Thrombocytosis in splenic trauma: In-hospital course and association with venous thromboembolism.

INTRODUCTION: Thrombocytosis is common following elective splenectomy and major trauma. However, little is known about the in-hospital course of platelet count (PC) and incidence of thrombocytosis after splenic trauma. Extreme thrombocytosis (PC>1000×109) is associated with increased risk of venous thromboembolism (VTE) in primary thrombocytosis leading to the use of acetylsalicylic acid (ASA) for risk reduction, but the need for this agent in splenic trauma is undefined. METHODS: Retrospective cohort study of all patients with splenic trauma between April 1, 2010 and March 31, 2014. The in-hospital course of PC was assessed based on splenic injury management type. The association of management type with thrombocytosis was evaluated using a multivariable logistic regression model adjusting for potential confounders. The association of thrombocytosis, extreme thrombocytosis, and ASA use for the outcome of VTE was explored. RESULTS: 156 patients were eligible, PC initially increased in all patients with the highest peak after total splenectomy. The incidence of thrombocytosis was 41.0% (64/156). Thrombocytosis was more likely following splenectomy compared with spleen preserving strategies independent of length of stay, injury grade, ISS, age and transfusion (OR 7.58, 95% CI: 2.26-25.45). Splenectomy was associated with extreme thrombocytosis (OR 10.39, 95% CI: 3.59-30.07). CONCLUSIONS: Thrombocytosis in splenic trauma is more likely after splenectomy than with spleen preserving strategies. Splenectomy is associated with extreme thrombocytosis. There was insufficient data in our study to determine the use of ASA as primary prevention of VTE after splenic trauma.

Multicenter accuracy and interobserver agreement of spot sign identification in acute intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Rapid, accurate, and reliable identification of the computed tomography angiography spot sign is required to identify patients with intracerebral hemorrhage for trials of acute hemostatic therapy. We sought to assess the accuracy and interobserver agreement for spot sign identification. METHODS: A total of 131 neurology, emergency medicine, and neuroradiology staff and fellows underwent imaging certification for spot sign identification before enrolling patients in 3 trials targeting spot-positive intracerebral hemorrhage for hemostatic intervention (STOP-IT, SPOTLIGHT, STOP-AUST). Ten intracerebral hemorrhage cases (spot-positive/negative ratio, 1:1) were presented for evaluation of spot sign presence, number, and mimics. True spot positivity was determined by consensus of 2 experienced neuroradiologists. Diagnostic performance, agreement, and differences by training level were analyzed. RESULTS: Mean accuracy, sensitivity, and specificity for spot sign identification were 87%, 78%, and 96%, respectively. Overall sensitivity was lower than specificity (P<0.001) because of true spot signs incorrectly perceived as spot mimics. Interobserver agreement for spot sign presence was moderate (k=0.60). When true spots were correctly identified, 81% correctly identified the presence of single or multiple spots. Median time needed to evaluate the presence of a spot sign was 1.9 minutes (interquartile range, 1.2-3.1 minutes). Diagnostic performance, interobserver agreement, and time needed for spot sign evaluation were similar among staff physicians and fellows. CONCLUSIONS: Accuracy for spot identification is high with opportunity for improvement in spot interpretation sensitivity and interobserver agreement particularly through greater reliance on computed tomography angiography source data and awareness of limitations of multiplanar images. Further prospective study is needed.