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Management of Airway, Hoarseness, and Vocal Cord Dysfunction After Esophagectomy
Laura Dooley and Ashok R. Shaha
6
Introduction
Vocal cord paralysis (VCP) can have a great impact on the quality of life. Change in voice quality and loudness can affect even the nonprofessional voice user. At times VCP can also be life
threatening—airway obstruction due to bilateral
paralysis with the urgent need for a tracheostomy
or recurrent aspiration pneumonia from inability
to fully protect the airway.
The etiology of unilateral VCP can be separated into a few main categories. Nonlaryngeal malignancy and iatrogenic (surgical trauma) account
for about 50 % of all causes of vocal cord immobility followed by an idiopathic etiology, nonsurgical trauma, and intubation-related etiologies.
Common nonlaryngeal malignancies such as lung
cancer with spread of disease into the aortopulmonary window, thyroid, esophageal, and skull
base lesions are frequently found when working
up unilateral vocal cord dysfunction. Nonlaryngeal malignancy is commonly cited as the most
common cause of unilateral VCP; however, iatrogenic nerve injury is likely the most common
cause for otolaryngology referral [1]. Common
A. R. Shaha ()
Department of Head and Neck Surgery, Memorial Sloan
Kettering Cancer Center, New York, NY, USA
e-mail: shahaa@mskcc.org
L. Dooley
Department of Surgery, Memorial Sloan Kettering
Cancer Center, New York, NY, USA
e-mail: dooleyl@mskcc.org
iatrogenic surgical procedures causing unilateral
vocal cord paresis include anterior cervical spine
procedures, Ivor-Lewis esophagectomies, gastric pull-up, thyroidectomy, thymectomy, neck
dissection, carotid endarterectomy, mediastinoscopy, and cardiothoracic surgery (CABG, pulmonary lobar resection). Endotracheal intubation,
prolonged nasogastric tube placement, and even
esophageal stethoscope placement have been implicated in vocal cord dysfunction [1]. Bilateral
paralysis is overwhelmingly due to iatrogenic
injury (82 %) and is mainly seen after total thyroidectomy.
This chapter will focus on unilateral and bilat-
eral adult VCP in the setting of esophagectomy.
Vocal Fold Dysfunction
The incidence of recurrent laryngeal nerve
(RLN) injury after esophagectomy has been reported to be anywhere between 2 and 20 % [2].
It is more often associated with cervical anastomoses and three-field LN dissection, especially
when removal of bulky proximal tumors or extensive lymph node dissection is required [2].
There are three possible mechanisms for injury
to the nerve: traction, dissection, and transection.
Frequently, injuries from retraction of the RLN,
inadvertently clamping the nerve, or stripping the
nerve of its blood supply can occur, causing the
patient symptoms, albeit more likely of a transient nature. Injury to the RLN during esophagectomy is more common on the left side due to
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_6,
© Springer Science+Business Media New York 2015
65
66 L. Dooley and A. R. Shaha
the mediastinal direction of the nerve as it courses around the arch of the aorta.
Differentiating the paralyzed cord from the
cord that is paretic after surgery can be difficult. This is especially true when the nerve was
not directly visualized and preserved at the time
of surgery. When RLN injury does occur, it increases the incidence of perioperative pulmonary
complications. Pneumonia in this setting is common, most likely due to aspiration, not only of
food and liquids at meals but aspiration of saliva,
as the patient no longer has a competent glottis
and cannot fully close the airway to clear secretions [2].
While up to 40 % of patients with vocal fold
dysfunction in the immediate postoperative setting will resolve their symptoms, the other 60 %
will have persistent dysfunction [2]. Patients
with persistent VCP, who complained of severe
hoarseness at 1 year postoperatively from inability to close the glottis during exertion, showed
debilitation in performance status and pulmonary
function at 3 years post-op [3]. Even in those who
do not complain of hoarseness and dysphonia, approximately one-half of them have a decrease in
phonation time [4]. Up to 20 % of all esophagectomy patients will report severe hoarseness due
to permanent recurrent nerve paralysis, resulting in poor quantity of food intake at 24 months
postoperatively, restricted daily activity, and difficulty in talking at 60 months or more after the
operation [5]. Persistent RLN paralysis continues
to deteriorate the patient’s quality of life until it
is adequately treated. In the setting of RLN sacrifice or iatrogenic injury, early treatment of the
paralyzed cord should be undertaken.
