How Turbinates Funtion
The roles of the turbinates and how their absence causes symptoms of ENS
The nasal turbinates are elongated bony structures, covered with nasal mucosa, that project off the nasal side walls and stretch across the entire nasal airway. In adults – the inferior turbinate is about the size of an index finger and the middle turbinate is about the size of the small finger. They are the most important mucosal and moisture secreting structures of the nose and they serve to heat regulate (to body temperature), humidify (to 98% humidity), to filter, to pressurize, elevate and streamline the air that flows through the nose. They provide most of the nasal mucosa for the air to flow over and by doing so they act as the radiators, the humidifiers and filters of the nose. The unique air-conditioning and processing conditions that the turbinates supply are not important only for proper lung function but also for keeping the health, function and integrity of the rest of the nasal mucosa, which is essentially the organ-system of the nose, as it covers all the inner nasal chambers and sinus cavities. The turbinates, in particularly the inferior ones, also play a crucial role in protecting the pharynx and larynx from the effect of direct insult of airflow and dryness.
The turbinates are also heavily innervated with pressure sensing receptors (of the trigeminal cranial nerve) that sense the airflow and thus notify the brain that enough air is traversing the nose to sustain life. If too much of these receptors are gone nasal breathing becomes unsatisfying, even though there is no structural blockage. This is called ‘paradoxical obstruction’ and is very common in ENS. This lack of airflow sensation causes much distress and morbidity to the sense of well being.
The turbinates, especially the inferior ones, also provide most of the nasal resistance to the lungs. The lungs need some resistance to allow them to reach their proper inflation and deflation rates during inhalation and exhalation. The nose supplies 50% of the entire resistance to the lungs. The turbinates supply most of these 50%. The function of nasal resistance is poorly researched and understood. It is well known from clinical observation that too little nasal resistance can cause similar pulmonary breathing difficulties and shortness of breath as too much resistance. Healthy nasal breathing is essential for maintaining all aspects of physical and mental health.
The turbinates also trap more than 75% of the water vapor returning from the lungs upon exhalation and thus help protect the body from dehydration.
The poorly understood naso-pulmonary reflex may also play a role in causing pulmonary restriction in ENS patients.
The implication of turbinectomies in causing ENS
Sometimes the turbinates become chronically swollen in such a way which causes too much nasal obstruction. ENT and plastic surgeons can decrease their volume using the surgical procedure known as a turbinectomy. However this is a wide code-name that might mean anything from minimal reduction to complete resection of an entire turbinate. While careful and judicial conservative reductions of a turbinate’s volume can be beneficial to the patient, an aggressive turbinectomy, in which most or all of the main turbinal body is resected, can be a devastating procedure that causes ENS.In many patients, ENS-type like symptoms develop even after what seems to be conservative reductions of the turbinates, especially if they include the anterior portion of the inferior turbinates, which are essentially a vital part of the inner nasal valve. However these symptoms will not be as severe as in over aggressive reductions of the turbinates.
When taking nasal anatomy and physiology into account it is very easy to see how over resection of nasal inferior and/or middle turbinates (also known as ‘conchae’) will cause the nasal chambers to be too empty, too wide and too dry, resulting in a marked decline of all nasal functions and sensations and this has a profound effect on the sufferer’s quality of life and sense of well-being.
The term “empty nose syndrome” was originally coined in the early 1990s by Dr. E.B. Kern (MD.) who was at the time head of the otolaryngology ward in the Mayo Clinic in Rochester, Minnesota, USA. He and his colleagues began to notice that more and more patients who had undergone aggressive resections of their inferior or middle turbinates seemed to develop symptoms of nasal obstruction and shortness of breath even though their noses appeared to be wide open, following partial or total turbinectomies. Other hallmark symptoms were chronic nasal dryness, difficulty concentrating, and often clinical depression. They found that all these symptoms and more, in all the patients examined, developed only after their inferior or middle turbinate were over aggressively resected.
All the patients had CT scans that showed abnormally wide and empty looking nasal cavities, thus they called it – “Empty Nose Syndrome”.
ENS is often referred to also as ‘secondary atrophic rhinitis’, because it is believed that the over exposed and wide cavities may become atrophic over time (‘secondary’= caused by surgery or other medical intervention, or direct trauma to the nose, as opposed to ‘primary’ which develops because of systemic illnesses). However, developing an atrophic mucosa on top of ENS is not a prerequisite for diagnosing a post-turbinectomy patient with ENS.
In ENS the mucosa in the over exposed cavities, where the turbinates were over resected, becomes chronically dry and in some cases even atrophic. But, unlike in atrophic rhinitis, this dryness or atrophy is caused directly by the direct impact of over turbulent and dry airflow and not because of chronic inflammation of the mucosa that occurs in atrophic rhinitis. So, perhaps a more accurate description, when comparing the two, would be to say that ENS symptoms can appear do be similar to those of atrophic rhinitis, but unlike the latter the dryness or atrophy in ENS is not of a progressive inflammatory sort.
From a histological point of view the clinical picture in ENS tends to resemble a form of rhinitis sicca with perhaps some limited areas of atrophic mucosa, usually at the front of the nose, rather than full blown atrophic rhinitis. Of course, atrophic rhinitis in itself, or ozena, can both result in ENS too.