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Anesth Analg 2002;94:1633-1638 © 2002 International Anesthesia Research Society
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Abstract |
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The amount of emboli formed (percentage of total emboli area to the right atrial area [%Ae]) after tourniquet release in invasive procedures of the medullary cavity is empirically much larger than that in noninvasive procedures, even if the tourniquet duration is similar. Thus, we compared %Ae between arthroscopic reconstruction of the anterior cruciate ligament (ACL, n = 20) and total knee arthroplasty (TKA, n = 20). The right atrium was continuously monitored by transesophageal echocardiography to assess %Ae. Peak %Ae ± SD (ACL, 4.1% ± 3.4%; TKA, 20.7% ± 16.7%) appeared 30–40 s after tourniquet release in both groups. However, %Ae in the TKA group was always larger than the peak %Ae in the ACL group. In addition, although the ETCO2 significantly increased after tourniquet release in both groups, increase of ETCO2 (1.1% ± 0.3%) in the ACL group was significantly larger than that in the TKA group (0.5% ± 0.2%). An increase in ETCO2 was inversely proportional to peak %Ae (P < 0.01; r = 0.703). Therefore, the present data suggest that the risk of acute pulmonary embolism after tourniquet release may be more frequent during TKA than ACL.
IMPLICATIONS: We compared emboli formation after tourniquet release in patients undergoing arthroscopic reconstruction of the anterior cruciate ligament (ACL, n = 20) and total knee arthroplasty (TKA, n = 20) using transesophageal echocardiography. The present data suggest that the risk of acute pulmonary embolism after tourniquet release could be more frequent during TKA than ACL.
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Introduction |
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In patients undergoing arthroscopic knee surgery using transesophageal echocardiography (TEE), the amount of emboli (percentage of total emboli area to the right atrial area [%Ae]) was dependent on tourniquet time (Ttq), and the emboli found were likely fresh thrombus and not fat because the arthroscopic knee surgery did not invade the medullary cavity (1). Similarly, Parmet et al. (2) also reported that the emboli after tourniquet deflation in orthopedic surgery might be fresh thrombus. However, several reports (3–5) suggest that the emboli after tourniquet release may be fatty marrow. Based on clinical observations, we suspect that the %Ae after tourniquet release in procedures invading the medullary cavity (e.g., total knee arthroplasty [TKA]) are more frequent than in noninvasive procedures (e.g., arthroscopic surgeries) even if the tourniquet duration is the same.
Fatal or near fatal pulmonary embolism immediately after tourniquet deflation in orthopedic surgery has been reported (6–8). These acute pulmonary emboli occurred in invasive procedures of the medullary cavity, especially TKA. Although a number of cases of emboli formation have been reported in arthroscopic surgical procedures, the patients had already had deep venous thrombus (6), or the embolism occurred a few days after the procedures (9,10). Demers et al. (11) reported that the risk of deep vein thrombosis was significantly increased among patients with tourniquet application for more than 60 min. As it usually takes more than 60 min to complete TKE, the incidence may be more frequent in patients undergoing this procedure. However, despite the similar surgical duration in reconstruction of the anterior cruciate ligament (ACL), fatal or near fatal pulmonary embolism immediately after tourniquet deflation has been rarely reported. In this study we used TEE to compare the amount of pulmonary emboli formed in patients undergoing ACL reconstruction and TKA.
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Methods |
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With University Ethical Committee approval and informed consent, 40 patients scheduled for ACL reconstruction (ACL group, n = 20) or TKA (TKA group, n = 20) by the same orthopedic surgeons were studied. Patient demographic data and type of surgery are shown in Table 1. Patients with apparent vascular disease and coagulopathy, history of pulmonary embolism, apparent deep vein thrombosis, or ASA physical status
III were excluded from the study. However, when patients were medicated with nonsteroidal antiinflammatory drugs, those whose bleeding time, prothrombin time, and activated partial thromboplastin time were within normal ranges were included.
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Anesthesia was induced with propofol 1.0–1.5 mg/kg, ketamine 0.5 mg/kg, and fentanyl 2 µg/kg and maintained with propofol 5–8 mg · kg-1 · h-1, ketamine 0–0.5 mg · kg-1 · h-1, and fentanyl 4–8 µg/kg. The trachea was intubated after muscle relaxation was induced by succinylcholine 0.8 mg/kg IV. Muscle relaxation was maintained with an IV bolus of vecuronium 0.08 mg/kg, and then a further 1 mg was given IV every 30 min. A four-chamber view of the heart was obtained by a 5.0-MHz multi-plane TEE transducer (UST-5280S-5, Aloka Co Ltd, Tokyo, Japan), and then the right atrium (RA) was monitored in the center of the screen. Routine monitoring (ETCO2 [%], SpO2 [%], electrocardiogram, and noninvasive blood pressure monitors [mm Hg]) was also applied. A pneumatic tourniquet was placed around the thigh of the operative limb, inflated (300 mm Hg) after the application of an Esmarch bandage, and deflated after skin closure.
