Anesthesia and analgesia
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Anesthesia and analgesia · Aug 2002
Randomized Controlled Trial Clinical TrialPostoperative pain relief using intermittent injections of 0.5% ropivacaine through a catheter after laparoscopic cholecystectomy.
Postoperative pain has been an important limiting factor for ambulatory laparoscopic cholecystectomy. We anesthetized 40 ASA physical status I-II patients using propofol for the induction and sevoflurane in oxygen and air for the maintenance of anesthesia. At the end of the anesthesia, the patients were randomized into one of two groups: Group P (Placebo) and Group R (0.5% Ropivacaine). Twenty milliliters of normal saline or ropivacaine, respectively, were injected intraperitoneally at the end of surgery via a catheter placed in the bed of the gall bladder. Postoperatively, intermittent injections (10 mL) of the study solution were given when required for pain. Ketobemidone 1-2 mg was given IV as rescue medication. Pain was assessed using a visual analog scale at 1, 2, 3, 4, 8, 12, 16, and 20 h after surgery and once each day for 1 wk at rest (deep pain), shoulder and incision sites, and pain during coughing. Recovery was assessed by the time to transfer from Phase 1 to 2, the ability to walk, drink, and eat, and the ability to void. Plasma concentrations of ropivacaine were measured in eight patients. Time to ability to walk, defecation, driving a car, and return to normal activities were also recorded through a questionnaire sent home with the patient. During the first 4 postoperative h, patients in Group R had lower scores for deep pain and during coughing compared with Group P (P < 0.05). No differences were found in the postoperative consumption of ketobemidone. Median times to recovery at home were similar between the groups. By the seventh day, 93% of the patients had returned to normal activities of daily living. We conclude that the early postoperative pain after ambulatory laparoscopic cholecystectomy could be relieved using intermittent injections of ropivacaine 0.5% into the bed of the gall bladder. ⋯ Early postoperative pain can be relieved by intermittent injections of ropivacaine 0.5% through a catheter placed in the bed of the gall bladder after ambulatory laparoscopic cholecystectomy.
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Anesthesia and analgesia · Aug 2002
Comparative Study Clinical Trial Controlled Clinical TrialEarly postoperative respiratory acidosis after large intravascular volume infusion of lactated ringer's solution during major spine surgery.
In this study, we compared the effects of large intravascular volume infusion of 0.9% saline (NS) or lactated Ringer's (LR) solution on electrolytes and acid base balance during major spine surgery and evaluated the postoperative effects. Thirty patients aged 18-70 yr were included in the study. General anesthesia was induced with 5 mg/kg thiopental and 0.1 mg/kg vecuronium IV. Anesthesia was maintained with oxygen in 70% nitrous oxide and 1.5%-2% sevoflurane. In Group I, the NS solution, and in Group II, the LR solution were infused 20 mL. kg(-1). h(-1) during the operation and 2.5 mL. kg(-1). h(-1), postoperatively. Electrolytes (Na+, K+, Cl-) and arterial blood gases were measured preoperatively, every hour intraoperatively and at the 1st, 2nd, 4th, 6th, and 12th hours postoperatively. In the NS group, pHa, HCO3 and base excess decreased, and Cl- values increased significantly at the 2nd hour and Na+ values increased at the 4th hour intraoperatively (P < 0.001). The values returned to normal ranges at the 12th hour postoperatively. In the LR group, blood gas analysis and electrolyte values did not show any significant difference intraoperatively, but the increase in PaCO2 and the decrease in pHa and serum Na+ was significant at the 1st hour postoperatively. Although intraoperative 20 mL. kg(-1). h(-1) LR infusion does not cause hyperchloremic metabolic acidosis as does NS infusion, it leads to postoperative respiratory acidosis and mild hyponatremia. ⋯ The infusion of large-volume lactated Ringer's solution does not cause hyperchloremic metabolic acidosis as does 0.9% saline during major surgery, but leads to postoperative mild hyponatremia and respiratory acidosis.
