Podcasts about d dimer

covid-19 real benefits mystery ideal helpful unraveling thick haulers initial d long haulers d dimer why should we care

Play Episode Listen Later Jul 14, 2024 13:22

The JournalFeed podcast for the week of July 8-12, 2024.These are summaries from just 2 of the 5 articles we cover every week! For access to more, please visit JournalFeed.org for details about becoming a member.Tuesday Spoon Feed:GRACE-4 is packed with practice-changing recommendations for patients with alcohol withdrawal syndrome (AWS), alcohol use disorder (AUD), and cannabinoid hyperemesis syndrome (CHS).Friday Spoon Feed:A “D-dimer only” pathway in patients with suspected pulmonary embolism (PE) was safely used to determine need for imaging without clinical decision rules, but there are some concerns with this approach.

pe aws aud chs d dimer

December 20th, 2023 Guest: Thomas E. Levy, MD

Healthy by Nature Show

Play Episode Listen Later Dec 20, 2023 59:49

Thomas E. Levy, MD is a Board-certified cardiologist, a bar-certified attorney and the author of several groundbreaking books: Magnesium: Reversing Disease Death by Calcium: Proof of the toxic effects of dairy and calcium supplements. Levy is also one of the world's leading vitamin C experts and wrote Curing the Incurable: Vitamin C, Infectious Diseases, and Toxins, 3rd Edition. During the pandemic, he told us how to prevent and treat covid without the scary and relatively useless drugs being recommended. Read his short article and the FREE e-book, Rapid Virus Recovery. He offered to send you Hidden Epidemic if you email him and ask for it (televymd@yahoo.com). On today's show we discussed several of his new and interesting articles: Root Canals Cause Breast Cancer--Frequently Heart Failure or Therapy Failure? Toxins Cause Cardiomyopathy ( Dr. Levy mentioned that far infrared sauna is a way to reduce the offending heavy metal toxins.) Persistent Spike Protein Syndrome: Rapid Resolution with Ultraviolet Blood Irradiation…Dr. Levy mentioned the D-Dimer test to check on the risk of clotting.

board md levy infectious diseases toxins curing hidden epidemic d dimer e levy thomas e levy rapid virus recovery

Unraveling the D-dimer Mystery: What Long Haulers Should Know

True Health Recovery

Play Episode Listen Later Sep 7, 2023 1:08 Transcription Available

Hey listeners! Ever heard of D-dimer? It's time to dive deep and learn why this is super important for folks dealing with long Covid.www.drhughwegwerth.com/What we're discussing today:What's D-dimer?A simple check to measure fibrin in your bloodstream. It's like getting a sneak peek into what's happening inside your veins!The Latest Research:D-dimer increases were found in 25% of people with long Covid.A high D-dimer indicates more fibrin in the bloodstream, which can make your blood thicker.Why Should We Care?Thick blood can be a breeding ground for diseases.The rise in D-dimer is linked to Covid 19.Real-life Story:We share a snapshot from one of our clients with long Covid.Initial D-dimer level: 1.48 (signaled by a red arrow).Ideal level: Below 0.49 (highlighted by a green arrow on the right).Benefits of the D-dimer Test:A before-and-after look at treatment progress.Helpful in tracking the reduction of long Covid symptoms and understanding lab results.

DrBeen#58 MTHFR Gene Mutation and the Risk of Clotting

FLCCC Alliance

Play Episode Listen Later Jul 6, 2023 21:21

DrBeen#58 MTHFR Gene Mutation and the Risk of Clotting In the United States, 20-40% of whites and hispanics have MTHFR gene mutation (C677T). This mutation leads to reduced function of MTHFR enzyme to 65% of normal. The second most common mutation leads to reduced function of MTHFR enzyme, to 30% of normal. The result of these performance issues is reduced methyl groups' availability for methylation functions. The likelihood of clotting in the cardiovascular system increases because of the endothelial impaired function, clotting factor abnormalities, and increased levels of reactive oxygen species (ROS). DrBeen: Medical Education Onlinehttps://www.drbeen.com/ FLCCC | Front Line COVID-19 Critical Care Alliancehttps://covid19criticalcare.com/ URL list from Tuesday, June 6, 2023 Homocysteine and MTHFR Mutations | Circulationhttps://www.ahajournals.org/doi/10.1161/circulationaha.114.013311 preprints202303.0418.v2.pdffile:///C:/Users/s_mob/Downloads/preprints202303.0418.v2.pdf Folate, MTHFR Gene and Heart Healthhttps://www.gbhealthwatch.com/GND-Cardiovascular-Diseases-MTHFR.php Folate Insufficiency Due to MTHFR Deficiency Is Bypassed by 5-Methyltetrahydrofolate - PMChttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7564482/ Frontiers | Prognostic Genetic Markers for Thrombosis in COVID-19 Patients: A Focused Analysis on D-Dimer, Homocysteine and Thromboembolismhttps://www.frontiersin.org/articles/10.3389/fphar.2020.587451/full Methylenetetrahydrofolate Reductase Deficiency - Medical Genetics Summaries - NCBI Bookshelfhttps://www.ncbi.nlm.nih.gov/books/NBK66131/ Contribution of genotypes in Prothrombin and Factor V Leiden to COVID‐19 and disease severity in patients at high risk for hereditary thrombophilia - Kiraz - 2023 - Journal of Medical Virology - Wiley Online Libraryhttps://onlinelibrary.wiley.com/doi/abs/10.1002/jmv.28457 Do MTHFR polymorphisms make you more susceptible to COVID-19? - MTHFR Support Australiahttps://mthfrsupport.com.au/2021/08/do-mthfr-polymorphisms-make-you-more-susceptible-to-covid-19/ Acute Macular Neuroretinopathy Associated With COVID-19 Infection: Is Double Heterozygous Methylenetetrahydrofolate Reductase (MTHFR) Mutation an Underlying Risk Factor? - PMChttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9968507/ Methylenetetrahydrofolate reductase - Wikipediahttps://en.wikipedia.org/wiki/Methylenetetrahydrofolate_reductase Disclaimer:This video is not intended to provide assessment, diagnosis, treatment, or medical advice; it also does not constitute provision of healthcare services. The content provided in this video is for informational and educational purposes only. Please consult with a physician or healthcare professional regarding any medical or mental health related diagnosis or treatment. No information in this video should ever be considered as a substitute for advice from a healthcare professional.

covid-19 united states risk journal downloads mthfr thrombosis clotting homocysteine c users mthfr gene d dimer prothrombin mthfr gene mutation c677t

D-Dimer (DDI) Lab Values

Lab Values Podcast (Nursing Podcast, normal lab values for nurses for NCLEX®) by NRSNG

Play Episode Listen Later Jun 12, 2023 2:34

Objective: Determine the significance and clinical use of D-Dimer in clinical practice Lab Test Name: D-Dimer- DDI Description: Measurement of D-Dimer evaluates the amount of byproduct produced as part of fibrinolysis D-dimer (DDI) is a product of fibrinolysis D-dimer levels are elevated in the setting of clot breakdown, and will be significantly elevated in the setting of Disseminated Intravascular Coagulation (DIC). Indications: Identify and monitor Disseminated Intravascular Coagulation (DIC) Rule out a blood clot: Pulmonary Embolism (PE) Deep Vein Thrombosis (DVT) Stroke Normal Therapeutic Values: Normal – ≤ 250 ng/mL Collection: Light blue lab tube What would cause increased levels? Increased Surgery Trauma Infection Cancer Heart attack Pregnancy Deep Vein Thrombosis (DVT) Disseminated Intravascular Coagulation (DIC) What would cause decreased levels? Indicates a lack of the substance that is released during the breakdown of a blood clot (i.e. lack of blood clots, or lack of fibrinolysis)

values ddi d dimer

Ep 213 - Sensitivity and Specificity (CAN 10)

The St.Emlyn's Podcast

Play Episode Listen Later Apr 17, 2023 11:23

The latest CAN is one of our brand-new 'revision editions' -- brief podcasts aimed at covering the essentials of critical appraisal for medical students and junior doctors preparing for exams. With the help of Gregory Yates, an academic doctor based in Manchester, this episode introduces two core concepts: sensitivity and specificity. These are two ways of thinking about the accuracy of a diagnostic test. Knowing the sensitivity and specificity of an investigation will give you a decent idea of how it should be used in the emergency department. Sensitivity (Sn) describes the chance that a test will be positive if your patient has the condition you're testing for. Some people call it the 'true positive rate' or alternatively the positivity in disease (PID) rate. If you need a hand remembering it, you can always remember that PID is a sensitive issue. Meanwhile, specificity (Sp) considers the chance of a test being negative if the patient doesn't have the condition you're testing for. It's the 'true negative rate' or alternatively the negativity in health (NIH) rate. There are times when we particularly need a test to have a high sensitivity. This is generally when we want to be particularly confident that a test accurately identifies everyone with the relevant condition because we really don't want to miss it. We need a high sensitivity to rule out disease. (Sn-uff it out). At other times, we need to be confident that a patient with a positive test actually has the disease - for example, if the treatment is unpleasant or involves exposing patients to risk. In that case, we want a high specificity to rule in disease. (Sp-in it in). In this CAN, we use D-Dimer as an example of a very sensitive investigation: it's positive in nearly 100% of cases of venous thromboembolism. Specificity describes the likelihood that the test will be negative if your patient does not have the disease. We use HbA1c as an example of a highly specific investigation: it's rarely used in the emergency department, but if it's elevated, we can be almost certain that the patient is diabetic. HbA1c is almost never (

manchester sensitivity nih sn specificity pid hba1c d dimer

Healthy Blood Flow Mastery: Boost Your Wellness with Effective Tools, Practices, and Education with Dr. Christine Schaffner | Episode184

The Spectrum of Health with Dr. Christine Schaffner

Play Episode Listen Later Mar 2, 2023 15:35

Today's Spectrum of Health podcast episode is short but packed full of pearls straight from Dr. Christine! She talks about healthy blood flow and takes a deep dive into the factors that can impact healthy blood flow, such as EMF, modern-day toxicity, and spike proteins. Dr. Christine also shares some tools and practices, such as ozone and meditation, that can help create a more oxygen-rich environment within the body. Listen in to learn more about today's conversation on healthy blood flow and how to optimize it for yourself: (0:00:02) - Factors that affect healthy blood flow (0:14:46) - The importance of being educated about the markers of blood flow (0:10:40) - Benefits of meditation on your health To get the full show notes - www.drchristineschaffner.com/Episode184

D Dimer

Lab Values Podcast (Nursing Podcast, normal lab values for nurses for NCLEX®) by NRSNG

Play Episode Listen Later Oct 15, 2022 2:37

Get a free nursing lab values cheat sheet at NURSING.com/63labs Objective: Determine the significance and clinical use of D-Dimer in clinical practice Lab Test Name: D-Dimer- DDI Description: Measurement of D-Dimer evaluates the amount of byproduct produced as part of fibrinolysis D-dimer (DDI) is a product of fibrinolysis D-dimer levels are elevated in the setting of clot breakdown, and will be significantly elevated in the setting of Disseminated Intravascular Coagulation (DIC). Indications: Identify and monitor Disseminated Intravascular Coagulation (DIC) Rule out a blood clot: Pulmonary Embolism (PE) Deep Vein Thrombosis (DVT) Stroke Normal Therapeutic Values: Normal – ≤ 250 ng/mL Collection: Light blue lab tube What would cause increased levels? Increased Surgery Trauma Infection Cancer Heart attack Pregnancy Deep Vein Thrombosis (DVT) Disseminated Intravascular Coagulation (DIC) What would cause decreased levels? Indicates a lack of the substance that is released during the breakdown of a blood clot (i.e. lack of blood clots, or lack of fibrinolysis)

nursing ddi d dimer

Q&A 7/26/22 Simple Lab Tests that Can Make a Big Difference

The Balancing Point Podcast

Play Episode Listen Later Sep 9, 2022 31:21

PODCAST HIGHLIGHTS: 03:19 Simple Lab Testing 04:18 Ideal Functional Ranges 07:20 White Blood Cells 10:25 Hemoglobin 12:06 RDW 14:17 MCV 15:13 Platelets 20:05 hs-CRP 20:55 Homocysteine 21:19 D-Dimer 23:25 Fibrinogen 24:09 GGT 24:48 Ferritin 25:49 Can high platelets lead to menstrual cramps https://youtu.be/6V3L-DhKLEs Transcript from Webinar: Welcome to another edition of "Ask Dr. Neiters" here...... Continue Reading →

simple tests big difference crp platelets white blood cells ferritin hemoglobin homocysteine mcv ggt fibrinogen d dimer rdw

Life-Threatening Decline in Medical Care

AMERICA OUT LOUD PODCAST NETWORK

Play Episode Listen Later Jul 31, 2022 56:33

Truth For Health with DrLee4America – The ER doctor refused to order a current D-Dimer blood test for the presence of blood clots — calling it “irrelevant” — even though the patient's clinical presentation had clear signs of another blood clot in her leg. Only after confirming the blood clot in her leg with an ultrasound, and with continued pressure from the...

decline medical care life threatening d dimer

Life-Threatening Decline in Medical Care

TRUTH FOR HEALTH

Play Episode Listen Later Jul 31, 2022 56:33

decline medical care life threatening d dimer

Q&A#52 If a person has been vaccinated would it be wise for them to have a D-dimer test to check for any blood clotting conditions (July 7, 2022)

FLCCC Alliance

Play Episode Listen Later Jul 24, 2022 2:48

Dr. Pierre Kory and Dr. Keith Berkowitz discuss their thoughts on whether patients should have a D-dimer test to check for blood clotting issues. Formed by leading critical care specialists in March 2020, the Front Line COVID-19 Critical Care Alliance (FLCCC) has developed highly effective treatment protocols that aim to prevent and treat COVID-19 at all stages of the disease. We are a 100% donor-supported 501(c)(3) non-profit organization — our work would not be possible without you. Your gifts help us expand our reach and share the latest research available, for the health and well-being of all. To donate online, click here: https://covid19criticalcare.com/network-support/support-our-work/ To follow FLCCC, click here: https://covid19criticalcare.com/follow-flccc-2/ To learn more about our protocols, click here: https://covid19criticalcare.com/covid-19-protocols/ To register for weekly webinars, click here: https://geni.us/FLCCC_Webinar_Register To buy FLCCC gear, click here: https://supportflccc.store

covid-19 blood wise conditions formed vaccinated clotting pierre kory front line covid flccc d dimer critical care alliance flccc

Q&A 5/17/22 D-Dimer, micro-clotting, Nattokinase, Serrapeptase, Long COVID Symptoms

The Balancing Point Podcast

Play Episode Listen Later May 24, 2022 49:21

Podcast Highlights: 06:11 High D-Dimer test results while in ER 45:42 Type of magnesium recommended for long-COVID heart problems. 47:14 Which brands of nattokinase and serrapeptase do you recommend? 48:10 What do you think about Health Concerns supplement – Serramend? Transcript from Webinar: Hi there. Welcome to another edition of “Ask Dr. John.” We’re [...]Read More »

covid-19 er micro symptoms long covid health concerns clotting covid symptoms nattokinase d dimer serrapeptase

Why We Must Spread the WHOLE Truth About the Jabs Even if Some of It Sounds Crazy

