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Acid reflux (gastro-oesophageal reflux disease; GORD)

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Image edited by Dr.Dt.E.Bihter Gürler

Gastro-oesophageal reflux disease (also known as GORD, gastroesophageal reflux disease, GERD or acid reflux disease) is a disease of the distal oesophagus and stomach. It involves the inflammation and damage of the lower oesophageal mucosa due to the spontaneous and involuntary reflux of gastric contents, including ingested food, gastric acid, and occasionally pancreatic and biliary secretions.1,2 GORD classically produces symptoms of heartburn and dyspepsia.

The image below demonstrates ulceration of the distal end of the oesophagus seen on endoscopy.

Figure 1: Inflamed oesophagus due to GORD. 

Incidence

Gastro-oesophageal reflux disease (GORD) is common in the Australian community. Data from the United Kingdom and United States suggest that approximately 20% of the population will experience symptoms of heartburn and acid reflux at least once per week, and that these symptoms are a frequent reason for general practice appointments.3 Similar high rates have also been demonstrated in Australia. Furthermore, approximately 80% of the population will have experienced symptoms of heartburn at some point in their lives.2,4

GORD is usually considered a disease of adults, with more than 50% of people with gastro-oesophageal reflux disease aged between 45 and 64.4,5

Gastro-oesophageal reflux disease can also present in infants and children. This must be distinguished from physiological reflux – a benign and self-limiting condition common in infants during the first year of life.2 However, gastro-oesophageal reflux and gastro-oesophageal reflux disease are more common in infants than older children and adults due to both the immaturity of the oesophagus and stomach, as well as a higher fluid intake.6,7

Predisposing Factors

A combination of genetic influences, lifestyle factors and dietary behaviour are thought to be involved in the development of GORD.8

Predisposing factors with a higher risk of developing GORD include:8-10

  • Obesity;
  • Cigarette smoking;
  • High caffeine intake;
  • Excess alcohol ingestion;
  • Eating large meals (especially late at night), or meals high in fat or chocolate. However, the evidence linking specific foods with GORD is lacking;
  • Hiatus hernia;
  • Pregnancy; and
  • Some drugs (particularly anti-hypertensives, anti-angina medications, and NSAIDs).

Impaired salivation, for example due to Sjogren’s syndrome, anticholinergic medications or oral radiation therapy, may exacerbate the symptoms of GORD.5 Likewise, GORD may exacerbate symptoms of asthma.10

Children

Reflux occurs in children when intra-abdominal pressures exceed those across the lower oesophageal sphincter (LOS). Transient relaxation of the sphincter is the major mechanism of reflux in infants, children and adults.2 Abdominal straining (leading to increased intra-abdominal pressures) and delayed gastric emptying may exacerbate reflux. The former is responsible for approximately 50% of episodes of reflux in infants and children. Immaturity of the digestive system, hereditary factors and food sensitivities may also contribute to reflux in children.11 Furthermore, neurological impairments may predispose to the development of gastro-oesophageal reflux.2

Macroscopic Features

Anatomic changes depend on the cause, duration and severity of reflux.4 Prolonged reflux causes inflammation (oesophagitis) and changes to the underlying mucosa.10 The oesophagus ranges from having a normal macroscopic appearance to diffuse or linear hyperaemia with superficial erosions to frank ulceration with or without hiatus hernias and strictures.12

Barrett’s oesophagus can appear macroscopically as tongues or patches of red velvety mucosa extending upwards from the gastro-oesophageal junction.12 Note, however, that symptoms correlate poorly with endoscopic evidence of injury to the mucosa.8

Microscopic Features

Oesophagitis may be seen as inflammation with red friable mucosa and ulceration in severe cases. There are three characteristic microscopic changes:

  1. Presence of inflammatory cells in the epithelial layer.
  2. Basal zone hyperplasia greater than 20% of epithelial thickness.
  3. Elongation of lamina propria papillae with congestion extending to top third of the epithelial layer.

