80
Correspondence
anaesthetic, but had then developed a twitching of his left arm which subsequently resolved. A diagnosis of a focal seizure with retained consciousness was made by a consultant physician who did not consider that an EEG or CT scan were indicated in the absence of focal signs or unprovoked seizures. To date the patient has suffered no further episodes. We believe this case to be of interest for three reasons. Firstly, this report would seem to be the first describing a purely focal event occurring without loss of consciousness. Seizures in the postoperative period following enflurane anaesthesia are well documented [ 141. However, there has been only one previous report of a seizure without loss of consciousness, and this consisted of generalised myoclonic jerks [5]. Secondly, there is the possibility of an interaction with methocarbamol which is promoted for the treatment of acute musculoskeletal disorders, and has a plasma half-life of 2 h [6]. There have been two cases of convulsions following methocarbamol reported to the Committee on Safety of Medicines (Personal communication Ms S. Faithful, Wyeth Laboratories). It seems unlikely, given the short half-life, that methocarbamol was exerting any pharmacological effect in the patient reported at the time of the anaesthetic. However, since he had suffered a focal seizure, a continuing electrical susceptibility to a recurrence may have remained at the time enflurane was administered. Thirdly, there is evidence that diazepam may potentiate
enflurane induced electroencephalographic seizure activity [3], and some have concluded that phenytoin or valproate should be used to treat enflurane induced seizures [5]. In our case diazepam eventually controlled the seizure, although only after repeated doses totalling 30 mg. Whilst it is possible the patient is harbouring a focal structural lesion, we think this unlikely. He has not developed any focal signs on follow-up, and his seizures only occurred when he was exposed to known epileptogenic drugs. Unusual reactions to drugs may have implications for the anaesthetic technique. Royal Berkshire Hospital. Reading RGI 5AN
T.J. PARKE R.H. JAGO
References [I] ALLANMWB. Convulsions after enflurane. Anaesthesia 1984; 39 605-6. [2] YAZJI NS, SEEDRF. Convulsive reaction following enflurane anaesthesia. Anaesthesia 1984; 39 1249. [3] KRUCZEKM,ALBINMS,WOLFS, BERTON1 JM. Postoperative seizure activity following enflurane anesthesia. Anesthesiology 1980; 53: 175-6. [4] NICOLL JMV. Status epilepticus following enflurane anaesthesia. Anaesthesia 1986; 41: 927-30. [5] JENKINS J, MILNEAC. Convulsive reaction following enflurane anaesthesia. Anaesthesia 1984; 39 44-5. [6] GOODMAN LS, GILMAN A, eds. The pharmacological basis of therapeutics, 4th edn. Macmillan, 1970: 226-9.
Methaemoglobinaernia and pulse oximetry We were interested to read the letter ‘Prilocaine associated methaemoglobinaemia and pulse oximeter’ by Marks and Desgrand (Anaesthesia 1991; 46: 703). The authors state that after surgery had begun the patient appeared dusky and ‘the pulse oximeter showed a saturation of 75%’. They also make the observation that the methaemoglobin level was 6.6%. These statements are misleading because in the presence of severe methaemoglobinaemia, the pulse oximeter reading tends towards 85%. Pulse oximeter readings in the presence of methaemoglobin causes a shift towards 85% and do not usually go below this value. The reason this shift occurs is explained by the fact that methaemoglobin absorbs strongly at both the oxyhaemoglobin wavelength (940 nm) and deoxyhaemoglobin wavelength (660 nm). The pulse oximeter determines the ratio of pulsatile absorbances at these two wavelengths and as the ratio approaches unity, the pulse oximeter saturation becomes 85%. Hence in situations of severe methaemoglobinaemia, the patient may have drastically reduced saturation in the presence of less alarming oximeter saturation readings. Furthermore, studies in dogs indicate that pulse oximeters begin to show
spurious readings at a methaemoglobin level of about 30-35%, at which values the readings are 82-85% and then become virtually, independent of the methaemoglobin level [ 1, 21. Therefore, the cited patients’ methaemoglobin level was not significant enough substantially to alter pulse oximeter readings and hence another explanation must exist for her observed saturation reading of 75%. Southwestern Medical Center, Dallas, Texas 75235-9068, USA
L. DELWOOD D. OFLAHERTY E.J. PREJEAN M. POPAT A.H. GIESECKE
References [I] BARKER SJ, TREMPERKK, HYATT J. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 1989; 7 0 1 12-7. [2] DELWOOD L, OFLAHERTYD, PREIEANEJ. Methemoglobinemia and its effects on pulse oximetry. Critical Care Medicine 1991; 19 988.
