Tourniquet use during surgery allows for a nearly bloodless operative field and improved visualization but poses several important challenges for anesthesia. Its application produces significant physiological and metabolic effects that must be carefully managed by the anesthesiologist. When applied, a tourniquet halts arterial inflow and venous outflow, producing distal limb ischemia. Upon release, a washout of metabolites such as lactate, carbon dioxide, and potassium occurs, which may cause transient metabolic acidosis, hyperkalemia, and hypotension (1). The magnitude of these changes depends on the pressure, duration, and area of occlusion.
Tourniquet pain, a phenomenon that occurs during tourniquet application, is particularly common in patients under regional anesthesia or light sedation. This pain typically begins 30 to 45 minutes after inflation and is described as a dull, burning discomfort arising from unmyelinated C-fiber activation and ischemia (2). Patients under general anesthesia do not consciously perceive this pain, but autonomic responses such as tachycardia and hypertension may still occur, indicating insufficient anesthetic depth. Management strategies include deepening anesthesia, administering opioids, or using adjuncts such as dexmedetomidine to mitigate these responses.
The moment of tourniquet release demands particular attention from the anesthesiologist. Deflation often causes abrupt changes in blood pressure, heart rate, and, in some cases, arrhythmias. These changes reflect the systemic effects of reperfusion and redistribution of blood volume, rather than the local metabolic washout described earlier. While these changes are usually self-limiting, they can be exaggerated in patients with cardiovascular compromise or hypovolemia (3). Proactive measures include optimizing intravascular volume prior to release, closely monitoring arterial pressure, and gradually deflating the cuff to allow for controlled reperfusion. While most patients tolerate these changes well, preparation is essential in those with limited cardiac reserve.
Beyond immediate hemodynamic changes, the ischemia–reperfusion cycle can trigger a systemic inflammatory response. Oxygen-free radicals and cytokines released during reperfusion can injure cell membranes and vascular endothelium (3). Experimental and animal studies suggest that certain anesthetic agents, such as propofol and volatile agents, may reduce oxidative stress and lipid peroxidation during reperfusion, though evidence in human surgery remains limited. These protective effects highlight the anesthesiologist’s role not just in intraoperative management but also in modulating postoperative recovery and tissue protection.
Safe tourniquet practice involves minimizing both pressure and duration. Nerve injury, the most feared complication, is associated with prolonged inflation times exceeding two hours and excessive cuff pressure. For upper extremities, pressures should typically be kept at 100 to 150 mmHg above systolic, and at 100 to 200 mmHg above for lower extremities. During long cases, intermittent deflation permits reperfusion and reduces the risk of ischemic complications (3).
Modern tourniquet systems with limb occlusion pressure monitoring allow for individualized pressure control, thereby lowering the risk of nerve and muscle damage. Conversely, newer surgical and anesthetic techniques, such as wide-awake local anesthesia with no tourniquet (WALANT), aim to eliminate the need for tourniquets by combining local anesthetics with epinephrine to achieve hemostasis without ischemia (4).
Anesthesia for surgery involving a tourniquet requires an understanding of the physiologic, metabolic, and neurologic consequences of ischemia and reperfusion. Optimal management involves minimizing tourniquet time and pressure, anticipating systemic changes, and tailoring anesthetic choice and monitoring to each patient’s comorbidities. By carefully planning and collaborating with the surgical team, anesthesiologists can ensure safe and effective outcomes while minimizing complications associated with tourniquet use.
References
- Kumar K, Railton C, Tawfic Q. Tourniquet application during anesthesia: “What we need to know?”. J Anaesthesiol Clin Pharmacol. 2016;32(4):424-430. doi:10.4103/0970-9185.168174
- Bostankolu E, Ayoglu H, Yurtlu S, et al. Dexmedetomidine did not reduce the effects of tourniquet-induced ischemia-reperfusion injury during general anesthesia. Kaohsiung J Med Sci. 2013;29(2):75-81. doi:10.1016/j.kjms.2012.08.013
- Estebe JP, Davies JM, Richebe P. The pneumatic tourniquet: mechanical, ischaemia-reperfusion and systemic effects. Eur J Anaesthesiol. 2011;28(6):404-411. doi:10.1097/EJA.0b013e328346d5a9
- Kurtzman JS, Etcheson JI, Koehler SM. Wide-awake Local Anesthesia with No Tourniquet: An Updated Review. Plast Reconstr Surg Glob Open. 2021;9(3):e3507. Published 2021 Mar 26. doi:10.1097/GOX.0000000000003507
