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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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35 Primary Dysphagia: A Case-Based Approach to Diagnosis…
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Fig. 35.1 Picture of
classic achalasia barium
swallow with bird’s beak
appearance. Image
courtesy of James
Callaway, MD
485
ing persistence of a column after 5 min. Following the barium
swallow, further testing is indicated in the form of an esophagogastroduodenoscopy to assess for pseudoachalasia and
high- resolution manometry to conrm pathologic motility. Highresolution manometry provides the gold standard of diagnosis and
is useful for differentiating the types of achalasia from one another
(Fig.35.2) [2]. The Chicago Classication for diagnosis of achalasia includes an IRP >15 and the absence of peristalsis in type I
achalasia.
Clinical Vignette continued: The patient undergoes highresolution manometry which demonstrates an IRP of 19 and
absence of peristalsis consistent with type I achalasia. The patient
undergoes an EGD demonstrating retained food particles in the
esophagus as well as LA grade B esophagitis. The EGD passes
through the LES with some difculty and characteristic “pop”
through the distal esophagus.
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Fig. 35.2 HRM of type I achalasia. Image courtesy of James Callaway, MD
M. W. Romine and A. D. Parmar
Treatment for achalasia includes surgical and nonsurgical
interventions. Nonsurgical options include use of botox injections
at the lower esophageal sphincter and endoscopic dilation.
Surgical interventions include a laparoscopic Heller myotomy
and per oral endoscopic myotomy (POEM) [3].
The denitive treatment of type I achalasia is Heller myotomy
or POEM.Both procedures are safe and provide excellent palliation of symptoms [4]. The choice of procedure to perform includes
patient preference, equipment and technical ability to perform
POEM, and degree of esophagitis. All POEM patients should be
consented for the possibility of conversion to a laparoscopic
Heller myotomy as complications may arise during POEM.
Clinical Vignette conclusion: The patient elects to undergo
POEM for treatment of her type I achalasia. She is discharged
home on postoperative day 1 with improvement in her symptoms
on a pureed diet. She returns to the clinic three weeks later reporting continued improvement in her swallowing function with no
further dysphagia symptoms.
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487
Case 2
Clinical Vignette: A 63-year-old female presents to the emergency
department after experiencing squeezing chest pain during dinner
in which she was drinking red wine. She reports the pain was so
severe that she regurgitated undigested food. The pain is midsternal, and she reports the pain resolved spontaneously shortly after
arrival to the emergency room. She reports similar episodes of
pain in the past which resolved quickly and were less intense. Her
past medical history is notable for hypertension, anxiety, depression, and gastroesophageal reux disease. Family history is notable for a grandmother who had a myocardial infarction at age 66.
A cardiac work-up in the emergency department is negative.
While drinking a cold glass of water in the emergency room, she
begins having the same pain again.
This patient has classic symptoms of both angina and diffuse
esophageal spasm (DES). Differentiating diffuse esophageal
spasm from angina can be challenging for clinicians and patients
alike, as the symptoms and patient population can be similar
between the two diagnoses. Pain from DES can be quite intense,
substernal and can last anywhere from several minutes to several
hours. However, in contrast to classic angina, the pain with DES
typically resolves spontaneously. DES is also typically identied
in patients between the ages of sixty to eighty, who may also be at
risk for cardiac disease. Ultimately, based on this signicant overlap in clinical symptoms, all patients with these symptoms should
be promptly evaluated for myocardial infarction, especially in
those with established cardiac risk factors.
In the above patient, there are several historical features that
are suggestive of an esophageal, and not cardiac, etiology. In prior
instances of the patient’s pain, her pain began following the ingestion of food and/or drink. Classic triggers of DES include ingestion of hot and cold substances as well as alcoholic beverages; in
particular, red wine. For this patient, she has additional comorbidities of gastroesophageal reux disease, anxiety, depression,
and hypertension, all of which predispose her to DES.Finally, this
patient’s history of regurgitation of food during or after the
episode of pain is another clinical feature that is suggestive of
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M. W. Romine and A. D. Parmar
DES.These associations with enteral intake would be atypical of
cardiac disease and is also a useful distinguishing clinical symptom between DES and hypercontractile (jackhammer) esophagus.
Clinical Vignette continued: Suspecting an esophageal disor-
der, a barium swallow is obtained as seen in Fig. 35.3.
Diagnostic evaluation of DES is typical for the work-up of
other esophageal motility disorders. A barium swallow is the most
useful rst test, followed by high-resolution manometry (HRM).