Symptoms of Unilateral Vocal Cord Dysfunction
The symptoms of unilateral vocal cord dysfunction are related to lateral displacement (abduction) of the vocal cord causing glottic insufficiency as the cords no longer meet in midline
during adduction. The most commonly reported
symptom is a change in the patient’s voice, usually hoarseness, though it can vary from vocal
fatigue and decreased volume to complete aphonia. A breathy weak voice results from air escape
during phonation due to the lateralized cord. The
voice can also sound “wet” when secretions are
retained in the pyriform sinus due to the inability
to create a forceful cough. Swallowing difficulties are also seen along with a weak and ineffective cough. When the superior laryngeal nerve is
also involved or injured, the patient will also lose
sensation in the ipsilateral larynx, making the
risk for aspiration higher. Injury to the superior
laryngeal nerve is most common in high skull
base lesions or surgery when the proximal vagal
nerve is injured but can occasionally occur during esophagectomy and other procedures in the
superior neck. With time, most patients compensate and will obtain a stronger voice, although
it will not return to what the patient reports as
their “normal” preoperative voice. The larynx attempts to compensate by supraglottic hyperfunction; where structures of the supraglottic larynx
(false vocal cords or arytenoids) constrict to oppose each other. The supraglottic larynx can also
constrict in the anterior to posterior direction
with the epiglottis folding back and meeting the
arytenoids cartilages to close the larynx. This hyperfunction attempts to mimic the closure of the
true vocal cords.
Another common complaint from patients
with VCP is reporting the feeling of being short
of air or breath. This is mainly reported during
conversation and is due to ineffective glottis closure, resulting in air leak and inability to project
the voice. In an attempt to compensate, patients
will strain the laryngeal musculature causing
vocal fatigue. This lack of valsalva mechanism,
which requires a closed glottis, makes exertional
activity difficult (lifting, pushing, and straining).
Symptoms of Bilateral Vocal Cord Dysfunction
The clinical presentation of bilateral vocal cord
dysfunction is different from unilateral dysfunction. The main complaint with bilateral dysfunction is shortness of air or stridor, with patients
developing biphasic stridor immediately on ex-
676 Management of Airway, Hoarseness, and Vocal Cord Dysfunction After Esophagectomy
tubation or within several hours. These patients
often have a normal voice. Usually the cords are
fixed in a paramedian position with just a 1–3mm gap [1]. Patients can many times compensate and maintain adequate oxygen saturations
remarkably well especially at rest. However, if a
patient is struggling and working hard (may see
retractions) to pull air through the narrowed glottis, they can quickly decompensate and require
intervention. In this setting, the oxygen saturation is not a good representation of the patient’s
overall condition and many times is a late marker
of decompensation.
Evaluation of the Vocal Cords
Evaluation of the vocal cords and larynx after
esophagectomy should be undertaken on postoperative day 1, in the setting of a hoarse patient
or one in whom the nerves were put at risk or
knowingly sacrificed. Appropriate evaluation of
the vocal cords to rule out dysfunction requires
fiberoptic laryngoscopy; this can be done by a
trained person, at the bedside. While visualizing
the vocal cords, it is useful to have the patient
perform an eee-sniff maneuver, where the patient
alternates between phonating an “e” sound and
sniffing vigorously. This causes the vocal cords
to adduct and abduct maximally and is a good
way to test for paresis [1]. Some residual adduction may be seen due to bilateral innervations of
the interarytenoid muscle. Another useful technique is to measure the patient’s maximal phonation time. This is done by having the patient take
a deep breath and phonate the “ee” vowel sound
for as long as possible. Normal maximal phonation time is at least 25 s. With vocal cord paresis
or paralysis, this is usually reduced to less than
10 s [1]. Underlying chronic obstructive pulmonary disease (COPD) and asthma can influence
this and must be taken into account.
