General

SARS-CoV-2 is a SARS-1 Evolution with Pulmonary Intravascular Coagulopathy

edited April 28 in General
Here’s an interesting post on comparing SARS-CoV-2 being the Michael Bay Transformer sequel to SARS-1
When you reach the point of ICU you probably have an extended pulmonary intravascular coagulopathy and your chances are not high since you have the prothrombotic phenotypic genetic response to COVID19.
At some point we will have to determinate the inflammatory mediators to determinate the intensity of the inflammatory cascade reaction leading to pulmonary vascular thrombosis by serum testing or genetic testing healthy patients to see if they can be infected without any mortality risk or if they are highly inflammatory responders.

https://www.facebook.com/jenniferkastenmd/posts/129795248673422?__tn__=K-R

COVID-19 and blood clots: the evidence, and why it's important for everything from to how to manage a ventilator, to what makes COVID unique. Today we'll look at:
- A new series of autopsies from Italy showing lungs full of clots [resulting in the equivalent of a middle school dance: oxygen on one wall, blood on the other]
- A new clinical term: Pulmonary Intravascular Coagulopathy, which might be the calling card of COVID
- How elevated the clotting risk really is in COVID, and how some patients are basically reverse hemophiliacs
- A paper comparing SARS-1 to our SARS-CoV-2 for clots [the sequel is always worse]
- And lastly: what this means for mechanically ventilated patients, and how it can explain the 'Not Normal ARDS' physiology

ITALIAN AUTOPSIES SHOW LUNGS WHERE BLOOD AND AIR CAN'T MEET

Investigators performed a series of 38 autopsies in Milan and Bergamo (1). The findings reinforced the smaller American series already published: the smallest capillaries are full of fibrin thrombi (clots), which significantly restrict the ability of oxygen to diffuse across into red blood cells- which is the entire purpose of the lungs. If blood and oxygen aren't meeting up, get a new DJ because the party is pretty much a bust.

Of the patients who had an important clotting factor measured, the values were screamingly high: more than 10x the normal range. 33/38 patients showed the fibrin thrombi, which is a much elevated rate over typical ARDS patients. [The picture shows a thrombus from their series, with the virus next door.]

THE CLOTTING IS SO UNIQUE, COVID HAS COINED A NEW TERM: PULMONARY INTRAVASCULAR COAGULOPATHY

Researchers in Ireland observed a 3-fold higher risk of clotting in a series of 83 mainly Caucasian patients, versus the Chinese data (2). (The risk of clotting is related to race: people of African descent are the highest risk, followed by Caucasians, with Asians the least likely (3)). Very importantly: the patients did not develop clots absolutely everywhere (a process called DIC, disseminated intravascular coagulopathy, which occurs in a wide array of critical illnesses). Instead, the deadly coagulation occurs predominantly in the lungs.

Why? They hypothesize that since the ACE-2 receptors are on the lining of blood vessels ("endothelium") as well as in lung cells, the teeming, extra-high viral loads in the lungs spillover into the endothelium and infect it, too. That makes the endothelial cells upset, and kicks off an inflammatory cascade which results in clotting.

ICU PATIENTS MAKE CLOTS EVEN WHEN ON PROPHYLAXIS, AND SOME ARE 'REVERSE HEMOPHILIACS'

It's no news that patients in ICUs are prone to making blood clots. They're in bed and not moving around (DON'T JUDGE, IT'S BEEN A HARD MONTH FOR US ALL), and they're ill, with numerous pro-coagulable factors released in their bloodstream. For that reason, most ICU patients are treated for clots before they can develop (typically, with Low Molecular Weight Heparin).

For COVID, everyone started anti-coagulating after a study in China (4), which showed that 25% of a series of 81 patients developed deep venous thromboses (DVTs), and 40% of those patients died- a rate of clotting which is 2x normal. In France (5) 26 patients were screened for DVTs with ultrasound in: 69% were positive, even though many of them were already on anticoagulation at the low 'preventive' dose. So they stepped up therapy to TREATMENT anti-coagulation, not just prevention and still- they still clotted. 56% developed DVTs, and 6 patients had an even more worrisome pulmonary embolism. In the Netherlands (6) researchers observed a rare phenomenon in COVID-19 patients: heparin resistance, where patients need an ultra-high dose of heparin to prevent clotting. They found that the virus caused the patients to make very high levels of Factor VIII (which is the same Factor many hemophiliacs are missing).

SARS-CoV-2 IS THE MICHAEL BAY OF CLOTTING

Have you ever watched a bloated, meaningless, sequel? Where they took all the good ideas from the original and said "this but more!"? That's the new coronavirus re: clotting. The original SARS definitely caused a similar picture (small clots in the vessels of the lungs, DVTs). About 30% of the patients in the largest series made DVTs, and there were five strokes. Compare that to the French data above (56% on therapy). The data is scantier on MERS, but it seemed to be more garden-variety DIC (7).

VERY INTERESTING, I GUESS, BUT ALSO, WHY IS THIS IMPORTANT?

I see you looking at your watch, trying politely to leave. Congrats! You made it to the end of the post! It's important because it validates all those countless clinical observations that "this isn't normal ARDS." I posted earlier about Dr. Cameron Kyle-Siddell's videos- the "is it like HAPE?" guy- and while no, it's not like HAPE, he was asking good questions. There are some very encouraging early anecdotes of doctors using this information to treat desperately failing patients, patients maxed out on the ventilator, with ANTI-COAGULATION (specifically, tPA) as a a way to open up those capillaries and let oxygen and the blood meet, marry, and diffuse.

