Tuesday Nov 15, 20059:30 – 11:00LectureEsophageal Physiology, Motility and Related PathologicConditionsArnold Wald, M. D. ...
movement of the bolus through the pharynx (the pharyngeal stage of swallowing) isreferred to as the transfer stage. This s...
Normal Esophageal Motility                                     Figure 1:          Primary Peristalsis                     ...
Figure 2The schematic above relates manometric pressure measurements to bolusmovement as shown videographically. The traci...
Table 1: Common Causes of Oropharyngeal Dysphagia Structural Abnormalities                      Neuromuscular Abnormalitie...
abnormality whereas dysphagia for both liquids and solids suggests a motilitydisorder. Many patients with a peptic strictu...
A suggested diagnostic approach to a patient with dysphagia is as followsThe following case histories serve to illustrate ...
Zenker’s Diverticulum: An example ofa disorder involving dysfunction of theupper esophageal sphincterEpidemiologyZenker’s ...
Case History #2A 78 year-old man presents with dysphagia and a 10 pound weight loss during thepast 18 months. He is a form...
Incomplete LES relaxation       Not Necessary             Increased LES pressure             Intraesophageal pressures exc...
Mechanism by which botulinum toxin A blocks release of acetylcholine atneuromuscular junction.        From:   Arnon: JAMA,...
Surgical myotomy is best for young patients and for those who do not respond topneumatic dilation. Either results in good ...
Epidemiology of GERDGastroesophageal reflux disease (GERD) is the most common condition arising fromthe GI tract. The most...
•   With respect to decreased esophageal clearance mechanisms, this can occur       because of weak or absent peristaltic ...
The choice of available diagnostic tests, as with dysphagia, is decided on the basis ofthe clinical question. Available te...
Question                              Best Diagnostic TestDoes patient have sigificant acid reflux?    Esophageal pH with ...
Total Fundoplication                       Efficacy of Therapies for GE Reflux                       Antacids     Prokinet...
The diagnosis of BE is made by endoscopic recognition and confirmed by biopsies ofthe affected area. In essence, it is the...
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Lecture

  1. 1. Tuesday Nov 15, 20059:30 – 11:00LectureEsophageal Physiology, Motility and Related PathologicConditionsArnold Wald, M. D. (walda@upmc.edu)Learning Objectives 1. Discuss the normal physiology of swallowing from the mouth to the stomach. 2. Compare the normal and abnormal neuromuscular activity of the esophagus. 3. Understand the symptoms of esophageal disorders with particular attention to dysphagia and its evaluation. 4. Understand the difference between dysphagia and odynophagia, including the underlying causes of each. 5. Distinguish the physiologic and clinical differences between structural and functional causes of dysphagia. 6. Explain the predominant pathophysiologic mechanisms underlying gastroesophageal reflux. 7. Discuss pathophysiology and management of achalasia.Suggested ReadingsArora AS, Conklin JL. Practical approaches to dysphagia caused by esophagealmotor disorders. Current Gastroenterology Reports, 2001;3:191-9.Sontag SJ. Gastroesophageal reflux disease. In Clinical Practice of Gastroenterology.LJ Brandt Ed. Churchill Livingstone, Philadelphia 1999; pp 21-33.Function of the EsophagusThe primary physiologic function of the esophagus is to transport a food bolus fromthe mouth to the stomach. This lecture reviews the process of swallowing andtransportation via the esophagus to the stomach, beginning with the transfer of abolus from the pharynx to the upper esophagus and continuing with the movementof material into the stomach.Pathologic conditions of the esophagus will be reviewed here. These frequentlyinvolve disturbance of normal swallowing and of esophageal motility. Otherdisorders of the esophagus are covered in the pathology lectures for this course.Physiology of SwallowingOropharyngeal PhaseThe initial stages of the act of swallowing – the so-called oropharyngeal phase,involve neuromotor function in the mouth and pharynx. After the ingested bolus issuitably prepared by chewing and mixing with saliva or liquid , it is movedvoluntarily from the mouth into the pharynx on initiation of a swallow. The 55
