Consortium Protocol
Consortium Protocol
Consortium Protocol
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) literature. We
should not re-invent the wheel but learn from the experience of others. This is a very dynamic situation;
therefore, we will be updating the guideline as new information emerges. Please check on the EVMS
website for updated versions of this protocol.
“If what you are doing ain’t working, change what you are doing”
Dr AB (NYC).
Note: A falling SaO2 despite respiratory symptoms should be a trigger to start anti-inflammatory
treatment (see Figure 2).
Note: Early termination of ascorbic acid and corticosteroids will likely result in a rebound effect with
clinical deterioration (see Figure 3).
14. Escalation of respiratory support (steps); Try to avoid intubation if at all possible, (see Figure 4)
• Accept “permissive hypoxemia” (keep O2 Saturation > 84%); follow venous lactate and
Central Venous O2 saturations (ScvO2) in patents with low arterial O2 saturations
• 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 repositioning-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.
Keep driving pressures < 15 cmH2O.
• Moderate sedation to prevent self-extubation
• Trial of inhaled Flolan (epoprostenol)
• Prone positioning.
There is widespread concern that using HFNC could increase the risk of viral transmission. There is
however, no evidence to support this fear. HFNC is a better option for the patient and the health
care system than intubation and mechanical ventilation. CPAP/BiPAP may be used in select
patients, notably those with COPD exacerbation or heart failure.
A sub-group of patients with COVID-19 deteriorates very rapidly. Intubation and mechanical
ventilation may be required in these patients.
• A sub-group of patients will develop MAS. This appears to be driven by SARS-CoV-2 induced
inflammasome activation and increased IL-1 β production (see Figure 5). [54,55]
• A ferritin > 4400 ng/ml is considered diagnostic of MAS. Other diagnostic features include
increasing AST/ALT and increasing CRP. [56]
• “High dose corticosteroids.” Methylprednisolone 120 mg q 6-8 hourly for at least 3 days,
then wean according to Ferritin, CRP, AST/ALT (see Figure 6). Ferritin should decrease by at
least 15% before weaning corticosteroids.
• Consider plasma exchange.
• Anakinra (competitively inhibits IL-1 binding to the interleukin-1 type I receptor) can be
considered in treatment failures.
17. Monitoring
• Daily: PCT, CRP, IL-6, BNP, Troponins, Ferritin, Neutrophil-Lymphocyte ratio, D-dimer and Mg.
CRP, IL-6 and Ferritin track disease severity closely (although ferritin tends to lag behind CRP).
Thromboelastogram (TEG) on admission and repeated as indicated.
• In patients receiving IV vitamin C, the Accu-Chek™ 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.
The above pathologies are not novel, although the combined severity in COVID-19 disease is
considerable. Our long-standing and more recent experiences show consistently successful treatment if
traditional therapeutic principles of early and aggressive intervention is achieved, before the onset of
advanced organ failure. It is our collective opinion that the historically high levels of morbidity and
mortality from COVID-19 is due to a single factor: the widespread and inappropriate reluctance amongst
intensivists to employ anti-inflammatory and anticoagulant treatments, including corticosteroid therapy
early in the course of a patient’s hospitalization. It is essential to recognize that it is not the virus that is
killing the patient, rather it is the patient’s overactive immune system. The flames of the “cytokine fire”
are out of control and need to be extinguished. Providing supportive care (with ventilators that
themselves stoke the fire) and waiting for the cytokine fire to burn itself out simply does not work… this
approach has FAILED and has led to the death of tens of thousands of patients.
The systematic failure of critical care systems to adopt corticosteroid therapy resulted from the
published recommendations against corticosteroids use by the World Health Organization (WHO), the
Centers for Disease Control and Prevention (CDC), and the American Thoracic Society (ATS) amongst
others. A very recent publication by the Society of Critical Care Medicine and authored one of the
members of the Front Line COVID-19 Critical Care (FLCCC) group (UM), identified the errors made by
these organizations in their analyses of corticosteroid studies based on the findings of the SARS and
H1N1 pandemics. Their erroneous recommendation to avoid corticosteroids in the treatment of COVID-
19 has led to the development of myriad organ failures which have overwhelmed critical care systems
across the world.
Our treatment protocol targeting these key pathologies has achieved near uniform success, if
begun within 6 hours of a COVID19 patient presenting with shortness of breath or needing ≥
4L/min of oxygen. If such early initiation of treatment could be systematically achieved, the
need for mechanical ventilators and ICU beds will decrease dramatically.
It is important to recognize that “COVID-19 pneumonia” does not cause ARDS. The initial phase of
“oxygenation failure” is characterized by normal lung compliance, with poor recruitability and near
normal lung water (as measured by transpulmonary thermodilution). This is the “L phenotype” as
reported by Gattonini and colleagues. [57-60] Treating these patients with early intubation and the
ARDNSnet treatment protocol will cause the disease you are trying to prevent i.e. ARDS. These patients
tolerate hypoxia remarkable well, without an increase in blood lactate concentration nor a fall in central
Patients in whom the cytokine storm is not “dampened” will progress into the “H phenotype”
characterized by poor lung compliance, severe oxygenation failure and PEEP recruitability (see Figure 7).
Progression to this phase is exacerbated by ventilator induced lung injury (VILI). The histologic pattern
of the “H Phenotype” is characterized by an acute fibrinous and organizing pneumonia (AFOP), with
extensive intra-alveolar fibrin deposition called fibrin “balls” with absent hyaline membranes.
Corticosteroids seem to be of little benefit in established AFOP. High dose methylprednisolone should
be attempted in the “early phase” of AFOP, however many patients will progress to irreversible
pulmonary fibrosis with prolonged ventilator dependency and ultimately death. [61,62]
it is important to recognize that COVID-19 patients present with a variety of phenotypes, likely
dependent on genetic heterogeneity, age, viral load, immunological and nutritional status, and co-
morbidities (see Figure 5). COVID-19 patients may develop a “thrombophilic phenotype” presenting with
severe thrombo-embolic disease with little evidence of lung parenchymal involvement. This suggests
that mildly symptomatic patients may benefit from anticoagulation. Furthermore, Vitamin D
insufficiency exacerbates the cytokine storm and likely increases the risk of death.
Finally, it is important to acknowledge that there is no known therapeutic intervention that has
unequivocally been proven to improve the outcome of COVID-19. This, however, does not mean we
should adopt a nihilist approach and limit treatment to “supportive care”. 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.
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