COVID Medical questions Q & A.

[Snaggy]

<apologies for the morbid question>

how does the assignment of cause of death work, in particular when covid-19 and co- or pre-existing conditions come into play?

clarification: are there multiple causes of death assigned?

thanks

Death Certificates are often done with surprisingly little deliberation by doctors, within pretty loose guidelines. A coroner can refuse to accept the document and ask for a revision, Doesn't happen that often.

The format is

- main cause of death and how long present
- due to, and how long present
- due to, and how long present
-Other conditions contributing to above.
-Any Surgeries performed for above and when



So for COVID, the doctor might put as primary cause
-either pneumonia or respiratory failure, present for days
-due to Novel Coronavirus, present weeks
Other conditions, Diabetes Mellitus Type 2, COPD or whatever else

Or maybe Coronavirus would be listed first
Or, maybe it would be
-Respiratory failure, due to ARDS, due to COVID
There could be a fair number of more or less correct ways.

It's important for Coronavirus to be in those top three for epidemiologic purposes.


What happens if the doctor thinks a fatal pneumonia could have been caused by Coronavirus but didn't get a test?

He should put the pneumonia as "due to Coronavirus", but not every Doc would, depending on the level of their suspicions, and that certificate would probably not be challenged either way.



CDC believes this is happening, because the deaths in the "Pneumonia and Influenza" category, not attributed to Coronavirus, is about 1-2% higher than expected.

Death Certificates can be disturbingly imprecise or even inaccurate because many thousands of doctors and coroners have their own ideas on how they should be done.

 

[Snaggy]

So, how long can the viruses live in the donated blood? In other words, is there a length of time when you would feel that our donated blood supply is safe?

I don't think there is that much known yet, but apparently viral RNA is found in blood early in the infection. This reference doesn't really provide much information. Blood is refrigerated, plasma is even frozen.

https://www.sciencedirect.com/science/article/pii/S0887796320300146

I don't think our blood supply will be COMPLETELY safe from COVID for the foreseeable future as no commercial PCR assay for COVID in bloodbanks is available.

 

[wannabe]

I don't think there is that much known yet, but apparently viral RNA is found in blood early in the infection. This reference doesn't really provide much information. Blood is refrigerated, plasma is even frozen.

https://www.sciencedirect.com/science/article/pii/S0887796320300146

I don't think our blood supply will be COMPLETELY safe from COVID for the foreseeable future as no commercial PCR assay for COVID in bloodbanks is available.

Thanks for the article. It was really interesting. Sadly, it really just confirmed what you said about our bloodbank inventory not being safe any time soon.

 

[Beanzy]

Have certain blood types been more representative among Covid-19 victims and survivors?

 

[bojangle]

What do you think about these breathing techniques for covid patients? Any merit to them?

https://www.reddit.com/r/awesome/comments/fu9hfo/doctor_from_queens_hospital_gives_breathing/

 

[Snaggy]

Have certain blood types been more representative among Covid-19 victims and survivors?

https://www.webmd.com/lung/news/20200320/blood-type-may-affect-covid19-risk-study

I would call this an unproven assertion, but Type A has been suggested

 

[Snaggy]

What do you think about these breathing techniques for covid patients? Any merit to them?

https://www.reddit.com/r/awesome/comments/fu9hfo/doctor_from_queens_hospital_gives_breathing/

Looks like something we'd say to prevent atelectasis, maybe even like incentive spirometry, the thing where you inhale and try to float the ball that you get in the hospital after surgery.

COVID doesn't give you a lobar pneumonia or segmental atelectasis though. OTOH, strategies to ventilate these patients with ARDS include low levels of PEEP and low tidal volumes to keep the alveoli inflated but not to hyperinflate the lungs and damage the alveoli further. Preferentially, they're ventilated prone to minimize fluid in the lung bases.

I'd say minimally helpful at best.

This is what we do when we can't do much. Hand people straws to give hope and a sense of control over their destiny.

