Surgical Management of Achalasia

Abstract

Esophageal achalasia is a primary esophageal motility disorder characterized by lack of peristalsis and by incomplete or absent relaxation of the lower esophageal sphincter in response to swallowing. The cause of the disease is unknown. The goal of treatment is to eliminate the functional outflow obstruction at the level of the gastroesophageal junction, therefore allowing emptying of the esophagus into the stomach. They include the laparoscopic Heller myotomy with partial fundoplication, pneumatic dilatation, and peroral endoscopic myotomy. Esophagectomy is considered as a last resort for patients who have failed prior therapeutic attempts. In this evidence and experience‐based review, we will illustrate the technique and results of the surgical treatment of esophageal achalasia and compare it to the other available treatment modalities.

Full text

Ann Gastroenterol Surg. 2020;4:343–351.
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1 | INTRODUCTION
Esophageal achalasia is a rare disease that affect s approximately one
in 100 00 0 people, regardless of gender or race. However, in some
geographical locations such as Brazil, it is much more common in
connection to the high prevalence of Chagas disease.1 The incidence
of achalasia increases with patient age.2 In addition, it seems that the
prevalence of this disease is increasing, probably due to improve-
ments in diagnostic modalities.3
In normal conditions, the lower esophageal sphincter (LES) relaxes
in response to swallowing. This physiological mechanism is dependent
on neurogenic control of the esophagus and LES through the myenteric
plexus, combining excitatory acetylcholine neurons, inhibitor nitric
oxide, and VIP neurons. Idiopathic achalasia is due to the degeneration
of inhibitory neurons, which are involved in the relaxation of LES. As a
result, the LES does not relax properly in response to swallowing, and it
is often hyp ertensive. In a ddition, there i s a lack of esophageal p eristalsis.
The lack of peristalsis and the impaired LES relaxation impair the
transit of t he food bolus from th e esophagus into the s tomach, leading
eventually to dilatation of the esophageal body. Almost every patient
experi ences dysphagia , which often lea ds to weight loss. Reg urgitation
of undigested food is also a common ailment, and may cause compli-
cations such as hoarseness, coughing, wheezing, and pneumonia. Up
to 50% of patients with achalasia also experience heartburn, which
is caused by fermentation of retained food in the esophagus. Chest
discomfor t or pain can also occur, and they are caused by esopha-
geal distension, which usually increases while eating.4 The severity of
achalasia symptoms is evaluated using the Eckardt score.
2 | PREOPERATIVE WORK-UP
A comprehensive evaluation of ever y patient should be carried out
to confirm the initial diagnosis suggested by the symptoms, and
Received: 27 Januar y 2020
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Revised: 3 Ap ril 2020
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Accepted: 13 Ap ril 2020
DOI: 10.10 02/ag s3.1 234 4
REVIEW ARTICLE
Surgical management of achalasia
Kamil Nurczyk1,2 | Marco G. Patti1,3
This is an op en access article under t he terms of the Creat ive Commons Attributio n License, which permits use, dist ribution and reproduc tion in any medium,
provide d the orig inal work is proper ly cited .
© 2020 The Authors . Annals of Gastroenterological Surgery published by John Wiley & Sons Australia, Ltd on behal f of The Japanese Society of
Gastroenterological Surgery
1Department of Surgery, University of North
Carolina at Chapel Hill, Chapel Hill, NC, USA
22nd Department of Gener al and
Gastrointest inal Surgery, and Surgical
Oncology of the Aliment ary Tract, Medic al
University of Lublin, Lublin, Poland
3Department of Medicine, University of
North Carolina at Chapel Hill, Ch apel Hill,
NC, USA
Correspondence
Marco G. P atti, D epartment of Me dicine and
Surger y, University of Nor th Carolina, 4 030
Burnett Womack Building, 101 Manning
Drive 7081, Chapel Hill, NC 27599-7081,
USA.
