Heartburn, regurgitation and non-cardiac chest pain

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1 Heartburn, regurgitation and non-cardiac chest pain

Case

A 52-year-old male presents with intermittent, retrosternal burning. This tends to occur after meals, but occasionally is worsened by exercise. He gets relief with drinking water and with antacids. The symptom has been present for years, but has become progressively more severe over the past 6 months. He has also developed what he describes as ‘slow swallowing’, which on further questioning sounds like mild dysphagia to solids that happens about once a week. He has gained 10 kg in the past year and has no evidence of gastrointestinal bleeding. His examination is unremarkable except for mild obesity (BMI = 31) and his stool has no occult blood. He had a normal exercise stress test as part of a recent executive physical.

He is started on omeprazole 20 mg daily and scheduled for an upper endoscopy due to his dysphagia and duration of disease. The endoscopy is performed after he was on the omeprazole for 4 weeks and demonstrates a 3 cm hiatal hernia with a lower oesophageal ring of about 15 mm diameter. There is no evidence of Barrett’s oesophagus. Dilation is performed to 20 mm. On follow-up questioning, he states that his reflux symptoms are 90% improved on the omeprazole and his dysphagia has resolved. He is counselled on dietary changes including, most importantly, smaller meals with lower fat content with a goal to improve both his weight and reflux symptoms. In 4 months, he returned with recurrent symptoms after stopping his omeprazole. He was counselled that he probably would need long-term maintenance, and the surgical and medical options were reviewed. He elected to remain on omeprazole and quickly became asymptomatic.

History

‘Indigestion’ is a commonly used but poorly understood term that means different things to different patients. Careful questioning may allow the examiner to determine if the patient is describing heartburn, acid regurgitation, belching, bloating, abdominal pain, halitosis or even flatus. Some patients even use the work ‘gas’ to describe indigestion.

Heartburn, regurgitation and, to a lesser extent, chest pain are symptoms that imply oesophageal disease. The type of oesophageal disease responsible for these symptoms can often be anticipated on the basis of history alone. Physical examination rarely contributes to the diagnosis. Heartburn and regurgitation will be discussed together as they often co-exist in patients with gastro-oesophageal reflux disease (GORD). Chest pain does not imply a particular disease process, but rather a group of disorders and will be discussed separately.

In this chapter, the features of and approach to symptoms best described as heartburn and regurgitation will be outlined and associated symptoms supporting the diagnosis of GORD and its complications will be discussed. Thereafter, a practical guide to the use of investigations to confirm the clinical diagnosis will be presented as well as an outline of the principles of clinical management. Similarly, a practical approach to the diagnosis and management of chest pain will be discussed.

Heartburn

Heartburn is a pain or discomfort typically described as burning in nature. Its primary position is usually lower retrosternal, deep to the xiphisternum. Heartburn commonly radiates upwards, retrosternally, occasionally as far as the neck. There may be associated epigastric pain.

The timing of heartburn is characteristic. It occurs intermittently, either postprandially or when the patient bends forward or lies flat in bed, when the gastric contents are level with, or above, the lower end of the oesophagus. When it occurs postprandially, it is most commonly in the early postprandial period, 5 to 30 minutes after a meal. The postural changes that initiate heartburn do so by raising the level of the gastric contents above the level of the gastro-oesophageal junction. The duration of an individual attack, when untreated, rarely exceeds an hour.

Factors that precipitate an attack vary considerably from patient to patient. For some, the size of the meal is important, such that it will occur with large meals but not small meals. For others, particular foodstuffs will precipitate an attack. Foodstuffs more commonly incriminated include curries, garlic, red wine, fatty foods, chocolate and citrus juice. The combination of a meal and lying down can be additive in effect. Some patients will describe waking from sleep with severe heartburn a few hours after retiring to bed, particularly following dietary indiscretions. Attacks may occur when the patient lies on the right side but not on the left side or supine. Exercise, either isometric, including straining, or isotonic, such as brisk walking or running, can trigger heartburn. Retrosternal burning pain that is triggered by exercise needs to be closely scrutinised to ensure that symptoms of coronary ischaemia are not being overlooked.

Response to medication is often predictive of whether the patient’s complaints are secondary to GORD and, therefore, qualify as heartburn. Retrosternal burning pain that is not at least partially relieved by appropriate medication is unlikely to be caused by the reflux of acid into the oesophagus, unless there is some other strong evidence supporting reflux as the cause of the symptom. Heartburn is usually relieved within several minutes by antacids. Discomfort relieved within much shorter periods or after much longer periods is less likely to be secondary to gastro-oesophageal reflux. Similarly, heartburn usually improves with agents that diminish gastric secretion of acid such as H2-receptor antagonists and proton pump inhibitors, although relief with these agents is not as immediate as the relief produced by antacids.

