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7/27/2019 2. ENT Esophagology 2014A
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September 10, 2012
EsophagologyDr. Calavera
OUTLINEI. Esophageal AnatomyII. DysphagiaIII. Diagnostic Tools
IV. AchalasiaV. Non-achalasia motility disorders
a. Diffuse esophageal spasm f. Barrett’sEsophagus
b. Scleroderma g. EsophagealAtresia
c. Esophageal strictures h.Zenker’s Diverticulum
d. Esophageal rings & webs i. CausticIngestion
e. GERD j. Foreign BodyIngestion
ESOPHAGEAL ANATOMY
• Muscular tube connectingthe pharynx to stomach
o Esophagus beginswhere the inferiorpharyngeal constrictormerges with thecricopharyngeus
o [2013A] Starts at (inferiorborder of the cricothyroidcartilage) at the level of C6 orC7 all the way down to T10
o [2013A]Tube that connects thepharynx to the stomach
o Upper esophagealsphincter (UES)
o Lower esophagealsphincter (LES)
• 18 to 26 cm in length
Probst: The esophagus begin at the upper esophagealsphincter, located at the level of the C6 and C7 vertebrae(inferior border of the cricoid cartilage). The esophagusterminates at the gastric cardia in the plane of the T10vertebra.
3 Physiologic Constrictions
Anatomical Landmarks (Adult)The landmarks will be from the central incisors to thecardia, which is around 40cm.The 1st constriction willbe 16 cm from central incisors; 2nd constriction, if webase it on the aorta, will be 23cm from the centralincisors; left main stem bronchus will be 27cm;diaphragmatic hiatus will be 38cm; and cardia will be40cm from central incisors.
Upper
• Upper esophageal sphincter (area of cricopharyngeus)
Probst: in the area of the esophageal inlet between the cricoidcartilage and the cricopharyngeal part of the constrictorpharyngis inferior muscle.
Middle
• Area where left mainstem bronchus and aortacrosses esophagus anteriorly
Probst: where the aortic arch crosses over the trachealbifurcation.
Lower
• Lower esophageal sphincter (area whereesophagus enters cardia of stomach)
Probst: where the esophagus pierces the diaphragm
These physiologic constrictions are important becausethese are the sites where suspected foreign bodies areusually found in foreign body ingestions.
Four LayersProbst: The wall structure of the esophagus adheres to thepattern of the gastrointestinal tract as a whole, consisting of several layers:
• Mucosa (Stratified, non keratinized squamousepithelium)
• Submucosa
• Muscularis Propria (inner circular and outerlongitudinal)
• Adventitia; no serosa
Mucosa
• Esophageal liningo Nonkeratinized, stratified squamous epithelium
• Gastric liningo Columnar epithelium (rugae)
• The Z-line
o Junction of the squamous epithelium(esophagus) and columnar epithelium(stomach)
• Barrett’s Esophagus
o Cephalad movement of the gastric mucosa(enters or crosses the Z-line into theesophageal mucosa
Muscularis Propria
• Skeletal and smooth muscleo Skeletal muscle (proximal
1/3)o Mixed (Middle 1/3)o Smooth muscle (Distal
1/3)
Probst:Upper fourth of the esophgus –Striated fibersSecond fourth – Mixed striated andsmoothLower Half – Smooth fibers
• Inner circular
• Outer longitudinal layers
•
Innervation mainly by Vagusnerveo Auerbach’s (myenteric) plexus
- B/w the 2 muscle layers, the inner circular and the outer longitudinal muscle layer)
- Controls esophageal peristalsis- ACh mediates contraction- NO mediates relaxation
o Meissner’s plexus
- Submucosal layer- Sensory input- Pain sensation overlap w/ heart &
respiratory system
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CM- 16
- 23
- 27
- 31
- 35
- 39
Distancefrom theincisors(40cm)
Cervical
Thoracic
Abdominal
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Probst: Neurovascular supplyBlood Supply – Cervical part of esophagus receives most of its blood supply from the inferior thyroid artery (lesser amountfrom the branches of the subclavian and vertebral arteries).Thoracic part of the esophagus is supplied by the aorta andintercostals arteries. Abdominal part of the esophagus by theleft gastric artery and left inferior phrenic artery
Lymphatic drainage – posterior mediastinum and pulmonaryhilumNerve Supply – Upper cervical part of the esophagus is
supplied by the branches from the recurrent laryngeal nerveand lower part with the unnamed branches from the vagusnerve. Below the tracheal bifurcation is the esophagealplexus, formed by the two vagus nerves.
