Clinical Approach To Gastroesophageal-reflux disease (GERD) presenting As Chest Pain

 

Ravinder PS Makkar, MBBS, MD
Medical Advisor, Department of Medical Assistance
International SOS, New Delhi, India

G.K. Sachdev, MBBS, MD, DM, DNB, FRCP
Professor of Medicine and Gastroenterology, Department of Medicine
Maulana Azad
Medical College, New Delhi, India

Corresponding author

E-mail: ravinder.makkar@internationalsos.com

 

Abstract:

Gastroesophageal-reflux disease (GERD) is probably the most common cause of non-cardiac chest pain in clinical practice. Most patients with GERD induced chest pain have other related symptoms (e.g. retrosternal burning, sour eructations, water brash, or regurgitation) when questioned closely, but about 10% may have only chest pain as there presenting complaint. Patients with unexplained chest pain should be considered to have a cardiac cause for their pain until proven otherwise. Coronary artery disease should be given ample consideration early in the diagnostic protocol because the implications of this diagnosis are more profound than are those of GERD. Patients with typical GERD symptoms should be evaluated by an upper GI endoscopy, while in others, tests like 24-hour pH monitoring or esophageal manometry can confirm the esophageal origin of the chest pain. When reflux is suspected as the cause, a therapeutic trial of proton pump inhibitors is appropriate. Antireflux surgery is indicated only if acid reflux is proved beyond doubt and is resistant to medical therapy. Also an important part of therapy is reassurance and careful explanation to the patient of the esophageal and not the cardiac origin of the chest pain.


Key words: Atypical symptoms; chest pain; gastroesophageal reflux disease, GERD

Introduction

Chest pain is one of the commonest clinical complaints encountered by the general practitioners and family physicians in their clinical practice. Besides being cardiac in origin, recurrent chest pain mimicking angina pectoris can arise from the esophagus. Esophageal disorders especially gastroesophageal-reflux disease (GERD) are probably the most common cause of non-cardiac chest pain (1). Nearly 30% of all patients with chest pain undergoing coronary angiography for coronary artery disease have normal angiograms and up to 60% may have esophageal disease for their symptoms (2). Many patients with esophageal chest pain complain of other esophageal symptoms when questioned closely, but about 10% may have only chest pain as there presenting complaint (3).

Pathophysiology of chest pain in GERD

The specific mechanisms that produce esophageal chest pain are not well understood. Chest pain that arises from esophagus has commonly been attributed to the stimulation of chemo-receptors (acid, pepsin, bile) or mechano-receptors (distension, spasms) although thermo-receptors may also be involved (4,5). Acid sensitivity produces pain presumably by direct stimulation of sensory nerve endings in the lamina propria or possibly in the epithelium itself. Although current opinion holds that esophageal pain is conveyed to the spinal cord by sympathetic fibers at the same level as the input from the heart and the gall bladder, afferent impulses may also ascend to the central system by way of the vague nerve (6). Acid infusion may also cause reflux coronary spasm in some patients with coronary artery disease (7).

Many patients with suspected esophageal chest pain have esophageal motility disorders (e.g. nutcracker esophagus) (8,9), which might cause distal esophageal spasm thus causing inhibition of blood flow for a critical period of time, leading to myoischemia. This myoischemia might be the cause of the esophageal chest pain (10). Studies suggest the esophageal dysmotility may represent an epiphenomenona of a chronic pain syndrome rather than the direct cause of complaints (11).

Other potential causes of esophageal chest pain include the excitation of temperature receptors and lamina distension. The ingestion of cold liquids can produce severe chest pain (12). Distension of stretch receptors of distal esophagus by acute food impaction or carbonated beverages may lead to chest pain when sensitized to gastroesophageal acid (13). Altered pain perception may also contribute to the patients' reaction to pain stimuli (14).

Clinical features of GERD induced chest pain

Intermittent anterior chest pain is the sine-qua-non of this syndrome. Chest pain is usually described as squeezing or burning, substernal in location and radiating to the back, neck, jaw or arms, making it sometimes indistinguishable from cardiac chest pain. It can be triggered by ingestion of very hot or very cold liquids. It frequently awakens the patient from sleep and may worsen during periods of emotional stress. The pain episode may last from minutes to hours and even persist intermittently for several days. Symptoms may abate spontaneously and may be eased with antacids but relief of severe chest pain may require narcotics or nitroglycerine. Most patients with esophagitis have associated other esophageal symptoms (e.g. epigastric or retrosternal burning sensation, sour eructations, water brash, or regurgitation) when closely questioned, but about 10% may have chest pain as their only complaint (3).

Clues suggesting esophageal origin of chest pain -

Management of GERD with chest pain

Coronary artery disease should be given ample consideration early in the diagnostic protocol in patients presenting with chest pain because the implications of this diagnosis are more profound than are those of GERD. Patients with unexplained chest pain should be considered to have a cardiac cause for their pain until proven otherwise, and should be evaluated by an ECG and Exercise stress test before a GI evaluation. Further more, because inferior myocardial ischemia may present with only GI symptoms, patients without chest pain but with dyspnoea or fatigue on exertion or presence of significant cardiac risk factors (hypertension, diabetes mellitus, hyperlipidemia, smoking, sedentary lifestyle or family history of coronary artery disease) should be evaluated for coronary heart disease before undergoing GI evaluation.

Patients presenting with typical GERD symptoms can be evaluated by an upper GI endoscopy to confirm the reflux. While in patients who do not have the typical reflux symptomatology, 24-hour esophageal-pH monitoring (15,16) indicating reflux, or 24-hour ambulatory esophageal-manometry indicating ineffective esophageal contractions (17) can confirm the esophageal origin of the chest pain (18).

 

Following recognition of an esophageal cause of chest pain, an important part of therapy is a careful and repeated explanation of this relationship to the patient. Given a positive diagnosis of an esophageal disorder patients return to a more normal life style (19) in contrast to the those patients who have been given reassurance following a negative cardiological assessment; these patients appear to remain unconvinced that their coronary arteries are normal and continue to be disabled (20).

More specific therapy for chest pain of esophageal origin depends on the pathophysiology of the pain. GERD induced chest pain is helped by antacids, H2 blockers or proton pump inhibitors (21). Proton pump inhibitors (PPI) have shown better results than H2 blockers or prokinetic agents. Infact in patients with non-cardiac chest pain, the administration of PPI could serve as a first approach towards the management of many patients (22).

PPI are the best drugs available for treating GERD since they decrease acid reflux in more than 80% patients and heal esophagitis in 30-85% of patients. Aggressive medical therapy with omeprazole 20-40 mg/day for 3 months and documented acid suppression can improve symptoms in nearly 75% of GERD related chest pain. It is likely that that the newer PPI (esomeprazole 50 mg/day) is more efficacious in controlling gastric acid than standard doses of other PPIs (23). Considering the cost and benefit analysis, the following approach can be followed for management of patients of GERD presenting with chest pain.

 

References:


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21. Jones MP. Acid suppression in gastro-oesophageal reflux disease: Why? How? How much and when? Postgrad Med J 2002; 78(922):465-8.

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First Published July 14th 2004

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