The time course, severity and frequency of heartburn will vary considerably from patient to patient. Some patients have the recent onset of symptoms, while others will have symptoms dating back over many years; some describe symptoms as occasional only, while others are inconvenienced many times a day. It is important to ask about nocturnal symptoms since those patients may have more severe mucosal disease, a poorer health-related quality of life and more difficult to treat disease. Heartburn is very common, reported by one-third of the population at least once a month; 10% have daily heartburn. Only a minority of those with reflux symptoms present for medical care.

Regurgitation

Regurgitation is the second ‘typical’ symptom of GORD. Patients with regurgitation often, but not always, also have heartburn. Although the two symptoms can be closely linked temporally, heartburn tends to be more frequent.

Regurgitation describes the intermittent, sudden and often spontaneous sensation of material moving from the stomach proximally towards the oesophagus and throat. Individual patients tend to regurgitate about the same volume of bolus each time. The usual precipitants of heartburn for a particular patient are also the precipitants of acid regurgitation. They include meals (especially larger meals), assumption of a horizontal posture, rises in intraabdominal pressure, and belching. Food regurgitation is described as the predominant form of regurgitation by some patients. This will obviously occur mostly after eating. Regurgitation occurring within the first 30–60 minutes after a meal usually will not be acidic in character, while regurgitation occurring more distant in time from a meal will usually be acidic. Regurgitation may persist in a treated patient even if the heartburn has resolved with acid suppression.

‘Waterbrash’ is a term used to describe the sudden appearance of a volume of salty or tasteless fluid in the mouth. It is the result of salivary gland stimulation in response to gastro-oesophageal reflux or peptic ulcer disease. At times, it is difficult to distinguish from regurgitation, but since both are reflux symptoms, that distinction is not always critical. There are several other symptoms that can be confused with regurgitation. Rumination is the effortless return of food into the oesophagus or mouth. This usually occurs during meals and the food is often reswallowed. Patients with bulimia are also occasionally misdiagnosed as having GORD. Finally, burping and belching involve the ‘reflux’ of air, not liquids, and can also be confused with regurgitation. Patients with rumination, bulimia and aerophagia (excessive belching and burping) can usually be diagnosed with a carefully taken history and will, at times, have false positive ambulatory reflux testing.

Complications of acid regurgitation

Severe acid regurgitation can be associated with other problematic symptoms including choking attacks, cough, asthma, hoarseness of voice, a foul taste in the mouth in the morning, bad breath, a sore tongue, dental caries and nasal aspiration. Some patients complain of waking up episodically with a sensation of choking such that they will cough vigorously, but rarely produce sputum, get up out of bed and even go to an open window to catch their breath. These symptoms subside fairly rapidly. For some, the history suggesting episodic tracheal aspiration will be less dramatic. They may describe a chronic cough, perhaps worse in the morning, but without sudden exacerbations. When that is the case, other causes of cough will need to be considered and excluded as part of a respiratory work-up. Asthma usually has an allergic basis but, occasionally, can be precipitated by gastro-oesophageal reflux. Such patients may present later in life without any obvious cause for obstructive airways disease. In these patients, the symptoms of gastro-oesophageal reflux are commonly not severe. Acid regurgitation can result in a chemical laryngitis and cause hoarseness of voice. Usually the regurgitation occurs at night so hoarseness is most evident in the morning, and gradually settles as the day passes. Similarly, waking up with a foul taste in the mouth or bad breath can be attributed to nocturnal gastro-oesophageal reflux. Nasal aspiration is a particularly unpleasant consequence of regurgitation, again usually occurring at night.

Problems with swallowing

Dysphagia

The sensation of obstructed swallowing is unusual in patients with heartburn and regurgitation and, when present, is worthy of special clinical attention. Oesophageal stenosis secondary to severe, long-standing erosive peptic oesophagitis is the most common cause of reflux-induced dysphagia. An undiagnosed oesophageal carcinoma should be considered in appropriate clinical settings. It is the implied severity of the reflux disease and the possibility of malignancy that makes investigation by barium swallow and upper gastrointestinal endoscopy mandatory in these patients. The features of dysphagia usually associated with a benign stenosis secondary to peptic oesophagitis are:

There are patients with symptoms of dysphagia and reflux for whom an organic cause will not be found by endoscopy or barium swallow; dysphagia in these cases may be caused by a motor disorder of the oesophageal body. It is usually not clear whether this dysmotility is due to chronic reflux or if motility is the primary problem. If confirmation is required (after more serious disease has been excluded by barium testing or endoscopy), an oesophageal manometry and ambulatory reflux test may be required. Alternatively, resolution of dysphagia after a trial of proton pump inhibitor therapy is nearly diagnostic of a reflux association.

