Would you look at that! A study talking about harmful affects of hyperoxia.

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Veneficus

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I bet even a nurse could do it.

You said this. I want it known I had nothing to do with it.


You aren't witholding oxygen; you simply aren't administering it unless it's indicated.

If you transport a person who isn't in pain and don't give them narcotics, are you witholding analgesia?

Are you withholding defibrillation when you don't shock someone with a strong pulse and a a nice NSR?

I like this logic.
 

ExpatMedic0

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treat the monitor and not the patient, I love it
 
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Veneficus

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treat the monitor and not the patient, I love it

Wouldn't be a problem if people knew how to treat patients, but alas quantitative monitoring has replaced clinical ability.
 

Bullets

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Or people with a GED and 1,000 hours of vocational training, for that matter.

I don't know....titrate to Sp02?

"When the red blinky number is more than 92, you don't need to do anything"

"If the red blinky number is between 88-92, use the plastic nose prong things"

"If the red blinky number is below 88, use the facemask and enough oxygen to keep the bag attached to it inflated".

Doesn't seem so hard.

I bet even a nurse could do it.


You aren't witholding oxygen; you simply aren't administering it unless it's indicated.

If you transport a person who isn't in pain and don't give them narcotics, are you witholding analgesia?

Are you withholding defibrillation when you don't shock someone with a strong pulse and a a nice NSR?

I use this when people use the "it can't hurt" logic. I suggest putting every patient on the AED because they might go into cardiac arrest. Usually ends the conversation
 

usalsfyre

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treat the monitor and not the patient, I love it
Treat the monitor, treat the patient, treat the paramedic's discomfort....it's all BS. Clinically correlating history, physical exam and any diagnostics you have is the only way you can effectively treat a pt. Unfortunately most of our educators don't know how to do this.
 

ExpatMedic0

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I do agree that o2 is in fact a drug, and in theory should not be administered unless required, and also at the proper rate.
What concerns me is its suggested an Sp02 dectector,(which is not always so reliable) dictates everything. These are all tools which combined with a providers assessment should be used to formulate a deferential diagnosis and a treatment plan.
Majority of providers in the USA are BLS according to statistics I have read. No carbon monoxide detection ability, no capongraphy, no biology, anatomy, or physiology ect. A variable plethora of diseases and conditions could happen in which the circumstance may dictate to provide more o2.

Yes, you could turn the tables and say the exact opposite, and the harmful effects of to much o2, free radicals, ect.. I understand this. But in a protocol driven, "mother may I" BLS system... which will help the most amount of people?
 
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Veneficus

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I do agree that o2 is in fact a drug, and in theory should not be administered unless required, and also at the proper rate.
What concerns me is its suggested an Sp02 dectector,(which is not always so reliable) dictates everything. These are all tools which combined with a providers assessment should be used to formulate a deferential diagnosis and a treatment plan.
Majority of providers in the USA are BLS according to statistics I have read. No carbon monoxide detection ability, no capongraphy, no biology, anatomy, or physiology ect. A variable plethora of diseases and conditions could happen in which the circumstance may dictate to provide more o2.

Yes, you could turn the tables and say the exact opposite, and the harmful effects of to much o2, free radicals, ect.. I understand this. But in a protocol driven, "mother may I" BLS system... which will help the most amount of people?

I am not sure a plethora, perhaps a few.

But then you must also consider whether this desaturation can be corrected simply by adding oxygen when taking into account your patient.

Anemia is a good example, you could increase sat to 100% with so much oxygen flames are shooting out your tailpipe and it will not change your patient's condition.
 

Carlos Danger

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You said this. I want it known I had nothing to do with it.
:cool:

treat the monitor and not the patient, I love it

And the alternative you offer is what, treat every patient the exact same way, no matter what the monitor says?

Let's just give everyone 15 lpm of oxygen, a liter of LR, and 5 of morphine. Because it will hurt very few, and will help many. I know that isn't what you wrote, but it is where your logic leads.....

