GASTROESOPHAGEAL REFLUX DISEASE (GERD): THE PATIENT, THE DISEASE AND ITS MANAGEMENT

DR. TAOPHEEQ BAMIDELE RABIU, MBchB (IFE)
ABSTRACT

This paper reviews the current concepts in gastroesophageal reflux disease. It provides a synopsis of the disease, the affected individual and comprehensive control measures that have evolved over centuries of continuous study of the condition.

INTRODUCTION

Gastroesophageal reflux disease (GERD) is the most common cause of indigestion. It is commonly known as heartburn and essentially represents the backflow of gastric and/or duodenal contents into the oesophagus without associated vomiting or belching.

It is a disease that has been with man over the ages but about which there have seen several misconceptions until very recently when a lot of progress has been made in its understanding. GERD could be very disturbing to the affected individual and as such, holistic approach needs to be taken in its management.

THE PATIENT

GERD affects up to 30% of the general population! It is slightly more common in women with most affected individuals above 50 years of age. Many are obese and the women are often multiparous (2) . it is more common in Caucasians than blacks (2).

Heartburn occurs 1 to 2 hours after eating and often gets worse with vigorous exercise, bending or lying down. The patient may report relief by using antacids or setting upright. If asked, he may recall regurgitating without associated nausea or belching.He may also have hypersalivation or ‘waterbrash’ that presents as a feeling of fluid accumulation in the throat without a sour or bitter taste. Odynophagia, possibly followed by a dull substernal ache as a result of long term reflux dysphagia from oesophageal spasn, stricture or oesophagitis may also occur.

The patient may have occasional regurgitation of bitter fluids with chronic pain that may mimic angina pectoris, radiating to the neck, jaw and arm. Recurrent chest infections from aspiration of regurgitated gastric contents may occur especially in children who may also have failure to thrive and forceful vomiting. In advanced disease, haematemesis and malaena stools (results of bleeding) may occur, as may weight loss and iron-deficiency anemia.

THE DISEASE PATHOPHYSIOLOGY

Occasional episode of gasto-oesohpageal reflux are common in health however the reflux is followed by oesephageal peristaltic waves which clear the gullet, alkaline saliva neutralizes the residual acid, and symptoms do not occur. GERD develops when the oesophageal mucosa is persistently exposed to gastric and duodenal contents, resulting in symptoms.

Ledrum (1937) postulated that a localized thickening exists in the lower end of the oesophagus. However, centuries of continous study gave no evidence of such an anatomical sphincter (2). Rather, a physiological sphincter, about 3.5cm long, has been demonstrated in the lower end of the oesophagus. The resting pressure in this sphincter in subjects without reflux is 15 to 20 mmHg. When suddenly challenged by an increase in intra-abdominal/intra-gastric pressure, as in straining (Valsalva manouvre), the pressure increases further to exceed the new level of intragastric pressure, thereby preventing reflux. This is called the “adaptive sphincter response”(2).

It has been demonstrated that this adaptive response is lacking in individuals with gastroesophageal reflux thus strengthening the present position that the Lower Oesophageal Sphincter (LOS) is the most important factor in the control of GE reflux and that where the sphincter is incompetent, no other factor seems capable of preventing reflux.

The LOS in Caucasians lie partly below and partly above the diaphragmatic oesophageal hiatus. Thus, it yields to forces that tend to produce reflux than a sphincter that lies entirely in the positive intra-abdominal pressure environment. This may explain the higher incidence of GERD in Caucasians as compared to blacks in which the LOS is intra-abdominal (2).

Sliding hiatus hernia is a very important cause of reflux. In fact, it used to be traditionally referred to as GERD. However reflux can occur in the absence of a hernia and hiatus hernia need not cause symptom.

Other important factors in the development of reflux include defective oesophageal peristalsis, defective gastric emptying, increased intra-abdominal pressure as from pregnancy and obesity, weakness of the right diaphragmatic crus from increasing age or fat deposition, congenitally “short” oesophagus and dietary factors like the ingestion of fat, chocolate, alcohol and coffee (1,2), Sitting or lying on right or left side have also been shown to lower LOS pressure but there is only little evidence t incriminate smoking or NSAIDs, as causes of GERD (1).

