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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
dose of ≥60 Gy are known to significantly increase the risk of esophageal
injury (Qiao et al., 2005). In the acute
setting, the radiation induces mucosal
necrosis and submucosal edema. Clinically, the discovery of ulcers, strictures,
or fistulas is common in the setting of
chronically induced radiation injury
with the microscopic finding of submucosal fibrosis. Current treatment strategies focus on mitigating the impact of
esophagitis through analgesics, antiemetics, nutritional supplements, and,
when necessary, the placement of a
gastrostomy tube. Significant effort has
been directed at developing biological
modifiers with the potential to act as
radioprotectors, but much additional
work remains before any such agent
becomes an integral part of radiotherapeutic management (Bradley & Movsas, 2004).
Figure 15 –9. Schatzki’s-B- ring (white
arrows) in an individual with solid food
dysphagia. Also present are high-grade
esophagitis (white arrowheads) with ulcera-
tion (black asterisk
hernia. Treatment with proton-pump inhibitors resolved the dysphagia and healed
the esophagitis. Dilation and surgical
reduction of the hernia were unnecessary.
) and a small hiatal
ESOPHAGEAL WEBS AND RINGS
Esophageal webs and rings are another
frequent cause of esophageal phase
dysphagia. An esophageal B-ring, or
Schatzki’s ring, is one of the most common causes of solid food dysphagia in
adults (Figure 15–9). Schatzki’s rings
can be found in up to 14% of patients
on fluoroscopic swallow evaluations
(DeVault, 1996). They occur at the
esophagogastric junction (EGJ) and
have squamous esophageal mucosa
on the proximal margin and columnar
gastric mucosa on the distal margin of
the ring. They usually occur in the presence of an HH and frequently become
symptomatic when the diameter of the
lumen is <13 mm. Esophageal dilation
is the treatment of choice.
Compared to the B-ring, or Schatzki’s
ring, which is membranous and occurs
at the EGJ, the esophageal A-ring is a
thick muscular ring that is present 2 cm
above the EGJ (Figure 15–10). It marks
the upper border of the LES. Esophageal A-rings are an infrequent cause of
dysphagia. Treatment with dilation is
usually unsuccessful, and the treatment
of choice is injection of botulinum toxin
into the muscular ring.
Esophageal webs are mucosal constrictions that occur above the EGJ.
Unlike B-rings, or Schatzki’s rings, they
have squamous mucosa on both sides.
An esophageal web usually occurs in
the proximal esophagus. A web in the
postcricoid region may be associated
with Plummer-Vinson syndrome. Dilation is curative. Other, less frequent,
Figure 15–10. Barium esophagram dis-
https://t.me/medicina_free
playing an esophageal A-
arrow
). Also present is a hiatal hernia
(white arrowheads) and a Schatzki’s
ring (black arrow ).
B-
ring (white
causes of esophageal dysphagia include
vascular rings, diverticula, and large
esophageal varices.
ESOPHAGEAL MOTILITY
DISORDERS
Esophageal motility disorders are defined as an abnormality of EGJ outflow
and/or derangement of peristalsis
(Yadlapati et al., 2021). Despite typically occurring as the consequence of
a benign etiology, with minimal associated mortality, these disorders can
induce considerable detrimental impact
on the patient’s quality of health (Mittal
& Vaezi, 2020).
Esophageal motility disorders represent a heterogeneous spectrum of pathological entities despite having some
shared symptomatic overlap, including dysphagia, chest pain, heartburn,
15. ESOPHAGEAL PHASE DYSPHAGIA
and regurgitation. The pathogenesis of
esophageal motility disorders is broadly
classified as the consequence of a local
disease process (primary) or a systemic
disease process (secondary). When
evaluating any patient with symptoms
of dysphagia/obstructive symptoms,
it is important to rule out structural
abnormality, such as neoplastic disease,
with esophagoscopy, before pursuing
a functional esophageal investigation
(Gyawali et al., 2020). In the absence of
apparent mucosal or structural abnormalities, high-resolution manometry
(HRM) is frequently the next step, as
endoscopic examination provides limited sensitivity for esophageal motility
disorders (Rohof & Bredenoord, 2017).
The introduction and advancement
within HRM technology has significantly improved the understanding
and visualization of esophageal physiologic function. Further, HRM has facilitated the development of classification
schemes for esophageal motility disorders, most notably being the Chicago
Classification (Yadlapati et al., 2021).
While HRM remains the gold standard
for the diagnosis of esophageal motility disorders, the Chicago Classification
version 4.0 (CCv4.0) advocates for supportive diagnostic testing, particularly
where HRM findings prove inconclusive (Yadlapati et al., 2021). Recommended supportive testing includes
conventional timed barium esophagram (TBE) with concurrent 13-mm
barium tablet and/or the functional
lumen imaging probe (FLIP) system.
