“…However, case reports of large pulmonary vein thrombosis have now emerged in severe COVID-19, 47 , 48 which provides a plausible mechanism to explain the propensity for systemic manifestations such as embolism to the kidney and brain, and might also explain the cutaneous manifestations of severe COVID-19 pneumonia. 12 , 23 Figure 3 Tricompartmental dysregulation and the severe systemic impact of COVID-19 (A) Immunothrombosis disrupts the terminal pulmonary arterioles (one of the dual blood supplies) and also eliminates anastomoses between the small bronchial artery and the distal pulmonary arteriole or capillary and vein, eliminating the wash-through effect of the pulmonary venules by the bronchial artery, which maintains venous patency in pulmonary embolism. Clot formation within pulmonary venules that are distal to the capillary networks provides a source from which systemic embolisation can occur.…”
Section: Tricompartmental Model Of Severe Covid-19mentioning
confidence: 99%
“…We also consider how immunothrombosis of the pulmonary venous drainage territory in COVID-19 might contribute to impaired oxygenation and also predispose to clot propagation, with ensuing systemic embolisation leading to manifestations such as cryptogenic stroke, renal infarction, peripheral artery occlusion, and cutaneous vasculitis. 12 We hope that our synthesis of data provides a robust model for better understanding of novel betacoronavirus infections, with implications for improved therapeutic approaches.…”
The emergent 21st century betacoronaviruses, including SARS-CoV-2, lead to clinicopathological manifestations with unusual features, such as early-onset chest pain, pulmonary infarction, and pulmonary and systemic thromboembolism that is pathologically linked to extensive capillary, arteriolar, and venular thrombosis. Early ground glass opacities detected by CT, which are reminiscent of lung infarcts associated with pulmonary embolism, point to a novel vascular pathology in COVID-19. Under physiological conditions, normal parenchymal oxygenation is maintained by three sources: the alveolus itself and dual oxygen supply from the pulmonary and bronchial artery circulations. We propose a model in which these three components are disrupted in COVID-19 pneumonia, with severe viral alveolitis and concomitant immunothrombotic obstruction of the pulmonary and bronchiolar circulation. Tricompartmental disruption might have two main consequences: systemic clot embolisation from pulmonary vein territory immunothrombosis, and alveolar-capillary barrier disruption with systemic access of thrombogenic viral material. Our model encompasses the known pathological and clinical features of severe COVID-19, and has implications for understanding patient responses to immunomodulatory therapies, which might exert an anti-inflammatory effect within the vascular compartments.
“…However, case reports of large pulmonary vein thrombosis have now emerged in severe COVID-19, 47 , 48 which provides a plausible mechanism to explain the propensity for systemic manifestations such as embolism to the kidney and brain, and might also explain the cutaneous manifestations of severe COVID-19 pneumonia. 12 , 23 Figure 3 Tricompartmental dysregulation and the severe systemic impact of COVID-19 (A) Immunothrombosis disrupts the terminal pulmonary arterioles (one of the dual blood supplies) and also eliminates anastomoses between the small bronchial artery and the distal pulmonary arteriole or capillary and vein, eliminating the wash-through effect of the pulmonary venules by the bronchial artery, which maintains venous patency in pulmonary embolism. Clot formation within pulmonary venules that are distal to the capillary networks provides a source from which systemic embolisation can occur.…”
Section: Tricompartmental Model Of Severe Covid-19mentioning
confidence: 99%
“…We also consider how immunothrombosis of the pulmonary venous drainage territory in COVID-19 might contribute to impaired oxygenation and also predispose to clot propagation, with ensuing systemic embolisation leading to manifestations such as cryptogenic stroke, renal infarction, peripheral artery occlusion, and cutaneous vasculitis. 12 We hope that our synthesis of data provides a robust model for better understanding of novel betacoronavirus infections, with implications for improved therapeutic approaches.…”
The emergent 21st century betacoronaviruses, including SARS-CoV-2, lead to clinicopathological manifestations with unusual features, such as early-onset chest pain, pulmonary infarction, and pulmonary and systemic thromboembolism that is pathologically linked to extensive capillary, arteriolar, and venular thrombosis. Early ground glass opacities detected by CT, which are reminiscent of lung infarcts associated with pulmonary embolism, point to a novel vascular pathology in COVID-19. Under physiological conditions, normal parenchymal oxygenation is maintained by three sources: the alveolus itself and dual oxygen supply from the pulmonary and bronchial artery circulations. We propose a model in which these three components are disrupted in COVID-19 pneumonia, with severe viral alveolitis and concomitant immunothrombotic obstruction of the pulmonary and bronchiolar circulation. Tricompartmental disruption might have two main consequences: systemic clot embolisation from pulmonary vein territory immunothrombosis, and alveolar-capillary barrier disruption with systemic access of thrombogenic viral material. Our model encompasses the known pathological and clinical features of severe COVID-19, and has implications for understanding patient responses to immunomodulatory therapies, which might exert an anti-inflammatory effect within the vascular compartments.
