The flipped classroom approach to didactic education resulted in a small improvement in knowledge retention and was preferred by anesthesiology residents.

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Our results demonstrating higher glucose and lactate with sevoflurane in the human brain compared with propofol could reflect greater neuronal activity with sevofluane resulting in enhanced glutamate-neurotransmitter cycling, increased glycolysis, and lactate shuttling from astrocytes to neurons or mitochondrial dysfunction. Further, the association between emergence delirium and lactate suggests that anesthesia-induced enhanced cortical activity in the unconscious state may interfere with rapid return to "coherent" brain connectivity patterns required for normal cognition upon emergence of anesthesia.

P roton magnetic resonance spectroscopy ( 1 HMRS) can track biochemical abnormalities that precede or are directly associated with pathologic changes. When 1 HMRS was used in studies on the rodent brain, isoflurane anesthesia was characterized by a higher concentration of lactate, glutamate, and glucose compared with propofol. In this study, 1 HMRS was used to characterize the cerebral metabolic status in children undergoing general anesthesia for a routine magnetic resonance imaging (MRI) scan.The 59 children, aged 2 to 7 years, were scheduled for an MRI under general anesthesia. They were randomized to receive either propofol (group P) or sevoflurane (group S) anesthesia. All received an inhalational mask induction for 1 to 2 minutes with sevoflurane. Children given propofol anesthesia were converted to an intravenous propofol infusion with oxygen via a nasal cannula; the average infusion rate was 165 T 17 Kg/kg per minute. In group S, the airway was secured, and sevoflurane was titrated to 1 to 1.5 minimum alveolar concentration (3.1%). All children received intravenous normal saline (10Y20 mL/kg) during the procedure. The 1 HMRS scans were acquired in the parietal cortex after about 60 minutes of anesthesia. During emergence from anesthesia, each child was assessed using the Pediatric Anesthesia Emergence Delirium (PAED) scale. Total recovery time was defined as the time from arrival to the recovery room until the patient met postanesthetic modified Aldrete recovery score criteria for discharge home.The final analysis included 50 children, 23 in group P and 27 in group S. The 2 groups did not differ in age, weight, or sex or in the frequency of indications for brain MRI (seizure disorders, headaches, and workup for developmental delay or attentiondeficit/hyperactivity disorder). In group P, 20 (87%) of 23 scans were interpreted as B normal.[ In group S, 23 (85%) of the 27 scans were considered to be normal. The average total duration of anesthesia was 65.5 T 15.5 minutes in group P and 61.3 T 10.2 minutes in group S. Mean arterial pressures were 68 T 7 and 61 T 8 mm Hg in groups P and S, respectively, a statistically significant difference (P = 0.001). Average heart rates were lower (87 T 14 beats/min) in group P than in group S (100 T 13 beats/min; P = 0.001). All children recovered without complications, with shorter time for recovery in the group P patients compared with those in group S (42 T 17 and 53 T 15 minutes; P = 0.02). The average total PAED score in group S was 7.0 T 5.7, and in group P, 3.9 T 4.7, indicating more agitation and delirium with sevoflurane (P = 0.037). Concentrations of taurine, glucose, and lactate were higher in group S patients compared with group P children, when controlling for age. Lactate was 2-fold higher and glucose 1.2-fold higher in the parietal cortex of children given sevoflurane compared with propofol. Lactate and glucose correlated positively and total creatine correlated negatively with the score on the PAED.Routine use of sevoflurane and propofol in children undergo...

Aim: End-tidal CO 2 (Et CO2 ) is the standard in operative care along with pulse oximetry for ventilation assessment. It is known to be less accurate in the infant population than in adults. Many neonatal intensive care units (NICU) have converted to utilizing transcutaneous CO 2 (tcP CO2 ) monitoring. This study aimed to compare perioperative Et CO2 to tcP CO2 in the pediatric perioperative population specifically below 10 kg, which encompasses neonates and some infants. Methods: After IRB approval and parental written informed consent, we enrolled neonates and infants weighing less than 10 kg, who were scheduled for elective surgery with endotracheal tube under general anesthesia. P CO2 was monitored with Et CO2 and with tcP CO2 . Venous blood gas (Pv CO2 ) samples were drawn at the end of the anesthetic. We calculated a mean difference of Et CO2 minus Pv CO2 (Delta Et CO2 ), and tcP CO2 minus Pv CO2 (Delta tcP CO2 ) from end-of-case measurements. The mean differences in the NICU and non-NICU patients were compared by t-tests and Bland–Altman analysis. Results: Median age was 10.9 weeks, and median weight was 4.4 kg. NICU (n=6) and non-NICU (n=14) patients did not differ in Pv CO2 . Relative to the Pv CO2 , the Delta Et CO2 was much greater in the NICU compared to the non-NICU patients (−28.1 versus −9.8, t=3.912, 18 df, P =0.001). Delta tcP CO2 was close to zero in both groups. Although both measures obtained simultaneously in the same patients agreed moderately with each other (r =0.444, 18 df, P =0.05), Bland–Altman plots indicated that the mean difference (bias) in Et CO2 measurements differed significantly from zero ( P <0.05). Conclusions: Et CO2 underestimates Pv CO2 values in neonates and infants under general anesthesia. TcP CO2 closely approximates venous blood gas values, in both the NICU and non-NICU samples. We, therefore, conclude that tcP CO2 is a more accurate measure of operative Pv CO2 in infants, especially in NICU patients.

