The reflux of gastric contents into the oesophagus probably occurs intermittently in everyone, particularly after eating. However, the oesophagus usually reacts to this by initiating a peristaltic wave that clears its contents back into the stomach. We are not aware of this happening. It is when we become aware of it, usually because of symptoms of burning retrosternal pain (heartburn) and/or regurgitation of the contents into the mouth (water brash), that we call the condition gastro-oesophageal reflux and think of it as a medical disorder. In fact, gastro-oesophageal reflux is a very common disorder in societies living aWestern lifestyle, with symptoms occurring once or twice a month in about one-third of the community, and symptoms occurring daily in approximately 5% of the community.
The reason why gastro-oesophageal reflux develops is unknown, but it certainly appears to be a disease associated with the Western lifestyle, and most clinicians believe that such things as overeating (and its consequence of obesity), alcohol and smoking are important factors that are strongly associated with the problem. Factors that normally prevent gastro-oesophageal reflux have all been implicated in its pathogenesis.
Lower oesophageal sphincter
This is a high-pressure zone interposed between the positive pressure environment of the abdomen, and the negative pressure of the thorax. This sphincter relaxes when a peristaltic wave approaches it with a bolus, and then contracts again when the bolus has passed through into the stomach. In patients with severe gastro-oesophageal reflux disease, the lower sphincter often has no recordable tone, and thus appears to be patulous. However, many patients with reflux disease have normal tone in their lower oesophageal sphincter, and a loss of tone may be a consequence of damage from the acid and other gastric contents that are contained in the refluxate. Even if low tone is not an initiating factor of abnormal reflux, it is certainly a perpetuating factor.
Oesophageal peristaltic activity
Many patients with gastro-oesophageal reflux disease have disordered motility in the oesophagus and consequently clear refluxed material poorly. However, once again this may be a consequence, and a perpetuating factor, of reflux rather than an initial cause of reflux damage.
Hiatus hernia and loss of normal anatomy
In the general population, hiatus hernia has captured the imagination, perhaps because it is alliterative and therefore easy to say, and it is a suitably harmless condition, so that a multitude of what are really dietary indiscretions can be ascribed to the hernia! There is undoubtedly a strong association between hiatus hernia and gastro-oesophageal reflux; a majority of (but not all) patients with severe reflux disease have a sliding hiatus hernia. Conversely, there are many more patients who are shown to have a hiatus hernia on barium meal examination than there are patients with symptomatic reflux disease. Hiatus hernia is considered in more detail later in this chapter.
Gastric contents usually contain gastric juice and food and sometimes duodenal content. Although much has been written about bile in refluxate (pancreatic juice has been all but ignored), its actual role remains uncertain. What has been shown is that if gastric acid is eliminated, the great majority of patients lose their symptoms, so it seems that acid is by far the most important constituent of the refluxate.
Most patients with gastro-oesophageal reflux have a normal oesophageal mucosa. However, in severe forms of the disease erosions occur, leading to ulceration that can become confluent. As with any inflammatory process, healing is associated with the development of fibrous tissue, and if enough fibrous tissue forms, like any scar, it will contract, leading to narrowing and foreshortening of the oesophagus (so-called stricture formation).
In a small proportion of patients, the oesophageal mucosa takes protective measures into its own hands and replaces the squamous mucosa with gastric (columnar) mucosa. This is often called Barrett's oesophagus, after the Australian-born surgeon Norman Barrett who first described it. Patients who develop Barrett's oesophagus often lose their symptoms, so this might be thought a particularly successful ploy on the part of the oesophagus. Unfortunately, the columnar mucosa is unstable and is regarded as a premalignant condition. Indeed, the incidence of adenocarcinoma in the region of the gastro-oesophageal junction is steadily increasing in Western countries and it is thought that this is through the mechanism of Barrett's oesophagus.
Very occasionally, a gastric ulcer can develop in the gastric mucosa of the oesophagus and it is then called a Barrett's ulcer, to distinguish it from ulcers that occur in inflamed squamous mucosa. Although adenocarcinoma occurring in a Barrett's oesophagus and, to a lesser extent, stricture formation, are the two most important complications of gastro-oesophageal reflux, probably the most common complication is chronic blood loss leading to iron-deficiency anaemia. This is seen most frequently in a hospital setting in bed-bound patients. Respiratory problems such as chronic infections (common in children) and asthma, occasionally may also be complications of gastro-oesophageal reflux disease.
