Gastroesophageal reflux disease

Mohammed A Al-Karawi

Home

About us

Instructions

Submission

Advertise

Contact

Users Online: 138

ARTICLES

Year : 1995 | Volume : 1 | Issue : 1 | Page : 20-24

Gastroesophageal reflux disease

Mohammed A Al-Karawi
Department of Gastroenterology, Riyadh Armed Forces Hospital, P.O. Box 7897, Riyadh, Saudi Arabia

Click here for correspondence address and email

Abstract

In this review of gastroesophageal reflux disease (GERD), we discuss the different aspects of physiology and pathophysiology and then the approach to diagnosis outlining the advantages and disadvantages of each method.
The last part of this review covers the management of GERD and advances in this subject with special concentration on other aspects of management such as lifestyle changes followed by drug management.

How to cite this article:
Al-Karawi MA. Gastroesophageal reflux disease. Saudi J Gastroenterol 1995;1:20-4

How to cite this URL:
Al-Karawi MA. Gastroesophageal reflux disease. Saudi J Gastroenterol [serial online] 1995 [cited 2022 Jul 6];1:20-4. Available from: https://www.saudijgastro.com/text.asp?1995/1/1/20/34062

In the last 10 years gastrointestinal motility and the study of its physiological and pathophysiological aspects have grown rapidly to a special section in gastroenterology. This has been facilitated by the development of sophisticated computer guided technology and the development of potent drugs affecting gastrointestinal motility. In addition to endoscopy, gastroenterologists have now better tools to evaluate gastrointestinal motility and its effect on organs applying 24-hour pH monitoring, manometry, isotope studies etc. It has been proven that motor abnormalities play an important role in both functional and organic categories of dyspepsia. In the last few years, gastroesophageal reflux disease has been very well studied with clear understanding of the pathophysiology, the available possibilities for effective management, and the limitations of diagnostic procedures and therapeutic modalities.

Physiology

The swallowing act is a complex action divided into a voluntary or oral stage, pharyngeal stage and esophageal stage which brings the food from the mouth into the stomach with propulsive waves transporting the food through the esophagus into the stomach.

The lower esophageal sphincter "LES" is an important barrier between the esophageal environment and the gastric acid environment. It relaxes to pass the food bolus but is continuously contracted to prevent reflux of gastric content into the esophagus. The stomach plays an important role in providing a resovoir for food, then mixing the food and grinding it with gastric secretions, and finally controlling the emptying of the grinded food into the duodenum through the pylorus. The stomach seems to have its own electropysiological pattern utilizing carefully regulated and coordinated contractions for mixing the food and its emptying. The small bowel also plays a very essential role in digestion with the initial mixing of food products with digestive secretions such as bile and pancreatic juice and finally absorbing the digested food through its surface and then propelling nonabsorbable dietary contents and debris from its lumen.^{[1],[2],[3],[4],[5]} All of this active intake, transport and digestion activities are co-related with a series of electrical, mechanical and chemical events. In every part of the gastrointestinal tract, gastrointestinal motility has its own identity from propulsive movements to mixing which varies from part to part. All of these facts have important therapeutic implications. Motility of the upper gastrointestinal tract is controlled by neurogenic, hormonal, myogenic and paracrine systems. The neurogenic control is primarily an intrinsic nervous system in the gut wall while the extrinsic control of the gut is a sympathetic and parasympathetic activity. In both forms. acetylcholine is the primary neurotransmitter which has stimulatory effect, speeding the passage of food through the gut.

A variety of hormonal peptides can affect the gastrointestinal motility. Myogenic control is also regulated by different potentials. All these systems regulate the passage of food through the lumen of the gut making it available for the body for absorption and later on to be evacuated outside the body. They interact to achieve proper digestion but it seems that the nervous system plays a dominant role in controlling all the above mentioned mechanisms.

Pathophysiology

Gastrointestinal motility disorders in general constitute an important part of gastroenterological practice, and gastroesophageal reflux disease is associated with considerable morbidity in the general population. It is estimated that about 5% of the population will have five reflux episodes or more per day and a good portion of those have established GERD.

