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28 Normal Physiologic Findings After Esophageal Myotomy
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in their study “Dor vs Toupet Fundoplication After Laparoscopic
Heller Myotomy: Long-Term Randomized Controlled Trial
Evaluated by High-Resolution Manometry”, compared the ndings of esophageal manometry for two groups of patients postmyotomy. Group A had Dor fundoplication while group B had
Toupet fundoplication. Their ndings showed that the “integrated
relaxation pressure” (IRP) and basal lower esophageal sphincter
(LES) pressure were within normal parameters in both groups at
6 and 24months. Early on, specically at the very rst month, the
IRP was signicantly higher (p<0.001) in Dor (9.78±4.20mmHg)
compared to that Toupet (5.91± 3.04 mmHg). At 6–24months,
however, there was no statistically signicant difference between
the two groups. A similar pattern was found for the basal LES
pressure at 1month and at 6–24 months [13]. In none of these
scenarios, patients showed symptoms of concern. On the other
hand, POEM was reported to have signicant improvement of
LES relaxation pressure and enhanced esophageal bolus clearance as measured by HRM over 1–12month period post- myotomy
[14].
Recurrence of dysphagia might be a sign of stricture, incomplete myotomy, or recurrence. Manometry would differentiate
among all three by indicating an increase in IRP and failure of
LES to relax. In cases of an incomplete myotomy, the patients
might experience short-term symptomatic relief or no relief. This
will be accompanied with an unsatisfactory postoperative IRP
results, classically >10mmHg.
391
Esophageal pH Study andEndoscopic Findings
Post-Myotomy
It was shown in different studies that in short-term follow-up,
POEM is non-inferior and, in some case, even potentially more
effective than LHM in relieving dysphagia. The downside of
POEM is that it was associated with a higher incidence of postoperative gastroesophageal reux [15].
Using esophageal pH studies, it was found that acid exposure
was signicantly higher among patients who underwent POEM
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A. A. Karam and M. Al Mahroos
compared to those who underwent LHM.The percentage of acid
reux reported was up to 48% in POEM vs 14% in
LHM. Interestingly, this was reported for all the parameters
encountered including total reux time, upright reux, supine
reux, postprandial reux and DeMeester scores [16]. Regardless
of the degree of reux observed in pH studies, in most cases, it
was not clinically signicant gastroesophageal reux disease
(GERD). The recent Lyon consensus indicates that the diagnosis
of GERD requires more objective endoscopic ndings such as
severe esophagitis, long segment of esophageal mucosa with
intestinal metaplasia or stenosis, or the time of esophageal acid
exposure is >6% of the time studied through the 24-h pH monitoring [17].
A meta-analysis done by Repici A. etal. found that the average
rate of esophagitis post-POEM was found to be 35% during the
rst 2 years. However, the majority of cases (92%) had mild
esophagitis, while only minority of cases were considered moderate to severe [16]. In contrast, esophagitis post-LHM, regardless
of severity, was found to be approximately 7.6%, and the majority
were classied as mild (48.5%) [18].
The lack of anti-reux procedure in POEM is thought to be the
primary cause of the increase in the incidence of acid exposure to
esophageal mucosa. However, the clinical implication of such
higher reux incidence appeared to be less relevant. When performing POEM, the peri-esophageal anti-reux barriers like suspensory ligaments and angle of His are preserved which can help
reduce incidence of clinically signicant GERD afterwards.
References
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and survival. A population-based study. Neurogastroenterol Motil.
2010;22:e256–61.
2. Zhong C, Tan S, Ren Y, Lü M, Peng Y, Fu X, Tang X.Quality of life following Peroral endoscopic myotomy for esophageal achalasia: a systematic review and meta-analysis. Ann Thorac Cardiovasc Surg.
2020;26:113–24.
28 Normal Physiologic Findings After Esophageal Myotomy
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3. Townsend CM, Beauchamp RD, Evers BM, Mattox KL.Sabiston textbook of surgery: the biological basis of modern surgical practic. 20th ed.
