conspiracy or clotting problems?

 

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These clots noticed by undertakers were reported two years ago on conspiracy sites.

Now, even back in 2021 I knew that the AZ vaccine caused blood clots, but I figured my chance of dying of covid because I was high risk was worth it.

But even here in the Philippines, we didn't give the AZ to young people

We didn't get the mRNA vaccines offered to us free by the USA back in Jan 2021 because the authorities

and here if an athlete or young man drops dead, it is assumed to be bangungot.

so when did the medical literature first report the problem of blood clots in covid?

But this German study of autopsies on covid deaths in May 2020 show a high incidence of blood clots and pulmonary emboli.

Results: Median patient age was 73 years (range, 52 to 87 years), 75% of patients were male, and death occurred in the hospital (n = 10) or outpatient sector (n = 2). Coronary heart disease and asthma or chronic obstructive pulmonary disease were the most common comorbid conditions (50% and 25%, respectively). Autopsy revealed deep venous thrombosis in 7 of 12 patients (58%) in whom venous thromboembolism was not suspected before death; pulmonary embolism was the direct cause of death in 4 patients. Postmortem computed tomography revealed reticular infiltration of the lungs with severe bilateral, dense consolidation, whereas histomorphologically diffuse alveolar damage was seen in 8 patients. In all patients, SARS–CoV-2 RNA was detected in the lung at high concentrations; viremia in 6 of 10 and 5 of 12 patients demonstrated high viral RNA titers in the liver, kidney, or heart.

In all 12 cases, the cause of death was found within the lungs or the pulmonary vascular system. However, macroscopically differentiating viral pneumonia with subsequent diffuse alveolar damage (a histologic diagnosis) from bacterial pneumonia was not always possible. Typically, the lungs were congested and heavy, with a maximum combined lung weight of 3420 g in case 11. The mean combined lung weight was 1988 g (median, 2088 g). Standard lung weights for men and women are 840 g and 639 g, respectively (13, 14). Only cases 6 and 9 presented with a relatively low lung weight: 550 g and 890 g, respectively (Appendix Table 1, available at Annals.org). The lung surface often displayed mild pleurisy and a distinct patchy pattern, with pale areas alternating with slightly protruding and firm, deep reddish blue hypercapillarized areas. On the cutting surfaces, this pattern was also visible (Figure 2). The consistency of the lung tissue was firm yet friable. In 8 cases, all parts of the lungs were affected by these changes. Cases 6, 7, and 9—occurring in the 3 women of the case series—presented with changes compatible with focal purulent bronchopneumonia. Macroscopically, no changes were observed outside the lungs and respiratory tract, except for splenomegaly in 3 cases, which suggested a viral infection.

Discussion In this autopsy study of 12 consecutive patients who died of COVID-19, we found a high incidence of deep venous thrombosis (58%). One third of the patients had a pulmonary embolism as the direct cause of death. Furthermore, diffuse alveolar damage was demonstrated by histology in 8 patients (67%)....

Other researchers have described coagulopathy as a common complication in patients with severe COVID-19 (5, 6, 19). In a recent study of 191 patients with COVID-19, 50% of those who died had coagulopathy, compared with 7% of survivors. D-dimer levels greater than 1000 µg/L were associated with a fatal outcome (6).

Steroids were used early to stop the pulmonary symptoms, but I don't remember reading that maybe covid patients needed blood thinners. Did I miss it?

a more recent report confirms the problems of blood clots leading to death in covid:

Science daily has a report from Brazilian docs that suggested that covid killed via clots:

Scientists from the University of São Paulo have discovered that severe COVID-19 is primarily caused by damage to the small blood vessels in the lungs, a result of SARS-CoV-2 infection. Blood clot formation (thrombosis) in the small blood vessels of the lungs is an early result of severe COVID-19, often occurring before the breathing difficulties caused by widespread damage to the air sacs, according to a Brazilian study reported in an article published in the Journal of Applied Physiology. Post-mortem examinations of nine individuals who passed away from severe COVID-19 revealed a distinct pattern of changes in lung blood vessel structure and thrombosis. For the first time, the article describes sub-cellular aspects of the endothelial damage and associated thrombotic phenomena caused by the infection. It notes the impact of acute inflammation on lung microvascular circulation as the key factor in severe COVID-19, contributing to a deeper understanding of the pathophysiology of the disease and the development of novel therapeutic strategies. “This study furnished the final proof of what we’d been pointing out since the very start of the pandemic – that severe COVID-19 is a thrombotic disease. The virus SARS-CoV-2 has a tropism for [is attracted to] the endothelium, the layer of cells that lines blood vessels. When it invades endothelial cells, it first affects microvascular circulation. The problem starts in the capillaries of the lungs [the tiny blood vessels that surround the alveoli], followed by clotting in the larger vessels that can reach any other organ,” said pulmonologist Elnara Negri

so was heparin in the treatment guidlines?

