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September 10, 2012 Esophagology Dr. Calavera OUTLINE I. Esophageal Anatomy II. Dysphagia III. Diagnostic Tools IV. Achalasia V. Non-achalasia motility disorders a. Dif fus e esopha gea l spasm f. Bar rett’s Esophagus b. Sc leroderma g. Es ophageal Atresia c. Esophageal strictures h. Zenker’s Diverticulum d. Esophageal rings & webs i. Caustic Ingestion e. GERD j. Foreign Bod y Ingestion ESOPHAGEAL ANATOMY Muscular tube connect ing the pharynx to stomach o Esophagus begins where the inferior pharyngeal constrictor merges with the cricopharyngeus o [2013A] St arts at (inferior border of the cricot hyroid cartilage) at the level of C6 or C7 all the way down to T10 o [2013A]Tube that connects the pharynx to the stomach o Upper esophageal sphincter (UES) o Lower esophageal sphincter (LES) 18 to 26 cm in length Pr obst: The es ophagu s begi n at the up per esophageal sphincter, located at the level of the C6 and C7 vertebrae (in fer ior bor der of the cri coi d car til age). The esopha gus ter min ates at the gast ric cardi a in the plane of the T10 vertebra. 3 Physiologic Constrictions Anatomical Landmarks (Adult) The landmarks will be from the central incisors to the cardia, which is around 40cm.The 1 st constriction will be 16 cm from central incisor s; 2 nd constrictio n, if we base it on the aorta, will be 23cm from the central incisors; left main stem bronchus will be 27cm; diaphragmatic hiatus will be 38cm; and cardia will be 40cm from central incisors. Upper Upper esophageal sphincter (area of  Probst: in the area of the esophageal inlet between the cricoid car til age and the cri cop har yng eal par t of the con str ict or pharyngis inferior muscle. Middle Ar ea where lef t mai nst em br onc hus and aor ta crosses esophagus anteriorly Probst : whe re the aor tic arc h crosses over the trache al bifurcation. Lower Lower eso phag eal sp hincte r (a rea wh ere esophagus enters cardia of stomach) Probst: where the esophagus pierces the diaphragm These physiologic constrictions are important because these are the sites where suspected foreign bodi es are usually found in foreign body ingestions. Four Layers Probst: The wall structure of the esophagus adheres to the pattern of the gastrointes tinal tract as a whole, consis ting of several layers: Mucosa (St ratif ied , non kerat inized squamous epithelium) Submucosa Mu scul ar is Pr op ri a (i nner ci rcul ar and outer longitudinal) Adventitia; no serosa Mucosa Esophageal lining o Nonkeratinized, stratified squamous epithelium Gastric lining o Columnar epithelium (rugae) The Z-line o  Junction of the squamous epithelium (e sop hagus) and co lumnar ep ith eli um (stomach) Barrett’s Esophagus o Cephalad movement of the gastr ic muc osa (e nters or crosses the Z- line into the esophageal mucosa Muscularis Propria Skeletal and smooth muscle o Skeletal muscle (proximal 1/3) o Mixed (Middle 1/3) o Smoo th musc le (D is tal 1/3) Probst: Upper fourth of the esophgus – Striated fibers Second fourth – Mixed striated and smooth Lower Half – Smooth fibers Inner circular Outer longitudinal layers Innervat ion mainly by Vagus nerve o Auerbach’s (myenteric) plexus - B/w the 2 muscle layers, the inner circular and the outer longitudinal muscle layer) - Controls esophageal peristalsi s - ACh medi ates contraction - NO mediates relaxati on o Meissner’s plexus - Submucosal layer - Sensory input  CM - 16 - 23 - 27 - 31 - 35 - 39 Distance from the incisors (40cm) Cervical Thoracic Abdominal

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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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