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134
Fig. 12.4 Developing the
retroesophageal window
using blunt dissection. A
Penrose drain can be used
for anterior retraction of
the esophagus once this
window is fully developed
Fig. 12.5 Running
horizontal mattress closure
of the hiatus
K. R. Chhabra and C. N. Paranjape
However, there are no large, multicenter randomized trials of mesh versus primary
repair, and no robust trials comparing the results of various types of mesh. We use
mesh selectively based on the mobility of the crura and for defects >5cm. When
using mesh, biologic material (such as Phasix ST or Bio-A, at our center) is preferred over permanent to reduce the risk of erosion into the esophagus (Fig.12.6).
Following hiatal closure, a fundoplication is typically performed. We perform
fundoplication by placing a marking suture 6cm lateral and 6cm caudal to the angle
of His (Fig.12.7). A 54 Fr bougie is then passed through the esophagus into the
stomach. The surgeon passes their left hand posterior to the esophagus, then brings
the fundus with the marking suture through this space to perform a shoeshine
maneuver (Fig.12.8). If the patient has normal esophageal manometry, we perform
12 Robotic Paraesophageal Hernia Repair
Fig. 12.6 Absorbable
mesh is used selectively to
reinforce the posterior
hiatal closure
Fig. 12.7 A marking
suture placed 6cm lateral
and 6cm distal to the
Angle of His can facilitate
creating a fundoplication
135
a loose and oppy Nissen fundoplication. If the patient’s motility is abnormal or
unclear, we perform a partial (Toupet) fundoplication. A recent meta-analysis indicated that fundoplication in the setting of paraesophageal hernia repair may be associated with reduced recurrence of GERD (relative risk [RR] 0.64, p=0.07) and
paraesophageal hernia (RR 0.53, p= 0.06), although these results did not reach
statistical signicance.16 We often perform a gastropexy suture to further anchor the
stomach in the abdomen.
We perform a completion endoscopy at the conclusion of every case. We pay particular attention to the ease of the scope’s passage through the lower esophageal sphincter, as well as the appearance of the fundoplication on retroexed view. We also perform
a transversus abdominus plane (TAP) block under laparoscopic visualization.
136
Fig. 12.8 Shoeshine
maneuver prior to
completing the
fundoplication
K. R. Chhabra and C. N. Paranjape
Postoperative Care
Postoperatively patients are allowed a clear liquid diet on postoperative day zero
with the following exceptions: no carbonation, no gelatins, no chewing gum, no
straws, and no caffeine. Patients are typically discharged home on the day of surgery or the day afterward on a full liquid diet for 2weeks. We continue proton pump
inhibitors for 2weeks after surgery then attempt to wean them in the outpatient
setting. We routinely measure gastrointestinal quality-of-life scores in the preoperative and postoperative setting, including the GERD-HRQL and Eckardt scores.
Patients are also encouraged to work with a registered dietician preoperatively and
postoperatively to optimize diet choices.
References
1. Kim J, Hiura GT, Oelsner EC, et al. Hiatal hernia prevalence and natural history on noncontrast CT in the Multi-Ethnic Study of Atherosclerosis (MESA). BMJ Open Gastroenterol.
2021;8(1):e000565. https://doi.org/10.1136/bmjgast- 2020- 000565.
2. Stylopoulos N, Gazelle GS, Rattner DW. Paraesophageal hernias: operation or observation?
Ann Surg. 2002;236(4):492–501.
3. Kohn GP, Price RR, DeMeester SR, etal. Guidelines for the management of hiatal hernia. Surg
Endosc. 2013;27(12):4409–28. https://doi.org/10.1007/s00464- 013- 3173- 3.
4. Markar SR, Menon N, Guidozzi N, etal. EAES Multidisciplinary Rapid Guideline: systematic
review, meta-analysis, GRADE assessment and evidence-informed recommendations on the
surgical management of paraesophageal hernias. Surg Endosc. 2023;37(12):9013–29. https://
doi.org/10.1007/s00464- 023- 10511- 1.
5. Mungo B, Molena D, Stem M, Feinberg RL, Lidor AO.Thirty-day outcomes of paraesophageal hernia repair using the NSQIP database: should laparoscopy be the standard of care? J Am
Coll Surg. 2014;219(2):229–36. https://doi.org/10.1016/j.jamcollsurg.2014.02.030.
6. Kooiker P, Monnett S, Thompson S, Richmond B. Robotic-assisted versus laparoscopic
repair of type II, III and IV hiatal hernias: a retrospective study comparing adverse outcomes.