The FLIP system was recently approved by the U.S. Food and Drug
Administration (FDA) and consists of
a distensible balloon encasing a catheter with multiple pairs of impedance
355
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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
electrodes (Savarino et al., 2020). The
FLIP catheter is placed transorally
immediately after sedated upper endoscopy (Bianca et al., 2020). Transnasal
placement is possible in the sedated
patient, but most available normative
data are based on transoral placement
(Savarino et al., 2020). The catheter is
advanced such that the EGJ is identified, with a few sensors in the stomach
and the remainder in the esophageal
lumen. The catheter is then connected
to a mechanical pump, which regulates
the inflation (distension) of the balloon
using a solution of known conductivity
and volume. The FLIP system quantifies
the LES and esophageal distensibility
(opening and compliance) function and
can determine the directionality of peristalsis (antegrade or retrograde) (McMahon etal., 2007; Mittal & Vaezi, 2020).
Within the CCv4.0 classification
scheme, primary esophageal motility
disorders are distinguished by objective
HRM measurements and classified as
resulting from EGJ outflow obstruction
(EGJOO), achalasia, or esophageal peristalsis (Yadlapati et al., 2021). Esophageal peristalsis disorders are further
classified as resulting from either
increased (distal esophagus spasm
[DES] and hypercontractile esophagus)
or decreased (ineffective esophageal
motility [IEM] and absent contractility)
esophageal contractility.
characterized by degeneration of the
myenteric plexus, resulting in impaired
relaxation of the EGJ and the loss of
organized peristalsis (Yadlapati et al.,
2021). The incidence of achalasia is estimated to range between 0.03 and 2.92
per 100,000 people (Duffield et al., 2017;
Samo et al., 2017). Clinical presentation
notable for dysphagia for solids and
liquids without oropharyngeal transfer difficulties occurs in roughly 90% of
patients, regurgitation in 75%, weight
loss in 60%, chest pain in 50%, and
heartburn in 40% (Khashab et al., 2020;
Vela et al., 2004). Diagnosis is made by
HRM and TBE. The classical finding
on esophagram is a dilated tortuous
esophagus with a “bird’s beak” appearance at the LES (Figure 15–11). Endoscopy examination should be performed
to exclude a neoplastic disease process
that can present with a similar appearance on fluoroscopy (pseudoachalasia).
According to specific HRM criteria, the
DISORDERS OF
ESOPHAGOGASTRIC
JUNCTION OUTFLOW
Achalasia
Achalasia is a primary esophageal
motor disorder of unknown etiology
Figure 15 –11. Barium esophagram dis-
playing a dilated, tortuous esophagus
with a “bird’s beak” appearance at the
lower esophageal sphincter (white arrow )
in an individual with achalasia.
15. ESOPHAGEAL PHASE DYSPHAGIA
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357
CCv4.0 defines three subtypes of achalasia: Type I, akin to classic achalasia;
Type II, seen with panesophageal pressurization; and Type III, or spastic, achalasia (Yadlapati et al., 2021). Current
treatment options include botulinum
toxin injection, pneumatic dilation, laparoscopic Heller myotomy, and peroral
endoscopic myotomy (POEM) (Khashab et al., 2020). Up to 5% of patients
with end-stage disease might require
esophagectomy (Vela et al., 2004). The
achalasia subtype has been demonstrated to impact outcomes, with achalasia Type II proving most amenable to
treatment and Type III proving most
resistant (Khashab et al., 2020). Recently,
it has been observed that Type III achalasia (and EGJOO) is significantly more
likely to be associated with the use of
opioids compared with achalasia Types
I and II and should be considered a
possible underlying etiology and guide
management (Babaei et al., 2019; Ratuapli et al., 2015; Richter, 2021).
Esophagogastric Junction
Outflow Obstruction
The CCv4.0 defines EGJOO as an elevated median integrated relaxation
pressure (IRP) in the primary and secondary position and ≥ 20% swallows
with elevated intrabolus pressure in
the supine position, with evidence of
peristalsis (Yadlapati et al., 2021). The
incidence of EGJOO ranges from 3.2%
to 11%, with a female predilection, and
typically occurs later in life (59–69 years
of age) (Richter & Clayton, 2019). The
etiology of primary/idiopathic EGJOO
remains unknown, although there is
speculation that it may be a precursor to or a variant of achalasia (Scherer
et al., 2009). The clinical presentation
of EGJOO is varied but includes dysphagia, chest pain, heartburn, and/or
regurgitation (Samo et al., 2017). An
isolated finding of EGJOO on HRM
should be considered clinically inconclusive (Yadlapati et al., 2021). A percentage of asymptomatic individuals
undergoing HRM will be discovered
to meet diagnostic criteria for EGJOO.
