The mucosal temperature postop has been shown to increase by average 0.9C (+3.0%) on both nasal expiration and inspiration, with the T°C difference between the nasal expiration and nasal inspiration being a constant 4C both preop and postop. This finding was true for all intranasa compartments: internal nasal valve, nasal cavity and inferior turbinate (Seresirikachorn 2024).
An ENS patient who is a member of the ENS fb group, has previously undergone both an aggressive turbinate reduction and aggressive septoplasty. He performed his own T°C measurements of the internal nasal valve (INV), using FLIR One Gen 3 thermal camera similar to the one used in Seresirikachorn 2024 study. His study showed that, on mouth breathing, there was a significant leak of air from the nose and that placing intranasal cotton plugs helped both reduce that air leak by about 60% and lower intranasal temperature by about 4%, with the difference between inhalation and exhalation being a constant 4.5C both with cotton and without. On nasal inhalation, this ENS patient used cotton plugs to effectively lower the intranasal T°C by about 0.6C (2.1%). However the exhalatory intranasal T°C stayed at 33.3C despite the cotton placement.
Seresirikachorn 2024 set the preoperative normal T°C for INV at 31.50C on nasal exhalation and 27.7C on nasal inhalation. This ENS patient with nasal cotton plugs in place, experienced 33.3C on nasal exhalation and 26.5C on nasal inhalation. While cotton plugs helped lower inhalationary T°C, they seemed ineffective with exhalatory T°C, leading to chronically high and damaging T°C on nasal exhalation, in absence of normal mucosal function and secretions. While +3-4% intranasal T°C increase may seem insignificant, that T°C increase appears to be detrimental to the histological structures of nasal mucosa, including cilia, ciliated cells, respiratory epithelium, goblet cells and basal cells. High Intranasal T°C leads to more mucosal dryness and atrophy, overheating of nasal cavities, septal burning, trigeminal pain and, ultimately, respiratory distress. Though there is no permanent solution to the destructive overheating of the nasal cavities from ENS, some patients find some relief in breathing clean cold air and/or refrigerator cooled supplemental oxygen. This shows again that nasal airflow resistance and intact mucosa are critical for adequate cooling of the nasal cavities and adjacent parts of the nervous system (e.g. ganglion block) and possibly even frontal parts of the brain.
Humidification of Lungs and Nasal Mucosa via water/vapor recycling in the nasal cavities
The nose provides 60-70% of total air humidification for the lungs, including 15% from inferior turbinates (Naftali 2005). On expiration, as air passes through the nose, it gives up heat to the cooler nasal mucosa. This cooling causes water vapor condensation and 33% return of both heat and moisture to the mucosal surfaces (White 2015). The sensation of pharyngeal dryness often reported by ENS patients is due to an airflow that is insufficiently humidified obviously yielding a drying of the airway mucosa (Scheithauer 2010). Intranasal dryness triggers the mucosal degradation and atrophy that leads to deterioration of the ENS condition and, ultimately, death. Additionally, dryness in the lungs leads to formation of more alveoli dead space, further hindering proper gas exchanges in the lungs.
