Dr pawan kumar Anesthesiologist

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Dr pawan kumar Anesthesiologist is now on WhatsApp.

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Breaking News: *Major cause of death in Covid-19 is Thrombosis, Not Pneumonia!*

It seems that the disease is being attacked wrongly worldwide?

Thanks to autopsies performed by the Italians ... it has been shown that it is not pneumonia ... but it is: disseminated intravascular coagulation (thrombosis).

Therefore, the way to fight it is with antibiotics, antivirals, anti-inflammatories and anticoagulants.

The protocols are being changed here since noon!

According to valuable information from Italian pathologists, ventilators and intensive care units were never needed.

If this is true for all cases, we are about to resolve it earlier than expected.

Important and new about Coranovirus:

Around the world, COVID-19 is being attacked wrongly due to a serious pathophysiological diagnosis error.

The impressive case of a Mexican family in the United States who claimed they were cured with a home remedy was documented:
three 500 mg aspirins dissolved in lemon juice boiled with honey, taken hot.

The next day they woke up as if nothing had happened to them!

Well, the scientific information that follows proves they are right!

This information was released by a medical researcher from Italy:
Thanks to 50 autopsies performed on patients who died of COVID-19, Italian pathologists have discovered that IT IS NOT PNEUMONIA, strictly speaking, because the virus does not only kill pneumocytes of this type, but uses an inflammatory storm to create an endothelial vascular thrombosis.

As in disseminated intravascular coagulation, the lung is the most affected because it is the most inflamed, but there is also a heart attack, stroke and many other thromboembolic diseases.

In fact, the protocols left antiviral therapies useless and focused on anti-inflammatory and anti-clotting therapies.

These therapies should be done immediately, even at home, in which the treatment of patients responds very well.

The later performed less effective.
In resuscitation, they are almost useless.

If the Chinese had denounced it, they would have invested in home therapy, not intensive care!

DISSEMINATED INTRAVASCULAR COAGULATION (THROMBOSIS):

So, the way to fight it is with antibiotics, anti-inflammatories and anticoagulants.

An Italian pathologist reports that the hospital in Bergamo did a total of 50 autopsies and one in Milan, 20, that is, the Italian series is the highest in the world, the Chinese did only 3, which seems to fully confirm the information.

Previously, in a nutshell, the disease is determined by a disseminated intravascular coagulation triggered by the virus; therefore, it is not pneumonia but pulmonary thrombosis, a major diagnostic error.

We doubled the number of resuscitation places in the ICU, with unnecessary exorbitant costs.

In retrospect, we have to rethink those chest X-rays that were discussed a month ago and were given as interstitial pneumonia; in fact, it may be entirely consistent with disseminated intravascular coagulation.

Treatment in ICUs is useless if thromboembolism is not resolved first. If we ventilate a lung where blood does not circulate, it is useless, in fact, nine (9) patients out of ten (10) die.

Because the problem is cardiovascular, not respiratory.

It is venous microthrombosis, not pneumonia, that determines mortality.

Why thrombi are formed❓

Because inflammation, according to the literature, induces thrombosis through a complex but well-known pathophysiological mechanism.

Unfortunately what the scientific literature said, especially Chinese, until mid-March was that anti-inflammatory drugs should not be used.

Now, the therapy being used in Italy is with anti-inflammatories and antibiotics, as in influenza, and the number of hospitalized patients has been reduced.

Many deaths, even in their 40s, had a history of fever for 10 to 15 days, which were not treated properly.

The inflammation did a great deal of tissue damage and created ground for thrombus formation, because the main problem is not the virus, but the immune hyperreaction that destroys the cell where the virus is installed. In fact, patients with rheumatoid arthritis have never needed to be admitted to the ICU because they are on corticosteroid therapy, which is a great anti-inflammatory.

This is the main reason why hospitalizations in Italy are decreasing and becoming a treatable disease at home. By treating her well at home, not only is hospitalization avoided, but also the risk of thrombosis.

It was not easy to understand, because the signs of microembolism disappeared!

With this important discovery, it is possible to return to normal life and open closed deals due to the quarantine, not immediately, but it is time to publish this data, so that the health authorities of each country make their respective analysis of this information and prevent further deaths. useless!

The vaccine may come later.

Now we can wait.
In Italy, as of today, protocols are changing.

According to valuable information from Italian pathologists, ventilators and intensive care units are not necessary.

Therefore, we need to rethink investments to properly deal with this disease.

