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245
uoroscopic guidance can be used to aid in the usage of the dilators. Multiple achalasia balloon sizes exist as 30, 35, and 40mm
[18]. There are variable reports on the success of pneumatic
dilation. Overall, pneumatic dilation is 60% effective when using
the smallest 30mm balloon, but using the 35mm balloon increases
the success rate to near 90% [12]. Pneumatic dilation has been
shown to be successful in about 60% of patients at 5 years after
several treatments; however, symptom relief decreases over time.
Some situations like age less than 40years can predict poor success of dilation [19]. If there is failure of symptom improvement
with the rst two treatments, pneumatic dilation will unlikely
resolve symptoms. In patients with high LES pressure (more than
15–30mmHg), or if the LES pressure did not drop to more than
50% from the pretreatment numbers, pneumatic dilation will
likely fail. Complications associated with pneumatic dilation
include perforation (incidence of 1.6%), bleeding, and reux [16].
The risk of perforation increases with the increase in balloon size.
However, dilation to 35 mm and even 40mm is relatively safe
when it is preceded by an initial 30mm dilation [20].
Surgical myotomy is referred to as a Heller myotomy. It was
originally described by Ernest Heller in 1914 and can provide
relief of symptoms in approximately 85–100% of patients. Recent
minimally invasive approaches to this operation have made it better tolerated by patients. A study reported that the therapeutic success rate of this approach is 93% and 90% after 1 and 2years,
respectively [21]. In the current era, it can be performed either
laparoscopically or robotically. The procedure involves the mobilization of the distal esophagus and proximal stomach with a
myotomy that must include the inner muscular circular bers. The
external longitudinal bers and the internal circular bers can be
divided using variable methods as hook cautery, ultrasonic dissection, or blunt dissection. The myotomy should be extended 6cm
onto the esophagus and at least 2cm onto the gastric muscle [6].
During a Heller myotomy, fundoplication may be performed. It
is thought that adding a fundoplication to the myotomy will prevent
reux since the LES mechanism is lost [22]. A systematic review
found after a mean follow-up of 26.6months that the rates of reux
and esophagitis following myotomy with fundoplication are 16.8%
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L. Serrano et al.
and 7.6%, respectively [23]. However, both the addition of a fundoplication and best type of fundoplication have been debated. Dor
fundoplication (anterior 180-degree fundoplication) provides reux
prevention, avoids dissection posterior to the esophagus, and covers
the exposed mucosa of the myotomy. Toupet fundoplication (posterior 270-degree fundoplication) is believed to provide a greater
antireux mechanism. The sutures placed on the cut end of the
muscle also help keep the myotomy open. Unlike Dor fundoplication, there is no coverage of the myotomy with the Toupet fundoplication [24, 25]. Intraoperative endoscopy is recommended to assess
for completion of myotomy and rule out leak.
Peroral endoscopic myotomy (POEM) was rst introduced by
Dr. Inoue in 2009. POEM is performed entirely endoscopically.
The procedures begins with a mucosotomy and accessing the submucosal space. This spaced is used to start the submucosal tunnel,
usually begining in the mid to upper esopahgus. This submucosal
tunnel will then go roughly 3 cm past the LES. The myotomy is
then created roughly from 2 cm distal to the LES on the gastric side,
to within 2–3 cm of the origional mucosotomy. Thus the myotomy
can be extremely long when performing a POEM, making it an
excellent treatment choice for type III achalasia. At the completion
of the case the mucosotmy is closed with endoscopic clips. POEM
has good efcacy in most patients with achalasia. It is rapidly gaining traction as another gold-standard treatment for achalasia. A systematic review compared the clinical success of POEM against
pneumatic dilation (PD). The clinical success with POEM was
superior to PD at 12, 24, and 36months. In addition, POEM was
superior to PD in type I, II, and III achalasia, and pooled odds ratio
of clinical success at 12 and 24months were signicantly higher
with POEM. However, pooled odds ratio of GERD was signicantly higher with POEM [26]. Another systematic review compared the risk of GERD and esophagitis after POEM against
laparoscopic Heller’s myotomy and fundoplication (LHM). The
pooled rate of abnormal acid exposure according to pH studies was
39.0% after POEM and 16.8% after LHM, and the rate of esophagitis was 29.4% after POEM and 7.6% after LHM [23].
