Texas Aggie Doctor Reports — Clinical Pearls Covid 19 for ER practitioners

The following information is from a front line ER doctor using the handle of ‘nawlinsag’ on a Texas Aggie web site.  I’ve included the link below. I’ve also included the complete text of his post in full in hopes medical professionals and lay people could get the most benefit from his observations of the course of COVID-19 in a small front line Louisiana hospital.

Short form: This is not the flu.  It is a horror show of death and disablement that is crowding out all other medical care including an immediate downgrade of life saving cardiac care.  Only on in seven people put on ventalators in this hospital is surviving, and then only after 10-t0-12 days of ventalator support.



I just spent an hour typing a long post that erased when I went to change the title so I apologize to the grammar and spelling police. This one will not be proofread and much shorter.

I am an ER MD in New Orleans. Class of 98. Every one of my colleagues have now seen several hundred Covid 19 patients and this is what I think I know.

Clinical course is predictable.
2-11 days after exposure (day 5 on average) flu like symptoms start. Common are fever, headache, dry cough, myalgias(back pain), nausea without vomiting, abdominal discomfort with some diarrhea, loss of smell, anorexia, fatigue.

Day 5 of symptoms- increased SOB, and bilateral viral pneumonia from direct viral damage to lung parenchyma.

Day 10- Cytokine storm leading to acute ARDS and multiorgan failure. You can literally watch it happen in a matter of hours.

81% mild symptoms, 14% severe symptoms requiring hospitalization, 5% critical.

Patient presentation is varied. Patients are coming in hypoxic (even 75%) without dyspnea. I have seen Covid patients present with encephalopathy, renal failure from dehydration, DKA. I have seen the bilateral interstitial pneumonia on the xray of the asymptomatic shoulder dislocation or on the CT’s of the (respiratory) asymptomatic polytrauma patient. Essentially if they are in my ER, they have it. Seen three positive flu swabs in 2 weeks and all three had Covid 19 as well. Somehow this ***** has told all other disease processes to get out of town.

China reported 15% cardiac involvement. I have seen covid 19 patients present with myocarditis, pericarditis, new onset CHF and new onset atrial fibrillation. I still order a troponin, but no cardiologist will treat no matter what the number in a suspected Covid 19 patient. Even our non covid 19 STEMIs at all of our facilities are getting TPA in the ED and rescue PCI at 60 minutes only if TPA fails.

CXR- bilateral interstitial pneumonia (anecdotally starts most often in the RLL so bilateral on CXR is not required). The hypoxia does not correlate with the CXR findings. Their lungs do not sound bad. Keep your stethoscope in your pocket and evaluate with your eyes and pulse ox.

Labs- WBC low, Lymphocytes low, platelets lower then their normal, Procalcitonin normal in 95%
CRP and Ferritin elevated most often. CPK, D-Dimer, LDH, Alk Phos/AST/ALT commonly elevated.
Notice D-Dimer- I would be very careful about CT PE these patients for their hypoxia. The patients receiving IV contrast are going into renal failure and on the vent sooner.

Basically, if you have a bilateral pneumonia with normal to low WBC, lymphopenia, normal procalcitonin, elevated CRP and ferritin- you have covid-19 and do not need a nasal swab to tell you that.

A ratio of absolute neutrophil count to absolute lymphocyte count greater than 3.5 may be the highest predictor of poor outcome. the UK is automatically intubating these patients for expected outcomes regardless of their clinical presentation.

An elevated Interleukin-6 (IL6) is an indicator of their cytokine storm. If this is elevated watch these patients closely with both eyes.

Other factors that appear to be predictive of poor outcomes are thrombocytopenia and LFTs 5x upper limit of normal.

I had never discharged multifocal pneumonia before. Now I personally do it 12-15 times a shift. 2 weeks ago we were admitting anyone who needed supplemental oxygen. Now we are discharging with oxygen if the patient is comfortable and oxygenating above 92% on nasal cannula. We have contracted with a company that sends a paramedic to their home twice daily to check on them and record a pulse ox. We know many of these patients will bounce back but if it saves a bed for a day we have accomplished something. Obviously we are fearful some won’t make it back.

We are a small community hospital. Our 22 bed ICU and now a 4 bed Endoscopy suite are all Covid 19. All of these patients are intubated except one. 75% of our floor beds have been cohorted into covid 19 wards and are full. We are averaging 4 rescue intubations a day on the floor. We now have 9 vented patients in our ER transferred down from the floor after intubation.