Freedom Discourse

Play Episode Listen Later May 8, 2022 17:42

Back in 2013, I was approached by a prominent Christian movie producer about working with them on a new major project. It seemed like a wonderful opportunity that was right up my alley. But as we discussed the project further, it became clear that they were pushing a watered-down, milquetoast version of the Gospel that was meant to ease people into the faith."We can't just walk around with hypodermic needles full of fire and brimstone and hope to reach people," he told me. "Sometimes it's best to feed them Flintstones Vitamins of the Bible so we can ease them into the faith."I wholeheartedly disagreed and did not join the project. We parted friends and I wished them the best, but I am much more of a fire and brimstone kind of guy, at least when it comes to spreading the truth. The Bible is wonderful as it is. We don't need to water it down. They produced their series and it was very successful. I could only watch some of it because they accomplished their mission of putting out a very safe telling of the Biblical narrative.The reason I bring this up is that we are faced with similar arguments being made about the Covid jabs. There is thankfully a growing number of Americans who are starting to see parts of the truth. Most importantly, they're realizing they've been lied to from the start, that the vaccines are neither safe nor effective, and the powers-that-be seem to have an agenda that doesn't really tie into healthcare other than using it as a vehicle for their machinations.There are three camps of vaccine skeptics in America today. The first camp is somewhat indifferent. They aren't getting jabbed or if they already have been, they're not getting the boosters. But otherwise, they don't talk about it. They take on the "buyer beware" attitude that releases them from being compelled to tell anyone what they know about the jabs.The second group is the largest. Most of you who are reading this or listening to the latest episode of End Medical Tyranny fall into this category. You're willing to share some of the truth such as VAERS data or lack of efficacy studies. You may even occasionally share some of the more controversial topics such as the belief that Covid and the jabs are two parts of a bioweapon. But the "crazy" stuff isn't worth sharing even if you believe some or all of it.I totally understand the thinking of people in this camp. It's a strategic choice to focus on what's mostly demonstrable rather than speculative. You believe if you tell people that there have been over a million adverse reactions reported to the CDC, you have the database to prove it. But if you say something like the jabs can induce acquired immune deficiency syndrome, you may lose their attention. They may start thinking you're a wacko conspiracy theorist. You may blow the opportunity to change a heart and mind.In other words, you believe in using the Flintstones Vitamins version of sharing vaccine skepticism. I hold zero grudges towards you if you're in that camp. In fact, you may actually be right in your strategy. My experience is different, but that's anecdotal.For me, I want to spread everything we know. I want to tell them about the long conversation I had with Dr. Sherri Tenpenny about vaccine shedding last May. Why? Because this May, vaccine shedding was proven. It sounds crazy to think that people who are heavily vaccinated may be shedding some elements of their injections, or possibly the reactions from the body itself, onto the people around them. But just because it sounds crazy doesn't mean it's not true, nor does it mean we shouldn't be sharing it.There are lines. I'm not in favor of sharing every theory that pops up. I assess each one and determine whether or not it's viable. If it seems possible, I'll explore further. If it then seems likely, I'll share it. Sometimes, I'll pass on sharing information until I can get more corroboration. For example, I haven't talked about the "snake venom" theory. It may be real, but I haven't seen enough evidence to make it seem likely. So in a way, I suppose I still have one foot in camp two. My appetite to share EVERY hypodermic needle of a conspiracy theory about the jabs isn't unquenchable.Here are some of the more controversial topics that I stick in my "hypodermic needle of vaccine truth" that I share with as many people as possible:The jabs hamper or even annihilate the natural immune system. This is by design to force people after they've been injected enough times to be completely dependent on future jabs. If they do enough damage, their bodies will no longer be able to defend themselves against diseases. They'll have to get on a ceaseless vaccine regimen that will make them permanently beholden to government just to survive.Shedding is real. There has been plenty of evidence of this from as early as last March. The fact that it was "debunked" by "scientists" long before enough time had passed for them to study it tells me this was likely known from the start.Blood clots are now fully acknowledged. What's not discussed nearly enough are the micro clots that are the likely causes for nearly every major ailment that follows both Covid infections and the jabs. The only way to detect micro clots is through a D-Dimer test. It's conspicuous that knowing this, Big Pharma's doctors have knowingly avoided testing people using the only technology that could reveal the truth.The fact that they are pushing to inject every man, woman, and child on earth tells me with a 99% certainty that the powers-that-be who are behind The Great Reset have very specific plans surrounding the jabs. Whether it's for control, depopulation, a combination of the two, or something even worse, I cannot say for certain. All I know for sure is that they wouldn't be so aggressively promoting jabs that clearly do not work if they weren't part of a nefarious agenda.I watch the other "fringe" theories as well, though I rarely spread them. It's not because I'm shy about it or I fear being called a conspiracy theorist (a label I do not consider to be pejorative). It's because I haven't seen enough data telling me they're likely. Theories about graphene hydroxide, 5G, snake venom, nanotechnology, and several others are all possible. As soon as I believe they're likely, I'll definitely share them. Until then, I'll watch closely and wait for more evidence.Through all of this, I haven't fully explained why I believe sharing all of the truth is better than simply sharing the less controversial stuff for the sake of strategy. I've seen the difference between coaxing and adamantly demanding that people wake up. I believe that anyone who I couldn't "ease into" a state of vaccine skepticism may have been better served with a hypodermic needle full of vaccine truth. Conversely, anyone who we wake up with the Flintstones Vitamin version likely would have still been woken up by the hypodermic needle.To me, we can convince ourselves that it's better to not sound like a conspiracy theorist for the sake of better spreading the truth, but I challenge that notion. I believe that easing in for the sake of strategy is an excuse that allows us to not get labeled as crazy. This brings us to the argument Senator Ron Johnson made on this very topic. According to the Wisconsin Examiner:In a video interview published on the right-wing social media platform Rumble, Sen. Ron Johnson said it "may be true" that vaccines against COVID-19 cause AIDS. Johnson was being interviewed by anti-vaccine lawyer Todd Callender, who alleged that the shots induce AIDS and that the FDA knew so when the vaccines were approved for emergency use. "The way to approach this is from a criminal point of view because that's what has happened. And until we start holding people accountable, [Dr. Anthony] Fauci number one, you're going to see people still falling out, still getting sick," Calendar said. "You've got more than a hundred doctors here, all of whom will tell you that these shots caused vaccine-induced AIDS. they purposefully gave people AIDS. They knew this."Johnson responded that it's possible the allegations are true, but that anti-vaccine activists need to wait for public opinion to be on their side before criminally charging health officials. "Let me challenge you there, that's way down the road," Johnson said. "You've gotta do one step at a time. Everything you say may be true, but right now the public views the vaccines as largely safe and effective, that vaccine injuries are rare and mild. That's the narrative, that's what the vast majority of the public accepts. So until we get a larger percentage of the population with their eyes open to ‘woah, these vaccine injuries are real, why?' You've got to do it step by step, you can't leap to crimes against humanity, you can't leap to another Nuremberg trial." Senator Johnson made the case for easing people in, yet the Wisconsin Examiner and others in corporate media still pounced on the notion that he believes vaccine-induced AIDS may be real. Don't get me wrong. Senator Johnson has done more to expose the truth about the vaccines than anyone else on Capitol Hill, so I don't want to be too critical of him or ignore his unique position that must be protected. All I'm saying is that trying to sound "sane" while talking about this stuff will not keep the wolves from pouncing and it won't help reach more people with the truth.Here's the segment of the interview in question:If you take the Flintstones Vitamin approach to spread vaccine truth, I'm okay with that. I disagree, but at least you're doing more than most in corporate and even conservative media. We need the truth to come out now.If you've been jabbed or if you may be experiencing vaxxing shedding from those around you, Dr. Vladimir Zelenko has the nutraceuticals for you. Check out Z-DTox now to make your immune system clean, resilient, and resistant. This is a public episode. If you would like to discuss this with other subscribers or get access to b

Episode 11 - Pulmonary Embolism: Part 1 - The Age-Adjusted D Dimer

Network Five Emergency Medicine Journal Club

Play Episode Listen Later Dec 12, 2021 25:01

Theme: Pulmonary Embolism.Participants: Dr Kevin Lai (senior emergency physician), Dr Arwen Morath (emergency physician), Dr Pramod Chandru, Naveendran Rajendran, Harry Hong, Samoda Wilegoda Mudalige, Kit Rowe and Caroline Tyers. Discussion:Robert-Ebadi, H., Robin, P., Hugli, O., Verschuren, F., Trinh-Duc, A., & Roy, P. et al. (2021). Impact of the Age-Adjusted D-Dimer Cutoff to Exclude Pulmonary Embolism. Circulation, 143(18), 1828-1830. https://doi.org/10.1161/circulationaha.120.052780. Presenter: Naveendran Rajendran - ED Resident at Westmead Hospital. Summary: This was a multinational, prospective, diagnostic outcome study designed to determine the impact of the use of age-adjusted D-dimer on clinical practice in the outpatient setting. This study follows on from the ADJUST-PE study released in 2014, which established the safety of using an age-adjusted D-dimer cut-off retrospectively. The primary outcome was the incidence of symptomatic thromboembolic events in the period following which a PE had been excluded in a patient based on a negative D-dimer (with the age-adjusted cut-off), and a low pre-test probability. The secondary outcome looked at the number of D-dimer results which sat between the conventional cut-off of 0.5 and the age-adjusted value in the whole cohort, as well as more specifically in those aged over 75 years (to determine the diagnostic yield of the age-adjusted cut-off). Of the 1421 patients with a low pre-test probability for PE and a D-dimer below 0.5, only 1 was found to have a non-fatal PE. The proportion of patients with D-dimers that fell between the conventional cut-off of 0.5 and the age-adjusted cut-off was 301 of 1507 patients, with 0 identified thromboembolic events noted during follow-up. This translates to a 20% increase in the number of negative D-dimer tests using the age-adjusted cut-off, with an even more pronounced increase of 67% in the group of patients over the age of 75. Take-Home Points: The age-adjusted D-dimer is a potential tool to assist with risk-stratifying patients presenting with possible PE. Previous concerns regarding various assays may have limited the implementation of an age-adjusted D-dimer in prior years. Further audits to quantify the impact of utilizing the age-adjusted D-dimer (with regards to imaging, treatment, costs, etc.) are required. References: Righini M, Van Es J, Den Exter P. Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: The ADJUST-PE Study. Journal of Vascular Surgery. 2014;59(5):1469.Credits:This episode was produced by the Emergency Medicine Training Network 5 with the assistance of Dr Kavita Varshney and, Deepa Dasgupta. Music/Sound Effects Got My Love by LiQWYD & Markvard | https://www.liqwydmusic.com, https://soundcloud.com/markvard, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution 3.0 Unported License, https://creativecommons.org/licenses/by/3.0/deed.en_US. Medical Examination by MaxKoMusic | https://maxkomusic.com/, Music promoted by https://www.free-stock-music.com, Creative Commons Attribution-ShareAlike 3.0 Unported, https://creativecommons.org/licenses/by-sa/3.0/deed.en_US. Shine by LiQWYD | https://www.liqwydmusic.com, Music promoted by https://www.free-stock-music.comCreative Commons Attribution 3.0 Unported License, https://creativecommons.org/licenses/by/3.0/deed.en_US. Sound effects from https://www.free-stock-music.com. Thank you for listening!Please send us an email to let us know what you thought.You can contact us at westmeadedjournalclub@gmail.com.You can also follow us on Facebook, Instagram, and Twitter!See you next time,Caroline, Kit, Pramod, Samoda, and Shreyas.~

music sound impact journal shine pe previous circulation adjusted unported unported license pulmonary embolism liqwyd vascular surgery shreyas pramod maxkomusic westmead hospital d dimer

The Significance of D-dimer blood test

The Neil Haley Show

Play Episode Listen Later Oct 22, 2021 48:00

Today on The Neil Haley Show, Rev. Winn Henderson and Neil will interview Dr. Robert Young, he will discuss The Significance of D-dimer blood test.

rev significance blood tests robert young d dimer

The Significance of the D-dimer blood test in Covid-19 disease

Freedom From Addiction

Play Episode Listen Later Oct 21, 2021 47:12

In this podcast, we talk with Dr. Robert Young who explains the significance of the D-dimer blood test as it relates to Covid-19 disease. Dr. Young is a world-class scientific investigator and expert especially on microscopic and submicroscopic elements of the human blood. He has written and published hundreds of scientific papers. You can find out more about Dr. Young at www.drrobertyoung.com/blog.

covid-19 young disease significance blood tests robert young d dimer

EMS Troponin | Distal DVT Risk | POCUS COVID-19 | Antivirals Pedi Flu | D-dimer for VTE COVID-19

mero ej actualizado d dimer

Play Episode Listen Later Oct 16, 2021

It's the JournalFeed Podcast for the week of October 11-15, 2021. We cover EMS drawing the first troponin en route, the danger of distal DVT, POCUS for COVID-19, antivirals for sicker children in the hospital, and the utility of D-dimer in COVID-19 patients.

covid-19 risk ems pedi pocus dvt distal antivirals troponin d dimer

Dímero D

LAS PODEROSAS CÉLULAS NK

Play Episode Listen Later Sep 29, 2021 8:14

Límites EJ, Kok SJ. D Dimer. [Actualizado el 14 de julio de 2021]. En: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 enero-. Disponible en: https://www.ncbi.nlm.nih.gov/books/NBK431064/ --- Send in a voice message: https://anchor.fm/las-poderosas-celulas-nk/message

#40 JournalChat // Professor Beverley Hunt on Clearing COVID Clots and D-dimer Decisions

covid-19 professor decisions hunt clearing icu roundup clots heparin critically ill patients d dimer

Play Episode Listen Later Sep 29, 2021 23:28

Trying to keep up with the medical literature but... As it's change-over time, you are far more preoccupied with finding where the staff toilet is, the code for this, and where on earth you can buy coffee?Your ears are in the right placeIn Ep40 we get our favourite Haematology Professor, Beverley Hunt OBE, to discuss our last Round Up's key articles. Including:Do we REALLY believe the idea that we should give treatment dose anticoagulant to moderate Covid but a prophylactic dose to patients in ICU?Therapeutic Anticoagulation with Heparin in Critically Ill Patients with Covid-19 | NEJMShould we be using D-dimers in pregnancy?D-dimer to rule out venous thromboembolism during pregnancy: A systematic review and meta-analysisThe DiPEP studyAnd are age-adjusted D-dimers the way to go?Multi-center implementation of automated age-adjusted D-dimer results reduces unnecessary PE imagingListen to find out. Rate us on Apple Podcasts. Enjoy.

#38 Journal Round Up with Dr David McCreary// COVID updates + D-dimer madness + Smoking cessation + Maximising Commutes + Kiwis for constipation & more.

