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Anesth Analg 2006;102:937-942
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000195233.80166.14

GENERAL ARTICLES

Postoperative Upper Airway Obstruction After Recovery of the Train of Four Ratio of the Adductor Pollicis Muscle from Neuromuscular Blockade

Matthias Eikermann, MD*, Manfred Blobner, MD{dagger}, Harald Groeben, MD*, Christopher Rex, MD{ddagger}, Thomas Grote*, Markus Neuhäuser, PhD§, Martin Beiderlinden, MD*, and Jürgen Peters, MD*

*Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen; {dagger}Klinik für Anästhesiologie, Technische Universität München; {ddagger}Klinik für Anästhesiologie und Operative Intensivmedizin, Kreiskliniken Reutlingen; and §Institut für Medizinische Informatik, Biometrie und Epidemiologie, Germany

Address correspondence and reprint requests to Matthias Eikermann, MD, Visiting Assistant Professor of Medicine, Division of Sleep Medicine, Sleep Disorders Program, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115. Address e-mail to meikermann{at}rics.bwh.harvard.edu.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Anesthetics, and even minimal residual neuromuscular blockade, may lead to upper airway obstruction (UAO). In this study we assessed by spirometry in patients with a train-of-four (TOF) ratio >0.9 the incidence of UAO (i.e., the ratio of maximal expiratory flow and maximal inspiratory flow at 50% of vital capacity [MEF50/MIF50] >1) and determined if UAO is induced by neuromuscular blockade (defined by a forced vital capacity [FVC] fade, i.e., a decrease in values of FVC from the first to the second consecutive spirometric maneuver of ≥10%). Patients received propofol and opioids for anesthesia. Spirometry was performed by a series of 3 repetitive spirometric maneuvers: the first before induction (under midazolam premedication), the second after tracheal extubation (TOF ratio: 0.9 or more), and the third 30 min later. Immediately after tracheal extubation and 30 min later, 48 and 6 of 130 patients, respectively, were not able to perform spirometry appropriately because of sedation. The incidence of UAO increased significantly (P < 0.01) from 82 of 130 patients (63%) at preinduction baseline to 70 of 82 patients (85%) after extubation, and subsequently decreased within 30 min to values observed at baseline (80 of 124 patients, 65%). The mean maximal expiratory flow and maximal inspiratory flow at 50% of vital capacity ratio after tracheal extubation was significantly increased from baseline (by 20%; 1.39 ± 1.01 versus 1.73 ± 1.02; P < 0.01), and subsequently decreased significantly to values observed at baseline (1.49 ± 0.93). A statistically significant FVC fade was not present, and a FVC fade of ≥10% was observed in only 2 patients after extubation. Thus, recovery of the TOF ratio to 0.9 predicts with high probability an absence of neuromuscular blocking drug-induced UAO, but outliers, i.e., persistent effects of neuromuscular blockade on upper airway integrity despite recovery of the TOF ratio, may still occur.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Upper airway obstruction (UAO) is a common cause of postoperative hypoxemia (1–4) and can be induced by a variety of drugs administered during general anesthesia (5–9), including neuromuscular blocking drugs (NBDs) (5,9). To detect the residual effects of NBDs on upper airway function, neuromuscular monitoring is recommended (5,10,11), and a recovery of the train-of-four (TOF) ratio of adductor pollicis muscle to 0.9–1.0 generally avoids the residual effects of NBD (5,11–13). However, there is evidence that upper airway dysfunction, i.e., misdirected swallowing (11) and partial UAO (5), may occur even with recovery of the TOF ratio to 0.9 in some individuals (5,11). This supports the view that pharyngeal muscles are susceptible to NBD (9,14,15) and implies that the effects of partial paralysis on upper airway integrity cannot be completely excluded from TOF ratio readings. Thus, it may be useful to consider additional methods to detect the effects of minimal neuromuscular blockade on upper airway integrity.

Several arguments suggest that spirometry may be a viable method for that purpose. First, UAO can be detected by spirometry, and a ratio of maximal expiratory flow and maximal inspiratory flow at 50% of vital capacity (MEF50/MIF50 ratio) of more than unity is an established measure of UAO (5,16,17). Second, there is evidence that spirometry can also be used to detect the respiratory effects of partial neuromuscular blockade (18). In fact, we recently found that a fade of forced vital capacity (FVC), i.e., a decrease in values of FVC by ≥10% with the second spirometric maneuver compared to the first, indicates respiratory effects of partial paralysis (18). Although we did not observe a FVC fade at baseline or with recovery of the TOF ratio to unity in that study, FVC fade was always observed at a TOF ratio of 0.5 and was still present during recovery of the TOF ratio until 0.9. Thus, a FVC fade observed during recovery from NBD is unlikely to be a random effect but can be used as an additional method of monitoring the respiratory effects of residual paralysis (18).

