E. DE ROBERTIS

ESPOSITO G

PIAZZA, ORNELLA

SERVILLO G

TUFANO R.

English

Archivio della Ricerca - Università di Salerno

Finally, they suggested the use of much higher infusionrates of insulin, because it would lead to an increase in theinfusion rate of glucose. In contrast to their data2 (which usedvariable infusion rates of both insulin and glucose) we actu-ally measured plasma insulin concentrations, which werereported to be in the supra-physiological range of 600–800 pmol litre1. We are not aware of any scientific evi-dence suggesting that the infusion rate of insulin describedin our paper was too low. On the contrary, it cannot beexcluded that their higher and varying insulin infusionrates may have led to a higher and more unpredictablerate of intracellular glucose usage, thus creating the neces-sity to check plasma glucose more frequently. To answer thisinteresting suggestion, a dose–response study in cardiacsurgical patients is required. Such a study should bedesigned to investigate the effect of different high concen-trations of insulin on the metabolic rate of glucose perio-peratively.H. B. Van Wezel*C. J. ZuurbierJ. van DijkF. J. HoekE. de JongeB. A. de MolAmsterdam, The Netherlands*E-mail: H.B.vanwezel@amc.uva.nl1 Visser L, Zuurbier CJ, Hoek FJ, et al. Glucose, insulin andpotassium applied as perioperative hyperinsulinaemic normoglycae-mic clamp: effects on inflammatory response during coronary arterysurgery. Br J Anaesth 2005; 95: 448–572 Carvalho G, Moore A, Qizilbash B, Lachapelle K, Schricker T.Maintenance of normoglycemia during cardiac surgery. AnesthAnalg 2004; 99: 319–24doi:10.1093/bja/aei627Laryngospasm during subarachnoid blockEditor—We thank Dr Chincholkar for his interest in our casereport.1 To answer the questions raised by Dr Chincholkar,2the level of block before the dressing was opened was T11,bilaterally to sharp pain. It may have been higher, but we didnot test further as the level was satisfactory for the dressingremoval. Only part of the outer layer of the dressing wasremoved, the patient’s leg was supported at his calf and thewound was not handled at any point. Thus, it is unlikely thatremoval of the dressing was the cause of laryngospasm. Ittook at least 3 min for the laryngospasm to break, that is, notimmediately after the surgeons stopped removing the dres-sings. The measures described in our case report namelyfluid loading and atropine prevented any further develop-ment of a high parasympathetic tone and this in our opinionexplains the further uneventful course of the anaesthetic.We employed sharp pain as a modality of testing as mostclinicians would do. We do agree that a simple pin prick testmay not equate to the complex mechanisms involved inperception of surgical pain, but this is the most commonmethod of testing the level of block for regional anaesthesiain most clinical settings. Temporal summation is blocked insubarachnoid blocks3 but not so well in epidural blocks.4We disagree that the onset of bilateral blocks in lateralposition is slow. There are multiple factors governing thespread and onset of subarachnoid block.5 Dr Chincholkarquotes a study of regional anaesthesia for Caesarean section6but the complex changes during pregnancy are not compar-able to our male patient undergoing foot surgery. Instead,I would draw his attention to a study,7 where the onsetof bilateral sensory block to T10 with bupivacaine 0.5%(15 mg) with glucose 8% was a median of 2 min (range2–10 min). The dose is slightly higher than the bupivacaine0.5% (12.5 mg) with glucose 8% that we used. In our patient,the block was performed in the right lateral position andthe patient was turned supine immediately and hence it isunlikely that the block was unilateral.We too were perplexed when confronted with laryngo-spasm during a spinal anaesthetic. What we did was tofollow ‘ABC’ as in any emergency. Haemodynamic opti-mization involved bolus of intravenous fluid, atropine andephedrine. In our opinion, the laryngospasm responded tothe above measures, which were mostly vagolytic.K. SubramaniWeston-Super-Mare, UKE-mail: ksubramani9@hotmail.com1 Subramani K, Paul A. Laryngospasm during subarachnoid block.Br J Anaesth 2005; 94: 668–702 Chincholkar MG. Laryngospasm during subarachnoid block. Br JAnaesth 2005; 95: 2773 Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Zbinden AM. Spinalanaesthesia inhibits central temporal summation. Br J Anaesth 1997;78: 88–94 Curatolo M, Petersen-Felix S, Arendt-Nielsen L, Fischer M,Zbinden AM. Temporal summation during extradural anaesthesia.Br J Anaesth 1995; 75: 634–55 Hocking G, Wildsmith JA. Intrathecal drug spread. Br J Anaesth 2004;93: 568–786 Lewis NL, Ritchie EL, Downer JP, Nel MR. Left lateral vs. supine,wedged position for development of block after combined spinal-epidural anaesthesia for Caesarean section. Anaesthesia 2004; 59:894–87 Whiteside JB, Burke D, Wildsmith JAW. Comparison of ropivacaine0.5% (in glucose 5%) with bupivacaine 0.5% (in glucose 8%) for spinalanaesthesia for elective surgery. Br J Anaesth 2003; 90: 304–8doi:10.1093/bja/aei628S100B in Guillain–Barré syndromeEditor—Guillain–Barré syndrome (GBS), a subacute inflam-matory demyelinating polyneuropathy, is the most commoncause of acute neuromuscular paralysis. Up to one-third ofpatients with GBS require mechanical ventilation (MV)Correspondence141in the ICU,1 although outcome is generally good,2 acutemortality remains relatively high and 20% of hospitalizedpatients may have a long-term disability.3Serum protein S100B is a recognized marker of traumaticbrain injury. We observed an increase in S100B levels intwo GBS patients, pointing to a potential acute influence ofperipheral neuropathy on levels not related to CNS injury.Serum S100B was measured from venous blood samplesin two GBS patients requiring MV, on admission to ICU andafter 10 days. S100B values >0.2 mg litre1 are consideredabnormal. The patients were examined by a neurologist andthe diagnosis was based on the National Institute of Neuro-logical and Communicative Disorders and Stroke diagnosticcriteria.4The first patient was treated with a total of 10 plasmaexchanges and steroids and required 13 days of MV. Thepatient was discharged from hospital at 40 days withseverely limited lower limb activity and confined to bed.On admission, the S100 serum level was raised at0.495 mg litre1, and at 10 days the level had reduced to0.093 mg litre1.The second patient was treated with plasma exchange andsteroids. The patient recovered spontaneous ventilation after62 days and was discharged, still confined to a chair, 90 daysafter SGB onset. On ICU admission, the S100B serum levelwas very high (2.61 mg litre1), and was still abnormal10 days later (0.891 mg litre1).The serum S100B increases observed in these two GBSpatients exceed those attributed to brain tissue damagepatients with mild traumatic head injury.5 The physiologicalrole of this neuroprotein is not yet clear, but in GBS it mayact as a regeneration stimulus or as marker of neuronaldamage. A comparison of CSF and serum levels of S100Bwould be useful for the understanding of the role played bythis protein in GBS. S100B in GBS might be an expressionof neurotrophic and neuroprotective activity but no conclu-sion should be made without extensive and focused clinicaland experimental studies.O. Piazza*G. EspositoE. De RobertisG. ServilloR. TufanoNaples, Italy*E-mail: orpiazza@unina.it1 Sharshar T, Chevret S, Bourdain F, Raphaël J. Early predictors ofmechanical ventilation in Guillain-Barré syndrome. Crit Care Med2003; 31: 278–832 Henderson RD, Lawn ND, Fletcher DD, McClelland RL, Wijdicks EF.The morbidity of Guillain-Barré syndrome admitted to the intensivecare unit. Neurology 2003; 60: 17–203 Dornonville de la Cour C, Andersen H, Stalberg E,Fuglsang-Frederiksen A, Jakobsen J. Electrophysiological signs ofpermanent axonal loss in a follow-up study of patients withGuillain-Barré syndrome. Muscle Nerve 2005; 31:70–74 National Institute of Neurological and Communicative Disordersand Stroke ad hoc Committee (NINCDS). Criteria for diagnosisof Guillain-Barré syndrome. Ann Neurol 1978; 3: 565–65 Ingebrigtsen T, Waterloo K, Jacobsen EA, Langbakk B,Romner B. Traumatic brain damage in minor head injury: relationof serum S-100 protein measurements to magnetic resonanceimaging and neurobehavioral outcome. Neurosurgery 1999; 45:468–75doi:10.1093/bja/aei629Correspondence142

S100B in Guillain-Barre syndrome.

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S100B in Guillain-Barre syndrome.

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