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Montoro-Huguet, M.A. Dietary and Nutritional Support in Esophageal Diseases. Encyclopedia. Available online: (accessed on 06 December 2023).
Montoro-Huguet MA. Dietary and Nutritional Support in Esophageal Diseases. Encyclopedia. Available at: Accessed December 06, 2023.
Montoro-Huguet, Miguel A.. "Dietary and Nutritional Support in Esophageal Diseases" Encyclopedia, (accessed December 06, 2023).
Montoro-Huguet, M.A.(2022, November 24). Dietary and Nutritional Support in Esophageal Diseases. In Encyclopedia.
Montoro-Huguet, Miguel A.. "Dietary and Nutritional Support in Esophageal Diseases." Encyclopedia. Web. 24 November, 2022.
Dietary and Nutritional Support in Esophageal Diseases

The esophagus is the centerpiece of the digestive system of individuals and plays an essential role in transporting swallowed nutrients to the stomach. Diseases of the esophagus can alter this mechanism either by causing anatomical damage that obstructs the lumen of the organ (e.g., peptic, or eosinophilic stricture) or by generating severe motility disorders that impair the progression of the alimentary bolus (e.g., severe dysphagia of neurological origin or achalasia). In all cases, nutrient assimilation may be compromised. In some cases (e.g., ingestion of corrosive agents), a hypercatabolic state is generated, which increases resting energy expenditure.

esophagus esophageal adenocarcinoma enteral nutrition parenteral nutrition

1. Introduction

The esophagus is a hollow muscular tube of 18 to 26 cm that acts as a conduit for the transport of food from the oral cavity to the stomach [1]. This organ has a sphincter at each end that joins the hypopharynx above to the stomach below. Structurally, the esophageal wall is composed of four layers: innermost mucosa, with an inner “skin-like” lining of stratified squamous epithelium; submucosa; muscularis propria; and outermost adventitia. The neuroanatomical control of esophageal function is highly complex [2]. It involves parasympathetic and sympathetic nerves ultimately responsible for peristalsis and sensation perception, affecting chemoreceptors located in the esophageal mucosa and submucosa and/or mechanoreceptors in the esophageal musculature [1][2][3]. Disruption of these mechanisms due to anatomical or structural damage (macro- or microscopic) or severe dysfunction of esophagus neuromuscular function seriously affects the organ’s ability to perform its purpose [4]. This means that macro- and micronutrients do not reach the stomach, leading to varying degrees of malnutrition and, in the most severe cases, dehydration, electrolyte depletion, and starvation.

2. Dietary and Nutritional Support in Esophageal Diseases

2.1. Severe Oropharyngeal Dysphagia

Oropharyngeal dysphagia (OD) is a prevalent condition that is recognized by the World Health Organization (WHO) in the International Classification of Diseases [5]. Patients with OD have difficulty transferring food from the mouth to the pharynx and report the feeling of an obstruction in the neck. The most severe cases are accompanied by coughing, choking, drooling, and violent nasal regurgitation when attempting to swallow liquids or solids. A history of aspiration pneumonia is common in such cases, and gradual and progressive weight loss is the norm.
Clinical conditions in which OD may develop include older age, neurodegenerative diseases (Parkinson’s disease, Alzheimer’s, motor neuron disease), previous stroke, traumatic brain injury, and head and neck cancer [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]. Approximately 50–75% of patients with OD present impaired safety of swallowing with bolus penetration into the laryngeal vestibule, and 20–25% of these experience aspiration into the airway [5][21][22]. A thorough history and physical examination are essential to identify the underlying etiology, considering iatrogenic, infectious, metabolic, myopathic, neurologic, and structural causes. The diagnostic evaluation includes laboratory tests, imaging tests to exclude brain damage, fiberoptic endoscopic evaluation of swallowing (nasoendoscopy), nasopharyngeal laryngoscopy, videofluoroscopy, and manometry [23][24][25][26][27].
The goal of managing OD in patients is to improve food transfer, prevent aspiration, and ensure adequate supply of the caloric–protein requirements. Treatment includes swallow rehabilitation therapy and nutritional support. In this strategy, it is essential to generate “Units Specialized in the Management of Swallowing Disorders”, where registered dieticians or nutritionists, neurogastroenterologists, geriatricians, experts in endocrinology and nutrition, and skilled nursing staff can collaborate following a multidisciplinary protocol.
Some dietary interventions may help to improve swallowing and minimize the risk of aspiration:
For those patients who do not show adequate tolerance of liquids, the use of certain additives with thickening properties may be helpful in improving their swallowing ability. The European Society for Swallowing Disorders (ESSD) has described the evidence in the literature on the effect that bolus modification has upon the physiology, efficacy, and safety of swallowing in adults with OD of diverse etiologies [5]. These studies show that increasing the viscosity from liquid to nectar and pudding reduces the prevalence of penetrations and aspirations, suggesting that patients with OD do indeed benefit from taking fluids with increased viscosity, which reduces the risk of laryngeal penetration and/or aspiration [5][28][29];
The transfer of the food bolus can be improved if the mouthfuls are small in volume;
Alternation of solid and liquid boluses can also facilitate transfer;
For those patients with severe dysphagia of neurological origin, the assistance of a caregiver may be critical, and the meals should be administered during times of maximal attentiveness;
Finally, for those patients who are refractory to all these measures or at high risk for aspiration (e.g., severe neuromuscular dysfunction), enteral nutrition should be provided, preferably by endoscopic, percutaneous gastrostomy. If the patient also has gastroparesis, a double lumen feeding tube can be attempted, whereby one is placed in the stomach to aspirate the gastric remnant (e.g., biliary reflux) and the other in the duodenum for nutrient perfusion.

