2 Dysphagia must be distinguished from globus sensation Globus is a sensation of a lump in the throat in which food transport is not limitedglobus is not related to swallowing and, in fact, may improve with swallowing
7 Oropharyngeal dysphagia abnormality related to the movement of a food bolus from the hypopharynx to the esophagusarises from disease of the upper esophagus, pharynx, or UES.
8 typically present with difficulty initiating a swallow and immediately experience coughing, choking, gagging, or nasal regurgitation when attempting to swallow
9 most common caused by disruptions in swallowing secondary to neuromuscular dysfunction this setting, the symptoms may be more severe when swallowing liquidsThe history and physical examination should focus on neurologic signs and symptoms
11 Rarely, structural abnormalities caused such as ♥ cervical osteophytes♥ hypopharyngeal diverticulum (Zenker's diverticulum)♥ tumors♥ postcricoid webstypically note difficulty with a solid food bolus leaving the mouth
12 Oropharyngeal swallow is best assessed by videofluoroscopy, also known as the modified barium swallowVideofluoroscopy not only serves to confirm the presence of oropharyngeal dysfunctionIt can also assess the degree of aspiration
13 Esophageal dysphagiathe difficulty in propagating food down the esophagusarises within the body of the esophagus either due to a mechanical or a motility disturbance.
14 Esophageal Disease States AchalasiaNonachalasia Motility DisordersStricturesRings/WebsGastroesophageal Reflux DiseaseExtraesophageal GERD
17 Achalasia a primary esophageal motility of unknown cause characterized by insufficient LES relaxation and loss of esophageal peristalsishereditary, degenerative, autoimmune, and infectious factors as possible causes
18 Pathologic changes occur in the myenteric plexus consist of a patchy inflammatory infiltrate of T lymphocytes, eosinophils, and mast cellsloss of ganglion cells and myenteric neural fibrosis
19 selective loss of post-ganglionic inhibitory neurons, nitric oxide and vasoactive intestinal polypeptideThe postganglionic cholinergic neurons are spared, leading to unopposed cholinergic stimulation.
20 This produces high basal LES pressures, and the loss of inhibitory input results in insufficient LES relaxationAperistalsis along the esophageal body—a process mediated by nitric oxide.
21 m/c symptoms of achalasia include ♥ dysphagia for solid & liquid♥ regurgitation♥ chest painPatients with achalasia localize their dysphagia to the cervical or xiphoid areas.
22 Initially, the dysphagia may be for solids only most patients have dysphagia for solids and liquids at time of presentationRegurgitation occurs in 75% of achalasia and becomes a greater problem as the esophagus dilates with progression of disease
23 Choking and Coughing may awaken the patient from sleep Chest pain 40%Weight loss 60% (minimal loss)barium esophagram with fluoroscopy is the best initial diagnostic study
24 This test will reveal a loss of primary peristalsis in the distal two thirds of the esophagus In the upright position, there will be poor emptyingwith retained food and saliva producing a heterogeneous air-fluid level at the top of the barium column.
26 The esophagus may be dilated (Figure 80-18). esophagus is dilated with a "bird's beak" tapering of the distal esophagusRetained secretions form the heteroge-nous air-fluid level seen at the top of the barium column.
34 Manometric findings in achalasia The aperistalsis is manifested by isobaric contractions without propagationThe LES pressure, which is elevated, shows minimal relaxation with swallowing.
35 Abnormal LES relaxation in all achalasia 70% - 80% of patients absent/ incomplete LES relaxation with swallowsbaseline LES pressure is usually elevated but may be normal in up to 45% of patients