Philadelphia, PA: Elsevier Saunders; 2017. p.1015–8.
4. Barker JR, Franklin RH.Heller's operation for achalasia of the cardia. A
study of the early and late results. Br J Surg. 1971;58(6):466–8.
5. Korean Society of Neurogastroenterology and Motility. 2019 Seoul consensus on esophageal achalasia guidelines. J Neurogastroenterol Motil.
2020;26(2):180–203.
6. Yoo C, Levine MS, Redfern RO, etal. Laparoscopic Heller myotomy and
fundoplication: ndings and predictive value of early postoperative radiographic studies. Abdom Imaging. 2004;29(6):643–7.
7. Rubesin S, E, Mary Kennedy BA, Levine MS, Rosato EF, Laufer I.Distal
esophageal ballooning following Heller myotomy. Radiology.
1988;167(2):345–7.
8. Gockel I, Rabe SM, Niebisch S. Before and after esophageal surgery:
which information is needed from the functional laboratory. Visc Med.
2018;34(2):116–2.
9. Rieder E, Dunst CM, Kastenmeier AS, Makris KI, Swanstrom
LL. Development and technique of per oral endoscopic myotomy
(POEM) for achalasia. Eur Surg. 2011;43(3):140–5.
10. Harmath C, Horowitz J, Berggruen S, etal. Fluoroscopic ndings postperoral esophageal myotomy. Abdom Imaging. 2015;40:237–45.
11. Pannu D, Yang D, Abbitt PL, Draganov PV.Prospective evaluation of CT
esophagram ndings after peroral endoscopic myotomy. Gastrointest
Endosc. 2016;84:408–15. https://doi.org/10.1016/j.gie.2016.02.022.
12. Townsend CM, Beauchamp RD, Evers BM, Mattox KL.Sabiston textbook of surgery: the biological basis of modern surgical practice. 20th ed.
Philadelphia, PA: Elsevier Saunders; 2017. p.1015–8.
13. Torres-Villalobos G, Coss-Adame E, Furuzawa-Carballeda J, et al. Dor
vs Toupet fundoplication after laparoscopic Heller myotomy?: long-term
randomized controlled trial evaluated by high-resolution manometry. J
Gastrointest Surg. 2018;22:13–22.
14. Teitelbaum EN, Soper NJ, Santos BF, etal. Symptomatic and physiologic
outcomes one year after peroral esophageal myotomy (POEM) for treatment of achalasia. Surg Endosc. 2014;28:3359–65.
15. Schlottmann F, Luckett DJ, Fine J, Shaheen NJ, Patti MG.Laparoscopic
Heller myotomy versus peroral endoscopic myotomy (POEM) for achalasia: a systematic review and meta-analysis. Ann Surg. 2018;267:451–
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16. Repici A, Fuccio L, Maselli R, etal. GERD after per-oral endoscopic
myotomy as compared with Heller’s myotomy with fundoplication: a
systematic review with meta-analysis. Gastrointest Endosc.
2018;87(4):934.e18–43.e18.
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17. Gyawali CP, Kahrilas PJ, Savarino E, etal. Modern diagnosis of GERD:
the Lyon consensus. Gut. 2018;67:1351–62.
18. Sanaka MR, Thota PN, Parikh MP, et al. Peroral endoscopic myotomy
leads to higher rates of abnormal esophageal acid exposure than laparoscopic Heller myotomy in achalasia. Surg Endosc. 2019;33:2284–92.
A. A. Karam and M. Al Mahroos
Part V
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Pathology/Symptom Based
Barrett’s Esophagus:
https://t.me/medicina_free
AReview ofCurrent
29
Literature
JustinEagleston, LaurenYoder,
andKshitijKakar
Introduction
The denition of Barrett’s esophagus (BE) is “the condition in
which metaplastic columnar epithelium replaces the stratied
squamous epithelium that normally lines the distal esophagus and
predisposes to cancer development” [1–5]. The change in epithelium to columnar is a consequence of continued and recurrent
esophageal epithelial injury, most commonly from gastroesophageal reux disease (GERD) (Fig.29.1).
