Representatives for Haematology at the Universities of Cape Town and Witwatersrand have expressed concern about protocols and a YouTube video that did the rounds last week about the use of antiplatelet agents and thrombolysis in the treatment of patients with moderate to severe COVID-19. In the video, Dr Jaco Laubscher from Stellenbosch Mediclinic gives a presentation in which he argues that COVID-19 is a vascular and not a respiratory disease, affecting vulnerable endothelium which leads to hyper-coagulability and impaired fibrinolysis. To manage this, he proposes the use of multiple antiplatelet agents and early thrombolysis.
But in a statement, the haematologists say although there is some agreement that coagulation and endothelial dysfunction are likely to form a key part of the pathophysiology of COVID-19, they don’t think that this treatment should be recommended unless they have a clinical trial comparing low molecular weight heparin with what is being proposed. The statement is signed by Prof Vernon Cloete, Chair and Head of the Division of Clinical Haematology in the Department of Medicine at UCT; Prof Jessica Opie, Head of Haematology Pathology at UCT and the NHLS, and Prof Barry Jacobson of the Department of Molecular Medicine and Haematology, Faculty of Health Sciences at Wits.
They point out that the risks of massive bleeding are very high if thrombolysis PLUS two antiplatelet agents are used.
“We are concerned about a greater than 10% risk of intracranial haemorrhage in particular when using thrombolysis (not adding the additional risk of two antiplatelet agents). We need to know what that risk is in COVID patients before we can recommend or even consider use in all moderate/severe patients. We have not seen information on bleeding in patients treated with these protocols yet,” they write.
They also don’t agree with the statement that it is a vascular rather than a lung disease, saying although thromboembolism is an important expression of the disease, it is only one of a variety of expressions.
“There is no doubt that COVID-19 has a variety of expressions, whether a haemophagocytic syndrome type phenotype associated with a cytokine storm, a more neurological phenotype, lung disease and/or gastrointestinal effects, etc. Whether the different effects are mediated by different genotypes, e.g. perforin gene polymorphisms or mutations, giving rise to haemophagocytosis and macrophage activation syndromes, or other genetic or environmental predispositions remain to be seen.
“The theories suggested on pathophysiology need further exploration, as is being pursued in many places around the world and we think that aggressive therapy with thrombolysis and dual anti-platelet therapy should be withheld until safety and efficacy has been proven in a clinical trial,” they noted.
“Nevertheless, we appreciate the opportunity for robust debate and for the time spent by colleagues for interesting presentations. We acknowledge that there may be desperate cases, where, within the framework of ethical patient management, certain patients could be managed with personalised treatments, but although it may be well meant, we advise against using anything in mild/moderate cases without solid evidence,” they conclude.
