Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialChoice of electrocardiography lead does not affect the usefulness of the T-wave criterion for detecting intravascular injection of an epinephrine test dose in anesthetized children.
Accidental intravascular injection of an epinephrine-containing test dose increases T-wave amplitude of lead II electrocardiogram (EKG) in anesthetized children. We designed this study to test whether the choice of EKG lead would affect the usefulness of simulated intravascular test dose. We studied 32 ASA physical status I infants and children (aged 6-49 mo) undergoing elective surgeries during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen. When hemodynamic stability was obtained, all subjects received IV saline 0.1 mL/kg, followed 4 min later by an IV test dose (0.1 mL/kg) consisting of 1% lidocaine with 1:200,000 epinephrine (epinephrine 0.5 microg/kg) via a peripheral vein to simulate the intravascular injection of the test dose. Heart rate and systolic blood pressure were recorded every 20 and 60 s, respectively, and leads II (n = 32), V(5) (n = 32) and either lead I (n = 15) or III (n = 17), choosing the one with greater preinjection T-wave amplitude, were continuously recorded for 4 min after the saline and the test dose injections. An IV test dose produced significant increases in heart rate, systolic blood pressure, and T-wave amplitude of all EKG leads studied in all subjects, whereas IV saline elicited no changes in these variables. Maximal increases in T-wave amplitude of leads II, I, III, and V(5) were 158% +/- 69%, 175% +/- 78%, 147% +/- 89%, and 170% +/- 72%, respectively (mean +/- SD, P > 0.05). There was no significant difference in temporal changes in T-wave amplitude among the 4 leads, and sensitivity and specificity were 100% on the basis of the T-wave criterion irrespective of the lead examined. Our results indicate that leads II, I, III, and V(5) of EKG are equally effective for detecting intravascular injection of the epinephrine-containing test dose in sevoflurane-anesthetized children. ⋯ To determine whether an epidurally administered local anesthetic has been accidentally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that increases in T-wave amplitude in leads I, II, III, and V(5) of the electrocardiogram are equally sensitive and specific for detecting intravascular injection of the epinephrine-containing test dose in sevoflurane-anesthetized infants and children.
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Anesthesia and analgesia · Aug 2003
Randomized Controlled Trial Clinical TrialThe effect of small dose fentanyl on the emergence characteristics of pediatric patients after sevoflurane anesthesia without surgery.
We designed this study to measure the effect of a small dose of IV fentanyl on the emergence characteristics of pediatric patients undergoing sevoflurane anesthesia without any surgical intervention. Thirty-two ASA physical status I or II pediatric outpatients receiving sevoflurane anesthesia for magnetic resonance imaging scans were enrolled and assigned in a random and double-blinded manner to receive either placebo (saline) or 1 micro g/kg IV fentanyl 10 min before discontinuation of their anesthetic. The primary outcome measure was the percentage of patients with emergence agitation. We also evaluated the duration of agitation and time to meet hospital discharge criteria. Patients who received fentanyl had a decreased incidence of agitation (12% versus 56%) when compared with placebo. There was no significant difference in time to meet hospital discharge criteria. We conclude that the addition of a small dose of fentanyl to inhaled sevoflurane anesthesia decreases the incidence of emergence agitation independent of pain control effects. ⋯ The addition of a small dose of fentanyl given to patients undergoing nonsurgical sevoflurane anesthesia resulted in a significant decrease in emergence agitation in a prospective, randomized, and controlled trial involving pediatric patients.
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Anesthesia and analgesia · Aug 2003
Postoperative pain experience: results from a national survey suggest postoperative pain continues to be undermanaged.
Postoperative pain can have a significant effect on patient recovery. An understanding of patient attitudes and concerns about postoperative pain is important for identifying ways health care professionals can improve postoperative care. To assess patients' postoperative pain experience and the status of acute pain management, we conducted a national study by using telephone questionnaires. A random sample of 250 adults who had undergone surgical procedures recently in the United States was obtained from National Family Opinion. Patients were asked about the severity of postsurgical pain, treatment, satisfaction with pain medication, patient education, and perceptions about postoperative pain and pain medications. Approximately 80% of patients experienced acute pain after surgery. Of these patients, 86% had moderate, severe, or extreme pain, with more patients experiencing pain after discharge than before discharge. Experiencing postoperative pain was the most common concern (59%) of patients. Almost 25% of patients who received pain medications experienced adverse effects; however, almost 90% of them were satisfied with their pain medications. Approximately two thirds of patients reported that a health care professional talked with them about their pain. Despite an increased focus on pain management programs and the development of new standards for pain management, many patients continue to experience intense pain after surgery. Additional efforts are required to improve patients' postoperative pain experience. ⋯ A survey of 250 US adults who had undergone a recent surgical procedure asked about their postoperative pain experience. Approximately 80% of patients experienced pain after surgery. Of these patients, 86% had moderate, severe, or extreme pain. Additional efforts are required to improve patients' postoperative pain experience.
