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Esophagitis Clinical Presentation

  • Author: Deepika Devuni, MBBS; Chief Editor: BS Anand, MD  more...
 
Updated: Nov 12, 2015
 

History

The history findings vary based on the type of esophagitis. Esophageal food impaction can be the initial presentation of eosinophilic esophagitis; proton-pump inhibitor therapy-responsive eosinophilic esophagitis may be a risk factor for esophageal food impaction.[46]

Symptoms of reflux esophagitis

The most common complaint in patients with esophagitis is heartburn (dyspepsia), a burning sensation in the midchest caused by the contact of stomach acid with the esophageal mucosa. Symptoms often are maximal while the person is supine, bending over, or wearing tight clothing or after the person has eaten a large meal. The patient may complain of water brash, a bitter taste of refluxed gastric contents often associated with heartburn.[1]

The American College of Gastroenterology (ACG) published updated guidelines for the diagnosis and treatment of GERD in 2005. According to the ACG guidelines, regurgitation, heartburn, or both are the symptoms most specific for GERD. The guidelines state that for patients with symptoms of uncomplicated GERD, the diagnosis of GERD may be assumed and empirical therapy begun. Patients who show signs of GERD complications or other illness or who do not respond to therapy should be considered for further diagnostic testing.[47]

Other common symptoms of esophagitis include upper abdominal discomfort, nausea, bloating, and fullness. Less common symptoms of esophagitis include dysphagia, odynophagia, cough, hoarseness, wheezing, and hematemesis.

The patient may experience chest pain indistinguishable from that of coronary artery disease. Pain is often midsternal, with radiation to the neck or arm, and may be associated with shortness of breath and diaphoresis. Chest pain may be relieved with nitrates if esophageal spasm is involved, further confounding diagnostic evaluation.

Infants with gastroesophageal reflux are at greater risk of aspiration. Symptoms include weight loss, regurgitation, excessive crying, backache, respiratory distress, and apnea.

Symptoms of infectious esophagitis

Infectious esophagitis is primarily seen in patients who are immunocompromised. The most common causes of infectious esophagitis are fungal (Candida species), herpetic (herpes simplex virus), and viral (cytomegalovirus [CMV]). A history of immunosuppression, steroid therapy, recent antibiotic use, or systemic illness supports the diagnosis. Although patients may be asymptomatic, typical symptoms include the following:

  • Onset of difficult or painful swallowing (ie, dysphagia, odynophagia)
  • Heartburn
  • Retrosternal discomfort or pain
  • Nausea, vomiting
  • Fever, sepsis
  • Abdominal pain
  • Epigastric pain
  • Hematemesis (occasionally)
  • Anorexia, weight loss (depends on chronicity and severity of underlying illness)
  • Cough

Candida esophagitis is usually manifested clinically by dysphagia and/or odynophagia in a patient with 1 or more predisposing factors for the condition. Symptoms are variable in severity, ranging from mild difficulty in swallowing to such intense odynophagia that the patient is unable to eat or swallow saliva. Other patients may present with chest pain or GI tract bleeding; occasionally, patients are asymptomatic.

Herpes esophagitis is most commonly seen in immunocompromised patients with AIDS, an underlying malignancy, or a debilitating illness or in patients who have been treated with radiation, steroids, or chemotherapy.[48] However, it occasionally occurs as an acute self-limiting disease in otherwise healthy patients who have no underlying immunologic problems. Patients with herpes esophagitis typically present with an acute onset of severe odynophagia. Other presenting findings include dysphagia, chest pain, and upper GI tract bleeding.

CMV esophagitis is usually manifested by the development of severe odynophagia, dysphagia, or both, in patients with AIDS. In affected individuals, evidence of CMV infection may be present in other organs or tissues, such as the retina, liver, and colon. Occasionally, odynophagia may be so severe that the patients develop sitophobia (fear of eating), and parenteral alimentation is required.

Patients with HIV ulcers typically present with acute onset of severe odynophagia, dysphagia, or both. If the ulcers develop at the time of seroconversion, a characteristic maculopapular rash may be seen on the upper half of the body.

