Anaesthesia, 1979, Volume 34, pages 147-151
Nitrous oxide and the middle ear
I. DAVIS, J.R.M. MOORE
A gradual increase in the volume of the induced gas space follows artificial pneumoperitoneum in dogs and cats with sulphur hexafluoride (SF,).' The volume change occurs because the rate of diffusion of nitrogen from the blood in to the pneumoperitoneum exceeds the rate of loss of SF, from the pneumoperitoneum to blood. The volume increases in artificial pneumothoraces during nitrous oxide anaesthesia are well-known.2 In these cases the rate of diffusion of nitrous oxide inwards exceeds the rate of diffusion of nitrogen outwards. The effect of similar anaesthesia on a non-compliant gas space causes rapid increases in pressure in the air-filled cisternal spaces of dogs following N 2 0 admini~tration.~ Similar effects occur in the middle ear during N 2 0 anaesthesia in patients4 Measurements in middle ear gas pressure and composition in cats and in man have confirmed these finding^.^." The effect is independent of airway pressure, and temporary or permanent hearing loss has occurred in several patients following N 2 0 anaesthesia.'. * Tympanic membrane graft displacement is commonly seen in middle ear surgery under N20anaesthesia, yet the agent is used almost universally in this work. The possible effects of N 2 0excretion into the middle ear cavity suggest that the gas should be withdrawn some minutes before the middle ear is ~ l o s e d . ~ * ~It- " has also been suggested that N 2 0 anaesthesia may be hazardous for the hearing of patients with
AND
S.K. LAHIRI
polyethylene struts or surgical reconstructions for chronic ear disease.8 The present study was undertaken because of the occurrence of a marked hearing loss following N 2 0 anaesthesia in one such patient. Its purpose was to confirm the effects of the gas on the normal middle ear, to compare the effect with that of non-N20anaesthesia and to explore the time course of the events observed. Case history The patient, a 43-year-old woman, had a left stapedectomy for otosclerosis about 10 years ago and a standard 4.5-mm Schucknecht gelfoam and stainless steel prosthesis was inserted. Figure l(a) shows her audiogram at postoperative review; the upper trace is her (normal) sensorineural level and the lower is her hearing level to air conduction. The functional result of surgery was good with complete closure of the conductive gap. A year later she had a hysterectomy under general anaesthesia and immediately after operation complained of severe deterioration in her hearing. Her complaint was confirmed by audiometry which showed a 20-25 dB conductive loss-Figure I(b)-which has persisted to the present. The anaesthetic sequence was thiopentone, alcuronium, intubation and ventilation with N 2 0 and O2 to which 0.5% halothane was added.
I. Davis, MB, BS, FFARCS, Senior Registrar, J.R.M. Moore, BSc, MB, ChB, FRCS (Ed), Senior Registrar and S.K.Lahiri, MB, BS, FFARCS, Consultant Southmead Hospital, Bristol, BSIO 5NB 0003-2409/79/0200-0147S02.00 01979 Blackwell Scientific Publications
147
Frecquency (Hz) Fig. 1. Audiograms of the patient. (a) At follow-up after stapedectomy. (b) Following nitrous oxide anaesthesia.
