Anesthesia and analgesia
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Anesthesia and analgesia · Apr 2002
Randomized Controlled Trial Clinical TrialPerioperative small-dose S(+)-ketamine has no incremental beneficial effects on postoperative pain when standard-practice opioid infusions are used.
Several studies report that when small-dose racemic ketamine, an N-methyl-D-aspartate receptor antagonist, is administered perioperatively, opioid consumption is reduced postoperatively. S(+)-ketamine has a higher affinity for the N-methyl-D-aspartate receptor and less-serious side effects than racemic ketamine. Thirty patients scheduled for elective arthroscopic anterior cruciate ligament repair were enrolled in this randomized, double-blinded clinical trial designed to determine the preemptive effect of S(+)-ketamine on postoperative analgesia requirements in a setting of clinically relevant perioperative analgesia. Total IV anesthesia was induced and maintained with remifentanil (0.125-1.0 microg x kg(-1) x min(-1)) and a propofol target-controlled infusion (target 2-4 microg/mL). The Ketamine group received a bolus of 0.5 mg/kg S(+)-ketamine before incision, followed by a continuing infusion of 2 microg x kg(-1) x min(-1) until 2 h after emergence from anesthesia. The Control group received NaCl in the same sequence. After IV morphine provided pain relief down to < or =3 on a visual analog scale scored from 0 to 10, patients were connected to a patient-controlled analgesia device. There were no significant differences between the two groups in terms of total morphine consumption or VAS scores, either at rest or with movement. In our study, S(+)-ketamine did not contribute to postoperative pain reduction, possibly because of the clinically routine perioperative opioid analgesia. ⋯ Small-dose S(+)-ketamine had no positive effect on postoperative analgesia when administered perioperatively for elective arthroscopic anterior cruciate ligament repair. Unlike investigations of the racemic mixture of ketamine, our study methods included timely standard-practice perioperative opioid analgesia, which seems to make supplemental analgesia unnecessary.
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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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Recent advances in acute pain mechanisms and management have implicated the N-methyl D-aspartate receptor-ion channel complex in the development of postoperative hyperalgesia and acute opioid tolerance. N-methyl D-aspartate receptor antagonists such as ketamine have been used increasingly in clinical studies in an effort to minimize acute postoperative pain and reduce opioid requirements. A mixture of ketamine and an opioid administered in the same solution and syringe would be a practical and useful technique for postoperative epidural analgesia, continuous IV infusion, or patient-controlled IV analgesia. We investigated the stability of a morphine sulfate and racemic ketamine solution in saline at pH 5.5-7.5 over a period of 4 days. Our study demonstrates that the ketamine-morphine mixture at a clinically relevant concentration seems to be stable at room temperature, at a wide range of pH values, for at least 4 days. ⋯ Small-dose ketamine is used with increasing frequency in the acute postoperative setting as an adjunct to traditional opioid analgesics. We show that a racemic ketamine and morphine solution at a clinically relevant concentration seems to be stable at room temperature at a wide range of pH values for at least 4 days.
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Anesthesia and analgesia · Apr 2002
Case ReportsBlood patch therapy for spontaneous intracranial hypotension: safe performance after epidurography in an unconscious patient.
Epidurography was useful for identifying the epidural space and determining the likely spread of an epidural blood patch in an unconscious patient with spontaneous intracranial hypotension.
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Anesthesia and analgesia · Apr 2002
Calibrated pneumoperitoneal venting to prevent N2O accumulation in the CO2 pneumoperitoneum during laparoscopy with inhaled anesthesia: an experimental study in pigs.
Nitrous oxide (N2O) accumulates in the CO2 pneumoperitoneum during laparoscopy when N2O is used as an adjuvant for inhaled anesthesia. This may worsen the consequences of gas embolism and introduce a fire risk. In this study, we quantified the pneumoperitoneal gas venting necessary to prevent significant contamination by inhaled N2O. Four domestic pigs (26-30 kg) were anesthetized and ventilated with 66% N2O in oxygen. A CO2 pneumoperitoneum was insufflated and maintained at a pressure of 12 mm Hg. Each animal underwent three experimental conditions, in random sequence, for 70 min each: 1) no pneumoperitoneal leak, 2) leak of 2 L every 10 min (12 L/h), and 3) leak of 4 L every 10 min (24 L/h). Every 10 min, pneumoperitoneal gas samples were analyzed for fractions (FPn) of N2O and CO2. Without leaks, FPnN2O increased continually and reached 29.58% +/- 3.15% at 70 min. With leaks of 2 and 4 L every 10 min (12 and 24 L/h), FPnN2O reached a plateau of <10% after 30 min. We conclude that calibrated pneumoperitoneal venting of 12 or 24 L/h is enough to prevent the constitution of potentially dangerous pneumoperitoneal gas mixtures if venting is constant. ⋯ External venting calibrated at four or eight initial pneumoperitoneal volumes per hour with compensation by fresh CO2 is sufficient to prevent nitrous oxide buildup of more than 10% in the pneumoperitoneum during laparoscopy with inhaled general anesthesia if venting is constant.