TITLE:
Esophagology and Esophagoscopy
SOURCE: Grand Rounds Presentation, The University of Texas Medical Branch
DATE: October 27, 2011
RESIDENT PHYSICIAN: Benjamin Walton,
MD
FACULTY PHYSICIAN: Michael Underbrink, MD
DISCUSSANT: Michael Underbrink, MD
SERIES EDITOR: Francis B. Quinn, Jr., MD
ARCHIVIST: Melinda Stoner Qui=
nn,
MSICS
"This material was prepared by resident physicians in partial
fulfillment of educational requirements established for the Postgraduate
Training Program of the UTMB Department of Otolaryngology/Head and Neck Sur=
gery
and was not intended for clinical use in its present form. It was prepared =
for
the purpose of stimulating group discussion in a conference setting. No
warranties, either express or implied, are made with respect to its accurac=
y,
completeness, or timeliness. The material does not necessarily reflect the
current or past opinions of members of the UTMB faculty and should not be u=
sed
for purposes of diagnosis or treatment without consulting appropriate
literature sources and informed professional opinion."
The Otolaryngologist needs to be familiar with the esophagus, its anatomy, disease process, diagnostic evaluation, and treatment. The esophagus is somewhat unique in that its location is not confined to the head and neck.<= span style=3D'mso-spacerun:yes'> It is an organ system that travers= es several specialty divisions. = The Otolaryngologist is an important member in the treatment team for esophageal abnormalities w= hich also includes the Gastroenterologist and Cardiothoracic surgeon. New advancements in endoscopic technology have further expanded the role of the Otolaryngologist in the fi= eld of esophagology. In-office esophagoscopy has become a safe and reliable tool in diagnosis and treatmen= t of various esophageal abnormalities.
The esophagus is a vertical muscular tube that extends= from the hypopharynx to the stomach. It is generally 23-25 cm in length and passes through the neck, superior mediastinum and posterior mediastinum anterior to the cervical and thoracic vertebrae. The esophagus gene= rally has a slight left curve in its descent before returning to the midline. In the superior mediastinum, the esophagus runs posterior to the trachea in contact with the common carotid arteries. Importantly, the recurrent laryngeal nerves run along the esophagus in the tracheoesophageal groove. Some esophageal patho= logy may compress or infiltrate these nerves causing hoarseness. Generally, the thoracic duct lies = to the left of the esophagus. The esophagus passes posterior and to the right of the descending aorta on its = way down to the stomach until the inferior mediastinum where the esophagus pass= es anterior and slightly to the left of the aorta. The left main bronchus crosses ant= erior and indents the esophagus below the arch of the aorta. The Aorta, left main stem bronchus= and diaphragm are three sites of external compression. These three anatomical locations a= re sights of esophageal compression and can be seen on routine esophagoscopy.<= span style=3D'mso-spacerun:yes'> In the thorax, the right vagus ner= ve descends posterior to the esophagus and the left vagus nerve descends anteriorly. The muscles of the esophagus consist of an inner circular layer of muscle continuous with the inferior constrictor muscles of the pharynx and an outer longitudinal layer. Between these two laye= rs, the Auerbach’s myenteric plexus sits. This nervous plexus is responsible= for peristalsis. The outer longit= udinal layer of muscle is arranged in fascicles at its proximal sight attaching to= the cricoid. More distally, the fascicles blend to form a uniform layer surrounding the esophagus. The outer longitudinal muscle laye= r is composed of striated muscle in the upper third, mixed striated and smooth muscle in the middle third, and smooth muscle in the lower third of the esophagus. Unlike the other o= rgans composing the digestive tract the outer coat of the esophagus is a loose fibroelastic tissue rather than a strong serosa.
The esophagus is lined by a non-keratinzed stratified squamous epithelium which covers a thin lamina propria. The muscularis mucosae is a smooth muscle arranged longitudinally deep to the lamina propria. This muscle generally thickens dow= n in the lower third of the esophagus. A submucosal layer consists of thick collagenous and coarse elastic fibers. This layer contains mucus glands a= nd Meissner’s plexus.