When viewing the larynx through the fiberoptic laryngoscope, the examiner should also
evaluate for tracheobronchitis, laryngeal edema
from intubation irritation, and arytenoid dislocation. All of these can cause hoarseness in the
postoperative setting that is unrelated to RLN
injury. Laryngeal edema and tracheobronchitis
are common causes of hoarseness in the recently intubated patient due to the contact irritation
from the endotracheal tube, especially in patients
with a history of reflux, tobacco exposure, and
chronic cough—patients with chronic irritation
of the larynx. It can cause dysphagia and aspiration when severe, especially in the compromised
and susceptible patient. Laryngeal edema is selflimiting and should resolve with time; however,
a short course of steroids can be given to hasten
recovery in the appropriate patient. Antibiotics
are rarely indicated except in the setting of complicated tracheobronchitis that is believed to be
secondarily infected. Arytenoid dislocation is a
controversial topic with most parties believing it
is a rare entity. Arytenoid dislocation is mainly
seen as a result of traumatic intubation and can be
the etiology of the voice dysfunction. To evaluate
for arytenoid dislocation, the professional looks
for a difference in vocal fold level or height and
the absence of the jostle sign. The jostle sign is a
brief lateral movement of the arytenoid cartilage
on the immobile side during glottis closure that is
caused by contact from the mobile arytenoid. The
evaluation for arytenoid dislocation is best done
with videostroboscopy in a clinic setting.
When the vocal cord is not functioning
postoperatively, at times it is difficult to know
whether the nerve has been cut accidently or is
nonfunctioning due to trauma and stretch, as paralysis and paresis present the same. A laryngeal
electromyography (EMG) in this setting can provide prognostic information. A denervated nerve
will show fibrillation potentials, absent or decreased motor unit potentials, and positive waves
while normal or polyphasic waves are seen during reinnervation of the vocal cord and predict
recovery for most patients [8]. Knowing whether
the cord is paralyzed permanently is important
in the counseling of the patient as well as offering therapeutic interventions. An abnormal EMG
can also help differentiate from cricoarytenoid
dislocation, which should have a normal EMG.
However, the best way to test for cricoarytenoid
dislocation is observation and palpation of the
posterior glottis during direct laryngoscopy in the
operating room.
68 L. Dooley and A. R. Shaha
Table 6.1 Products for vocal cord injections
Material Length of effect Comments
TMa
Gelfoam
TMa
Zyplast
Cymetra
alloderm
Fat 2
Fascia 3 months Effects last up to 1 year
Teflon
Radiesse
hydroxylapatite)
Radiesse
a
Rarely used anymore
(Bovine collagen) 4–6 months Allergy testing required
TM
(Micronized
TM
)
TMa
TM
voice (Ca
TM
voice gel 1–2 months Temporary
4–6 weeks Long track record, short duration
2–4 months No allergy, longer prep time, expensive, unpredictable
+ years Autologous, for
Permanent Long lasting, granuloma formation, migration, VF stiffness
2 + years possibly
permanent
reabsorbtion
giving, donor site morbidity, unpredictable
length
Long lasting
Whether or not the vocal cord is paralysed or
just paretic, a good course of action is to involve
the speech pathologist to evaluate swallowing in
order to avoid silent aspiration. A modified barium swallow is warranted in all patients. Identifying aspiration will decrease the risk of respiratory
complications from 18 to 11 % [2]. Occasionally,
aspiration can be treated with specialized maneuvers that can create a safe swallow, such as
the supraglottic swallow (patients are instructed
to tightly hold their breath while swallowing,
then to cough immediately after the swallow and
before resuming breathing) or turning the head
to the affected side during the swallow to help
approximate the vocal cords during swallowing.
The speech therapist can teach these maneuvers
and evaluate their effectiveness during their evaluation.
Treatment of Unilateral Vocal Cord Dysfunction
Treatment of patients with vocal cord dysfunction should be tailored to the individual. It is acceptable to observe a patient with a weak voice
who is not found to be aspirating. However,
those who are aspirating or are not tolerating the
deficit from the nonfunctioning vocal cord are
candidates for intervention, either temporary or
permanent, based on the surgeon’s knowledge of
the status of the nerve. In all patients, referral to
a speech or voice therapist for voice strengthening, breath support, swallowing exercises, proper
vocal use, and psychological support is appropriate. Best results are obtained when the patient
sees the speech therapist prior to intervention as
well as after surgical intervention.
Injection Augmentation
The injection of material into the vocal cord is an
excellent method of improving vocal cord function for weeks to months. With numerous products in the market currently (see Table 6.1 ), there
are several options in material whose duration of
action is variable and treatment can be individually tailored to the patient’s needs. Teflon is rarely used anymore due to its propensity to migrate
and form granulomas. Newer synthetic agents
have many times replaced teflon, fat (due to its
inconsistent reabsorption), and bovine collagen
(due to proposed need for allergy testing). Injections are an excellent option to improve voice and
dysphagia while awaiting return of vocal cord
function, usually up to 6 months. Longer lasting injections can also be considered in the setting where the RLN was known to be sacrificed.
