Search

Background Significant numbers of patients are seen for surgery and anesthesia with a history of chronic cocaine use. However, little is known about how cocaine use influences anesthetic physiology and pharmacology. The purpose of this study was to investigate the effect of chronic cocaine exposure on the minimum alveolar concentration (MAC) of isoflurane in sheep. Methods Isoflurane MAC was determined at baseline in 12 sheep using a standard protocol. The animals were subsequently exposed to cocaine for 18 days. Cocaine exposure consisted of a continuous subcutaneous cocaine infusion at 0.2 mg.kg-1.h-1, twice daily 4-mg/kg intravenous boluses and repeated hourly 4 mg/kg cocaine boluses for 8 h on day 18. Minimum alveolar concentration determinations were repeated again on days 15, 18, and on day 28 after 10 days of cocaine abstinence. Results Compared to baseline MAC (1.53 +/- 0.12%) cocaine exposure significantly increased isoflurane MAC on days 15 (1.91 +/- 0.14%) and 18 (1.78 +/- 0.13%; P = .005). MAC decreased after discontinuation of cocaine and was not different from baseline on day 28 (1.67 +/- 0.11). Conclusions In sheep, chronic cocaine exposure resulted in a reversible increase in isoflurane MAC. This finding contrasts with studies of other central nervous system stimulants, which have demonstrated a decrease in MAC after chronic drug exposure.

Opioid addiction therapy includes successful detoxification, rehabilitation, and sometimes methadone maintenance. However, the patient may have physical, mental, and emotional pain while trying to achieve abstinence. A new detoxification technique that incorporates general anesthesia uses a high-dose opioid antagonist to compress detoxification to within 6 h while avoiding the withdrawal.After Institutional Review Board approval and detailed informed consent, 20 patients, American Society of Anesthesiologists status I-II, addicted to various opioids underwent anesthesia-assisted rapid opioid detoxification. After baseline hemodynamics and withdrawal scores were obtained, anesthesia was induced. After testing with 0.4 mg intravenous naloxone, 4 mg nalmefene, was infused over 2 to 3 h. After emergence, severity of withdrawal was scored before and after administration of 0.4 mg intravenous naloxone. After 24 h, patients began outpatient follow-up treatment while taking oral naltrexone.All 20 patients were successfully detoxified with no adverse anesthetic events. After the first post-treatment test dose of 0.4 mg naloxone, 13 of 20 patients had no signs of withdrawal and hemodynamic changes were minimal. Withdrawal scores were always very low and similar before and after detoxification. Three of 17 patients (18%) available for follow-up have remained abstinent from opioids since treatment (or = 18 months). Four other patients are clean after brief relapses.Anesthesia-assisted opioid detoxification is an alternative to conventional detoxification.

Background Opioid addiction therapy includes successful detoxification, rehabilitation, and sometimes methadone maintenance. However, the patient may have physical, mental, and emotional pain while trying to achieve abstinence. A new detoxification technique that incorporates general anesthesia uses a high-dose opioid antagonist to compress detoxification to within 6 h while avoiding the withdrawal. Methods After Institutional Review Board approval and detailed informed consent, 20 patients, American Society of Anesthesiologists status I-II, addicted to various opioids underwent anesthesia-assisted rapid opioid detoxification. After baseline hemodynamics and withdrawal scores were obtained, anesthesia was induced. After testing with 0.4 mg intravenous naloxone, 4 mg nalmefene, was infused over 2 to 3 h. After emergence, severity of withdrawal was scored before and after administration of 0.4 mg intravenous naloxone. After 24 h, patients began outpatient follow-up treatment while taking oral naltrexone. Results All 20 patients were successfully detoxified with no adverse anesthetic events. After the first post-treatment test dose of 0.4 mg naloxone, 13 of 20 patients had no signs of withdrawal and hemodynamic changes were minimal. Withdrawal scores were always very low and similar before and after detoxification. Three of 17 patients (18%) available for follow-up have remained abstinent from opioids since treatment (< or = 18 months). Four other patients are clean after brief relapses. Conclusions Anesthesia-assisted opioid detoxification is an alternative to conventional detoxification.

The cardiovascular effects of 3 and G per cent alveolar concentrations of diethyl ether in nine healthy young volunteers during the first and fifth hours of anesthesia were studied. Pac* was maintained at 35–39 torr and esophagcal temperature at 36 ± 0.5 C. Cardiac output was unchanged or increased at 3 and 6 per cent ether during the first hour; heart rate increased while stroke volume fell. During the fifth hour of anesthesia, cardiac output increased at both 3 and 6 per cent ether, heart rate increased further, and stroke volume rose to the awake value. Total peripheral resistance was initially unchanged but fell with duration of anesthesia. The ratio of cardiac output to oxygen consumption was unchanged at one hour and increased at five hours. Base excess fell slightly initially and slightly more by five hours.

The clinical signs of anesthetic depth (heart rate, mean arterial pressure, pupil diameter, pupil reactivity to light, tearing, and eye movement) were correlated with anesthetic dose in healthy young volunteers. During halothane, halothane—nitrous oxide, Forane, or Forane–nitrous oxide anesthesia at normal PaCO2 (controlled ventilation), only hypotension in the first hour of anesthesia correlated with anesthetic dose. After five hours of halothane or halothane–nitrous oxide, blood pressure remained constant as anesthetic concentration increased. During cyclopropane, diethyl ether, and fluroxene anesthesia, only pupillary dilatation and reduced pupil reactivity to light correlated with anesthetic dose. When nitrous oxide was added to halothane, ether, or fluroxene, mean arterial pressure rose and pupils dilated. During halothane–oxygen anesthesia with spontaneous ventilation, the rise in PaCO2 allowed less hypotension and increased heart rate. Tidal volume decreased and respiratory rate increased as anesthesia deepened. During Forane–oxygen anesthesia with spontaneous respiration, mean arterial pressure, tidal volume, and minute ventilation decreased as anesthesia deepened. In healthy surgical patients anesthetized with halothane or Forane only, incision of the skin modified the clinical signs significantly. While surgery continued, this change in clinical signs persisted during Forane anesthesia, but returned to control during halothane anesthesia.

The ability of leukocytes to kill tumor cells appears central to the defense against neoplastic growth. The authors determined the effect of thiopental on this phenomenon in vitro by incubating 51Cr-labelled YAAC-1 tumor cells obtained from the peritoneal cavities of syngeneic A/JAX white mice with immune leukocytes from the peritoneal cavities of allogeneic C57/black mice. Tumor-cell death was quantitated by the amount of 51Cr released into the medium following tumor-cell lysis. Thiopental, in concentrations used during routine anesthesia, inhibited tumor-cell killing in a dose-related manner. Inhibition of cytotoxicity ranged from 8.6 per cent at 2.8 x 10(-5) M thiopental to 38.1 per cent at 8.5 x 10(-5) M thiopental. Moreover, this inhibitory effect was additive to that previously demonstrated with halothane, and was related to the duration of exposure to the anesthetic. It is postulated that thiopental and other anesthetics contribute to the inhibition of leukocyte responsiveness observed in patients with malignancies who have undergone surgical procedures.

Fine-screen filters were studied in a simulated clinical situation wherein ten units of outdated concentrated erythrocytes were rapidly transfused per filter to determine flow rates and effectivenesses of debris removal. Preliminary studies to evaluate flow rates with outdated whole blood indicated