Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 566 - файл
.pdf
16 Endoscopic Evaluation oftheBariatric Surgery Patient
https://t.me/medicina_free
76. Lennon AM, Kapoor S, Khashab M, etal. Spiral assisted ERCP is equivalent to single balloon assisted ERCP in patients with Roux-en-Y anatomy. Dig Dis Sci. 2012;57:1391–8.
77. Shah RJ, Smolkin M, Yen R, et al. A multicenter, U.S. experience of
single- balloon, double-balloon, and rotational overtube assisted enteroscopy ERCP in patients with surgically altered pancreaticobiliary anatomy
(with video). Gastrointest Endosc. 2013;77:593–600.
78. Ceppa FA, Gagne DJ, Papasavas PK, et al. Laparoscopic transgastric
endoscopy after Roux-en-Y gastric bypass. Surg Obes Relat Dis.
2007;3:21–4.
79. Martinez J, Guerrero L, Byers P, etal. Endoscopic retrograde cholangiopancreatography and gastroduodenoscopy after Roux-en-Y gastric
bypass. Surg Endosc. 2006;20:1548–50.
80. Schreiner MA, Chang L, Gluck M, et al. Laparoscopy-assisted versus
balloon enteroscopy-assisted ERCP in bariatric post-Roux-en-Y gastric
bypass patients. Gastrointest Endosc. 2012;75:748–56.
81. Baron TH. Approaches to ERCP in patients with Roux-en-Y gastric
bypass anatomy. Gastroenterol Hepatol (N Y). 2019;15(11):622–4.
233
Part IV
https://t.me/medicina_free
Foregut Motility Disorders
Achalasia
https://t.me/medicina_free
17
LuisSerrano, JoelRichter,
ChristopherDuCoin,
andAbdul- RahmanFadiDiab
Case Presentation
A 30-year-old female presents to the ofce with progressive dysphagia to solids and liquids for the past 6 months. She describes
food “sticking” in her mid-chest area and complains of heartburn
and food regurgitation after eating. She reports a 28-pound weight
loss over the last 6 months and has been seeing a psychologist for
an “eating disorder” for the past year. She recently saw a gastroenterologist who performed an upper endoscopy and noted a
L. Serrano
HCA Florida Osceola Surgical Care Specialists, Kissimmee, FL, USA
e-mail: luis.serrano@hcahealthcare.com
J. Richter · C. DuCoin (*) · A.-R. F. Diab
Division of Gastrointestinal Surgery, Department of Surgery, University
of South Florida Morsani College of Medicine, Tampa, FL, USA
e-mail: jrichte1@usf.edu; cducoin@usf.edu; abduldiab@usf.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_17
237
238
https://t.me/medicina_free
mildly dilated esophagus and difculty traversing the esophagogastric junction. The gastroenterologist has now ordered a timed
barium swallow (TBS) and a high-resolution manometry (HRM).
What do we expect to see on TBS and HRM? What are our treatment options?
L. Serrano et al.
Introduction
Achalasia is an esophageal motility disorder characterized by failure of the lower esophageal sphincter (LES) mechanism to relax
and by disruption of the peristaltic mechanism of the body of the
esophagus. Both conditions need to be present to conrm the
diagnosis of achalasia. In addition, these symptoms must not be
related to other structural or mechanical causes [1]. Achalasia is
an uncommon disease that can often be challenging to diagnose
and can pose a long and at times frustrating diagnostic process for
both the physician and the patient. The reported annual incidence
is 1in 100,000, and the disease has a prevalence of 10 per 100,000
[2, 3]. Achalasia is equally distributed between men and women.
It has a bimodal distribution with most patients diagnosed between
the ages of 20–40 and 60–70; however, it can also be seen in children [4].
Pathophysiology
Several theories exist that attempt to explain the origin of achalasia; however, no clear explanation has yet to be proven. The fact
that it is uncommon in siblings and that it manifests later in life
suggests external sources as a possible triggering agent for the
development of achalasia. Concepts of viral infections and autoimmune causes have been studied with no consistent evidence to
explain the origins of achalasia. As of now, achalasia remains as
an idiopathic condition [5].
The normal anatomic function of the esophagus is to allow a
food bolus to pass from the oropharynx to the stomach. The bolus
moves through the esophagus which transitions from proximal
17 Achalasia
https://t.me/medicina_free
239
skeletal to distal smooth muscle and traverses both the upper
(UES) and the lower esophageal sphincters (LES). These sphincters act as toned muscle that functions to prevent gastric contents
from reuxing back into the esophagus and thus preventing aspiration. The muscular function of the esophagus is controlled by
the myenteric plexus which contains inhibitory and excitatory
neurons. In patients with achalasia, there is a functional loss of the
nitric oxide (NO) secreting inhibitory neurons in the myenteric
plexus. This loss results in the inability of the LES to relax and
failure of peristalsis in the esophageal body [6].
