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15. Aggarwal N, Thota PN, Lopez R, et al. A randomized double-blind
placebo- controlled crossover-style trial of buspirone in functional
dysphagia and ineffective esophageal motility. Neurogastroenterol Motil.
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16. Monrroy H, Cisternas D, Bilder C, etal. The Chicago classication 3.0
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21. Wang D, Wang X, Yao Y, Xiaowen X, Wang J, Jia Y, Hong X.Assessment
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22. Savarino E, Gemignani L, Pohl D, etal. Oesophageal motility and bolus
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A. Banks-Venegoni et al.
Distal Esophageal Spasm
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SarahSamreen andDmitryOleynikov
Introduction
Distal esophageal spasm (DES) is an idiopathic disorder and is
the most frequently studied esophageal motility disorder aside
from achalasia. It used to be commonly known as diffuse esophageal spasm, but in 2003, Sperandio etal. [1] concluded that due to
the limited nature of the disorder, diffuse esophageal spasm is a
misnomer and the name “distal” esophageal spasm is more appropriate. The Chicago classication of esophageal motility disorders has since adopted the new name. Due to the rarity of this
disorder, the true prevalence in the general population is unknown;
however, prevalence is 3–9% in symptomatic patients [2]. The
disorder is most often seen in women and most commonly diag-
S. Samreen
University of Texas Medical Branch, Galveston, TX, USA
e-mail: sasamree@utmb.edu
D. Oleynikov (*)
Department of Surgery, Monmouth Medical Center,
Long Branch, NJ, USA
e-mail: dmitry.oleynikov@rwjbh.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_19
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nosed in the 60s to early 70s age range [3, 4]. This may also be
secondary to delay in diagnosis due to a lack of physician and
public awareness.
Even though the complete neuromuscular physiology is
unclear, it is thought to be caused by an impaired neurologic
inhibitory pathway due to muscular hypertrophy and degeneration of the branches of the vagus nerve. This allows for premature,
repetitive, and simultaneous esophageal smooth muscle contractions [5] most notably in the lower two-thirds of the esophagus.
Another suggested pathway is the impairment of inhibitory innervation secondary to deciency of tissue nitric oxide (NO) [6] once
again leading to simultaneous contractions and possibly abnormal
relaxation of the esophagogastric junction. This is supported by
the fact that healthy subjects administered NO scavenger demonstrate simultaneous contractions in the distal esophagus, which is
reversed by the replacement of NO [7]. Since achalasia has a similar pathophysiologic mechanism, some authors have suggested
that even though uncommon DES may progress to or overlap with
achalasia [8–11]. Some studies employing intraluminal ultrasound or computed tomography (CT) have demonstrated thicker
lower esophageal sphincter (LES) and esophageal smooth muscle
layer in patients with DES [12, 13]. It is unclear if these ndings
are the primary cause or secondary to chronically increased neuronal stimulation.
S. Samreen and D. Oleynikov
Symptoms andDiagnosis
DES can present with various esophageal symptoms that range
widely in severity and frequency. Tutuian etal. [4] demonstrated
the most common symptoms by analyzing 71 patients with a
manometric diagnosis of DES.They found dysphagia to be the
most common symptom (32%), followed by chest pain (22%),
typical GERD symptoms (20%), and atypical GERD symptoms
(13%). When correlated with manometry, dysphagia may be associated with impaired bolus transit, whereas chest pain may be
associated with strong esophageal contraction amplitudes.
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However, patients rarely present with a single symptom and most
commonly have a combination of several symptoms. Thirty percent of the patients may have some weight loss [3] due to modication of dietary habits.
Symptoms are often triggered by ingestion of solids or uids,
emotional stress, or even exertion. Chest pain can radiate to the
back, jaw, bilateral chest, and shoulders and thus can be confused
with cardiac angina. Hence, it is prudent to prioritize cardiac
investigation and rule out more-prevalent and life-threatening cardiovascular disease as the cause of chest pain, before attributing
symptoms to less dangerous and rare disorder like DES [14].
The workup of DES consists of upper endoscopy, pH monitoring, esophageal manometry, and esophagography. Esophageal
manometry is considered the gold standard, especially since the
introduction of high-resolution manometry (HRM). It is important to remember that due to the intermittent nature of DES,
spasm-attributed motility may not always be observed during
esophageal manometry. Hence, a negative study does not always
rule out the diagnosis of DES.
According to the Chicago classication v4.0, a conclusive
manometric diagnosis of DES is dened by premature contractions in more than 20% of swallows, coupled with a normal lower
esophageal sphincter pressure [15]. Premature contractions are
indicated on manometry as low distal latency (DL) of <4.5seconds, in the setting of a DCI greater than 450 mmHg.s.cm. DL is
dened as the time between the swallow- induced upper esophageal sphincter relaxation and the contractile deceleration point
(CDP) in the distal esophagus where propagation velocity slows
down [16].
Barium esophagram may demonstrate a “corkscrew” or “rosary
bead” pattern of simultaneous contractions, sometimes also
referred to as pseudodiverticulosis. This is caused by tertiary contractions indicating advanced disease. However, these ndings are
neither specic nor sensitive and are not necessary for diagnosis.