Recent developments have contributed to clear understanding and recognition that abnormal gastrointestinal motility is an important pathophysiological factor in GERD and chronic dyspepsia [Figure - 1]. A key role in the development of GERD has been attributed to the LES as a barrier against retrograde flow of gastric content. The loss of its efficacy coupled with deficient gastric emptying are important factors in the development of GERD. The reflux process results from the retrograde movement of the acidic gastric contents through LES. These episodes are more frequent and longer duration than the normal, thus breaking the defence barrier of esophageal mucosa and inducing esophagitis. The severity (grade) of esophagitis depends on the duration of reflux and the ability of the esophagus in clearing the refluxate. Indeed, it has been shown that the grade of esophagitis is directly related to esophageal pH and total reflux time.^[6]

The reflux episodes are related to transient spontaneous lower esophageal sphincter relaxation, transient changes in intra-abdominal pressure, or spontaneous free reflux across hypotonic lower esophageal sphincter in the presence of hiatus hernia.^[7],[8] On the other hand, reflux disease can present in different ways mimicking other diseases such as myocardial infarction. Further, it has now been proven that a good proportion of patients with asthma have reflux disease and asthmatic attacks can be aggravated by refluxate reaching the bronchial tree.^[5],[9],[10]

In most patients, GERD is mild and intermittent but it can progress in severity and lead to serious complications including bleeding, respiratory disorders, stricture formation and the development of Barret's lesions which can give rise to adenocarcinoma of the lower esophagus.

The severity of reflux esophagitis can be graded according to Savary Miller classification where Grade I represents tiny isolated erosions and red streaks, Grade II shows esophagitis with literally confluent erosions, Grade III depicts circumferential erosions at the level of squamous columnar junction and Grade IV when induced strictures, ulcers or Barret's lesions have developed in the esophagus. Tytgat, however, describe five grades of esophagitis.^[11],[12]

Diagnostic Approach

With advanced technical development specially in computers, gastroenterologists have now an array of diagnostic procedures available for evaluating patients with suspected GERD. Even with this array of diagnostic procedures available at our disposal, the golden standard in medicine is still valid whereby proper careful history and medical examination are the most important diagnostic aids. This is to be complimented by objective tests to assess the severity of GERD.

Endoscopy has an essential role in the diagnosis of GERD specially to assess the damage to the mucosa. Unfortunately, it can be negative in mild cases. In our study of 142 patients with GERD we found that only about one third of them with positive history of GERD could be confirmed by endoscopy, and with the use of additional objective tests such as 24-hour pH monitoring, we were able to detect a further third. It is very clear that endoscopy enables the gastroenterologist to assess the extent and severity of mucosal lesion, confirm the presence of esophagitis, facilitate the possibility to take biopsies, and perform dilatation if needed. ^{[11],[13],[14]}

Prolonged 24-hour esophageal pH monitoring

Prolonged 24-hour esophageal pH monitoring is at present the gold standard for specific and sensitive diagnosis of GERD [Figure - 2]. The procedure can provide a quantitative measure of reflux duration and frequency, relate symptoms to episodes of reflux and give accurate information on the capacity of esophagus to clear refluxate from its lumen. This helps not only in establishing accurate diagnosis but also evaluate potential therapeutic approaches and their success or failure. Different studies have demonstrated the high diagnostic yield of 24-hour pH monitoring in GERD. This is not only used for evaluating GERD but also to confirm certain suspected diagnoses such as achalasia, whereby no acid reflux in its physiological pattern can be demonstrated. The effects of different positions and patient's conditions on the esophageal pH monitor are evaluated. For example, if the patient is in the supine position, the reflux may increase. On the other hand, the patient can indicate the pain episodes he experiences and it can be correlated to the time of reflux on the computer sheets.^[15],[16] Even in infants the 24- hour pH monitoring can be of great value and help in the diagnosis and treatment, preventing severe complications in these patients. ^{[17],[18],[19]} In recent years, prolonged 24-hour pH monitoring has proved to be of great value in cases of non cardiac chest pains and asthma. It is interesting to find that there is a direct relationship between the degree of esophagitis and the total acid exposure time. It is now accepted that the percentage of overall time with pH below four is the single best determinant of gastroesophageal reflux. In addition, the duration of esophageal acid exposure shows significant correlation with the severity of esophagitis. Prolonged acid clearance is observed in patients with severe esophagitis, both during the day and in the night. ^[11],[19]

Radiological Examinations

Radiography is not frequently used for diagnosing GERD but rather for excluding other conditions in the differential diagnosis. Unfortunately, radiographic procedures have shown no correlation between the radiographic identification of hiatus hernia and reflux episodes. Radiology shows a high incidence of false positive and false negative results. In patients with GERD only severe esophageal lesions such as stricture formation can be visualized by radiological examination.^[20]

