Diagnosis: Primary atrophic rhinitis, or ozena Primary atrophic rhinitis, or ozena, is a chronic nasal disease that is characterized by progressive mucosal atrophy with resorption of the underlying bone and formation of thick, foul-smelling crusts. In 1876, Fraenkel described these clinical findings as a separate entity of the nose.1 The disease is uncommon in the United States but appears to be endemic in subtropical and temperate countries. In affected areas, such as Egypt, the annual incidence among ear, nose, and throat outpatients is 1%.2 The exact etiology of atrophic rhinitis remains elusive, although several pathogenetic factors have been suggested. Bacterial organisms, including Klebsiella ozaenae, nontoxic Corynebacterium diphtheriae, and Coccobacillus, have been reported to cause atrophic rhinitis; however, some of them may secondarily invade damaged mucosa.3 Iron and vitamin A deficiency are also purported causes.4 Han-Sen5 found 84% symptomatic improvement in patients treated with high doses of vitamin A. The disease is more common in women than in men, supporting a hormonal theory, mainly estrogen deficiency.6 Autonomic imbalance, poor pneumatization of the maxillary sinus, collagen disorder, and heredity have also been investigated as causative factors.7 Mickiewicz et al8 found atrophic rhinitis in workers exposed to phosphorite and apatite dusts. Lacking a definitive agent or cause, it seems likely that separate factors work simultaneously in causing atrophic rhinitis. The presenting symptoms are most commonly nasal obstruction, headache, epistaxis, anosmia, and halitosis. The paradoxical complaint of nasal obstruction, despite a large nasal cavity, may be attributable to crusting or to the absence of nasal turbinates as a sensor organ to airflow. On physical examination, the nasal cavities are found to be lined with adherent crusts that are yellow-green to gray-black. The crusts, which are foul smelling, are one of the hallmarks of the disease and the most distressing symptom. Most frequently the inferior turbinate and less commonly the middle turbinate are atrophied. The nasal passage is excessively open, making the nasopharynx clearly visible via anterior rhinoscopy. Pathologic examination shows chronic inflammation, with atrophy and fibrosis. Squamous metaplasia of the respiratory epithelium, ciliary destruction, and arteritis obliterans are also prominent features.9 The turbinate’s atrophy can sometimes be seen even in a simple radiograph of the nose and sinuses, although a computed tomographic scan better demonstrates the atrophic changes in the facial region, as in the present case. Cultures from nasal secretions can yield multiple microorganisms, including Proteus, Escherichia coli, Staphylococcus aureus, and pneumococci. Klebsiella ozaenae, an encapsulated gram-negative rod, is most often associated with, and isolated in, atrophic rhinitis.10 Primary atrophic rhinitis occurs in a previously healthy nose. Absence of the intranasal structures can also result from the destruction associated with infectious diseases such as tuberculosis, syphilis, and leprosy and with granulomatous disorders such as sarcoid and Wegener granulomatosis, as well as after nasal surgery. Postoperative radiologic changes in the intranasal structures usually do not show resection of all the turbinates. Therapy is directed toward reducing the amount of crusting, thus relieving the associated foul odor, and toward clearing secondary bacterial infections. The mainstay of medical treatment is antibiotic use and regular cleaning of the nasal cavity with syringes filled with sodium bicarbonate, balanced physiologic saline, or 25% glucose in glycerin, with routine mechanical crust removal under rigid endoscopic guidance. Topical aminoglycosides are used in mild cases; however, superimposed bacterial sinusitis requires systemic antibiotic therapy. Tetracycline has traditionally been used to treat this disease, with recent studies also suggesting the use of ciprofloxacin. Vasoconstrictive nose drops should be avoided because the vascular supply is already compromised. Several surgical procedures have been used to try to narrow the nasal cavity. The procedure described by Taylor and Young11 involves bilateral closure of the nostrils one side at a time at a 3-month interval, and the modification of Gadre et al12 includes partial nostril closure. The partial closure seems to reduce the amount of crusting, while facilitating nasal endoscopy, which will help the physician decide the appropriate time to reverse the closure (usually in 3 to 5 years). Several artificial grafts have been used as implants to decrease the nasal lumen patency, but all of them have demonstrated an extrusion rate of up to 80%.13 With no known cure, all available treatment modalities are empirical and directed toward symptomatic relief. Residents and fellows in otolaryngology are invited to submit quiz cases for this section and to write letters to the ARCHIVES commenting on cases presented. Quiz cases should follow the patterns established. See “Instructions for Authors.” Material for CLINICAL PROBLEM SOLVING: RADIOLOGY should be mailed to the Editor. Reprints are not available from the authors. References 1. Chand MSMacArthur CJ Primary atrophic rhinitis: a summary of four cases and review of the literature. Otolaryngol Head Neck Surg 1997;116554- 558PubMedGoogle ScholarCrossref 2. Shehata MA Atrophic rhinitis. Am J Otolaryngol 1996;1781- 86PubMedGoogle ScholarCrossref 3. Ferguson JLMcCaffrey TVKern EBMarin WJ Effect of Klebsiella ozaenae on ciliary activity in vitro: implications in the pathogenesis of atrophic rhinitis. Otolaryngol Head Neck Surg 1990;102207- 211PubMedGoogle Scholar 4. Bernat I Ozaena and iron deficiency. BMJ 1968;3315PubMedGoogle ScholarCrossref 5. Han Sen C The ozena problem: clinical analysis of atrophic rhinitis in 100 cases. Acta Otolaryngol 1982;93461- 464PubMedGoogle ScholarCrossref 6. el-Barbary A el-SYassin AFouad Hel-Shennawy M Histopathological and histochemical studies on atrophic rhinitis. J Laryngol Otol 1970;841103- 1112PubMedGoogle ScholarCrossref 7. Zohar YTalmi YPStrauss M et al. Ozena revisited. J Otolaryngol 1990;19345- 349PubMedGoogle Scholar 8. Mickiewicz LMikulski TKuzna-Grygiel WSwiech Z Assessment of the nasal mucosa in workers exposed to the prolonged effect of phosphorite and apatite dusts. Pol J Occup Med Environ Health 1993;6277- 285PubMedGoogle Scholar 9. Goodman WSDe Souza FM Atrophic rhinitis. Otolaryngol Clin North Am 1973;6773- 782PubMedGoogle Scholar 10. Dudley JP Atrophic rhinitis: antibiotic treatment. Am J Otolaryngol 1987;8387- 390PubMedGoogle ScholarCrossref 11. Taylor MYoung A Histopathological and histochemical studies on atrophic rhinitis. J Laryngol Otol 1961;55574- 590PubMedGoogle ScholarCrossref 12. Gadre KCBhargava KBPradhan RYLodaya JDIngle MV Closure of the nostrils (Young’s operation) in atrophic rhinitis. J Laryngol Otol 1971;85711- 714PubMedGoogle ScholarCrossref 13. Shehata MDogheim Y Surgical treatment of primary chronic atrophic rhinitis (an evaluation of silastic implants). J Laryngol Otol 1986;100803- 807PubMedGoogle ScholarCrossref
Archives of Otolaryngology - Head & Neck Surgery – American Medical Association
Published: Aug 1, 2005
Keywords: radiology specialty
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