Play Episode Listen Later Sep 8, 2021 60:37

JournalSpotting is back from its summer break.Jon & Barney are joined by Dr. Dave McCreary all the way from Australia. Dave runs the RCEM podcast and joins JournalSpotting to bridge the chasm between A&E and medics and share some evidence-based pearls.We cover:Why COVID is still *****How does the delta variant present and does my microchip work?Have we figured out how to anticoagulate in COVID-19?More evidence for age-adjusted D-dimers?Do you use D-Dimers in Pregnancy?Do we still need to create arbitrary bridging protocols for surgery?Is that double shot espresso really causing your patients AF?How effective is smoking cessation at improving lung cancer survival?Does smoking cessation improve mental health symptoms?Can an app save my back pain?Which central line is safest for chemo?Kiwis for constipation?Is this podcast making me any smarter?For full episode details and show notes, head to journalspotting.comGet in touch @JournalSpotting on Twitter, Instagram, or Facebook.or email us journalspotting@gmail.com

Vertigo Exam | Silver Nitrate for Epistaxis | CVT | RVD on CTPA | D-dimer Pregnancy

The GenerEhlist - CCFP Exam & Canadian Primary Care Medicine

Play Episode Listen Later Aug 21, 2021

It's the JournalFeed Podcast for the week of August 16-20, 2021. We cover detecting central vertigo on exam, silver nitrate for recurrent epistaxis, cerebral venous thrombosis, spotting RV dysfunction in PE on CT, and D-dimer in pregnancy.

pregnancy silver pe rv exam vertigo nitrate epistaxis d dimer ctpa

CCFP 105 Topics: Deep Vein Thrombosis

Play Episode Listen Later Jul 11, 2021 20:33

Written By: Caleb Dusdal Peer Review By: Sarah Donnelly https://thegenerehlist.ca/ccfp-exam-105-topics-podcast/ Objective One: In patients complaining of leg pain and/or swelling, evaluate the likelihood of deep venous thrombosis (DVT) as investigation and treatment should differ according to the risk. Objective Two: In patients with high probability for thrombotic disease (e.g., extensive leg clot, suspected pulmonary embolism) start anticoagulant therapy if tests will be delayed. Objective Three: Identify patients likely to benefit from DVT prophylaxis. Objective Four: Utilize investigations for DVT allowing for their limitations (e.g., Ultrasound and D-dimer). Objective Five: In patients with established DVT, use oral anticoagulation appropriately, (e.g., start promptly, watch for drug interactions, monitor lab values and adjust dose when appropriate, stop warfarin when appropriate, provide patient teaching). Objective Six: Consider the possibility of an underlying coagulopathy in patients with DVT, especially when unexpected. Objective Seven: Use compression stockings in appropriate patients, to prevent and treat post-phlebetic syndrome.

family medicine ultrasounds dvt vte deep vein thrombosis d dimer thrombus cfpc

Bonus Episode

Network Five Emergency Medicine Journal Club

Play Episode Listen Later Apr 7, 2021 68:55

Theme: Bonus Episode. Participants: Dr Pramod Chandru, Kit Rowe, Shreyas Iyer, Caroline Tyers and, Samoda Wilegoda Mudalige. Discussion 1:Chandru, P., Priyambada Mitra, T., Dutt Dhanekula, N., Dennis, M., Eslick, A., Kruit, N., & Coggins, A. Out of hospital cardiac arrest in Western Sydney: an analysis of outcomes and estimation of future eCPR eligibility - not yet available online. Take-Home Points: This paper was a prospective observational study of consecutive out-of-hospital of cardiac arrests (OOHCAs) at Westmead Hospital over a 3-year period. It looked at the feasibility of setting up an ECMO service for refractory OOHCAs (i.e. for patients who have received CPR for 20 minutes or longer, between the ages of 18 and 70 years, and had a VF arrest). This study had 17 patients who would have qualified as true refractory OOHCAs (none of whom survived to hospital discharge). This proportion of patients was similar to other studies that have been undertaken on this topic, which also demonstrated a survival to hospital discharge with good neurological recovery of around 35-40% with the use of ECMO CPR. The 2CHEER study performed out of Melbourne is also a good reference for this subject - this was one of the first RCTs for the use of ECMO CPR in a pre-hospital setting (see reference below). Westmead Hospital will be one of the centers involved in the upcoming RESET trial looking at the implementation of ECMO CPR. Discussion 2:Bima, P., Pivetta, E., Nazerian, P., Toyofuku, M., Gorla, R., & Bossone, E. et al. (2020). Systematic Review of Aortic Dissection Detection Risk Score Plus D‐dimer for Diagnostic Rule‐out of Suspected Acute Aortic Syndromes. Academic Emergency Medicine, 27(10), 1013-1027. https://doi.org/10.1111/acem.13969. Take-Home Points: This meta-analysis suggested a sensitivity of 97.6-99.9% for an aortic dissection risk score of 0-1 and a negative D-dimer (

FAST for PED | REALITY RCT | MENDS2 RCT | HOT-ICU RCT | Auto Age-Adjusted D-dimer

Ridgeview Podcast: CME Series

Play Episode Listen Later Apr 3, 2021

It’s the JournalFeed Podcast for the week of Mar 29 - Apr 2, 2021. We cover FAST exam for pediatric trauma, transfusion threshold in acute MI, dexmedetomidine vs propofol, PaO2 targets: 60 vs 90mm Hg, and an EHR auto age-adjusted D-dimer.

reality auto adjusted hg ehr d dimer

Stroke Alert March 2021

Stroke Alert

Play Episode Listen Later Mar 12, 2021 17:08

On Episode 2 of the Stroke Alert podcast, host Dr. Negar Asdaghi highlights two featured articles from the March 2021 issue of Stroke. This episode also features a conversation with Dr. Joan Montaner from Neurovascular Research Laboratory at the Universitat Autònoma in Barcelona, Spain, to discuss his article “D-Dimer as Predictor of Large Vessel Occlusion in Acute Ischemic Stroke.” Dr. Negar Asdaghi: Can your microRNA profile predict your future risk of stroke? Is stroke that wake-up call to finally live a healthier lifestyle, better diet, exercise more, and stop smoking? Can a simple blood test improve our clinical predictive models for presence of a large vessel occlusion in patients with suspected ischemic stroke? We have the answers and much more in today's podcast. You're listening to Stroke Alert. Stay with us. Dr. Negar Asdaghi: From the Editorial Board of Stroke, welcome to the Stroke Alert Podcast. My name is Negar Asdaghi. I'm an Associate Professor of Neurology at the University of Miami, Miller School of Medicine, and the host of the monthly Stroke Alert Podcast. In today's podcast, I'm going to interview the senior author of the study on the values of D-dimer and predicting the presence of large vessel occlusion in stroke. But first with these two articles. Dr. Negar Asdaghi: DNA noncoding sequences and introns, once thought to represent the, quote, junk DNA, quote, have been found to play an important role in the modulation of gene expression at the post transcriptional level through coding for regulatory molecules, such as microRNAs, or miRNA. Whether the presence of certain miRNAs can signal a future risk of development of stroke is unknown. In their paper titled “Circulatory MicroRNAs as Potential Biomarkers for Stroke Risk: The Rotterdam Study,” Dr. Michelle Mens and colleagues from the Department of Neurology, University Medical Center, in Rotterdam, Netherlands, discuss their findings related to microRNA samples collected between 2002 and 2005 from over 1900 stroke-free participants of the Rotterdam Study. Participants were assessed for incident stroke through continuous monitoring of medical records until January 1, 2016. Dr. Negar Asdaghi: At baseline, using next-generation sequencing, they measured expression levels of over 2083 miRNAs in plasma samples. During a mean follow-up of close to 10 years, the incidence of stroke was 7% in their study population, and they found, in total, 39 miRNAs were at least nominally related with that incidence of stroke. In their fully adjusted model, they found significant association between expression level of three particular microRNAs and risk of stroke, with the hazard ratio ranging between 1.1 to 2.6. Interestingly, the area under the curve for the longitudinal predictive models improved when the miRNA data was added to the vascular risk factor model. And in conclusion, they found miRNA 6124, 5196-5p and 4292 were associated with future risk of stroke in their population. The elevated levels of these miRNAs may serve as plasma biomarkers for predicting future risk of stroke in combination with other known vascular risk factors for stroke. Dr. Negar Asdaghi: So, speaking of vascular risk factors, let's move on to our second paper for today's podcast. There's a growing emphasis on adherence with pharmaceutical interventions, such as diabetic and blood pressure treatments, statin therapy, to control the risk factors for stroke and prevent recurrent vascular events. All the while, the non-pharmaceutical interventions, such as smoking cessation, diet control, and increased physical activity, seem to represent the somewhat easy or implied aspect of our secondary preventive efforts. But how well are stroke survivors doing with regards to making these healthy lifestyle modifications? In the March issue of Stroke, Dr. Chelsea Liu and colleagues from Johns Hopkins School of Public Health presented their findings on lifestyle and behavioral changes pertaining to cardiovascular health in the study titled, “Change in Life's Simple 7 Measure of Cardiovascular Health After Incident Stroke: The REGARDS Study.” Dr. Negar Asdaghi: So, this was a population-based, epidemiological study of over 7,000 stroke-free participants between 2003 and 2007, who had data on Life's Simple 7, what the author called “LS7 measures,” which studied seven different domains. Four of them behavioral, including smoking, diet, physical activity, body mass index, and three medication-controlled, including blood pressure, total cholesterol, and fasting glucose, both at study entry and their follow-up visit. At which point, either they did not have a stroke or had an ischemic stroke and were included if that stroke had happened more than one year before the follow-up visit. And so the study authors hypothesized that those with a stroke would have had a significant improvement in their Life's Simple 7 data poststroke as compared to the stroke-free participants. Dr. Negar Asdaghi: But what they found was completely the opposite. At 10 years follow-up, a total of 149 patients had suffered a stroke in their study. On a scale of zero to 14 at study entry, all participants scored low or relatively low in these seven simple measures, but those participants who would ultimately suffer a stroke scored significantly lower at baseline. What was alarming, though, was that after adjusting for all confounders, at follow-up, participants who had experienced an ischemic stroke showed a significantly further decline in their total LS7 score at 10-year follow-up. And the greatest declines were noted in behavioral domains, most notably physical activity and diet scores. The authors noted a non-significant improvement, in other words, improvement in weight in the BMI score among stroke survivors, but they caution that that may indeed be actually related to muscle loss, a downstream effect of decreased physical activity poststroke, rather than representing active dietary interventions with weight loss. So, in summary, this important paper highlights, on a population level, the urgent need for behavioral interventions to improve secondary prevention after a stroke event up and beyond our efforts to improve medication adherence. Dr. Negar Asdaghi: So now moving on from secondary preventative measures to the acute phase, our next paper discusses ways in which we can improve our diagnostic accuracy in the acute setting. Identification of large vessel occlusions is the first step in determining patients' eligibility for endovascular thrombectomy, a highly effective treatment to improve outcomes in acute ischemic stroke. But without vascular imaging, which may not be readily available in the small or community hospitals, the decision to transfer patients to thrombectomy-capable centers is entirely dependent on clinical scales, which, as we all know, may have suboptimal sensitivity and specificity. So the question is, could a simple blood test improve the predictive capabilities of our current clinical scales for presence of a target LVO, or large vessel occlusion? Joining me now is Dr. Joan Montaner from Neurovascular Research Laboratory at the Universitat Autònoma in Barcelona, who is the senior author of the study titled “D-Dimer as Predictor of Large Vessel Occlusion in Acute Ischemic Stroke.” Good morning, Joan, all the way from the sunny Florida to the beautiful Barcelona. Good to have you with us, and thank you for joining us. Dr. Joan Montaner: Hello. Nice to talk with you on blood biomarkers for stroke management. Dr. Negar Asdaghi: Thank you, Joan. Your study touches on the importance of improving the ways in which the systems of care are set up in triage and transfer of patients with thrombectomy-capable centers. Can you please tell us briefly about the stroke systems of care in Catalonia where you practice and where your study is based out of? And what clinical scales are currently used for transfer of patients with suspected acute stroke to a comprehensive stroke center? Dr. Joan Montaner: Yes, Catalonia, it's a region of about 7.5 million inhabitants. And when we did this study, most of the comprehensive stroke centers were located in Barcelona itself, in the capital. So it's true that there are several areas of the region that are far away from Barcelona. It took more than two hours to bring some patients from those distant regions to Barcelona. That's why we began to use these clinical scales that you are talking about. Mainly they are RACE, it's like a simplification of the NIHSS subscale. And, in fact, a large study RACE card that was presented last year in the European Stroke Conference was done to try to see if we could, by using these scales, RACE, select the right patients to come directly to the thrombectomy centers instead of going to the closest hospital. But, unfortunately, the results were neutral. So, we were a little bit disappointed, and we think, as you were saying, that these neurological scales are suboptimal, probably not enough sensitivity and specificity for identifying LVO. That's why we think that these biomarkers could improve the accuracy of those scales. Dr. Negar Asdaghi: Perfect. I totally agree with you. And now, before you tell us about the biomarkers, can you just briefly tell us about the Stroke-Chip study, your study population, and what prompted you to look at these various biomarkers that you addressed in the paper? Dr. Joan Montaner: Stroke-Chip was a lot, it was really a massive collaborative effort among all the public hospitals in this network here in Catalonia. We were able to collect more than 1,300 patients in this particular study that we are talking about. Dr. Anna Ramos-Pachón and Elena Cancio were leading the analysis on the relation of these biomarkers with LVO. But I have to say that this was not the original intention of our study. Really, and perhaps we were naive at that time, we were looking for biomarkers to differentiate ischemia from hemorrhagic strokes or from stroke mimicking conditions to try to give TPA or TNK in the ambulance. But, as I was saying, perhaps that was a little bit naive, and we know how difficult that would be and perhaps with some liabilities. That's why it came this idea of, "Well, if we use those markers, not for giving a drug in the ambulance, but for doing triage and sending the patient to the right hospital, that could be more simple and more useful even." Dr. Negar Asdaghi: Thank you very much. Can you briefly tell us about the study? What were your inclusion criteria? Dr. Joan Montaner: Well, in this study, we selected all consecutive acute stroke patients attending the stroke unit of all these hospitals. We were including all stroke suspicions, if their symptoms onset happened within six hours. So, it's really hyperacute patients. And we were able to collect, like this, more than 1,300 patients. And then at the hospital, with the angio CT or duplex, we were able to categorize those with LVO, and we measured a panel of different biomarkers in the blood stream of those patients and trying to associate which of these markers were related with having or not having an LVO. Dr. Negar Asdaghi: Very interesting. So tell us, please, your study's main finding? Dr. Joan Montaner: The main finding, what we liked more, let's say, of our results was that some of those markers, specifically NT-proBNP and D-dimer, were really high among patients with a large vessel occlusion. When we combined these results, for example, having high levels of D-dimer, those patients above fourth quartile of D-dimer with more stroke severity, patients with NIH of more than 10, the accuracy was really good. It was very specific, 93% specificity, 34% sensitivity, to predict an LVO. So this means that without almost any mistake, you select more than one third of the patients that have an LVO, that could be very useful. To bring those patients, we were talking from far away of these thrombectomy centers, to the right place. And perhaps we could be doing a thrombectomy one or two hours before with these technologies. Dr. Negar Asdaghi: Perfect. So basically, just to reiterate what you're saying, is that D-dimer, as non-specific as it is and as important as it is to note that it can be elevated in the setting of aging or increase NIH Stroke Scale severity, this increase in D-dimer noted in patients with LVO was just not a factor of just age simply or increased severity of the stroke scale. Can you tell us about your multivariate analysis and what other factors you adjusted for in your final model? Dr. Joan Montaner: You are right that D-dimer can be modified by many things, as you were saying. That's why we took a lot of care about the multivariate analysis and all factors, all clinical factors that were related with LVO were included in the model. And finally, only eight NIH Stroke Scale scores D-dimer and the vast history of atrial fibrillation were included in the model. Odds ratio for D-dimer was 1.59 that I think it's quite acceptable. And it's true that in that model, NT-proBNP was not included anymore, probably because it's related with a fee. So, that's something interesting if perhaps in the ambulance, you don't know about the story, the history of a patient, of a fee, we could use NT-proBNP, so I think this opens the possibility of using different clinical neurological scales biomarkers in combination to make the prediction of LVO. Dr. Negar Asdaghi: Yes. Very, very exciting results for sure. So what is our main takeaway from your study? Are we thinking that D-dimer or a particular level of elevations of D-dimer will one day become the, quote, Troponin equivalent of LVO for stroke? Dr. Joan Montaner: Well, it sounds nice, but I know it's several technical issues here. You are right that there is variability among labs in the measurement of D-dimer so now what we are doing is really, in a prospective study called BIO-FAST in the south of Spain, in Seville, in a large network of ambulances, we are measuring D-dimer, but in a rapid fashion with a rapid point of care test in the ambulance itself. We think that we are not going to have a magic biomarker. Not that Troponin you are talking about. Probably we need to combine it with others. We think that the marker of brain damage would add a lot on top of D-dimer, probably D-dimer is very good for the clot burden, but we think other markers could improve the accuracy of the test. And we are measuring them together with these. Our dream would be really to have cost utility study in the future and to see if really we are able to randomize patients based on these biomarkers in the ambulance, will have an impact on outcome if we are able really to do thrombectomies much faster. Dr. Negar Asdaghi: Well, we certainly look forward to covering your future studies on this topic of biomarkers. Dr. Joan Montaner, thank you for joining us and congratulations on your work. Dr. Joan Montaner: Thanks a lot. Dr. Negar Asdaghi: And this concludes our podcast. Don't forget to check online for the full list of publications, including two papers on the state of pediatric thrombectomy and a study on the association between stroke and subsequent risk of suicide that are published online ahead of their presentations at the International Stroke Conference. Until our next podcast, stay alert with Stroke Alert.

