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Anesth Analg 2001;93:776-780
© 2001 International Anesthesia Research Society

GENERAL ARTICLES

The Relationship Between Pneumatic Tourniquet Time and the Amount of Pulmonary Emboli in Patients Undergoing Knee Arthroscopic Surgeries

Kazuyoshi Hirota, MD*, Hiroshi Hashimoto, MD*, Shizuko Kabara, MD*, Toshihito Tsubo, MD*, Yutaka Sato, MD{dagger}, Hironori Ishihara, MD*, and Akitomo Matsuki, MD*

*Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan; and {dagger}Department of Anesthesiology, Seihoku Central Hospital, Goshogawara, Japan

Address correspondence and reprint requests to Dr. K. Hirota, Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki 036-8562, Japan. Address e-mail to masuika{at}cc .hirosaki-u.ac.jp.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Near-fatal pulmonary embolism can occur immediately after tourniquet release after orthopedic surgeries. In this study, we determined the relationship between tourniquet time and the occurrence of pulmonary emboli in 30 patients undergoing arthroscopic knee surgeries, by using transesophageal echocardiography. The right atrium (RA) was continuously monitored by transesophageal echocardiography, and the number of emboli present was assessed with the following formula: Amount of emboli = 100 x [(total embolic area in the RA after tourni-quet release) - (total area of emboli or artifact in the RA before tourniquet release)]/(RA area).

The area was assessed 0–300 s after tourniquet release by using image-analysis software. The peak amount of emboli appeared approximately 50 s after tourniquet release. In addition, there was a significant correlation between amount of emboli (Ae [%]) and tourniquet time (Ttq [min]): (Ae = 0.1 x Ttq - 1.0, r = 0.795, P < 0.01). This study suggests that acute pulmonary embolism may occur within 1 min of tourniquet release and that the number of emboli is dependent on Ttq.

IMPLICATIONS: We studied the relationship between tourniquet time and number of pulmonary emboli in 30 patients undergoing arthroscopic knee surgeries, by using transesophageal echocardiography. These data suggest that acute pulmonary embolism may occur within 1 min of the tourniquet release and that the number of emboli is related to tourniquet time.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Tourniquet for surgery of the extremities is widely used to achieve a bloodless surgical field. However, fatal or near-fatal pulmonary embolism after deflation or second application with the Esmarch bandage in orthopedic surgeries has been reported (1–3). In addition, pulmonary embolism and venous thrombosis may occur even after arthroscopic knee surgery (4). Demers et al. (5) reported that the risk of deep vein thrombosis was significantly higher among patients with tourniquet application for more than 60 min. Therefore, some reports (6,7) suggest routine use of thromboprophylaxis, such as low-molecular-weight heparin.

Two articles (8,9) indicate that transesophageal echocardiography (TEE) is useful for the detection of pulmonary embolism. In this study with TEE, we determined the relationship between pneumatic tourniquet time (Ttq) and number of pulmonary emboli in patients undergoing arthroscopic knee surgery.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After our University Ethical Committee approval and with informed consent, 30 patients scheduled for elective arthroscopic knee surgery were studied. Patient demographic data and type of surgery are shown in Table 1. Patients with vascular disease and coagulopathy, history of pulmonary embolism, deep vein thrombosis, or ASA physical class >=III were excluded from the study. However, when the patients were medicated with nonsteroidal antiinflammatory drugs, patients whose bleeding time, prothrombin time, and activated partial thromboplastin time were within normal ranges were included.


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  		Table 1. Patient Characteristics
 
Anesthesia was induced with propofol 1.0–1.5 mg/kg, ketamine 0.5 mg/kg, and fentanyl 2 µg/kg. The trachea was intubated after muscle relaxation induced by succinylcholine 0.8 mg/kg IV. Anesthesia was 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. Vecuronium 0.08 mg/kg was administered before insertion of the TEE probe, 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 multiplane 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 was also used. A pneumatic tourniquet was placed around the thigh of the operative limb, inflated (300 mm Hg) after the application of the Esmarch bandage, and deflated after skin closure.