36 Esophagus is dilated with retained fiuid and debris.
37 Asynchronous contraction and Nonperistaltic Fibrotic and atrophic Nonrelaxation of LESAsynchronous contraction and NonperistalticFibrotic and atrophicRetention and stagnation of chronic foodRetention esophagitis
38 All should upper endoseopy to exclude Pseudoaehalasia arising from a tumor at the GEJ Pseudoaehalasia may mimic with classic achalasia both clinically and manometricallysuspected in older age with short duration of symptoms and more significant weight loss
39 Therapy 1.Medical therapy 2.Pneumatic dilation of the LES 3.Surgical myotomy4.Botulinum toxin injection
40 The two most effective treatments graded pneumatic dilation and surgical myotomy
41 1.Medical therapyNitrates, calcium channel blockers (nifedipine)Cause smooth muscle relaxation but with limited success
42 -good short-term results 2.Pneumatic dilation of the LES-good short-term results-2% to 5% risk of perforation- performed endoscopy uses air pressure to dilate and disrupt thecircular muscle fibers of the LES
43 Balloon dilators,: three diameters (3, 3.5, and 4 cm) are positioned over a guidewireAfter pneumatic dilation gastrograffin studyby barium swallow to exclude esophageal perforationrelief of symptoms in 50% to 93%
45 3.Surgical myotomy-fail repeated pneumatic dilations-an anterior myotomy across the LES(Heller's myotomy) usually associated with an antire-flux procedure-laparoscopy
46 good-to-excellent response rate of 80% to 94% A potential complication of myotomyis GERD, which occurs in 10% to 20%
47 4.Botulinum toxin injection -Inhibits release of excitatory acetylcholine from nerve endings (thus causing lower LES pressures)-Good short-term results, but long term efficacy unknow-Effective in about; 85% ofpatients
48 However, symptoms recur in more than 50% of patients after 6 months do not improve LES relaxation or improve peristalsisdo not provide complete symptom reliefThe clinical response is short actingefficacy decreases with time.
50 Nonachalasia Motility Disorders Other described primary motility disorders of the esophagusDefined based on the presence of specific manomctrie criteria
51 Most often noted on manometry in patients with chest pain or dysphagia2.1 Diffuse esophageal spasm (DES)2.2 Scleroderma orprogressive systemic sclerosis (PSS)2.3 Other systemic conditions
52 Diffuse Esophageal Spasm Repetitive, high amplitude contractions of smooth muscle portion of the esophagusThe striated portion and LES relaxation normally.Histopathology : muscular hypertrophy with lymphocytic infiltration of Auerbach’plexus
53 S&S: dysphagia and chest pain (substernal) or esophageal colic with may occur with or without swallowing.Trigger by emotional stress, hot or cold liquids and GE reflux
54 DES may present with chest pain if the contraction amplitudes are high dysphagia if the contraction amplitudes are low.
55 Investigate: CXR, cardiac evaluation, barium study and manometry LES relaxation is also normal in DESThe classic finding on esophagogramis the "corkscrew" esophagus
73 Strictures defined as any loss of lumen area within the esophagus The normal esophagus measures 20 mm in diameterThe predominant clinical symptom of strictures is dysphagia, which is usually when the lumenal diameter is less than 15 mm.
74 Even less severe strictures can cause intermittent dysphagia to large food piece ; meat and bread There are multiple intrinsic and extrinsic causes for esophageal strictures
79 Treatment esophageal dilation. There are several different types: of dilators, including:(1) mercury-filled, rubber Maloney dilators; (2) wire-guided rigid Savary-Gilliard dilators; (3) balloon dilators that can either be through-the-scope (TT8) or wire guided
80 Maloney bougies are used in uncomplicated, short, straight strictures The wire-guided Savary-Gilliard and TTS balloons are both best suited for long, tight, or tortuous strictures.
81 Complications of esophageal dilation perforation (0.5%)bleeding (0.3%)bacteremia (20%-50% )Those with radiation-induced or malignant strictures are at higher risk of perforation.To minimize the risk of perforation, the "rule of. threes" applies.
82 That is, no more than three sequential dilators should be performed per session. The goal of esophageal dilation is to obtain an objective diameter of greater than 15 mmApproximately 90% of; patients dilated to 15 mm have no recurrence at; 24 months
83 Refractory esophageal strictures are defined by lack of response to two or more dilations. The causes, for refractory strictures can includeongoing insults from pills or nonsteroida] antiinfkunmatory drugs(NSAlDs)uncontrolled acid refluxinadequate lumen diameter with dilations
84 PPIs are superior to H-2 blockers in preventing the recurrence of acid-related strictures The treatment of refractory strictures includes the elimination of the offending agents (pills and acid) and gentle dilation to 15 mm.
