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ICU Doctor: Top 10 Things I learned Treating Coronavirus Patients | Coronavirus Intensive Care

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ICU Doctor: Top 10 Things I learned Treating Coronavirus Patients | Coronavirus Intensive Care

ICU Doctor: Top 10 Things I learned Treating Coronavirus Patients | Coronavirus Intensive Care
#coronavirus #covid19 #covid_19

Coronavirus | COVID-19 YouTube Video Playlist:


Some intensive care units in various hospitals throughout this county have designated units for COVID-19 patients. As an intensive care doctor, I’ve been seeing a lot of COVID-19 patients in our designated Coronavirus ICU. It's one thing to read about Coronavirus in the medical literature, but to be actually seeing real patients with this disease is another experience altogether. There are a lot of things I’ve learned, but for this video, I’ll focus on the top 10 that stand out to me.

So, starting at the bottom with number 10, is, signs/symptoms. The most common symptoms that I’m seeing are fever, cough, shortness of breaths, and body/muscle aches. I haven’t seen many patients with the other symptoms we often hear about, such as loss of taste and smell, or nausea, and diarrhea. I have not seen any rashes related to Coronavirus, probably because I only see adult patients. I will say that even though confusion and delirium are very common in the ICU in general, there does seem to be more of that with Coronavirus.

A lot of COVID-19 patients who require hospitalization have low levels of vitamin D. And this is consistent with what we are seeing in a lot of recent studies that have been coming out. But of course, correlation doesn’t necessarily mean causation, so does it just so happen that a lot of patients who have moderate or severe COVID, happen to have low vitamin D levels? Maybe, maybe not. And does that mean that we should give every hospitalized patient with Coronavirus big doses of vitamin D when they hit the door? Maybe. And does that mean people, in general, should supplement with vitamin D? And what is the ideal level of vitamin D for the population, especially when it comes to COVID-19? Should we be targeting the current general recommendation for everyone, irrespective of COVID-19, with a goal of 20 ng/ml? or should we aim for higher, like 30, or perhaps 40? No one knows for sure the answers to these questions. But there are studies being done on this. And as we speak there are 3 RCT for vitamin D and Coronavirus.

This virus is VERY contagious. One of my patients was in the hospital for unrelated reasons. She actually had sepsis due to infarcted gut, meaning part of her intestine was not getting enough blood flow. It was severe enough to the point that some of the tissue in her intestine had died. When this happens, the bacteria that live in the intestine can then invade the walls of the intestine, and get into the bloodstream. This is bad news because these bacteria can then spread throughout the body, and this is known as sepsis. Besides antibiotics, this treated with surgery, where the dead gut tissue is removed, meaning part of the intestine is taken out. And this is what happened to her. And she got better. But after she initially got better, she started having more difficulty with her breathing. Her oxygen levels were dropping, despite us giving her more and more oxygen. So we got a CXR, and later a CT scan of the chest, which showed bilateral infiltrates, meaning areas of inflammation in both lungs. And this is the pattern we typically see with COVID-19 pneumonia, where it tends to go to the periphery of the lungs and also more so at the bottom of the lungs.

Vitamin D3 (Cholecalciferol) and Vitamin D2 (Ergocalciferol) and Calcitriol
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Does Vitamin D help with Immunity?
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Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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#coronavirus #covid19 #covid_19
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How to Treat Coronavirus Patients in the ICU (Intensive Care Unit) | Covid-19

How to Treat Coronavirus Patients in the ICU (Intensive Care Unit) | Covid-19

Coronavirus | COVID-19 YouTube Video Playlist:

#coronavirus #covid19 #covid_19

Coronavirus (COVID-19) has brought unprecedented challenges regarding the ability to generate timely evidence, all while this pandemic overwhelms hospitals and health care workers.

About 5% of patients with coronavirus require admission to the intensive care unit and mechanical ventilation.

Based on the recent epidemiological models, Coronavirus is going to hit all the areas in the USA.

Every ICU is preparing for the surge, there are a number of changes that intensive care units are making, including ours.

We are preparing anesthesiologists (who are not CCM trained) and nurse anesthetists, to help us manage patients with COVID-19. Even though they are not CCM trained, we have a lot of overlap of knowledge, especially when it comes to managing ventilators, and we have a lot of overlap with certain procedures.