Luckily we are part of a larger hospital group. Our main teaching hospital repurposed space to open 50 new Covid 19 ICU beds this past Sunday so these numbers are with significant decompression. Today those 50 beds are full. They are opening 30 more by Friday. But even with the “lockdown”, our AI models are expecting a 200-400% increase in covid 19 patients by 4/4/2020.


worldwide 86% of covid 19 patients that go on a vent die. Seattle reporting 70%. Our hospital has had 5 deaths and one patient who was extubated. Extubation happens on day 10 per the Chinese and day 11 per Seattle.

Plaquenil which has weak ACE2 blockade doesn’t appear to be a savior of any kind in our patient population. Theoretically, it may have some prophylactic properties but so far it is difficult to see the benefit to our hospitalized patients, but we are using it and the studies will tell. With Plaquenil’s potential QT prolongation and liver toxic effects (both particularly problematic in covid 19 patients), I am not longer selectively prescribing this medication as I stated on a previous post.

We are also using Azithromycin, but are intermittently running out of IV.

Do not give these patient’s standard sepsis fluid resuscitation. Be very judicious with the fluids as it hastens their respiratory decompensation. Outside the DKA and renal failure dehydration, leave them dry.

Proning vented patients significantly helps oxygenation. Even self proning the ones on nasal cannula helps.

Vent settings- Usual ARDS stuff, low volume, permissive hypercapnia, etc. Except for Peep of 5 will not do. Start at 14 and you may go up to 25 if needed.

Do not use Bipap- it does not work well and is a significant exposure risk with high levels of aerosolized virus to you and your staff. Even after a cough or sneeze this virus can aerosolize up to 3 hours.

The same goes for nebulizer treatments. Use MDI. you can give 8-10 puffs at one time of an albuterol MDI. Use only if wheezing which isn’t often with covid 19. If you have to give a nebulizer must be in a negative pressure room; and if you can, instruct the patient on how to start it after you leave the room.

Do not use steroids, it makes this worse. Push out to your urgent cares to stop their usual practice of steroid shots for their URI/bronchitis.

We are currently out of Versed, Fentanyl, and intermittently Propofol. Get the dosing of Precedex and Nimbex back in your heads.

One of my colleagues who is a 31 yo old female who graduated residency last may with no health problems and normal BMI is out with the symptoms and an SaO2 of 92%. She will be the first of many.

I PPE best I have. I do wear a MaxAir PAPR the entire shift. I do not take it off to eat or drink during the shift. I undress in the garage and go straight to the shower. My wife and kids fled to her parents outside Hattiesburg. The stress and exposure at work coupled with the isolation at home is trying. But everyone is going through something right now. Everyone is scared; patients and employees. But we are the leaders of that emergency room. Be nice to your nurses and staff. Show by example how to tackle this crisis head on. Good luck to us all.

50 thoughts on “Texas Aggie Doctor Reports — Clinical Pearls Covid 19 for ER practitioners”

  1. What they are seeing is ARDS cases that are advanced on admission. No remdesivir available, it sounds. Hydroxychloroquine is not helping at this advanced stage. Cytokine storm should be rare. Maybe they are getting a cluster of L type virus.

  2. I can see why the public is being kept in the dark about the specifics. I’m not a doctor but even I can read this as being a global disaster on a scale we have never experienced in our lifetimes, and I’m including WW2.

    In a month there won’t be a need to declare official shutdowns, people will be too frightened to leave their houses.

  3. Here is an example that sounds like those cases in the post above.

    54 your old diabetic woman worked in a pediatric clinic.

    Her illness kept getting worse over a few days. She tested negative for the flu and then eventually found out she had pneumonia. A lung X-ray prompted her doctor to order a COVID-19 test.

    Three days later, her test result came back positive. And within minutes of arriving at the hospital, the 54-year-old woman became Tucson’s first known coronavirus-related fatality.

    Testing was slow and she was not treated with hydroxychloroquine.

    When she started to develop a fever on March 15, Anderson immediately made an appointment with her doctor. Her family said she wasn’t experiencing any cough or shortness of breath at this point.