Access into and out of the esophagus is controlled by =
two sphincters. The upper esophageal sphincter (UE=
S) is
a high pressure zone. It cons=
ists
of an inner circular layer of muscle that is thicker at the cricoids
blending with the cricopharyn=
geal
muscle. The lower esophageal
sphincter is no one distinct muscle.
It is generally 3 cm in length and has a resting tone of 15-45 mm
Hg. This resting tone is impo=
rtant
to keep in mind as pathology such as achalasia distorts its resting tone.
Swallowing, also known as primary peristalsis is the mechanism in which a bolus of food is passed from the oral cavity into the stomach. A tight coordination= of multiple muscle factors works to push the bolus down. Any problem with a muscle group in= this process can lead to dysphagia. The UES, esophageal body, and LES work in a coordinated behavior to transfer fo= od through the esophagus. There = are three main phases in swallowing known as the oral phase, oropharyngeal phase and esophageal phase. The oral phase of swallowing is voluntary; however, the esophageal phase is not. Bolus passage through the mouth in= to the pharynx is known as the oropharyngeal phase. This phase predicates on very prec= ise timing of the opening and closure of various portions of the pharynx for pr= oper swallowing and airway protection. The larynx elevates in this phase allowing the epiglottis to seal the airway. The food bolus then p= asses through the relaxed UES. The = UES then closes and peristalsis begins as progressive circular contractions pro= pel the bolus down the esophagus through a relaxed LES. Normal esophageal pressures during peristalsis can range from 30 to 180 mm Hg. There is a secondary peristalsis t= hat occurs in the esophagus. Seco= ndary peristalsis is progressive contraction in the esophageal body stimulated by sensory receptors rather than by swallowing. This mechanism clears food that ha= s been poorly cleared by primary peristalsis.
Through precise movement and coordinated muscular acti= vity, the food bolus travels into the stomach.&n= bsp; However, any process that disrupts this coordinated activity can cau= se dysphagia. Dysphagia is defin= ed as a sensation of food being delayed in its normal passage from the mouth to t= he stomach. As it is defined, th= ere are multiple reasons a patient can have dysphagia. One way to further define dysphagi= a is to understand the differences in sensation. Patients who generally complain of difficulty with initiating a swallow have what is termed oropharyngeal dysphagia. Patients who compl= ain that food “sticks” after swallowing have what is termed esophag= eal dysphagia. Important in the evaluation of dysphagia is a good, thorough clinical history. Distinguishing the type of dysphag= ia can be helpful in creating a specific diagnosis. Patients complaining of solid food= dysphagia often have a structural lesion. Intermittent solid food dysphagia may represent an esophageal ring.<= span style=3D'mso-spacerun:yes'> Dysphagia to solids and liquids li= kely represents a motility disorder as the cause of dysphagia.
Or= opharyngeal dysphagia is sometimes termed transfer dysphagia. The oropharyngeal phase of swallowing is where precise movements of the orophar= ynx, hypopharynx, and esophagus allow both transfer of food and airway protection. This type of dysp= hagia generally arises from diseases of the upper esophagus, pharynx, or UES.&n= bsp; Patient generally will present with complaints of difficulty initiat= ing a swallow with immediate cough, gag, or nasal regurgitation. Patients with complaints of dyspha= gia to the throat or cervical area are less likely to have primary esophageal dysphagia as studies have shown 30% of patients who localize their difficul= ty to the cervical or throat area have esophageal dysphagia. Oropharyngeal dysphagia is most co= mmonly caused by neuromuscular dysfunction. There are many causes of oropharyngeal dysphagia. Neuromuscular causes include CVA, amyotrophic lateral sclerosis, Parkinson’s disease, Myasthenia gravis, and Tardive dyskinesia. Struc= tural causes include cervical osteophytes, zenker’s diverticulum, tumors, a= nd post-cricoid webs.