The barium swallow in Fig.35.3 demonstrates the classic “corkscrew” or “rosary bead” appearance seen in patients with diffuse
esophageal spasm. While this barium swallow demonstrates the
classic appearance, less than 5% of patients will have these
ndings on barium swallow [5]. The Chicago Classication crite-
Fig. 35.3 Barium
esophagram
demonstrating
corkscrew appearance
classically seen in
Diffuse Esophageal
Spasm. Image courtesy
of James Callaway, MD
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489
ria for the diagnosis of DES includes a normal IRP and a shortened distal latency (≥20% of swallows are premature, for
example, distal latency <4.5 s). Figure35.4 demonstrates the clas-
sic HRM ndings of DES.A screening esophagogastroduodenoscopy should also be performed to rule out malignancy, take
biopsies if indicated, and evaluate for other pathology.
The mainstay of treatment of DES is medical management,
with surgical intervention rarely required. Agents used include
calcium channel blockers, phosphodiesterase inhibitors, and
Fig. 35.4 Classic HRM ndings of diffuse esophageal spasm. Image courtesy of James Callaway, MD
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botox. Treatment of underlying or associated conditions such as
reux and anxiety can also aid in the treatment of DES.Surgical
therapy such as POEM for DES is reserved for medically refractory disease, but there are few long-term studies documenting the
durable effect of surgical therapy on DES [6].
Clinical Vignette conclusion: The patient undergoes HRM conrming DES. She is subsequently started on calcium channel
blockers and a proton pump inhibitor with improvement in her
symptoms.
M. W. Romine and A. D. Parmar
Case 3
Clinical Vignette: A 74-year-old male with Parkinson’s disease
for the last 5 years presents to the clinic with complaints of difculty swallowing. He reports it is difcult to initiate a swallow
and feels a lump in the back of his throat with swallowing. He has
associated symptoms of coughing and an unintentional weight
loss of 15 pounds. He has been hospitalized for pneumonia within
the past month. Currently, he lives in a nursing home.
Dysphagia is a relatively common problem in the elderly with
an estimated prevalence of greater than 30% in nursing home
patients [7]. The initiation of swallowing is a complex process,
involving the coordination of greater than 30 muscles of the oropharynx and neck. Understanding the components of the swallowing process is critical to characterizing disorders of swallowing.
Briey, the swallowing process is broken down into three components: (1) the oral preparation phase, (2) the pharyngeal phase,
and (3) the esophageal phase [8]. Oropharyngeal dysphagia is a
broad term that encompasses a large variety of disease conditions
affecting phases one and two of the swallowing process.
This patient has difculty transferring food from the oral cavity to the pharynx and a globus sensation than can be characteristic symptoms of oropharyngeal dysphagia. Other symptoms of
oropharyngeal dysphagia include odynophagia, coughing, and a
choking sensation. Clinicians should be aware that globus sensation can be a diagnosis on its own, but has specic diagnostic
criteria including the sensation of a nonpainful lump or foreign
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491
body within the throat in the absence of other esophageal motility
disorders, GERD, or anatomical abnormality [9]. Patients frequently localize symptoms to the throat. Symptoms can occur
with both solids and liquids and usually occur with most swallowing attempts. In severe cases, patients may need to extend their
neck to aid with bolus transfer or digitally insert the bolus into
their throat.
Oropharyngeal dysphagia can begin in the oral preparation
phase. The oral phase involves bolus preparation in the swallow
process and involves chewing and bolus formation with the hard
palate and tongue. As this phase is the voluntary phase in the
swallowing process, a wide variety of conditions can affect this
phase of swallowing. Disease processes such as poor dentition,
cerebrovascular disease affecting voluntary mastication and neuromotor function, inability to produce saliva, and disease conditions resulting in oropharyngeal mucosal breakdown can all affect
the oral preparation phase.
The pharyngeal phase is largely reexive and involves complex neuromuscular coordination to propel the bolus into the
pharynx, relax the upper esophageal sphincter, and elevate the larynx to thereby close at the epiglottis to prevent aspiration. As this
is a complex neuromuscular event, neuromuscular diseases tend
to affect the pharyngeal phase. This patient’s history of Parkinson’s
disease places him at risk for disorders with the pharyngeal phase
of swallowing. Amyotrophic lateral sclerosis (ALS), myasthenia
gravis, and other neurodegenerative diseases can affect the pharyngeal phase of swallowing. Mechanical obstructions such as
tumors, osteophyte formation, and diverticular formation affect
this phase as well.
As the differential diagnosis of oropharyngeal dysphagia is
quite broad, the work-up and management varies based on the
etiology. A careful history can help guide the work-up. The presence of a globus sensation, odynophagia, halitosis, coughing, gagging, timing of symptoms in relation to a meal, and regurgitation
is strongly suggestive on history to be related to oropharyngeal
dysphagia. In addition, a past medical history of cerebrovascular
or neurodegenerative disease should raise the specter of this disease.
