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Dysphagia. Dr.Krisana Thaitong. 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 . Dysphagia. Oropharyngeal dysphagia

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dysphagia

Dysphagia

Dr.Krisana Thaitong

dysphagia2
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
dysphagia3
Dysphagia
  • Oropharyngeal dysphagia
  • Esophageal dysphagia
slide5

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
slide6

Esophageal dysphagia

Solids only

Solids & liquids

Mechanical obstruction

Motility disorder

Intermittent

progressive

Intermittent

progressive

  • Rings/Webs
  • Strictures
  • Achalasia
  • Esophageal
  • spasm
  • Malignancy
  • Scleroderma
oropharyngeal dysphagia
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.
slide8
typically present with difficulty initiating a swallow and immediately experience coughing, choking, gagging, or nasal regurgitation when attempting to swallow
slide9
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
neuromuscular dysfunction
Neuromuscular dysfunction
  • Cerebrovascular accidents
  • Amyotrophic Lateral Sclerosis (AML)
  • Parkinson's dis­ease
  • Myasthenia gravis
  • Tardive dyskinesia.
slide11
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
slide12
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
esophageal dysphagia
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.
esophageal disease states
Esophageal Disease States
  • Achalasia
  • Nonachalasia Motility Disorders
  • Strictures
  • Rings/Webs
  • Gastroesophageal Reflux Disease
  • Extraesophageal GERD
slide15
Neoplasia
  • Esophageal Diverticula
  • Foreign Bodies
  • Pill-Induced Injury
  • Infectious Esophagitis
  • Caustic Injury
achalasia
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
slide18
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
slide19
selective loss of post-ganglionic inhibitory neurons, nitric oxide and vasoactive intestinal polypeptide
  • The postganglionic cholinergic neurons are spared, leading to unopposed cholinergic stimulation.
slide20
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.
slide21
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.
slide22
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
slide23
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
slide24
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.
slide26
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.

slide28
chronic disease be massive with sigmoid-like tortuosity

sigmoid-like tortuosity with large amount of retained debris.

late-stage achalasia

slide29
smooth tapering of the lower esophagus leading to closed LES, resembling a bird's beak
  • presence of epiphrenie diverticulum may suggest achalasia
slide31
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.
manometry
Elevated resting LES pressure (>35 mmHg )

Incomplete LES relaxation

Absence of peristalsis

Manometry
slide34

Manometric findings in achalasia

The aperistalsis is manifested by isobaric contractions without propagation

The LES pressure, which is elevated, shows minimal relaxation with swallowing.

slide35
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
slide37
Nonrelaxation of LES
  • Asynchronous contraction and Nonperistaltic
  • Fibrotic and atrophic
  • Retention and stagnation of chronic food
  • Retention esophagitis
slide38
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
therapy
Therapy
  • 1.Medical therapy
  • 2.Pneumatic dilation of the LES
  • 3.Surgical myotomy
  • 4.Botulinum toxin injection
slide40
The two most effective treatments
  • graded pneumatic dilation and surgical myotomy
slide41
1.Medical therapy
    • Nitrates, calcium channel blockers (nifedipine)
    • Cause smooth muscle relaxation but with limited success
slide42
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

slide43
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%
slide45
3.Surgical myotomy

-fail repeated pneumatic dilations

-an anterior myotomy across the LES

(Heller's myotomy) usually associated with an antire-flux procedure

-laparoscopy

slide46
good-to-excellent response rate of 80% to 94%
  • A potential complication of myotomy

is GERD, which occurs in 10% to 20%

slide47
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

slide48
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.
nonachalasia motility disorders
Nonachalasia Motility Disorders
  • Other described primary motility disorders of the esophagus
  • Defined based on the presence of specific manomctrie criteria
slide51
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

diffuse esophageal spasm
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
slide53
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
slide54
DES may present with chest pain if the contraction amplitudes are high
  • dysphagia if the contraction amplitudes are low.
slide55
Investigate: CXR, cardiac evaluation, barium study and manometry
  • LES relaxation is also normal in DES
  • The classic finding on esophagogram