Journal Review Day with Drs. Chris Solie and Abby Elliott

Play Episode Listen Later Jan 22, 2021 73:39

In this podcast Dr. Chris Solie, an ER physician with EMPAC, and Dr. Abby Elliott, with Lakeview Clinic, cover a variety of topic areas from six journal articles. If you like to skip to the conclusion part of the article, this podcast is for you. Enjoy the podcast! Objectives: Upon completion of this podcast, participants should be able to: Differentiate if chest pulmonary CTs are necessary when patients present with suspected venous thromboembolism (VTE). Name at least 2 benefits of nighttime antihypertensive dosing for patients. Assess when cardioversion would be deemed necessary for individuals experiencing A-fib. Identify the risks of short-term steroid use. Identify the relevance of lumbar MRI and its findings. Summarize the findings that IV contrast causing acute kidney injury is a myth. CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity. Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks. You may contact the accredited provider with questions regarding this program at rmccredentialing@ridgeviewmedical.org. Click on the following link for your CME credit: CME Evaluation: "Journal Review Day - with Drs. Chris Solie and Abby Elliott" (**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.) DISCLOSURE ANNOUNCEMENT The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics. Any re-reproduction of any of the materials presented would be infringement of copyright laws. It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented. Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event. SHOW NOTES: Journal Article 1: "Diagnosis of Pulmonary Embolism with d-Dimer Adjusted to Clinical Probability" PEs and DVTs can be elusive. There are rising numbers of chest pulmonary CTAs being done with lower yields. These can result in increased cost and health risks. In this study, the adjusted d-dimer was looked at to see if the number of CTs being ordered can be reduced. The Wells criteria was used to place patients into low, moderate or high clinical pretest probability for venous thromboembolism of VTE. In the podcast, "clinical pretest probability" is referred to as risk. Of the entire 2000 patients enrolled, the diagnosis of VTEW was only made in 7%. Participants that qualified as low risk numbered 1742 and 1200 of these had d-dimer less than 1000. No VTWE was found in these patients for the next 90 days. For those with a d-dimer between 500 and 999, none had a VTE at 90 days. In moderate-risk groups with d-dimer less than 500, none had VTE at 90 days. Combining low-risk patients with a d-dimer less than 1000, non of these patients had evidence of VTE at 90 days. Even in the 467 patients with a d-dimer greater than 1000, only 87 had a VTE. Moderate- or high-risk patients are not applicable for this study. According to the article, if the d-dimer is greater than 1000, and the patient is low-risk, there was a 20% incidence of VTE. While it is an impressive study, it is one peice of data and should not replace clinical gestalt and decision making when truly concerned about the presence of VTE. Journal Article 2: "Bedtime Hypertension Treatment Improves Cardiovascular Risk Reduction: The Hygia Chronotherapy Trial" HTN is difficult to manage in many patients. This was a large study out of Spain of approximately twenty thousand patients. Patients were selected to take their medication either in the AM or nighttime and 48-hour blood pressure monitoring was performed. Patients were followed for 6 years. Night time dosed patients had significantly lower cardiovascular event rates than the daytime group, as well as better blood pressure management. There is little evidence to not advise nighttime antihypertensive dosing for patients, unless there would be compliance concerns. Medications that would not be tolerated, or specific medications, like diuretics, that can disrupt sleep. This was an impressive study that demonstrates a rather simple maneuver to effect a remarkable change in cardiovascular risk. Bear in mind, diet and lifestyle may also contribute to the results, but those were not assessed in this study. Journal Article 3: "Early or Delayed Cardioversion in Recent-Onset Atrial Fibrillation" A-Fib is a common presentation in primary care practice and in Emergency Departments. In this study of early cardioversion strategy vs delayed, 437 patients, aged 18 and above, were reviewed. Necessary criteria included A-fib bit less than 36-hours and hemodynamic stability. The conclusion was that neither strategy delayed or early cardioversion was an inferior approach. A large number of patients in this study spontaneously converted to normal sinus rhythm without demonstrating higher rates of stroke. However, this study was not powered to assess risk of long-term stroke, and this remains unknown. Though based on other studies referenced today, it's known that a patient cardioverted after 12-hours of A-fib has an increased risk of stroke. Psychologically, being in A-fib can be disturbing for the individual, and remaining in A-fib is not always desirable from the patient perspective. There are also potential logistical and cost considerations with delayed approach including numerous repeat clinics and ER visits for a small number of patients. Journal Article 4: "Short-term Use of Oral Corticosteroids and Related Harms Among Adults in the United States: Population-based Cohort Study" An impressive review of three hundred thousand patients was performed. Corticosteroids were given for mostly musculoskeletal, respiratory and allergic issues. Sepsis, VTE and fracture were monitored for over a 90-day time period and statistically significant higher rates of all of these were noted. Bear in mind, this was a study without true placebo, and patients essentially compared their experience on steroids to their experience not on steroids. It should probably be followed up with a prospective trial to help further validate these concerning findings. Still, this study only looked at 3 different complications and the numbers here are pretty striking, with 205 of adults receiving steroids. There are a number of studies which have shown no evidence of benefit in the use of steroids for a variety of indications, including conditions, such as urticaria and even anaphylaxis. Journal Article 5: "No Association Between MRI Changes In The Lumbar Sone and Intensity of Pain, Quality of Life, Depressive and Anxiety Symptoms in Patients With Low Back Pain" In this study, out of Poland, patients were referred for a lumbar spine MRI by neurologists, surgeons or other specialists, but not by primary care. These MRIs were graded in the study based on criteria derived from the reading radiologists. The endpoint of the study was to compare the severity of MRI findings with the patient's self-assessment and scoring of pain, quality of life, etc. The study ultimately showed there was no correlation. However, age and BMI, and total MRI scores did correlate. Physically active patients had better scores. Learning new ways of coping with pain and helping our patients with this reality can equal a more efficient use of time and money. Per this study, medications or a reassuring MRI, does not correlate to resolution of pain. Of course, MRIs are often indicated in the setting of significant neurologic findings and emergencies, but outside of those settings, some patients may not be convinced that an MRI is not necessary. Using articles like this one can assist to better counsel patients and reduce unnecessary MRIs. Journal Article 6: "Contrast Associated Acute Kidney Injury Is A Myth: Yes" IV contract is often blamed for acute kidney injury, or AKI. It turns out, like many time honored beliefs in medicine, this is not likely the case. While attempting to research and write a paper on this subject, the investigators quickly discovered that ample data already exists that shows CIN or contrast induced nephropathy, appears to be more a myth than truth. One senior author of this paper demonstrated in a pool of thousands of patients in two other separate studies that there's no association between contrast and AKI. Another investigator who is a cardiologist demonstrated actually less incidence of AKI in a cohort of patients. So, while personal clinical experience and Gestalt should not be ignored, we also must maintain a desire to debunk dogma that is unfounded time and again in the scientific literature. With regard to AKI from IV contrast, maybe there will be a prospective randomized trial looking at this, but there seems to be a preponderance of evidence already to suggest it may not be necessary. Thanks for listening. Sources/Links: Kearon C, de Wit K, Parpia S, et al. Diagnosis of Pulmonary Embolism with d-Dimer Adjusted to Clinical Probability. N Engl J Med. 2019;381(22):2125-2134. doi:10.1056/NEJMoa1909159 Available: https://www.nejm.org/doi/10.1056/NEJMoa1909159?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed Hermida RC, Crespo JJ, Domínguez-Sardiña M, et al. Bedtime hypertension treatment improves cardiovascular risk reduction: the Hygia Chronotherapy Trial. Eur Heart J. 2020;41(48):4565-4576. doi:10.1093/eurheartj/ehz754 Available: https://academic.oup.com/eurheartj/article/41/48/4565/5602478 Pluymaekers NAHA, Dudink EAMP, Luermans JGLM, et al. Early or Delayed Cardioversion in Recent-Onset Atrial Fibrillation. N Engl J Med. 2019;380(16):1499-1508. doi:10.1056/NEJMoa1900353 Available: https://www.nejm.org/doi/full/10.1056/NEJMoa1900353 Airaksinen, K. E., Grönberg, T., Nuotio, I., Nikkinen, M., Ylitalo, A., Biancari, F., & Hartikainen, J. E. (2013). Thromboembolic Complications After Cardioversion of Acute Atrial Fibrillation. Journal of the American College of Cardiology, 62 (13), 1187-1192. doi:10.1016/j.jacc.2013.04.089 Waljee AK, Rogers MA, Lin P, et al. Short term use of oral corticosteroids and related harms among adults in the United States: population based cohort study. BMJ. 2017;357:j1415. Published 2017 Apr 12. doi:10.1136/bmj.j1415 Available: https://www.bmj.com/content/357/bmj.j1415 Yao, T., Huang, Y., Chang, S., Tsai, S., Wu, A. C., & Tsai, H. (2020). Association Between Oral Corticosteroid Bursts and Severe Adverse Events. Annals of Internal Medicine, 173 (5), 325-330. doi:10.7326/m20-0432 Babińska, A., Wawrzynek, W., Czech, E., Skupiński, J., Szczygieł, J., & Łabuz-Roszak, B. (2018). No association between MRI changes in the lumbar spine and intensity of pain, quality of life, depressive and anxiety symptoms in patients with low back pain. Neurologia I Neurochirurgia Polska . doi:10.5603/pjnns.a2018.0006 Available: file:///C:/Users/E55983/Downloads/No_association_between_MRI_changes_in_the_lumbar_s.pdf Ehrmann, S., Aronson, D., & Hinson, J. S. (2018). Contrast-associated acute kidney injury is a myth: Yes. Intensive Care Medicine, 44 (1), 104-106. doi:10.1007/s00134-017-4950-6 Available: file:///C:/Users/E55983/Downloads/Ehrmann2018_Article_Contrast-associatedAcuteKidney.pdf Davenport, M. S., Perazella, M. A., Yee, J., Dillman, J. R., Fine, D., Mcdonald, R. J., Weinreb, J. C. (2020). Use of Intravenous Iodinated Contrast Media in Patients with Kidney Disease: Consensus Statements from the American College of Radiology and the National Kidney Foundation. Radiology, 294 (3), 660-668. doi:10.1148/radiol.2019192094

united states spotify learning apple pain podcasts er spain healthcare night bear journal patients mcdonald medical identify poland stitcher iv dom diagnosis published medications drs chang physically mri american colleges steroids assess contrast czech bmi intensity internal medicine davenport cin objectives moderate huang gestalt wu cardiology differentiate hypertension cme radiology emergency departments sepsis annals aki babi tsai mris psychologically yee bmj ctas summarize cts aronson depressive afib yao hinson new england journal of medicine corticosteroids pulmonary embolism vte sardi national kidney foundation dillman z39 intensive care medicine anxiety symptoms ehrmann weinreb journal article cme/ce ridgeview solie d dimer dvts cardioversion abby elliott drs chris

#15 Disseminated Intravascular Coagulation (DIC) and fibrin related markers

Ask Stago

Play Episode Listen Later Dec 22, 2020 8:13

Welcome to Ask Stago, the weekly podcast for Hemostasis laboratory professionals.   This week, with our expert Paul Riley, Scientific Business Development Manager, Cécile Hourquet and Audrey Carlo will cover the usage of fibrin related markers in the diagnosis of disseminated intravascular coagulopathy.   Litterature: Baglin T. Disseminated intravascular coagulation: diagnosis and treatment. BMJ 1996; 312: 683-7 Iba T, Di Nisio M, Thachil J, Wada H, Asakura H, Sato K, Kitamura N, Saitoh D. Revision of the Japanese Association for Acute Medicine (JAAM) disseminated intravascular coagulation (DIC) diagnostic criteria using antithrombin activity. Crit Care. 2016 Sep 14;20:287 Taylor FB Jr, Toh CH, Hoots WK, Wada H, Levi M; Scientific Subcommittee on Disseminated Intravascular Coagulation (DIC) of the International Society on Thrombosis and Haemostasis (ISTH). Towards definition, clinical and laboratory criteria, and a scoring system for disseminated intravascular coagulation. Thromb Haemost. 2001 Nov;86(5):1327-30 JAAM; Iba T, Di Nisio M, Thachil J, Wada H, Asakura H, Sato K, Kitamura N, Saitoh D. Revision of the Japanese Association for Acute Medicine (JAAM) disseminated intravascular coagulation (DIC) diagnostic criteria using antithrombin activity. Crit Care. 2016 Sep 14;20:287 Boral BM, Williams DJ, Boral LI. Disseminated Intravascular Coagulation. Am J Clin Pathol 2016; 146: 670-80 Wada H, Sakuragawa N. Are fibrin-related markers useful for the diagnosis of thrombosis? Semin Thromb Hemost 2008; 34: 33-8 Toh JMH, Ken-Drorb G, Downey D, Abram ST. The clinical utility of fibrin-related biomarkers in sepsis Blood Coagulation and Fibrinolysis 2013, 24:00–00 Gris JC, Cochery-Nouvellon E, Bouvier S, Jaber S, Albanese J, Constantin JM, Orban JC, Morel J, Leone M, Deras P, Elotmani L, Lavigne-Lissalde G, Lefrant JY. Clinical value of automated fibrin generation markers in patients with septic shock: a SepsiCoag ancillary study. Br J Haematol. 2018 Nov;183(4):636-647 (Singh N, Prasad Pati H, Tyagi S, Datt Upadhyay A, Saxena R. Evaluation of the Diagnostic Performance of Fibrin Monomer in Comparison to D-Dimer in Patients With Overt and Nonovert Disseminated Intravascular Coagulation. Clin Appl Thromb / Hemost 2015; 1-6.). (Park KJ, Kwon EH, Kim HJ, Kim SH. Evaluation of the diagnostic performance of fibrin monomer in disseminated intravascular coagulation. Korean J Lab Med. 2011; 31: 143-7.).

