Gastro-Oesophageal Reflux Disease (GORD)
What is it?
Heartburn, the cardinal symptom of gastro-oesophageal reflux disease, is experienced by 15 – 20% of adults at least once a week.
The patient’s history and response to an empiric trial with a proton pump inhibitor (PPI) are used to diagnose GORD in primary care. Endoscopy often provides limited diagnostic information as most patients with GORD will not have visible lesions.
The role of endoscopy is therefore limited to investigating patients with possible complications of GORD, e.g. erosive oesophagitis or Barrett’s oesophagus. PPIs are the mainstay of treatment for GORD but should be prescribed at the lowest effective dose or “as needed” for patients with mild to moderate forms of GORD.
The patient’s history and response to an empiric trial with a proton pump inhibitor (PPI) are used to diagnose GORD in primary care. Endoscopy often provides limited diagnostic information as most patients with GORD will not have visible lesions.
The role of endoscopy is therefore limited to investigating patients with possible complications of GORD, e.g. erosive oesophagitis or Barrett’s oesophagus. PPIs are the mainstay of treatment for GORD but should be prescribed at the lowest effective dose or “as needed” for patients with mild to moderate forms of GORD.
Gastro-oesophageal reflux disease (GORD) and its complications
Reflux of the stomach's contents into the oesophagus is a regular physiological event that occurs in many people after eating. When gastric reflux causes a person to have symptoms and/or complications, they are said to have gastro-oesophageal reflux disease (GORD); the Montreal definition. This patient-centred definition frames GORD as a range of disorders, including
- non-erosive reflux disease,
- erosive oesophagitis,
- Barrett’s oesophagus and, most seriously,
- oesophageal adenocarcinoma.
Between 15 – 20% of adults experience heartburn, the cardinal symptom of GORD, at least once a week. GORD is clinically significant when symptoms are present two or more days a week.1 Proton pump inhibitors (PPIs) are used in the short term to help diagnose GORD, allow healing of erosive lesions, and provide long-term symptom control on an “as needed” or daily basis. If a patient has an uncertain diagnosis or symptoms that do not respond to treatment, they may need to be referred for further investigation.
The pathophysiology of GORD
The most common cause of gastric reflux is periodic relaxation of the lower oesophageal sphincter. This exposes the easily damaged squamous mucosa of the oesophagus to acid, proteolytic enzymes (e.g. pepsin and trypsin) and bile salts.
Repeated exposure to gastric reflux can cause oesophagitis that is visible on endoscopy in some people, although approximately two-thirds of people with GORD will not have visible signs of this. For many people, GORD symptoms result from abnormal spaces in the mucosa's epithelium, causing excessive nerve endings and peripheral sensitisation stimulation. Without any reflux of gastric fluid, gas reflux can also be experienced as heartburn. In people with GORD symptoms that do not respond to PPI treatment, gas reflux may be causing distension of mechanoreceptors in the oesophageal wall.
Acid production by the stomach is highest when empty, but patients often experience GORD when acid production is lowest after a meal. This is because after eating, an unbuffered volume of acid is formed in the proximal region of the stomach, referred to as the acid pocket.
GORD can be caused or exacerbated by:
- Hiatus hernia; occurs when the oesophageal junction is displaced. Nearly all patients with severe GORD have a hiatus hernia which can be diagnosed on endoscopy.
- Central obesity; increases the pressure gradient between the abdomen and thorax, increasing the number of reflux episodes and the likelihood of hiatus hernia.
- Impaired oesophageal or gastric clearance; slow material moving down the digestive tract.
Stress is reported to be a causative factor for symptoms by 60% of people with GORD. Symptoms of GORD may be aggravated by diet and lifestyle, e.g. high-fat foods, spicy foods, caffeine, alcohol and smoking.
Risk factors for GORD
The risk of GORD is increased in people who consume more than seven standard alcoholic drinks per week. The risk is also increased in people with a first-degree relative with a history of heartburn. The genetics of GORD are poorly understood, and multiple genes are likely to be involved. Up to half of the pregnant women will experience symptoms related to GORD (see: “GORD during pregnancy”). GORD is also more prevalent in people confined to bed for extended periods.
