Indigestion and Heartburn

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[edit] Indigestion and Heartburn

Leonor Fernandez


Indigestion and heartburn are terms patients sometimes use when referring to a variety of symptoms that involve the upper gastrointestinal (GI) tract. Dyspepsia, as defined by the medical profession, refers to persistent or recurrent pain or discomfort centered in the upper abdomen for greater than 1 month with symptoms more than 25% of the time.[1] The prevalence of dyspepsia is very high, up to 20% to 40% of adults in some studies, and accounts for up to 2% to 5% of primary care visits.[2]

Clinically it is difficult to distinguish between the various causes of dyspepsia. The subclassification of types of dyspepsia into “dysmotility-like,” “refluxlike,” and “ulcerlike,” which had been proposed in the past, has poor discriminant value for each disease.[2] The current consensus is to treat patients having “classic” reflux symptoms (see A) with a strategy that targets the reflux physiology. The remaining patients are considered dyspeptic. When these dyspeptic patients are studied by endoscopy, approximately 15% to 25% have peptic ulcer disease, 5% to 15% have gastroesophageal reflux disease (GERD), less than 2% have gastric cancer, and 50% to 60% have no endoscopic abnormalities (with their clinical picture then termed nonulcer dyspepsia).[1][2] The algorithm describes the features that help the physician evaluate reflux and dyspepsia, and then outlines a management strategy for each.


[edit] Image:B0323008283500297_g00000a.jpg History.

Although dyspepsia is centered in the upper abdomen, many patients report symptoms elsewhere in the abdomen as well. Indeed, there is considerable overlap between patients who experience dyspepsia and those who experience irritable bowel syndrome, and many patients who start out with symptoms centered in the upper abdomen may describe a change in the primary location over time to the lower abdomen, or vice versa. The location and quality of discomfort may be even more difficult to ascertain when the patient is of a different cultural or linguistic background than the physician.

Classic gastroesophageal reflux symptoms, in contrast, include epigastric or substernal burning, belching, and regurgitation. The pain often radiates to the back. It usually occurs postprandially, and is aggravated by certain foods (see H), by certain drugs (see C), and by bending over or lying down. The extent of reflux does not appear to correlate well with symptoms: many patients with extensive acid reflux as documented by endoscopy or pH monitoring do not report current symptoms.[3]

Biliary colic should be considered, but this is usually manifested by more prolonged episodes of pain, lasting hours, accompanied often by nausea. There have been reports of Oddi's sphincter dysfunction causing similar symptoms. Less common diagnoses to consider include gastroparesis (often diabetic), ischemic heart disease, metabolic disorders (e.g., hypercalcemia), pancreatitis, and others (see Chapter 103 ).


[edit] Image:B0323008283500297_g00000b.jpg Physical.

The physical examination should include attention to the patient's weight, presence of jaundice, and presence of any abdominal masses, organ enlargement, or lymphadenopathy.


[edit] Image:B0323008283500297_g00000c.jpg Medications.

Several medications may worsen dyspepsia or GERD. These include antibiotics, nonsteroidal antiinflammatory drugs (NSAIDs), niacin, potassium chloride, iron, corticosteroids, quinidine, colchicine, narcotics, estrogen, progestins, aminophylline, calcium channel blockers, and even acetaminophen according to a recent report.


[edit] Image:B0323008283500297_g00000d.jpg Laboratory Tests.

Laboratory tests that may be considered include a complete blood count (CBC) and amylase. Liver function tests may occasionally be useful. Since both dyspepsia and asymptomatic gallstones are common, there may be many patients with both. Therefore it is not recommended to look for gallstones (e.g., with ultrasound) unless the history is suggestive of biliary colic.


[edit] Image:B0323008283500297_g00000e.jpg Alarm Symptoms.