“…Proposed mechanisms relate to immune dysregulation, complement activation, clotting pathway activation or viral dissemination with direct systemic endothelial infection. 13 Although tests for factor VIII and protein S were not carried out in this case, the patient had a D-dimer of 20733, severe acute kidney injury and persistent uraemia requiring haemodialysis, in addition to bilateral segmental and subsegmental pulmonary emboli, all of which point to excessive coagulation. This may also help to explain the patient's persistent asymmetrical polyneuropathy.…”
Section: Case Report Differential Diagnosismentioning
A range of neurological manifestations associated with COVID-19 have been reported in the literature, but the pathogenesis of these have yet to be fully explained. The majority of cases of peripheral nervous system disease published thus far have shown a symmetrical pattern. In contrast, we describe the case of a patient with asymmetrical predominantly upper-limb sensorimotor polyneuropathy following COVID-19 infection, likely due to a multifactorial pathological process involving critical illness neuropathy, mechanical injury and inflammatory disease. His presentation, management and recovery contribute to the understanding of this complex condition and informs rehabilitation approaches.
“…Research into COVID-19 and its systemic effects has demonstrated a definitive increased risk of mortality secondary to diffuse alveolar damage and the development of immunothrombi in the pulmonary vasculature. In addition, COVID-19 has been directly linked to inflammatory and vasculitic processes affecting the skin, pulmonary vasculature and a Kawasaki-like disease phenomenon [3]. The proposed mechanisms for these include upregulation of pro-inflammatory cytokines, complement activation, endothelial damage/dysfunction.…”
Section: Discussionmentioning
confidence: 99%
“…There is a breath of knowledge emerging in recent times regarding the severe acute respiratory syndrome coronavirus 2 (SARs-CoV-2), also known as COVID-19, and its multi-systemic effects on the human body. There is evidence to support its link with vasculitic processes such as pulmonary vasculitis, Kawasaki's disease and cutaneous vasculitis [3]. In addition, COVID-19 infection has also been associated with increased risk of arterial and venous thrombosis, which is treated currently with anticoagulation [4].…”
Pulmonary artery pseudoaneurysms are uncommon and can cause severe, life-threatening haemoptysis. We present a case of a 74-year-old gentleman who was being treated for COVID-19 pneumonitis and a concomitant segmental pulmonary artery thrombus with conventional treatment and anticoagulation. The patient developed significant haemoptysis during admission. A repeat computed tomography pulmonary angiogram revealed an 8 mm left upper lobe pulmonary artery pseudoaneurysm. Anticoagulation was withheld and the pseudoaneurysm was successfully treated with endovascular embolisation with an AmplatzerÂź IV plug, leading to resolution of the haemoptysis. To our knowledge this is the first case of a pulmonary artery pseudoaneurysm secondary to COVID-19.
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