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factors are suspected to be implicated in these changes, including
but not limited to proportion of visceral body fat, intra-abdominal
pressure, dietary composition (high-fat diet), changes in gastrointestinal hormonal levels (leptin, ghrelin, GLP-1), and diabetes
mellitus [3, 4]. Changes in the microbiome are also being studied
for their potential role in altered function of the GI tract in obese
patients, but appear to play a more signicant role in the distal
portions [5]. In this chapter, we will focus on these interactions as
it pertains to the anatomic and physiologic integrity of the esophagus and stomach.
R. Lamm and F. Palazzo
Esophagus
Esophageal peristalsis and functionality of the lower esophageal
sphincter (LES) have been suspected to be altered in obese and
morbidly obese patients for several years [6]. Kuper etal. in 2009,
using traditional manometric testing, identied morbidly obese
patients as having dysfunction of the LES and altered esophageal
motility, even in the absence of GERD symptoms [6].
The advent of high-resolution manometry (HRM) and the
methodological classication of esophageal dysmotility disorders
with the Chicago Classication allow for more reliable ndings
with reproducible/consistent nomenclature [3].
Esophageal Dysmotility
While there are numerous factors responsible for the onset of dysmotility disorders, obesity has been implicated in the dysfunction
at numerous critical portions of normal esophageal peristalsis (see
Fig.3.1).
Esophageal dysmotility is common in morbidly obese patients.
Utilizing HRM, Kristo etal. found that the prevalence of esophageal motility disorders, as classied by the Chicago algorithm,
was 34% among obese patients [7]. In this study, a signicant
proportion of the disorders were outow obstruction and a novel
hypercontractile disorder, which they referred to as jackhammer
esophagus. These ndings mirrored previous studies, which found
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Fig. 3.1 High-resolution manometry (HRM) and the effects of morbid obesity. UES upper esophageal sphincter, LES lower esophageal sphincter
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Fig. 3.2 Increased transdiaphragmatic pressure causing hiatal hernia. UES
upper esophageal sphincter, LES lower esophageal sphincter
high rates of dysmotility, specically hypercontractile abnormalities, in obese patients [8, 9].
The presumed mechanism of esophageal dysmotility arises
from the increased pressure from excess adipose tissue
characteristic of obese patients [7]. This creates a gradient, which
exceeds the normal force from the intra-abdominal cavity and
intra- thoracic cavity, a phenomenon referred to as increased transdiaphragmatic pressure (TP) (see Fig.3.2). The increased pressure opposes the forward-owing peristalsis, which may cause
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compensatory increases in contractile forces resulting in dysmotility or simply disrupting the natural peristalsis. More evidence needs to be elucidated for the exact mechanism. However,
some speculate esophageal motility derangements are secondary
to the measurable changes in LES pressure, presence of hiatal hernias, and increased gastric pressure, all of which are discussed
later in this chapter.
The increasing use of bariatric surgery with the potential
impact that some of the more common procedures (sleeve gastrectomy) may have on esophageal motility makes it critically
important for clinicians and patients to have a better understanding of esophageal motility of morbidly obese patients at baseline.
There is evidence that a variety of dysmotility disorders can
occur after or as a result of bariatric surgical procedures [10].
These are described in dedicated chapters later in this manual
(Chaps. 27, 29, 41, and 42).
R. Lamm and F. Palazzo
Integrity oftheLower Esophageal Sphincter (LES)
Perhaps the most profound of the effects of obesity is its alteration of the lower esophageal sphincter (LES) and the implications of those alterations. Normal resting pressure at the LES is
10–26mmHg [11]. During swallowing, LES pressure initially
rises to 45mmHg and then slowly relaxes to the resting pressure
over 2–3s [11]. LES length, dened as the distance between the
upper and lower borders of LES, is usually in the range of
3–4cm in healthy adults [12]. This pressure and length are adequate to protect the esophagus from reuxing acid produced in
the stomach.