Não há (Translation by automatic device).

LET'S PUBLISH URGENTLY! "
Wish this is true.👆🏼

Interesting Facts Revealed!

Excerpt:

In COVID- 19

Best summary today:

1.-Why there is high ferritin level ?

2.-Why there is very high DDimer levels disproportionate with the severity of infection?

3.-Why ARDS in those are nearly
Not responding to high PEEP and Fio2 levels?

4.-Why all CT chest patterns are exclusively Ground glassing and associated with rapid and marked hypoxemia disproportionates with the geographical CT findings size ?

5.- Why Early Chinese protocol for Covid includes high dosing of systemic steroids which is questioned and rejected by WHO ?

6.- Why body immune response aganist Covid is not like other respiratory viruses by lymphocytosis ( Cytotoxic T cells and Natural killer cells) , insteadly body prefers to reacts against covid by phagocytosis ( monocytosis ) ?

7.- Why Covid Attacking mature red blood cell while it is one of body cells that dose not contain nucleus and DNA ?

8.-Why Critically ill Patients are responding well to anticoagulation , Hydroxycholoquine and novel antiviral Favipiravir ?

The following molecular pathogenesis is the only one for the time being that can answer all these questions .

COVID -19 may not cause pneumonia either typical or atypical or classical ARDs . It seems like we are dealing with a presumed wrong disease.

The Key pathogenic molecular step of SARS-Cov2 is to attack the 1-Beta Chain of Hemoglobin and hunting the porphyrins dissociating the iron form it and releasing iron into the circulation.

Thus Hb looses its capacity to bind with oxygen , so oxygen is not supplied to major organs. That is why we see resistant hypoxia coupled with very rapid multi-organ failures.

Moreover The free iron released into the circulation is so toxic as it causes a powerful oxidative damage to the lungs .

Free iron toxicity causes inflammation of alveolar macrophages- leads to CT scan characteristic changes.

The body try to compensate this by elevating the rate of Hb synthesis which explains why Hb is high in those patients.

Other compensatory mechanisms to deal with such iron load is increasing ferritin production ( iron store ) which explains the very high ferritin levels observed in those patients.

Therefore the cause of monocytosis is the body needs to excess macrophages to engulf the excess iron load .

And the cause of Lymphopenia is the WBCs differentiation favored twards monocytes line rather than lymphocytes line.

This makes ferritin a bad prognostic marker (too much iron means too much Hb lost its O2 carrying capacity) .

Also this iron load and increased Hb production lead to increased blood viscosity with recurrent and diffuse micro and macro circulatory thrombosis that is why there is high levels of DDimer in those patients and this explains the cause of sudden deterioration and death in some sporadic cases

This disseminated thrombosis is proved by postmortem examinations of ARDS victims ( it is not a real ARDS) .

This theory could explain why we are loosing patients so rapidly and why mechanical ventilation is not so much effective in treatment and using ARDS mechanical ventilation protocol is not causing any benefit. actually it could be futile and causing more lung damage.

On the other hand this is crucially explains the very rapid and good response of those patients to full therapeutic anti coagulation.

Chloroquine as antimalarial drugs is working by protecting Hb against invasion by malaria parasites .It is doing the same here but just protecting the Hb against invasion by the virus.

The chemical components in chloroquine phosphate compete with the porphyrin and bind to the viral protein, thereby inhibiting the viral protein's attack on heme or binding to the porphyrin.

Favipiravir is the latest anti-novel coronavirus drug with specific therapeutic effects.

In Favipiravir, the most critical ligand is 1RP, which is 6 - fluoro - 3 - oxo - 4 - (5 - O - phosphono - beta - D - ribofuranosyl ) - 3, 4 - dihydropyrazine - 2 - carboxamide.

Favipiravir cannot be bind to E2 glycoprotein and Nucleocapsid, and its binding energy to viral envelope protein, ORF7a, orf1ab is higher than that to porphyrin.

It is useful to note that the binding energy of Envelope protein and Favipiravir is more than 2700 times the binding energy of porphyrin.

The primary function of Envelope protein is to help the virus enter host cells, which shows that Favipiravir can effectively prevent the virus from infecting human cells.

* Recommendations :-
According to these clinical observations ,correlations and understandings :-

1- Hydroxychloquine , Favipiravir and early full anti coagulation therapy should be involved as early as possible in our National Management Protocol of Covid-19 .