Nitrous oxide should not be used during laparoscopy nor during other abdominal operations I write to second Dr G . Verheecke’s questioning of the wisdom of the use of nitrous oxide during laparoscopic cholecystectomy (Anaesthesia 1991; 46: 698). For 25 years anaesthetists (and ‘anaesthesiologists’!) seem to have ignored, and seem to be continuing to ignore, the important work of Eger and his team at the University of California as quoted by Dr Verheecke. Eger showed that the administration of nitrous oxide makes the intestines increase in size because nitrous oxide, with its high solubility, gets into the bowel faster than the normal bowel
gases (nitrogen and methane) can get out. There have been even more recent papers confirming Eger’s ideas, yet anaesthetists all over the world continue to administer nitrous oxide as if it were required by our religion, even in operations when we know that its administration is going to make the bowel size greater and, therefore, make the surgeons’s job harder! Dr Verheecke asks ‘Why not avoid nitrous oxide by using total intravenous anaesthesia’? That may be all very well, but I would ask too, ‘Why not use old-fashioned
Correspondence
anaesthetic, but had then developed a twitching of his left arm which subsequently resolved. A diagnosis of a focal seizure with retained consciousness was made by a consultant physician who did not consider that an EEG or CT scan were indicated in the absence of focal signs or unprovoked seizures. To date the patient has suffered no further episodes. We believe this case to be of interest for three reasons. Firstly, this report would seem to be the first describing a purely focal event occurring without loss of consciousness. Seizures in the postoperative period following enflurane anaesthesia are well documented [ 141. However, there has been only one previous report of a seizure without loss of consciousness, and this consisted of generalised myoclonic jerks [5]. Secondly, there is the possibility of an interaction with methocarbamol which is promoted for the treatment of acute musculoskeletal disorders, and has a plasma half-life of 2 h [6]. There have been two cases of convulsions following methocarbamol reported to the Committee on Safety of Medicines (Personal communication Ms S. Faithful, Wyeth Laboratories). It seems unlikely, given the short half-life, that methocarbamol was exerting any pharmacological effect in the patient reported at the time of the anaesthetic. However, since he had suffered a focal seizure, a continuing electrical susceptibility to a recurrence may have remained at the time enflurane was administered. Thirdly, there is evidence that diazepam may potentiate
enflurane induced electroencephalographic seizure activity [3], and some have concluded that phenytoin or valproate should be used to treat enflurane induced seizures [5]. In our case diazepam eventually controlled the seizure, although only after repeated doses totalling 30 mg. Whilst it is possible the patient is harbouring a focal structural lesion, we think this unlikely. He has not developed any focal signs on follow-up, and his seizures only occurred when he was exposed to known epileptogenic drugs. Unusual reactions to drugs may have implications for the anaesthetic technique. Royal Berkshire Hospital. Reading RGI 5AN
T.J. PARKE R.H. JAGO
References [I] ALLANMWB. Convulsions after enflurane. Anaesthesia 1984; 39 605-6. [2] YAZJI NS, SEEDRF. Convulsive reaction following enflurane anaesthesia. Anaesthesia 1984; 39 1249. [3] KRUCZEKM,ALBINMS,WOLFS, BERTON1 JM. Postoperative seizure activity following enflurane anesthesia. Anesthesiology 1980; 53: 175-6. [4] NICOLL JMV. Status epilepticus following enflurane anaesthesia. Anaesthesia 1986; 41: 927-30. [5] JENKINS J, MILNEAC. Convulsive reaction following enflurane anaesthesia. Anaesthesia 1984; 39 44-5. [6] GOODMAN LS, GILMAN A, eds. The pharmacological basis of therapeutics, 4th edn. Macmillan, 1970: 226-9.
Methaemoglobinaernia and pulse oximetry We were interested to read the letter ‘Prilocaine associated methaemoglobinaemia and pulse oximeter’ by Marks and Desgrand (Anaesthesia 1991; 46: 703). The authors state that after surgery had begun the patient appeared dusky and ‘the pulse oximeter showed a saturation of 75%’. They also make the observation that the methaemoglobin level was 6.6%. These statements are misleading because in the presence of severe methaemoglobinaemia, the pulse oximeter reading tends towards 85%. Pulse oximeter readings in the presence of methaemoglobin causes a shift towards 85% and do not usually go below this value. The reason this shift occurs is explained by the fact that methaemoglobin absorbs strongly at both the oxyhaemoglobin wavelength (940 nm) and deoxyhaemoglobin wavelength (660 nm). The pulse oximeter determines the ratio of pulsatile absorbances at these two wavelengths and as the ratio approaches unity, the pulse oximeter saturation becomes 85%. Hence in situations of severe methaemoglobinaemia, the patient may have drastically reduced saturation in the presence of less alarming oximeter saturation readings. Furthermore, studies in dogs indicate that pulse oximeters begin to show
spurious readings at a methaemoglobin level of about 30-35%, at which values the readings are 82-85% and then become virtually, independent of the methaemoglobin level [ 1, 21. Therefore, the cited patients’ methaemoglobin level was not significant enough substantially to alter pulse oximeter readings and hence another explanation must exist for her observed saturation reading of 75%. Southwestern Medical Center, Dallas, Texas 75235-9068, USA
L. DELWOOD D. OFLAHERTY E.J. PREJEAN M. POPAT A.H. GIESECKE
References [I] BARKER SJ, TREMPERKK, HYATT J. Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 1989; 7 0 1 12-7. [2] DELWOOD L, OFLAHERTYD, PREIEANEJ. Methemoglobinemia and its effects on pulse oximetry. Critical Care Medicine 1991; 19 988.
Nitrous oxide should not be used during laparoscopy nor during other abdominal operations I write to second Dr G . Verheecke’s questioning of the wisdom of the use of nitrous oxide during laparoscopic cholecystectomy (Anaesthesia 1991; 46: 698). For 25 years anaesthetists (and ‘anaesthesiologists’!) seem to have ignored, and seem to be continuing to ignore, the important work of Eger and his team at the University of California as quoted by Dr Verheecke. Eger showed that the administration of nitrous oxide makes the intestines increase in size because nitrous oxide, with its high solubility, gets into the bowel faster than the normal bowel
gases (nitrogen and methane) can get out. There have been even more recent papers confirming Eger’s ideas, yet anaesthetists all over the world continue to administer nitrous oxide as if it were required by our religion, even in operations when we know that its administration is going to make the bowel size greater and, therefore, make the surgeons’s job harder! Dr Verheecke asks ‘Why not avoid nitrous oxide by using total intravenous anaesthesia’? That may be all very well, but I would ask too, ‘Why not use old-fashioned
