Wuhan Coronavirus

[T-Rock]

Thanks JJ BPK! I'm guessing since that article seems footnoted fairly well with links to scientific articles, the prisoner must not have written it. Lol

Edited to add:

From what I can tell, it appears the author of the article on "Harvard to the Big House" blog originated from "Medium(dot)com" and was posted by "@siradrianbond" whoever that is.

[mugwump]

This coming weekend (Feb 8/9) will be interesting. When this first started three epidemiological curves of infection rates were predicted from SARS/MERS experience showing optimistic, expected, and worst-case plots of the growth of total cases. Basically, they predicted scenarios when the total number of infections would peak and then flatten and decline. The virus has blown past the optimistic and expected peaks. The pessimistic number should be achieved Thurs/Fri. If we hear of flat numbers this weekend that would be sublime---the disease will taper off in China and contagion pressure will ease. If not, we're looking at pandemic, most likely. Even then, we probably need to wait til the end of of the month to understand what's going to happen here in NA.

There's going to be a long hard look at the Wuhan's Institute of Virology when the dust settles. And, I hope, forensic accounting investigations of the top WHO cats.

Everyone is holding their breath and looking at Lagos, Mumbai, Mexico City.

How dangerous this truly is is all over the map. They need the total number of cases to make that estimate and they just don't have the data (lies, exhaustion, insufficient test supplies, lack of resource). Epidemiologists were totally counting on Hong Kong (considered first-world reliable) to report hard data on the prevalence of mild/asymptomatic cases. They're just not seeing them, at least not yet. So that's disappointing, and a blow to the hopes that this is a mild infection that's only culling the weak.

The fatalities aren't dying quickly, many taking 5-7 days to succumb. This is leading a lot of amateurs (and unsophisticated docs) to say "200 deaths, 12,000 cases, that's <2%--bad but severe-flu bad, not catastrophic." The problem is those 200 folks who died contracted the disease 10-15 days ago, when there were only 4,000 cases. Meaning a 5% death rate. Less good. The people who exhibit symptoms today are going to contribute to fatality stats in a week or so. If you see new cases flatten this weekend while deaths keep increasing, it's expected--within reason.

The bottom line is, no one knows how serious this is. It could be less than 1%, maybe much less if there are lots and lots of mild cases. Or it could be >5%, which would be bad bad bad to the supply chain and heartbreaking on the personal level.

The top three medical supply producers (China, India, Thailand) have halted all exports to conserve supplies for local use. No masks, gowns, IV sets, O2 cannulae...Every time I hear some US health administrator boasting about their preparedness I wince. Hubris. Gods. Eek. STFU

Social distancing remains the only option and it's a legitimate and successful tactic. Avoid all crowds as much as possible. Wash hands like an obsessive-compulsive at an STD clinic. Hand sanitizer. "Gel in, gel out" as the medicos say. Doorknobs/handles, handrails, grocery cart handles, elevator buttons, etc...all are enemies. Use your elbows and shoulders to open doors. Shoes and outerclothes off outside. Don't touch your face. Plan on wanting to stay indoors for extended periods.

Good luck to us all.

[InTheBlack]

Originally Posted by mugwump

Good luck to us all.

Mug, are you doing all your posting in this thread now, not the original Pandemic Flu thread?

I'll repeat a couple of items:
1) Where can we find info on "how to use" ACE2 inhibitors if the hospitals are full and someone is sick? Better case is there are beds but you have to provide your own meds, or you can contact an MD for advice.

2) what should one ask his MD for NOW, in the way of a prescription for a supply of ACE2 inhibitor, to put it in our disaster med kit?

3) Is alcohol hand sanitizer sufficient to kill virii?

I see there are BAC based hand sanitizers (Benzalkonium Chloride), and one using something they call BAC-D which claims to have an ionic charge added to it, which disrupts cell walls. And to remain active on the skin for hours.

