I’m a new listener from Canada and despite my lack of scientific background, I’m finding your podcast riveting.
I have a question about what post-ventilator life is like for people who end up sick enough from COVID-19 that they need one.
For those who get off the ventilator, what is their quality of life? I heard on your “parking lot interview” with Daniel Griffin that in addition to lung, patients may have issues with heart, kidneys, and liver. So, afterward, are they just walking away and getting back to their normal life, or are they now seriously chronically ill?
I’m sure there’s a range of outcomes based on pre-COVID health, but let’s say someone who is in either terrific health or average? There may not be enough experience with COVID-19 yet, but would knowledge based on pneumonia or influenza cases be relevant in trying to predict?
I am a layman who has been listening to the podcast for the past two months. I love the clear, well-informed and science-based discussion you have every few days. You guys are the eye of the storm these days.
In the last episode (TWiV 606), Daniel Griffin spoke about the blood clotting issues in patients with COVID-19. He mentioned putting patients on high doses of Heparin to stop the blood coagulating. There was also a Washington Post article on the same subject. Young and middle-aged people, barely sick with covid-19, are dying of strokes
My question is: should adults with COVID-19 symptoms immediately start taking aspirin as a precaution? Or is the anti-inflammatory effect too dangerous?
Dear TWiV folks,
Is there any evidence that those with existing blood clotting disorders are at higher risk for blood clots while infected by COVID-19?Â I and (at least) four of my family members, have Protein S Deficiency.Â Some of us are on anticoagulants for the duration and others of us are not. What would you recommend to those with Protein S and C Deficiencies and Factor 5?Â How do your recommendations change for those on anticoagulants vs. those who are not?
I hope you all are and remain healthy physically, mentally, and emotionally.
Thank you for all you do,
Stephanie RiCharde, PhD
University of Lynchburg
Long time listener and big fan. Neurology resident in NYC. Listening to this week’s episode and very curious what Dr. Griffin thinks of looking for smaller peripheral emboli with VQ scans as well as the CT PE scans to get a better idea of the chronicity of some of these PEs. As a prelim medicine intern some of my oncology patients with hypercoaguability would have hypoxia (especially with exertion) out of proportion to their CT findings but with many smaller/distal/chronic appearing clots better visualized w VQ scans. I suspect they would be challenging to get for COVID patients logistically (what isn’t hard now?) but I wonder if having better ideas of the timeline of clotting would help us prevent hospitalizations if it led us to consider for example prophylactic apixaban for outpatients with covid or suspected covid.
Thank you a million times over for what you do, I recommend the show to everyone.
Hello TWIV Team,
I saw some early reports that people with COVID-19 have low circulating eosinophil counts and eosinopenia could be an indicator of severe COVID-19:
Daniel Griffin in TWIV 603 mentioned that he’s seeing a lot of eosinophils (among other inflammatory cells) in his bronchoalveolar lavages, so I was wondering if you could clarify why we’re seeing decreased eosinophils in the blood but increased eosinophils in the lungs. Are the eosinophils migrating from the blood to the lungs? If so, why are they doing that if eosinophils are not typically associated with the clearance of a viral pathogen?
Thanks for all the work you guys do!
CMDB PhD Candidate
P.S. I will also send this email to Immune if you’d rather answer it there.
I have a question for Dr. Griffin:
In TWiV 603 Dr. Griffin described how severe cases of Covid-19 can lead to low blood oxygen saturation even with oxygen therapy, which would normally prompt physicians to intubate. He also said that because of the bad prognosis of intubated patients with covid-19 some doctors are now delaying or even avoiding intubation, even if it means tolerating low oxygen saturation. They face a dichotomy:
- intubation leading to possible death or
- tolerating hypoxia with possible long term consequences for tissue.
In a recent TWiV it was explained that fevers in mechanically ventilated patients must be treated to avoid additional demand for oxygenation. I wonder if the same logic would apply to inducing hypothermia (instead of preventing fever) to reduce the demand for oxygen to avoid intubation or maybe reduce the risk associated with hypoxia.
I discovered your pod(s) thanks to Science Vs. They are awesome!
– T.B. (It is 11ºC in Madrid)
PS: The following Stat article describes the low blood oxygen saturation. Interestingly, CO2 does not seem elevated so some gas exchange must be taking place.