  2. 2. movement of the bolus through the pharynx (the pharyngeal stage of swallowing) isreferred to as the transfer stage. This stage of swallowing is highly integrated andcoordinated through a rapid series of events that occur less than 1 second afterswallowing is initiated.When the person decides toforce a bolus from the oralcavity into the oropharynx;1) the soft palate is elevatedagainst the posteriorpharyngeal wall, therebysealing off the nasopharynxand preventing regurgitationinto the nasal cavity,2) the afferent nerveendings in the oropharynxand pharynx are stimulatedon initiation of theswallowing act, and3) the bolus is pushed intothe proximal pharynx,initiating a reflex action thatcannot be aborted;4) the posterior pharyngealconstrictor muscles contractsequentially in a caudad direction,5) forcing the food bolus into the hypopharynx (pyriform sinuses) and6) through the receptively relaxed upper esophageal sphincter (cricopharyngeus).As swallowing begins,7) the cricopharyngeus muscle relaxes at the same time8) a pharyngeal peristaltic wave propels the bolus in a caudad direction.Within 2 seconds of the initiation of the swallow, the bolus is completely cleared fromthe pharynx and hypopharynx, including the recesses of the pyriform sinuses,through the UES into the upper esophagus.In the esophagus, an integrated mechanism transports material by peristalticcontractions into the stomach via coordinated relaxation of the lower esophagealsphincter (LES). The normal tone of the LES helps prevent reflux of gastric contentsback into the esophagus. The esophagus has no storage capacity and there is nomeaningful retention of food or liquids under normal circumstances. 56
  3. 3. Normal Esophageal Motility Figure 1: Primary Peristalsis Secondary PeristalsisAt rest, the normal esophagus is quiescent, with no spontaneous contractions, andboth sphincters are tonically contracted. Swallows trigger relaxation of the upperand lower esophageal sphincters and give rise to a peristaltic contraction travelingsmoothly through the striated and then the smooth muscle portion of the esophagus(Figure 1, left). Each location along the esophageal axis contracts with a latencythat increases gradually from the upper esophagus to the LES. The velocity of theperistaltic wave is slower in the striated muscle and faster in the smooth muscle.Contractions reach the striated muscle segment within 2 seconds after the onset ofthe swallow, traveling at a speed of about 3 cm per second; in the smooth musclesegment, the velocity of propagation may be as fast as 5 cm per second.Contractions in the distal one third of the esophagus are usually stronger (50-150mmHg) than those in the upper third (40-120 mmHg), and both are stronger thanthose in the middle third where they are relatively weak (20-80 mmHg), probablyoccurring at the transition between the striated and smooth muscle esophagus.If material is refluxed into the esophagus from the stomach, distension of theesophagus triggers peristaltic contractions which sweep the bolus into the stomach(Figure 1, right). This occurs in the absence of swallowing and is termed secondaryperistalsis.Manometric pressure waves can be correlated with movement of a bolus through theesophagus (Figure 2). 57
  4. 4. Figure 2The schematic above relates manometric pressure measurements to bolusmovement as shown videographically. The tracings from the video images on theright show the distribution of the barium column at the times indicated above theindividual tracings and by arrows on the manometric record. (Kahrilas, et al, Gastro1988;94:73)Esophageal PathophysiologyClinical symptomsFour symptoms are classically associated with diseases of the esophagus. These aredysphagia, odynophagia, heartburn, and chest pain. Other symptoms such aswheezing, cough, hoarseness, laryngitis and sore throat may be associated withgastro-esophageal reflux disease (GERD) but are not specific to the esophagus.DysphagiaDysphagia is defined as difficulty in swallowing and is perhaps the most specificsymptom of esophageal disease. When dysphagia is accompanied by painfulswallowing, it is called odynophagia; these two conditions are distinct and should notbe considered synonymous.There are two types of dysphagia;1. Oropharyngeal dysphagia - defined as the inability to initiate swallowing ortransfer a bolus from the mouth to the esophagus. It is caused by neuromusculardisorders or structural abnormalities of the striated muscles of the oropharynx orupper esophageal sphincter (UES) (Table 1). 58
