Faculty Bibliography

SUMMARY By all criteria studied (quality of pain relief, length of stay in the PACU, side effects and patient satisfaction), a femoral nerve block is an excellent alternative to routine narcotic pain medication in patients undergoing hip arthroscopy. DATA Purpose: To evaluate the utility of femoral nerve blocks in post-operative pain control after hip arthroscopy. Methods: Forty consecutive patients scheduled for hip arthroscopy were randomized into two groups for postoperative pain control. Half were to receive routine intravenous narcotics for pain scores of seven or above in the PACU, the other half were to receive a femoral nerve block in the PACU for the same pain scores. Data was compared with respect to patient sex, age, nausea, overall satisfaction with analgesia, and duration of time in the PACU. Results: Thirty-six patients had initial pain scores of seven or greater. Sixteen were randomized to receive post-operative morphine, and twenty to receive a femoral nerve block. There were no significant differences between the two groups with respect to sex or age of the patients. Patients who received morphine had a significantly longer time to discharge from the PACU (216 mins) than the femoral nerve block group (177 mins). The morphine group was also significantly more likely to report post-operative nausea (75%) than the femoral nerve block group (10%). Patients receiving femoral nerve blocks were significantly more likely to be satisfied with their post-operative pain control (90%) than those who had received morphine (25%). All of the patients receiving femoral nerve block stated that they would have the block again if they needed another hip arthroscopy

BACKGROUND AND OBJECTIVE: Chlorhexidine is recommended by several anesthesiology societies for antisepsis before regional anesthesia, but there is concern it may be neurotoxic. We evaluated the cytotoxicity of chlorhexidine and povidone-iodine in human neuronal and rat Schwann cells. METHODS: Human SH-SY5Y neuroblastoma and rat RSC96 Schwann cells were incubated with serial dilutions of 2% chlorhexidine gluconate and 10% povidone-iodine for 10 minutes, and viability was assessed with the MTT colorimetry assay and a fluorescent assay using calcein and ethidium. Cell morphology during antiseptic incubation was observed under light microscopy. To estimate the amount of antiseptic a needle carries through tissues, tritium radioactivity was measured in an animal injection model. RESULTS: Chlorhexidine at all tested concentrations significantly decreased viability compared with controls in both SH-SY5Y and RSC96 cells (P < 0.001). Povidone-iodine significantly decreased viability for both cells at concentrations of 0.2% or higher (P < 0.001). At the same dilutions of 1:200, 1:150, and 1:100, chlorhexidine was more cytotoxic than povidone-iodine for both cells (P< 0.001). During chlorhexidine treatment, both cell types became rounded and shriveled. Less dramatic changes were observed with povidone-iodine. In the injection model, 1.75% +/- 1.29% of the maximum amount of radioactive contamination was carried through tissues. CONCLUSIONS: Chlorhexidine gluconate and povidone-iodine were cytotoxic to SH-SY5Y (neuronal) and RSC96 (Schwann) cells. Chlorhexidine was more potent than povidone-iodine at more dilute concentrations. However, the toxicity of the two was not different at concentrations used clinically. When using either of these agents for antisepsis before regional anesthesia, it is prudent to allow adequate drying time after application.

ABSTRACT: Simulation-based training is becoming an accepted tool for educating physicians before direct patient care. As ultrasound-guided regional anesthesia (UGRA) becomes a popular method for performing regional blocks, there is a need for learning the technical skills associated with the technique. Although simulator models do exist for learning UGRA, they either contain food and are therefore perishable or are not anatomically based. We developed 3 sonoanatomically based partial-task simulators for learning UGRA: an upper body torso for learning UGRA interscalene and infraclavicular nerve blocks, a femoral manikin for learning UGRA femoral nerve blocks, and a leg model for learning UGRA sciatic nerve blocks in the subgluteal and popliteal areas

A potentially life-threatening arrhythmia appeared on the preinduction electrocardiogram of an asymptomatic young woman prior to spine surgery. The patient was evaluated by electrophysiology and had a rare accessory pathway, a Mahaim Fiber

BACKGROUND: To our knowledge, no study to date has compared the use of spinal and general anesthesia in patients undergoing operative fixation of an unstable ankle fracture. The purpose of this study was to assess the effects of anesthesia type on postoperative pain and function in a large cohort of patients. METHODS: Between October 2000 and November 2006, 501 patients who underwent surgical fixation of an unstable ankle fracture were followed prospectively. Patients receiving spinal anesthesia were compared with a cohort who received general anesthesia. All patients were evaluated at three, six, and twelve months postoperatively with use of standardized, validated general and limb-specific outcome instruments. Standard and multivariable analyses comparing outcomes at these intervals were performed. RESULTS: Four hundred and sixty-six patients (93%) who had been followed for a minimum of one year met the inclusion criteria. Compared with the general anesthesia group, the spinal anesthesia group had a greater mean age (p = 0.005), higher classification on the American Society of Anesthesiologists system (p = 0.03), and a greater number of patients with diabetes (p = 0.02). There was no difference in sex distribution between the groups. At three months, patients who received spinal anesthesia had significantly better pain scores (p = 0.03) and total scores on the American Orthopaedic Foot and Ankle Society outcome instrument (p = 0.02). At six months, patients in the spinal anesthesia group continued to have better pain scores (p = 0.04), but there was no longer a difference in total scores (p = 0.06). At twelve months, no difference was detected between the groups in terms of functional or pain scores. There was no difference in complication rates between the groups. CONCLUSIONS: Patients who undergo fixation of an ankle fracture under spinal anesthesia seem to experience less pain and have better function in the early postoperative period. We recommend that, unless there is a specific contraindication, patients should be offered spinal anesthesia when undergoing operative fixation of an ankle fracture. LEVEL OF EVIDENCE: Therapeutic Level II. See Instructions to Authors for a complete description of levels of evidence

