Guidelines for the pediatric perioperative anesthesia environment. American Academy of Pediatrics. Section on Anesthesiology.

The American Academy of Pediatrics proposes the following guidelines for the pediatric perioperative anesthesia environment. Essential components are identified that make the perioperative environment satisfactory for the anesthesia care of infants and children. Such an environment promotes the safety and wellbeing of infants and children by reducing the risk for adverse events.

Exposure of postoperative nurses to exhaled anesthetic gases.

UNLABELLED: The National Institute of Occupational Safety and Health (NIOSH) has established recommended exposure limits of 25 parts per million (ppm) as a time-weighted average for nitrous oxide and a ceiling of 2 ppm for volatile anesthetics. We quantified exposure of postanesthetic nurses to exhaled anesthetic gases. This study was conducted in the postanesthesia care unit (PACU) of a medium-sized hospital. PACU air exchanges averaged 8 vol/h; however, much of this air was recirculated. We evaluated 50 adults anesthetized with either isoflurane (n = 19) or desflurane (n = 31). Roughly half the patients were tracheally extubated in the operating room, whereas the others were extubated just after admission to the PACU. Exhaled anesthetic gases were sampled through a 20-m hose attached to the participating nurses' shoulders (breathing zone). We also evaluated nursing exposure to exhaled anesthetic gases during recovery of 15 patients who had been anesthetized with nitrous oxide. Exposure was quantified with lapel dosimeters. Anesthetic and recovery durations were each approximately 1 h, with most patients being tracheally extubated in the PACU. Breathing-zone anesthetic concentrations in the patients given isoflurane exceeded NIOSH recommendations in 37% of the patients, representing 12% of recovery time. Breathing-zone anesthetic concentrations in the patients given desflurane, however, exceeded NIOSH limits in 87% of the patients, representing 49% of recovery time. Altogether, noncompliant episodes were detected in 68% of these patients, representing 35% of the entire recovery duration. Breathing-zone anesthetic concentrations in the patients given nitrous oxide exceeded NIOSH limits in 53% of the patients. Our data suggest that postoperative nurses' exposure to exhaled anesthetic gases exceeds NIOSH limits under some circumstances. IMPLICATIONS: Some epidemiological evidence suggests that exposure to waste anesthetic gases may be associated with reproductive toxicity. Accordingly, the National Institute of Occupational Safety and Health has established recommended exposure limits for nitrous oxide and volatile anesthetics. Our data suggest that exposure of healthcare personnel may exceed recommended levels in poorly ventilated postanesthesia care units.

A clinical evaluation of an operational postanesthesia care unit source control system.

Various air safety hazards in the PACU and a number of attempts to cope with the hazards have been addressed (see J Peri Anesth Nurs 11:207, 1996). This article presents a clinical evaluation of an operational source control system developed specifically for use in the PACU. The criterion for evaluation was the degree to which the source control system could reduce the concentration of waste anesthetic gases released into the environment by the patient. The N2O molecule is a thousand times smaller than droplet nuclei that carry infectious respiratory disease. Thus, containment of waste gases may also indicate containment of pathogens. Twenty-two postsurgical patients were studied. The control group was given routine care with supplemental oxygen by nasal prong. The experimental group was given supplemental oxygen and had exhalent scavenged via the source-control system. Waste gas concentrations were monitored, and a criterion was applied to the data to determine the effectiveness of the source control group when compared to nasal prong group. The nasal prong group exceeded the compliance criterion 58% of the time. The source control group exceeded the compliance criterion at no time during the study. From these results, the source control system is effective at reducing concentrations of waste anesthetic gases allowed into the atmosphere of a room. Application of the source control to the PACU environment could prove valuable in addressing air safety hazards.

An evaluation of air safety source-control technology for the post anesthesia care unit.

A new source-control system designed specifically to address the most important air safety hazards in the post anesthesia care unit (PACU) is presented--the transmission of bloodborne and respiratory pathogens, and occupational exposure to waste anesthetic gases. The controversy arising from research in the 1970s, 1980s, and 1990s regarding waste anesthetic gases, government regulations that responded to air safety hazards, and the resulting de facto use of scavenging systems in almost all operating rooms across the United States is discussed. However, a similar concern does not apply to the PACU although its unique characteristics make it an especially high-risk environment for air safety hazards.

