Esophageal Structure and FunctionThe esophagus is a hollow muscular tube coursingthrough the posterior mediastinum joining thehypopharynx to the stomach with a sphincter ateach end. It functions to transport food and fluidbetween these ends, otherwise remaining empty.
Gastroesophageal Reflux2 conditions for Reflux Episode to occur: 1. Gastro-intestinal contents must be “ready” to reflux 2. The anhireflux mechanism at the lower end of the esophagus must be compromised. Gastro-intestinal contents are most likely to reflux1. When gastric volume is increased . after meals . in the presence of pyloric obstruction or gastric stasis syndrome . in acid hypersecretory states
2. When gastric contents are located near thegastroesophageal due to: . Recumbence . bending down . Presence of hiatus hernia3. When gastric pressure is increased . Obesity . Pregnancy . Ascitis . Tight binders/ girdles Normal antireflux mechanism Consist of LES and the anatomic configuration of gastroesophageal junction.
Situations that predisposes togastroesophageal reflux: 1. Reflux occur when the gradient of pressure between LES and the stomach is lost. 2. It can be caused by increased intragastric pressure or by transient or sustained decrease in LES tone. 3. Decrease in sphincter tone maybe due to muscle weakness. 4. Inappropriate sphincter relaxation mediated by inhibitory nerves.
5. Secondary causes of. LESIncompetence include 5.1 Scleroderma- like diseases 5.2 Myopathic type of chronic intestinal pseudoobstrution syndrome 5.3 pregnancy 5.4 smoking 5.5 smooth muscle relaxant Ex. Beta-adrenergenic agents Aminoplylline Nitrates Calcium channel blockers
6. Destruction of Sphinter by 6.1 Surgical Resection 6.2 Myotomy 6.3 Baloon dilatation 6.4 Esophagitis7. Abnormal activity of the diaphragmatic crural muscleswhich surrounds the esophageal hiatus in the diaphragm.8. Changes in hiatal hernia.
Complications of Reflux:1. Esophagitis- develops when mucosal defenses that normally counteract the effect of the injurious agents on esophageal mucosa succumb to the onslaught of refluxed acid pepsin or bile.Causing: . Erosive esophagitis . Peptic stricture . Replacement of Squamous epithelium of esophagus by columnar epithelium ( Barret’s esophagus)
Major Esophageal Symtoms are:1. Heartburn (pyrosis)- a discomfort or burning sensation behindthe sternum that arises the epigastrium and may radiate towardthe neck. Heartburn is an intermittent symptoms, most commonlyexperienced after eating, during exercise, and while lyingrecumbent.2. Regurgitation- effortless return of food or fluid into thepharynx without nausea or retching. Patients report a sour orburning fluid in theThroat or mouth that may also contain undigested foodparticles. Bending, belching, or maneuvers that increaseintraabdominal pressure can provoke regulation.
3. Chest pain- is a common esophageal symptoms withcharacteristics similar to cardiac pain, which closely mimics anginapectoris. Features suggesting esophageal pain include pain that isnonexertional, prolonged, interrupts sleep, is meal-related, isrelieved with antacids, and is accompanied by heartburn,dysphagia, or regurgitation.4. Esophageal dysphagia- a feeling of food “sticking” or even loggingin the chest.5. Odynophagia- is pain either caused by or exacerbated byswallowing. Odynophagia is more common with pill or infectiousesophagitis than with reflux esophagitis and should prompt asearch for these entities. When odynophagia does occur in GERD,it is likely related in an esophageal ulcer or deep erosion.
Diagnostic TestEndoscopy- also known as esophagogastroduodenoscopy EGD isthe best for the evaluation of the proximal gastrointestinal tract.Radiography – Contrast radiography of theesophagus, stomach, and duodenum can demonstrate bariumreflux, hiatal hernia, mucosalgranularity, erosions, ulceration, and strictures.
Endoscopic ultrasound (EUS) - instrument combine anendoscope with an ultrasound transducer to create atransmural image of the tissue surrounding the endoscope tip.The key advantage of EUS over alternative radiologic imagingtechniques is much greater solution attributable to theproximity of the ultrasound transducer to the area beingexaminedEsophageal manometry - or motility testing, entailspositioning a pressure sensing catheter within the esophagusand then observing the contractility following test swallows.The upper and lower esophageal sphincters appear as zonesof high pressure that relax on swallowing while theintersphincteric esophagus exhibits peristaltic contractions.Manometry is used to diagnose motility disorders (achalasia,diffuse esophageal spasm) and to assess peristaltic integrityprior to the surgery for reflux disease.