Pathophysiology of GORD

The oesophagus and the stomach are separated by a high-pressure zone produced by tonic contraction of specialised smooth muscle of the lower oesophageal sphincter (LOS) and the phasic contraction of the cural diaphragm. In normal individuals, this functional barrier is maintained except to allow antegrade flow with swallowing and retrograde flow with belching and vomiting. Reflux is likely when the LOS has a very low basal pressure. In patients with a weak sphincter, increases in intraabdominal pressure can easily overcome that pressure and produce pathological amounts of reflux. On the other hand, most patients with reflux have relatively normal pressure and it is felt that the LOS tends to relax at inappropriate times, leading to reflux (transient LOS relaxations). Hiatus herniation predisposes to reflux as a result of a dissociation of a weak LOS with the added pressure provide by the diaphragm. In addition, a hernia predisposes to inadequate clearance of gastric contents away from the lower oesophagus.

Most of the fluid volume of refluxate is promptly cleared from the oesophagus by one or more swallows. Small amounts of residual acid are neutralised by weakly alkaline saliva with subsequent swallows. Clearance is delayed during sleep when swallowing is less reliably triggered by reflux. Smoking exacerbates the effects of reflux by inhibiting salivation, thereby delaying acid clearance.

Repeated and prolonged exposure to gastric secretions can result in erosion and ulceration of the oesophageal mucosa. The occurrence of injury, expressed as erosive oesophagitis, is dependent on three factors: (1) duration of exposure; (2) the chemical composition of the refluxate; and (3) the natural resistance of the individual. Thereby, we can explain several well-known clinical observations. First, the severity of oesophagitis tends to be worse when oesophageal acidification is prolonged, and reducing gastric acid secretion promotes healing of peptic oesophagitis. Secondly, two patients with similar levels of reflux, as measured by pH monitoring, may have marked differences in mucosal appearance at endoscopy. One may have severe erosive oesophagitis while the other, a normal-looking mucosa. The role of bile and pancreatic juice in producing oesophagitis in patients with an intact LOS and pylorus is limited. This mechanism is of considerable importance in patients without an intact pylorus.

Heartburn, on the other hand, is dependent primarily on mucosal sensitivity, not mucosal ulceration. Thus, some patients with symptomatically severe heartburn may have no peptic oesophagitis, while others with no heartburn can present with a peptic stricture secondary to long-standing peptic oesophagitis. Therefore, the severity of heartburn is a poor predictor of oesophagitis. This is a particular problem in older patients who often present with advanced oesophageal damage despite relatively modest symptoms.

Investigation of Heartburn and Acid Regurgitation

Upper gastrointestinal endoscopy

The finding of peptic oesophagitis at endoscopy confirms that symptoms of heartburn and regurgitation are due to GORD. On the other hand the absence of oesophagitis in no way excludes GORD. Patients with typical symptoms that occur occasionally and that are completely controlled by simple measures, such as attention to lifestyle (see below) or antacids, do not need upper endoscopy. On the other hand, patients with reflux symptoms and alarm features (such as vomiting, bleeding, weight loss or dysphagia) should always be investigated. In addition, certain patients (particularly older patients with chronic symptoms) should undergo endoscopy to screen for Barrett’s oesophagus.

The characteristic endoscopic signs of reflux oesophagitis are shown in Table 1.1 and Figure 1.1. As mentioned above, there is only a weak correlation between the severity of oesophageal acidification and the degree of peptic oesophagitis. On the other hand, it is clear that more severe grades of esophagitis are more difficult to heal. Oesophagitis should never be diagnosed based on anything short of mucosal erosion and never should be based on erythema of the distal oesophagus. The diagnostic endoscopic examination is always carried as far as the first part of the duodenum looking for incidental pathology. The finding of a chronic duodenal ulcer is significant as this may be the underlying cause of gastro-oesophageal reflux symptoms (see Ch 5).

Table 1.1 Classification of reflux at endoscopy (Los Angeles—LA—System)

Grade Feature
Grade A At least one mucosal break (erosion) each ≤ 5 mm
Grade B At least one mucosal break > 5 mm but not continuous between the tops of two mucosal folds
Grade C At least one mucosal break that is continuous between the tops of 2 mucosal folds, but which is not circumferential (< 75%)
Grade D Circumferential mucosal break (≥ 75%)
image

Figure 1.1 Endoscopic view of linear erosive peptic oesophagitis (Grade D) of the distal oesophagus.

From plate 20-4 of the online edition of the Merck Manual, with permission from Dr D Martin.

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