New study: Atomatic IT reduction during septoplasty is wrong
I've always thought that the claim that mucosal turbinate hypertrophy was irreversible after being chronic for a long time, was not necessarily true, and if the causes for the hypertrophy are properly addressed they will shrink, making turbinate reductive surgeries unnecassery and un-indicated. All the ENT needs to do is to find the underlying cause, treat it and be patient as to let the turbinates shrink back to their normal size. The following study proves this line of thought, and suggests that the common practice of reducing turbinates automatically when performing a septoplasty is unnecassery and given the risks of ENS should be stopped, even when done conservatively, given that if the septum is the problem causing the hypertrophy, with time, approximately a year following surgery, the turbinates will shrink all by themselves, to suite the size of the post of cavities. Dr. Houser, do you agree? Arch Otolaryngol Head Neck Surg. 2008 Apr;134(4):419-23. Effect of septoplasty on inferior turbinate hypertrophy.Kim DH, Park HY, Kim HS, Kang SO, Park JS, Han NS, Kim HJ. Department of Otolaryngology, Ajou University School of Medicine San 5, Wonchon-dong, Youngtong-gu, Suwon 443-721, South Korea. ENTKHJ@ajou.ac.kr. OBJECTIVE: To measure the effect of septoplasty on the volume of inferior turbinate in patients with a deviated nasal septum. DESIGN: In this retrospective analysis, patients who underwent septoplasty without turbinate surgery from May 1, 2003, through April 30, 2006, were studied. The thicknesses and cross-sectional areas of mucosa and conchal bones were measured with computed tomography before the operations and at least 1 year after the operations. SETTING: University hospital. PATIENTS: A total of 20 patients who presented with a chief concern of nasal obstruction. MAIN OUTCOME MEASURES: The thicknesses of the medial mucosa, bone, and lateral mucosa and the cross-sectional area of turbinate before and after septoplasty were compared using the Wilcoxon signed rank -*test*-('"). P < .05 was considered statistically significant. RESULTS: The medial mucosa and cross-sectional area of the inferior turbinate on the concave side of the septum were significantly decreased by septoplasty (both, P = .01), and the medial mucosa and cross-sectional area of the inferior turbinate on the convex side of the septum were significantly increased by septoplasty (P = .01). The thicknesses and cross-sectional areas of the conchal bone on the concave and convex sides of the septum were not affected by septoplasty. CONCLUSION: After septoplasty, inferior turbinate hypertrophy, especially in the medial mucosa, may reverse.

I read this article when it came out and I found it fascinating. I does run counter to our teaching that a compensatory hypertrophied IT needs to be reduced at the time of septoplasty. It is the type issue that would require a great deal of counselling with patients: expect you previously open side to now be blocked up for a year or so. Valid info.

Compensatory hypertrophy is a fascinating issue and I think it should serve as a good model to explain ENS: Why does the turbinate on the concave side of the septum expand? - because the nose cannot stand having even one of it's sides too open. Say a septum has suddenly become seriously deviated because of a direct blow to the face, leaving one side of the nose now with an over patent airway - basically with ENS. The IT, or MT, depending where the concave is exactly, will quickly hypertrophy to fill in the gap. Of course, when the turbinates have been resected they cannot compensate like this any more, and ENS remains permanent. If the turbinators were right and the nose can function fine with over enlarged cavities - then the turbinates on the concave side would not hypertrophy. It's as simple as that - and that is the main argument that should be put to them. Why does the opposite turbinate, on the convex side, shrink? - because the nose cannot tolerate mechanical obstruction, so the turbinate shrinks to allow normal size air passage. What happens on the concave side, in particular, should be used as the best natural proof that nature provides us for the existence of ENS and the the critical role of airflow dynamics in it: When a septum is deviated and causes a concave side. But all the turbinates are there and the nose is disease free. The mucosa is in good condition and does not lack any nerve receptors. If ENS was only or mostly about a loss of nerve receptors then why should the turbinate on the concave side hypertrophy? Answer: The fact that it hypertrophies proves beyond doubt that having nerve endings and receptros intact is not enough to prevent ENS. Because if the air passage is too wide the air will not come enough into smooth motion of regular contact with the mucosa and thus the nerves won't get a strong and constant enough stimuli of breathing. Therefore, narrowing the over open passage increases the friction, the transduction (which should be the key word in explaining ENS) between the airflow and the mucosa on the nasal wall - which is what requested for sending the brain a proper breathing feedback from the nose.

ah but the nerves are vital as they are the mechanism by which the airflow is sensed to allow the info to be processed and then direct any changes in the bloodflow, etc. that leads to turbinate hypertrophy/reduction. It comes back to a combo - structure determining flow, and nerves sensing flow. The intimate interplay is complex and essential for proper health. If either are significantly disturbed then the system can crash.

