GORD, Hiatus Hernia, Reflux and Barrett's Oesophagus
Gord is usually associated with excessive exposure of the oesophagus to gastric acid. Acid reflux occurs through a relatively incompetent lower oesophageal sphincter that is commonly associated with hiatus hernia. Under normal circumstances acid reflux is prevented by the contraction of the lower oesophageal sphincter together with muscular activity within the lower oesophagus which clears the refluxed contents back to the stomach.
The role of hiatus hernia.
The lower oesophageal sphincter between the oesophagus and the stomach is normally supported by the diaphragm. If the diaphragm is weakened, the stomach moves up into the chest reducing the effectiveness of the lower oesophageal sphincter and allowing acid and gastric contents to escape upwards in the oesophagus, resulting in heartburn
Those with higher acid secretion may develop symptoms, whereas those who have lower acid secretion will not. Many people hiatus hernia have no symptoms and require no treatment because if does not interfere with the function of the lower oesophageal sphincter.
Medical treatment of GORD
The objectives are:
- To achieve symptomatic relief.
- Reduce the risk of complications and improve quality of life.
- Heal oesophageal ulceration.
- Lifestyle modifications
As surveys have indicated, individuals blame a combination of lifestyle factors as the cause of their heartburn. These need to be addressed and will vary between such individuals. In general, avoidance of high fat diets, excessive coffee and alcohol and other caffeine containing drinks together with stopping smoking is important.
- Elevation of the bed head
As reflux episodes occur as frequently while upright as when prone, elevation of the bed head has little to offer in terms of therapeutic response, particularly since the advent of proton pump inhibitor therapies.
III. Weight loss
There is equally little evidence that weight loss will result in the improvement of symptoms unless there is avoidance of the particular lifestyle factors that precipitate episodes of acid reflux. There are however other major health benefits from weight reduction.
- Drugs / medication
Medications that might exacerbate reflux disease include anticholinergic drugs, antidepressants such as Amitriptyline, aspirin, non-steroid inflammatory drugs, coxibs, tetracycline, slow release potassium and biphosphonates for treatment of osteoporosis. Prescription of alternatives may be required.
If symptoms are mild or an endoscopy has shown a normal oesophagus or minimal inflammation, then it would be appropriate to begin with H2 Receptor Antagonist therapy either once or twice daily.
If symptoms are inadequately controlled, then “step up” therapy becomes mandatory, with the use of proton pump inhibitors. It must be recognised that once this level of therapy is reached, treatment is likely to be lifelong and therefore endoscopy prior to embarking on such therapy is mandatory.
If symptom control is achieved with normal doses of PPI’s then there is a virtue in determining if a smaller dose of PPI will achieve the same effect as “step down” therapy.
If this is unsuccessful then reversion to normal dose therapy is required.
In general terms, intermittent or every second or third day therapy with PPI’s is largely unsuccessful because of the time taken to achieve acid inhibition, although intermittent therapy with an H2RA is frequently helpful due to the rapid response in terms of acid control. The latter however, is only useful in mild disease.
Persistence of retrosternal pain despite adequate therapy
The advent of powerful proton pump inhibitors has made 24 hour ambulatory pH monitoring less relevant. In those whose symptoms don’t respond to high dose PPI therapy, other factors should be considered:
- Could it be cardiac ischaemia?
- Is there a musculo-skeletal contribution (Tietze’s syndrome) associated with tenderness over the costochondral junctions and frequently thoracic back pain?
- Could it be dysmotility?
Surgical treatment of GORD
The traditional anti-reflux surgery is now done laparascopically. Although there are prospects for endoscopic day only procedures, at this time they remain relatively experimental.
The major indication for surgery is for volume reflux where gastric contents reflux into the mouth without significant heartburn as the symptoms of acid reflux are almost universally controlled with acid suppression, If a patient has volume reflux, a prokinetic agent may be useful prerequisite to considering fundoplication, particularly if there is any suggestion of dysmotility. However, the presence of established dysmotility remains an almost certain contraindication to fundoplication.
Anti-reflux surgery for heartburn has no place for patients who have failed to respond to acid inhibition.
It should be recognised that some years after initially successful fundoplication, acid reflux may recur and warrant acid suppression.
After fundoplication patients in general will be unable to burp and may initially have mild dysphagia.
Barrett’s Oesophagus is present when the normal squamous mucosa of the lower oesophagus is replaced by columnar epithelium, which contains intestinal metaplasia. At endoscopy columnar mucosa will appear with a salmon pink colour which is quite distinct from the normal lighter coloured squamous mucosa. However it is necessary to take biopsies and have them examined by an experienced pathologist to determine if the intestinal metaplasia is present, since fundic and cardiac mucosa has the same appearance at endoscopy.
The recent development of high resolution and magnification endoscopy has improved the ability to detect abnormal mucosa and to target biopsies.
Chromo-endoscopy using either vital dyes, which are taken up by the tissues or surface agents which allow easier definition of mucosal patterns have also been advocated. The combination of magnification and chromo-endoscopy is currently advocated by has not been proven to be of benefit in the detection of Barrett’s Oesophagus of the targeting of biopsies to detect the presence of dysplasia.
Many, but by no means all patients with Barrett’s Oesophagus will have a long history of significant heartburn. The sequence of development in Barrett’s Oesophagus is thought to be that gastro esophageal reflux causes oesophageal ulceration and subsequent replacement of normal squamous lining by columnar epithelium containing intestinal metaplasia. There is some evidence that control of reflux ulceration will prevent the development of Barrett’s Oesophagus.
Barrett’s patients with intestinal metaplasia in their lower oesophagus have and increased risk of developing oesophageal cancer. Progression to cancer will go through a series of dysplastic changes. Mild dysplasia may progress but equally is frequently noted to disappear. Once severe dysplasia is present and this has been confirmed by a second expert pathologist, then a significant proportion of patients will already have developed carcinoma of the oesophagus even if not visually apparent. Further, there is a high likelihood of invasive carcinoma developing with the next few years.