Cause Of Dysphagia In Patients Research Articles

The cause of dysphagia in patients with esophageal atresia: a systematic review and meta-analysis

Dysphagia is the most common symptom in patients with esophageal atresia (EA) of all ages. There is no study addressing the direct relation between dysphagia and surgical results. Therefore, a systematic review was performed to define the relationship between surgical complications and dysphagia in patients with EA. The systematic review was drafted under PRISMA guidelines. Systematic literature search was performed for the period 2000 (Jan) to 2019 (Dec)-20years-in the databases: MEDLINE, EMBASE, and PubMed. Statistical analysis was performed using Comprehensive Meta-Analysis Version 3.0 software. Among 767 articles, 486 abstracts were screened for the inclusion criteria. The full-texts of 64 articles were assessed for eligibility. The sub-group analysis could be performed in 4 articles for anastomotic strictures. Heterogeneity was calculated by I2 statistic as 18,487 and pooled odds ratio was measured under the fixed effect model (Q = 3.68; P = 0.298, I2 = 18,487). There was no significant relationship with an odds ratio of 1.37 between anastomotic stricture (AS) and dysphagia (95% CI 0.631-2.973, p = 0.426). There was no publication bias for the data (Begg's test, p = 0.496; Egger's tests, p = 0.335). This meta-analysis did not reveal a significant relationship between AS and dysphagia in children with EA. Since many other factors contribute to dysphagia, comprehensive variable information such as detailed standardized registry systems for rare diseases for pooling analysis is needed regarding other potential factors including surgical complications.

Dysphagia in a patient with ankylosing spondylitis: A case report

BACKGROUNDAnkylosing spondylitis (AS) is a systematic and rheumatic disease, which causes multiple symptoms. However, dysphagia due to the formation of a giant anterior cervical osteophyte is rare in patients with AS.CASE SUMMARYWe present the case of a 65-year-old male patient who was diagnosed with AS and visited the hospital with a complaint of progressive dysphagia. The appropriate imaging examinations indicated that a giant anterior cervical osteo-phyte at C3-4 caused esophageal compression, which led to dysphagia. An operation for resection was performed without complications.CONCLUSIONThis case demonstrates that a large cervical osteophyte may be the cause of dysphagia in patients with AS, and early accurate diagnosis and surgical treat-ment are very important for the improvement of symptoms. Anterior cervical discectomy and fusion are extremely effective and should be taken into consideration.

Research progress on the application status of dysphagia assessment scale and functional training for patients with oral and maxillofacial tumors

This article summarizes the causes of dysphagia in patients with oral and maxillofacial tumors, the application of dysphagia assessment scale; and the current status of functional training for those patients, so as to provide the reference for delivering clinical and continued nursing care for the patients with dysphagia. Key words: Review; Dysphagia; Oral and maxillofacial tumor; Assessment scale; Functional training

Severe dysphagia due to rapidly progressive pharyngoesophageal segment stenosis in systemic sclerosis

Purpose To describe a case of pharyngo-esophageal segment involvement by systemic sclerosis resulting in severe and rapid progressive dysphagia refractory to management. Case report A 69-year-old female with known systemic sclerosis presented with progressive solid and liquid food dysphagia. Serial video fluoroscopic swallowing studies demonstrated progressive hypopharyngeal and upper esophageal sphincter stenosis along with oropharyngeal dysphagia. Attempted esophagogastroduodenoscopy by gastroenterology using a 5.4 mm diameter gastroscope failed to pass through the hypopharynx. Operative laryngoscopy demonstrated a 3 mm hypopharyngeal lumen extending for 2 cm into the cervical esophagus. The stenosis was cannulated and dilated to 10 mm, but remained refractory to further dilations. The patient was unable to maintain any oral intake and required percutaneous gastrostomy placement. Conclusions Involvement of the pharyngo-esophageal segment is an underreported cause of severe dysphagia in patients with systemic sclerosis. Early recognition is necessary to prevent complete stenosis.