Weight loss, hematemesis, odynophagia, dysphagia, anemia, and melena are considered alarm symptoms that suggest more serious pathology, such as complications from GERD, gastric cancer, and duodenal ulcer.[1][4] Complications from GERD include esophagitis of various degrees, peptic esophageal strictures, and intestinal metaplasia of the esophagus (Barrett's esophagus).[5]

Dysphagia often suggests the presence of erosive esophagitis or strictures. Odynophagia usually signifies severe esophagitis. The majority of patients with GERD do not have endoscopic evidence of esophagitis.[3] The prevalence of complications is associated with increasing age, male sex, duration of symptoms (>5 years), and conditions such as Zollinger-Ellison syndrome and scleroderma. The presence of gastric cancer is associated with a family history of gastric cancer, and positive Helicobacter pylori serology.


[edit] Image:B0323008283500297_g00000f.jpg Age.

Gastroenterologists generally agree that referral for endoscopy is indicated in older patients with new onset dyspepsia. In the United States and western Europe, the incidence of gastric cancer is less than 1 per 100,000 before the age of 45 but then increases significantly, so this is the recommended age threshold. A lower age threshold is recommended in Japanese and other populations where gastric cancer is more common in younger age groups, or in patients with a family history of gastric cancer or other risk factors, such as pernicious anemia or known gastric polyps.

Image:B0323008283500297_g024001.jpg


[edit] GERD

[edit] Image:B0323008283500297_g00000g.jpg Extraesophageal or “Atypical” Symptoms.

Extraesophageal or “atypical” symptoms may include chest pain simulating angina, hoarseness, sore throat, asthma, and cough, especially nighttime cough (see Chapter 72 ). Patients may not necessarily report heartburn symptoms at all with these conditions. The association between GERD and asthma is complex, since it is not necessarily causal. Antireflux treatment improved asthma symptoms in 69% of subjects, reduced asthma medication use in 62%, but did not improve spirometry in a recent review that combined data from several studies.[6]


[edit] Image:B0323008283500297_g00000h.jpg Lifestyle Changes.

Lifestyle changes or nonpharmacologic measures may have a modest benefit. These include raising the head of the bed 6 inches, avoidance of precipitating agents (alcohol, spicy foods, citrus, chocolate, peppermint, coffee, fatty meals, tobacco), avoidance of meals for 3 hours prior to recumbency, and withdrawal of medications that may exacerbate symptoms. Antacids are not effective agents to heal esophagitis, but do help symptoms quickly. Alginic acid forms a viscous solution that floats over the gastric pool and acts as a mechanical barrier. It is not effective when the patient is lying down.


[edit] Image:B0323008283500297_g00000i.jpg Treatment (see Chapter 101 ).

H2-blockers are all equally effective but often require very high doses to heal esophagitis; mild esophagitis heals in 75% to 90% of cases whereas severe heals in only 40% to 50%.[7] Proton pump inhibitors (PPIs) are potent long-acting inhibitors of acid secretion and are highly efficacious in the healing of all grades of esophagitis. PPIs may promote gastric atrophy in patients who are infected with H. pylori, and this atrophy may be a precursor to gastric cancer.[8] The clinical significance of this finding is unclear, however, since the use of PPIs has not been associated with an increase in stomach cancer. Nonetheless, for this reason some have advocated the testing and treatment of all patients with H. pylori who are maintained on PPIs for more than a short time. Prokinetic agents are generally viewed as second line and used as a complement to H2-blockers or PPI or when dysmotility is suspected. Cisapride interacts with several medications and may result in QT prolongation and risk of torsades. Step-down therapy may be considered when symptoms stabilize: consider discontinuation of medications, or lower doses, and change from PPIs to H2-blockers. In general, the symptoms should guide pharmacologic therapy unless severe asymptomatic esophagitis or Barrett's esophagus has been documented.


[edit] Image:B0323008283500297_g00000j.jpg Endoscopy.