You can get 2% BAC disinfectant by the gallon at any big box hardware store, in the janitorial supply section.

[mugwump]

I’m not really posting much anywhere since the first flurry because I don’t have any inside gouge. I’m following the suggestion to post here.

Chinese docs on Weibo were begging for injectable ACE2 inhibitors but those are not available in the US. No real use, normally. The Celestials obvs make it for something but I don’t know what. There are reagent grade samples sold here but I think my daughter or one of her colleagues figured it cost about $12.5K per 500mg dose, two doses per day x 10 days. They sell in micrograms and you administer in grams. “A mite dear” as granny used to say.

So, nothing to ask for.

ACE1 inhibitors for the cytokine storm are an unknown to me. I’ve seen no talk of their use. Those are as common as mud...lisinopril and the like.

There’s a cocktail of old school AIDS antivirals that’s supposed to work against the virus but now we’re fighting supply chain voids and I just assume none will be around. Leronlimab, Abbvie’s alluvia, I think and some ebola antiviral I can't remember the name of. Lisinopril/ACE1 for h5n1 was a possibility because it worked, it’s common as mud and just as cheap, but aids antiretrovirals for someone without aids would be a stretch. Maybe a scrip from a medical marijuana hack with a few gold eagles jingling in your hand. Dunno. But all this stuff is made in India/Thailand/China so a scrip might be useless anyway.

Hand gel works. Bar soap with good method for >20 seconds works. Social distancing works. Buy bar/liquid soap. The gougers are on the purell.

Hand sanitizer is 62-65% ethanol. If you can’t get bulk purell buy 151 rum and dilute The water %age is an important part of the process I hear. All the Purell looks to be gone on amazon (I wasn’t exhaustive) with that ‘available March 5th’ joke, same as masks, gloves. Pro tip: it’s not going to be available March 5 Maybe on a local shelf.

I know nothing first hand about BAC. Maybe that is what the Chinese are spraying on every surface in the vids? It’s still available on amazon and claims efficacy so ???



The good news is youngsters are currently underrepresented in the Chinese dead. They are catching it but not dying. So there’s that. There are also decent odds this won’t be terribly virulent, will be contained, at least here, blah blah.

That said just be ready for supply chain disruption. China has its hooks into Nigeria via debt/infrastructure and thousands were going back and forth. If Lagos starts to burn it’ll be magnitude 9 on the cable news Richter scale. Investor panic. Payments late on Hamptons vacay homes. Kias on Wall and Broad instead of range rovers.

My daughter keeps telling me that critical meds are short now, any worse and people die. get that 90 days ASAP, even if nothing develops twitter could kill you. Sorry to ramble

[Divemaster]

Macau stops shaking it's money maker. They will be closing their casinos for two weeks (I expect it will be longer).

Macau just got its 10th case. Hong Kong is at 15 with one death. The fatality was a 39 yr old male.

Most HK land crossings with the mainland are closed. The 2-3 remaining open are naturally seeing increased traffic, which puts more pressure on the ability to conduct medical screening. HK medical workers went on strike to protest the lack of a total closure.

The ferry service between HK & Macau has temperature screening at the customs and immigration points.

Some hotels in HK are taking temps of new guest arrivals and turning away those who come up hot.

If Hong Kong is closed entirely, no in/out international flights or shipping, the impact to global markets will be not good.

[InTheBlack]

Mug - Prayers for you. Don't ring the bell !!! You still have knowledge, you can still do good.

Questions for all:

I don't know the difference between ACE1 and ACE2, but reading indicates ACE2 is the choice. I thought the ACE2 class was a commonly used oral drug? If so, what are some brand & generic names? Or is it still a researchers' unicorn ?

I have dug out my notes from October 2006 in the Pandemic Flu thread.

Statins, like Zocor, 20mg twice a day at first hint of symptoms, and once a day for family members who are asymptomatic. Seems like 10-12 day course probably reasonable risk.