The post anesthesia care unit: unique contribution, unique risk.

The environment in the postanesthesia care unit (PACU) is unique in the modern hospital. It was born of necessity and continues of necessity. The modern PACU has evolved from a simple room designed to house a single patient and a nurse to a modern, bustling room of great proportions. Today's PACU is an open ward, probably the only one left in the modern hospital, and contains many immunocompromised patients, including pediatric patients; knowledge of the patient's medical history may be sketchy or brief. Patients undergo cough-inducing procedures and exhale waste anesthesia gases. The PACU has a high ratio of health care workers (HCWs) to patients. HCWs, often in their childbearing years, function in close proximity to the patient's face. These environmental conditions coupled with the epidemic proportions of tuberculosis in the United States, the increase in incidence of hepatitis C virus, the consequences of human immunodeficiency virus, and the possible adverse effects of waste anesthesia gases result in a milieu that is a risk to both patients and HCWs that cannot be managed with air exchange controls alone. This article reviews the historical contribution of the PACU and the factors in the PACU environment that increase the vulnerability of HCWs and patients to respiratory diseases, bloodborne pathogens, and adverse effects of waste anesthetic gases.

The postanesthesia care unit: a high-risk environment for bloodborne and infectious respiratory pathogens.

The PACU is a high-risk environment for exposure to infectious diseases. A confluence of risk factors unique to the PACU increases the probability for exposure of personnel to both bloodborne and airborne pathogens. These risk factors include frequent coughing in the PACU, blood-contaminated saliva in the PACU, air mixing maximized in the PACU, high patient census and rapid patient turnover, inadequate patient histories, and the proximity of the postanesthesia nurse to the patient's face. Both the Occupational Safety and Health Administration and the Centers for Disease Control have issued recommended procedures for limiting occupational exposure of personnel to these hazards.

Bupivacaine toxicity in lightly anesthetized pigs with respiratory imbalances plus or minus halothane.

BACKGROUND AND OBJECTIVES: Changes in acid base balance within the body, oxygen delivery to tissue, and carbon dioxide elimination, as well as general anesthetics, influence the toxicity of local anesthetics. The objective of this study was to test the hypothesis that light halothane anesthesia, hypercapnia, and hypoxia act together to alter the central nervous system and cardiovascular toxicity of bupivacaine. METHODS: Three groups of 2-week-old pigs were lightly anesthetized with N2O in O2 and paralyzed with pancuronium. One group (n = 6) was made hypercapnic (group A; PaCO2 > or = 60 mg Hg), another group (n = 6) was made hypercapnic and hypoxic (group B; F1O2 = 0.1, PaCO2 = 66.8 +/- 9.91 mm Hg, PaO2 = 29.2 +/- 3.53 mm Hg), and another group (group C; n = 5) was made hypercapnic and hypoxic and given 0.5% halothane (PaCO2 = 68.54 +/- 4.18, PaO2 = 31.06 +/- 1.96). Bupivacaine was infused intravenously at 1 mg.kg-1.min-1 until the animals developed cardiac asystole. RESULTS: Arrhythmias, seizures, isoelectric electroencephalogram (isoEEG), and asystole were readily identified in groups A and B. None of the animals given halothane had seizures, but they did exhibit the other three toxic endpoints. The doses of bupivacaine producing asystole were significantly less in group C than in group A (7.9 +/- 1.8 versus 17.7 +/- 2.2 mg.kg-1). The doses of bupivacaine that produced isoEEG were significantly lower in groups B and C than in group A (8.9 +/- 6.2, 5.0 +/- 1.1, 14.6 +/- 3.2 mg/kg, respectively). Doses of bupivacaine producing all toxic endpoints except seizures were lower in group B animals than in group A, but only the isoEEG doses were statistically different (arrhythmias 2.3 +/- 1.1 versus 3.7 +/- 1.1; isoEEG 8.9 +/- 6.2 versus 14.6 +/- 3.2; asystole 12.1 +/- 7.5 versus 17.7 +/- 2.2 mg.kg-1). No differences in seizure pattern or type of arrhythmia were detected. Mean arterial pressure decreased during bupivacaine infusion, the rate of decrease was fastest (P < .05) in the animals receiving halothane and slowest in the hypercapnic animals. Mean arterial pressure in group A increased significantly compared to control (to 135.5 +/- 14.4% of control; P < .01) before decreasing. Heart rate decreased and the differences over time among groups differed significantly. CONCLUSIONS: Bupivacaine is significantly more lethal, as judged by the doses producing asystole, in young pigs that are hypercapnic, hypoxic, and receiving halothane than in young pigs that are hypercapnic.

