PETERSEN-FELIX, S.

ZBINDEN, A. M.

RERO DOC Digital Library

704 BRITISH JOURNAL OF ANAESTHESIAparative trial. Program and Abstracts of the Association forPractitioners in Infection Control Educational Conference,1984.5. Craven DE, Lichtenberg DA, Kunches M. A randomizedstudy comparing a transparent polyurethane dressing to a drygauze dressing for peripheral intravenous catheter sites.Infection Control 1985; 6: 361-366.6. Hoffman KK, Weber DJ, Samsa GP, Rutala WA. Trans-parent polyurethane film as an intravenous catheter dressing.A meta-analysis of the infection risk. Journal of the AmericanMedical Association 1992; 267: 2072-2076.Sir,—Drs Kitching and Rice describe an interesting case ofpuerperal extradural abscess after normal delivery withoutextradural analgesia. A similar case was described by Male andMartin [1], who reported an extradural abscess that developed 6days after normal delivery in a 22-yr-old woman who also had notreceived extradural analgesia. This patient had been admitted 10days before delivery suffering from infective hepatitis withhepatocellular dysfunction and jaundice, whereas the patientdescribed by Drs Kitching and Rice was presumably healthy.I agree that it is possible for an extradural abscess to occur afterextradural catheterization without a causal relationship existing.However, I would emphasize several points. The incidence ofspontaneous extradural abscess in the general hospital populationis estimated at 0.2-1.2 per 10000 which, indeed, is greater than thereported incidence of extradural abscess after lumbar extraduralanalgesia in obstetric patients, as pointed out by Drs Kitching andRice. However, these populations are not equivalent. Closerinspection of reports within the general population demonstratesa high incidence of co-existing chronic disease, which is a riskfactor for compromised immunity, and a predilection for the olderage group, the majority of cases being patients older than 50 yr[2, 3]. In contrast, the average parturient is young and relativelyhealthy compared with the general population. Therefore a directcomparison of relative incidence between the obstetric populationand the general population is inappropriate and statisticallyunsound.I believe there is strong evidence of a causal relationshipbetween the use of extradural anaesthesia and the development ofan extradural abscess in our patient. This is supported by a closetemporal relationship, correspondence of the location of theabscess and the site of extradural catheter insertion, and growth ofthe likely infective organism from a skin lesion at the puncturesite.Whilst Drs Kitching and Rice have demonstrated that extra-dural abscess can develop in the puerperium without obviouscause, I believe that extradural catheterization remains a riskfactor for development of this serious condition in obstetrics andin other specialties, and would reiterate the importance ofmeticulous aseptic technique when performing these procedures.Drs Vasdev and Leicht make pertinent comments regardingaseptic technique for extradural catheter insertion. However, Iwould draw to attention possible neonatal complications that mayarise from maternal transdermal absorption of iodine from iodine-containing skin disinfectants. Neonatologists in our institutionhave shown recently that mothers exposed to topical iodine-containing antiseptics immediately before delivery had concen-trations of iodine in their breast milk twice those of non-exposedmothers, and that this appeared to be linked to an increasedincidence of transient neonatal hypothyroidism [4]. Iodineabsorption would probably be minimized by the practice ofrinsing off the iodine with 70% alcohol as recommended byVasdev and Leicht, but in our delivery suite it is now policy toavoid completely the use of iodine-containing skin disinfectants.We have favoured polyurethane dressings such as Tegaderm(3M) as dressings for extradural catheter sites because of theirexcellent fixation properties. Vasdev and Leicht cite evidence thatthese dressings may increase bacterial colonization, which indeedis of concern; we are currently reappraising usage in our practice.W. D. NGAN KEEWellington School of MedicineWellington, New Zealand1. Male CG, Martin R. Puerperal spinal epidural abscess.Lancet 1973; 1: 608-609.2. Hlavin ML, Kaminski HJ, Ross JS, Ganz E. Spinal epiduralabscess: a ten-year perspective. Neurosurgery 1990; 27:177-184.3. Danner RL, Hartman BJ. Update of spinal epidural abscess:35 cases and review of the literature. Reviews of InfectiousDiseases 1987; 9: 265-274.4. Tracey MB, Richardson VF. Breast milk iodine levels andmaternal iodine exposure. The cause of transient neonatalhypothyroidism? Paediatric Society of New Zealand AnnualGeneral Meeting, October 16, 1991.THE LARYNGEAL MASK AND INTRAOCULAR SURGERYSir,—We were interested in the article of Lamb, James andJanicki on the effect of the laryngeal mask airway (LMA) [1] onintraocular pressure [2]. In their conclusion, the authors men-tioned the potential risk