2.2. Achalasia

Achalasia is a relatively rare primary motor esophageal disorder characterized by the ab sence of relaxations of the lower esophageal sphincter (LES) and of peristalsis along the esophageal body. This esophageal motility disorder is thought to result from the progressive degeneration of ganglion cells in the myenteric plexus of the esophageal wall. The gold standard test for diagnosing achalasia is high-resolution manometry (HRM) of the esophagus. HRM should be the next test after first excluding the possibility of mechanical obstruction by endoscopy [30]. The incidence of achalasia ranges from 0.3 to 3.0/100,000 adults, and the prevalence ranges from 1.8 to 12.6/100,000 [30][31]. However, there appears to be striking international variations and significant differences within countries [32] and, in any case, the incidence and prevalence seem to be increasing in very different geographic areas [30][32]. The disease occurs with equal frequency in men and women and is more common with advanced age [33]. Clinically, it manifests as mixed dysphagia (solids and liquids), initially paradoxical and intermittent, and is ultimately progressive, causing marked dilatation of the esophagus. In this phase, regurgitation, sialorrhea, and nocturnal coughing outbreaks are common, reflecting slight bronchoaspiration. If the disorder is not corrected, the dysphagia becomes disabling, and the patient is destined to severe malnutrition with an estimated average weight loss of 20 ± 16 pounds [34].

2.3. Eosinophilic Esophagitis

Eosinophilic esophagitis (EoE) is a chronic, immune-mediated disorder that involves the esophagus. Its pathogenesis appears to depend largely upon delayed, cell-mediated hypersensitivity, and it is one of the most prevalent esophageal diseases and the leading cause of dysphagia and food impaction in children and young adults [35]. The incidence of EoE appears to be increasing, approaching that of inflammatory bowel disease [36][37]. Approximately 70% of children and adults affected by the disease are male, and the average age of presentation in the adult population is 34 years (range 14 to 77 years) [38].
Dietary therapy is an effective first-line treatment for EoE in children and adults. The selection of foods to be eliminated, the duration of restriction, and how restricted foods should be reintroduced have been controversial topics over time.
The patient or their caregivers should be informed about the pros and cons of each available option before planning;
When available, a registered dietician or nutritionist who is familiar with food allergies is a very valuable part of the patient’s care team;
A diet based on the empirical elimination of six foods (milk, wheat, egg, soy/legumes, nuts, fish/seafood) (6-FED) was initially considered the gold standard for the management of EoE [39][40][41]. The 6-FED followed by an endoscopic procedure before reintroducing a food and after checking histological healing showed that cow milk (especially in children < 10 years old), wheat, egg, legumes and, to a lesser extent, soy were the most common food triggers for EoE in both children and adults [41]. Nevertheless, this dietary approach did not become popular for patients and caregivers due to the need for numerous endoscopies and the high level of restriction for almost a year [39];
The most commonly used empiric elimination diet in the patients is the 4-FED, which involves the elimination of cow milk, hen eggs, soy–legumes, and wheat. This approach achieves histologic remissions in up to 54% and 64% of adults and children, respectively [42][43];
Studies of 4-FED demonstrated that around half of responders had one or two food triggers (usually milk and wheat) [42]. Following these findings, some authors advocate starting with a two-food (cow milk and wheat) elimination diet, and in the case of nonresponse, sequentially escalating the diet to 4-FED and then 6-FED. This strategy achieves 43%, 60%, and 75% histologic remission rates, respectively [44]. Therefore, an empirical staged elimination diet, starting with one or two food groups, represents a pragmatic dietary approach for children and adult patients with EoE [45];
Of interest, Spanish authors have investigated the tolerance of sterilized cow milk (boiled instead of UHT-processing) regarding maintenance of EoE remission, health-related quality of life (HRQoL), nutritional intake, and allergic sensitization in patients of all ages with milk-triggered EoE. Notably, the results of this elegant study demonstrate that sterilized milk did not trigger EoE in two-thirds of patients with documented milk-induced EoE in either the short or long term [46];
The highest success rates in symptomatic and histologic improvement are seen with the elemental diet. However, even in children, this diet is the most difficult to follow. This diet should be restricted to patients who have not responded to any other approach, when seeking a nutrient supply that cannot be achieved by any other means, or the patient manifests a desire to initiate treatment in this way and if resources allow it.

2.4. Caustic Injuries

Caustic ingestion continues to be a severe problem, often with devastating consequences, and involves children and adults affected by alcoholism, mental disorders, or suicidal intention. The most affected parts are the oropharyngeal cavity, larynx, esophagus, and stomach [47]. The severity and extent of esophageal and gastric damage are determined by the ingested substance’s corrosive properties (pH), concentration and amount ingested (in adults, a normal sip is 30–50 mL, a large gulp is 60–90 mL), physical form of the agent (solid or liquid), and duration of contact with the mucosa [47][48][49][50][51][52][53][54]. Most patients present with mild injuries that recover without sequelae. However, patients who have ingested a significant amount of strong alkali or acid, usually due to a suicide attempt or psychiatric illness, are at obvious risk of developing severe complications, such as perforation, mediastinitis or peritonitis. Other sequelae such as fistula formation (tracheobronchial, aortoenteric), hemorrhage, or pulmonary complications lead to a state of systemic inflammatory response and increase the basal energy expenditure [the amount of energy required to maintain the body’s normal metabolic activity], creating an imbalance between the nutrient intake and the real (increased) needs, thus contributing to malnutrition [55].
The evaluation of the degree and extent of the injury is a critical point in decision-making related to nutritional support. Thus, CT of the neck, thorax, and abdomen should be per-formed 3–6 h after ingestion to classify the severity of the lesions in a non-invasive manner [52][56]. In turn, endoscopy should be performed in the first 24–48 h, especially when CT is not available, administering of intravenous contrast is contraindicated, or CT shows signs of wall necrosis, but the interpretation of the findings is uncertain (grade 2 CT). Endoscopy performed under these conditions allows grading the lesions from lesser to greater severity (Zargar classification) and has been shown to have prognostic value [53][54]. Both examinations, together with the patient’s clinical condition, allow scholars to guide the nutritional management according to the following postulates:
(1)In asymptomatic patients without oral burns and a history of low-volume, accidental ingestion of low-concentration acid or alkali, upper endoscopy is not necessary. Such patients may be discharged from the hospital, and a diet based on soft foods or liquids for the first 24–48 h is recommended;
(2)Patients who have ingested a substance with a high risk of esophageal injury (high-concentration acid or alkali or a high volume (>200 mL) of a low-concentration acid or alkali) should be hospitalized. Nutritional support should be initiated with hemodynamic stabilization and the restoration of fluids, electrolytes, and acid–base balance [56];
(3)Corrosive ingestion injuries up to Zargar 2A-grade 1-CT (low-grade injuries) do not cause long-term sequelae and do not require advanced nutrition. Oral feeding should be reintroduced as soon as patients are swallowing normally, and they should be discharged quickly from the hospital (usually within the first 24–48 h) [56][57];
(4)Patients with grade 2A-CT esophageal injuries have a low risk (<20%) of stricture formation [58]. Oral nutrition is usually well tolerated and should be introduced as soon as pain diminishes, and patients can swallow. Oral liquids are allowed after the first 48 h if the patient is able to swallow saliva. If patients are unable to tolerate oral liquids, early enteral feeding is provided through a nasojejunal tube or jejunostomy;
(5)Patients with grade 2-CT lesions will develop stricture in 80% of cases. Pain, sialorrhea, and odynophagia are frequent during the acute phase and can severely limit swallowing, making oral feeding impossible. Such cases may benefit from nutritional support by the nasoenteral route, jejunostomy and, as a last resort, exclusive parenteral nutrition. The decision to adopt one procedure over another is dependent on how long before the patient is expected to be able to restart feeding and their tolerance [55][58]. Kochhar et al. compared the nutritional parameters of 53 and 43 patients with severe acute corrosive injury supplied with nasoenteral tube (NETF) or jejunostomy feeding (JF), respectively. NETF was found to be as effective as JF in maintaining nutrition, and the rate of complications was similar (including the development of strictures). However, NETF provided a lumen for dilatation that was useful as a guide for performing the procedure [59];
(6)Signs of perforation (e.g., mediastinitis, peritonitis), major metabolic disorders, and CT evidence of transmural necrosis of the esophagus or stomach (grade 3-CT) in patients are indications for emergency surgery. In all these cases, the surgeon disrupts the continuity of the gastrointestinal tract to save the patient’s life, making oral feeding virtually impossible.
(7)Esophageal strictures are the most common complication of caustic esophageal ingestion and can affect the esophagus, stomach, and other locations in the digestive tract. They usually develop within 2 months (3 weeks to 1 year) and multiple strictures appear in some cases [60].

