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41. Lee J, Huprich J, Kujath C, etal. Esophageal diameter is decreased in some patients with eosinophilic esophagitis and might increase with top­ical corticosteroid therapy. Clin Gastroenterol Hepatol. 2012;10:481–6.
42. Hirano I, Moy N, Heckman MG, Thomas CS, Gonsalves N, Achem SR.Endoscopic assessment of the oesophageal features of eosinophilic oesophagitis: validation of a novel classication and grading system. Gut. 2013;62:489–95.
43. Dellon ES, Gibbs WB, Fritchie KJ, etal. Clinical, endoscopic, and histo­logic ndings distinguish eosinophilic esophagitis from gastroesophageal reux disease. Clin Gastroenterol Hepatol. 2009;7:1305–13.
44. Gentile N, Katzka D, Ravi K, etal. Oesophageal narrowing is common and frequently under-appreciated at endoscopy in patients with oesopha­geal eosinophilia. Aliment Pharmacol Ther. 2014;40:1333–40.
45. Menard-Katcher C, Swerdlow MP, Mehta P, Furuta GT, Fenton LZ.Contribution of esophagram to the evaluation of complicated pediat­ric eosinophilic esophagitis. J Pediatr Gastroenterol Nutr. 2015;61(5):541–
6.
46. Hejazi RA, Reddymasu SC, Sostarich S, McCallum RW.Disturbances of esophageal motility in eosinophilic esophagitis: a case series. Dysphagia. 2010;25(3):231–7.
47. Aceves SS, Newbury RO, Chen D, et al. Resolution of remodeling in eosinophilic esophagitis correlates with epithelial response to topical cor­ticosteroids. Allergy. 2010;65:109–16.
48. Kuchen T, Straumann A, Safroneeva E, etal. Swallowed topical cortico­steroids reduce the risk for long-lasting bolus impactions in eosinophilic esophagitis. Allergy. 2014;69:1248–54.
49. Moawad FJ, Cheatham JG, DeZee KJ.Meta-analysis: the safety and ef­cacy of dilation in eosinophilic oesophagitis. Aliment Pharmacol Ther. 2013;38:713–20.
50. Ortiz V, Garcia-Campos M, Saez-Gonzalez E, delPozo P, Garrigues V.A concise review of opioid-induced esophageal dysfunction: is this a new clinical entitiy? Dis Esophagus 2018;31(5).
51. Gonzalez ES, Bellver VO, Jaime FC, etal. Opioid-induced lower esopha­geal sphincter dysfunction. J Neurogastroenterol Motil. 2015;21:618–20.
52. Wu SD, Zhang ZH, Jin JZ, etal. Effects of narcotic analgesic drugs on human Oddi’s sphincter motility. World J Gastroenterol. 2004;10:2901–
4.
53. Dorn S, Lembo A, Cremonini F.Opioid-induced bowel dysfunction: epi­demiology, pathophysiology, diagnosis, and initial therapeutic approach. Am J Gastroenterol. 2014;2:31–7.
54. Kahrilas PJ, Bredenoord AJ, Fox M, etal. Expert consensus document: advances in the management of oesophageal motility disorders in the era of high-resolution manometry: a focus on achalasia syndromes. Nat Rev Gastroenterol Hepatol. 2017;14:677–88.
M. A. Harrison et al.
21 Secondary Esophageal Motility Disorders: Diagnosis…
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55. Meneghelli UG, Peria FM, Darezzo FMR, etal. Clinical, radiographic, and manometric evolution of esophageal involvement by Chagas’ dis­ease. Dysphagia. 2005;20(1):40–5.
56. Silva LC, Vicentine FPP, Herbella FAM. High resolution manometric ndings in patients with Chagas' disease esophagopathy. Asian Pac J Trop Med. 2012;5(2):110–2.
57. Oliveria RB, Troncon LEA, Dantas RO, Meneghelli UG.Gastrointestinal manifestations of Chagas’ disease. Am J Gastroenterol. 1998;93:884–9.
58. Rezende JM.The digestive tract in Chagas’ disease. Mem Inst Oswaldo Cruz. 1984;79:97–106.
59. Oliveira RB, Rezende Rilho J, Dantas RO, Lazigi N.The spectrum of esophageal motor disoders in Chagas’ disease. Am J Gastroenterol. 1995;90:1119–24.
60. Dantas RO, Deghaide NHS, Donadi EA.Esophageal motility of patients with Chagas’ disease and idiopathic achalasia. Dig Dis Sci. 2001;46:1200–6.
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Esophagogastric Junction
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Outow Obstruction
KellyM.Herremans, J.ChristianBrown, andAlexanderL.Ayzengart
Case Scenario
67-year-old woman presented with a 3-year history of dysphagia (mostly to solids), associated with occasional regurgitation of undigested food and substernal chest pain. Her workup included a diagnostic upper endoscopy, timed barium esophagram, and high­resolution manometry. Manometry was consistent with esophago­gastric junction outow obstruction and demonstrated elevated lower esophageal sphincter integrated relaxation pressure of
18.8mmHg (Fig.22.1). Peristalsis was normal with 100% bolus
clearance. No evidence of intraluminal mucosal pathology, stric­tures, or external compression was noted on endoscopy. Timed barium esophagram showed retention of liquid contrast at 1min and eventual passage of the barium tablet after 5min, but no evi­dence of hiatal hernia, gastric volvulus, or esophageal diverticulum.