The %Ae was assessed as reported previously (1). Briefly, the TEE was performed by an anesthesiologist skilled in echocardiography, and a blinded anesthesiologist, who did not know the patient group, calculated the %Ae using the following formula: %Ae = 100 x ([Total area of emboli in the RA after release of tourniquet] - [Total area of emboli or artifact in the RA before tourniquet release]) / (the RA area).
The total area of emboli implies that the sum of each embolic area was measured by the MacSCOPE 2.56 (Mitani Corp, Fukui, Japan), which is an image processing and analysis program. The area during the end-expiratory pause and end-systolic phase of the cardiac cycle was assessed 0, 10, 20, 30, 40, 50, 60, 120, 180, 240, and 300 s after tourniquet release. The infusion rate of propofol and ketamine and fluid administration did not change until the assessment was finished.
All data are expressed as mean ± SD. Statistical analysis was performed by one- or two-way repeated-measures analysis of variance followed by Student-Newman-Keuls test using Sigma Sat for Windows (Jandel Scientific Software, Chicago, IL). A P < 0.05 was considered significant. The relationship between Ttq and the %Ae measured by TEE was assessed by Pearson’s correlation coefficient, and a least squares linear regression line was fitted using GraphPad Prism 1.03 (GraphPad Software Inc, San Diego, CA). In addition, the relationship between peak emboli formation and changes in ETCO2 and SpO2 (values between pre- and posttourniquet release) were also examined by the curve-fitting program using GraphPad Prism 1.03.
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Results |
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TEE detected emboli in all patients in both groups. Typical images are shown in Figure 1. The peak emboli formation appeared around 30–40 s after tourniquet release in both groups ( Fig. 2). In the ACL group, %Ae in the RA returned to the baseline 2 min after release, whereas in the TKA group, there was no return to baseline over the measurement period. In addition, %Ae in the TKA group was always significantly larger than that in the ACL group during the assessment period.
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%Ae, defined in Methods, was dependent on Ttq, and there was a significant correlation between the two variables in the ACL group (Fig. 3; r = 0.616; P < 0.01) but no correlation in the TKA group.
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ETCO2 (%) significantly increased after tourniquet release in both groups (Table 2). However, the increased ETCO2 in the ACL group was significantly larger than that in the TKA group (Table 2, Fig. 4). Using one-phase exponential kinetics (one-phase exponential decay, Y = Span x (1 - e-Kx) + Plateau, start at Span + Plateau and decay to Plateau with a rate constant K), an increase in ETCO2 (
ETCO2 [%] = [maximal ETCO2 after the release] - [ETCO2 before tourniquet release]) was inversely proportional to peak %Ae in the RA (Fig. 4; P < 0.01; r = 0.703).
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Systolic and diastolic blood pressures 5 min after tourniquet release significantly decreased, and heart rates significantly increased, in both groups (Table 2), but these hemodynamic changes were within clinically acceptable ranges (<20%). In addition, after emergence from general anesthesia in the postanesthetic care units, no patient in either group showed any symptoms of pulmonary embolism such as tachypnea, restlessness, hypoxemia, hypotension, and distension of cervical veins.
SpO2 (%) decreased 1 and 3 min after tourniquet release but by <1% in both groups (Table 2). There was no correlation between peak %Ae and the decrease in SpO2.
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Discussion |
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The present study showed that a pulmonary embolism might occur after tourniquet release in patients undergoing ACL reconstruction or TKA. In patients undergoing intramedullary guided TKA, Parmet et al. (2) found that the emboli (in blood aspirated from the femoral vein of the operative limb after tourniquet release) could be fresh thrombus and not necessarily fat. Moreover, they also observed emboli formed after tourniquet release in patients undergoing extramedullary guided TKA, which is a less-invasive procedure for the medullary cavity (12). In addition, several articles (13,14) suggest prothrombotic effects of tourniquet application. However, in the present study, the %Ae formed in the TKA group was much larger than that in the ACL group, despite similar Ttq between the two groups. In addition, there was a significant correlation between the %Ae and Ttq in the ACL group, similar to our previous report in patients undergoing arthroscopic surgery, whereas there was no correlation in the TKA group. Therefore, it is likely that the emboli, at least in the TKA group, may have included not only thrombus but also other echogenic materials. Several articles (3–5,15,16) suggest that pulmonary embolism occurring during orthopedic surgery may result from fat embolism caused by invasion of the medullary cavity. In addition, McGrath et al. (17) suggested that air emboli was another possibility in their TKA group because they occasionally observed this by TEE after tourniquet release. In the present study, we did not aspirate blood from the femoral vein on the operative side to identify the emboli because we feel it would have been difficult to obtain consent for cannulation of the femoral vein, especially in patients in the ACL group.
