Empty nose syndrome (ENS) is a poorly understood and rare iatrogenic disorder resulting from the destruction of normal nasal tissue. In severe forms, it can be debilitating. In this article, the authors elucidate the distinction between ENS and atrophic rhinitis, and provide a systematic approach to the diagnosis and management of ENS. They urge a judicious and cautious approach to turbinate resection, to help better prevent this sequela of nasal surgery. They state that patients with ENS can be rehabilitated and their quality of life substantially improved with nasal augmentation as a means to help restore nasal anatomy toward the premorbid state.
Empty nose syndrome (ENS) is an iatrogenic disorder most often recognized for the presence of paradoxic nasal obstruction despite an objectively wide, patent nasal fossa. The term “empty nose syndrome” was initially coined to describe certain symptoms associated with tissue loss and radiographic findings of a paucity of normal anatomic structures in the nasal cavities. It has been referred to in the literature, erroneously, as a form of atrophic rhinitis. Because the understanding of ENS has progressed, it is important to appreciate its distinction from atrophic rhinitis, as well as the manifestations, diagnosis, and treatment of this debilitating disorder.
Explanation of atrophic rhinitis
Atrophic rhinitis is a chronic, degenerative condition characterized by inflammation and atrophy of the nasal and paranasal mucosa and structures. It is primarily a clinical diagnosis and should be considered in patients who have chronic rhinosinusitis and significant crusting, especially subsequent to repetitive nasal trauma or injuries. The classic constellation of symptoms of atrophic rhinitis includes thick and adherent crusting, foul odor (or fetor ), and nasal obstruction. The hardened crusts that develop have classically been referred to as rhinitis atrophicans cum foetore , or ozena . In the majority of cases, these symptoms are late sequelae of a chronic underlying inflammatory state in which much of the damage to the nasal and paranasal mucosa has already taken place. A keen clinical suspicion on the part of the otolaryngologist aids in early diagnosis of this disease. There may be a link between infections (eg, measles, scarlet fever, and diphtheria) and atrophic rhinitis; a sharp decrease in the incidence of atrophic rhinitis has been noted in countries in which a concurrent decrease in such infections was noted, despite unchanged sanitation.
It is important to note that two distinct conditions have been widely cited in the literature: primary and secondary atrophic rhinitis. Primary atrophic rhinitis is often spontaneous in onset and has a slowly progressing, debilitating course. Often, no underlying etiology is discovered, although inheritable or infectious causes are proposed mechanisms. Although spontaneous in onset, primary atrophic rhinitis likely reflects a microvascular paucity in blood flow that has been present for a prolonged period of time. Secondary atrophic rhinitis is much more commonly encountered and usually develops after specific insults, such as trauma, irradiation, reductive nasal surgery, or granulomatous disease. In secondary entities, nasal crusting, enlarged nasal cavities, resorption of the turbinates, mucosal atrophy, and paradoxic nasal congestion are encountered. Less commonly reported symptoms include facial pain and pressure, anosmia, and intermittent epistaxis. Physical and nasal endoscopic examination will always yield abnormalities of the nasal sidewall. A retrospective review of 242 patients showed the partial and complete absence of inferior turbinate (IT) tissue in 62% and 37% of patients, respectively. The absence of the middle turbinate (MT) was found in 57% of patients, and 32% of patients had either no recognizable or very small remnants of turbinate tissue. All patients had discolored (yellow, brown, or green) crusts covering the sidewalls and floor of the nose.
Histopathologic analysis of nasal mucosa may serve as confirmatory evidence of atrophic rhinitis. Universally, atrophy of serous and mucinous glands, loss of cilia and goblet cells, and inflammatory cell infiltrates are seen. Endarteritis obliterans and dilatation of capillaries increase the fragility of the epithelium and reflect the microvascular changes present. Pathogenic organisms, most commonly Klebsiella ozaenae , but also Staphylococcus aureus , Proteus mirabilis , and Escherichia coli may be found on nasal cultures.
Computed tomography (CT) scans of the nose and paranasal sinuses may reveal characteristic findings, including:
- 1.
Mucosal thickening of the paranasal sinuses
- 2.
Loss of definition of the ostiomeatal complex
- 3.
Hyperplasia of the maxillary sinus
- 4.
Enlargement of the nasal cavities with destruction of the lateral nasal wall
- 5.
Bony destruction of the IT and MT.
