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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1033_Библиотеки_им_академика_М_И_Перельмана
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M. A. Harrison et al.
improve the symptomatology of GERD, but it is unknown whether
it will improve motor abnormalities. Prokinetic agents (metoclopramide, bethanecol, domperidone) have proven to increase the
rate of gastric emptying, increase the LES pressure, and esophageal clearance of reux [29]. Endoscopic thermal ablation has
been shown to decrease esophageal acid exposure and decreases
the frequency of transient LES relaxation, but its impact on dysmotility is unclear [30]. Fundoplication, either the laparoscopic
gold standard or transoral incisionless fundoplication (TIF), can
be effective in improving esophageal acid exposure, but should be
viewed with caution in the setting of signicant dysmotility [31,
32]. A partial fundoplication, such as a Toupet, is a more appro-
priate choice than Nissen fundoplication (360°) with esophageal
dysmotility.
Case #3
Patient Information
A 42-year-old male presents to the emergency department with
chest pain and intermittent dysphagia to solid foods. His medical
history is signicant for asthma and multiple episodes of food
impactions in the past. Endoscopy during his hospitalization with
proximal esophageal biopsies reveals 40 eosinophils/high powered eld on microscopic evaluation.
Manometry
Figure 21.3 shows the HRM for this patient. Manometry
reveals esophagogastric junction outow obstruction (EGJOO)
secondary to distal esophageal eosinophilic esophagitis (EoE)
stricture. There is evidence of increased intrabolus pressures;
mean DCI of 5200mmHg/s/cm and median IRP of 16mmHg.
Manometry normalized with treatment of EoE and esophageal
balloon dilation.
Background
Eosinophilic esophagitis (EoE) is one of the most common
conditions diagnosed during the assessment of feeding problems
in children and during the evaluation of dysphagia and food
impaction in adults [33]. Estimated prevalence of EoE is between
1 and 5 per 10,000 persons in the United States and Europe, with
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Fig. 21.3 High Resolution Manometry in Eosinophilic Esophagitis. Mean
DCI: 5200mmHg/s/cm, and Median IRP: 16mmHg
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an increasing prevalence in Asia and a 3:1 male:female predominance [34–38].
EoE is currently dened as a chronic, immune-mediated or
antigen-mediated esophageal disease characterized by symptoms
related to esophageal dysfunction and eosinophil predominant
inammation, with the most dominant antigens being food-based
[33]. Additionally, esophageal mucosal eosinophilia of at least 15
eosinophils per high power eld is present. This is thought to
approach a sensitivity of 100% and specicity of 96% for establishing histologic diagnosis [39]. Eosinophils can release cytokines, growth factors, and other proteins resulting in chronic
inammation. This will affect the esophageal motility via the
inhibitory or excitatory pathways. This can lead to abnormal
esophageal relaxation or contraction. Symptoms include: feeding
problems, vomiting and abdominal pain in children, dysphagia,
chronic reux, and food impaction in adolescents and adults.
Esophageal dysfunction is most often related to stricturing and
brosis. While this is not always detectable endoscopically, this
can be seen using an intraluminal balloon device [40]. Contrast
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M. A. Harrison et al.
esophagography in patients with abnormal esophageal-wall compliance often reveals that the esophageal caliber is decreased and
the esophagus is diffusely less distensible [41]. The most common
endoscopic ndings are white specks (representative of eosinophilic exudates), mucosal edema, linear furrows, esophageal
rings, and strictures [42, 43]. Strictures in patients with EoE may
be lengthy, tapered, and commonly escape detection during
endoscopy but are evident in contrast esophagram. Two recent
studies reported that 71% of adults and 55% of children with
eosinophilic esophagitis did not have esophageal narrowing recognized at the time of endoscopy, but did have evidence of narrowing at the time of esophagography [44–46].
Manometry may be used in patients with EoE during the work up since dysphagia is one of the most common clinical symptoms.
EoE can mimic all of the categories of esophageal motility. A
recent small study by Hejazi et al. found that one patient had
manometric ndings including non-peristaltic contractions and
incomplete relaxation of the LES, suggesting achalasia. One had
total aperistalsis with contraction amplitudes <10 mmHg and a
weak LES pressure, criteria suggesting scleroderma. Two had low
amplitude (<30mmHg) non-peristaltic contractions limited to the
mid esophagus. Criteria for nutcracker esophagus were met in 2
patients. Isolated low LES pressure was observed in four patients
who were also receiving proton pump inhibitors, and the remainder had normal esophageal motility ndings [46]. This illustrates
the heterogeneity in manometric ndings in EoE.
Management of these patients includes alleviation of symptoms, control of inammation, and restoration of function. Diet,
pharmaceutical agents, and dilation can be used to reach these
goals [33]. Pharmaceutical agents include the use of proton pump
inhibitors and topical glucocorticoids, which specically decrease
brosis through the reduction of inammatory cells [47]. Topical
glucocorticoids may also reduce the frequency of subsequent food
impactions [48]. Esophageal dilation can alleviate esophageal
narrowing particularly in older teenagers and adults. Perforation
rates of less than 1% have been seen in several large series [49].
In patients with eosinophilic esophagitis, dilation should be
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performed gradually over multiple sessions, with an expectation
that 75% of patients will have chest pain after the procedure [33].
Case #4
Patient Information
A 42-year-old female presents to the ofce with complaints of
chest pain associated with regurgitation and dysphagia to both
solids and liquids. Her medical history is signicant for chronic
back and knee pain, and she takes chronic opioids for this pain.