Email: Marco_patti@med.unc.edu
Abstract
Esophageal achalasia is a primary esophageal motility disorder characterized by
lack of peristalsis and by incomplete or absent relaxation of the lower esophageal
sphincter in response to swallowing. The cause of the disease is unknown. The goal
of treatment is to eliminate the functional outflow obstruction at the level of the
gastroesophageal junction, therefore allowing emptying of the esophagus into the
stomach. They include the laparoscopic Heller myotomy with partial fundoplication,
pneumatic dilatation, and peroral endoscopic myotomy. Esophagectomy is consid-
ered as a last resort for patients who have failed prior therapeutic attempts. In this
evidence and experience-based review, we will illustrate the technique and results of
the surgical treatment of esophageal achalasia and compare it to the other available
treatment modalities.
KEYWORDS
dor fundoplication, esophageal achalasia, heller myotomy, peroral endoscopic myotomy,
pneumatic dilatation

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should include: esophagogastroduodenoscopy (EGD), barium swal-
low, esophageal manometry, and in some cases ambulator y 24-hour
pH monitoring.
Usually, the evaluation begins with an EGD to exclude other
causes of dysphagia such as a peptic stricture or a tumor. Typical
findings are esophageal dilation and presence of retained food.
Sometimes candidiasis of the esophageal mucosa is present. It is
worth mentioning that gastroesophageal junction cancer infiltrat-
ing the LES may mimic achalasia. This misleading condition, called
pseudo-achalasia, should be ruled out in elderly patients, with short
duration of symptoms and marked weight loss.5
The barium swallow of ten shows the characteristic “bird beak”
sign (narrowing at the level of the gastroesophageal junction), de-
layed passage of the contrast into the stomach, an air-fluid level, and
tertiary contractions of the esophagus.
The gold st andard for the diagnosis of achalasia is the high-res-
olution esophageal manometry (HRM). It enables the measurement
of the pressure, leng th, and relaxation of the lower and upper
esophageal sphincters and assessment of esophageal peristalsis. To
confirm the diagnosis of achalasia, it is necessary to document lack
of esophageal peristalsis and partial or absent LES relaxation. The
Chicago classification introduced by Pandolfino6 and his colleagues
distinguishes three types of achalasia. Type I involves aperistalsis
and absence of esophageal pressurization; type II is associated
with aperistalsis and pan-esophageal pressurization in at least
20% of swallows; and in type III there are premature spastic con-
tractions (distal latency <4.5 seconds) in at least 20% of swallows.
What makes the Chicago classification useful is that it can also help
predicting treatment outcome. In fac t, many studies have shown
higher success rates in patients with type II achalasia.7, 8 It has been
speculated that type II achalasia is an initial phase of the disease
process with pan-esophageal pressurization, while type I rep-
resents a later phase with complete absence of any contrac tion.7
Type III achalasia, characterized by premature spastic contractions,
is associated with decreased response to surgical treatment .7 It is
speculated that it may represent a recognizably different patholog-
ical process which is not a part of the progression from t ype II to
type I achalasia, rather being a variant of distal esophageal spasm
which involves the LES.7
Ambulatory pH monitoring is not necessary in the work-up of
patients with achalasia. It should be performed only in patients with
heartburn and dysphagia who are considered to have gastroesoph-
ageal reflux refrac tory to medical treatment. In these patients, this
test will distinguish GERD from achalasia.9 Interestingly, up to 50%
of patients who end up having a diagnosis of achalasia have been
treated for prolonged periods of time with proton pump inhib-
itors on the assumption that abnormal reflux was present.10 The
pH monitoring study should also be performed af ter treatment to
rule out pathologic gastroesophageal reflux (GER), which is often
asymptomatic.11 In patients who are asymptomatic, particularly
if young, we do prescribe acid-reducing medications. In patients
found to have erosive esophagitis, we also prescribe acid-reducing
medications.
3 | SURGICAL TREATMENT OF
ESOPHAGEAL ACHALASIA
3.1 | Evolution of surgery for esophageal achalasia
In 1914, the first transabdominal ex tramucosal cardioplasty was de-
scribed by Heller. He performed the myotomy both on the anterior
and posterior walls of the cardia.12 Groeneveldt and Zaaijer simpli-
fied the procedure by performing one myotomy only.13 In the 1940s
and 1950s, the transabdominal approach was the most commonly
used, while few surgeons favored a left trans-thoracic approach.14
Until the 1960s, the focus of treatment was on the relief of the
dysphagia by the myotomy and no consideration was given to the
possibility of post-myotomy reflux. In 1956, Nissen popularized a
360-degree fundoplication to control gastroesophageal reflux and
this inspired Dor to propose a 180-degree anterior fundoplication
in 1962 that could be added to the myotomy.15 In 1963, Toupet de-
scribed a partial posterior fundoplication.