Esophageal dysphagia encompasses a large number of causes. It is often best to g= roup these causes into four main categories. Causes of esophageal dysphagia are grouped into motility abnormaliti= es, strictures, rings and webs, and eosinophilic esophagitis.
Esophageal motility disorders have undergone several classification systems. The l= atest system consists of 4 major patterns: inadequate relaxation of the LES, atypical disorders of LES relaxati= on , hypercontraction disorders, and hypocontraction disorders. Disorders of inadequate relaxation= of the LES include classical Achalasia and atypical disorders of LES relaxation. Classical achalas= ia is a primary esophageal motility disorder.&nb= sp; It generally is of unknown etiology; however, Chagas disease caused = by infection with the Trypanosoma cruzi protozoa. Histological examination shows pat= chy inflammatory infiltrates of T cells, eosinophils, and mast cells into the Auerbach’= ;s myenteric plexus. These patie= nts present with dysphagia to solids and liquids. Most patients try to accommodate t= his dysphagia with several maneuvers. 75% of these patients present with regurgitation and 60% of these patients complain of weight loss. However, in most patients, this loss is generally minimal. Diagnosis of achalasia is done wit= h a barium esophagram with fluoroscopy. The esophagram reveals the classic “bird’s beak” tapering of the distal esophagus. Esophageal manometry reveals aperistalsis in the body of the esophag= us with baseline elevation of LES pressure.&n= bsp; There is currently no cure for Achalasia. Treatments generally include pneum= atic dilation and surgical myotomy. Importantly, all patients considered for dilation must be surgical candidates as dilation incurs a 2-5% risk of perforation. Surgical treatment includes the Heller’s myotomy which is an anterior myotomy across the LES. This procedure is often done with = an anti-reflux procedure. Alternatively, non-surgical candidates can be treated with botulinum toxin injections into the LES. This treatment is effective in 85% of the patients. However, its long term efficacy is= not good as 90% patients have symptom return in 6 months.
The spectrum of esophageal dysphagia disorders of uncoordinated contraction includes diffuse esophageal spasm. Diffuse esophageal spasm is the pr= esence of simultaneous and repetitive contractions in the esophageal body. Unlike achalasia, patients with dif= fuse esophageal spasm have some normal peristalsis. Often, these patients are diagnosed after substantial work-up for cardiac-related disorders is negative. The barium esophagram shows the cl= assic “corkscrew esophagus.” Treatment of this disorder includes nitrates and calcium channel blockers.
Hypercontraction esophageal disorders include nutcrack= er esophagus and isolated hypertensive LES.&n= bsp; Nutcracker esophagus is more commonly seen of the two hypercontracti= le disorders. Generally, these patients present with noncardiac chest pain. Esophageal manometry reveals high-amplitude peristalsis. M= any experts believe that nutcracker esophagus is not a true primary motility disorder.
Di= sorders of hypocontraction include ineffective esophageal motility. Ineffective esophageal motility is diagnosed when esophageal manometry reveals contraction amplitudes of less = than 30 mm Hg in 30% or more of wet swallows.&n= bsp; There is a higher incidence in patients with GERD.
It is important to remember that there are also other factors that can cause motility disorders.= There are many systemic conditions that can cause secondary motility disorders. Most commonly, scelorderma or progressive systemic sclerosis can cause esophageal dysmotility. Also, hypothyroi= dism, diabetes mellitus, and amyloidosis can cause dysmotility.