is the "corkscrew" esophagus

radiographic
Radiographic
  • Classic “corkscrew”
  • Beaklike taper
  • Increase in esophageal wall thickness
slide57
Manometrie :simultaneous and repetitive contractions in the esophageal body
  • but in contrast to achalasia, some normal peristalsis is maintained
slide58
Typical : corkscrew pattern
  • Manometry : prolong, high amplitude nonperistaltic
  • Both UES and LES normal,but elevate LES pressure may be found.
slide59
"Nutcracker" esophagus is another common manometrie diagnosis in noncardiac chest pain
  • defined by high-amplitude peristalsis
slide60
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
treatment
Treatment
  • 1.Reassuring the disease is not heart disease.
  • 2.Medication : nitroglycerine, calcium blocker, anticholinergic, PPI (Rx GERD)

(not completely effective)

slide62
3.Surgery:
    • 3.1 Dilation: help only in LES dysfunction, improve dysphagia temporarily
    • 3.2 Surgical myotomy
scleroderma
Scleroderma
  • progressive systemic sclerosis (PSS)
  • Secondary motility disorders arc commonly a result of systemic conditions
  • The most common condition affecting esophageal motility
slide64
Esophageal motor disturbances occur in several of the collagen vascular diseases
    • Dermatomyositis
    • Polymyositis
    • Lupus erythematosus
    • Scleroderma (extremely common)
slide65
Characterized by :
  • Smooth muscle atrophy and collagen deposition in the submucosa
  • Decrease peristalsis and LES resting pressure
  • Refulx esophagitis, ulceration, bleeding
radiography
Radiography
  • Dilate esophagus with decreased motility (unlike achalasia, persistent patent GE junction and no air fluid level)
slide68
Endoscopy:
  • Reflux esophagitis
other systemic conditions
Other systemic conditions
  • results in esophageal hypomotility
    • hypothyroidism
    • diabetes mellitus
    • amy-loidosis
investigation
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
treatment71
Treatment
  • Standard antireflux medicine
  • In patients with intractable symptoms gastroesophageal reflux surgery should be considered
strictures
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.
slide74
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
slide75
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
slide76
Extrinsic strictures
    • Pulmonary/mediastinai malignancies
    • Anomalous vessels and aneurysms
    • Metastatic submucosal infiltration (breast cancer, mesothelioma, adenoeareinoma of gastric eardia)
slide77
Intrinsic strictures are most common, with acid/ peptic cause accounting for the majority of cases (60%-70%)
treatment79
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

slide80
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.
slide81
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.
slide82
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
slide83
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
slide84
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.
slide85
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.
rings webs
Rings/Webs
  • common findings on upper endoscopy,
  • many are asymptomatic
  • Symptoms can include intermittent solid

food dysphagia, aspira­tion, and regurgitation.

slide88
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.
slide89
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.
slide90
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
slide91
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
slide92
Treatment of symptomatic esophageal webs consists of mechanical disrup­tion
  • This can be accomplished with bougie or balloon dilators.
slide93
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
slide94
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
slide95
Recurrent symptoms requiring repeat dilation is not uncommon, and some authors recommend maintaining the patient on acid suppression given the possible association with GERD
slide96
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.
slide97
"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
treatment99
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
gastroesophageal reflux disease
Gastroesophageal Reflux Disease
  • chronic symptoms or mucosal damage caused by the abnormal reflux of gastric contents into the esophagus.
  • Reflux esophagitisrefers to a subgroup of GERD that involves histopathologically characteristic changes in the esophageal mucosa
slide102
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%
pathophysiology
Pathophysiology
  • Transient relaxation of the GE sphincter
  • Esophageal motility disorders
  • Delayed gastric emptying
  • Hiatal hernia
  • Acidic gastric contents
  • Bile acids (more severe eophagitis )
slide107
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
slide108
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
slide109
severe GERD and related complications have a permanent structural alteration
    • low LES pressure
    • a large hiatal hernia
slide110
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
slide111
Classic symptoms of GERD are heartburn
  • defined as a retrosternal burning discomfort, and acid regurgitation
  • Symptoms often occur after meals
slide112
Other in typical reflux are dysphagia, odynophagia, and belching
  • Atypical GERD symptoms include asthma, chest pain, cough, laryngitis, and dental erosions.
slide113
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 abnormal24-hour pH monitoring.
slide114
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.
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