RadiesseTM Voice Gel for temporary injections
(does not contain calcium hydroxylapatite) and
RadiesseTM Voice for long-term injections have
become popular at our institution due to the ease
of preparation and injection and consistent longterm results. Vocal fold injections can be considered routinely in patients with a glottis gap up to
3 mm, after which the gap is difficult to fully correct [6]. These procedures do not interfere with
696 Management of Airway, Hoarseness, and Vocal Cord Dysfunction After Esophagectomy
spontaneous recovery, and the injection can be
repeated as needed. Vocal cord injection will not
compromise future laryngeal framework surgery
if required [6, 7].
Multiple techniques have been described
for vocal cord injections. The intended injection location is in the paraglottic space or to the
medial or lateral aspect of the thyroarytenoid
muscle, depending on the material used. Placement of the injection lateral to the vocal process
will allow the process to rotate medially [8, 9].
Care to avoid a superficial injection into Reinke’s
space is paramount as a superficial injection can
impair or cause loss of the vibratory function of
the vocal fold, with worsening of voice. In the
correctly selected patient, an in the office awake
injection (transcutaneous or per-oral approach)
has equal results as to those that are placed in the
operating room under general anesthesia via direct laryngoscopy with telescopic or microscopic
guidance [8]. Cummings and colleagues reported
and 88 % subjective improvement of dys
an 85
phagia and aspiration after hydroxylapatite medialization thyroplasty [7].
-
Framework Surgery for Unilateral Vocal Cord Dysfunction
Framework surgery for unilateral vocal fold dysfunction is a standard treatment for long-term
VCP in the nonradiated neck, with medialization
laryngoplasty (type 1 thyroplasty) and arytenoid
adduction being the most widely performed procedures. Any framework surgery must be carefully considered in the radiated neck as chondroradionecrosis is a devastating though rare complication. Many times, long-lasting injections, even
when needing to be repeated, are a safer option
than framework surgery in this special population.
Medialization laryngoplasty is a long-term solution that medializes the paralyzed vocal cord to
allow contact during vocalization with the contralateral cord. The procedure can be and usually
is done under local anesthesia. A window is created in the thyroid cartilage preserving the inner
perichondrium, and an implant (preformed or
carved by the surgeon) is placed in the middle
third of the vocal cord. Placement can be tailored
specifically for each patient based on where the
cord has lateralized and where the greatest glottis gap is located. Voice quality can be measured
intraoperatively since the procedure is done
under local anesthesia and adjustments in placement and size of the implant can be done while
the patient is in the operating room. Due to the
trauma and placement of a foreign body, a good
voice on the operating room table can and will
become rough and breathy due to edema in the
subsequent days. It is recommended the patient
be observed overnight in the hospital in case of
significant airway edema and three doses of IV
steroids be given. While medialization laryngoplasty is expected to be a permanent solution to
medialize the vocal cord, the procedure can be
reversed and the implant removed or adjusted as
needed.
Arytenoid adduction can be an added procedure for selected cases, mainly those with a large
posterior gap and vocal processes that do not
contact during phonation. Arytenoid adduction is
done by suturing the muscular process of the immobile arytenoid to the anterior cricoid cartilage.
This lowers the position of the vocal process,
medializes and stabilizes the vocal process, and
rotates the arytenoid cartilage [1]. In the properly
selected patient, arytenoid adduction is an important adjunct.
Treatment of Bilateral Vocal Paralysis
The initial management and concern in bilateral
vocal paralysis is securing the airway. In a patient
with stridor and who is in distress, intubation is
the best method of securing the airway while a
more definitive plan can be discussed and agreed
upon. Reintubation with the administration of
steroids can be done for 48–72 h with a subsequent trial of re-extubation versus tracheostomy.
A temporary tracheostomy can be undertaken in a
controlled situation if cord function is not thought
to return within the next several days. Permanent tracheostomy while an excellent means of
securing the airway is many times unacceptable
70 L. Dooley and A. R. Shaha
to the patient since there are alternative options
available. Long-term surgical options to improve
airway can be undertaken, however, they come at
the price of voice and swallowing. Any opening
or widening of the airway to create better flow
will allow greater air escape during phonation. It
can also compromise swallowing and lead to aspiration pneumonia in the susceptible patient as
the vocal cords will not fully adduct.
