1. The Raw Facts About Esophagitis Crystal Byerly, MEd., PA-C Seton Hill University PA Program Assistant Professor And Family Practice PA

2. Learning Objectives Recall the etiological findings of esophagitis Describe and identify the varied clinical manifestations of esophagitis Identify the various etiologies of and risk factors for esophagitis Explain the appropriate diagnostic testing for esophagitis Demonstrate knowledge of the treatment strategies of esophagitis Restate the complications of esophagitis

3. Esophagitis Esophagitis is a general term for any inflammation, irritation, or swelling of the esophagus, the tube that leads from the back of the mouth to the stomach.

4. Most common types of Esophagitis Reflux Esophagitis/GERD Infectious esophagitis Candidiasis HSV CMV Eosinophilicesophagitis Pill Induced esophagitis Radiation esophagitis Caustic esophagitis Esophageal cancer

5. Diseases of esophagus clinical manifestations Dysphagia, heartburn, and odynophagia are symptoms with a high degree of specificity for the esophagus Chest pain, though common in esophageal disease, has a much longer differential diagnosis list

6. Dysphagia Dysphagia means difficulty swallowing. an alarm symptom because it raises concern for the presence of a peptic stricture or adenocarcinoma arising in Barrett's esophagus

7. Heartburn Heartburn is a symptom complex characterized by episodic substernal pain that is worse after meals and on reclining and is relieved, at least temporarily, by antacids. Relief by antacids is especially important because it links the pain with acidity. The quality of the discomfort is often burning, and it commonly radiates toward the mouth. Heartburn is frequently accompanied by complaints of a bitter taste in the mouth (regurgitation) or a welling up in the mouth of a salty tasting (salivary derived) fluid (water brash).

8. When substernal pain relieved by antacids recurs at least once per week over an extended period, the history alone permits the diagnosis of gastroesophageal reflux disease (GERD). Unfortunately, patients often use the term “heartburn” inaccurately, and even “burning” substernal pain lacks specificity for GERD without coincident relief by antacids. As a result, GERD is overdiagnosed, and “treatment failures” often reflect misdiagnoses

9. Odynophagia Odynophagia means painful swallowing and implies an acute and severe form of esophagitis, typically with mucosal ulceration. Odynophagiais experienced substernally as an aching or stabbing pain that is aggravated by the act of swallowing, even swallowing saliva. It is common in esophagitis caused by infection, pills, and radiation but rare in esophagitis caused by reflux

10. Upper Endoscopy/EGD For most upper gastrointestinal lesions the sensitivity (about 90%) specificity (nearly 100%) are far higher than those of barium radiography (about 50 and 90%, respectively)

11. Endoscopy advantages The major advantages of endoscopy over contrast radiography in evaluation of diseases of the alimentary tract include direct visualization more accurate and sensitive evaluation of mucosal lesions the ability to obtain biopsy specimens from superficial lesions the ability to perform therapeutic interventions.

12. B, Digital photograph from esophagogastroduodenoscopy confirms the presence of an ulcerated submucosal mass within the duodenum.

13. Non-Invasive radiologic evaluation methods:Flouroscopic procedures However, a variety of fluoroscopic contrast studies remain useful because of their relatively noninvasive and low-cost nature. The videofluoroscopic swallowing study and barium esophagram are efficient and effective noninvasive means of excluding significant pathologic changes in patients with dysphagia = “Ba swallow”

14. Real-time fluoroscopic contrast studies can provide valuable physiologic evaluation, serve as a problem-solving tool when endoscopy is equivocal or contraindicated, and are useful in evaluating for suspected leak, perforation, or fistula. Depending on the specific indication, either barium or water-soluble iodinated contrast material may be used.

15. Reflux Esophagitis Gastroesophageal reflux disease (GERD) is a condition in which the stomach contents (food or liquid) leak backwards from the stomach into the esophagus (the tube from the mouth to the stomach). This action can irritate the esophagus, causing heartburn and other symptoms. AKA: Peptic esophagitis; GERD; Heartburn - chronic; Dyspepsia

16. When the sphincter of muscle fibers called the lower esophageal sphincter, or LES, doesn't close well, food, liquid, and stomach acid can leak back into the esophagus. This reflux may cause symptoms, or can even damage the esophagus.

17. GERD risk factors The risk factors for reflux include hiatal hernia Pregnancy Scleroderma Obesity Cigarettes Alcohol Certain meds: Anticholinergics Beta blockers, CCB Bronchodilators Dopamine Sedatives/anxiety meds, tricyclic antidepressants

18. GERD sx Recurrent heartburn, when properly defined (see earlier), is the hallmark of GERD and enables the diagnosis to be made by the history alone. The heartburn associated with GERD typically occurs once or twice per day and lasts from a few minutes to an hour or more if untreated.