Strictures can occur along the entire length of the esophagus and cause dysphagia in patients.= A stricture is defined as a loss of lumen area within the esophagus. The normal diamete= r of the esophagus is 20 mm, and generally symptoms of dysphagia occur when the diameter of the lumen is less than 15 mm.&= nbsp; Generally strictures are defined under two broad categories. Strictures are generally either classified as intrinsic or extrinsic. Intrinsic strictures include peptic acid-induced, pill-induced, chemical, post-NG intubation, infectious esophagitis, sclerotherapy-induced, irradiation-induced, esophageal/gastric malignancies, congenital, systemic inflammatory disease and epidermolysis bullosa. Extrinsic causes of strictures inc= lude pulmonary/mediastinal malignancies, anomalous vessels and aneurysms, and metastatic submucosal infiltration by breast cancer, mesothelioma, and adenocarcinoma of the gastric cardia. The foundation of treatment of esophageal strictures is esophageal dilation. There are several t= ypes of esophageal dilator available and include the Maloney bougies and Savary-Gilliard dilators. Rec= ently balloon dilators have become increasingly more popular in esophageal dilation. Esophageal dilation= is not without complications. Mo= st commonly, bacteremia occurs in 20-50% of patients. Esophageal dilation incurs a 0.5% = risk of perforation. Also, there i= s a 0.3% risk of bleeding. Radiat= ion and malignancy-induced strictures are at greater risk of perforation. To safely dilate the esophagus, ma= ny experts agree to follow the “rule-of-threes.” In one setting for esophageal dila= tion, one should not dilate more than three times in one session. The goal of dilation is to get the esophageal objective diameter of greater than 15 mm. Studies have shown that 90% = of patients in whom the esophagus is dilated to 15 mm do not have recurrence of their dysphagia at 24 month f= ollow-up. Esophageal strictures that d= o not resolve after standard treatment are termed refractory esophageal strictures. Often the causes = of these strictures include nonsteroidal anti-inflammatory drugs, pill injury, uncontrolled acid reflux, and inability to achieve adequate lumen diameter = by dilation. Treatment for refra= ctory strictures includes removing the offending agent and gentle dilation to 15 mm. Studies have shown intralesional steroid injections are safe and may be effective in refractory strictures.
Rings or webs are structural abnormalities that are of= ten found incidentally in asymptomatic patients. An esophageal web is defined as a circumferential lesion of the esophagus that can consist of either mucosa or muscle. Esophageal rings gene= rally occur in the distal esophagus. There are two major types of esophageal ring. A B ring or Schatzki’s ring occurs at the distal margin of the LES. Schatzki’s ring is the most = common cause of intermittent solid food dysphagia and food impaction in the general population. There is controve= rsy among experts in regards to the cause of Schatzki’s ring. There is also an entity known as a= n A ring which is a muscular ring that occurs generally at the proximal margin = of the LES 2 cm proximal to the squamocolumnar junction. Webs generally only occupy part of= the lumen. Esophageal webs are al= ways mucosal unlike rings and mostly occur in the proximal esophagus. For rings and webs, barium esophag= ram is the most sensitive diagnostic tool. Interestingly, esophageal webs may be related to a specific syndrome known as Plummer-Vinson or Paterson-Kelly Syndrome. Two Gastroenterologists in the US = and two Otolaryngologists in the UK noted the association of proximal esophageal webs, iron-deficiency anemia and dysphagia.
One of the newer pathology that has become more and mo= re relevant in esophagology is eosinophilic esophagitis. On esophagoscopy, there are findin= gs of multiple esophageal rings. Diagnosis of eosinophilic esophagitis is made by biopsy showing esophageal eosinophilia. Defi= nitive diagnosis requires greater than 15 eosinophils per high-power field of muco= sa that then does not clear after appropriate treatment with a PPI. In many patients, this finding is associated with other atopic diseases including eczema and asthma. There is often a strong family his= tory of atopy as well. In the pedi= atric and adolescent population, eosinophilic esophagitis is increasingly recogni= zed as the cause of dysphagia and food impaction in young adults. In the pediatric population, dieta= ry modification and food elimination are effective treatment. Often times, dilation is necessary= in the older population.