comparison clinical evaluation revision international society fdp markers bmj dic thrombosis coagulation ddi paul riley hemostasis disseminated d dimer fibrin lab life fibrinolysis

EM Quick Hits 23 – Clinical Probability Adjusted D-dimer, ARDS Part 2, Pharyngitis Mimics, Barotrauma, Vertigo, CPR Gender-Based Differences

pages questioning exclusion offs indications european society vte coagulation david jim european heart journal hemostasis d dimer

Play Episode Listen Later Oct 27, 2020 48:46

In this month's EM Quick Hits podcast we have Salim Rezaie on clinical probability adjusted D-dimer for pulmonary embolism, Bourke Tillmann on ARDS for the ED Part 2, Brit Long & Michael Gottlieb on pharyngitis mimics, Justin Hensley on the many faces of barotrauma, Hans Rosenberg & Peter Johns on assessment of continuous vertigo and Justin Morgenstern & Jeannette Wolfe on gender-based differences in CPR... The post EM Quick Hits 23 – Clinical Probability Adjusted D-dimer, ARDS Part 2, Pharyngitis Mimics, Barotrauma, Vertigo, CPR Gender-Based Differences appeared first on Emergency Medicine Cases.

gender differences clinical cpr vertigo probability adjusted ards mimics michael gottlieb d dimer barotrauma pharyngitis salim rezaie justin morgenstern hans rosenberg

TWiV 673: Wake up and smell the pandemic

This Week in Virology

Play Episode Listen Later Oct 18, 2020 160:48

Daniel Griffin provides a clinical report on COVID-19, we debunk the Great Barrington Declaration, and discuss smell and taste changes as early indicators of the pandemic, vascular disease and thrombosis in SARS-CoV-2 infected humans and rhesus macaques, and the ability of the swine pathogen SADS-CoV to infect human respiratory tract cells. Subscribe (free): iTunes, Google Podcasts, RSS, email Become a patron of TWiV! Links for this episode Daniel’s COVID-19 testing strategy calculator (and medRxiv preprint) US COVID-19 mortality rates (JAMA) Final remdesivir report (NEJM) Hydroxychloroquine for COVID-19 (NEJM) Tech position with Dr. Rosenfeld Biological safety officer position at CUMC Support MicrobeTV at Parasites Without Borders Smell and taste changes as early pandemic indicators (Nat Comm) Vascular disease and thrombosis in SARS-CoV-2 infected macaques (Cell) SADS-CoV can infect human airway cells (PNAS) Letters read on TWiV 673 Timestamps by Jolene. Thanks! Weekly Science Picks Dickson – The Age of Nature Brianne – Virologist, Immunologist, Science Communicator pins and Virus Earrings Alan – Sharks, Squalene, and a SARS-CoV-2 Vaccine Rich – 6th Annual Science Mill Benefit Vincent – The Evolution of Infectious Disease by Paul Ewald Intro music is by Ronald Jenkees Send your virology questions and comments to twiv@microbe.tv

covid-19 coronavirus pandemic viruses wake viral smell sars cov infectious diseases virology us covid immunologist thrombosis science communicator anosmia d dimer twiv daniel griffin pnas letters

TWiV 673: Wake up and smell the pandemic

This Week in Virology

Play Episode Listen Later Oct 18, 2020 160:48

covid-19 coronavirus pandemic viruses wake viral smell sars cov infectious diseases virology us covid immunologist thrombosis science communicator anosmia d dimer twiv daniel griffin pnas letters

#4 D-Dimer and its cut-offs for VTE exclusion

Ask Stago

Play Episode Listen Later Oct 6, 2020 7:52

Welcome to Ask Stago, the Podcast providing expert answers to your expert questions. In today’s episode, with François Depasse our Clinical Development Director, we will discuss the selection of a cut-off for D-dimer assay in venous thromboembolism exclusion diagnosis. Sources: Pernod G, Maignan M, Marlu R. Questioning the use of an age-adjusted D-dimer threshold to exclude venous thromboembolism: analysis of individual patient data from two diagnostic studies: comment. J Thromb Haemost 2016; 14: 2553–4. Stavros V Konstantinides, Guy Meyer, Cecilia Becattini, Héctor Bueno, Geert-Jan Geersing, Veli-Pekka Harjola, Menno V Huisman, Marc Humbert, Catriona Sian Jennings, David Jiménez, Nils Kucher, Irene Marthe Lang, Mareike Lankeit, Roberto Lorusso, Lucia Mazzolai, Nicolas Meneveau, Fionnuala Ní Áinle, Paolo Prandoni, Piotr Pruszczyk, Marc Righini, Adam Torbicki, Eric Van Belle, José Luis Zamorano, ESC Scientific Document Group, 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC), European Heart Journal, Volume 41, Issue 4, 21 January 2020, Pages 543–603, https://doi.org/10.1093/eurheartj/ehz405.

#14 JournalChat// Bloody COVID, with Thrombosis Expert Prof Beverley Hunt

Play Episode Listen Later Jul 6, 2020 36:53

Are you trying to keep up with the COVID literature but by the time you've read one article you realise it was from one month ago and therefore is currently irrelevant?Here we have the Brilliant Professor Beverley Hunt to help us wade through the literature, learn from her experience and figure out how we should be treating our COVID-19 patients relating to their bloody sticky blood.Don't forget to subscribe to the podcast, and get regular emails by signing up on our website. Also on our website are the awesome Podpoint Graphics by Kosta for this episode and others!www.JournalSpotting.com01:00 Introduction to hosts / what we are talking about03:30 Professor Beverley explains her role in COVID crisis05:00 Why the blood is so sticky06:40 How we have come to understand this08:50 Rates & Cause of thrombosis - immunothrombosis11:10 Why Dexamethasone helps12:50 What thromboses do we see in patients?15:10 Which patients are most at risk16:35 And in pregnancy?18:45 Which blood tests are useful? And the D-Dimer?24:25 Which dose of LMWH? Call for trials27:50 Rates of bleeding with LMWH29:45 Are the thrombosis rates higher than other conditions?30:45 OP / discharge Tx33:20 Key Take Home Points for Bloody COVID - Thromboprophylaxis on D1 admission! - Enter your patients into trials - Don't over treat with LMWH - Sometimes the best is what existed before and had good evidence35:00 An OBE for COVID?35:15 Thank yous and sign offsWant more info on Professor Hunt? Just google her name or find her on Twitter @bhwords.Follow us on twitter @JournalSpotting, Facebook or Instagram.Subscribe to regular JournalSpotting emails on our website!

covid-19 prof hunt rates bloody d1 obe kosta thrombosis d dimer lmwh

Episode 507: Increasing the D-dimer threshold for patients with low clinical pretest probability effectively rules out PE (PEGeD)

POEM of the Week Podcast

Play Episode Listen Later May 3, 2020 8:09

Dr. Ebell and Dr. Wilkes discuss the POEM titled ' Increasing the D-dimer threshold for patients with low clinical pretest probability effectively rules out PE (PEGeD) '

patients increasing clinical poem threshold probability wilkes d dimer pretest

#06 Covid Zone 2- Coronavirus literature updates 22nd April 2020

covid-19 donald trump coronavirus recovery treatments literature 5g barney stat turbulent jogging bmj cui jigglypuff transmision coagulopathy d dimer

Play Episode Play 40 sec Highlight Listen Later Apr 22, 2020 50:41

Welcome to the COVID-ZONE--------------------------- Journalspotting is here to bring you important clinical updates on coronavirus. Get in touch: journalspotting@gmail.com Twitter @JournalSpotting ----------------------------In today's episode:#Transmision models: out with the old and in with the new- Turbulent gas clouds- Barney's Jigglypuff work shelf- Presymptomatic transmission- Jogging with COVID-19#Treatment update: Remdesivir, convalescent plasma, RECOVERY trial- Remdesevir: NEJM paper, orphan status, STAT news#Cover your face(mask)- BMJ analysis - How good are cotton masks?#Coagulopathy & COVID-19- Cui et al + D-Dimer pooled analysis- ISTH Interim guidance- The dutch anticoagulateCovid rants- Donald Trump cuts WHO funding - 5G conspiracy + app ideasCovert Covid Distractions- Explicit lyric warning!!

D-dimer-DVT, Epi for Peds OHCA, Lidocaine vs Amio Peds Arrest, 5 Ways to Connect with Patients

The Elective Rotation: A Critical Care Hospital Pharmacy Podcast

Play Episode Listen Later Feb 22, 2020

This week on JournalFeed, we cover clinical pretest probability adjusted D-dimer for DVT, epinephrine for pediatric out-of-hospital cardiac arrest, lidocaine vs amiodarone for pediatric arrest, and five evidence-based ways to connect with your patients, and more.

patients arrest peds dvt lidocaine ohca d dimer

475: Can D-dimer results be improved by adjusting cutoffs for renal dysfunction?

Play Episode Listen Later Feb 6, 2020 2:51

Show notes at pharmacyjoe.com/episode475. In this episode, I ll discuss whether D-dimer results can be improved by adjusting cutoffs for renal dysfunction. The post 475: Can D-dimer results be improved by adjusting cutoffs for renal dysfunction? appeared first on Pharmacy Joe.