2.5. Gastroesophageal Reflux Disease

The passage of gastric contents into the esophagus (gastroesophageal reflux [GR]) is a normal physiologic process. Physiologic reflux episodes typically occur postprandially, are short-lived, asymptomatic, and rarely occur during sleep. The term gastroesophageal reflux disease (GERD) is applied to patients with bothersome symptoms suggestive of reflux with or without oesophagitis.

2.5.1. Foods That Contribute to the Triggering or Worsening of Symptoms

In the etiopathogenesis of GERD, there is an imbalance between aggressive factors (number and duration of reflux episodes and acidity of the refluxed material) and defensive factors (esophageal acid clearance and mucosal integrity). Without a doubt, the most important pathogenic factor is incompetence of the lower esophageal sphincter (LES). The three dominant pathophysiologic mechanisms causing esophagogastric junction incompetence are transient LES relaxations, a hypotensive LES, and anatomic disruption of the gastroesophageal junction, often associated with a hiatal hernia. Knowledge of these mechanisms is essential as it has been postulated that some foods that stimulate gastric acid secretion (e.g., caffeine, alcohol) or decrease LES tone (e.g., fatty meals, cocoa, chocolates, and alcohol) should be significantly reduced in the usual dietary intake of a person with GERD [61][62][63][64][65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82].

2.5.2. Overweight and Obesity

Epidemiological studies show that obesity is a risk factor for GERD because of multiple factors, including increased (1) intra-abdominal pressure, (2) gastroesophageal sphincter gradient, and (3) incidence of hiatal hernia as well as impaired gastric emptying and the output of bile and pancreatic enzymes [61][64][65][66]. Overweight/obesity increases the risk for GERD symptoms by 1.2–3-fold, and 60% of the overweight or obese population report having GERD [67]. In addition, there is evidence that obesity, especially central obesity, increases the risk of complications such as peptic esophagitis, BE, and adenocarcinoma of the esophagus [68][69][70].

2.5.3. Food and Reflux Symptoms during Sleep

Postprandial reflux is common in patients with GERD, and patients frequently present with nocturnal symptoms or wake up in the morning with symptoms suggestive of peptic laryngitis. For this reason, it is very common for physicians to advise their patients not to go to bed shortly after dinner and to wait at least 2–3 h after their last meal [61][83][84][85][86].
New evidence indicates the following:
Elevation using a foam wedge causes a statistically significant decrease in the time that distal esophageal pH is less than 4 compared with the flat position. [87][88];
Elevating the head of the bed is an easy and effective way to alleviate the symptoms of acid regurgitation. Furthermore, this intervention results in more effective relief of symptoms than taking medications alone [89][90];
Elevation using a foam wedge causes a statistically significant decrease in the time that distal esophageal pH is less than 4 compared with the flat position. [87][88];
Elevating the head of the bed is an easy and effective way to alleviate the symptoms of acid regurgitation. Furthermore, this intervention results in more effective relief of symptoms than taking medications alone [89][90];
Elevating the head of the bed may be useful for relieving acid regurgitation among esophageal cancer patients after surgery [89];
The use of a wedge-shaped pillow (WSP) alleviates reflux symptoms in patients with esophageal cancer following esophagectomy and reconstruction. Likewise, the combined treatment (antisecretory drugs + WSP) also reduces the severity of esophagitis [91];
Several studies show that sleeping with the head of the bed elevated or on a wedge reduces GER and lying left-side down reduces GER versus lying right-side down and supine [92]. The left lateral position is a suitable alternative to prone for the postural management of infants with symptomatic GER [93];
Finally, bed head elevation by reducing the time of acid exposure also alleviates the consequences of nocturnal supraesophageal reflux, including perennial nasopharyngitis, cough, and asthma [94].

2.5.4. Dietary, Barrett’s Esophagus, and Cancer Risk

About 10–15% of patients with gastroesophageal reflux disease develop BE. This is considered a premalignant condition because it can progress from metaplasia to high-grade dysplasia and eventually to adenocarcinoma [95]. The incidence of esophageal adenocarcinoma and its precursor, BE, have increased greatly (~500%) over the past 40 years and continue to rise [96][97][98]. Although the reasons are not clear, advanced age, male gender, obesity, smoking, and alcohol have been identified as risk factors [99][100][101][102][103][104][105]. Hence, increased cell turnover and eventual carcinogenesis are likely precipitated by increased intragastric pressure but are also affected by the complex interaction of increased insulin resistance in patients with increased fat mass [101].

