British Journal of Anaesthesia 1992; 69: 661-665
CORRESPONDENCE
L. N. YADDANAPUDI L. KASHYAP A. MALLICK
As we stated in our study, in most instances the decrease in saturation values in the group receiving manual ventilation occurred before effective hand ventilation rather than during subsequent LMA insertion. Clearly, for these patients, using this procedure, effective hand ventilation could not prevent hypoxaemia as it had already occurred. The concluding sentence of our paper, "Manual ventilation at induction of anaesthesia was not effective in preventing hypoxaemia." was intended to be taken in the context of the findings of our study. G. W. A. GILLIES
Glasgow VOCAL CORD MOVEMENT ON INDUCTION OF ANAESTHESIA Sir,—In the recent fibrcoptic study of movements of the human vocal cords during induction of anaesthesia [1], the authors observed significantly greater decreases in the angle between the cords on induction with thiopentone than with propofol. The decreases were attributed to reflex adduction of the cords and were thought to imply that the tendency to laryngeal spasm was greater with thiopentone. An antithetical interpretation may possibly be more appropriate. The decreased angle between the vocal cords could have resulted, not from active reflex adduction, but from drug-induced paresis of the intrinsic laryngeal muscles, giving a result similar to that of classical bilateral mechanical injury to the recurrent laryngeal nerves, namely, narrowing of the glottis. Because of the oblique axis of the cricoid facet of the cricoarytenoid joint [2], when the tonic postural activity in the cricoarytenoid muscles is impaired, the arytenoid droops passively so that the vocal process points downward and medially towards its fellow of the opposite side. There is then a tell-tale convergence of the vocal processes as viewed from above, whereas with active adduction the arytenoids do not sag and the vocal processes point almost directly forward. If the reported narrowing of the rima glortidis with induction happened to be of the passive variety, it would imply that thiopentone diminished the activity of the laryngeal muscles more than did propofol, which is of course the reverse of what the authors inferred. It would be interesting to know if their videotape pictures show the direction of the vocal processes clearly enough to decide which is the correct interpretation.
New Delhi, India 1. Haynes SR, Allsop GW, Gillies GWA. Arterial oxygen saturation during induction of anaesthesia and laryngeal mask insertion: prospective evaluation of four techniques. British Journal of Anaesthesia 1992; 68: 519-522. 2. Brain AIJ, McGhee TD, McAteer EJ, Thomas A, Abu-Saad MAW, Bushman JA. The laryngeal mask airway; development and preliminary trials of a new type of airway. Anaesthesia 1985; 40: 356-361. Sir,—Thank you for an opportunity to respond to the letter from Drs Yaddanapudi, Kashyap and Mallick. I was most interested to hear of their findings. I would agree that their low incidence of difficulty with insertion of the laryngeal mask airway (LMA) may reflect the. improved conditions achieved with neuromuscular block, assuming that they applied a similar criterion for difficulty. I believe that the likely explanation for the marked differences in results between their study and ours for arterial oxygen saturation values associated with insertion of the LMA after manual ventilation lies in the fact that the two studies have followed different designs. Our patients were premedicated with temazepam, anaesthesia was induced with fentariyl andpropofol and the lungs ventilated with five tidal breaths of 100% oxygen before insertion of the LMA. Their patients were unpremedicated, anaesthesia was induced with thiopentone and suxamethonium and the lungs ventilated manually with 33% oxygen for 1 min before LMA insertion.
B. R. FINK
Seattle 1. Barker P, Langton JA, Wilson IG, Smith G. Movements of the vocal cords on induction of anaesthesia with thiopentone or propofol. British Journal of Anaesthesia 1992; 69: 23-25. 2. Sonesson B. Die funktionelle Anatomic des Cricoarytaenoidgelenkes. Zeitschrift fur Anatomic und Entwicklungsgeschichte
1959; 121: 292-303. Sir,—Dr Fink's hypothesis is that thiopentone may cause a greater reduction in the activity of the intrinsic laryngeal muscles than propofol, producing drug-induced paresis of these muscles. In the design of our study, we did not attempt to measure the activity of the intrinsic laryngeal muscles and therefore we cannot draw any conclusions relating to this point. However, if thiopentone produced paresis of the intrinsic muscles, then we should have expected the vocal cords to have assumed the cadaveric position, similar to that seen after administration of neuromuscular blocking drugs. In fact, we observed that in some patients, who received thiopentone, the vocal cords closed completely. In a recent study by Drummond [1], the influence of thiopentone on upper airway muscles was investigated. He concluded that, after the use of thiopentone for induction of anaesthesia, there was a change in the pattern of activity of the upper airway muscles, rather than a reduction in the magnitude of their activation.
