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Wise et al.

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surgery causes nerve damage that if improperly healed, results in failure to return to a normal physiologic state. 221 Differences in nerve recovery after surgery may explain why only some patients develop ENS despite identical turbinate surgeries. Indeed, certain surgeons have identified patients with unilateral ENS symptoms while their normal sensing side looks like a mirror image in terms of absent inferior turbinate tissue. Diagnosis is made based on history, physical exam, and the cotton test, where a piece of slightly moist cotton is placed in the nasal cavity for 10 to 30 minutes with alleviation of symptoms, validating the diagnosis. 223 Other conditions that present with nasal dryness and crusting should be ruled out (ie, atrophic rhinitis, sarcoidosis, etc.). The Empty Nose Syndrome 6-Item Questionnaire has documented validity in identifying ENS patients. 229 Surgery for submucosal expansion of the internal nasal mucosa can often bring relief for patients. 223 It has also been reported that depression and anxiety are prevalent among ENS patients. 230 Atrophic rhinitis is a chronic, degenerative condition characterized by inflammation and atrophy of the nasal and paranasal mucosa. 231 Primary atrophic rhinitis runs a protracted course. It can occur spontaneously with unknown etiology, but it is also associated with a bacterial infection, almost exclusively Klebsiella ozaenae . In a study examining 45 patients diagnosed with primary atrophic rhinitis, all nasal cultures were positive for Klebsiella ozaenae . 231 Mucosal injury is hypothesized to result from prolonged microvascular or ischemic injury. 231-233 Secondary atrophic rhinitis is far more common and usually develops following direct injury from trauma, irradiation, reductive nasal or sinus surgery, or in certain rare granulomatous diseases. 231,234 Secondary atrophic rhinitis is also associated with a bacterial infection, but Staphylococcus aureus, Proteus mirabilis , and Escherichia coli are the more common pathogens, with Klebsiella ozaenae rarely isolated. 231 Atrophic rhinitis presents as thick, adherent nasal crusting, nasal congestion, foul odor, and atrophy of mucosal and turbinate surfaces, with severe cases having complete absence of recognizable anatomic landmarks, septal perforations, or saddle nose deformity. 231-233 Hyposmia, epistaxis, and facial pain or pressure may also occur. Histological examination of intranasal tissue demonstrates squamous metaplasia, glandular atrophy, and diffuse endarteritis obliterans in both types of atrophic rhinitis. 231 Diagnosis is established from clinical examination, nasal biopsy, and nasal cultures for associated bacteria. Both atrophic rhinitis and ENS patients complain of nasal congestion. For atrophic rhinitis patients, this is often a result of significant nasal crusting, although as the disease progresses and mucosa and turbinate tissue is lost, the widened nasal cavity can very closely resemble that of an ENS patient. The pathophysiology of the paradoxical sensation of nasal congestion at this point is the same in both disease states, although the origin of the inciting event differs. In the literature, ENS has repeatedly been described erroneously as a form or subset of atrophic rhinitis. ENS results from iatrogenic removal of turbinate tissue and is not associated with a bacterial infection whereas atrophic rhinitis results from a chronic, often idiopathic inflammatory process associated with bacterial infection that progresses to resorption of turbinate tissue. Atrophic rhinitis patients suffer from heavy crusting whereas ENS patients exhibit only minor crusting or no crusting.

Author Manuscript Author Manuscript Author Manuscript Author Manuscript

Int Forum Allergy Rhinol . Author manuscript; available in PMC 2020 June 10.