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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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Fig. 18.1 Weak esophageal contractile force with normal peristalsis
A. Banks-Venegoni et al.
Fig. 18.2 Failed swallow
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Fig. 18.3 Delayed esophageal bolus clearance by impedance data
tion into his throat mostly at night while supine. He denies
dysphagia or shortness of breath. Diet modication and antacid therapy have not provided symptomatic improvement.
UGI suggested slightly dilated distal esophagus without delay
in passage of contrast or tablet into the stomach and small sliding hiatal hernia. EGD demonstrated normal appearing esophagus with small hiatal hernia and without eosinophilia. pH
study conrms GERD by elevated DeMeester score of 21 and
high percent time spent in reux at 6.8%. Heartburn and cough
were associated with reux events by symptom association
probability (SAP) of 98% and 99%. HRM demonstrates normal UES resting and relaxation pressures, normal LES resting
and relaxation pressures, weak DCI with mean of
398 mmHg·s·cm, abnormal peristalsis with 50% weak and
60% failed swallows, and 40% incomplete bolus clearance
(Figs.18.4 and 18.5). The patient was treated for his GERD
with laparoscopic hiatal hernia repair and Toupet fundoplication with resolution in preoperative symptoms.
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Fig. 18.4 Weak and ineffective esophageal contraction
A. Banks-Venegoni et al.
Fig. 18.5 Delayed esophageal bolus clearance by impedance data
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Fragmented Peristalsis
Fragmented peristalsis (FP) is dened by the Chicago
Classication v3.0 (CC3.0) in 2014 by HRM demonstrating
greater than or equal to 50% of fragmented contractions (each
with >5cm break in the 20mmHg isobaric contour) with a normal
distal contractile integral (DCI) and normal lower esophageal
sphincter (LES) relaxation pressure [2]. The CC3.0 simplied the
descriptions of peristaltic function and retired the terms dened in
the 2012 Chicago Classication (CC2.0), namely “weak peristalsis with small breaks” and “weak peristalsis with large breaks,” by
making contractile vigor (based solely on DCI) independent of
contraction pattern (based on latency and breaks). The new classication clarifying diagnostic criteria subsequently not only
reduced the number of diagnoses classied as minor motility disorders, but also reduced the number of patients diagnosed with a
minor motility disorder [2, 16].
The pathophysiology of FP is unknown but thought to be due
to an abnormality of esophageal peristalsis at the transition zone
between the proximal and distal contractile segments. This results
in a break of the contractile contour that causes incomplete bolus
transit [1, 17]. Of note, a normal esophageal peristalsis topography already consists of three natural troughs: one dividing proximal skeletal muscle from distal smooth muscle, one dividing the
distal smooth muscle into two contraction segments, and one
between the distal smooth muscle segment and LES [18]. The rst
trough of the esophagus is also the most distinctive on topography
as it signies the transition zone (also termed intersegmental
trough) between the proximal and distal contractile segments,
which corresponds to the interface between different muscle ber
types and neural control mechanism [1, 19, 20]. A transition zone
with a measurement of 2cm or 1s in size was identied as the
95th percentile in asymptomatic patients [19]. To correlate these
measurements with actual bolus clearance, a high-resolution
impedance manometry study revealed that incomplete bolus transit was only found in 16% of the patients with breaks <5cm, as
opposed to 100% of the patients with breaks exceeding 5cm in
length, which became the basis for the denition of FP [17].
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A. Banks-Venegoni et al.
Since the new classication, there have been no studies that
examined the prevalence of FP in asymptomatic patients. One
study that specically looked at the difference in prevalence
between CC3.0 and CC2.0 examined minor disorders of peristalsis and noted a prevalence of 15% in healthy volunteers
(down from 25.2% of CC2.0) and 33.3% in symptomatic
patients (up from 24.5% in CC2.0) [16]. The study suggested
an increase in the prevalence of minor disorders of peristalsis
with abnormal results as the diagnostic criteria became more
stringent and less asymptomatic patients were diagnosed. A
study by Dan Wang et al. from China, assessed patients presenting with a predominant symptom of dysphagia and a normal EGD and found fragmented peristalsis had a prevalence of
16.1% [21].
