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GERD is one of the most common diseases encountered by GPs and gastroenterologists. It affects both genders across all ethnicities and across all ages (see Figure 1). The high prevalence of GERD carries significant impact on a health system’s economy. Long-term management includes costs of medications, medical appointments, surgeries, as well as potential compli-cations like oesophageal stricture or oesophageal adenocarcinoma. For individuals, persistent and troublesome symptoms can affect the frame of mind, enjoyment of food, social activity and work productivity, ultimately altering the quality of life.1,2

PHYSIOLOGIC GASTROESOPHAGEAL REFLUX VS GERDGastroesophageal reflux is a physio-logical movement occurring as a result of constantly changing pressures between the stomach and oesophagus. The inherent relaxation of the lower oesophageal sphincter (LES) allows the stomach contents to travel upwards into the distal oesophagus, where it is immediately cleared back into the stomach, not causing any symptoms. GERD happens when frequent or prolonged exposure of oesophageal mucosa to the stomach’s acidic content affects the barriers protecting the oesophagus and causes bothersome

GASTROESOPHAGEAL REFLUX DISEASE AND DYSPHAGIA

It is not often that dysphagia is discussed in the context of gastroesophageal reflux. This article presents an overview of gastroesophageal reflux disease (GERD), focusing on its relation to swallowing difficulties.

Bogna Nicinska RDSpecialist Diabetes Dietitian, Oviva

Dietitian by day, writer by night, Bogna has experience in research, community and acute care. Prior to Oviva, Bogna worked at Imperial College Healthcare NHS Trust as a Nutrition Support Dietitian.

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Figure 1: Prevalence of gastroesophageal reflux worldwide,3

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symptoms. Up to 70% of GERD patients develop a non-erosive reflux disease (NERD) which typically remains unchanged. However, around 10% of patients with NERD might progress to erosive reflux disease (ERD).2,4,5

GERD RISK FACTORSHigh BMI, large waist circumference, limited physical activity, high fat intake and consumption of carbonated drinks are several risk factors predisposing to GERD. The role of alcohol and smoking as risk factors is unclear, although both are associated with progression to oesophageal malignancy. Medications, such as calcium channel blockers, anticholinergics, nonsteroidal anti-inflammatory drugs (NSAIDs), potassium supplements, tetracycline and bisphosphonates, may exacerbate GERD symptoms and prolong the treatment. Other GERD risk factors include pregnancy, hiatus hernia, family history and decrease in the prevalence of Helicobacter pylori infection.2,6

GERD AND DYSPHAGIAIn most cases, GERD can be diagnosed clinically based on comprehensive history and symptomatology. According to the World Gastroenterology Organisation (WGO), pre-sence of symptoms twice or more times a week is suggestive of GERD.2 However, with some patients, pH monitoring or an esophagogastroduodenoscopy (EGD) might be required.4,7 The most common typical symptoms

of GERD are heartburn and regurgitation. Nevertheless, patients might display atypical symptoms such as asthma, chronic cough, hoarseness, laryngitis, chest pain, epigastric pain or globus sensation.2 Dysphagia can occur as a direct complication of GERD or as an indirect consequence of prolonged GERD and its treatment. Alternatively, it can be part of a disorder mimicking GERD (see Table 1). As the usual assessment of dysphagia is based on biased (culture, beliefs, ethnicity) self-reporting with yes/no answers, researchers in Brazil decided to use a validated Eating Assessment Tool (EAT-10) instead, to determine the prevalence of dysphagia in patients with GERD. A total of 147 patients (age, 20-70 years; women, 72%) complaining of heartburn and regurgitation, without oesophageal stricture, previous oesophageal surgery, or other diseases were evaluated. Twenty-seven patients had oesophagitis. Results of the 147 patients were compared with those of 417 healthy volunteers (women, 62%; control group) aged 20-68 years. The prevalence of dysphagia was noted in 56% of the patients with oesophagitis and 47% of the patients without oesophagitis. Moreover, 20% of the patients had a diagnosis of ineffective oesophageal motility.5

In the context of GERD, oesophageal and functional (non-obstructive) dysphagia are discussed. Oesophageal dysphagia embraces all the disorders originating below Upper Oesophageal Sphincter (UES), which means the

Table 1: Mechanisms of dysphagia in gastroesophageal reflux disease (GERD)4

Dysphagia directly related to GERD• Erosive oesophagitis• Reflex-induced peptic stricture• Oesophageal adenocarcinoma from Barrett’s oesophagus