PWE-084 Dysphagia in Patients with Non-Erosive Gatro-Oesophageal Reflux Disease: Abstract PWE-084 Table 1

Introduction Dysphagia is commonly reported by patients with NERD. 1 In the absence of mechanical obstruction or erosions, the mechanism underlying dysphagia in NERD is unclear. Impaired oesophageal motility with delayed bolus clearance, increased resistance at the OGJ or impairment of mucosal integrity could potentially underlie this symptom. The aim of this study was to evaluate these potential causes of dysphagia in NERD patients. Methods All adult patients, presenting to the Upper GI Physiology unit between January 2014 and October 2015, with typical GERD symptoms, normal OGD, acid exposure time > 4.2%, no major manometric abnormalities and no structural, systemic or neurologic abnormalities were included. A composite dysphagia score was prospectively recorded (0–45). Motility was evaluated using HRM and Chicago classification 2015. Bolus clearance was assessed on 24 h pH-MII using bolus exposure time and post-reflux peristaltic wave (PSPW) score. Mucosal integrity was evaluated using Mean Nocturnal Baseline Impedance (MNBI). Results Out of the 76 eligible patients, 17 patients (8 M:9 F) with typical NERD and dysphagia symptoms (Group A) and 26 patients (15 M:11 F) with NERD only symptoms (Group B) fulfilled the inclusion criteria. Mean age for both groups was 49 years. Acid exposure time and number of reflux episodes between groups were similar (NS). The median composite dysphagia score for Group A was 19.5 (range 3.5–45). Minor oesophageal motility abnormalities were identified in 10/17 patients from Group A and 12/26 patients from Group B (P > 0.05). The median IRP was 6 mmHg in group A and 7 mmHg in group B (NS). There was no statistically significant difference in the bolus exposure time and PSPW index. Mucosal integrity evaluated with baseline impedance (MNBI) was slightly low in the distal oesophagus, without difference between groups. MNBI in the proximal oesophagus was normal and not different between groups (Table). Conclusion 40% of NERD patients reported dysphagia; majority reporting moderately severe symptoms. Impairment of oesophageal motility, bolus clearance and mucosal integrity do not seem to explain the pathophysiology of dysphagia in these patients. Esophageal hypersensitivity to mechanical stimulation and/or hypervigilance remained as potential causes of dysphagia in patients with NERD. Reference 1 Locke 3rd GR, et al. Prevalence and clinical spectrum of gastroesophageal reflux: A population-based study in Olmsted County, Minnesota. Gastroenterology 1997; 112 (5):1448–1456. Disclosure of Interest None Declared

Dysphagia after laparoscopic total fundoplication: anterior or posterior gastric wall fundoplication?

The occurrence of severe dysphagia after laparoscopic total fundoplication is currently an important factor associated with loss of quality of life in patients undergoing this modality of treatment for gastroesophageal reflux disease. Compare the incidence and evaluate the causes of severe postoperative dysphagia in patients undergoing laparoscopic total fundoplication (LTF) without short gastric vessels division, using the anterior gastric wall (Rossetti LTF) or anterior and posterior gastric walls (Nissen LTF). Analysis of the data of 289 patients submitted to LTF without short gastric vessels division from January 2004 to January 2012, with a minimum follow-up of 6 months. Patients were divided in Group 1 (Rossetti LTF - n = 160) and Group 2 (Nissen LTF - n = 129). The overall incidence of severe postoperative dysphagia was 3.11% (4.37% in group 1 and 1.55% in group 2; P = 0.169). The need for surgical treatment of dysphagia was 2.5% in group 1 and 0.78% in group 2 (= 0.264). Distortions of the fundoplication were identified as possible causes of the dysphagia in all patients taken to redo fundoplication after Rossetti LTF. No wrap distortion was seen in redo fundoplication after Nissen LTF. The overall incidence of severe postoperative dysphagia did not differ on the reported techniques. Only Rossetti LTF was associated with structural distortion of the fundoplication that could justify the dysphagia.

