Please distribute this to every family member you know, have them
copy this and present this procedure to their admitting/treating
physician
This is from a document I just received.
It fully documents the procedures I have been recommending for some
time. This time, it is a highly respected Doctor in the midst of the
fight against COVID-19. For those of you that want the source article, click here and share to everyone you know. Ventilators are killing almost 90% of patients who go on one. The Doctors have been treating the wrong disease. Click Here for Original Source:
E. VIrginia Medical School Protocol
Please note: every single word beneath this line is from Doctor Marik’s protocol.
EVMS CRITICAL CARE
COVID-19 MANAGEMENT PROTOCOL
Developed
and updated by Paul Marik, MD Chief of Pulmonary and Critical Care
Medicine Eastern Virginia Medical School, Norfolk, VA April 2, 2020
URGENT!
Please circulate as widely as possible. It is crucial that every
pulmonologist, every critical care doctor and nurse, every hospital
administrator, every public health official receive this information
immediately.
This is our recommended approach to COVID-19 based on
the best (and most recent) available literature including the Shanghai
Management Guideline for COVID. We should not re-invent the wheel, but
learn from the experience of others around the world. It is important to
recognize that COVID-19 does not cause your “typical ARDS”... this
disease must be treated differently and it is likely we are exacerbating
this situation by causing ventilator induced lung injury. This is a
very fluid situation; therefore, we will be updating the guideline as
new information emerges. Please check on the EVMS website for updated
versions of this protocol.
EVMS COVID website: https://www.evms.edu/covid-19/medical_information_resources/ Short url: evms.edu/covidcare
Dr. AB (NYC).
“
We
have zero success for patients who were intubated. Our thinking is
changing to postpone intubation to as long as possible, to prevent
mechanical injury from the ventilator. These patients tolerate arterial
hypoxia surprisingly well. Natural course seems to be the best.”
This is not your “typical ARDS”. Mechanical Ventilation may be doing harm. We need to think of alternative treatment strategies.
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A few General thoughts:
1.
We are all inhabitants of the same planet and we are all in this
together. The medical community needs to get off their “high pedestal”
and act decisively and immediately; there is no time to lose. Patients
are dying needlessly.
2. It is likely that 40-80% of the
population across the world will become infected with this virus. It is
therefore unrealistic for us to expect this will just go away. Our goal,
therefore, should be to reduce the mortality in those who are at
greatest risk of dying. This requires those at risk to diligently
“socially distance” themselves. Once they become infected, we should
treat aggressively to prevent disease progression.
3. The course
of the disease is quite predictable. Acute respiratory failure occurs on
day 6-8 concomitant with the cytokine storm and hypercoagulable state.
In those patients requiring supplemental oxygen, we need to be very
aggressive to prevent disease progression and mechanical ventilation.
Once intubated, the mortality is high.
4. This is not your
“typical” ARDS... but something else (weird). Chest CT shows bilateral,
discreet, irregular, multilobar infiltrates and not the typical
dependent air-space consolidation (“sponge lung”) characteristic of
“typical” ARDS. Physiologically “COVID-19 ARDS” is different; our
preliminary data suggests that lung water (EVLWI) is normal or only
marginally increased (therefore by definition this is NOT ARDS).
Furthermore, lung compliance is quite good yet there is severe hypoxia
(due to shunting). This suggest microvascular and/or macrovascular
disease... or some other alternative explanation. In addition, pulmonary
embolism appears to be very common in these patients and may be the
cause of sudden death.
5. It is important to stress that there is
no known drug/treatment that has been proven to improve the outcome of
COVID. This, however, does not mean we should adopt a nihilist approach.
Furthermore, it is likely that there will not be a single “magic
bullet” to cure COVID-19. Rather, we should be using multiple
drugs/interventions that have synergistic and overlapping biological
effects, that are safe, cheap and “readily” available. The impact of
COVID-19 on middle- and low-income countries will be enormous; these
countries will not be able to afford expensive designer molecules.
6.
Preliminary data suggests that chloroquine and hydroxychloroquine
decrease the duration of viral shedding. In addition, chloroquine has
favorable immunomodulating properties including inhibition of PAI-1
expression. These agents are now FDA approved for the treatment of
COVID- 19. These agents (if available) could be used to mitigate/curtail
the spread of this virus and could be used in elderly patients with
comorbidities at risk of progression and death.
7. Zinc (Zn++)
inhibits viral RNA dependent RNA polymerase (replicase). Chloroquine and
hydroxychloroquine are potent Zn ionophores that increase intracellular
Zn concentrations.