improved adjusting dysfunction renal cand cutoffs d dimer

Deca Only For HRT - A Comprehensive Overview And My Personal Blood Work

More Plates More Dates

Play Episode Listen Later Feb 1, 2020 27:52

There's been a growing amount of hype around the "Deca only cycle". While it is most commonly referred to as the Deca only cycle, it is actually based on the compound Nandrolone being used on its own. The decanoate ester being abbreviated as "Deca" has just become synonymous nowadays in the bodybuilding community with Nandrolone itself. Seeing the potential merits of Nandrolone as a makeshift hormone replacement therapy alternative to Testosterone, I stopped using Testosterone and instead started using Nandrolone on its own with exogenous Estradiol for 3 months and paid over $1000 for an elaborate blood panel to assess how it affected my health markers. https://youtu.be/kLScNddgkks How Nandrolone Could Potentially Be A Superior HRT Alternative To Testosterone The primitive thought process is that Nandrolone used in conjunction with Testosterone will lead to horrible side effects, but Nandrolone used on its own will just result in all of the benefits of steroids with a near absence of the androgenic or estrogenic side effects associated with Testosterone use. In reality, it's a lot more nuanced than that. The reason why I found this experiment worth pursuing is the lack of androgenicity of Nandrolone in the body. Nandrolone 5α-reduces in tissues that express 5α-reductase to the much less androgenic metabolite Dihydronandrolone (DHN). Nandrolone is basically the only anabolic steroid that is going to maintain 100% anabolic activity of the Nandrolone in muscle tissue where you want it, but also be converted into a much less androgenic metabolite with a lower binding affinity in certain areas of the body where you wouldn't want Nandrolone to bind. The two areas of concern for most individuals being hair follicles and skin. By converting to DHN in these areas, Nandrolone (and by extension DHN) causes less hair loss and acne than Testosterone (and by extension DHT). In addition, some men are genetically predisposed to high levels of aromatization and estrogen receptor expression and can't even use TRT doses of Testosterone without experiencing estrogenic side effects. Nandrolone is not a potent substrate for aromatase, and mainly converts to a weaker estrogen called Estrone (Estradiol is about 10-fold more potent than Estrone). Nandrolone is also mildly estrogenic on its own via its ability to act as an estrogen receptor alpha (ERα) agonist [R]. Overall, Nandrolone is much less androgenic and estrogenic than Testosterone, and may provide symptom relief in those seeking a viable hormone replacement therapy alternative. In this context, Nandrolone may also have great potential as an efficacious alternative to Testosterone as an anabolic agent for some individuals who are prone to androgenic and/or estrogenic side effects. The Neurotoxicity And Cardiotoxicity Of Nandrolone Based on the limited data available, Nandrolone has shown to be more deleterious to cardiovascular and neurological health than testosterone. https://www.youtube.com/watch?v=Gv_v0mJy6Bg By extrapolating the data, we start to get a clearer picture as to why this likely is. Nandrolone is mildly estrogenic on its own, and it does not aromatize nearly enough to create as much Estradiol as Testosterone does. Comparing the effect of testosterone with that of 19-nortestosterone (Nandrolone) and Stanozolol (Winstrol) on neurotoxicity we can clearly see that Estrogen is what protects neurons in the brain, not Testosterone itself. In this study, a physiologic dosage of Testosterone was neuroprotective [R]. Testosterone only amplified neurotoxicity at supraphysiological dosages. The neuroprotective effect of a physiologic dosage of Testosterone was completely eliminated when the aromatase inhibitor Anastrozole (Arimidex) was co-administered, suggesting that the intrinsic toxicity of Testosterone as an androgen is only counterbalanced by its aromatization into 17β-estradiol. As opposed to testosterone, Nandrolone does not appear to aromatize sufficiently into estrogen. As you would expect, Nandrolone was neurotoxic at every single dose evaluated regardless of Arimidex being co-administered or not. If Nandrolone was inherently able to provide enough estrogen receptor alpha (ERα) activation to balance out its androgenicity without even requiring aromatization (it acts as an estrogen on its own to some extent), we would see a neuroprotective effect at equivalent dosages to a physiologic concentration of Testosterone when no AI is used, but that does not appear to be the case either. The anti-androgen flutamide attenuated the neurotoxicity of all three androgens, thus further reinforcing that physiologic dosages of androgens without a sufficient amount of opposing estrogens, or supraphysiological dosages of androgens may facilitate neuronal death. I suspect that the same applies for the inherent cardiotoxicity of Nandrolone as well. Just because you can get your Estradiol levels up to 15 pg/mL with a gram of Deca only, that ratio of androgens to estrogen in the body is way off of what would otherwise be optimal for health based on what I've seen. This is reinforced by the fact that Flutamide (an anti-androgen) was able to attenuate the neurotoxicity of Nandrolone. By preventing Nandrolone from binding to androgen receptors, it is no longer able to transcribe its effects in tissues. Hair loss and acne are one thing, cardiotoxicity and neurotoxicity are another thing and should ultimately take precedence obviously. However, just because Nandrolone monotherapy cannot produce a sufficient ratio of androgens to estrogens, that doesn't mean that there isn't a potential loophole. That loophole is exogenous Estradiol administration. Exogenous Estradiol Use With Nandrolone Only Cycles As we've seen, Estrogen produced via aromatase is what provides neuroprotection from the androgenicity of Testosterone, not the Testosterone itself. We also know that Nandrolone is not able to produce enough estrogenic activity in the body to facilitate this same level of neuroprotection. I theorize that Nandrolone in conjunction with exogenous Estradiol to replace this otherwise missing component could attenuate a significant amount of the deleterious impact Nandrolone has on the heart and brain. In addition, by providing a sufficient amount of exogenous estrogen, libido, muscle growth, fat loss, and several other aspects of health and performance should be more optimized. It isn't a coincidence that cardiovascular disease rates skyrocket once women hit menopause and stop producing Estrogen properly. The same negative effects will apply in men with low Estrogen levels. The lack of sufficient Estrogen is often addressed in Deca only cycles by adding an adjunct anabolic steroid that aromatizes into Estrogen or Estrogen analogs. Obviously for those seeking to minimize androgenic side effects, the ideal way to go about achieving sufficient Estrogen receptor activation is probably not going to be by adding more steroids to their protocol. This is where exogenous Estradiol comes into play, and I believe the majority of Deca only cycles would be more sustainable from a health perspective, and successful in a bodybuilding context as well with its inclusion. I have yet to see one person on a Deca only cycle achieve a sufficient Estradiol level relative to their Nandrolone dosage via a sensitive assay Estradiol blood test. The following blood test result was submitted by an individual on over 1000 mg per week of Deca only. Over a gram of androgens relative to a 19.2 pg/mL Estradiol level is far from ideal in my opinion. I had a good conversation with Vigorous Steve as well about his Deca only cycle experience. He told me that his Estradiol was 12 pg/mL on 1000 mg of Deca per week after 4 weeks, and he ended up adding 25 mg DHEA per day just to bring it up to 25 pg/mL. When it comes to Nandrolone use on its own, most would benefit from more Estrogen in my opinion. My Weekly Nandrolone And Estradiol Dosage For "HRT" Most guys doing Deca only cycles are evaluating Nandrolone at dosages of 600 mg or higher per week for short blasts. My experiment was based on its potential as an alternative long term HRT option for those prone to androgenic side effects. Or alternatively, its potential as a compound to swap to periodically throughout the year from TRT to reverse some of the androgenic side effects of Testosterone and DHT while still maintaining the same amount of muscle mass. Every blood test I've seen of Deca only cycle users was on high doses of Nandrolone without a sufficient amount of Estrogen. I wanted to see how Nandrolone on its own at a "therapeutic dose" would affect my blood work if I had a sufficient amount of Estrogen provided through exogenous Estradiol. Long-term, the only way Nandrolone monotherapy could be even relatively safe in a cardiovascular context would be with exogenous Estradiol supplementation from what I've seen. And even then, I'm sure it has major drawbacks that will likely accumulate over the years. With that being said, it is still something I wanted to explore nonetheless, as it is one of the few compounds that can actually support supraphysiological muscle growth with a relatively minimal impact on androgenic alopecia. Oral micronized Estradiol tablets have quite a few drawbacks. A few of the most notable drawbacks are that oral Estrogen pills can be somewhat liver toxic, they spike SHBG through the roof, and they result in the production of clotting factors in the blood that do not develop with forms of administration that skip the first pass. The two most viable methods of administration that skip the first pass are transdermal topical application, or injection. I chose to topically apply transdermal Estradiol gel (Estrogel) for this experiment. I used 100 mg of Nandrolone phenylpropionate (NPP) per week split into daily injections using an insulin pin rotating between my glutes and ventroglutes. I also applied 2.5 grams of transdermal Estrogel (delivering 1.5 mg Estradiol) to my inner thighs every day for over 3 months straight. Blood Pressure Changes On Nandrolone One of the first things I noticed was that it was a struggle to keep my blood pressure in check on NPP, even at the mild dose I was using. What that was caused by exactly, I'm not sure. I assumed it was Aldosterone prior to this blood work. When I'm on Testosterone, even when I was using TRT as high as 200 mg per week, I could keep my blood pressure at 110/70 with ease. Even if I ate terribly, I could still hold 115/75 without even trying on Testosterone. Within the first week of switching to NPP it became way harder to control my systolic blood pressure. My diastolic blood pressure was fine for the entire 3 months, but my systolic blood pressure would consistently be around 125-128. That is not normal for me, and is borderline stage 1 hypertension. The fact that I even had to try to lower my blood pressure showed to me that Nandrolone is a lot harder to manage in this regard. This is consistent with almost every single person I know who has blasted high doses of Deca. They all had significant issues with blood pressure. Most of the guys who thought they had normal blood pressure were actually stage 1 hypertensive and didn't even realize that their results were indicative of cardiovascular stress. My 125-128 systolic occurred without being in a calorie surplus, without any weight changes, and on what I would consider a very low dose of NPP. The exact same diet, weight, lifestyle, etc. would have me at 110/70 on TRT. Muscle Growth And Strength On Nandrolone I maintained my muscle and do not feel that there was a substantial difference between the anabolic potency of Nandrolone compared to Testosterone. At the very least, the anabolic activity of Nandrolone is comparable to Testosterone, but the androgenic activity is far less than that of Testosterone. In certain contexts for certain individuals, Nandrolone will be the desirable alternative because of this. Reduced Libido On Nandrolone - Deca Dick? My libido was extremely subdued on NPP. That's one of the most obvious things I noticed during my experiment. I had a libido and would still want to have sex, but my libido was much lower than it is on regular TRT. On TRT I can barely go one day without sex before it starts to consume my mind. On Nandrolone only, I can easily go a couple days barely even thinking about it. However, when it came time to get the job done, I could still get the job done and stay hard the entire time without any issues in erection quality. It was a bit harder to reach orgasm though. On top of the lack of androgenicity causing a reduction in libido, Nandrolone also has progestogenic activity and binds to the Progesterone receptor. Excessive Progesterone is notorious for killing libido and causing erectile dysfunction, and it seems that Nandrolone has similar effects in many individuals via this pathway in conjunction with its 5α-reduction into DHN. My drive was also lower, and I felt less aggressive overall. In many individuals Testosterone and DHT levels will strongly influence libido, drive, aggression, motivation and productivity. Personally, even if I have that support via DHT or DHT derivatives, the increased motivation and drive is actually more counterproductive in a work productivity context because my libido gets way too high. Even when I had high testosterone levels and 0 DHT in my body I still had sex on my mind far more than I would like. When that happens, I can barely get anything done, and then I end up depleting myself of energy for the day through excessive sex. The subdued and normalized libido on Nandrolone is welcomed for me because of this. I don't think this is necessarily just because I'm a good responder to Nandrolone, I think it has more so to do with the fact that I was using exogenous Estrogen during this experiment with the Nandrolone. Despite androgens driving aggression and drive, libido and erection quality is largely dictated by adequate Estrogen levels. With all that being said, DHT (with sufficient Estrogen via Testosterone aromatization) is blatantly better for sexual support than Nandrolone, and testosterone itself, even if you completely inhibited 5α-reductase and nuked DHT, still provides better libido and erection quality than Nandrolone does at equivalent "therapeutic" doses for the majority of people. My Blood Work Results On A Deca Only Cycle For HRT I don't like taking shots in the dark when it comes to something that I see potential in. There is a lot of theory thrown back and forth in the community on Deca only cycles, and I needed to see for myself how Nandrolone in conjunction with exogenous Estradiol would impact my personal blood work. I wanted to check markers of oxidative stress, inflammation, kidney function, Aldosterone, Prolactin, hormone levels via sensitive assay testing, and an array of other health markers that are often debated about but very infrequently actually tested for to reinforce statements made. Expectedly, high dose Deca only cycle blasts will almost always result in low HDL levels, subpar Estradiol levels, and an array of other out of range values that are less common and are more individual dependent. To date I have yet to see someone get their blood work checked with exogenous Estradiol being used in conjunction with Nandrolone at a "therapeutic" dose. This is what I wanted to evaluate. Complete Blood Count with Differential/Platelets I was actually expecting far worse from my blood test results. At a "therapeutic" dose, it doesn't seem like my hematology was negatively affected at all. Comprehensive Metabolic Panel In my metabolic panel, nothing was really off to the point that would cause concern. My BUN being high is likely just the result of being muscular and having a high protein diet. Lipid Panel Going into the lipid panel, we can see the number one most common blood test result among steroid users. My HDL is low. LDL is also borderline high, but not overly concerning when I can see that my Triglycerides are pretty low. The reason why my HDL was too low was that my Estrogen levels were too low. Again, this just reinforces the fact that Nandrolone does not sufficiently aromatize into Estrogen. I will get into my Estrogen level and why it was still too low even with Estrogel administration later once we get to that part of the blood test results, but my HDL could have been in range if my Estrogen level was in check. If I didn't use the Estrogel my HDL likely would have been in the single digits. I know I can get my HDL into the reference range if my estradiol levels were doubled, which I have the leeway to do. Iron And Total Iron Binding Capacity Getting into Iron and TIBC we can see that everything looks pretty normal here. Total Testosterone And Free Testosterone Expectedly, by assessing my Total Testosterone level via liquid chromatography with tandem mass spectrometry (LC/MS-MS) and my Free Testosterone level via equilibrium ultrafiltration, we can see that my Testosterone levels were crashed. Both the total and the free were lower than a healthy female. This is what you should see in your blood work if you’re on just Nandrolone. The only Testosterone being produced in my body was indirectly via the trace amounts of androgens produced in my adrenal cortex, which is why the value wasn't completely bottomed out at 0. I've mentioned many times the importance of getting high sensitivity testing done for hormone levels and how Nandrolone will register as Testosterone in primitive garbage blood tests. This is another great example of this. In addition to high sensitivity testing, I had the same blood tested using electrochemiluminescence immunoassay (ECLIA) for my Total Testosterone level, and direct analog enzyme immunoassay (EIA) for my Free Testosterone level. These were the test results using the exact same blood sample with the terrible default assays that doctors will use to determine how to treat you, and that labs will give you in the majority of your blood work panels. According to ECLIA and EIA, I have a normal Total Testosterone and Free Testosterone level. Hilarious. This just one example of why getting accurate hormone testing is critical. My Testosterone levels are actually in the gutter, but the stupid primitive tests that doctors and labs give out as defaults for people is so f*cking stupid that it can't even tell the difference between Testosterone and 19-nortestosterone in my blood. Renin Activity and Aldosterone My renin activity and Aldosterone appeared to be normal. This is one of the main things I wanted to check because there's a lot of speculation around the effect Nandrolone is going to have on Aldosterone levels. When it comes to the Deca only cycle, there's something going on that throws off homeostatic mechanisms that regulate blood pressure that does not appear to be Estrogen related or Aldosterone related. At least based on my blood work, my Aldosterone was definitely not at a level that could imply any kind of negative effect on blood pressure. My Aldosterone level was low if anything. Granted, some markers in the serum can be relatively worthless when compared to actual tissue concentrations, but at least based on my blood work, Aldosterone does not appear to be the culprit. The first thing many jump to when explaining blood pressure regulation is the effect Nandrolone supposedly has on spiking Aldosterone through the roof, but it just doesn't appear to be the case in my experience as you can see yourself here. Vitamin B12 and Folate My B12 and Folate levels were normal. Pregnenolone Pregnenolone appeared to be normal and within the reference range for men which is notable, as many assume that Nandrolone will shut down the production of precursor steroids. That does not appear to be the case either. I assumed precursor hormone levels like Pregnenolone would be less affected than many seem to think as most circulating Pregnenolone is derived from the adrenal cortex. Dihydrotestosterone (DHT) Expectedly, my DHT was very low. This is because I have almost no Testosterone being produced to 5α-reduce into DHT. If my Testosterone is low, my DHT will be low as well. DHT Backdoor Pathway Contrary to popular belief, there is a backdoor pathway via Pregnenolone that can create DHT as well, which contributes to the chunk of DHT I have in my blood. Hemoglobin A1c Hemoglobin A1c appeared to be normal at 5.1%. Thyroxine (T4) My Free T4 was 1.28 ng/dL, which is acceptable. DHEA-Sulfate My DHEA was in range and actually on the high end of normal. Being on exogenous Nandrolone or Testosterone does not shut down DHEA production. Cortisol Cortisol was "normal" apparently, although it looks a bit high to me. I believe this result was mostly sleep hygiene related rather than entirely Nandrolone related. Thyroid Stimulating Hormone (TSH) My TSH is too high. I've never had a TSH this high before. I have had a TSH in the 2's before, this isn't the first time, but never this high. However, based on my resting heart rate and my morning waking temperature and my mid-day temperature, my metabolic rate seems to be the same as it usually is on TRT, and I have had no standout hypothyroidism symptoms. Luteinizing Hormone (LH) and Follicle Stimulating Hormone (FSH) Expectedly, LH and FSH were undetectable. Prolactin My Prolactin was on the low end of normal. This was another interesting health marker to see on Nandrolone, as many will often jump to assuming that Nandrolone spikes Prolactin levels through the roof. That does not appear to be the case though. Prostate-Apecific Antigen (PSA) My PSA level was normal, and did not change from my previous blood work on Testosterone for TRT. D-Dimer My D-Dimer was normal. A friend of mine had a very high D-Dimer level on a Deca only cycle and he wanted me to check mine to see if there was a pattern. It looks like the elevated D-Dimer was case-specific for him and was probably caused by something completely unrelated, as my D-Dimer is normal. C-Reactive Protein C-Reactive Protein is one of the primary markers we have for assessing inflammation in the body. A C-Reactive Protein level of 0.34 mg/L is not overly concerning, although I would like to see it below 0.3 mg/L. I had undetectable C-Reactive Protein levels in the past on TRT, and on Nandrolone it jumped up to 0.34, which is notable. Estradiol, Sensitive My Estradiol (E2) level determined via LC/MS-MS was only 15.4 pg/mL, despite administering 2.5 grams of Estrogel per day. This was disappointing, as I would have liked to see my E2 at least around 30 pg/mL based on the amount of Estrogel I was applying daily. Evidently, my inner thigh was not absorbing the Estrogel very well. This is one of the recommended areas of application, but my results were not even close to in line with the average blood levels found in the Estrogel pharmacokinetics studies. With daily administration of 2.5 g or 5 g Estrogel (corresponding to 1.5 mg or 3 mg estradiol, respectively), mean serum estradiol concentrations of approximately 80 pg/ml (294 pmol/L) and 150 pg/ml (551 pmol/L), respectively, are maintained. Administration of Estrogel also results in increased serum estrone concentrations, producing a physiological estradiol/estrone ratio of approximately one. Therefore, serum concentrations of both estradiol and estrone and the serum estradiol/estrone ratio provided by ESTROGEL® are consistent with physiological levels observed during the follicular phase of the normal menstrual cycle. My inner thigh isn't very hairy at all as I manscape fairly regularly, so I expected at least a 40 pg/mL E2 based on the amount of Estrogel I was applying. I was overly generous with my dose based on the off chance that I would encounter an absorption issue, and my E2 was still way below where I expected it to be. Based on the pharmacokinetics outlined by Merck, 80 pg/mL is the average E2 level for someone applying 2.5 grams of Estrogel per day. There's no way I could have predicted that I would have an absorption issue so problematic that it would result in five times lower absorption than the average. If my E2 was closer to 30 pg/mL, I expect that my HDL would have been pushed into the reference range, and all Estradiol driven physiologic functions likely would have been more optimized. To me, this just reinforced further that Nandrolone is a subpar source of Estradiol as I was using a high dose of transdermal E2 and still could barely reach a satisfactory E2 level. To increase my E2 levels for similar future experiments I will either have to find a better application area, add some DMSO to my Estrogel to increase absorption, or consider Estradiol injections instead. Homocysteine My Homocysteine level was higher than I would like. Normally my Homocysteine is closer to 8-8.5 umol/L. Earlier in the year when I did a shorter Nandrolone experiment for a month using 200 mg per week (double the dose I used for this experiment) I had a Homocysteine level around 8.5, so I doubt this spike was Nandrolone related. This is one of the main markers I always have my eye on because I am homozygous for the C667T polymorphism. Gamma-Glutamyl Transferase (GGT) My GGT looked good. I was worried that this would be cranked through the roof as it is a marker of oxidative stress. Magnesium My magnesium level looked okay. Copper and Zinc My zinc level looked okay. My copper level may be a bit low, which I am now addressing by eating an ounce of beef liver every day. Progesterone My Progesterone was normal, which is notable as it is another precursor hormone that many assume drops to zero when exogenous anabolic steroids are present in the body. Insulin My insulin level was good. Estrone Expectedly, my Estrone was a bit high. This can be a major problem with exogenous Estradiol and Nandrolone unfortunately. Estrone Level Increase From Exogenous Estradiol The ratio of Estrone-to-Estradiol is skewed with massive elevations in Estrone with oral Estrogen administration. Fortunately, this unhealthy ratio can be avoided for the most part with transdermal Estradiol administration. High levels of serum Estrone sulfate (E1S) were found after long-term oral estrogen treatment of commonly prescribed dosages, whereas there was a small increase in E1S levels after transdermal Estradiol (E2) therapy. The mean maximum E1S levels were more than 20-fold higher with oral estradiol (E2) when compared with the 0.05 mg/day transdermal estradiol patch. This is consistent with the 20-fold higher dose of E2 when compared with the transdermal dose [R]. Estrone Level Increase From Nandrolone Nandrolone also significantly elevates concentrations of Estrone in plasma [R]. During a pilot study evaluating the possible beneficial effect of Nandrolone Decanoate (ND) on bone metabolism in patients with rheumatoid arthritis there was a significant increase in the serum levels of Estrone [R]. Despite the fact that Estrone can convert to Estradiol, we can clearly see that the amount this actually happens in the body is minimal based on the consistently skewed ratios of androgens to Estradiol in the blood test results of Deca only users (or Nandrolone in general). Ferritin My Ferritin level is too low. This is likely the result of phlebotomizing too frequently in 2019. Estriol My Estriol level was undetectable, which was expected. Triiodothyronine (T3) My Free T3 level was 2.7 pg/mL. It's not low enough for me to be overly concerned, however, it is suboptimal and should be in the low 3's at least. This is something I will need to address moving forward. With that being said, I like to look at my resting heart rate as well as my body temperature for a more accurate assessment of my metabolism, and both are where I want them to be. My waking temperature has consistently been 98 degrees Fahrenheit, and my midday temperature has consistently been 98.6 degrees Fahrenheit. Sex Hormone-Binding Globulin Expectedly, my sex hormone-binding globulin (SHBG) was low. While this isn't as relevant for a Nandrolone only user as Nandrolone has a very low affinity for SHBG, this is a value I would still like to see in the reference range, especially if I was on TRT. If I had the Estradiol level I was shooting for, I'm confident that my SHBG would have been in the reference range. My Overall Experience On Nandrolone And Exogenous Estrogen For HRT I was expecting to see a bunch of red flags in my blood work, but nothing really stood out as a major concern to me except for the spike in systolic blood pressure, and the high Estrone level. A before and after echocardiogram and calcium scoring would have been nice to see, but unfortunately I can only afford to do so much in these experiments, and the blood work was expensive enough as is. I felt good throughout the entire experiment, I maintained my physique, my libido and penis were functional, and my blood work looked pretty good considering that each issue was something more so related to my Estradiol administration than the Nandrolone itself. Estrone being out of range is a concern, as I would need to use even more exogenous Estradiol to achieve what I would consider a more therapeutic E2 level, which would likely push my Estrone up even higher. The difficulty in controlling the blood pressure spike is also a huge concern and could be a deal breaker. If I gave this experiment more time, it is entirely possible that certain things would have become problematic that appeared to be fine during my three month assessment, like my libido or sense of well-being. It is also possible that despite maintaining a healthy Estrogen level, the same neurological and cardiovascular issues we see in a significant amount of the Nandrolone data could still accumulate over time. In addition, healthy looking serum levels of Estradiol may not necessarily reflect adequate localized Estrogen receptor activation in each tissue. With Testosterone, there is a regulated amount of aromatization occurring in each tissue to satisfy however much Estrogen receptor (ER) activation we need. In the context of Deca only cycles, or Nandrolone monotherapy, there's nothing else I can refer to other than serum levels, my libido, sense of well-being, other cardiovascular health markers, etc. In other words, just because you feel good and your Estrogen levels look good on paper, that doesn't mean that an exogenously administered source of Estrogen is providing the same therapeutic ER activation in all tissues like it would if it were regulated via aromatase. With that being said, you could also argue the opposite as adequate receptor activation via exogenous hormone therapy is essentially all HRT boils down to to begin with in the context of any hormone. More than 95% of our endogenous Testosterone is produced in the testes. Testosterone is supplied to target tissues in the blood, just like most other hormones in the body. If you inject exogenous Testosterone, it then goes into the blood and is supplied to target tissues. If you inject anything it goes into the blood and then is carried to the areas that it is needed. Estrogen replacement has been deemed satisfactory for fulfilling the same functions as endogenously produced Estrogen in women for years, and synthetic Estrogen analogs are handed out like candy to millions of young girls (including teenagers). Is it healthy? Estrogen analogs like Ethinyl Estradiol probably aren't ideal for regulating Estrogen dependent functions, and they definitely aren't ideal for developing women who haven't fully matured. However, there is tons of data to support the fact that exogenous Estradiol is well-tolerated, has a strong safety profile, and can still fulfill physiologic functions sufficiently. In an ideal world, this would be a regulated process in the body in each tissue (aromatization). My experiments do not necessarily reflect what I believe are best practice with these hormones, which should be noted. This was an experiment, and not something that I would recommend someone else do. Using an exogenous progestogen with estrogel certainly isn't what I would consider an optimal HRT protocol, or what is indicative of an ideal means of providing androgenic and estrogenic support in tissues. With that being said, I don't see a better way to go about utilizing Nandrolone on its own for HRT. Should it even be considered as an HRT alternative though? That's the question, and I believe it is largely going to be individual dependent, with a significant amount of users having poor outcomes in one aspect or another. I do believe there are a minority of individuals who are very prone to androgenic and/or estrogenic side effects from exogenous Testosterone use that may benefit from exploring Nandrolone though, and it should not be discarded as a potentially viable alternative simply because it is not the primary bioidentical hormone that men produce.

