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.