Anesth Analg 2006;102:750-754
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000197695.24281.df
PEDIATRIC ANESTHESIA
Upper Airway Collapsibility in Anesthetized Children
Ronald S. Litman, DO,
Joseph M. McDonough, MS,
Carole L. Marcus, MBBCh,
Alan R. Schwartz, MD, and
Denham S. Ward, MD, PhD
Department of Anesthesiology, University of Rochester, Rochester, New York; Department of Anesthesiology and Critical Care, Division of Pulmonary Medicine, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania; Johns Hopkins Hospital, Johns Hopkins University School of Medicine, Baltimore, Maryland
Address correspondence and reprint requests to Ronald S. Litman, DO, Department of Anesthesiology, The Children’s Hospital of Philadelphia, 34th Street and Civic Center Boulevard, Philadelphia, PA 19104. Address e-mail to Litmanr{at}email.chop.edu.
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Abstract
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We sought to establish the feasibility of measuring upper airway narrowing in spontaneously breathing, anesthetized children using dynamic application of negative airway pressure. A secondary aim was to compare differences in upper airway collapsibility after the administration of sevoflurane or halothane. Subjects were randomized to either drug for inhaled anesthetic induction. Each was adjusted to their 1 MAC value (0.9% for halothane and 2.5% for sevoflurane) and a blinded anesthesia provider held the facemask without performing manual airway opening maneuvers but with inclusion of an oral airway device. Inspiratory flows were measured during partial upper airway obstruction created by an adjustable negative pressure-generating vacuum motor inserted into the anesthesia circuit. Critical closing pressure of the pharynx (Pcrit) was obtained by plotting the peak inspiratory flow of the obstructed breaths against the corresponding negative pressure in the facemask and extrapolating to zero airflow using linear correlation. Fourteen children were enrolled, seven in each anesthetic group. Two children in the halothane group did not develop flow-limited airway obstruction despite negative pressures as low as –9 cm H2O. Pcrit for sevoflurane ranged from –6.7 to –11.6 (mean ± sd, –9.8 ± 1.9) cm H2O. Pcrit for halothane ranged from –8.1 to –33 (mean ± sd, –19.4 ± 9.3) cm H2O (sevoflurane versus halothane, P = 0.048). We conclude that when using dynamic application of negative airway pressure, halothane appears to cause less upper airway obstruction than sevoflurane at equipotent concentrations.
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Introduction
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Anesthetic-induced upper airway obstruction is a common and serious cause of hypoxemia. Although the prevalence of this problem is widely appreciated, little is known about the effects of inhaled anesthetics on upper airway patency in adults (1,2), and even less is known about the characteristics of upper airway patency during anesthesia in children (3–5).
The primary aim of this study was to establish the feasibility of characterizing pharyngeal collapse in children using a previously described method called dynamic application of negative airway pressure (DNAP) (6). A secondary aim was to compare differences in upper airway collapse after the administration of sevoflurane or halothane.
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Methods
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This study, which was performed at Strong Memorial Hospital (Rochester, NY) and The Children’s Hospital of Philadelphia, was approved by the respective institutions’ IRBs. Consent was obtained from parents of all participating children, and assent was obtained from children older than 7 yr, when appropriate. Healthy children, 4 to 12 yr of age, who were scheduled for elective surgery, were eligible to participate. Exclusion criteria included significant medical disease, history of obstructive sleep apnea syndrome, obesity (>90th percentile for weight), and cases in which there were contraindications to inhaled anesthesia (e.g., malignant hyperthermia susceptibility) or if the attending anesthesiologist did not feel that mask induction of general anesthesia was appropriate. In addition, in an effort to exclude children with possible airway abnormalities, children undergoing ear-nose-throat (e.g., adenotonsillectomy) procedures were not eligible for study.
After the consent process, each subject was randomized to receive halothane or sevoflurane for inhaled induction of general anesthesia. All children received premedication with oral midazolam syrup (0.5 mg/kg, maximum 15 mg) 15–30 min before induction of general anesthesia, which consisted of sevoflurane or halothane in 70% N2O. Monitoring included electrocardiography, capnography, pulse oximetry, and intermittent automated arterial blood pressure measurements. After loss of consciousness, the N2O was discontinued, an IV catheter was inserted with infusion of lactated Ringer’s solution at a weight-appropriate maintenance rate, and the inhaled anesthetic was adjusted downward to achieve a 1 MAC (minimum alveolar concentration) level using end-tidal measurements. For halothane we used 0.9% (7) and for sevoflurane we used 2.5% (8). In all subjects, a standard Guedel type oral airway device was inserted to alleviate any airway-obstructing effects of variable tonsil and adenoid size that might be present between patients. All subjects lay supine with their heads resting on a small folded blanket and their heads and necks maintained in the neutral position.