Non-steroidal anti-inflammatory drugs (NSAIDs), some antibiotics (e.g. tetracyclines), iron supplements and potassium supplements can irritate the oesophagus and cause heartburn. The likelihood of GORD and its complications (see below) is increased in people who are obese, have chronic respiratory disease (e.g. asthma), or have connective tissue disease (e.g. scleroderma).
In people with systemic sclerosis, atrophy of the muscularis mucosa and submucosal fibrosis result in oesophageal and gastrointestinal dysfunction.7 The relationship between GORD and asthma needs to be clarified, and a review on the subject could not conclude whether GORD precedes asthma or triggers GORD.8
In people with systemic sclerosis, atrophy of the muscularis mucosa and submucosal fibrosis result in oesophageal and gastrointestinal dysfunction.7 The relationship between GORD and asthma needs to be clarified, and a review on the subject could not conclude whether GORD precedes asthma or triggers GORD.8
The complications of GORD
Chronic exposure of the oesophagus to gastric reflux can result in several complications requiring long-term management.
- Erosive oesophagitis occurs when excessive gastric reflux causes necrosis of the oesophageal mucosa, resulting in erosions and ulcers. This is diagnosed with endoscopy and graded A to D (least to most severe) according to the Los Angeles classification. People with erosive oesophagitis have a five times greater risk of progressing to Barrett’s oesophagus.
- Barrett’s oesophagus is a complication of chronic GORD involving metaplasia of the lining of the lower oesophagus following exposure to gastric reflux. This results in the squamous epithelium being replaced by a specialised columnar-lined epithelium. The risk of Barrett’s oesophagus increases with age, and it is more likely in males and people who are obese to have a poor diet or smoke. The prevalence of Barrett’s oesophagus in the general population has been estimated at 1.6%. The lifetime risk of a person with Barrett’s oesophagus developing oesophageal adenocarcinoma is less than 2%.
- Peptic stricture is a narrowing of the oesophagus that results from the healing and fibrosis of inflammatory lesions following long-term exposure to gastric reflux. There has been a substantial decline in the prevalence of peptic strictures due to the use of PPIs. Peptic stricture is likely higher in older people with chronic GORD or people with dysphagia. Peptic strictures are classified as simple or complex, depending on their length and degree of contraction. They are generally treated using invasive techniques that physically dilate the oesophagus.
- The risk of oesophageal adenocarcinoma is correlated with symptoms' frequency, severity and duration. People with frequent symptoms of GORD, i.e. more than three times per week, are approximately 17 times more likely to develop oesophageal adenocarcinoma than those without GORD. People with severe symptoms occurring for more than 20 years are over 40 times more likely to develop adenocarcinoma than those without GORD.10
People with Barrett’s oesophagus have a significantly increased risk of developing adenocarcinoma, but very few people with Barrett’s oesophagus die from this form of cancer.
Diagnosing GORD
The characteristic features of GORD are heartburn and regurgitation. The meaning of heartburn may not be apparent to all patients, and providing a description is known to increase GORD detection rates. Heartburn is a burning feeling that rises from the stomach or lower chest towards the neck and frequently occurs after eating. It may also be associated with bending, lying down or straining. Approximately two-thirds of people with GORD report upper abdominal pain or discomfort. Regurgitated food is generally swallowed but can sometimes be of sufficient quantity to be mistaken as vomit. Patients may also experience water brash. This sudden and rapid saliva production fills the mouth and may be associated with nausea. The patient’s history may reveal triggers for GORD symptoms, which can be avoided.