Reflux Testingreflux testing can demonstrate excessive esophageal exposure torefluxed gastric juice, the physiologic abnormality of GERD. This canbe done by ambulatory 24- to 48-hour esophageal pH recording usingeither a wireless pH-sensitive transmitter that is anchored to theesophageal mucosa or with a transnasally positioned wire electrodewith the tip stationed in the distal esophagus. Either way, the outcomeis expressed as the percentage of the day that the pH was less than 4(indicative of recent acid reflux), with values exceeding 5% indicativeof GERD. Reflux testing is useful with atypical symptoms or aninexplicably poor response to therapy. Intraluminal impedancemonitoring can be added to pH monitoring to detect reflux eventsirrespective of whether or not they are acidic, potentially increasingthe sensitivity of the stud
Hiatal HerniaHiatus hernia is a herniation of viscera, most commonly thestomach, into the mediastinum through the esophageal hiatusof the diaphragm. Four types of hiatus hernia aredistinguished with type I, or sliding hiatal hernia comprisingat least 95% of the overall total. A sliding hiatal hernia is onein which the gastroesophageal junction and gastric cardiaslide upward as a result of weakening of thephrenoesophageal ligament attaching the gastroesophagealjunction to the diaphragm at the hiatus. True to its name,sliding hernias enlarge with increased intraabdominalpressure, swallowing, and respiration. The incidence of slidinghernias increases with age and conceptually, results fromwear and tear: increased intraabdominal pressure fromabdominal obesity, pregnancy, etc., and hereditary factorspredisposing to the condition. The main significance ofsliding hernias is the propensity of affected individuals tohave GERD.
Types II, III, and IV hiatal hernias are all subtypes ofparaesophageal hernia in which the herniation into themediastinum includes a visceral structure other than thegastric cardia. With type II and III paraesophageal hernias,the gastric fundus also herniates with the distinction beingthat in type II, the gastroesophageal junction remains fixedat the hiatus, while type III is a mixed sliding/paraesophagealhernia. With type IV hiatal hernias, viscera other than thestomach herniate into the mediastinum, most commonly thecolon. With type II and III paraesophageal hernias, thestomach inverts as it herniates and large paraesophagealhernias can lead to an upside down stomach, gastric volvulus,and even strangulation of the stomach. Because of this risk,surgical repair is often advocated for large paraesophagealhernias
GERDWith respect to the esophagus, the spectrum of injuryincludes esophagitis, stricture, Barretts esophagus, andadenocarcinoma . Of particular concern is the rising incidenceof esophageal adenocarcinoma, an epidemiologic trend thatparallels the increasing incidence of GERD.
PathophysiologyEsophagitis occurs when refluxed gastric acid and pepsincause necrosis of the esophageal mucosa causing erosions andulcers.Three dominant mechanisms of esophagogastric junctionincompetence are recognized:(1) transient LES relaxations (a vagovagal reflex in which LES relaxation is elicited by gastric distention),(2) LES hypotension, or(3) anatomic distortion of the esophagogastric junction inclusive of hiatus hernia.
Complications1. The complications of GERD are related to chronic esophagitis (bleeding and stricture) and the relationship between GERD and esophageal adenocarcinoma. However, both esophagitis and peptic strictures have become increasingly rare in the era of potent antisecretory medications.2. Conversely, the most severe histologic consequence of GERD is Barretts metaplasia with the associated risk of esophageal adenocarcinoma, and the incidence of these lesions has increased, not decreased in the era of potent acid suppression.
Treatment: Gastroesophageal Reflux Disease (GERD)1. Lifestyle modifications are routinely advocated as GERD therapy. Broadly speaking, these fall into three categories:(1) avoidance of foods that reduce lower esophageal sphincter pressure, making them "refluxogenic" (these commonly include fatty foods, alcohol, spearmint, peppermint, tomato-based foods, possibly coffee and tea);(2) avoidance of acidic foods that are inherently irritating; and(3) adoption of behaviors to minimize reflux and/or heartburn. In general, minimal evidence supports the efficacy of these measures. However, clinical experience dictates that subsets of patients are benefitted by specific recommendations, based on their unique history and symptom profile. A patient with sleep disturbance from nighttime heartburn is likely to benefit from elevation of the head of the bed and avoidance of eating before retiring,
but those recommendations are superfluous for a patient without nighttime symptoms. The most broadly applicable recommendation is for weight reduction. Even though the benefit with respect to reflux cannot be assured, the strong epidemiologic association between obesity and GERD and the secondary health gains of weight reduction are beyond dispute. 2. The dominant pharmacologic approach to GERD management is with inhibitors of gastric acid secretion and abundant data support the effectiveness of this approach. Pharmacologically reducing the acidity of gastric juice does not prevent reflux, but it ameliorates reflux symptoms and allows esophagitis to heal. The hierarchy of effectiveness among pharmaceuticals parallels their antisecretory potency. Proton pump inhibitors (PPIs) are more efficacious than histamine2 receptor antagonists (H2RAs), and both are superior to placebo. No major differences exist among PPIs and only modest gain is achieved by increased dosage.
3. Reflux symptoms tend to be chronic, irrespective of esophagitis.Thus, a common management strategy is indefinite treatment withPPIs or H2RAs as necessary for symptom control. The side effectsof PPI therapy are generally minimal. Vitamin B12, calcium, and ironabsorption may be compromised and susceptibility to entericinfections, particularly Clostridium difficile colitis increased withtreatment. Consequently, as with any medication, dosage should beminimized to that necessary.4. Laparoscopic Nissen fundoplication, wherein the proximal stomachis wrapped around the distal esophagus to create an antirefluxbarrier, is a surgical alternative to the management of chronic GERD.Just as with PPI therapy, evidence on the utility of fundoplication isstrongest for treating esophagitis and controlled trials suggest similarefficacy to PPI therapy. However, the benefits of fundoplicationmust be weighed against potential deleterious effects, includingsurgical morbidity and mortality, postoperative dysphagia, failure orbreakdown requiring reoperation, an inability to belch, and increasedbloating, flatulence, and bowel symptoms after surgery.
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