Endoscopy is the best method to determine the presence of any mucosal damage and to rule out Barrett's esophagus. Biopsies are necessary, since areas that look like columnar epithelium may not in fact always represent the histologic precursor for adenocarcinoma.[3] A recent study suggests that the frequency of symptoms (of heartburn and reflux), their occurrence at night (relative risk of 11 compared with asymptomatic persons), and their duration were all highly associated with risk of esophageal adenocarcinoma.[9] Endoscopy is very dependent on operator skill; according to some studies it is preferred by patients to barium swallow (see D and E). It is more expensive, but allows direct tissue sampling and therapy such as stricture dilation.


[edit] Image:B0323008283500297_g00000k.jpg Antireflux Surgery.

Antireflux surgery may be considered in younger patients with severe GERD who would require lifelong medical treatment, and in those patients with strictures or recurrent symptoms on therapy. In expert hands surgery has an efficacy of approximately 90%.[4] Manometry is important preoperatively to confirm normal esophageal peristalsis. Several other tests are used less frequently than in the past (e.g., the acid infusion [Bernstein] test, scintigraphy) because of their lower sensitivity and specificity, and are best ordered, if necessary, by the GI specialist.


[edit] Image:B0323008283500297_g00000l.jpg Barium Swallow.

Barium swallow is especially useful in patients with dysphagia. It is more sensitive for subtle strictures and rings than endoscopy, but its sensitivity for mild reflux esophagitis was only 24% in one study.[7] Moreover, it does not allow for any histologic diagnosis or grading.


[edit] Image:B0323008283500297_g00000m.jpg Esophageal pH Monitoring.

Esophageal pH monitoring (24 hour) is considered the gold standard for the diagnosis of GERD, although this has been questioned recently. A pH monitor is placed at the lower esophagus, and pH is recorded over 24 hours. It is probably most helpful in patients who have persistent symptoms despite treatment and a normal endoscopy, as a way to correlate symptoms with episodes of reflux. It is also used by some to diagnose reflux as the cause of non-cardiac chest pain, although some advocate that an empiric 1-week trial of treatment with high-dose PPI (60 mg per day) may be less costly and less invasive. This “omeprazole test” had 78% sensitivity and 86% specificity in one study.[10]


[edit] Image:B0323008283500297_g00000n.jpg Barrett's Esophagus.

Recent practice guidelines[11] on the diagnosis, surveillance, and treatment of Barrett's esophagus suggested that follow-up should be based on the histologic grade seen in the multiple biopsy samples that should be obtained. As with any guideline, these need to be interpreted in light of the individual patient's situation, such as the potential to prolong life expectancy and the patient's eligibility for therapy. The cost-effectiveness and the efficacy of this surveillance have not yet been determined.


[edit] Dyspepsia
[edit] Image:B0323008283500297_g00000o.jpg Empiric Treatment.

Empiric treatment of dyspepsia is perhaps the most common management strategy followed by primary care physicians, usually with H2-blockers or prokinetic agents. Prokinetic agents may in fact be more effective for dyspepsia.[2] There is some limited evidence[12] that empiric treatment of dyspepsia with H2-blockers in younger patients may be as expensive as early endoscopy and result in lesser patient satisfaction (in part because of a high recurrence rate of symptoms requiring subsequent visits and endoscopy.) The empiric treatment strategy has also been criticized because it may promote long-term use of an ineffective medication and mask the symptoms of malignant ulcers.


[edit] Image:B0323008283500297_g00000p.jpg Helicobacter Pylori.