Barrett’s esophagus is the most significant outc= ome of chronic GERD. This condition predisposes patients to the development of esophageal adenocarcinoma. The histopathology of Barrett̵= 7;s is such that normal stratified squamous epithelium of the distal esophagus is replaced by intestinal columnar metaplasia. Studies find that 6-12% of patients undergoing endoscopy for GERD have Barrett’s esophagus and in this population the risk of esophageal adenocarcinoma is 0.5% annually. Current endoscopic surveillance guidelines require four quadrant biopsies at 2 cm intervals along the entire length of Barrett’s esophagus every 3 years. As will be discussed later, there = is a distinct role of the Otolaryngologist in this practice.
Dr. Jonathan Aviv has developed a guideline for patien= ts who present in the clinic with the chief complaint of dysphagia. Up to 10% of patients who see an O= tolaryngologist are presenting with laryngopharyngeal reflux. LPR is present in up to 50% of pat= ients with hoarseness and in 51% of patients who present with dysphagia. It is important to have a step-by-= step process in the work-up and management of these patients. Dr. Aviv divides patients into two categories. Patient who prese= nt with cough, throat clearing and hoarseness but deny dysphagia are separated from patients who present with a chief complaint of dysphagia. Dr. Aviv has helped to devel= op a testing system that utilizes laryngeal sensory testing. The endoscope delivers a discrete = pulse of air to the epithelium innervated by the internal branch of the superior laryngeal nerve to elicit the laryngeal adductor reflex. This air pulse is 50 ms in width a= nd is delivered by a channel associated with the flexible laryngoscope. Normal sensory threshold is less t= han 4 mm Hg air pulse pressure. Mod= erate deficit is defined as 4.1-60. mm Hg air pulse pressure. Severe deficit is defined as great= er than 6.1 mm Hg air pulse pressure.
Patients complaining of cough, throat clearing or hoar= seness first undergo flexible laryngoscopy with laryngeal sensory testing. Patients with findings of LPR and = no sensory deficits are then started on standard PPI treatment for 6-8 weeks w= ith follow-up. Any patients with persistent symptoms afterward, are asked to undergo trans-nasal esophagoscopy. Those patients= with LPR and asymmetrical sensory deficit undergo imaging to rule out a neoplasm. If the imaging is negative, those patients undergo trans-nasal esophagoscopy. Patients with tumors or malignancy= found under imaging or initial evaluation or referred to the appropriate physicia= n.
Patients who present with a chief complaint of dysphag= ia are offered a flexible endoscopic evaluation of swallowing with sensory testing (FEESST). This testing assess= es both airway protection and bolus transport of patients. The testing utilizes laryngeal sen= sory testing and endoscopic swallowing evaluation. The first phase of the testing inv= olves flexible laryngoscopy where the anatomy of the nasopharynx, tongue base, hypopharynx, larynx and vocal folds are evaluated. The physician should assess proper velopharyngeal closure, vocal fold mobility, baseline secretion management, pharyngeal muscle strength, and laryngeal elevation. The second phase of the test invol= ves laryngeal sensory testing of the laryngopharynx. The third phase of testing is the = motor evaluation of swallowing with the administration of food consistencies vary= ing from thin liquids to solids. Patients undergoing this testing generally require a trans-nasal esophagoscopy for further evaluation.