Clinical Presentation
Achalasia presents with a variety of signs and symptoms. The most
common clinical complaints are dysphagia, regurgitation, chest pain,
and some degree of weight loss. Less common symptoms include
epigastric pain, heartburn, and respiratory symptoms secondary to
aspiration of regurgitated food and saliva. Patients can present with a
single symptom or multiple symptoms. Dysphagia can be for both
liquids and solids; however, solids are usually affected rst, and then
liquids become affected. Dysphagia is caused by failed propulsion of
food bolus due to lack of peristalsis and inability of the LES to relax.
Heartburn symptoms are related to either retained acidic food in the
distal esophagus or to food undergoing the process of fermentation in
the esophagus. Physical exam adds little value to the clinical picture;
nonetheless, a focused exam can help rule out other conditions that
can mimic achalasia as cancer [6].
The Eckardt score is a fast and simple scale (Table17.1), that
aids in making the diagnosis of achalasia and in assessing the
Table 17.1 Eckardt score
Score Dysphagia Regurgitation Chest pain Weight loss (kg)
0 None None None None
1 Occasional Occasional Occasional <5
2 Daily Daily Daily 5–10
3 Every meal Every meal Every meal >10
240
https://t.me/medicina_free
severity of the disease. It is also a tool that can be used clinically
to assess the effectiveness of treatments. It consists of four
components addressing degrees of dysphagia, regurgitation,
chest pain, and weight loss in kilograms (kg). Each category can
receive a score of 0–3 for a maximum of 12 points. If a patient
has a score of more than 4 the diagnosis of achalasia should be
considered [7].
L. Serrano et al.
Diagnostic Workup
If the diagnosis of achalasia is suspected, the workup should
start with a barium swallow where the classic “bird’s beak”
image is seen. We favor the timed barium swallow (TBS) to
increase the diagnostic capability of the radiologic evaluation of
the esophagus, as this test assesses both esophageal anatomy
and upright emptying. To perform a TBS, the patient is given
8ozs of barium in the upright position and lms are obtained at
1- and 5-min intervals (Fig.17.1). At this point, the esophagus is
cleaned of the contrast by drinking water. Lastly, a 13mm barium pill is swallowed and an additional X-ray is obtained 5min
later. The 13mm size has been historically used because 13mm
is the size diameter where esophageal strictures are symptomatic [8]. Retention of the barium tablet at 5min is considered
abnormal as well as a liquid barium column greater than 5cm at
the 1-min interval and 2cm at 5-min interval [9, 10]. A key criteria is liquid retention which shows an 85% accuracy for the
diagnosis of achalasia and hold up of the pill which shows a
100% accuracy in achalasia patients [10].
Esophagogastroduodenoscopy (EGD) is a mandatory workup
for achalasia to aid with the diagnosis and to rule out pseudoachalasia. Pseudoachalasia is dened as an invasive tumor, usually
adenocarcinoma, or an extrinsic compression that mimics the
symptoms and the imaging studies of achalasia. In patients with
achalasia, there can be a wide variety of ndings from normal
esophageal anatomy to a markedly dilated esophagus with
retained food particles on EGD.In addition, increased resistance
can be encountered during passage of the scope through the gas-
17 Achalasia
https://t.me/medicina_free
241
Fig. 17.1 Barium swallow shows a persistently narrowed region at the end
of the esophagus (the lower esophageal sphincter) with a positive bird’s beak
sign and a dilated esophagus above the narrowed region
troesophageal junction, which should alert the endoscopist to the
possibility of achalasia. In some cases, puckering of the GE junction can be appreciated by the endoscopist [11].
EGD and TBS aid in the diagnosis of achalasia; however, the
nal diagnosis is not made until conrmatory high-resolution
manometry (HRM) is performed. HRM is considered the gold
standard in the diagnosis of achalasia. HRM can distinguish
242
https://t.me/medicina_free
Fig. 17.2 High-resolution manometry (HMR) exemplifying the difference
between achalasia types I, II, and III
L. Serrano et al.
between three different types of achalasia [12]. HRM evaluates
the esophageal motility using a catheter with 36 pressure sensors
spaced every 1cm along its length. The catheter is placed into the
nose and advanced into the stomach. Once in place, the patient
completes 10 swallows of 5ml of saline that are then mapped in a
pressure and time chart (Fig.17.2) [13].