Background A wealth of data shows neuronal demise after general anesthesia in the very young rodent brain. Here we apply proton magnetic resonance spectroscopy (1HMRS), testing the hypothesis that neurotoxic exposure during peak synaptogenesis can be tracked via changes in neuronal metabolites. Methods 1HMRS spectra was acquired in the brain (thalamus) of neonatal rat pups 24- and 48 h after sevoflurane exposure on post-natal day (PND) 7 and 15, and in unexposed, sham controls. A repeated measure ANOVA was performed to examine if changes in metabolites were different between exposed and unexposed groups. Sevoflurane-induced neurotoxicity on PND7 was confirmed by immunohistochemistry. Results In unexposed PND7 pups (N=21), concentration of NAA ([NAA]) increased by 16% from PND8 to PND9, whereas in exposed PND7 pups (N=19), [NAA] did not change and concentration of choline compounds ([GPC+PCh]) decreased by 25%. In PND15 rats, [NAA] increased from PND16 to PND17 for both the exposed (N=14) and unexposed (N=16) groups. Two-way ANOVA for PND7 pups demonstrated changes over time observed in [NAA] (p=0.031) and [GPC+PCh] (p=0.024) were different between those two groups. Conclusions We demonstrated that normal [NAA] increase from PND8 to PND9 was impeded in sevoflurane-exposed rats when exposed at PND7; however, not impeded when exposed on PND15. Furthermore, we showed that non-invasive 1HMRS is sufficiently sensitive to detect subtle differences in developmental time trajectory of [NAA]. This is potentially clinically relevant since 1HMRS can be applied across species, and may be useful in providing evidence of neurotoxicity in the human neonatal brain.

Brain growth across childhood is a dynamic process associated with specific energy requirements. A disproportionately higher rate of glucose utilization (CMRglucose) compared with oxygen consumption (CMRO2) was documented in children's brain and suggestive of non-oxidative metabolism of glucose. Several candidate metabolic pathways may explain the CMRglucose-CMRO2 mismatch, and lactate production is considered a major contender. The ~33% excess CMRglucose equals 0.18 μmol glucose/g/min and predicts lactate release of 0.36 μmol/g/min. To validate such scenario, we measured the brain lactate concentration ([Lac]) in 65 children to determine if indeed lactate accumulates and is high enough to (1) account for the glucose consumed in excess of oxygen and (2) support a high rate of lactate efflux from the young brain. Across childhood, brain [Lac] was lower than predicted, and below the range for adult brain. In addition, we re-calculated the CMRglucose-CMRO2 mismatch itself by using updated lumped constant values. The calculated cerebral metabolic rate of lactate indicated a net influx of 0.04 μmol/g/min, or in terms of CMRglucose, of 0.02 μmol glucose/g/min. Accumulation of [Lac] and calculated efflux of lactate from brain are not consistent with the increase in non-oxidative metabolism of glucose. In addition, the value for the lumped constant for [18F]fluorodeoxyglucose has a high impact on calculated CMRglucose and use of updated values alters or eliminates the CMRglucose-CMRO2 mismatch in developing brain. We conclude that the presently-accepted notion of non-oxidative metabolism of glucose during childhood must be revisited and deserves further investigations.

Magnetic resonance (MR) imaging is generally considered a safe procedure. Contraindications include the presence of foreign objects in or on the body, which may be subject to electromagnetic fields associated with the MR system. Most of these objects are well known and are routinely screened for prior to the procedure. The authors report an unusual adverse event that appears to have been caused by a unique combination of factors involving an identification bracelet, an item not previously known to present any risks. To the authors' knowledge, this is the first report in the literature of a severe electrical thermal burn that required surgical intervention. Identification bracelets may need to be removed or padded to prevent direct contact with the patient's skin during all MR imaging examinations for patients unable to communicate, such as those requiring sedation or general anesthesia. (c) RSNA, 2010.