Pulmonary embolism with endovascular thrombolysis for thrombosed hemodialysis arteriovenous access
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AIMS: Acute thrombosis of hemodialysis (HD) arteriovenous access is an urgent problem for HD patients and is commonly managed by endovascular thrombolysis. Pulmonary embolism (PE) is a recognized complication of HD access thrombosis and thrombolysis but the risk and outcomes are unclear. This study aims to determine the incidence, predictors, and outcomes of PE after endovascular thrombolysis of HD arteriovenous access in patients presenting with acute thrombosis. MATERIALS AND METHODS: A single-center retrospective study was performed for all adult chronic kidney disease patients undergoing arteriovenous access thrombolysis between January 1, 2012, and December 31, 2014. Investigation for PE with CT pulmonary angiography or ventilation/perfusion scintigraphy (V/Q scan) was performed as clinically directed by the managing clinicians. In cases diagnosed with PE, the pulmonary embolism severity index (PESI) was calculated. RESULTS: A total of 48 (median age 68) patients underwent 74 thrombolysis procedures. Thrombolysis techniques were divided into pharmacological (44.6%), mechanical (17.6%), or pharmacomechanical (37.8%). Clinical success was achieved in 56/74 (75.7%) of procedures. Five episodes of thrombolysis for access thrombosis (6.8%) were associated with clinically symptomatic PE. The PESI score ranged from 51 to 127. All patients with PE were managed with 3 - 6 months of anticoagulation and recovered clinically. There were no statistically significant differences in baseline characteristics, methods of thrombolysis, or clot burden in patients that developed a PE. CONCLUSION: There is a clinically significant risk of symptomatic PE after arteriovenous access thrombolysis for access thrombosis in HD patients.
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Monitoring Unfractionated Heparin (UFH) therapy: which Anti-Factor Xa assay is appropriate?

INTRODUCTION: Anti-Factor Xa (Anti-Xa) assays specifically determine the anticoagulant activity of UFH by measuring the ability of heparin-bound Antithrombin (AT) to inhibit a single enzyme, Factor Xa (FXa). Recent improvements in the automation, cost-effectiveness and accessibility of the assay to clinicians, have resulted in the Anti-Xa assay becoming a part of daily clinical practice in many institutions. OBJECTIVES: We hypothesized that different Anti-Xa assays have different applicability for use in clinical settings, depending on the amount of UFH administered. This was investigated in a tertiary paediatric institution. MATERIALS AND METHODS: Samples were collected from children receiving Low-dose of UFH of at least 10 IU/kg/h, with or without a previous bolus of up to 25 IU/kg/h, within the previous 6 h in the PICU and HDU. High-dose UFH population consisted of children undergoing Cardiac Catheterization (CC), who received a bolus of UFH of 100 IU/kg body weight, 30 min prior to sampling. RESULTS AND CONCLUSIONS: The Anti-Xa activity for a given dose of UFH was found to vary significantly based on the Anti-Xa assay and the population being monitored. Our study suggests that the MODIFIED COMATIC Anti-Xa assay provides the best physiological measure of the UFH effect in children, as it does not introduce sources of error, such as exogenous AT, which may increase the measured ant Factor Xa activity, nor Dextran Sulphate which can displace plasma protein bound heparin and once again leading to falsely elevated assay results. Further studies that include assessment of clinical outcomes are required to confirm the applicability of use of this particular assay in monitoring UFH therapy.