2.5.5. Complications Contributing to Malnutrition

Esophageal reflux may result in several complications, including esophagitis, upper gastrointestinal bleeding, anemia, peptic ulcer, peptic stricture, dysphagia, cancer of gastric cardia, and Barrett´s esophagus. All of these can adversely affect nutritional status via various mechanisms (Figure 1).
Figure 1. Precipitating factors of GERD, complications, and effects on nutritional status.

3. Conclusions

Anatomical or swallowing disorders of the esophagus adversely affect nutritional status. Severe dysphagia of neurological origin and sequelae following the ingestion of corrosive agents can have devastating repercussions and require advanced nutritional support. In other cases, it is the food itself that negatively affects esophageal function (e.g., EoE or GERD). Finally, lifestyle and Western dietary patterns generate obesity. Experimental and epidemiological evidence supports the concept that obesity and other harmful habits, such as smoking or alcoholism, increase the risk of BE and esophageal adenocarcinoma. Registered dietitians or nutritionists should have a comprehensive knowledge of all these mechanisms and work interdisciplinarily with gastroenterologists to correct any macro- or micronutrient deficiencies. In some cases, the selective exclusion of foods will be necessary (e.g., EoE) though without the deterioration of nutritional status. This is a challenge for professionals with expertise in human nutrition and dietetics.