  5. 5. Table 1: Common Causes of Oropharyngeal Dysphagia Structural Abnormalities Neuromuscular Abnormalities • Zenker’s diverticulum • Stroke • Cricopharyngeal bar • Multiple Sclerosis • Postcricoid web • Parkinson’s disease • Tumor • Cerebral palsy • Enlarged Thyroid • Myopathies and muscular • Cervical Osteophyte dystrophies • Motor neuron diseaseTherapeutic options for oropharyngeal dysphagia include: • Swallowing therapy o Retraining o Bolus size and consistency adjustment o Specific swallowing maneuvers • Esophageal dilation • Surgical Myotomy of UES ± closure of Zenker’s diverticulumSevere cases may require temporary or prolonged cessation of oral feeding togetherwith nutrition support via a gastric or jejunal feeding tube (PEG, PEJ) orintravenously (TPN).2. Esophageal dysphagia reflects difficulty in moving material through theesophagus and is caused by neuromuscular disorders of esophageal smooth muscleor by mechanical obstruction of the esophagus (Table 2). Table 2: Common Causes of Esophageal Dysphagia Structural Abnormalities Motility Abnormalities • Peptic stricture • Achalasia • Esophageal (Schatzki’s) ring • Diffuse esophageal spasm • Carcinoma • Ineffective esophageal motility • Webs • Gastroesophageal reflux (most • Benign tumors likely • Osteophytes from ineffective esophageal motility) • Scleroderma or other collagen vascular disordersWhen esophageal dysphagia is clinically suspected, it is important to differentiatebetween dysphagia for solids or for liquids. This suggests diagnostic possibilities anddirects the work-up (Table 3). Dysphagia for solid foods suggests a structural 59
  6. 6. abnormality whereas dysphagia for both liquids and solids suggests a motilitydisorder. Many patients with a peptic stricture or a carcinoma initially havedysphagia for solids which progresses to liquids as the lumen narrows. Intermittentdysphagia for solid foods, which does not progress over time, is more characteristicof an esophageal ring or web.The presence of dysphagia for both solids and liquids suggests the presence of anesophageal motility disorder (Table 2). These disorders invariably affect esophagealsmooth muscle function; often, the LES in involved as well. Table 3: Esophageal Dysphagia: Symptoms Suggest DiagnosisDiagnostic Evaluation of DysphagiaThe choice of available diagnostic tests is generally decided on the basis of theclinical question. Question Best Diagnostic TestWhat is the structure and function of the Barium esophagogram using both liquidsesophagus? and a solid bolusWhat is the integrity of the mucosa Endoscopy with biopsiesand/or the cause of luminal narrowing?What is the motor function of the Esophageal manometryesophagus and LES? 60
  7. 7. A suggested diagnostic approach to a patient with dysphagia is as followsThe following case histories serve to illustrate the more common clinicalconditions related to esophageal pathophysiology. Each case will bediscussed in greater detail in class.Case History #1A 67 year-old woman presents with dysphagia, choking and coughing for the past 15months. She is a nonsmoker who has been well until the onset of these symptoms.Her dysphagia is characterized by difficulty in swallowing, initially for solids but nowequally for liquids and solids. Frequently, she coughs when trying to eat. In the last15 months, she has noticed a gurgling sensation on swallowing. On occasion, sheawakens from sleep because of forceful coughing and choking.She denies heartburn, odynophagia, chest pain, shortness of breath or vomiting.She has no neck or chest pain and no hoarseness.Her physical examination is unremarkable. What is the mechanism behind her symptoms; structural? motility? 61
  8. 8. Zenker’s Diverticulum: An example ofa disorder involving dysfunction of theupper esophageal sphincterEpidemiologyZenker’s diverticulum is an uncommondisorder affecting both men and women,most of whom are older. It is believed tobe a late manifestation of cricopharyngealdysfunction which may be idiopathic butis also thought to be associated withgastroesophageal reflux.PathophysiologyThe primary abnormality concerns that ofUES relaxation. Most recent studiessuggest that the resistance of the UES toopening is increased associated withreduced muscle compliance. As a result,increased pharyngeal pressures arenecessary to open the UES duringswallowing. This results in protrusion ofhypopharyngeal mucosa between the oblique fibers of the inferior pharyngealconstrictor and the transverse fibers of the cricopharyngeal muscle. With time, theprotrusion elongates to produce the diverticulum.In fully developed Zenker’s diverticulum, oropharyngeal dysphagia is the result ofUES dysfunction whereas accumulation of food and fluid in the pouch can lead toaspiration with recurrent pulmonary infections. Other symptoms include halitosis, agurgling sound while swallowing and coughing episodes.Diagnostic EvaluationThe best study is a modified barium swallow using cineradiology to assess transfer ofa bolus from mouth to esophagus. This may show a prominent cricopharyngeal bar,a diverticulum of various sizes and preferential filling of the diverticulum withcontrast (see figure-arrow).TreatmentThe treatment is usually surgical myotomy to reduce UES pressure together withdiverticulectomy or reduction of the pouch using a plication technique. UESmyotomy alone is insufficient if the diverticulum is large; diverticulectomy withoutmyotomy does not correct the underlying problem and will lead to recurrence of thepouch. 62