The patient recently refused general anaesthesia for an orthopaedic operation lest her deafness became even more severe. Materials and methods The patients selected for the study were scheduled for genito-urinary surgery which was likely to last for an hour or more. The procedure was approved by the local ethical committee, and informed consent was obtained from each patient. Those with anatomically and functionally normal ears were admitted to the study though several had to be rejected later on because satisfactory sealing of the external acoustic meatus could not be achieved or could not be maintained during the surgical procedure. Measurements of middle ear pressure were made with the Peters Impedance Bridge AP 62, the operating principle of which is fully discussed elsewhere.12The apparatus measures the efficiency of the ear drum in converting sound pressure energy (SPE) to mechanical energy (ME) for transfer by ossicular movement to the inner ear. Sound waves entering the external ear impinge on the tympanic membrane and cause it to vibrate. The conversion of SPE to ME is most efficient when the drum is able to vibrate freely: minimal constraint of free vibration occurs when the pressures in the external canal and the middle ear cavity are equal. Under these conditions reflection of sound from the drum is minimal. Any inequality of external and middle ear pressures causes the drum to become stiffened, less efficient in converting SPE to ME, and more efficient as a sound reflector-
a state of affairs detected by the impedance bridge. The patient's external canal is fitted with a seal through which the bridge delivers a pure tone at 250 Hz while a microphone records SPE in the enclosed meatal space. Air pressure in the space is varied by an air pump and monitored by a manometer over the range -200 to 400mm H 2 0 in a timed sequence. When middle ear pressure is normal, meatal pressures at the extremes of the range stiffen the drum to the extent that its energy-converting efficiency is near zero, sound reflection is maximal, and hence SPE levels in the canal are maximal. When the pressures on each side of the drum are equalised, converting efficiency is maximal and the detected SPE level in the canal is minimal. Thus alterations in middle ear pressure are detected and measured by the pressure that has to be applied to the meatal space to minimise the observed SPE levels. When middle ear pressure is not atmospheric, restoration of the drum to its normal position by altering meatal pressure also changes middle ear volume-and hence middle ear pressure. However, the volume displacement of the adjusted drum is negligible in relation to middle ear volume. During the study intratympanic pressures were measured at 2-min intervals. The traditional unit for middle ear pressure measurement is millimetres of water (mm H20*). Results Figure 2 shows middle ear pressure changes in
* 1 m m H 2 0 = 10 Pa or 0.01 kPa.
Nitrous oxide and the middle ear 5oc
67 % Nitrous oxide
400 I
0, 30C
E L
?
3
e
20c
a
Ioc
F'
C
I
I
30
60
I 90
Time (min)
Fig. 2. Middle ear pressure rise and passive venting.
five patients anaesthetised with 67% N 2 0 using a Magill system following lumbar epidural block and a sleep dose of Althesin. Maximal pressure was attained between 30 and 40 rnin (mean 33 rnin) and ranged from 230 to 420 mm H 2 0 (mean 313 mm H20).The mean rate of rise was 9.5 mm H 2 0 per minute. Passive venting of the middle ear gas through the pharyngotympanic tube then followed. The measured pressure reductions at venting were typically between 80 and 130 mm H,O. Figure 3 shows the results obtained in two further studies. Patient A was anaesthetised with Althesin and maintained on 1-2% halothane in oxygen delivered by a Magill system. The maximum intratympanic pressure of 95 mm HzO was achieved after 55 rnin and no passive venting was detected during the 65 rnin of the operation. Patient B was intubated after
149
Althesin and alcuronium and ventilated with 1-2% halothane in oxygen for 30 min: over the period middle ear pressure rose from 10 to 45 mm H20. Halothane was then discontinued and ventilation maintained at the same minute volume with 67% N 2 0 in 0 2 .The intratympanic pressure rose over the succeeding 35 min to 400 mm H20 and passive venting followed. The mean rate of rise of pressure was 10.3 mm H20min. Figure 4 shows the decline in middle ear pressure in five further patients after N 2 0 withdrawal. Each patient was anaesthetised with a sleep-dose of Althesin after the establishment of lumbar epidural blockade and breathed 67% N 2 0in O2from a Magill system until peak middle ear pressures were reached and passive venting demonstrated. The time to the peak pressure was 10-25 min (mean 19 min); the peak pressure ranged from 225 to 350 mm H20with a mean of 249 mm H 2 0 . The mean rate of rise was 13 mm H20/per min. Immediately after venting was observed the N20was withdrawn and unconsciousness maintained by intermittent, small, doses of Althesin while the patient breathed oxygen-enriched air (approximately 30% 0 2 )until the end of surgery. The range of reduction in middle ear pressure over the succeeding 35-50 min of surgery was 10-90 mm
500 400
r
1 .d !'\
3o01
i. ,r-.-.-\/'.. c
\
100
0
\L--. ......... ..................