  1. Madanick, R.; Orlando, R.C. Anatomy, Histology, Embryology, and Developmental anomalies of the esophagus. In Sleisenger and Fordtran´s. Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management; Feldman, M., Friedman, L., Brandt, L.J., Eds.; Saunders & Elsevier: Philadelphia, PA, USA, 2016; pp. 689–700.
  2. Pandolfino, J.E.; Kharilas, P.J. Esophageal Neuromuscular Function and Motility Disorders. In Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management; Feldman, M., Friedman, L., Brandt, L.J., Eds.; Saunders & Elsevier: Philadelphia, PA, USA, 2016; pp. 732–761.
  3. Parkman, H.P. Modern Approaches for Evaluation and Treatment of GI Motility Disorders. In Gastroenterology Clinics: Esophagus; Elsevier: Philadelphia, PA, USA, 2020; pp. 1–498.
  4. Gavaghan, M. Anatomy and physiology of the esophagus. AORN J. 1999, 69, 370–386.
  5. Newman, R.; Vilardell, N.; Clavé, P.; Speyer, R. Effect of Bolus Viscosity on the Safety and Efficacy of Swallowing and the Kinematics of the Swallow Response in Patients with Oropharyngeal Dysphagia: White Paper by the European Society for Swallowing Disorders (ESSD). Dysphagia 2016, 31, 232–249.
  6. Takizawa, C.; Gemmell, E.; Kenworthy, J.; Speyer, R. A Systematic Review of the Prevalence of Oropharyngeal Dysphagia in Stroke, Parkinson’s Disease, Alzheimer’s Disease, Head Injury, and Pneumonia. Dysphagia 2016, 31, 434–441.
  7. Barczi, S.R.; Sullivan, P.A.; Robbins, J.A. How should dysphagia care of older adults differ? Establishing optimal practice patterns. Semin. Speech Lang. 2000, 21, 347–364.
  8. Ekberg, O. Dysphagia: Diagnosis and Treatment; Springer Publishing: Berlin, Germany, 2012.
  9. Daniels, S.K.; Brailey, K.; Priestly, D.H.; Herrington, L.R.; Weisberg, L.A.; Foundas, A.L. Aspiration in patients with acute stroke. Arch. Phys. Med. Rehabil. 1998, 79, 14–19.
  10. Martino, R.; Foley, N.; Bhogal, S.; Diamant, N.; Speechley, M.; Teasell, R. Dysphagia after stroke: Incidence, diagnosis, and pulmonary complications. Stroke 2005, 36, 2756–2763.
  11. Kalf, J.; de Swart, B.; Bloem, B.; Munneke, M. Prevalence of oropharyngeal dysphagia in Parkinson’s disease: A meta-analysis. Park. Relat. Disord. 2012, 18, 311–315.
  12. Simons, J.A. Swallowing Dysfunctions in Parkinson’s Disease. Int. Rev. Neurobiol. 2017, 134, 1207–1238.
  13. Sato, E.; Hirano, H.; Watanabe, Y.; Edahiro, A.; Sato, K.; Yamane, G.; Katakura, A. Detecting signs of dysphagia in patients with Alzheimer’s disease with oral feeding in daily life. Geriatr. Gerontol. Int. 2014, 14, 549–555.
  14. Langmore, S.E.; Olney, R.K.; Lomen-Hoerth, C.; Miller, B.L. Dysphagia in patients with frontotemporal lobar dementia. Arch. Neurol. 2007, 64, 58–62.
  15. Homer, J.; Alberts, M.J.; Dawson, D.V.; Cook, G.M. Swallowing in Alzheimerʼs disease. Alzheimer Dis. Assoc. Disord. 1994, 8, 177–189.
  16. Haverkamp, L.J.; Appel, V.; Appel, S.H. Natural history of amyotrophic lateral sclerosis in a database population Validation of a scoring system and a model for survival prediction. Brain 1995, 118, 707–719.
  17. Mackay, L.E.; Morgan, A.S.; Bernstein, B.A. Swallowing disorders in severe brain injury: Risk factors affecting return to oral intake. Arch. Phys. Med. Rehabil. 1999, 80, 365–371.
  18. Mélotte, E.; Maudoux, A.; Panda, R.; Kaux, J.-F.; Lagier, A.; Herr, R.; Belorgeot, M.; Laureys, S.; Gosseries, O. Links Between Swallowing and Consciousness: A Narrative Review. Dysphagia 2022, 30, 1–23.
  19. García-Peris, P.; Parón, L.; Velasco, C.; de la Cuerda, C.; Camblor, M.; Bretón, I.; Herencia, H.; Verdaguer, J.; Navarro, C.; Clavé, P. Long-term prevalence of oropharyngeal dysphagia in head and neck cancer patients: Impact on quality of life. Clin. Nutr. 2007, 26, 710–717.
  20. Berg, M.G.A.V.D.; Rütten, H.; Rasmussen-Conrad, E.L.; Knuijt, S.; Takes, R.P.; Van Herpen, C.M.L.; Wanten, G.J.A.; Kaanders, J.H.A.M.; Merkx, M.A.W. Nutritional status, food intake, and dysphagia in long-term survivors with head and neck cancer treated with chemoradiotherapy: A cross-sectional study. Head Neck 2014, 36, 60–65.
  21. Clavé, P.; Shaker, R. Dysphagia: Current reality and scope of the problem. Nat. Rev. Gastroenterol. Hepatol. 2015, 12, 259–270.
  22. Rofes, L.; Arreola, V.; Romea, M.; Palomera, E.; Almirall, J.; Cabré, M.; Serra-Prat, M.; Clavé, P. Pathophysiology of oropharyngeal dysphagia in the frail elderly. Neurogastroenterol. Motil. 2010, 22, 851-e230.
  23. Ahuja, N.K.; Chan, W.W. Assessing Upper Esophageal Sphincter Function in Clinical Practice: A Primer. Curr. Gastroenterol. Rep. 2016, 18, 7.
  24. Cock, C.; Omari, T. Diagnosis of Swallowing Disorders: How We Interpret Pharyngeal Manometry. Curr. Gastroenterol. Rep. 2017, 19, 11.
  25. Omari, T.I.; Ciucci, M.; Gozdzikowska, K.; Hernández, E.; Hutcheson, K.; Jones, C.; Maclean, J.; Nativ-Zeltzer, N.; Plowman, E.; Rogus-Pulia, N.; et al. High-Resolution Pharyngeal Manometry and Impedance: Protocols and Metrics—Recommendations of a High-Resolution Pharyngeal Manometry International Working Group. Dysphagia 2019, 35, 281–295.
  26. Boaden, E.; Nightingale, J.; Bradbury, C.; Hives, L.; Georgiou, R. Clinical practice guidelines for videofluoroscopic swallowing studies: A systematic review. Radiography 2020, 26, 154–162.
  27. Luan, S.; Wu, S.-L.; Xiao, L.-J.; Yang, H.-Y.; Liao, M.-X.; Wang, S.-L.; Fan, S.-N.; Ma, C. Comparison studies of ultrasound-guided botulinum toxin injection and balloon catheter dilatation in the treatment of neurogenic cricopharyngeal muscle dysfunction. NeuroRehabilitation 2021, 49, 629–639.
  28. Trimble, J.; Patterson, J. Cough reflex testing in acute stroke: A survey of current UK service provision and speech and language therapist perceptions. Int. J. Lang. Commun. Disord. 2020, 55, 899–916.