85 Intralesional steroids injected before dilation are safe and probably effective for refractory stricturesSurgery may be considered in those who fail to respond to aggressive medical therapy and dilation.
87 Rings/Webs common findings on upper endoscopy, many are asymptomatic Symptoms can include intermittent solidfood dysphagia, aspiration, and regurgitation.
88 Rings are circumferential, can consist of mucosa or muscle, and most commonly occur in the distal esophagusEsophageal webs occupy only part of the esophageal lumen, are always mucosal, and are usually located in the proximal esophagus.
89 Esophageal webs can be found as 5% of asymptomatic individuals When symptomatic, usually dysphagiairon deficiency was noted by gas-troenterologistsPlummer and Vinson in the United States, as well as otolaryngologists Paterson and Kelly in the United Kingdom.
90 Plummer-Vinson or Paterson-Kclly syndrome to the triad of proximal esophageal webs, iron deficiency anemia, and dysphagiaBarium radiography is the most sensitive test to diagnose esophageal webs
91 endoscopic visualization, web will appear as a thin, eccentric lesion with normal-appuaring mucosa Some webs are located so proximally that routine passage of the endoscope through the UES with fracture the web
92 Treatment of symptomatic esophageal webs consists of mechanical disruption This can be accomplished with bougie or balloon dilators.
93 Schatzki's ring (B ring) occurs at the GEJ at the distal margin of the LES most common cause of intermittent solid food dysphagia and food impactionThe presence of symptoms depends on the luminal diameter
94 If the ring diameter is less than 13 mm, the patient will have symptoms If greater than 20 mm the patient will almost never have symptomsBetween 13 and 20 mm, which accounts for the majority of Sehatzki's rings, symptoms are variableThe pathogenesis of esophageal rings is controversial
95 Recurrent symptoms requiring repeat dilation is not uncommon, and some authors recommend maintaining the patient on acid suppression given the possible association with GERD
96 The second type of esophageal ring is the A ring", which is a muscular ring most commonly detected on barium swallowThis lower esophageal muscular ringrarely symptomatic and occurs at the proximal margin of the LES approximately 2 cm proximal to SGM.
97 "Ringed" esophagus is a rare condition that occurs in young men The syndrome consists of endoscopie findings of multiple esophageal rings in patients with dysphagiaThe cause is unclearGERD. congenital abnormality, and possible allergic conditions have been implicated
99 TreatmentTreatment consists of dilation with bougienage and possibly acid suppressionMany of these patients require more than one treatment session to obtain a desired esophageal lumen of 15 mmThey are also at higher risk of painful deep mucosal tears
101 Gastroesophageal Reflux Disease chronic symptoms or mucosal damage caused by the abnormal reflux of gastric contents into the esophagus.Reflux esophagitis refers to a subgroup of GERD that involves histopathologically characteristic changes in the esophageal mucosa
102 Nonerosive reflux disease (NERD) refers to endoseopy-negative patients with typical GERD symptoms NERD accounts for approximately 50% of patientsReflux esophagitis for 30% to 40%Barrett's esophagus in the remaining 10% to 20%
106 Pathophysiology Transient relaxation of the GE sphincter Esophageal motility disordersDelayed gastric emptyingHiatal herniaAcidic gastric contentsBile acids (more severe eophagitis )Lower esophageal sphincter works in conjunction with diaphragm to create a physical barrierPt.s with gastroparesis have predisposition to refluxAcidic gastric material, and duration of exposure primary offending agents in gastritis60% of pts reflux both gastric and duodenal juices. Bile acid reflux leads to more severe eophagitis despite adequate suppression of gastric acid secretion
107 normal antireflux barrier between the stomach and the esophagus is impaired transient / permanently defects in the esophagogastric barrier such as LES incompetence, TLESR, and hiatal hernia in the development of GERD
108 TLESRs are short relaxations of the LES that do not occur in response to swallow TLESRs are the primary mechanism for gastroesophageal reflux in healthy persons and in those with mild GERD
109 severe GERD and related complications have a permanent structural alteration low LES pressurea large hiatal hernia
110 Symptoms develop when the offensive factors in the gastroduodenal contents overcome several lines of esophageal defenseAs more components of esophageal defense break down, the severity of reflux increases
111 Classic symptoms of GERD are heartburn defined as a retrosternal burning discomfort, and acid regurgitationSymptoms often occur after meals
112 Other in typical reflux are dysphagia, odynophagia, and belching Atypical GERD symptoms include asthma, chest pain, cough, laryngitis, and dental erosions.