Once steady-state levels of the inhaled anesthetic were achieved (after approximately 10 min) with an Fio2 of 1.0, the vaporizers on the anesthesia machine were covered with a sheet (to mask the identity of the inhaled anesthetic) and an experienced "blinded" anesthesiologist or nurse anesthetist entered the room to manage the child’s airway during the application of negative pressure. The anesthetic analyzer monitor was partially covered to conceal the identity of the anesthetic from the person managing the airway during pharyngeal pressure measurements. The anesthesiology provider managing the airway was continuously observed and instructed to keep the child’s head and neck in a neutral position, with the mouth in the closed position around the oral airway, and without applying chin lift or jaw thrust. No attempt was made to partition oral and nasal breathing.
The critical closing pressure of the pharynx (Pcrit) was measured in each child using DNAP, a methodology we previously described in adults (6). An adjustable negative pressure-generating vacuum motor (VirtuosoTM; Respironics, Murrysville, PA) was inserted into the expiratory limb of the circle breathing circuit. A pressure transducer (Validyne, Northridge, CA) was inserted into the facemask to continuously measure and record mask pressure. A pneumotachometer (Hans Rudolph, Kansas City, MO) was connected to the facemask to continuously measure ventilatory flow. All data were stored automatically into a computerized data acquisition program (Testpoint; Keithley Instruments, Cleveland, OH).
Three approximate target values of negative pressure, –3, –6, and –9 cm H2O, were applied randomly, based on a previously generated unblinded, randomization scheme, separated by 1-min recovery periods. Each negative pressure trial was repeated once, for a total of 6 negative pressure applications per subject. The negative pressure was held for a minimum of 5 breaths and then released. If complete upper airway obstruction (i.e., no inspiratory flow) was detected during a negative pressure trial, that application of DNAP was immediately terminated. Additional prospective termination criteria included oxygen saturation below 94% at any time and any other unexpected clinical aberration (none occurred in any child). After the last application, the child resumed routine anesthetic care at the discretion of the attending anesthesiologist before beginning surgery.
Each subject’s pressure and flow curves were examined during the DNAP episodes (Fig. 1) (Microcal Origin v. 6.0, Northampton, MA). The presence of upper airway narrowing was confirmed by examining the shape of the inspiratory flow curve (i.e., plateau instead of a rounded peak) to confirm the presence of flow limitation (9). The peak flow values from the initial 3 breaths were measured (10) and plotted against their corresponding airway pressure levels (mask pressure) to generate a scatter plot that included all DNAP episodes for that subject. Pcrit was derived by extrapolating the pressure-flow curve (Microcal Origin v. 6.0, Northampton, MA) to the point of zero flow (Fig. 2) (9).
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Figure 1. Pressure and flow curves during dynamic application of negative airway pressure (DNAP). The top trace demonstrates mask pressure (Pmask), which is decreased to approximately –6 cm H2O. The bottom trace demonstrates inspiratory (downward) flattening, which indicates flow limitation (i.e., partial upper airway obstruction) during application of negative airway pressure. Note the progressive decrease in inspiratory flow from breath to breath during DNAP, indicating lack of a central activation response.
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Figure 2. Derivation of critical closing pressure of the pharynx (Pcrit) by plotting peak inspiratory flow versus mask pressure (Pmask) during dynamic application of negative airway pressure. Using linear correlation, Pcrit is the value at which peak inspiratory flow becomes equal to zero.
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Sample size analysis for the comparison between anesthetics was based on unpublished pilot data that demonstrated a mean Pcrit of –8.75 cm H2O with a standard deviation of 1.25 in similar experimental conditions. To detect a clinically meaningful difference, which we assumed to be 25% (2.2 cm H2O), we required 7 subjects per group with an 
of 0.05 and power of 0.8, using analysis of variance. Comparisons between groups were performed by using Student’s t-tests for analysis of continuous, normally distributed data, and the Mann-Whitney U-test for comparison of the Pcrit values, in which the variances of the groups were dissimilar.
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Results
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Fourteen children were enrolled, seven in each anesthetic group. Two children who received halothane did not develop flow-limited airway obstruction at DNAP levels as low as –9 cm H2O, indicating that upper airway narrowing leading to a decrease in flow did not occur, and thus, in these children, we were unable to measure Pcrit. In the remaining children who underwent data analysis, Pcrit for sevoflurane ranged from –6.7 to –11.6 (mean ± sd = –9.8 ± 1.9) cm H2O; Pcrit for halothane ranged from –8.1 to –33 (mean ± sd = –19.4 ± 9.3) cm H2O (sevoflurane versus halothane, P = 0.048) (Table 1, Fig. 3). There were no adverse or other unexpected events during the conduct of the negative pressure measurements.