Intra-epithelial eosinophils are believed to be present early, and intra-epithelial neutrophils are markers of more severe injury (e.g. ulceration).12

The image below is of Barrett’s oesophagus. Note the replacement of normal oesophageal squamous epithelium with metaplastic columnar epithelium, and the presence of mucosal glandular structures in the metaplastic epithelium.8,12 Barrett’s oesophagus predisposes to the development of adenocarcinoma, thus dysplastic changes may also be seen in the oesophagus.12

Figure 2: Barrett’s oesophagus

Natural History

Over time, oesophageal exposure to gastric acid in gastro-oesophageal reflux disease can lead to a number of complications:4

  • Reflux oesophagitis, which may be mild or erosive;
  • Peptic stricture: Present in up to 10% of patients with untreated gastro-oesophageal reflux disease;
  • Development of Barrett’s oesophagus.

Approximately 11% of patients with GORD will develop Barrett’s oesophagus (replacement of the squamous mucosa of the distal oesophagus by metaplastic columnar epithelium in response prolonged exposure to acid and/or bile). Patients at higher risk are those with long-standing or severe reflux disease. Barrett’s oesophagus is significant due to the 30-40 fold higher relative risk of developing adenocarcinoma of the oesophagus.4,12

Children

In infants and children, mild gastro-oesophageal reflux symptoms usually resolve within the first 12 months of life. By 1-2 years of age, the oesophageal mechanisms have matured so that increased intra-abdominal pressures are no longer transmitted as reflux.6 A more solid diet and increased upright posture also helps to prevent reflux.7 However, a small percentage of children will go on to develop true GORD, and these children may require treatment to prevent complications.2

Clinical History

You should consider GORD in any patient presenting with predominant or frequent (more than once a week) heartburn until proven otherwise.13

The following are common symptoms of GORD:4,5,10

  • Heartburn;
  • Dysphagia;
  • Acid regurgitation;
  • Upper gastrointestinal bleeding;
  • Nausea and vomiting;
  • Belching;
  • Epigastric pain which can radiate through to the back;
  • ‘Waterbras’ (excess salivation due to reflex salivary gland stimulation as acid enters the oesophagus).

You should elicit a detailed history of the symptoms, including their onset, duration, and aggravating and relieving factors.

Classically patients will describe a worsening of heartburn (a burning retrosternal discomfort) 30-60 minutes after meals, with aggravation on bending, stooping, or lying down, and relief with antacids.10 Patients also may complain of pain on eating or drinking (odynophagia), especially on drinking hot liquids or alcohol.5 This is caused by oesophagitis or strictures within the lower oesophagus. Dysphagia may be the presenting complaint of patients with erosive oesophagitis, oesophageal dysmotility, strictures, or adenocarcinoma of the oesophagus.5

Family history and information about lifestyle factors may be useful for supporting the diagnosis of GORD. Regurgitation of food and acid into the mouth (acid brash) gives a bitter, acid taste; this tends to occurparticularly when the patient is lying flat or bending. Aspiration into the lungs is unusual, but cough, nocturnal asthma, and even waking with choking from regurgitation and aspiration can occur.9,10 Note that patients with GORD may present with chest pain, not unlike the presentation of patients with angina.4

The correlation between heartburn and severity of oesophagitis is poor. Some patients with severe oesophagitis may not present with symptoms but instead with bleeding (haematemesis) or anaemia.5

Infants and children

The most common symptoms of GORD in children are vomiting and regurgitation.There are, however, a large number of conditions that can cause vomiting and regurgitation (effortless spilling of gastric contents) in children.2 More serious causes, such as foreign bodies, pyloric stenosis, bowel obstruction and inflammatory bowel disease, should be excluded.