22
K. M. Herremans · J. C. Brown · A. L. Ayzengart (*) Department of Surgery, University of Florida Health, Gainesville, FL, USA e-mail: kelly.herremans@surgery.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_22
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Fig. 22.1 Findings of EGJOO on HRM
Introduction
K. M. Herremans et al.
Esophagogastric junction outow obstruction (EGJOO) is classi­ed as a major esophageal motility disorder by the Chicago Classication of Esophageal Motility Disorders, version 4.0, and is dened by recently rened ndings on high-resolution manom­etry (HRM) and its associated protocol incorporating patient posi­tioning and provocative swallowing. EGJOO is characterized by an elevated integrated relaxation pressure (IRP) with preserved or weak peristalsis, such that the criteria of achalasia are not met. IRP is considered elevated when above the threshold of 15mmHg, albeit this is technology-specic.
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Etiology
Findings of EGJOO are not uncommon and are reported in up to 14% of HRM studies. It is more commonly found in women (51– 88%) and the average age of diagnosis is between 56 and 69years old. Etiologies of EGJOO vary signicantly and include mechan­ical, inammatory, medication-related, and functional causes. Secondary causes of EGJOO include a wide range of pathologies (Table22.1). Functional, or idiopathic, EGJOO is diagnosed once secondary causes have been excluded.
Table 22.1 Secondary Causes
Secondary Causes of EGJOO
Mechanical Inammatory Medication-related
• Hiatal hernia
• Gastric volvulus
• Distal esophageal – Stricture – Schatzki ring – Web – Diverticulum
Esophageal varices
• Vascular compression
• Malignancy
• Postsurgical
• Reux esophagitis
• Eosinophilic esophagitis
• Systemic sclerosis
• Amyloidosis
• Chronic opioid use
• Antipsychotics
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K. M. Herremans et al.
Clinical Presentation
Patients diagnosed with EGJOO present with a variety of symp­toms. The most common symptom prompting HRM evaluation is dysphagia (46%), but other symptoms include chest pain (32%), heartburn (20%), nausea, and vomiting (19%). However, patients typically present with a combination of symptoms. EGJOO may also be found incidentally on routine preoperative evaluation for anti-reux procedures. Therefore, large volume foregut centers may report higher incidence of EGJOO.
Diagnosis
The diagnosis of EGJOO is made based on HRM ndings of an elevated median IRP above 15mmHg with intact peristalsis. It is differentiated from achalasia based on the presence and degree of peristalsis. IRP measurement is representative of the deglutitive esophagogastric junction relaxation and is recorded as a median pressure (mmHg) of ten test swallows.
Additional information from HRM studies may be utilized to help support the diagnosis of EGJOO and identify patients who would benet from intervention. Findings of delayed bolus transit combined with patient symptoms of dysphagia and chest pain are highly predictive of clinically relevant EGJOO. Elevated distal contractile integral (DCI) >11,000 mmHg-cm-s in addition to elevated IRP is predictive of symptom persistence after lower esophageal sphincter (LES) directed therapy. Though further research is needed, panesophageal pressurization during rapid drink challenge is found to be related to increased severity of symptoms and likelihood of progression to achalasia.
Additional methods for evaluation of EGJOO include endos­copy, timed barium esophagram (TBE), computed tomography (CT), and endoscopic functional luminal imaging probe (EndoFLIP). If not previously performed, endoscopy should be completed to assess for secondary causes of outlet obstruction. Thorough endoscopic evaluation, including forward and retro-
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exed views, is necessary to evaluate for secondary causes such as hiatal hernia, postsurgical changes, strictures, rings, gastric and esophageal tumors, and esophagitis. Endoscopic ultrasound may also be used to further elucidate obstructive etiologies if suspi­cious ndings are noted on endoscopy. TBE serves a dual purpose in the evaluation of EGJOO, as it may be used to rule out second­ary causes, but may also be used to indicate clinically relevant disease. This test is particularly useful in differentiating EGJOO from untreated achalasia. Addition of a barium tablet may be used to supplement barium esophagram. Delay in passage of barium tablet further indicates functional or anatomical obstruction. CT imaging may be used to evaluate secondary causes of EGJOO. However, CT should be considered on an individual basis as it has been found to yield little additional information. Endoscopic FLIP topography is a relatively new method that has been employed to assess esophageal motility. The EndoFLIP probe uses high-resolution impedance planimetry to measure the relationship between luminal dimensions and distensive pressure during volumetric distension. It may be utilized trans-nasally in an awake patient, but also can be used as a quick 5-min adjunct to endoscopy or in the intraoperative setting. Despite limited adop­tion in clinical settings, EndoFLIP may be used as a complemen­tary tool to assess EGJ dynamics. It is recommended that data from multiple testing modalities should be evaluated and utilized on a case-by-case basis in order to determine the etiology of patient’s EGJOO.