-
30
.....
60
Timeiminl
Fig. 3. Anaesthesia with and without nitrous oxide. (a) 1-2% halothane in oxygen. (b) As (a) for 30 min, then 67% nitrous oxide.
Time (minl
Fig. 4. Middle ear pressure during nitrous oxide elimination.
150
I. Davis, J.R.M. Moore and S.K.Lahiri
H 2 0 with a mean of 36 mm H 2 0 over the initial 35 min. The mean rate of fall of pressure in this period was 1 mm H20/min. Further passive venting was seen in two of the five cases, and a marked rise in middle ear pressure occurred in one patient 10 min after NzO administration ceased. Discussion The release of nitrous oxide into the middle ear cavity during anaesthesia is a consequence of its rate of diffusion exceeding that of nitrogen by some twenty times. Under identical conditions the relative rates of diffusion of the agents used in the study and N2 (Dagent/DN,) are functions of solubility (Blood/Gas Partition Coefficient, L) and molecular weight (MW). Thus for NzO
Values for the agents are shown in Table 1 but it must be recalled that their partial pressures at the blood/gas interface are not the same. Table 1. Physical values of the agents Agent Nitrous oxide Oxygen Halothane Nitrogen
MW 44 32
D agentlDN2
197
0.47 0.03 2.3
23.5 1.7 54
28
0.016
1
(For explanation of abbreviations see 'Discussion'.)
Nitrous oxide at high partial pressure in the blood diffuses into the middle ear cavity much more rapidly than nitrogen can diffuse out. Since the middle ear cavity is a poorly-compliant gas-filled space, the pressure of the contained gas volume increases. Samples of middle ear gas during nitrous oxide anaesthesia in cats were found to be between 21 and 23% by volume which are values consistent with the pressure increases demonstrated. The rate and range of the pressure rises in the present study
are of the same order as those measured by other^^^^ but less than those found in the maxillary sinuses of patients with chronic or recurrent tonsillar d i s e a s e Passive venting of the middle ear in normal subjects has been reportedI3 to occur at pressures of 150-300 mm H 2 0 . The present study indicates the upper limit to be somewhat higher: in the eleven patients in which it was clearly demonstrated the range was 225-420 mm H 2 0 . Inhalation anaesthesia without nitrous oxide (halothane in 0 2 )might be expected to produce a minor rise in the intra-tympanic pressure since small quantities of both agents would enter the space more rapidly than nitrogen could leave it. Such a change was found in the two cases in which this technique was used (Fig. 3) but others6# found stable middle ear pressures. The rate of rise of middle ear pressure in the one patient ventilated with nitrous oxide was close to that seen during spontaneous ventilation with the agent (compare Fig. 3 patient B with Fig. 2) and probably reflects rapid blood equilibration with inspired gas under both sets of conditions. After withdrawal of nitrous oxide the rate of fall of intratympanic pressure was initially about 10% of the rate of rise. In one of five patients N 2 0 was still leaving the blood for the middle ear cavity 10 min after its administration to the patient had ceased. A similar effect was noted by others* 20 min after withdrawal of the gas. The choice of model for the study did not allow the pressure changes during N 2 0 elimination to be followed for a sufficient period. I n another studys it was noted that it took about 1 hr before middle ear pressure reached atmospheric pressure. In one case the return to normal intratympanic pressure was followed by the development of a sub-atmospheric pressure of -285 mm H 2 0 attributed to the rate of loss of N 2 0 exceeding that of gain of nitrogen by the middle ear. The occurrence of increases in intratympanic pressure rises long after N 2 0 withdrawal, and the possibility of sub-atmospheric pressures later, may have significant implications for the fate of inlay and onlay tympanic membrane grafts, and for the stability of replaced o r reconstructed middle ear components. Since intratympanic pressure can be rapidly and measurably altered it is possible that nitrous