19. This symptom pattern recurs, but with considerable variation in frequency and severity. However, neither the frequency, severity, nor duration of heartburn predicts disease severity on endoscopy.

20. Diagnostic evaluation Reflux Esophagitis The damage in GERD is best assessed by upper endoscopy and esophageal biopsy. Endoscopy may reveal friability, erosions, ulcers, strictures, or Barrett's esophagus in a third of subjects. In the other two thirds, endoscopic findings are normal but esophageal biopsy may show basal cell hyperplasia, edema, or inflammatory findings

21. Esophageal pH monitoring, the “gold standard” for identifying acid reflux, is performed by fixing a small pH probe in the esophagus, 5 cm above the LES, and recording all episodes in which esophageal pH drops to less than 4 over a 24- to 48-hour period

22. Treatment trial over endoscopy Currently, the preferred method for establishing GERD as the cause of symptoms (e.g., chest pain, wheezing) is an empirical trial of acid suppression with a PPI (e.g., omeprazole, 20 mg twice daily), which normalizes esophageal acidity in approximately 95% of subjects.

23. Treatment of Reflux Esophagitis The goals of treatment are to relieve symptoms and prevent relapse and complications. All patients should be advised about lifestyle modifications that help reduce symptoms and prevent relapse. Antacids or antacid-alginate combinations are recommended for safe, prompt, inexpensive relief of heartburn.

24. Lifestyle modifications Elevate the head of the bed 6 inches Stop smoking Stop excessive alcohol consumption Reduce dietary fat Reduce meal size Avoid bedtime snacks Lose weight (if overweight) Avoid: chocolate, carminatives (spearmint, peppermint), coffee (caffeinated and decaffeinated), tea, cola beverages, tomato juice, citrus fruit juices

25. H2 Blockers Examples of histamine antagonists available in the United States include ranitidine (Zantac®), famotidine (Pepcid®), cimetidine (Tagamet®), and nizatidine (Axid®). These medications are usually taken by mouth once or twice per day. Cimetidine, ranitidine, and famotidine are available in prescription and non-prescription strengths.

27. PPI Tx options dexlansoprazole (Rx) - Dexilant, Kapidex GERD Tx: 30 mg daily x 4wks Erosive EsophagitisTx: 60 mg daily x 8wks Maintenance: 30 mg daily DEXILANT is the first and only acid reflux disease treatment that gives you two releases of medicine in one pill. DEXILANT releases one shift of medicine within an hour of taking pill. Then, around 4–5 hours later, DEXILANT releases a second shift of medicine.

28. So which is better? PPI or H2B? Heartburn relief rate in a symptom relief study shows PPI to have more rapid sx relief and more effective in healing esophagitis PPI relief 11.5% per week H2 relief 6.4% per week

29. Combination and Intermittent Therapy Intermittent (on-demand) therapy with an H2 receptor antagonist or proton pump inhibitor may be successful in some patients with mild to moderate heartburn without moderate-severe esophagitis. The optimal approach for prescribing intermittent therapy has not been established. In some instances, a bedtime dose of a histamine H2-receptor antagonist (e.g., ranitidine, 300 mg) is added to PPI therapy to reduce the possibility of nocturnal acid breakthrough.

30. Safety and Maintenance of Antisecretory therapy Is it necessary for your patients to get Bone density studies? H Pylori screenings?

31. NissenFundoplication When indicated, the operative procedure of choice is laparoscopic Nissenfundoplication, with a success rate of about 90%

32. Endoscopic GERD therapies Three novel endoscopic therapies— Stretta, EndoCinch, and Enteryxprocedures —are approved by the U.S. Food and Drug Administration for the treatment of GERD. All can initially reduce or eliminate reliance on drug therapy in about 30 to 50% of GERD patients, but safety and durability are of major concern and thus none is currently recommended.

33. The Stretta procedure involves thermocoagulation of the LES region, EndoCinch provides suture plication of the gastric cardia, and Enteryx involves injection of a biopolymer into the LES muscle as a bulking agent.

35. Complications The two major complications of GERD are peptic stricture formation and Barrett's esophagus (frequency, 5 to 15%)

36. Peptic Stricture Peptic stricture is a lumen-narrowing lesion that occurs in erosive esophagitis secondary to edema, inflammation, or fibrosis of the distal end of the esophagus Strictures produce dysphagia for solids Diagnosis is by Ba swallow or EGD Strictures may respond to medical therapy for GERD alone. However, when strictures are fibrotic, dilation is typically required at various intervals. PPI therapy is useful after dilation to reduce recurrent stricturing and the need for more frequent dilation.