GORD should be suspected in infants and children who present with the following symptoms:

  • Infants: Feeding difficulties (including refusing to feed, pulling away, comfort feeding, crying during feeding), failure to thrive or malnutrition, colic, irritability, cough, cyanotic episodes, apnoeic episodes, sleep disturbances (restless during sleep and night time wakening), hiccoughing.11
  • Children: Complaints of a ‘bad taste’ in the mouth, nausea, dysphagia or odynophagia, heartburn, haematemesis (coffee ground vomit), recurrent chest infections, weight loss, hoarseness of the voice, chronic cough or asthma.2

Like adults, the number and degree of symptoms does not necessarily correlate with the severity of reflux. Symptoms vary largely with age. Older children are more likely to describe typical symptoms of heartburn, chest pain and a sick or sour taste in the mouth. Serious presentations of GORD include apnoea and recurrent chest infections secondary to aspiration.2

Clinical Examination

GORD is not associated with specific findings on physical examination. There may be weight loss as a consequence of dysphagia, or weight gain as a result of eating to relieve symptoms.9

General Investigations

The diagnosis of GORD can often be made without performing investigations, especially in young patients with typical symptoms and without concerning features such as vomitingweight loss or anaemia.Patients with a history of uncomplicated GORD can undergo empirical treatment (including lifestyle modification) without further investigations.14 However, specific investigations are indicated in patients with atypical features, if complications are suspected, or if there is no response to therapy.

Common investigations include:14

  • Barium swallow and meal: Ingestion of a radio-labelled dye may help visualise reflux, hiatus hernia and strictures. Simple oesophagitis cannot be seen. The disadvantage of this technique is that biopsy is not possible.
  • Oesophagogastroscopyupper gastrointestinal endoscopy: A fibre-optic telescope passed through the mouth allows for direct visualisation of the lining of the oesophagus, as well as a biopsy if necessary. This allows for the diagnosis of Barrett’s oesophagus and other complications, including malignancy. Endoscopy and biopsy are considered the best investigations for detecting complications, but a normal examination cannot exclude the diagnosis of GORD.

Specific Investigations

Ambulatory 24-hour oesophageal pH monitoring is unnecessary in most patients, but may be recommended for documentation and quantitation of reflux. It should be performed when there is uncertainty regarding the role of reflux in causing a patient’s symptoms, or when surgery is being considered.5 Oesophageal motility studies may occasionally be useful in assessing suitability for surgical intervention.4

Investigations in children

There is no single test for the diagnosis of GORD in children. If physiological reflux is suspected, further diagnostic tests are not indicated. Thorough history and examination is also usually sufficient to make the diagnosis of typical GORD in children.7 However, investigations are sometimes performed according to the age of the child, availability of tests and severity of symptoms.

Possible investigations include:

  • Barium studies: The most widely used but with poor accuracy. This helps diagnose other structural abnormalities such as pyloric stenosis, intestinal rotation or hiatus hernia.7
  • Radionucleotide scintigraphy
  • Upper gastrointestinal endoscopy and biopsies: This investigation is indicated in patients with complications. Biopsies also serve a diagnostic purpose in children.4
  • 24-hour intra-oesophageal pH monitoring: This is the gold standard for detecting reflux, but not necessarily disease.
  • Oesophageal manometry: This is most useful prior to anti-reflux surgery.4,14

Prognosis

With appropriate treatment, the prognosis for patients with GORD is excellent, as symptoms almost invariably resolve and oesophageal inflammation can heal in the majority of patients. However, recurrence of disease is common if therapy is stopped. Surgery is available for severe cases.6

The presence of Barrett’s oesophagus signifies that the patient is at a much higher chance of developing adenocarcinoma of the oesophagus (30-40 times that of the general population).12

An increased risk of developing oesophageal adenocarcinoma is associated with male sex, smoking, obesity, age, and the frequency and severity of reflux symptoms.8 These patients require more aggressive treatment and follow-up.9 However, the overall absolute risk of developing adenocarcinoma is still low and only 2-3 percent of affected individuals die from adenocarcinoma of the oesophagus.8

Children

As aforementioned, the majority of children will grow out of their condition and long-term complications of gastro-oesophageal reflux are rare.6 Reflux during childhood can lead to failure to thrive, pulmonary disease (primary aspiration pneumonia) and oesophagitis.