Tuberculous esophagitis occurs primarily in patients with advanced pulmonary or mediastinal tuberculosis or in immunocompromised patients who have disseminated tuberculosis or other mycobacterial diseases.

Next

Physical Examination

The physical examination usually is not helpful in confirming the diagnosis of uncomplicated esophagitis. However, the examination may reveal other potential sources of chest or abdominal pain.

Perform a rectal examination (eg, stool guaiac) to identify the presence of occult bleeding.

Examine the oral cavity (for thrush or ulcers). Oropharyngeal candidiasis is commonly associated with esophageal candidiasis; therefore, the presence of oral thrush may be helpful in suggesting the diagnosis of Candida esophagitis in the appropriate clinical setting. Nevertheless, only 50-75% of patients with Candida esophagitis have oropharyngeal disease, and some patients with oropharyngeal candidiasis and dysphagia are found to have other types of esophagitis; therefore, the correct diagnosis cannot always be suggested on the basis of clinical presentation.

Look for signs of immunosuppression and skin signs of systemic disease (eg, telangiectasias and sclerodactyly in scleroderma).

Although the presence of herpes labialis (cold sores) or herpetic lesions of the oropharynx should suggest the presence of herpetic esophagitis in the appropriate clinical setting, most patients have no concurrent oropharyngeal herpetic lesions. Moreover, some patients with odynophagia and oral herpes eventually are found to have Candida esophagitis. Therefore, the presence of other herpetic lesions is not accurately predictive of herpes esophagitis in patients with odynophagia. There are rare reports of concomitant herpetic and candidal esophagitis.[26]

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Contributor Information and Disclosures
Author

Deepika Devuni, MBBS Resident Physician, Department of Internal Medicine, University Of Connecticut School of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

John W Birk, MD, FACG Associate Professor of Medicine, Director, Gastroenterology and Hepatology Fellowship Program, University of Connecticut School of Medicine; Chief, Division of Gastroenterology, University of Connecticut Health Center

John W Birk, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Sajid Ansari, MD Consulting Staff, Department of Gastroenterology, St Anthony's Medical Center

Sajid Ansari, MD is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and Missouri State Medical Association

Disclosure: Nothing to disclose.

Simmy Bank, MD Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF Associate Professor of Clinical Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Professor of Clinical Medicine, Hofstra Medical School

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, and New York Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chin Hung Chung, MBBS, FRCS(Glasg), FHKAM(Surgery) Chief of Service, Department of Accident and Emergency, North District Hospital, Hong Kong

Chin Hung Chung, MBBS, FRCS(Glasg), FHKAM(Surgery) is a member of the following medical societies: American College of Surgeons and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

Steven C Dronen, MD, FAAEM Chair, Department of Emergency Medicine, LeConte Medical Center

Steven C Dronen, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

James Li, MD Former Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Board of Directors, Remote Medicine

Disclosure: Nothing to disclose.

Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Chun-hing Ludwig Tsoi MB, ChB, MPH, MRCP, FRCS(Edin), Senior Medical Officer, Accident and Emergency Department, Tseng Kwan O Hospital, Hong Kong; Chairman, Committee on Training, Hong Kong St John Ambulance

Chun-hing Ludwig Tsoi is a member of the following medical societies: Royal College of Physicians of the United Kingdom and Royal College of Surgeons of Edinburgh

Disclosure: Nothing to disclose.

References
  1. Dellon ES, Gibbs WB, Fritchie KJ, Rubinas TC, Wilson LA, Woosley JT, et al. Clinical, endoscopic, and histologic findings distinguish eosinophilic esophagitis from gastroesophageal reflux disease. Clin Gastroenterol Hepatol. 2009 Dec. 7(12):1305-13; quiz 1261. [Medline]. [Full Text].

  2. Howden CW, Hornung CA. A systematic review of the association between Barrett's esophagus and colon neoplasms. Am J Gastroenterol. 1995 Oct. 90(10):1814-9. [Medline].