Downloaded from http://bja.oxfordjournals.org/ at University of Birmingham on July 5, 2015
HYPOXAEMIA AND INSERTION OF THE LARYNGEAL MASK AIRWAY Sir,—In their study on arterial saturation during induction of anaesthesia and insertion of the laryngeal mask airway (LMA), Haynes, Allsop and Gillies [1 ] have observed a 3 % failure rate and 18% rate of difficulty of insertion of the LMA. This has been attributed to inadequate depth of anaesthesia with propofol. As part of an ongoing investigation, we have studied arterial saturation during the insertion of the LMA under neuromuscular block as described by Brain and co-workers [2], in 20 ASA I adult, unpremedicated patients undergoing elective surgery. Arterial saturation was monitored using a Horizon 1000 pulse oximeter (Mermen Medical) in the 3-s updating mode. Patients' lungs were not prcoxygenated. Anaesthesia was induced with i.v. thiopentone 3-5 mg kg"1 and 66% nitrous oxide in oxygen administered via a tightly fitting face mask and Bain system at 6 litre min"1 from the time of the loss of eyelash reflex. The patients were given suxamethonium l.Smgkg" 1 and the lungs were ventilated manually for 1 min. We had difficulty in insertion of the LMA in one patient and no failures. The average time for securing the airway from the end of manual ventilation was 33.5 (SD 7.73) s. The low rates of difficulty and failure are probably explained by the use of a neuromuscular blocking drug. In cases where the requirements of surgery necessitate controlled ventilation, we feel that insertion of the LMA under neuromuscular block is a viable alternative to insertion under propofol or inhalation anaesthesia. In our study, the median values of SpOi at various times were: preinduction, 98% (range 95-100%); smallest value from cessation of manual ventilation to securing the airway, 98% (93-100%); smallest value in the subsequent 3 min, 99% (96-100 %). A decrease in 5p Ol to less than the preinduction value occurred in seven of 20 patients, compared with 19 of 25 in the manual ventilation group of Haynes and colleagues. None of our patients had an SpOt less than 90% at any time. This can be attributed to the early and effective administration of manual ventilation for 1 min immediately after suxamethonium. In the light of our observations, we cannot agree with the authors' conclusion that manual ventilation at induction of anaesthesia does not prevent hypoxaemia.
CORRESPONDENCE
L. N. YADDANAPUDI L. KASHYAP A. MALLICK
As we stated in our study, in most instances the decrease in saturation values in the group receiving manual ventilation occurred before effective hand ventilation rather than during subsequent LMA insertion. Clearly, for these patients, using this procedure, effective hand ventilation could not prevent hypoxaemia as it had already occurred. The concluding sentence of our paper, "Manual ventilation at induction of anaesthesia was not effective in preventing hypoxaemia." was intended to be taken in the context of the findings of our study. G. W. A. GILLIES
Glasgow VOCAL CORD MOVEMENT ON INDUCTION OF ANAESTHESIA Sir,—In the recent fibrcoptic study of movements of the human vocal cords during induction of anaesthesia [1], the authors observed significantly greater decreases in the angle between the cords on induction with thiopentone than with propofol. The decreases were attributed to reflex adduction of the cords and were thought to imply that the tendency to laryngeal spasm was greater with thiopentone. An antithetical interpretation may possibly be more appropriate. The decreased angle between the vocal cords could have resulted, not from active reflex adduction, but from drug-induced paresis of the intrinsic laryngeal muscles, giving a result similar to that of classical bilateral mechanical injury to the recurrent laryngeal nerves, namely, narrowing of the glottis. Because of the oblique axis of the cricoid facet of the cricoarytenoid joint [2], when the tonic postural activity in the cricoarytenoid muscles is impaired, the arytenoid droops passively so that the vocal process points downward and medially towards its fellow of the opposite side. There is then a tell-tale convergence of the vocal processes as viewed from above, whereas with active adduction the arytenoids do not sag and the vocal processes point almost directly forward. If the reported narrowing of the rima glortidis with induction happened to be of the passive variety, it would imply that thiopentone diminished the activity of the laryngeal muscles more than did propofol, which is of course the reverse of what the authors inferred. It would be interesting to know if their videotape pictures show the direction of the vocal processes clearly enough to decide which is the correct interpretation.