  9. 9. Case History #2A 78 year-old man presents with dysphagia and a 10 pound weight loss during thepast 18 months. He is a former heavy smoker who had undergone a coronarybypass graft 10 years earlier.His dysphagia began insidiously and he reports difficulty in both solids and liquids.On occasion, he regurgitates foamy white bland tasting material. Increasingly,eating became more deliberate and he often stands up during a meal to relieve thesensation of retrosternal fullness. Over the past 6 months, he has noted a steadyweight loss that reached 10 pounds at the time he presented to the officeHis physical examination is unremarkable except for a well-healed scar over thesternum. What is the mechanism behind his symptoms; structural? motility?Achalasia: An example of a disorder involving esophageal motilityEpidemiologyAchalasia is an uncommon but worldwide disorder affecting both genders and allages. The etiology is unknown although an autoimmune mechanism is plausible.An achalasia-like condition is Chagas disease which occurs in South America and iscaused by an immune response to a parasite (Trypanosoma cruzi), which damagesthe myenteric plexus of the esophagus. A similar mechanism in response to anunknown agent(s) is hypothesized for achalasia.PathophysiologyPresumably, an inciting event produces damage or death to myenteric gangliacontaining the inhibitory neurotransmitters, nitric oxide and vasoactive intestinalpolypeptide (VIP) in the esophageal smooth muscle and LES. This results in loss ofperistalsis as well as incomplete relaxation of the LES. The LES is not able to relaxproperly due to an unopposed cholinergic stimulation. This produces a functionalmechanical obstruction at the LES and slowly progressive dilation of the esophagus.As the disease advances there is retention of ingested food and saliva and symptomsof regurgitation.Diagnostic evaluationA characteristic barium esophagram shows a dilated esophagus, a column of bariumextending high into the chest and a characteristic “bird’s beak” narrowing at theregion of the LES.Esophageal manometry reveals 4 characteristic findings, only two of which arenecessary for the diagnosis of achalasia.Manometric criteria for achalasia Necessary Absence of esophageal peristalsis 63
  10. 10. Incomplete LES relaxation Not Necessary Increased LES pressure Intraesophageal pressures exceed intragastric pressuresTreatmentNo treatment restores neuronal loss or peristalsis. Thus, efforts are directed towardsdecreasing LES pressure to reduce functional obstruction. This can be done bydisrupting the LES mechanically or reducing LES tone pharmacologically. Muscle Disruption: Pneumatic dilation LES myotomy (Heller myotomy) Treatment Of Achalasia Balloon Dilation Esophagogastric Myotomy Muscle Relaxation: Botulinum toxin injection Nitrates Calcium channel blockers 64
  11. 11. Mechanism by which botulinum toxin A blocks release of acetylcholine atneuromuscular junction. From: Arnon: JAMA, Volume 285(8).February 28, 2001.1059-1070Release of acetylcholine at the neuromuscular junction is mediated by the assemblyof a synaptic fusion complex (SNARE proteins) which fuses to allow release of Achinto the synaptic cleft. Botulinum A toxin cleaves SNAP-25 protein (a dockingprotein) to block the release. When injected into the LES, this release is blockedlocally which decreases LES pressure. Best used as a temporary bridge to moredefinitive therapies or for patients who cannot tolerate the potential morbidity ofmuscle disruption. 65
  12. 12. Surgical myotomy is best for young patients and for those who do not respond topneumatic dilation. Either results in good to excellent results with acceptablemorbidity rates. SUGGESTED ALGORITHM FOR TREATMENT OF ACHALASIA Low surgical risk High surgical risk/unwilling to have surgeryLaparoscopic myotomy Graded Pneumatic Botulinum Toxin (80-100 units) DilationFailure Success Failure Success Failure SuccessLow surgical risk Repeat botulinum toxinFailure Success Failure SuccessLow surgical risk Nifedipine/IsordilCase History #3A 52 year-old woman presents with dysphagia over the past 3 months. She is amoderate smoker who underwent a cholecystectomy 13 years earlier and ahysterectomy 1 year later, both for benign diseases.Her dysphagia began approximately 3 months ago when she began to notice thatsolid foods would stick in the region of the lower substernal area. Gradually, shebegan to eat semi-solid foods to avoid symptoms. Liquids passed without difficulty.Although she changed her diet, her appetite was maintained and she lost no weight.Further history reveals that she has had intermittent heartburn for many years forwhich she used antacids and more recently over-the-counter Cimetidine. Shereports no cold intolerance, tightening of skin or change in bowel habits.Her physical examination is unremarkable except for well-healed surgical scars. What is the mechanism behind her symptoms; structural? motility?Peptic Stricture: An example of a complication of gastroesophageal (GE) reflux. 66