  3. Uygun I. Caustic oesophagitis in children: prevalence, the corrosive agents involved, and management from primary care through to surgery. Curr Opin Otolaryngol Head Neck Surg. 2015 Dec. 23 (6):423-32. [Medline].

  4. Lowe RC, Wolfe MM. The pharmacological management of gastroesophageal reflux disease. Minerva Gastroenterol Dietol. 2004 Sep. 50(3):227-37. [Medline].

  5. O'Rourke A. Infective oesophagitis: epidemiology, cause, diagnosis and treatment options. Curr Opin Otolaryngol Head Neck Surg. 2015 Dec. 23 (6):459-63. [Medline].

  6. Patel NC, Caicedo RA. Esophageal infections: an update. Curr Opin Pediatr. 2015 Oct. 27 (5):642-8. [Medline].

  7. Rothenberg ME. Biology and treatment of eosinophilic esophagitis. Gastroenterology. 2009 Oct. 137(4):1238-49. [Medline].

  8. Winstead NS, Bulat R. Pill Esophagitis. Curr Treat Options Gastroenterol. 2004 Feb. 7(1):71-76. [Medline].

  9. Fields J, Go JT, Schulze KS. Pill properties that cause dysphagia and treatment failure. Curr Ther Res Clin Exp. 2015 Dec. 77:79-82. [Medline].

  10. Liacouras CA, Ruchelli E. Eosinophilic esophagitis. Curr Opin Pediatr. 2004 Oct. 16(5):560-6. [Medline].

  11. Mann NS, Leung JW. Pathogenesis of esophageal rings in eosinophilic esophagitis. Med Hypotheses. 2005. 64(3):520-3. [Medline].

  12. Oyoshi MK. Recent research advances in eosinophilic esophagitis. Curr Opin Pediatr. 2015 Dec. 27 (6):741-7. [Medline].

  13. Johnson JB, Boynton KK, Peterson KA. Co-occurrence of eosinophilic esophagitis and potential/probable celiac disease in an adult cohort: a possible association with implications for clinical practice. Dis Esophagus. 2015 Nov 6. [Medline].

  14. Bradley J, Movsas B. Radiation esophagitis: Predictive factors and preventive strategies. Semin Radiat Oncol. 2004 Oct. 14(4):280-6. [Medline].

  15. Quarto G, Sivero L, Somma P, De Rosa G, Mosella F, Nunziata G, et al. A case of infectious esophagitis caused by human papilloma virus. Minerva Gastroenterol Dietol. 2008 Sep. 54(3):317-21. [Medline].

  16. Haron E, Vartivarian S, Anaissie E, Dekmezian R, Bodey GP. Primary Candida pneumonia. Experience at a large cancer center and review of the literature. Medicine (Baltimore). 1993 May. 72(3):137-42. [Medline].

  17. Levine MS, Macones AJ Jr, Laufer I. Candida esophagitis: accuracy of radiographic diagnosis. Radiology. 1985 Mar. 154(3):581-7. [Medline].

  18. Walsh TJ, Hamilton SR, Belitsos N. Esophageal candidiasis. Managing an increasingly prevalent infection. Postgrad Med. 1988 Aug. 84(2):193-6, 201-5. [Medline].

  19. Kliemann DA, Pasqualotto AC, Falavigna M, Giaretta T, Severo LC. Candida esophagitis: species distribution and risk factors for infection. Rev Inst Med Trop Sao Paulo. 2008 Sep-Oct. 50(5):261-3. [Medline].

  20. Vidal AP, Pannain VL, Bottino AM. [Esophagitis in patients with acquired human immunodeficiency syndrome: an histological and immunohistochemistry study]. Arq Gastroenterol. 2007 Oct-Dec. 44(4):309-14. [Medline].

  21. Bianchi Porro G, Parente F, Cernuschi M. The diagnosis of esophageal candidiasis in patients with acquired immune deficiency syndrome: is endoscopy always necessary?. Am J Gastroenterol. 1989 Feb. 84(2):143-6. [Medline].

