Journal of Otology & RhinologyISSN: 2324-8785

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Research Article, J Otol Rhinol Vol: 3 Issue: 4

Atrophic Rhinitis - Empty Nose Syndrome: A Clinical, Endoscopic and Radiological Entity

Jean Jacques Braun1,2*, Christian Debry1, Alessio Imperiale3,Frédéric de Blay2, Benjamin Rock4, Francis Veillon5 and Sophie Riehm5
1Service ORL et CCF, Hôpital de Hautepierre, Strasbourg cedex, France
2Service de pneumologie, d’allergologie et de pathologie respiratoire del’environnement, Nouvel hôpital civil, Strasbourg cedex, France
3Service de Biophysique et de Médecine Nucléaire, Hôpital Hautepierre,Strasbourg cedex, France
4University of Exeter and Peninsula College of Medicine and Dentistry, Royal Cornwall Hospital, Cornwall, England
5Service de Radiologie 1, Hôpital de Hautepierre, Strasbourg cedex, France
Corresponding author : Jean Jacques Braun
8 quai Kellermann, 67000 Strasbourg, France
Tel: +33(0)388221307; Fax: +33(0)388324681;
E-mail: [email protected]
Received: April 22, 2014 Accepted: July 02, 2014 Published: July 12, 2014
Citation: Jean Jacques Braun, Christian Debry, Alessio Imperiale, Frédéric de Blay, Benjamin Rock, Francis Veillon, Sophie Riehm (2014) Atrophic Rhinitis - Empty Nose Syndrome: A Clinical, Endoscopic and Radiological Entity. J Otol Rhinol 3:4. doi:10.4172/2324-8785.1000169


Atrophic Rhinitis - Empty Nose Syndrome: A Clinical, Endoscopic and Radiological Entity

Background: Atrophic rhinitis results from progressive atrophy of the nasal mucosa and underlying bone. Empty nose syndrome is often described as post-turbinectomy iatrogenic atrophic rhinitis. For some authors a distinction should be drawn between these two conditions.

Purpose: The aim of this article is to review the literature (PubMed, EMBASE, Google: Atrophic Rhinitis, Ozaena, Empty Nose Syndrome) and to present a representative series of 21 cases of the two conditions in a compressed overview.

Clinical, endoscopic, radiological features: The clinical symptoms include nasal obstruction, epistaxis, impaired olfaction, purulence and crusting. Endoscopy and computed tomography show mucosal and osteochondral modifications with an enlargement of the nasal cavities up to the choanae.

Aetiologies: By combining the results of clinical, endoscopic, imaging and additional investigations if necessary, it may be possible to differentiate between primary or idiopathic forms and secondary forms of atrophic rhinitis to optimize diagnostic work-up and patient management.

Keywords: Atrophic rhinitis; Empty nose syndrome; Ozaena; CT; MRI


Atrophic rhinitis; Empty nose syndrome; Ozaena; CT; MRI


AR: Atrophic Rhinitis; ENS: Empty Nose Syndrome; CT: Computed Tomography; MRI: Magnetic Resonance Imaging


Atrophic rhinitis (AR) results from progressive atrophy of the nasal mucosa and underlying bone; its symptoms including nasal obstruction, epistaxis, anosmia/cacosmia, purulence, crusting and chronic inflammatory disease of the upper airway [1-8]. Empty nose syndrome (ENS) is often described as post-turbinectomy iatrogenic AR. Some authors argue that a distinction should be drawn between ENS and AR, even though the two entities may present with similar symptomatologies and endoscopic and imaging findings [7]. According to a review of the literature (PubMed, EMBASE, Google: Atrophic Rhinitis, Ozaena, Empty Nose Syndrome) it seems more sensible to combine AR and ENS within a single clinical, endoscopic and radiological entity referred to as AR. The aetiologies and medical backgrounds enable one to distinguish between primary AR (ozaena) the incidence of which has decreased over the last century and secondary AR resulting variously from trauma, surgery, infection, granulomatous or other systemic diseases or radiation exposure. Knowledge of the underlying aetiology has a major influence on the diagnosis and treatment of AR [4-8].

