SoulSlaveAG2005 said:

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In last 3 weeks our shipments of convalescent plasma have increased 3 fold from September. An other week of this and we will be back to shipping same numbers from July.

Hospitals are drinking it, but feedback I have heard from docs and co-workers that family was in hospital, said they improved noticeably w/n 24 hrs of transfusion.

Hope it keeps working

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BadMoonRisin said:

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SoulSlaveAG2005 said:

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In last 3 weeks our shipments of convalescent plasma have increased 3 fold from September. An other week of this and we will be back to shipping same numbers from July.

Hospitals are drinking it, but feedback I have heard from docs and co-workers that family was in hospital, said they improved noticeably w/n 24 hrs of transfusion.

Hope it keeps working

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Wow that's great news. Im a regular donor now, thanks in part to you and your helpfulness about donating during a pandemic.

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Infection_Ag11 said:

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Keegan99 said:

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The standard of care early on was, I believe, "vent early, vent hard", no?

And part of the motivation was to protect doctors and nurses?

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Marcus is probably a better person to pose this question to, but this disease was initially being managed as we've always managed ARDS. High PEEP, low TV, etc. Many have come to believe the pathophysiology of this disease is related more to intrapulnonary right to left shunts related to microthrombi (that's oversimplified but the point is it's different than primary parenchymal pneumonia). Because of the physiological cascade that follows, you end up with the body selectively shutting off certain alveolar segments with lots of physiologic dead space (places blood isn't getting to) and these areas are very hard to recruit with increased ventilatory pressure. In traditional pneumonia, these air spaces fill with fluid and debris but can be propped open with improved gas exchange by higher pressure. In COVID19, it seems the increased pressure is just shunted to the remaining functional alveoli with gives these alveoli much higher pressures that you think you're exposing them to and this results in worsening lung damage. So many critical care physicians have been trying to delay intubation with high flow, probing and letting patients ride at lower O2 and then if they require intubation they are using lower PEEP.

With respect to intubating as a means of protecting practitioners, I can only say that such a practice would be both highly unethical and not particularly effective at achieving the intended goal. While intubation does represent a closed respiratory system, the process of intubation is very high risk for the person doing the intubating. Moreover, all precautions must still be used given potential fomite and secretion transmission as well as the common complication of unintentional interruption of the respiratory system (patient pulling the tube, accidentally disconnecting the vent, etc.)

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Infection_Ag11 said:

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Some of the skin manifestations of this disease have been pretty interesting. Acral ischemia, livedo, leukocytoclastic vasculitis, etc. I haven't seen this but some have reported diffuse urticaria as well as a dengue like morbilliform rash.

My least favorite skin thing is probably pyoderma gangrenosum. Some hospitalist always swabs it, it always grows staph or pseudomonas and I get to decide if this thing is really secondarily infected or just colonized. It's especially fun when it's a nasty MDR pseudomonas and they want to use Zerbaxa or colistin or some *****

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