    On March 19, her doctor ran the flu and strep tests that came back negative, and did a chest X-ray. The next day, the radiology report showed that Anderson had pneumonia. Her doctor was concerned that the infection patterns on her lungs were consistent with coronavirus.

    She was tested for COVID-19 on Friday, March 20.

    “She thought it was pneumonia and she just complained of back pain,” said her sister Melanie Meza.

    On Monday morning, Anderson received a call from her doctor saying that her coronavirus test was positive and that she should go to the emergency room right away. By now, she was having more trouble breathing.

    She died before she was treated at the hospital. Testing with fast results or treatment while waiting.

  4. Taking the numbers cited, that works out to a mortality rate of 0.0071 among people exhibiting symptoms (1 out of 7 of those requiring critical care). Based on the Diamond Princess experience (“experiment”?) (8% of passengers and crew exhibiting symptoms, 100% assumed exposed based on the timeline), that works out to a mortality rate of 0.0006 for the general population. Or, potentially, 198,000 in the United States.

  5. I pose one question. There has been a lot of talk of the treatment value of Chloroquin and its associated meds. There has been at least one post in Doximity with comments by other medical persons suggesting this medication is more a PREVENTIVE than a treatment. Both of the two comments I recall reading were people with RA (Rheumatoid Arthritis) patients on this group of drugs and realized that during the 5 years (in one case at least) they had NOT had, colds, flu and other viral inflammatory problems. Perhaps someone ought to consider using this series of medications as a prophylaxis not a treatment. I am well aware a “series of two” is not valid but this class of drugs was, early on, used prophylacticaly against Malaria, I believe.

  6. I love the smell of panic in the morning.

    Trent’s ER doctor certainly uses some of the right terms, so let’s assume he (she?) is genuine. According to the CDC, up to 810,000 hospitalizations for influenza happen every year. If we generously assume the flu season is 200 days long, that is an average of up to 4,000 new admissions every day, with a peak obviously much higher than that. And yet the hospitals cope, and the flu season usually passes with no more than a snippet at the end of the local news, after the latest cute cat video.

    Show me the bodies!

    What would be truly informative would be to see the daily reported total “All Causes” deaths for the last year for the US, or for a State, or even for a major city. Are we seeing total daily deaths rising significantly because of this virus? But that data is very hard to find. What we do know is that typically about 7,800 people die every day in the US from All Causes. Daily deaths from this Panic Virus are tiny in comparison — especially when we remember that many of the virus deaths would have occurred anyway to the old sick patients.

    As someone pointed out — there is a difference between dying with the virus and dying from the virus.

    In the meantime, the economic impact of the over-reaction to the virus are devastating to a very much larger number of healthy people.

  7. “What would be truly informative would be to see the daily reported total “All Causes” deaths for the last year for the US, or for a State, or even for a major city. Are we seeing total daily deaths rising significantly because of this virus?”

    You are an unserious person, and have been for two months now.

    From my link:
    “[H]ere is the most important data point: in Bergamo, people are dying at 14 times the rate of a normal year. In the 8th-16th of March period, 330 deaths in 2020 vs 23 in the same period in 2019.
    The essay contains other data points regarding the cities I managed to find the data online: in total, 6 towns in Northern Italy registered a total of 613 deaths over the last ~3 weeks compared to 73 over the same period last year: 8.4 times as much!”

  8. I’ve mostly stopped reading any of the medical “data” available. I’m as far as I can be from a position where what I think matters to anyone. I can remember reading just before this got hot about a young child with the flu that suddenly died after exhibiting mild symptoms for a few hours and have avoided many similar. I’m not saying this is just the flu, but the plural of anecdote isn’t data.

    There are too many contradictory reports to make sense of or to give weight to one over another. There are the cruise ship numbers which seem to be in sharp contrast to the numbers from Italy. The numbers from China are worse than useless. And then there are no end of “experts” that have found the surest way onto the front page is some dire pronouncement. What none of them do is change what I should do. If it turns out to be a blip, fine. If it’s the end of the world, well, we’re all along for the ride, like it or not.

    I’ll do my best to avoid getting this, at least partly to avoid giving it to anyone else or consuming resources that could go to someone else, but mostly to stay alive a little longer and avoid pain. I’d really like to avoid being one of the “lucky” ones that survives a long stint on a ventilator but I’d rather survive than not.