Dysphagia indirectly related to GERD

• Hiatus hernia• Oesophageal hypomotility• Postfundoplication dysphagia• Dysphagia following radiofrequency ablation of Barrett’s

oesophagus

Dysphagia from disorders mimicking GERD

• Pill oesophagitis• Eosinophilic oesophagitis• Achalasia and oesophageal outflow obstruction• Infectious oesophagitis• Lichen planus• Acute oesophageal necrosis (black oesophagus)• Caustic oesophagitis

symptoms onset occurs following the swallow, not during the swallow (as in the case of oropharyngeal dysphagia). Patients with reflux-associated dysphagia exhibit difficulty in opening the UES, a longer time for the bolus to pass through the sphincter and a delayed airway closure relative to the bolus arrival at the UES. As per Rome IV criteria, functional dysphagia can be diagnosed upon tests for eosinophilic oesophagitis, GERD and major motor disorders are negative. It is the sensation of abnormal bolus transit through the oesophagus in the absence of any abnormalities. The main causes for its occurrence are mentioned changes in oesophageal motility, dysfunction of UES and hypersensitivity in patients with GERD.8-10

Patients experiencing dysphagia with GERD or with suspicion of GERD should undergo further invasive investigation (oesophageal function testing, barium radiography and endoscopic functional lumen imaging probe called endo-FLIP), for evaluation of potentialcomplications such as stricture or malignancy (see Figure 2).

MANAGEMENT OF GERD AND DYSPHAGIA IN GERD PRESENTATIONGERD therapy is primarily focused on pharmacological interventions and lifestyle changes. If those fail, some patients may under-go surgery called fundoplication. Therapy of dysphagia in GERD presentation, similarly, con-centrates on pharmacological acid suppression and potential fundoplication. The lifestyle interventions in GERD include:• weight loss (in individuals with high BMI);• avoiding large meals or meals before

bedtime;• avoidance of tea/coffee (acid production),

alcohol, chocolate and foods high in fat (decreasing LES pressure), peppermint, citrus, carbonated drinks and spicy foods;

• smoking cessation;• head-of-the-bed elevation.11,12

In 2018, researchers from Moscow invest-igated the effect of dietary fibre on GERD/NERD patients. Their prospective study revealed that dietary fibres have the ability to bind nitric

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Figure 2: Algorithm for evaluation of dysphagia

oxide contained in food, which may diminish its negative effect on LES pressure. In practice, it suggests that increased fibre intake can lead to a decrease in the number of gastroesophageal refluxes.13

PHARMACOLOGICAL INTERVENTIONStomach acid secretion is regulated by neural (acetylcholine), hormonal (gastrin) and paracrine (histamine, somatostatin) mechanisms. The major circulating stimulus of acid secretion is gastrin, which mobilises histamine ensuring the proper secretion of hydrogen chloride (HCl). The most common pharmaceuticals are over the counter antacids, which offer rapid but transient action. Following GERD diagnosis, it is likely that H2-receptor antagonists (H2RAs) or Proton pump inhibitors (PPIs) will be prescribed. H2RAs partially suppress basal and meal-stimulated acid secretion for approximately 10 h/day when given twice/day at recommended doses. Regrettably, H2RAs present limited efficacy in more complex disorders such as erosive oesophagitis. PPIs on the other hand,

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secrete hydrogen ions into the gastric lumen in exchange for potassium ions. Once-daily PPI therapy inhibits maximal acid output by about 66% after five days. Moreover, PPI has been proven beneficial in both healing erosive oesophagitis and dysphagia relief. In a cohort of 12,000 patients, once-daily dosage of PPI resolved dysphagia in 83% of the patients.14,15

Being aware of pharmacological limitations of H2RAs and PPIs, such as a delay onset of action, incomplete acid suppression and the need for ingestion before a meal to achieve maximum efficacy, a new era of medication is on its way. This includes the development of potent H2-receptor agonists, gastrin agonists, non-benzimidazole PPI, extended and delayed release PPIs, a PPI combination, new agents with longer half-lives and a new generation of PPIs. Clinical benefits and side effects of new medications need yet to be determined.16,17

SURGERYIn some cases of persistent GERD, significant hiatus hernia or mucosal damage, anti-reflux surgery called a Nissen fundoplication, might be considered. However, fundoplication carries a higher risk of post-operative dysphagia compared to pharmacological intervention. Up to two thirds of patients develop dysphagia postfundoplication.18 A study by Hasak et al concluded that most patients with early (six weeks after anti-reflux surgery) postfundoplication dysphagia resolve with time and require no intervention, and those with clinically significant late (>six weeks after surgery) postfundoplication dysphagia benefit from endoscopic dilation.19

SUMMARYGERD is one of the most common diseases encountered by doctors on the appointment. Dysphagia occurs in 50% of these patients and it is important they undergo further investigations for evaluation of potential stricture or malignancy. The therapy focuses primarily on acid suppression through pharmacological intervention or, if necessary, a surgery. The limitations of current treatment are recognised, and new improved ways of action are being developed.