At the beginning of the 1990s, minimally invasive techniques
were introduced for the treatment of esophageal diseases. The first
laparoscopic cardiomyotomy was performed by Cuschieri in 1991.16
In 1992, Pellegrini et al described the outcomes of myotomy per-
formed through a lef t thoracoscopic approach, showing excellent
results in about 90% of patients.17 However, it soon became evident
that the procedure led to abnormal gastroesophageal reflux in 60%
of patients.18 Their findings determined a switch to a laparoscopic
approach combined with a partial fundoplication.19 In 1993, Ancona
et al repor ted the technique of a laparoscopic esophageal myotomy
and Dor fundoplication developed at the University of Padua.20
The same year the laparoscopic and open approach were compared
showing that, while the outcomes were similar, the minimally in-
vasive approach was associated with a shorter hospit al stay, less
post-operative discomfort, and faster return to regular activities.21
Finally, at the end of 20th century, the laparoscopic Heller myotomy
(LHM) with fundoplication became the standard of care worldwide
(Table 1).
3.2 | Laparoscopic Heller myotomy
The treatment of esophageal achalasia is palliative, and it focuses
on decreasing the outflow resistance of the GEJ caused by the dys-
functional LES. LHM has been the gold standard therapy for most
esophageal achalasia patients.29, 30 SAGES guidelines describe it as a
safe and low-risk treatment method for resolving symptoms and im-
proving quality of life.31 This statement is based on strong evidence
showing excellent and durable results. 27,31,32,33
The evolution of achalasia treatment clearly shows that a fundo-
plication is required to prevent postoperative GERD.34,35 In 2003,
Falkenback et al presented data from a prospec tive randomized
trial in 20 open Heller myotomy patients comparing those with and
without total fundoplication, at more than 3-year follow-up.36 By pH
monitoring evaluation, they documented pathologic GER in 13.1%

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of patients with no fundoplication and 0.15% in the fundoplication
group. In addition, Richards and colleagues,23 in a prospective and
randomized double-blind trial with 6-month follow-up, proved the
superiority of LHM and anterior partial fundoplication versus LHM
alone in terms of postoperative GER, by reporting 47.6% pathologic
reflux after LHM alone, and only 9% after LHM with Dor fundopli-
cation. Campos et al,37 in a large meta-analysis, showed a higher rate
of pathologic postoperative GER in patients after LHM alone versus
LHM with fundoplication (32% vs 9%). These findings helped confirm
that a fundoplication is necessary to control pathologic GER after
myotomy.
Determining whether to perform a total or partial fundoplication
was not clear from the start. Topart et al,38 in a 10-year follow-up
evaluation of patients after LHM with total fundoplication, showed
that 82% of the patients had recurrence of symptoms. In contrast,
Rossetti et al39 described excellent outcomes regarding dysphagia
symptoms relief in more than 90% of patients, showing no patho-
logic GER at mean follow-up of 83 months. In 2008, Rebecchi and
Year Author Importance
1991 Shimi et al16 Dr Cuschieri's group from the University of D undee in
United Kingdom performed the first laparoscopic Heller
myotomy
1992 Pellegrini et al17 Dr Pellegrini from the University of California described
the new technique of thoracoscopic Heller myotomy and
performed the first minimally invasive cardiomyotomy in
the USA
1993 Ancona et al20 The group from the University of Padua in Italy was f irst to
report the technique of laparoscopic Heller myotomy with
Dor fundoplication.