    The information above would be useful if I was a doctor trying to treat this, assuming it’s true. Don’t see how I can use it.

    Glad to see Trent is back.

  9. What the ER doc above is seeing might be a different strain of the virus, the L type.

    As for chloroquine, I agree that it is preventative but there are also small series showing good response when taken early. The Tucson case I linked to shows the consequences of delay, especially in testing and getting results. That woman might be alive if she was put on hydroxychloroquine while waiting for test results,.

  10. “If you can keep your head when all about you
    Are losing theirs … You’ll be a Man, my son”

    Here is a very interesting item which seems to have been given little attention in the panic-stricken media. Read the whole thing:

    Short version — the English academic wallah whose model study had so panicked our Anglophile bureaucrats and a media seeking for a stick with which to beat the President has now backtracked. He originally predicted that 550,000 people would die in the UK from the Panic Virus; his revised prediction is down to 20,000 — or possibly a lot less.

    In the meantime, people have lost their jobs, businesses are going bust. Taking the virus seriously should not involve economic suicide.

  11. National differences in defining what is a CV19 “death” are such that we should rely only on American statistics at this point. We have a sufficient CV19 database at this point to do that. Some nations define a CV19 death as EXCLUDING comorbidities (diabetes, heart disease) which might have contributed to the death, and instead always attribute it to the cormorbidity without doing an autopsy to confirm the cause of death.

    Probably all or almost all hospitals in the US attribute the death of a CV19 victim to CV19 even if the victim had several comorbidities, because the latter hadn’t killed the victim yet.

    I’ve ignored foreign statistics on the lethality rate of CV19 for more than a week based on this definitional difference.

  12. >>I thought Trent had been banned. Welcome back.

    I’ve been taking care of the homestead and putting a lot of Coronavirus bandwidth into e-mails and social media with friends and family.

    I only mirror here with materials that I am sure will get the Silicon Valley techlord “Get Smart” cone of silence.

  13. The first comment that popped up after reading the article is Mike K who makes the statement “hydroxychloroquine isn’t effective at this stage.” But the original post never mentioned it Mike’s conclusion is without justification.

    After listing a smorgasbord of symptoms, the OP notes that all of these people have WuFlu and asserts “Essentially if they are in my ER, they have it.”

    Could be true. But when they are reporting someone with a cracked skull died, and for some inexplicable reason, was tested for WuFlu, turned up positive, he is reported as a WuFLu death. Seems to me that everything is being attributed to the WuFlu. Ok, we have a half million cases with 22k dead. Even if you take the numbers at face value, nobody has presented any numbers that say these cases and deaths are in excess of a normal flu season. The numbers are quite small compared to the ordinary flu. The idea that there is this massive swamping of the health care system doesn’t seem to comport with that data. Of course, you never actually hear any official numbers on overall seasonal mortality which would shed some light on this.

  14. “Probably all or almost all hospitals in the US attribute the death of a CV19 victim to CV19 even if the victim had several comorbidities, because the latter hadn’t killed the victim yet”

    If that’s the standard we are going to use, then the flu kills approximately zero people.

    We’ve known for weeks now that lots of people are dying without being tested. It’s not a secret.

    If someone with diabetes gets coronavirus and then develops pneumonia and dies, I think it’s fair to say they died of coronavirus.

  15. “But when they are reporting someone with a cracked skull died, and for some inexplicable reason, was tested for WuFlu, turned up positive, he is reported as a WuFLu death”
    That’s absurd. Show one case where that happened.

  16. Almost all CV-19 fatalities are caused either by pneumonia (the vast majority) or multiple organ failure (far behind in second place).

  17. The first comment that popped up after reading the article is Mike K who makes the statement “hydroxychloroquine isn’t effective at this stage.” But the original post never mentioned it Mike’s conclusion is without justification.

    I am reading many sources and am coming to the conclusion that they may be correct about the failure of the chloroquine drugs when they are given at late stages.

    You are welcome to draw your own conclusions but I would ask your back ground and qualifications beside being “skeptical.”

    Lots of recent info to process.

    Tell us your experience. I’m all ears.

  18. As for my comment being about something ‘the original post never mentioned it ”

    Plaquenil which has weak ACE2 blockade doesn’t appear to be a savior of any kind in our patient population. Theoretically, it may have some prophylactic properties but so far it is difficult to see the benefit to our hospitalized patients, but we are using it and the studies will tell.

