Anesth Analg 2002;94:1152-1154
© 2002 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Vasospasm After Use of a Tourniquet: Another Cause of Postoperative Limb Ischemia?
Rodrigo R. Gazmuri*,
Juan A. Muñoz*,
Juan P. Ilic*,
Ricardo M. Urtubia*, and
Roberto R. Glucksmann
*Intensive Care & Anesthesia Unit, Trauma Unit, Mutual de Seguridad Hospital, C.CH.C. Santiago, Chile
Address correspondence to Rodrigo R Gazmuri, MD, Intensive Care and Anesthesia Unit, Mutual de Seguridad Hospital, C.CH.C., Alameda 4848, Santiago, Chile. Address e-mail to rgazmuri{at}entelchile.net
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Abstract
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IMPLICATIONS:Two previously reported causes of postoperative limb ischemia after use of a tourniquet, compartment syndrome and arterial thromboembolism, require aggressive and invasive management. We report another probable cause that can be managed nonsurgically: vasospasm.
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CASE REPORT
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Tourniquets are often used in orthopedic surgery to provide a bloodless surgical field. However, they are not devoid of complications. We report a case of prolonged reversible postoperative ischemia of the lower limb associated with the intraoperative use of a thigh tourniquet, probably caused by vasospasm.
A previously healthy 40-yr-old man was operated on for a tibiofibular synostosis caused by the faulty consolidation of a leg fracture sustained a year earlier and treated orthopedically. He did not smoke and was not taking any medication.
The surgery consisted of resecting the bony bridge between the distal ends of the left tibia and fibula. The patient agreed to a regional anesthesia, which consisted of a combined spinal-epidural at the L3-4 level. A 26-gauge pencil point spinal trocar was advanced through a 16-gauge Tuohy needle and 1.8 mL of 0.75% hyperbaric bupivacaine was injected in the subarachnoid space, followed by the introduction of a 16-gauge catheter in the epidural space through a 16-gauge Tuohy needle. No pain or paresthesias were reported. The anesthesia achieved a T10 level.
After the limb was exsanguinated with an elastic bandage, a properly sized left thigh tourniquet was positioned and the pressure set to 300 mm Hg with an automatic inflation device (Zimmer A.T.S.TM 1500; Zimmer, Dover, OH), which worked properly before the case and in the ensuing ones. The incision was made longitudinally over the anterior surface of the distal third of the left leg. The surgery was uneventful, with a total duration of ischemia of 35 min. Immediately after tourniquet deflation we noted the left foot was pale and cold with no posterior tibial and dorsalis pedis arteries palpable pulses.
A Doppler ultrasound performed in the operating room revealed absent dorsalis pedis artery flow and minimal posterior tibial artery flow. An immediate vascular evaluation suggested an arterial color Doppler duplex ultrasound was needed; it was performed 5 h after the spinal anesthesia and showed a pattern of acute arterial insufficiency with no collateral circulation, consistent with vasospasm below the knee. Normal triphasic flow in the left common femoral, superficial femoral, and popliteal arteries with abnormal biphasic flow in the posterior tibial artery and abnormal monophasic flow in the dorsalis pedis artery were demonstrated (Fig. 1–3). The ankle/brachial index was 0.41 (normal value, 1–1.15), consistent with lower limb ischemia. Right lower limb examination was normal (Fig. 4, 5).
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Figure 2. Doppler Duplex ultrasound of the left posterior tibial artery showing abnormal biphasic flow.
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Figure 3. Doppler Duplex ultrasound of the left dorsalis pedis artery showing abnormal monophasic flow.
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Figure 5. Doppler ultrasound of the right posterior dorsalis pedis artery showing normal triphasic flow.
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Unfortunately, we could not perform Doppler duplex ultrasound frequently so we resorted to clinical evaluations, gradually documenting improvement of foot perfusion. The spinal anesthesia lasted approximately 2.5 h and we did not use the epidural catheter. The patient never reported foot pain.
During the 6 h after the Doppler duplex ultrasound the left foot slowly recovered color and temperature. The posterior tibial artery pulse was clearly palpable 11 h after the spinal anesthesia, followed 6 h later by normalization of the dorsalis pedis artery pulse as well. A control Doppler duplex ultrasound performed 30 h after the spinal anesthetic reported normal triphasic flow of the left leg arteries. No atherosclerotic plaques or vascular calcifications were evident by Doppler ultrasound examinations.