The lack of normal anatomic turbinate tissue together with atrophic rhinitis symptoms has erroneously been termed “the empty nose” in much of the literature. The idea that the presence of these conditions indicates that a patient has ENS has been propagated by the occurrence of paradoxic nasal congestion, the most common presenting symptom of atrophic rhinitis. The cause of paradoxical nasal obstruction is unclear, but atrophy of the olfactory epithelial receptors leading to anosmia, along with atrophy of pain and temperature receptors, is likely a contributing factor. Furthermore, the lack of anatomic nasal barriers and an adequate mucociliary elevator as the result of atrophic nasal mucosa results in substantially decreased nasal airflow. Investigators believe that some degree of nasal airflow resistance is necessary to balance pulmonary inspirations. The resulting lack of or offset of this balance may contribute to a subjective sense of inadequate nasal airflow, nasal breathing, and subsequent nasal congestion.
The management of atrophic rhinitis
Atrophic rhinitis can be a crippling disease. Medical treatment has aimed at reducing symptoms and complaints to allow the afflicted patient a better quality of life. Treatment of atrophic rhinitis is not so much controversial as it is varied. Several approaches have been used that are either primarily medical, primarily surgical, or a combination of both approaches. Aggressive nasal hygiene with regular intranasal irrigation remains the standard of conservative therapy and assists by producing minimizing crusting and restoring nasal hydration. Commonly used irrigation solutions include normal saline solution, sodium bicarbonate, aminoglycoside topical therapy, and plain water. Systemic or topical antibiotic irrigations are generally reserved for patients who have atrophic rhinitis that is the result of acute infection or that is indicated by positive cultures. Such antibiotics include tetracycline, aminoglycosides, and ciprofloxacin. Vasodilators and topical steroids may also provide palliative results.
A variety of surgical procedures exist to address the symptoms of atrophic rhinitis. Surgical principles for atrophic rhinitis have a long and plentiful developmental history. In 1873, Rouge recommended curettage and removal of the entire atrophic mucosa in the nose. In 1900, Gersuny injected paraffin under the nasal mucosa, which heralded the era of implants. In 1948, Rethi constructed a baffle from the septum to obstruct the nasal cavities and also used transplantation of Stensen’s duct, which had originally been reported by Wittmaack in 1919. In 1967, Young described a staged method of bilateral closure of the nostrils that had been performed in a small number of patients. This was done by raising skin flaps within the nostrils and suturing the folds together to allow effective closure of the nostril. Unilateral closure was first completed, and at the time of closure of the contralateral nostril, the opportunity was taken to re-open and examine the previously sutured nasal cavity. Young reported that crusting and purulent debris had disappeared upon such re-opening and that with time the nasal mucosa returned to a pink, healthy appearance. Regeneration of ciliated epithelium and mucous glands was found on histologic examination. In 1971, Gadre and colleagues reported on a modification of Young’s procedure and demonstrated the disappearance of crusting at six months after such modified procedures. Serial endoscopic examinations over several years showed some mucosal regeneration when modifications of Young’s original procedure were used.
A multitude of implant material has been used to augment intranasal volume. In 1923, Eckert-Mobius used macerated spongy beef bone. In 1947, Proud implanted acrylic resin in the septum and Eyries extended this technique to include the lateral nasal wall. In 1980, Chatterji modified Saunders’s autogenous bone-graft technique from 1958. Chatterji used a single, long piece of bone to enhance the biologic activity of the underlying nasal mucosa. The use of dermofat and placental grafts similarly is based on this theory of “biologic activation,” with the underlying tissue responses reversing and rejuvenating the existing atrophic conditions of nasal cavities. Goldenberg and colleagues placed plastipore implants in submucosal pockets in the floor of the nose and septum in a small number of patients. They reported excellent results in the majority of their patients, with complete resolution of symptoms up to 24 months after surgery. Overall, the use of implants has been promising, but extrusion of artificial implants has been reported in up to 80% of cases.
In general, the surgical principle of using implants in cases of atrophic rhinitis is directed at reducing the volume of the nasal fossae and, when using autogenous implantation, enhancing biologic activity of the affected nasal mucosa. The slower the absorption of the implant, as in the use of a single, long piece of graft, the greater the biologic effect. The rationale of narrowing the nasal lumen is that a decreased amount of airflow will occur with inspiration, thus resulting in less drying, crusting, and subsequent damage to the nasal mucosa. The explanation further involves contributions to the shape and position of the nostrils, the valvular action of the lateral nasal cartilages, the size and function of the turbinates, and underlying mucosal changes and blood flow.