  22. Sam JW, Levine MS, Rubesin SE, Laufer I. The "foamy" esophagus: a radiographic sign of Candida esophagitis. AJR Am J Roentgenol. 2000 Apr. 174(4):999-1002. [Medline].

  23. Prasad GA, Alexander JA, Schleck CD, Zinsmeister AR, Smyrk TC, Elias RM, et al. Epidemiology of eosinophilic esophagitis over three decades in Olmsted County, Minnesota. Clin Gastroenterol Hepatol. 2009 Oct. 7(10):1055-61. [Medline].

  24. Nurko S, Rosen R, Furuta GT. Esophageal dysmotility in children with eosinophilic esophagitis: a study using prolonged esophageal manometry. Am J Gastroenterol. 2009 Dec. 104(12):3050-7. [Medline].

  25. McColl KE. Review article: Helicobacter pylori and gastro-oesophageal reflux disease--the European perspective. Aliment Pharmacol Ther. 2004 Dec. 20 Suppl 8:36-9. [Medline].

  26. Chen LI, Chang JM, Kuo MC, Hwang SJ, Chen HC. Combined herpes viral and candidal esophagitis in a CAPD patient: case report and review of literature. Am J Med Sci. 2007 Mar. 333(3):191-3. [Medline].

  27. DeGaeta L, Levine MS, Guglielmi GE, Raffensperger EC, Laufer I. Herpes esophagitis in an otherwise healthy patient. AJR Am J Roentgenol. 1985 Jun. 144(6):1205-6. [Medline].

  28. Levine MS, Laufer I, Kressel HY, Friedman HM. Herpes esophagitis. AJR Am J Roentgenol. 1981 May. 136(5):863-6. [Medline].

  29. Levine MS, Loevner LA, Saul SH, Rubesin SE, Herlinger H, Laufer I. Herpes esophagitis: sensitivity of double-contrast esophagography. AJR Am J Roentgenol. 1988 Jul. 151(1):57-62. [Medline].

  30. Shortsleeve MJ, Levine MS. Herpes esophagitis in otherwise healthy patients: clinical and radiographic findings. Radiology. 1992 Mar. 182(3):859-61. [Medline].

  31. Borowitz SM. Diagnosis: herpes simplex esophagitis. Clin Pediatr (Phila). 2007 Jul. 46(6):557-9. [Medline].

  32. Geagea A, Cellier C. Scope of drug-induced, infectious and allergic esophageal injury. Curr Opin Gastroenterol. 2008 Jul. 24(4):496-501. [Medline].

  33. Baroco AL, Oldfield EC. Gastrointestinal cytomegalovirus disease in the immunocompromised patient. Curr Gastroenterol Rep. 2008 Aug. 10(4):409-16. [Medline].

  34. Buckner FS, Pomeroy C. Cytomegalovirus disease of the gastrointestinal tract in patients without AIDS. Clin Infect Dis. 1993 Oct. 17(4):644-56. [Medline].

  35. Bonacini M, Young T, Laine L. Histopathology of human immunodeficiency virus-associated esophageal disease. Am J Gastroenterol. 1993 Apr. 88(4):549-51. [Medline].

  36. Bonacini M, Young T, Laine L. The causes of esophageal symptoms in human immunodeficiency virus infection. A prospective study of 110 patients. Arch Intern Med. 1991 Aug. 151(8):1567-72. [Medline].

  37. Calore EE, Cavaliere JM, Perez NM, Campos Sales PS, Warnke KO. Esophageal ulcers in AIDS. Pathologica. 1997 Apr. 89(2):155-8. [Medline].

  38. Edwards P, Wodak A, Cooper DA, Thompson IL, Penny R. The gastrointestinal manifestations of AIDS. Aust N Z J Med. 1990 Apr. 20(2):141-8. [Medline].

  39. Levine MS, Loercher G, Katzka DA, Herlinger H, Rubesin SE, Laufer I. Giant, human immunodeficiency virus-related ulcers in the esophagus. Radiology. 1991 Aug. 180(2):323-6. [Medline].