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Anesthesia and analgesia · Aug 2003
Lidocaine attenuates cytokine-induced cell injury in endothelial and vascular smooth muscle cells.
Local anesthetics have been reported to attenuate the inflammatory response and ischemia/reperfusion injury. Therefore, we hypothesized that pretreatment with local anesthetics may protect endothelial and vascular smooth muscle (VSM) cells from cytokine-induced injury. Human microvascular endothelial cells and rat VSM cells were pretreated with lidocaine or tetracaine (5-100 microM for 30 min) and then exposed to the cytokines tumor necrosis factor-alpha, interferon-gamma, and interleukin-1beta for 72 h. Cell survival and integrity were evaluated by trypan blue exclusion and lactate dehydrogenase release. The role of adenosine triphosphate-sensitive potassium (KATP) channels, protein kinase C, or both in modulating local anesthetic-induced protection was evaluated with the mitochondrial KATP antagonist 5-hydroxydecanoate, the cell-surface KATP antagonist 1-[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenyl]sulfonyl-3-methylthiourea (HMR-1098), and the protein kinase C inhibitor staurosporine. Lidocaine attenuated cytokine-induced cell injury in a dose-dependent manner. Lidocaine (5 microM) increased cell survival by approximately 10%, whereas lidocaine (100 microM) increased cell survival by approximately 60% and induced a threefold decrease in lactate dehydrogenase release in both cell types. In contrast, tetracaine did not attenuate cytokine-induced cell injury. 5-hydroxydecanoate abolished the protective effects of lidocaine, but staurosporine and HMR-1098 had no effect on the lidocaine-induced protection. This study showed that lidocaine, but not tetracaine, attenuates cytokine-induced injury in endothelial and VSM cells. Lidocaine-induced protection appears to be modulated by mitochondrial KATP channels. ⋯ This study demonstrates that lidocaine attenuates cytokine-induced injury of endothelial and vascular smooth muscle cells via mechanisms involving adenosine triphosphate-sensitive potassium channels. Protection of the vasculature from cytokine-induced inflammation may preserve important physiological endothelial and vascular smooth muscle functions.
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Anesthesia and analgesia · Aug 2003
gamma-Aminobutyric acid-A receptors contribute to isoflurane neuroprotection in organotypic hippocampal cultures.
The mechanisms by which anesthetics such as isoflurane reduce cell death in rodent models of cerebral ischemia remain incompletely defined. Reduction in glutamate excitotoxicity explains some but not all of isoflurane's neuroprotection. Because isoflurane potentiates gamma-aminobutyric acid (GABA) receptor-mediated ion fluxes and GABA(A) receptor agonists have neuroprotective effects, we hypothesized that GABA(A) receptors contribute to isoflurane neuroprotection. As a model of cerebral ischemia and recovery, we used rat hippocampal slice cultures. Survival of CA1, CA3, and dentate neurons was examined 2 and 3 days after 1-h combined oxygen-glucose deprivation (OGD) at 37 degrees C. To define the role of GABA(A) receptors in mediating protection, the effect of 1% isoflurane on cell survival was examined in the presence of the GABA(A) antagonist bicuculline during OGD. Cell death was measured with propidium iodide fluorescence. Isoflurane and the selective GABA(A) agonist muscimol (25 micro M) reduced cell death after OGD to values similar to slices not exposed to OGD, with the exception that muscimol did not reduce cell death in CA3 neurons 2 days after OGD. The GABA(A) antagonist bicuculline reduced the neuroprotective effects of isoflurane on hippocampal neurons 2 and 3 days after OGD. We conclude that GABA(A) receptors contribute to neuroprotection against OGD produced by isoflurane in the hippocampal slice model. Based on this and other studies, it is likely that neuroprotection produced by isoflurane is multifactorial and includes actions at both GABA(A) and glutamate receptors and possibly other mechanisms. ⋯ Isoflurane is neuroprotective in rodent brain ischemia models, but the mechanisms for this effect remain incompletely defined. In organotypic cultures of rat hippocampus, we show that protection of CA1, CA3, and dentate neurons by 1% isoflurane from death caused by oxygen and glucose deprivation involves GABA(A) receptors.