Laser transverse cordectomy is the most commonly used procedure to widen the airway. A
laser is used to transect the true vocal fold anterior to the vocal process, and the incision is extended laterally to involve the false vocal fold.
This detaches the thyroarytenoid muscle from
the arytenoid and allows the thyroarytenoid to
contract anteriorly, which will create a posterior
space. This can be repeated on the contralateral
vocal cord as well if needed. Unilateral cordectomy will enlarge the airway a couple millimeters;
however, patients see a reduction in their shortness of breath and most have an acceptable voice
[10, 11].
The other routinely used procedure is a laser
arytenoidectomy, where the entire arytenoid
is removed along with a small wedge from the
posterior vocal fold. This is usually modified
and either the posterior or lateral aspect of the
arytenoid is left in place. The results of this technique have been reported to be comparable to the
transverse cordotomy and may possibly cause
less vocal dysfunction due to less disruption of
the membranous vocal fold.
While these procedures can allow for decannulation, they still only provide a marginal airway and have a worse voice quality than can
be obtained with a tracheostomy. Tracheostomy
would remain the best option for acute airway
distress in the setting of bilateral VCP.
These patients are best managed in a team
environment with the consultant’s role being
to maintain the airway, perform a full work-up,
avoid aspiration, and continue with long-term
follow-up. Long-term follow-up is important as
those who were compensating and not aspirating
without intervention may subsequently require
future intervention as the vocal cord ages and
undergoes normal age related changes (bowing).
Repeat injections or augmentation to framework
surgery may also be required in the setting of the
aging larynx.
Key Summary Points
1. Symptoms of vocal cord dysfunction are primarily related to voice changes, air movement, and aspiration. Voice changes include
changes in phonation and “breathy” voice.
2. Unilateral vocal cord injury must be differentiated from bilateral injury. While unilateral
injury causes voice changes and increased
risk for aspiration, bilateral injury can cause
stridor and can be an airway emergency.
3. Treatment for unilateral injury includes
observation, temporary medialization procedures, and more definitive surgical reconstruction.
4. Treatment for bilateral injury includes initially
securing the airway. Permanent tracheostomy
or surgical intervention may be needed for
those patients in whom spontaneous recovery
does not occur.
References
1. Bailey BJ, Johnson JT. Head and neck surgery—otolaryngology. 4th ed. Baltimore: Lippincott Williams &
Wilkins; 2006.
Low DE, Bodnar A. Update on clinical
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documentation, and management of complications
associated with esophagectomy. Thorac Surg Clin.
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Y, Kawachi K, Kusano C, Aikou T. Does hoarseness of
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Am Coll Surg. 1999;188(3):231–6. PMID: 10065810.
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I, Takayama T. Phonatory function following esophagectomy for esophageal cancer. Hepatogastroenterology. 2004;51(60):1717–21. PMID 15532812.
5. Baba M, Aikou T, Natsugoe S, Kusano C, Shimada M,
Nakano S, Fukumoto T, Yoshinaka H. Quality of life
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PMID:9595229.
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6. Mallur PS, Rosen CA. Vocal fold injection: review of
indications, techniques and materials for augmentation. Clin Exp Otorhinolaryngol. 2010;3(4):177–82.
Eisele DW, Smith
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neck surgery. 2nd ed. Philadelphia: Mosby, an
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Comparison of outcomes and complications between
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RV. Complications in head and
CR, Klein AM, Johns MM 3rd.
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A, Harris AT, Henshaw P,
Severe Reux-Induced
Esophagitis
Carlotta Barbon, Benedetto Mungo, Daniela Molena
and Stephen C. Yang
7
Introduction
Reflux-induced esophagitis is a condition characterized by inflammation of the esophageal
squamous epithelium, caused by persistent and
prolonged gastroduodenal reflux. The damage to
the mucosa can progress to the point of becoming
extremely debilitating, causing pain, esophageal
dysfunction, and an overall diminished quality of
life. Moreover, it may lead to severe complications, such as ulcers, bleeding, strictures, metaplasia, and epithelial dysplasia, which can eventually evolve to esophageal adenocarcinoma.
