Effects of acetaminophen for intravenous regional anesthesia consumption and delayed tourniquet pain onset time. In the pilot study that was conducted we discovered that some of the cases faced a delay in surgery as the motor block was not achieved even after IVRA. Therefore, we did not asses onset and recovery time of motor block in this study. Further studies are therefore required to know the effects on motor block. It is known that by increase in pH of local anesthetics improves the nerve penetration and rate of onset of blockade [2], we investigate pH of each solution used in this study. The pH of lidocaine-normal saline solution was 6.16 (Group C), and that of lidocaine-normal saline-ketorolac mixture was 6.28 (Group K) and the pH value of lidocaine-intravenous acetaminophen mixture was 5.88 (Group P). Although the pH of lidocaine- intravenous acetaminophen mixture was lower than other groups, onset time of sensory block was much faster in Group P compared to Group C. This effect may be as a result of acetaminophen's antinociceptive effect at pheripheral site. NSAIDs are widely used concomitantly with IVRA to improve the quality of anesthesia. It is known that the analgesic effect of NSAID is attributed to inhibition of the isoenzyme COX-2 [8] that is primarily associated with inflammation. Cytokines and growth factors enhance the expression and synthesis of COX-2, mainly at inflammatory sites, producing prostaglandins that mediate inflammation, pain and fever [9]. Reuben et al. demonstrated that ketoroloac added to lidocaine improved control of tourniquet pain and postoperative pain [6]. The study also suggested that reduction of postoperative pain is as a result of residual ketorolac in the operative arm, and its redistribution to the systemic circulation after tourniquet deflation [7]. Studies have indicated that optimal dose of ketorolac for IVRA was 20 mg [7], but we used 10 mg of ketorolac, as 30 mg of ketorolac was shown to be equipotent with 1 g of intravenous acetaminophen [10]. In this study, postoperative pain and postoperative analgesic consumption were decreased in Group K than Group C but was ineffective in decreasing tourniquet pain and onset time of sensory block. Ketorolac 10 mg when added to IVRA may be insufficient to reduce tourniquet pain but its anti-inflammatory effect and systemic circulation after tourniquet deflation may reduce postoperative pain. The main mechanism of analgesic effect of acetaminophen is demonstrated to be through its action on central nervous system mediated by inhibition of prostaglandin synthesis [11,12]. Acetaminophen is also shown to inhibit cyclooxygenase (COX) enzyme in vivo [13,14]. In a recent study, paracetamol added to lidocaine for IVRA improved quality of anesthesia and delayed tourniquet pain onset time, reduced intraoperative and postoperative analgesic consumption [15] in which paracetamol 300 mg was added to 40 ml solution for IVRA similar to present study. Sen H et al. [15] compared the IVRA lidocaine and paracetamol 360 Vol. 58, No. 4, April 2010 mixture with IVRA lidocaine plus intravenous acetaminophen whereas the present study compared the effects of IVRA lidocaine and acetaminophen mixture vs IVRA lidocaine and ketorolac mixture. The results of this study were comparable to the previous study, except that, in this study intravenous acetaminophen for IVRA did not significantly reduce intraope- rative analgesic consumption. The time points of intraoperative analgesic administration were also different. Sen H et al. [15] used fentanyl for decreasing tourniquet pain when VAS > 4 but in the present study VAS > 3 was the cut-off pain score, thus intraoperative analgesics were administered in more number of patients than study conducted by Sen H et al. [15]. Several studies have demonstrated the peripheral antinoci- ceptive effect of acetaminophen. Lee et al. [16] have suggested that acetaminophen selectively suppressed peripheral prosta- glandin E2 release and increased COX-2 gene expression in a clinical model of acute inflammation. In another study, acetaminophen may also interfere with the delivery of peripheral β-endorphins and help in reducing the pain [17]. Canbay et al. [18] have studied that 50 mg of intravenous aceta- minophen pretreatment is effective in reducing the pain on propofol injection. Dani et al. [19] suggested that paracetamol exhibits local antinociceptive effects by modulating cannabi- noid receptors. There were few limitations in this study. The dose of intra- venous acetaminophen 300 mg was fixed for the reason that when intravenous acetaminophen over 300 mg was mixed then the total volume of IVRA solution would be too large and would be difficult to control the concentration of lidocaine. We anticipate that larger doses of acetaminophen would increase the efficacy of analgesic during IVRA but optimal dose of acetaminophen could not be determined. Another limitation is that motor block and delayed postoperative pain after patient discharge from postanesthesia care unit were not assessed. The variability in intraoperative pain or postoperative pain depending on the type of surgery performed such as carpal tunnel syndrome, close reduction of radius fracture, ganglion excision etc, could not be standardized (Table 2). In conclusion, this study indicated that the addition of intra- venous acetaminophen to lidocaine in IVRA significantly shortens the onset time of sensory block, but not intravenous ketorolac. The addition of both drugs may not affect intraoperative anal- gesia and tourniquet pain. However, both drugs would improve postoperative analgesia in postanesthesia care unit. References 1. Brill S, Middleton W, Brill G, Fisher A. Bier’s block; 100 years old and still going strong! Acta Anaesthesiol Scand 2004; 48: 117-22. 2. Choyce A, Peng P. A systematic review of adjuncts for intravenous www.ekja.org