Anesthesia and analgesia for minor injuries to children.

Today's children are rambunctious, playful, and aggressive and are provided through the miracles of modern technology with ample opportunities to injure themselves. As such, they are a source of both joy and terror to their parents. It is a "given" that many of them will injure themselves in the course of growing up. When they come to us in the ED waiting room, they are typically very frightened and usually in pain. We are fortunate that we have techniques and drugs to alleviate this pain and to attenuate their fear. It is our responsibility as anesthesiologists to ensure that these drugs and techniques are used appropriately and cause no further harm. We hope the information contained in this chapter may be of benefit in achieving this goal.

Respiratory frequency and artifact affect the capnographic baseline in infants.

We sought to determine the effect of rebreathing on the capnographic waveform baseline. In anesthetized infants, we studied the effect of respiratory frequency (f) and breathing circuit type (Bain, n = 6, and pediatric circle, n = 4) on capnography of respiratory gas aspirated from the circuit for mass spectrometry (PCO2asp) and flowing through an infrared analyzer (PCO2f-t). As f increased, measured values of PiCO2asp and PiCO2f-t increased in both Bain and circle groups, with the exception of PiCO2f-t values that remained zero in the circle group. PETCO2 decreased as f increased in the circle groups, but remained constant in the Bain groups. These data suggest that artifact, most likely due to parabolic distortion of CO2 plugs traversing long sampling catheters, makes up a significant percentage (8%-36%) of the aspiration capnographic baseline elevation depending on f and breathing circuit type. Despite increases in PiCO2 as f increased, PETCO2 does not increase in Bain circuits due primarily to an increase in minute ventilation (Ve) that offsets the increase in the PiCO2 to provide balance in the CO2 mass relationship (PETCO2 approximately VCO2/Ve+PiCO2). These findings are useful in the correct interpretation of elevated capnographic baseline in infants.

Severe hypoxia enhances central nervous system and cardiovascular toxicity of bupivacaine in lightly anesthetized pigs.

Toxic systemic reactions to bupivacaine usually involve a number of factors, including hypoxia and acidosis. The objective of this study was to test the hypothesis that cardiovascular and central nervous system responses to bupivacaine overdose are proportional to the severity of hypoxia. The central nervous system and cardiovascular toxicity of bupivacaine was examined in three groups of pigs breathing 30%, 15%, or 10% O2, 70% N2O, and He (FIO2 = 0.15 and 0.1 groups). The 18 2-week-old pigs (6 animals per treatment) were paralyzed with pancuronium and their lungs ventilated mechanically. During the intravenous infusion of bupivacaine 2 mg.kg-1.min-1, four readily identified toxic endpoints (seizures, arrhythmias, isoelectric electroencephalogram, asystole) were observed in all animals, with the exception that 1 pig in the FIO2 = 0.3 group and 1 in the FIO2 = 0.15 group had no arrhythmias. Bupivacaine doses producing seizures, isoelectric EEG, and asystole were significantly less in the FIO2 = 0.1 groups as compared to the other groups. Arrhythmias occurred before seizures in all animals in the FIO2 = 0.1 group but in only 1 of 5 and 2 of 5 animals in the FIO2 = 0.15 and 0.3 groups, respectively. There was no significant difference between the arrhythmic dose of bupivacaine in the FIO2 = 0.3 versus 0.1 animals (8.4 +/- 2.4 vs. 4.0 +/- 1.4 mg.kg-1), but the dose was significantly less in the FIO2 = 0.1 animals than in the FIO2 = 0.15 animals (12.5 +/- 5.6 mg.kg-1). Arterial pH was stable in all three groups during bupivacaine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory gas monitoring in the pediatric patient.