In the present study, no patients showed any symptoms of acute pulmonary embolism. Thus, we could not determine which is the greatest risk of acute pulmonary embolism, size of emboli, frequency of emboli, or %Ae. Berman et al. (18) reported that only patients who had had echogenic materials of more than 0.5 cm maximum in diameter after tourniquet release in TKA revealed postoperative clinical pulmonary embolism. Thus, the size of emboli may be the most important factor. However, as Markel et al. (5) reported using a canine model that histologically marked the %Ae that obstructed the pulmonary vasculature during TKA, even when TEE revealed a sustained embolic shower, the %Ae (even embolic debris) may also be relevant. In addition, as TEE showed embolic showers in TKA patients, these patients could have asymptomatic pulmonary embolism, and the embolism might deteriorate postoperative pulmonary functions, although we did not evaluate this in the present study.
Because the peak %Ae appeared within one minute after tourniquet release in both the ACL and TKA groups, acute pulmonary embolism may occur within one minute after tourniquet release, and the emboli in the ischemic area could mostly be removed during the initial recirculation after deflation of the tourniquet. However, in the TKA group, larger levels of emboli than at the peak in the ACL group were detected until the end of TEE monitoring (five minutes after tourniquet release). In the ACL group, emboli were not detected two minutes after release. Thus, in the TKA group, the risk of acute pulmonary embolism could remain even several minutes after release.
McGrath et al. (17) reported that the incidence of pulmonary embolism in patients undergoing surgery of the lower extremity was unrelated to the type of surgical procedure and duration of tourniquet inflation. However, in the present study, the %Ae in TKA group was four- to five-fold larger than in ACL group, and there was a significant correlation between the %Ae and tourniquet duration in the ACL group. Thus, the incidence of pulmonary embolism may be related to the type of surgical procedure and would correlate with Ttq in some types of surgery (e.g., arthroscopic surgery).
In the present study, ETCO2 increased significantly after tourniquet deflation. This may have resulted from metabolic acidosis caused by acid metabolites washed from the ischemic area. In addition, using a one-phase exponential decay, the ETCO2 inversely correlated with peak %Ae. This may imply an increase in dead space of the lung. Because TKA patients (mean, 71.3 years old) were much older than ACL patients (mean, 26.7 years old), metabolic acidosis-induced cardiac depression may be more likely in TKA patients. Thus, the ventilation:perfusion ratio could increase in TKA patients more than that in ACL patients. However, because a reduction in blood pressure after tourniquet deflation was not significantly different between the two groups in the present study (e.g., systolic blood pressure, 147 ± 17 to 119 ± 19 in the TKA group and 139 ± 20 to 127 ± 22 in the ACL group), changes in pulmonary blood flow would not be different between the two groups. Therefore, the difference in ETCO2 between the two groups may have been due to the amount of pulmonary emboli.
In the present study, there was a big age difference between groups. However, because it is rare that young and old patients undergo TKA and reconstruction of the ACL, respectively (1,9,12), it is very difficult to match the age between groups. Thus, in general, the between-group comparison may not be appropriate. However, %Ae could be affected by surgical procedures rather than age. Therefore, we believe that the data between groups could be comparable.
As demonstrated in our previous report, the echogenic materials detected before tourniquet release may be propofol that is a lipid-based emulsion because lipids can be detected by TEE. However, as we did not change the infusion rate of propofol and fluid, the image was consistent, and the amount was small. Therefore, it is unlikely that the lipid image profoundly affected our results.
In conclusion, the present study suggests that an acute pulmonary embolism might occur within one minute after tourniquet release. Because the peak %Ae in the TKA group was much larger than that in the ACL group, the risk of pulmonary embolism after tourniquet release could be larger in invasive procedures for the medullary cavity compared with noninvasive procedures.
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Acknowledgments |
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The authors thank DG Lambert, Phd, (University Department of Anesthesia, Critical Care and Pain Management, Leicester Royal Infirmary, UK) for his valuable comments.
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References |
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