1995 Ancona et al21 Randomized trial comparing outcomes of laparoscopic and
open Heller myotomy demonstrating the benefits of a
minimally invasive approach
1998 Pat ti et al18 A comparison of thoracoscopic and laparoscopic Heller
myotomy indicating high rate of postoperative reflux in
patients after myotomy without fundoplication
1999 Patti et al19 Study showing long-term outcomes of laparoscopic and
thoracoscopic Heller myotomy indicating that laparoscopic
Heller myotomy with Dor fundoplication should be
considered the treatment of choice
2001 Melvin et al22 First case report of robotically assisted Heller myotomy
2004 Richards et al23 A randomized controlled s tudy that confirmed the
importance of adding an antireflux procedure to
laparoscopic Heller myotomy in order to avoid
postoperative reflux
2006 Torquati et al24 A repor t that conf irmed good long-term outcomes of
laparoscopic Heller myotomy with Dor fundoplication in
terms of symptom control and occurrence of postoperative
reflux
2008 Rebecchi et al25 A randomized controlled trial that compared laparoscopic
Heller myotomy with total and par tial fundoplication
and indicated higher rate of dysphagia s ymptoms after
total fundoplic ation with no significant difference in
postoperative reflux rate
2012 Rawlings et al26 A randomized s tudy demonstr ating the equivalence
of anterior and posterior partial fundoplication after
laparoscopic Heller myotomy in terms of symptom control
and postoperative reflux
2019 Costantini27 A report of 25-y experience at a single surgical center
showing good long-term outcomes of laparoscopic Heller
myotomy with Dor fundoplication
2019 Werner et al28 First randomized controlled trial comparing outcomes of
laparoscopic Heller myotomy with Dor fundoplication and
peroral endoscopic myotomy demonstrating equivalence
of both techniques in symptom control but higher rates of
esophagitis after POEM
TABLE 1 Evolution of Minimally
Invasive Surgery for Esophageal Achalasia

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colleagues25 published data from their prospective randomized trial
comparing the outcome of a LHM with a Dor or Nissen fundoplica-
tion. They found that at 5-year follow-up the postoperative patho-
logic GER ratio was similar in both groups. However, patients after
total fundoplication had increased dysphagia rate when compared
to those after Dor (15% vs 2.8%). Based on these findings, it is clear
that a total fundoplication should not be performed in patients with
achalasia after LHM, and LHM with partial fundoplication should be
the treatment of choice.27
The best type of partial fundoplication (anterior or posterior)
after LHM remains undetermined. A multicenter prospective trial
by Rawlings et al26 indicated that at 1-year follow-up both proce-
dures were equivalent in terms of symptom control and rates of
pathologic GER. Kumagai and colleagues40 compared outcomes of
LHM with Dor and Toupet fundoplication, finding no significant
difference in postoperative pathologic GER and Eckardt score at
1-year follow-up. Since there is no evidence for the superiority
of one type of partial fundoplication over the other, the choice
should belong to the surgeon. Some prefer the partial anterior
Dor fundoplication, which requires limited hiatal dissection and
allows coverage of the exposed mucosa,33,41,42 while others be-
lieve that a partial posterior fundoplication may keep the edges
of the myotomy separated, reducing the probability of recurrent
dysphagia.43,44
3.3 | Technical aspects of LHM
Our technique for a laparoscopic Heller myotomy has been previ-
ously described in the literature.45 It consists of a 8 cm myotomy
extending for 2.5 cm onto the gastric wall and a Dor fundoplication.
3.4 | LHM vs other treatment options
Medical therapy and endoscopic botulin injection have limited effec t
and are indicated for patients who are not fit for other treatment
modalities.46 Other options commonly used are pneumatic dilat ation
(PD) and the peroral endoscopic myotomy (POEM) (Table 2).
In 2015, a large European randomized controlled trial comparing
LHM and PD was published.58 It showed no significant difference in
success rate between the two treatment s, with 8 4% and 82% suc-
cess after 5 years for LHM and PD, respectively. However, 25% of
patients treated with PD required additional dilat ations. It is in fact
known that patients treated with PD eventually require additional
dilatations over time to control the symptoms. This was well shown
in this randomized trial. In 2017, Ehlers et al64 also showed that LHM
was associated with a lower rate of reintervention and readmission.