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Discussion
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Complications are sometimes associated with use of a tourniquet. Among these the most feared, (although very infrequent) is death caused by pulmonary embolism from leg vein thrombi before tourniquet inflation (1) or after tourniquet deflation (2,3). Frequently, hemodynamic alterations are observed after tourniquet release, including hypotension, bradycardia, or even asystole (4). Neurologic deficits ("tourniquet paralysis"), caused usually by high tourniquet pressure and/or prolonged ischemic times, are sometimes observed (5,6).
There are two main causes of postoperative ischemia associated with the use of a tourniquet after orthopedic surgery: 1) thrombosis and/or embolism from a ruptured atherosclerotic plaque inside a major artery caused by tourniquet-associated limb manipulation (7,8) and 2) compartment syndrome (9,10). Thrombosis usually occurs in vascular-damaged patients with advanced atherosclerosis. Compartment syndrome appears typically with swollen limb resulting from edema and usually accompanies a long procedure and high inflating tourniquet pressures (9). None of the above circumstances were present in our patient. Direct artery trauma by the surgical procedure was excluded because of the location of the surgery and because it affected both main calf arteries.
We cannot prove that the ischemia was caused by vasospasm, but the clinical context, the spontaneous reversibility of the process, the lack of demonstrable thromboembolic phenomena (no cardiovascular risk factors and no atherosclerotic plaques on color Doppler duplex ultrasound examinations), and the absence of a compartment syndrome strongly suggests this etiology. It affected the arterial circulation distal to the tourniquet placement by a mechanism we are not able to elucidate, perhaps involving humoral factors overriding the sympathetic blockade-mediated vasodilation of the continuing spinal anesthetic. We did not perform angiographic studies because we documented clinical improvement of the foot perfusion after the first Doppler duplex ultrasound.
We are not aware of any similar cases reported in the literature and thus we would like to call attention to another possible cause of postoperative ischemia that does not require surgical or invasive management after use of a tourniquet. Thus, whenever an ischemic complication occurs after its use we suggest to exclude thromboembolic phenomena and compartment syndrome and to aggressively treat the limb ischemia as vasospasm using vasodilators. Also, we suggest identifying a subset of patients who might be more susceptible to vasospasm (i.e., patients who smoke or those who have Raynaud’s phenomenon).
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Acknowledgments
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We are grateful to Alejandro G. Cabrera, MD for interpreting and explaining the color Doppler ultrasound images for us and to Raúl J. Gazmuri, MD for revising the manuscript.
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References
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Boogaerts JG. Lower limb exsanguination and embolism. Acta Anaesthesiol Belg 1999; 50: 95–8.[Medline]
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Berman AT, Parmet JL, Harding SP et al. Emboli observed with the 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]
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McGrath BJ, Hsia J, Epstein B. Massive pulmonary embolism following tourniquet deflation. Anesthesiology 1991; 74: 618–20.[ISI][Medline]
-
Gielen M. Cardiac arrest after tourniquet release. Can J Anaesth 1991; 38 (4 Pt 1):541.
-
Aho K, Sainio K, Kianta M, Varpanen E. Pneumatic tourniquet paralysis. J Bone Joint Surg Br 1983; 65: 441–3.
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Mohler LR, Pedowitz RA, Lopez MA, Gershuni DH. Effects of tourniquet compression on neuromuscular function. Clin Orthop 1999; 359: 213–20.
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Hagan PF, Kaufman EE. Vascular complication of knee arthroplasty under tourniquet. Clin Orthop 1990; 257: 159–61.
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Kobayashi S, Isobe K, Koike T, et al. Acute arterial occlusion associated with total knee arthroplasty. Arch Orthop Trauma Surg 1999; 119: 223–4.
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Hirvensalo E, Tuominen H, Lapinsuo M, Helio H. Compartment syndrome of the lower limb caused by a tourniquet: a report of two cases. J Orthop Trauma 1992; 6: 469–72.[Medline]
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Ananthanarayan C, Casro C, McKee N, Sakotic G. Compartment syndrome following intravenous regional anesthesia. Can J Anaesth 2000; 47: 1094–8.[Abstract]
Accepted for publication January 9, 2002.
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Abstract
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