Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2005
Comparative StudyThe comparative neurotoxicity of intrathecal lidocaine and bupivacaine in rats.
There is a considerable difference in the number of reports of neurologic injury in the literature between lidocaine and other local anesthetics. Few in vivo animal studies have produced convincing results showing a difference in neurotoxicity among anesthetics. We investigated whether lidocaine and bupivacaine differ with respect to sensory impairment and histologic damage when equipotent doses of the two are administered intrathecally in rats. First, to determine relative anesthetic potency, rats intrathecally received 20 muL of saline, 0.625%, 1.25%, 2.5%, or 5% lidocaine, or 0.125%, 0.25%, 0.5%, or 1.0% bupivacaine, and were examined with the tail-flick test for 90 min. The potency ratio calculated was approximately 1:4.70 (95% confidence interval, 3.65-6.07) for lidocaine/bupivacaine. In the next experiment, 45 rats intrathecally received 20 muL of saline, 2.13% bupivacaine (approximately 1.5 mg/kg), or 10% lidocaine (approximately 6.9 mg/kg), and were examined for persistent functional impairment and morphologic damage. Rats given lidocaine developed significantly more prolonged tail-flick latencies than those in other groups 4 days after injection and incurred more morphologic damage than those given saline or bupivacaine. In conclusion, although the doses of anesthetics administered were larger than those used clinically, the present results suggest that bupivacaine is less neurotoxic than lidocaine when administered intrathecally at equipotent concentrations in the rat model. ⋯ Bupivacaine induces less severe functional impairment and morphologic damage than lidocaine when the two anesthetics are intrathecally administered at equipotent concentrations in the rat.
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Anesthesia and analgesia · Aug 2005
The efficacy and safety of pain management before and after implementation of hospital-wide pain management standards: is patient safety compromised by treatment based solely on numerical pain ratings?
Inadequate analgesia in hospitalized patients prompted the Joint Commission on Accreditation of Healthcare Organizations in 2001 to introduce standards that require pain assessment and treatment. In response, many institutions implemented treatment guided by patient reports of pain intensity indexed with a numerical scale. Patient safety associated with treatment of pain guided by a numerical pain treatment algorithm (NPTA) has not been examined. We reviewed patient satisfaction with pain control and opioid-related adverse drug reactions before and after implementation of our NPTA. Patient satisfaction with pain management, measured on a 1-5 scale, significantly improved from 4.13 to 4.38 (P < 0.001) after implementation of an NPTA. The incidence of opioid over sedation adverse drug reactions per 100,000 inpatient hospital days increased from 11.0 pre-NPTA to 24.5 post-NPTA (P < 0.001). Of these patients, 94% had a documented decrease in their level of consciousness preceding the event. Although there was an improvement in patient satisfaction, we experienced a more than two-fold increase in the incidence of opioid over sedation adverse drug reactions in our hospital after the implementation of NPTA. Most adverse drug reactions were preceded by a documented decrease in the patient's level of consciousness, which emphasizes the importance of clinical assessment in managing pain. ⋯ Although patient satisfaction with pain management has significantly improved since the adoption of pain management standards, adverse drug reactions have more than doubled. For the treatment of pain to be safe and effective, we must consider more than just a one-dimensional numerical assessment of pain.
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Anesthesia and analgesia · Aug 2005
Case ReportsBrown-Séquard syndrome following removal of a cerebrospinal fluid drainage catheter after thoracic aortic surgery.
Neurological deficit remains a devastating complication of thoracic aortic surgery despite advances in methods to protect the spinal cord from ischemia. Various techniques have been used, including the combination of cerebrospinal fluid (CSF) drainage and distal aortic perfusion to decrease the incidence of postoperative neurological deficit. These deficits are usually bilateral and result in paraplegia. In this case report we present a patient with Type B aortic dissection and thoracoabdominal aortic aneurysm repair with insertion of a lumbar CSF drainage catheter. Postoperatively, the patient developed unilateral neurological features consistent with Brown-Séquard syndrome after removal of the CSF catheter. The lumbar cerebrospinal fluid catheter was reinserted and the CSF was drained. Medullary T6-7 signal abnormalities were seen on spinal cord magnetic resonance imaging, and we suggest that the spinal cord suffered a direct injury during catheter removal. The patient had an uneventful recovery. ⋯ We describe a patient who developed unilateral neurologic features suggestive of Brown-Sequard syndrome following removal of a cerebrospinal fluid catheter after thoracic aortic surgery. We suggest that the spinal cord was injured during catheter removal. The catheter was reinserted and the patient had a full neurologic recovery.
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Anesthesia and analgesia · Aug 2005
The inhibitory effects of sevoflurane on angiotensin II- induced, p44/42 mitogen-activated protein kinase-mediated contraction of rat aortic smooth muscle.
Sevoflurane dilates blood vessels and reduces arterial blood pressure in a dose-dependent manner. Angiotensin II (Ang II) is one of the primary regulators of vascular tension and arterial blood pressure, and the p44/42 mitogen-activated protein kinases (p44/42 MAPK) are involved in Ang II-mediated vascular smooth muscle contraction. We designed this study to examine the effects of sevoflurane on Ang II-induced, p44/42 MAPK-mediated contraction of rat aortic smooth muscle. The effects of the p44/42 MAPK kinase (MEK1/2) inhibitor, PD 098059 (10(-5) molar [M], 5 x 10(-5) M and 10(-4) M), and sevoflurane (1.7%, 3.4%, and 5.1%) on Ang II-induced contraction and p44/42 MAPK phosphorylation were tested in rat aortic smooth muscle, using isometric force measurement and Western blot analysis, respectively. Ang II induced both a transient contractile response and phosphorylation of p44/42 MAPK, which were significantly attenuated by PD 098059 (P < 0.05-0.01). Sevoflurane inhibited Ang II-induced contractile response in a dose-dependent manner (P < 0.05 and 0.01 in response to 3.4% and 5.1% sevoflurane, respectively). Sevoflurane also dose-dependently depressed Ang II-elicited p44/42 MAPK phosphorylation (P < 0.01 in response to 3.4% and 5.1% sevoflurane). These results suggest that the inhibitory effect of sevoflurane on Ang II-induced vasoconstriction is, at least in part, caused by the inhibition of the p44/42 MAPK-mediated signaling pathway. ⋯ The present study demonstrates that sevoflurane can dose-dependently inhibit both angiotensin II (Ang II)-induced contraction and p44/42 MAPK phosphorylation of rat aortic smooth muscle. These data suggest that sevoflurane-produced inhibition of Ang II-induced vasoconstriction is, at least in part, caused by depression of the p44/42 MAPK-mediated signaling pathway.
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Anesthesia and analgesia · Aug 2005
Comment Letter Clinical TrialLidocaine toxicity in volunteer subjects undergoing awake fiberoptic intubation.