Parents of soon-to-be-anesthetized children frequently express concern about their child's safety because they have heard that "anesthesia is the most dangerous part of the operation." Although I don't believe that statement was ever true, it is even less true today. With the development of reliable capnography and volatile agent measurement in infants and children, we have significantly reduced the risks associated with anesthesia. I think we can, and should, confidently reassure parents that the "anesthesia part of the operation" has been made much safer and that the child's breathing (as well as heart beat, temperature, oxygenation, etc.) will be vigilantly monitored by the anesthesiologist using both human senses and the latest in monitoring equipment.

End-tidal carbon dioxide pressure in neonates and infants measured by aspiration and flow-through capnography.

In 25 anesthetized, intubated, artificially ventilated, and paralyzed healthy neonates and infants, end-tidal PCO2 (PETCO2) measured by remote multiplexed mass spectrometry was 1.86 +/- 1.58 mm Hg lower than arterial PCO2 (PaCO2). PETCO2 measured by a flow-through cuvette was 1.02 +/- 1.64 mm Hg lower than PaCO2. The difference between the two methods of capnography was not significant. Values for PETCO2 obtained by mass spectrometry changed -0.43 +/- 1.43 mm Hg from baseline after 15 minutes of aspiration at a sample flow rate of 240 ml/min. Values for PETCO2 obtained with flow-through capnography changed -0.17 +/- 2.17 mm Hg from baseline after 15 minutes. In both methods, the changes from baseline in PETCO2 over time were not significant. These results suggest that both methods of capnography studied are reliable and may be used safely in neonates despite high sample flow rates and added apparatus dead space (0.6 ml for tracheal tubes less than or equal to 4.0 mm OD and 4.9 ml for tracheal tubes greater than 4.0 mm OD).

A rodent model for studying four well defined toxic endpoints during bupivacaine infusion.

An animal model with four well defined endpoints for studying the cardiotoxicity and neurotoxicity of bupivacaine is described. Five male Wistar rats (264-324 g) were anesthetized, tracheostomized and ventilated, and ECG and EEG leads were placed. Femoral arteries and veins were then cannulated. Twenty minutes before bupivacaine infusion, 0.1 mg/kg pancuronium was given intravenously, and anesthesia was adjusted to halothane 0.5%, 30% O2 and 70% N2O. Bupivacaine infusion was then begun at 2 mg/kg/minute. Bupivacaine doses producing the following endpoints were then determined: (1) first ventricular arrhythmia (ARR), (2) seizures (SZ), (3) isoelectric EEG (ISO EEG), and (4) asystole (ASYS). The doses of bupivacaine (in mg/kg +/- SD) precipitating AAR, SZ, ISO EEG and ASYS were 4.22 +/- 1.87, 7.08 +/- 1.55, 11.05 +/- 5.15 and 20.4 +/- 6.49 mg/kg, respectively. These endpoints were present and readily determined in all animals. The doses of bupivacaine producing ARR and SZ were not significantly different (p greater than 0.05). The doses producing SZ, ISO EEG and ASYS were significantly different from each other (p greater than 0.05, ANOVA and the Duncan test). These results indicate that it is possible to study, in the anesthetized and paralyzed rat that is intensely monitored, many of the variables associated with local anesthetic toxicity currently of clinical interest. The use of a constant local anesthetic infusion allows ready observation of the progression of toxic signs.

Cardiovascular and central nervous system effects of co-administered lidocaine and bupivacaine in piglets.

The toxic profile of bupivacaine (1 mg/kg/minute) when administered intravenously alone or with lidocaine (1 mg/kg loading dose, then 1 mg/kg/minute) was examined in 12 2-day-old pigs anesthetized with 70% N2O/30% O2 and paralyzed with 0.15 mg/kg pancuronium. Bupivacaine doses producing arrhythmias, seizures, isoelectric EEG and asystole were about 24% lower in the lidocaine plus bupivacaine group (n = 6) than in the bupivacaine group (n = 6). However, the incidence of cardiac arrhythmias in the combination local anesthetic group (3/6) was half that in the bupivacaine group (6/6). Administration of lidocaine with bupivacaine under conditions of this study apparently reduces the risk of cardiac arrhythmias and acts along with bupivacaine to produce seizures, cerebral depression (isoelectric EEG) and asystole.

Bupivacaine toxicity in young pigs is age-dependent and is affected by volatile anesthetics.