Stages Of DeglutitionProbst: Normal swallowing requires coordinated interaction of various anatomic structures in the oral cavity, pharynx, larynxand esophagus. From a functional standpoint, the voluntarilyinitiated oral phase of swallowing is distinguished from aninvoluntary pharyngeal phase and esophageal phase whichare controlled through reflux mechanism. Bolus is transportedin the stomach within 7-10 seconds.
• Oralo Voluntary movement of food from mouth into
the pharynx
Probst: Food is broken down and moistened to form abolus that is moved toward the oropharynx. This isaccompanied by pressing food against the hard palatewith the tongue
• Pharyngealo Transport of food through the pharynx
Probst: Bolus comes in contact with receptors in thethroat. Afferent impulses for this reflex travel through theglossopharyngeal and vagus nerve while efferent neuronsthat supply the pharyngeal muscles arise from cranialnerves V3, VII, IX, X and XII. The velum is then elevatedto close of the nasopharynx. The larynx is also sealed of
by the elevation of the epiglottis. This is accompanied bya reflex adduction of the vocal cords, allowing food topass through the piriform sinuses toward the esophaguswhile bypassing the larynx.
• Esophagealo Passage of the bolus through the esophagus
Probst: Swallowing begins with a primary peristalticwave, which reflexly initiated in response tomovement of the bolus through the pharynx (CNIX, X). Secondary peristalsis is additionallytriggered in the esophagus by the pressure of thebolus against the esophageal wall.
DYSPHAGIA• Greek dys (difficulty, disordered) and phagia (to
eat)
• Sensation that food is hindered in its passage fromthe mouth to the stomach
• Most patients complain that food:o “sticks,” “hangs up”, or “just won’t go down
right”
• Anatomically classified into two separate clinicalcategories:o Oropharyngealo Esophageal
• Psychiatric disorders can amplify this symptomo If there is no structural or mechanical
abnormalities seen, it is more often than not psychological. One concrete example would betaking the ENT exam. If you know you belongto the 23 failing at the moment, you most
probably will have dysphagia as well.
• Three questions are crucial:1. What type of food or liquid causes
symptoms?o Mechanical vs neuromuscular defecto Primarily solids
o Structural lesion – peptic stricture,ring, or malignancy
o Both solid and liquido Motility disorder – achalasia, or
scleroderma2. Is the dysphagia intermittent orprogressive?
o Esophageal rings tend to causeintermittent solid food dysphagia
o Strictures and cancer causeprogressive dysphagia3. Does the patient have heartburn?
o Complications of GERD – esophagitis,stricture, or Barrett’s esophagus
Dysphagia can be subdivided into oropharyngeal andesophageal. If esophageal dysphagia is particularly on thesolids only, consider mechanical obstruction: if intermittent –esophageal ring, if progressive – stricture / malignancy. If dysphagia is to both solids and liquids, consider motility disorders: if intermittent – esophageal spasm, if progressive –achalasia / scleroderma.
DIAGNOSTIC TOOLS
Esophagogram
• Double-contrast barium esophagogram
• Usually the first specific diagnostic test in theevaluation of esophageal dysphagia
• Detect subtle narrowing and esophageal webs thatmay not be appreciated on endoscopy
Endoscopy
• Procedure of choice to evaluate the mucosa of theesophagus
• Detection of structural abnormalities
• Flexible esophagoscopyo Used by GI serviceo Mode of entry: transorallyo Usual diameters of probes approaching 1cm
o Advantageo allows the insufflation of air to distend the
esophagus and more easily see all of themucosa
o magnified view, suction, irrigation, andbiopsy ports
o Disadvantage: requires intravenous sedationsetting
Rigid Esophagocscopy
• Used by otolaryngologists
• Requires general anesthesia
• Examine the full extent of the esophagus
• View is not magnified
• Esophagus is not distended• Allow use of instrumentation
• Particularly used to remove foreign bodies in theesophagus
• The risks of general anesthesia and the rigidesophagoscopy
Transanal Esophagoscopy• Uses a smaller diameter endoscope
• Flexible esophagoscopy
• Topical anesthesia (optional if patient is tolerant)
• “Easily” performed clinic procedure
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History
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• Patient can return to work after the appointment
• Allows the insufflation of air to distend theesophagus and more easily see all of the mucosa
• Angulation of 180deg retroflexes the tip to seelesser curve
FEES
• Functional Endoscopic Evaluation of Swallowing(FEES)
• Assess risk or presence of aspiration in patientswith swallowing disorders (stroke patients,aspiration)
• No risk of repeated exposure to radiation
• Uses flexible nasal endoscope for viewingstructures, insert to the nasal passage down to the
throat, let the patient take in gelatin, or gulp incolored fluid and visualize if it enters the larynx and not the esophagus.
