Chapter 4a
REFLUX OESOPHAGITIS
1. DEFINITION
Reflux oesophagitis disease means the presence of regurgitation of gastric contents into the oesophagus with endoscopic or histological evidence of oesophageal inflammation with or without associated symptoms. It attracts ICD 10AM Code K21.
It is necessary here to make a number of distinctions:
• GASTRO-OESOPHAGEAL REFLUX DISEASE is an end result, clinical and pathological, of the reflux of gastroduodenal contents into the oesophagus.
• GASTRO-OESOPHAGEAL REFLUX is the movement of gastric contents into the oesophagus. Such a process is frequent in normal individuals and generally has no adverse consequences.
• REFLUX OESOPHAGITIS is a condition in which there are histological or even visual changes in the oesophagus, such as erosions, inflammation, ulceration as a result of reflux. There may be no symptoms.
• HEART BURN/DYSPEPSIA often takes the form of a lower retrosternal burning discomfort. It may be due to reflux oesophagitis which may also be symptomless. Heartburn/dyspepsia may also occur in the absence of endoscopic or histological changes in the oesophagus.
Oesophagitis and dyspepsia may be regarded as independent variables.
2. PREVALENCE
This is extremely difficult to determine with any precision. We may consider:-
1. What is the prevalence of dyspepsia?
2. What is the prevalence of reflux disease in dyspeptics?
3. What is the prevalence of reflux disease in the symptom free?
4. What is the prevalence of dyspepsia in reflux disease?
1. The prevalence of dyspepsia is readily determined. Representative figures are 20-40% in Europe and 22% in the U.S. with slightly higher figures in females than males and in the young.
2. The prevalence of reflux disease in dyspeptics has been extensively studied and is about 10%. Strangely, in spite of much work on developing categories of dyspepsia symptoms and their significance, they are of little discriminant value in the nature of dyspepsia whether ulcerlike, dysmotilitylike, refluxlike or non-specific (1).
3. Reflux itself is both frequent and normal in the symptom free.
However, reflux episodes are as a rule, brief, more likely after meals and occur during the day rather than during sleep. Reflux disease is not uncommon in the symptom free but the data are unclear.
4. The prevalence of dyspepsia in reflux disease leads to question of the prevalence of symptoms in those with reflux disease. Unfortunately, although it is widely held that reflux disease may be symptomless, good data on its prevalence have not been found.
3. PATHOGENESIS OF GASTRO-OESOPHAGEAL REFLUX
This is multifactorial. The principal factors protecting the oesophagus from reflux of gastric contents are:-
a. The lower oesophageal sphincter (LES),
b. The crura of the diaphragm which enclose the lower oesophagus, c. The acute angulation of the oesophageal junction with the stomach producing a flap valve,
d. The anchored gastro-oesophageal junction (2). Oesophageal clearing is impaired in patients with hiatus hernia.
The lower sphincter is served by excitatory and inhibitory fibres. The excitatory impulses are mediated by acetyl choline; the inhibitory by vasoactive intestinal polypeptide (VIP) and nitric oxide. The tone of the LES is inhibited by fatty meals, belching, smoking and xanthine containing drinks, coffee, tea, cola. Numerous humoral factors influence the sphincter
REFLUX OESOPHAGITIS 23 tone. There is good evidence that the tone in the LES is lower in patients with gastro-oesophageal reflux disease than in controls. In a study of 184 patients with reflux disease who received extensive investigations including endoscopy, manometry and oesophageal pH monitoring, patients with oesophagitis had lower oesophageal sphincter pressures, more frequent reflux episodes and longer periods of acid contact with the oesophagus (2)
4. RISK FACTORS FOR REFLUX OESOPHAGITIS There are numerous. The major ones are:- hiatus hernia, obesity, pregnancy, drugs, alcohol, tobacco, gastric distension, heredity, naso gastric intubation.
4.1 Hiatus Hernia
The evidence for an association is very strong. A number of studies have reported a prevalence of hiatus hernia of 50-94% in patients with gastro- oesophageal reflux disease, prevalence in controls around 13%. Those with reflux oesophagitis have a 16.5 fold increase in the prevalence of hiatus hernia (2). Conversely, oesophagitis is, at the most, uncommon in the absence of a hiatus hernia. Recent studies clearly indicate that the presence of a hiatus hernia is associated with significantly increased susceptibility to reflux by reducing sphincter pressure (3).
