Belgian guidelines concerning central neural blockade in patients with drug-induced alteration of coagulation: an update.
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Biomedical subjects
Publications and source records attributed to F Singelyn.
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The analgesic efficacy of tenoxicam, a newer injectable non-steroidal anti-inflammatory drug, for post-operative analgesia after abdominal or orthopaedic surgery in ASA Grade I/II patients is reported. Two hundred and fifty-six patients received a single dose of tenoxicam 40 mg intravenous (i.v.) at the end of surgery and this was repeated 24 h later. These patients were compared, with respect to pain or adverse events, with 258 patients that received placebo. All patients were monitored for the next 72 h. Overall, tenoxicam provided reliable analgesia with comparable pain scores at rest, moving and coughing. The cumulative rescue PCA-morphine consumption was always lower in the tenoxicam treated patients and was most marked at 4 and 24 h after the second injection of tenoxicam. This effect was more pronounced after abdominal surgery. The intravenous administration of tenoxicam was associated with a low incidence of adverse events and a high tolerability.
This study was designed to evaluate hypoxemia and platelet aggregation in man following intravenous administration of clonidine. With Institutional approval and following informed consent, 20 patients (ASA I-II) without spontaneous or drug-induced coagulation disorder undergoing elective total hip replacement were studied. They were randomly divided into two groups. Group A (n = 10) received an IV loading dose of 4 micrograms/kg of clonidine in 30 minutes followed by an infusion of 1 microgram/kg/h till the end of the procedure. Group B (n = 10) received saline. Platelet aggregation was assessed before infusion and at the end of both the loading dose and the infusion. PaO2 was measured before anesthesia (FIO2 = 0.21), before femoral cementation (FIO2 = 0.40), 2 min. after prosthesis implantation (FIO2 = 1), before the end of the procedure (FIO2 = 0.40) and in the recovery room (spontaneous breathing with FIO2 = 0.21). Plasma clonidine levels were assessed at the end of both the loading dose and the infusion. At any time considered, no statistical differences were noted between the groups for platelet aggregation and PaO2. We conclude that intravenous clonidine does not clinically promote platelet aggregation nor hypoxemia in man.
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