Like IEM, patients with FP often have a wide range of symptoms that can include cough, heartburn, dysphagia, or regurgitation. Retrospectively, FP has been associated with GERD and
Barrett’s esophagus [1, 22, 23]. Using HRM, recent studies show
that failed peristalsis and fragmented peristalsis had a higher signicant correlation with reux burden as opposed to weak peristalsis, which further supports the new metrics found in CC3.0 [24].
There is no pharmacologic intervention that will restore the
break in esophageal peristalsis or improve symptoms. Therefore,
unless GERD is identied, symptomatic patients with FP are
challenging to treat. In GERD patients undergoing fundoplication without dysphagia symptoms but had a preoperative diagnosis of fragmented peristalsis, current evidence showed no
correlation from these diagnoses with post-fundoplication dysphagia in short- term follow-up [25, 26]. However, the question
regarding whether to perform a total versus partial fundoplication in GERD patients with dysphagia from FP remains controversial. Newer provocative maneuvers such as multiple rapid
swallows (MRS) demonstrate contraction reserve, which detects
abnormalities in inhibitory and excitatory esophageal motor
function. When the contraction following the last swallow is
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weak in an MRS maneuver, an impaired integrity of neural excitation and muscle is predicted. Patients with abnormal MRS
contraction have increased risk of prolonged bolus transit and
poor bolus clearance. MRS evaluation can help identify patients
who are at higher risk for post-fundoplication dysphagia [27–
29].
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Patient Scenario
1. HG is a 76-year-old male presenting with reux symptoms for
20years that have worsened over the past 6months. Symptoms
consist of bloating, chest pain, chronic cough, regurgitation of
saliva and mucus when supine, and spicy food intolerance. He
denies abdominal pain, dysphagia, emesis, food impaction,
heartburn, hematemesis, nausea, or odynophagia. Lifestyle
modications including decreased meal size, avoiding spicy
foods, not eating 5h prior to bedtime, and elevating the head
of the bed have provided minimal symptomatic relief. The
patient has taken a PPI for years with some relief. UGI demonstrated delayed distention in the distal esophagus secondary to
multiple, persistent tertiary contractions, and insufcient primary peristaltic waves with moderate esophageal dysmotility.
EGD identied mild esophagitis conrmed on biopsy and
grade II ap valve. pH study revealed a normal DeMeester
score of 0.6 and normal % time spent in reux at 0.1%.
Heartburn was not correlated to reux events. HRM demonstrated normal UES resting and relaxation pressures, normal
LES resting and relaxation pressures, normal LES length, normal DCI, 70% fragmented peristaltic waves, and 100% incomplete bolus clearance (Figs.18.6 and 18.7). The patient was
counseled that his symptoms were due to esophageal stasis
and was instructed to continue lifestyle modications that help
with esophageal emptying.
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A. Banks-Venegoni et al.
a
b
Fig. 18.6 Fragmented swallows
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Fig. 18.7 Esophageal stasis and delayed clearance by impedance data
Editors’ Note
IEM
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IEM in a patient with longstanding GERD and a hiatal hernia.
The study of the LES reveals a shortened length and a large
hiatal hernia. The LES pressure is low at 11mmHg and relaxes
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A. Banks-Venegoni et al.
completely. The esophageal body study demonstrates normal
peristalsis and low contraction amplitudes (DEA 16 mmHg,
DCI of 56). Bolus transit is fair at 50%. Overall, the patient has
IEM, hiatal hernia, and hypotensive LES.Also, the UES is dysfunctional with non-coordinated contractions and does not
relax.
IEM with dysphagia/heartburn: dysphagia of solid food only
sticking to the mid-lower chest for the past 2–3 years occurring
about once a week that improves with smaller bites; heartburn
presenting as a burning sensation for the past 10–12 years occurring 3–4 times a week with certain foods late at night that goes
away with Tums; also complains of a raspy voice and cough.