The fact is, Sp02 monitoring is an extremely valuable and (usually) accurate tool that should be used to guide oxygen therapy.

What else do you go by? Waiting for the skin to turn blue or the mental status to change before giving oxygen is not a good strategy, IMO. There is no other indicator of oxygenation that is more objective or reliable than Spo2.

Everyone brings up CO poisoning, but that is a rare problem that affects a tiny % of patients. And I don't think it's hard for a BLS provider to understand that if someone is pulled out of a house fire unresponsive, then oxygen is probably a good idea because Sp02 isn't reliable in that case.

I do agree that o2 is in fact a drug, and in theory should not be administered unless required, and also at the proper rate.
What concerns me is its suggested an Sp02 dectector,(which is not always so reliable) dictates everything.

No one is suggesting that Sp02 should dictate everything. But when it comes to titrating oxygen, it is absolutely the right tool for the job.

How do you know when your patient is in a shockable rhythm? You look at your monitor.

How do you know for sure that your ETT is properly placed? You look at your monitor.

How do we know when our patients need antihypertensive therapy? You look at your monitor.

We use the objective measurements that "monitors" give us all the time, as major determinants of treatment in our most critical clinical decisions. So I'm not sure why pulse oximetry is so often looked at differently by paramedics.

Majority of providers in the USA are BLS according to statistics I have read. No carbon monoxide detection ability, no capongraphy, no biology, anatomy, or physiology ect.
Right. Which is exactly why the simplest, most objective measurement should be used.


A variable plethora of diseases and conditions could happen in which the circumstance may dictate to provide more o2.
Right. And 99% of these will manifest in a low Spo2.


Yes, you could turn the tables and say the exact opposite, and the harmful effects of to much o2, free radicals, ect.. I understand this. But in a protocol driven, "mother may I" BLS system... which will help the most amount of people?

I don't think it's been definitely determined that short periods of high flow oxygen are harmful to anyone. Neonates are probably the most susceptible population to complications of hyper-oxygenation, and even they receive high-flow O2 for brief periods of time.

The thing is, interventions need to prove themselves helpful before they are implemented, not proved harmful in order to be withheld. Doing it that way is backwards; it's exactly why we're still backboarding everyone and giving epi in cardiac arrest.

I don't think there is a big problem with BLS providers not knowing when to give oxygen. I think most patients who really need oxygen are usually pretty obvious, even to BLS folks. When you combine the obvious signs of air hunger with Sp02, I think the chances of missing something important are slim.
 
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Veneficus

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I think your post here really opens up a can of more problems than it addresses. But it makes for good discussion.


And the alternative you offer is what, treat every patient the exact same way, no matter what the monitor says?.

A majority of my time is spent on shock patients of one form or another. A vast majority are septic shock. From both research and experience, I can tell you, by the time you actually see clinical signs of shock, you are behind.

I would offer this is true of oxygenation and just about every disease process known. I can think of no exception.

However, we must first acknowledge that US EMS education is based around late stage findings, that in modern times these are a minority of patients. I did a poll on this a few days back. I think the results are telling that there are not a lot of end stage critical patients still surviving.

Which brings us to education...yet again... In order to initiate preclinical monitoring, you have to have a suspicion of a disease process. Some 40% of neonatal sepsis goes undiagnosed in early stages. The obvious clinical signs and even basic detection like reduced urine output or increased serum creatinine is either too late for treatment or unreliable because of physiologic parameters.

early geriatric sepsis diagnosis I am told by my collegues who deal primarily with that is even worse, for similar reasons.

So first you must educate on how to suspect.

Then you would need to institute a major paradigm shift in EMS function from emergency treatment to diagnosis.

You would then need to determine what very expensive monitors and tests would be done in the field, along with all the nightmares that come with that, like labratory oversight.

Is that where we want EMS to go in determining sublinical presentation? Is it even viable to do that? WHat is the benefit?