New Delhi, India 1. Haynes SR, Allsop GW, Gillies GWA. Arterial oxygen saturation during induction of anaesthesia and laryngeal mask insertion: prospective evaluation of four techniques. British Journal of Anaesthesia 1992; 68: 519-522. 2. Brain AIJ, McGhee TD, McAteer EJ, Thomas A, Abu-Saad MAW, Bushman JA. The laryngeal mask airway; development and preliminary trials of a new type of airway. Anaesthesia 1985; 40: 356-361. Sir,—Thank you for an opportunity to respond to the letter from Drs Yaddanapudi, Kashyap and Mallick. I was most interested to hear of their findings. I would agree that their low incidence of difficulty with insertion of the laryngeal mask airway (LMA) may reflect the. improved conditions achieved with neuromuscular block, assuming that they applied a similar criterion for difficulty. I believe that the likely explanation for the marked differences in results between their study and ours for arterial oxygen saturation values associated with insertion of the LMA after manual ventilation lies in the fact that the two studies have followed different designs. Our patients were premedicated with temazepam, anaesthesia was induced with fentariyl andpropofol and the lungs ventilated with five tidal breaths of 100% oxygen before insertion of the LMA. Their patients were unpremedicated, anaesthesia was induced with thiopentone and suxamethonium and the lungs ventilated manually with 33% oxygen for 1 min before LMA insertion.
B. R. FINK
Seattle 1. Barker P, Langton JA, Wilson IG, Smith G. Movements of the vocal cords on induction of anaesthesia with thiopentone or propofol. British Journal of Anaesthesia 1992; 69: 23-25. 2. Sonesson B. Die funktionelle Anatomic des Cricoarytaenoidgelenkes. Zeitschrift fur Anatomic und Entwicklungsgeschichte
1959; 121: 292-303. Sir,—Dr Fink's hypothesis is that thiopentone may cause a greater reduction in the activity of the intrinsic laryngeal muscles than propofol, producing drug-induced paresis of these muscles. In the design of our study, we did not attempt to measure the activity of the intrinsic laryngeal muscles and therefore we cannot draw any conclusions relating to this point. However, if thiopentone produced paresis of the intrinsic muscles, then we should have expected the vocal cords to have assumed the cadaveric position, similar to that seen after administration of neuromuscular blocking drugs. In fact, we observed that in some patients, who received thiopentone, the vocal cords closed completely. In a recent study by Drummond [1], the influence of thiopentone on upper airway muscles was investigated. He concluded that, after the use of thiopentone for induction of anaesthesia, there was a change in the pattern of activity of the upper airway muscles, rather than a reduction in the magnitude of their activation.
Downloaded from http://bja.oxfordjournals.org/ at University of Birmingham on July 5, 2015
HYPOXAEMIA AND INSERTION OF THE LARYNGEAL MASK AIRWAY Sir,—In their study on arterial saturation during induction of anaesthesia and insertion of the laryngeal mask airway (LMA), Haynes, Allsop and Gillies [1 ] have observed a 3 % failure rate and 18% rate of difficulty of insertion of the LMA. This has been attributed to inadequate depth of anaesthesia with propofol. As part of an ongoing investigation, we have studied arterial saturation during the insertion of the LMA under neuromuscular block as described by Brain and co-workers [2], in 20 ASA I adult, unpremedicated patients undergoing elective surgery. Arterial saturation was monitored using a Horizon 1000 pulse oximeter (Mermen Medical) in the 3-s updating mode. Patients' lungs were not prcoxygenated. Anaesthesia was induced with i.v. thiopentone 3-5 mg kg"1 and 66% nitrous oxide in oxygen administered via a tightly fitting face mask and Bain system at 6 litre min"1 from the time of the loss of eyelash reflex. The patients were given suxamethonium l.Smgkg" 1 and the lungs were ventilated manually for 1 min. We had difficulty in insertion of the LMA in one patient and no failures. The average time for securing the airway from the end of manual ventilation was 33.5 (SD 7.73) s. The low rates of difficulty and failure are probably explained by the use of a neuromuscular blocking drug. In cases where the requirements of surgery necessitate controlled ventilation, we feel that insertion of the LMA under neuromuscular block is a viable alternative to insertion under propofol or inhalation anaesthesia. In our study, the median values of SpOi at various times were: preinduction, 98% (range 95-100%); smallest value from cessation of manual ventilation to securing the airway, 98% (93-100%); smallest value in the subsequent 3 min, 99% (96-100 %). A decrease in 5p Ol to less than the preinduction value occurred in seven of 20 patients, compared with 19 of 25 in the manual ventilation group of Haynes and colleagues. None of our patients had an SpOt less than 90% at any time. This can be attributed to the early and effective administration of manual ventilation for 1 min immediately after suxamethonium. In the light of our observations, we cannot agree with the authors' conclusion that manual ventilation at induction of anaesthesia does not prevent hypoxaemia.