Folge 10 - Obstruktiver Schock, D-Dimer, Triagierungsapps

Fasttrack - Der Notfallpodcast

Play Episode Listen Later Jan 29, 2020 61:23

In dieser Folge schliessen wir unsere kleine Schockreihe mit einem Interview zum obstruktiven Schock ab. Passend dazu hat Marius für uns das Wichtigste zum D-Dimer zusammengefasst. Ausserdem haben wir noch zwei Interviews geführt zu der Zukunft der Triagierung. Zum Einen sprechen wir darüber mit dem Geschäftsführer der Firma In4medicine die die Apps SMASS bzw.SMED entwickelt hat, zum anderen gibt es noch eine Stellungname der DGINA zu diesem wichtigen Thema.

interview thema zukunft gesch passend marius wichtigste schock ausserdem zum einen smed d dimer

D Dimer Cutoffs

Corpsey

Play Episode Listen Later Jan 8, 2020 9:38

Mel explores the wonderful world of age and pre-test probability cutoffs for D Dimer and a BIG thought by Dr. Jeffery Kline. See: CorePendium: Venous Thromboembolism Chapter and a recent NEJM paper to be reviewed on march EMA.Allpart of EMRAP.org

nejm cutoffs d dimer em rap

D-dimer Adjusted for Clinical Probability of PE, Work Schedules of Hospitalists, Inappropriate Fluoroquinolone Prescribing, Utilization and Outcomes of Lytics in Acute PE

Last Week in Medicine

Play Episode Listen Later Dec 2, 2019 24:07

Can you get away with a higher d-dimer value in patients with a low pre-test probability for PE? Does working more days in a row improve patient outcomes? How often are people inappropriately prescribing fluoroquinolones? How often are people using systemic lytics vs catheter directed lytics in acute PE, and what are the outcomes?Music from https://filmmusic.io"Sneaky Snitch" by Kevin MacLeod (https://incompetech.com)License: CC BY (http://creativecommons.org/licenses/by/4.0/)

music pe clinical kevin macleod outcomes schedules inappropriate acute probability utilization adjusted prescribing hospitalists pulmonary embolism sneaky snitch antibiotic stewardship fluoroquinolones thrombolysis d dimer

EM Quick Hits 5 Ludwig’s Angina, Transient Monocular Vision Loss, D-dimer for PE Workup in Pregnancy, Pediatric Nasal Foreign Bodies, Trimethoprim Drug Interactions, Airway Management in Cardiac Arrest

AAEM: The Journal of Emergency Medicine Audio Summary

Play Episode Listen Later Jun 4, 2019 42:42

In this EM Quick Hits Podcast: Ludwig's Angina Emergency Management - Approach, Airway, Imaging, Transient Monocular Vision Loss (TMVL), D-dimer in the Work-up of Pulmonary Embolism in Pregnancy, Management of Pediatric Nasal Foreign Bodies: Tips and Tricks, Sulfamethoxazole-Trimethoprim Drug Interactions and Airway Options in Cardiac Arrest - LMA for all?... The post EM Quick Hits 5 Ludwig’s Angina, Transient Monocular Vision Loss, D-dimer for PE Workup in Pregnancy, Pediatric Nasal Foreign Bodies, Trimethoprim Drug Interactions, Airway Management in Cardiac Arrest appeared first on Emergency Medicine Cases.

work management tricks pregnancy ludwig pediatric imaging nasal cardiac arrest transient airway angina pulmonary embolism vision loss foreign bodies drug interactions airway management workup d dimer trimethoprim

JEM May 2019 Podcast Summary

Play Episode Listen Later May 27, 2019 52:16

Podcast summary of articles from the May 2019 edition of the Journal of Emergency Medicine from the American Academy of Emergency Medicine. Topics include Age Adjusted D-dimer for DVT, Whole Blood Transfusions, Pediatric Concussions, Antipsychotic medications, Foreign Body Aspirations and board review on Foreign Body Ingestions. Guest speaker is Dr. Julia Coppi.

D-dimer: Common Assay, Challenges Abound, Caution Advised

JALM Talk Podcast

Play Episode Listen Later Mar 19, 2019 7:54

Venous thromboembolism, or VTE, is a serious medical condition characterized by a blood clot in a vein, also known as deep vein thrombosis. If the clot breaks free from the vein, it can cause a life-threatening pulmonary embolism by blocking blood supply to the lungs. Over 100,000 Americans may die from VTE per year. If recognized quickly, VTE may be effectively treated with anticoagulant therapy; however, it can be difficult to detect when VTE is occurring and when treatment is warranted, thus the clinical laboratory plays an important role in performing diagnostic tests for VTE.

americans challenges abound venous vte assay d dimer caution advised

Diagnostic utility of D-dimer concentrations in dogs with pulmonary embolism | VETgirl Veterinary Continuing Education Podcasts

VETgirl Veterinary Continuing Education Podcasts

Play Episode Listen Later Nov 5, 2018 6:42

In today's VETgirl online veterinary continuing education podcast, we review the use of D-dimers in predicting the presence or absence of pulmonary emboli in dogs. Pulmonary embolism (PE) refers to an obstruction of a pulmonary vessel, which could be caused by a blood clot, tissue, infectious material, parasites, foreign bodies, or other material (Goggs). There are a variety of diseases known to increase risk for PE's in our canine patients, including immune-mediated diseases such as IMHA, protein-losing nephropathies, hyperadrenocorticism, neoplasia, sepsis, and cardiac disease, as well as the use of certain medications like steroids. Unfortunately, the diagnosis of PE can be challenging due to non-specific clinical and radiographic changes. Probably many of us have seen an IMHA patient become acutely dyspneic with minimal radiographic changes, a situation where you may highly suspect a PE! In human medicine, CT or pulmonary angiography are the gold standard for antemortem diagnosis (Torbicki), but there have been various studies in both humans and in dogs evaluating the use of D-dimers as a tool to rule out a PE.

dogs podcasts pe utility diagnostic continuing education veterinary pulmonary pulmonary embolism concentrations d dimer goggs vetgirl

Diagnostic utility of D-dimer concentrations in dogs with pulmonary embolism | VETgirl Veterinary Continuing Education Podcasts

VETgirl Veterinary Continuing Education Podcasts

Play Episode Listen Later Nov 5, 2018 6:42

dogs podcasts pe utility diagnostic continuing education veterinary pulmonary pulmonary embolism concentrations d dimer goggs vetgirl

JEM October 2018 Podcast Summary

AAEM: The Journal of Emergency Medicine Audio Summary

Play Episode Listen Later Oct 28, 2018 43:49

Podcast summary of articles from the October 2018 edition of Journal of Emergency Medicine from the American Academy of Emergency Medicine. Topics include intranasal vasoconstrictors, pre-oxygenation with NIPPV and nasal cannula, cardiac glycoside toxicity, age adjusted D-dimer for pulmonary embolism, antibiotic use after abscess drainage, and board review on immune checkpoint inhibitor toxicities. Guest speaker is Dr. Matthew Addis.

american medicine academy journal emergency pe american academy oxygen immune oncology emergency medicine antibiotics cardiac checkpoint jem adjusted pulmonary toxicology inhibitor abscess intranasal bipap epistaxis podcast summary embolism digoxin d dimer nippv aaem preoxygenation heent