  13. 13. Epidemiology of GERDGastroesophageal reflux disease (GERD) is the most common condition arising fromthe GI tract. The most characteristic symptom is heartburn. A small minority ofaffected persons seeks medical attention and even fewer have complications. Othercommon symptoms include regurgitation, belching and “water brash”, but patientsmay also have atypical presentations including chest pain, hoarseness, loss of dentalenamel, chronic cough, and asthma. Slowly progressive dysphagia for solidssuggests a peptic stricture in the esophagus whereas liquid and solid dysphasiasuggests a reflux related motility disorder.PathophysiologyThe primary abnormality in GERD is excessive ‘reflux’ of stomach contents into theesophagus at inappropriate times and for an inappropriately long duration andfrequency. Damage caused by acid, enzymes and other gastric juice constituentsmay lead to esophageal mucosal damage and subsequent symptoms andcomplications.Four major physiologic mechanisms act to prevent and protect the esophagus fromthe damaging effects of gastroesophageal reflux. These are, according to theirdegree of importance: 1. Lower esophageal sphincter (LES) competence, 2. Esophageal clearance mechanisms, 3. Gastric emptying, and 4. Esophageal mucosal integrity.The most important parameter in preventing gastric regurgitation is LEScompetence, which consists of LES pressure and the location of the sphincteradjacent to the diaphragmatic crus.Normally, when gastric contents reflux into the esophagus during periods of transientLES relaxation, primary or secondary peristalsis clears the majority of refluxant whilethe alkaline saliva neutralizes residual acid. Gravity also promotes esophagealclearance, returning refluxed material to the stomach without peristalsis when thepatient is in the upright position. The constant emptying of gastric contents ensuresthat gastric stasis and/or subsequent increase in gastric pressure with resulting GERis minimized. The esophagus also secretes bicarbonate, has a cellular mechanism toactively transport H+ out of epithelial cells, and secretes mucin and epidermal growthfactor in response to acid and pepsin. • With respect to LES function in GE reflux, at least 3 mechanisms have been demonstrated: 1. Transient LES (TLES) relaxations occur in all persons via a neural reflex which is mediated through the brainstem. Gastric distrension, upright posture and meals high in fat increase the frequency of TLES which in turn can result in increased reflux into the lower esophagus. 2. Decreased LESP weakens the GE barrier to reflux and is associated with more severe esophageal changes. 3. Some patients have low normal LESP but do not increase pressures in response to increased abdominal pressure. This mechanisms are illustrated as follows: Three Mechanisms of LESP Incompetence 67
  14. 14. • With respect to decreased esophageal clearance mechanisms, this can occur because of weak or absent peristaltic esophageal contractions or decreased production of saliva whose alkanility serves to neutralize acid in the esophagus • Delayed gastric emptying increases the risk of excessive reflux of gastric contents (see lecture on gastric physiology) • The final line of defense of the esophageal mucosa is its intrinsic resistance to acid, pepsin and bile acids. Such factors such as epidermal growth factor (EGF) and intracellular electrolyte movement helps to maintain esophageal epithelial integrity and may be inadequate in some patients with reflux esophagitis.Hiatal hernias are noted in 42% of all patients with symptoms of reflux, but in 60%to 80% of patients with endoscopic esophagitis or peptic strictures. Patients withlarge hiatal hernias associated with relatively low LES pressures are susceptible toreflux episodes following sudden increases in intra-abdominal pressure. These refluxepisodes probably occur because the LES does not tonically contract in response tointra-abdominal pressure events so that transmitted intragastric pressures easilyovercome the LES, which is located in the negative atmosphere of the thoraciccavity. Once gastroesophageal reflux occurs, esophageal peristalsis clears theesophageal contents into the hiatal hernia, which then acts as a reservoir of gastriccontents awaiting further intra-abdominal pressure events, transient LES relaxations,or free reflux events to repeat the reflux cycle.Diagnostic Testing in suspected GERD 68