During HRM, patients with achalasia will have several characteristics, including failed LES relaxation with swallowing and a
hypertensive LES baseline in about 50% of patients. There are
three subtypes of achalasia based on the ndings of HRM, classied according to the Chicago classication [14]. The combination
of TBS and HRM has been studied and together they increase the
diagnostic accuracy for achalasia to nearly 100% [10].
Chicago Classication
The Chicago classication is the universal method of interpreting
HRM.It was initially published in 2009 and updated in the 2015
consensus to version 3.0 (v3.0). It is important to understand the
parameters reported by HRM.These include the UES, the body of
the esophagus, the LES, and the intrabolus pressure pattern. The
esophageal body is evaluated by both contraction strength and
17 Achalasia
https://t.me/medicina_free
243
peristalsis. Contraction strength is expressed by the distal
contractile index (DCI). A normal DCI is between 450 and
8000mmHg×cm×s. The DCI can be subclassied as failed if
less than 100 mmHg × cm × s, ineffective if 100–
450 mmHg × cm × s or hypercontractile when greater than
8000mmHg×cm×s (Table17.2). Peristalsis is evaluated by the
distal latency (DL), which measures the period from the beginning of the contractile wave to the contractile deceleration point.
LES function is expressed by the integrated relaxation pressure
(IRP) and basal pressure (BP) of the LES.Lastly, the intrabolus
pressure pattern corresponds to areas of the esophagus with a
pressure greater than 30mmHg. Based on the manometric ndings, esophageal motility disorders are categorized as either distal
disorders with esophagogastric junction outow obstruction or
major disorders and minor disorders of peristalsis [13, 14].
Achalasia falls into the esophagogastric junction outow
obstruction group. In achalasia, there are two issues with the
esophagus as follows: (1) incomplete relaxation of the LES
expressed as an elevated IRP greater than 15mmHg and (2) some
degree of failed peristalsis. Achalasia is further subdivided into
three categories based on the manometry ndings, specically
based on the type of peristalsis irregularity. Achalasia type I
involves an elevated IRP and 100% failed esophageal contractions. Type II achalasia is the most common type and has an elevated IRP; however, there is panesophageal pressurization in at
least 20% of the swallows. Type III achalasia has similar characteristics of IRP and LES, but there are more than 20% spastic
contractions on swallows (Fig.17.2) [15]. Achalasia can evolve
into stage IV achalasia, also known as sigmoid type or end-stage
achalasia. It consists of a severely enlarged and tortuous esophagus that on imaging resembles a sigmoid colon. There is no mano-
Table 17.2 Distal contractile index (values in mmHg×cm×s)
Failed Ineffective Normal Hypercontractile
<100 100–450 450–8000 >8000
244
https://t.me/medicina_free
metric equivalent for stage IV achalasia; thus, the diagnosis is
made based on descriptive ndings on EGD and barium swallow
rather than manometry [16].
An additional subtype of the EGJ obstructive condition that is
like achalasia but does not meet criteria for achalasia is called
esophagogastric junction outlet obstruction (EGJOO). It is characterized by elevated IRP and failed relaxation of the
LES.However, normal esophageal contractility is preserved [17].
L. Serrano et al.
Treatment
Achalasia cannot be cured. At best treatment is palliative as the
disease persists even after all treatment modalities. It is thus vital
to discuss with patients the goals and expectations regarding treatment and that interventions are not for cure but rather to improve
quality of life and prevent complications such as megaesophagus.
As mentioned above, achalasia encompasses two problems, the
esophagogastric obstruction and the dysmotility of the esophagus.
Currently, there is no treatment for the dysmotility portion of this
disease. Treatments efforts are therefore focused toward the
obstruction of the distal esophagus [4, 17].
Treatment strategies can be medical, endoscopic, and/or surgical. Medical management with calcium channel blockers like
nifedipine or nitrates has shown limited success and is reserved
for patients who cannot tolerate a more invasive approach.
Botulinum toxin injection is a temporary treatment modality
for achalasia. Typically, 100units of botulinum toxin are injected
into four quadrants of LES.This relaxes the LES by blocking the
release of acetylcholine. It is particularly benecial in older
patients that would otherwise not tolerate more invasive procedures [17]. The limitation of botulinum toxin is its short duration
of action with only 3–6 months of symptom relief and limited
success in subsequent injections [16].
Pneumatic dilatation is the most efcient nonsurgical treatment available. Pneumatic dilators are preferentially performed
since they can split the circular bers of the esophagus which
translates into a more effective treatment. Both endoscopic and
Соседние файлы в папке @xirurgi_2025