ACE2 seemed to be "new" vs flu in 2006 -- No dosage info.

By now, doesn't WHO etc have a medical protocol for treating SARS & MERS etc which specifies drugs & dosage etc ? I am searching but the web is full of spam; need to find a portal to real physician information.

Wondering if "vasodilatory shock" is synonymous with ARDS (acute respiratory distress syndrome). Not sure if this article contains useful knowledge:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6067786/
Angiotensin II: a new therapeutic option for vasodilatory shock

Angiotensin II (Ang II), part of the renin–angiotensin–aldosterone system (RAS), is a potent vasoconstrictor and has been recently approved for use by the US Food and Drug Administration in high-output shock.

Though not a new drug, the recently published Angiotensin II for the Treatment of High Output Shock (ATHOS-3) trial, as well as a number of retrospective analyses have sparked renewed interest in the use of Ang II, which may have a role in treating refractory shock.

We describe refractory shock, the unique mechanism of action of Ang II, RAS dysregulation in shock, and the evidence supporting the use of Ang II to restore blood pressure.

Evidence suggests that Ang II may preferentially be of benefit in acute kidney injury and acute respiratory distress syndrome, where the RAS is known to be disrupted.

Additionally, there may be a role for Ang II in cardiogenic shock, angiotensin converting enzyme inhibitor overdose, cardiac arrest, liver failure, and in settings of extracorporeal circulation.
********

Don't know about dehydration & fluids. How many liters of IV bags might be needed? What type of fluid? Is subcutaneous administration feasible in adults (I know how to do that).

Goldpharma.com still exists, but maybe it only allows drug searches if you register first. I can't get anything but the home page to show.

[InTheBlack]

More from the 2006 thread:
Get vaccinated for HiB and Pneumovax II. Sometimes this is a combined shot.

[Divemaster]

Ferry service between Hong Kong & Macau is suspended as of 0000 04 FEB HK time.

turbojet.com.hk/en/routing-sailing-schedule/hong-kong-macau/sailing-schedule-fares.aspx

[InTheBlack]

Gone down the rabbit hole.

1) US Dept Health & Human Services
Chemical Hazards Emergency Medical Management
Home > Medical Countermeasures Database > Statins
https://chemm.nlm.nih.gov/countermeasure_statins.htm

Above article on statins. Cites lots of research articles. Opinions seem to be mixed as to whether statins lower mortality.

edit: No dosing information for ARDS:
"2. Chemical Defense therapeutic area(s)
— including key possible uses

Statins can be used as anti-inflammatory treatment for acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) induced by pulmonary agent such as phosgene."


2) You have to register here, but you can do so as a non-medical pro. Site provides info & Continuing Education credits for the medical field.

Everything you could ever want to know about diagnosing & treating ARDS:
Drugs & Diseases > Critical Care
Acute Respiratory Distress Syndrome
Updated: Oct 17, 2018

https://emedicine.medscape.com/article/165139-overview

ALSO:
Drugs & Diseases > Critical Care
Acute Respiratory Distress Syndrome Questions & Answers
Updated: Oct 17, 2018

https://emedicine.medscape.com/artic...ns-and-answers

[InTheBlack]

Long post. PART 1
Trying to treat ARDS in the field seems futile.

My summary drawn from:
https://emedicine.medscape.com/article/165139-overview
Acute Respiratory Distress Syndrome
Updated: Oct 17, 2018
*****

Early use Corticosteriods seem NOT to improve mortality, but I have not necessary seen the latest study data on that.

FLUIDS: "Type one reflects primarily acute lung injury without antecedent systemic processes like sepsis or pancreatitis. Type two is acute lung injury with an overwhelming systemic insult like sepsis.

Important to note, type one patients benefit from a fluid-restrictive management strategy (infra vide)"


VENTILATION: One item is that those positive-pressure breathing masks (CPAP) so many people have can, so some extent, substitute for a real ventilator. Lots of technical issues in the pressure curves and oxygen saturation, but in the field helping respiration might be the best you can do.

