TWiV 608: Daniel Griffin’s COVID-19 clinical report

May 1, 2020

Daniel Griffin updates the clinical situation with COVID-19 patients, followed by analysis of the remedesivir clinical trial results, and answers listener questions.

Hosts: Vincent Racaniello and Rich Condit

Guest: Daniel Griffin

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Download TWiV 608 (35 MB .mp3, 57 min)
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Intro music is by Ronald Jenkees.

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8 comments on “TWiV 608: Daniel Griffin’s COVID-19 clinical report

  1. michelle May 1, 2020

    I have a friend who has DAD as sequelae to previous ARDS from H1N1 infection (ca. 2016). She survived on ECMO for nearly a month at that time (and was about 30 years old). She has the classic signs of DAD – asthma-like symptoms and greatly diminished exercise capacity. Unfortunately, she is also working-poor with spotty access to health insurance. What recommendations are being made in local county medical centers in poorer areas like Yavapai County, AZ, for dealing with the onset of clinical symptoms for covid-19 in people with such serious preexisting conditions?

    Best Regards,

  2. Adrianne May 2, 2020

    Thank you so much for continuing to bring quality information and really thoughtful discussion to those of us who cannot find it really anywhere else.

    I have a question regarding the clotting issues rearing their ugly heads with COVID discussed across a few episodes.
    I’m a physician in Texas, and trained in a very busy level 1 trauma center in a surgical subspecialty. The swirl of controversy around hypercoaguulability and tendency of trauma patients to clot and embolize (and the pesky Coumadin bridge that extended their admission, not to mention extra radiation blasts with all the additional fine cut chest CTs) never ended. There was a shift of perspective later in my training that I found at least theoretically to be very powerful that I am curious about in our present situation.
    It occurred to the STICU thinktank that in polytraumatized patients (who very likely sustained chest/trunk injury, even if not deemed significant still present) that what we interpret to be an embolic event because of perhaps a culture of fear in our hospital system today – very likely was not a clot that had originated distally and been “thrown” to the lungs, but could very possibly have originated in the lungs, which we think respond in an similar manner to practically every other tissue in the body to injury… by bleeding – inflaming – clotting /effort to heal. So maybe what we assumed to be embolic events quite possibly were simply the result of damage to lung tissue that we have a tendency to compartmentalize into all the glorious associated lung /respiratory metrics. I know Inam preaching to the choir – but we know it matters when trying to not rob a sick patient or whatever reserve they might have left – whether they are truly helped by aggressive anticoagulation or if we do it because the hospital gets bad marks if something that even smells like a clot isn’t hit hard with all our impressive armory to make patients bleed really easily and for a long time.

    A doc friend of mine who eventually was found to have COVID told me that the only reason he actively sought out care is because he broke two ribs purely from the violent, persistent dry cough. I’d imagine the lungs in these patients are subject to trauma from not only uncontrollable cough, but the cell lysis and cascading/ inflammatory train and also vent injury that we know is occurring especially in lung tissue. It seems to be ground zero: I wonder what your thoughts are on the possibility that what look like emboli might not have traveled anywhere except through the viral lysed/destroyed cell membrane in a very damaged lung tissue. And, does that thought potentially impact treatment if this “embolus” is found/read incidentally?

  3. Priscilla May 2, 2020

    V/Q scans -> ventilation /perfusion
    Abbreviating perfusion with Q, from the formula for flow: Q= A • v
    or flow = area • velocity

    Excellent podcast as usual! Thank you.

  4. Melinda Kreisberg May 6, 2020

    Thank you for covering remdesivir with respect to the viral course within infection. I am a PhD in Microbiology and Immunology and keep debating with colleagues remdesivir given that when patients ‘go south’ the viral load is quite low and the disease at this point is primarily immune maladaptive. Hearing the discussion was quite helpful and I have sent the link (as well as previous links to TWiV) to several colleagues. We teach at a small, state-assisted university in WV. Currently the institution has announced plans to reopen fully in the fall. That said, they have not indicated the ‘how’ nor do they seem interested in soliciting information from our micro/immuno-trained faculty (we have 3 at our institution of 2400 students). What are your opinions on the potential of reopening higher ed and remaining safe while so doing. I certainly understand the financial ramifications but am interested if, as several of you teach and at very different institutions, you have insight on how or if your institutions plan to address the pandemic. Thank you! I found TWiV through the ASM and have listened to IMMUNE and TWiP. I have used TWiV and IMMUNE in class this semester and plan to incorporate them and TWiP more formally next year.

    PS it is rainy and chilly in WV- barely 50F. Would love to see the sun and make some Vitamin D!