We are left then with only the reality that in order to institute effective treatment, and EMS patient must have deteriorated to the point where immediate transport supercedes all treatment.

I think this is why there is such a focus on clinical correlation in EMS.

What does an early stage sick person look like?

They look near normal.

This is the biggest conundrum of modern EMS. They are expected to determine sick vs. not sick. But without the means to reliably do it until the patient is really sick.

Let's just give everyone 15 lpm of oxygen, a liter of LR, and 5 of morphine. Because it will hurt very few, and will help many. I know that isn't what you wrote, but it is where your logic leads.....

This attitude and practice is endemic at every level of medicine. It is not unique to EMS.

It is the very premis of guidline based medicine.

The fact is, Sp02 monitoring is an extremely valuable and (usually) accurate tool that should be used to guide oxygen therapy..

As opposed to what? I have too much respect for you to think you are equating oxygen saturation with tissue oxygenation in a sick and compensating person.

To do so would make an assumption totally eliminating oxygen dissociation curves and the factors that influence them.

You cannot possibly be suggesting that?


What else do you go by? Waiting for the skin to turn blue or the mental status to change before giving oxygen is not a good strategy, IMO. There is no other indicator of oxygenation that is more objective or reliable than Spo2.

As I detailed above, I don't think that is your opinion at all. It is the best indicator of heme saturation, which is only one component of oxygenation.

Everyone brings up CO poisoning, but that is a rare problem that affects a tiny % of patients. And I don't think it's hard for a BLS provider to understand that if someone is pulled out of a house fire unresponsive, then oxygen is probably a good idea because Sp02 isn't reliable in that case..

Because it is an effective stawman.

Forget CO, go back to anemia, a symptom of multiple disease processes, saturation 100%, ineffective tissue oxygenation. Hemorrhage, saturation 100%. MI, saturation 100%. Stroke, saturation 100%. other ischemic location, the same. Do I need to continue?

Tissue Oxygenation, inadequete if not 0.

Effect of increasing oxygen even with decreased Spo2? 0, likely harmful.

No one is suggesting that Sp02 should dictate everything. But when it comes to titrating oxygen, it is absolutely the right tool for the job.

It is the only tool in BLS, and likely the most common in ALS. It defaults to being the best in the same manner that an only child is a favorite.

How do you know when your patient is in a shockable rhythm? You look at your monitor..

After determining unresponsiveness, pulselessness, or obvious clinical signs.

None of us have hooked up a normal looking patient and found vfib or pulseless vtach.

How many EMS providers have electively cardioverted a stable rhythm? I will bet not many.

How do you know for sure that your ETT is properly placed? You look at your monitor.

After clinical indicators like seeing the tube pass the chords, breath sounds, etc.

How do we know when our patients need antihypertensive therapy? You look at your monitor..

After a clinical complaint that correlates.

We use the objective measurements that "monitors" give us all the time, as major determinants of treatment in our most critical clinical decisions. So I'm not sure why pulse oximetry is so often looked at differently by paramedics.

Because we have more than 1 type of monitoring that gives us more accurate data.

Right. Which is exactly why the simplest, most objective measurement should be used.

Even if it doesn't detect subclinical condition?


Right. And 99% of these will manifest in a low Spo2.

And already be clinically evident.

COPD a great example, how many will have a low SPO2 and not be clinically compensating or outright decompensating?

How many COPD patients are administered oxygen based on ABG in the hospital? Most liekly all of them. The same for home prescription O2 as well. ( I know a few social exceptions or I would say all of them)

EMS does not have ABG.


I don't think it's been definitely determined that short periods of high flow oxygen are harmful to anyone. Neonates are probably the most susceptible population to complications of hyper-oxygenation, and even they receive high-flow O2 for brief periods of time..

There is more than ample evidence that subclinical damage is done. Not witnessing overt clinical damage in the emergent environment and calling that reasonable negates any argument that monitoring devices should be used to initiate treatment of subclinical conditions based on the idea there is no overt clinical sign.