Laparosc Endosc Robot Surg. 2023; https://doi.org/10.1016/j.lers.2023.12.004.
12 Robotic Paraesophageal Hernia Repair
7. O’Connor SC, Mallard M, Desai SS, etal. Robotic versus laparoscopic approach to hiatal
hernia repair: results after 7 years of robotic experience. Am Surg. 2020;86(9):1083–7. https://
doi.org/10.1177/0003134820943547.
8. Nocera F, Wilhelm A, Schneider R, etal. Robot-assisted vs. laparoscopic repair of complete
upside-down stomach hiatal hernia (the RATHER-study): a prospective comparative single
center study. Br J Surg. 2021;108(Supplement_4):znab202.001. https://doi.org/10.1093/bjs/
znab202.001.
9. Ma L, Luo H, Kou S, etal. Robotic versus laparoscopic surgery for hiatal hernia repair: a
systematic literature review and meta-analysis. J Robot Surg. 2023;17(5):1879–90. https://doi.
org/10.1007/s11701- 023- 01636- 5.
10. Watson DI, Thompson SK, Devitt PG, etal. Five year follow-up of a randomized controlled trial
of laparoscopic repair of very large hiatus hernia with sutures versus absorbable versus nonabsorbable mesh. Ann Surg. 2020;272(2):241. https://doi.org/10.1097/SLA.0000000000003734.
11. Analatos A, Håkanson BS, Ansorge C, Lindblad M, Lundell L, Thorell A.Hiatal hernia repair
with tension-free mesh or crural sutures alone in antireux surgery: a 13-year follow-up of
a randomized clinical trial. JAMA Surg. 2023; https://doi.org/10.1001/jamasurg.2023.4976.
12. Oor JE, Roks DJ, Koetje JH, etal. Randomized clinical trial comparing laparoscopic hiatal
hernia repair using sutures versus sutures reinforced with non-absorbable mesh. Surg Endosc.
2018;32(11):4579–89. https://doi.org/10.1007/s00464- 018- 6211- 3.
137
Management ofAchalasia: ADisease
Hard toSwallow
MollyBelisle, SanaKhan, NicholasCalvo, AlexLynch,
andAbubakerA.Ali
Introduction
Achalasia originates from the Greek a- (not) khalasis (relaxation), translating to
failure of relaxation [1]. It is a rare esophageal motility disorder characterized by
impaired relaxation of the lower esophageal sphincter (LES) with absent or spastic contractions of the esophagus [2]. Relaxation of the esophageal smooth muscle
is impaired by a loss of inhibitory nerve function of the esophageal myenteric
plexus. The prevailing hypothesis is that of an autoimmune reaction targeting an
unknown antigen within the esophageal myenteric neurons in genetically predisposed patients. This is challenged by ndings that antibodies against myenteric
neurons identied in patients with achalasia do not selectively target esophageal
myenteric neurons and have also been identied in patients with gastroesophageal
reux disease (GERD) [3]. Infectious and degenerative hypotheses have also been
postulated, but no theory has been denitively accepted. The annual incidence of
achalasia is estimated at 1–5 cases per 100,000 individuals [4]. There is no predilection for sex or race. Achalasia can occur at any age, but its incidence and prevalence show an age- related increase, predominantly affecting patients over the age
of 60 [4]. The most common symptoms of achalasia are dysphagia, regurgitation
of undigested food, heartburn, chest pain, and weight loss [2]. The evaluation of a
patient suspected to have achalasia involves the barium esophagram and upper
endoscopy to rule out structural causes of dysphagia and a denitive diagnosis is
made with high- resolution manometry [5]. Endoluminal functional lumen imaging probe (EndoFLIP) measures the dimensions, movement, and pressure inside
the esophagus and can be used as an adjunct to high-resolution manometry for
diagnosis in equivocal cases [6]. Medical and surgical treatments aim to palliate
symptoms of achalasia as there is no curative therapy available. Treatment involves
13
M. Belisle · S. Khan · N. Calvo · A. Lynch · A. A. Ali (*)
Wayne State University, Detroit, MI, USA
e-mail: aaali@med.wayne.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
S. Samreen et al. (eds.), The SAGES Manual of Robotic Surgery,
https://doi.org/10.1007/978-3-031-86927-3_13
139
140
nonsurgical management such as LES botulinum toxin injection and pneumatic
dilation, and surgical management such as per-oral endoscopic myotomy and
laparoscopic Heller myotomy [1].