The amount of emboli (Ae) was assessed by a blinded anesthesiologist who was skilled in echocardiography, and it was calculated with the following formula:

equation


where TAafter = total area of emboli in the RA after tourniquet release and TAbefore = total area of emboli or artifact in the RA before tourniquet release.

The total area of emboli implying the sum of each emboli area was measured by MacSCOPE 2.56 (Mitani Corporation, Fukui, Japan), which is an image-processing and -analysis program. The monochrome image was taken into the image-analysis program. The emboli were described as whitish particles, and the other area in the atrium was black. Thus, these two areas were distinguished by the concentration. Then the program proceeded with the calculation of the emboli area and the ratio of total emboli area to the atrial area. 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 the tourniquet release. During assessment, the infusion rate of propofol, ketamine, and fluid did not change. All data are expressed as mean ± SD. Statistical analysis was by repeated-measures analysis of variance followed by Fisher’s protected least significant difference test by use of Stat View II (Abacus Concept, Inc., Berkeley, CA). P < 0.05 was considered significant. The relationship between the Ttq and Ae measured by TEE was examined by Pearson’s correlation coefficient, and a least-square linear regression line was fitted by using GraphPad Prism 1.03 (GraphPad Software Inc., San Diego, CA). In addition, the relationship between the Ttq and changes in {Delta}ETCO2 and {Delta}SpO2 (values between pre- and posttourniquet release) were also examined by the curve-fitting program with GraphPad Prism 1.03.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The TEE detected emboli in all patients (Fig. 1). The peak amount of emboli appeared approximately 40–50 s after tourniquet release (Fig. 2). The percentage of emboli area in the RA returned to the baseline 2 min after the release. In addition, the Ae defined in Methods was dependent on Ttq, and there was a significant correlation between the two variables: Ae = 0.1 x Ttq - 1.0 (Fig. 3, r = 0.795, P < 0.01).



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  		Figure 1. Transesophageal echocardiography (TEE) clearly detected the emboli after tourniquet deflation. Pictures are TEE images of right atrium before (A) and after (B) tourniquet release.

 


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  		Figure 2. Time course of the percentage of embolic area in the right atrium after tourniquet release. *P < 0.01 versus Time 0. All data are mean ± SD.

 


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  		Figure 3. Linear correlation between duration of tourniquet inflation and peak percentage of area of emboli in the right atrium (r = 0.795, P < 0.01).

 
Systolic and diastolic blood pressures 5 min after tourniquet release significantly decreased from 136.1 ± 17.6 mm Hg to 125.4 ± 19.0 mm Hg and 75.0 ± 12.3 mm Hg to 68.0 ± 11.5 mm Hg, respectively, and heart rates significantly increased from 77.4 ± 17.0 to 82.9 ± 19.6 bpm P < 0.01), but the hemodynamic changes were within a clinically acceptable range. In addition, no patient had any symptoms of pulmonary embolism.

The ETCO2 significantly increased after tourniquet release (Table 2). By use of one-phase exponential kinetics (one-phase exponential association: Y = Ymax x [1 - e-Kx], start at 0 and ascend to Ymax with a rate constant K), an increase in ETCO2 ({Delta}EtCO2 [%] = [maximal ETCO2 after the release] - [ETCO2 before tourniquet release]) was Ttq dependent and saturable (Fig. 4, P < 0.01, r = 0.653, maximal {Delta}ETCO2 = 1.36% ± 0.18%).


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  		Table 2. Changes in ETco2 and Spo2 After Tourniquet Release
 


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  		Figure 4. Relationship between duration of tourniquet inflation and maximal increase in {Delta}ETCO2 after tourniquet deflation (P < 0.01, r = 0.653).