Clinical Features

The clinical symptoms of AR include an almost constant sensation of nasal obstruction (inability to perceive airflow); a dry nose and sometimes a dry throat, often with crusting rhinitis (rhinitis sicca); impaired olfaction, ranging from hyposmia to anosmia and cacosmia in cases of ozaena; epistaxis and more rarely atypical dyspnoea; pain at the root of the nose with a sensation of mid-face fullness and, occasionally, systemic symptoms of fatigue, insomnia, anxiety or depression [1,2,4,6-9].
In a clinical examination, AR is diagnosed by nasal endoscopy; enlargement of the nasal cavities up to the choanae; dry, dystrophic, atrophic and sometimes crusted or ulcerated mucosa of the nasal cavities and, in some cases, the nasopharynx; absence, hypoplasia or atrophy of the inferior and/or middle turbinates, with a variable degree of destruction of the sinonasal walls and even of the perisinusal structures; the sequelae of prior sinonasal surgery (particularly turbinate surgery); septal perforation; osteochondral erosions; synechiae and visible nodular lesions suggesting Wegener’s granulomatosis or sinonasal sarcoidosis which must be confirmed by the appropriate clinicopathological work-up [1-8].
Rhinomanometry will reveal abnormally high nasal airflow rates and much-reduced resistance. Acoustic rhinomanometry will confirm the enlargement of the nasal cavities with wider cross-sectional area than normal [3-5,10].
Microbiological tests may be relevant if there is associated suppuration related to Klebsiella ozaenae and Corynebacterium diphteriae which have been implicated in ozaena, Staphylococus aureus, Proteus mirabilis or Escherichia coli [1,2,11].
Histology is more relevant for diagnosing the underlying aetiology of secondary AR than for confirming the diagnosis of AR itself [1,2,4,7,12].

Radiological Imaging

At our knowledge there is no review in the literature about the imaging features and the different aetiologies of AR.
Computed tomography (CT) enables the accurate analysis of osteochondral structures (the turbinates, septum, sinonasal walls, osteomeatal complex, sinuses and skull base) and can confirm an endoscopic diagnosis of AR. Furthermore, CT may provide clues to the underlying aetiology (sinonasal sarcoidosis or Wegener’s granulomatosis, for example), although histological confirmation will be required [2,4,12-18]. Magnetic resonance imaging (MRI) may provide a more detailed picture of sinonasal mucosal structures and the extent of the disease process in some cases [12,16]. 18F-FDG PET CT may be used for diagnosis assessement but also to monitor treatment response in difficult cases of sarcoidosis with AR [18].
Imaging features which may depend on the underlying aetiological process include atrophy of the nasal or even nasopharyngeal mucosa (sometimes with mucosal thickening of the maxillary sinuses, which are often hypoplastic and have poorly visible osteomeatal complexes); turbinoseptal synechiae; nodular lesions affecting the inferior turbinates and septum in cases of sarcoidosis; destructive nasal osteochondral lesions involving the turbinates, septum and sinonasal walls and which may sometimes extend into the paranasal sinuses, adjacent tissues or even the skull base; absent or malformed sinonasal structures (the turbinates, sinusal walls or sinuses); sclerotic lesions or bone remodelling in cases of Wegener's granulomatosis or following radiotherapy; and cervicothoracic, musculoskeletal and intracranial lesions in the context of systemic diseases of which AR is just one of the manifestations. Independently of the aetiology the most common imaging feature is an enlargement of the nasal cavities up to the choanae [6,7,14-16,18].

Disease Mechanism and Aetiologies of Atrophic Rhinitis

Atrophic abnormalities of the nasal mucosal and osteochondral structures (the turbinates, septum and sinonasal walls) can profoundly alter nasal physiology and thus impair the organ's respiratory, secretory, ciliary and olfactory functions [1,2,5,9].
These structural alterations are probably related to a combination of genetic and environmental factors and result in chronic inflammation, impaired drainage of nasal secretions and bacterial colonization - all of which may profoundly alter the patient’s quality of life [1-4,8,9].
Porcine progressive AR which serves as an animal model of the human condition is thought to be caused by infectious and toxic phenomena involving thermolabile exotoxins from Pasteurella multocida (together with Bordetella bronchisepta, in some cases) [1].
By combining the results of clinical, endoscopic, imaging and additional investigations if necessary, it may be possible to differentiate between (i) primary or idiopathic forms of AR in which chronic progressive mucosal and osteochondral lesions of unknown aetiology may significantly impair quality of life and (ii) secondary forms in which AR is a manifestation of a local, locoregional or systemic disease process or an after-effect of sinonasal surgery, craniofacial radiotherapy or traumatic or chemical injury [1-16,18-28].

