What causes turbinate dysfunction?

Updated: Jun 24, 2021
  • Author: Sanford M Archer, MD, FACS; Chief Editor: Arlen D Meyers, MD, MBA  more...
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The etiology of turbinate dysfunction is multifactorial. Because the turbinates have a very rich blood supply and are governed by the parasympathetic nervous system, anything that affects either of these 2 systems affects the turbinates and, hence, the nose. [3]

Allergic rhinitis is the most common cause of turbinate dysfunction. Allergic rhinitis is due to environmental allergens that come in contact with the nasal membranes, causing an inflammatory reaction and resultant congestion and increased drainage. This category is so large that any nonallergic cause of turbinate dysfunction is known as vasomotor rhinitis. Vasomotor is a term that indicates the neurovascular control of the nasal membranes. Causes of vasomotor rhinitis include, but are not limited to, the use of cardiovascular and antihypertensive drugs, female hormones, changes in temperature, and rhinitis of disuse.

Any medication a patient takes that stimulates the parasympathetic nervous system can also affect the turbinate mucosa and cause congestion. Female hormones, specifically progesterone, may have a similar effect; therefore, congestion can frequently be experienced during the premenstrual phase of the menstrual cycle and the third trimester of pregnancy. Some female hormone replacement therapy and oral contraceptives that have a higher concentration of progesterone may have similar effects, although a 2006 small clinical study did not demonstrate that effect. [4]

Condensation rhinitis is well known to snow skiers and is due to the reaction of the nasal membranes to the colder outside environment. An equivalent example is that of taking a cold beverage can outside on a hot day and finding condensation developing on the outside of the can.

Rhinitis of disuse occurs in patients who no longer use their noses for airflow (eg, patients who have undergone laryngectomy) or those who abuse topical nasal decongestants (rhinitis medicamentosum). In the first case, the underlying pathophysiology is rebound inflammation due to a lack of feedback from the normal nasal airflow. In the second case, a rebound vasodilation of the turbinates occurs as a response to the topical sympathomimetics.

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