Acute Lung Injury Puns

I am an ICU nurse in Florida, and last year it was so upsetting to see so many young (20s) people in my ICU with ARDS (acute respiratory distress syndrome) needing the highest levels of care, seemingly from vaping. Since some time has gone by and I have seen fewer of these cases come through, I can’t help but think it is because the cause of this has been figured out and eliminated. So does anyone know why it was? It honestly could be as simple as vitamin E oil in the mix, causing lipoid pneumonia. Anyway, any word out there on a cause?

Omega-3 fatty can effectively improve the respiratory function and promote the recovery of acute lung injury (ALI) patients (PubMed Article)👇

https://pubmed.ncbi.nlm.nih.gov/32883303/

Abstract

Background: Several randomized controlled trials (RCTs) have compared the treatment of acute lung injury (ALI) with omega-3 fatty, yet the results remained inconsistent. Therefore, we attempted this meta-analysis to analyze the role of omega-3 fatty in the treatment of ALI patients.

Methods: We searched PubMed databases from inception date to October 31, 2019, for RCTs that compared the treatment of ALI with or without omega-3 fatty. Two authors independently screened the studies and extracted data from the published articles. Summary mean differences (MD) with 95% confidence intervals (CI) were calculated for each outcome by fixed- or random-effects model.

Results: Six RCTs with a total of 277 patients were identified, of whom 142 patients with omega-3 fatty acid treatment and 135 patients without omega-3 fatty treatment. Omega-3 fatty treatments significantly improve the PaO2 (MD = 13.82, 95% CI 8.55-19.09), PaO2/FiO2 (MD = 33.47, 95% CI 24.22-42.72), total protein (MD = 2.02, 95% CI 0.43-3.62) in ALI patients, and omega-3 fatty acid treatments reduced the duration of mechanical ventilation (MD = - 1.72, 95% CI - 2.84 to - 0.60) and intensive care unit stay (MD = - 1.29, 95% CI - 2.14 to - 0.43) in ALI patients.

Conclusions: Omega-3 fatty can effectively improve the respiratory function and promote the recovery of ALI patients. Future studies focused on the long-term efficacy and safety of omega-3 fatty use for ALI are needed.

Keywords: Acute lung injury; Meta-analysis; Omega-3 fatty; Review; Treatment.

Hey, anyone has experience with acute lung injury following sct?

Dads been in and out of hospital and icu due to low oxygen levels. Steroids help, but the problem returns whenever they start to taper. This time round they haven't even began to taper and his oxygen levels dropped drastically again... We had only been home a few days. He's over 4 months post transplant now.

Doctors probably gonna start etanercept next. Any experience with that or any other meds? I read a couple of papers but seems there are no promising ways to resolve this.

Thanks! ++

https://physoc.onlinelibrary.wiley.com/doi/full/10.1113/expphysiol.2007.040048

It seems that an enzyme/protein, ACE2 (not ACE) which binds to the ACE2 receptor which is found in the cell membrane, is protective in lung tissue against ARDS.
diagram of ACE2 activity scroll down in link

It is known that the ACE2 receptor is the binding site of nCoV.

A couple thoughts… Those with more receptors are likely more prone to initial infection as well as proliferation of the virus with in the lungs.

Receptors are known to respond to physiological condition by upregulating (expressing more of) or downregulating (expressing less of), depending on the availability of the ligand that binds to them. Angiotensin II (vasoconstrictor) is converted to angiotensin 1-7 (vasodilator) by ACE2.

Is it possible that people who live in highly air-polluted areas have more ACE2 receptors due to the constant assault to their lungs which would be clamoring for protection? Is it possible that increased need for ACE2 enzyme/protein binding converting angiotensin II (vasoconstrictor) to angiotensin 1-7 (vasodilator) drives the upregulation of ACE2 receptors?

The paper also outlines how binding by the virus is thought to induce downregulation of receptors, likely due to some sort of agonist (signaling) effect. This would mean less receptors available to be triggered by the protective ACE2 enzyme/protein to convert angiotensin II (vasoconstrictor) to angiotensin 1-7 (vasodilator) and less ultimate protection. This makes me think of the cases of late ARDS.

Perhaps those that fare best when infected have few receptors for child viral particles to bind to and lower levels of angiotensin II (vasoconstrictor) in the lungs ample available ACE2 enzymes/proteins to bind to the receptors which provides protection to the lungs. I have not yet found what drives basal levels of enzyme/protein ACE2, other than that it ACE2 acts on angiotensin I and II as a part of the negative feedback loop of the RAAS.

It seems that it would make sense that selective pressure would allow a virus such as this to initially take hold only in susceptible populations.

I am not a scientist (or a doctor), however I have long enjoyed reading scholarly articles and enjoy discussion about their content.

Thoughts?

Edits inc

https://www.atsjournals.org/doi/full/10.1513/AnnalsATS.201612-974LE

I stumbled upon this article today. While the report is vague on a few details like location, brand and usage, as it is form 2 years ago, it seems like this may have been one of the first cases reported about “vape lung”. In fact, the reporters speculate it is the first case of its kind.

"A relatively healthy 54-year-old man was admitted to the hospital through the emergency department (ED) for acute onset of dyspnea and hemoptysis. He had never smoked cigarettes but had been vaping cannabis oil approximately once weekly for several years."

"Dyspnea is the medical term for shortness of breath, sometimes described as 'air hunger.'"

"Hemoptysis is the coughing up of blood or blood-stained mucus from the bronchi, larynx, trachea, or lungs. In other words, it is the airway bleeding."

As of yet, there has been no definitive link between any of the cases beyond vaping; no link in brand, type of device, or user behavior. From my own reading over the past couple days, you could lump some of the cases into two categories: Chemical Exposure, and Long term use.

1. You risk injury from being exposed to vitamin E acetate, additional chemicals from pesticides or from metals particles that can be inhaled from faulty cheap hardware and fake carts. The risk of damaging the cart increases if a single cart is reused and refilled repeatedly. Chemical exposure can cause injury in a short time period.
2. You risk injury in the long term, as mentioned in this report, from a build-up over time from long term use. This is also similar to the case with Adam Hergenreder, the 18-year-old with “70-year-old lungs”. Long Term use also increases your chances of running into the risks of chemical exposure.

It is hard to determine if this patient had suffered from long term use, or if they eventually got a bad cart that tips his system and destroyed his lungs. They suspected that because some of his symptoms cleared up while he was in the hospital, it was from exposure to something more recent, but they list him as a long term user.

I myself had recently switched to vaping mostly out of convenience but also because of just feeling like joints and bowls were turning my lungs brown. I had been coughing up weed for years, but when I switched to vaping, that has cleared up. Now I am concerned about what I am sacrificing just to be able

DOI/PMID/ISBN: 10.1097/ALN.0000000000002687

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