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33 Eosinophilic Esophagitis
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and the exclusion of other causes of esophageal eosinophilia such
as a parasite infection or allergic vasculitis [16].
Patients with suspected EoE are evaluated by endoscopy.
Characteristic endoscopic ndings of EoE include exudates, mucosal edema, linear furrows, rings, and strictures (Figs.33.1 and 33.2)
Fig. 33.1 Panels (a) and (b) show stacked, circular rights on endoscopy in a
patient with eosinophilic esophagitis giving a trachea-like appearance
Fig. 33.2 Vertical lines termed “linear furrows” (arrow) on endoscopy in a
patient with eosinophilic esophagitis
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T. J. James and N. A. Bildzukewicz
[3, 17]. The stacked, circular esophageal rings give the esophagus
the appearance of a trachea. “Crepe paper esophagus,” where the
esophageal mucosa appears thin and fragile, has also been described
in patients with EoE [17]. An endoscopic reference score (EREFS)
assessing the characteristic endoscopic ndings of EoE has been
developed and validated to standardize diagnosis and grade disease
severity (Table33.1) [17].
During endoscopy, biopsies should be obtained from the proximal, mid, and distal esophagus. The sensitivity of biopsies for
diagnosis of EoE increases with number of biopsies taken, with
sensitivity reaching 100% when ve or more biopsies are obtained
[18, 19]. A threshold of 15 or more eosinophils per high power
eld is required for diagnosis (Fig.33.3) [11].
Contrast imaging is a useful adjunct to endoscopy in the diagnosis of EoE. While not a diagnostic modality alone, barium
esophagography can reveal ring-like stricturing and esophageal
narrowing that may be missed on endoscopy (Fig.33.4) [20].
Table 33.1 The endoscopic reference score (EREFS) classication system
developed by Hirano etal. to standardize EoE diagnosis and disease severity
Grade
0 Grade 1 Grade 2 Grade 3
Exudates None Mild (lesions
involving <10%
of esophageal
surface area)
Rings None Mild (subtle
circumferential
ridges)
Edema Absent Mild (loss of
clarity of vascular
markings)
Furrows Absent Mild (vertical
lines present
without visible
depth)
Strictures Absent Present
Severe (lesions
involving >10%
of esophageal
surface area)
Moderate
(distinct rings
that do not
impair passage
of a diagnostic
endoscope)
Severe (absence
of vascular
markings)
Severe (vertical
lines with
mucosal depth)
Severe (distinct
rings that do not
permit passage
of a diagnostic
endoscope)
ab
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Fig. 33.3 Low-power (a) and high-power (b) view of esophageal mucosa
with increased number of eosinophils in a patient with eosinophilic
esophagitis
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Fig. 33.4 Ring-like stricturing demonstrated on barium esophagogram in a
patient with eosinophilic esophagitis
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T. J. James and N. A. Bildzukewicz
Treatment
Treatment goals of EoE are to control symptoms and decrease
inammation. The three treatment modalities for EoE are diet
modication, medication, and esophageal dilation.
Dietary modication involves elimination of allergenic foods
that can trigger EoE.The original and most comprehensive elimination diet is an elemental (or amino acid based) diet, which eliminates all potential food allergens. Elemental diets are restrictive
and often difcult to follow, thus more selective elimination diets
have been developed for better patient satisfaction and compliance. Two common diets are the “6-food elimination diet” and the
“4-food elimination diet,” selectively eliminating foods that have
been identied as the most commonly allergenic (namely, wheat,
milk, soy, nuts, eggs, and seafood) [21–23]. Allergen testing such
as radioallergosorbent testing, skin-prick testing, and atopy-patch
testing have aided in the development of more personalized elimination diets for patients with EoE [24]. Disease relapse is common upon trigger food reintroduction [25].
Medications for EoE include proton pump inhibitors (PPIs)
and topical glucocorticoids. Patients with EoE were previously
thought to not respond to PPIs, under the assumption that the sole
mechanism of PPI was gastric acid suppression [11]. However,
some patients with EoE were noted to have symptomatic improvement with PPIs, and this population was termed “PPI-responsive
esophageal eosinophilia” [26]. Further research into the mechanisms of PPIs found anti-inammatory effects in addition to acid
suppression, proposing a potential mechanism of treatment in
patients with EoE [27]. Patients with EoE are typically treated
with full-dose PPI and evaluated for symptomatic improvement
after eight weeks. If symptoms persist, patients are considered
refractory to PPI and are trialed with different treatment options.
In addition to PPIs, topical glucocorticoids (GCs) have been
shown to successfully manage symptoms in patients with EoE,
but their use is not yet FDA-approved. Histological response to
GCs in patients with EoE can be seen by decreased eosinophil
counts [28]. The two GCs used for EoE are uticasone and
budesonide. Fluticasone is administered via a metered dose
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inhaler, and budesonide is a swallowed liquid. Patients typically
respond to GCs within several days, but relapse is common when
the treatment is stopped [29]. The dose is titrated while monitoring symptoms to identify a maintenance dose that is individualized to the patient.