Nitrous oxide and the midde ear oxide has therapeutic possibilities in some middle ear diseases. It has been notedI4 that although NzO anaesthesia usually causes temporary impairment of middle ear function, measurable improvement is seen in a small proportion of cases. Further work to clarify this aspect is in progress. Conclusions During NzO anaesthesia the middle ear pressure increases rapidly: the rate of increase is about 10 mm H20per minute. Maximum pressures are reached in about 30 min and are limited in normal ears by passive venting. Non-nitrous oxide anaesthesia does not cause a substantial increase in intratympanic pressure. After nitrous oxide anaesthesia the middle ear pressure decreases slowly: initially the rate of fall is about 1 mm HzO/min. Intratympanic pressure may continue to rise up to 20 min after withdrawal of the gas. If nitrogen is not replaced at a sufficient rate, elimination of nitrous oxide may allow the creation of a considerable subatmospheric pressure. These effects may well be significant for the fate of tympanic membrane grafts and middle ear prostheses and reconstructions. The use of nitrous oxide anaesthesia for this kind of surgery, and for operations on patients who have had middle ear reconstructive procedures is therefore questionable; alternative techniques excluding nitrous oxide may be preferable. Summary
EAR; middle ear pressure. SURGERY; middle ear. Acknowledgments The authors thank Mr R.K. Roddie, Consultant ENT Surgeon, for help and advice and Mr R.C.L. Feneley, Consultant Urologist, for allowing them to study patients in his care.
References 1. TENNEY, S.M., CARPENTER, F.G. & RAHN, H. (1953) Gas transfers in a sulfur hexafluoride
pneumoperitoneum. Journal of Applied Physiology, 6,201. 2. HUNTER,A.R. (1955) Problems of anaesthesia in artificial pneumothorax. Proceedings of the Royal Society of Medicine, 48. 765. L.J. & EGER,E.I., 11. (1965) Change in 3. SAIDMAN,
4.
5.
6.
7.
cerebrospinal fluid pressure during pneumoencephalography under nitrous oxide anesthesia. Anesthesiology, 26, 67. THOMSEN, K.A., TERKILDSEN, K. & ARNFRED,I. (1965) Middle ear pressure variations during anesthesia. Archives of Otolaryngology, 82, 609. MATZ,G.J., RATTENBORC, C.G. & HOLADAY, D.A. (1967) Effects of nitrous oxide on middle ear pressure. Anesthesiology, 28, 948. RASMUSSEN, P.E. (1967) Middle ear and maxillary sinus during nitrous oxide anaesthesia. Acta Otolaryngologica, 63, 7. WAUN,J.E., SWEITZER, R.S. & HAMILTON, W.K. (1967) Effect of nitrous oxide on middle ear mechanics and hearing acuity. Anesthesiology, 28,
846. M.E. & BARTLETT, P.C. (1976) Hearing 8. PATTERSON,
impairment caused by intratympanic pressure changes during general anesthesia. Laryngoscope, 86, 399. R.S. (1973) A Synopsis of 9. LEE,J.A. & ATKINSON, Anaesthesia. 7th edn, p. 561. John Wright, Bristol. A.R.DEC. (1971) Aspects of anaesthesia 10. DEACOCK,
A case of hearing deficit following nitrous oxide anaesthesia is reported. The mechanism and time course of nitrous oxide-induced intratympanic pressure changes are described and contrasted with the effects of non-nitrous oxide anaesthesia. The rate of increase is about 10 mm HzO/min. The possibility that nitrous oxide may cause displacement of tympanic membrane grafts both outwards and inwards, or disrupt the reconstructed middle ear conducting mechanism, is raised again.
13.
Key words
14.
ANAESTHETICS, GASES; nitrous oxide.
151
11.