The management of atrophic rhinitis
Atrophic rhinitis can be a crippling disease. Medical treatment has aimed at reducing symptoms and complaints to allow the afflicted patient a better quality of life. Treatment of atrophic rhinitis is not so much controversial as it is varied. Several approaches have been used that are either primarily medical, primarily surgical, or a combination of both approaches. Aggressive nasal hygiene with regular intranasal irrigation remains the standard of conservative therapy and assists by producing minimizing crusting and restoring nasal hydration. Commonly used irrigation solutions include normal saline solution, sodium bicarbonate, aminoglycoside topical therapy, and plain water. Systemic or topical antibiotic irrigations are generally reserved for patients who have atrophic rhinitis that is the result of acute infection or that is indicated by positive cultures. Such antibiotics include tetracycline, aminoglycosides, and ciprofloxacin. Vasodilators and topical steroids may also provide palliative results.
A variety of surgical procedures exist to address the symptoms of atrophic rhinitis. Surgical principles for atrophic rhinitis have a long and plentiful developmental history. In 1873, Rouge recommended curettage and removal of the entire atrophic mucosa in the nose. In 1900, Gersuny injected paraffin under the nasal mucosa, which heralded the era of implants. In 1948, Rethi constructed a baffle from the septum to obstruct the nasal cavities and also used transplantation of Stensen’s duct, which had originally been reported by Wittmaack in 1919. In 1967, Young described a staged method of bilateral closure of the nostrils that had been performed in a small number of patients. This was done by raising skin flaps within the nostrils and suturing the folds together to allow effective closure of the nostril. Unilateral closure was first completed, and at the time of closure of the contralateral nostril, the opportunity was taken to re-open and examine the previously sutured nasal cavity. Young reported that crusting and purulent debris had disappeared upon such re-opening and that with time the nasal mucosa returned to a pink, healthy appearance. Regeneration of ciliated epithelium and mucous glands was found on histologic examination. In 1971, Gadre and colleagues reported on a modification of Young’s procedure and demonstrated the disappearance of crusting at six months after such modified procedures. Serial endoscopic examinations over several years showed some mucosal regeneration when modifications of Young’s original procedure were used.
A multitude of implant material has been used to augment intranasal volume. In 1923, Eckert-Mobius used macerated spongy beef bone. In 1947, Proud implanted acrylic resin in the septum and Eyries extended this technique to include the lateral nasal wall. In 1980, Chatterji modified Saunders’s autogenous bone-graft technique from 1958. Chatterji used a single, long piece of bone to enhance the biologic activity of the underlying nasal mucosa. The use of dermofat and placental grafts similarly is based on this theory of “biologic activation,” with the underlying tissue responses reversing and rejuvenating the existing atrophic conditions of nasal cavities. Goldenberg and colleagues placed plastipore implants in submucosal pockets in the floor of the nose and septum in a small number of patients. They reported excellent results in the majority of their patients, with complete resolution of symptoms up to 24 months after surgery. Overall, the use of implants has been promising, but extrusion of artificial implants has been reported in up to 80% of cases.
In general, the surgical principle of using implants in cases of atrophic rhinitis is directed at reducing the volume of the nasal fossae and, when using autogenous implantation, enhancing biologic activity of the affected nasal mucosa. The slower the absorption of the implant, as in the use of a single, long piece of graft, the greater the biologic effect. The rationale of narrowing the nasal lumen is that a decreased amount of airflow will occur with inspiration, thus resulting in less drying, crusting, and subsequent damage to the nasal mucosa. The explanation further involves contributions to the shape and position of the nostrils, the valvular action of the lateral nasal cartilages, the size and function of the turbinates, and underlying mucosal changes and blood flow.
The manifestation and symptoms of empty nose syndrome
“Empty nose syndrome,” or more precisely, “the empty nose syndrome of Stenkvist,” is a term first coined by Eugene Kern and Monika Stenkvist at the Mayo Clinic in 1994 to describe certain symptomatology and the type of images appearing on sinus CT scans after tissue loss. It is commonly referred to in the literature as an iatrogenic form of atrophic rhinitis, though it is important to note the two are distinct clinical entities. Patients who have ENS present most commonly after undergoing IT resection. MT resection or even the presence of normal turbinate tissue and intranasal volume are also associated with ENS. There is a paucity of literature surrounding the evolution and diagnosis of this disorder, so that some otolaryngologists doubt the existence of ENS. Few patients develop ENS following turbinate resection, but this debilitating complication requires astute diagnosis and clinical suspicion on the part of the otolaryngologist.