NEJM wrote about it in Aug 2021 CONCLUSIONS In critically ill patients with Covid-19, an initial strategy of therapeutic-dose anticoagulation with heparin did not result in a greater probability of survival to hospital discharge or a greater number of days free of cardiovascular or respiratory organ support than did usual-care pharmacologic thromboprophylaxis. ,

LINK letter to the editor suggests no problem with clots:

The incidences of prospectively diagnosed acute pulmonary embolism among patients who were hospitalized for Covid-19 were relatively low: 1.3% (29 of 2226) among noncritically ill patients and 5.1% (55 of 1089) among the critically ill. These incidences were similar to those observed in other prospective trials involving patients with Covid-19.3

well, heparin like meds only stop the clots, so if given late you have to wait for the body to remove the clots. Did they use medicine to disssolve clots? I'll have to look that up.

how about an easy anti thrombotic medicine we use all the time: Aspirin? LINK2022 Jan 1; Further evidence for the use of aspirin in COVID-19

if you took aspirin prior to getting covid, or very early when you got sick, your chances of living were better

The coronavirus disease (COVID)-19 is associated with cytokine storm attendant with very high levels of inflammation biomarkers, hypercoagulability marked by elevated levels of d-dimer, and fibrinogen, modest consumption of coagulation factors, and mild abnormalities in platelet count, platelet activation and prothrombin time [1]. Therefore, patients with COVID-19 are at risk for multiorgan thrombotic and thromboembolic events that can rapidly lead to critical lung illness and death. Patients with COVID-19 have benefited from concomitant treatment with antiinflammatory, antiviral, and anticoagulant agents. Currently available therapies that are directly targeting the virus may exhibit limited effectiveness over time due to continuous mutations into new variant forms [2]. Observational studies have demonstrated the potential efficacy of adjunctive therapy of low-dose aspirin (81–100 mg per day) in patients with COVID-19. In an earlier small observational cohort study of adult patients with COVID-19 by Chow et al., aspirin use (n = 98) at least seven days before hospitalization or within 24 h of hospitalization compared to no aspirin use (n = 314) was significantly associated with lower intensive care unit (ICU) admission, risk of mechanical ventilation, and in-hospital mortality. There were no differences in overt thrombosis or major bleeding between groups [3]. In another recent observational study, among 730 patients on antiplatelet therapy, 645 patients were treated with either oral or intravenous aspirin during hospitalization. Compared to 6986 patients on no antiplatelet therapy, patients on antiplatelet therapy had lower in-hospital mortality and a shorter duration of mechanical ventilation. ,

they also discuss giving it nebulized and in influenza patients

another article discussing nuances here.

treatment last october guideines said:There is insufficient evidence for the Panel to recommend either for or against routine screening for venous thromboembolism (VTE) in patients with COVID-19 who do not have signs or symptoms of VTE, regardless of the status of their coagulation markers. For hospitalized patients with COVID-19 who experience rapid deterioration of pulmonary, cardiac, or neurological function or sudden, localized loss of peripheral perfusion, the Panel recommends evaluating the patients for thromboembolic disease (). Anticoagulant Treatment for Thrombosis When diagnostic imaging is not possible, the Panel recommends that patients with COVID-19 who are highly suspected to have thromboembolic disease be treated with therapeutic anticoagulation (). The Panel recommends that patients with COVID-19 who require extracorporeal membrane oxygenation or continuous renal replacement therapy or who have thrombosis related to catheters or extracorporeal filters be treated with antithrombotic therapy as per the standard institutional protocols for those without COVID-19 (). Antithrombotic Therapy for Nonhospitalized Patients Without Evidence of Venous Thromboembolism In nonhospitalized patients with COVID-19, the Panel recommends against the use of anticoagulant and antiplatelet therapy (i.e., aspirin, P2Y12 inhibitors) for the prevention of VTE or arterial thrombosis, except in a clinical trial (). This recommendation does not apply to patients with other indications for antithrombotic therapy. Antithrombotic Therapy for Hospitalized, Nonpregnant Adults Without Evidence of Venous Thromboembolism The Panel recommends against using anticoagulant or antiplatelet therapy to prevent arterial thrombosis outside of the usual standard of care for patients without COVID-19 (). In hospitalized patients, low-molecular-weight heparin (LMWH) or unfractionated heparin (UFH) is preferred over oral anticoagulants (). Because these types of heparin have shorter half-lives, their effects can be reversed quickly. They can also be administered intravenously or subcutaneously, and they have fewer drug-drug interactions than oral anticoagulants. When heparin is used, LMWH is preferred over UFH.

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