37. Barrett’s esophagus Barrett's esophagus is replacement of reflux-damaged squamous epithelium in the distal part of the esophagus by metaplastic, specialized columnar epithelium. It is found in 10 to 15% of patients with GERD, principally in white individuals. The lesion is suspected on endoscopy by the presence of reddish epithelium extending from the stomach into the tubular lumen of the esophagus

38. Barrett’s esophagus

39. Confirmation is by biopsy. Barrett's metaplasia is a premalignant lesion that increases the risk for esophageal adenocarcinoma 30- to 125-fold over that of the general population.

40. Factors that increase the risk for malignancy in Barrett's esophagus include: white race, male sex, alcohol and tobacco use, obesity, and its length.

41. When Barrett's esophagus is identified on endoscopy, it generally follows a benign course (life expectancy similar to that of the general population) and remains unchanged for years to decades irrespective of the type or extent of treatment. Nonetheless, the presence of Barrett's esophagus carries up to a 10% lifetime risk for the development of esophageal adenocarcinoma, so periodic endoscopy and biopsy are currently recommended for surveillance.

42. Patients with Barrett's esophagus and heartburn or erosive esophagitis are treated like other patients with GERD without Barrett's esophagus.

43. Barrett’s tx Endoscopic surveillance, though not proved to increase survival, allows detection of phenotypic (dysplasia) and genetic abnormalities before progression to adenocarcinoma and permits cancer to be detected at a stage (T0 to T2) for potentially curative esophagectomy. Currently, endoscopic surveillance is recommended every 2 to 3 years, with four-quadrant jumbo biopsy specimens obtained every 2 cm throughout the length of Barrett's esophagus

44. Infectious Esophagitis most commonly found in patients who are immunocompromised: usually from cancer chemotherapy, post-transplant antirejection medication, and acquired immunodeficiency syndrome (AIDS) (especially with CD4 counts <200 mm3) Candida albicans herpes simplex virus type 1 (HSV-1) CMV

45. Odynophagia Odynophagia is characteristic and may be severe. Dysphagia, weight loss, and gastrointestinal bleeding are common. Complications are infrequent but may include tracheobronchial fistula, perforation, and hemorrhage.

46. Candida esophagitis Multiple biopsies of ulcerated areas with routine histologic evaluation provide a definitive diagnosis. Candida esophagitis is characterized on endoscopy by numerous small white-yellow mucosal plaques containing microorganisms, inflammatory cells, and necrotic mucosa biopsy demonstrate Candida pseudohyphae

48. Tx Candida esophagitis In non-AIDS patients, Candida esophagitis may be treated with oral nystatin, 1 to 3 million units four times a day, or clotrimazole (Mycelex troches), 100-mg tablets dissolved in the mouth three to five times a day, but patients with AIDS require an azole antifungal such as oral or intravenous fluconazole (Diflucan), 100 to 200 mg/day for 10 to 14 days

49. HSV esophagitis HSV esophagitis on endoscopy begins as numerous vesicles that ulcerate to yield small (<2 cm), shallow, volcano-shaped ulcers A positive biopsy specimen from the ulcer edge demonstrates the characteristic cytopathic effect of HSV within squamous epithelial cells—eosinophilicintranuclear occlusions.

50. Tx HSV esophagitis HSV esophagitisis treated with a nucleoside analogue such as Acyclovir (Zovirax), 200 to 400 mg orally five times a day or 250 mg/m2 intravenously every 8 hours for 2 weeks. Valacyclovir (Valtrex) and famciclovir (Famvir) are alternatives; for resistant cases, intravenous foscarnet, 60 mg/kg every 8 hours for 2 to 4 weeks, is effective

51. CMV esophagitis CMV esophagitis is characterized by large (>2 cm), deep, often linear ulcers; a positive biopsy specimen from the ulcer base demonstrates the characteristic cytopathic effect of CMV within fibroblasts and endothelial cells—basophilic intranuclear inclusions

52. Tx CMV esophagitis CMV esophagitisis treated with intravenous ganciclovir, 5 mg/kg every 12 hours for 2 to 4 weeks; for resistant cases, foscarnet is administered intravenously at 60 mg/kg every 8 hours for 2 to 4 weeks.