M. Belisle et al.
Pathophysiology
The esophagus is a muscular hollow tube that transports food from the mouth into
the stomach using gravity and peristalsis. The transfer of food from the esophagus
into the stomach is controlled by the lower esophageal sphincter (LES), a 2–4cm
thickened circular muscle layer at the distal end of the esophagus. The LES prevents
reux of gastric contents back into the esophagus by maintaining a resting sphincter
tone of 10–30mmHg. Relaxation of the LES facilitates passage of food into the
stomach. This is triggered by swallowing and esophageal wall distention that activates nonadrenergic noncholinergic neurotransmitters, most commonly nitric oxide
and vasoactive intestinal peptide (VIP) [3].
Achalasia is characterized by the functional impairment of inhibitory postganglionic neurons in the myenteric plexus ganglion cells of the distal esophagus
and the lower esophageal sphincter [7]. The inciting event is unknown, but is
hypothesized to be autoimmune in nature, possibly triggered by a viral infection.
Individuals with achalasia are more likely to have concurrent autoimmune diseases compared to the general population with an increased prevalence of serum
neural autoantibodies [2]. The progressive degeneration of postganglionic neurons in the distal esophagus is caused by an inammatory response, largely by
T-cell lymphocytes [8]. The inammation of the myenteric plexus impairs the
release of nitric oxide and VIP, resulting in unopposed cholinergic stimulation
that impairs esophageal and LES relaxation while increasing contractility of the
esophagus [2].
Clinical Features
The development of symptoms of achalasia is insidious, with patients typically
experiencing symptoms for years prior to seeking formal evaluation [9]. The most
common symptoms are progressive dysphagia to both solids and liquids, heartburn
from fermentation of carbohydrates in the esophagus, regurgitation of undigested
food, which can be mistaken for vomiting, weight loss, and chest pain [10].
Regurgitation of food while lying at can lead to pulmonary sequelae such as cough
and pneumonia [2]. The Eckardt symptom score (ESS) is a widely used tool in clinical and research settings to evaluate symptom severity by measuring weight loss in
kilograms, chest pain, regurgitation, and dysphagia [11].
Many patients with achalasia are initially misdiagnosed with GERD. The
American College of Gastroenterology recommends a diagnostic workup for achalasia in patients suspected of having GERD who do not respond to acid-suppressive
therapy [5].
13 Management ofAchalasia: ADisease Hard toSwallow
141
Diagnosis
Once achalasia is suspected in patients with the symptoms described above, diagnostic modalities, including the barium esophagram, upper endoscopy, manometry,
and Endoip, can be used to conrm the diagnosis.
Barium esophagram is a complementary study that can show a dilated esophagus
with a classic “bird-beak” appearance of a narrow gastroesophageal junction in latestage disease. Timed barium esophagram (TBE) is a simple and cost-effective study
that can identify aperistalsis and delayed emptying of barium into the stomach,
allowing for the assessment of post-therapy results. A retrospective cohort study by
Blonski etal. used TBE with liquid barium to differentiate untreated achalasia from
other groups of gastroesophageal junction outow obstruction and non-achalasia
dysphagia with a 79.5% predictive accuracy. This accuracy was improved to 100%
using tablet barium. However, they noted that patients with non-achalasia dysphagia
also retained liquid and tablet barium 39.3% of the time [12]. Barium esophagram
is not specic for achalasia and should not be used alone in diagnosis [5].
Upper endoscopy is used to rule out more common structural disorders of the
esophagus, including strictures and neoplastic processes. In patients with achalasia,
upper endoscopy can show a dilated esophagus with retained food products. The
LES can be traversed by the scope with gentle pressure, unlike in cases of esophageal obstruction by stricture or neoplasm [5]. Patients with achalasia have an
increased risk of developing esophageal cancer due to chronic stasis, typically squamous cell type. Those with alarming clinical features such as symptoms of less than
6months duration, elderly patients with new-onset dysphagia, rapid weight loss, or
abnormal endoscopic evaluation raising suspicion for malignancy should undergo
further evaluation with endoscopic ultrasound and ne-needle aspiration [13].
Manometry is used to conrm the diagnosis. Manometry ndings of achalasia
are incomplete relaxation of the lower esophageal sphincter and absence of peristalsis in the distal two-thirds of the esophagus. High-resolution manometry (HRM) has
largely replaced conventional manometry due to superior specicity and is the gold
standard test for diagnosing achalasia [5]. The Chicago Classication is a system
that uses HRM ndings to diagnose achalasia and further divides it into three clinically relevant subtypes that vary in treatment types and response. An elevated
median integrated relaxation pressure, along with failed peristalsis or spasm on
HRM, is consistent with a diagnosis of achalasia. Type I achalasia is characterized
by absent peristalsis and pressurization in the distal esophagus, type II by absent
peristalsis but with panesophageal pressurization, and type III by abnormal peristalsis with premature contraction [14]. Heller myotomy is indicated for type I and II
achalasia, while type III achalasia has shown the best response with peroral endoscopic myotomy. Patients with type II achalasia have the best prognosis with treatment and patients with type III have the worst [1].