Accordingly, the aim of this study was to determine both the incidence of UAO (MEF50/MIF50 ratio >1) (5,16,17) induced by neuromuscular blockade (FVC fade) (15) and by other factors (no FVC fade) in patients with TOF ratio >0.9.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After approval by the local ethics committee and written informed patient consent, 142 healthy male patients (aged 55 ± 14 yr, mean± sd) of normal weight (72 ± 12 kg) scheduled for elective major abdominal surgery (assuming duration >100 min and 3 NBD doses required to achieve surgical relaxation) were enrolled. Patients with a history of neuromuscular, cardiovascular, pulmonary, renal, hepatic, or neurological disorders were excluded. Twelve of 142 patients were secondarily excluded because the duration of surgery was shorter than expected (i.e., <100 min, n = 8) or because their core temperature at the time of scheduled tracheal extubation was less than 35.5°C (n = 4).

Respiratory function and patients' ability to swallow normally were assessed before induction (more than 30 min after midazolam administration, i.e., preinduction baseline), after tracheal extubation (TOF ratio: 0.9 or more), and 30 min later (recovery room) with the patient's upper body raised (30°) and knees flexed (20°–30°). MEF50/MIF50, FVC, peak expiratory flows, and peak inspiratory flows were measured using spirometry (EasyOne® Spirometer; ndd-Medizintechnik, Zürich, Switzerland) (19) in an air-conditioned room at constant humidity and temperature by a series of 3 repetitive maneuvers. Because subject cooperation is essential to achieve valid spirometric measurements (20), we trained the patients to perform spirometric tests before assessment of baseline values. Furthermore, they were coached throughout each maneuver verbally and via body language so as to maximize their effort.

FVC fade, used to reveal residual blockade, was defined as a decrease in values of FVC from the first to second consecutive spirometric maneuver performed 60 s apart by 10% or more, reflecting impaired neuromuscular transmission (18). The time interval to identify FVC fade from the beginning of the first to the beginning of the second spirometric maneuver was 60 s. Patients were assisted by an investigator to seal the mouthpiece. If a patient, previously trained in performing spirometric measurements, did not perform the maneuver adequately or was unable to seal the mouthpiece, despite being assisted by an investigator, this particular series of measurements was excluded (18).

Postoperatively we assessed patients' ability to swallow normally by asking them to swallow and to indicate whether swallowing was impaired (5). The effects of NBD on peripheral skeletal muscle were measured by accelerometry (TOF-Watch©-SX Monitor; Organon Teknika, Eppelheim, Germany). Every 15 s this device measured, in each volunteer, the acceleration of a transducer taped to the thumb in response to supramaximal TOF ulnar nerve stimulation (2 Hz) (12).

For safety, we also continuously monitored heart rate (electrocardiograph), arterial oxygen saturation (pulse oximetry), and end-expiratory carbon dioxide concentration.

At least 30 min before being transported to the operating room (OR) patients received small doses of midazolam (3.75–7.5 mg per os (21,22). After positioning on the operating table with the upper body raised (30°) and knees flexed (20°–30°) baseline spirometric measurements were performed. Propofol (1.5–2.5 mg/kg) and fentanyl (4–8 µg/kg) were given for induction, and anesthesia was maintained with propofol (5–10 mg/kg) and remifentanil (up to 30 µg/kg). An intubating dose of cisatracurium (0.1 mg/kg) or rocuronium (0.6 mg/kg) was subsequently administered. NBD doses of 0.025 mg/kg (cisatracurium) and 0.15 mg/kg (rocuronium), respectively, were given as soon as T1 (first twitch in TOF) amplitude had recovered to 20% of baseline, until closure of the abdominal wall muscle fascia.

At the end of surgery neuromuscular blockade was not reversed but spontaneous recovery was allowed until the TOF ratio reached 0.9 in all patients. Tracheal extubation was performed if the following criteria were met: recovery of the TOF ratio to 0.9 or more, recovery of consciousness (eye opening on demand), adequate spontaneous ventilation, and a core temperature of 35.5° or more. Subsequently, we tested respiratory function within 5 min after tracheal extubation in the OR and again 30 min later in the recovery room. For postoperative analgesia, patients received piritramid before tracheal extubation and repeated doses of piritramid up to 7.5 mg between the second and third series of spirometry, if required.