To avoid unnecessary investigation and
treatment, the CCv4.0 recommends that
a distinction be made between a clinically irrelevant manometric observation
and symptomatic EGJOO (Yadlapati
etal., 2021). In symptomatic patients,
the priority is ruling out any secondary
cause of EGJOO, which reportedly can
be discovered in 13% to 66% of cases
(Richter & Clayton, 2019). Commonly
encountered causes for secondary
EGJOO include a large HH, esophageal
stricture/ring, opioid use, or esophageal/gastric neoplasm. In the absence
of secondary etiology, a diagnosis of
primary/idiopathic EGJOO requires
confirmation with an abnormal TBE
with barium pill and/or FLIP test (Yadlapati et al., 2021). Treatment options are
similar to that of achalasia and include
botulinum toxin injection, pneumatic
dilation, or surgical myotomy (Richter & Clayton, 2019). In symptomatic
patients found to have a normal TBE
and/or FLIP, treatment ranges from
reassurance, calcium channel blockers,
and PPIs to simple esophageal dilation.
DISORDERS OF PERISTALSIS
Distal Esophageal Spasm
The diagnosis of distal esophageal
spasm (DES) is made on HRM and is
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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
defined by the CCv4.0 as ≥20% premature contractions and distal contractile
integral (DCI) of >450 mmHg/s/cm
3
(Yadlapati et al., 2021). Using TBE can
provide diagnostic support, as it can
identify tertiary contraction or a rosary
bead or corkscrew esophagus associated with DES (Figure 15–12).
It is believed that distal esophageal spasm results from an imbalance
between the nitrogenic inhibitory
pathway and the cholinergic excitatory
pathway in the myenteric plexus (Gorti
et al., 2020). It is rare, with a prevalence
of between 3% and 9% of symptomatic patients, with a slight female predominance and a mean age of onset of
60 years (Khalaf et al., 2018). The most
common symptoms of DES include
dysphagia, heartburn, and noncardiac
chest pain (Almansa et al., 2012). Treatment of DES is challenging, given that
the etiology remains unknown. Pharmacological treatment is directed at
symptom control and includes nitrates,
phosphodiesterase-5 inhibitors, cal-
Figure 15–12. Barium esophagram dis-
playing a corkscrew esophagus in an
individual with distal esophageal spasm.
cium channel blockers, and tricyclic
antidepressants (Khalaf et al., 2018).
Where acid reflux is suspected to be
driving spasticity, treatment should
focus on antireflux management, especially as antispasmodic therapy has the
potential to augment gastroesophageal
reflux and worsen symptoms (Patel et
al., 2022). Endoscopic options include
POEM, botulinum toxin injection, and
esophageal dilation (Khalaf et al., 2018).
Hypercontractile Esophagus
Hypercontractile esophagus is the
HRM version of the old nutcracker
esophagus and is defined as ≥20%
hypercontractile swallows in the supine
position (DCI >8,000 mmHg/s/cm
(Chicago Classification Version 4.0 and
Its Impact on Current Clinical Practice
— Gastroenterology & Hepatology,
n.d.; Yadlapati et al., 2021). Esophageal
hypercontractility is either limited to
the esophageal body or can also incorporate the LES but is rarely limited to
the LES (Kahrilas et al., 2015). A variant of form characterized on HRM as
having prominent, high-amplitude,
repetitive contractions is aptly known
as jackhammer esophagus (Yadlapati
et al., 2021). The etiology of hypercontractile esophagus remains unknown,
although it likely involves an excess of
cholinergic drive with asynchrony of
circular and longitudinal muscle contractions (Khalaf et al., 2018). An association with GERD has been reported,
although causality remains uncertain.
Hypercontractile esophagus remains
a rare diagnosis, with an occurrence
ranging from 1.5% to 3% on HRM in
motility centers (de Bortoli et al., 2021).
Medical treatment is considered first,
3
)
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359
with the goal of decreasing symptoms.
Antireflux medication is used to treat
comorbid GERD, although it has not
been shown to have a significant effect
on pain relief (Borjesson et al., 2003).
Sildenafil has been shown to decrease
the amplitude of peristaltic contractions in patients with hypertensive
peristalsis and may be considered a
treatment option (Lee et al., 2003). Trazodone, selective serotonin reuptake
inhibitors, tricyclic antidepressants, or
botulinum toxin injections may also be
considered. There is also some evidence
that POEM has the potential to nullify
the hypercontractile segment of smooth
muscle esophagus and potentially help
symptoms (de Bortoli et al., 2021).
Ineffective Esophageal Motility
and Absent Contractility
With the introduction of the CCv4.0,
the diagnostic criteria of IEM have been
made more restrictive (Richter, 2021)
and are now defined as ≥70% ineffective swallows (DCI >100 mmHg/s/cm
and <450 mmHg/s/cm
3
) or ≥50% failed
swallows (DCI <100 mmHg/s/cm
3
3
).
