Theories concerning the etiology of tourniquet trelated pain have identified nerve ischemia and compression as the main sources of noxious stimuli during the maintenance of tourniquet inflation. Unmyelinated C fibers, whose function is preserved during prolonged tourniquet inflation, have been recognized to represent an important nociceptive pain pathway. Increase in C fiber action potential frequency by hypoxia and other metabolic perturbations suggests their activation secondary to ischemia and compression. Considering the important role of C fibers in the neuropathologic mechanisms of tourniquet-related pain, the decrease of their activity may reduce pain. Clonidine has been found to prolong the action of local anesthetics in peripheral nerve blocks, although it is unlikely that the prolongation of the block is caused by decreased local anesthetic systemic absorption due to clonidine induced vasoconstriction. This effect of clonidine could be mediated directly at the peripheral nerve, because the drug has been shown to inhibit impulse conduction inprimary afferents and especially in C fibers Ketamine, on the other hand, acting via a peripheral mechanism, enhances the duration of local anesthetic and analgesic actions of bupivacaine during infiltration anesthesia in surgical patients. Anatomical studies showed the presence of peripheral N-methyl-D-aspartate (NMDA) and other glutamate receptors associated with unmyelinated sensory axons, suggesting that activation of these receptors leads to increased primary afferent activity and, thus, to pain. This finding raises the possibility that the block of NMDA receptors on peripheral unmyelinated sensory axons could be the basis of peripheral ketamine-induced analgesia. The present study compares the effects of a low dose of clonidine or ketamine separately added to intravenous regional anesthesia (IVRA) with lidocaine to prevent tourniquet pain.
Anyone who has had a tourniquet on the thigh inflated to 100 mm Hg above systolic blood pressure for more than a few minutes appreciates tourniquet pain. Although the mechanism and neural pathways for this severe aching and burning sensation defy precise explanation, unmyelinated, slow-conduction C fibers, which are relatively resistant to local anesthetic blockade, probably play a critical role. Tourniquet pain gradually becomes so severe over time that patients may require substantial supplemental analgesia, if not general anesthesia, despite a regional block that is adequate for surgical incision. Even during general anesthesia, tourniquet pain is often manifested as a gradually increasing mean arterial blood pressure beginning about ¾ to 1 h after cuff inflation. Signs of progressive sympathetic activation include marked hypertension, tachycardia, and diaphoresis. The likelihood of tourniquet pain and its accompanying hypertension may be influenced by many factors, including anesthetic technique (intravenous regional > epidural > spinal > general anesthesia), intensity and level of regional anesthetic block, choice of local anesthetic (hyperbaric spinal with tetracaine > isobaric bupivacaine), and supplementation of the block with opioids.