In obese patients, due largely to the increased transdiaphragmatic pressure, LES resting pressure and length are both signicantly decreased. HRM LES resting pressures in obese patients
are signicantly decreased, measuring ≤6mmHg [13–18]. Jung
etal. showed that obesity also contributes to LES length shortening to ≤1cm [19]. Both of these contribute to the breakdown of
protection from esophageal reux from the stomach, resulting in
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gastroesophageal reux disease (GERD) and its sequelae. This
problem is so prevalent in the obese patient population that when
studied Klaus etal. found that patients with obesity were twice as
likely to have mechanically defective LES complexes as compared
to healthy adults [13]. Besides resting LES pressures, one study
found that there were independently increased LES relaxations in
obese patients during the postprandial phase [6]. Consequently,
the prevalence of LES disruption is evident in the obese patient
population.
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Integrity oftheHiatal Crura
As alluded to earlier, obesity increases transdiaphragmatic pressure (TP) both at rest and during strain. We have described in the
previous section the impact this has on the contractility of the
esophagus. In addition, chronically increased TP can result in
macroscopic anatomic changes to the diaphragmatic crura resulting in the development of a hiatal hernia. A hiatal hernia is dened
as the migration of the LES and/or stomach and, in some cases,
additional intra-abdominal organs, normally located below the
diaphragm through the hiatus in the diaphragm and above the diaphragm [20].
Rates of hiatal hernias in patients having a BMI ≥ 30 vary
based on the modality of diagnosis with up to 23% being diagnosed on esophagogastroduodenoscopy (EGD) [20] and 40% on
upper gastrointestinal (UGI) contrast studies [21]. Data from preoperative bariatric EGD studies have found hiatal hernias in up to
52% of patients with BMI ≥ 30 [22, 23]. Evidence shows that
higher TP is directly correlated with increasing BMI and waist
circumference [13, 24]. Most current data illustrate correlative
data between obesity and hiatal hernia occurrence. However,
recent models in dogs show that the presence of increased abdominal pressure increased the diameter of the hiatal opening in the
diaphragm, and esophageal shortening can disrupt the integrity of
the LES/crura and force the foregut into the chest causing the
migration or hernia [25] (see Fig.3.2).
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R. Lamm and F. Palazzo
Stomach
Some of the obesity-related factors that play a key role in inducing changes to the esophageal function—TP—also have an impact
on the stomach. Higher intra-abdominal pressure increases intragastric pressure, which contributes to gastric contents physically
crossing the EGJ [14, 26] and contributes to the propulsion of the
stomach from the intra-abdominal cavity into the intra-thoracic
cavity [21]. However, there are a few stomach-specic pathophysiologic changes worth noting in the obese population.
Regulation ofAppetite
Ghrelin is an orexigenic hormone produced by endocrine cells in
the stomach after stimulation by the vagus nerve causing an
increase in appetite [27]. Obesity has been shown to be correlated
with higher levels of ghrelin, proposed to be the result of altered
stimulation from the vagus nerve in obese patients [27–29]. The
overall effect is appetite stimulation, increased intake, and weight
gain. This is supported by the fact that, in most bariatric procedures, the exclusion of the fundus results in decreased ghrelin
secretion, which contributes to weight loss [29]. In addition, studies have shown decreased satiety and feelings of fullness correlated with altered appetite-regulating hormone pathways, which
include feedback from the stomach in obese patients [30].
Gastric Size andMotility
Obesity also affects the size and function of the stomach itself.
One large study involving >500 patients showed that obese
patients had larger fasting gastric volume [31]. In addition, some
studies have shown that patients with obesity have larger stomachs on ultrasound, CT scan, and at direct visualization at the time
of surgery [32]. These data were correlated with a delayed feeling
of satiety, as well as increased levels of hunger leading to higher
consumption [31].