Pathophysiology
Reflux-induced esophagitis is caused by gastroesophageal reflux disease (GERD), a chronic
condition in which the esophagus is pathologi-
S. Yang ()
Division of Thoracic Surgery, Department of Surgery,
Johns Hopkins Hospital, Baltimore, MD, USA
e-mail: asyang@jhmi.edu
C. Barbon · B. Mungo · D. Molena
Department of Surgery, Johns Hopkins Hospital,
Baltimore, MD, USA
e-mail: carlotta.barbon@gmail.com
B. Mungo
e-mail: bmungo1@jhmi.edu
D. Molena
e-mail: dmolena2@jhmi.edu
cally exposed to gastric contents, such as acid
and pepsin, and to alkaline reflux of duodenal
origin, composed of bile salts and pancreatic secretions [1].
GERD is extremely common in the western world, where it is estimated to affect about
10–20 % of the population, especially overweight, middle age, white males, whereas it is
less prevalent in Asia [2]. It represents one of
the most widespread outpatients’ diseases in the
USA and has become a serious burden for the
health care system, and it is likely to increase in
the near future due to rising obesity and bad eating habits [3].
Physiologically, several defensive mechanisms protect the esophagus from reflux, with
the lower esophageal sphincter (LES) being the
most important. This contributes to the creation
of a high-pressure zone between the stomach and
the esophagus and, together with the intrinsic
esophageal, cardial musculature, and the crural
diaphragm, prevents the upward transit of lower
digestive contents in the esophageal lumen.
GERD develops as a consequence of the overcoming of the aforementioned barriers, through
different mechanisms [4], such as
• Incompetence of the LES;
• Transient lower esophageal sphincter release
(TLESR), mediated by vagal reflexes trig-
gered by gastric distension;
• Peristaltic dysfunction;
• Ineffective esophageal acid clearance;
• Weak esophageal contractions;
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_7,
© Springer Science+Business Media New York 2015
73
74 C. Barbon et al.
Table 7.1 Los Angeles classification of esophagitis
A One (or more) mucosal break< 5 mm that does not extend between the peaks of two mucosal folds
B One (or more) mucosal break> 5 mm long without continuity between the peaks of two mucosal folds
C One (or more) mucosal break continuous between the peaks of two or more mucosal folds but involving
less than 75
D Mucosal breaks involving at least 75 % of the esophageal circumference
% of the circumference
• Delayed gastric emptying, which shows an
increased risk in patients with diabetes and
scleroderma [5];
• Increased intra-abdominal pressure;
• Decreased production of saliva, which has the
capability of buffering the acid.
Specific conditions such as hiatal hernia and
obesity [4] can predispose to the development of
GERD as well as several habits such as smoking, alcohol, and caffeine use, medications that
decrease the LES tone (Ca2+channel blockers,
anticholinergics, beta-agonists including inhalers, narcotics, nitrates, theophylline, opioids,
neuroleptics, benzodiazepines, tricyclic antidepressants), and hormones such as estrogen and
progesterone [6].
Erosive esophagitis is present in only one-
third of patients with GERD symptoms [7], and
the frequency and severity of reflux episodes
poorly predict its occurrence [8,9].
In the past, chemical damage was thought to
be the cause of esophageal erosion, but recent
data suggest that it is an inflammatory-mediated process that triggers esophagitis. Cytokines
released in response to acid reflux may attract
immune cells, which are ultimately responsible
for the mucosal damage. This hypothesis would
explain the high interindividual variability in response to acid reflux and shed light on different
healing patterns, leading to normal esophageal
mucosa in some patients, whereas inducing a
metaplastic process in others. Individual immune
response and signaling pathways, which determine cell proliferation and differentiation, may
play a role: It has been hypothesized that acid
and bile salts could selectively modulate the expression of certain intestinal transcription factors
(i.e., CDX2) in esophageal cells, thus triggering
the metaplastic evolution. A complex molecular
integration, beyond the mere chemical damage,
would contribute to explain why not only the cor-
rosive acidic reflux, but also the apparently less
harmful alkaline reflux is capable of triggering an
esophageal inflammatory response [10].
The inflammatory response could also affect
the overall esophageal function, causing dysmotility [11], which might account for the tendency of esophagitis to self-exacerbate through
a vicious feedback. In fact, impaired motility
affects the ability of the esophagus to clear the
refluxed acid content, leading to worsening of
esophagitis.
Classification
Esophagitis is classified according to Los Angeles criteria [12], introduced in 1994 (Table 7.1).
Grades A and B are the most common and,
compared to C and D, have an increased response to proton pump inhibitors (PPIs) (as high
as 90 %). On the other hand, the most severe
grades only heal in 50 % of the cases [13], have a
higher tendency to relapse when medications are
withdrawn, and have a fourfold increased risk at
2 years of developing Barrett’s esophagus (BE),
with respect to A and B grades [14,15].
