Summary.  Background:  It is uncertain whether reactive thrombocytosis is associated with an increased risk of venous thromboembolism. This study assessed the incidence of reactive thrombocytosis, defined as platelet count ≥ 500 × 109 L−1, at intensive care unit discharge and its association with subsequent venous thromboembolism. Methods and Results:  This cohort study involved linkage of routinely collected intensive care unit, laboratory, radiology and death registry data of critically ill patients admitted to the intensive care unit between January 2009 and March 2010. The census date for survival and radiologically confirmed venous thromboembolism was 31 October 2011. Of the 1446 patients who survived to intensive care unit discharge, 139 patients had reactive thrombocytosis (9.6%, 95% confidence interval [CI] 8.2–11.2%). Twenty‐nine patients developed venous thromboembolism after discharge (2%, 95% CI 1.4–2.9%; 67 per 100 person‐years, 95% CI 45–97) and the median time to develop venous thromboembolism was 25 days (interquartile range 8–148). Reactive thrombocytosis was associated with an increased risk of subsequent venous thromboembolism (hazard ratio 5.3, 95% CI 1.7–16.4), after adjusting for other covariates. Platelet counts explained about 34% of the variability in the risk of venous thromboembolism and had a relatively linear relationship with the risk of venous thromboembolism when the platelet counts were > 400 × 109 L−1. Venous thromboembolism after intensive care unit discharge was associated with an increased risk of mortality (hazard ratio 2.0, 95% CI 1.1–3.9), after adjusting for reactive thrombocytosis. Conclusions:  Reactive thrombocytosis during the recovery phase of critical illness was associated with an increased risk of subsequent venous thromboembolism.

SUMMARY AimIt is uncertain whether hypocalcaemia is associated with an increased risk of bleeding. This study assessed the dose-related relationship between ionised calcium concentrations and in vitro clot strength measured by maximum amplitude (MA) on the thromboelastograph (TEG). MethodsA total of 610 patients who were at risk of bleeding or had active bleeding between 2010 and 2014 were considered in this retrospective cohort study. A scatter plot with Pearson correlation coefficient (r) and multiple linear regression was used to assess the dose-related relationship between ionised calcium concentrations and MA on the TEG. ResultsThe mean ionised calcium of the patients was 1·10 mmol L −1 (interquartile range: 1·04-1·17) and 235 (38·5%) of them had hypocalcaemia (<1·1 mmol L −1). Hypocalcaemia was more common in patients with significant coexisting coagulopathy. Ionised calcium concentrations (r = 0·285, 95% confidence

Object The authors assessed the risk factors and outcomes associated with blood-brain barrier (BBB) disruption in patients with severe, nonpenetrating, traumatic brain injury (TBI) requiring decompressive craniectomy. Methods At 2 major neurotrauma centers in Western Australia, a retrospective cohort study was conducted among 97 adult neurotrauma patients who required an external ventricular drain (EVD) and decompressive craniectomy during 2004–2012. Glasgow Outcome Scale scores were used to assess neurological outcomes. Logistic regression was used to identify factors associated with BBB disruption, defined by a ratio of total CSF protein concentrations to total plasma protein concentration > 0.007 in the earliest CSF specimen collected after TBI. Results Of the 252 patients who required decompressive craniectomy, 97 (39%) required an EVD to control intracranial pressure, and biochemical evidence of BBB disruption was observed in 43 (44%). Presence of disruption was associated with more severe TBI (median predicted risk for unfavorable outcome 75% vs 63%, respectively; p = 0.001) and with worse outcomes at 6, 12, and 18 months than was absence of BBB disruption (72% vs 37% unfavorable outcomes, respectively; p = 0.015). The only risk factor significantly associated with increased risk for BBB disruption was presence of nonevacuated intracerebral hematoma (> 1 cm diameter) (OR 3.03, 95% CI 1.23–7.50; p = 0.016). Although BBB disruption was associated with more severe TBI and worse long-term outcomes, when combined with the prognostic information contained in the Corticosteroid Randomization after Significant Head Injury (CRASH) prognostic model, it did not seem to add significant prognostic value (area under the receiver operating characteristic curve 0.855 vs 0.864, respectively; p = 0.453). Conclusions Biochemical evidence of BBB disruption after severe nonpenetrating TBI was common, especially among patients with large intracerebral hematomas. Disruption of the BBB was associated with more severe TBI and worse long-term outcomes, but when combined with the prognostic information contained in the CRASH prognostic model, this information did not add significant prognostic value.