Atypical symptoms of GORD include angina-like chest pain, cough, hoarseness or throat changes, wheezing, frequent belching and nausea. Several other conditions can cause gastrointestinal symptoms that may be mistaken for GORD. These include gastric ulcer disease, and functional dyspepsia (dyspepsia without an apparent cause), and approximately 40% of patients with irritable bowel syndrome will have regurgitation. Helicobacter pylori infection should be considered in patients who present with dyspepsia. The possibility of medicine-induced symptoms should also be considered if the patient is taking medicines that cause dyspepsia or that have a mechanism of action that is more likely to result in reflux, e.g. theophylline, nitrates, calcium-channel blockers, beta-blockers, alpha-blockers, benzodiazepines, tricyclic antidepressants and anticholinergics, which can all reduce oesophageal sphincter pressure and exacerbate the symptoms of GORD.
Low, or absent, gastric acid production (achlorhydria) impairs protein digestion, can cause symptoms similar to GORD, and is more common in older people.
A therapeutic trial can be used to diagnose GORD.
A therapeutic trial of PPIs in a patient with symptoms suggestive of GORD has comparable sensitivity and specificity for diagnosing GORD as measuring the presence of oesophageal acid directly with a pH monitor in a secondary care setting. This approach suits younger patients with no red flags and mild, long-term symptoms. It is unlikely that prescribing a higher dose of a PPI will benefit patients with uncomplicated GORD as in a primary care setting omeprazole 20 mg, daily is generally considered to be as effective as omeprazole 40 mg, daily.
A therapeutic trial of PPIs in a patient with symptoms suggestive of GORD has comparable sensitivity and specificity for diagnosing GORD as measuring the presence of oesophageal acid directly with a pH monitor in a secondary care setting. This approach suits younger patients with no red flags and mild, long-term symptoms. It is unlikely that prescribing a higher dose of a PPI will benefit patients with uncomplicated GORD as in a primary care setting omeprazole 20 mg, daily is generally considered to be as effective as omeprazole 40 mg, daily.
The role of endoscopy
The role of endoscopy is limited in diagnosing GORD as most patients with GORD will not have oesophageal abnormalities on endoscopy. However, endoscopy is the investigation with the highest specificity for oesophagitis caused by GORD as it can differentiate between mucosal lesions caused by infective oesophagitis, peptic ulcer disease, malignancy and other abnormalities of the gut.1 Endoscopy is also the most sensitive technique for diagnosing Barrett’s oesophagus and is used to identify peptic strictures.
The role of endoscopy is limited in diagnosing GORD as most patients with GORD will not have oesophageal abnormalities on endoscopy. However, endoscopy is the investigation with the highest specificity for oesophagitis caused by GORD as it can differentiate between mucosal lesions caused by infective oesophagitis, peptic ulcer disease, malignancy and other abnormalities of the gut.1 Endoscopy is also the most sensitive technique for diagnosing Barrett’s oesophagus and is used to identify peptic strictures.
Endoscopic assessment is indicated:
- Promptly in patients with red flags, whether or not empiric treatment is initiated
- Where there are diagnostic uncertainty, e.g. non-specific or atypical symptoms, or when other diagnoses are being considered, e.g. infective or medicine-induced oesophagitis or malignancy.
- When the patient's symptoms do not respond to PPI treatment or worsen despite treatment
- Before surgical intervention for GORD, e.g. fundoplication
Endoscopy may also be appropriate for patients with GORD that have multiple risk factors for oesophageal adenocarcinoma, e.g. chronic GORD, frequent symptoms, age over 55 years (local guidelines may vary), males, European ethnicity, a history of smoking, hiatus hernia, increased body mass index and intra-abdominal distribution of fat.
Managing patients with GORD
The management of GORD is determined by the severity of the patient’s symptoms and the likelihood of complications. If the patient’s symptoms are mild, lifestyle changes and antacids may provide benefits before a diagnostic trial with PPIs is tried (see below). However, there is no evidence that changes in lifestyle alone will allow the healing of established oesophagitis.