By allowing anesthesiologists and nurse anesthetists to help in this manner, it will help other intensivists like myself handle the surge of patients coming our way.

And because they are helping us, that is the main reason for me making this video, so that they can watch this and be better equipped to handle the surge with us.

“Knowing, and implementing all of the info in this video does not guarantee you save a COVID-19 patient living in the ICU, but, it will give you the best chance of doing so”

If a patient with COVID-19 is coming to your ICU, they most certainly have pneumonia, and they probably have acute respiratory distress syndrome (ARDS) as well.

Patients with severe disease who require ICU admission are likely to have high oxygen requirements.
Although both High flow oxygen and noninvasive positive pressure ventilation have been used for COVID-19, the safety of these is uncertain, and they are considered aerosol-generating procedures that warrant specific isolation precautions.

Most patients who require ICU admission have ARDS, and they will likely have a better outcome if intubated sooner rather than later. That is another reason why it likely better to skip Hi-Flow oxygen and NIPPV and jump straight to intubation.

Acute Respiratory Distress Syndrome (ARDS)
ARDS is a clinical diagnosis, based on non-cardiogenic pulmonary edema, with bilateral patchy infiltrates on chest imaging and a PaO2/FiO2 ratio of less than 300.

In ARDS, there is this crazy, chaotic inflammatory response within the lungs, with damage to the alveoli and surrounding capillaries, which leads to excess protein and fluid accumulation in interstitial and alveolar spaces.

That means decreased lung compliance, increased V̇/Q̇ mismatch, and increases in shunt and dead-space ventilation.

Patients with ARDS are at high risk of mortality, which increases with ARDS severity. With that said, mortality is usually the result of the underlying disease that triggered ARDS, rather than refractory hypoxemia.

The severity of ARDS is important because it’s going to determine how we manage patients with ARDS.

With ARDS, the alveoli fill up with protein and fluid. This leads to at least partial alveolar collapse, and decreased lung compliance, with shunt physiology.

Increasing the PEEP minimizes the repeated opening and closing of distal airways and alveoli. It also improves the homogeneity of the lung parenchyma by reducing drastic differences in regional lung compliance.

What is the ideal level of PEEP?
No one knows for sure. Typically for ARDS, we set the initial PEEP between 10 to 15. Sometimes all the way to 20 if they have severe disease. You don’t want to go too high though, because this increases the risk of pneumothorax.
The recommendation is to give COVID-19 patients steroids only if they have ARDS.

Critically ill patients with coronavirus often develop septic shock. And for shock, we give IVF and vasopressors. But ARDS patients generally do better when you keep them in a negative fluid balance state.

COVID-19 patient, who is in shock and ARDS, what should you do?
Based on my experience of treating ARDS patients who are in shock, my recommendation would be to use minimal fluid possible and to start vasopressors early. In my experience, patients tend to respond better to albumin than crystalloids, especially if they have low albumin levels. Either way, you’re going to want to assess fluid resuscitation responsiveness, and if they don’t respond well to fluids, just stick with the vasopressors.

Note: To get the proper details please watch the video from first to last without skipping.

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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Critical care doctor explains what coronavirus intensive care is really like | Covid-19 UK

Critical care consultant in the Royal Gwent Hospital, Dr David Hepburn, explains what intensive care is really like for coronavirus patients - and says 'it could be any of us'. (Subscribe:

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ICU doctor on Trump's COVID-19 diagnosis

President Trump and first lady Melania Trump have tested positive for COVID-19. Dr. Thomas Yadegar, a pulmonologist and medical director of the intensive care unit at Providence Cedars-Sinai Tarzana Medical Center, joins CBSN Los Angeles to discuss about the medical symptoms Mr. Trump could face with COVID-19.
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What happens when you’re in the ICU with COVID-19

A look at how sick someone has to be to be taken to the ICU, what the treatment might be and what recovery could look like.

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ICU Doctor With COVID-19 Discharged After Returning as Patient to the Unit He Trained In

He’s used to treating critically ill patients. But when he became infected with COVID-19, one critical care doctor found himself as a patient in an ICU.

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Coronavirus intensive care: inside a London hospital as doctors fight to save lives - BBC News

BBC News has been given rare access to a leading London hospital's Intensive Care ward as medical staff treat seriously ill coronavirus patients.

