Empty Nose Syndrome

Empty nose syndrome (ENS) was originally described by Dr. Eugene Kern in the 1990s to describe symptoms suffered by some patients who had received a partial and/or total middle and/or inferior turbinate reductions or resections. Turbinates serve as radiator fins in the nose that project off the side of the nose to help filter and humidify the air. Turbinate reduction or resection has been a common procedure that is practiced throughout the world. In the absolute great majority, the surgery provides improvedment in nasal airflow. Those patients that benefit from turbinate reduction surgery routinely require less use of medications and report better breathing on nasal and sinus surveys. Surgical benefits of turbinate reduction include: improvements in nasal breathing, decreased use of nasal medications, and improvements in validated quality of life survey instruments. Despite excellent results in most patients, there is a small subset of patients who have reported nasal crusting/dryness, poor nasal airflow and significant impact on sleep and quality of life measures after over aggressive turbinate surgery.

Empty nose syndrome patients mainly complain of obstructed nasal passages and not being able to get a full breath in through the nose despite having wide open nasal passages. Other less reported symptoms include nasal crusting, inhaling too much cold air and suffocation symptoms that affect sleep. In severe cases, patients can develop physcological or psychiatric conditions such as anxiety about their lack of nasal airflow, depression and sleep disorders.

Turbinates and the Nasal Cycle

Nasal turbinates also contain a significant amount of erectile tissue (tissue that swells), particularly within the anterior aspect of the inferior turbinate, thought to allow precise regulation of nasal airflow. In particular, this erectile tissue is thought to be essential for the nasal cycle, in which one nostril becomes congested while the other side is decongested. The true importance of the nasal cycle is unknown, but it is thought that the nasal cycle may be important for reducing the risk of pressure ulcers during sleep. Nasal cycle duration is longer than in wakefulness, and changes from side to side of the nasal cycle frequently coincide with changes in posture during sleep, tend to occur during REM sleep (the deepest part of sleep), never occur during slow wave sleep, and maybe absent in patients with severe nasal obstruction. The inferior turbinates contain a significant amount of autonomic innervation (the part of the nervous system that functions automatically). As a result, it is reasonable to think that patients with autonomic nerve damage to the inferior turbinates may have abnormalities and/or difficulties during sleep.


Recent research suggests that the feeling of nasal congestion is likely related to the body sensing different levels of pressure and/or temperature in each nasal cavity. These pressure and temperature receptors are likely located on the turbinate structures themselves, typically within the surface mucosal layer. With over-aggressive resection (surgically removing) of these turbinate structures, particularly with resection of the mucosal layer of the turbinates, people with ENS lose the ability to feel their nasal breathing. Furthermore, exquisite control of the diameter of the inferior turbinates is necessary to maintain laminar airflow (air moving through organized streamlines) that allows greater volumes of air to flow through the nose per a given breath. Without control of the diameter of the nasal airway, or with altered structures such as a septal perforation (a hole through the wall that separates the nasal cavity from right and left sides), nasal airflow becomes turbulent (disorganized streams of airflow) which limits the volume of airflow through the nose. Finally, the mucosal layer of the turbinates is an important immune-system organ, providing the first line of defense against bacteria and other pathogens that are inhaled. Through our own immune defense systems, the mucosal layer of our turbinate epithelium maintains a population of harmless bacteria that helps to crowd out dangerous bacteria from entering the nose. Patients with ENS lose these regulators of the bacterial population, and dangerous and harmful bacteria slowly colonize the nose. These bacteria can cause crusting, bleeding, worsening nasal congestion, and worsening dryness of the remaining nasal lining which leads to a vicious cycle and worsens the symptoms associated with ENS.

How do we treat empty nose syndrome?
Empty nose syndrome can be treated with topical therapies that attempt to moisturize the nose. Unfortunately, many of these therapies are probably harmful and provide limited benefit. For example, repeated saline irrigations or saline gel provide temporary relief of nasal dryness but wash out the proteins and mucins in the mucus layer lining the nasal cavity. These proteins include host defense peptides such as lactoferrin, human beta-defensins, and others that regulate the usual bacteria that exist within the nose. Washing these proteins away also interferes with the nose’s ability to protect the nasal mucosa from dangerous bacteria, such as Klebsiella ozenae. Humidifiers are helpful since oxygen transfer in the alveoli of our lungs is most efficient at 100% humidity, however, most commercial humidifiers become rapidly contaminated with fungus. Constant fungal exposure in the setting of ENS is likely more harmful than the benefit gained from using a humidifier. More helpful than a humidifier is living in a warm, humid climate, particularly with salty air, such as close to a tropical beach. Antibiotic nasal irrigations are often necessary in advanced forms of ENS to kill and deter growth of harmful bacteria such as Klebsiella species. Certain creams and oral therapies have been tried as well to hypertrophy (increase the size) of any remaining turbinate tissue. These include estrogen creams (turbinates enlarge during pregnancy) and recently medications like Viagra. Phosphodiesterase inhibitors such as Viagra are known to cause nasal congestion, possibly by inducing hypertrophy of nasal mucosa.


Surgery for ENS has typically involved using implants or bulking materials to increase the size of any remaining turbinate tissue, or to increase nasal resistance by implanting materials in other locations (such as the nasal septum) in an attempt to recreate a nasal turbinate. These implants have been partially successful in reducing the turbulence of nasal airflow that occurs. However, these implants do not reproduce the humidification or immune protection aspects of the original turbinate mucosa. The choice of implant is also difficult for surgeons. Initially surgeons prefer to use absorbable materials such as hyaluronic acid to see if patients will benefit from an implant. Later, more permanent implants such as with Gore-Tex or acellular dermis have been tried. Many patients report modest benefit with these implant options. Recently, a few centers have started implementing platelet-rich plasma combined with acellular extracellular matrix implants for the therapy of ENS.

More questions? Drop us a line!