  40. Levine MS, Woldenberg R, Herlinger H, Laufer I. Opportunistic esophagitis in AIDS: radiographic diagnosis. Radiology. 1987 Dec. 165(3):815-20. [Medline].

  41. Raufman JP. Infectious esophagitis in AIDS: what have we learned in the last decade?. Am J Gastroenterol. 1995 Nov. 90(11):1914-5. [Medline].

  42. Sor S, Levine MS, Kowalski TE, Laufer I, Rubesin SE, Herlinger H. Giant ulcers of the esophagus in patients with human immunodeficiency virus: clinical, radiographic, and pathologic findings. Radiology. 1995 Feb. 194(2):447-51. [Medline].

  43. Villanueva JL, Torre-Cisneros J, Jurado R, Villar A, Montero M, López F, et al. Leishmania esophagitis in an AIDS patient: an unusual form of visceral leishmaniasis. Am J Gastroenterol. 1994 Feb. 89(2):273-5. [Medline].

  44. Yangco BG, Kenyon VS. Epidemiology and infectious complications of human immunodeficiency virus antibody positive patients. Adv Exp Med Biol. 1993. 335:235-40. [Medline].

  45. Mimidis K, Papadopoulos V, Margaritis V, Thomopoulos K, Gatopoulou A, Nikolopoulou V, et al. Predisposing factors and clinical symptoms in HIV-negative patients with Candida oesophagitis: are they always present?. Int J Clin Pract. 2005 Feb. 59(2):210-3. [Medline].

  46. Hiremath GS, Hameed F, Pacheco A, Olive A, Davis CM, Shulman RJ. Esophageal food impaction and eosinophilic esophagitis: a retrospective study, systematic review, and meta-analysis. Dig Dis Sci. 2015 Nov. 60 (11):3181-93. [Medline].

  47. DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol. 2005 Jan. 100(1):190-200. [Medline].

  48. Amaro R, Poniecka AW, Goldberg RI. Herpes esophagitis. Gastrointest Endosc. 2000 Jan. 51(1):68. [Medline].

  49. Nonevski IT, Downs-Kelly E, Falk GW. Eosinophilic esophagitis: an increasingly recognized cause of dysphagia, food impaction, and refractory heartburn. Cleve Clin J Med. 2008 Sep. 75(9):623-6, 629-33. [Medline].

  50. Dellon ES, Gonsalves N, Hirano I, et al. ACG clinical guideline: evidenced based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis (EoE). Am J Gastroenterol. 2013 May. 108(5):679-92; quiz 693. [Medline].

  51. Hakansson B, Montgomery M, Cadiere GB, et al. Randomised clinical trial: transoral incisionless fundoplication vs. sham intervention to control chronic GERD. Aliment Pharmacol Ther. 2015 Dec. 42 (11-12):1261-70. [Medline].

  52. Wilheim AB, Miranda-Filho Dde B, Nogueira RA, Rêgo RS, Lima Kde M, Pereira LM. The resistance to fluconazole in patients with esophageal candidiasis. Arq Gastroenterol. 2009 Jan-Mar. 46(1):32-7. [Medline].

  53. Straumann A, Conus S, Degen L, Felder S, Kummer M, Engel H, et al. Budesonide is effective in adolescent and adult patients with active eosinophilic esophagitis. Gastroenterology. 2010 Nov. 139(5):1526-37, 1537.e1. [Medline].

  54. Reuters Health. Elimination diet helps adult eosinophilic esophagitis: study. Medscape Medical News. February 15, 2013. Available at http://www.medscape.com/viewarticle/779438. Accessed: March 4, 2013.

  55. Lucendo AJ, Arias A, González-Cervera J, et al. Empiric 6-food elimination diet induced and maintained prolonged remission in patients with adult eosinophilic esophagitis: A prospective study on the food cause of the disease. J Allergy Clin Immunol. 2013 Mar. 131(3):797-804. [Medline].

  56. Agency for Healthcare Research and Quality. Comparative Effectiveness of Management Strategies for Gastroesophageal Reflux Disease. AHRQ: Agency for Healthcare Research and Quality. Available at http://effectivehealthcare.ahrq.gov/healthInfo.cfm?infotype=rr&ProcessID=1&DocID=42. Accessed: January 30, 2009.