Manometry
Figure 21.4 shows the HRM for this patient. Manometry
reveals hypercontractile esophagus. Mean DCI is 10,500mmHg/s/
cm and median IRP is 8mmHg.
Background
Opioids have become the most widely prescribed analgesia in
western countries. The effect of opioids on stomach, small intestine, and colon motility has been well characterized, but the
effects on esophageal motility are still unclear [50]. Data suggest
Fig. 21.4 High Resolution Manometry in Opioid-Induced Esophageal Dysmotility. Mean DCI: 10500mmHg/s/cm, Median IRP: 8mmHg. This is classied by the Chicago 3.0 classication as hypercontractile esophagus.
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that long-term use of opioids can cause esophageal motility dysfunction, reecting symptoms similar to motility disorders, such
as achalasia and functional esophagogastric junction (EGJ) outow obstruction [51]. This is termed opioid-induced esophageal
dysfunction (OIED) [50].
There are multiple theories for how opioids act on the receptors in the esophagus. The μ-opioid receptor stimulation can be
associated with symptoms of dysphagia and heartburn. Opioids
decrease peristaltic activity and alter the function of the lower
esophageal sphincter, mediated mainly by μ-opioid receptors.
While the pathophysiologic mechanism is not well understood,
one mechanism could be the impairment of the nitric oxide pathwa y.
While symptoms can vary, the predominant symptom in most
patients is dysphagia, especially to liquids, with sudden onset.
Other symptoms include weight loss, regurgitation, and chest
pain.
According to the Chicago classication and published studies
on the use of opioids and esophageal motility, the main opioidrelated esophageal disorders are EGJ outow obstruction and type
3 achalasia, along with distal esophageal spasm and hypercontractile esophagus. Impaired LES relaxation and reduced distal
latency in the manometry, observed in EGJ outow obstruction
and type 3 achalasia, can be more frequent in patients undergoing
long-term opioid therapy [50].
Limited data exist in the management of OIED. The withdrawal of the opioid is the rst line measure, given that studies
have observed a reversal of motility dysfunction after the withdrawal of the drug [50]. If the drug cannot be withdrawn, it should
be reduced to the minimum effective dosage. Other options
include calcium channel blockers, aimed to decrease LES pressure, which have led to little improvement [52]. Other available
options include the injection of botulinum toxin. This could be a
valid temporary and more rational option for patients who cannot
withdraw from opioids. A small number of patients have been
treated with pneumatic dilation and per-oral endoscopic myotomy, both with poor results [53, 54].
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Case #5
Patient Information
A 55-year-old male from Bolivia, with a history of congestive
heart failure secondary to dilated cardiomyopathy presents to
clinic complaining of dysphagia to solids, regurgitation, and constipation.
Manometry
Figure 21.5 shows the manometry for this patient. Manometry
reveals Achalasia associated with Chagas disease, with elevated
IRP and aperistalsis.
Background
Chagas disease is a tropical infectious disease caused by the
protozoan Trypanosoma cruzi. A large proportion of individuals
develop chronic disease many years after the acute phase, often
without detectable parasitemia [55]. Gastrointestinal dysfunction occurs in 10–15% of patients with Chagas disease. The
Fig. 21.5 Manometry in Chagas Disease. Mean DCI: 5mmHg/s/cm, Median
IRP: 35mmHg. This is classied by the Chicago 3.0 classication as Type 1
Achalasia secondary to Chagas disease (Used with permission, courtesy of
Dr. Asyia Ahmad)
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pathology of the esophageal dysfunction caused by Chagas disease is the loss of the myenteric plexus of the esophagus [55].
The symptoms are characterized by slowly progressive dysphagia, malnutrition, and weight loss. Some patients may also experience regurgitation, heartburn, chest pain, and pulmonary
complications due to elementary aspiration [56]. Severity of
symptoms is secondary to the degree of denervation that the
patient experiences [55].
Manometry shows partial or absent lower esophageal sphincter
relaxation and simultaneous contractions in the esophageal body
[57–60]. The esophageal manifestations of the disease are very
similar, although not completely equal, to those of idiopathic type
II achalasia.
Silva etal. observed that the LES was hypotensive or normotensive in the majority of patients with impaired relaxation found
in a minority of patients. Aperistalsis was seen in 100% of the
patients, and the upper esophageal sphincter had impaired relaxation in a signicant number of patients. In both Chagas disease
esophagopathy (CDE) and Type II achalasia, the main feature is
aperistalsis of the esophageal body. Additionally, the LES shows
a failure to relax [56].
Treatment is similar to that of Type II achalasia. The mainstay
of treatment is pneumatic dilation and myotomy. However,
Meneghelli etal. evaluated the manometric evolution of esophageal involvement and found that worsening of dysphagia was not
associated with the longer duration of dysphagia. Patients whose
disease did not worsen had dysphagia for a longer time, suggesting that the duration of this symptom may not be associated with
changes in the severity of the disease. This is contrary to idiopathic achalasia, where the natural history is progression of dysphagia. While some patients chose to make lifestyle modications
for mild symptom of dysphagia without esophageal dilation,
when there is worsening of the dysphagia or an increase in esophageal diameter, patients are more likely to accept invasive treatment, such as myotomy [55].
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Summary
The causes and prevalence of secondary esophageal motility disorders range from autoimmune to infectious, and common to very
rare. A good clinical understanding of these conditions, and their
manometric ndings and management, is essential to providing
optimal care in these patients.
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