A comparison between the GlideScope Video Laryngoscope and direct laryngoscope in paediatric patients with difficult airways - a pilot study.

The GlideScope Video Laryngoscope may improve the view seen at laryngoscopy in adults who have a difficult airway. Manikin studies and case reports suggest it may also be useful in children, although prospective studies are limited in number. We hypothesised that the paediatric GlideScope will result in an improved view seen at laryngoscopy in children with a known difficult airway, compared to direct laryngoscopy. Eighteen children with a history of difficult or failed intubation were prospectively recruited. After inhalational induction, each patient had laryngoscopy performed using a standard blade followed by GlideScope videolaryngoscopy. The GlideScope yielded a significantly improved laryngoscopic view, both with (p = 0.003) and without (p = 0.004) laryngeal pressure. The mean (SD) time taken to achieve the optimal view was 20 (8)s using conventional laryngoscopy and 26 (22)s using the GlideScope (p = 0.5). The GlideScope significantly improves the laryngoscopic view obtained in children with a difficult airway.

Cerebral blood flow velocity increases when propofol is changed to desflurane, but not when isoflurane is changed to desflurane in children.

BACKGROUND: Children may exhibit delayed emergence following maintenance of anesthesia with propofol or isoflurane. Desflurane is often used towards the end of procedures to facilitate emergence. This study evaluated the effect on middle cerebral artery blood flow velocity (Vmca) in anesthetized children when propofol or isoflurane was substituted with desflurane. METHODS: Forty-two healthy children aged 1-6 years were enrolled. A standardized anesthetic induction was used. Anesthesia was maintained with remifentanil (0.5 microg.kg(-1) bolus followed by an infusion of 0.2 microg.kg(-1).min(-1)) and a randomly selected sequence of propofol/desflurane/propofol, desflurane/propofol/desflurane, isoflurane/desflurane/isoflurane or desflurane/isoflurane/desflurane. Propofol was administered to maintain a steady-state serum concentration of 3 microg.ml(-1). Desflurane and isoflurane were administered at age-corrected 1 MAC. Hemodynamic stability was maintained. Transcranial Doppler sonography was used to measure Vmca. Hemodynamic variables as well as Vmca were measured 30 min after skin incision and repeated 30 min after each change in anesthetic maintenance agent. RESULTS: The mean age and weight was 2.3 +/- 1.3 years and 13.0 +/- 3.7 kg, respectively. The Vmca (mean) increased by 35% from 37.7 +/- 10.5 cm s(-1) to 57.8 +/- 14.6 cm s(-1) (P < 0.0001) when propofol was changed to desflurane but was unaffected when desflurane replaced isoflurane. CONCLUSION: When propofol is changed to desflurane, cerebral blood flow velocity increases significantly in normal children. This cerebral vasodilatory effect may have important implications in the neurosurgical setting.

The effect of sevoflurane on cerebral blood flow velocity in children.

BACKGROUND: Sevoflurane is a suitable agent for neuroanesthesia in adult patients. In children, cerebrovascular carbon dioxide reactivity is maintained during hypo- and normocapnia under sevoflurane anesthesia. To determine the effects of sevoflurane on middle cerebral artery blood flow velocity (Vmca) in neurologically normal children, Vmca was measured both at different MAC values and at one MAC over a specified time period, using transcranial Doppler sonography. METHODS: Twenty-six healthy children undergoing elective urological surgery were enrolled (16 patients in part I and 10 in part II). In part I of the study anesthesia comprised sevoflurane 0.5, 1.0 and 1.5 MAC in 30% oxygen and a caudal epidural block. Once steady state had been reached at each sevoflurane MAC level, three measurements of Vmca, mean arterial pressure (MAP) and heart rate (HR) were recorded. In part II of the study patients received sevoflurane 1.0 MAC over a 90-min period, with the same variables being recorded at 15-min intervals. RESULTS: Vmca did not vary significantly at 0.5, 1.0 and 1.5 MAC sevoflurane. There was a significant decrease in MAP between 0.5 MAC and 1.0 MAC sevoflurane (P < 0.005) and also between 1.0 MAC and 1.5 MAC (P < 0.01). There was no significant change in Vmca over 90 min at 1.0 MAC sevoflurane. CONCLUSION: Sevoflurane does not significantly affect cerebral blood flow velocity in healthy children at working concentrations.

The effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during propofol anesthesia.

Nitrous oxide (N(2)O) increases cerebral blood flow when used alone and in combination with propofol. We investigated the effects of N(2)O on cerebrovascular CO(2) reactivity (CCO(2)R) during propofol anesthesia in 10 healthy children undergoing elective urological surgery. Anesthesia consisted of a steady-state propofol infusion and a continuous caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Randomization determined the sequence order of N(2)O (N(2)O/air or air/N(2)O) and end-tidal (ET)CO(2) concentration (25, 35, 45, and 55 mm Hg) using an exogenous source of CO(2). At steady state, three sets of measurements of middle cerebral artery blood flow velocity, mean arterial blood pressure, and heart rate were recorded. A linear preservation of CCO(2)R was observed above 35 mm Hg of ETCO(2), irrespective of N(2)O. A decrease in CCO(2)R to 1.4%-1.9% per millimeters of mercury was seen in the hypocapnic range (ETCO(2) 25-35 mm Hg) with both air and N(2)O. We conclude that N(2)O does not affect CCO(2)R during propofol anesthesia in children. When preservation of CCO(2)R is required, the combination of N(2)O with propofol anesthesia in children would seem suitable. The cerebral vasoconstriction caused by propofol would imply that hyperventilation to ETCO(2) values less than 35 mm Hg may not be required because no further reduction in cerebral blood flow velocity would be achieved.

Effect of nitrous oxide on cerebrovascular reactivity to carbon dioxide in children during sevoflurane anaesthesia.

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.

The effect of nitrous oxide on cerebral blood flow velocity in children anesthetized with propofol.

BACKGROUND: Propofol for maintenance of anesthesia by continuous infusion is gaining popularity for use in pediatric patients. Nitrous oxide (N2O) has been shown to increase cerebral blood flow velocity (CBFV) in both children and adults. To determine the effects of N2O on middle cerebral artery blood flow velocity (Vmca) during propofol anesthesia in children, Vmca was measured with and without N2O using transcranial Doppler (TCD) sonography. METHODS: Thirty ASA I or II children aged 18 months to 6 years undergoing elective urological surgery were enrolled. Anesthesia comprised propofol aimed at producing an estimated steady-state serum concentration of 3 micro g.ml-1 and a caudal epidural block. A transcranial Doppler probe was used to measure middle cerebral artery blood flow velocity. Each patient was randomized to receive a sequence of either Air/N2O/Air or N2O/Air/N2O in 35% oxygen. Fifteen min after each change in the N2O concentration, three measurements of cerebral blood flow velocity, blood pressure and heart rate were recorded. Ventilatory parameters and EtCO2 were kept constant throughout the study period. RESULTS: CBFV increased by 12.4% when air was replaced by N2O, and returned to baseline when N2O was subsequently removed. There was a 14% decrease in CBFV when N2O was replaced with air, which increased to baseline when air was subsequently replaced with N2O. Mean heart rate and blood pressure remained constant throughout the study period. CONCLUSION: The effects of nitrous oxide on CBFV are preserved in children during propofol anesthesia.

The effect of nitrous oxide on cerebral blood flow velocity in children anaesthetised with desflurane.

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.