UK Efficacy and Mechanism Evaluation Programme and National Institutes of Health.

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SummarySafe vascular access is integral to anaesthetic and critical care practice, but procedures are a frequent source of patient adverse events. Ensuring safe and effective approaches to vascular catheter insertion should be a priority for all practitioners. New technology such as ultrasound and other imaging has increased the number of tools available. This guidance was created using review of current practice and literature, as well as expert opinion. The result is a consensus document which provides practical advice on the safe insertion and removal of vascular access devices.

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Patients with COVID-19 have a coagulopathy and high thrombotic risk. In a cohort of 69 intensive care unit (ICU) patients we investigated for evidence of heparin resistance in those that have received therapeutic anticoagulation. 15 of the patients have received therapeutic anticoagulation with either unfractionated heparin (UFH) or low molecular weight heparin (LMWH), of which full information was available on 14 patients. Heparin resistance to UFH was documented in 8/10 (80%) patients and sub-optimal peak anti-Xa following therapeutic LMWH in 5/5 (100%) patients where this was measured (some patients received both anticoagulants sequentially). Spiking plasma from 12 COVID-19 ICU patient samples demonstrated decreased in-vitro recovery of anti-Xa compared to normal pooled plasma. In conclusion, we have found evidence of heparin resistance in critically unwell COVID-19 patients. Further studies investigating this are required to determine the optimal thromboprophylaxis in COVID-19 and management of thrombotic episodes. Keywords Thrombosis • Intensive care • COVID-19 • Heparin Highlights• Heparin resistance with unfractionated heparin or suboptimal anti-Xa peak with low molecular weight heparin appeared common in COVID-19 intensive care unit patients that received therapeutic anticoagulation. • In-vitro spiking of COVID-19 samples from patients in intensive care unit with low molecular weight heparin failed to recover the anti-Xa level as would have been predicted. • COVID-19 patients have high factor VIII and fibrinogen with low antithrombin which could contribute to the picture seen. • Further studies are needed to confirm our findings and also describe the mechanism of heparin resistance in these patients as well as optimal management of thrombosis in COVID-19.