About this Course
During these challenging times, we’ve been working closely with our partners to develop new courses that share vital information about COVID-19 with learners from around the world. Most recently, Stanford University published COVID-19 Training for Healthcare Workers, a course offering a unified, evidence-based approach to addressing the novel coronavirus that will be free to learners through July 28, 2021.
COVID-19 is rapidly spreading across the globe and all providers must be prepared to recognize, stabilize, and treat patients with novel coronavirus infection. Following the completion of this short course physicians, nurses, and other healthcare professionals will have a unified, evidenced-based approach to saving the lives of patients with COVID-19, including those who are critically ill.
Learning modules are broken into short videos presented in a richly illustrated and compelling manner. The course is self-paced and providers can schedule their learning to fit with their schedules. Topics include symptoms and signs in patients with COVID-19, early stabilization of patients, preventing the need for intubation, and ventilator management. The best evidence and guidelines are summarized while accompanying handouts provide written learning points and links to online resources. Simple infographics are available for providers to utilize within their care facilities to educate and promote optimal care across their entire institution.
To learn more about our other programs and find additional resources, please visit Stanford Emergency Medicine International (https://emed.stanford.edu/specialized-programs/international.html), The Stanford Center for Health Education (https://healtheducation.stanford.edu/), and our Digital Medic Initiative (https://digitalmedic.stanford.edu/our-work/covid-19-resources
Special Promotion: Enroll for Free!
This course includes a certificate and the fee is waived.
Discount applied at checkout. One-time use only. Offer valid until 7/28/2021, while supplies last.
S V Mahadevan
Dr. S.V. Mahadevan is a Professor of Emergency Medicine at Stanford University School of Medicine. He was the ED Medical Director and Associate Chief from 2000-2012 and served as the founding department chair in emergency medicine from 2015-2017. Dr. Mahadevan currently serves as Director of Global Affairs and Strategy for Stanford Medicine and Stanford Health Care, and the Director of South Asia Outreach, Center for Asian Health Research and Education (CARE). He has written, traveled, and taught widely, presenting over 500 invited lectures worldwide and authoring over 150 journal articles, book chapters, and multimedia publications. He is the lead editor of the textbook, An Introduction to Clinical Emergency Medicine, which was awarded the 2006 American Medical Writer’s Association Award: Physician’s Category as the top medical textbook in the United States for all specialties. Dr. Mahadevan founded Stanford Emergency Medicine International (SEMI) in 2000, and has been instrumental in setting up India’s first international paramedic training institute, Nepal’s first EMS system, India’s first guidelines for prehospital care, Cambodia’s first emergency medicine strengthening program and Myanmar’s first emergency medicine training program.
Dr. Strehlow is a Clinical Associate Professor of Emergency Medicine/Surgery at the Stanford University School of Medicine and Director of the Clinical Decision Unit. He is actively involved in the development of Emergency Medicine internationally and co-directs the Stanford Emergency Medicine International (SEMI) program and fellowship. Dr. Strehlow has been actively involved in the development of emergency medicine and emergency medical services across the globe including in countries such as India, Nepal, and Cambodia. He has received multiple teaching awards including the American College of Emergency Physicians (ACEP) Rising Star Speaking Award and the Stanford University Emergency Medicine Teaching Award.
COVID Autopsy Findings – What Doctors Are Learning From Autopsy Findings of COVID Patients
Are You Protected from DELTA Variant? (DEPENDS on THIS)
Are You Protected from DELTA Variant? (DEPENDS on THIS) There are lots of factors that determine your level of protection from Delta Variant. Are you vaccinated? If so, which one? Have you had COVID already? Did you have COVID and the vaccine? Are you immunocompromised? Will the booster shot give you more protection? Since the Delta COVID Variant is still fairly new, there are still many questions.
OVID Autopsy Findings – What Doctors Are Learning From Autopsy Findings of COVID Patients
Once the COVID is deeply embedded in the body, it begins to cause more severe disease. This is where the direct attack on other organs with ACE2 receptors can occur, including heart muscle, kidneys, blood vessels, liver, and the brain. Early findings, including those from multiple covid autopsies and biopsy reports, show that viral particles can only be found in the nasal passages and throat and 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 covid patients had meningitis.
So the covid is sometimes going to all these different organs by attaching to the ACE2 receptors there, but that’s not even the whole story.
⏩ Timestamps, click to skip ahead – COVID Autopsy Findings
00:00 – Common Symptoms of COVID
01:40 – What we know about COVID
02:25 – Early findings of Multiple Autopsy and Biopsy Reports of COVID
03:02 – Microscope Picture of the COVID and Kidney Cells
03:20 – COVID Autopsy Findings
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Because in some COVID 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 many 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 covid invades the capillaries. It means that it serves as the trigger for the onslaught of inflammation AND clotting. Early covid autopsy results are also showing widely scattered clots in multiple organs. In one study from the Netherlands, 1/3rd hospitalized with COVID got clots despite 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 through blood clots – Yes!
4) Indirectly cause damage due to 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, 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. For example, blood clots travel to the toes and cause blockages in blood flow, meaning ischemia or infarction can cause gangrene. 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 covid patients with APS have catastrophic APS, where these patients can have strokes, seizures, heart attacks, kidney failure, ARDS, skin changes like the ones I mentioned. In addition, viral infectious diseases, particularly those of the respiratory tract, have been reported as CAPS 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 cholesterol levels, smoking, diabetes, age, chemotherapy, and infection degree. All of these contribute toward developing arterial thrombosis.
Many patients with severe COVID have labs resembling DIC, such as increased PT/INR, increased PTT, and decreased platelet levels. But the reason these COVID patients who developed clots in the study I mentioned earlier, the reason they don’t have DIC is actually 2 reasons, one, they didn’t have extensive bleeding. Two, they did not have low fibrinogen levels. And if it’s truly DIC, you would have both of those things.
Doctor Mike Hansen, MD
Internal Medicine | Pulmonary Disease | Critical Care Medicine
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