Data are expressed as mean ± sd. We tested the hypotheses that after major abdominal surgery UAO (MEF50/MIF50 ratio >1) would develop despite the recovery of TOF to 0.9 or more (primary criterion) and that patients with UAO would show a clinically significant FVC fade (10% or more) 5 and 30 min after surgery (secondary end-point). Using a hierarchical sequence, the 2 main criteria could be tested with an {alpha}-error of 5% without adjustment for multiple testing (23). A power analysis based on data reported previously (5,18) revealed that a sample size of 80 patients would be sufficient to detect a FVC fade in patients with UAO. In particular, based on published data (5), we expected an incidence of postoperative UAO of 50% and calculated that a number of 80 patients would provide a power of 99% (type 1 error [{alpha}] = 0.05) to detect UAO (MEF50/MIF50 ratio >1) postoperatively. With respect to the secondary criterion (FVC fade) we considered a difference to be detected of 10% between the first and the second FVC maneuver and a between-patient variation ({sigma} (2) of the differences of 15% (18). From these data we calculated that 40 patients with UAO would provide a sufficient power to detect a clinically significant FVC fade (power: 0.8, {alpha} = 0.05).

We also calculated with an exploratory intention the negative predictive value of the TOF ratio of 0.9 for NBD-induced UAO. Values derived from spirometry were not used for analysis if patients were not able to appropriately perform (18) a series of 3 spirometric measurements within 5 min after a scheduled measurement. Wilcoxon's test and McNemar's test were used, as appropriate. SPSS version 10.0 (SPSS Inc., Chicago, IL) was used for statistical analysis.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
At baseline all 130 patients were able to appropriately perform spirometric measurements. Immediately after tracheal extubation and 30 min later, 48 and 6 of 130 patients, respectively, were not able to appropriately perform spirometry because of sedation, but all patients indicated adequately, at all measurement points, whether or not the ability to swallow normally was impaired.

The incidence of UAO (MEF50/MIF50 ratio >1) increased significantly (P < 0.01) from 82 of 130 patients (63%) at preinduction baseline to 70 of 82 patients (85%) after tracheal extubation and subsequently decreased within 30 min to values observed at preinduction baseline (80 of 124 patients, 65%). The mean MEF50/MIF50 ratio after tracheal extubation was significantly increased from preinduction baseline by 20% (1.73 ± 1.02 versus 1.39 ± 1.01; P < 0.01), and subsequently decreased significantly to values that did not differ significantly from preinduction baseline values (1.49 ± 0.93), as depicted in Figure 1.


Figure 146
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  		Figure 1. Upper airway function (maximal expiratory flow (MEF50)/maximal inspiratory flow (MIF50), and pulmonary function [forced vital capacity (FVC), peak inspiratory (PIF) and expiratory (PEF) flow], before induction of anesthesia, after tracheal extubation, and 30 min later. Mean ± sd from 130, 82, and 124 patients who were able to appropriately perform spirometry at baseline, postoperatively, and 30 min later, respectively. MIF50/MIF50 ratio increased significantly after tracheal extubation but within 30 min significantly recovered to preinduction values. All variables of pulmonary function decreased significantly after extubation, were improved significantly after 30 min, but were still significantly less than preinduction values. * P < 0.05 versus preinduction; # P < 0.05 versus after extubation (operating room).

 

A statistically significant fade of FVC was not observed, and FVC fade of 10% or more was observed in only 2 of 70 patients with UAO after tracheal extubation and also in 1 of these 2 patients 30 min later (Table 1).


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  		Table 1. Signs and Symptoms of Partial Paralysis in Patients with Upper Airway Obstruction

 

With a TOF ratio of 0.9 (inclusion criterion) a clinically significant FVC fade was observed postoperatively in only 2 of 70 patients with UAO. Accordingly, the negative predictive value of a TOF ratio of 0.9 for absence of NBD-induced UAO was 97%.

Patients' inability to swallow normally was observed in 4 patients with UAO after tracheal extubation and also in 1 of these 4 patients 30 min later (Table 1). One patient showed both signs and symptoms of partial neuromuscular blockade, FVC fade, and inability to swallow normally both postoperatively and 30 min later. In patients without UAO, FVC fade was not observed and only 1 patient indicated an impaired ability to swallow normally.