    I’m sure you must know that “Plaquenil” is hydroxychloroquine. Right ?

  19. Trent, lf you look at the least entry in that thread, you will see the recommendations for hydroxychloroquine.

    My son is a paramedic and is diabetic so I got him a supply to use if he is exposed. So far he has not been.

    He has three teenagers and they have enough so that all can go to prophylaxis if any have early symptoms.

    From that thread, it sounds like it should be begun early to be effective,.

  20. >>If someone with diabetes gets coronavirus and then develops pneumonia and dies, I think it’s fair to say they died of coronavirus.

    Germany’s low death rate from COVID-19 is primarily due to the fact their medical system is attributing most COVID-19 fatalities to the various co-morbidities of the infected.

    Additionally, a lot of nations are not testing for, so are not counting, whether “Death by Pneumonia by unknown causes” are in fact COVID-19 fatalities as China, Germany and now it looks like Italy are doing.

    The USA is not without guilt in ‘morbidity shifting’ in this regard as I’ve heard from various people talking to several different American doctors saying that they’re admitting patients as “community-acquired pneumonia” in order to avoid public outcry and freak-out for the last couple of months. Which means they’re not being counted as COVID-19 cases or deaths either.

    Over all, I think Tom Holsinger is correct regards only counting on US morbidity & mortality data.

    Just remember in a pandemic, US public health data is not going to be ‘high fidelity’ for a whole lot of reasons.

  21. Pandemic! That means lots of people are going to be dying — lots more than normal.

    The estimable blogger Hector Drummond has tracked down an official source of data for weekly deaths registered in England & Wales.

    From Jan 1 through 13 March, a total of 128,271 people had died in England & Wales from all causes. Here is a comparison of that total with the totals at the same point in the preceding 5 years:
    2019 – 2,522 fewer deaths than in 2020
    2018 – 14,500 more deaths than in 2020
    2017 – 5,136 more deaths than in 2020
    2016 – 3,750 fewer deaths than in 2020
    2015 – 11,139 more deaths than in 2020

    Through mid-March, total English deaths were unexceptional, within the range seen in prior years. It will be useful to follow this data source.

  22. Trent, I’m glad to hear your anecdote regarding morbidity shifting. The wildly different reports coming from nations that share common genetics and levels of wealth make no sense at all and I had attributed it to something along those lines. It seems to me then that the most accurate estimates are going to be on the high end of the fatality rates as everything COVID related is recorded in those figures.

    Hiding causes of death off the books during a pandemic seems grossly irresponsible as it prevents people and governments from making data based decisions.

  23. International comparisons of many kinds of statistics are fraught with traps for naive observers. Look at crime stats, literacy stats, income and standard-of-living stats, health-outcomes stats, etc. Why would epidemiological data be any different?

  24. I have been on anti-malarial (preventive) drugs twice–1998 for several months in Costa Rica and 2007 -2009in the Dominican Rep. I can’t recall now what drug it was. I wonder if chloroquine was the standard preventive med. then?

  25. John, quinine in some form has been sused as preventative for malaria for at least 150 years. Here is the Wikipedia entry for development of the Gin and Tonic.

    “The cocktail was introduced by the army of the British East India Company in India. In India and other tropical regions, malaria was a persistent problem. In the 1700s Scottish doctor George Cleghorn studied how quinine, a traditional cure for malaria,[14] could be used to prevent the disease.[15] The quinine was drunk in tonic water, however the bitter taste was unpleasant.[15] British officers in India in the early 19th century took to adding a mixture of water, sugar, lime and gin to the quinine in order to make the drink more palatable, thus gin and tonic was born.[16] Soldiers in India were already given a gin ration, and the sweet concoction made sense.[17] Since it is no longer used as an antimalarial, tonic water today contains much less quinine, is usually sweetened, and is consequently much less bitter.[18]”

  26. I find it difficult to imagine why Putin would go around in a hazmat suit, and shut down Moscow, if Russia didn’t think the coronavirus was kind of a big deal. Ditto for Modi ordering everyone in India to remain at home for 3 weeks. Are they supposedly caught up in a groundless hysteria?