"The use of positive end-expiratory pressure (PEEP) to diminish alveolar collapse and the use of low tidal volumes and limited levels of inspiratory filling pressures appear to be beneficial in diminishing the observed VALI.

"Generally, oxygen concentrations higher than 65% for prolonged periods (days) can result in DAD, hyaline membrane formation, and, eventually, fibrosis.

ARDS is uniformly associated with pulmonary hypertension"

MORBIDITY PREDICTORS:
"Indices of oxygenation and ventilation, including the PaO2/FiO2 ratio, do not predict the outcome or risk of death. The severity of hypoxemia at the time of diagnosis does not correlate well with survival rates. However, the failure of pulmonary function to improve in the first week of treatment is a poor prognostic factor.

Peripheral blood levels of decoy receptor 3 (DcR3), a soluble protein with immunomodulatory effects, independently predict 28-day mortality in ARDS patients.

In a study comparing DcR3, soluble triggering receptor expressed on myeloid cells (sTREM)-1, TNF-alpha, and IL-6 in ARDS patients, plasma DcR3 levels were the only biomarker to distinguish survivors from nonsurvivors at all time points in week 1 of ARDS. [11] Nonsurvivors had higher DcR3 levels than survivors, regardless of APACHE II scores, and mortality was higher in patients with higher DcR3 levels."

PRESENTATION:
"With the onset of lung injury, patients initially note dyspnea with exertion. This rapidly progresses to severe dyspnea at rest, tachypnea, anxiety, agitation, and the need for increasingly high concentrations of inspired oxygen.

Physical Examination

Physical findings often are nonspecific and include tachypnea, tachycardia, and the need for a high fraction of inspired oxygen (FiO2) to maintain oxygen saturation. The patient may be febrile or hypothermic. Because ARDS often occurs in the context of sepsis, associated hypotension and peripheral vasoconstriction with cold extremities may be present. Cyanosis of the lips and nail beds may occur.

Examination of the lungs may reveal bilateral rales. Rales may not be present despite widespread involvement."

"Because cardiogenic pulmonary edema must be distinguished from ARDS, carefully look for signs of congestive heart failure or intravascular volume overload, including jugular venous distention, cardiac murmurs and gallops, hepatomegaly, and edema."


COMPLICATIONS:
"ventilator-associated pneumonia (VAP) and line sepsis. The incidence of VAP in ARDS patients may be as high as 55% and appears to be higher than that in other populations requiring mechanical ventilation. Preventive strategies including elevation of head of the bed, use of subglottic suction endotracheal tubes, and oral decontamination."

"Renal failure is a frequent complication of ARDS, particularly in the context of sepsis. Renal failure may be related to hypotension, nephrotoxic drugs, or underlying illness. Fluid management is complicated in this context, especially if the patient is oliguric. Multisystem organ failure, rather than respiratory failure alone, is usually the cause of death in ARDS.

Other potential complications include ileus, stress gastritis, and anemia. Stress ulcer prophylaxis is indicated for these patients. Anemia may be prevented by the use of growth factors (erythropoietin)."

FIELD EXPEDIENT WORKUP ITEMS:
"Approach Considerations

Acute respiratory distress syndrome (ARDS) is defined by the acute onset of bilateral pulmonary infiltrates and severe hypoxemia in the absence of evidence of cardiogenic pulmonary edema. Workup includes selected laboratory tests, diagnostic imaging, hemodynamic monitoring, and bronchoscopy. ARDS is a clinical diagnosis, and no specific laboratory abnormalities are noted beyond the expected disturbances in gas exchange and radiographic findings.

Laboratory Tests

In ARDS, if the partial pressure of oxygen in the patient’s arterial blood (PaO2) is divided by the fraction of oxygen in the inspired air (FiO2), the result is 300 or less. For patients breathing 100% oxygen, this means that the PaO2 is less than 300.