The hallmark complaint of a patient who has been afflicted with ENS is paradoxic nasal obstruction. On physical examination, large, patent nasal fossae may be present as the result of the lack of turbinate tissue, but patients report a subjective feeling of “stuffiness,” for lack of a better descriptor. This sensation may be coupled with “emptiness,” a term patients use to describe the subjective inability to sense airflow, mainly seen following total inferior turbinectomy. Another common and perplexing symptom of paradoxic nasal obstruction is shortness of breath or difficulty breathing. Patients with this symptom tend to overbreathe and often slip into hyperventilation because they feel a relentless sense of dyspnea. This condition is perhaps the most severe form of paradoxic obstruction and may worsen with strain or physical activity.
The term “paradoxic obstruction” describes the subjective feeling of poor breathing despite objective patency, which typically is overly patent. A lack of nasal resistance leads to poor pulmonary function because the body strains to sense airflow, because the nasal resistor is essential to proper pulmonary function. The nasal resistor has been cited as centrally important in providing wider opening of the peripheral bronchioles and enhancing alveolar ventilation. These actions allow for better gas exchange, higher negative thoracic pressure, and overall improved venous cardiac and pulmonary backflow. This claim is strengthened by clinical research that indicates that normal rates of nasal resistance to expiration help to maintain lung volumes and may indirectly determine arterial oxygenation. In fact, the symptoms may be so bothersome that the patient relates a sense of suffocation. As a result, the patient who has ENS becomes preoccupied with nasal symptoms, resulting in the inability to concentrate (aprosexia nasalis), fatigue, irritability, anxiety, and depression. Many times, this constellation of symptoms is overlooked because the physician does not have a clear explanation for paradoxic obstruction in the presence of a widely patent nasal cavity. Crusting and pain may be present with ENS. Dryness is a constant subjective complaint and can typically be observed objectively as well. This may lead to atrophic rhinitis, though as previously stated in this article, the two entities are separate disorders.
Although the term “empty nose syndrome” was originally coined to describe radiographic findings, the diagnosis of ENS relies heavily on clinical suspicion and physical examination. The onset of ENS’s manifestations varies widely, ranging from months to years after turbinate surgery. Most commonly, ENS is encountered after IT resection; however, ENS can occur after MT resection and in patients who have seemingly normal turbinate tissue. In all cases of ENS, patients have had some type of turbinate procedure performed during their lifetimes.
Overall, ENS seems most commonly associated with mucosal destructive surgeries. From personal experience and examination of the literature regarding turbinate excision, the authors estimate that approximately 20% of patients with IT resection will develop full-blown ENS and that a greater percentage suffers from at least dryness ( Table 1 ). The syndrome does not occur after most turbinate procedures, even total removal. The authors are not certain why some patients develop ENS whereas others do not. One thought is that a “two hit” phenomenon that must take place, in which (1) the tissue is excised or damaged and (2) the sensory nerves to the area manage to regenerate poorly. Poor nerve growth following tissue destruction is a known risk for many forms of surgery. For example, there is a 26.4% incidence of hypoesthesia at the surgical site after inguinal herniorrhaphy. Indeed, the turbinates are recognized as a source of nerve growth factor. Thus, damage to turbinate tissue may predispose the nose to poor nerve regrowth and healing, leading to a significantly decreased sensation of airflow.
| Study | n | Resection Degree | Postoperative Complications and Patient Complaints (% of Patients) | Follow-up |
|---|---|---|---|---|
| Martinez et al, 1983 | 29 of 40 | Total |
| 2 months–5 years |
| Moore et al, 1985 | 18 a | Total |
| 2–7 years |
| Ophir et al, 1985 | 150 | Total |
| 2.5 years (mean) |
| Ophir, 1990 | 38 | Total |
| 2.8 years (mean) |
| Ophir et al, 1992 | 186 | Total |
| 12 years (mean) |
| Courtiss and Goldwyn, 1990 | 25 | Partial |
| 13 years (mean) |
| Wight et al, 1990 | 16 b | Total |
| 14–29 months |
| Carrie et al, 1996 | 14 c | Total |
| 7–8 years |
| Salam and Wengraf, 1993 | 20 | Total |
| 6 months |
| Oburra, 1995 | 34 | Total |
| 2 years and more |
| Berenholz et al, 1998 | 42 | Total |
| 3–10 months |
| Passàli et al, 1999 | 62 | Partial, surface electrocautery |
| 1–4 years |
| 58 | Partial, cryotherapy |
| 1–4 years | |
| 54 | Partial, laser cautery |
| 1–4 years | |
| 69 | Submucosal resection (−) outfracture |
| 1–4 years | |
| 94 | Submucosal resection (+) outfracture |
| 1–4 years | |
| 45 | Total |
| 1–4 years | |
| Gendeh, 2000 | 15 | Total |
| 3–6 months |
| 21 | Partial |
| 3–6 months |
a According to Moore and Kern (2001), the patients in this study were 18 of the 40 patients that Martinez reported on two years previously.