H. pylori has been found to be an etiologic agent for gastric cancer, gastritis, and duodenal ulcer (DU), although its role in nonulcer dyspepsia remains uncertain. Recent guidelines by the American Gastroenterological Association[1] suggest a “test and treat” strategy, where all patients with dyspepsia and positive H. pylori test should be treated. In this way all those who had dyspepsia as a presentation of their ulcer diathesis would be treated, but at the cost of also treating others with infection but without peptic ulcer disease (PUD). Two large recent studies on the efficacy of treating H. pylori infection in this setting have yielded mixed results. One study[13] found that dyspepsia symptoms resolved at 1 year in 21% of patients who received a metronidazole-based eradication regimen and in only 7% of those treated with omeprazole alone, while the other study[14] found no significant difference between similarly randomized patients.[5] In both studies, however, more than 70% of the patients did not get significant relief with eradication of H. pylori. Some authors advocate the use of H. pylori testing for the purpose of risk stratification in patients under 45 years of age with dyspeptic symptoms (excluding those with classic GERD). They suggest that an endoscopy is not warranted when the H. pylori is negative and the young patient does not use NSAIDs; the likelihood of significant findings on endoscopy in such circumstances is extremely low. In those that are positive for H. pylori, they believe treatment may benefit the 15% to 25% who have ulcers (or are destined to develop them).[1]


[edit] When To Refer

Patients should be referred to a gastroenterologist if they have “alarm” symptoms (as defined above). If a patient above the age of 45 or with risk factors for gastric cancer experiences new onset of dyspepsia, a referral should be considered as well. There is controversy regarding the need to refer patients with reflux symptoms for greater than 5 years, although physicians should be mindful of their increased risk for esophageal cancer. The benefit of surveillance, however, remains unproven. Patients with extraesophageal symptoms consistent with GERD may benefit from an otolaryngology referral. Any patient with Barrett's esophagus should be followed by a GI specialist. There is controversy regarding the cost-effectiveness and utility of referring a young patient with dyspepsia and no alarm symptoms. A more prompt referral is in order if the patient would benefit a lot from the reassurance value of an endoscopy. As the cost of endoscopy declines, the cost-effectiveness of prompt endoscopy increases.


[edit] REFERENCES

  1. 1.0 1.1 1.2 1.3 1.4 American Gastroenterological Association Medical Position Statement: Evaluation of dyspepsia. Gast 1998; 114:579 - 581.
  2. 2.0 2.1 2.2 2.3 RS Fisher, HP Parkman: Management of nonulcer dyspepsia. N Engl J Med 1998; 339:1376 - 1381.
  3. 3.0 3.1 3.2 JE Richter: Long-term management of GERD and its complications. Am J Gastroenterol 1997; 92 (4 Suppl):30S - 35S.
  4. 4.0 4.1 PJ Kahrilas: Gastroesophageal reflux disease. JAMA 1996; 276:983 - 988.
  5. 5.0 5.1 LS Friedman: Helicobacter pylori and nonulcer dyspepsia. N Engl J Med 1998; 339:1930 - 1932.
  6. SK Field, LR Sutherland: Does medical antireflux therapy improve asthma in asthmatics with GERD? A critical review of the literature. Chest 1998; 114 (1):275 - 283.
  7. 7.0 7.1 KR DeVault, DO Castell: Guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Arch Intern Med 1995; 155:2165 - 2173.
  8. EJ Kuipers,et al.: Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med 1996; 334:1018 - 1022.
  9. J Lagergren, R Bergström, A Lindgren,et al.: Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma. N Engl J Med 1999; 340:825 - 831.
  10. R Fass, MB Fennerty, JJ Ofman,et al.: The clinical and economic value of a short course of omeprazole in patients with non-cardiac chest pain. Gastroenterology 1998; 115:42 - 49.
  11. RE Sampliner: Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus. Am J Gastroenterol 1998; 93 (7):1028 - 1032.
  12. PB Bytzer, JM Hansen, OB Schaffalitzky de Muckadell: Empirical H2-blocker therapy or prompt endoscopy in the management of dyspepsia. Lancet 1994; 343:811 - 816.
  13. K McColl,et al.: Symptomatic benefit from eradicating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med 1998; 339:1869 - 1874.
  14. AL Blum,et al.: Lack of effect of treating Helicobacter pylori infection in patients with nonulcer dyspepsia. N Engl J Med 1998; 339:1875 - 1881.
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