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Thread: Coronavirus

  1. #1501
    Bogley BigShot oldno7's Avatar
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    between biden and rice--we really need there well thought out leadership in a time of crisis.

    "tens of thousands"--got it.


    Susan Rice: Trump's lack of coronavirus leadership 'has cost tens of thousands of American lives'


    “Even I am not prepared to say that, and maybe I should, but it’s just inconceivable to me to have to state a proposition that the president of the United States is willfully trying to kill Americans,” Rice told the Washington Post's Jonothan Capehart during a recent edition of his podcast. "I don’t want to say that. I don’t want to believe that. But I do think he’s playing politics."

    According to the Obama-era official, Trump has shown a lack of leadership during a time of national crisis.

    https://www.washingtonexaminer.com/n...american-lives
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  3. #1502
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  4. #1503
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  5. #1504
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  6. #1505
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  7. #1506
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  9. #1507
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  10. #1508
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  11. #1509
    Quote Originally Posted by BasinCruiser View Post
    Of course he does. Trump only has Fauci there for optics. Trump knows.

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  14. #1511
    #LetsGoBrandon BasinCruiser's Avatar
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  16. #1512
    Bogley BigShot oldno7's Avatar
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  17. #1513
    Bogley BigShot oldno7's Avatar
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  19. #1514
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  20. #1515
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  21. #1516

    Coronavirus

    He’s starting to paint a positive picture.



  22. #1517
    #LetsGoBrandon BasinCruiser's Avatar
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    #PumpUpThoseNumbers

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  23. #1518
    #LetsGoBrandon BasinCruiser's Avatar
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    Ummmm. That’s going to be a big, gigantic : No.

    Tell me again why we have #2A.


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  25. #1519

    Coronavirus

    Light at the end of the tunnel in New York?



  26. #1520
    ephemeral excursionist blueeyes's Avatar
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    Intersting article on how a hospital in Queens is handling COVID-19 patients.

    https://journals.lww.com/em-news/blo...spx?PostID=508

    Things I find of interest is of course all the correlation to lab values but more specifically how it talks about the kidney damage.

    "A side note about acute kidney injury (AKI): There appears to be a disproportionate number of patients with AKI from COVID-19 compared with typical viral pneumonia. This may suggest another contributing factor, possibly a microangiopathic component."

    I am not kidding when I say it is alarming to me the kidney damage from this viral infection.

    Also the proposed treatment of Chloroquine and Azythromicn...this maybe effective but can cause complications

    "Hydroxychloroquine and thiamine:*These are being recommended on the floors. The data available so far are mixed, but we don't have much. It would be worth considering starting chloroquine or hydroxychloroquine for critically ill patients, depending on availability. Antiviral therapy may be effective primarily early in the disease course, before the development of ARDS. Initiating this in the ED is probably the best bet, but this is not routine practice at this time. Remdesivir is emerging as a frontrunner for antiviral therapy, but it is not widely available at this time. It may end up doing more harm than good, but we will know more with further investigation. Our current dosing on the floors is thiamine 200 mg IV Q12 x 6 days and chloroquine 500 mg BID x 5 days. See below for QTc considerations. Also consider G6PD for patients getting chloroquine; that is why it should be sent with labs at admission.

    Azithromycin:*We are not starting this on everyone. Keep in mind that both azithromycin (although mild) and chloroquine are going to prolong the QT, so be careful and aggressively replete Mg and K as needed. The efficacy has yet to be proven."

    These medications mess with the heart and need to be carefully administered. Especially in patients with heart issues and this virus starts affecting the heart because if you are not perfusing O2 it causes the heart to work harder.

    But the most interesting thing to me is that they present with thrombocytopenia means they have low platelets why?? Some patients over respond to the infection their immune system causes a cytokine storm. This makes them use up all of their platelets and coagulation factors. They are hypercoagulable. Person who had normal platelets are now clotting all over the place. Usually we have negative feedback system that keeps us from doing this but the cytokine storm effectively stops this negative feed back loop. This puts a patient at risk for DIC

    Why does this matter? DIC probably one of the most intersting responses of the body to trauma if you ask me.

    Disseminated Intravascular Coagulation basically your body starts using up all your available clotting factors to the point you have nothing left and start bleeding internally and you can bleed externally.


    The link below has some really good information on COVID-19.


    https://emcrit.org/ibcc/covid19/


    "Most patients with COVID seem to be extremely hypercoagulable.* This would support a potential role for heparin anticoagulation, and also bolster the safety of heparin administration (some patients appear*heparin-resistant –*again suggesting that heparin is probably fairly*safe*here."


    "COVID produces a form of disseminated intravascular coagulation (DIC) which is usually marked by hypercoagulability.

    The exact causes of this are unclear and likely numerous.* They could include the following:

    (1) Inflammation (e.g. IL-6) stimulates up-regulation of fibrinogen synthesis by the liver (Carty 2010).

    (2) Virus may bind directly to endothelial cells.

    There is likely a bi-directional, synergistic relationship between DIC and cytokine storm (wherein each exacerbates the other).

    DIC appears to be a driver of disease severity.* As might be expected, it is a strong prognostic factor for poor outcome (Tang et al. 2020).

    Microthrombi have been reported as autopsy findings in patients with COVID-19 (Luo et al.)"

    And from the same source

    "stage III (hyperinflammation phase / cytokine storm)

    Clinically:* Patients deteriorate with progressive disseminated intravascular coagulation and multi-organ failure (e.g. vasodilatory shock, myocarditis).* Laboratory abnormalities include marked elevation of D-dimer, C-reactive protein, and ferritin.* Patients may initially respond well to intubation and ventilation during stage II, but subsequently develop increasing levels of inflammation, which leads to clinical deterioration.

    Biologically:* The adaptive immune response spirals into an immunopathological dysregulated cytokine storm.* This likely represents a form of virus-induced hemophagocytic lymphohistiocytosis (HLH)"

    Just some research I have been doing. Wanting to understand lab values and disease progress.

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