Abstract
Background: The frequent occurrence of thromboembolic events in patients infected with the severe acute respiratory syndrome CoV2 (SARS-CoV-2) virus is a well-recognized fact in the medical literature, but less data is available about possible hemorrhagic incidents. Methods: We report the case of a 76-year-old patient who suffered from a mild COVID-19 infection in September 2021 and after four weeks, experienced a completely spontaneous popliteal hematoma followed by deep vein thrombosis (DVT). Therapy with low molecular weight heparins (LMWH) was started, but subsequently, the patient developed a massive sub-pectoral and calf hematoma leading to moderate post-hemorrhagic anemia and acute kidney injury. This patient was treated completely conservatively. Conclusions: Considering the continuous spread of the infection with various, continuously evolving strains of this virus and the extended use of LWMH in clinical practice, such cases were seldom described in the medical literature, but should be considered as a potential cause for hemorrhagic events.
Highlights
It is a general consensus that the infection with the severe acute respiratory syndromeCoV-2 (SARS-CoV-2) virus is associated with an increased risk for thromboembolic events such as deep vein thrombosis (DVT) or even pulmonary embolism (PE), numerous scientific researches being published about this topic [1,2,3,4]
Responsible mechanisms are considered: (a) an increased release of the vasoconstrictor angiotensin II, mediated by the virus, (b) a decreased level of angiotensin which acts as a vasodilator, (c) the sepsis-induced release of cytokines that can even result in an exuberant “cytokine storm”, and (d) inflammatory responses that may trigger a coagulopathy in COVID-19
The case presented in this paper is peculiar because the patient developed a completely spontaneous popliteal hematoma a month after he tested positive for a SARS-CoV-2 infection, and experienced a mild form of this disease without pneumonia
Summary
It is a general consensus that the infection with the severe acute respiratory syndrome. (a) an increased release of the vasoconstrictor angiotensin II, mediated by the virus, (b) a decreased level of angiotensin which acts as a vasodilator, (c) the sepsis-induced release of cytokines that can even result in an exuberant “cytokine storm”, and (d) inflammatory responses that may trigger a coagulopathy in COVID-19. Medicina 2022, 58, 230 release of cytokines that can even result in an exuberant “cytokine storm”, and (d) inflammatory responses that may trigger a coagulopathy in COVID-19. Pro-inflammatory cytokines are critically involved in abnormal clot formation and platelet hyperactivation and play an important role in the downregulation of important physiological anticoagulant mechanisms. It has been determined that mor necrosis factor reached increased levels in the majority of patients with severe outpro-inflammatory cytokines such as interleukin 6 (IL-6), IL-17A, and tumor necrosis factor comes [2,3,5].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