The endoluminal functional luminal imaging probe (EndoFLIP) is an adjunctive study that provides a three-dimensional image of the esophageal lumen by
measuring diameter, volume, and pressure changes [15]. It can be used to diagnose achalasia in patients where manometry is inconclusive and intraoperatively
142
to assess treatment results. Upper endoscopy may be required to guide the
EndoFLIP catheter into the stomach if it is unable to be passed through the gastroesophageal junction [16].
M. Belisle et al.
Endoscopic Functional Luminal Imaging Probe (EndoFLIP)
Endoscopic functional luminal imaging probe (EndoFLIP) is a balloon-based catheter that uses impedance planimetry technology to assess the cross-sectional area
and distensibility of any sphincter and has been used to determine esophagogastric
junction (EGJ) geometry, physiology, and pressure in response to volume distension
[17]. A growing body of literature suggests that EndoFLIP can be used in the diagnosis of achalasia and a tool to measure the effectiveness of therapeutic intervention
[16]. Manometry remains the current gold standard to diagnose achalasia; however,
there are times when obtaining accurate manometric results is not possible or the
results do not correlate with patient symptoms. If the EGJ cannot be traversed with
the probe, which can occur in a large hiatal hernia (50%) and achalasia (24%), precise conclusions cannot be determined. Likewise, a large hiatal hernia can show
elevated integrated relaxation pressure (IRP), yet the LES relaxation may not be
impaired, due to the anatomic angulation of the EGJ secondary to the intrathoracic
position of the stomach. Multiple studies have shown that the distensibility index
(DI) in patients with achalasia falls below 1mm2/mmHg, which was supported by
Law etal., who found that patients with DI <0.8 have a 99% probability of having
a diagnosis of achalasia. They also found that values of DI of 0.8–1.3 had a 95%
probability of having achalasia and not a hiatal hernia. Thus, for patients with symptoms of dysphagia and upper endoscopy or esophagram consistent with achalasia,
the EndoFLIP DI value can provide additional conrmation of improvement with
myotomy. Of note, a DI >2.3mm2/mmHg with 30cc in the 8cm balloon was consistent with 99% probability of having a hiatal hernia and DI 1.4–2.2mm2/mmHg
had a 94% probability of having a hiatal hernia and not achalasia [17].
Treatment
Pharmacotherapy
Calcium channel blockers and nitrates are the mainstay medical therapies for achalasia. However, their use is limited due to adverse effects and poor long-term symptom relief. Beta-agonists, anticholinergics, and phosphodiesterase inhibitors have
also shown efcacy in treating achalasia but are not widely used due to poor tolerance. All agents for achalasia are usually taken before meals due to the short duration of relief.
Nitrates release nitric oxide, which leads to smooth muscle relaxation at the
lower esophageal sphincter. Isosorbide dinitrate is the most common agent for achalasia. It transiently improves dysphagia, but its efcacy is limited by tachyphylaxis
13 Management ofAchalasia: ADisease Hard toSwallow
143
and side effects such as headache, palpitations, and dizziness [18, 19]. Calcium
channel blockers inhibit calcium inux into smooth muscle cells, which leads to
smooth muscle relaxation. Nifedipine is the agent of choice and reduces sphincter
pressures but does not alter esophageal emptying. The main side effects are headaches and peripheral edema [18, 19].
Pharmacotherapies are the least effective treatment option for achalasia and
carry a high incidence of adverse effects. Furthermore, there is a lack of high- quality
literature evaluating these agents. Thus, several societies recommend reserving
pharmacotherapy for poor endoscopic or surgical candidates or for patients who
have failed botulinum toxin injection [5, 20, 21].
Endoscopic Treatment
Botulinum Toxin Injection
Botulinum toxin works to decrease LES pressure by inhibiting the presynaptic
release of acetylcholine. A total of 80–100 units of botulinum toxin is injected into
four quadrants at the lower esophageal sphincter. In a meta-analysis, Leyden etal.
showed that 78% of patients treated with a single injection of botulinum toxin injection had initial remission of symptoms. However, 52% were in remission at 6months
and 38% in remission at 12months [22]. Zaninotto etal. injected botulinum toxin
twice 1 month apart, which showed 78% remission at 6months, 60% at 12months,
and 34% at 24months [23]. Botulinum toxin injections have poor long-term efcacy compared to alternative therapies [22, 23]. Thus, its use is limited to patients
who are not candidates for pneumatic dilation or myotomy. Repeat injections are
often required in patients undergoing sole treatment by botulinum toxin injection.
