Robert B. Steinberg

Intravenous Regional Anesthesia Using Lidocaine and Ketorolac

Nonsteroidal antiinflammatory drugs (NSAIDs) interfere with the synthesis of inflammatory mediators and can supplement postoperative pain relief.We postulated that using the parenterally available NSAID ketorolac (K) as a component of intravenous regional anesthesia (IVRA) would suppress intraoperative tourniquet pain and enhance postoperative analgesia. Sixty patients were assigned randomly and blindly to receive either intravenous (IV) saline and IVRA with 0.5% lidocaine, IV K and IVRA 0.5% lidocaine, or IV saline and IVRA 0.5% lidocaine with K. The patients who received IVRA K reported significantly less intraoperative tourniquet pain, with lower verbal analog pain scores at 15 and 30 min after tourniquet inflation. Similarly, IVRA-K patients experienced less postoperative pain with lower visual analog scale (VAS) pain scores at 30 and 60 min, and required no fentanyl for control of early postoperative pain in the postanesthesia care unit (PACU). They also required fewer analgesic tablets in the first 24 h (1.9 +/- 1.4 Tylenol No. 3 Registered Trademark tablets compared to the other two groups, 4.6 +/- 1.3 and 3.0 +/- 1.1; P < 0.05). We conclude that K improves IVRA with 0.5% lidocaine both in terms of controlling intraoperative tourniquet pain and by diminishing postoperative pain. (Anesth Analg 1995;81:110-3)

The dose-response relationship of ketorolac as a component of intravenous regional anesthesia with lidocaine.

Ketorolac (K) is a useful addition to lidocaine for IV regional anesthesia (IVRA).However, the minimal dose of K that is effective for this purpose has not been established. We added 0, 5, 10, 15, 20, 30, and 60 mg of K to 0.5% lidocaine IVRA for either carpal tunnel release or tenolysis. Pain was assessed in the postanesthesia care unit by using a visual analog scale. The duration of analgesia (time to first request for pain relief) and the use of Tylenol No. 3 tablets (T3) were measured. A linear dose-response relationship was observed between the dose of K and the duration of analgesia (r = 0.988) up to 20 mg of K. Similarly, the number of T3 tablets used was inversely related to the dose of K (r = 0.960) over the same range. There were no significant differences among the groups who received 20, 30, or 60 mg of K. We conclude that 20 mg of K is the optimal dose for inclusion with 0.5% lidocaine for IVRA under the conditions of our study. Implications: The antiinflammatory drug ketorolac is a useful addition to lidocaine for IV regional anesthesia. This study showed that 20 mg of ketorolac is equally effective as 60 mg in this context. However, smaller doses provided less effective pain relief, and a linear dose-response relationship was demonstrated. (Anesth Analg 1998;86:791-3)

A dose-response study of intravenous regional anesthesia with meperidine.

UNLABELLED Intravenous regional anesthesia (IVRA) with meperidine in doses > or = 100 mg provides effective postoperative analgesia. However, this technique is associated with excessive opioid-related side effects, which limit its clinical usefulness. The minimal dose of meperidine that is effective for IVRA has yet to be established. We added 0, 10, 20, 30, 40, or 50 mg of meperidine to 0.5% lidocaine IVRA for either carpal tunnel or tenolysis surgery. Pain and sedation scores and the incidence of side effects were assessed in the postanesthesia care unit. The duration of analgesia, defined as the time to first request for pain medications, and use of acetaminophen/codeine (T3) tablets were measured. The duration of analgesia increased, in a dose-dependent manner, in the groups that received 0, 10, 20, and 30 mg of meperidine. There was no significant difference in the duration of analgesia for patients receiving > or = 30 mg of meperidine. T3 use was similar in the groups that received 0, 10, and 20 mg of meperidine and in the groups that received 30, 40, and 50 mg. T3 use was significantly lower in the larger dose groups. The incidence of sedation and of all other side effects was significantly higher in the groups that received 30-50 mg of meperidine compared with those that received smaller doses. We conclude that doses of meperidine large enough to produce the most effective postoperative analgesia with IVRA lidocaine causes a significant incidence of side effects, thus limiting its clinical usefulness. IMPLICATIONS Meperidine may be a useful addition to 0.5% lidocaine for i.v. regional anesthesia. We showed that 30 mg is the optimal dose of meperidine with respect to postoperative analgesia. However, this dose caused a significant incidence of sedation, dizziness, and postoperative nausea and vomiting.