That arguement is a manipulation of evidence based medicine in order to serve a preconceived purpose.

I call shenanigans on it. Double standard.

The thing is, interventions need to prove themselves helpful before they are implemented, not proved harmful in order to be withheld. Doing it that way is backwards; it's exactly why we're still backboarding everyone and giving epi in cardiac arrest..

Oversimplified and example of double standard. You just argued that adding oxygen over the short term has not proven to be harmful so it should be ok.

Plus, no novel treatment could ever be initiated, nor any treatment unresponsive to proven therapy in a populaiton.

It also requires all therapies to undergo scrutiny, which is not the case at current.

Furthermore, it means that no patient would be responsive to said treatments which is a very difficult statement to prove.

I don't think there is a big problem with BLS providers not knowing when to give oxygen. I think most patients who really need oxygen are usually pretty obvious, even to BLS folks. When you combine the obvious signs of air hunger with Sp02, I think the chances of missing something important are slim.

I agree, but I think the argument is that the obvious signs are so profound that SPo2 is merely confirmatory and in the absense of confirmation you would treat based on clinical symptoms.

Again I will use COPD as the example, most COPD patients have developed compensatory mechanisms, pursed lips, barrel chest, you know the drill.

What made them call you today?

Something changed. So they have clinical symptoms and maybe an spo2 of 94%. What is their normal? 95? 96? 97? you don't know.

But they have a complaint, have requested aid, clinical signs, and perhaps an inconclusive data point.

Your first decision point is: oxygen or not?

an ABG would answer this quantitatively. SPo2 will not.
 

mycrofft

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I was skimming the exchanges above when this popped out:

"The thing is, interventions need to prove themselves helpful before they are implemented, not proved harmful in order to be withheld"

I say both, in an ideal world. It isn't one or the other. But proving helpful beyond empirics is very tough without studies, and the placebo/amiodorone/lidocaine study in Oregon is an example of how sticky that is. Plus, give me a small grant , some interns and some rats, and I can show you any medication is potentially harmful. Or even a large grant!

(As an aside, if they had to have tested O2 as they have other meds, imagine the price?).
 

Carlos Danger

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Forget CO, go back to anemia, a symptom of multiple disease processes, saturation 100%, ineffective tissue oxygenation. Hemorrhage, saturation 100%. MI, saturation 100%. Stroke, saturation 100%. other ischemic location, the same. Do I need to continue?

I just spent a significant amount of time typing a detailed response, during which I came the realization that it is probably better not to have EMT’s rely on Sp02.

You guys win. :cool:

In all seriousness, I think as I was typing the following, I realized that we were quickly getting beyond a level of understanding that could be expected of EMT-B’s.

As opposed to what? I have too much respect for you to think you are equating oxygen saturation with tissue oxygenation in a sick and compensating person.

To do so would make an assumption totally eliminating oxygen dissociation curves and the factors that influence them.

You cannot possibly be suggesting that?

As opposed to having no idea whatsoever is going on with oxygenation.

Of course Sp02 doesn’t tell you what’s going on at the tissue level, or account for the many factors that affect oxygen delivery and dissociation at the tissues.

What it does, however, is give quantitative information about what is one of the most important variables in the D02 equation, hemoglobin saturation.

Hemoglobin saturation is, coincidentally, pretty much the only factor in the D02 equation that can be manipulated by the EMT-B.

In a critically ill patient encountered in the prehospital setting, I think it is safe to assume that oxygen delivery to the vital tissues is low.

And in that case, ensuring that the Ca02 is as high as possible is no small thing.
But I guess we’re getting off topic here.


I don't think it's been definitely determined that short periods of high flow oxygen are harmful to anyone. Neonates are probably the most susceptible population to complications of hyper-oxygenation, and even they receive high-flow O2 for brief periods of time..

There is more than ample evidence that subclinical damage is done. Not witnessing overt clinical damage in the emergent environment and calling that reasonable negates any argument that monitoring devices should be used to initiate treatment of subclinical conditions based on the idea there is no overt clinical sign.