The influence of age and volatile anesthetic agents on plasma concentrations and toxic effects of bupivacaine were studied in 2-day-old, 2-week-old, and 2-month-old pigs. Bupivacaine was infused at a constant rate while the pigs' ECGs and EEGs were recorded. Six pigs in each age group were lightly anesthetized with 70% N2O/30% O2 during the bupivacaine infusion, and twelve 2-day-old pigs were anesthetized with 70% N2O/30% O2 plus either 0.5 X MAC halothane or isoflurane. Two-day-old pigs were more resistant than older pigs to the toxic effects of bupivacaine despite higher plasma concentrations at all sample times. All pigs given N2O alone or N2O plus halothane had ventricular dysrhythmias, but only one pig in the N2O plus isoflurane group had a ventricular dysrhythmia. Threshold doses of bupivacaine for dysrhythmias in the N2O alone and N2O plus halothane groups did not differ. Seizures occurred in all pigs in the N2O alone group, in none of the N2O plus halothane group, and in two of the N2O plus isoflurane group. The doses required to depress cardiac index and cause asystole were less in the groups receiving halothane and isoflurane. It was concluded that N2O plus halothane and N2O plus isoflurane increase the lethality of bupivacaine while preventing early warning signs of toxicity.

Accuracy of end-tidal PCO2 measurements using a sidestream capnometer in infants and children ventilated with the Sechrist infant ventilator.

To determine the accuracy of end-tidal PCO2 (PETCO2) measurements analyzed with a sidestream capnometer in infants and children whose lungs were ventilated with a Sechrist infant ventilator and an Ayre's t-piece, we compared PETCO2 measurements obtained from the proximal (PETCO2-p) and distal (PETCO2-d) ends of the tracheal tube to arterial PCO2 (PaCO2) in 37 healthy infants and children between 1.3 and 24.5 kg. Both PETCO2-p and PETCO2-d accurately approximated PaCO2, however, the mean (+/- SD) arterial to end-tidal PCO2 difference (delta(a-ET)PCO2) was significantly greater with proximal (1.27 +/- 1.54 mmHg) than with distal sampling (0.64 +/- 1.64 mmHg) (P less than 0.01). In the subgroup of patients who weighted less than 12 kg, the delta(a-ET)PCO2 using proximal gas sampling (1.94 +/- 1.29 mmHg) was also significantly greater than it was using distal sampling (0.74 +/- 1.31 mmHg) (P less than 0.001). We conclude that although statistically different, both proximal and distal estimates of PETCO2 provide acceptable estimates of PaCO2 in healthy infants and children who are ventilated with a Sechrist infant ventilator and an Ayre's t-piece system.

Alveolar dead space does not affect indirect Fick cardiac output determinations.

We examined the influence of three variables (different breathing circuits, breath selected for analysis, and alveolar dead space ventilation) on the accuracy of noninvasive cardiac output determinations with the Fick CO2 (indirect) equation. We compared noninvasive determinations with invasive thermodilution measurements over a wide range of cardiac outputs in 17 2-mo-old pigs anesthetized with halothane and nitrous oxide and paralyzed with either pancuronium or d-tubocurare. We found that rebreathing and nonrebreathing circuits provide accurate cardiac output determinations and that the optimal breath for analysis with either the rebreathing or nonrebreathing technique appears to depend on the cardiac output. When alveolar dead space was increased by using positional changes and the intracardiac administration of glass beads, there was still a good correlation between noninvasive and invasive cardiac output determinations. We conclude that both rebreathing and nonrebreathing techniques of indirect Fick cardiac output determinations correlate well with thermodilution measures over a wide range of cardiac outputs and alveolar dead space/tidal volume fractions.

Thiopental attenuates dysrhythmias in children: comparison of induction regimens.

Anesthesia was induced in 91 children using one of three induction regimens: (a) thiopental, atropine, and succinylcholine (T group); (b) halothane, atropine, and succinylcholine (H group); and (c) halothane, thiopental, atropine, and succinylcholine (H/T group). The incidence of dysrhythmias was significantly greater in the H group (85%) than in the T group (6%) and H/T group (20%). Fewer dysrhythmias occurred in the H/T group compared to the H group despite similarly prolonged QTc intervals in both groups. We conclude that induction of anesthesia with thiopental is appropriate and reduces the incidence of cardiac rhythm disturbances in children and that administration of thiopental to children during induction of anesthesia with halothane, atropine, and succinylcholine may reduce the incidence of cardiac dysrhythmias.