 
The SpO2 (%) significantly decreased 1 min after tourniquet release, but only by 0.7% (Table 2). In addition, there was no correlation between time and decreases in SpO2.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
This study showed that pulmonary embolism may occur after tourniquet release in patients undergoing arthroscopic surgeries. Two reports (10,11) suggest that the pulmonary embolism occurring during orthopedic surgery may result from fat embolism caused by invasion of the medullary cavity. However, not all arthroscopic surgeries in this study included invasive procedures of the medullary cavity. Moreover, Rozencwaig et al. (12) reported fatal pulmonary embolism after knee arthroscopy.

In patients undergoing intramedullary guided total knee arthroplasty, Parmet et al. (13) found that the emboli (in blood-aspirated from the femoral vein of the operated limb after tourniquet release) could be fresh thrombus and not necessarily fat. Moreover, they also observed the emboli after tourniquet release in patients undergoing extramedullary guided total knee arthroplasty, which is a less invasive procedure for the medullary cavity (14). In addition, several papers (15,16) suggest prothrombotonic effects of tourniquet application. Air emboli were another possibility suggested by McGrath et al. (4); they occasionally observed these after tourniquet release. In this study, because invasive procedures for the medullary cavity were not included, the high echocardiographic densities are, in our opinion, unlikely to be mainly air and may represent fresh thrombus, although we did not aspirate the blood from the femoral vein on the operated side to confirm the thrombus because we believed that it would be difficult to obtain consent for cannulation of the femoral vein.

Our data showed that the peak amount of emboli appeared approximately 40–50 seconds after tourniquet release and that emboli were not detected by TEE two minutes after release. This implies that acute pulmonary embolism may occur within one minute of tourniquet release and that the thrombi in the ischemic area could be removed during initial recirculation after tourniquet release. However, when Demers et al. (5) determined the incidence of deep vein thrombosis after knee arthroscopy, by using contrast venography, deep vein thrombosis was detected in 33 of 184 patients approximately one week after surgery. Only 20 patients had symptoms, whereas 13 were asymptomatic, although no patients presented with suspected pulmonary embolism. Moreover, Schippinger et al. (7) reported either deep vein thrombosis or pulmonary embolism in 12 of 101 patients five weeks after knee arthroscopy, despite the fact that all patients received a once-daily injection of low-molecular-weight heparin 5000 IU as thromboprophylaxis. These data suggest the possibility of pulmonary embolism more than one month after surgery, although in our study patients did not show any clinical symptoms of pulmonary embolism or deep vein thrombosis before or after discharge.

McGrath et al. (4) 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 this study, there was a significant correlation between the number of emboli and tourniquet duration. Similarly, Demers et al. (5) showed that the risk of deep vein thrombosis was significantly increased among patients having a tourniquet applied for more than 60 minutes. We believe that because McGrath et al. included any lower extremity surgeries that used a tourniquet with invasive (e.g., knee replacement) and noninvasive (e.g., diagnostic arthroscopy) procedures for the medullary cavity, they could not detect the correlation between the amount of emboli and tourniquet duration. Although McGrath et al. stated that the incidence of the embolism was unrelated to the type of surgical procedure, we noticed that the amount of emboli in patients undergoing knee arthroplasty was extremely large compared with that in arthroscopy patients. Thus, the difference of study designs may explain the discrepancy between the report of McGrath et al. and these data. In addition, we therefore suggest that the duration of tourniquet inflation may be a risk factor for pulmonary embolism.

In this study, there was a time-dependent increase in {Delta}ETCO2 that may have resulted from metabolic acidosis due to acid metabolites washed from the ischemic area. Our data were well described by a one-phase exponential, implying that the increase in ETCO2 may be limited. Perhaps the difference between ETCO2 and PaCO2 was increased by a reduction in pulmonary blood flow caused by the emboli, whose amount depended on tourniquet duration, or by metabolic acid from the ischemic area which may have caused a decrease in cardiac contractility and blood pooling in the ischemic area.