A majority of patients with acute and chronic pain experience breakthrough pain above their baseline, despite a fixed regimen. The characteristics of current short-acting oral medications are not optimal because they often peak too late and last beyond the duration of pain. Oral absorption limits the onset time, whereas the development of newer routes can shorten onset times. A number of medications, both opioid and nonopioid, are being developed for intranasal delivery with promising results. In addition to the intranasal administration route being efficacious, it also provides better patient satisfaction by allowing the patient to titrate their own pain medication. There are legitimate concerns for abuse and addiction with these medications, which will need to be minimized with proper dispensing modifications. A number of nonopioid agents are also entering the market that will allow for multimechanistic analgesic plans. Although ketamine is not a common component of current pain treatment plans, the development of an intranasal formulation may potentially produce wider acceptance. Many traditional medications, including ibuprofen and acetaminophen, have been developed for parenteral administration. Intravenous ibuprofen or diclofenac can be administered for a longer duration and have a lower bleeding risk then ketorolac. Intravenous acetaminophen can provide balanced analgesia when nonsteroidal anti-inflammatory drugs are contraindicated, as is common in the postoperative period. The role of individual agents in each specialty is not currently clear, but the future treatment of pain, both acute and chronic, is brighter with the addition of these formulations

BACKGROUND: In addition to inhibiting the excitation conduction process in peripheral nerves, local anesthetics (LAs) cause toxic effects on the central nervous system, cardiovascular system, neuromuscular junction, and cell metabolism. Different postoperative neurological complications are ascribed to the cytotoxicity of LAs, but the underlying mechanisms remain unclear. Because the clinical concentrations of LAs far exceed their EC(50) for inhibiting ion channel activity, ion channel block alone might not be sufficient to explain LA-induced cell death. However, it may contribute to cell death in combination with other actions. In this study, we compared the cytotoxicity of six frequently used LAs and will discuss the possible mechanism(s) underlying their toxicity. METHODS: In human SH-SY5Y neuroblastoma cells, viability upon exposure to six LAs (bupivacaine, ropivacaine, mepivacaine, lidocaine, procaine, and chloroprocaine) was quantitatively determined by the MTT-(3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetra-odium bromide) colorimetry assay and qualitatively confirmed by fluorescence imaging, using the LIVE/DEAD assay reagents (calcein/AM and ethidium homodimer-1). In addition, apoptotic activity was assessed by measuring the activation of caspase-3/-7 by imaging using a fluorescent caspase inhibitor (FLICA). Furthermore, LA effects on depolarization- and carbachol-stimulated intracellular Ca(2+)-responses were also evaluated. RESULTS: 1) After a 10-min treatment, all six LAs decreased cell viability in a concentration-dependent fashion. Their killing potency was procaine < or = mepivacaine < lidocaine < chloroprocaine < ropivacaine < bupivacaine (based on LD(50), the concentration at which 50% of cells were dead). Among these six LAs, only bupivacaine and lidocaine killed all cells with increasing concentration. 2) Both bupivacaine and lidocaine activated caspase-3/-7. Caspase activation required higher levels of lidocaine than bupivacaine. Moreover, the caspase activation by bupivacaine was slower than by lidocaine. Lidocaine at high concentrations caused an immediate caspase activation, but did not cause significant caspase activation at concentrations lower than 10 mM. 3) Procaine and chloroprocaine concentration-dependently inhibited the cytosolic Ca(2+)-response evoked by depolarization or receptor-activation in a similar manner as a previous observation made with bupivacaine, ropivacaine, mepivacaine, and lidocaine. None of the LAs caused a significant increase in the basal and Ca(2+)-evoked cytosolic Ca(2+)-level. CONCLUSION: LAs can cause rapid cell death, which is primarily due to necrosis. Lidocaine and bupivacaine can trigger apoptosis with either increased time of exposure or increased concentration. These effects might be related to postoperative neurologic injury. Lidocaine, linked to the highest incidence of transient neurological symptoms, was not the most toxic LA, whereas bupivacaine, a drug causing a very low incidence of transient neurological symptoms, was the most toxic LA in our cell model. This suggests that cytotoxicity-induced nerve injury might have different mechanisms for different LAs and different target(s) other than neurons