Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2005
Clinical TrialThe effects of sevoflurane and hyperventilation on electrocorticogram spike activity in patients with refractory epilepsy.
We investigated the effects of sevoflurane and hyperventilation on intraoperative electrocorticogram (ECoG) spike activity in 13 patients with intractable epilepsy. Grid electrodes were placed on the brain surface and ECoG was recorded under the following conditions: 1) 0.5 minimal alveolar anesthetic concentration (MAC) sevoflurane, 2) 1.5 MAC sevoflurane, and 3) 1.5 MAC sevoflurane with hyperventilation. The number of spikes per 5 min and the percentage of leads with spikes were assessed in each condition. In 4 patients with chronically implanted-subdural electrodes, the leads with seizure onset and with spikes during the interictal periods in the awake state were compared with those during sevoflurane anesthesia at 0.5 MAC and 1.5 MAC. The number of spikes and the percentage of leads with spikes were significantly more under 1.5 MAC sevoflurane anesthesia compared with those under 0.5 MAC sevoflurane (P < 0.05). The induction of hyperventilation significantly increased the number of spikes and percentage of leads with spikes (P < 0.05). With 0.5 MAC sevoflurane, the leads with spikes were similar to those at seizure onset in the awake state, whereas with 1.5 MAC sevoflurane, spikes were similar to those occurring during interictal periods in the awake state. These results indicate that sevoflurane and hyperventilation can affect the frequency and extent of ECoG spike activity in patients with intractable epilepsy. Careful attention should be paid to the concentration of sevoflurane used and ventilatory status when intraoperative EcoG is used to localize epileptic lesions. ⋯ Electrocorticogram can be used to define the location and extent of epileptic foci during epilepsy surgery. However, electrocorticogram can be affected by anesthetic technique. The present study found that sevoflurane concentration and hyperventilation affected the frequency and the extent of electrocorticogram spike activity in epileptic patients.
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Anesthesia and analgesia · Aug 2005
Clinical TrialPredictive factors of early postoperative urinary retention in the postanesthesia care unit.
Urinary retention is a common postoperative complication associated with bladder overdistension and the risk of permanent detrusor damage. The goal of this study was to determine predictive factors of early postoperative urinary retention in the postanesthesia care unit (PACU). We prospectively collected, in 313 adult patients, variables including age, gender, previous history of urinary tract symptoms, type of surgery and anesthesia, intraoperative administration of anticholinergics, amount of intraoperative fluids, IV morphine titration, and bladder volume on entry to the PACU. For each patient, bladder volume was measured by ultrasound on entry and before discharge from the PACU. Urinary retention was defined as a bladder volume larger than 600 mL with an inability to void within 30 min. Predictive factors were identified by multivariate analysis. The incidence of urinary retention in the PACU was 16%. In the multivariate analysis only the amount of intraoperative fluids (>or=750 mL; P = 0.02; odds ratio = 2.3), age (>or=50 yr; P = 0.008; odds ratio = 2.4), and bladder volume on entry to PACU (>or=270 mL; P = 0.0001; odds ratio = 4.8) were found to independently increase the risk of urinary retention. Considering the clinical impact of undiagnosed postoperative urinary retention, these results suggest systematic evaluation of bladder volume with a portable ultrasound device in the PACU, especially in patients with risk factors. ⋯ In this observational study, the ultrasound monitoring of bladder volume in the postanesthesia care unit (PACU) revealed that postoperative urinary retention occurred with an incidence of 16%. Age (>or=50 yr), amount of intraoperative fluid volume (>or=750 mL), and bladder volume on entry to PACU (>or=270 mL) were independent predictive factors for this complication.
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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.