University College Hospital has one of the UK’s biggest intensive care facilities.

The latest official figures say that 439 people in the UK have died in hospital from the effects of Coronavirus up to 5pm on Sunday.

It brings the total number of deaths in hospital from the disease to 5,373. These figures do not account for people who have died in the community or in a care home.

This special report is by our medical correspondent Fergus Walsh and cameraman Adam Walker.

Produced for the BBC News at Six and presented by Huw Edwards.

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Overview of Critical Care Management of COVID Patients in the ICU by Dr. Bassily-Marcus, MD

Overview of Critical Care Management of COVID Patients in the ICU by Dr. Bassily-Marcus, MD

Coronavirus (COVID-19) Update: Critical Care Management

Noninvasive ventilation (NIV) , working with dying patients’ families, use of experimental therapies, and more. Derek Angus MD, MPH, FRCP, Distinguished Professor and Chair of Critical Care Medicine at the University of Pittsburgh, provides a COVID-19 ICU management update. Originally broadcast on Wednesday, April 1, 2020 at 13:00 CST (GMT-05:00).

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Topics discussed in this interview:
0:00 Introduction

2:00 Say you have 100 patients come into the hospital with COVID-19. It looks like about a third end up in the intensive care unit. How do they do once they're in the intensive care unit?

7:00 There's been some tension about early intubation versus waiting. Do you want to comment on that or just not enough information?

8:16 There are reports of people who are developing acute respiratory distress syndrome (ARDS) and deteriorating very quickly. Do you have a sense of that in your ICU?

9:56 There's been some reports that for the people who get intubated they appear to stay on mechanical ventilation for a longer period of time than people's other experience with ARDS but again, this is observational information.

12:52 Case-fatality once you're intubated is high. From looking at the various reports, talking to your colleagues, do you have a sense of what it is?

15:05 As someone who runs a lot of ICUs, what's your greatest fear?

17:48 What's your sense of the clinical trials? Where will they be successful? Should they be tried in very sick people or is the goal to try some of them in less sick people to prevent those people from needing the intensive care unit?

22:27 Do you have a sense - is it going to be the antivirals, is it going to be this so-called cytokine storm that we can intervene with, will it be chloroquine? Do your instincts tell you that there is going to be a big gain with one of these new therapies?

26:45 Do you understand the exuberance around chloroquine?

29:00 Are there any clinical trials focused on preventing mildly ill patients from needing ICU care or have most of them been focused on the more ill patients?

32:10 Visitation is remarkably limited and their loved ones are dying and are going to die. Either they're on a ventilator or they've been appropriately extubated to spend their last few hours in comfort. How do you imagine that playing out in the US?

38:39 How soon do you think we'll get results from the randomized trials?

40:58 What is the primary outcome in most of the trials?

41:52 Would you use one ventilator for two patients if ventilators are scarce?

42:45 What do you think the 900,000 physicians who aren't intensivists need to know?

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Inside an ICU during coronavirus: how doctors and nurses are coping as they battle to save patients

Hospitals are still crowded with the desperately ill. People are dying in their hundreds every day. We are nearing the peak of the crisis, say scientists - but how long that peak will last, no one can say. (Subscribe:

It's left to intensive care wards to carry on the battle to keep the worst affected people alive. Like Epsom and St Helier hospital - which was hit early on with a wave of patients. Our health and social care correspondent Victoria Macdonald has spent the day there with intensive care staff - and has spoken to doctors and nurses about how they've been managing to cope.

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Italian doctor on treating COVID-19 patients

Infectious disease specialist Dr. Giovanni Guaraldi discusses lessons being learned by Italian doctors about the new virus – with advice for Canadian physicians.