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Anesthesia and analgesia · Aug 2002
Randomized Controlled Trial Clinical TrialOral tizanidine, an alpha2-adrenoceptor agonist, reduces the minimum alveolar concentration of sevoflurane in human adults.
Tizanidine, an alpha2-adrenoceptor agonist, has an antinociceptive effect in animals. In humans premedicated with oral tizanidine, the increase in blood pressure associated with laryngoscopy and intubation was attenuated, and the amount of midazolam required for loss of consciousness was significantly reduced. We speculated that the oral administration of tizanidine might reduce the minimum alveolar anesthetic concentration (MAC) of sevoflurane. Fifty-two ASA physical status I-II patients, aged 24-56 yr, were randomly allocated into two groups: a Control group (n = 26) and a Tizanidine group (n = 26). As premedication, the Control group received a placebo, and the Tizanidine group received 4 mg of oral tizanidine 90 min before surgical skin incision. Anesthesia was induced in all patients by using vital capacity rapid inhaled induction with sevoflurane (5%). Loss of consciousness was defined as both the loss of the eyelid reflex and the lack of a response to a verbal command. MAC was determined by a technique adapted from the conventional up-down method for quantal responses. The MAC of sevoflurane was 2.2% +/- 0.2% in the Control group and 1.8% +/- 0.2% in the Tizanidine group (P = 0.0004). The time to loss of consciousness in the Tizanidine group (60.2 +/- 22.5 s) was significantly shorter than that in the Control group (73.7 +/- 26.3 s) (P = 0.03). The oral administration of tizanidine 4 mg successfully reduced the MAC of sevoflurane by 18% in human adults. ⋯ Oral tizanidine (4 mg), an alpha2-adrenoceptor agonist, reduces the minimum alveolar concentration of sevoflurane by 18%.
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Anesthesia and analgesia · Aug 2002
Clinical TrialImpairment of hepatosplanchnic oxygenation and increase of serum hyaluronate during normothermic and mild hypothermic cardiopulmonary bypass.
Hepatic sinusoidal endothelial cells (SECs) are more vulnerable to hypoxia or hypothermia than hepatocytes. To test the hypothesis that hepatic venous desaturation during cardiopulmonary bypass (CPB) leads to impairment of SEC function, we studied the plasma kinetics of endogenous hyaluronate (HA), a sensitive indicator of SEC function, and hepatosplanchnic oxygenation during and after CPB. Twenty-five consecutive patients scheduled for elective coronary artery bypass graft surgery, who underwent normothermic (>35 degrees C; n = 15) or mild hypothermic (32 degrees C; n = 10) CPB participated in this study. A hepatic venous catheter was inserted into each patient to monitor hepatosplanchnic oxygenation and serum levels of HA concentration. Hepatic venous oxygen saturation decreased essentially to a similar degree during normothermic and mild hypothermic CPB. Hepatosplanchnic oxygen consumption and extraction increased during normothermic (P < 0.05), but not mild hypothermic, CPB. Both arterial and hepatic venous HA concentrations showed threefold increases during and after CPB in both groups. A positive correlation was found between hepatosplanchnic oxygen consumption and arterial HA concentrations during CPB, suggesting a role of changes in hepatosplanchnic oxygen metabolism in the mechanisms of increases in serum HA concentrations. The failure of the liver to increase HA extraction to a great degree suggests that a functional impairment of the SEC may contribute to the observed increase of serum HA. ⋯ Hepatic sinusoidal endothelial cells (SECs) are pivotal in the regulation of sinusoidal blood flow. This study showed that SEC function might be impaired during and after cardiopulmonary bypass, irrespective of the temperature management.
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Anesthesia and analgesia · Aug 2002
Case ReportsPersistent left superior vena cava identified after cannulation of the right subclavian vein.
We report the case of a patient with a chest radiograph suggestive of intraarterial placement of a central venous catheter. On investigation, the catheter was located in a previously undiagnosed persistent left superior vena cava.