POEM is particularly useful in patients with type III achalasia,
due to long segments of spastic contractions and POEM’s ability
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247
to create a long myotomy [27]. POEM is well tolerated with good
symptomatic improvement. Some potential complications include
both pneumothorax and pneumoperitoneum which are decreased
by using CO2 instead of air for insufation. Another possible
complication is bleeding within myotomy tunnel or inadvertent
mucosotomy [16, 17, 28]. A study compared rates of serious
adverse events following POEM against laparoscopic Heller’s
myotomy (LHM), and they reported rates of 2.7% and 7.3% for
POEM and LHM, respectively. POEM is as safe as LHM if not
even safer [29].
Unlike a Heller myotomy, POEM does not include an antireux procedure such as a Dor or Toupet fundoplication. Due to the
lack of an antireux operation, post-POEM patients can experience gastrointestinal reux disease up to 50% of the time.
Evidence of reux can even be seen in asymptomatic patients. For
this reason, it is good practice to follow POEM patients for reux
using endoscopy. Some advocate treating patients with a proton
pump inhibitor (PPI) post-POEM to prevent acid reux complications such as peptic stricture, Barrett’s esophagus, and esophageal
cancer [28]. Since its inception, POEM has gained acceptance and
been utilized as a treatment modality around the world.
Esophagectomy is reserved as a last resort for end-stage achalasia with megaesophagus. Myotomy, either surgical or endoscopic, will relax the LES, but there is currently no therapy for the
aperistalsis seen in achalasia. In these instances, esophagectomy
should be considered in patients that have already undergone an
appropriate myotomy with resting low LES pressures, a dilated or
megaesophagus, and persistent symptoms [6].
Achalasia is a complex disease that requires a combined
approach of a primary care physician, a gastroenterologist, and a
surgeon for the diagnosis, treatment, and follow-up of such
patients. The diagnosis can occasionally be challenging. It is crucial to understand the pathophysiology, the diagnostic algorithm,
and the treatment options. At best, the interventions are palliative
and not therapeutic, and the risk of disease progression is always
present. A key aspect in the treatment of achalasia is having a
well-informed and continuous dialog with the patient, so that they
are fully informed regarding realistic treatment expectations.
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Editors’ Note
L. Serrano et al.
Type 1 achalasia
Type 2 achalasia
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Type 3 achalasia
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10. Blonski W, Kumar A, Feldman J, Richter JE.Timed barium swallow:
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11. Ates F, Vaezi MF.The pathogenesis and management of achalasia: current status and future directions. Gut Liver. 2015;9(4):449–63. https://doi.
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12. Moonen A, Boeckxstaens G.Current diagnosis and management of achalasia. J Clin Gastroenterol. 2014;48(6):484–90. https://doi.org/10.1097/
MCG.0000000000000137.
13. Ju H, Ma Y, Liang K, Zhang C, Tian Z. Function of high-resolution
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Surg Endosc. 2016;30(3):1094–9. https://doi.org/10.1007/s00464- 015-
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14. Schlottmann F, Herbella FA, Patti MG.Understanding the Chicago classication: from tracings to patients. J Neurogastroenterol Motil.
2017;23(4):487–94. https://doi.org/10.5056/jnm17026.
15. Kahrilas PJ, Bredenoord AJ, Fox M, etal. The Chicago classication of
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16. Stefanidis D, Richardson W, Farrell TM, etal. SAGES guidelines for the
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analysis. Neurogastroenterol Motil. 2019;31(7):e13548. https://doi.
org/10.1111/nmo.13548.
21. Boeckxstaens GE, Annese V, des Varannes SB, etal. Pneumatic dilation
versus laparoscopic Heller’s myotomy for idiopathic achalasia. N Engl J
Med. 2011;364(19):1807–16. https://doi.org/10.1056/NEJMoa1010502.