In 2010, Dr Inoue from Japan described a novel endoscopic tech-
nique – POEM.47 The myotomy was performed endoscopically by
the creation of a long submucosal tunnel (mean length about 12 cm),
followed by transection of the circular fibers for about 8 cm-6 cm on
the esophagus and 2 cm onto the gastric wall. Many retrospective
studies from the United States, Asia, and Europe confirmed the
initial experience, showing excellent relief of symptoms but a very
high rate of post POEM pathologic reflux.65,66,67 Schlottmann et al,61
in a meta-analysis of 54 studies, compared 5834 patients who un-
derwent a LHM with 1958 patients treated with POEM, with an
average follow-up of 24 months. Their study indicated that POEM
was slightly more effective than LHM, since the improvement rate
of dysphagia was described in 92.7% of patients after POEM, and
90.0% of patients from LHM group. However, a signific ant differ-
ence was found in terms of pathologic GER. Ambulatory pH moni-
toring showed pathologic reflux in 48% of patients after POEM, but
in only 11% of patient s after LHM. Esophagitis was present in 22% of
patients after POEM and in 12% after LHM. Kumbhari et al reported
a higher rate of clinical response to POEM in patients with type III
achalasia when compared to LHM with partial fundoplication (98.0%
vs 80.8%).68 The reason for these different outcomes is probably
due to the fact that POEM allows a proximally ex tended myotomy.
At the end of 2019, the result s of a prospective European mul-
ticenter randomized trial comparing 109 patients who underwent
LHM with 112 patients after POEM were published.28 At a 3-month
follow-up, the rate of reflux esophagitis was 20% after LHM but 57%
after POEM. The study indicated the equivalence of the two proce-
dures in terms of symptom relief at 2-year follow-up, which was not
surprising as POEM allows an excellent division of the muscle fibers.
Overall, GER remains a major concern for POEM, particularly since
there are data showing the onset of denovo Barrett's esophagus and
reflux stricture after treatment.69 In addition, in 2019 the first case
of esophageal cancer following POEM was reported.70
In patient s with end stage of achalasia, many exper ts recommend
an esophagectomy as primary treatment.71,72 However, esophagec-
tomy is associated with longer hospitalization, risk of pneumonia,
anastomotic leak, recurrent laryngeal nerve injury, bleeding, chy-
lothorax, and death.72,73 Considering the satisfactory results of a
myotomy, and the high morbidit y and mor talit y associated with an
esophagectomy, LHM should always be considered as the first-line
treatment option even in end-stage achalasia, reserving esophagec-
tomy for patients who have failed other treatment options.
4 | FOLLOW-UP
Achalasia patients have an increased risk of squamous cell cancer
after treatment, usually 10 to 50 times higher than the general popu-
lation.74,75,76 In addition, some studies have shown that adenocarci-
noma can occur after treatment due to pathologic gastroesophageal
reflux77, 78 . Interestingly the group that designed the 2018 ISDE
achalasia guidelines specifically said: “We make no recommenda-
