated (closed circles) as those in whom H. pylori infection persisted (open circles). (Adapted from Labenz et al. [16].) References: [16]. Labenz J, Blum AL, Bayerdorffer E, et al. Curing Helicobacter pylori infection in patients with in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 1997 112 1442-1447