12.
for middle ear surgery and blood loss during stapedectomy. Proceedings of the Royal Society of Medicine, 64, 1226. THORNTON, J.A. & LEVY,C.J. (1974) Techniques of Anaesthesia. p. 272. Chapman and Hall, London. BROOKS,D.N. (1976) Acoustic impedance. In: Scientific Foundations of Otolaryngology (eds R. Hinchcliffe & D. Harrison), p. 281. Heinemann, London. THOMSEN, K.A. (1957) Studies on the function of the eustachian tube in a series of normal individuals. Acta Otolaryngologica, 48, 5 16. PEACOCK, M.R. (1977) The effect of anaesthesia on middle ear function (a preliminary report.) Journal of Laryngology and Otology, 91, 81.
Nitrous oxide and the middle ear
I. DAVIS, J.R.M. MOORE
A gradual increase in the volume of the induced gas space follows artificial pneumoperitoneum in dogs and cats with sulphur hexafluoride (SF,).' The volume change occurs because the rate of diffusion of nitrogen from the blood in to the pneumoperitoneum exceeds the rate of loss of SF, from the pneumoperitoneum to blood. The volume increases in artificial pneumothoraces during nitrous oxide anaesthesia are well-known.2 In these cases the rate of diffusion of nitrous oxide inwards exceeds the rate of diffusion of nitrogen outwards. The effect of similar anaesthesia on a non-compliant gas space causes rapid increases in pressure in the air-filled cisternal spaces of dogs following N 2 0 admini~tration.~ Similar effects occur in the middle ear during N 2 0 anaesthesia in patients4 Measurements in middle ear gas pressure and composition in cats and in man have confirmed these finding^.^." The effect is independent of airway pressure, and temporary or permanent hearing loss has occurred in several patients following N 2 0 anaesthesia.'. * Tympanic membrane graft displacement is commonly seen in middle ear surgery under N20anaesthesia, yet the agent is used almost universally in this work. The possible effects of N 2 0excretion into the middle ear cavity suggest that the gas should be withdrawn some minutes before the middle ear is ~ l o s e d . ~ * ~It- " has also been suggested that N 2 0 anaesthesia may be hazardous for the hearing of patients with
AND
S.K. LAHIRI
polyethylene struts or surgical reconstructions for chronic ear disease.8 The present study was undertaken because of the occurrence of a marked hearing loss following N 2 0 anaesthesia in one such patient. Its purpose was to confirm the effects of the gas on the normal middle ear, to compare the effect with that of non-N20anaesthesia and to explore the time course of the events observed. Case history The patient, a 43-year-old woman, had a left stapedectomy for otosclerosis about 10 years ago and a standard 4.5-mm Schucknecht gelfoam and stainless steel prosthesis was inserted. Figure l(a) shows her audiogram at postoperative review; the upper trace is her (normal) sensorineural level and the lower is her hearing level to air conduction. The functional result of surgery was good with complete closure of the conductive gap. A year later she had a hysterectomy under general anaesthesia and immediately after operation complained of severe deterioration in her hearing. Her complaint was confirmed by audiometry which showed a 20-25 dB conductive loss-Figure I(b)-which has persisted to the present. The anaesthetic sequence was thiopentone, alcuronium, intubation and ventilation with N 2 0 and O2 to which 0.5% halothane was added.
I. Davis, MB, BS, FFARCS, Senior Registrar, J.R.M. Moore, BSc, MB, ChB, FRCS (Ed), Senior Registrar and S.K.Lahiri, MB, BS, FFARCS, Consultant Southmead Hospital, Bristol, BSIO 5NB 0003-2409/79/0200-0147S02.00 01979 Blackwell Scientific Publications
147
Frecquency (Hz) Fig. 1. Audiograms of the patient. (a) At follow-up after stapedectomy. (b) Following nitrous oxide anaesthesia.