Stopped taking Protonix almost 2 months ago.
Interpretation: The study of the LES reveals a shortened length
and a small sliding hiatal hernia. The LES pressure is negligible.
The hiatus appears tighter. With viscous materials, the LES was in
the hiatus and showed minimal relaxation. The esophageal body
study demonstrates 80% ineffective swallows (40% weak and
40% failed swallows) and amplitudes of only 35mmHg (DCI
225). There are increased velocities seen with some swallows.
Bolus transit is poor (10%). Overall, the patient has a small sliding hiatal hernia, hypotensive LES, and poor esophageal clearance with IEM.
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265
References
1. Porter RF, Kumar N, Drapekin JE, Gyawali CP.Fragmented esophageal
smooth muscle contraction segments on high resolution manometry: a
marker of esophageal hypomotility. Neurogastroenterol Motil.
2012;24:763–e353.
2. Kahrilas PJ, Bredenoord AJ, Fox M, Gyawali CP, Roman S, Smout AJ,
Pandolno JE.The Chicago classication of esophageal motility disorders, v3.0. Neurogastroenterol Motil. 2015;27:160–74.
3. Carlson DA, Crowell MD, Kimmel JN, etal. Loss of peristaltic reserve,
determined by multiple rapid swallows, is the most frequent esophageal
motility abnormality in patients with systemic sclerosis. Clin
Gastroenterol Hepatol. 2016;14:1502–6.
4. Mittal RK.Regulation and dysregulation of esophageal peristalsis by the
integrated function of circular and longitudinal muscle layers in health and
disease. Am J Physiol Gastrointest Liver Physiol. 2016;311:G431–43.
5. Triadalopoulos G, Tandon A, Shetler KP, etal. Clinical and pH study
characteristics in reux patients with and without ineffective oesophageal
motility (IEM). BMJ Open Gastroenterol. 2016;3:e000126.
6. Shetler KP, Bikhtii S, Triadalopoulos G.Ineffective esophageal motility:
clinical, manometric, and outcome characteristics in patients with and
without abnormal esophageal acid exposure. Dis Esophagus. 2017;30:1–8.
7. Bennett MC, Patel A, Sainani N, Wang D, Sayuk GS, Gyawali CP.Chronic
cough is associated with long breaks in esophageal peristaltic integrity on
high-resolution manometry. J Neurogastroenterol Motil. 2018;24:387–94.
8. Rengarajan A, Bolkhir A, Gor P, etal. Esophagogastric junction and esophageal body contraction metrics on high resolution manometry predict
esophageal acid burden. Neurogastroenterol Motil. 2018;30(5):1647–54.
9. Gyawali CP, Sifrim D, Carlson DA, etal. Ineffective esophageal motility:
concepts, future directions, and conclusions from the Stanford 2018 symposium. Neurogastroenterol Motil. 2019;31(9):e13584.
10. Morozov S, Isakov V, Konovalova M.Fiber-enriched diet helps to control
symptoms and improves esophageal motility in patients with non-erosive
gastroesophageal reux disease. World J Gastroenterol. 2018;24:2291–9.
11. Pauwels A, Vandingenen N, Vanuytsel T, etal. The effect of an osteopathic intervention on the respiratory diaphragm on lower esophageal
function in healthy volunteers and patients with non-erosive reux disease. Gastroenterology. 2018;154:S-238.
12. Chen C-L, Yi C-H, Liu T-T, Orr WC.Effects of mosapride on secondary
peristalsis in patients with ineffective esophageal motility. Scand J
Gastroenterol. 2013;48:1363–70.
13. Scheerens C, Tack J, Rommel N.Buspirone, a new drug for the management of patients with ineffective esophageal motility? United European
Gastroenterol J. 2015;3:261–5.
14. The 5-HT1A receptor agonist buspirone improves esophageal motor
function and symptoms in systemic sclerosis: a 4-week, open-label trial.
Arthritis Res Ther. 2016;18:195.
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