  15. 15. The choice of available diagnostic tests, as with dysphagia, is decided on the basis ofthe clinical question. Available tests include barium swallow, endoscopy, esophagealpH monitoring and esophageal manometry AMBULATORY pH STUDYESOPHAGEAL pH PROBE BRAVO (wireless pH probe) pH RECORDING 69
  16. 16. Question Best Diagnostic TestDoes patient have sigificant acid reflux? Esophageal pH with “DeMeester score”Are symptoms due to acid reflux? Esophageal pH with “symptom index”Why is patient having dysphagia? Barium esophagram with liquids and solidsHas acid reflux caused damge to Endoscopy with biopsyesophageal mucosa?Treatment of GERDTreatment options for GERD include; • Lifestyle modifications • Acid suppression and promotility medications • Surgical antireflux proceduresPhase 1 therapy, which involves life-style and dietary modifications, is the initial stepfor treatment of all patients with GERD. The head of the bed should be elevated 6”with bed blocks or a wedge under the shoulders. This practice uses gravity todecrease esophageal acid contact time when reflux occurs. An empty stomachbefore going to sleep reduces the stimulus for nocturnal reflux. Reduction in dietaryfat decreases reflux frequency in patients with GERD. Patients should stop smokingand avoid esophageal irritants, such as citrus products and coffee. Potentiallyharmful medications should be avoided. For instance, nitrates, theophylline, andcalcium channel blockers may reduce LES pressure, whereas doxycycline, quinidine,and NSAIDs may cause mucosal injury.Acid suppression is the backbone of pharmacologic therapy for GERD. The twoclasses of drugs commonly used are H2 receptor antagonists (H2 RAs) and theproton pump inhibitors (PPIs). Promotility drugs improve esophageal andgastric emptying and may be useful in some patients. However, these drugsfrequently are required indefinitely and are expensive..Otherwise healthy patientsunder the age of 50 may be more effectively treated and perhaps at reduced costwith anti-reflux surgery compared to a lifetime of medical therapy. Other indicationsfor anti-reflux surgery include difficult to manage strictures, severe bleeding fromesophagitis, and aspiration symptoms.The principle of surgery is to restore an effective GE barrier to eliminate GE reflux.The most common operation is a fundoplication in which the hernia, if present, isreduced and the fundus of the stomach is wrapped around the GE junction at thelevel of the diaphragmatic crus. The fundoplication is then anchored to the upperportion of the esophageal hiatus. 70
  17. 17. Total Fundoplication Efficacy of Therapies for GE Reflux Antacids Prokinetics H2RAs PPIs Surgery Eliminate + ++ +++ ++++ ++++ Symptoms Heal Esophagitis 0 + +++ ++++ ++++Manage or Prevent 0 0 ++ +++ +++ ComplicationsMaintain Remission 0 + ++ +++++ ++++Esophageal strictureThis most often occurs in the distal esophagus where GERD does most of its damageand is typically less than 1 cm in length. Dysphagia is often insidious in onset, thetypical patient has dysphagia for several years. Profound weight loss is uncommon,in contrast to patients with esophageal cancer.The diagnosis is often made with barium contrast studies and/or endoscopy withbiopsy and brush cytology specimens. Treatment using various dilating devices andwith aggressive acid suppression therapy is often effective. In some patients,surgery may be required.Barrett’s Esophagus (BE)This is a condition in which columnar intestinal-like epithelium replaces thesquamous epithelium which normally lines the distal esophagus. This develops whenGE reflux damages the squamous mucosa and the injury heals through a metaplasticprocess. The abnormal epithelium that characterizes BE is an incomplete form ofintestinal metaplasia (called specialized metaplasia) and its importance is that itpredisposes patients to an increased risk of developing adenocarcinoma. 71
  18. 18. The diagnosis of BE is made by endoscopic recognition and confirmed by biopsies ofthe affected area. In essence, it is the recognition that the squamocolumnar junction(called the Z line) now lies proximal to the gastroesophageal junction.If the segment is ≥ 3 cm, it is known as long-segment BE whereas if it is less than 3cm, it is known as short-segment BE. Although it seems logical that the risk ofdeveloping adenocarcinoma is proportionate to the length of BE, this is unproven andboth are managed in a similar fashion.Management consists of periodic endoscopic surveillance with multiple biopsies. Thefinding of high grade dysplasia often prompts esophagectomy although nonsurgicalmeans of treatment are currently under investigation. It is unproven as to whetheraggressive antireflux therapy, either medical or surgical, reduces the risk of cancer. NOTES 72
  19. 19. NOTES 73

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