I will defer to you on this, because you are obviously more familiar with the research and with the relevant physiology than I am.

My point was not that prehospital oxygenation is not harmful, just that my argument for Sp02 monitoring did not depend on that. I had other rationale that I felt justified my position.


The thing is, interventions need to prove themselves helpful before they are implemented, not proved harmful in order to be withheld. Doing it that way is backwards; it's exactly why we're still backboarding everyone and giving epi in cardiac arrest..
Oversimplified and example of double standard. You just argued that adding oxygen over the short term has not proven to be harmful so it should be ok.

Plus, no novel treatment could ever be initiated, nor any treatment unresponsive to proven therapy in a populaiton.

It also requires all therapies to undergo scrutiny, which is not the case at current.

Furthermore, it means that no patient would be responsive to said treatments which is a very difficult statement to prove.

Oversimplified, sure, but not a double standard.

All I meant was that routine treatments should be evidence-based, and that the burden of proof rests on the intervention, rather than on those who choose not to adopt an unproven practice.

Of course investigational or novel therapies require a different standard.

It's not a double standard because at no point was was I arguing in favor of routine oxygenation at all.

In fact the whole point of my "lets use Sp02" was that I thought it could minimize prehospital oxygen administration.
 

Rialaigh

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After seeing the sheer number of people that live at home with an o2 sat of 85% or less and almost no short term ill effects and very few long term effects I really have no issue bringing someone into the ER satting 88% on room air. If they are breathing 18 times a minute and are not complaining of any shortness of breath (etc) and I think that their chief complain is not hypoxia related. If they are a chronic COPD patient I have no issue at all bringing them in on room air at 85% if they say they feel like they normally do every other day (lets say their complaint is hip pain or something clearly unrelated).

Oxygen is great to calm panicked people, to arouse lethargic people, and to slow breathing in hyperventilating patients. I think it is sooooo over used in EMS, the hospital, doctors offices, and everywhere else.
 

ShockableAsystole

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A very interesting thread! In getting to grips with some of the differences between UK and US practices myself, this particular topic came up as particularly archaic. Reading the UK's British Thoracic societies oxygen guidelines may in fact give some of you MI's.

The biggest problem I see here is a knee jerk reaction to change. The evidence is thin, on both sides and more is needed, but the evidence is stacking and the studies are being done. Doing things because we've always done them is no longer acceptable.
 

PaddyWagon

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In my recent basic class there were two themes when it came to oxygen:
One was that the NREMT test expected high flow and that's what our scenarios worked with; Two was that in the reality of evidence based care and in a dense urban area most patients would be offered oxygen because it made them feel a bit safer, like they see on TV all the time, and in the short transfer times it wouldn't matter if they got a bit much.

That's book learnin' for ya.
 
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Veneficus

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A very interesting thread! In getting to grips with some of the differences between UK and US practices myself, this particular topic came up as particularly archaic. Reading the UK's British Thoracic societies oxygen guidelines may in fact give some of you MI's.

The biggest problem I see here is a knee jerk reaction to change. The evidence is thin, on both sides and more is needed, but the evidence is stacking and the studies are being done. Doing things because we've always done them is no longer acceptable.

If you include the multiple animal studies and the basic science studies on reactive oxygen the evidence against using oxygen is not that thin.
 

RocketMedic

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I was accidentally the Oxygen Guy today, BiPaped a dude with pneumonia, a lot of pulmonary edema and deep in septic shock from SpO2 76% to 93%.
 

KellyBracket

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I am inclined to believe in the potential harm of hyperoxia, and am quick to dial down the FiO2 in my patients, but the available clinical evidence seems, well, thin.

The authors apparently tend to agree on the current state of the literature - I lightly edited their review of the clinical evidence:
1. Acute myocardial infarction. ... While the small number of included studies limited the interpretation of these reviews and none of the original studies obtained a statistically significant result, they highlight provocative data that merits further urgent investigation.