Although a hiatus hernia can exist without gastrooesophageal reflux, and vice versa, it is nevertheless common to consider the two entities together. The reason for this is the strong association between reflux and the most common type of hiatus hernia (i.e. a sliding hiatus hernia). A sliding hiatus hernia (Barium swallow and meal demonstrating a sliding hiatus hernia. This oesophagus is ‘shortened’ and the stomach is drawn up into the chest.) is so called because it fulfils the definition of a sliding hernia (i.e. the viscus forms part of the wall of the hernial sac). This is because there is an unperitonealised area (bare area) at the back of the stomach. Thus, when the gastro-oesophageal junction passes up through the hiatus, there is a sac of peritoneum on the front and sides of the hernia, but not posteriorly. The loss of the acute angle of entry of the oesophagus into the stomach removes one of the anatomical barriers to reflux, and clearly makes reflux more likely to occur. However, it probably requires some measure of deficiency in other antireflux mechanisms of the lower oesophagus before reflux occurs with hiatus hernia. Why a sliding hiatus hernia occurs is unknown, but it is probably some combination of attenuation of hiatal attachments combined with the upwards pull of the longitudinal muscle of the oesophagus. A sliding hiatus hernia, as such, probably never causes symptoms; any symptoms are almost certainly the result of associated gastrooesophageal reflux.
A para-oesophageal hiatus hernia (X-ray demonstrating a barium-filled fundus of stomach in the chest and alongside the oesophagus. This is a para-oesophageal or rolling hiatus hernia.) occurs when the gastro-oesophageal junction remains in its normal position, but part of the anterior wall of the stomach rolls up alongside the oesophagus and into the mediastinum (it is sometimes called a rolling hiatus hernia). Such a hernia has a complete peritoneal sac. These hernias can sometimes be huge and involve virtually all of the stomach, so that the gastro-oesophageal junction and the pylorus lie alongside each other. In spite of their size, these hernias are, somewhat surprisingly, occasionally asymptomatic. Symptoms associated with them include pain and discomfort after meals, and episodes of more acute pain that are probably associated with intermittent twisting of the stomach. Patients sometimes present as an acute emergency, with strangulation of the hernia. If the condition is discovered coincidentally (often by a chest X-ray that shows a fluid level in the mediastinum behind the heart), provided the hernia is asymptomatic, then it seems reasonable to leave it, instructing the patient to seek urgent medical attention if pain and/or vomiting should develop. However, it should be noted that some clinicians believe all hernias should be repaired, if the patient is regarded as fit for surgery. In reality, a para-oesophageal hernia alone is quite uncommon, because usually the gastrooesophageal junction also slides up into the chest. The condition is then called a mixed hiatus hernia and the patient is likely to have some symptoms, usually gastrooesophageal reflux.
The type of operation carried out for hiatus hernia varies with the type of hernia. Sliding hiatus hernia, when gastro-oesophageal reflux is the problem, is treated by bringing the gastro-oesophageal junction back into the abdomen, narrowing the hiatus with sutures by approximating the muscle pillars of the hiatus posterior to the oesophagus, and performing an antireflux operation, usually a fundoplication. With paraoesophageal hiatus hernia, the contents of the sac are reduced, the hiatus is narrowed, as described above, and the fundus of the stomach is fixed with sutures to the diaphragm. If reflux is thought to be a problem, an antireflux procedure is carried out. Some surgeons advocate an antireflux procedure in all circumstances. Today, all of these procedures are usually undertaken laparoscopically.
The majority of patients present with retrosternal burning pain occurring after eating, and more particularly after eating certain foods. For example, many patients find such things as pastries, sweet biscuits, tomato sauce and fatty foods as likely to cause heartburn. Certain types of activity also sometimes bring on heartburn (e.g. stooping while gardening or lifting heavy objects). Heartburn is nearly always temporarily relieved by taking antacids. Some patients find that their heartburn is worse when they are lying down, and they then tend to wake with the problem during the night. Many patients are also aware that if they overeat or indulge in more alcohol than is their custom, then their problem is worse. Regurgitation of either gastric contents, or sour or bitter fluid into the mouth, is a symptom in some patients and occasionally such patients wake at night coughing and spluttering, having inhaled a small amount of the refluxate. Although unusual, some patients present with the complications of their reflux disease, having never experienced heartburn or regurgitation, or at least only having experienced it in a very mild way. Most often in this setting the presentation is difficulty in swallowing, but other presentations may be tiredness from iron-deficiency anaemia, recurrent respiratory infections, hoarseness of voice, halitosis and loss of enamel on the teeth.
The great majority of patients with reflux either never go to the doctor with their problem at all, or are relatively simply treated with antacids and changes to their lifestyle, such as weight reduction, reducing alcohol intake and avoiding foods that exacerbate the problem. In some patients, the addition of intermittently administered acid-lowering drugs, such as H2 receptor blockers, also ameliorates their symptoms.