Primary Forms of AR

Primary AR (also known as ozaena) has become increasing rare over the last century. Middle-aged patients (particularly those of Mediterranean, Indian, Chinese or African ethnicity) may develop an atrophic process that involves the nasal structures (often extending to the nasopharynx) and is associated with crusting and disabling cacosmia. Klebsiella ozaenae and (sometimes) Corynebacterium diphtheriae are frequently present, although the organisms' aetiological roles remain subject to debate. Rare cases of ozaena have been reported in children (Figure 1) [1,11,16].
Figure 1: Axial CT image of a 7-year-old child with ozaena, showing voluminous nasal cavities, atrophy of nasal and nasopharyngeal mucosa, absent turbinates, a frayed appearance of the septal mucosa, mucosal thickening of the right maxillary and lysis of the sinusal walls.
Non-ozaenic primary AR can affect adults and children and may in some cases be familial (i.e. several cases in the same family or in twins [1,4,28]) or congenital, with turbinate agenesis or hypoplasia; malformations of the sinonasal walls and sinuses; congenital anosmia or primary dystrophic rhinobronchial mucosa (Figure 2).
Figure 2: Congenital AR in an 11-year-old child. Coronal T2 weighted MRI showing bilateral agenesis of the turbinates, voluminous nasal cavities, wide opening of the ethmoid aircells into the nasal cavities, normal-appearing septal mucosa, thickening of the left maxillary sinus mucosa and agenesis of the olfactory bulbs and sulci, in association with congenital anosmia.
Figure 3: AR and sinonasal sarcoidosis. Coronal gadoliniumenhanced fat-saturated T1-weighted MRI showing sequelae of sinonasal sarcoidosis: several nodular or pseudonodular lesions affecting both sides of the septum and the right inferior turbinate and atrophy of the left inferior turbinate and middle turbinates extending to involve the sinonasal walls on both sides and thickening of the mucosa of maxillary and ethmoid sinuses (no surgery had been performed).
Figure 4: AR associated with a Wegener’s granulomatosis. Coronal CT image showing a combination of bony destruction (involving the inferior and middle turbinates, anterior ethmoid aircells) and sclerosis (involving the sinus walls and hard palate).
Figure 5: AR in relapsing polychondritis. Axial CT image demonstrating septal perforation, absence of the inferior turbinates, and partial lysis of the sinusal wall of the left maxillary sinus. Nasogastric tube in the right nasal cavity.
Figure 6: AR in Crohn’s disease. Axial CT showing destructive involvement of the nasal pyramid, turbinates, septum and sinonasal walls and opacification of the maxillary sinuses.
Figure 7: AR in a cocaine user. Axial CT image demonstrating extensive destruction of the sinonasal structures with a large sinonasal cavity.
Figure 8: AR in Lethal Midline Granuloma (Stewart’s granuloma). Coronal CT images showing extensive destruction of the sinonasal structures, with orbital wall and ethmoidal roof lysis.
Figure 9: AR as a complication of craniofacial radiotherapy. Axial CT shows significant remodeling of the sinusal walls and the skullbase. Hypoplasia of the turbinates is seen.
Table 1: Secondary forms of Atrophic Rhinitis.

Secondary Forms of AR

The secondary forms of AR are summarized in a table with the main clinical, endoscopic and radiological features.
When considering these different aetiologies, the physician's diagnosis of AR is based on the case history, endoscopic findings, radiological features and (where necessary) additional investigations (biopsies, microbiological tests, biochemical assays and rhinomanometry); this is especially true for secondary AR.
The distinction between primary AR and the different aetiological forms of secondary AR is not only academic but also has therapeutic and prognostic importance. For example, management of primary AR and irreversible end-stage AR is not the same as management of secondary AR related to sarcoidosis, tuberculosis or Wegener’s granulomatosis, which require specific, early treatment.


The treatment for iatrogenic AR is essentially preventive (e.g. conservative sinonasal surgery). Nasal turbinate surgery is reserved for resistant, well-documented nasal obstruction.
In cases of AR caused by a systemic disease, the appropriate specific treatment should be initiated as soon as possible, in order to minimize the progressive, irreversible destruction of sinonasal structures. So for the systemic diseases the treatment is guided by disease severity and organ involvement often after discussion with a multidisciplinary team. The appropriate specific treatment may include antibiotics (multiagent treatment for tuberculosis) corticosteroids (sarcoidosis, Wegener’s granulomatosis); immunosuppressive or cytotoxic drugs like methotrexate, cyclophosphamide, azathioprine, infliximab for different connective tissue diseases often in association with corticosteroids.
Symptomatic medical treatments for AR include nasal lavage, mucous membrane humidification, topical ointments, antibiotics, antimicrobials and crenotherapy, removal of crusts by ENT clinician and elimination of environment and workplace promoting factors.
Surgery may be indicated in some cases of AR, in order to decrease the overall volume of the nasal cavities whilst preserving the remaining mucosa and/or promoting the regeneration of normal mucosa. This surgery may involve the intranasal injection of hyaluronic acid gel, submucosal implantation of cartilage, methacrylate, hydroxyapatite or Teflon or even medialization of the sinonasal wall or septal mucoperichondrial flap [2,4,5,7,8,15,17,26,27-31].
Nevertheless there is no evidence from randomized trials concerning the long-term benefits or risks of different treatment modalities for AR [32].


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