An observation of 50% to 70% ineffective swallows is considered inconclusive for a definitive diagnosis and
requires further confirmatory testing,
such as poor bolus transit on impedance or barium esophagram. About 45%
of patients with manometric IEM will
have normal transit of barium through
the esophagus (Shakespear et al., 2004).
Absent contractility is defined as 100%
failed peristalsis (DCI <100 mmHg/s/
3
cm
), with a normal median IRP in the
upright position (Yadlapati et al., 2021).
The clinical relevance of IEM remains
under debate as studies have failed to
demonstrate a significant correlation
between the diagnosis and esophageal
symptoms, but the finding has been
associated with a higher esophageal
reflux burden (Gyawali et al., 2019;
Richter, 2021; Shetler et al., 2017; Xiao
et al., 2014). Treatment of both conditions remains challenging and, in the
absence of a pharmacological agent for
esophageal contractility augmentation,
remains directed at addressing underlying GERD and symptomatic relief.
SYSTEMIC (SECONDARY)
CAUSES OF ESOPHAGEAL
PHASE DYSPHAGIA
Connective Tissue Disease
Various connective tissue diseases can
affect the esophagus. Systemic sclerosis
(scleroderma), polymyositis, dermatomyositis, and systemic lupus erythematosus can all affect esophageal motility
to varying degrees. Scleroderma affects
the smooth muscle portion of the esophagus, while sparing the proximal skeletal portion. The LES is often affected
and may become hypotensive and
incompetent. Severe GERD is frequent.
In contrast to scleroderma, the inflammatory myopathies affect the proximal
skeletal muscle portion of the esophagus. The cricopharyngeus and pharyngeal musculature may be involved. The
distal esophagus and LES are spared, so
associated GERD is less common than
with scleroderma.
Patients with Sjögren’s syndrome (an
autoimmune disease that affects moisture-producing glands) often complain
of dysphagia. Although esophageal peristalsis may be affected, patients often
develop severe swallowing problems
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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
because of xerostomia. Pills, breads, and
other dry foods can be extremely difficult to consume. Salivary bicarbonate is important in neutralizing even
physiologic amounts of reflux. All patients with Sjögren’s syndrome can lack
this important buffering capacity and
are prone to develop severe GERD.
Other systemic diseases affecting
the esophagus include diabetes mellitus, Parkinson’s disease, and hypothyroidism. The autonomic dysfunction
associated with diabetes can result in
esophageal dysmotility with delayed
esophageal emptying and in gastroparesis with delayed gastric emptying. Parkinson’s disease can result in
oropharyngeal and esophageal phase
swallowing problems. Hypothyroidism can produce esophageal dysmotility and LES dysfunction that should
normalize with thyroid replacement
therapy (Eastwood et al., 1982).
Esophageal Neoplasms
The majority of esophageal tumors are
malignant. Squamous cell carcinoma
used to be the most common esophageal cancer. Adenocarcinoma, however,
has now overtaken squamous cell cancer as the most frequent esophageal
malignancy. Adenocarcinoma of the
esophagus is the most rapidly expanding cancer in the United States. Early
diagnosis by endoscopy and biopsy
is critical. Benign esophageal tumors
include leiomyomas, papillomas, cysts,
fibrovascular polyps, lipomas, hemangiomas, and granular cell tumors. The
most common presenting symptom
for all esophageal tumors is dysphagia. Patient localization for the site of
dysphagia is often inaccurate. Esopha-
goscopy is advised for all patients with
solid food dysphagia to rule out esophageal neoplasia and its premalignant
precursors.
CONCLUSION
The causes of esophageal phase dysphagia are diverse, and a detailed
understanding of esophageal pathology is necessary to properly evaluate
and manage patients presenting with
dysphagia. Even patients complaining
of suprasternal dysphagia symptoms
localized in the neck may have esophageal pathology. Esophageal manometry
and fluoroscopic studies can be useful in detecting anatomic and motility abnormalities. A low threshold
for esophageal endoscopy should be
maintained so neoplasms or potentially treatable infectious causes are not
missed. Endoscopy is mandatory for
any patient with solid food dysphagia
to rule out esophageal dysplasia and
carcinoma.
STUDY QUESTIONS
1. What is the most common cause of
esophagitis?
2. Match each of the following esophageal motility disorders with the
description that best fits:
a. Achalasia
b. IEM
c. DES
d. Hypercontractile esophagus
(1) High-amplitude nonperistaltic
esophageal contractions
(2) Absence of esophageal
peristalsis
15. ESOPHAGEAL PHASE DYSPHAGIA
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361
(3) High-amplitude esophageal
contractions, peristaltic
Low-amplitude esophageal
(4)
contractions, peristaltic
3. Does scleroderma affect the proximal esophagus?
4. What is one medication that is a
common cause of pill-induced
esophagitis?
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