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Management
EGJOO is a heterogeneous disorder composed of both mechani­cal and functional motor abnormalities. As a result, management strategies for the treatment of EGJOO are as diverse as its under­lying causes. Appropriate diagnosis, as identied during clinical evaluation, denes the practical treatment modality. However, thorough review of these individual clinical entities and their associated treatment outcomes is beyond the scope of this chapter.
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A portion of manometrically identied EGJOO lacks a discrete mechanical obstruction and is classied as functional, or idio­pathic, EGJOO (iEGJOO). Some indicate that iEGJOO is a vari­ant phenotype of achalasia; the cardinal feature of impaired lower esophageal sphincter relaxation occurs, but with intact peristalsis. Although tailoring the therapeutic modality to the underlying eti­ology is likely critical to achieving successful long-term treatment outcomes, a paucity of evidence exists to support an optimal approach.
For patients with incidentally found EGJOO on HRM, watch­ful waiting is an appropriate option as many resolve without inter­vention. Differentiating between patients with nil-to-mild symptoms and moderate-to-severe symptoms helps to delineate between further management options. In patients with mild or atypical symptoms, expectant management may be recommended initially, as overall spontaneous resolution rate is approximately 40%.
Patients with signicant dysphagia and severe chest pain are less likely to have symptom resolution without intervention. Manometric ndings of DCI >11,000mmHg-cm-s, delayed bolus transit, intrabolus pressure greater than 24mmHg, and panesoph­ageal pressurization on rapid drink test help to distinguish clini­cally signicant disease. Delayed barium passage as well as retention of barium tablet during further workup may also assist in identifying patients who would benet from intervention.
K. M. Herremans et al.
Treatment
Clinical evidence regarding the treatment of EGJOO remains sparse as a result of the rarity of this disease. However, due to the overlap with achalasia, multiple therapeutic options have been applied with varying success. If a patient’s presentation includes the aforementioned severe symptoms or evaluation ndings, tar­geted lower esophageal sphincter (LES) therapy is warranted and treatment options must be tailored to patient’s symptoms, comor­bidities, surgical candidacy, and physician expertise.
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Pharmaceutical treatments have been explored with mixed out­comes. Medications frequently trialed are calcium channel block­ers, PPI’s, nitrates, antispasmodics, and prokinetics. Initiation of pharmacologic treatment is a practical starting point given their safety prole and known outcomes in achalasia. However, it has been reported that only 50% of patients with EGJOO exhibit any response to therapy. Acotiamide is a new prokinetic medication that has been heralded for its preliminary results in functional dyspepsia and subsequently EGJOO with up to 83% of patients showing symptomatic improvement. In the United States, it remains in clinical trials at the time of this publication.
Botulinum toxin may also be injected into the LES. The effect is transient and decremental with subsequent injections. Botulinum toxin injections are inferior to myotomy and should be reserved for poor surgical candidates as resultant scarring from injections may obscure esophageal surgical planes if additional interventions need to be carried out.
Bougie dilation may be reserved for EGJOO secondary to inammatory or peptic strictures, but pneumatic dilation is pre­ferred in functional EGJOO.Pneumatic dilation is a safe, effec­tive option for patients with clinically signicant EGJOO. Of note, age less than 40 and male gender were associated with lower rates of sustained symptomatic improvement following pneu­matic dilation. However, clinical improvement is typically achieved through repeat dilations. Pneumatic dilation is non­inferior to myotomy in the treatment of EGJOO, though patient characteristics should be considered.
Heller myotomy, performed laparoscopically or robotically, is a successful and sustainable treatment option in EGJOO with 90–100% success in symptom resolution. Classically, a full­thickness myotomy is created at least 5–6 cm proximal and 2–3cm distal to the esophagogastric junction. At the time of oper­ation, a partial fundoplication is typically performed to reduce postoperative GERD. Heller myotomy remains an excellent option for the treatment of EGJOO in patients who are deemed appropriate surgical candidates.
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K. M. Herremans et al.
Peroral endoscopic myotomy (POEM) is a relatively new tech­nique that may be used to perform LES myotomy in EGJOO.In this procedure, a long submucosal tunnel is created using a com­bination of hydrodissection and electrocautery, followed by an endoscopic myotomy of the circular muscle bers. The myotomy length can extend beyond 15cm proximal and 3cm distal to the esophagogastric junction and can be tailored to the underlying esophageal disease. Short-term data are promising (>90% success rate), but future long-term outcomes require further analysis. Notably, patients undergoing POEM have signicant rates of symptomatic reux and esophagitis following the procedure.
Conclusion
Given the heterogeneity of EGJOO and its unclear clinical sig­nicance, a progression of treatment modalities from the least invasive to the most invasive (i.e., surgery) is a reasonable thera­peutic approach (Fig.22.2). An eventual progression to the POEM
Fig. 22.2 Treatment Algorithm