    When all this is over, no matter when that happens, or how awful or mild what happens next will be, the consensus for deaths will soar because flu-like models will be applied to estimate the deaths attributable to the virus. The apples to oranges comparison with flu have been a massive obstacle to a rapid response because confirmed positive tests vs. statistical population models is guaranteed to downplay the danger.

  27. I wonder if chloroquine was the standard preventive med. then?

    It is in all malaria zones except those with chloroquine resistant strains, often in the south Pacific islands. I was signed up for a military history trip to Guadalcanal about 15 years ago. We were warned that it was a chloroquine resistant malaria zone. The trip was eventually cancelled because of some local revolution in the area.

    I was all ready to to go as one guide was to be Mitchell Paige.

  28. We’ve already seen that Putin is into costumes. He might be trying to get people’s attention and convince them to take precautions as he should.

    India is an ongoing health disaster and really doesn’t need any more. When the U.S has about 20,000 more deaths from Wuhan Virus, we’ll approach the number of Indians that die every year from rabies.

    Given that any discussion of the flu should include the 1918-19 epidemic, the comparison is entirely appropriate. At worst, it’s the difference between Red Delicious and Granny Smith, it’s all down to magnitude.

  29. MCS: No, the “just the flu” folks claim (still!), that coronavirus is similar to, or even much milder(!!!), than the seasonal flu, not Spanish flu. If they allowed for Spanish flu death numbers, they’d actually take it seriously, which they don’t.

    Another frustrating aspect of JTF folks is they completely downplay any serious risk from coronavirus while claiming people are running around panicking about some Black Death level event, when no one has ever done anything of the sort. People have been warning that we need to prepare in order to prevent Spanish flu level impacts, and have faced nothing but ridicule and contempt from the JTF side.

  30. Lots of “just the flu” folks out there and they tend to be very noisy. Meanwhile I watch the remorseless exponential growth in the number of cases watching for signs of a slowdown. I don’t really expect to see much change for another week or so, and the increased testing complicates the issue, but there is always hope.

  31. The US seems to be clinging fairly well to a doubling period of 2.9 days. If the isolation measures do not bite into that rate soon things will go completely out of control within 2-3 weeks.

  32. Any estimate of the rate is confounded by increasing testing. You can’t say that it doubled in 3 days because you don’t have any idea how many were actually infected 3 days ago. There are ways of estimating it but they are all very sensitive to initial assumptions. In other words, an educated guess.

    We know that the number of people that have tested positive are not anywhere near the number of people that actually have it. Then as the number of test increase, false positives will start to assert themselves unless the infection rate is pretty high. A 1% false positive rate is 10,000 per million and most tests are a lot closer to 95% or less.

  33. @MCS,

    The modelers model death rates and hospitalizations, not the actual number of infections. That lessens the testing problems and models things that will directly influence public policy.

  34. With no end to models and assumptions and estimates that will be fought over in journals from now until they run out of pixels.

    I was specifically talking about the idea that you could take the numbers reported in media, draw a line thorough the points and reach any kind of valid conclusion.

  35. Straight up info: Hydroxychloroquine and chloroquine work by allowing zinc into cells. Normally its blocked by the cell wall. Zinc shuts down viral replication. That’s really enough clues, but I’ll spell it out. You need to, as the Chinese have done start this treatment right away, waiting makes the treatment much less effective.

  36. The guys over at PowerLine are citing a very positive study of 80 patients on the hydroxychloroquinine/Azithromycin “protocol.”


    BTW, I’ve been taking Zinc-Magnesium-Aspartate (ZMA) with the intent to flood my system with zinc. That’s supposed to support natural steroid conversion enzymes but maybe the extra zinc will help against viruses too.

    BTW Gavin; “the English academic wallah” is the long way of saying “boffin.”

  37. Please STOP this foolishness about zinc & chloroquine! This stuff keeps being posted, and this is simply not the case. Now, if you are REALLY interested in looking for a natural element, a trace element that may be beneficial in this illness: learn about Selenium.

    You do not HAVE CELL WALLS! No, actually you did give us a clue. Only plants have cell walls, you must be a vegetable. But which one? And while zinc is a trace element that is important, and it does benefit some respiratory viruses (I was a strong advocate for Zicam, found it beneficial as did patients of mine), but you (and whoever keeps posting this over at ZH … I assume you are the same person) ought to consider learning physiology, biochemistry, and pathophysiology before spouting something you likely read on some OTHER website.