TOF ratio at the time of tracheal extubation was 0.94 ± 1.1, and the first spirometric measurement after extubation was performed 10 ± 9 min after TOF ratio of 0.9 had been achieved. TOF ratios at the time of extubation did not correlate with the increase of the MEF50/MIF50 ratio from baseline.

FVC was decreased from predicted values even at preinduction baseline and amounted to 3.5 ± 0.98 L (mean ± sd), i.e., 89% ± 17% of predicted (24) values. After tracheal extubation, all pulmonary function variables were significantly decreased. FVC, peak expiratory flows, and peak inspiratory flows amounted to 65% ± 34%, 66% ± 38%, and 53% ± 32% of preinduction baseline values, respectively. Although values increased subsequently for 30 min, all variables of pulmonary function were still significantly less than preinduction baseline and amounted to 77% ± 37%, 71% ± 49%, and 65% ± 45% of baseline, respectively.

Duration of anesthesia was 205 ± 79 min. A total dose of 19 ± 7 mg cisatracurium (n = 40) and 112 ± 37 mg rocuronium (n = 42) were given to facilitate surgical relaxation.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
This is the first report on the incidence of postoperative UAO. The main finding is that UAO is observed in most patients after abdominal surgery despite recovery of the TOF ratio to 0.9. A statistically significant FVC fade at this point of recovery from neuromuscular blockade was not observed. A FVC fade of 10% or more occurred in only 2 individuals with postoperative UAO.

Although single doses of NBD with an intermittent duration of action can occasionally evoke residual paralysis in the postanesthesia care unit (13), an increased recovery time from neuromuscular blockade is to be expected after repeated doses of nondepolarizing muscle relaxants (25). Thus, we speculated that the probability of detecting the respiratory effects of NBD after recovery of the TOF ratio, if present, would be increased after administration of repeated NBD doses. Therefore, we only studied patients after long-term abdominal surgery where at least 3 doses of NBD were given intraoperatively.

A transportable spirometer was used to allow repeated measurements of respiratory function at different locations, i.e., in the OR and in the recovery room (19). Recent data suggest that respiratory effects of NBD can be detected spirometrically by a decrease (fade) in FVC from the first to the second consecutive spirometric measurement (18). Detection of FVC fade requires a specific technique of data analysis. In cases of large variability of conventional spirometric measurements, the American Thoracic Society (ATS) committee on standards of pulmonary function testing recommends performing up to 8 maneuvers and excluding outliers so as to achieve 3 acceptable forced respiratory curves (20). However, this approach would have excluded a test for FVC fade because a fade of pulmonary function cannot be discriminated from an outlier. Therefore, in accordance with a previous study (18), we used a different approach to achieve acceptable spirometric measurements. If a patient appropriately trained in performing spirometric measurements did not perform the maneuver adequately or if a patient was unable to seal the mouthpiece despite the investigator's assistance, the particular series of measurements was excluded (18). These patients were considered as being unable to appropriately perform spirometric measurements at this specific measurement point. We also assessed patient ability to swallow normally because this muscle function test is easy to perform and is a sensitive symptom of partial neuromuscular blockade (5).

We found a frequent incidence of significant UAO. Several arguments suggest that UAO is predominantly a result of the composite effects on upper airway integrity of midazolam premedication and anesthetics rather than those evoked by the residual effects of NBD and/or surgery. The absence of FVC fade and TOF fade, as observed in 68 of 70 patients with UAO, suggests the absence of NBD-induced UAO in almost all patients after recovery of the TOF ratio to 0.9. The latter is also suggested by the absence of impaired ability to swallow normally, which was also observed in 66 of 70 patients with UAO. Moreover, the incidence and degree of postoperative UAO markedly exceeded the incidence and degree observed in awake volunteers even with profound partial neuromuscular blockade (TOF ratio: 0.5) (5), which may also suggest that NBD were not the main cause of postoperative UAO in our study.

UAO was observed even before anesthesia, suggesting the effects of midazolam premedication on upper airway integrity (6,7). Even though UAO after orally administered midazolam has been reported (6), its frequent incidence was quite surprising, particularly as only small doses were administered (21,22), ensuring that all patients could expend enough effort to perform spirometry appropriately. The clinician should consider that UAO is to be expected frequently when drugs for premedication are administered. Enhanced monitoring may be required even before the patients have entered the OR, particularly patients at risk to develop UAO, e.g., those with obstructive sleep apnea.

Thus, after recovery of the TOF ratio to 0.9, postoperative UAO is most likely a result of anesthetics and/or the effects of midazolam premedication rather than the result of residual NBD effects.

