This study assessed the effect on coagulation tests of fresh frozen plasma (FFP), given according to guidelines compared with higher doses in critically ill patients. Group 1 (10 patients) received 12.2 ml/kg and group 2 (12 patients) 33.5 ml/kg FFP. Prothrombin time, activated partial thromboplastin time and factors I-XII were measured before and after FFP infusion. Factor levels of 30 IU/dl (1 g/l for fibrinogen) were considered haemostatic. A retrospective review showed 10 of 22 (five in group 1 and five in group 2) patients had not required FFP. Of those that needed FFP, one of five in group 1 and seven of seven in group 2 had coagulation factor levels above the target post-FFP. Increments for group 1 versus 2 were: fibrinogen 0.4 vs. 1.0 g/l, FII 16 vs. 41*, FV 10 vs. 28*, FVII 11 vs. 38*, FVIII 10 vs. 17, FIX 8 vs. 28*, FX 15 vs. 37*, FXI 9 vs. 23 and FXII 30 vs. 44 IU/dl* (*P < 0.01). In vivo recovery of coagulation factors was the same for both groups and the observed increments correlated with the dose of FFP. In conclusion, coagulation screens were poor predictors of coagulation factor levels and current guidelines on the use of FFP result in predictably small increments in coagulation factors in critically ill patients and should be reviewed.

Summary Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐tissue factor activated (LD‐TFA) Rotem and LD‐TFA waveform analysis. Thirty‐six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P < 0·05), VII, X, XI and XII, antithrombin and protein C (P < 0·01) was decreased in sepsis compared with controls. The mean factor VIII and fibrinogen level (P < 0·001) was increased. CAT in platelet rich and poor plasma showed a prolonged lag time (P < 0·02), decreased peak thrombin (P < 0·02) and delayed time to peak thrombin (P < 0·001) in sepsis patients, however, the endogenous thrombin potential was equivalent in sepsis and controls. In LD‐TFA Rotem, septic patients had delayed clot times (P = 0·04) but an increased maximum velocity of clot formation (P < 0·01) and area under the clot elasticity curve (P < 0·01). LD‐TFA waveform analysis showed a delayed onset time but an increased rate of clot formation (P < 0·005). In conclusion, global tests of haemostasis suggest that in this patient group, activation of haemostasis is delayed but once initiated thrombin generation and clot formation are normal or enhanced.

The incidence of bacteraemia following a single stage PDT was similar to other manipulations of the aerodigestive tract such as intubation, insertion of an LMA or tooth brushing. We suggest that routine antibiotic prophylaxis is unnecessary for this procedure.

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