ICU resources for COVID-19

Marik Protocol; Front Line COVID-19 Critical Care Working Group Protocol; Farid Jalali's beautiful detective work hypothesising about exactly what is happening in the lungs of COVID-19 patients; Vitamin D to stabilize the endothelium . . .

Robin Whittle rw@firstpr.com.au .   2020-04-09  Last update 2020-05-27 15:00 UTC

To the main COVID-19 page of this site: http://aminotheory.com/cv19/ , concerning nutritional supplements - especially vitamin D and boron - for all adults and some children ASAP, so their immune system will not be thrown into deadly sepsis by COVID-19.  This begins with links to research showing a sharp dichotomy between generally mild symptoms for people with vitamin D 25OHD levels of 30ng/ml or more, and much greater rates of serious symptoms and death for those with 25OHD levels below 30ng/ml.

If everyone in the world was already replete in vitamin D alone (with the current very poor boron status) or boron replete (with the current poor vitamin D status) then I believe that very few people would be dying of COVID-19.

Be sure to read the Disclaimer!




#2020-Jalali-b

Farid Jalali's hypothesis of vascular damage and shunting via diffuse pulmonary-bronchial anastomoses

Be sure to read this beautiful detective work which offers the best explanation yet for many perplexing aspects of COVID-19.  The first link is to a video podcast with PDF and discussion and the second is to a text and graphic presentation with comments by Cameron Kyle-Sidell MD:

https://emcrit.org/emcrit/pathophysiology-of-covid19/

https://rebelem.com/covid-19-acute-lung-injury-a-proposed-
model-
v1-0-via-farid-jalali-md/




Cameron Kyle-Sidell's appreciative comments begin with:

I applaud Dr. Jalali for proposing a model for COVID-19 injury based on seemingly sound physiologic principles.  This model does provide explanations for anecdotal observations made by bedside physicians treating COVID-19 patients.  For example, the presence of dorsal-predominant shunting would explain why proning leads to marked oxygenation improvement that is not sustained once the patient returns to the supine position.

This work highlights the importance of protecting the integrity of the endothelium and limiting vasoconstriction, which is caused by excessive angiotensin II, resulting from SARS-CoV-2 destroying the ACE2 receptors.  See the next item.

#2020-Kim

Vitamin D and Endothelial Function

Your COVID-19 patients are (according to Philippino and Indonesian research I cite here cv19/) generally seriously deficient in vitamin D.  Surely you can improve their chances of survival with vitamin D supplements. 

Cholecalciferol (D3) takes days to convert to 25OHD in the liver - and the liver may not be functioning well.  So high dose oral D3 - such as 50,000 or 100,000IU, ideally with a meal including fats - when they arrive in hospital, is one way to start.  If you can do oral of IV 25OHD (calcifideol = Rayaldee) then this would be faster.  Most immune system cells require plasma 25OHD for their internal synthesis of 1,25OHD to activate their internal (intracrine) vitamin D receptor signaling.  So the whole of immune regulation depends on a good 25OHD level. 

Other cells, such as endothelial cells, require 1,25OHD calcitriol at their membrane bound vitamin D receptors, and so may not rely directly on plasma 25OHD levels. 

Please see this recent review article:

Vitamin D and Endothelial Function
Do-Houn Kim et al. Nutrients 2020, 12(2), 575
https://www.mdpi.com/2072-6643/12/2/575


Adequate vitamin D activation of endothelial cells achieves numerous functions:
NO is a primary vasoactive substance that works as a potent vasodilator in addition to other vasoprotective properties such as protection from vessel inflammation and lesion formation.

Endothelium-derived NO acts on adjacent vascular smooth muscle cells in a paracrine manner and induces vascular muscle relaxation . . .

. . . protects the vessel from developing atherosclerosis by inhibiting platelet adherence and aggregation, and leukocyte activation.

COVID-19 Protocol for early intervention to reduce cytokine storm and so reduce or eliminate the deadly hypercoagulative state

The website of the Front Line COVID-19 Critical Care Working Group is:

https://covid19criticalcare.com

Please follow all the links to protocol, press release and other documents there, as well as documents linked from theirs:

General Adaptation in Critical Illness: Glucocorticoid Receptor-alpha Master Regulator of Homeostatic Corrections
Meduri & Chrousos
https://www.frontiersin.org/articles/10.3389/fendo.2020.00161/full

Outcomes of Metabolic Resuscitation Using Ascorbic Acid, Thiamine, and Glucocorticoids in the Early Treatment of Sepsis
Jose Iglesias et al.
https://www.sciencedirect.com/science/article/abs/pii/S0012369220304554

https://sci-hub.tw/10.1016/j.chest.2020.02.049


The original website was: recoverywithoutwalls.com/covidprotocol/

The protocol concerns the early use of methylprednisolone, low molecular weight heparin, IV vitamin C and hydroxychloroquine, before to reduce or prevent the development of the cytokine storm which causes the hypercoagulative state which is what harms and kills people.  Other elements are nasal cannula oxygen with prone positioning and avoidance of incubation as much as possible.   In late April, they added optional vitamin D to their ICU protocol.

An excellent write-up by Caitlin Dickson: news.yahoo.com/...doctors-question-how-we-use-ventilators-123733204.html

The Marik Protocol

The basis for the abovementioned Task Force Protocol:

www.evms.edu/covid-19/medical_information_resources/

EMCrit discussion on timing of corticosteroids

Josh Farkas and commenters discuss the timing and strength of corticosteroid use with COVID-19:

https://emcrit.org/pulmcrit/steroid-covid/

Dr Cameron Kyle-Sidell's videos on how different COVID-19 is from what he trained for

His impassioned video:  www.youtube.com/watch?v=g3ka8lo_fZ8 .  A later interview with John Whyte in which he mentions that his view of what was good for the patient was incompatible with the guidelines followed by the rest of his ICU team, so he resigned his position to work in the ER: www.medscape.com/viewarticle/928156 .

L. Gattinoni et al. on L and H "phenotypes"

www.esicm.org/wp-content/uploads/2020/04/684_author-proof.pdf


#2020-Jalali-a

Dr Farid Jalali's COVID-19 diagram concerning cytokine storm and resulting hypercoagulative state


Farid Jalali twitter.com/farid__jalali tweeted a detailed diagram twitter.com/farid__jalali/status/1247036001349849088 depicting the cytokine storm turning a moderately PAI-1 elevated coagulative state, which apparently can be controlled with heparin, into a hypercoagulable Progressive Thrombotic Cascade.  The long progression of this thrombosis apparently enables the oxygen levels to drop slowly enough that the patient copes with it better than would be the case with normal ARDS.  This leads to microvascular thrombosis in the lungs, heart, kidney, gut, pancreas, skin and CNS - and so frequently to death.

He states that COVID-19 is cytopathic to the endothelium and that this degenerates (as far as I know, in the absence of vitamin C etc. treatment) into the Severe COVID-19 cytokine storm.  This makes me think that the vitamin C, corticosteroid etc. treatment prevents the virus and the consequent (at least in these patients) immune response doing so much harm to the endothelium.





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