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What Doctors Are Learning From Autopsy Findings of New CORONAVIRUS Patients

What Doctors Are Learning From Autopsy Findings of New CORONAVIRUS Patients

⏩ Timestamps, click to skip ahead!
00:00 - Common Systoms of COVID
01:40 - What we know about COVID
02:25 - Early findings of Multiple Cutopsy and Biopsy Reports of COVID
03:02 - Microscope Picture of the Coronavirus and Kidney Cells
03:20 - COVID Autopsy Findings

Once the SARS-CoV-2 virus is deeply embedded in the body, it begins to cause more severe disease. This is where the direct attack on other organs that have ACE2 receptors can occur, including heart muscle, kidneys, blood vessels, liver, and the brain. Early findings, including those from multiple autopsies and biopsy reports, show that viral particles can be found not only in the nasal passages and throat, but also in tears, stool, kidneys, liver, pancreas, and heart. One case report found evidence of viral particles in the CSF, meaning the fluid around the brain. That patient had meningitis.

So the coronavirus is sometimes going to all these different organs by means of attaching to the ACE2 receptors that are there, but that’s not even the whole story.

Because in some COVID-19 cases, by the time the body’s immune system figures out the body are being invaded, it's like unleashing the military to stomp out the virus, and in that process, there’s a ton of collateral damage. This is what we refer to as the cytokine storm. When the COVID gets into the alveolar cells, meaning the tiny little air sacs within the lungs, it makes a ton of copies of itself and goes onto invading more cells. The alveoli’s next-door neighbor is guessed who, yeah, the tiniest blood vessels in our body, capillaries. And the lining of those capillaries is called the endothelium, which also has ACE2 receptors. And once the coronavirus invades the capillaries. It means that it serves as the trigger for the onslaught of inflammation AND clotting. Early autopsy results are also showing widely scattered clots in multiple organs. In one study from the Netherlands, 1/3rd of hospitalized with COVID 19 got clots despite already being on prophylactic doses of blood thinners. So not only are you getting the inflammation with the cytokine storm, but you’re also forming blood clots, that can travel to other parts of the body, and cause major blockages, effectively damaging those organs.

So it can cause organ damage by
1) Directly attacking organs by their ACE2 receptor - Yes!
2) Indirectly attacking organs by way of collateral damage from the cytokine storm - Yes!
3) Indirectly cause damage to organs by means of blood clots - Yes!
4) Indirectly cause damage as a result of low oxygen levels, improper ventilator settings, drug treatments themselves, and/or all of these things combined - Yes!

Endothelial cells are more vulnerable to dying in people with preexisting endothelial dysfunction, which is more often associated with being a male, being a smoker, having high blood pressure, diabetes, and obesity. Blood clots can form and/or travel to other parts of the body. When blood clots travel to the toes, and cause blockages in blood flow there, meaning ischemia or infarction, that can cause gangrene there. And lots of times patients with gangrene require amputation, and “COVID toes”

So is antiphospholipid antibody syndrome, the cause of all these blood clots in patients with severe COVID? Maybe. Some patients with APS have what’s called catastrophic APS, where these patients can have strokes, seizures, heart attacks, kidney failure, ARDS, skin changes like the ones I mentioned. Viral infectious diseases, particularly those of the respiratory tract, have been reported as being the triggers for CAPS.

Various factors increase the risk of developing arterial thrombosis. Classically, the cardiovascular-dependent risk factors implicated in clotting have been hypertension, meaning high blood pressure, high levels of cholesterol, smoking, diabetes, age, chemotherapy, and degree of infection. All of these contribute toward developing arterial thrombosis.

A lot of patients with severe COVID 19 have certain labs that resemble DIC, such as increased PT/INR, increased PTT, decreased levels of platelets. But the reason why these Coronavirus patients who developed clots in the study I mentioned earlier, the reason why they don’t have DIC, is actually 2 reasons, one, they weren’t having extensive bleeding, and two, they did not have low fibrinogen levels. And if its truly DIC, you would have both of those things.

Anyway, you can probably glean from this video why it's so hard for doctors to figure out what is going on with this virus. Between the variable ways this disease can present in different patients, and the different ways that organs can suffer damage, yeah, this is really, really really, complicated.

Are BLOOD CLOTS the reason why COVID-19 patients are dying?
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Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine

113 - The Recovery Process of ICU COVID-19 Patients

Patients who have spent time in the ICU because of COVID-19 face a long recovery. Comprehensive rehabilitation that starts early and continues after release can make all the difference in getting patients back to day-to-day activities. Johns Hopkins physiatrist Dr. April Pruski talks with Stephanie Desmon about the team of physical, occupational, and speech therapists, psychologists and more performing early interventions with COVID-19 patients and what recovery looks like after the ICU.

