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Sugammadex 2.0 mg kg(-1) administered at reappearance of T(2) was significantly faster in reversing rocuronium-induced blockade than neostigmine was in reversing cisatracurium-induced block.

The widespread use of metal stents and drug-eluting stents has shown the extent to which patients with unstable coronary perfusion depend on antiplatelet drugs, and how their risk of late thrombosis depends on the long-term use of agents such as clopidogrel. It has also been shown that the risk of surgical bleeding, if antiplatelet drugs are continued, is lower than that of coronary thrombosis if they are withdrawn. Thus, except for low-risk settings, the practice of withdrawing antiplatelet drugs 5-10 days prior to surgical procedures should be changed. The following suggestions are meant to provide a guideline in this respect. Most of the current surgical procedures may be performed while on low-dose aspirin treatment. Except when bleeding may occur in closed spaces (e.g. intracranial surgery, spinal surgery in the medullary canal, surgery of the posterior chamber of the eye) or where excessive blood loss is expected, where only clopidogrel should be discontinued; in all other cases the surgical procedures should be carried out in the presence of dual antiplatelet agents (if prescribed). Aspirin may be discontinued only in subjects at low risk of thrombosis, and at high risk of intraoperative bleeding. Operations associated with an expected excessive blood loss should be postponed unless vital. When prescribed for acute coronary syndrome or during stent re-endothelialization, clopidogrel should not be discontinued before a noncardiac procedure. For elective procedures, surgery should be postponed until the end of the indication for clopidogrel. After the operation, clopidogrel should be resumed within the 12-24 h. Cardiac procedures should be postponed for at least 4 days after clopidogrel withdrawal. The thrombotic risk of preoperative withdrawal of antiplatelet drugs overwhelms the benefit of regional or neuraxial blockade. Antiplatelet treatment replacement by heparin or low-molecular weight heparin does not provide protection against the risk of coronary artery or stent thrombosis. Haemostasis requires that at least 20% of circulating platelets have a normal function. As the effects of antiplatelet agents are not reversible by other drugs, fresh platelets are the only manner to rapidly restore normal haemostasis. Aprotinin decreases postoperative bleeding and transfusion rates in patients undergoing CABG and on clopidogrel during the days preceding surgery.

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A controlled, parallel group study of the analgesic efficacy of flupirtine maleate, was compared against diclofenac sodium in 40 orthopaedic patients with post-operative pain. Clinically, both drugs were of equal analgesic efficacy. A mathematical model has been developed, however, to evaluate the speed, intensity and duration of the analgesic effect and provides data which significantly favour flupirtine maleate in the treatment of these patients.

We have examined the in vitro effects of increasing concentrations of propofol (5-70 micrograms ml-1), ketamine (10(-6)-10(-3) mol litre-1) and thiopentone (10(-5)-8 x 10(-4) mol litre-1) on the release of preformed histamine and de novo synthesized mediators (peptide leukotriene C4 (LTC4) or prostaglandin D2 (PGD2] from human basophils and mast cells isolated from lung parenchyma and skin tissue and from heart fragments. Propofol, ketamine and thiopentone failed to induce the release of histamine and de novo synthesis of LTC4 from basophils. Propofol induced histamine release from lung (mean 8.6 (SEM 1.6)%) and skin mast cells (3.8 (1.5)%), but not from heart mast cells. Ketamine caused release of histamine from lung (6.2 (0.9)%) and skin mast cells (2.5 (1.5)%). Thiopentone caused a small amount of histamine release from lung mast cells (3.1 (1.2)%). Propofol, ketamine and thiopentone did not induce de novo synthesis of PGD2 and LTC4 from lung and skin mast cells. These results demonstrate that general anaesthetics induce only histamine release selectively from human mast cells.

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