Trans-nasal esophagoscopy is quickly growing in its importance in esophagology. T= he technique is an important advance in the care of patients with reflux, dysphagia, and esophageal pathology. Advances in technology allow for brilliant illumination and excellent image quality. The endoscope = is capable of air-insufflation and irrigation along with a 2 mm working channel. For trans-nasal esophagoscopy there is no conscious sedation required. This is a decided advantage for the general population as the risk of sedation is negated. Relatively new to esophagoscopy, T= NE has a long list of indications which continues to grow. These indications are divided into esophageal and extra-esophageal indications. According to the ASGE and ACG, indications for TNE include: esophageal symptoms persisting despite adequate therapy, dysphagia, odynophagia, weight loss, anorexia, radiologically-demonstrated lesions, acute injury after caustic ingestion, greater than 5 years symptoms of GERD or GERD and greater than 50 years old, continuous anti-reflux therapy, foreign body evaluation and possible remova= l, cirrhosis screening for varices, and guide-wire placement of esophageal manometry. Therapeutic indica= tions include: dilation of strictur= es, placement of a feeding tube, botox treatment of achalasia, laser therapy, a= nd placement of wireless pH telemetry capsules. Relative extra-esophageal indicati= ons include: globus pharyngeus, c= hronic cough, cervical dysphagia, asthma or COPD, odynophagia, hemoptysis, LPRD, a= nd head and neck cancer. Trans-n= asal esophagoscopy performs a limited evaluation of the upper gastrointestinal t= ract and often does not view the distal stomach or duodenum. A study by Wildi et al shows that patients with reflux symptoms without abdominal complaints including daily = pain and nausea with a history of ulcer disease are highly unlikely to have a ma= jor disease involving the stomach or duodenum.= Their study shows that daily abdominal pain and nausea with a histor= y of ulcer disease is a strong predictor of major gastric and duodenal diseases.=
The technique for trans-nasal esophagoscopy is
straight-forward and requires little set-up. It is preferable that patients be =
NPO
for 3 hours. The technique do=
es not
require any IV or conscious sedation; however, adequate topical nasal
anesthesia and decongestion is required.&n=
bsp;
Many authors agree that there should be minimal hypopharyngeal
anesthesia to prevent secretion build-up and subsequent coughing or aspirat=
ion
of the secretions. The
esophagoscope can be held in a variety of manners. Most utilize either the standard o=
r the
fishing pole technique. The
lubricated esophagoscope is passed through the nare and then inserted into =
the
esophagus. There are generall=
y two
techniques to intubate the esophagus.
The first technique asks the patient to burp, then the scope is pass=
ed
posterior to the cricoids and into the cervical esophagus. The other technique involves the p=
atient
tucking their chin toward the chest and then swallowing. The esophagoscope tip is then pass=
ed
above the arytenoids or into the left pyriform. Gentle pressure is then applied as=
the
scope is passed through the esophagus.&nbs=
p;
Any excessive resistance that is found in intubating the esophagus
should terminate the procedure. The
patient should then undergo a bariums swallow or modified barium swallow.
During esophagoscopy, there are several landmarks that= were mentioned earlier. The aorta compresses the esophagus generally 24 mm from the nasal ala. The left mainstem bronchus compres= ses the esophagus at 26 mm from the nasal ala.= The third major esophageal landmark is the diaphragm which compresses the esophagus at 41 mm from the nasal ala.
As discussed earlier, Barrett’s esophagus is a predisposing factor for developing adenocarcinoma of the esophagus. Esophageal carcinoma is the fastest growing cancer of the USA and Western Europe in the past 25 years. Unfortunately, esophageal carcinom= a is generally detected in an advanced stage when symptoms occur. The 5 year survival rate for sympt= omatic patients is less than 10% in advanced stages. Early stage adenocarcinoma of the esophagus has a much better survival rate with 5 year survival rates reachi= ng 90%. Saeian et al studi= ed the accuracy of trans-nasal esophagoscopy in the detection of Barrett’s metaplasia and dysplasia. TNE utilizes a 2 mm working channel and the biopsies are generally smaller. The study took 32 patients with Barrett’s metaplasia who underwent quadrant biopsies with standard eq= uipment and TNE biopsy forceps at least 1 week apart. Two pathologists blinded to the st= udy evaluated the specimens. The = study found excellent agreement in the quality of both biopsy specimens. Trans-nasal esophagoscopy allows f= or a safe and effective manner to detect and survey Barrett’s metaplasia in patients. One of the best advantages is the ability to perform the procedure without conscious sedation. This is often the c= ause of most complications from esophagogastroduedenoscopy.