113 There is no diagnostic gold .standard for detecting GERD Classic symptoms of acid regurgitation and heartburn are specific but not sensitive for the diagnosis of GERDas determined by abnormal 24-hour pH monitoring.
114 initial empiric trial of antisecretory therapy in a patient with classic GERD symptoms Further diagnostic should be doneif there is a failure to respond to an empiric courseif alarm signs such as dysphagia, odynophagia, weight loss, chest pain, or choking are present.
115 Atypical symptoms Atypical chest pain Hoarseness Nausea Cough OdynophagiaAsthmaGlobus sensationOnset after age 45Recurrent laryngitisRecurrent sore throatSubglottic stenosisDental enamel loss
116 Endoscopy is the technique of choice to evaluate GERD Reflux esophagitis is present when erosions or ulcerations are present at SCMThere are many grading systems to characterize the severity of esophagitis,the most common of which is theLos Angeles classification
117 The presence of esophagitis and the finding of Barrett's esophagus are diagnostic of GERD 24-hour pH monitoring has long been thought to be the gold standard for the diagnosis of GERDlimitations that remain underappreciated.
118 Results are normal in 25% of patients with erosive esophagitis and 33% of patients with nonerosive reflux disease
119 Radiologic Finding Only 1/3 of patients have radiologic findings ErosionsUlcerationsStricturesHiatal herniaThickening of mucosal foldsNot the test of choice for diagnosis
120 6 cm long distal esophageal stricture with nodularity—c/w esophagitis
121 EsophagogramExtensive linear superficial ulcerations and erosions involving the distal 1/3 of the esophagus.
122 Endoscopy Useful for diagnosing complications of GERD Barrett’s EsophagitisStricturesNot sensitive for GERD itselfOnly 50% of patients manifest evidence on endoscopy
130 LIFESTYLE MODIFICATION Head of bed elevated six inchesDecreased fat intakeSmoking cessationWeight lossAvoidance of recumbency for 3 hours post-prandiallyAvoidance of large meals and trigger foodsAvoidance of exacerbating medicationsMeds: calcium channel blockers, beta-agonists, alpha agonists, theophylline, nitrates and some sedatives
131 The goals of treatment in GERD are to relieve symptomsheal esophagitisprevent recurrence of symtomsprevent complicationsA variety of lifestyle modifications are recommended in the treatment off GERD.
132 These includeavoidance of precipitating foods(fatty foods, alcohol, caffeine)avoidance of recumbency for 3 hours postprandiallyelevation of the head of the bedsmoking cessationweight loss
133 Histamine receptor antagonists (H2RAs) in standard doses achieve complete symptom relief in 60% of patients and heal esophagitis in bout 50%
134 PPIs are superior to H2RAs in both healing rosive esophagitis and symptoms relief, with healing 90% GERD is a chronic relapsing disease with almost universal recurence of symptoms after treatment withdrawalrequires maintenance therapy in many patients
135 longterm therapy with PPIs is again superior to H2RAs, with remission maintained in 80% and 50% of patients, respectively
136 "step-down" therapy is recommended Antireflux surgery, now laparoscopie approach, remains an option for carefully selected patients with well documented GERD
137 Surgical Treatment Nissen fundoplication Total or partial Their aim is to:Restore normal anatomy (intra-abdominal segment of esophagus)Re-creating an appropriate high-pressure sound at the esophagogastric junctionMaintaining this repair in the normal anatomic position
140 Extraesophageal GERDPatients with GERD may present with symptoms other heartburn and regurgitationThis includes asthma, chest pain, chronic cough, laryngitis, and dental erosions
141 lack of the classic heartburn and regurgitation symptoms Esophagitis/Barrett's esophagus is usually not presentan empiric trial of bid PPIs is indicated as initial treatment because there is no definitive diagnostic gold standard for GERD.