There is only a weak correlation between degree of damage, esophagitis grade, and symptoms severity; however, there seems to be a link
between erosive esophagitis and contact time
with acidic juice.
Symptoms
Typical symptoms of GERD are heartburn and
regurgitation. Other common symptoms are dysphagia, epigastric pain, bloating, belching, and
nausea.
Symptoms are typically worsened by heavy
meals, after the ingestion of certain foods, espe-
757 Severe Reflux-Induced Esophagitis
cially fatty ones, coffee, tea, spices, and acidic
foods such as tomatoes and citrus fruits. They are
often present at night when lying down, because
this position impairs upper digestive clearance.
For this reason, nocturnal reflux is usually associated with increased complications, severe
esophagitis, and intestinal metaplasia (BE) [16].
Extra-esophageal, or atypical, symptoms such
as chest pain, chronic cough, laryngitis, asthma,
and hoarseness can also be present and muddy the
clinical picture of GERD; respiratory symptoms
are due both to the reflux itself and to the bronchospasm induced by vagal stimulation. Their
response to PPIs and antireflux surgery (ARS) is
not as satisfactory as that of typical symptoms.
Only one-third of patients with erosive esophagitis have symptoms [7], and some people with
a rich constellation of symptoms do not show
esophagitis (nonerosive reflux disease—NERD).
There is a strong correlation between longstanding esophageal reflux disease and adenocarcinoma, and the risk is associated with disease
severity, frequency, and duration [17]. As a consequence, an endoscopy should always be performed in the case of alarm symptoms such as
weight loss, dysphagia, gastrointestinal blood
loss, anemia, chest pain, and epigastric mass on
palpation [18,19].
It is paramount to perform a differential diagnosis, in order to exclude conditions with overlapping symptoms, such as cardiac disease, gallbladder diseases, gastrointestinal tumors, peptic
ulcers, eosinophilic esophagitis, infections, functional heartburn, and benign esophageal disorders such as achalasia, distal esophageal spasm,
nutcracker esophagus, and diverticula.
Mortality in esophagitis is linked to its complication, mostly to adenocarcinoma. It is otherwise infrequent, having been reported in the year
2000 to be as low as 0.46/100,000 [20]. The most
frequent causes of mortality, besides neoplastic
degeneration, are hemorrhage (38 %), ulcer perforation or esophageal rupture (29 %), aspiration
pneumonia (19 %), and complications of ARS
(11 %) [20].
Diagnosis
The goal of diagnostic tests is to assess the following:
• the presence and degree of esophagitis;
• the underlying cause of reflux esophagitis;
and
• the presence of complications.
The gold standard for detection of esophagitis is
endoscopy. Patients presenting with typical reflux symptoms are commonly given an empiric
course of PPIs; endoscopy is performed in those
who fail or have an unsatisfying response to medical treatment. Upper endoscopy shows esophagitis only in 1/3 of patients with GERD symptoms
[7] and is even less frequent after treatment with
PPIs [21]. It is important to study the anatomy
of the gastroesophageal junction (GEJ) (presence
of hiatal hernia or diverticula), to rule out complications and to obtain esophageal and gastric
biopsies to exclude the presence of concurrent
diseases (i.e.,Helicobacter pylori infection or
eosinophilic esophagitis). Moreover, endoscopic
ultrasound (EUS) is at times useful to assess the
degree of esophageal wall involvement.
Twenty-four hours pH monitoring is the
only technique capable of objectively detecting
the presence of acidic reflux. It is helpful in case
of symptoms with a negative endoscopy. Moreover, it should always be performed before ARS,
both as a definitive confirmation test and as a
predictor of surgical outcomes.
Impedance monitoring allows detection of
both acidic and alkaline reflux, adding sensitivity
to pH monitoring. It is particularly useful when
performed in patients on PPI therapy, in which
reflux becomes mostly nonacidic [22].
Esophageal manometry is used to evaluate
LES function and esophageal peristalsis and to
rule out the presence of esophageal motility disorders.
Barium esophagram is not helpful for the
detection of esophagitis itself, but it rather reveals severe complications such as strictures and
Schatzki’s rings and gives information on esophageal anatomy. It can also indicate the presence
of a hiatal hernia, or other pathologic disease processes (e.g., neoplasms).