PubMed · 11949650
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L Ng, H Hopwood. 2002. Colour coding for piped Entonox hoses.. https://doi.org/10.1046/j.1365-2044.2002.2575_5.x
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The aim of this study was to determine the effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane. Eighteen healthy children scheduled for elective surgery were enrolled into the study. Anaesthesia was induced using sevoflurane, and a caudal block was performed following tracheal intubation. Anaesthesia was maintained with 1 age-adjusted MAC desflurane. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomised to receive a sequence of either air/nitrous oxide/air or nitrous oxide/air/nitrous oxide in 30% oxygen. Fifteen minutes after each change in the nitrous oxide concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Neither the addition nor removal of nitrous oxide caused any significant changes in middle cerebral artery blood flow velocity, heart rate or blood pressure. This may be due to a more potent cerebral vasodilatory effect of desflurane in children.
BACKGROUND: Sevoflurane and nitrous oxide have intrinsic cerebral vasodilatory activity. To determine the effects of nitrous oxide on cerebrovascular reactivity to carbon dioxide (CCO(2)R) during sevoflurane anaesthesia in children, middle cerebral artery blood flow velocity (V(mca)) was measured over a range of end-tidal carbon dioxide concentrations (E'(CO(2))), using transcranial Doppler (TCD) ultrasonography. METHODS: Ten children aged 1.5-6 yr were anaesthetized with sevoflurane and received a caudal block. Patients were allocated randomly to receive either air-nitrous oxide or nitrous oxide-air. Further randomization determined the sequence of E'(CO(2)) (25, 35, 45, and 55 mm Hg) and sevoflurane (1.0 then 1.5 MAC or 1.5 then 1.0 MAC) concentrations. Once steady state had been reached, three measurements of V(mca), mean arterial pressure (MAP), and heart rate (HR) were recorded. RESULTS: Cerebrovascular carbon dioxide reactivity was reduced in the 25-35 mm Hg E'(CO(2)) range on the addition of nitrous oxide to 1.5 MAC, but not 1.0 MAC sevoflurane. A plateau in CCO(2)R of 0.4-0.6% per mm Hg was seen in all groups between E'(CO(2)) values of 45 and 55 mm Hg. Mean HR and MAP remained constant throughout the study period. CONCLUSIONS: Cerebrovascular carbon dioxide reactivity is reduced at and above an E'(CO(2)) of 45 mm Hg during 1.0 and 1.5 MAC sevoflurane anaesthesia. The addition of nitrous oxide to 1.5 MAC sevoflurane diminishes CCO(2)R in the hypocapnic range. This should be taken into consideration when hyperventilation techniques for reduction of brain bulk are being contemplated in children with raised intracranial pressure.
Sharp debridement is the most efficient method for clearing the woundbed in the exudation and granulation phase of wound healing. At our clinic the anaesthetic lidocaine-prilocaine cream, EMLA, has been used as an analgesic for sharp debridement since 1994. A review of patients' records was conducted, including ulcer size, dose of cream used, analgesic efficacy and complications. During a 6-year period a total of 1084 patients were treated for leg ulcers, decubitus ulcers, abscess revisions, anal and coccyx fistulae, postoperative wounds, diabetic ulcers and burns. Doses ranging from 3 to 150 g cream were applied for 45-60 min. In all patients except three the analgesia was adequate for debridement. We observed no allergic reactions, no clinical symptoms of local anaesthetic toxicity or methaemoglobinaemia. In 12 patients (1.1%) a burning sensation was reported directly after the application of EMLA cream to the ulcer, which, however, subsided within 15-20 min. In our experience, sharp debridement in percutaneous analgesia with EMLA is efficient, economical, safe, and tolerable for the patient.