Ketorolac as an adjunct to patient-controlled morphine in postoperative spine surgery patients

Background and Objectives. This randomized double-blind study was designed to determine whether administration of ketorolac either on schedule or as a component of patient-controlled analgesia (PCA) to patients who have undergone spinal stabilization would decrease PCA morphine use, decrease side effects, and/or enhance analgesia. Methods. Eighty inpatients undergoing spine stabilization by one surgeon were evaluated after excluding patients with contraindications to the use of ketorolac or morphine. All patients received PCA morphine. The patients were divided into four groups, which were given either intravenous saline (control group); intravenous ketorolac 15 mg every 6 hours; intravenous ketorolac 30 mg every 6 hours; or ketorolac added to the PCA morphine on a milligram per milligram basis. The outcome measures included pain scores, 24-hour morphine use, level of sedation, and side effect profile at six times during the first 24 postoperative hours. Results: The total dose of morphine (P

Intraarticular Morphine in the Multimodal Analgesic Management of Postoperative Pain After Ambulatory Anterior Cruciate Ligament Repair

Reconstruction of the anterior cruciate ligament (ACL) is associated with a considerable degree of postoperative pain.Our customary multimodal approach to postoperative analgesia after ambulatory ACL surgery includes perioperative nonsteroidal antiinflammatory drugs, pre- and postincisional intraarticular (IA) bupivacaine (B), and postoperative cryotherapy using an external cooling system. This study was designed to determine whether the addition of IA morphine (MS) provides improved postoperative analgesia. One hundred patients scheduled for elective ambulatory ACL repair received our standard multimodal therapy. After surgery, patients were randomized to one of four study groups. Group 1 received 30 mL of 0.25% B IA. Group 2 received 30 mL of normal saline IA and 5 mg of MSIA. Group 3 received 30 mL of 0.25% bupivacaine IA and 5 mg of MS IV. Group 4 received 30 mL of 0.25% B IA and 5 mg of MS IA. The addition of IA B postoperatively provided prolonged analgesia and decreased postoperative pain and analgesic requirements. The addition of MS to IA B did not provide additional postoperative analgesia. We conclude that patients undergoing ambulatory ACL repair using our standard multimodal analgesic regimen failed to receive additional postoperative analgesia when MS was added to the IA B. Implications: Patients receiving a multimodal analgesic regimen of perioperative nonsteroidal antiinflammatory drugs, intraarticular bupivacaine, and external cooling did not receive any additional analgesia from intraarticular morphine. (Anesth Analg 1998;86:374-8)

The effect of cyclooxygenase-2 inhibition on acute and chronic donor-site pain after spinal-fusion surgery.

BACKGROUND AND OBJECTIVES The development of chronic pain after spinal-fusion surgery represents a significant source of morbidity. One of the predictive factors for the development of chronic postsurgical pain is inadequate acute postoperative pain management. Further, the up-regulation of cyclooxygenase-2 (COX-2) after surgery may result in neuro-plastic changes that may contribute to a progression from acute to chronic pain. The goal of this prospective, randomized, double-blind study was to examine the effect of perioperative COX-2 inhibition on acute and chronic donor-site pain in patients undergoing spinal-fusion surgery. METHODS Eighty patients scheduled to undergo instrumented posterior spinal fusion were randomized to either receive celecoxib 400 mg 1 hour before surgery, and then 200 mg every 12 hours after surgery for the first 5 days or receive matching placebo at similar time intervals. Patients were administered morphine via patient-controlled analgesia pump for the first 24 hours, and then acetaminophen and oxycodone tablets. Patients were asked to quantify their average pain on postoperative days 1 to 5. At 1 year after surgery, patients were questioned about the presence and subjective characteristics of any residual donor-site pain. RESULTS Patients administered celecoxib reported lower pain scores and less opioid use during the first 5 postoperative days. Chronic donor-site pain was significantly higher (P<.01) in the placebo group (12 of 40, or 30%) compared with the celecoxib group (4 of 40, or 10%) at 1 year after surgery. CONCLUSIONS The administration of celecoxib for the first 5 days after spinal-fusion surgery resulted in improved analgesia and a reduction in chronic donor-site pain at 1 year after surgery.

Postoperative modulation of central nervous system prostaglandin E2 by cyclooxygenase inhibitors after vascular surgery.