Critical Care Management of COVID-19 Patients (Faisal N. Masud, MD) April 16, 2020

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April 16, 2020
HMDHVC GRAND ROUNDS CONFERENCE

Critical Care Management of COVID-19 Patients: What Non-Intensivist Need to Know

Houston Methodist DeBakey Heart & Vascular Center, Grand Rounds Conference featuring Faisal N. Masud, MD, Deepa Gotur, MD, Daniela M. Moran, MD, Divina M. Tuazon, MD, and Steven H. Hsu, MD, as they discuss “Critical Care Management of COVID-19 Patients: What Non-Intensivist Need to Know.

INTRODUCTION: Dipan J. Shah, MD

MODERATOR: Faisal N. Masud, MD, FCCP, FCCM
Medical Director, Center for Critical Care, Houston Methodist Hospital
Vice Chair for Quality and Patient Safety, Professor of Clinical Anesthesiology
Medical Director, CVICU, Houston Methodist DeBakey Heart & Vascular Center

PANELIST: Steven H. Hsu, MD
Daniela M. Moran, MD
Deepa Gotur, MD
Divina M. Tuazon, MD
_________________________________
Presented by Houston Methodist DeBakey Heart & Vascular Center.

A DeBakey CV Education event

Building on Dr. Michael E. DeBakey’s commitment to excellence in education, Houston Methodist DeBakey CV Education is an epicenter for cardiovascular academic and clinical educational programs that support the provision of optimal care to patients suffering from cardiovascular conditions and diseases.

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This Doctor's DIY Home ICU Tips May Help Save Covid Patients

This cardiologist from Sunshine Hospital, Gachibowli is demonstrating how you can set up an 'ICU' at home for Covid-19 patients.
#Covid19India #Doctor

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Inside UCHealth's COVID-19 ICU

UCHealth gave Denver7 a look inside its COVID-19 intensive care unit.

Homemade ICU for COVID-19 Patients | Dr. Sanjeev Kumar | Sunshine Hospitals

Dr. Sanjeev Kumar, DM Cardiology at Sunshine Hospitals, speaks about how you can create an ICU at home for family members with symptoms. Do tune in!

#covid19 #covid_19 #icu #quarantine #covidathome #stayhome #covidpatient #covid #coronavirus #treatment

Coronavirus Autopsy Report Analysis by Dr. Mike | COVID-19 Autopsy

Coronavirus Autopsy Report Analysis by Dr. Mike | COVID-19 Autopsy
#coronavirus #covid19 #covid_19

⏩ Timestamps, click to skip ahead!
00:00 - Introduction
01:00 - Current Positive COVID Cases Details
02:05 - New Studies of COVID and Autopsy Report Analysis of a COVID Patient

Coronavirus | COVID-19 YouTube Video Playlist:


Coronavirus is the virus responsible for the COVID-19 outbreak. Wuhan, China has been the epicenter of this epidemic, but some experts, like Dr. Anthony Fauci, are now saying that we are on the verge of a pandemic.

Before I get to the Coronavirus autopsy report of a patient with COVID-19, its important to understand the context of the numbers of total people infected, total people with coronavirus pneumonia, number of people who developed ARDS, and the total number of deaths.

When looking at the numbers, we should realize that they are almost certainly being underreported in China, and there are multiple reasons for that, which I won't get into right now.

Although these are not concrete numbers, its what we have to go by at this point. The percentage of people.

Also, up to this point, there has not been any pathology reported on this disease because of limited access to autopsy and biopsy reports.

But finally, we now have a new case report study in Lancet Respir Med, published Feb 17, that has autopsy reports for a patient who died from COVID-19.

Pathological findings of COVID-19 associated with acute respiratory distress syndrome.

A patient is a 50-year-old man from China, who visited Wuhan Jan 8–12. On Jan 14, he developed a dry cough and some mild chills, so this is day 1 of the illness. However, he did not initially seek medical attention and kept working until Jan 21. He then went to a medical clinic on Jan 21, because by that time, he had developed worsening symptoms. He had fever, chills, fatigue, cough, and shortness of breath.
On Jan 22 (day 9 of illness), the Beijing Centers for Disease Control (CDC) confirmed by reverse real-time PCR assay that the patient had COVID-19.