 

[Snaggy]

https://dgalerts.docguide.com/sars-cov-2-detected-blood-donations-kidney-disease-linked-hospital-death-patients-covis-19-and?nl_ref=newsletter&pk_campaign=newsletter&nl_eventid=36283&nl_campaignid=3720&pw_siteID=25&ncov_site=covid-19

-COVID RNA found in 4 out of 2500 blood bank products in Wuhan. One sample positive at the "very limit of detection".

-Kidney Failure emerging as a dire complication in hospitalized patients.

-The REALLY bad news?

In Italy, FIVE WEEKS after ICU admission, 58% of patients were still intubated, 16% were discharged, and 26% died.

That's terrible for so many reasons

 

[Snaggy]

American Thoracic Society gives some recommendations.

They endorsed Hydroxychloroquine, while acknowledging that there is little evidence that it works. That's what everybody is saying. See comment above about straws and hope.

 

[wannabe]

American Thoracic Society gives some recommendations.

They endorsed Hydroxychloroquine, while acknowledging that there is little evidence that it works. That's what everybody is saying. See comment above about straws and hope.

Did you get a chance to listen to the latest TWIV podcast? The physician from New York mentioned that he was seeing some benefits with starting with steroids prior to using Plaquenil.

Edit: he mentioned that he has been way too busy to publish his findings.

I feel bad for the people with lupus who are now having a tough time getting the drug.

 

[Snaggy]

A few care reports I've read also included steroid use. Based on the results in Influenza pneumonia(ineffective) and other causes of ARDS, I dunno, but the Hail Mary still wins games I guess.

I think you'd need a LOT of patients to prove anything, more than any single hospital has so far. Plus controls, protocols, but lets hope.

Government is getting all the plaguenil it can. Taking it away from SLE patients isn't good and might cause some to suffer. If it actually works, good trade off, but...

 

[wannabe]

Next question. Since testing is still pretty hard to get, assuming that you are experiencing the symptoms and are forced to just suck it up and recover at home, how long should you assume that you are going to be contagious? In other words, once the symptoms pass, how long should you continue to self-quarantine?

 

[Snaggy]

Next question. Since testing is still pretty hard to get, assuming that you are experiencing the symptoms and are forced to just suck it up and recover at home, how long should you assume that you are going to be contagious? In other words, once the symptoms pass, how long should you continue to self-quarantine?

The question that hasn't been answered yet is how much functional infectious virus are people shedding later in the disease. The test looks for RNA.

This is current CDC rec on when to stop isolation on people staying home with the illness. These patients aren't likely to get the 2 negative tests that hospitalized patients are getting, or antibody tests either.

https://www.cdc.gov/coronavirus/2019-ncov/hcp/disposition-in-home-patients.html

 

[Beanzy]

What is causing the high morbidity rate among blacks? Pre-existing conditions? Higher incidence of Blood Type A? Arrival in the hospital too ill and too late?

 

[Snaggy]

What is causing the high morbidity rate among blacks? Pre-existing conditions? Higher incidence of Blood Type A? Arrival in the hospital too ill and too late?

African Americans have more Hypertension, tobacco abuse, obesity, diabetes and heart disease, all true, and all risk factors for worse COVID outcomes. They're also pretty common in all Americans, especially older ones.

Might be much more interesting though.

Couple of things, the SARS-2 Coronavirus caused an epidemic in 2002 and is similar to COVID 19 in it's cellular target site, the ACE2 receptor, and a fair amount of ACE2/SARS research has appeared since then. Right now, a flurry of half-baked medical reports and articles are reigniting interest in Coronaviruses and ACE2 tropism, some pearls, some not.

ACE2 receptors are part of a complex hormonal system, called RAS or RAAS, that regulates blood pressure, renal and cardiac function, potassium and sodium balance, inflammation, lipid metabolism and other things and are found in lung, kidney, heart and the cells lining the vascular system.

There is genetic and racial variation in RAAS function. African Americans have significantly worse response to blood pressure meds that target the RAAS. Certain ACE2 receptor genetic variants have ethnic distributions. Other medical conditions are also related to RAAS and ACE2 receptors in the lungs. Some people that survived SARS-2 eighteen years ago have shown persistent abnormalities in RAAS related physiology.