Which patients should be investigated further? Patients with typical heartburn that can be treated easily with occasional antacids do not require further investigation. Patients with atypical symptoms, or patients in whom high-level therapy such as proton-pump inhibitors are required to control symptoms, should first undergo an endoscopy. If erosive oesophagitis is found, further investigation is not warranted. If the patient has a normal oesophagus on endoscopy, then monitoring of the oesophagus over a prolonged time, usually 24 hours, is indicated in order to obtain a pH profile, which can then be correlated with the patient's symptoms. If an abnormality is seen on endoscopy, then it is biopsied and sent for histology.
Simple treatment has already been described and is well known to most people. High-level therapy consists of either the prolonged taking of proton-pump inhibitors (e.g. omeprazole, lanzoprazole) or antireflux surgery. The advantage of drug therapy is its low morbidity, while its disadvantages are the need to take the therapy lifelong, and therefore its cost and the unknown effect of chronic administration of the drug over a long period. If regurgitation is a major problem, protonpump inhibitors are less effective because they do not stop gastro-oesophageal reflux occurring, but merely reduce the acid in the refluxed material.
The advantage of operative therapy is that it cures the problem, while its disadvantages are the morbidity of the operation itself and the fact that it usually leaves the patient unable to belch effectively. This leads to a feeling of being bloated after eating, and patients sometimes have to modify their eating habits to a degree (usually to smaller meals). In fact, patients who are trying to lose weight sometimes see this as a positive outcome from their operation.
It is important to realise, when discussing high-level management such as lifelong proton-pump inhibition or surgery, that we are referring only to the small group of patients who are at the severe end of the reflux spectrum. The indications for surgery are really dictated by the patient's problems from the reflux. When the patient suffers complications such as severe dysphagia from stricture formation or recurrent respiratory problems from spillover into the larynx, then the balance is strongly tilted towards surgery. However, such complications occur in a small minority of patients. The majority of patients at the severe end of the reflux spectrum have reflux symptoms that are spoiling their enjoyment of life and they then have a choice of drug therapy to control their symptoms, or surgery.
In the past, the pain associated with surgery and the prolonged period away from normal activity afterwards tended to put people off having an operation. However, the advent of laparoscopic surgery has changed this. Nevertheless, laparoscopic antireflux surgery is not without problems, so it should still only be offered to patients at the severe end of the reflux spectrum. Furthermore, it is only suitable in patients with reasonably straightforward disease and is best avoided in patients with shortened oesophagus (relatively rare), and in patients who have had previous upper abdominal operations in the area of the oesophagus and stomach. Patients undergoing laparoscopic antireflux surgery should also be aware that there is approximately a 2%conversion rate to open operation because of difficulties that may be encountered during the laparoscopic procedure. Open operation can be undertaken via either the abdominal or the thoracic route. Most operations today are undertaken abdominally because the morbidity from the procedure is substantially less through this route.
The most common operation performed is one where the fundus of the stomach is drawn around behind the oesophagus and then stitched to itself in front of the oesophagus. This is called a fundoplication (Fundoplication: The stomach is wrapped around the lower oesophagus and controls acid reflux.) and although the way in which it works is not entirely clear, it is known that this wrapping of the oesophagus is extremely effective in its antireflux action. As already mentioned, it is so effective that it holds gas in the stomach as well as other stomach contents. Furthermore, even with the vigorous antiperistalsis of vomiting, it usually prevents retropulsion of gastric contents into the oesophagus.
Complications specific to antireflux surgery are usually related to dysphagia, which occurs if the wrap is too tight, the oesophageal hiatus is made too narrow, the gastro-oesophageal junction is pulled through the wrap, or para-oesophageal herniation occurs alongside the wrap. In some patients, the wrap seems to break down with time and the incidence of recurrent reflux is about 15% over many years. It is possible to undertake further antireflux surgery in such circumstances, although surgery is usually more difficult the second time around.
Post-operative management is relatively standard, with oral fluids being commenced immediately, and a soft diet introduced when the patient is able to tolerate it. Discharge usually occurs 6–8 days after open surgery or 2–3 days after laparoscopic surgery. Because patients feel so well after laparoscopic surgery, they have to be advised to not do anything that raises their intraabdominal pressure to high levels (such as heavy lifting) for about 8 weeks, to allow the hiatus to adequately seal with fibrous tissue. Otherwise there is a tendency for an early para–oesophageal hiatus hernia to occur.
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