There are multiple procedures that can be performed in= the unsedated patient through trans-nasal esophagoscopy. Biopsies can be safely performed u= sing a 1.8 mm cupped forceps through the working channel of the scope. Biopsies can be safely taken in an= y area of the upper aerodigestive tract with proper topical anesthesia. TNE can be utilized to place wirel= ess pH probes. The esophagoscope can localize the upper and lower esophageal sphincters and determine the accura= te position of the pH probes. Generally, the distal pH sensor is 6 cm above the squamocolumnar junction. The hypopharyngeal = sensor is placed 1 cm above the proximal border of the upper esophageal sphincter. The working channe= l of the scope can be used to pass a flexible laser wire. Often, the KTP laser is utilized.<= span style=3D'mso-spacerun:yes'> This technique is most often used = for laryngeal and hypopharyngeal lesions. Esophageal dilation can be safely performed without sedation. Generally this is performed with a= guide wire placed through the trans-nasal esophagoscope. A Savary dilator or hydrostatic ba= lloon dilator can be utilized in dilation. The Savary dilator utilized a guide wire which is placed under direct visualization with the esophagoscope. The esophagoscope is then removed while the guide wire is kept in pl= ace. The guide wire is then extracted t= hrough the oral cavity with a Kelly clamp. The dilator is then passed over the gui= de wire. Balloon dilation is a n= ewer technique that allows for visualization of the dilation. Unfortunately, the working channel= of the trans-nasal esophagoscope is too small for passing the balloon through = the channel. In a similar fashion= to the Savary dilator, a guide wire is passed under direct visualization of the esophagoscope through the working channel.= The esophagoscope is then removed with the guidewire in place. The balloon is passed over the gui= de wire with the esophagoscope to allow for direct visualization of the balloon passage.
Trans-nasal esophagoscopy can also be utilized to perf= orm a secondary trachea-esophageal puncture.&nbs= p; A secondary TEP can be safely performed using TNE in the office. The technique utilizes an 18 gauge needle, a TEP dilatory, local anesthesia and a 15 blade scalpel.
Botulinum toxin injections can be safely performed in patients using trans-nasal esophagoscopy.&= nbsp; Botulinum toxin inject= ions are useful in the treatment of patients with achalasia, hypertensive lower esophageal sphincter, distal esophageal spasm, nutcracker esophagus, and obstructing muscular rings. T= he technique involves an endoscopic sclerotherapy needle through the working channel of the scope. 100 uni= ts of Botulinum toxin is suspended into 4 ml of sterile saline. In preparing the needle, one must account for the dead space in the long injection needle. 0.5 ml of toxin is injected into t= he LES musculature with 2 injections per quadrant as the esophagus is divided into= 4 quadrants.
Esophagology is an important aspect in the world of the
Otolaryngologist. Otolaryngol=
ogists
often see patients with both extra-esophageal and esophageal complaints.
That was an excellent talk, ve=
ry
well done, and I think that this information is becoming more and more
important as we delve into this new technology that we've become accustomed
to. The esophagus is a diffic=
ult
structure because it’s partitioned and based on the anatomical region=
s,
it is the province of different specialists, the gastroenterologist, the
thoracic surgeon, and the otolaryngologist.
Many esophageal problems prese=
nt
first to the otolaryngologist, in the form of dysphagia, regurgitation, and=
laryngopharyngeal reflex symptoms.<=
span
style=3D'mso-spacerun:yes'> Thus it is important for us =
to
gain a good knowledge of the anatomy and physiology of this structure as we=
go
forward into practice with our transnasal esophagoscpes.
My second point is about Dr. A=
viv's
sensory testing, which is a wonderful thing. Unfortunately the pump porti=
on of
the apparatus is no longer available to us, and it would have been helpful =
to
measure sensation before administering a barium swallow, so as to avoid
aspiration in the insensate portion of the swallowing mechanism. We generally start with a thick ba=
rium
bolus, but some aspiration is always present.