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M. W. Romine and A. D. Parmar
Clinical Vignette: Based on this patient’s history of Parkinson’s
and symptoms, he undergoes videouoroscopy to assess for swallowing abnormalities. This conrmed oropharyngeal dysphagia
with aspiration.
The initial work-up of oropharyngeal dysphagia should include
videouoroscopy due to the ability to observe a dynamic swallow
from oropharynx to the stomach. Videouoroscopy can evaluate
for silent aspiration, presence of failed swallows, and help guide
the need for further testing. Fiberoptic endoscopic evaluation of
swallowing (FEES) is also helpful in evaluating oropharyngeal
dysphagia but is more invasive. FEES can detect aspiration,
impairment of pharyngeal swallowing, and evaluate for mechanical obstructions or mucosal lesions that may affect swallow function. Treatment of oropharyngeal disease varies depending on the
underlying etiology, thus making accurate diagnosis the most
important part of the management process.
Clinical Vignette: Ultimately, due to the progressive nature of
his Parkinson’s disease, the patient underwent placement of a
percutaneous endoscopic gastrostomy tube for feeding access and
nil per os to help prevent future aspiration events.
References
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2015;313(18):1841. https://doi.org/10.1001/jama.2015.2996.
2. Vaezi MF, Pandolno JE, Yadlapati RH, Greer KB, Kavitt RT.ACG clini-
cal guidelines: achalasia. Am J Gastroenterol. 2020;115(9):1393–411.
https://doi.org/10.14309/ajg.0000000000000731.
3. Kahrilas PJ, Bredenoord AJ, Fox M, etal. The Chicago classication of
esophageal motility disorders, v3.0. Neurogastroenterol Motil.
2015;27(2):160–74. https://doi.org/10.1111/nmo.12477.
4. Werner YB, Hakanson B, Martinek J, etal. Endoscopic or surgical myot-
omy in patients with idiopathic achalasia. N Engl J Med.
2019;381(23):2219–29. https://doi.org/10.1056/NEJMoa1905380.
5. Almansa C, Heckman MG, DeVault KR, Bouras E, Achem SR.Esophageal
spasm: demographic, clinical, radiographic, and manometric features in
108 patients: esophageal spasm features in 108 patients. Dis Esophagus.
2012;25(3):214–21. https://doi.org/10.1111/j.1442- 2050.2011.01258.x.
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6. Filicori F, Dunst CM, Sharata A, et al. Long-term outcomes following
POEM for non-achalasia motility disorders of the esophagus. Surg
Endosc. 2019;33(5):1632–9. https://doi.org/10.1007/s00464- 018- 6438- z.
7. Roy N, Stemple J, Merrill RM, Thomas L.Dysphagia in the elderly: preliminary evidence of prevalence, risk factors, and socioemotional effects.
Ann Otol Rhinol Laryngol. 2007;116(11):858–65. https://doi.
org/10.1177/000348940711601112.
8. Christmas C, Rogus-Pulia N.Swallowing disorders in the older population. J Am Geriatr Soc. 2019;67(12):2643–9. https://doi.org/10.1111/
jgs.16137.
9. Aziz Q, Fass R, Gyawali CP, Miwa H, Pandolno JE, Zerbib F.Esophageal
disorders. Gastroenterology. 2016;150(6):1368–79. https://doi.
org/10.1053/j.gastro.2016.02.012.
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Persistent Dysphagia After
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Prior Anti-Reux Procedure
JenniferF.Preston
andNathanielJ.Soper
Introduction
The incidence of dysphagia following anti-reux procedures is
widely variable in the literature [1]. Dysphagia in the early postoperative period is common and can usually be managed with
dietary modications and allowing time for inammation and
swelling to decrease [2]. Persistent dysphagia, dened as dysphagia that is still present 3 months after an anti-reux procedure, can
have multiple etiologies and requires a calculated, algorithmic
approach to evaluation. In this chapter, we will outline the
approach to evaluation of persistent dysphagia for surgical fundoplication and magnetic sphincter augmentation.
There is limited literature on dysphagia following transoral
incisionless fundoplication (TIF). In fact, persistent dysphagia
following TIF has not been documented in the literature [3–5].
Therefore, TIF will not be included in this chapter as reporting an
evidence-based approach to evaluation is not possible at this time.
36
J. F. Preston (*) · N. J. Soper
College of Medicine Phoenix, University of Arizona, Phoenix, AZ, USA
e-mail: Jennifer.preston@bannerhealth.com; Sopern@email.arizona.edu
© 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_36
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