He was immediately admitted to the isolation ward and received supplemental oxygen through a face mask.

He was given several different medications, which included the inhaled version of interferon alfa-2b, lopinavir plus ritonavir as antiviral therapy, and Moxifloxacin, to prevent secondary bacterial infection.

He was also given a steroid, methylprednisolone, to attenuate lung inflammation.

On day 12 of illness, after the initial presentation, his symptoms did not improve, other than his fever, which he received medication for.

His chest x-ray on day 12 showed progressive bilateral infiltrates. He repeatedly refused ventilator support in the intensive care unit repeatedly, apparently because he suffered from claustrophobia.

His oxygen saturation values decreased to 60%, and the patient had a cardiac arrest. At that point he was intubated with mechanical ventilation, he had chest compressions and epinephrine.

Unfortunately, they are unable to revive him.

An autopsy is done, and biopsy samples were taken from the lung, liver, and heart.

The heart tissue was essentially normal.

The liver biopsy of this patient showed moderate microvascular steatosis and
mild lobular and portal activity, indicating the injury could have been caused by either Coronavirus infection or as a result drug-induced liver injury.

Histological examination of lung tissue showed diffuse alveolar damage with cellular fibromyxoid exudates, along with the desquamation of pneumocytes and hyaline membrane formation.

These findings are consistent with acute respiratory distress syndrome ( ARDS ).

Interstitial mononuclear inflammatory infiltrates, dominated by lymphocytes, was seen in both lungs. There were multinucleated syncytial cells with atypical large alveoli characterized with prominent nucleoli, consistent with viral cytopathic-like changes.

These pathological features of COVID-19 greatly resemble those seen in SARS and Middle Eastern respiratory syndrome (MERS) coronavirus infection.

Acute Respiratory Distress Syndrome ( ARDS )
To watch the video please visit this link:

Dr. Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
Website:

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#coronavirus #covid19 #covid_19

Dexamethasone for Coronavirus (COVID-19) - GOOD NEWS! ???? | Coronavirus Medicine

Dexamethasone for Coronavirus | Coronavirus Medicine

Dexamethasone is being called a “Major Breakthrough” based on a recent RCT in the UK. Dexamethasone (Decadron), is an example of a glucocorticoid. Glucocorticoids are sometimes referred to as corticosteroids. Other examples of glucocorticoids include Hydrocortisone, Methylprednisolone, Prednisolone, Prednisone, Betamethasone, and Triamcinolone. Glucocorticoids are a class of steroid hormones that bind to the glucocorticoid receptor in the body. Cortisol (hydrocortisone) is the glucocorticoid we naturally make in our body. It is essential for life, and it regulates or supports various cardiovascular, metabolic, and homeostatic functions. It also plays a big role in our immune system, especially when it comes to reducing certain aspects of inflammation.

This is why we use them all the time in medicine. We sometimes give these steroids for asthma, COPD, rheumatologic type diseases, and countless more diseases. Sometimes we give steroids for meningitis, and also for some forms of cancer. We give them in the early course of severe ARDS, acute respiratory distress syndrome, whether that ARDS is due to infection such as pneumonia, or vaping lung injury, or whatever the cause.

For severe ARDS, we typically give methylprednisone, at a dose of 1 mg/kg per day. So for most people, that ends being around 80 mg per day. This is the equivalent of 15 mg of dexamethasone for covid 19. The idea here is to suppress the cytokine storm that is taking place, meaning that massive amount of inflammation that causes lung damage and can indirectly cause damage to other organs as well. Our body naturally makes cortisol in our adrenal glands, specifically, in the zona fasciculate of the adrenal cortex. The adrenal gland then secretes cortisol into the bloodstream, and travels to different tissues of the body, and then binds to the glucocorticoid receptor inside cells. It then stimulates the cell to make more anti-inflammatory proteins and reduces the number of pro-inflammatory proteins being made. But giving someone glucocorticoids (steroids) who has an infection is somewhat of a tricky thing because the fear is that if you suppress the body’s immune system, it has the potential to make the infection worse. But sometimes the body’s immune system does more damage than the actual infection. For example, in cases of meningitis that is due to streptococcus or tuberculosis, we give steroids because the medical evidence shows that they have better outcomes when we do so.