Endoscopic dilation is usually reserved for patients who have
failed conservative therapy. Dilation can temporarily relieve
symptoms caused by esophageal remodeling, but it has no effect
on the underlying inammatory process of the disease [30].
Dilation is typically performed gradually over multiple sessions,
limiting each dilation to 3mm due to the risks of mucosal tear
(around 9%) or perforation (around 1%) [31]. Techniques to help
mitigate perforation include assessing for resistance when passing
the endoscope or dilators and subsequently inspecting the esophagus prior to dilation [30]. Patients can experience chest pain and
bleeding after esophageal dilation [30].
Investigational treatments for EoE include monoclonal antibodies against EoE-specic cytokines and prostaglandin D2
receptor antagonists [32, 33].
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Follow-up
EoE is not pre-malignant [34]. Some providers choose to perform
surveillance endoscopy in EoE patients annually to assess treatment response and/or disease progression.
Conclusion
In summary, EoE is a chronic immune disorder characterized by
eosinophil-mediated esophageal dysfunction. EoE affects both
children and adults and can present similarly to GERD.Diagnosis
is made by characteristic endoscopic ndings and >15 eosinophils
per high power eld on esophageal biopsy. Treatment includes
dietary modication to eliminate trigger foods, medication including PPIs and topical glucocorticoids, and endoscopic dilation for
symptom management.
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T. J. James and N. A. Bildzukewicz
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27. Wolf WA, Dellon ES.Eosinophilic esophagitis and proton pump inhibitors: Controversies and implications for clinical practice. Gastroenterol
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28. Konikoff MR, Noel RJ, Blanchard C, etal. A randomized, double-blind,
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32. Hirano I, Dellon ES, Hamilton JD, etal. Efcacy of dupilumab in a phase
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T. J. James and N. A. Bildzukewicz
Paraesophageal Hernias
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34
IsaacR.Kriley, ShaoxuBing,
andRuchirPuri
Introduction
Denition, Incidence, Prevalence, andRisk Factors
Hiatal hernias occur when intraabdominal organs pass through the
esophageal hiatus, which is formed by the right and left diaphragmatic crura. Hiatal hernias are classied as four types: (1) sliding
hernias, in which the GEJ migrates above the diaphragm and the
gastric fundus remains below the diaphragm; (2) the GEJ remains
in its normal anatomic location, but some portion of the gastric
fundus herniates above the diaphragm; (3) both the GEJ and the
gastric fundus herniate above the diaphragm; and (4) hernias that
include organs besides the stomach, such as omentum, colon, or
small bowel [1]. Type I hiatal hernias represent over 95% of hiatal
hernias, while paraesophageal hernias (PEH) account for <5%,
and more than 90% of PEH are type III.The true incidence and
prevalence of PEH are unknown as most are asymptomatic and
never come to clinical attention. Risk factors for PEH include
body mass index, sex, and age [2]. There is a direct relationship
I. R. Kriley · S. Bing · R. Puri (*)
Department of Surgery, UF Health Jacksonville, Jacksonville, FL, USA
e-mail: ruchir.puri@jax.u.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_34
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between increasing body mass index (BMI) and PEH; those with
a BMI greater than 25 kg/m2 have 1.93 odds of having a PEH
compared to people with BMI less than 25 kg/m2. Men are more
likely to have PEH (odds ratio 1.36), and those over 50 years old
are more likely to have PEH (odds ratio 2.17). This chapter
focuses on the evaluation and management of hiatal hernia types
II–IV, PEH.
I. R. Kriley et al.
Etiology
The etiology of paraesophageal hernias is somewhat elusive. The
crura and ligaments of the hiatus have been investigated on microscopic, ultrastructural, and molecular levels for characteristics
associated with PEH.In the elderly, the inferior leaf of the phrenoesophageal ligament is attenuated or absent, which might explain
the prevalence of PEH among older patients [3]. Elastin is an
extracellular matrix protein that allows tissues to be temporarily
deformed and was found to be reduced by 50% in the phrenoesophageal ligament among patients with hiatal hernias [3, 4].
Collagen is a protein that provides strength to tissue. Conicting
results about the quantity of collagen in the phrenoesophageal
ligament have been reported [5, 6]. Supporting the role of collagen in PEH and suggesting a genetic component is the observation of a single nucleotide polymorphism in COL3A1 that is
associated with hiatal hernias among male patients. COL3A1
codes for type III collagen and mutations in the gene cause types
III and IV Ehlers-Danlos syndrome [7]. Though a causative gene
was not identied, a genetic component of PEH is further supported by the observation that 23 of 38 family members over ve
generations in Ireland had radiographic evidence of a hiatal hernia
and the mode of inheritance was autosomal dominant [8].
Structural deciencies of the crura have been observed by light
and electron microscopy among patients with hiatal hernia and
include dilation of the intermyobrillar spaces, swelling of the
sacrotubular structures, focal degeneration of myobrils, extended
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