J. Eagleston
Trihealth Good Samaritan Hospital, Cincinnati, OH, USA
Carolinas Medical Center, Charlotte, NC, USA
L. Yoder
Trihealth Good Samaritan Hospital, Cincinnati, OH, USA
e-mail: lauren_yoder@trihealth.com
K. Kakar (*)
Trihealth Bethesda North Hospital, Cincinnati, OH, USA
© 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_29
397
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Fig. 29.1 Epithelial injury as a result of GERD as seen on endoscopy
J. Eagleston et al.
History
Norman Barrett is credited for identifying reux changes within
the distal esophagus in 1950 [6]. However, his initial description
was that of peptic ulcers and belief that the stomach had herniated
through the esophageal hiatus and the mucosal change was actually normal stomach epithelium. Looking back in history we nd
that Albers in 1839 also identied peptic ulcer disease within the
esophagus [6]. It was in 1948 that Allison described several types
of hiatal hernias. At the time, it was believed that esophageal
ulcers were due to a congenital shortening of the esophagus.
However, Allison believed that a short esophagus was actually
acquired due to sliding hiatal hernias causing incompetence of the
gastric cardia and resulting in recurrent gastric reux. In 1950,
Barrett described circumferential and longitudinal strictures of
the distal esophagus associated with reux esophagitis [6]. In
1953, Allison and Johnstone described a segment of columnar
29 Barrett’s Esophagus: AReview ofCurrent Literature
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399
epithelium lining the esophagus between the squamocolumnar
junction and the stomach in an article titled “The Oesophagus
Line with Gastric Mucous Membrane” [7]. This description of
gastric mucosa within the esophagus was thought to be heterotopic and not normal, but it was not understood that this change
was acquired and metaplastic. In this paper, Barrett’s ulcers are
described as chronic esophageal ulcers within the gastric mucosa
of the esophagus. These ulcers were more likely to bleed and/or
perforate than peptic ulcers of the esophagus. Additionally, one
patient died of gastric cancer and there is a description of cardiac
mucosa within the esophagus with goblet cells. Later in 1957,
Barrett wrote “The Lower Esophagus Lined by Columnar
Epithelium.” It was this paper where he suggests the term “columnar epithelium”, but the etiology was still thought to be congenital
and due to “the result of a failure of the embryonic lining of the
gullet to achieve normal maturity.” [8]. By dening the columnar
epithelium within the esophagus, Barrett’s ulcers were then
known as Barrett’s esophagus. By the 1960s, Barrett and Allison
recognized that the columnar epithelium was due to gastric reux.
In 1961, Hayward wrote an editorial describing the transformation of squamous into columnar epithelium and felt this was metaplastic [9]. The important aspects of this paper are as follows: (1)
He denes the esophagogastric junction anatomically, as the end
of the tube (2). He advocates for eliminating the vague anatomic
term “cardia.” (3) He recognizes that during normal swallowing
the mucosa can slide approximately 2cm (4). He proposes that
columnar epithelium between the squamous and oxyntic mucosa
was a normal and necessary transition to protect between the acidproducing gastric mucosa and the esophageal squamous mucosa.
This location was determined to be the “junctional” epithelium. In
patients with reux it was noted that the junction became more
proximal due to the acid causing injury to the squamous epithelium which then would heal in a metaplastic fashion. Hayward
felt the proximalization of the junctional mucosa had the following implications: (1) Carcinoma of the cardia should be considered an esophageal cancer variant (2). Reux injury leads to the
proximalization of the junctional epithelium and this is not congenital ectopic tissue (3). Congenital ectopic tissue should involve
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resection; however, if the tissue was acquired, surgery to correct
reux might lead to regression of the junctional epithelium. In
1970, Cedric Bremner surgically created an incompetent lower
esophageal sphincter causing reux in dogs. This resulted in proof
that the columnar lined esophagus could be acquired and was
related to gastric reux [10]. Back in 1951, Bosher and Tayler
were the rst to describe goblet cells within the columnar esophageal mucosa [11]. In 1952, Morson and Belcher described an
esophageal adenocarcinoma surrounded by intestinal epithelium
with goblet cells [12].
