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Dysphagia Dr.Krisana Thaitong.

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1 Dysphagia Dr.Krisana Thaitong

2 Dysphagia must be distinguished from globus sensation
Globus is a sensation of a lump in the throat in which food transport is not limited globus is not related to swallowing and, in fact, may improve with swallowing

3 Dysphagia Oropharyngeal dysphagia Esophageal dysphagia

4 Dysphagia

5 Oropharyngeal dysphagia
Oropharyngeal dysphagia Esophageal dysphagia Neuromuscular dysfunction Achalasia Nonachalasia Motility Disorders Strictures Rings/Webs GERD Extraesophageal GERD Cerebrovascular accidents Amyotrophic Lateral Sclerosis (AML) Parkinson's disease Myasthenia gravis Tardive dyskinesia. Neoplasia Esophageal Diverticula Foreign Bodies Pill-Induced Injury Infectious Esophagitis Caustic Injury

6 Mechanical obstruction
Esophageal dysphagia Solids only Solids & liquids Mechanical obstruction Motility disorder Intermittent progressive Intermittent progressive Rings/Webs Strictures Achalasia Esophageal spasm Malignancy Scleroderma

7 Oropharyngeal dysphagia
abnormality related to the movement of a food bolus from the hypopharynx to the esophagus arises 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 liquids The history and physical examination should focus on neurologic signs and symptoms

10 Neuromuscular dysfunction
Cerebrovascular accidents Amyotrophic Lateral Sclerosis (AML) Parkinson's dis­ease Myasthenia gravis Tardive dyskinesia.

11 Rarely, structural abnormalities caused such as
♥ cervical osteophytes ♥ hypopharyngeal diverticulum (Zenker's diverticulum) ♥ tumors ♥ postcricoid webs typically note difficulty with a solid food bolus leaving the mouth

12 Oropharyngeal swallow is best assessed by videofluoroscopy, also known as the modified barium swallow Videofluoroscopy not only serves to confirm the presence of oropharyngeal dysfunction It can also assess the degree of aspiration

13 Esophageal dysphagia the difficulty in propagating food down the esophagus arises within the body of the esophagus either due to a mechanical or a motility disturbance.

14 Esophageal Disease States
Achalasia Nonachalasia Motility Disorders Strictures Rings/Webs Gastroesophageal Reflux Disease Extraesophageal GERD

15 Neoplasia Esophageal Diverticula Foreign Bodies Pill-Induced Injury Infectious Esophagitis Caustic Injury

16 1. Achalasia

17 Achalasia a primary esophageal motility of unknown cause
characterized by insufficient LES relaxation and loss of esophageal peristalsis hereditary, 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 cells loss of ganglion cells and myenteric neural fibrosis

19 selective loss of post-ganglionic inhibitory neurons, nitric oxide and vasoactive intestinal polypeptide The 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 relaxation Aperistalsis along the esophageal body—a process mediated by nitric oxide.

21 m/c symptoms of achalasia include
♥ dysphagia for solid & liquid ♥ regurgitation ♥ chest pain Patients 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 presentation Regurgitation 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 emptying with retained food and saliva producing a heterogeneous air-fluid level at the top of the barium column.

25 Achalasia

26 The esophagus may be dilated (Figure 80-18).
esophagus is dilated with a "bird's beak" tapering of the distal esophagus Retained secretions form the heteroge-nous air-fluid level seen at the top of the barium column.

27

28 chronic disease be massive with sigmoid-like tortuosity
sigmoid-like tortuosity with large amount of retained debris. late-stage achalasia

29 smooth tapering of the lower esophagus leading to closed LES, resembling a bird's beak
presence of epiphrenie diverticulum may suggest achalasia

30 Bird’s beak deformity at LES

31 Esophageal manometry can be used to diagnosis
In the body of the esophagus, aperistalsis is always present all swallows are typically with low contraction amplitudes.

32 Manometry Elevated resting LES pressure (>35 mmHg )
Incomplete LES relaxation Absence of peristalsis 

33 Manometry

34 Manometric findings in achalasia
The aperistalsis is manifested by isobaric contractions without propagation The 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 swallows baseline 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 LES Asynchronous contraction and Nonperistaltic Fibrotic and atrophic Retention and stagnation of chronic food Retention 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 manometrically suspected 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 myotomy 4.Botulinum toxin injection

40 The two most effective treatments
graded pneumatic dilation and surgical myotomy

41 1.Medical therapy Nitrates, 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 the circular muscle fibers of the LES

43 Balloon dilators,: three diameters
(3, 3.5, and 4 cm) are positioned over a guidewire After pneumatic dilation  gastrograffin study by barium swallow to exclude esophageal perforation relief of symptoms in 50% to 93%

44 Pneumatic dilation of the LES

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 myotomy is 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% of patients

48 However, symptoms recur in more than 50% of patients after 6 months
do not improve LES relaxation or improve peristalsis do not provide complete symptom relief The clinical response is short acting efficacy decreases with time.