  29. Blonski, W.; Slone, S.; Richter, J.E. Update on the Diagnosis and Treatment of Achalasia. Dysphagia 2022, 18, 1–13.
  30. Sadowski, D.C.; Ackah, F.; Jiang, B.; Svenson, L. Achalasia: Incidence, prevalence and survival. A population-based study. Neurogastroenterol. Motil. 2010, 22, e256–e261.
  31. Podas, T.; Eaden, J.; Mayberry, M.; Mayberry, J. Achalasia: A critical review of epidemiological studies. Am. J. Gastroenterol. 1998, 93, 2345–71998.
  32. Marlais, M.; Fishman, J.R.; Fell, J.M.E.; Haddad, M.J.; Rawat, D.J. UK incidence of achalasia: An 11-year national epidemiological study. Arch. Dis. Child. 2011, 96, 192–194.
  33. Fisichella, P.M.; Raz, D.; Palazzo, F.; Niponmick, I.; Patti, M.G. Clinical, radiological, and manometric profile in 145 patients with untreated achalasia. World J. Surg. 2008, 32, 1974–1979.
  34. A Patel, D.; Naik, R.; Slaughter, J.C.; Higginbotham, T.; Silver, H.; Vaezi, M.F. Weight loss in achalasia is determined by its phenotype. Dis. Esophagus 2018, 31, doy046.
  35. Hruz, P.; Straumann, A.; Bussmann, C.; Heer, P.; Simon, H.-U.; Zwahlen, M.; Beglinger, C.; Schoepfer, A.M.; Swiss EoE Study Group. Escalating incidence of eosinophilic esophagitis: A 20-year prospective, population-based study in Olten County, Switzerland. J. Allergy Clin. Immunol. 2011, 128, 1349–1350.e5.
  36. Navarro, P.; Arias, Á.; Arias-González, L.; Laserna-Mendieta, E.J.; Ruiz-Ponce, M.; Lucendo, A.J. Systematic review with meta-analysis: The growing incidence and prevalence of eosinophilic oesophagitis in children and adults in population-based studies. Aliment. Pharmacol. Ther. 2019, 49, 1116–1125.
  37. Croese, J.; Fairley, S.K.; Masson, J.W.; Chong, A.K.; Whitaker, D.A.; Kanowski, P.A.; Walker, N.I. Clinical and endoscopic features of eosinophilic esophagitis in adults. Gastrointest. Endosc. 2003, 58, 516–522.
  38. Hurrell, J.M.; Genta, R.M.; Dellon, E.S. Prevalence of esophageal eosinophilia varies by climate zone in the United States. Am. J. Gastroenterol. 2012, 107, 698–706.
  39. Gonsalves, N.; Yang, G.; Doerfler, B.; Ritz, S.; Ditto, A.M.; Hirano, I. Elimination Diet Effectively Treats Eosinophilic Esophagitis in Adults; Food Reintroduction Identifies Causative Factors. Gastroenterology 2012, 142, 1451–1459.e1.
  40. Lucendo, A.J.; Arias, A.; González-Cervera, J.; Yagüe-Compadre, J.L.; Guagnozzi, D.; Angueira, T.; Jiménez-Contreras, S.; González-Castillo, S.; Rodríguez-Domíngez, B.; De Rezende, L.C.; et al. Empiric 6-food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic esophagitis: A prospective study on the food cause of the disease. J. Allergy Clin. Immunol. 2013, 131, 797–804.
  41. Molina-Infante, J.; Arias, A.; Barrio, J.; Rodríguez-Sánchez, J.; Sanchez-Cazalilla, M.; Lucendo, A.J. Four-food group elimination diet for adult eosinophilic esophagitis: A prospective multicenter study. J. Allergy Clin. Immunol. 2014, 134, 1093–1099.e1.
  42. Kagalwalla, A.F.; Wechsler, J.B.; Amsden, K.; Schwartz, S.; Makhija, M.; Olive, A.; Davis, C.M.; Manuel-Rubio, M.; Marcus, S.; Shaykin, R.; et al. Efficacy of a 4-Food Elimination Diet for Children With Eosinophilic Esophagitis. Clin. Gastroenterol. Hepatol. 2017, 15, 1698–1707.e7.
  43. Molina-Infante, J.; Arias, A.; Alcedo, J.; Garcia-Romero, R.; Casabona-Frances, S.; Prieto-Garcia, A.; Modolell, I.; Gonzalez-Cordero, P.L.; Perez-Martinez, I.; Martin-Lorente, J.L.; et al. Step-up empiric elimination diet for pediatric and adult eosinophilic esophagitis: The 2-4-6 study. J. Allergy Clin. Immunol. 2018, 141, 1365–1372.
  44. Aceves, S.S.; Alexander, J.A.; Baron, T.H.; Bredenoord, A.J.; Day, L.; Dellon, E.S.; Falk, G.W.; Furuta, G.T.; Gonsalves, N.; Hirano, I.; et al. Endoscopic approach to eosinophilic esophagitis: American Society for Gastrointestinal Endoscopy Consensus Conference. Gastrointest. Endosc. 2022, 96, 576–592.
  45. Furuta, G.T.; Katzka, D.A. Eosinophilic Esophagitis. N. Engl. J. Med. 2015, 373, 1640–1648.
  46. Dhar, A.; Haboubi, H.N.; Attwood, S.E.; Auth, M.K.H.; Dunn, J.M.; Sweis, R.; Morris, D.; Epstein, J.; Novelli, M.R.; Hunter, H.; et al. British Society of Gastroenterology (BSG) and British Society of Paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN) joint consensus guidelines on the diagnosis and management of eosinophilic oesophagitis in children and adults. Gut 2022, 71, 1459–1487.
  47. González-Cervera, J.; Arias, A.; Navarro, P.; Juárez-Tosina, R.; Cobo-Palacios, M.; Olalla, J.M.; Angueira-Lapeña, T.; Lucendo, A.J. Tolerance to sterilised cow’s milk in patients with eosinophilic oesophagitis triggered by milk. Aliment. Pharmacol. Ther. 2022, 56, 957–967.
  48. Contini, C.S.S. Caustic injury of the upper gastrointestinal tract: A comprehensive review. World J. Gastroenterol. 2013, 19, 3918–3930.
  49. Cabral, C.; Chirica, M.; de Chaisemartin, C.; Gornet, J.-M.; Munoz-Bongrand, N.; Halimi, B.; Cattan, P.; Sarfati, E. Caustic injuries of the upper digestive tract: A population observational study. Surg. Endosc. 2012, 26, 214–221.
  50. Kluger, Y.; Ben Ishay, O.; Sartelli, M.; Katz, A.; Ansaloni, L.; Gomez, C.A.; Biffl, W.; Catena, F.; Fraga, G.P.; Di Saverio, S.; et al. Caustic ingestion management: World society of emergency surgery preliminary survey of expert opinion. World J. Emerg. Surg. 2015, 10, 1–8.
  51. Mowry, J.B.; Spyker, D.A.; Cantilena, L.R., Jr.; McMillan, N.; Ford, M. Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 31st Annual Report. Clin. Toxicol. 2014, 52, 1032–1283.
  52. Montoro-Huguet, M.A. Esophagogastric lesions caused by caustics. Gastroenterol. Hepatol. 2000, 23, 436–447.
