Effect of nitrous oxide exposure during surgery on the homocysteine concentrations of children.

BACKGROUND: Nitrous oxide converts vitamin B12 to its nonmetabolically active form, inhibits methionine synthase, and results in an elevation of plasma total homocysteine (tHcy). The authors investigated the effect of nitrous oxide anesthesia on the plasma tHcy concentrations in children the morning after surgery and whether blood concentrations of folate and vitamins B12 and B6 were associated with any potential increase. METHODS: The authors measured plasma tHcy concentrations in 32 children before and 24 h after initial exposure to nitrous oxide (≥ 2 h). Genotype for methylenetetrahydrofolate reductase C677T and blood concentrations of folate, vitamins B12 and B6, and methylmalonic acid were measured before surgery. RESULTS: The median age of participants was 11 months (3-126 months). The median (first, third quartile) postoperative plasma tHcy concentration was significantly higher than the preoperative concentration (6.4 [4.7, 8.9] vs. 5.1[4.1, 6.4] µM, P < 0.0001), a 25% (2%, 42%) relative increase. Six of 28 (21%) children with normal, age-appropriate, preexposure plasma tHcy concentrations had postoperative plasma tHcy concentrations greater than the cutoff values. The duration of nitrous oxide exposure was associated positively with the rise in plasma tHcy concentration (R2 = 0.696, P = < 0.001). CONCLUSION: Exposure to ≥ 2 h nitrous oxide is associated with a small, albeit statistically significant, increase in postoperative plasma tHcy concentrations the morning after surgery in young children. The clinical significance of this increase is unknown.

Cerebrovascular reactivity to carbon dioxide is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane.

PURPOSE: Maintenance of cerebrovascular reactivity to CO(2) (CCO(2)R) is important during neurosurgical anesthesia. This study was designed to determine the effect of different desflurane concentrations on CCO(2)R in children. METHODS: Children undergoing urological surgery were enrolled. Anesthesia was induced with sevoflurane in air/oxygen. After intubation, sevoflurane was switched to desflurane. Analgesia was provided with an epidural neuraxial block. Mechanical ventilation was adjusted to an initial EtCO(2) of 30 mmHg. Exogenous CO(2) was used to achieve an EtCO(2) of 40 and 50 mmHg. Patients were randomized to the sequence of desflurane concentration (1.0 and 1.5 MAC) and the EtCO(2). Transcranial Doppler was used to measure middle cerebral artery blood flow velocity (Vmca). Five minutes were allowed to reach steady state after each change in EtCO(2) and 15 min after changing the desflurane concentration. RESULTS: Sixteen patients were studied. The mean age and weight were 3.5 +/- 1.5 yr and 14.4 +/- 3.1 kg, respectively. Mean arterial pressure remained stable throughout the study, while at an EtCO(2) of 50 mmHg, heart rate decreased at both desflurane concentrations (P < 0.05). At 1.0 MAC, Vmca increased from 30 to 40 mmHg (P < 0.05), but not from 40 to 50 mmHg EtCO(2). At 1.5 MAC, Vmca increased between 30 and 50 mmHg (P < 0.05). CONCLUSION: CCO(2)R is preserved during hypocapnia in children anesthetized with 1.0 MAC, but not with 1.5 MAC desflurane. The lack of further increase in Vmca at higher EtCO(2) concentrations implies that desflurane may cause significant cerebral vasodilatation in children. This may have important implications in children with reduced intracranial compliance.

Cerebral blood flow velocity in children anaesthetized with desflurane.

BACKGROUND: Desflurane allows for rapid emergence and changes in depth of anaesthesia which makes it especially suitable for neuroanaesthesia. This study was designed to determine the effects of different desflurane concentrations on cerebral blood flow velocity (CBFV) in healthy children. METHODS: Twenty children, aged 1-7 years undergoing urological surgery were studied. Anaesthesia was induced with sevoflurane in oxygen. After tracheal intubation, sevoflurane was discontinued and ventilation with desflurane in air/oxygen was initiated and normoventilation maintained. A caudal block was performed. The patients were randomized to receive three different desflurane concentrations (0.5, 1.0 and 1.5 MAC). Fifteen minutes were allowed to reach steady-state at which time CBFV was measured by transcranial Doppler sonography. Mean arterial pressure (MAP) and heart rate (HR) were simultaneously recorded at 1-min intervals. RESULTS: Cerebral blood flow velocity increased from 0.5 to 1.0 MAC (P < 0.05), but not from 1.0 to 1.5 MAC. HR increased from 0.5 to 1.0 (P < 0.001) and from 1.0 to 1.5 MAC (P < 0.001), whereas the MAP decreased only from 0.5 to 1.0 MAC (P < 0.001). CONCLUSIONS: Desflurane in concentrations of 1.0 and 1.5 MAC in children increases CBFV significantly when compared with 0.5 MAC. These changes were associated with a significant increase in HR and decrease in MAP.