142 Confirm diagnosis of GERD when If treatment failsfull investigationambulatory pH testingConfirm diagnosis of GERD whensymptoms relieve by specific antireflux therapy
145 Neoplasia uncommon when present is typically malignant. The two main culprits areesophageal squamous cell carcinomaesophageal adenocarcinoma.
146 Benign Esophageal Tumors and Cysts Benign tumors are rare (< 1 %)Classified in two groupsMucosalExtramucosal (intramural)
147 More useful classification: 60% of benign neoplasms are leiomyomas20% are cysts5% are polypsOthers (< 2 percent)
148 Leiomyomas Most common benign tumor of the esophagus Intramural Occur between years of age with no gender preponderance
149 80% occur in the middle and lower third of the esophagus, rare in the cervical region Obstruction and regurgitation may occur in large lesionsBleeding is a more common symptom of the malignant form of the tumor: leiomyosarcoma
152 Malignant Tumors of the Esophagus Usually are in advanced stages at the time of diagnosis (involving the muscular wall and extending into adjacent tissues)Alcohol consumption and cigarette smoking seem to be the most consistent risk factors
153 Esophageal squamous cell carcinoma Esophageal squamous cell carcinoma (95% of all esophageal cancers) is a disease of men (5: 1)most often in the upper and midthoracic segmentsleast frequently in the cervical esophagus
154 Adenocarcinoma approximate 8% of primary esophageal cancers Most often occur in the distal third of the esophagus in the 6th decade of life.Male to female ratio is 3:1Patients with Barretts metaplasia are 40 times more likely to develop adenocarcinoma
155 Clinical Presentation Dysphagia is the presenting complaint in 80-90% of patients with esophageal carcinomaEarly symptoms are sometimes nonspecific retrosternal discomfort or indigestion
156 As the tumor enlarges, dysphagia becomes more progressive. Later symptoms include weight loss, odynophagia, chest pain and hematemesis
163 TreatmentSurgical resection is the standard treatment for early esophageal cancer in Stages I, II and most cases of III
164 During the past decade, outcomes with surgery have improved resulting in a better 5 year survival due to:Better staging techniquesIncreased rate of curative resectionA decreased rate of postoperative deathPalliative endoscopic measures
174 Barium swallow is an excellent test Many small diverticula are asymptomaticpatients with large diverticula should be offered treatment
175 Another option for extremely large diverticula The classic treatmentopen surgical resection of the diverticulum with division of the cricopharyngcus musclesAnother option for extremely large diverticuladiverticulopexysuspension of the diverticulum in a cranial direction.
176 Midesophageal diverticula are most commonly asymptomatic, occur in the midesophagus Traction diverticuli form as a result of external pulling of the esophageal wallfrom neighboring inflammatory orfibrotic tissue, such as adjacent tuberculous mediastinitis
177 Traction diverticuli are located in the middle third of the esophagus. Midesophageal traction diverticula are the only true diverticula in the esophagus
178 Epiphrenic diverticula, located near the diaphragmatic hiatus, occur in the distal esophagus near the LESThese diverticula are often the result of a motility disorder such as achalasia or DES
179 manometric studies in patients with epiphrenic diverticulum to rule out an associated motility disorderMost diverticula are asymptomatic, but occasionally chest pain or regurgitation can be prominent symptoms
186 Foreign BodiesThe esophagus is one of the locations where intervention is often requiredUnderlying alterations in the lumen of the esophagus play an important role in the risk of a swallowed object becoming lodged
187 The esophagus has several areas of physiologic narrowing the upper esophageal sphincterthe level of the aortic archthe diaphragmatic hiatus/LES where a foreign body can become impacted.
188 The key to the management of foreign bodies is understanding that different foreign bodies require different interventionsIt is important to distinguish a true foreign body from a food impaction.
189 A trial of pharmacologic therapy with A trial of pharmacologic therapy with .1 to 2 mg of glucagon given intravenously, which relaxes the LES, can be given but is rarely successful in relieving a food' impaction.