  53. Ryu, H.H.; Jeung, K.W.; Lee, B.K.; Uhm, J.H.; Park, Y.H.; Shin, M.H.; Kim, H.L.; Heo, T.; Min, Y.I. Caustic injury: Can CT grading system enable prediction of esophageal stricture? Clin. Toxicol. 2010, 48, 137–142.
  54. Zargar, S.A.; Kochhar, R.; Nagi, B.; Mehta, S.; Mehta, S.K. Ingestion of corrosive acids. Spectrum of injury to upper gastrointes-tinal tract and natural history. Gastroenterology 1989, 97, 702–707.
  55. A Zargar, S.; Kochhar, R.; Nagi, B.; Mehta, S.K. Ingestion of strong corrosive alkalis: Spectrum of injury to upper gastrointestinal tract and natural history. Am. J. Gastroenterol. 1992, 87, 337–341.
  56. Chibishev, A.; Markoski, V.; Smokovski, I.; Shikole, E.; Stevcevska, A. Nutritional therapy in the treatment of acute corrosive intoxication in adults. Mater. Socio Medica 2016, 28, 66–70.
  57. Chirica, M.; Resche-Rigon, M.; Zagdanski, A.M.; Bruzzi, M.; Bouda, D.; Roland, E.; Sabatier, F.; Bouhidel, F.; Bonnet, F.; Munoz-Bongrand, N.; et al. Computed Tomography Evaluation of Esophagogastric Necrosis After Caustic Ingestion. Ann. Surg. 2016, 264, 107–113.
  58. Chirica, M.; Kelly, M.D.; Siboni, S.; Aiolfi, A.; Riva, C.G.; Asti, E.; Ferrari, D.; Leppäniemi, A.; Broek, R.P.G.T.; Brichon, P.Y.; et al. Esophageal emergencies: WSES guidelines. World J. Emerg. Surg. 2019, 14, 26.
  59. Bruzzi, M.; Chirica, M.; Resche-Rigon, M.; Corte, H.; Voron, T.; Sarfati, E.; Zagdanski, A.-M.; Cattan, P. Emergency computed tomography predicts caustic esophageal stricture formation. Ann. Surg. 2019, 270, 109–114.
  60. Chirica, M.; Resche-Rigon, M.; Bongrand, N.M.; Zohar, S.; Halimi, B.; Gornet, J.M.; Sarfati, E.; Cattan, P. Surgery for caustic injuries of the upper gastrointestinal tract. Ann. Surg. 2012, 256, 994–1001.
  61. Chowdhury, S.D.; George, G.; Ramakrishna, K.; Ramadass, B.; Pugazhendhi, S.; Mechenro, J.; Jeyaseelan, L.; Ramakrishna, B.S. Prevalence and factors associated with gastroesophageal reflux disease in southern India: A community-based study. Indian J. Gastroenterol. 2019, 38, 77–82.
  62. Kaltenbach, T.; Crockett, S.; Gerson, L.B. Are lifestyle measures effective in patients with gastroesophageal reflux disease? Arch. Intern. Med. 2006, 166, 965–971.
  63. DeVault, K.R.; Castell, D.O. American College of Gastroenterology. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am. J. Gastroenterol. 2005, 100, 190–200.
  64. Dagli, U.; Kalkan, I.H. The role of lifestyle changes in gastroesophageal reflux diseases treatment. Turk. J. Gastroenterol. 2017, 28, 33–37.
  65. Sethi, S.; Richter, J.E. Diet and gastroesophageal reflux disease. Curr. Opin. Gastroenterol. 2017, 33, 107–111.
  66. Ayazi, S.; Hagen, J.A.; Chan, L.S.; Demeester, S.R.; Lin, M.W.; Ayazi, A.; Leers, J.M.; Oezcelik, A.; Banki, F.; Lipham, J.C.; et al. Obesity and gastroesophageal reflux: Quantifying the association between body mass index, esophageal acid exposure, and lower esophageal sphincter status in a large series of patients with reflux symptoms. J. Gastrointest. Surg. 2009, 13, 1440–1447.
  67. Maev, I.V.; Yurenev, G.L.; Mironova, E.M.; Yureneva-Thorzhevskaya, T.V. Phenotype of obesity and gastroesophageal reflux disease in the context of comorbidity in patients with cardiovascular diseases. Ter. Arkh. 2019, 91, 126–133.
  68. Bischoff, S.C.; Barazzoni, R.; Busetto, L.; Campmans-Kuijpers, M.; Cardinale, V.; Chermesh, I.; Eshraghian, A.; Kani, H.T.; Khannoussi, W.; Lacaze, L.; et al. European guideline on obesity care in patients with gastrointestinal and liver diseases—Joint European Society for Clinical Nutrition and Metabolism / United European Gastroenterology guideline. United Eur. Gastroenterol. J. 2022, 10, 663–720.
  69. Chang, P.; Friedenberg, F. Obesity and GERD. Gastroenterol. Clin. N. Am. 2014, 43, 161–173.
  70. A Corley, D.; Kubo, A. Body mass index and gastroesophageal reflux disease: A systematic review and meta-analysis. Am. J. Gastroenterol. 2006, 101, 2619–2628.
  71. Hampel, H.; Abraham, N.S.; El-Serag, H.B. Meta-analysis: Obesity and the risk for gastroesophageal reflux disease and its complications. Ann. Intern. Med. 2005, 143, 199.
  72. Nam, S.Y.; Choi, I.J.; Ryu, K.H.; Park, B.J.; Kim, H.B.; Nam, B. Abdominal visceral adipose tissue volume is associated with increased risk of erosive esophagitis in men and women. Gastroenterology 2010, 139, 1902–1911.e2.
  73. Chung, S.J.; Kim, D.; Park, M.J.; Kim, Y.S.; Kim, J.S.; Jung, H.C.; Song, I.S. Metabolic syndrome and visceral obesity as risk factors for reflux oesophagitis: A cross-sectional case-control study of 7078 Koreans undergoing health check-ups. Gut 2008, 57, 1360–1365.
  74. Nadaleto, B.F.; Herbella, F.A.; Patti, M.G. Gastroesophageal reflux disease in the obese: Pathophysiology and treatment. Surgery 2016, 159, 475–486.
  75. Park, S.K.; Lee, T.; Yang, H.J.; Park, J.H.; Sohn, C.I.; Ryu, S.; Park, D.I. Weight loss and waist reduction is associated with im-provement in gastroesophageal disease reflux symptoms: A longitudinal study of 15 subjects undergoing health checkups. Neuro. Gastroenterol. Motil. 2016, 29, e13009.
  76. De Groot, N.L.; Burgerhart, J.S.; Van De Meeberg, P.C.; De Vries, D.R.; Smout, A.J.P.M.; Siersema, P.D. Systematic review: The effects of conservative and surgical treatment for obesity on gastro-oesophageal reflux disease. Aliment. Pharmacol. Ther. 2009, 30, 1091–1102.
  77. Djärv, T. Physical activity, obesity and gastroesophageal reflux disease in the general population. World J. Gastroenterol. 2012, 18, 3710–3714.
