Gastroesophageal reflux disease (GERD) is defined as the presence of symptoms or complications that are directly related to the retrograde flow of gastric contents into the esophagus.1 

A certain degree of reflux is normal.

Reflux into the esophagus is prevented by the anti-reflux barrier made up of multiple components, including the lower esophageal sphincter, the extrinsic crural diaphragm, and the supporting structures of the gastroesophageal flap valve.

When these protective components are compromised, the deleterious effects are additive, resulting in increasing numbers of reflux events and increasingly abnormal esophageal reflux exposure. When gastric juice enters the esophagus, protective factors help clear the refluxate from the esophagus and protect the epithelium. Breakdown of these protective forces promotes reflux disease. However, complications and symptoms can also occur in individuals with a normal reflux burden, when there is either poor epithelial resistance or increased visceral sensitivity.

The pathogenesis of gastroesophageal reflux disease (GERD) involves interactions in reflux exposure, epithelial resistance, and visceral sensitivity.

This balance among reflux exposure, epithelial resistance, and visceral sensitivity can be altered by perturbations in physiologic and anatomical factors that either promote or impede reflux into the esophagus, or protect or injure the epithelium from exposure to gastric juice.

The gastric refluxate is a noxious material that injures the esophagus.

 Esophageal exposure to gastric refluxate is the primary determinant of disease severity. This exposure arises via compromise of the anti-reflux barrier and reduced ability of the esophagus to clear and buffer the refluxate, leading to reflux disease. However, complications and symptoms also occur in the context of normal reflux burden, when there is either poor epithelial resistance or increased visceral sensitivity. Reflux therefore develops via alterations in the balance of aggressive and defensive forces.1

 

These exist in a continuum that determines severity of reflux disease. It is important to consider this balance in attempting to understand mechanisms of pathogenesis in each patient.

 

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1. Reduced lower esophageal sphincter (LES) tone as in scleroderma and pregnancy

2. Frequent transient LES relaxations (TLESRs) that permit bathing of the esophagus by acid or nonacidic fluid.

3. Reductions in esophageal body motility or salivary secretion prolong fluid exposure.

3. Increased intragastric pressure promotes gastroesophageal reflux in obese patients.

4. The role of hiatal hernias is controversial—most reflux patients have hiatal hernias, but most with hiatal hernias do not report excess heartburn.

5. Disturbed gastric motility may contribute to gastroesophageal reflux in up to one-third of cases. 

 

 

     

    Management based on the frequency and severity of symptoms and the presence of erosive esophagitis or Barrett’s esophagus on upper endoscopy'

    1. Mild Intermittent Symptoms (fewer than two episodes per week and no evidence of erosive esophagitis)

    Along with appropriate diet and lifestyle modification recommendations, you prescribe omeprazole.

    Erosive esophagitis, Barrett's esophagus

     

●We suggest lifestyle and dietary modification in all patients with GERD (Grade 2C). (See 'Lifestyle and dietary modification' above.)

●In patients with mild and intermittent (less than two episodes per week) symptoms of GERD who are naïve to treatment and no evidence of erosive esophagitis or Barrett’s esophagus, we suggest as needed low-dose histamine 2 receptor antagonists (H2RAs) (table 1) (Grade 2B). Concomitant antacids, and/or sodium alginate can be used if symptoms occur less than once a week. In patients with continued symptoms, we increase the dose of H2RAs to standard dose, twice daily for a minimum of two weeks. (See 'Antacids' above and 'Overall approach' above.)

●If symptoms of GERD persist, we discontinue H2RAs and initiate once-daily proton pump inhibitors (PPIs) at a low dose (Grade 2B) and then increase to standard doses if required for symptom control (table 1). We make gradual incremental changes in therapy at two- to four-week intervals. Once symptoms are controlled, therapy should be continued for at least eight weeks. (See 'Histamine 2 receptor antagonist' above and 'Overall approach' above.)

●In patients with erosive esophagitis, we recommend initial acid suppressive therapy with standard-dose PPI once daily (table 1) (Grade 1A). (See 'Overall approach' above and 'Proton pump inhibitors' above.)

●In patients with frequent (two or more episodes per week), severe symptoms that impair quality of life or Barrett’s esophagus, we suggest initial therapy with standard-dose PPI once daily (Grade 2B). (See 'Overall approach' above and 'Proton pump inhibitors' above.)

●Referral to a subspecialist is warranted for patients who fail to respond to once-daily PPI therapy and patients who cannot tolerate long-term PPIs or want to discontinue therapy. (See 'PPI refractory symptoms' above.)

●We discontinue acid suppression in all patients with GERD whose symptoms resolve completely with treatment with the exception of those with severe esophagitis on upper endoscopy and Barrett's esophagus. (See 'Duration of acid suppression' above.)

●In patients with recurrent symptoms within three months of discontinuing acid suppression, we continue long-term maintenance therapy with a PPI. However, if symptoms occur after three or more months, we use repeated eight week courses of previously effective acid suppressive therapy (algorithm 1) (see 'Recurrent symptoms' above).

●Management of GERD in pregnancy includes lifestyle and dietary modification followed by pharmacologic therapy with antacids and sucralfate. Antacids containing sodium bicarbonate and magnesium trisilicate should be avoided in pregnancy. In patients who fail to respond, similar to nonpregnant patients, H2RAs and then PPIs are used to control symptoms. (See 'Pregnancy and lactation' above and 'Mild and intermittent symptoms' above.)

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Pts without alarm features are generally treated empirically.

Individuals >45 years can be tested for the presence of H. pylori. Pts positive for the infection are treated to eradicate the organism. Pts who fail to respond to H. pylori treatment, those >45 years old, and those with alarm factors generally undergo upper GI endoscopy.

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(If alarm features, risk factors for Barrett’s esophagus, or abnormal gastrointestinal imaging are present,

Further Evaluation)

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Weight reduction; elevation of the head of the bed; and avoidance of large meals, smoking, caffeinealcohol, chocolate, fatty food, citrus juices, and NSAIDs may prevent GERD. Antacids are widely used. Clinical trials suggest that proton pump inhibitors (omeprazole) are more effective than histamine receptor blockers (ranitidine) in pts with or without esophageal erosions. H. pylori eradication regimens are discussed in Chap. 147. Motor stimulants like metoclopramide and erythromycin may be useful in a subset of pts with postprandial distress.

Surgical techniques (Nissen fundoplication, Belsey procedure) work best in young individuals whose symptoms have improved on proton pump inhibitors and who otherwise may require lifelong therapy. They can be used in the rare pts who are refractory to medical management. Clinical trials have not documented the superiority of one over another.

Dietary exclusion of gas-producing foods (i.e., low FODMAP [fermentable oligosaccharide, disaccharide, monosaccharide, and polyol] diets), and therapies to modify gut flora can reduce symptoms but efficacy is unproven.

Consider a trial omeprazole; if no response, 24-h ambulatory luminal pH monitoring; if negative, esophageal manometry may show motor disorder. Trial of imipramine, 50 mg PO qhs, may be worthwhile. Consider psychiatric evaluation in selected cases

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Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.

 

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