BACKGROUND The clinical availability of injectable cyclooxygenase inhibitors allows examination of the importance of cyclooxygenase 1 and 2 after surgery. The authors hypothesize that spinal prostaglandin E2 increases with lower extremity vascular surgery and that spinal prostaglandin E2 decreases with intravenous postsurgical administration of either a mixed cyclooxygenase 1/2 inhibitor (ketorolac) or a cyclooxygenase 2 selective inhibitor (parecoxib). METHODS Thirty patients undergoing elective lower extremity revascularization under continuous spinal anesthesia had cerebrospinal fluid obtained at baseline and then up to 6 h after the start of surgery. Four hours after surgical incision, patients were randomized to receive intravenous parecoxib 40 mg, ketorolac 30 mg, or preservative-free normal saline. Patients were administered intravenous fentanyl in the postanesthesia care unit and acetaminophen/oxycodone on the surgical ward to control pain. RESULTS Cerebrospinal fluid prostaglandin E2 concentrations were increased during and after surgery. After surgery, intravenous parecoxib 40 mg rapidly decreased cerebrospinal fluid prostaglandin E2, and intravenous ketorolac 30 mg also reduced cerebrospinal fluid prostaglandin E2 compared with placebo, but not as much as parecoxib. Postanesthesia care unit pain scores were reduced in the two drug groups compared with placebo, and surgical ward pain scores were also decreased for both drug groups, especially with parecoxib. No patient receiving parecoxib required postoperative intravenous fentanyl. Acetaminophen/oxycodone consumption was reduced in both drug groups compared with placebo, more so with parecoxib. CONCLUSIONS Cerebrospinal fluid prostaglandin E2 is elevated in patients after lower extremity vascular surgery. Postsurgical intravenous administration of the cyclooxygenase 1/2 inhibitor ketorolac, and especially the cyclooxygenase 2 inhibitor parecoxib, reduces cerebrospinal fluid prostaglandin E2 concentration and postoperative pain.

An evaluation of the analgesic efficacy of intravenous regional anesthesia with lidocaine and ketorolac using a forearm versus upper arm tourniquet.

UNLABELLED Intravenous regional anesthesia (IVRA) using a forearm tourniquet may be a potentially safer technique compared with using an upper arm tourniquet. Ketorolac is a useful adjuvant to lidocaine for IVRA. In this study, we assessed the analgesic efficacy of administering IVRA lidocaine and ketorolac with either a forearm or upper arm tourniquet for outpatient hand surgery. Upper arm IVRA was established using 40 mL of a solution containing 200 mg of lidocaine and ketorolac 20 mg (0.5 mg/mL). Forearm IVRA was established using 20 mL of a solution containing 100 mg of lidocaine and ketorolac 10 mg (0.5 mg/mL). Onset and duration of sensory block as well as postoperative pain and analgesic use were recorded. The patients who received forearm IVRA had a significantly longer period during which they required no analgesics (701 +/- 133 min) compared with 624 +/- 80 min for the upper arm IVRA ketorolac patients (P = 0.032). Onset of sensory block was similar between the two groups; however, recovery of sensation was significantly longer in the Forearm IVRA (22 +/- 5 min) group compared with the Upper Arm IVRA (13 +/- 3 min) group (P < 0.05). There were no differences in postoperative analgesic use or pain scores between the two groups. We conclude that forearm IVRA with lidocaine and ketorolac provides safe and effective perioperative analgesia for patients undergoing ambulatory hand surgery. This technique results in a longer duration of sensory block and prolonged postoperative analgesia compared with upper arm IVRA while using one-half the doses of both lidocaine and ketorolac. IMPLICATIONS Forearm tourniquet intravenous regional anesthesia (IVRA) with 50% less lidocaine and ketorolac provides for both a longer duration of sensory block and prolonged postoperative analgesia compared with upper arm IVRA.

Acute toxic delirium in a patient using transdermal fentanyl.

ecent advances in transdermal drug systems permit continuous delivery of medications to R patients for a variety of indications. The development of such a system for fentanyl (Duragesic, Janssen Pharmaceutica) has greatly expanded the use of systemic fentanyl for patients with chronic pain. Using this device, serum concentrations of fentanyl reach a plateau after approximately 18 h and tend to remain stable thereafter (1). Few complications have been reported, of which nausea and somnolence are the most common (1,2). We report a case of acute toxic delirium in a patient who used transdermal fentanyl patches for 24 days.

Gastric perforation associated with the use of celecoxib.

NONSTEROIDAL antiinflammatory drugs (NSAIDs) are among the most commonly used drugs in the treatment of musculoskeletal disease. NSAIDs inhibit prostaglandin biosynthesis by inhibiting the enzyme cyclooxygenase (COX), the rate-limiting enzyme of prostaglandin synthesis. 1 NSAIDs impair prostaglandin-dependent mucosal protective mechanisms, including gastric blood flow and secretion of gastric mucus, bicarbonate, and surfactant-like phospholipid. 2,3 Two distinct COX isozymes exist: COX-1 is a constitutive enzyme expressed in many tissues, including the gastric mucosa, whereas COX-2 is an inducible enzyme expressed in fibroblasts, macrophages, and other inflammatory mediators. 4,5 Most currently marketed NSAIDs inhibit both COX-1 and COX-2 enzymes with approximately equal potency. Therefore, these NSAIDs inhibit both the inflammatory response (COX-2) as well as the maintenance of regular cellular physiology (COX-1). Selective COX-2 inhibitors were developed with the goal of providing effective antiinflammatory and analgesic activity without causing gastrointestinal side effects. We report a case in which gastric perforation developed after the administration of celecoxib, a new selective COX-2 NSAID, in a patient recovering from a gastric ulcer.