In addition to hypoxemia, arterial blood gases often initially show a respiratory alkalosis. However, in ARDS occurring in the context of sepsis, a metabolic acidosis with or without respiratory compensation may be present.

As the condition progresses and the work of breathing increases, the partial pressure of carbon dioxide (PCO2) begins to rise and respiratory alkalosis gives way to respiratory acidosis. Patients on mechanical ventilation for ARDS may be allowed to remain hypercapnic (permissive hypercapnia) to achieve the goals of low tidal volume and limited plateau pressure ventilator strategies aimed at limiting ventilator-associated lung injury."

MANAGEMENT:
" A study by Martin-Loeches et al concluded that the early use of corticosteroids was also ineffective in patients with the pandemic H1N1 influenza A infection, resulting in an increased risk of superinfections. [23] This finding was also echoed in a study by Brun-Buisson et al, who found no evidence of benefit associated with corticosteroids in patients with ARDS secondary to influenza pneumonia but did find that early corticosteroid therapy may be harmful. [24]

Numerous pharmacologic therapies, including the use of inhaled synthetic surfactant, intravenous (IV) antibody to endotoxin, ketoconazole, simvastatin, and ibuprofen, have been tried and are not effective. [25]

A study that examined the use and outcomes associated with rescue therapies in patients with ARDS determined that these therapies offered no survival benefit. [26] The study also determined that rescue therapies are most often used in younger patients with more severe oxygenation deficits.

Inhaled nitric oxide (NO), a potent pulmonary vasodilator, seemed promising in early trials, but in larger controlled trials, it did not change mortality rates in adults with ARDS. [27, 28] A systematic review, meta-analysis, and trial sequential analysis of 14 randomized controlled trials, including 1303 patients, found that inhaled nitric oxide did not reduce mortality and results in only a transient improvement in oxygenation. [29]

Although no specific therapy exists for ARDS, treatment of the underlying condition is essential, along with supportive care, noninvasive ventilation or mechanical ventilation using low tidal volumes, and conservative fluid management.

Because infection is often the underlying cause of ARDS, early administration of appropriate antibiotic therapy broad enough to cover suspected pathogens is essential," ...
...

"With the development of the National Institutes of Health (NIH)–sponsored ARDS Clinical Trials Network, several large well-controlled trials of ARDS therapies have been completed. Thus far, the only treatment found to improve survival in ARDS is a mechanical ventilation strategy using low tidal volumes (6 mL/kg based upon ideal body weight).

The main concerns are missing a potentially treatable underlying cause or complication of ARDS. In these critically ill patients, pay careful attention to early recognition of potential complications in the intensive care unit (ICU), including pneumothorax, IV line infections, skin breakdown, inadequate nutrition, arterial occlusion at the site of intra-arterial monitoring devices, DVT and pulmonary embolism (PE), retroperitoneal hemorrhage, gastrointestinal (GI) hemorrhage, erroneous placement of lines and tubes, and the development of muscle weakness."

[InTheBlack]

Long post. PART 2

FLUID MANAGEMENT : too detailed to summarize here.

" Noninvasive Ventilation and High-Flow Nasal Cannula

Because intubation and mechanical ventilation may be associated with an increased incidence of complications, such as barotrauma and nosocomial pneumonia, alternatives to mechanical ventilation such as a high-flow nasal cannula or noninvasive positive-pressure ventilation (NIPPV) may be beneficial in patients with ARDS. "
SNIPPED MORE DETAILS

"Mechanical Ventilation

The goals of mechanical ventilation in ARDS are to maintain oxygenation while avoiding oxygen toxicity and the complications of mechanical ventilation. Generally, this involves maintaining oxygen saturation in the range of 85-90%, with the aim of reducing the fraction of inspired oxygen (FiO2) to less than 65% within the first 24-48 hours. Achieving this aim almost always necessitates the use of moderate-to-high levels of positive end-expiratory pressure (PEEP)."
SNIPPED DETAILS