The patient recently refused general anaesthesia for an orthopaedic operation lest her deafness became even more severe. Materials and methods The patients selected for the study were scheduled for genito-urinary surgery which was likely to last for an hour or more. The procedure was approved by the local ethical committee, and informed consent was obtained from each patient. Those with anatomically and functionally normal ears were admitted to the study though several had to be rejected later on because satisfactory sealing of the external acoustic meatus could not be achieved or could not be maintained during the surgical procedure. Measurements of middle ear pressure were made with the Peters Impedance Bridge AP 62, the operating principle of which is fully discussed elsewhere.12The apparatus measures the efficiency of the ear drum in converting sound pressure energy (SPE) to mechanical energy (ME) for transfer by ossicular movement to the inner ear. Sound waves entering the external ear impinge on the tympanic membrane and cause it to vibrate. The conversion of SPE to ME is most efficient when the drum is able to vibrate freely: minimal constraint of free vibration occurs when the pressures in the external canal and the middle ear cavity are equal. Under these conditions reflection of sound from the drum is minimal. Any inequality of external and middle ear pressures causes the drum to become stiffened, less efficient in converting SPE to ME, and more efficient as a sound reflector-
a state of affairs detected by the impedance bridge. The patient's external canal is fitted with a seal through which the bridge delivers a pure tone at 250 Hz while a microphone records SPE in the enclosed meatal space. Air pressure in the space is varied by an air pump and monitored by a manometer over the range -200 to 400mm H 2 0 in a timed sequence. When middle ear pressure is normal, meatal pressures at the extremes of the range stiffen the drum to the extent that its energy-converting efficiency is near zero, sound reflection is maximal, and hence SPE levels in the canal are maximal. When the pressures on each side of the drum are equalised, converting efficiency is maximal and the detected SPE level in the canal is minimal. Thus alterations in middle ear pressure are detected and measured by the pressure that has to be applied to the meatal space to minimise the observed SPE levels. When middle ear pressure is not atmospheric, restoration of the drum to its normal position by altering meatal pressure also changes middle ear volume-and hence middle ear pressure. However, the volume displacement of the adjusted drum is negligible in relation to middle ear volume. During the study intratympanic pressures were measured at 2-min intervals. The traditional unit for middle ear pressure measurement is millimetres of water (mm H20*). Results Figure 2 shows middle ear pressure changes in
* 1 m m H 2 0 = 10 Pa or 0.01 kPa.
Nitrous oxide and the middle ear 5oc
67 % Nitrous oxide
400 I
0, 30C
E L
?
3
e
20c
a
Ioc
F'
C
I
I
30
60
I 90
Time (min)
Fig. 2. Middle ear pressure rise and passive venting.
five patients anaesthetised with 67% N 2 0 using a Magill system following lumbar epidural block and a sleep dose of Althesin. Maximal pressure was attained between 30 and 40 rnin (mean 33 rnin) and ranged from 230 to 420 mm H 2 0 (mean 313 mm H20).The mean rate of rise was 9.5 mm H 2 0 per minute. Passive venting of the middle ear gas through the pharyngotympanic tube then followed. The measured pressure reductions at venting were typically between 80 and 130 mm H,O. Figure 3 shows the results obtained in two further studies. Patient A was anaesthetised with Althesin and maintained on 1-2% halothane in oxygen delivered by a Magill system. The maximum intratympanic pressure of 95 mm HzO was achieved after 55 rnin and no passive venting was detected during the 65 rnin of the operation. Patient B was intubated after
149
Althesin and alcuronium and ventilated with 1-2% halothane in oxygen for 30 min: over the period middle ear pressure rose from 10 to 45 mm H20. Halothane was then discontinued and ventilation maintained at the same minute volume with 67% N 2 0 in 0 2 .The intratympanic pressure rose over the succeeding 35 min to 400 mm H20 and passive venting followed. The mean rate of rise of pressure was 10.3 mm H20min. Figure 4 shows the decline in middle ear pressure in five further patients after N 2 0 withdrawal. Each patient was anaesthetised with a sleep-dose of Althesin after the establishment of lumbar epidural blockade and breathed 67% N 2 0in O2from a Magill system until peak middle ear pressures were reached and passive venting demonstrated. The time to the peak pressure was 10-25 min (mean 19 min); the peak pressure ranged from 225 to 350 mm H20with a mean of 249 mm H 2 0 . The mean rate of rise was 13 mm H20/per min. Immediately after venting was observed the N20was withdrawn and unconsciousness maintained by intermittent, small, doses of Althesin while the patient breathed oxygen-enriched air (approximately 30% 0 2 )until the end of surgery. The range of reduction in middle ear pressure over the succeeding 35-50 min of surgery was 10-90 mm
500 400
r
1 .d !'\
3o01
i. ,r-.-.-\/'.. c
\
100
0
\L--. ......... ..................
