Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2002
Randomized Controlled Trial Clinical TrialThe interaction between propofol and clonidine for loss of consciousness.
Clonidine premedication reduces the intraoperative requirement for opioids and volatile anesthetics. Clonidine also reduces the induction dose of IV anesthetics. There is no information, however, regarding the effect of oral clonidine premedication on the propofol blood concentrations required for loss of consciousness, and the interaction between propofol and clonidine. We randomly administered target effect-site concentrations of propofol ranging from 0.5 to 5. 0 microg/mL by using computer-assisted target-controlled infusion to 3 groups of healthy male patients: Control (n = 35), 2.5 microg/kg Clonidine (n = 36), and 5.0 microg/kg Clonidine (n = 36) groups. Nothing was administered to the Control group. Clonidine (2.5 or 5.0 microg/kg) was administered orally 90 min before the induction of anesthesia in the Clonidine groups. After equilibration between the blood and effect-site for 15 min, a verbal command to open their eyes was given two times to the patients. Arterial blood samples for analysis of the serum propofol and clonidine concentrations were taken immediately before verbal commands were given. Measured serum propofol concentrations in equilibrium with the effect-site at which 50% of the patients did not respond to verbal commands (EC50 for loss of consciousness) were determined by logistic regression. The EC50 +/- SE values in the Control, 2.5 microg/kg Clonidine, and 5.0 microg/kg Clonidine groups were 2.67 +/- 0.18, 1.31 +/- 0.12, and 0.91 +/- 0.13 microg/mL, respectively. The EC50 in the 2.5 and 5.0 microg/kg clonidine groups was significantly smaller than that in the Control group (P < 0.001). The use of a response surface modeling analysis indicated that there was an additive interaction between measured arterial propofol and clonidine concentrations in relation to loss of consciousness. These results indicate that propofol and clonidine act additively for loss of consciousness. ⋯ Oral clonidine 2.5 and 5.0 microg/kg premedication decreases the propofol concentration required for loss of consciousness.
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Anesthesia and analgesia · Apr 2002
The origin of the spinal subdural space: ultrastructure findings.
Previous studies of samples from cranial meninges have created doubts about the existence of a virtual subdural space. We examined the ultrastructure of spinal meninges from three human cadavers immediately after death to see whether there is a virtual subdural space at this level. The arachnoid mater had two portions: a compact laminar portion covering the dural sac internal surface and a trabecular portion extending like a spider web around the pia mater. There was a cellular interface between the laminar arachnoid and the internal layer of the dura that we called the dura-arachnoid interface. There was no subdural space in those specimens where the dura mater was macroscopically in continuity with the arachnoid trabecules. In the specimens where the dura mater was separated from the arachnoid, we found fissures in between the neurothelial cells that extended throughout the interface. We hypothesize that the subdural space would have its origin within the dura-arachnoid interface when the neurothelial cells break up, creating in this way a real subdural space. ⋯ The subdural space was not seen under transmission electron microscopy in samples of human spinal meninges where surgical manipulation was avoided. Scanning electron microscopy in other samples showed the presence of broken neurothelial cells giving up fissures that extended along the dura-arachnoid interface. These findings may explain the origin of a real subdural space.
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Anesthesia and analgesia · Apr 2002
Randomized Controlled Trial Clinical TrialPostoperative analgesia with continuous sciatic nerve block after foot surgery: a prospective, randomized comparison between the popliteal and subgluteal approaches.
To compare the posterior popliteal and subgluteal continuous sciatic nerve block for anesthesia and acute postoperative pain management after foot surgery, 60 ASA physical status I and II patients undergoing elective orthopedic foot surgery were randomly assigned to either a Subgluteal group (n = 30) or Popliteal group (n = 30). Before surgery and after performing a femoral nerve block with 15 mL of 2% mepivacaine, we performed the sciatic nerve block with 20 mL of 0.75% ropivacaine using either a subgluteal or posterior popliteal approach, and the placement of a catheter came afterward. In the recovery room, the catheter was connected to a patient-controlled analgesia pump to infuse 0.2% ropivacaine (basal infusion rate of 5 mL/h, incremental bolus of 10 mL, and a lockout time of 60 min). There were no technical problems in catheter placement. Intraoperative efficacy of nerve block was similar in the two groups. Postoperative catheter displacement and occlusion were recorded in four patients in the Popliteal group and two patients in the Subgluteal group (P = 0.67). Both approaches provided similar postoperative analgesia. We conclude that the subgluteal approach is as effective and safe as the previously described posterior popliteal approach for continuous sciatic block and can be considered a useful alternative to anesthesia and acute postoperative analgesia after foot procedures. ⋯ Comparing two different approaches for continuous sciatic nerve block after orthopedic foot surgery, this prospective, randomized study demonstrated that the subgluteal approach is as effective and safe as the previously described posterior popliteal approach, and can be considered a useful alternative to anesthesia and acute postoperative analgesia after foot procedures.
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Anesthesia and analgesia · Apr 2002
Intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension.
Sympathetic hyperactivity during sudden intracranial hypertension leads to cardiovascular instability, myocardial dysfunction, and neurogenic pulmonary edema. Because spinal anesthesia is associated with sympatholysis, we investigated the protective effects of intrathecal lidocaine in a rodent model. Halothane-anesthetized rats were given a 10-microL intrathecal injection of saline (n = 10) or lidocaine 1% (n = 6). A subdural balloon catheter was inflated for 60 s to produce intracranial hypertension. Hemodynamics were monitored, and hearts and lungs were harvested for histological examination. In Saline versus Lidocaine-Treated rats, peak mean arterial blood pressure during balloon inflation was 115 +/- 4 mm Hg versus 78 +/- 8 mm Hg (P < 0.05), mean arterial blood pressure 30 min after balloon deflation was 47 +/- 2 mm Hg versus 67 +/- 3 mm Hg (P < 0.05), and lung weight was 1.54 +/- 0.03 g versus 1.41 +/- 0.04 g (P < 0.05), respectively. Cardiac dysrhythmias and electrocardiographic changes were more frequent in the Saline-Treated group (P < 0.05). Saline-Treated rats had extensive, hemorrhagic pulmonary edema, whereas the Lidocaine-Treated rats had only patchy areas of lung abnormality. Histological changes in the myocardium were rare, and no difference was found between the two groups. We conclude that intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension. ⋯ In a rat model of intracranial balloon inflation, intrathecal lidocaine prevented cardiovascular collapse and neurogenic pulmonary edema. Descending neural pathways are involved in the development of cardiopulmonary complications associated with acute intracranial hypertension.
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Anesthesia and analgesia · Apr 2002
Prolonged intravenous remifentanil infusion for labor analgesia.
A 34-h remifentanil infusion was administered for labor analgesia in a patient with thrombocytopenia and renal insufficiency. Compared with other opioids, remifentanil may produce fewer cumulative effects during prolonged infusion because of its unique metabolism.