22. Richards WO, Torquati A, Holzman MD, etal. Heller myotomy versus
Heller myotomy with dor fundoplication for achalasia. Ann Surg.
2004;240(3):405–15. https://doi.org/10.1097/01.
sla.0000136940.32255.51.
23. Repici A, Fuccio L, Maselli R, etal. GERD after per-oral endoscopic
myotomy as compared with Heller’s myotomy with fundoplication: a
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2018;87(4):934–943.e18. https://doi.org/10.1016/j.gie.2017.10.022.
24. Patel DA, Lappas BM, Vaezi MF.An overview of achalasia and its subtypes. Gastroenterol Hepatol. 2017;13(7):411–21.
25. Rawlings A, Soper NJ, Oelschlager B, etal. Laparoscopic dor versus
Toupet fundoplication following Heller myotomy for achalasia: results of
a multicenter, prospective, randomized-controlled trial. Surg Endosc.
2012;26(1):18–26. https://doi.org/10.1007/s00464- 011- 1822- y.
26. Ofosu A, Mohan BP, Ichkhanian Y, etal. Peroral endoscopic myotomy
(POEM) vs pneumatic dilation (PD) in treatment of achalasia: a metaanalysis of studies with ≥ 12-month follow-up. Endosc Int Open.
2021;9(7):E1097–107. https://doi.org/10.1055/a- 1483- 9406.
27. Hamer PW, Holloway RH, Heddle R, Devitt PG, Thompson SK.Type III
achalasia—a clinical description. Dis Esophagus. 2017;30(8):1–6.
https://doi.org/10.1093/dote/dox051.
28. Inoue H, Minami H, Kobayashi Y, et al. Peroral endoscopic myotomy
(POEM) for esophageal achalasia. Endoscopy. 2010;42(4):265–71.
https://doi.org/10.1055/s- 0029- 1244080.
29. Werner YB, Hakanson B, Martinek J, etal. Endoscopic or surgical myotomy in patients with idiopathic achalasia. N Engl J Med.
2019;381(23):2219–29. https://doi.org/10.1056/NEJMoa1905380.
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Minor Disorders
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ofEsophageal Motility
AmyBanks-Venegoni, JustinHsu,
andGregoryFritz
Ineective Esophageal Motility
Ineffective esophageal motility (IEM) is a manometric diagnosis
that is dened as greater than or equal to 50% ineffective swallows that can be combinations of failed or weak (distal contractile
integral <450mmHg·s·cm) swallows with a normal lower esophageal sphincter relaxation pressure of less than 15mmHg·s·cm [1].
It is associated with impaired bolus transit through the esophagus
and nonobstructive dysphagia. This disorder is reportedly found
in as high as 30% of patients undergoing high-resolution manometry (HRM) and as many as 17% of asymptomatic patients [2].
IEM has been found to have a higher prevalence in smooth muscle
disorders like scleroderma and other diseases that affect neuron
function like Parkinson’s disease and ALS [3]. The pathophysiology of IEM has therefore been investigated and theorized to arise
18
A. Banks-Venegoni (*)
Spectrum Health Medical Group and Corewell Health West-Department
of Surgery, Michigan State School of Medicine, East Lansing, MI, USA
e-mail: Amy.banksvenegoni@Corewellhealth.org
J. Hsu · G. Fritz
Corewell Health General Surgery Residency, Michigan State School of
Medicine, East Lansing, MI, USA
e-mail: Justin_Hsu@med.unc.edu; Gregory.fritz@Corewellhealth.org
© Society of American Gastrointestinal and Endoscopic Surgeons
(SAGES) 2023
A. D. Patel et al. (eds.), The SAGES Manual of Physiologic
Evaluation of Foregut Diseases,
https://doi.org/10.1007/978-3-031-39199-6_18
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A. Banks-Venegoni et al.
from a combination of neuronal factors that disrupt the circular
muscle contraction, esophageal shortening (from longitudinal
muscle contraction), and esophageal muscle tone that participate
in primary esophageal peristalsis [4]. Impaired secondary peristalsis that is triggered by esophageal distension may also play a
signicant role in the underlying cause of IEM.