Lifestyle treatment strategies include:
- Avoiding foods that cause symptoms, e.g. alcohol, coffee and spicy, fatty or acidic foods
- Avoiding eating three to four hours before sleeping
- Weight loss for obese or overweight patients
- Smoking cessation
- Raising the head of the bed, if this can be done safely. Extra pillows should not be used as they may increase abdominal pressure.
Discussing the patient’s stress or anxiety levels and suggesting relaxation techniques may improve symptoms or assist the patient in avoiding triggers for GORD, e.g. alcohol.
Review the use of any medicines which may be contributing to symptoms.
Due to their rapid onset, over-the-counter antacids can be used for the occasional treatment of patients with mild or intermittent symptoms of GORD. However, these are not appropriate for the long-term management of GORD.
Proton pump inhibitors are the first-line treatment for GORD
Multiple studies have found PPIs to be the most potent class of acid-suppressive medicine and the most effective class of medicine in treating GORD. For example, a meta-analysis found that PPIs were more effective than H2-receptor antagonists at treating erosive oesophagitis, especially in patients with severe disease.
When initiating PPI treatment, it is a good idea to discuss with patients the expected duration of treatment. For patients with mild GORD, the regimen should be regularly reviewed with the goal of treatment being lifestyle control of symptoms with minimal reliance on medicines. Patients with severe GORD are likely to require long-term treatment with PPIs and may require surgery.
The patient's age should be considered when recommending a treatment regimen, as younger patients may be exposed to a greater lifetime risk of adverse effects from long-term PPI use. The possibility of the patient developing rebound acid secretion following treatment withdrawal should also be discussed. This occurs due to increased gastrin production, which is released to compensate for the decreased acidity of the stomach when PPIs are taken.
PPIs can be purchased in limited quantities, without a prescription, as a “Pharmacist only” medicine. Patients should be asked about any use of medicines for their GORD symptoms before PPIs are prescribed. Patients who self-administer PPIs could potentially develop rebound acid secretion, complicating the clinical picture.
Antacids can be prescribed as “rescue” medication for rebound acid secretion.
Many patients will experience reflux after PPIs are withdrawn due to rebound acid secretion. This can be indistinguishable from the ongoing symptoms of GORD. Patients can be prescribed “rescue” medication to help them manage symptoms that may arise after stopping the PPI. If symptoms cannot be managed, or continue for longer than one or two weeks, reconsider the decision to withdraw the PPI.
Antacids can be prescribed as “rescue” medication for rebound acid secretion.
Many patients will experience reflux after PPIs are withdrawn due to rebound acid secretion. This can be indistinguishable from the ongoing symptoms of GORD. Patients can be prescribed “rescue” medication to help them manage symptoms that may arise after stopping the PPI. If symptoms cannot be managed, or continue for longer than one or two weeks, reconsider the decision to withdraw the PPI.
Medicines containing antacids and anti-foaming agents are likely the most effective treatment for rebound acid secretion. Liquid preparations are often more effective, but chewable tablets may be more convenient for some patients. Some products contain significant amounts of sodium and should be used carefully or avoided in patients with heart failure (see below). To avoid interactions, these medicines should not be used within two hours of taking any regular medicines for other conditions.
The following medicines are currently partially subsidised* and may be prescribed for adults:
- Mylanta P or Acidex oral liquid, 10–20 mL, as required, up to four times daily, usually after meals and at night. Prescribe Acidex with caution in people with heart failure.
- Gaviscon Double Strength tablets, 1–2 tablets chewed as required, up to four times daily, after meals and half an hour before bed. Prescribe Gaviscon Double Strength with caution in people with heart failure.
- Aluminium hydroxide tablets are an alternative antacid that is fully subsidised but do not contain an anti-foaming agent. Prescribe Alu-tab 600 mg tablets, one tablet, up to four times daily, between meals and at bedtime.
Note:
Medical conditions MUST always be diagnosed by a medical professional.
The following information is structured to provide basic information to HWH Support Workers and Clinical Care Managers.
Medical conditions MUST always be diagnosed by a medical professional.
The following information is structured to provide basic information to HWH Support Workers and Clinical Care Managers.