SOURCES
1) Luca Carsana, Aurelio Sonzogni, Ahmed Nasr, Roberta Rossi, Alessandro Pellegrinelli, Pietro Zerbi, Roberto Rech, Riccardo Colombo, Spinello Antinori, Mario Corbellino, Massimo Galli, Emanuele Catena, Antonella Tosoni, Andrea Gianatti, Manuela Nebuloni. "Pulmonary post-mortem findings in a large series of COVID-19 cases from Northern Italy." PRE-PRINT on Medrxiv.org.

2) Fogarty H, Townsend L, Ni Cheallaigh C, Bergin C, Martin-Loeches I, Browne P, Bacon CL, Gaule R, Gillett A, Byrne M, Ryan K, O'Connell N, O'Sullivan JM, Conlan N, O' Donnell JS. COVID-19 Coagulopathy in Caucasian patients. Br J Haematol. 2020 Apr 24.

3) White RH, Keenan CR. Effects of race and ethnicity on the incidence of venous thromboembolism. Thromb Res. 2009;123 Suppl 4:S11-7.

4) Cui S, Chen S, Li X, Liu S, Wang F. Prevalence of venous thromboembolism in patients with severe novel coronavirus pneumonia. J Thromb Haemost. 2020 Apr 9.

5) Llitjos JF, Leclerc M, Chochois C, Monsallier JM, Ramakers M, Auvray M, Merouani K. High incidence of venous thromboembolic events in anticoagulated severe COVID-19 patients. J Thromb Haemost. 2020 Apr 22.

6) Beun R, Kusadasi N, Sikma M, Westerink J, Huisman A. Thromboembolic events and apparent heparin resistance in patients infected with SARS-CoV-2. Int J Lab Hematol. 2020 Apr 20.

7) Giannis D, Ziogas IA, Gianni P. Coagulation disorders in coronavirus infected patients: COVID-19, SARS-CoV-1, MERS-CoV and lessons from the past. J Clin Virol. 2020 Apr 9;127:104362.

Comments

  • edited November -1
    blue skies, smling at me. Nothing but blue skies for me .......
  • edited November -1
    I wonder if Aspirin will be the first choice if people show positive for Covid-19 but not symptomatic enough for the hospital. It also explains the high rate for strokes in people who are only mildly symptomatic. One of the earliest predictors of hospitalization is low O2 sats even with people with mild symptoms with the prescription now to get people with low O2 sats into the hospital early.
  • edited April 28
    Aspirin works differently than heparin or oral anticoagulants. It is a platelet aggregation inhibitor. That said, it is interesting in theory (just as HCQ was "interesting" in vitro) and very low risk to give, but studies are needed.

    Famotidine (Pepcid) is being assessed in a small clinical trial in a NYC hospital alongside other studies of more well-known potential treatments for COVID-19, including Gilead Sciences’ remdesivir and the antimalarial drug hydroxychloroquine. Again, a very low risk drug that I'm not worried about people dying from.

    But, as could be predicted, famotidine has been hoarded up and may now be hard to find. With ranitidine off the market due to contamination of the active pharmaceutical ingredient from China, more heartburn will ensue.
  • edited April 30
    I guess it depends on the cause of the coagulopathy. This could be DIC
  • edited April 30
    SCCRENDO | April 29, 2020
    I guess it depends on the cause of the coagulopathy. This could be DIC

    Don’t you have petechia and all capillaire affected?
    Didn’t read for covid specific coagulopathy if there are cases affecting outside the lungs
  • edited April 30
    Neither did I. That is why I asked
  • edited April 30
    We got a lot of fake docs up in here
  • edited November -1
    Is Orthopod the new name for facdoc or whatever his name was?

    As Slim Shady would say
    Will the real Magic8ball please stand up.

    Who is next to come back or change EaglesPDX?

    You guys have been stuck in your houses too long and are losing your minds or been smoking dope and drinking booze or Clorox and have lost it.
  • edited April 30
    Yes he is Maxxer aka Fake Doc aka FactDoc
  • edited April 30
    Hey Mario Brothers. Where did you suddenly spring from? Go back to watching Foxnews and yelling at the TV
  • edited April 30
    Hey old fart go back to your ocean view house and take a chill pill.
  • edited November -1
    I am there enjoying the view. Now stop harassing people trying to have a constructive conversation. Feel free to contribute in a constructive manner. Otherwise you would do us all a favor by yelling at your TV
  • edited April 30
    Fake news. Fake doc.
    You are an EVIL liar.

    Hidden AGENDA telling other to scream at TV and you scream at Tesla to help your position on TSLA short
  • edited November -1
    Hey Magic no balls. Get back on your meds. But to play your game. Explain to me why as a TSLA shareholder I would want to short the stock? I think I would sell my stock first. But who knows?
  • edited April 30
    Lying again.

    SCCRENDO = lying = fake

    No proof of your tsla stock = no stock

    Only saying you have to hide your agenda you have been pushing undercover of a liberal fake doctor.
    Go join your pretending gang. FISHEV leading you all.
  • edited April 30
    @MB8, I know for a FACT that SCC is in fact a physician. So it's you who is a liar.
  • edited April 30
    @rxlawdude. Thanks for the defense. But I cannot take the poor fellow too seriously sans his Seroquel
  • edited May 2
    This discussion was interesting until the uneducated trolls started polluting the forums again


    New researches seems to point out that some specific patients develop DIC, new treatment for these sub patients will need to act on coagulation cascade
  • edited November -1
    Thought so. Thanks
  • edited May 28
    Interesting. I didn't hear about the Italian findings.
  • Another WW_spd meltdown?
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