    There simply is too much we don’t know about this bug. I have been digging into a great many resources for two months, and am still astounded at the differences that are exhibited. From a nothing-burger to many infected, to total devastation to others who were totally healthy without significant health problems before. I still wrestle a lot with is isolation/distancing vs. economic harm. There is NO EASY SOLUTION, and politics is not longer about true LEADERSHIP but about acquisition of wealth, power, and status. While I was glad to see Trump in the WH (rather than the Hildabeast) he needs to absolutely SHUT HIS MOUTH after he pulls his foot out of it. He can beat Biden without campaigning IF he doesn’t keep saying STUPID STUFF about this illness.

    We are all going to suffer from this in various ways. No matter what approach is tried, as we don’t have a crystal ball, picking up the pieces afterwards is going to be a huge effort. Consider learning how to be a bit more gentle, peaceable, and teachable. There will be more than enough finger pointing to go around, and it won’t solve anything. It will simply turn into an extended blame game rather than truly getting things operating again.

    Consider carefully, this is going to be a long, dark journey. No magical uniform farts are going to be blasted into the air to remove this disease.

  38. I couldn’t read all the comments, in ways as part of self-preservation. But enjoyed the insight from the original post, except that we have markedly reduced the PEEP, actually – may have been why we were having such a high mortality once intubated. Not sure – though we have also been reducing intubations as a general rule and proning early, often, etc.

  39. It is a curious aspect of the 20th/21st century to repose great therapeutic/prophylactic (or conversely, malignant) powers in dietary items, typically with equivocal or no evidence apart from testimonials of dubious merit.

    For my part, I’m advocating as the ultimate cure for what ails you: sticking a yam up your butt. It’s one of those things THEY don’t want you to know about, but I knew this guy who used to be really sick all the time, and then one day he got a yam …

  40. This stuff keeps being posted, and this is simply not the case.

    Are you also complaining about the hydroxychloroquine ? I have had doubts about Zinc. I just want to figure out where you are coming from.

    Here is a modest size series with remdesivir, that shows reasonably good response in serious cases (Half on ventilators ).

    There is no time to wait for randomized trials.

    While I was glad to see Trump in the WH (rather than the Hildabeast) he needs to absolutely SHUT HIS MOUTH after he pulls his foot out of it.

    Examples ? Should he not have the briefings? Are they too long ? I might agree there. Should he not be talking about reopening the economy ?

    Your comment has a tone of TDS or NT about it. I’m just asking for clarification.

    We’ve had a troll here talking about needing a million hospital beds.

  41. Are you also complaining about the hydroxychloroquine ? I have had doubts about zinc.

    As a chemist, I am extremely skeptical about the putative relationship of hydroxychloroquine and zinc(II). The former exhibits zero structural characteristics of a chelator of the latter. Besides that, chelation would involve presumably involve more than one molecule of hydroxychloroquine. What’s the concentration of hydroxychloroquine at the therapeutic dose? Maybe … micromolar? Let’s see, 10^-6 squared is … zip; 10^-6 cubed is less than zip. Intracellular concentration of zinc(II)? No idea, but let’s say, 1 mM, which is doubtless a gross over-estimation. That imputes a stability constant of 10^9 (bis(chelate)) or 10^-12 (tris(chelate)) for 50% chelation of zinc(II) under these conditions. Evidence for this?

    Some other mechanism than chelation, perhaps? OK. Lay it on me. I remain to be persuaded. Seriously. Not to say that there isn’t another mechanism – there could be – but chelation? Uh … no. I don’t think so.

    But here’s a perhaps more trenchant question: why motivated anyone initially to combine hydroxchloroquine with a zinc(II) salt? Was there some defensible rationale, or were they simply throwing random crap at the wall to see what would stick?

    Not to say, again, that the combination might not be efficacious – maybe it is, and until contrary evidence arises, sure, let’s try it, since desperate times and all that – but then, by the same token, wearing an onion on your belt might be efficacious too. In each case the question eventually has to come down to: evidence?

  42. That imputes a stability constant of 10^9 (bis(chelate)) or 10^-12 (tris(chelate)) for 50% chelation of zinc(II) under these conditions.

    Sorry, on reading my comment I realized I’d recast the original sentence and had failed to update it accordingly.

    Should read: “10^15 (bis(chelate)) or 10^21 (tris(chelate)).

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