The indications for TNE (trans=
nasal
esophagoscopy) are all over the place, and I think that as more and more
otolaryngologists are doing TNE the
indications become softer and softer, but the important thing is that if you
treat empirically for things that you think might be reflex with dysphagia =
or
silent reflex you might consi=
der
assessing the esophagus or at least advising the patient to undergo TNE after about three months of
treatment because the inciden=
ce of
adenocarcinoma in Barrett's esophagus is going up.
Our problem is "When do we
refer this patient to a gastroenterologist?" Generally, if during the TNE=
you
see something you're worried about or don't understand you're probably bett=
er
off putting the referral in.
Now, I like to look into the stomach, peek into the duodenum, but if=
I
see anything suggestive of peptic ulcer disease, of if my biopsy for H. pyl=
orii
comes back positive, I'll go =
ahead
and refer to our gastroenterologist.
It is unusual, however, for that type of patient, one with abdominal
pain and ulcer symptoms, to come to the otolaryngologist.
Amin MR, Postma GN, =
Setzen
M, Koufman JA. “Transna=
sal
esophagoscopy: A position statement from the American Bronchoesophagological
Association (ABEA).”
Aviv JE. “Prospective, Randomized Out= come Study of Endoscopy Versus Modified Barium Swallow in Patients with Dysphagia.” The Laryngoscope. 2000; 110:<= span style=3D'mso-spacerun:yes'> 564-574.
Aviv JE. “The Office Dysphagia Consult: Diagnosis, Managemen= t, and Coding.” Presented at AAO-HNSF Annual Meeting, October 2009.
Aviv JE, Murry T, Co=
hen M,
Zschommler, Gartner C.
“Flexible Endoscopic Evaluation of Swallowing and Sensory
Testing: Patient Characterist=
ics
and Analysis of Safety in 1,340 Consecutive Examinations.” Ann Otol Rhinol Laryngol.
Chheda NN, Postma GN= . “Transnasal Esophagoscopy.&#= 8221; Flint: Cummings Otolaryngology: Head & Neck Surgery, 5th<= /sup> ed. Mosby, 2010.
Dale OT, Alhamarneh =
O, Young
K, Mohan S. “Laryngeal sensory te=
sting
in the assessment of patients with laryngopharyngeal reflux.” The Journal of Laryngology & Otology. 2010; 124: 330-332.
Falcone
MT, Garrett CG, Slaughter JC, Vaezi M.&nbs=
p;
“Transnasal esophagoscopy findings: Interspecialty comparison.”<=
span
style=3D'mso-spacerun:yes'> Otolaryngology-Head and Neck Su=
rgery. 2009; 140: 812-815.
Ford CN. “Evaluation and Management of Laryngopharyngeal Reflux.” JAMA. 2005; 294: 1534-15400.
Kahrilas PJ, Pandolf= ino JE. “Esophageal Neuromu= scular Function and Motility Disorders.”&nb= sp; Feldman: Sleisenger= and Fordtran’s Gastrointestinal and Liver Disease, 9th ed.= Saunders, 2010.
Koufman JA, Aviv JE, Casiano RR, Shaw GY. “Laryngopharyngeal reflux:
Position statement of the Committee on Speech, Voice, and Swallowing Disord=
ers
of the American Academy of Otolaryngology–Head and Neck Surgery.̶=
1; Otolaryngol Head Neck Surg.=
2002; 127: 32-35.
Long JD, Orlando RC.= “Anatomy, Histology, Embryol= ogy, and Developmental Anomalis of the Esophagus.” Feldman: Sleisenger and Fordtran’s Gastrointestinal and Liver Disease, 9th ed. Saunders, 2010.
Postma GN, Cohen JT, Belafsky PC, Halum SL, Supta S=
K,
Bach KK, Koufman JA. “T=
ransnasal
Esophagoscopy: Revisited (over 700 Consecutive Cases).” The Laryngoscope. 2005; 115: 321-323.
Postma GN, Belafsky = PC, Aviv JE. Atlas of Transnasal Esophagoscopy. 1st edition.= Lippincott Williams & Wilkins, 2007.
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