-
30
.....
60
Timeiminl
Fig. 3. Anaesthesia with and without nitrous oxide. (a) 1-2% halothane in oxygen. (b) As (a) for 30 min, then 67% nitrous oxide.
Time (minl
Fig. 4. Middle ear pressure during nitrous oxide elimination.
150
I. Davis, J.R.M. Moore and S.K.Lahiri
H 2 0 with a mean of 36 mm H 2 0 over the initial 35 min. The mean rate of fall of pressure in this period was 1 mm H20/min. Further passive venting was seen in two of the five cases, and a marked rise in middle ear pressure occurred in one patient 10 min after NzO administration ceased. Discussion The release of nitrous oxide into the middle ear cavity during anaesthesia is a consequence of its rate of diffusion exceeding that of nitrogen by some twenty times. Under identical conditions the relative rates of diffusion of the agents used in the study and N2 (Dagent/DN,) are functions of solubility (Blood/Gas Partition Coefficient, L) and molecular weight (MW). Thus for NzO
Values for the agents are shown in Table 1 but it must be recalled that their partial pressures at the blood/gas interface are not the same. Table 1. Physical values of the agents Agent Nitrous oxide Oxygen Halothane Nitrogen
MW 44 32
D agentlDN2
197
0.47 0.03 2.3
23.5 1.7 54
28
0.016
1
(For explanation of abbreviations see 'Discussion'.)
Nitrous oxide at high partial pressure in the blood diffuses into the middle ear cavity much more rapidly than nitrogen can diffuse out. Since the middle ear cavity is a poorly-compliant gas-filled space, the pressure of the contained gas volume increases. Samples of middle ear gas during nitrous oxide anaesthesia in cats were found to be between 21 and 23% by volume which are values consistent with the pressure increases demonstrated. The rate and range of the pressure rises in the present study
are of the same order as those measured by other^^^^ but less than those found in the maxillary sinuses of patients with chronic or recurrent tonsillar d i s e a s e Passive venting of the middle ear in normal subjects has been reportedI3 to occur at pressures of 150-300 mm H 2 0 . The present study indicates the upper limit to be somewhat higher: in the eleven patients in which it was clearly demonstrated the range was 225-420 mm H 2 0 . Inhalation anaesthesia without nitrous oxide (halothane in 0 2 )might be expected to produce a minor rise in the intra-tympanic pressure since small quantities of both agents would enter the space more rapidly than nitrogen could leave it. Such a change was found in the two cases in which this technique was used (Fig. 3) but others6# found stable middle ear pressures. The rate of rise of middle ear pressure in the one patient ventilated with nitrous oxide was close to that seen during spontaneous ventilation with the agent (compare Fig. 3 patient B with Fig. 2) and probably reflects rapid blood equilibration with inspired gas under both sets of conditions. After withdrawal of nitrous oxide the rate of fall of intratympanic pressure was initially about 10% of the rate of rise. In one of five patients N 2 0 was still leaving the blood for the middle ear cavity 10 min after its administration to the patient had ceased. A similar effect was noted by others* 20 min after withdrawal of the gas. The choice of model for the study did not allow the pressure changes during N 2 0 elimination to be followed for a sufficient period. I n another studys it was noted that it took about 1 hr before middle ear pressure reached atmospheric pressure. In one case the return to normal intratympanic pressure was followed by the development of a sub-atmospheric pressure of -285 mm H 2 0 attributed to the rate of loss of N 2 0 exceeding that of gain of nitrogen by the middle ear. The occurrence of increases in intratympanic pressure rises long after N 2 0 withdrawal, and the possibility of sub-atmospheric pressures later, may have significant implications for the fate of inlay and onlay tympanic membrane grafts, and for the stability of replaced o r reconstructed middle ear components. Since intratympanic pressure can be rapidly and measurably altered it is possible that nitrous