Botulinum toxin injection is well tolerated, with mild side effects occurring in only
8% of procedures. These included transient chest pain and heartburn. Severe complications include acute mediastinitis, but this is rare [24]. There are concerns that
repetitive botulinum injections can result in a brotic reaction that obscures the
submucosal plane and increases the complication rates of future myotomy [25].
However, more recent studies call these concerns into question [26]. While there is
not yet a consensus, some organizations believe that botulinum toxin injection does
not signicantly affect myotomy outcomes [5].
Pneumatic Dilation
Pneumatic dilation is a nonsurgical option for achalasia that functions to dilate the
LES using air pressure, disrupting the sphincter’s circular muscle layer. The procedure can be performed under endoscopic or uoroscopic guidance. There is variability in technique, but typically a 3cm transparent polyethylene balloon is inated
to 10–12psi for 60s. The most serious complication is perforation, which can occur
in 2–4% of patients [27, 28]. These can be managed with observation, covered
stents, or operative intervention depending on the nature of the perforation. Some
advocate limiting its use only to patients who are surgical candidates due to the risk
of perforation and subsequent operation [5]. Symptom remission for a single
144
M. Belisle et al.
pneumatic dilation at 1 year has been reported in the range of 55–90% [23, 27, 28].
Pneumatic dilation is preferred to botulinum toxin injection due to improved longterm efcacy [23]. A randomized control trial by Boeckxstaens etal. showed similar
long-term remission rates at 2, 5, and 10years between pneumatic dilation and laparoscopic Heller myotomy [28–30]. However, 25% of pneumatic dilation patients
required repeat dilation after 5years. Further studies and meta-analyses have demonstrated the noninferiority of pneumatic dilation to laparoscopic Heller myotomy
[31]. Thus, some advocate that either treatment can be used for the initial treatment
of achalasia. However, like botulinum toxin injection, there is concern that scarring
and inammation from pneumatic dilation can complicate future myotomy [32].
Per-oral Endoscopic Myotomy (POEM)
POEM is a hybrid therapy performed under general anesthesia to create a surgical
myotomy. First, the gastroesophageal junction is identied, and then diluted methylene blue is injected 10–15cm proximally. Next, a 1.5cm longitudinal incision is
made on the mucosa to create a submucosal tunnel. A myotomy is then performed
along the circular muscle bers, extending 2–3cm onto the gastric cardia. The
endoscope is then withdrawn and passed through the gastroesophageal junction to
assess the adequacy of the myotomy. Finally, the mucosal incision is closed with
endoscopic clips, endoscopic sutures, or endoscopic stents.
POEM is indicated for patients who are surgical candidates but wish to avoid
surgery or those who failed prior treatments. Patients undergoing POEM achieved
2-year clinical success rates of 80–90% [33, 34]. POEM has been found to be superior to pneumatic dilation for treatment-naive patients [33]. However, Werner etal.
showed similar rates of treatment success for naive patients treated with POEM
compared to laparoscopic Heller myotomy with Dor fundoplication [34]. POEM
can also be used as salvage therapy after the failure of laparoscopic Heller myotomy. Saleh etal. found that patients with recurrent symptoms after laparoscopic
Heller myotomy had 1-year treatment success rates of 62% with POEM compared
to 27% with pneumatic dilation [35]. It should be noted that there are signicantly
increased rates of postoperative GERD associated with POEM compared to other
therapies. Other less common adverse effects include mucosal perforation, pneumomediastinum, pneumoperitoneum, and Candida esophagitis.
Heller Myotomy andIts Evolution
The surgical treatment of achalasia is not a cure; instead, its goal is to enhance the
functionality of the EGJ, facilitating the emptying of the esophageal contents in the
absence of peristalsis [36]. The rst documented treatment of dysphagia was in 1674
with anterograde dilation using a whalebone [37]. It was not until centuries later that
the concept of cardioplasty of the EGJ was rst proposed by Gottstein in 1901. In
1914, Ernst Heller went on to describe an “extramucosal cardioplasty” involving an
anterior and posterior 8cm vertical esophageal myotomy for the treatment of idiopathic dilation of the esophagus. Zaaijer modied this technique using only an