Post COVID-19 sequelae: venous thromboembolism complicated by lower GI bleed

Kumar, Malini Ashok; Madhavan, Krishnaswamy; Arul, Judah Nijas

doi:10.1136/bcr-2020-241059

Cited by 21 publications

(29 citation statements)

References 3 publications

(4 reference statements)

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“…Endothelial injury, either due to virus invasion or in the context of profound inflammation increased levels of coagulation factors, hypoxia, due to respiratory impairment or anti-platelel factor 4 (PF4)-immune complexes, has been implicated in acute COVID-19 pathogenesis, predisposing to coagulopathy and thromboembolic complications in large blood vessels and microcirculation [ 53 , 72 , 73 ]. Thromboembolism may also complicate the post-COVID period in the context of a hypercoagulate state [ 74 ]. An increased risk of developing pulmonary thromboembolism, deep vein thrombosis, and thrombosis in other systems manifested by active bleed, has been recorded in patients who have recovered from COVID-19 [ 74 ].…”

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

“…Thromboembolism may also complicate the post-COVID period in the context of a hypercoagulate state [ 74 ]. An increased risk of developing pulmonary thromboembolism, deep vein thrombosis, and thrombosis in other systems manifested by active bleed, has been recorded in patients who have recovered from COVID-19 [ 74 ]. Follow-up of at least 30 days post-discharge is required, while patients at high-risk for thrombosis should receive anticoagulation medications for a prolonged period [ 74 ].…”

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

“…An increased risk of developing pulmonary thromboembolism, deep vein thrombosis, and thrombosis in other systems manifested by active bleed, has been recorded in patients who have recovered from COVID-19 [ 74 ]. Follow-up of at least 30 days post-discharge is required, while patients at high-risk for thrombosis should receive anticoagulation medications for a prolonged period [ 74 ]. A recent study from Ireland found increased D-dimer levels (>500 ng/mL) in 25.3% of 150 COVID-19 patients, including 60 with a history of hospitalization, up to four months after initial diagnosis [ 75 ].…”

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

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Post-COVID Syndrome: An Insight on Its Pathogenesis

2021

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Post-COVID syndrome is increasingly recognized as a new clinical entity in the context of SARS-CoV-2 infection. Symptoms persisting for more than three weeks after the diagnosis of COVID-19 characterize the post-COVID syndrome. Its incidence ranges from 10% to 35%, however, rates as high as 85% have been reported among patients with a history of hospitalization. Currently, there is no consensus on the classification of post-COVID syndrome. We reviewed the published information on post-COVID syndrome, putting emphasis on its pathogenesis. The pathogenesis of post-COVID syndrome is multi-factorial and more than one mechanism may be implicated in several clinical manifestations. Prolonged inflammation has a key role in its pathogenesis and may account for some neurological complications, cognitive dysfunction, and several other symptoms. A multisystem inflammatory syndrome in adults (MIS-A) of all ages has been also described recently, similarly to multisystem inflammatory syndrome in children (MIS-C). The post-infectious inflammatory pathogenetic mechanism of MIS-A is supported by the fact that its diagnosis is established through serology in up to one third of cases. Other pathogenetic mechanisms that are implicated in post-COVID syndrome include immune-mediated vascular dysfunction, thromboembolism, and nervous system dysfunction. Although the current data are indicating that the overwhelming majority of patients with post-COVID syndrome have a good prognosis, registries to actively follow them are needed in order to define the full clinical spectrum and its long-term outcome. A consensus-based classification of post-COVID syndrome is essential to guide clinical, diagnostic, and therapeutic management. Further research is also imperative to elucidate the pathogenesis of post-COVID syndrome.

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Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

Section: Pathogenesis Of Post-covid Syndromementioning

confidence: 99%

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Post-COVID Syndrome: An Insight on Its Pathogenesis

2021

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“…Given her positive serology, it is reasonable to assume that at some point before her STEMI, she was infected with COVID-19; however, she was completely asymptomatic. Cardiac injury from COVID-19 is not well understood, however, the majority of cases reported involve patients with a severe form of the disease, usually requiring hospitalization [11][12][13][14][15][16][17]. COVID-19 is associated with hypercoagulability both during acute infection and after recovery 14 [11].…”

Section: Discussionmentioning

confidence: 99%

“…However, the literature review does show the possibility of coronary artery thrombosis secondary to endothelial damage from prolonged severe coronary vasospasm in patients without evidence of atherosclerotic plaque rupture [5][6][7][8][9][10][11]. More recently, coronavirus disease 2019 (COVID-19) has been shown to be associated with various thromboembolic phenomena, however, the majority of cases involving acute coronary artery occlusion have been observed in hospitalized patients with concurrent respiratory failure [12][13][14][15][16][17]. Post-infection coronary artery thrombosis in a recovered asymptomatic patient has yet to be reported.…”

Section: Introductionmentioning

confidence: 99%

ST-Elevation Myocardial Infarction in a 23-Year-Old Female: The Mystery of Thrombus Formation

Sikandar¹,

Butler²,

Battula³

et al. 2021

Cureus

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Acute ST-elevation myocardial infarction (STEMI) is rarely seen in young adults, however, when encountered, the underlying cause is either a genetic condition leading to early-onset coronary artery disease (CAD), an acquired pro-thrombotic condition, or an idiopathic condition like spontaneous coronary artery dissection (SCAD). Our case describes a healthy 23-year-old female who presented with sudden onset severe angina and was found to have a laminated thrombus in the left anterior descending coronary artery (LAD), with no evidence of intraluminal dissection or plaque rupture. Although the underlying etiology of thrombus formation remains unknown, coronavirus disease 2019 (COVID-19) related thrombotic event is the prime suspect. In addition, another culprit that cannot be excluded is phentermine-induced coronary vasospasm, a commercially available medication for weight loss. This report addresses current literature on acute coronary syndromes in young adults and reviews the potential etiologies for coronary artery thrombosis, which led to a near-fatal acute coronary syndrome in our patient.

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