Esophageal Manometry• Measures intraluminal pressures
o LES, esophageal body & UES
• With each swallowo Strengtho Timingo Sequence of pressure events
• Indicated for patients who need recurrentintraluminal pressure assessment
o Achalasia
o Diffuse esophageal spasm
ACHALASIA• Primary esophageal motility disorder
o Insufficient LES relaxation (contracted LES)
o Loss of esophageal peristalsis
• Pathologico Loss of ganglion of ganglion cell in the
myenteric plexuso Infiltration of T lymphocytes, eosinophils, and
mast cellso Selective loss of post ganglionic inhibitory
neurons, which contain both nitric oxide andvasoactive intestinal polypeptide
• Symptomso Dysphagia to solids and liquido Regurgitationo Chest pain
Achalasia Diagnosis
• Barium esophagogram withfluoroscopyo Best initial diagnostic studyo Findings:
- Proximal esophagealdilatation
- Distal esophagealconstriction (Closed LES)
- Loss peristalsis- Bird’s beak sign
• Esophageal manometryo Establish the diagnosis using pressure
- Absent or incomplete LESrelaxation
- Pressure in the LES would behigh
- Loss of peristalsis
NON-ACHALASIA MOTILITY DISORDERSDIFFUSE ESOPHAGEAL SPASM (DES)
• Simultaneous and repetitive contractions in theesophageal body
• Normal LES relaxation
• Dysphagia if contraction amplitudes are low
• Chest pain if contraction amplitudes are high
• Diagnosis:o Esophagogram
- “corkcrew” esophaguso Manometry
- Simultaneous and repetitive contractions inthe esophageal body
• Treatmento Medications that relax the esophagus
- Nitrates and calcium-channel blockers
SCLERODERMA
• Connective tissue disease
• Peristalsis is absent in the distaltwo-thirds
• Mild dilation of the distal esophagus
• LES becomes incompetent
• Associated with:o
Aspiration pneumoniao Reflux esophagitis with
Barrett’s esophagus
STRUCTURAL DEFECTSESOPHAGEAL STRICTURES
• Loss of lumen area
• Dysphagia main symptom
• Worse with large food piecessuch as meat and bread
• Acid/peptic strictureaccounting for the majority of cases (60%-70%).