Echogenic materials such as emboli were detected even before tourniquet release in this study. We used propofol as the main anesthetic. Because it is a lipid-based emulsion, the lipid may be detected before tourniquet release. However, because 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 the results.

In conclusion, this study suggests that acute pulmonary embolism might occur within one minute of tourniquet release and that the amount of emboli is dependent on duration of tourniquet inflection.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. McGrath BJ, Hsia J, Epstein B. Massive pulmonary embolism. Anesthesiology 1991; 74: 618–20.[Web of Science][Medline]
  2. Valli H, Rosenberg PH, Kytta J, Nurminen M. Arterial hypertension associated with the use of a tourniquet with either general or regional anaesthesia. Acta Anaesthesiol Scand 1987; 78: 349–53.
  3. Kato S, Okada K, Sakuramoto C, et al. Fatal pulmonary embolism during knee surgery under epidural anesthesia. Masui 1997; 46: 393–6.[Medline]
  4. McGrath BJ, Hsia J, Boyd A, et al. Venous embolization after deflation of lower extremity tourniquets. Anesth Analg 1994; 78: 349–53.[Web of Science][Medline]
  5. Demers C, Marcoux S, Ginsberg JS, et al. Incidence of venographically proved deep vein thrombosis after knee arthroscopy. Arch Intern Med 1998; 158: 47–50.[Abstract/Free Full Text]
  6. Nassif JM, Ritter MA, Meding JB, et al. The effect of intraoperative intravenous fixed-dose heparin during total joint arthroplasty on the incidence of fatal pulmonary emboli. J Arthroplasty 2000; 15: 16–21.[Web of Science][Medline]
  7. Schippinger G, Wirnsberger GH, Obernosterer A, Babinski K. Thromboembolic complications after arthroscopic knee surgery: incidence and risk factors in 101 patients. Acta Orthop Scand 1998; 69: 144–6.[Web of Science][Medline]
  8. Sermeus L, Van Hemelrijick J, Vandommele J, Van Aken H. Pulmonary embolism confirmed by transoesophageal echocardiography. Anaesthesia 1992; 47: 28–9.[Web of Science][Medline]
  9. Berman AT, Parmet JL, Harding SP, et al. Emboli observed with use of transesophageal echocardiography immediately after tourniquet release during total knee arthroplasty with cement. J Bone Joint Surg Am 1998; 80: 389–96.[Abstract/Free Full Text]
  10. Djelouah I, Lefèvre G, Ozier Y, et al. Fat embolism in orthopedic surgery: role of bone marrow fatty acid. Anesth Analg 1997; 85: 441–3.[Web of Science][Medline]
  11. Murphy P, Edelist G, Byrick RJ, et al. Relationship of fat embolism to haemodynamic and echocardiographic changes during cemented arthroplasty. Can J Anaesth 1997; 44: 1293–300.[Web of Science][Medline]
  12. Rosencwaig R, Shilt JS, Ochsner JL Jr. Fatal pulmonary embolus after knee arthroscopy. Arthroscopy 1996; 12: 240–1.[Web of Science][Medline]
  13. Parmet JL, Horrow JC, Singer R, et al. Echogenic emboli upon tourniquet release during total knee arthroplasty: pulmonary hemodynamic changes and embolic composition. Anesth Analg 1994; 79: 940–5.[Abstract/Free Full Text]
  14. Parmet JL, Horrow JC, Pharo G, et al. The incidence of venous emboli during extramedullary guided total knee arthroplasty. Anesth Analg 1995; 81: 757–62.[Abstract]
  15. DeLee JC. Complications of arthroscopy and arthroscopic surgery: results of national survey. Arthroscopy 1985; 1: 214–20.[Medline]
  16. Small NC. Complications in arthroscopy: the knee and other joints. Arthroscopy 1986; 2: 253–8.[Medline]
Accepted for publication May 1, 2001.




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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 2001 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press