Manometry

Manometry is mainly utilized to locate the LES, measure its pressure and to investigate the motility of the esophagus [Figure - 3]. It has helped in identifying the drugs which affect the LES pressure resulting in increased reflux. Therefore, manometry can provide information on the etiological factors of reflux esophagitis; despite that it is not of great importance in comparison with 24-hour pH measurements. It cannot confirm the diagnosis of reflux or exclude it by simply measuring the LES pressure or esophageal motility. It is mainly utilized for monitoring the effects of medical treatment and surgical repair and assessing patients with evidence of multisystem diseases such as scleroderma, connective tissue disease and chronic intestinal pseudo obstruction.^[21]

Gastroesophageal Scintigraphy

By giving a meal mixed with radio active substance and with the use of extended monitoring by means of gamma camera, gastroesophageal scintigraphy is very simple and non-invasive procedure but it is more valuable in assessing gastric emptying and esophageal clearance. Its reliability and validity in GERD remain greatly disputed.^[22]

Ultrasound

This examination is also very easy to perform but it is mainly used for assessing the stomach and the gastric emptying. It has the advantage of being free of radiation and that it can be repeated without hazard. On the other hand it cannot detect esophagitis, and small hiatus hernia will not be diagnosed by ultrasound. It can however provide additional information for the assessment of GERD.^[23]

Management

Proper management of GERD depends on three essential principles. Firstly, enhancement of refluxate clearance from the esophagus. Secondly, prevention of reflux to the esophagus and Thirdly, reducing the effect of refluxate on the mucosa. To achieve these three goals a strategy has to be designed according to the severity of GERD. The following steps are proposed:

1. Changes in the lifestyle such as avoiding heavy fatty meals, alcohol and smoking. Reduction of weight, and encouragement of physical activity.

2. Dietary modifications: Small meals which contain high protein and low fat are advised. No late meals before sleeping. The reduction of total calorie intake is recommended in order to reduce weight. Food products which lower the sphincter pressure such as fats, chocolates, spearmint and peppermint should be avoided. Even food products which can irritate the esophageal mucosa such as citrus, tomato and coffee should be avoided.

3. Sleeping position: The head of the bed should be elevated which will improve the esophageal clearance and reduce the episodes of reflux.

4. Smoking: It has been shown that smoking can reduce the LES pressure. Therefore, the patient should be advised to stop smoking.

5. Drugs affecting LES pressure. Many of the routinely used drugs can reduce the LES pressure. It is therefore advisable to avoid these drugs whenever possible. They include theophylline, anticholinergic, progesterone, diazepam, morphine, beta-adrenergic agonist and alpha-adrenergic antagonists, calcium channel blockers specially nifedipine. Others such as doxycycline, potassium supplements and quinidine can also cause esophageal ulcerations.

6. Drug therapy - Many drugs have been used to achieve the three principal goals of management. For very mild reflux antacids and sucralfate can be very effective. These can be supplemented by H2-receptor antagonists to reduce the direct effect on the mucosa. On the other hand, a drug which can improve and enhance esophageal clearance through increasing LES pressure is now available. Cisapride increases the LES pressure and enhances the motility for better clearing of refluxate from the esophagus. In severe cases of esophagitis, proton-pump inhibitors (Omeprazole) might be indicated. Unfortunately, GERD, even on initial successful treatment with omeprazole, can recur quickly within the first six months. Sucralfate might be useful as it binds bile salt and adhere to damaged gastrointestinal mucosa. The overall efficacy of sucralfate is similar to H2 receptor blockers. ^{[24],[25],[26],[27],[28]}

Lastly, surgery still has a place in the management of GERD specially in young patients with severe disease and in patients with large hiatus hernia and severe GERD, unresponsive to medicaltherapy.