"Positive end-expiratory pressure and continuous positive airway pressure

ARDS is characterized by severe hypoxemia. When oxygenation cannot be maintained despite high inspired oxygen concentrations, the use of CPAP or PEEP usually promotes improved oxygenation, allowing the FiO2 to be tapered." SNIPPED DETAILS OF HOW TO CONFIGURE THE APPARATUS

"Prone positioning

Some 60-75% of patients with ARDS have significantly improved oxygenation when turned from the supine to the prone position. The improvement in oxygenation is rapid and often substantial enough to allow reductions in FIO2 or level of CPAP. The prone position is safe, with appropriate precautions to secure all tubes and lines, and does not require special equipment. The improvement in oxygenation may persist after the patient is returned to the supine position and may occur on repeat trials in patients who did not respond initially.
snip

However, a subsequent randomized controlled trial in which patients with severe ARDS were placed in the prone position early and for at least 16 hours a day showed a significant mortality benefit. [48] In this study, patients with severe ARDS (PaO2/FiO2 of < 150) were randomized to prone position after 12-24 hours of stabilization. The 28-day mortality rate was 16% in the prone group and 32.8% in the supine group. Patients were turned manually. A specialized bed was not required."

"Nutritional Support

Institution of nutritional support after 48-72 hours of mechanical ventilation usually is recommended. Enteral nutrition via a feeding tube is preferable to IV hyperalimentation unless it is contraindicated because of an acute abdomen, ileus, GI bleeding, or other conditions.

A low-carbohydrate high-fat enteral formula including anti-inflammatory and vasodilating components (eicosapentaenoic acid and linoleic acid) along with antioxidants has been demonstrated in some studies to improve outcome in ARDS. [52, 53]"

"Activity Restriction

Patients with ARDS are on bed rest. Frequent position changes should be started immediately, as should passive—and, if possible, active—range-of-motion activities of all muscle groups. Elevation of the head of the bed to a 45° angle is recommended to diminish the development of VAP.


THE MEDICATION SECTION SHOULD BE READ IN FULL BY THOSE INTERESTED, recall that you need to register:
https://emedicine.medscape.com/artic...139-medication

"Medication Summary

No drug has proved beneficial in the prevention or management of acute respiratory distress syndrome (ARDS).

Early administration of corticosteroids to septic patients does not prevent the development of ARDS.

Numerous pharmacologic therapies, including the use of inhaled or instilled synthetic surfactant, intravenous (IV) antibody to endotoxin, ketoconazole, and ibuprofen, have been tried and are not effective.

Statins, which also appeared to have promise in small studies, also did not show benefit in a recently published randomized trial in 60 patients with acute lung injury (ALI). [57]"

[
BUT THE REFERENCED ABSTRACT SAYS IT DID HELP, IF I UNDERSTAND IT CORRECTLY:

NOTE 57:
https://reference.medscape.com/medli...tract/20870757

A randomized clinical trial of hydroxymethylglutaryl- coenzyme a reductase inhibition for acute lung injury (The HARP Study).
Am J Respir Crit Care Med. 2011; 183(5):620-6 (ISSN: 1535-4970)

Craig TR; Duffy MJ; Shyamsundar M; McDowell C; O'Kane CM; Elborn JS; McAuley DF

RATIONALE: There is no effective pharmacological treatment for acute lung injury (ALI). Statins are a potential new therapy because they modify many of the underlying processes important in ALI.

OBJECTIVES: To test whether simvastatin improves physiological and biological outcomes in ALI.
SNIP

CONCLUSIONS: Treatment with simvastatin appears to be safe and may be associated with an improvement in organ dysfunction in ALI. These clinical effects may be mediated by a reduction in pulmonary and systemic inflammation. Clinical trial registered with www.controlled-trials.com (ISRCTN70127774).