A rare cause of dysphagia: compression of the esophagus by an anterior cervical osteophyte due to ankylosing spondylitis

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatological disease affecting the axial skeleton with various extra-articular complications. Dysphagia due to a giant anterior osteophyte of the cervical spine in AS is extremely rare. We present a 48-year-old male with AS suffering from progressive dysphagia to soft foods and liquids. Esophagography showed an anterior osteophyte at C5-C6 resulting in esophageal compression. The patient refused surgical resection of the osteophyte and received conservative therapy. However, after 6 months there was no improvement in dysphagia. This case illustrates that a large cervical osteophyte may be the cause of dysphagia in patients with AS and should be included in the diagnostic workup in early stages of the disease.

Esophageal Diameter Is Decreased in Some Patients With Eosinophilic Esophagitis and Might Increase With Topical Corticosteroid Therapy

The rapid response to topical corticosteroids makes it hard to implicate fibrosis as the cause of dysphagia in patients with eosinophilic esophagitis (EoE). We examined surrogates of esophageal expansion using minimal and maximal esophageal diameter (EDmin and EDmax) in barium swallow examinations. Eleven patients evaluated at Mayo Clinic, Rochester (8 female, median age 40, median diagnosis 36 months, median symptom duration 132 months) underwent barium esophagrams to determine EDmin and EDmax before and after 6 weeks of topical corticosteroid therapy. We assessed parameter reproducibility (in healthy volunteers), baseline EDmin and EDmax, postcorticosteroid changes in EoE patients, and correlation with clinical response. EDmin and EDmax were reproducible, with nonsignificant variance in the 2 esophagrams in control subjects (P = .44 and P = .66, respectively). Baseline EDmax was reduced in EoE at 19 mm (range, 13-26 mm) vs 24 mm (range, 19-29 mm) in controls (P = .004). About 50% of the EoE patients had EDmax and min values within the 10th to 90th percentile of controls (45% and 55%, respectively). Clinical improvement by Mayo Dsyphagia Questionnaire did not correlate with postcorticosteroid luminal change (P = .19 for EDmax; P = .75 for EDmin). Median increases in postcorticosteroid EDmax and EDmin were not statistically significant (P = .15 and .1, respectively). However, they were significant in patients with abnormal baseline EDmax (n = 6; 2 mm; P = .01) and EDmin (n = 5; 3 mm; P = .02). Esophageal diameter is a reproducible parameter that is frequently decreased in EoE, but normal in approximately 50% of patients. Those with narrowing might respond to steroids, but it is unclear if narrowing causes dysphagia.

An increasingly recognized cause of dysphagia in patients with severe atopic dermatitis

An increasingly recognized cause of dysphagia in patients with severe atopic dermatitis

Mitochondrial Neurogastrointestinal Encephalomyopathy: Evidence of Mitochondrial DNA Depletion in the Small Intestine

Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is an autosomal recessive disease clinically defined by gastrointestinal dysmotility, cachexia, ptosis, ophthalmoparesis, peripheral neuropathy, white-matter changes in brain magnetic resonance imaging, and mitochondrial abnormalities. Loss-of-function mutations in thymidine phosphorylase gene induce pathologic accumulations of thymidine and deoxyuridine that in turn cause mitochondrial DNA (mtDNA) defects (depletion, multiple deletions, and point mutations). Our study is aimed to define the molecular basis of gastrointestinal dysmotility in a case of MNGIE. By using laser capture microdissection techniques, we correlated histologic features with mtDNA abnormalities in different tissue components of the gastrointestinal wall in a MNGIE patient and ten controls. The patient's small intestine showed marked atrophy and mitochondrial proliferation of the external layer of muscularis propria. Genetic analysis revealed selective depletion of mtDNA in the small intestine compared with esophagus, stomach, and colon, and microdissection analysis revealed that mtDNA depletion was confined to the external layer of muscularis propria. Multiple deletions were detected in the upper esophagus and skeletal muscle. Site-specific somatic point mutations were detected only at low abundance both in the muscle and nervous tissue of the gastrointestinal tract. Analysis of the gastrointestinal tract from 10 controls revealed a non-homogeneous distribution of mtDNA content; the small intestine had the lowest levels of mtDNA. Atrophy, mitochondrial proliferation, and mtDNA depletion in the external layer of muscularis propria of small intestine indicate that visceral myopathy is responsible for gastrointestinal dysmotility in this MNGIE patient.