Patients with IEM often have a wide range of symptoms that
include cough, heartburn, regurgitation, chest pressure, and dysphagia which makes the diagnosis difcult. The typical workup to distinguish the etiology of these symptoms includes
esophagogastroduodenoscopy (EGD), upper GI contrast study
(UGI), pH testing, and high-resolution manometry (HRM). IEM
impairs esophageal clearance and therefore can participate in the
pathophysiology of gastroesophageal reux disease (GERD) [5].
Patients with IEM and normal pH studies are younger than those with
abnormal pH testing, suggesting that IEM could be an early primary
event that subsequently leads to abnormal acid burden [6]; however,
further studies need to be performed to conrm this. Patients with
chronic cough have a higher likelihood of esophageal hypomotility,
lower contraction amplitude, and vigor [7]. Identication of severe
IEM (>70% ineffective peristalsis) provides supportive evidence for
a more severe GERD phenotype marked by supine acid burden [8].
There is no pharmacologic intervention that reliably restores
esophageal smooth muscle contractility or improves symptoms.
Therefore, unless GERD is identied, symptomatic patients with
IEM are challenging to treat. Dietary restriction and lifestyle changes
typically recommended to patients with GERD remain the mainstay
of clinical IEM management. With the hypothesis that dietary ber
binds nitric oxide (NO) contained in food and could reduce the
inhibitory effects of NO in the esophagus, psyllium (15g/day) was
reported to decrease esophageal dysphagia and increase LES resting
pressure in patients with GERD [9, 10]. However, effects on esopha-
geal contractility were not reported in this open-label study.
Alternative therapies are popular, as they decrease esophageal sensitivity and symptom perception and may benet esophageal contractility. A pilot study of patients with PPI refractory GERD
demonstrated signicant increase in esophageal contraction vigor
10min after an osteopathic intervention on the diaphragm, but longterm effects on esophageal symptoms are unknown [11].
18 Minor Disorders ofEsophageal Motility
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Conventional prokinetic agents (metoclopramide, domperidone)
have not been proven to be benecial in IEM.There are limited data
on newer prokinetic agents like mosapride, a 5HT-4 agonist, which
may facilitate secondary peristalsis induced by rapid air distension
in patients with IEM but had no improvement in primary and secondary esophageal contraction vigor [9, 12]. Buspirone, a mixed
partial 5HT-1A agonist and dopamine D2 receptor antagonist,
increased esophageal contraction amplitudes and decreased reux
symptoms in scleroderma patients [9, 13, 14], but was not more
effective than placebo in patients with IEM and dysphagia [15].
No specic management strategy has been favored over
another. Treatment options revolve around management of symptoms for each individual patient. If IEM patients are found to have
GERD refractory to pharmacologic management and are pursuing
antireux surgery, then a partial (270-degree) Toupet fundoplication is the surgical treatment of choice so as to not further exacerbate poor esophageal clearance.
255
Patient Scenarios
1. JV is a 66-year-old female presenting with dysphagia who pre-
viously was diagnosed with reux many years ago. She takes a
proton pump inhibitor (PPI) twice daily without symptomatic
improvement. Her main complaint is dysphagia to thicker food
groups and pills. She endorses early satiety without weight loss
and regurgitation of liquids when supine. She denies true heartburn-like symptoms or odynophagia. UGI showed small sliding hiatal hernia without reux. EGD conrmed hiatal hernia
without eosinophilia. pH study had a normal DeMeester score
of 0.5 with normal percent time spent in reux. HRM with normal upper esophageal sphincter (UES) pressures, normal lower
esophageal sphincter (LES) pressures, weak distal contractile
integral (DCI) with mean of 425mmHg·s·cm, abnormal peristalsis with 40% weak and 70% ineffective swallows, and 70%
incomplete bolus clearance (Figs. 18.1, 18.2, and 18.3). The
patient was treated with lifestyle modication only with moderate improvement in symptoms.
2. SB is a 65-year-old male presenting with burning sensation
and chest pressure after eating. He endorses liquid regurgita-
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