49 2.Nonachalasia Motility Disorders

50 Nonachalasia Motility Disorders
Other described primary motility disorders of the esophagus Defined based on the presence of specific manomctrie criteria

51 Most often noted on manometry in
patients with chest pain or dysphagia 2.1 Diffuse esophageal spasm (DES) 2.2 Scleroderma or progressive systemic sclerosis (PSS) 2.3 Other systemic conditions

52 Diffuse Esophageal Spasm
Repetitive, high amplitude contractions of smooth muscle portion of the esophagus The 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 DES The classic finding on esophagogram is the "corkscrew" esophagus

56 Radiographic Classic “corkscrew” Beaklike taper
Increase in esophageal wall thickness

57 Manometrie :simultaneous and repetitive contractions in the esophageal body
but in contrast to achalasia, some normal peristalsis is maintained

58 Typical : corkscrew pattern
Manometry : prolong, high amplitude nonperistaltic Both UES and LES normal,but elevate LES pressure may be found.

59 "Nutcracker" esophagus is another common manometrie diagnosis in noncardiac chest pain
defined by high-amplitude peristalsis

60 distal esophageal contraction amplitude less than 30 mmHg in 30% or more of wet swallows
a food bolus may not be effectively transported resulting in dysphagia

61 Treatment 1.Reassuring the disease is not heart disease.
2.Medication : nitroglycerine, calcium blocker, anticholinergic, PPI (Rx GERD) (not completely effective)

62 3.Surgery : 3.1 Dilation: help only in LES dysfunction, improve dysphagia temporarily 3.2 Surgical myotomy

63 Scleroderma progressive systemic sclerosis (PSS)
Secondary motility disorders arc commonly a result of systemic conditions The most common condition affecting esophageal motility

64 Esophageal motor disturbances occur in several of the collagen vascular diseases
Dermatomyositis Polymyositis Lupus erythematosus Scleroderma (extremely common)

65 Characterized by : Smooth muscle atrophy and collagen deposition in the submucosa Decrease peristalsis and LES resting pressure Refulx esophagitis, ulceration, bleeding

66 Radiography Dilate esophagus with decreased motility (unlike achalasia, persistent patent GE junction and no air fluid level)

67 Scleroderma Stricture from reflux esophagitis

68 Endoscopy: Reflux esophagitis

69 Other systemic conditions
results in esophageal hypomotility hypothyroidism diabetes mellitus amy-loidosis

70 Investigation Esophageal manometry and intraesophageal pH readings are the most sensitive means of detection Diminished contractions in LES and distal two thirds of the esophagus

71 Treatment Standard antireflux medicine
In patients with intractable symptoms gastroesophageal reflux surgery should be considered

72 3.Strictures .

73 Strictures defined as any loss of lumen area within the esophagus
The normal esophagus measures 20 mm in diameter The 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

75 Etiology of Esophageal Strictures Intrinsic strictures
Acid peptic Pill-induced Chemical/lye Post-nasogastric tube Infectious esophagitis Sclerotherapy Radiation-induced Esophageal/gastric malignancies Surgical anastomotic Congenital Systemic inflammatory disease Epidermolysis bullosa

76 Extrinsic strictures Pulmonary/mediastinai malignancies
Anomalous vessels and aneurysms Metastatic submucosal infiltration (breast cancer, mesothelioma, adenoeareinoma of gastric eardia)

77 Intrinsic strictures are most common, with acid/ peptic cause accounting for the majority of cases (60%-70%)

78 Strictures / Caustic Ingestion

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 mm Approximately 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 include ongoing insults from pills or nonsteroida] antiinfkunmatory drugs(NSAlDs) uncontrolled acid reflux inadequate 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 strictures Surgery may be considered in those who fail to respond to aggressive medical therapy and dilation.

86 4.Rings/Webs

87 Rings/Webs common findings on upper endoscopy, many are asymptomatic
Symptoms can include intermittent solid food dysphagia, aspira­tion, and regurgitation.