We used the TOF ratio of 0.9 as a measure of tracheal extubation readiness. However, at the time of extubation, e.g., the point of time we started spirometric measurements, TOF ratio varied among patients with a mean TOF ratio of 0.94. Thus, it is difficult to pinpoint the exact TOF value suggesting adequate recovery of upper airway integrity from residual paralysis. The absence of a correlation between TOF ratio at the time of tracheal extubation and MEF50/MIF50 ratio increase from baseline suggests the absence of relevant effects of partial paralysis with recovery of the TOF ratio to 0.9.

Accordingly, we recommend that recovery of TOF ratio of 0.9 can be used as an indication of sufficient recovery of upper airway integrity from the effects of NBD in clinical practice. However, it is useful to pay attention to outliers, i.e., patients with persistent effects of neuromuscular blockade on upper airway integrity despite recovery of the TOF ratio. In accordance with the results of studies in volunteers (5,11), we also found in this study that upper airway function may still be impaired in individuals despite recovery of the TOF ratio to 0.9–1.0. In fact, 2 and 4 volunteers presented with FVC fade and impaired ability to swallow normally after tracheal extubation, and even 1 and 2 patients still showed signs and symptoms of partial neuromuscular blockade 30 minutes later in the recovery room. Thus, other monitoring methods, e.g., assessment of FVC fade or testing the ability to swallow normally, may be useful to test for the effects of partial paralysis on upper airway integrity that cannot be detected sensitively by TOF monitoring. Administration of drugs that reverse neuromuscular blockade should be considered when signs or symptoms of partial paralysis (FVC fade, inability to swallow normally) occur, despite recovery of the TOF ratio.

In addition to postoperative UAO, we observed a perioperative decline in FVC, which was most likely induced by a combined effect of midazolam, anesthetics, and surgery. At preinduction baseline, paralleling the UAO, FVC preinduction values were less than predicted (19), which was most likely a result of the effects of midazolam premedication. Postoperatively, FVC was decreased further from preinduction baseline, but this decrease was partially reversed within 30 minutes. Therefore, we suggest that both midazolam premedication and anesthetics contribute to the postoperative pulmonary dysfunction we observed. Furthermore, abdominal surgery may have caused the persistent postoperative decrease of FVC. This is in accordance with the observation of others (26,27), who demonstrated that abdominal surgery induces a long-lasting decrease in lung volume, i.e., the so called "postoperative pulmonary restrictive syndrome" (26,27), lasting for up to 2 months.

Although FVC fade suggests, with a high positive predictive value, the respiratory effects of partial neuromuscular blockade (18), negative predictive value amounts to only 77% (18). Thus, despite the absence of TOF fade and FVC fade, we cannot completely exclude the potential effects of neuromuscular blockade on upper airway integrity, and the true incidence of patients with persistent effects of neuromuscular blockade on upper airway integrity may be somewhat more frequent than we observed. We studied patients presenting without any evidence or history of UAO. Thus, we assume that the MEF50/MIF50 ratio, which is a strong measure of UAO, was normal (i.e., <1) in all patients before midazolam was given. However, we cannot prove this assumption because we did not perform spirometric measurements before the patients received midazolam.

In summary, UAO is commonly observed after major abdominal surgery, even when TOF ratio has recovered to 0.9. Recovery of the TOF ratio to 0.9 predicts, with a high probability, the absence of NBD-induced UAO. Accordingly, recovery of the TOF ratio to 0.9 can be used in clinical practice as an indication of sufficient recovery of upper airway integrity from the effects of NBD but obviously not from the other effects of anesthesia. The combination of TOF monitoring with other monitoring methods, e.g., FVC fade or testing the ability to swallow normally, may increase the probability to detect outliers, i.e., patients with persistent effects of neuromuscular blockade on upper airway integrity despite recovery of the TOF ratio.


   Footnotes
 
Accepted for publication September 26, 2005.

Supported, in part, by a grant from GlaxoSmithKline, München, Germany, and departmental sources.


   References
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 Abstract
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 References
 

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M. Eikermann, F. M. Vogt, F. Herbstreit, M. Vahid-Dastgerdi, M. O. Zenge, C. Ochterbeck, A. de Greiff, and J. Peters
The Predisposition to Inspiratory Upper Airway Collapse during Partial Neuromuscular Blockade
Am. J. Respir. Crit. Care Med., January 1, 2007; 175(1): 9 - 15.
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press