Anesthesia and analgesia
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Anesthesia and analgesia · Jun 2003
Randomized Controlled Trial Clinical TrialPostoperative analgesia in children undergoing myringotomy and placement equalization tubes in ambulatory surgery.
We enrolled 120 children undergoing bilateral myringotomy and tube placement in this prospective, randomized, observer-blinded study. Patients were randomized into one of four groups: Group 1 (control) was plain acetaminophen 10 mg/kg orally, Group 2 was acetaminophen 10 mg/kg with 1 mg/kg of codeine orally, Group 3 was transnasal butorphanol 25 micro g/kg given immediately after the induction of anesthesia, and Group 4 was ketorolac 1 mg/kg given IM immediately after the induction of anesthesia. All children received oral midazolam (0.6 mg/kg) before surgery. A nurse blinded to the analgesic technique used assessed the child's behavior at the induction of anesthesia and in the postanesthesia care unit using a 4-point scale. Analgesic effectiveness was determined by assessing the child's pain at 5-min intervals using a modified 10-point objective pain scale. In the postanesthesia care unit, rescue pain medication was administered for an objective pain scale >or=4 or a behavior score >or=3. Our data suggest that IM ketorolac is a promising analgesic to be used in this surgical population. Time to first rescue analgesic was longest in the ketorolac group, and there was no associated postoperative vomiting or nausea. IM ketorolac given during surgery was the best analgesic regimen for these procedures. ⋯ We compared four different analgesics in the management of pain after placement of pressure equalization tubes during myringotomy in children and demonstrated that ketorolac or butorphanol provided superior analgesia when compared with acetaminophen with codeine or plain acetaminophen. Children who received ketorolac versus butorphanol had less vomiting in the 24 h after surgery.
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Anesthesia and analgesia · Jun 2003
Survival with full neurologic recovery after prolonged cardiopulmonary resuscitation with a combination of vasopressin and epinephrine in pigs.
We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery. ⋯ We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.
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Anesthesia and analgesia · Jun 2003
Clinical TrialThe effect of graded hypothermia (36 degrees C-32 degrees C) on hemostasis in anesthetized patients without surgical trauma.
The isolated effects of hypothermia on hemostasis have not been investigated in healthy humans. We cooled 16 anesthetized patients scheduled for elective intracranial surgery to 32 degrees C body core temperature and assessed prothrombin time (PT), activated partial thromboplastin time, thrombelastogram (TEG), closure time, and platelet count at 36 degrees C, 34 degrees C, and 32 degrees C body core temperature after the induction of anesthesia but before surgical intervention. Activated partial thromboplastin time, hematocrit, and closure time did not change, whereas PT and platelet count decreased during cooling. Platelet count decreased without a decrease in hematocrit; hence, a dilution by administered fluids seemed unlikely. The small decrease of platelet count is probably clinically irrelevant in patients with normal platelet count and function. The small decrease in PT indicates an alteration of the extrinsic pathway of coagulation. TEG measurements showed a delay of clot formation in temperature-adjusted measurements but showed no change if the test temperature was 37 degrees C. This indicates that hypothermia reduces plasmatic coagulation and platelet reactivity. However, the clot strength is not altered by hypothermia. All coagulation variables remained within the normal ranges. Our results may indicate that moderate short-term (4-h) hypothermia has only minor adverse effects in healthy humans. We can make no statement about the effects of hypothermia of longer duration. ⋯ This study investigated the isolated effects of hypothermia in healthy anesthetized humans. We found only minor effects of body temperature reduction to 32 degrees C on assessed coagulation variables, indicating only minor effects in otherwise healthy humans.
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Anesthesia and analgesia · Jun 2003
Clinical TrialPerioperative myocardial ischemia in patients undergoing sternectomy shortly after coronary artery bypass grafting.
Coronary revascularization reduces cardiac complications associated with noncardiac surgery in patients with severe coronary disease. However, patients undergoing emergency noncardiac surgery soon after coronary bypass operations may still be vulnerable to ischemic myocardial events. We prospectively evaluated the incidence of myocardial ischemia in 82 consecutive patents scheduled for sternectomy in the first (Group 1; 35 patients) or second (Group 2; 47 patients) week after coronary artery bypass graft (CABG) surgery. The interval between CABG surgery and sternectomy in Groups 1 and 2 was 6 days (range, 4-7 days) and 11 days (range, 8-14 days), respectively. Electrocardiographic (ECG) changes consistent with myocardial ischemia were assessed with a two-channel Holter system for 48 h. There were no between-group differences in updated Acute Physiology and Chronic Health Evaluation score, use of beta-blockers, or perioperative hemodynamic changes. The incidence of ECG changes consistent with myocardial ischemia was fivefold more frequent in Group 1 (22.85% versus 4.25%; P < 0.05). Of the ischemic patients in Group 1, 25% experienced a perioperative acute myocardial infarction (one was fatal). There were no infarcts in Group 2. Thus, patients appear to be prone to coronary events during sternectomy performed early after CABG surgery. Although the incidence of ischemia did not differ from that previously reported after CABG surgery alone, further investigation is required to determine whether the findings obtained in this high-risk population are generalizable to patients undergoing noncardiac surgery soon after uneventful CABG surgery. ⋯ This study demonstrates an increased incidence of myocardial ischemia when sternectomy for mediastinitis is performed within one week of coronary artery bypass graft surgery, and this ischemia is associated with a 25% incidence of myocardial infarction.
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Anesthesia and analgesia · Jun 2003
Case ReportsPostdural puncture headache: an imaging-guided management protocol.
We propose an imaging-based algorithm for the management of headache caused by the inadvertent puncture of dura that occurs sporadically during epidural analgesia. Its implementation can identify those postdural puncture headache cases that cannot benefit from epidural blood patches, and their unnecessary application can consequently be avoided.