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Otitis externa pathophysiology

Introduction

Overview

Overview

Otitis externa develops when the external ear canal becomes susceptible to bacterial or fungal infection by various mechanisms. Sudden invasive changes in humidity from a rapid intake of water into the ear canal can predispose the external ear to bacterial infection. This occurs by thinning of the cerumen in the ear canal and weakening an important protective barrier in the ear. The epithelial surface of the skin begins to degrade, allowing easier infiltration by bacteria. The pH of the ear canal is usually maintained at 5.0 by a combination of the cerumen and the mechanical construction of the ear; when this increases it renders the ear more favorable to bacterial reproduction. Increased moisture in the ear canal can also lead to otitis externa caused by otomycosis. The buildup of fungal debris in the ear canal epithelium leads to increasing pressure and inflammation. Surfer’s ear or exostosis of the ear canal predisposes to otitis externa by rendering the ear canal more prone water-bourne pathogens. Localized trauma can cause weakening of the ear canal epithelium and thinning of cerumen, predisposing infection. Otitis externa is associated with infectious, inflammatory ear and head conditions. Gross pathology for otitis externa will include erythema of the ear canal, along with eczema-like scaly, shedding of the skin. It also includes visible ear canal swelling, as well as potentially cellulitis of the pinna and otorrhea.

Pathogenesis

Pathogenesis

Otitis externa develops when the external ear canal becomes susceptible to infection due to a variety of causes.

Moisture-bourne infection

Exostosis

  • Surfer’s ear or exostosis of the ear canal raises the predisposition to otitis externa by rendering the ear canal more prone to trapping water and water-bourne pathogens.[5]

Dermatoses

Associated Conditions

Associated Conditions

Gross Pathology

Gross Pathology

References

References

  1. ↑ Wang MC, Liu CY, Shiao AS, Wang T (2005). “Ear problems in swimmers”. J Chin Med Assoc. 68 (8): 347–52. doi:10.1016/S1726-4901(09)70174-1. PMIDΒ 16138712.
  2. ↑ Kim JK, Cho JH (2009). “Change of external auditory canal pH in acute otitis externa”. Ann. Otol. Rhinol. Laryngol. 118 (11): 769–72. PMIDΒ 19999361.
  3. ↑ 3.0 3.1 Anwar K, Gohar MS (2014). “Otomycosis; clinical features, predisposing factors and treatment implications”. Pak J Med Sci. 30 (3): 564–7. doi:10.12669/pjms.303.4106. PMCΒ 4048507. PMIDΒ 24948980.
  4. ↑ Handzel O, Halperin D (2003). “Necrotizing (malignant) external otitis”. Am Fam Physician. 68 (2): 309–12. PMIDΒ 12892351.
  5. ↑ Trojanowska A, Drop A, Trojanowski P, RosiΕ„ska-Bogusiewicz K, Klatka J, Bobek-Billewicz B (2012). “External and middle ear diseases: radiological diagnosis based on clinical signs and symptoms”. Insights Imaging. 3 (1): 33–48. doi:10.1007/s13244-011-0126-z. PMCΒ 3292638. PMIDΒ 22695997.
  6. ↑ Rosenfeld RM, Schwartz SR, Cannon CR, Roland PS, Simon GR, Kumar KA, Huang WW, Haskell HW, Robertson PJ (2014). “Clinical practice guideline: acute otitis externa”. Otolaryngol Head Neck Surg. 150 (1 Suppl): S1–S24. doi:10.1177/0194599813517083. PMIDΒ 24491310.
  7. ↑ Saxby A, Barakate M, Kertesz T, James J, Bennett M (2010). “Malignant otitis externa: experience with hyperbaric oxygen therapy”. Diving Hyperb Med. 40 (4): 195–200. PMIDΒ 23111934.
  8. ↑ Hui CP (2013). “Acute otitis externa”. Paediatr Child Health. 18 (2): 96–101. PMCΒ 3567906. PMIDΒ 24421666.
  9. ↑ “Swimmer’s earΒ : MedlinePlus Medical Encyclopedia”.
  10. ↑ Schaefer P, Baugh RF (2012). “Acute otitis externa: an update”. Am Fam Physician. 86 (11): 1055–61. PMIDΒ 23198673.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]