88 Rings are circumferential, can consist of mucosa or muscle, and most commonly occur in the distal esophagus Esophageal 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 dysphagia iron deficiency was noted by gas-troenterologists Plummer 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 dysphagia Barium 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 impaction The 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 symptoms Between 13 and 20 mm, which accounts for the majority of Sehatzki's rings, symptoms are variable The 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 swallow This lower esophageal muscular ring rarely 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 dysphagia The cause is unclear GERD. congenital abnormality, and possible allergic conditions have been implicated

98 Esophageal Webs and Rings

99 Treatment Treatment consists of dilation with bougienage and possibly acid suppression Many of these patients require more than one treatment session to obtain a desired esophageal lumen of 15 mm They are also at higher risk of painful deep mucosal tears

100 5. Gastroesophageal Reflux Disease

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 patients Reflux esophagitis for 30% to 40% Barrett's esophagus in the remaining 10% to 20%

103 Barrett’s esophagus

104 Barrett’s esophagus with ulceration

105 Barrett’s esophagus

106 Pathophysiology Transient relaxation of the GE sphincter
Esophageal motility disorders Delayed gastric emptying Hiatal hernia Acidic gastric contents Bile acids (more severe eophagitis ) Lower esophageal sphincter works in conjunction with diaphragm to create a physical barrier Pt.s with gastroparesis have predisposition to reflux Acidic gastric material, and duration of exposure primary offending agents in gastritis 60% 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 pressure a large hiatal hernia

110 Symptoms develop when the offensive factors in the gastroduodenal contents overcome several lines of esophageal defense As 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 regurgitation Symptoms 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 GERD as 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 done if there is a failure to respond to an empiric course if alarm signs such as dysphagia, odynophagia, weight loss, chest pain, or choking are present.

115 Atypical symptoms Atypical chest pain Hoarseness Nausea Cough
Odynophagia Asthma Globus sensation Onset after age 45 Recurrent laryngitis Recurrent sore throat Subglottic stenosis Dental enamel loss

116 Endoscopy is the technique of choice to evaluate GERD
Reflux esophagitis is present when erosions or ulcerations are present at SCM There are many grading systems to characterize the severity of esophagitis, the most common of which is the Los 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 GERD limitations 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
Erosions Ulcerations Strictures Hiatal hernia Thickening of mucosal folds Not the test of choice for diagnosis

120 6 cm long distal esophageal stricture with nodularity—c/w esophagitis

121 Esophagogram Extensive linear superficial ulcerations and erosions involving the distal 1/3 of the esophagus.

122 Endoscopy Useful for diagnosing complications of GERD Barrett’s
Esophagitis Strictures Not sensitive for GERD itself Only 50% of patients manifest evidence on endoscopy

123 Gastroesophageal Reflux Disease

124 Esophagoscopy

125

126                                                                            stricture

127 1: esophageal structure
1: esophageal structure. White areas radiating proximally are linear erosion 2: baloon dilator 3: stricture is dilated

128 Ambulatory pH Mornitoring
Diagnostic gold standard pH monitor placed in esophagus above sphincter Patient symptom log Correlate symptoms with low pH Not readily available Time consuming inconvenient

129 TREATMENT Lifestyle modifications Antacids
Histamine H2 receptor antagonists Prokinetic Agents Proton Pump inhibitors Anti-reflux surgery Newer endoscopic treatments

130 LIFESTYLE MODIFICATION
Head of bed elevated six inches Decreased fat intake Smoking cessation Weight loss Avoidance of recumbency for 3 hours post-prandially Avoidance of large meals and trigger foods Avoidance of exacerbating medications Meds: calcium channel blockers, beta-agonists, alpha agonists, theophylline, nitrates and some sedatives

131 The goals of treatment in GERD are to
relieve symptoms heal esophagitis prevent recurrence of symtoms prevent complications A variety of lifestyle modifications are recommended in the treatment off GERD.

132 These include avoidance of precipitating foods(fatty foods, alcohol, caffeine) avoidance of recumbency for 3 hours postprandially elevation of the head of the bed smoking cessation weight 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 withdrawal requires 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 junction Maintaining this repair in the normal anatomic position

138

139 6.Extraesophageal GERD

140 Extraesophageal GERD Patients with GERD may present with symptoms other heartburn and regurgitation This 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 present an 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 fails full investigation ambulatory pH testing Confirm diagnosis of GERD when symptoms relieve by specific antireflux therapy

143 Extraesophageal GERD Laryngitis Asthma Chest pain Chronic cough
Dental erosions

144 7.Neoplasia

145 Neoplasia uncommon when present is typically malignant.
The two main culprits are esophageal squamous cell carcinoma esophageal adenocarcinoma.