ESOPHAGEAL STRICTURES SECONDARY TO CHRONIC CANDIDAL ESOPHAGITIS

Introduction: Candida esophagitis is a common cause of dysphagia in patients with AIDS. As the degree of immunosuppression worsens, the severity of esophagitis and the resistance to conventional treatments increase. Esophageal stricture is a rare complication of chronic candidal esophagitis. Case Report: A 34 y/o Caucasian female with AIDS (CD 4 count of 4) presented with worsening esophageal dysphagia over several months tolerating only a liquid diet. Physical examination revealed oral candidiasis despite treatment with fluconazole 200 mg po daily for 4 weeks. Esophagoscopy revealed candida throughout the oropharynx and severe candidal esophagitis in the proximal esophagus. An 8 mm stricture was noted 24 cm from the incisors, preventing advancement of the endoscope. The patient was started on amphotericin B IV, but 4 days later there was no decrease in oral candidiasis or improvement in her dysphagia. Subsequently, the patient was started on caspofungin IV for a total of 10 days with disappearance of her oral candidiasis. Repeat esophagosocpy revealed resolution of candidal esophagits, but the esophageal stricture persisted. Balloon dilation was performed from 8 mm to 12 mm. A large ulcer was noted distal to the stricture. A second 8 mm stricture was noted at 39 cm from the incisors, which was dilated to 12 mm. No further abnormalities were noted in the stomach or duodenum. Biopsies of the esophageal ulcer base and stricures revealed necrotic cells with degenerated yeast cells and hyphae suggestive of candida species. Im-munostains for CMV were negative. At the time of discharge, the patient was tolerating a mechanical soft diet. Discussion: Chronic candidal esophagitis with chronic inflammation may uncommonly progress to fibrosis and stricutre. Although a rare complication, esophageal stricture should be considered in an immunosuppresed patient who continues to have dysphagia despite appropriate antifungal treatments. Furthermore, candidal resistance to azoles should be suspected in patients who do not respond to conventional antifungal regimens and broader spectrum or newer antifungal treatments should be considered.

Oropharyngeal swallowing in craniocervical dystonia

Objective: To clarify the pathophysiology of dysphagia by electrophysiological methods. Method: Electrophysiological methods related to oropharyngeal swallowing were used to investigate 25 patients with cervical dystonia and 25 age matched...

Cricopharyngeal achalasia is a common cause of dysphagia in patients with mtDNA deletions.

To assess dysphagia, the authors examined 12 patients with Kearns-Sayre syndrome (KSS) or chronic progressive external ophthalmoplegia (CPEO) due to mitochondrial DNA (mtDNA) deletion by videofluoroscopy and manometry. Cricopharyngeal achalasia was documented in nine of 12 patients (75%), whereas deglutitive coordination problems were found in one patient. Cricopharyngeal myotomy may be an effective treatment in selected cases with severe cricopharyngeal obstruction.