  57. Donnellan C, Sharma N, Preston C, Moayyedi P. Medical treatments for the maintenance therapy of reflux oesophagitis and endoscopic negative reflux disease. Cochrane Database Syst Rev. 2005 Apr 18. CD003245. [Medline].

  58. Harrison L. Patients With Previous Food Allergies at Risk for Esophagitis. Medscape Medical News. Available at http://www.medscape.com/viewarticle/821762. Accessed: March 17, 2014.

  59. Maggadottir SM, Hill D, Brown-Whitehorn TF, Spergel JM. Development Of Eosinophilic Esophagitis To Food After Development Of IgE Tolerance To The Same Food. American Academy of Allergy, Asthma & Immunology (AAAAI) 2014 Annual Meeting. Available at http://www.jacionline.org/webfiles/images/journals/ymai/AAAAI_2014_Abstracts_Tuesday_March_4.pdf. Accessed: March 18, 2014.

  60. Malfertheiner P, Lind T, Willich S, Vieth M, Jaspersen D, Labenz J, et al. Prognostic influence of Barrett's oesophagus and Helicobacter pylori infection on healing of erosive gastro-oesophageal reflux disease (GORD) and symptom resolution in non-erosive GORD: report from the ProGORD study. Gut. 2005 Jun. 54(6):746-51. [Medline]. [Full Text].

  61. Medical Economics Staff. Physicians’ Desk Reference. 55th ed. Medical Economics Company: Montvale, NJ; 2001.

 
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Esophagitis. Location of fungal and viral infections in ulcers.
Peptic esophagitis. A rapid urease test (RUT) was performed on the esophageal biopsy sample. The result was positive for Helicobacter pylori.
Corrosive esophagitis. This is a vinegar-induced esophageal burn. The patient had a fish bone in her throat. She ingested vinegar in an attempt to dissolve the fish bone but to no avail; this led to corrosive esophagitis.
Infectious esophagitis. Candida esophagitis. Double-contrast esophagram shows linear plaquelike lesions in the esophagus, with normal intervening mucosa.
Infectious esophagitis. Two examples of advanced Candida esophagitis demonstrate a shaggy esophagus. In both images, the double-contrast esophagram shows a grossly irregular esophageal contour due to innumerable plaques and pseudomembranes, with the trapping of barium between lesions. Patients with this fulminant form of esophageal candidiasis are almost always found to have acquired immunodeficiency syndrome (AIDS).
Infectious esophagitis. Candida esophagitis with a foamy esophagus. This patient has a dilated esophagus with beaklike narrowing (arrow) at the gastroesophageal junction as a result of long-standing achalasia. Innumerable tiny bubbles are layering out in the barium column due to infection by the yeast form of candidiasis.
Infectious esophagitis. Herpes esophagitis. Double-contrast esophagram shows small, discrete ulcers (arrows) in the mid esophagus on a normal background mucosa. Note the radiolucent mounds of edema surrounding the ulcers. In the appropriate clinical setting, this appearance is highly suggestive of herpes esophagitis, since ulceration in candidiasis almost always occurs on a background of diffuse plaque formation.
Infectious esophagitis. Cytomegalovirus esophagitis in a patient with acquired immunodeficiency syndrome (AIDS). Double-contrast esophagram shows a large, flat ulcer in profile (large arrows) in the mid esophagus with a cluster of small satellite ulcers (small arrows). Because HIV esophagitis may produce identical radiographic findings, endoscopy is required to confirm the presence of cytomegalovirus before patients are treated.
Infectious esophagitis. Two examples of giant human immunodeficiency virus (HIV) esophageal ulcers (arrows) in patients with acquired immunodeficiency syndrome (AIDS). In A, the ulcer is seen in profile, whereas in B, the ulcer is seen en face. Endoscopy is required to exclude cytomegalovirus as the cause of this finding before treating patients.
 
 
 
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