Atypical symptoms
slide116
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

slide117
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.
slide118
Results are normal in 25% of patients with erosive esophagitis and 33% of patients with nonerosive reflux disease
radiologic finding
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
esophagogram
Esophagogram

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

endoscopy
Endoscopy
  • Useful for diagnosing complications of GERD
    • Barrett’s
    • Esophagitis
    • Strictures
  • Not sensitive for GERD itself
  • Only 50% of patients manifest evidence on endoscopy
ambulatory ph mornitoring
Ambulatory pH Mornitoring
  • Diagnostic gold standard
  • pH monitor placed in esophagus above sphincter
  • Patient symptom log
  • Correlate symptoms with low pH
treatment129
TREATMENT
  • Lifestyle modifications
  • Antacids
  • Histamine H2 receptor antagonists
  • Prokinetic Agents
  • Proton Pump inhibitors
  • Anti-reflux surgery
  • Newer endoscopic treatments
lifestyle modification
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
slide131
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.
slide132
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
slide133
Histamine receptor antagonists (H2RAs) in standard dosesachieve completesymptomrelief in 60% of patients and heal esophagitis in bout 50%
slide134
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
slide135
longtermtherapywithPPIsisagainsuperiorto H2RAs, with remission maintained in 80% and 50% of patients, respectively
slide136
"step-down" therapy is recommended
  • Antireflux surgery, now laparoscopie approach, remains an option for carefully selected patients with well documented GERD
surgical treatment
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
extraesophagea l gerd
Extraesophageal GERD
  • Patients with GERD may present with symptoms other heartburn and regurgitation
  • This includes asthma, chest pain, chronic cough, laryngitis, and dental erosions
slide141
lack of the classic heartburn and regurgitation symptoms
  • Esophagitis/Barrett's esophagus is usually not present
  • an empiric trial of bid PPIs is indicatedas initial treatment because there is no definitive diagnostic gold standard for GERD.
slide142
If treatment fails
    • full investigation
    • ambulatory pH testing
  • Confirm diagnosis of GERD when
    • symptoms relieve by specific antireflux therapy
extraesophagea l gerd143
Extraesophageal GERD
  • Laryngitis
  • Asthma
  • Chest pain
  • Chronic cough
  • Dental erosions
neoplasia
Neoplasia
  • uncommon
  • when present is typically malignant.
  • The two main culprits are
    • esophageal squamous cell carcinoma
    • esophageal adenocarcinoma.
benign esophageal tumors and cysts
Benign Esophageal Tumors and Cysts
  • Benign tumors are rare (< 1 %)
  • Classified in two groups
    • Mucosal
    • Extramucosal (intramural)
slide147
More useful classification:
    • 60% of benign neoplasms are leiomyomas
    • 20% are cysts
    • 5% are polyps
    • Others (< 2 percent)
leiomyomas
Leiomyomas
  • Most common benign tumor of the esophagus
  • Intramural
  • Occur between 20-50 years of age with no gender preponderance
slide149
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
malignant tumors of the esophagus
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
slide153
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
slide154
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
clinical presentation
Clinical Presentation
  • Dysphagia is the presenting complaint in 80-90% of patients with esophageal carcinoma
  • Early symptoms are sometimes nonspecific retrosternal discomfort or indigestion
slide156
As the tumor enlarges, dysphagia becomes more progressive.
  • Later symptoms include weight loss, odynophagia, chest pain and hematemesis
diagnosis
Diagnosis
  • Barium swallow
  • Esophagoscopy
  • Esophageal biopsy
  • Brushings for cytologic evaluation
treatment163
Treatment

