EuclidIt just seems like something is missing in this story.
Part of what is 'missing' is that, for testing to be of much practical value in any currently-relevant sense, it has to be conducted before the usual presenting symptoms manifest and then become serious enough to warrant 'hospitalization' (or being seen by "a doctor" instead of the usual feed-a-cold-starve-a-fever activity until things get worrisome.
And the testing has to be done progressively, perhaps no more than days apart, and carefully tracked ... but not in ways that violate the spirit of HIPAA or that could have data diverted or hijacked for private purposes.
As long as we have serological testing that requires serious phlebotomy, and swab tests that may be less than 2/3 specific, highly unpleasant to receive, and potentially dangerous to administer for proof of genomic presence, it isn't terrifically likely that large numbers of relatively asymptomatic will flock to ad hoc testing centers to fill out interminable paperwork.
One of the characteristics of the evolved human immune system is that it 'works' against a variety of pathogens, and the evolution of effective response to one given type does not necessarily address, or even work positively, against others. Development of fever (hyperthermia) is well-established to work against certain microorganisms that only thrive in a limited temperature range; development of malignant hyperthermia may be a conserved response, or an uncontrolled response to stimuli that aren't resolved in simple feedback. But fever is not a response that is meaningful in viral infection; neither is much of the immune response observed in progressive ARDS. This is part of the reason why "waiting" until fever is observed is both wrong and shortsighted in determining when to start testing for COVID-19; many of those at risk are severely, perhaps even irrecoverably compromised before they even present. Basing a relaxation of SIP/SD on testing conducted only on the frankly symptomatic is almost a recipe for disaster down the line. (Meanwhile there is some evidence that by the time frank symptoms of immune modulation are present, SARS-CoV-2 transmissibility may already be reduced, while on the other hand the likelihood of earlier spread sometime in the preceding 5 days or so may have been high.)
As noted earlier, one of the 'correct' approaches to restarting the economy is to continue SIP for the cohorts most at risk for ARDS, combined with reasonable and correct social distancing and transmission reduction in areas those cohorts may 'frequent'. This is going to be no fun at all for a large number of nursing homes and similar "assisted care" facilities that have traditionally run cheap and slipshod hospice-lite kinds of operations. Other social operations, involving mass gatherings or large groups, will have similar safeguards inherent in their 'new normal' operating models, for at least the duration of the initial 'opening' of the economy.
Since treatment is such a lethal joke so much of the time, and so many effective therapies appear to be just like power production from contained nuclear fusion or thorium, effective prevention of those at greatest risk while permitting acquired immunity in those less at risk in a reasonably short time is the only real strategy that does not involve the risk of extensive, and publicized, outbreaks of suffering and death.
Hopefully we learn for the next time.
This is stunning if true. This doctor says we are treating COVID-19 incorrectly. It correlates with why the death rate is so high for people on ventilators.
https://www.youtube.com/watch?v=Elgct0nOcKY&feature=emb_logo
EuclidThis is stunning if true. This doctor says we are treating COVID-19 incorrectly. It correlates with why the death rate is so high for people on ventilators. https://www.youtube.com/watch?v=Elgct0nOcKY&feature=emb_logo
Totally highlights how little we know and understand about Covid-19 and how to successfully treat it.
The lack of a acknowledged and scientifically tested treatment protocol is the real problem at this point in time.
Never too old to have a happy childhood!