•
Diagnosis:o Esophagogram
- Intial diagnostic study- Delineate the stricture
o Endoscopy (flexible /
rigid)- evaluate mucosa
Distal stricture Caustic ingestion Normal mucosaBarrett’s metaplasia
ESOPHAGEAL RINGS & WEBS
• Symptomso Intermittent solid food
dysphagiao Aspirationo Regurgitation
• Ringso Circumferentialo Involves either mucosa or
muscleo Most commonly occur in the distal esophaguso Schatzki’s ring occurs at the GEJ
• Webs
o Only part of the esophageal lumeno Always mucosalo Located in the proximal esophagus
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o Association with iron deficiency (Plummer
Vinson)- Considered in patients complaining of solid
food dysphagia with Fe deficiency, and onendoscopy there are webs in the proximalesophagus
- Triad: solid food dysphagia, Fedeficiency, webs
•
Diagnosiso Barium Esophagogram – most sensitive testo Endoscopic visualization
- Normal-appearing mucosa- Cervical webs are associated with
carcinoma
• Treatmento Endoscopic dilationo Large bougle/ balloon (15-20mm) so as to
fracture the ringo Refractory rings – the ff can be utilized:
Pneumatic dilation (large balloon)
Electrosurgical incision
Surgical resection
Treat GERD
GASTROESOPHAGEAL REFLUX DISEASE• GERD is recognized in about 10-15% of the
population
• Reflux esophagitiso Changes in the esophageal mucosa secondary
to the acid reflux from the stomacho Present in 30-40%
• Barrett’s esophagus
o 10%-20%
• Conditions that can lead to these are the defects in
the esophagogastric barries such aso LES incompetenceo Transient relaxation of LESo Hiatal hernia
• Classic symptom is heartburno Retrosternal burning discomfort and acid
regurgitationo Other symptoms are dysphagia, odynophagia
and belching
• Laryngopharyngeal reflux (LPR)o Hoarseness, throat clearing, dysphagia,
increased phlegm and globus sensation
• Diagnosis: Bravo pH probeo Size of a capsuleo Placed endoscopically down into the
esophagus to the level of LESo Transmits to a recording device and relay the
amount of acid in the LESo 48 hours of pH datao Falls off after 4-10 days, and discarded in the
rectumo Patients prefer this device over the catheter
based system due to reduced discomfort
Barett’s Esophagus
• Condition wherein stomach lining retrogradely
ascends to the esophagus, passing the Z-line• Potentially serious complication of long standing
GERD
• Stratified squamous epitheium of the distalesophagus is replaced by intestinal columnarmetaplasia
• 10-15% predisposes patients to the developmentof esophageal adenocarcinoma
ESOPHAGEAL ATERSIA WITH OR WITHOUTTRACEOESOPHAGEAL FISTULA
Most common: Esophageal atresia (EA) withtracheoesophageal fistula (TEF). Important to takenote: occurs in 87%!
ZENKER’S DIVERTICULUM
• Synonym – Hypopharyngeal diverticulum
• Esophageal diverticula are classified based on:1. Anatomic location2. Mechanism of origin (pulsion or traction)
• Pulsion type diverticulum
Probst: Pulsion diverticula – the mucosa herniatesthrough a weak point in the muscular coat due to a rise of intraluminal pressure. Traction diverticula – usually format the parabronchial sites due to scar traction followinglymphadenitis and involve all the lates of the esophagealwall.
• Herniation of esophageal mucosa occur at weakpoints in the posteroinferior hypopharyngeal wall,above cricopharyngeus
• Annual incidence of 2 per 100,00 people per year
• Male predominance (2-3 times)
• Long history of reflux esophagitis
• Treatment: Surgery
• Types of Zenker’s Diverticulum (Take note of these!):
1. Killian’s dehisence or triangle- Between the cricopharyngeal muscleand inferior constrictor muscle
2. Killian-Jamieson’s- Between the oblique and transverse
fibers of the cricopharyngeal muscle3. Laimer’s triangle
- Between the cricopharyngeal muscleand the most superior esophageal wallcircular muscles
• Diagnosiso History
- Progressive dysphagia – 90& of patientspresenting with ZD
- Regurgitation of food especially in the
morning and while lying down. [Probst]- Unprovoked aspiration- Noisy deglutition
Probst: Patients also complain of pronouncedhalitosis caused by food residues trapped in thediverticulum. Smaller diverticula are sometimesmanifested only by a foreign – body sensation ormaybe completely asymptomatic.
o Barium Esophagogram
Probst – Mirror examination or indirect laryngoscopywill occasionally show the pooling of saliva in thepiriform sinus, but only an imaging procedure canestablish the diagnosis. If reflux espphagits issuspected, the imaging study should besupplemented by ambulatory 24-hour pH-metry andesophageal manometry.
• Treatmento Surgery
- Cricopharyngeal myotomy
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o External- Cricopharyngeal myotomy- Diverticulum is excised and the defect
closed
Probst - The treatment of choice is surgery, using either andendoscopic or external approach.
Endoscopic Approach – The endoscope is advanced throughthe mouth toward the esophageal introitus. The muscularseptum formed by the cricopharyngeus is transacted usingeither conventional technique or CO2 laser, therebyreintegrating the diverticular pouch into the hypopharynx oresophagus. The endoscopic technique is particularly suitablefor older patients with high surgical risk.