146 Benign Esophageal Tumors and Cysts
Benign tumors are rare (< 1 %) Classified in two groups Mucosal Extramucosal (intramural)

147 More useful classification:
60% of benign neoplasms are leiomyomas 20% are cysts 5% are polyps Others (< 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 lesions Bleeding is a more common symptom of the malignant form of the tumor: leiomyosarcoma

150

151 Cancer

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 segments least 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 3:1 Patients 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 carcinoma Early 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

157 Diagnosis Barium swallow Esophagoscopy Esophageal biopsy
Brushings for cytologic evaluation

158 Barium

159 Barium

160 Cancer: apple core appearance

161 Current AJCC 2002 staging

162

163 Treatment Surgical 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 techniques Increased rate of curative resection A decreased rate of postoperative death Palliative endoscopic measures

165 Palliative endoscopic measures include
repeated dilation, laser/photo dynamic therapy ablation esophageal stent placement percutaneous gastrostomy tube placement

166 Neoadjuvant /adjuvant therapy
Neo-adjuvant Chemotherapy Neo-adjuvant Radiation Neo-adjuvant Chemo-Radiation Adjuvant Chemotherapy Adjuvant Radiation Adjuvant chemoradiation

167 8.Esophageal Diverticula

168 Esophageal Diverticula
is a sac that protrudes from the esophageal wall As in the rest of the Gl tract a true diverticulum is one that contains all layers of the wall.

169 Esophageal diverticula are most practically classified, based on anatomy, into four categories:
Zenker's diverticula midesophageal diverticula epiphrenic diverticula intramural pseudodiverticulosis.

170 Zenker's divertieulum referred to as an esophageal diverticulum
its location is proximal to the esophagus, above the UES, and it should be considered a hypopharyngeal diverticulum.

171 believed to form as a result of an area of weakness
Killian's triangle, which exists between the cricopharyngeal sphincter and the inferior pharyngeal constrictor muscle

172 Zenker’s diverticulum
Occurs in Killian’s area. Associated with failure of cricopharyngeal dilatation. Symptoms: regurgitation, dysphagia, weight loss.

173 Symptoms include oropharyngeal dysphagia regurgitation halitosis cough aspiration pneumonia

174 Barium swallow is an excellent test
Many small diverticula are asymptomatic patients with large diverticula should be offered treatment

175 Another option for extremely large diverticula
The classic treatment open surgical resection of the diverticulum with division of the cricopharyngcus muscles Another option for extremely large diverticula diverticulopexy suspension 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 wall from neighboring inflammatory or fibrotic 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 LES These 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 disorder Most diverticula are asymptomatic, but occasionally chest pain or regurgitation can be prominent symptoms

180

181 Midesophageal Diverticula

182 Epiphrenic Diverticula

183 Treatment Treatment consists of
managing the underlying motility disorder diverticulotomy with/without myotomy for symptomatic diverticula

184 9.Foreign Bodies

185 Foreign Bodies

186 Foreign Bodies The esophagus is one of the locations where intervention is often required Underlying 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 sphincter the level of the aortic arch the 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 interventions It 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.

190 10.Pill-Induced Injury

191 Pill-Induced Injury Pill-induced injury to the esophagus is an underappreciated entity. over 70 drugs are capable of producing injury to the esophagus Drugs 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 mucosa There is a wide spectrum of injury from 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.

194 11.Infectious Esophagitis

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
odynophagia pain swallowing immunodeficient 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 albicans cytomegalo virus (CMV) herpes simplex virus (HSV)

198 Treatment consists of antifungal therapy, most commonly with fluconazole100 to 200 mg/day for10 to 14 days In patients with only mild immunologic deficiencies, the topical antifungal agents clotrimazole and nystatm are reasonable alternatives

199 12.Caustic Injury

200 Caustic Injury Caustic 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 cleaners Electric dishwasher soap Hair relaxant Acids Bleaches Esophageal, pharyngeal, and laryngeal injuries can occur from ingestion of acids, bases, and bleaches Ingestion of bases causes the most severe injuries Bases – drain cleaners, ammonia, detergents Hair relaxers – no child proof packaging

202 Mechanism of injury Alkalis – pH > 7 Liquefaction necrosis
Acids – pH < 7 Coagulation necrosis Bleaches – pH = 7 Irritants Mechanism of injury differs Liquefaction necrosis – loosening of tissue with deep diffusion into the tissue, only neutralization by the burning tissue will stop the reaction Coagulation necrosis – formation of eschar which will limit the depth of burn Bleaches 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
Odynophagia Mucosal erythema, ulceration Drooling Tongue edema Stridor Hoarseness Esophageal Dysphagia Odynophagia Chest or back pain Gastric Epigastric pain or tenderness Vomiting Hematemesis

205 Radiography Radiologic exam Chest & neck radiographs Barium swallow
Will not reveal 1st and 2nd degree injuries Associated airway distress? Foreign bodies? Barium swallows not for acute management Delays endoscopy

206 Esophagoscopy Esophagoscopy in virtually all patients at hours post-ingestion < 24 hours – underestimation of injury > hours with risk of iatrogenic perforation – barium swallow Rigid vs. flexible debatable Endoscopy to upper limit of severe burn Signs and symptoms are not entirely predictive of esophageal injury 48-72 hrs – structural weakness in esophageal wall

207

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 avoided If 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

213 Thank You


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