BACKGROUND: The nasal septal deviation is a common cause of nasal obstruction. On the other hand, many septal deviations are asymptomatic. It seems a physiological adaptation occurs on both sides. Septal deviation leads to internal nasal asymmetry, which in turn causes compensatory change in turbinate morphology (e.g. turbinate hypertrophy respectively hypotrophy). This mechanism is investigated with the help of fluid dynamic experiments and functional rhinologic diagnostics. METHODS: Functional models of the nose (modified Mink's boxes) were used and assessment was made by acoustic rhinometry and rhinoresistometry, followed by flow dynamic investigations. Septal deviations of varying position, together with turbinates of differing grades of hypertrophy, were simulated and assessed. RESULTS AND CONCLUSIONS: We observed in models of septal deviation an increase in flow resistance on the ipsilateral side as a result of friction of flow particles in the narrowing. Furthermore, on the opposite side of the deviation, the enlargement of the stream channel did not generally lead to a reduction in flow resistance, but rather to a 'dead space', where only a slow-circling eddy was observed. This eddy causes an increase in turbulence. In vivo turbinate hypertrophy occurs to fill this dead space, thereby reducing turbulent flow without a significant increase in resistance. In cases of moderate septal deviation, compensatory mechanisms of the turbinates can lead to a normalization of nasal airflow and surgical therapy would not be indicated. Deviations in the anterior part of the septum seem to be more symptomatic, because the mechanism is missing and due to the physiological narrowing of the nasal isthmus. To differ between physiologic and pathologic deviation, functional diagnostics are needed. Copyright (c) 2006 S. Karger AG, Basel.
BACKGROUND: The nasal septal deviation is a common cause of nasal obstruction. On the other hand, many septal deviations are asymptomatic. It seems a physiological adaptation occurs on both sides. Septal deviation leads to internal nasal asymmetry, which in turn causes compensatory change in turbinate morphology (e.g. turbinate hypertrophy respectively hypotrophy). This mechanism is investigated with the help of fluid dynamic experiments and functional rhinologic diagnostics. METHODS: Functional models of the nose (modified Mink's boxes) were used and assessment was made by acoustic rhinometry and rhinoresistometry, followed by flow dynamic investigations. Septal deviations of varying position, together with turbinates of differing grades of hypertrophy, were simulated and assessed. RESULTS AND CONCLUSIONS: We observed in models of septal deviation an increase in flow resistance on the ipsilateral side as a result of friction of flow particles in the narrowing. Furthermore, on the opposite side of the deviation, the enlargement of the stream channel did not generally lead to a reduction in flow resistance, but rather to a 'dead space', where only a slow-circling eddy was observed. This eddy causes an increase in turbulence. In vivo turbinate hypertrophy occurs to fill this dead space, thereby reducing turbulent flow without a significant increase in resistance. In cases of moderate septal deviation, compensatory mechanisms of the turbinates can lead to a normalization of nasal airflow and surgical therapy would not be indicated. Deviations in the anterior part of the septum seem to be more symptomatic, because the mechanism is missing and due to the physiological narrowing of the nasal isthmus. To differ between physiologic and pathologic deviation, functional diagnostics are needed. Copyright (c) 2006 S. Karger AG, Basel.