There are few experts, little consensus, a very low signal to noise ratio, few good studies and a great deal of work to be done on this and COVID in general.

 

[Beanzy]

Do you find this poster accurate, Snaggy?

Found it on Claycord.

 

[Snaggy]

Do you find this poster accurate, Snaggy?

Found it on Claycord.

I don't see Primary Influenza Pneumonia that often, and it's usually a kid if I do. The cough with Influenza is almost always upper respiratory and bronchitis. With Influenza, I don't see people that are short of breath, just the kind of rapid breathing you see in people if they have a high fever. Flu people cough during the deep breath part of the exam, they have bronchial obstruction which generally doesn't make you hypoxic unless it gets very bad. Flu will give you a 102 or 103 temp pretty often. They usually wheeze at some point in the illness. Flu people look like they FEEL sick. They have miserable facial expressions. They don't look you in the eye, don't want to talk. Their body is fighting.

The four people I've seen in their cars that were pretty sick with COVID looked different. A couple were diaphoretic and they were truly laboring for air, but they were willing to talk. If I use my stethoscope, I have them lean over the steering wheel and I try to put my head on top of the car roof. I'm tall. The first two had wet rales. Their forced expirations weren't prolonged and it didn't make them cough and they moved air pretty normally. It's not a bronchial problem, it's alveolar, in the air sacs. If their O2 sats are down under 95%, I just send them to ER. They haven't had high fevers either, 101'ish. COVID patients, including the pictures I've seen, make eye eye contact, but they have this sort of anxious expression you see in ICU's. They don't look like they FEEL sick, more confused looking.

So yeah, to me I don't consider most flu patients short of breath, they are exchanging O2 and CO2 fine, just have bronchitis.

Cold patients will often have a watery, dripping runny nose at first. Flu doesn't. The cough in cold people is upper respiratory, with clearing of the throat and post nasal drip.

 

[wannabe]

Sorry, I have more questions. It's specific to the latest TWIV podcast episode. Unfortunately, Dr. SLO's thread is closed to questions, so I thought I would ask them here. I don't know if I heard it correctly, but I just wanted to confirm.

In the podcast, the doc from New York mentioned that he noticed that the patients that he puts on a ventilator have a 50% mortality rate, so they reduced the oxygen saturation rules for putting people on a ventilator down to 80% or less.

The part that had me confused was when he mentioned that they were treating for Acute Respiratory Distress Syndrome, but the patients reactions were more aligned to High Altitude Pulmonary Edema. Can you please explain the difference in how the two are treated? My google-fu wasn't strong enough to figure this one out.

 

[Snaggy]

The part that had me confused was when he mentioned that they were treating for Acute Respiratory Distress Syndrome, but the patients reactions were more aligned to High Altitude Pulmonary Edema. Can you please explain the difference in how the two are treated? My google-fu wasn't strong enough to figure this one out.

High Altitude Pulmonary Edema = HAPE

Wow, pulmonary physiology is incredibly complex, I'm not even sure if I understand this part of it enough to explain it but here goes.

Alveoli are small sacs in the lung which fill with air when you breath. Only a thin membrane separates the gas in the alveoli from the blood flowing through the capillaries. Across this membrane, gases cross, oxygen entering the blood, CO2 exiting. If the membrane is damaged, fluid will leave the bloodstream and enter the alveoli. That is what characterizes ARDS, gives the Ground Glass X-ray, and it interferes with gas exchange, leading to hypoxia.

ARDS is a syndrome, it isn't a single disease, any process injuring the alveolar membrane will allow fluid to leak out of the bloodstream and flood the air sacs/alveoli. The body appears to respond to the injury with inflammation, which will damage the membrane even more. HAPE causes ARDS, COVID causes ARDS.

Ventilators don't treat the ARDS, they only provide oxygen to keep the patient alive while you hope something else you're doing has the patient improve.

In HAPE, low oxygen in the air above 8000 feet causes constriction of the pulmonary blood vessels, increasing the pulmonary blood pressure. High pressure on the capillaries damages them and initiates the efflux of capillary fluid into the alveoli that can lead to ARDS. Drugs that dilate the pulmonary vessels reduces the pressure and reduces the edema in HAPE.