Well done TE! You should become a lecturer in ENS. Doctors should know this though - turbinates change in size and shape all the time. However, when they have become damaged I think the technical term would be they are "buggered".

really guys... you're quick... :lol: I didn't even have a chance to refine this complicated post before you responded... boy is this forum hot or what :?: :!: ... Doc, I am not saying that one is superior on the other. I am simply saying what I have said all the time - that you should not downplay the importance of either of those components. In most of your previous posts you were downplaying the role of aerodynamics - as you were suggesting that the integrity of the nerve endings was more important than the airflow pattern. I think you have traditionally been over suspicious towards the role of altered aerodynamics in creating ENS, because you were puzzled by patients that had over patent airways that didn't complain of ENS. I am now certain more than ever that those patients might not be aware of it (as for instance blaming their sleep apnea on what other doctors told them - the palette etc' as they always downplay the role of the nose) - so they will think that their problems are not from their noses, but if the nasal passages are over patent in certain key areas like - close enough to the nasal valve or in the mid-superior regions - be it from a deviated septum or a radical ethmoidectomy - and - the second condition - the turbinates in that area were over resected and cannot compensate by hypertrophy - than ENS will ALWAYS occur to some degree. For example, how many turbinectomised patients have developed asthma or bronchi-hyper-responsiveness (a possible complication admitted to even by Ophir), or chronic phryngittis or laryngitis and and don't realize that this has all originated from their over opened nose? especially as the doctors will relate only to the coin under the lamp - the throat or lungs themselves, and not look for the underlying cause as these all have symptomatic treatments. I think that the natural occurring phenomena of compensatory hypertrophy - both on the concave side and the convex side - proves beyond doubt that the communication between the airflow and nasal mucosa depends on both - the proper flow patterns and of course on the nerve endings being there to begin with. One cannot separate the two, true, but if you are adamant in blaming it all on one main cause - I would say that it is altered aerodynamics that cause ENS because when that occurs - even when the nerve receptors are intact - ENS will occur - otherwise turbinates on the concave side would not need to hypertrophy. Of course, if on top of that nerve receptors are lost or are paralysed by too much dryness, cold and irritants in the airflow, the ENS will become even worse - but that's just adding to the main and prime cause - the over patent airway. So you see, you can explain ENS alone by leaning only on the structural cause, but you cannot explain it alone by leaning on the nerve receptors loss. Because, although it is a necessary condition for airflow sensation to occur, loosing only the receptors will cause nasal obstruction - but this alone is not ENS. As there are many cases in which the nerves can be damaged resulting in obstruction, when the turbinates have not even been touched. It's enough for the nasal mucosa to be scorched, or to develop scar tissue for any other reason, anywhere in the anterior nose for an annoying loss of airflow sensation to occur. But - is that ENS? - No way. These patients are suffering - and may perhaps deserve a category of their own, but they are not suffering from ENS - as ENS is condition in which widening the passages too much causes paradoxical obstruction alone, while the nerve tissue can remain intact, as proven by the compensatory hypertrophy phenomena. If on top of that nerve tissue is lost, the obstruction will be even worse, but nerve loss alone is not ENS. This is why in many places in the literature ENS is referred to as "OPEN Nose syndrome" and not "Empty Nose syndrome", which is perhaps a more accurate way of explaining it, but "EMPTY" is pretty descriptive and accurate in pin-pointing the main cause too: One must relate to the element of "openness" or "emptiness" in explaining how ENS occurs. Further more - here is another "sensational" claim ( (8) ) of mine: It may be quite possible that when the passages in certain areas are over enlarged and the air flows through them too strongly - there is actually too much friction and over stimulation of the nerve endings. These are after all pain-receptors, and there is a thresh-hold in which the fine pleasant sensation of motion becomes painful. When this happens - the receptors will constrict the blood vessels and this is how the extreme sensation of dryness in ENS is caused, even in areas where the mucosa looks intact and no atrophy is seen and the receptros are all there. This is a straightforward case of structurally induced rhinitis sicca. In summary - ENS is primarily a case in which the airflow in critical areas loses it's natural laminar fashion and speed and becomes either - too turbulent or too fast or both or simply too much interms of volume for the mucosa to handle and this will cause the receptors to induce vascular constriction and rhinitis sicca that will in a vicious cycle only serve to reduce the sensativity of the receptros resulting in ever increasing sensation of obstruction. This is precisely why - the nose should be kept moist and warm at all times and why all ENS patients should strive towards narrowing their over-enlarged passages. As ENS can deteriorate and become worse even when properly managed.