8. Ascorbic acid has numerous proven
biological properties (anti-inflammatory, anti-oxidant, immune
enhancing, antiviral) that are likely to be of benefit in patients with
COVID-19 disease. Furthermore, it is important to stress that ascorbic
acid has proven synergistic effects when combined with corticosteroids.
Therefore, steroids are recommended in patients with COVID-19 and
respiratory failure. The benefit of ascorbic acid (without
corticosteroids) in patients with severe respiratory failure appears to
be limited. While the optimal dose of ascorbic acid is unknown, we
suggest 3 g IV q 6 hourly. It should be noted that in the presence of
free iron (released from ferritin) ascorbic acid may potentially have
pro-oxidant effects. Therefore, the trends in CRP and ferritin need to
be closely monitored; in those patients who ferritin AND CRP are
increasing, reducing the dose to 1.5g q 6 hourly should be considered.
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9.
Very recent data suggests that in addition to being a potent
anti-oxidant, melatonin may have direct antiviral effects against
COVID-19. In healthy people, melatonin levels plummet after the age of
40 years. This may partly explain the increased risk of death in
patients with COVID-19 who are over the age of 40. Melatonin may
therefore have a role in both the prevention and treatment of COVID-19.
10.
Vitamin D has important immune-enhancing effects. Much of the
population, especially the elderly have sub-optimal vitamin D levels,
particularly during the winter months. Low vitamin D levels have been
shown to increase the risk of developing viral upper respiratory tract
infections. Therefore, prophylactic vitamin D should be considered
especially in the elderly.
11. Quercetin is a plant phytochemical.
Experimental and early clinical data suggests that this compound has
broad antiviral properties (including against coronavirus) and acting at
various steps in the viral life cycle. Quercetin is a potent inhibitor
of heat shock proteins (HSP 40 and 70) which are required for viral
assembly. This readily available and cheap plant-derived compound may
play a role in the prophylaxis of COVID-19 in high risk populations.
Prophylaxis
While
there is very limited data (and none specific for COVID-19), the
following “cocktail” may have a role in the prevention/mitigation of
COVID-19 disease, especially amongst the most vulnerable citizens in our
community; i.e. those over the age of 60 years and those with medical
comorbidities. While there is no high level evidence that this cocktail
is effective; it is cheap, safe and should be readily available. So what
is there to lose?
• Vitamin C 500 mg BID
• Zinc 75-100 mg/day (acetate, gluconate or picolinate; do not use for more than 2 months)
• Quercetin 500-1000 mg/day
• Melatonin (slow release): Begin with 0.3mg and increase as tolerated to 1-2 mg at night
• Vitamin D3 1000-4000 u/day (optimal dose unknown; likely that those with baseline low 25-OH
vitamin D and those > 40o latitude will benefit the most)
Mildly Symptomatic patients (on floor):
• Vitamin C 500mg BID
• Zinc 75-100 mg/day
• Quercetin 500-1000 mg/day
• Melatonin 6-12 mg at night (the optimal dose is unknown)
• Vitamin D 1000- 4000 u/day
• Enoxaparin 40-60mg day (if not contraindicated; dose adjust with CrCl < 30ml/min)
• Observe closely.
• N/C 2L /min if required (max 6L/min; however, consider early t/f to ICU for escalation of care).
• Avoid Nebulization and Respiratory treatments. Use MDI if required.
• NO Bagging.
• Avoid non-invasive ventilation
• T/f EARLY to the ICU for increasing respiratory signs/symptoms.
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Respiratory symptoms (SOB; hypoxia: admit to ICU):
1. Chloroquine 500 mg PO BID for 5 days or hydroxychloroquine 400mg BID day 1 followed by 200mg BID for 4 days.
2.
Ascorbic acid (Vitamin C) 3g IV q 6 hourly until extubated and for at
least 4 days and up to 7 days (see dosage adjustment above and caution
with POC glucose testing).
3. Anticoagulation. COVID-19 results in
a hypercoagulable state with pulmonary micro- and macrovascular disease
playing a role in the hypoxia/pulmonary shunting. Unless
contraindicated we suggest FULL anticoagulation (on admission to the
ICU) with enoxaparin, i.e 1 mg kg s/c q 12 hourly (dose adjust with Cr
Cl < 30mls/min). The use of half-dose rTPA has also been suggested:
25mg of tPA over 2 hours followed by a 25mg tPA infusion administered
over the subsequent 22 hours, with a dose not to exceed 0.9 mg/kg
followed by full anticoagulation.