Transient complete esophageal obstruction after pneumatic dilation of the lower esophageal sphincter for achalasia

We report this case to draw to the attention of others another, albeit unusual, cause of dysphagia in patients with esophageal endoprosthesis in situ. It should be considered in the differential diagnosis of dysphagia in this group of patients, particularly if the dysphagia is unexplained or occurs after the endoprosthesis has been in situ for some months as in this case. Keymed, the manufacturer of the Atkinson tube, stated they were aware of only one other instance of this type of structural fatigue in the 9 years that this product has been on the market, but to our knowledge this has not been reported in the literature. Structural endoprosthesis fatigue has been de-

Peristaltic dysfunction associated with nonobstructive dysphagia in reflux disease

An evaluation was done of 325 consecutive patients who underwent esophageal manometry to investigate the relationship between solid food dysphagia and peristaltic dysfunction in gastroesophageal reflux disease. All patients with dysphagia were endoscoped to evaluate for mechanical obstruction. Manometry was done focusing on the incidence of peristaltic dysfunction (failed peristaltic sequences or sequences characterized by foci of hypotensive peristalsis). The major finding was that the severity of manometrically demonstrated peristaltic dysfunction in reflux patients correlated with the prevalence of dysphagia. After excluding patients with esophageal rings or strictures from the analysis, the overall prevalence of dysphagia was 39% among the 157 reflux patients. Within this group, 29% of patients with minimal peristaltic dysfunction experienced dysphagia compared to 78% of patients with severe peristaltic dysfunction. We conclude that peristaltic dysfunction should be considered along with mechanical obstruction as a potential cause of dysphagia in patients with gastroesophageal reflux disease.

Dysphagia due to mediastinal fibrosis in advanced pulmonary tuberculosis.

Dysphagia in patients with pulmonary tuberculosis may be due to tuberculous esophagitis or compression of the esophagus by enlarged mediastinal lymph nodes or mediastinal fibrosis. We studied the clinical and radiologic findings in nine patients with advanced pulmonary tuberculosis who presented with dysphagia. In each patient, dysphagia first occurred while the patient was on antituberculous therapy. Chest radiographs in each case showed extensive tuberculous disease of the lung, affecting especially the left upper lobe. In addition, dense mediastinal pleural fibrosis was seen along the medial aspects of the upper thorax. Tomograms did not show mediastinal lymph node enlargement. Barium esophagograms showed extrinsic compression and various degrees of narrowing of the supracarinal part of the esophagus. No mucosal abnormality was seen on esophagoscopy. On the basis of these findings, the compression of the esophagus in these patients was attributed solely to tuberculous mediastinal fibrosis. The dysphagia remained constant in all patients except one, in whom worsening dysphagia improved after balloon dilatation. We conclude that mediastinal fibrosis is a significant cause of dysphagia in patients with advanced pulmonary tuberculosis.

Neurohumoral, hormonal, and drug receptors for the lower esophageal sphincter

The lower esophageal sphincter (LES) is a specialized structure present at the junction of the esophagus with the stomach.‘” The LES keeps closed at rest and is responsible for a pressure barrier which separates the negative intrathoracic pressure in the esophagus from the above atmospheric pressure in the stomach, and it opens in response to swallowing to allow the passage of an ingested bolus into the stomach. l, * Impairment of closure of the sphincter at rest is thought to be an important factor in causing reflux esophagitis, and abnormalities in the degree, duration, and timing of sphincter relaxation is an important cause of dysphagia in patients with achalasia.ss In recent years there has been considerable interest in the physiology and pharmacology of the LES in order to understand the pathophysiology of sphincter incompetence and achalasia, and to search for appropriate therapeutic agents for their treatment.4,5*10-14 Because all neurotransmitters, hormones, or exogenous drugs produce their effects by binding with specific receptors,15-17 consideration of these receptors has been very useful in the study of both the pharmacology and physiology of the LES. Effects of an ever-increasing, potentially infinite, number of drugs are more easily understood when their actions are perceived in terms of a finite number of receptors. Information on the existence and precise location of these receptors is helpful in defining the mode of action of new drugs. Furthermore, characterization of the receptors using selective agonists or antagonists has enhanced our understanding of the nature of the neurons and neurotransmitters involved in the regulation of LES function. General Receptor Concepts