4.2 Obesity
Although widely regarded as associated with reflux, the data are sparse and conflicting. One detailed study of 55 massively obese patients found reflux symptoms in 73% especially in the older patients. On the other hand a study of 75 predominantly young and middle aged female candidates for obesity surgery found normal sphincter function. Clinical experience suggests a higher prevalence of reflux symptoms in obese middle aged women but good data on this are lacking. Essentially, objective changes in oesophageal function are confusing in obesity. It may be that dietary fat lowering LES pressure is the culprit (4).
4.3 Pregnancy
Symptomatic gastro-oesophageal reflux occurs in 30-50% of pregnant women. The mechanisms are debatable. It is not due to abnormal distension
and does not occur in males with ascites; it is most likely related to hormonal factors in pregnancy.
4.4 Anticholinergic drugs
These are widely held to predispose to gastro-oesophageal reflux disease.
Other drugs are nitrates, beta-adrenergics, diazepam and aminophylline. The relation with NSAIDs is complex. Two associated series of patients with ulcerative oesophagitis matched with hospital and with community controls showed no association with NSAID use (5), but another large study found an OR of 2 (1.3-3.0) for use of NSAIDs in patients with oesophagitis (6).
There is evidence from a very large VA study of an association of erosive oesophagitis and oesophageal stricture with painful arthritic conditions. The likelihood is that in those with reflux, NSAIDs produce ulceration and stricture by a local action. (7).
4.5 Alcohol
The effect of alcohol, even given IV has been widely studied. In essence, alcohol is associated with gastro-oesophageal reflux by the lowering of LES pressure and impaired oesophageal clearance.
4.6 Tobacco
That there is an association is clear; however, the data on mechanisms are conflicting. Smoking seems to be associated with an increased rate of reflux events and sphincteric pressures are probably lowered.
4.7 Gastric Distension
While it is clear that delayed gastric emptying is associated with reflux, the evidence is that while gastric distension produces reflux, it is not a factor in the usual patient with GER disease.
4.8 Heredity
It is now clear that there is a major hereditary factor in gastro- oesophageal reflux disease. The major evidence comes from a study of 8411 twin pairs over 55 years of age in the Swedish Twin Registry who underwent a detailed telephone interview for reflux disease symptoms. The data show an hereditability of 31% (0.23-0.38) for such symptoms (8).
REFLUX OESOPHAGITIS 25 4.9 Naso Gastric Intubation
Naso gastric intubation is associated with oesophageal reflux and oesophagitis. Although it is more often associated with prolonged e.g.
weeks of intubation in the recumbent position and even stricture formation, it may occur within 72 hours (4).
In summary Gastro-oesophageal reflux disease is frequent in all western societies studied but the prevalence in the lesser developed world is less clear and may be lower. It complicates gastro-oesophageal reflux which is a normal phenomenon but less well developed in the adult population. Its pathogenesis is complex and multifactorial and is almost always associated with hiatus hernia. Although it is regarded as having characteristic symptoms, objective data indicate that its symptoms are often non specific.
1. Talley NJ, Weaver AL, Tesmer DL, Zinmeister AD. Lack of discriminant value of dyspepsia subgroups in patients referred for upper endoscope. Gastroenterology 105,1378-86 (1993).
2. Sontag SJ, Schnell TG, Miller TQ et al. The importance of hiatus hernia in reflux oesophagitis compared with lower esophageal sphincter pressure on smoking. J Clin Gastroenterol. 13,628-43 (1991).
3. Kahrilas PJ, Lin S, Chen J, Manka M. The effect of hiatus hernia on gastro-oesophageal function pressure. Gut 44,476-87 (1999).
4. Horwhat JD, Wong RKH. Risk factors for gastoesophageal reflux disease. Types and mechanisms. In : Orlando RC ed. Gastroesophageal reflux disease. (Marcel Dekker , New York, 2000), pp. 27-83.
5. Ryan P, Hetzel DJ, Shearman DJ, McMichael A. Risk factors for ulcerative oesophagitis : a case control study. J. Gastroenterol. Hepatol. 10,306-12 (1995).
6. Voutilainen M, Sipponen P, Macklin J-P, Juhola M, Farkkila M. Gastroesophageal reflux disease : Prevalence, clinical, endoscopic and histopathological findings in 1128 consecutive patients referred for endoscopy due to dyspeptic and reflux symptoms.
Digestion 61,6-13 (2000).
7. El-Serag HB, Sonnenberg A. Association of oesophagitis and oesophageal strictures with diseases treated with non-steroidal anti-inflammatory agents. Am. J. Gastroenterol.
92,52-6 (1997).
Cameron AJ, Lagergren J, Henriksson, Nyren O, Lockett GR, Pedersen NI.
8.
Gastroesophageal reflux disease in monozygote and dizygote twins. Gastroenterology 122,55-9 (2002).
References
