Viral Coagulopathy in Patients With COVID-19: Treatment and Care.

COVID-19 has proven to be particularly challenging given the complex pathogenesis of SARS-CoV-2. Early data have demonstrated how the host response to this novel coronavirus leads to the proliferation of pro-inflammatory cytokines, massive endothelial damage, and generalized vascular manifestations. While SARS-CoV-2 primarily targets the upper and lower respiratory tract, other organ systems are also affected. SARS-CoV-2 relies on 2 host cell receptors for successful attachment: angiotensin-converting enzyme 2 and transmembrane protease serine 2. Clinicopathologic reports have demonstrated associations between severe COVID-19 and viral coagulopathy, resulting in pulmonary embolism; venous, arterial, and microvascular thrombosis; lung endothelial injury; and associated thrombotic complications leading to acute respiratory distress syndrome. Viral coagulopathy is not novel given similar observations with SARS classic, including the consumption of platelets, generation of thrombin, and increased fibrin degradation product exhibiting overt disseminated intravascular coagulation-like syndrome. The specific mechanism(s) behind the thrombotic complications in COVID-19 patients has yet to be fully understood. Parenteral anticoagulants, such as heparin and low-molecular-weights heparins, are widely used in the management of COVID-19 patients. Beyond the primary (anticoagulant) effects of these agents, they may exhibit antiviral, anti-inflammatory, and cytoprotective effects. Direct oral anticoagulants and antiplatelet agents are also useful in the management of these patients. Tissue plasminogen activator and other fibrinolytic modalities may also be helpful in the overall management. Catheter-directed thrombolysis can be used in patients developing pulmonary embolism. Further investigations are required to understand the molecular and cellular mechanisms involved in the pathogenesis of COVID-19-associated thrombotic complications.

Neuromuscular electrical stimulation reduces sludge in the popliteal vein.

BACKGROUND: The common peroneal nerve stimulator (CPNS) is a UK-approved device for reducing venous thromboembolism (VTE) risk. It resembles a wrist watch and is placed over the common peroneal nerve, discharging electricity at a rate of 1 impulse/s. It has been presumed that as blood flow slows, erythrocytes aggregate into ultrasound-detectable echogenic particles, described as venous sludge. The aim of the study was to determine whether the CPNS reduces venous sludge by using an ultrasound-derived gray-scale (0-255) venous sludge index (VSI). METHODS: Twenty-five healthy volunteers had their right popliteal vein video recorded using B-mode ultrasound at 22 frames/s in longitudinal and transverse views, standing and lying. This was performed first with the CPNS off and then with the CPNS on. The CPNS impulse intensity used was set from 1 to 7 for each individual, and the level was sufficient to cause an outward jerking movement of the foot. A single frame of the possible 154 frames, lasting 7 seconds, was selected using a random number generator for the image analysis. The "brightness" of the erythrocyte aggregates (pixels) within a circular sampling area was quantified using the VSI. The brighter the sample, the greater the sludge. RESULTS: Values are expressed as median (interquartile range). On standing with the device off, there was a significantly higher VSI (P < .0005) compared with lying (longitudinal view, 27.7 [18.8-41.4] vs 11.7 [5.5-17.5]; transverse view, 20.7 [13.6-32.2] vs 11.4 [6.3-15.9]). Activation of the CPNS significantly reduced all the VSI values (P < .0005) shown (longitudinal view, 2 [1.1-3.2] and 1.5 [0.5-3.1]; transverse view, 1.1 [0.6-2.7] and 0.8 [0.5-2.1]). CONCLUSIONS: The CPNS device significantly reduces venous sludge within the popliteal vein irrespective of whether the subject is standing or lying down or of the longitudinal or transverse position of the ultrasound transducer. The principal mode of action of the device in the claim that it may reduce venous thromboembolism risk may be through a reduction of venous sludge. However, the relationship between erythrocyte aggregation, venous stasis, and venous thromboembolism risk requires more investigation.