Nitrous oxide and the midde ear oxide has therapeutic possibilities in some middle ear diseases. It has been notedI4 that although NzO anaesthesia usually causes temporary impairment of middle ear function, measurable improvement is seen in a small proportion of cases. Further work to clarify this aspect is in progress. Conclusions During NzO anaesthesia the middle ear pressure increases rapidly: the rate of increase is about 10 mm H20per minute. Maximum pressures are reached in about 30 min and are limited in normal ears by passive venting. Non-nitrous oxide anaesthesia does not cause a substantial increase in intratympanic pressure. After nitrous oxide anaesthesia the middle ear pressure decreases slowly: initially the rate of fall is about 1 mm HzO/min. Intratympanic pressure may continue to rise up to 20 min after withdrawal of the gas. If nitrogen is not replaced at a sufficient rate, elimination of nitrous oxide may allow the creation of a considerable subatmospheric pressure. These effects may well be significant for the fate of tympanic membrane grafts and middle ear prostheses and reconstructions. The use of nitrous oxide anaesthesia for this kind of surgery, and for operations on patients who have had middle ear reconstructive procedures is therefore questionable; alternative techniques excluding nitrous oxide may be preferable. Summary
EAR; middle ear pressure. SURGERY; middle ear. Acknowledgments The authors thank Mr R.K. Roddie, Consultant ENT Surgeon, for help and advice and Mr R.C.L. Feneley, Consultant Urologist, for allowing them to study patients in his care.
References 1. TENNEY, S.M., CARPENTER, F.G. & RAHN, H. (1953) Gas transfers in a sulfur hexafluoride
pneumoperitoneum. Journal of Applied Physiology, 6,201. 2. HUNTER,A.R. (1955) Problems of anaesthesia in artificial pneumothorax. Proceedings of the Royal Society of Medicine, 48. 765. L.J. & EGER,E.I., 11. (1965) Change in 3. SAIDMAN,
4.
5.
6.
7.
cerebrospinal fluid pressure during pneumoencephalography under nitrous oxide anesthesia. Anesthesiology, 26, 67. THOMSEN, K.A., TERKILDSEN, K. & ARNFRED,I. (1965) Middle ear pressure variations during anesthesia. Archives of Otolaryngology, 82, 609. MATZ,G.J., RATTENBORC, C.G. & HOLADAY, D.A. (1967) Effects of nitrous oxide on middle ear pressure. Anesthesiology, 28, 948. RASMUSSEN, P.E. (1967) Middle ear and maxillary sinus during nitrous oxide anaesthesia. Acta Otolaryngologica, 63, 7. WAUN,J.E., SWEITZER, R.S. & HAMILTON, W.K. (1967) Effect of nitrous oxide on middle ear mechanics and hearing acuity. Anesthesiology, 28,
846. M.E. & BARTLETT, P.C. (1976) Hearing 8. PATTERSON,
impairment caused by intratympanic pressure changes during general anesthesia. Laryngoscope, 86, 399. R.S. (1973) A Synopsis of 9. LEE,J.A. & ATKINSON, Anaesthesia. 7th edn, p. 561. John Wright, Bristol. A.R.DEC. (1971) Aspects of anaesthesia 10. DEACOCK,
A case of hearing deficit following nitrous oxide anaesthesia is reported. The mechanism and time course of nitrous oxide-induced intratympanic pressure changes are described and contrasted with the effects of non-nitrous oxide anaesthesia. The rate of increase is about 10 mm HzO/min. The possibility that nitrous oxide may cause displacement of tympanic membrane grafts both outwards and inwards, or disrupt the reconstructed middle ear conducting mechanism, is raised again.
13.
Key words
14.
ANAESTHETICS, GASES; nitrous oxide.
151
11.
12.
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