Treatment Overview

Management of GORD requires a combination of lifestyle changes, medication, and occasionally, surgical intervention. The aims of treatment are to relieve symptoms, improve quality of life, heal erosive oesophagitis, and avoid complications.1 Below is an overview of the treatments available for GORD.  


Lifestyle factors

Patients should be educated on the typical triggers for GORD so that avoidance measures can be put in place. Studies have shown that the following lifestyle modifications will reduce acid exposure to the oesophagus, though the true effect of these changes is unknown:14

  • Elevation of the head of the bed
  • Smoking cessation
  • Decreased fat intake
  • Avoiding recumbency for three hours after eating

It is estimated that up to 50% of patients respond to simple antacids and general measures, including weight reduction; avoidance of ‘trigger’ foods (spicy or high fat foods); small, frequent meals; reduction in caffeine, alcohol and nicotine consumption; and sleeping on a wedge pillow or with the head of the bed elevated.15

Pharmacological management

  • Simple antacids (e.g. Mylanta) or alginates (e.g. Gaviscon) may be sufficient for patients with infrequent GORD.15 These agents are available over-the-counter and can be self-administered.14
  • Acid suppression is the mainstay of treatment for GORD. Both proton pump inhibitors (PPIs) and H2 receptor antagonists can be used, but studies have shown that the former produces more rapid responses and healing in a greater percentage of patients.14 A recent head-to-head trial showed that low-dose PPI pantoprazole (e.g. Somac) once daily was superior to standard-dose H2 receptor antagonist ranitidine (e.g. Zantac) in terms of complete symptom control. Both agents are safely tolerated.3 Note that cessation of these agents frequently leads to rapid return of symptoms so long-term maintenance therapy is often appropriate.14 Mild GORD may be treated with an over-the-counter formulation of pantoprazole (Somac Heartburn Relief) for up to 14 consecutive days.
  • Prokinetic agents can enhance emptying of the oesophagus and stomach, but tend to be used only as an adjunctive therapy for patients.5 Examples include metoclopramide, cisapride or domperidone. Dystonic reactions are a potential serious side effect of these medications.10
  • Mucosal protective agents such as sucralfate, which forms a protective barrier resistant to acid, pepsin and bile.5,15
  • Helicobacter pylorieradication: The role of pylori in GORD remains controversial. In some types of gastritis, treatment can improve reflux; however, in cases of generalised atrophic gastritis, a condition that usually results in less acid production, eradication may actually increase reflux. However, due to the risks of peptic ulceration and gastric carcinoma from this bacterium, eradication is usually recommended.8,10

Heartburn Treatment Plan Questionnaire

Step by Step

Part A
Is the patient experiencing:
YesNo
Heartburn (Burning feeling rising from the stomach or lower chest up towards the neck)
Regurgitation (The taste of food, acid or fluid coming back into the mouth)

References:

  1. Somac Heartburn Relief: Pharmacist Training Manual. Nycomed Pty Ltd. August 2008.
  2. Somac Heartburn Relief Tablets Consumer Medicine Information. July 2008.

This information will be collected for educational purposes, however, it will remain anonymous.

Surgery

Nissen fundoplication (preferably laparoscopically) is the most popular type of anti-reflux surgery, involving the wrapping of the upper stomach around the lower oesophagus, and the reduction of a sliding hiatus hernia when present.4,10 Fundoplication increases lower oesophageal sphincter pressure and may be particularly appropriate in patients requiring high dose proton pump inhibitor therapy who have persistently inadequate sphincter pressure in oesophageal motility studies.4 Controversy still exists regarding the long-term effectiveness of surgical intervention compared to chronic medical treatment.14 In addition, peptic strictures may require endoscopic dilatation.