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Figure 3. Box plots of the critical closing pressure of the pharynx (Pcrit) values obtained for halothane and sevoflurane. The limits of the boxes indicate the 25th and 75th percentiles. The whiskers indicate the lowest and highest values, and the small boxes indicate the mean of each group. Pmask, mask pressure. *P = 0.048 difference between groups.
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Discussion
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In the present study, we established the feasibility of measuring Pcrit in spontaneously breathing anesthetized children. Two children studied did not demonstrate upper airway obstruction (determined by lack of inspiratory flow limitation) at negative airway pressures as low as –9 cm H2O. Based on our results from sedated adults (6), we limited the most negative pressure to this modest level to prevent the possibility of complete upper airway obstruction at more negative pressure levels. Subsequent investigations using this methodology may require the use of more negative pressures to improve measurement precision.
The second aim of this study was to compare upper airway collapse during equipotent levels of halothane and sevoflurane. The Pcrit of children anesthetized with halothane was lower than that for children anesthetized with sevoflurane, implying that at approximately equipotent concentrations, halothane causes less depression of pharyngeal dilator muscle activity. This may translate clinically into a more patent upper airway during spontaneous ventilation. Our results are consistent with previous investigations of the respiratory effects of halothane and sevoflurane in children, which demonstrated that sevoflurane is a more potent respiratory depressant (11). On examination of the box plots, it appears that the range of Pcrit values obtained for halothane was larger than for sevoflurane. The cause for this larger range for halothane is not readily apparent. One possible explanation is that if halothane has less airway-collapsing properties than sevoflurane, it is possible then that Pcrit may be more dependent on patient factors such as gender and ethnicity.
There are several possible limitations inherent in the methodology of this study. The most important is the use of the oral airway device in all studied children. We included this in our protocol to negate the effects of the inherently variable size of tonsils and adenoids among patients. Although we purposely excluded children with a known diagnosis of sleep apnea, our clinical experience has shown that it is impossible to predict tonsil or adenoid size from patient to patient, and thus we chose to bypass this area of the upper airway to improve the internal validity of the study. This comes at the expense of external validity. Thus, we cannot make comparisons between our pharyngeal collapsibility pressures and that for other populations who were either not anesthetized, or in whom an oral airway device was not used. Furthermore, it limits airway collapsibility to the portion of the oropharynx caudad to the oral airway device. This distal portion of the upper airway has been implicated in the pathophysiology of propofol-induced obstruction in children (3,12).
Another limitation is the use of MAC as a determinant of equivalency between halothane and sevoflurane. MAC is an approximate value indicating potency of an anesthetic, primarily at the level of the spinal cord. Currently, we do not have an accurate indicator of equivalent anesthetic potency. The bispectral index (BIS) shows promise as a more precise pharmacodynamic measure, but its usefulness has not been validated in children (13) and pediatric studies demonstrate a wide range of BIS values at a given level of sedation (14) and possible differences in BIS response between anesthetics (15).
A third possible limitation is contained within the experimental protocol of the study. Before each DNAP application, subjects breathed at approximately atmospheric pressure. Previous investigators have determined that application of continuous positive airway pressure "shuts off" efferent input to the pharyngeal dilator muscles (16), thus negating differences in central output between measurements. In the present study, continuous positive airway pressure was not used before DNAP; however, we believe the likelihood of varying states of central output during the time frame of the measurements to be low and unlikely to influence accuracy of the measurements.
In summary, we have demonstrated the feasibility of using DNAP to measure pharyngeal collapsibility in anesthetized children. We also demonstrated that halothane causes relatively less upper airway obstruction than sevoflurane, at equipotent concentrations, in the portion of the upper airway distal to the oral airway device. DNAP is a promising method for characterizing upper airway collapse in anesthetized children for the future determination of patient- and anesthetic-related factors that impair upper airway patency.
The authors wish to acknowledge the expert technical assistance of Linda Palmer, R.N. William Voter (Strong Memorial Hospital, Rochester, NY) and Rosetta Chiavacci, B.S.N. (The Children’s Hospital of Philadelphia).
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Footnotes
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Accepted for publication October 25, 2005.
Supported by the individual departmental internal funding mechanisms of the Department of Anesthesiology, University of Rochester, and the Department of Anesthesiology and Critical Care, The Children’s Hospital of Philadelphia.
Presented, in part, at the annual meeting of the Association of University Anesthesiologists, Milwaukee, Wisconsin, May 2003.
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References
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Abstract
Introduction