b The initial group included twenty patients. Four patients had anterior radical trimming and only later had total resection, so those four patients were excluded from the results.
c This study is a six-year follow-up on fourteen patients from Wight’s 1990 initial study group (data also reported in this table).
Another thought is that unique patient anatomy leads to varying airflow disruption. Elad and Zhao have elegantly demonstrated such airflow disruption after IT resection in computer modeling of airflow through the nose. In general, the turbinates define and are intimately related to the nasal meati through which air flows. The meati that are formed between the turbinates, the septum, and the nasal floor and walls are very narrow and offer a mechanism of resistance to limit the total amount of airflow. This resistance also serves to increase the velocity of airflow, ensuring a mostly laminar pattern. As a result, a maximal conductive air–mucosal interface exists, which provides maximum sensation. Loss of turbinate tissue ultimately disrupts and destroys the meatal structure, causing turbulent, less efficient, and less sensate airflow.
The dry lining that results from a loss of physiologic humidification and heating may produce crusts that further impair the sensation of airflow. Passàli and colleagues demonstrated a disruption of nasal physiology (mucociliary clearance, IgA secretion rates, and general heating and humidification capacities) in 45 patients who had total inferior turbinectomies. Naftali and colleagues and Elad and colleagues used computational and computerized simulations to demonstrate that removal of the IT reduces overall heat and water vapor flux in the nose by 16% and that removal of the MT or removal of the IT and MT together reduces vaporization by 12% and 23%, respectively. An implant to the nose can be useful in either scenario because when the airflow is shifted toward more sensate tissue, less crusting occurs with a reduced dry air stream, and the airflow pattern is more normalized when a pseudo-turbinate created. Further research is needed to shed more light on the origin of ENS.
Because ENS is a recent area of interest and research, the literature does not elucidate a set diagnostic criterion, in particular because complaints of patients afflicted with ENS often are subjective. Houser uses the Sino-Nasal Outcome Test (SNOT-20), a validated 20-item survey that examines general nasal symptoms and can be used as a comparator before and after some type of intervention. Each item is scored from zero (no symptoms) to five (severe symptoms). Houser modified the existing SNOT-20 to include five additional, ENS-specific questions (SNOT-25). The SNOT-25, with Houser’s modifications, is shown in Table 2 . Patients are also asked to free text or expand on their responses. The SNOT-25 is a comprehensive assessment tool to aid with recognition and diagnosis of ENS patients.
| Scoring Range (0–5) | ||||||
|---|---|---|---|---|---|---|
| SNOT-20 and SNOT-25 Nasal Symptoms | 0 No Symptoms | 1 | 2 | 3 | 4 | 5 Severe Symptoms |
| 1. Need to blow nose | ||||||
| 2. Sneezing | ||||||
| 3. Runny nose | ||||||
| 4. Cough | ||||||
| 5. Postnasal discharge | ||||||
| 6. Thick nasal discharge | ||||||
| 7. Ear fullness | ||||||
| 8. Dizziness | ||||||
| 9. Ear pain | ||||||
| 10. Facial pain/pressure | ||||||
| 11. Difficulty falling asleep | ||||||
| 12. Waking up at night | ||||||
| 13. Lack of good night’s sleep | ||||||
| 14. Waking up tired | ||||||
| 15. Fatigue | ||||||
| 16. Reduced productivity | ||||||
| 17. Reduced concentration | ||||||
| 18. Frustration/restlessness/irritability | ||||||
| 19. Sadness | ||||||
| 20. Embarrassment | ||||||
| Houser Modification adds: | ||||||
| 21. Dryness | ||||||
| 22. Difficulty with nasal breathing | ||||||
| 23. Suffocation | ||||||
| 24. Nose is too open | ||||||
| 25. Nasal crusting | ||||||
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