Giving someone steroids for viral pneumonia, such as influenza, is more controversial because doing so generally leads to a worse infection. With that said, if the viral pneumonia is so bad to the point of causing severe ARDS, most doctors including myself will give steroids in that situation. This is why the general medical guidelines thus far recommend against giving steroids for COVID pneumonia unless the patient has severe ARDS. We’ve been waiting for RCT to come out for steroids and COVID-19, and here we are now. In March 2020, the RECOVERY (Randomized Evaluation of COVid-19 thERapY) trial was one of that RCT that actually looked at several different potential treatments for COVID-19, which included low-dose dexamethasone (a steroid treatment). This trial was done in the UK and had over 11,500 patients in it.

So this trial has not been peer-reviewed as of the making of this video and has not been published in a journal yet. So everything I know so far is based on what has been released to the general public. In this trial, over 2100 patients were randomized to receive dexamethasone 6 mg once per day for ten days and were compared with over 4300 patients randomized to standard care alone. So 6 mg of dexamethasone is the equivalent of 32 mg of methylprednisolone, so this is about half the dose we would typically use for someone with severe ARDS.

Among the patients who received standard care alone, 28-day mortality was highest in those who required mechanical ventilation (41%), intermediate in those patients who required oxygen only (25%), and lowest among those who did not require any supplementary oxygen (13%). For patients on ventilators, dexamethasone reduced mortality from 41% to 28%. For patients needing supplemental oxygen, it reduced mortality from 25% to 20%. There was no benefit among those patients who did not require supplemental oxygen. In other words, if someone only has mild disease, there is no point in giving dexamethasone. Based on these results, 1 death would be prevented by treatment of around 8 ventilated patients, and around 25 patients requiring oxygen alone. So these preliminary results, are significant but do not mean that dexamethasone is a miracle drug. It's certainly not a cure. But it does seem to help, based on these numbers. And dexamethasone could be of huge benefit in poorer countries with high numbers of Covid-19 patients, because the drug is very cheap & widely available.

Do Ventilators Save Coronavirus (COVID-19) Patient's Lives?

Do Ventilators Save Coronavirus (COVID-19) Patient's Lives?

Ventilators are not a cure, but instead are a form of life support.

Most COVID-19 Patients, who need a breathing tube, meaning mechanical ventilation, do not live. Based on a recent study, only 14% live. To understand why this is, let’s take a look at what intubation and mechanical ventilation really mean, and we also have to understand what COVID-19 does to the lungs.

When we intubate someone, meaning put a breathing tube down into their upper airway, and have that person on a ventilator, meaning mechanical ventilation, there are only 4 main reasons why we do that. So it’s sometimes its one, two, three, or all 4 of these reasons.

1. Indications for Intubation (at least one of following)
a. Hypoxia
b. Hypercapnia
c. Increased WOB
d. Reduced level of consciousness

2. COVID-19 patients who are intubated (mortality rate)
a. COVID-19 patients die because it triggers a chaotic inflammatory response within the lungs
b. ARDS
i. Causes (EVALI, Trauma, Pneumonia, Aspiration, Sepsis, blood transfusions)
ii. Diagnosis
1. Low paO2 to FiO2 ratio
2. Bilateral infiltrates on CXR or CT scan (GGO)

3. Non-cardiogenic
iii. keys to managing ARDS patients
1. LTVV and PEEP
2. What is PEEP?
3. Risk of PEEP
4. Prone positioning
5. Steroids
6. Paralysis
7. Different mechanical ventilation strategies
c. average length of mech ventilation: 17 days
d. the mortality rate for those who required intubation: 86% (based on a study done a few weeks ago in the Lancet)

3. Course for intubated patients
a. Get better, extubate
b. Don’t get better, trach
c. Don’t get better, extubate and die in peace/comfort
d. Get worse and die with a breathing tube in, connected to the ventilator

4. ECMO
a. What is ECMO?
b. 30% risk of bleeding
c. 5% risk of thromboembolism
d. Only 250 centers
e. Not accepting transfers

5. DNI/DNR
a. The patient and/or family decides on wishes
b. DNI
c. DNR
d. CPR for COVID-19 patients?
e. Teams determining code status based on SOFA scores

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