Discussion
The ventilation function of the ET includes active and passive openingwhich are key for the success of ME surgeries such as tympanoplasty and myringotomy with VTI.4,9,10Its dysfunction can lead to many ME diseases including COME, atelectasis and cholesteatoma formation.2,11,12 Nasopharyngeal obstructions such as adenoid hypertrophy, tumor compression and intratubular mucus retention mainly cause passive opening dysfunction while impaired contraction of the peritubular muscles, i.e., tensor veli palatini (TVP) and levator veli palatini (LVP) mostly leads to active opening dysfunction.13 The presence of passive opening is a good indication that the ET is free of obstruction while active opening indicates that the ET can be actively opened by effective contraction of the peritubular muscles.
In this study, most ears in the TP group had both active and passive ET ventilation function. Only 9.5%(2/21) ears failed in passive ET opening, 4.7%(1/21) ears could not balance the positive MEP and 14.3%(3/21) could not balance the negative MEP. Elner and colleagues14 explored the normal ETF in 102 healthy subjects and found that the ET was forced to open passively in all tested subjects, 5% of subjects could not equilibrate positive MEP and 7% could not equilibrate negative MEP. The results were comparable to ours and indicated that a few normal subjects with no ear diseases also had impaired ETF. We speculated these subjects were more susceptible to otitis media compared to those with good ETFand were thus more likely to develop ME diseases such as OME in the presence of infection, immunological and other induced factors.15
We evaluated both the active and passive ET ventilation function of 21 ears in the TP group and 51 ears in the COME group and classified those ears into four categories as mentioned before(Table 2). We found 88.2% ears in the COME group had either active or passive ventilation dysfunction of ET. The possible reasons for the ETD included: 1.Decreased contractility of the peritubular muscles in cases where ET could undergo only passive opening, with testing showing normal ET opening resistance; 2.Increased ET opening resistance with normal or even enhanced peritubular muscle function in cases where ET could only undergo active opening; 3. In cases with both active and passive opening failure, there was very high ET opening resistance which probably exceeded the maximum contractility of the peritubular muscles. So it is necessary to choose appropriate treatment according to various causes of poor ventilation of the ET. Rehabilitation of the peritubular muscle should be emphasized in the treatment of muscular abnormalities; and drugs to reduce mucosal edema, to promote mucus excretion or the use of surfactants are the possible treatment options to reduce increased ET opening resistance caused by mucosal inflammation.
Po is related to the opening resistance of the ET (mucosal factors, surface tension, viscosity of secretions, etc.).16When the resistance is increased, a higher positive MEP is needed to open the ET. If the resistance is greater than the maximum pressure that can be applied to force the ET to open passively, the tube will not be opened. Pc is assumed to represent the periluminal forces (pressure of the cartilage and other surrounding tissues, etc.) and is related to the protective function of the ET.17 Our results showed that 90.5% ears in the TP group had passive ET opening with a Po and Pc range of 215~480dapa and 25~160daPa respectively. This was comparable to the results reported by Takahashi.11 In contrast, only 25.5% of ears in the COME group had passive ET opening with their Po and Pc range close to that of the TP group. There was a significant difference in the proportion of the two groups(P<0.05). This indicated that a majority of COME patients had increased ET opening resistance which resulted in the inability to effectively open the ET.
ET is an elastic tubular structure composed of a mucosacovered lumen, cartilage, peritubular muscles and soft tissues. The opening of the ET begins at the cartilaginous anterior one-third segment of the ET lying at the nasopharyngeal orifice. Opening is triggered by contraction of the LVP which then spreads to the isthmus by contraction of TVP to open the posterior 2/3 of the tube. Tubal closure is brought about by the elastic recoil of the tube and peritubular tissues and relaxation of LVP and TVP although the direction followed is opposite to that seen on opening, i.e., closure begins from the tympanic end of the ET and relaxation of the TVP is followed by that of the LVP.18,19 This mechanism of tubal opening is able to explain the formation of the rebound wave we observed in our study. The appearance of this wave is assumed to reflect the extent of opening and the speed of closing. While no relevant literature has reported this phenomenon so far, in our study, we observed the rebound wave in most TP patients and the appearance of this rebound wave during swallowing was significantly lower in the COME group in comparison to the TP group (P<0.001, Table3). Thus, we could speculate that the contraction pattern of the peritubular muscles in COME patients might be different from normal and healthy subjects. It is a known fact that owing to chronic inflammation of the ME and ET, COME patients have associated mucosal edema and hyperplasia and narrowing of the ET lumen. As a result, the peritubular muscles require more effort to open the tube which in turn leads to a smaller opening. Moreover, since the contractile effort is increased, the peritubular muscles would also have decreased velocity of contraction and relaxation. Both decreased extent of tubal opening and decelerated closing thus leaded to the disappearance of the rebound wave.
The level of Pr after swallowing is an indicator of the active pressure equilibrating ability of the ET and many researchers have graded the ETF according to it.14,20 The higher Pr after several swallows is usually related to the poor active opening of ET. In our study, we observed that almost every swallow could trigger an ET opening in the TP group with active ET opening function with post-swallow Pr ranging from 0 to 50 daPa under positive MEP and -103 to 0 daPa under negative MEP respectively. In the COME group, not every swallow could open the ET effectively; only 2 ears had a Pr less than 50 daPa when given a positive MEP and most ears could not open actively under negative MEP. The mean positive-Pr was higher in the COME group compared to the TP group(P<0.001, Table3). Active opening of the ET is powered by contraction of the peritubular muscles (TVP, LVP and salpingopharyngeus) during swallowing or yawning.18,21We speculated the higher Pr in COME patients could be related to the low frequency of ET opening during 10 consecutive swallows which was 3.8 times compared to9.1 times in the TP group. This phenomenon was also observed by Van Heerbeck and colleagues,22they found the frequency of ET opening during 10 swallows dropped from 8.4 times to 2.7 times after inducing ET dysfunction in healthy subjects. One explanation for this phenomenon is that there is usually more secretions in a diseased ET lumen which accounts for the increased opening resistance. Consequently, with greater ET opening resistance, more muscular force would be required to open the ET. Additionally, after each swallow, the opening resistance may vary due to the changeable distribution of secretions in the lumen; the ET would only open actively under a circumstance where the resistance is relatively smaller.23 Another explanation is that the peritubular muscles suffer increased fatigue and muscle contraction abnormalities (e.g., fasciculations, hypercontractility and limited contractility) during successive deglutition which may cause ET to open not at all or only partially.24
The mean ET opening duration in the TP group was 0.50±0.13s in our study. Mondain25reported a mean duration of 0.43±0.18s in 120 normal ears using sonotubometry which closely resembles our results. Gaihede8 reported a mean ET opening duration of 0.34s in their pressure-equilibration test, however, there were only 4 healthy subjects included in hisstudy. We observed a significantly longer duration of ET opening in the COME group than in the TP group(P=0.004,Table 3), Poe and Alper26,27 also observed a longer duration of opening in patients with ETD compared to normal subjects using slow-motion endoscopy. The reason for this phenomenon has not been fully understood up till now though decreased contraction and relaxation speed of the peritubular muscles caused by increased afterload (ET opening resistance) could be the cause.