191 Pill-Induced InjuryPill-induced injury to the esophagus is an underappreciated entity.over 70 drugs are capable of producing injury to the esophagusDrugs commonly associated with pill-induced injury include potassium chloride tablets, doxycycline, quuudine, NSAIDs. iron, and alendronate
192 Pills can damage the esophagus by various mechanisms such as acidity, size, and contact time with esophageal mucosaThere is a wide spectrum of injuryfrom acute self-limited esophagitis to refractory strictures
193 The typical sites of pill-induced injury are at the level of the aortic arch and the distal esophagus, where there is anatomic narrowing.
195 Infectious Esophagitis Infectious esophagitis is common, especially in immunosuppressed hosts such as patients with human immunodeficiency virus (HIV), transplant patients, and chemotherapy patients.
196 The cardinal symptom of infectious esophagitis is odynophagiapainswallowingimmunodeficient patients can present with a variety of symptoms including heartburn, nausea, fever, or bleeding.
197 The three most common causes of infectious esophagitis are Candida albicanscytomegalo virus (CMV)herpes simplex virus (HSV)
198 Treatment consists of antifungal therapy, most commonly with fluconazole100 to 200 mg/day for10 to 14 daysIn patients with only mild immunologic deficiencies, the topical antifungal agents clotrimazole and nystatm are reasonable alternatives
200 Caustic InjuryCaustic ingestion can result in severe injury to the esophagus and stomach.Most ingestions occur accidentally in the pediatric population and the remainder in suicidal, psychotic, and alcoholic adults
201 Caustic Ingestion Esophagus, pharynx, larynx Bases ( most severe injuries )Drain cleanersElectric dishwasher soapHair relaxantAcidsBleachesEsophageal, pharyngeal, and laryngeal injuries can occur from ingestion of acids, bases, and bleachesIngestion of bases causes the most severe injuriesBases – drain cleaners, ammonia, detergentsHair relaxers – no child proof packaging
202 Mechanism of injury Alkalis – pH > 7 Liquefaction necrosis Acids – pH < 7Coagulation necrosisBleaches – pH = 7IrritantsMechanism of injury differsLiquefaction necrosis – loosening of tissue with deep diffusion into the tissue, only neutralization by the burning tissue will stop the reactionCoagulation necrosis – formation of eschar which will limit the depth of burnBleaches are irritants and generally there is no serious morbidity
203 Severity of burn Type Amount Concentration Time of contact Stricture formation
204 Signs and symptoms Pharyngeal or laryngeal Esophageal Gastric OdynophagiaMucosal erythema, ulcerationDroolingTongue edemaStridorHoarsenessEsophagealDysphagiaOdynophagiaChest or back painGastricEpigastric pain or tendernessVomitingHematemesis
205 Radiography Radiologic exam Chest & neck radiographs Barium swallow Will not reveal 1st and 2nd degree injuriesAssociated airway distress? Foreign bodies?Barium swallows not for acute managementDelays endoscopy
206 EsophagoscopyEsophagoscopy in virtually all patients at hours post-ingestion< 24 hours – underestimation of injury> hours with risk of iatrogenic perforation – barium swallowRigid vs. flexible debatableEndoscopy to upper limit of severe burnSigns and symptoms are not entirely predictive of esophageal injury48-72 hrs – structural weakness in esophageal wall
208 Management 1. Stable airway dexamethasone (adult 20 to 30 mg intravenous bolus, pediatric 0.5 to 1 mg/kg) can help prevent further deterioration
209 2. Acute airway obstruction Blind nasotracheal intubation should be avoidedIf direct visualization of the larynx for intubation is not possible because of edema and exudate, emergent cricothyrotomy or tracheotomy is a safer choice
210 Therapy Choice of therapy depends on the degree of injury. 1. First-degree burns of the esophageal mucosa require no further therapy
211 2. Second- and localized third-degree injuries without transmural necrosis: pharmacologic reduction or prevention of stricture formation and to maintain a conduit from the hypopharynx to the stomach by esophageal dilation, stenting, or reconstruction
212 3. Fourth-degree and even selected extensive third-degree esophageal burns: thoracotomy for direct examination of the esophageal wall esophagectomy