* References :-
-Data is collected and interpritated from different clinical observations and reviews of many doctors and intensivists and from the postmortem examination pictures of Covid-19 victims in USA and Europe.

-Wenzhong Liu and Hualan Li2 (2020):
COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism; School of Computer Science and Engineering, Sichuan University of Science & Engineering, Zigong, 643002, China;
School of Life Science and Food Engineering, Yibin University, Yibin,644000, China; Correspondence: [email protected];

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 15th 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 and recent information from Italy. 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 “typical ARDS”… this disease must be treated differently and it is likely that mechanical ventilation may be exacerbating this situation by causing ventilator induced lung injury (i.e. the ventilator may cause the disease we think we are treating). Patients suffer from oxygenation failure and not lung failure. Furthermore, this is predominantly an immune and clotting disorder and not a lung disease.
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.
EVMS COVID website: https://www.evms.edu/covid-19/medical_information_resources/ Short url: evms.edu/covidcare

“If what you are doing ain’t working, change what you are doing”

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.”

The course of COVID-19 and General Approach to treatment is illustrated below.


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. While there is no high level evidence that this cocktail is effective; it is cheap, safe and widely available.
• Vitamin C 500 mg BID and Quercetin 250-500 mg BID
• Zinc 75-100 mg/day (acetate, gluconate or picolinate). Zinc lozenges are preferred. After 1-2 months, reduce the dose to 30-50 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).

Mildly Symptomatic patients (at home):
• Vitamin C 500mg BID and Quercetin 250-500 mg BID (if available)
• Zinc 75-100 mg/day
• Melatonin 6-12 mg at night (the optimal dose is unknown)
• Vitamin D3 1000-4000 u/day
• Optional: Hydroxychloroquine 400mg BID day 1 followed by 200mg BID for 4 days

Mildly Symptomatic patients (on floor):
• Vitamin C 500mg BID and Quercetin 250-500 mg BID (if available)
• Zinc 75-100 mg/day
• Melatonin 6-12 mg at night (the optimal dose is unknown)
• Vitamin D3 1000-4000 u/day
• Methylprednisolone 40 mg daily
• Enoxaparin 40-60 mg daily
• Optional: Hydroxychloroquine 400mg BID day 1 followed by 200mg BID for 4 days
• N/C 2L /min if required (max 4 L/min; consider early t/f to ICU for escalation of care).
• Avoid Nebulization and Respiratory treatments. Use “Spinhaler” or MDI and spacer if required.
• Avoid non-invasive ventilation
• T/f EARLY to the ICU for increasing respiratory signs/symptoms.


Respiratory symptoms (SOB; hypoxia- requiring N/C ≥ 4 L min: admit to ICU):
Essential Treatment (dampening the STORM)
1. Methylprednisolone 80 mg loading dose then 40mg q 12 hourly for at least 7 days and until transferred out of ICU. Alterative approach: Hydrocortisone 50 mg q 6 hourly.
2. Ascorbic acid (Vitamin C) 3g IV q 6 hourly for at least 7 days and/or until transferred out of ICU. Note caution with POC glucose testing (see below).
3. Full anticoagulation: 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). Heparin is suggested with CrCl < 15 ml/min. Alternative approach: Half-dose rTPA: 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. On transfer to floor, consider reducing enoxaparin to 40-60 mg /day.

Note: Early termination of ascorbic acid and corticosteroids will likely result in a rebound effect (see graphic below).

Additional Treatment Components (the Full Monty)

4. Melatonin 6-12 mg at night (the optimal dose is unknown).
5. 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).
6. Optional: 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).
7. 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
8. 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).
9. Maintain EUVOLEMIA (this is not non-cardiogenic pulmonary edema). Due to the prolonged “symptomatic phase” with flu-like symptoms (6-8 days) patients may be volume depleted. Cautious rehydration with 500 ml boluses of Lactate Ringers may be warranted, ideally guided by non- invasive hemodynamic monitoring. Diuretics should be avoided unless the patient has obvious intravascular volume overload.
10. Early norepinephrine for hypotension. While the angiotenin II agonist Giapreza ™ has a limited role in septic shock, this drug may uniquely be beneficial in patients with COVID-19 (downregulates ACE-2).


11. Escalation of respiratory support (steps); Try to avoid intubation if at all possible
• Accept “permissive hypoxemia” (keep O2 Saturation > 84%)
• 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; see Figure)
• 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
• ?? 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 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 group of patients with COVID-19 deteriorates very rapidly (see graphic below). Intubation and mechanical ventilation may be required in these patients.