Surgical resection is the standard treatment for early esophageal cancer in Stages I, II and most cases of III

slide164
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
slide165
Palliative endoscopic measures include
    • repeated dilation,
    • laser/photo dynamic therapy ablation
    • esophageal stent placement
    • percutaneous gastrostomy tube placement
neoadjuvant adjuvant therapy
Neoadjuvant /adjuvant therapy
  • Neo-adjuvant Chemotherapy
  • Neo-adjuvant Radiation
  • Neo-adjuvant Chemo-Radiation
  • Adjuvant Chemotherapy
  • Adjuvant Radiation
  • Adjuvant chemoradiation
esophageal diverticula
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.
slide169
Esophageal diverticula are most practically classified, based on anatomy, into four categories:
    • Zenker's diverticula
    • midesophageal diverticula
    • epiphrenic diverticula
    • intramural pseudodiverticulosis.
slide170
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.
slide171
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
zenker s diverticulum
Zenker’s diverticulum
  • Occurs in Killian’s area.
  • Associated with failure of cricopharyngeal dilatation.
  • Symptoms: regurgitation, dysphagia, weight loss.
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Symptoms include
    • oropharyngeal dysphagia
    • regurgitation
    • halitosis
    • cough
    • aspiration pneumonia
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Barium swallow is an excellent test
  • Many small diverticula are asymptomatic
  • patients with large diverticula should be offered treatment
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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.
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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

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Traction diverticuli are located in the middle third of the esophagus.
  • Midesophageal traction diverticula are the only true diverticula in the esophagus
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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
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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
treatment183
Treatment
  • Treatment consists of
      • managing the underlying motility disorder
      • diverticulotomy with/without myotomy for symptomatic diverticula
foreign bodies186
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
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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.
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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.
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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.
pill induced injury
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
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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

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The typical sites of pill-induced injury are at the level of the aortic arch and the distal esophagus, where there is anatomic narrowing.
infectious esophagitis
Infectious Esophagitis
  • Infectious esophagitis is common, especially in immunosuppressed hosts such as patients with human immunodeficiency virus (HIV), transplant patients, and chemotherapy patients.
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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.
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The three most common causes of infectious esophagitis are
    • Candida albicans
    • cytomegalo virus (CMV)
    • herpes simplex virus (HSV)
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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
caustic ingestion
Caustic Ingestion
  • Esophagus, pharynx, larynx
  • Bases ( most severe injuries )
    • Drain cleaners
    • Electric dishwasher soap
    • Hair relaxant
  • Acids
  • Bleaches
mechanism of injury
Mechanism of injury
  • Alkalis – pH > 7
    • Liquefaction necrosis
  • Acids – pH < 7
    • Coagulation necrosis
  • Bleaches – pH = 7
    • Irritants
severity of burn
Severity of burn
  • Type
  • Amount
  • Concentration
  • Time of contact
  • Stricture formation
signs and symptoms
Pharyngeal or laryngeal

Odynophagia

Mucosal erythema, ulceration

Drooling

Tongue edema

Stridor

Hoarseness

Esophageal

Dysphagia

Odynophagia

Chest or back pain

Gastric

Epigastric pain or tenderness

Vomiting

Hematemesis

Signs and symptoms
radiography204
Radiography
  • Radiologic exam
    • Chest & neck radiographs
  • Barium swallow
    • Will not reveal 1st and 2nd degree injuries
esophagoscopy205
Esophagoscopy
  • Esophagoscopy in virtually all patients at 24-48 hours post-ingestion
  • < 24 hours – underestimation of injury
  • > 48-72 hours with risk of iatrogenic perforation – barium swallow
  • Rigid vs. flexible debatable
  • Endoscopy to upper limit of severe burn
management
Management
  • 1. Stable airway
      • dexamethasone (adult 20 to 30 mg intravenous bolus, pediatric 0.5 to 1 mg/kg) can help prevent further deterioration
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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
therapy209
Therapy
  • Choice of therapy depends on the degree of injury.
  • 1. First-degree burns of the esophageal mucosa require no further therapy
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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
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3. Fourth-degree and even selected extensive third-degree esophageal burns:
      • thoracotomy for direct examination of the esophageal wall esophagectomy