tion about routine endoscopy surveillance or endoscopy intervals
after any treatment”.79 In our center, we do recommend routine EGD
every 3 years or when symptoms recur. Unfortunately, there are no
precise guidelines regarding the timing and frequency of follow-up
EGD after intervention for achalasia. Even the 3-year time frame is
an arbitrary number that most but not all the insurance companies

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TABLE 2 Studies Comparing Different Treatment Modalities for Esophageal Achalasia
Source Year Design Procedures Group size [n] F
Complication rate
[%] LOS [d] Remission rate
Postoperative
GERD
Ancona21 1995 RC LHMD vs OHMD 34 (17 + 17) 6 0% (LHMD) vs 0%
(OHMD)
4 (LHMD) vs 10
(OHMD)
94.2%(LHMD) vs
100%(OHMD)
by pH: 0% (THM) vs
5.8% (OHMD)
Patti19 1999 RC THM vs LHMD/T 168 (35 + 133) 28 8.6% (THM) vs
5.2% (LHMD/T)
3 (THM) vs 2
(LHMD/T)
85% (THM) vs 93%
(LHMD/T)
by pH: 60% ( THM)
vs 17% (LHMD/T)
Richards 23 2004 RCT LHM vs LHMD 43 (21 + 22) 6 0% (LHM) vs 0%
(LHMD)
1 (LHM) vs 1
(LHMD)
LHM = LHMD (P = .79) by pH: 47.6% (LHM)
vs 9.1% (LHMD)
(P = .005)
Horgan48 2005 RC RAHM vs LHMD 121 (59 + 62) 18 0% (RAHM) vs
16% (LHMD)
1.5 (RAHM) vs
2.2 (LHMD)
92% (RAHM) vs 90% (LHMD)
(P = .5)
symptoms: 17%
(RAHM) vs 16%
(LHMD) (P = .9)
Mikaeli49 2006 RCT PD vs EBTI + PD 54 (27 + 27) 12 0% (PD) vs 0%
(EBTI + PD)
NA 62% (PD) vs 77% (EBTI + PD)
(P = .1)
NA
Kostic 50 2007 RC T PD vs LHMT 51 (26 + 25) 12 8% (PD) vs 0%
(LHMT)
0 (PD) vs 3
(LHMT)
77% (PD) vs 96% (LHMT)
(P = .0 47)
NA
Rebecchi25 2008 RCT LHMD vs LHMN 144 (72 + 72) 60 97% (LHMD) vs
85% (LHMN)
3.2 (LHMD) vs
3.6 (LHMN)
LHMD > LHMN (P = .001) symptoms: 5.6%
(LHMD) vs 0%
(LHMN)
by pH: 2.8% (LHMD)
vs 0% (LHMN)
(P > .05)
Bakhshipour51 2009 RCT EBTI + PD vs PD 34 (16 + 18) 12 0% (EBTI + PD) vs
0% (PD)
NA 87.5% (EBTI + PD) vs. 55.5%
(PD) (P = .53)
NA
Novais52 2010 RCT PD vs LHMD 94 (4 + 47) 3 4% (PD) vs 0%
(LHMD)
NA 73.8% (PD) vs 88.3% (LHMD)
(P = .08)
by pH: 31% (PD)
vs 4.7% (LHMD)
(P = .001)
Boeckxstaens53 2011 RCT PD vs LHMD 201 (95 + 106) 24 4% (PD) vs 12%
(LHMD)
NA 86% (PD) vs 90% (LHMD)
(P = .46)
NA
Rawlings26 2012 RCT LHMD vs LHMT 60 (36 + 24) 12 5.6% (LHMD) vs
8.3% (LHMT)
NA LHMD = LHMT (P > .05) by pH: 41.7%
(LHMD) vs 21.1%
(LHMT) (P = .152)
Shaligram54 2012 RC RAHM vs LHM vs
OHM
2683 (149 + 2116
+ 418)
1 4.02% (R AHM)
vs 5.19% (LHM)
vs 9.08%
(Open-HM)
2.42 (RAHM) vs
2.70 (LHM) vs
4.42 (OHM)
NA NA
Borges55 2014 RCT PD vs LHMD 92 (48 + 44) 24 4% (PD) vs 0%
(LHMD)
NA 54% (PD) vs 60% (LHMD)
(P = NS)
by pH: 27.7% (PD)
vs 4.7% (LHMD)
(P = .003)
(Continues)

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Source Year Design Procedures Group size [n] F
Complication rate
[%] LOS [d] Remission rate
Postoperative
GERD
Hamdy56 2015 RCT PD vs LHMD 50 (25 + 25) 12 8% (PD) vs 4%
(LHMD)
0 (PD) vs 3
(LHMD)
76% (PD) vs 96%(LHMD)
(P = .04)
symptoms: 28% (PD)
vs 16% (LHMD)
(P = .3)
Persson57 2015 RCT PD vs LHMT 53 (28 + 25) 60 0% (PD) vs 7%
(LHMT)
NA 64% (PD) vs 92% (LHMT)
(P = .016)
NA
Moonen58 2016 RCT PD vs LHMD 201 (96 + 105) 60 5% (PD) vs 11%
(LHMD)
NA 82% (PD) vs 84% (LHMD)
(P = .92)
by pH: 12% (PD)
vs 34% (LHMD)
(P = .14)
Chrystoja59 2 016 RCT PD vs LHMD/T 50 (25 + 25) 60 4.5% (PD) vs 13%