Upper endoscopy performed at the initial evaluation allows the
exclusion of mechanical obstruction, esophageal stenosis, or
esophagitis [6]. Twenty-four- or 48-h pH monitoring should be
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considered in patients having regurgitation or heartburn to exclude
GERD.
S. Samreen and D. Oleynikov
Treatment
There is no standardized treatment algorithm for DES.This is due
to the rarity of the diagnosis and a lack of clinical trials as well as
a lack of understanding of the underlying pathology of the disease. Symptom control is the main focus of treatment. The rst
step is to eliminate trigger foods or drinks from the diet. Proton
pump inhibitors (PPIs) and histamine receptor blockers are used
for patient’s complaining of GERD, which has the potential to
induce spasm. Peppermint oil has smooth muscle relaxing properties and has emerged as a potential treatment for patients with
dysphagia and non-cardiac chest pain [17, 18].
Smooth muscle relaxants may be effective in providing symptomatic relief in some cases. Nitrates cause smooth muscle relaxation through an increase in tissue NO. While not tested in a
controlled fashion, nitrates have shown manometrically to prolong the DL without an effect on the distal contraction amplitude
[7]. Phosphodiesterase-5 inhibitors work by blocking the breakdown of NO controlled by cyclic guanosine monophosphate,
leading to the reduction in the esophageal contractile amplitude
[19]. However, the high cost and lack of insurance coverage are a
barrier to the use of phosphodiesterase-5 inhibitors. Calcium
channel blockers are another drug therapy used in the management of DES, but the use is limited by side effects. Since visceral
hypersensitivity can be a major driver of symptoms, tricyclic antidepressants are effective at relieving chest pain in patients with
esophageal motility disorders [20–22].
Botox injection is currently the best-studied treatment in
patients with DES [23]. Botulinum toxin causes muscle relaxation
by inhibiting the release of acetylcholine from cholinergic neurons at the neuromuscular junction. Vanuytsel et al. [24] per-
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formed a prospective, double-blind, randomized controlled trial
comparing Botox injection vs. saline in patients with DES and
nutcracker esophagus. They gave botulinum toxin into the esophageal body above the esophagogastric junction and demonstrated
reduced symptoms, as well as stabilized unintentional weight loss
in those treated with botulinum toxin. Even though botox injections appear effective, the effect is temporary and there is concern
over complications. However, complications occur at a low rate of
7.9% and seem to be mild consisting mainly of chest pain, heartburn, and epigastric pain, except for one patient that had a fatal
case of mediastinitis after botox injection [25].
Esophageal dilation has a limited role in the management of
DES.Pneumatic dilation has been reported to have some success,
but it is unclear if the patients could have been more properly
categorized as spastic achalasia [26]. Also, pneumatic dilation has
a risk for esophageal perforation.
Peroral endoscopic myotomy (POEM) has emerged and shown
promise in the treatment of DES. It is especially effective for
achieving a long myotomy that is essential to prevent any spastic
remnants. However, the procedure can be technically challenging
due to hyperactive spastic contractions during the procedure [27].
Studies also seem to suggest that the success rates for POEM are
higher in classic achalasia than in patients with DES [28, 29].
Considering that patients with DES are usually older than patients
with achalasia, the fact that POEM is minimally invasive appears
attractive. The risks associated with POEM procedure include
bleeding, mucosal tears, pneumothorax, pneumo-peritoneum, and
worsening GERD [2]. Still, the results are favorable and continued research is needed.
Heller myotomy is a well-established treatment for achalasia.
However, its role in the management of DES is debatable at best.
Leconte etal. [30] performed long myotomy and anterior fundoplication on 20 patients with a diagnosis of DES. Dysphagia and
chest pain were signicantly improved in 18 and 20 patients,
respectively, after 50 months of median follow-up. All of these
procedures were performed via laparotomy. With the current
advancement in minimally invasive procedures performed via
either laparoscopy or robotically, newer studies, especially con-
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S. Samreen and D. Oleynikov
trolled trials, are necessary to determine if surgical management
is superior to endoscopic or medical treatment of DES.
Conclusion
In conclusion, accurate diagnosis of this condition is the most
important rst step. Once this is completed, then an escalation of
management should be started with medical management as the
rst step. This is followed by endoscopic management using
Botox and dilation, and then progression to myotomy, either
endoscopic or laparoscopic if the patient is a good candidate.
Because of the chronic nature of DES, these patients require prolonged follow-up in a partnership with gastroenterology and surgery is key in the ultimate symptomatic management of these
patients.
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S. Samreen and D. Oleynikov
Jackhammer Esophagus
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StuartA.Abel andJosephR.Broucek
Introduction
Jackhammer esophagus (JE) is a relatively new diagnosis that has
been distinguished from nutcracker esophagus and diffuse esophageal spasm (DES). JE was rst described in 2012 when esophageal hypercontractility without multipeaked contractions was
noted in association with esophagogastric junction outow
obstruction [1]. The denition of JE was dened more specically
by the Chicago Classication published in 2015 [2].
S. A. Abel (*)
Division of Upper GI and General Surgery, Department of Surgery, Keck
Medical Center of USC, University of Southern California,
Los Angeles, CA, USA
e-mail: Stuart.Abel@med.usc.edu
J. R. Broucek
Division of General Surgery, Department of Surgery, Vanderbilt
University Medical Center, Nashville, TN, USA
e-mail: Joseph.Broucek@vumc.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_20
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