ACE2 IS A PULMONARY VASODILATOR.

What the pulmonologists are saying is that the mechanism of pulmonary edema in COVID seems to be related to Pulmonary Hypertension/vessel constriction, in the same way that HAPE causes pulmonary edema. The cause of the pulmonary hypertension is different, but the result is the same, and maybe COVID pulmonary edema will respond to the same cheap blood pressure meds as HAPE.

We know COVID binds, enters and kills cells that express ACE2 receptors. ACE2 functions to regulate our circulatory system. The virus could hardly pick a more complex and vital target.

https://www.cureus.com/articles/29004-acetazolamide-nifedipine-and-phosphodiesterase-inhibitors-rationale-for-their-utilization-as-adjunctive-countermeasures-in-the-treatment-of-coronavirus-disease-2019-covid-19

https://journals.lww.com/shockjournal/Fulltext/2016/09000/Pulmonary_Angiotensin_Converting_Enzyme_2__ACE2_.3.aspx


I want to reread that second link a couple hundred times, maybe it will make sense to me then.
.

 

[wannabe]

High Altitude Pulmonary Edema = HAPE

Wow, pulmonary physiology is incredibly complex, I'm not even sure if I understand this part of it enough to explain it but here goes.

Alveoli are small sacs in the lung which fill with air when you breath. Only a thin membrane separates the gas in the alveoli from the blood flowing through the capillaries. Across this membrane, gases cross, oxygen entering the blood, CO2 exiting. If the membrane is damaged, fluid will leave the bloodstream and enter the alveoli. That is what characterizes ARDS, gives the Ground Glass X-ray, and it interferes with gas exchange, leading to hypoxia.

ARDS is a syndrome, it isn't a single disease, any process injuring the alveolar membrane will allow fluid to leak out of the bloodstream and flood the air sacs/alveoli. The body appears to respond to the injury with inflammation, which will damage the membrane even more. HAPE causes ARDS, COVID causes ARDS.

Ventilators don't treat the ARDS, they only provide oxygen to keep the patient alive while you hope something else you're doing has the patient improve.

In HAPE, low oxygen in the air above 8000 feet causes constriction of the pulmonary blood vessels, increasing the pulmonary blood pressure. High pressure on the capillaries damages them and initiates the efflux of capillary fluid into the alveoli that can lead to ARDS. Drugs that dilate the pulmonary vessels reduces the pressure and reduces the edema in HAPE.

ACE2 IS A PULMONARY VASODILATOR.

What the pulmonologists are saying is that the mechanism of pulmonary edema in COVID seems to be related to Pulmonary Hypertension/vessel constriction, in the same way that HAPE causes pulmonary edema. The cause of the pulmonary hypertension is different, but the result is the same, and maybe COVID pulmonary edema will respond to the same cheap blood pressure meds as HAPE.

We know COVID binds, enters and kills cells that express ACE2 receptors. ACE2 functions to regulate our circulatory system. The virus could hardly pick a more complex and vital target.

https://www.cureus.com/articles/29004-acetazolamide-nifedipine-and-phosphodiesterase-inhibitors-rationale-for-their-utilization-as-adjunctive-countermeasures-in-the-treatment-of-coronavirus-disease-2019-covid-19

https://journals.lww.com/shockjournal/Fulltext/2016/09000/Pulmonary_Angiotensin_Converting_Enzyme_2__ACE2_.3.aspx


I want to reread that second link a couple hundred times, maybe it will make sense to me then.
.

Dude! You totally rawk for taking the time to explain that to me! I think I understand the difference between HAPE and ARDS now. (At least in a big picture way.) I’ll try reading those white papers tomorrow to see if I can confuse myself more.

But, for now, I’m at least starting to understand why I heard early rumors of standard blood pressure meds helping. :thumbup Whether or not they do is still debatable, but the understanding on why they thought they would is there for me now.

Edit: it also helps me now understand why a patient with underlying high blood pressure is more likely to make the ARDS worse. *mind blown*