SummaryWe simultaneously evaluated platelet and fibrinolytic parameters to assess their individual and combined contributions to postoperative blood loss in cardiopulmonary (CP) bypass patients. Platelet count, platelet aggregability, hematocrit, plasminogen (PLG) concentration, alpha2-antiplasmin (AP) concentration, free protease activity (fPA), and antithrombin-III (AT-III) were measured in nine patients undergoing surgery using cardiopulmonary bypass. Chest tube drainage was used as the measure of postoperative blood loss. Hematocrit, platelet count, PT .G , AP and AT-TTT all decreased during CP bypass, with PLG and AT-III decreasing much more than dilution. During CP bypass, platelet aggregability to A DP did not change significantly from pre-bypass, but aggregability to arachidonic acid (AA) decreased significantly. Following protamine administration there was a large increase (83%) in fPA, the platelet count showed a further drop (from 61 % to 50% of pre-bypass levels) . and platelet aggregability decreased significantly (from 95% to 34% of prebypass levels for ADP, and from 55% to 11.9% for A A). Chest tube drainage during the first four postoperative hours correlated positively (p <0.05) with the combination of increase in free protease activity and decrease in platelet count. The total chest tube drainage correlated significantly with the combination of decrease in platelet count and the decrease in platelet aggregability. These combinations of changes correlated significantly with postoperative blood loss whereas the individual changes did not. These data indicate that during the early postoperative period the increased fibrinolytic activity and the decreased platelet count together contribute toward postoperative blood loss in CP bypass patients, and that during the entire first 24 hour period postoperatively the decreased platelet number and decreased platelet function are important contributors to blood loss.

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The menopausal transition is associated with increasing sleep disorders including sleep apnoea and restless leg syndrome. Insomnia is the most common and is recognised as a core symptom of the menopause. Guidelines to support decision making for women with sleep problems during the menopausal transition are lacking. Sleep problems are associated with negative impacts on healthcare utilisation, quality of life and work productivity. Sleep deprivation is a risk factor for cardiovascular disease, diabetes, obesity and neurobehavioral dysfunction. Declining oestrogen is implicated as a cause of menopausal sleep disruption. Vasomotor symptoms (VMS) and menopausal mood disturbance are also factors in the complex aetiology. VMS commonly precipitate insomnia and, due to their prolonged duration, they often perpetuate the condition. Insomnia in the general population is most effectively treated with cognitive behavioural therapy (CBT) (also effective in the menopausal transition.) The associations of menopausal sleep disturbance with VMS and depression mean that other treatment options must be considered. Existing guidelines outline effectiveness of hormone replacement therapy (HRT), CBT and antidepressants. HRT may indirectly help with sleep disturbance by treating VMS and also via beneficial effect on mood symptoms. The evidence base underpinning menopausal insomnia often references risks associated with HRT that are not in line with current international menopause guidelines. This may influence clinicians managing sleep disorders, leading to hesitation in offering HRT, despite evidence of effectiveness. Viewing sleep symptoms on an axis of menopausal symptoms – towards vasomotor symptoms or towards mood symptoms may help tailor treatment options towards the symptom profile.

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