of loss of airway control with the LMAduring general anaesthesia for intraocular surgery. This risk is nottheoretical, but a practical disadvantage of the method, as theanaesthetist does not have access to the patient's airway duringsurgery.We describe two patients who recently underwent intraocularsurgery under general anaesthesia (thiopentone, fentanyl, en-flurane in an oxygen-nitrous oxide mixture and vecuronium). Inboth patients, insertion of the LMA was easy and resulted in atight seal, which allowed mechanical ventilation (with peakinspiratory pressure less than 15 cm H2O) [3]. The LMA wassecured with adhesive strips. The surgical procedure for the firstpatient was initially uneventful, but the LMA was displacedslightly toward the end of the procedure. This resulted in amassive gas leak that led to a dramatic decrease in the expiratorytidal volume (less than 100 ml). Airway control was resumedtemporarily by pushing down the LMA, but the leak recurredalmost immediately. The LMA was then held in place by theanaesthetist's hand under the drapes and this allowed completionof the procedure. Hypoxia was not detected by pulse oximetry.Recovery was uneventful. In the second patient, a gas leak becameevident before the beginning of the procedure, but after drapes,instrumentation and microscope were in place. Because expiratoryflow was not detected in the breathing system, the drapes wereremoved hurriedly. The LMA was removed, the patient's lungswere ventilated using a face mask, additional thiopentone (150 mg)given i.v. and the trachea intubated. Hypoxia was not detected. Inboth patients there were no harmful consequences.We had chosen to control the airway during general anaesthesiafor intraocular surgery with the LMA because, as Lamb, Jamesand Janicki have shown, this could blunt any increase inintraocular pressure. However, a minor incident (displacement ofthe LMA) could be transformed into a potentially disastrousaccident. In our opinion, the inability of the anaesthetist to gainconvenient control of the patient's airway during the procedure isa major hazard. Because of our experience, we have discontinuedthe use of an LMA for airway control in intraocular surgery.J. RIP ARTR. COHENDYJ.-J. ELEDJAMCentre Hospitaller Universitaire de NimesF 30029, Nimes, France1. Brain AIJ. The laryngeal mask. A new concept in airwaymanagement. British Journal of Anaesthesia 1983; 55:801-805.2. Lamb K, James MFM, Janicki PK. The laryngeal maskairway for intraocular surgery: effects on intraocular pressureand stress responses. British Journal of Anaesthesia 1992; 69:143-147.3. Benumof JL. Laryngeal mask airway: indications andcontraindications. Anesthesiology 1992; 77: 843-846.BRAIN PARTIAL PRESSURES OF ISOFLURANE ANDNITROUS OXIDESir,—We read with interest the article by Dr Thornton andcolleagues [1], but wish to comment on the methods used.Thornton's group used isoflurane or nitrous oxide, changedrandomly in three consecutive 10-min periods. They do not statewhich anaesthesia system or what fresh gas flows they used.CORRESPONDENCE0.8-,3? 0 . 6 -CDcCOoCO- 0.2 H0.0r 8 0Iso N,0- 6 0if•5- 2010 20Time (min)30 40FIG. 1. Computer simulation of the brain partial pressures ofisoflurane (A) and nitrous oxide ( • ) during three 10-min periodsin which either isoflurane (0.65-0.70 % end-tidal) or nitrous oxide(60-65 % end-tidal) was administered. Time = Time after be-ginning of anaesthesia. Iso = Isoflurane.We have simulated an isoflurane-nitrous oxide-isofluraneanaesthesia period as described by Thornton and colleagues, withthe GUS computer simulation program (Gas Uptake Simulation,iMedEd Inc, Phoenix, Arizona, U.S.A.) using a circle system andfresh gas flows of 12 litre min"1. We agree that, when changingfrom isoflurane to nitrous oxide after the first 10-min period,stable end-tidal nitrous oxide values can be obtained within 5 min,after which the end-tidal partial pressure of isoflurane would notbe less than 5 % of the initial value as stated by Dr Thornton andcolleagues, but 0.23 vol% decreasing to 0.15 vol% at the endof the nitrous oxide period. Even with fresh gas flows of20 litre min"1, the residual end-tidal isoflurane washout from thebrain would be even slower (fig. 1). Five minutes after the changefrom isoflurane to nitrous oxide, the brain partial pressure wouldbe 0.38 vol%, decreasing to 0.24 vol% at the end of the nitrousoxide period. When, as in the first 10-min period, the end-tidalconcentration of isoflurane is changed from 0 to approximately0.70 vol%, a 10-min equilibration period does not produce stablebrain partial pressures of isoflurane.We would recommend longer equilibration periods in order toobtain stable conditions before measurements are performed.S. PETERSEN-FELIXA. M. ZBINDENUniversity of BerneSwitzerland1. Thornton C, Creagh-Barry P, Jordan C, LuffNP, Dore CJ,Henley M, Newton DEF. Somatosensory and auditoryevoked responses recorded simultaneously: differential effectsof nitrous oxide and isoflurane. British Journal of Anaesthesia1992; 