(LHMD/T)
NA 77% (PD) vs 100% (LHMD/T ) by pH: 10% (PD)
vs 0% (LHMD/T)
(P = .49)
Tor res -
Villalobos60
2018 RCT LHMD vs LHMT 73 (38 + 35) 24 2.6% (LHMD) vs
0% (LHMT)
2.54 (LHMD) vs
2.54 (LHMT)
100% (LHMD) vs 90%
(LHMT)
by pH: 10.5%
(LHMD vs 31.5%
(LHMT) (P = .111)
Schlottmann61 2018 M LHM vs POEM 7792 (5834 + 1958) 24 NA POEM (+1.03 d)
>LHMD
92.7% (POEM) vs 90% (LHM)
(P = .01)
by pH: 11.1% (LHM)
vs 47.5% (POEM)
(P < .0001)
EGD: 11.5% (LHM)
vs 22.4% (POEM)
(P < .0001)
Ponds62 2019 RCT POEM vs PD 133 (67 + 66) 24 0% (POEM) vs 2%
(PD)
NA 92% (POEM) vs 5 4% (PD)
(P < .001)
by EGD: 41%
(POEM) vs 7% (PD)
(P = .002)
Costantini63 20 19 CCS POEM vs LHMD 240 (140 + 140) 24 5% (POEM) vs
2.1% (LHMD)
2 (POEM) vs 3
(LHMD)
99.3% (POEM) vs 97.1%
(LHMD) (P < .12)
by pH: 38.4%
(POEM) vs 17.1%
(LHMD) (P < .01)
by EGD: 37.4%
(POEM) 15.2%
(LHMD) (P < .05)
Werner28 2019 RCT POEM vs LHMD 221 (109 + 112) 24 2.7% (POEM) vs
7.3% (LHMD)
POEM = LHMD
(95% CI,
−0.12-0.63)
83% (POEM) vs 81.7%
(LHMD) (P = .007 for
noninferiority)
by pH: 30% (POEM)
vs 30% (LHMD)
by EGD: 44%
(POEM) and 29%
(LHMD) (95% CI
1.03-3.85)
Abbreviations: CCS, case control study; EBTI, endoscopic botulin toxin injection; EGD, esophagogastroduodenoscopy; F, months of follow-up; LHM, laparoscopic Heller myotomy; LHMD, laparoscopic
Heller myotomy with Dor fundoplication; LHMD/T, laparoscopic Heller myotomy with Dor or Toupet fundoplication; LHMN, laparoscopic Heller myotomy with Nissen fundoplication; LHMT, laparoscopic
Heller myotomy with Toupet fundoplication; LOS, length of stay; M, meta-analysis; N A, dat a nonavailable; OHM, open Heller myotomy; OHMD, open Heller myotomy with Dor fundoplication; PD,
Pneumatic dilation; pH, pH-monitoring; POEM, peroral endoscopic myotomy; RAHM , robotically assisted Heller myotomy; RC, retrospective cohort; RCT, randomized controlled trial; THM, thor acoscopic
Heller myotomy.
TABLE 2 (Continued)

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accept. Some insurance companies will allow an EGD only if a patient
has recurrent symptoms.
5 | TREATMENT ALGORITHM FOR
ACHALASIA MANAGEMENT
POEM and LHM are equally effective and should considered in
every patient with achalasia. In our center, we do perform LHM
for patients with type I and t ype II achalasia. These patients are
often over weight and have a hiatal hernia so that the addition of a
fundoplication allows control of reflux in most patients. In patients
with type III achalasia, POEM should be considered as initial treat-
ment. In case of failure, we recommend PD as the second step
therapy. If pneumatic dilatation fails, it is reasonable to consider
POEM for those who underwent LHM initially and LHM for those
after POEM. Esophagectomy should be considered as a last resort
for patients with persisting symptoms after failure of other treat-
ment modalities.
DISCLOSURE
Conflict of Interests: Authors declare no conflict of interests for this
article.
ORCID
Kamil Nurczyk https://orcid.org/0000-0002-1855-0401
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How to cite this article: Nurczyk K, Patti MG. Surgical
management of achalasia. Ann Gastroenterol Surg. 2020;4:
34 3–351. https://doi.org/10.1002/ags3.12344