What This Study Adds to the Field
We have found, in a randomized, double-blind trial of 60
patients with ALI, that simvastatin was safe and showed
modest improvements in nonpulmonary organ dysfunction,
improvement in systemic organ dysfunction, and a reduction
in IL-8 in the airspaces of the lung.

FULL STUDY URL:
https://www.researchgate.net/publica...00000/download

]

[InTheBlack]

Deeper dive FWIW:
https://www.medscape.com/viewarticle/894046_1

The Relationship Between High-Dose Corticosteroid Treatment and Mortality in Acute Respiratory Distress Syndrome
A Retrospective and Observational Study Using a Nationwide Administrative Database in Japan

Takashi Kido; Keiji Muramatsu; Takeshi Asakawa; Hiroki Otsubo; Takaaki Ogoshi; Keishi Oda; Tatsuhiko Kubo; Yoshihisa Fujino; Shinya Matsuda; Toshihiko Mayumi; Hiroshi Mukae; Kazuhiro Yatera
Disclosures

BMC Pulm Med. 2018;18(28)


Conclusions
Our results suggest that high-dose corticosteroid treatment does not improve the prognosis of patients with ARDS, even in this era. However, this study has limitations owing to its retrospective and observational design.

[InTheBlack]

"Pharmacologic therapies such as β2 agonists, statins, and keratinocyte growth factor, which targeted pathophysiologic alterations in ARDS, were not beneficial and demonstrated possible harm."

FULL TEXT:
https://sci-hub.tw/10.1001/jama.2017.21907

ABSTRACT:
https://www.ncbi.nlm.nih.gov/pubmed/29466596

JAMA. 2018 Feb 20;319(7):698-710. doi: 10.1001/jama.2017.21907.
Acute Respiratory Distress Syndrome: Advances in Diagnosis and Treatment.
Fan E1,2,3,4, Brodie D5, Slutsky AS1,4,6.

FINDINGS:

Findings:

After screening 1662 citations, 31 articles detailing major advances in the diagnosis or treatment of ARDS were selected. The Berlin definition proposed 3 categories of ARDS based on the severity of hypoxemia: mild (200 mm Hg<Pao2/Fio2≤300 mm Hg), moderate (100 mm Hg<Pao2/Fio2≤200 mm Hg), and severe (Pao2/Fio2 ≤100 mm Hg), along with explicit criteria related to timing of the syndrome's onset, origin of edema, and the chest radiograph findings. The Berlin definition has significantly greater predictive validity for mortality than the prior American-European Consensus Conference definition. Clinician interpretation of the origin of edema and chest radiograph criteria may be less reliable in making a diagnosis of ARDS. The cornerstone of management remains mechanical ventilation, with a goal to minimize ventilator-induced lung injury (VILI). Aspirin was not effective in preventing ARDS in patients at high-risk for the syndrome. Adjunctive interventions to further minimize VILI, such as prone positioning in patients with a Pao2/Fio2 ratio less than 150 mm Hg, were associated with a significant mortality benefit whereas others (eg, extracorporeal carbon dioxide removal) remain experimental.

Pharmacologic therapies such as β2 agonists, statins, and keratinocyte growth factor, which targeted pathophysiologic alterations in ARDS, were not beneficial and demonstrated possible harm.

Recent guidelines on mechanical ventilation in ARDS provide evidence-based recommendations related to 6 interventions, including low tidal volume and inspiratory pressure ventilation, prone positioning, high-frequency oscillatory ventilation, higher vs lower positive end-expiratory pressure, lung recruitment maneuvers, and extracorporeal membrane oxygenation.

[InTheBlack]

None of these studies on statins vs ARDS seem to have started the drug before full-blown ARDS

Using them at the first signs of flu, when it is a deadly flu, and you cannot get lab tests etc, may still be a useful tactic.

[InTheBlack]

graph & numbers:

https://gisanddata.maps.arcgis.com/a...23467b48e9ecf6