53. Pill-Induced Esophagitis commonly develops in patients, particularly the elderly, who are taking medication improperly (i.e., while supine or with too little liquid). It also occurs in patients with a preexisting abnormality, such as a stricture, diverticulum, or motor disorder. Pills adhere to the esophageal mucosa and cause necrosis and ulceration by the topical release of caustic medication

55. Tx Pill-Induced Esophagitis Discontinuation of the offending medication and treatment with sucralfate suspension (1 g orally four times a day for 1 to 2 weeks) or a cocktail (equal parts viscous lidocaine, antacid, and diphenhydramine [Benadryl]) may control the symptoms. Once-a-day PPI therapy is useful to prevent aggravation by reflux. Education about the proper method of taking medication may prevent recurrence.

56. Radiation esophagitis occurs after chest radiation therapy severe esophagitis and ulceration can develop and lead to hemorrhage, perforation, or fistula. Substernalpain, odynophagia, and dysphagia are typical. Barium swallow and endoscopy can demonstrate the extent and severity of mucosal inflammation, ulceration, and luminal narrowing; endoscopy has the added benefit of biopsy for exclusion of infectious esophagitis

57. A liquid diet or intravenous fluids plus the treatments described for pill-induced esophagitis are helpful. Strictures may require dilation or even esophagectomy with colonic or jejunal interposition.

58. Eosinophilicesophagitis uncommon, immunologically mediated entity The disease is due to food allergy and can be manifested as chest pain or heartburn, but solid food dysphagia and food impaction are characteristic. Skin testing and a radioallergosorbent assay (RAST) for allergy should be performed to identify and remove the offending agent or agents—the most common being seafood, nuts, milk, eggs, and soy. Dietary changes

59. In the past, eosinophilicesophagitis was abbreviated as "EE" but, because of confusion with erosive esophagitis, many prefer the abbreviation "EoE". A panel of experts defined eosinophilicesophagitis as "a chronic, immune/antigen-mediated, esophageal disease characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation"

61. Caustic esophagitis occurs from accidental ingestion in children and from suicidal attempts in adults. Among the more common materials ingested are drain cleaners (sodium hydroxide), bleach (sodium hypochlorite), detergents (sodium tripolyphosphates), and disc batteries (sodium hydroxide). has the potential to cause acute ulceration, perforation, and later stricture formation

62. When perforation is excluded by contrast (diatrizoate [Gastrografin] and, if negative, barium) swallows, endoscopy may be of value to assess the esophageal injury, but passage of the scope beyond an area of severe injury is not recommended to avoid perforation. Emergency esophagogastrectomy is indicated for free perforation and mediastinitis

63. In the absence of these complications, esophagitis is treated supportively with intravenous fluids and prophylactic antibiotics. Steroids in tapering dosage are often given but are without proven efficacy

66. Esophageal Cancer Diagnostic evaluation starts with Endoscopy (EGD) Endoscopic ultrasound (EUS) The two major treatment options for early esophageal cancer are surgical esophagectomy and endoscopic therapy. The depth of tumor invasion into the wall of the esophagus is an important factor in selecting treatment.

67. Learning Objectives Recall the etiological findings of esophagitis Describe and identify the varied clinical manifestations of esophagitis Identify the various etiologies of and risk factors for esophagitis Explain the appropriate diagnostic testing for esophagitis Demonstrate knowledge of the treatment strategies of esophagitis Restate the complications of esophagitis

68. ANY QUESTIONS?? Thank you!

69. References http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0002138/ U.S. National Library of Medicine Orlando R. Diseases of the esophagus. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 140. www.uptodate.com Chiba N, De Gara CJ, Wilkinson JM, Hunt RH. Speed of healing and symptom relief in grade II to IV gastroesophageal reflux disease: a meta-analysis. Gastroenterology 1997; 112:1798. Fass R, Fennerty MB, Vakil N. Nonerosive reflux disease--current concepts and dilemmas. Am J Gastroenterol 2001; 96:303. Richter JE, Campbell DR, Kahrilas PJ, et al. Lansoprazole compared with ranitidine for the treatment of nonerosive gastroesophageal reflux disease. Arch Intern Med 2000; 160:1803. Richter JE, Peura D, Benjamin SB, et al. Efficacy of omeprazole for the treatment of symptomatic acid reflux disease without esophagitis. Arch Intern Med 2000; 160:1810. van Pinxteren B, Numans ME, Bonis PA, Lau J. Short-term treatment with proton pump inhibitors, H2-receptor antagonists and prokinetics for gastro-oesophageal reflux disease-like symptoms and endoscopy negative reflux disease. Cochrane Database Syst Rev 2000; :CD002095.