68: 508-514.Sir,—Thank you for inviting us to reply to the interesting letterfrom Drs Petersen-Felix and Zbinden. We have used a similarprogram, Narkup [1], which was produced at Northwick Park, toreproduce exactly the brain concentrations shown in their figure,when the alveolar concentrations of isoflurane and nitrous oxidewere maintained at 0.6% and 60%, respectively. Clearly, boththese programs use, for modelling of the "brain compartment",blood flow, mass and partition coefficient based on whole brainvalues. This is a good example of the need to know exactly whatassumptions are made in pharmacokinetic models. When Narkupis re-run using, for example, assumptions that the effectcompartment is in the cerebral grey matter (40 % of the brain),with a high proportion of the blood flow (say 70 %), then brainconcentrations are stable for the whole of the test periods. Ofcourse, we have no means of knowing if the above assumptions aretrue, but the writers of each program also do not know.The end-expiratory concentrations of both gases were measureddirectly either by the Capnomac, or by a mass spectrometer inboth our 1992 paper, and a previous study which used the samemethodology [2]j in both studies, end-expiratory concentrationhad decreased to less than 5 % of the original concentration before705the test period for the next gas. The anaesthetic was deliveredfrom a Manley MP3 (non-rebreathing) as a circle system wouldhave been inappropriate to produce the rapid changes inconcentration that we needed. Again, any computer modellingwould be dependent on assumptions about minute volume andcardiac output.The particular point about the three-period statistical con-struction that we chose [3] is that it effectively eliminates errorswhich are caused by carry-over from one period to another.C. THORNTOND. E. F. NEWTONNorthwick Park HospitalHarrow1. Lockwood GG, White DC. Effect of ventilation and cardiacoutput on the uptake of anaesthetic agents from differentbreathing systems: A theoretical study. British Journal ofAnaesthesia 1991; 66: 519-526.2. Newton DEF, Thornton C, Creagh-Barry P, Dore CJ. Earlycortical evoked response in anaesthesia: comparison of theeffects of nitrous oxide and isoflurane. British Journal ofAnaesthesia 1989; 62: 61-65.3. Ebbutt AF. Three period crossover designs for two treat-ments. Biometrics 1984; 40: 219-224.HYPERTONIC SOLUTIONS IN MASSIVE HAEMORRHAGESir,—We read with interest the case report by Dr Ngan Kee andtransfusion by Donaldson, Seaman and Park [1] and wouldcommend the authors on providing the reader with an excellentpractical approach to the initial management of the acutelybleeding, hypovolaemic patient. However, we feel that a dis-cussion on the crystalloid/colloid controversy should also nowinclude some comment on the use of hypertonic solutions.As the authors state, the success of initial resuscitation in theacutely hypovolaemic patient depends upon speed and adequacyof repletion. There has been increasing interest in the use ofhypertonic solutions in the prehospital management of patientswith traumatic hypovolaemic shock [2, 3]. The advantage ofhypertonic over isotonic solutions in early resuscitation is thatadequate resuscitation can be accomplished rapidly with smallvolumes through peripheral i.v. lines until conventional fluidtherapy can be initiated. The smaller volume of fluid may alsoreduce complications related to dilutional coagulopathy andthermal stress. Hypertonic saline—Dextran 70 has been shown toimprove mean arterial pressure, cardiac output, oxygen deliveryand urine output and to increase survival compared with Ringer'slactate solution in severely traumatized patients [3].Hypertonic solutions are still at an early stage of clinicalinvestigation and further work is required before their role in fluidresuscitation is evaluated fully [4, 5]. The anticipated problems ofacute hypernatraemia, hypervolaemia and venous injury have notmaterialized in the studies published so far [4].We would suggest that in acute massive haemorrhage wherevenous access may be limited and rapid restoration of arterialpressure is required, there may be a role for hypertonic solutions.We would be interested in the authors' views on this subject.J. BRIMACOMBEA. BERRYRoyal Perth HospitalPerth, Australia1. Donaldson MDJ, Seaman MJ, Park GR. Massive bloodtransfusion. British Journal of Anaesthesia 1992; 69: 621-630.2. Mattox KL, Maningas PA, Moore EE. Prehospital hy-pertonic saline/dextran infusion for post-traumatic hypo-tension. Annals of Surgery 1991; 213: 482-489.3. Holcroft J, Vassar M, Turner J. 3 % NaCl and 7.5 % dextran70 in the resuscitation of severely injured patients. Annals ofSurgery 1987; 206: 279-288.4. Dontigny L. Small-volume resuscitation. Canadian Journalof Surgery 1992; 35: 31-33.5. Vincent J-L. Fluids for resuscitation. British Journal ofAnaesthesia 1991; 67: 185-193.

BRAIN PARTIAL PRESSURES OF ISOFLURANCE AND NITROUS OXIDE

Abstract

Similar works

Full text

Available Versions

RERO DOC Digital Library