Acute upper limb ischemia in a patient with COVID-19

Kaur, Parminder; Qaqa, Firas; Ramahi, Amr; Shamoon, Yezin; Singhal, Monisha; Shamoon, Fayez; Maroules, Michael; Singh, Balraj

doi:10.1016/j.hemonc.2020.05.001

Cited by 61 publications

(61 citation statements)

References 8 publications

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“…Extensive workup including gene mutations and flow cytometry was performed and resulted in negative. The patient finally underwent limb salvage therapy through angioplasty with below-the-ankle amputation of the gangrenous tissue [9,10].…”

Section: Discussionmentioning

confidence: 99%

Acute Limb Ischemia in COVID-19 Disease: A Mysterious Coagulopathy

Anwar¹,

Acharya²,

Shabih³

et al. 2020

Cureus

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Severe coronavirus disease 2019 (COVID-19) as a respiratory tract infection has been noted to be a causative agent for acute respiratory distress syndrome, shock, and multiple organ failure. It is also being suggested that COVID-19 results in serious systemic coagulopathies similar to disseminated intravascular coagulation. We describe a case of severe arterial thrombosis induced by COVID-19 infection along with its pathological implications.

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Section: Discussionmentioning

confidence: 99%

Acute Limb Ischemia in COVID-19 Disease: A Mysterious Coagulopathy

Anwar¹,

Acharya²,

Shabih³

et al. 2020

Cureus

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“…Acute Limb Ischemia Acute upper or lower extremity ischemia has been identified as a COVID-19 arterial thrombotic complication, in some cases requiring surgical embolectomy [71,72]. In one case series, two young patients who had no comorbidities developed acute limb ischemia despite low molecular weight heparin prophylaxis [73].…”

Section: -Clinical Phenotypementioning

confidence: 99%

Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses

et al. 2020

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Purpose of Review To review current literature on endothelial dysfunction with previous coronaviruses, and present available data on the role of endothelial dysfunction in coronavirus disease-2019 (COVID-19) infection in terms of pathophysiology and clinical phenotype Recent Findings Recent evidence suggests that signs and symptoms of severe COVID-19 infection resemble the clinical phenotype of endothelial dysfunction, implicating mutual pathophysiological pathways. Dysfunction of endothelial cells is believed to mediate a variety of viral infections, including those caused by previous coronaviruses. Experience from previous coronaviruses has triggered hypotheses on the role of endothelial dysfunction in the pathophysiology of SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), which are currently being tested in preclinical and clinical studies. Summary Endothelial dysfunction is the common denominator of multiple clinical aspects of severe COVID-19 infection that have been problematic for treating physicians. Given the global impact of this pandemic, better understanding of the pathophysiology could significantly affect management of patients.

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“…Fever and upper and lower respiratory tract symptoms and signs (especially dry cough, and shortness of breath, but also fatigue, headache, myalgia, or diarrhea) are the main clinical manifestations of this disease 1,5,12 . Acute respiratory distress syndrome can be added to these 7,12 . Chinese authors report that about 20% of patients infected with SARS-CoV-2 have severe forms of the disease 17 .…”

Section: Coagulation Dysfunction Reflected In Clinical and Laboratorymentioning

confidence: 99%

“…Thrombotic events (venous and arterial thromboembolism) (ref. 7 ) occur more often in patients with more severe disease who also have other risk factors, such as male gender, advanced age, obesity, cancer, different comorbidities, and treatment in intensive care units 3 .…”

Section: Introductionmentioning

confidence: 99%

Coagulation disorders in SARS-CoV-2 infection

Mihăilă¹,

Mihaila²

2020

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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A better understanding of the pathogenetic mechanisms triggered by SARS-CoV-2 infection may contribute to a more effective management of patients with COVID-19. Coagulation dysfunction is a key pathogenetic element of this disease as well as a challenge for practitioners. Marked inflammatory process found in severe forms of COVID-19, the complement activation, the cytokine storm, and disruption of the renin-angiotensin-aldosterone system are involved in the onset of thrombotic microangiopathy and large vessel coagulopathy. Virus-induced procoagulant activity occurs at the systemic level. Intravascular microthrombi disrupt vascularization in various tissues and organs, contributing to the occurrence of multiorgan failure and explain the higher morbidity and all-cause mortality of patients. It is estimated that almost 20% of patients with COVID-19 have significant coagulation disorders, and about a quarter of those hospitalized in intensive care units are prone to develop thrombosis events under prophylactic anticoagulant treatment. Some of patients who have been immunized after healing from the SARS-CoV-2 infection have a hypercoagulable state and are prone to develop thrombosis. Hypercoagulability is supported by thrombelastographic analysis: patients have an acceleration of the propagation phase of blood clot formation and higher clot strength. Markers of coagulation dysfunction in SARS-CoV2 are: decreased platelet count, increased INR, presence of fibrin degradation products, and especially higher plasma levels of D-dimers, which predict unfavorable outcome in these patients. Age, pre-existing diseases and associated risk factors, together with careful monitoring of clinical evolution and laboratory parameters allow the choice of the best personalized prophylactic or curative anticoagulant treatment.

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Acute upper limb ischemia in a patient with COVID-19

Cited by 61 publications

References 8 publications

Acute Limb Ischemia in COVID-19 Disease: A Mysterious Coagulopathy

Acute Limb Ischemia in COVID-19 Disease: A Mysterious Coagulopathy

Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses

Coagulation disorders in SARS-CoV-2 infection

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