Overmod Euclid It just seems like something is missing in this story. Part of what is 'missing' is that, for testing to be of much practical value in any currently-relevant sense, it has to be conducted before the usual presenting symptoms manifest and then become serious enough to warrant 'hospitalization' (or being seen by "a doctor" instead of the usual feed-a-cold-starve-a-fever activity until things get worrisome. And the testing has to be done progressively, perhaps no more than days apart, and carefully tracked ... but not in ways that violate the spirit of HIPAA or that could have data diverted or hijacked for private purposes. As long as we have serological testing that requires serious phlebotomy, and swab tests that may be less than 2/3 specific, highly unpleasant to receive, and potentially dangerous to administer for proof of genomic presence, it isn't terrifically likely that large numbers of relatively asymptomatic will flock to ad hoc testing centers to fill out interminable paperwork. One of the characteristics of the evolved human immune system is that it 'works' against a variety of pathogens, and the evolution of effective response to one given type does not necessarily address, or even work positively, against others. Development of fever (hyperthermia) is well-established to work against certain microorganisms that only thrive in a limited temperature range; development of malignant hyperthermia may be a conserved response, or an uncontrolled response to stimuli that aren't resolved in simple feedback. But fever is not a response that is meaningful in viral infection; neither is much of the immune response observed in progressive ARDS. This is part of the reason why "waiting" until fever is observed is both wrong and shortsighted in determining when to start testing for COVID-19; many of those at risk are severely, perhaps even irrecoverably compromised before they even present. Basing a relaxation of SIP/SD on testing conducted only on the frankly symptomatic is almost a recipe for disaster down the line. (Meanwhile there is some evidence that by the time frank symptoms of immune modulation are present, SARS-CoV-2 transmissibility may already be reduced, while on the other hand the likelihood of earlier spread sometime in the preceding 5 days or so may have been high.) As noted earlier, one of the 'correct' approaches to restarting the economy is to continue SIP for the cohorts most at risk for ARDS, combined with reasonable and correct social distancing and transmission reduction in areas those cohorts may 'frequent'. This is going to be no fun at all for a large number of nursing homes and similar "assisted care" facilities that have traditionally run cheap and slipshod hospice-lite kinds of operations. Other social operations, involving mass gatherings or large groups, will have similar safeguards inherent in their 'new normal' operating models, for at least the duration of the initial 'opening' of the economy. Since treatment is such a lethal joke so much of the time, and so many effective therapies appear to be just like power production from contained nuclear fusion or thorium, effective prevention of those at greatest risk while permitting acquired immunity in those less at risk in a reasonably short time is the only real strategy that does not involve the risk of extensive, and publicized, outbreaks of suffering and death. Hopefully we learn for the next time.
Euclid It just seems like something is missing in this story.
The more testing the better. Look at nations that have an aggressive, coordinated national testing program and their death rates. Those are far better than our inadequate, incoherent program because of incompetent leadership from the WH which trusts fads and pals more than actual experts.
If this doctor is correct in his observations and conclusions, the implications could not be more profound. It means that all of the fatalities may have been actually caused by the incorrect treatment with ventilators.
It also means that none of the fatalities may have occurred had the proper treatment been administered.
It also means that the behavior of this virus effect is something that has never been seen before, and is thus unknown and unanticipated.
EuclidIt means that all of the fatalities may have been actually caused by the incorrect treatment with ventilators.
A child of 6 who read up on the actual mechanisms involved in ARDS would have understood this nearly immediately. People in the preservation industry posting on RyPN effectively pointed this out more than a month ago. The existing statistics richly illustrate the point -- when correctly framed and interpreted.
Meanwhile, to get a better appreciation for the true flavor of most of the various 'bridge' and homebuilt respirator "attempts", it pays to go to their various Web sites and look at the assumptions made in the designs, and some of the correspondence in their design processes. Very few of them aren't inherent death machines for anyone with ARDS ... to the point anyone with ARDS needed to be placed on a full intrusive ventilator in the first place.
But you're the one who keeps 'concluding' that there aren't any effective treatments for COVID-19 yet. What are your specific conclusions at present regarding how to keep people from progressing to ARDS and, once showing significant symptoms of it, from degrading into morbidity?
That is utter rubbish; the observance of specific cytokine storm was well documented as early as 2012, and effective palliative therapy for the condition (when specifically induced via interleukin-6) worked out by mid-2017. The condition itself, of course, was well known in the 1918-20 pandemic waves, even if its operative causes were little comprehended then. Specifically, the degenerative changes in lung tissue are, or ought to be, very well recognized (they were covered in a multiple-tape review series on pulmonary conditions as far back as the 1990s, so I can't expect they're unfamiliar even to pulmonologists who haven't been fully diligent in continuing education) as have the specific design of respirator equipment to work with various compromised lung tissue.
Where the controversy is in the 'behavior of the virus' is how SARS-CoV-2 specifically produces ARDS in patients at greater risk -- it does not appear identical to mechanisms in H1N1, for instance. Personally I think the 'cause' is triggering of some pathway signaled secondarily by ACE2 either when invaded or surface-degraded by viral binding and specialized subsequent infection ... but I have to wait for actual scientific work to be done, properly reviewed, and published to see. It was certainly 'unanticipated' that a novel virus that in effect targeted a major part of the RAAS would prove highly infectious, just as it was unanticipated before AIDS that a virus might selectively infect specific response cells in the immune system that proliferate upon "viral" infection effects. That does not extend to the part of COVID-19 that is a hyperimmune response to viral infection, specifically including treatment problems related principally to ARDS.
EXCELLENT CLARITY:
https://www.youtube.com/watch?v=Hx4sG2-Ma_Y
Ventilator = pressurizes lungs. Defeated by virus attacking red blood cells.
Hyperbaric Oxygen Therapy = pressurizes the air the patient breathes. Circumvents the effect of the virus attacking red blood cells.
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