12. Treatment of secondary HLH (increasing Ferritin, CRP and transaminases)

• “High dose corticosteroids.” Methylprednisolone 120 mg q 8 hourly for at least 3 days, then wean accruing to CRP, IL-6, Ferritin etc.
• Tocilizumab (IL-6 inhibitor) as per dosing guideline.
• Consider plasma exchange

13. 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. 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.


14. Post ICU management
a. Enoxaparin 40-60 mg s/c daily
b. Methylprednisone 40 mg day, the wean slowly
c. Vitamin C 500 mg PO BID
d. Melatonin 3-6 mg at night





A few General thoughts:

1. Severe COVID-19 disease results in a dysregulated immune response with aberrant CD4+ T cell activation. Patients have significantly elevated levels of IL-6, IL-10 and TNFα. Downregulating the cytokine storm is an essential component of the treatment of severe COVID-19 disease.
2. COVID-19 patients developed a severe hypercoagulable state (see Figures). This likely results in pulmonary micro- and macrovascular disease which may lead to hypoxia/pulmonary shunting. These patients have a markedly increased risk of pulmonary and cerebral emboli (see Figure).
3. This is not your “typical” ARDS… but something else. Chest CT shows bilateral, discreet, irregular, multilobar “ground-glass” infiltrates and not the typical dependent air-space consolidation (“sponge lung/baby lung”) characteristic of “typical” ARDS. Physiologically “COVID-19 ARDS” is different; our 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 disease and pulmonary vasoplegic resulting in marked V/Q mismatching (shunt). In addition, pulmonary embolism appears to be very common in these patients and may be the cause of sudden death (see Figure). The typical ARDS that develops over time (see Figures) is due mechanical ventilator induced lung injury and/or superadded bacterial pneumonia.
4. It is important to stress that there is no known drug/treatment that has been proven unequivocally 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.
5. Randomized controlled rials are not the answer to this catastrophic pandemic. It will likely take many months before these studies are completed and the results are available; many tens of thousands of patients will die from COVID-19 related complications in the intervening time. Furthermore, treating patients with placebo wold appear to be ethically unsound.
6. Good medical practice and the best interests of the patient require that physicians use legally available drugs according to their best knowledge and judgement. If physicians use a product for an indication not currently approved, they have the responsibility to be well informed about the product, to base its use on firm scientific rationale and on sound medical evidence, and to maintain records of the product's use and effects.
7. Zinc (Zn++) inhibits viral RNA dependent RNA polymerase (replicase).
8. Chloroquine and hydroxychloroquine have broad antiviral properties. In addition, these drugs are potent Zn ionophores and have favorable immunomodulating properties including inhibition of PAI-1 expression. These drugs may have a role in the EARLY viral replicative phase.
9. 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.
10. 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.

11. 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.
12. 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.


Premature discontinuation of Corticosteroids and Vitamin C (after 4 days), and the effect of reinitiation of this Vital Combination on CRP. Clinical course followed CRP profile.


Secondary HLH Rx with Vitamin C 3g IV q 6 and increased methylprednisolone (125 mg q 8 hourly)

CRP

AST




CT scan of Typical COVID-19 Patient


CTPA of 44 yr. old COVID + patient (with no risk factor for DVT/PE) presenting with severe tachycardia


“Cooperative” proning-repositioning of non-intubated patient


Thromboelastogram (TEG) of COVID-19 patient on admission to ICU Demonstrating marked hypercoagulable state

Medical Information/COVID Care Protocol - Eastern Virginia Medical School (EVMS), Norfolk, Hampton Roads The EVMS Medical Group is providing guidance for healthcare providers treating COVID-19 patients. This approach to COVID-19 is based on the best (and most recent) available literature and the Shanghai Management Guideline for COVID.

Covid 19 best protocol till date!

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Covid Mx protocol!

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Medical Information/COVID Care Protocol - Eastern Virginia Medical School (EVMS), Norfolk, Hampton Roads The EVMS Medical Group is providing guidance for healthcare providers treating COVID-19 patients. This approach to COVID-19 is based on the best (and most recent) available literature and the Shanghai Management Guideline for COVID.

Mechanical Ventilation Clearly explained ! Covid ICU management by PK Vines

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Mechanical Ventilation Clearly explained ! Covid ICU management by Mechanical Ventilation Clearly explained | Covid ICU management by PK Vines Welcome to my PKVines channel In this video you ...

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