The absorption of aspirin is reduced after coronary artery bypass grafting.

BACKGROUND: Despite treatment with the antiplatelet drug aspirin, some patients who undergo coronary artery bypass grafting (CABG) experience a thromboembolic event in the early postoperative period. The etiology of a reduced aspirin effect after CABG is still unsolved. Hence, we investigated whether patients who undergo CABG have a reduced absorption of aspirin after surgery, measured as levels of plasma salicylic acid (SA). METHODS: In total, 53 patients were included between October 2015 and May 2018. Blood samples where obtained at the day before surgery, and at the first (day 1) and second (day 2) postoperative day. A subgroup of 10 patients had additional blood samples obtained on day 1. Plasma SA was measured using liquid chromatography-electrospray-ionization tandem-mass spectrometry. Multiplate Analyzer (Roche, Roche Diagnostics, Mannheim, Germany) and VerifyNow Aspirin Test (Accumetrics, San Diego, Calif) were used to assess platelet aggregation as a measurement of the antiplatelet effect of aspirin. RESULTS: A comparison of the difference in change of SA concentration between the day before surgery with day 1 and day 2 showed a significantly reduced increase in SA plasma levels after intake of aspirin at day 1 and day 2 after surgery (P < .0001), including a significantly reduced SA increase in the subgroup at 2, 3, and 4 hours after intake of aspirin. Corresponding with a reduced effect of aspirin, neither Multiplate Analyzer arachidonic acid, nor VerifyNow Aspirin Test showed a significant reduction in platelet aggregation 1 hour after intake of aspirin at day 1 (P < .0001). This also accounted for the subgroup 2, 3, and 4 hours after aspirin intake on day 1. At day 2 the same pattern as preoperatively was detected. CONCLUSIONS: After CABG, the SA level and the effect of aspirin were reduced in the immediate postoperative period.

[Drowning-induced hyperfibrinolytic disseminated intravascular coagulation].

This article summarizes the current knowledge of drowning-induced hyperfibrinolytic disseminated intravascular coagulation. Drowning induces respiratory failure with ensuing cardiac arrest, hypoxaemia and ischaemia. A coagulopathy is induced by ischaemia, acidosis and hypothermia, and clinically the patient develops uncontrolled bleeding due to hyperfibrinolysis. A rapid diagnostic approach is required to recognize this hyperfibrinolytic state, since initiation of treatment with antifibrinolytics and fibrinogen concentrate may bring this life-threatening condition to cessation.