4. Thiamine 200mg q 12 (PO or IV).
5. Azithromycin 500 mg day 1 then 250 mg for 4 days (has immunomodulating properties including
downregulating IL-6; in addition Rx of concomitant bacterial pneumonia).
6. Melatonin 6-12 mg at night (the optimal dose is unknown).
7. Zinc 75-100 mg daily.
8. Magnesium: 2 g stat IV. Keep Mg between 2.0 and 2.4 mmol/l. Prevent hypomagnesemia (which
increases the cytokine storm and prolongs Qtc).
9. Broad-spectrum antibiotics if superadded bacterial pneumonia is suspected based on
procalcitonin levels and resp. culture (no bronchoscopy).
Co-infection
with other viruses appears to be uncommon, however a full respiratory
viral panel is still recommended. Superadded bacterial infection is
reported to be uncommon (however, this may not be correct).
10. Maintain EUVOLEMIA (this is not non-cardiogenic pulmonary edema).
11. Early norepinephrine for hypotension. While the angiotenin II agonist Giapreza TM has a limited
role in septic shock, this drug may uniquely be beneficial in patients with COVID-19
(downregulates ACE-2).
12. Optional: Atorvastatin 40-80 mg/day. Of theoretical but unproven benefit. Statins have been
demonstrated
to reduce mortality in the hyper-inflammatory ARDS phenotype. Statins
have pleotropic anti-inflammatory, immunomodulatory, antibacterial and
antiviral effects. In addition, statins decrease expression of PAI-1.
13. Optional: Tocilizumab (if available) may have a role in cytokine storm (specific IL-6 inhibitor).
14. Steroids:
a.
This topic is controversial. However, the only study on the use of
corticosteroids and COVID (from Wuhan) demonstrates a marked mortality
reduction with methylprednisolone (60mg daily). Steroids together with
vitamin C maybe necessary to down-regulate the cytokine storm.
b. During the early viral replicative stage, best to avoid.
c. During the hyperimmune/hypercoagulable phase (day 6-8 onward) in patients with
hypoxia: Hydrocortisone 50mg IV q 6 for 4 days is recommended (together with ascorbic
acid)
d. Patients may evolve into an HLH/cytokine vortex phase, marked by increasing ferrin,
CRP, IL-6 and worsening oxygenation. These patients may benefit from high dose methylprednisolone. (dose ?? 200-500 mg q 12).
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15.
Consider plasma exchange for cytokine storm/HLH picture (see steroids
below). The use of CVVH filters that remove cytokines should also be
considered.
16. Escalation of respiratory support (steps); Try to avoid intubation if at all possible
• Accept “permissive hypoxemia” (keep O2 Saturation > 86%)
• N/C 1-6 L/min
• High Flow Nasal canula (HFNC) up to 60-80 L/min
• Trial of inhaled Flolan (epoprostenol)
• Attempt proning (cooperative proning)
• Intubation ... by Expert intubator; Rapid sequence. No Bagging; Full PPE. Crash/emergency
intubations should be avoided.
• Volume protective ventilation; Lowest driving pressure and lowest PEEP as possible
• Moderate sedation to prevent self-extubation
• Trial of inhaled Flolan (epoprostenol)
• Prone positioning
• ?? ECMO < 60 yrs and no severe commodities/organ failure.
There
is widespread concern that using HFNC could increase the risk of viral
transmission. There is, however, no solid evidence to support this fear.
CPAP/BiPAP may be used in select patients, notably those with COPD exacerbation or heart failure.
17. Monitoring
•
Daily: PCT, CRP, IL-6, BNP, Troponins, Ferritin, Neutrophil-Lymphocyte
ratio, D-dimer, Mg, CRP and Ferritin are good biomarkers and track
disease severity.
• In patients receiving IV vitamin C, the
Accu-ChekTM POC glucose monitor will result in spuriously high blood
glucose values. Therefore, a laboratory glucose is recommended to
confirm the blood glucose levels.
• Monitor QTc interval if using
chloroquine/hydrochloroquine and azithromycin and monitor Mg++ (torsades
is uncommon in monitored ICU patients)
• No routine CT scans, follow CXR and chest ultrasound.
• Follow ECHO closely; Pts develop a severe cardiomyopathy.
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Typical CT scan of “COVID-9 ARDS”
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CTPA of 44 COVID + patient (with no risk factor for DVT/PE) presenting with severe tachycardia
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Found on Internet, source unknown (thank you, author)
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Proposed mechanism of hypercoagulable state.
Found on Internet, source unknown (thank you, author)
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THIS IS THE END OF DR. MARIK'S PROTOCOL. SHARE WITH EVERYONE
For More info on this GO TO: www.covid19prevention.com