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Gastric motility appears to be altered in obesity as well. The
overall effect of obesity on motility is controversial and likely
multifactorial. On one hand, some studies have observed increased
gastric emptying times in obese patients, which is believed to contribute to late satiety [31] and could very well predispose to
increase gastroesophageal reux. On the other hand, diabetes
mellitus (DM) contributes to decreased contractility via gastroparesis, which is thought to arise from damage to the vagus nerve
[33]. Krishnasamy etal. found that 20–50% of diabetic patients
suffer from gastroparesis [34]. Likely, both of these pathologic
states exist simultaneously and the overall effect is different for
each patient. To complicate things further, evidence exists to suggest an even stronger role of hormonal regulation on motility than
previously thought [35].
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Obesity asaRisk Factor forDened Pathologic
States
Gastroesophageal Reux Disease (GERD)
All of the aforementioned alterations in anatomy and physiology help contribute to an overall increased acid/alkaline exposure of the esophagus in the obese patient. Herbella et al.
showed that BMI was independently associated with the severity of GERD and that in most morbidly obese patients with
GERD, reux occurred despite normal or hypertensive esophageal motility [36]. Obese patients have a threefold increase in
total acid exposure events (dened as a number of times at
which pH<4 at LES) [37, 38]. This relationship has also been
shown to be reversible with weight loss both via lifestyle modications and bariatric surgery [39]. In other words, a portion
of GERD in obese patients can be attributed to increased transdiaphragmatic pressure; however, the majority of obese
patients have a pathophysiology completely independent of
isolated LES dysfunction (which argues against traditional
anti-reux surgery being effective in this patient population).
The pathologic effect of GERD is exacerbated by the fact that
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esophageal dysmotility, present in many obese patients, is
associated with decreased acid clearance, which increases total
acid exposure time [24].
R. Lamm and F. Palazzo
Barrett’s Esophagus (BE)
Linked to higher rates of GERD, perhaps the most consequential
physiologic change IN the foregut associated with obesity is
Barrett’s esophagus (BE). BE is the metaplastic change in mucosal cells lining the lower portion of the esophagus from stratied
squamous to simple columnar epithelium, a premalignant condition [40].
Studies have shown that while the rate of BE in the non-obese
population is close to 1.2%, it can reach as high as 9% in obese
patients [40, 41]. Other studies have shown that in obese women,
every 5kg/m2 increase in BMI leads to a 35% increase in the incidence of BE [39].
While all of the aforementioned mechanisms of increased acid
exposure contribute to this higher incidence of BE in obese
patients, other theories including decreased sensitivity to acid
exposure in obese patients leading to longer exposure times have
been proposed, also called silent reux [42].
Esophageal Adenocarcinoma (EAC)
With increased levels of BE reported in the obese population, it is
no surprise that higher levels of esophageal adenocarcinoma
(EAC) also exist as BE is a signicant risk factor for the development of EAC [43, 44] and cancers of the esophageal body and
stomach cardia [39].
Recent studies have also proposed that the local microbiome of
the foregut created by obesity and the hormonal changes it creates
could be a contributing factor leading to EAC; however, more
research into the topic is required [5].
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Conclusion
As the prevalence and incidence of obesity continue to steadily
increase, consideration of the effects of this disease on the anatomy and physiology of the foregut will become essential in health
care going forward. Clinicians caring for these patients will need
to be able to utilize a broader set of diagnostic tools and consider
more complex pathophysiologic pathways than those that are
accepted for non-obese patients. While preventive care for obesity, in the form of lifestyle modications, remains the gold standard for treating physicians, bariatric surgery to treat obesity and
reverse the pathophysiology discussed above is increasing in
popularity.
Foregut surgeons who want to properly and comprehensively
care for this patient population will need to embrace the importance of bariatric surgical options in the care of some of the disorders traditionally approached with standard—and likely
ineffective in obese patients—anti-reux procedures.
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