  78. De Bortoli, N.; Guidi, G.; Martinucci, I.; Savarino, E.; Imam, H.; Bertani, L.; Russo, S.; Franchi, R.; Macchia, L.; Furnari, M.; et al. Voluntary and controlled weight loss can reduce symptoms and proton pump inhibitor use and dosage in patients with gastroesophageal reflux disease: A comparative study. Dis. Esophagus 2014, 29, 197–204.
  79. Ness-Jensen, E.; Lindam, A.; Lagergren, J.; Hveem, K. Weight loss and reduction in gastroesophageal reflux. a prospective population-based cohort study: The HUNT study. Am. J. Gastroenterol. 2013, 108, 376–382.
  80. Singh, M.; Lee, J.; Gupta, N.; Gaddam, S.; Smith, B.K.; Wani, S.B.; Sullivan, D.K.; Rastogi, A.; Bansal, A.; Donnelly, J.E.; et al. Weight loss can lead to resolution of gastroesophageal reflux disease symptoms: A prospective intervention trial. Obesity 2013, 21, 284–290.
  81. Madalosso, C.; Gurski, R.R.; Jacques, S.M.C.; Navarini, D.; Mazzini, G.; Pereira, M.D.S. The impact of gastric bypass on gastroesophageal reflux disease in morbidly obese patients. Ann. Surg. 2016, 263, 110–116.
  82. Han, Y.; Jia, Y.; Wang, H.; Cao, L.; Zhao, Y. Comparative analysis of weight loss and resolution of comorbidities between laparoscopic sleeve gastrectomy and Roux-en-Y gastric bypass: A systematic review and meta-analysis based on 18 studies. Int. J. Surg. 2020, 76, 101–110.
  83. Qumseya, B.; Qumsiyeh, Y.; Sarheed, A.; Rosasco, R.; Qumseya, A. Barrett’s Esophagus in Obese Patient Post-Roux-en-Y Gastric Bypass: A Systematic Review. Obes. Surg. 2022, 32, 3513–3522.
  84. Duroux, P.; Bauerfeind, P.; Emde, C.; Koelz, H.R.; Blum, A.L. Early dinner reduces nocturnal gastric acidity. Gut 1989, 30, 1063–1067.
  85. Lanzon-Miller, S.; Pounder, R.E.; McIsaac, R.L.; Wood, J.R. The timing of the evening meal affects the pattern of 24-hour intragastric acidity. Aliment. Pharmacol. Ther. 1990, 4, 547–553.
  86. Orr, W.C.; Harnish, M.J. Sleep-related gastro-oesophageal reflux: Provocation with a late evening meal and treatment with acid suppression. Aliment. Pharmacol. Ther. 1998, 12, 1033–1038.
  87. Stanciu, C.; Bennett, J. Effects of posture on gastro-oesophageal reflux. Digestion 1977, 15, 104–109.
  88. Hamilton, J.W.; Boisen, R.J.; Yamamoto, D.T.; Wagner, J.L.; Reichelderfer, M. Sleeping on a wedge diminishes exposure of the esophagus to refluxed acid. Am. J. Dig. Dis. 1988, 33, 518–522.
  89. Pollmann, H.; Zillessen, E.; Pohl, J. Effect of elevated head position in bed in therapy of gastroesophageal reflux . Z. Gastroenterol. 1996, 34 (Suppl. S2), 93–99.
  90. Huang, H.C.; Fang, S.Y. A Systematic Review of the Literature Related to Elevating the Head of the Bed for Patients. With Gastroesophageal Reflux Disease: Applications in Patients After Esophageal Cancer Surgery. Hu Li Za Zhi 2016, 63, 83–93.
  91. Khan, B.A.; Sodhi, J.S.; Zargar, S.A.; Javid, G.; Yattoo, G.N.; Shah, A.; Gulzar, G.M.; Khan, M.A. Effect of bed head elevation during sleep in symptomatic patients of nocturnal gastroesophageal reflux. J. Gastroenterol. Hepatol. 2012, 27, 1078–1082.
  92. Huang, H.-C.; Chang, Y.-J.; Tseng, Y.-L.; Fang, S.-Y. Effect of Head-of-Bed Elevation on Nocturnal Reflux Symptoms of Esophageal Cancer Patients With Esophagectomy and Reconstruction. Cancer Nurs. 2021, 44, 244–250.
  93. Person, E.; Rife, C.; Freeman, J.; Clark, A.; Castell, D.O. A Novel Sleep Positioning Device Reduces Gastroesophageal Reflux. J. Clin. Gastroenterol. 2015, 49, 655–659.
  94. Tobin, J.M.; McCloud, P.; Cameron, D.J.S. Posture and gastro-oesophageal reflux: A case for left lateral positioning. Arch. Dis. Child. 1997, 76, 254–258.
  95. Scott, D.R.; Simon, R.A. Supraesophageal Reflux: Correlation of Position and Occurrence of Acid Reflux-Effect of Head-of-Bed Elevation on Supine Reflux. J. Allergy Clin. Immunol. Pract. 2015, 3, 356–361.
  96. Oh, D.S.; Demeester, S.R. Pathophysiology and treatment of Barrett’s esophagus. World J. Gastroenterol. 2010, 14, 3762–3772.
  97. Falk, G.W. Barrett’s oesophagus: Frequency and prediction of dysplasia and cancer. Best Pr. Res. Clin. Gastroenterol. 2015, 29, 125–138.
  98. Patti, M.G. Gastroesophageal reflux disease: From heartburn to cancer. World J. Gastroenterol. 2010, 16, 3743–3744.
  99. Thrift, A.P. Determination of risk for Barrett’s esophagus and esophageal adenocarcinoma. Curr. Opin. Gastroenterol. 2016, 32, 319–324.
  100. Heidarzadeh-Esfahani, N.; Soleimani, D.; Hajiahmadi, S.; Moradi, S.; Heidarzadeh, N.; Nachvak, A.S.M. Dietary Intake in Relation to the Risk of Reflux Disease: A Systematic Review. Prev. Nutr. Food Sci. 2021, 26, 367–379.
  101. Duggan, C.; Onstad, L.; Hardikar, S.; Blount, P.L.; Reid, B.J.; Vaughan, T.L. Association between markers of obesity and progression from Barrett’s esophagus to esophageal adenocarcinoma. Clin. Gastroenterol. Hepatol. 2013, 11, 934–943.
  102. Lynch, K.L. Is Obesity Associated with Barrett’s Esophagus and Esophageal Adenocarcinoma? Gastroenterol. Clin. N. Am. 2016, 45, 615–624.
  103. Matsuzaki, J.; Suzuki, H.; Kobayakawa, M.; Inadomi, J.; Takayama, M.; Makino, K.; Iwao, Y.; Sugino, Y.; Kanai, T. Association of Visceral Fat Area, Smoking, and Alcohol Consumption with Reflux Esophagitis and Barrett’s Esophagus in Japan. PLoS ONE 2015, 10, e0133865.
  104. Kubo, A.; Corley, D.A.; Jensen, C.D.; Kaur, R. Dietary factors and the risks of oesophageal adenocarcinoma and Barrett’s oesophagus. Nutr. Res. Rev. 2010, 23, 230–246.
  105. Filiberti, R.A.; Fontana, V.; De Ceglie, A.; Blanchi, S.; Grossi, E.; Della Casa, D.; Lacchin, T.; De Matthaeis, M.; Ignomirelli, O.; Cappiello, R.; et al. Alcohol consumption pattern and risk of Barrett’s oesophagus and erosive oesophagitis: An Italian case–control study. Br. J. Nutr. 2017, 117, 1151–1161.
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