COMPLICATIONS

Long standing cases of GERD may result in oesophagitis that could lead to benign oesophageal stricture especially in the elderly. Barret’s oesophagus, which is metaplasia of the normal squamous epithelium of the oesophagus to form columnar epithelium, may also occur. Almost all patients with Barret’s oesophagus have hiatus hernia and the metaplasia increases the risk of adenocarcinoma by 90 – 150 fold.(1)

Iron deficiency anaemia may occur as a consequence of chronic insidious blood loss from long-standing oesophagitis while recurrent chest infections may also occur, especially in children.

MANAGEMENT

A careful history and physical examination are essential to the diagnosis. Young patients with typical symptoms of gastroesophageal reflux, without worrying features such as dysphagia, weight loss or anaemia, can be treated empirically, investigation is advisable if patient presents in middle or late age, if symptoms are a typical or if a complication is suspected.

Endoscopy is the investigation of choice (1).
When, despite endoscopy, the diagnosis is unclear, 24 hours pH monitoring is indicated.
Other tests like oesophageal manometry and barium study may be indicated.

Treatment may be medical or surgical.

Effective management relieves symptoms by reducing reflux through gravity, strengthening the LOS, neutralizing gastric contents, and reducing intra-abdominal pressure. It should including a modification of the patient’s lifestyle and dietary habits to ensure optimal LOS pressure.

A stepwise approach (1) as shown below may be appropriate.

Changes in lifestyle include weight loss, avoidance of dietary items that worsens symptoms, elevation of the bed head in those with nocturnal symptoms, avoidance of late meals and giving up alcohol drinking and cigarette smoking.

Proton pump inhibitors (PPIs) (0meprazole and lansoprazole) are the treatment of choice for severe symptoms and for complicated disease.(1) Lansoprazole provides more effective and faster relief than omeprazole.(5)

The PPIs are clearly superior to H2RAs in their ability to control acid secretion and in the rate at which symptoms are lessened and lesions healed (3). It has also been shown that tolerance develop to H2RAs but not to PPIs during anti-secretory therapy (4)

.

Patients who fail to respond to medical therapy, those who are unwilling to take long term PPIs, those in whom mucosal histological changes supervene and those with pulmonary symptoms unresponsive to treatment should be considered for antireflux surgery.

The commonly done surgical procedures are
Nissen’s fundoplication in which the mobilized stomach is wrapped around the lower end of the oesophagus using non-absorbable sutures
Belsey operation (Mark IV) involving two-third circumference wrap of the oesophagus using the fundus.
Gastropexy in which the sromach is fixed to the linea alba (Boerema anterior gastropexy ) or to the median arcuate ligament of the diaphram (Hill Posterior gastropexy).
Surgery relieves symptoms but decreases survival more than medical treatment (6).

CONCLUSION

The patient with GERD need understanding, compassion and comprehensive care tailored to his/her individual need. Although heartburn and regurgitation are alleviated in most patients, proportions develop complications such as inability to vomit and abdominal bloating, the so called gas-bloat syndrome (1).

REFERENCES
  1. Gastroesophageal reflux disease, in, Davidson’s textbook of Medicine, 18th edition, pp. 623 – 626
  2. Gastro-oesophageal reflux, in, Badoe, Archampong and Jaja, Principles and practice of Surgery including pathology in the tropics, 2nd edition, 1986, pp 336-338
  3. Gut 1990; vol 31, pA1189
  4. Hatleback JG, Berstra A, Pharmacokinetic Optimization in the treatment of gasto-oesophageal reflux disease, Clin Pharmacokinet, 1996 vol 31, pp 386 – 406.
  5. Hoogerwerf WA, Pasricha PJ, Evid. Based Med. 2002;7,85.
  6. Ritcher JE, Evid. Based Med.,2002;7,26.

Edited by Dr Oluwadiya KS

NB: Dr Rabiu is now a Consultant Neurosurgeon with the LAUTECH Teaching Hospital, Osogbo