Management of Acid Reflux in Children

In most infants with gastro-oesophageal reflux, symptoms will disappear completely by 12 months of age. It is therefore important that medical or surgical treatments are only offered when absolutely necessary.2 Conservative management and lifestyle modification should be the mainstay of treatment. The overall goals of management of GORD in children are similar to adults: to eliminate symptoms, promote healing of oesophageal mucosa, manage or prevent complications, and maintain life-long remission.7

Treatment options for children include:

  • Infants with mild gastro-oesophageal reflux may respond well to simple thickening of their feeds. (Thickened formulas are commercially available).2Smaller volumes and lower osmolality of the feeds also decrease reflux.7 Keeping the child upright for 30 minutes following feeds or lying the child prone (but with an increased risk of SIDS) have also been shown to reduce reflux levels.7,11 In addition, reassurance of parents is an essential component of management. This will avoid unnecessary investigations and multiple drug treatments.
  • Acid suppressing agents may be appropriate in some infants, and in particular, in those with chronic respiratory disease or neurological disability. The agents used are similar to those for adults, and include simple antacids, proton pump inhibitors, and histamine-2 receptor antagonists. PPIs, particularly omeprazole and lansoprazole, have proven to be effective in infants and children with oesophagitis. However, long-term acid suppression is generally not recommended.6
  • Children with severe reflux disease, persistent vomiting, and failure to thrive may require continuous feeding through a nasogastric tube.
  • Nissen fundoplication may also be used in children, though the risks and complications of surgery must be carefully considered.11Surgery is often withheld until after 2-3 years of age.6

 

View the Reflux Information leaflet

 

 

More Information

 

For more information on acid reflux and heartburn and related investigations, treatments and supportive care, Acid Reflux and Heartburn.

 

References

  1. Ip S, Bonis P, Tatsioni A, et al. Comparative effectiveness of management strategies for gastroesophageal reflux disease [online]. Rockville, Md: Agency for Healthcare Research and Quality, US Department of Health and Human Services. 12 December 2005 [cited 15 March 2006]. Available online at: URL link
  2. Robinson MJ, Robertson DM (eds). Practical Paediatrics (5th edition). Parkville, VIC: Churchill Livingston; 2003. [Publisher]
  3. Talley N, Moore M, Sprogis A, Katelaris P. Randomised controlled trial of pantoprazole versus ranitidine for the treatment of uninvestigated heartburn in primary care. Med J Aust.2002; 177(8): 423-7. [Abstract | Full text]
  4. Braunwald E, Fauci AS, Kasper DL, et al. Harrison’s Principles of Internal Medicine (15th edition). New York: McGraw-Hill Publishing; 2001. [Publisher]
  5. Tierney LM, McPhee SJ, Papadakis MA (eds). Current Medical Diagnosis and Treatment (45th edition). New York: McGraw-Hill; 2006. [Publisher]
  6. Cezard J. Managing gastro-oesophageal reflux disease in children. 2004; 69(Suppl 1): 3-8. [Abstract]
  7. Chawla S, Divya S, Mahajan P, Kamat D. Gastroesophageal reflux disorder: A review for primary care providers. Clin Pediatr (Phila).2006; 45(1): 7-13. [Abstract]
  8. Fox M. Gastro-oesophageal reflux disease. Clinical review. BMJ. 2006; 332: 88-93. [AbstractFull text]
  9. Kumar P, Clark M (eds). Clinical Medicine (5th edition). Edinburgh: WB Saunders Company; 2002. [Publisher]
  10. Longmore M, Wilkinson I, Rajagopalan S. Oxford Handbook of Clinical Medicine (6th edition). Oxford: Oxford University Press; 2004. [Publisher]
  11. Reflux Infants Support Association Inc [online]. Fortitude Valley, QLD: RISA. Available from: URL link
  12. Cotran RS, Kumar V, Collins T, Robbins SL. Robbins Pathologic Basis of Disease (6th edition). Philadelphia: WB Saunders Company; 1999. [Publisher]
  13. Talley NJ, Vakil N. Guidelines for the management of dyspepsia. Am J Gastroenterol. 2005; 100(10): 2324-37. [Abstract]
  14. DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol.2005; 100(1): 190-200. [Abstract]
  15. Murtagh J. General Practice (3rd edition). Sydney: McGraw-Hill; 2003. [Publisher]

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Dates

Posted On: 18 September, 2003
Modified On: 23 November, 2018
Reviewed On: 17 March, 2007

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