References

1.	Code CF, Szurszewski JH, Kelly KA, et al. A concept of control of gastrointestinal motility. In: Code CF, Heidel H (Eds) Handbook of physiology, Section 6: the alimentary canal. Baltimore, Williams & Wilkins 1968; 5:2881-6.
2.	Despopoulos A. Silbernagl S. Color atlas of physiology. Stuttgart, Georg Thieme Verlag 1984.
3.	Daniel EE. A conceptual analysis of the pharmacology of gastrointestinal motility. In: Pharmacology of gastrointestinal motility and secretion. Holton P (Ed): Oxford. Pergamon Press 1973; 457-545.
4.	Sarna SK, Otterson MF. Gastrointestinal motility: some basic concepts. Pharmacology 1988; 36(Suppl.1):7-14.
5.	Minami H, McCallum RW. The physiology and pathophysiology of gastric emptying in humans. Gastroenterology 1984; 86:1592-610.
6.	DeMeester TR, Johnson LF, Joseph GJ. Patterns of gastroesophageal reflux in health and disease. Annals of Surgery 1976:184:459-69.
7.	Dent J, Dodds WJ, Friedman RH, et al. Mechanism of gastroesophageal reflux in recumbent asymptomatic human subjects. Journal of Clin Invest 1980; 65:256-67.
8.	Dent J, Holloway RH, Toouli J, Dodds WJ. Mechanisms of lower oesophageal sphincter incompetence in patients with symptomatic gastroesophageal reflux. Gut 1988; 29:1020-8.
9.	David P, Denis P, Nouvet G, et al. Lung function and gastroesophageal reflux during chronic bronchitis. Bulletin Europeen de Physiopathologie Respiratoire - Clinical Respiratory Physiology 1982: 18:81-6.
10.	Goodall RJR, Earis JE, Cooper DN, Bernstein A, Temple JG. Relationship between asthma and gastroesophageal reflux. Thorax 1981; 36:116.
11.	Savary M, Miller G. The esophagus. Handbook and atlas of endoscopy, Gassmann Verlag AG, Solothurn, Switzerland. 1978.
12.	Tytgat GNJ, Nio CY, Schotborgh RH. Reflux esophagitis. Scand J Gastroenterol 1990: 25(suppl.175):1-12.
13.	Lambert R. Therapeutic upper gastrointestinal endoscopy: past, present and future. Scand J Gastroenterol 1990: 25(Suppl.175):63-76.
14.	Masclee AAM, De Best ACAM, De Graaf R. Cluysenaer OJJ, Jansen JBMN. Ambulatory 24-hour pH-metry in the diagnosis of gastroesophageal reflux disease: determination of criteria and relation to endoscopy. Scand J Gastroenterol 1990; 25:225-30.
15.	Johnsson F, Joelsson B, Isberg PE. Ambulatory 24-hour intraesophageal pH monitoring in the diagnosis of gastroesophageal reflux disease. Gut 1987; 28:1145-50.
16.	Atkinson M, VanGelder A. Esophageal intraluminal pH recording in the assessment of gastroesophageal reflux and its consequences. Am J Dig Dis 1977; 22:365-70.
17.	Jolley SG, Johnson DH, Herbst JJ, et al. An assessment of gastroesophageal reflux in children by extended pH monitoring of the distal esophagus. Surgery 1978; 84:16-24.
18.	Newman LJ, Berezin S, San Filippo JA, et al. A new ambulatory system for extended esophageal pH monitoring. J Pediatr Gastroenterol Nut 1985; 4:707- 10.
19.	Collins JA, Watt PCH, Hamilton PW, et al. Assessment of oesophagitis by histology and morphometry. Histopathology 1989; 14:381-9.
20.	Swischuk LE, Hayden Jr CK, Fawcett HD, Isenberg JN. Gastroesophageal reflux: How much imaging is required? Radiographics 1988; 8:1137-45.
21.	Richter JE. Castell DO. Gastroesophageal reflux: pathogenesis, diagnosis and therapy. Ann Intern Med 1982:97:93-103.
22.	Fisher RS, Malmud LS. Roberts GS, Lobis IF. Gastroesophageal (GE) scintiscanning to detect and quantitate GE reflux. Gastroenterology 1976; 70:301-8.
23.	Bateman DN, Whittingham TA. Measurement of gastric emptying by real time ultrasound. Gut 1982; 23:524.
24.	Hetzel DJ. Dent J, Reed WD, et al. Healing and relapse of severe peptic esophagitis after treatment with omeprazole. Gastroenterology 1988; 95:903-12.
25.	Tytgat GNJ, Bianchi Porro G, Feussner H, et al. Working team report. Long term strategy for the treatment of gastro-oesophageal reflux disease. Gastroenterology International 1991; 4:21-32.
26.	Klinkenberg-Knol EC, Jansen JMBJ, Festen HPM, Meuwissen SGM. Lamers CBHW. Double blind multicentre comparison of omeprazole and ranitidine in the treatment of reflux oesophagitis. Lancet 1987; 1:349-51.
27.	Tytgat GNJ. Drug therapy of reflux oesophagitis: an update. Scand J Gastroenterol 1989: 24(Suppl. 168):38-49.
28.	Deakin M, Temple JG. Are we making progress in the drug treatment of oesophageal disease? J Clin Pharm and Therap 1988; 13:365-74.