External Transcervical Approach – The cricopharyngeus isexposed and divided through a cervical incision, and thediverticular pouch is removed. A post operative radiographshould always be taken to assess the integrity of theesophagus.
CAUSTIC INGESTION• The majority of caustic injuries occur in children
younger than 6 years of age and is entirelypreventable
• Alkaline substances are much more likely to induceinjury to the esophagus than acid chemicals
• Most common sites for burnso Cricopharyngeus (UES)
o Cardia (near LES)
• If there is a history of possible ingestion of causticagents, it is imperative that the presence orabsence of esophageal involvement be established
• Esophageal burn can be established only byesophagoscopyo Never passed beyond 1st visible esophageal
injuryo Generally done 24-48 hours after ingestion
Probst: Acids cause a coagulation necrosis with thedenaturation of proteins, alkalis cause a colliquative necrosiswith liquefaction of the necrotic tissue. Strictures caused byscarring are common sequelae of this type of injury.
• TYPE • COMMERCIAL
PRODUCTSulphuric BatteriesOxalic Paint thinnerHypochloric SolventPhosphoric Metal cleaner
Toilet cleaner
Alkali
<
• TYPE • COMMERCIALPRODUCT
Sodium hydroxide Drain cleanerPotassiumhydroxide
Oven cleaner
Sodium carbonate Washing products
Soapmanufacturing
Fig. Severe erosion secondary to acid ingestion
Probst:Symptoms – acute cases present with severe pain in themouth and the pharynx and possibly in retrosternal andepigastric areas. Drooling is also present. Esophagealperforation may occur and will present with subcutaneousemphysema in the neck or pneumomediastinum.Symptoms of intoxication such as renal and liver failure, electrolyteimbalance and hemolysis do not appear until 1 – 2 days afteringestion. Long term patients may develop stricture withprogressive dysphagia.
Diagnosis – Mirror examination initially – mucosa will appearerythematous and edematous and later may show epithelialdefects and a whitish fibrin coating. Radiographs of chest andabdomen to exclude perforation of esophagus or stomach.
Treatment – First priority is to treat for shock. It is importantto stabilize the airway, replace fluids, correct electrolyteimbalances, relieve pain and provide sedation. Treatmentshould also include high doses of corticosteroids as well asantibiotics to prevent long term infection. For long termpatients, esophageal strictures should be treated by dilation.If stricture cannot be expanded by dilation, stenotic segmentmaybe resected and gastic pull up or interpose a free segentof jejunum with microvascular anastamosis should beperformed.
FOREIGN BODY INGESTION• Most common cause: carelessness on part of
patient or parent
• Other factors: intoxication, unconsciousness, facialtrauma
• Important point in HISTORY is to BELIEVE thepatient
• Most common site of lodgement: level of cricopharyngeus (C7)
Probst: foreign bodies typically become lodged in thehypopharynx or in the upper constriction of theesophagus. Most patients are small children and olderpatients who have decreased sensation in the hardpalate.
Symptoms: Feeling of pressure, pricking sensation, or
pain in the hypopharynx or retrosternal area. Dysphagiamay also be present, depending on the size and locationof the foreign body.
• Diagnosticso Lateral Chest Radiographs
- For radiopaque foreign bodies- Include all areas from nose to anus
o Esophagogram- Barium-soaked cotton swallow- For radiolucent foreign bodies
Probst: Inspection and palpation will disclose anycutaneous emphysema caused by perforation of hypopharynx or esophagus due to sharp objects. This isfollowed by mirror observation of the hypopharynx. If thisfails to locate the foreign body, diagnostic imaging shouldalso be performed. The imaging procedure of choicedepends on the nature of the foreign body. If radiopaqueforeign body at hypopharynx or upper esophagealconstriction, soft tissues of the neck should be should beimaged with a lateral radiograph. Otherwise, an oralcontrast examination should be performed. Abdominalplain film can also show evidence of a foreign body insome cases.
• COIN INGESTIONo Level of cricopharyngeus (1st constriction)
o Level of aortic crossover (2nd constriction)
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Acid
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o Level of LES (3rd constrictions)
__________________END___________________
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