2. Acute ischemic stroke. Clinical trial data evaluating the effects of different inspired oxygen levels are even more sparse in acute ischemic stroke. ...

3. Neonatal resuscitation. ...Such is the evidence base that resuscitation guidelines in neonates now advise that the initial gas administered for ventilation should be air, and that oxygen should be titrated into the mixture according to clinical response so as to avoid hypoxemia.

4. Adult resuscitation following cardiac arrest ... The authors of [a retrospective cohort study] concluded that excessive oxygen has harmful potential during adult resuscitation post cardiac arrest, possibly via ischemic reperfusion damage to central nervous tissue.

5. Critical illness. Limited data are available describing the relationship between arterial oxygenation, morbidity, and mortality in critically ill patients. The complexity of separating “signal” from “noise” in this heterogeneous patient cohort makes this task challenging.

The study of ROSC patients mentioned in point 4 is available for free at Association Between Arterial Hyperoxia Following Resuscitation From Cardiac Arrest and In-Hospital Mortality. Unfortunately, the retrospective design limits the conclusions.

On the other hand, the oft-cited EMS study Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial was prospective, and showed a large clinical effect. Almost too large - you can read some criticisms of that study at COPD: Is EMS Killing Patients with Oxygen?. (Read part 1 too!)

In the future we may be able to suss out the individual oxygen levels that are appropriate for each patient, but in the meantime I'm not going to fret too much, and I think there are other worthy targets for EMS education these days. (Analgesics for abdominal pain, e.g.)

In the meantime, I may not give the uncomplicated MI patient the "standard of care" nasal cannula, but I'm also not going to worry about reactive oxygen species as I prep the hypoxic patient for intubation, with a NRB mask at 25 lpm, and a nasal cannula at 10 lpm!
 

mycrofft

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"Adult resuscitation following cardiac arrest ... The authors of [a retrospective cohort study] concluded that excessive oxygen has harmful potential during adult resuscitation post cardiac arrest, possibly via ischemic reperfusion damage to central nervous tissue."

Are we being ushered into a new generation of determination about exactly what causes death by asystole (or asphyxia) and where in that process we can best intervene?

I remember people pushing bicarb because, while it was not exactly "mother's milk", it was fairly benign and uncomplicated versus the perceived absolute need to overcome metabolic acidosis STAT. Someone had to say "Whoa, let's take a look at this some more...".

In this debate, though, let's remember the tech in the field with a twenty minute or less transport time to definitive care and potentially somewhat ineffective ventilation methods. DOES oxygen for that short period cross some threshold which is readily flown past lying in a hospital bed with a cannula up your nose?
 

KellyBracket

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In this debate, though, let's remember the tech in the field with a twenty minute or less transport time to definitive care and potentially somewhat ineffective ventilation methods. DOES oxygen for that short period cross some threshold which is readily flown past lying in a hospital bed with a cannula up your nose?

Well, that's the conclusion of "Effect of high flow oxygen on mortality .." Austin et al. found an absolute 5% increase in in-hospital mortality (or a 42% relative) after COPD patients received high-flow oxygen during the pre-hospital phase.

As I said, I find this result out-sized and implausible, but it's out there.
 

mycrofft

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Well, that's the conclusion of "Effect of high flow oxygen on mortality .." Austin et al. found an absolute 5% increase in in-hospital mortality (or a 42% relative) after COPD patients received high-flow oxygen during the pre-hospital phase.

As I said, I find this result out-sized and implausible, but it's out there.

If anything, the internet has made me cynical and despairing about "research" which is the reporting of an interesting hint some real research needs to be done on.

The biggest factor I think is poorly controlled (other than skewed/incomplete reporting/data) is the fact that the more desperately sick someone is, the more measures get thrown at them; since their outcomes are going to be worse, the measures get a skewed reportage of poor outcomes. A case can be made (and has been in the lay press) that being admitted to the ICU increases your chances of not leaving the hospital alive....OF COURSE.
 
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