[1032472]
Approximately 4 million children undergo general anesthesia each year. A number of studies have demonstrated that anesthetics can cause toxicity and neuronal apoptosis in the developing brain. Recent work has suggested that children exposed to inhalation anesthetics were twice as likely to develop behavioral or developmental disorders following exposure compared to controls. Although the exact mechanisms are unknown, it is likely that neurotoxicity associated with anesthetic exposure is multifactorial. Carbon monoxide -co- is a known neurotoxin that is potentially generated within anesthesia breathing systems. Low concentration, subclinical co exposure has been shown to impair the developing brain. Formation of co occurs in the breathing circuit when inhalation volatile anesthetic agents are degraded by strong alkalai carbon dioxide absorbents. Degradation is inversely proportional to the water content of the carbon dioxide absorbent and considerable co formation has been shown when inhalation anesthetics are used with dessicated or dried absorbent. The magnitude of co generation varies amongst the different inhalation anesthetics and co production during anesthesia has been shown to be indirectly related to fresh gas flow in the breathing circuit. There are numerous studies and anecdotal case reports that have demonstrated significant co production in the anesthesia circuit related to dried absorbent resulting in clinical signs of co toxicity and elevated carboxyhemoglobin -cohb- levels. Little is known, however, about co production during routine anesthetics with fresh, hydrated absorbent. We hypothesized that children are exposed to co routinely during general anesthesia and that the level of co produced is directly related to patient minute ventilation relative to fresh gas flow. In this study, we aimed to quantify co exposure during general endotracheal anesthetics in infants and children and define the variables associated with the level of production. Immediately before each procedure, both canisters of carbon dioxide soda lime absorbent were replaced in the anesthesia machine -aestiva/5, ge healthcare, with fresh, out-of-the-package absorbent -medisorb, ge healthcare, foreign country. An electrochemical carbon monoxide sensor -range 0-2000 ppm, resolution 1 +/- 2 ppm, bacharach inc,- underwent 2-point calibration -zero [ambient air] and 25 ppm [stock gas] - and was connected to a sampling port in the expiratory limb of the breathing circuit. The device uses the electrochemical oxidation principle and draws 150 ml/min with a 40 second response time. Each patient underwent induction of anesthesia via mask with sevoflurane -up to 8% baxter healthcare corporation, 70% nitrous oxide, and 30% oxygen. After an adequate facemask seal was achieved and exhaled carbon dioxide was detected, exhaled fibaselinefl co was measured and recorded continuously for the remainder of induction. An intravenous catheter was placed and venous blood was sampled for fibaselinefl carboxyhemoglobin -cohb- measurement via 6 wavelength co-oximetry -radiometer osm3 hemoximeter, foreign counrty. Following muscle relaxation with intravenous rocuronium -0. 6 mg/kg-, patients tracheas were intubated with either a cuffed or uncuffed tracheal tube such that there was no audible airway leak at less than 30 cm h2o. Mechanical ventilation was titrated to prospectively designated standard target ranges for tidal volume -10 ml/kg- and pco2 -40 mmhg- utilizing peak inspiratory pressures less than or equal to 30 cm h2o. Fresh gas flow was fixed at 1. 5 l/min -air, 0. 21% oxygen- and anesthesia was maintained with either sevoflurane -up to 3. 6%- or desflurane -up to 6%, baxter healthcare corporation, -based on the anesthesiologist's preference-. The carbon monoxide sensor sampling port was then switched to the inspiratory limb of the breathing circuit. Each patient was continuously monitored with pulse oximetry, end tidal co2, non-invasive blood pressure, electrocardiogram, and temperature measurement. We tracked inspired co concentration -ppm-, minute ventilation, and exhaled volatile anesthetic agent concentration every 5 minutes for one hour and recorded patient age, sex, and body weight. The anesthesiologist was permitted to adjust the concentration of inhaled anesthetic and minute ventilation as clinically necessary. However, the fresh gas flow remained fixed at 1. 5 l/min. At the 1-hour time point, venous blood was again sampled for cohb measurement.
Patient Sequence No: 1, Text Type: D, B5