Then in 1976, Paul used esophageal manometry to determine
the location of the lower esophageal sphincter. He then took biopsies of this location and found three different mucosal types: (1)
Specialized columnar epithelium with a villiform surface and
mucous glands, (2) Cardiac mucosa (Hayward’s junctional
mucosa) composed of strictly mucus cells, (3) Gastric fundic epithelium with parietal cells and mucus. If the specialized columnar
epithelium was present, it was always the most proximal and the
most distal was the gastric fundic epithelium [13]. Going forward,
endoscopy became more prevalent and Barrett’s esophagus was
being diagnosed via endoscopy rather than surgical resection.
Biopsies could not differentiate between normal gastric mucosa
and metaplastic esophageal epithelium until deeper biopsies were
taken. The deeper biopsies were able to pick up the dening characteristics of the esophagus (submucosal glands, circular and longitudinal muscularis, and less/lack of serosa).
Initially, in order to avoid a high false positive rate, a minimum
of 3 cm of columnar-lined esophagus was needed to diagnose
Barrett’s esophagus [14]. Endoscopists would not routinely
biopsy the columnar epithelium if it were less than 3 cm, nor
would they biopsy the columnar epithelium in patients without
severe symptoms of GERD [15]. The 3cm rule was challenged by
Spechler in 1994 and his group found 18% rate of intestinal metaplasia in the columnar-lined epithelium [16]. Patients without
signs and symptoms of GERD who had developed the columnar
metaplasia also appeared to be at risk and this was studied by
multiple other investigators [17–19]. Following this discovery, the
concept of short segment <3cm and long segment >3cm Barrett’s
29 Barrett’s Esophagus: AReview ofCurrent Literature
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esophagus was accepted. Barrett’s esophagus then became associated with any increased acid exposure which resulted in Barrett’s
esophagus being diagnostic for pathologic GERD without pH
testing [20]. Lastly, in 1997, Nandurkar standardized the use of
Alcian blue because the stain is able to better identify goblet cells.
After changing to Alcian blue, it was found that 50% of Barrett’s
would have been missed by standard H&E staining [21].
401
Epidemiology/Demographics
The mean age of diagnosis of Barrett’s esophagus is 55years and
Barrett’s is normally discovered during endoscopy [22, 23].
Barrett’s esophagus is two to threefold more common in men than
in women [24]. Approximately 5.6% of adults in the United States
have BE.However, the prevalence of BE in the general population
varies from 0.4% to greater than 20% depending on the population studied and what criteria are used to establish the diagnosis
[25–29]. In Western populations, the prevalence is highest in
Caucasians with Hispanics and Asians being affected at lower
rates and African-Americans being affected the least [30, 31].
Short segment BE is more prevalent than long segment BE [32,
33]. In 1999, Wong studied 889 patients undergoing upper endos-
copy who had biopsies taken at the gastroesophageal junction. He
found that 13.2% of patients had specialized intestinal metaplasia.
He also found the prevalence of short-segment BE to be 6.4% and
long-segment BE to be 1.6% [25].
Risk Factors
GERD is an independent risk factor for BE, conferring a vefold
increased risk of the development of Barrett’s at 5-year follow-up
studies [34]. There is debate as to whether a peptic stricture
increases the prevalence of BE; however, the prevalence of intestinal metaplasia appears to be similar in patients with and without
a stricture [35]. Obesity, and specically central obesity, is another
risk factor for GERD as well as BE [36, 37]. Patients with a BMI
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