It Is Time To ADJUST -D-Dimer – Podcast 10

YEMIOWA

Play Episode Listen Later Jul 11, 2018 23:03

d dimer

May 2018

RCEM Learning

Play Episode Listen Later May 1, 2018 91:58

This month we have Traumatic cardiac Arrest Part 1 & 2 , Do you know how and when to undertake a resuscitative thoracotomy in traumatic cardiac arrest? & Do you open the chest in blunt trauma? Do you know the basics well and do you rehearse and deliver the simple interventions quickly and effectively in traumatic arrest? | Should we have a geriatrician on the trauma team? | How do you make end of life decisions in the trauma bay? How do you avoid opiate overuse in elderly trauma patients? | Can we clinically predict which patients might benefit from thrombectomy for stroke | Can we use higher D-Dimer thresholds to avoid imaging low-risk patients for PE? | Does a greater occipital nerve block help with the treatment of migraine

d dimer

Cardiac Enzymes Plus D.Dimer/ESR/BNP/Tox for PodCast

Talk EM - Enhancing Clinical Excellence in EM

Play Episode Listen Later Apr 3, 2018 20:59

Join John Bielinski for live CME in 2019. www.Emergency-Medicine-Institute.com Demystifying Emergency Medicine Conference April 1-4, 2019 Marriott Key West Beachside Master labs/CXR and EKGs Urgent Care Medicine Conference July 8-11, 2019 The Lakefront Anchorage All aspects of urgent care medicine Critical Access Emergency Medicine Conference Oct 8-11, 2019 Yellowstone For critical access providers who are solo providers

cardiac cme enzymes esr cpk cxr d dimer troponins myoglobin

A Test in Context: D Dimer

JACC Podcast

Play Episode Listen Later Oct 30, 2017 24:48

Commentary by Dr. Valentin Fuster

context commentary d dimer valentin fuster

Podcast #249: D-Dimer

Emergency Medical Minute

Play Episode Listen Later Sep 6, 2017 3:45

Author: Michael Hunt, M.D. Educational Pearls In the recent YEARS study, investigators checked every patient with suspicion for PE with a D-dimer, using a modified Wells score for risk stratification. The goal of the study was to show that CT scan usage could safely reduced using this screening method. The Wells Criteria measures they used to stratify risk were: PE mostly likely dx, hemoptysis, and evidence of DVT. If the d-dimer was 1, but the patient had none of the Wells criteria, the patient did not get a CT. If the patient had any of the criteria, but the d-dimer was only 0.5, the patient did not get a CT scan. The investigators reduced CT usage by 14% using the new criteria, with no significant increase in morbidity and mortality. References: van der Hulle et al. Simplified diagnostic management of suspected pulmonary embolism (the YEARS study): a prospective, multicentre, cohort study. The Lancet. 2017

pe references simplified lancet dvt hulle d dimer

How to diagnose pulmonary embolism: Age-adjusted D-dimer, PERC rule and Wells score

Heart podcast

Play Episode Listen Later Apr 12, 2017 14:00

In this special episode, we bring you three interviews with key people behind clinical decision tools for prediction of pulmonary embolism. This topic is covered in a BMJ Learning module called 'Step by step: how to diagnose pulmonary embolism', which is a practical guide for GPs available at www.learning.bmj.com - direct URL: https://goo.gl/NyN3FQ. The program starts with an interview with Dr Phil Wells, who is the author of the Wells score for deep vein thrombosis and pulmonary embolism. This is followed by a discussion with Dr Gregoire le Gal, author of the paper on age adjusted D-dimer. The last interview is with Dr Jeff Kline, who is the author of the PERC rule. The interviews are conducted by Dr Kerstin de Witt lead author of the BMJ Learning module on how to diagnose a pulmonary embolism.

health interview education british heart debate medicine conference journal medical roundtable gps score gal diagnose cardiology witt adjusted perc bmj gregoire pulmonary embolism d dimer jeff kline phil wells bmj learning

The Aorta Will %$#@!& You UO - David Carr

SMACC

Play Episode Listen Later Apr 6, 2017 23:46

The talk focuses on why clinicians miss the diagnosis on aortic dissection. It breaks down the key pearls on history and physical exam that guide you into correctly suspecting a dissection. Aortic dissection is a challenging diagnosis that you can not afford to miss. The talk aims to give you the framework to avoid missing the diagnosis. I want to raise the bar so that the standard of care is not to miss a dissection when it presents atypically. The talk will also highlight strategies on what to do when you suspect the diagnosis. It will guide you to order the right imaging tests and begin the treatment promptly. Sit back and be ready to see dissections in a different light.

treatments controversies dissection david carr aorta aortic d dimer smaccdub

Journal Jam 9 – D-dimer to Rule Out Aortic Dissection

Hospital and Internal Medicine Podcast

Play Episode Listen Later Feb 7, 2017 46:12

The EM Cases Team is very excited to bring you not only a new format for the Journal Jam podcast but a new member of the team, Dr. Rory Spiegel, aka @EM_Nerd an Emergency Medicine physician from The University Maryland Medical Center in Baltimore, the founder of the EM Nerd blog and the co-host of the Annals of EM podcast. The new format sees Justin Morgenstern, Teresa Chan, Rory Spiegel and Anton Helman doing deep dives into the world's literature on specific practical questions while highlighting some important evidence-based medicine concepts. The question we ask in this Journal Jam podcast: Is there a role for D-dimer testing in the workup of aortic dissection in the ED? The post Journal Jam 9 – D-dimer to Rule Out Aortic Dissection appeared first on Emergency Medicine Cases.

journal baltimore emergency medicine annals aortic dissection d dimer teresa chan justin morgenstern anton helman emnerd

Pulmonary Embolism - part 1

Play Episode Listen Later Jun 3, 2016 17:50

The topics covered are D-Dimer testing, false positive over-diagnosis of PE on CT scanning, the ADJUST-PE study, and clinical signs and symptoms of a pulmonary embolism.

pe pulmonary embolism d dimer

D-Dimer (DDI)

Lab Values Podcast (Nursing Podcast, normal lab values for nurses for NCLEX®) by NRSNG

Play Episode Listen Later May 19, 2016 3:09

The post D-Dimer (DDI) appeared first on NURSING.com.

nursing d dimer lab values podcast

D-Dimer

Emergency Medical Minute

Play Episode Listen Later May 11, 2016 3:56

Age adjusted D-Dimer sensitivity and indications for a CT scan.

d dimer

Big Labs, Little People

Pediatric Emergency Playbook

Play Episode Listen Later Apr 1, 2016 31:34

It's a busy shift. Today no one seems to have a chief complaint. Someone sends a troponin on a child. Good, bad, or ugly, how are you going to interpret the result? And while we’re at it – what labs do I need to be careful with in children – sometimes the normal ranges of common labs can have our heads spinning! Read on to go from bread-and-butter pediatric blood work to answer the question – what’s up with troponin, lactate, d-dimer, and BNP in kids? A fundamental tenet of emergency medicine: We balance our obligation to detect a dangerous condition with our suspicion of the disease in given patient. Someone with a cough and fever may simply have a viral illness, or he may have pneumonia. Our obligation is to evaluate for the pneumonia. It’s ok if we “miss” the diagnosis of a cold. It could be bad if we don’t recognize the pneumonia. How do we decide? Another fundamental concept: The threshold. Depending on the disease and the particular patient, we have a threshold for testing, and the threshold for treating. Every presentation – and every patient for that matter – has a complicated interplay between what we are expected to diagnose, how much we suspect that particular serious diagnosis, and where testing and treating come into play. What's wrong with "throwing on some labs"? Easy to do right? They are but a click away… Often a good history and physical exam will help you to calibrate your investigational thresholds. This is especially true in children – the majority of pediatric ambulatory visits do not require blood work to make a decision about acute care. If your patient is ill, then by all means; otherwise, consider digging a bit deeper into the history, get collateral information, and make good use of your general observation skills. First, a brief word about basic labs. The punchline is, use a pediatric reference. If you don’t have a trusted online reference available during your shift, make sure you have something like a Harriett Lane Handbook accessible to you. Don’t rely on your hospital’s lab slip or electronic medical record to save you, unless you are sure that they use age-specific pediatric reference ranges to flag abnormal values. Believe it or not, in this 21st century of ours, some shops still use adult reference ranges when reporting laboratory values on children. Notable differences in basic chemistries Potassium: tends to run a bit higher in infants, because for the first year of life, your kidneys are inefficient in excreting potassium. BUN and creatinine: lower in children due to less muscle mass, and therefore less turnover (and usually lack of other chronic disease) Glucose: tends to run lower, as children are hypermetabolic and need regular feeding (!) Alkaline phosphatase: is always high in normal, growing children, due to bone turn over (also fond in liver, placenta, kidneys) Ammonia: high in infancy, due to immature liver, trends down to normal levels by toddlerhood ESR and CRP: low in healthy children, as chronic inflamation from comorbidities is not present; both increase steadily with age Thyroid function tests: all are markedly high in childhood, not as a sign of disease, but a marker of their increased metabolic activity Big Labs Troponin Reliably elevated in myocarditis, and may help to distinguish this from pericarditis (in addition to echocardiography) Other causes of elevated troponin in children include: strenuous activity, status epilepticus, toxins, sepsis, myocardial infarction (in children with congenital anomalies). Less common causes of troponemia are: Kawasaki disease, pediatric stroke, or neuromuscular disease. Don't go looking, if you won't do anything with the test. Brain natriuretic peptide (BNP) In adults, we typically think of a BNP < 100 pg/mL as not consistent with symptoms caused by volume overload. Luckily, we have data in children with congenital heart disease as well. Although each company's assay reports slightly different cut-offs, in general healthy pediatric values match healthy adult values. One exception is in the first week of life, when it is high even in healthy newborns, due to the recent transition from fetal to newborn circulation. Use of BNP in children has been studied in both clinic and ED settings. Cohen et al. in Pediatrics used BNP to differentiate acute heart failure from respiratory disease in infants admitted for respiratory distress. They compared infants with known CHF, lung disease, and matched them with controls. Later, Maher et al. used BNP in the emergency department to differentiate heart failure from respiratory causes in infants and children with heart failure and those with no past medical history. The bottom line is: BNP reliably distinguishes cardiac from respiratory causes of shortness of breath in children with a known diagnosis of heart failure. D-dimer To cut to the chase: d-dimer for use as a rule-out for pulmonary embolism has not been studied in children. The only data we have in using d-dimer in children is to prognosticate in established cases. It is only helpful to track therapy for children who have chronic clots. This is where our adult approach can get us into trouble. Basically, think of the d-dimer in children like it doesn’t even exist. It’s not helpful in our setting for our indications. An adult may have an idiopathic PE – in fact, up to a third of adults with PE have no known risk factor, which makes decision tools and risk stratification important in this population. Children with PE almost always have a reason for it. There is at least one identifiable risk factor in up to 98% of children with pulmonary embolism. The majority have at least two risk factors. If you’re suspecting deep venous thrombosis, perform ultrasonography, and skip the d-dimer. If you’re worried about PE, go directly to imaging. In stable patients, you may elect to use MR angiography or VQ scan, but most of us will go right to CT angiography. Radiation is always a concern, but if you need to know, get the test. This is yet another reminder that your threshold is going to be different in children when you think about PE – they should have a reason for it. After you have excluded other causes of their symptoms, if they have risk factors, and you are still concerned, then do the test you feel you need to keep this child safe. You are the test. Risk factors only inform you, and you’ll have to just pull the trigger on testing in the symptomatic child with risk factors. Lactate A sick child with sepsis syndrome? The short answer – yes. In the adult literature, we know that a lactate level above 4 mmol/L in patients with severe sepsis was associated with the need for critical care. This has been studied in children as well, and an elevated lactate in children – typically above 4 – was a predictor of prolonged ICU course and mortality in septic patients. The acute recognition and treatment of sepsis is first and foremost, clinical. And it’s all about perfusion and providing oxygen to the tissues. Lactate and other laboratory testing is not a substitute for clinical assessment – it should be used as an extension of your assessment. There are two main reasons for an elevated lactate: the stress state and the shock state. The stress state is due to hypermetabolism and an increase in glycolysis, as an example, in early sepsis. The shock state is due to tissue hypoxia, seen in septic shock. The confusion and frustration with lactate is that we often test the wrong people for it. We could use it to track treatment, and see if we can clear the lactate; decreased lactate levels are associated with a better outcome in adults. Serial clinical assessments are even more useful to gauge your success with treatment. We should use lactate to detect occult shock. Children compensate so well for shock, that subtle tissue hypoxia may not be detected until later. It may inform your decision for level of care, intensive care versus some other lower level. Have you every been in this situation: "Why, oh why, did we send a lactate?" There are times when a lactate is ordered – maybe by protocol or maybe accidentally – or maybe in retrospect, the patient didn’t need it. Here is a quick mnemonic to remember the reasons for an elevated lactate: LACTATES L – liver – any liver disease affects how lactate is metabolized by the Cori cycle A – albuterol (or for our international friends, salbutamol), beta-agonists like albuterol, increase lactate production via cyclic amp C – “can’t breathe” – respiratory distress and increased work of breathing shifts the ratio of aerobic and anerobic repiration T – toxins – all kinds of wonder drugs and recreational drugs do it – look up your patient’s list if you’re suspicious A – alcohol, not an infrequent offender T – thiamine deficiency – think of this in your cachectic or malnourished patients E – epinephrine – a by-product of the cori cycle, how lactate is metabolized. Difficult to interpret lactates when a patient is on an epinephrine drip. S – seizure or shock – most commonly septic, but can be any type: cardiogenic, bstructive, hypovolemic, distributive. Bottom line: high serum lactate levels have been associated with morbidity and mortality in children with sepsis and trauma, the two best-studied populations. A summary of how labs can help you – or hurt you – in pediatric emergency medicine: Have a good reference for normal values and always be skeptical of how your lab reports them. Troponin testing is great for the child with suspected cardiogenic shock, myocarditis, or in unwell children with congenital heart disease. BNP in children can be used just like you do in adults – to get a sense of whether the presenting symptoms are consistent with heart failure. D-dimer is mostly a waste of time in the PED. Lactate can be useful in the right patient – use it to risk-stratify the major trauma patient or the patient with sepsis that may be suffering from occult shock. And lastly, make sure that you are mindful of your threshold for testing, and our threshold for treatment. If will vary by disease and by the patient at hand. References Troponin Gupta SK, Naheed Z. Chest Pain in Two Athletic Male Adolescents Mimicking Myocardial Infarction. Pediatr Emer Care. 2014;30: 493-495. Kelley WE, Januzzi JL, Christenson RH. Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure. Clinical Chemistry. 2009; (55) 12:2098–2112. Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in Children: Elevated Troponin I Level Does Not Predict Outcome. Pediatr Cardiol. 2012; 33:1040–1045. Koerbin G, Potter JM, Abhayaratna WP et al. The distribution of cardiac troponin I in a population of healthy children: Lessons for adults. Clinica Chimica Acta. 2016; 417: 54–56. Liesemer K, Casper TC, Korgenski K, Menon SC. Use and Misuse of Serum Troponin Assays in Pediatric Practice. Am J Cardiol. 2012;110:284 –289. Newby KL et al. for the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. J Am Coll Cardiol. 2012; 60(23): 2427-2463. Schwartz MC, Wellen S, Rome JJ et al. Chest pain with elevated troponin assay in adolescents. Cardiology in the Young; 2013. 23: 353–360. BNP Auerbach SR, Richmond ME, Lamour JM. BNP Levels Predict Outcome in Pediatric Heart Failure Patients Post Hoc Analysis of the Pediatric Carvedilol Trial. Circ Heart Fail. 2010;3:606-611. Cohen S, Springer C, Avital A et al. Amino-Terminal Pro-Brain-Type Natriuretic Peptide: Heart or Lung Disease in Pediatric Respiratory Distress? Pediatrics. 2005;115:1347–1350. Fried I, Bar-Oz B, Algur N et al. Comparison of N-terminal Pro-B-Type Natriuretic Peptide Levels in Critically Ill Children With Sepsis Versus Acute Left Ventricular Dysfunction. Pediatrics. 2006; 118(4): 1165-1168. Koch A, Singer H. Normal values of B type natriuretic peptide in infants, children, and adolescents. Heart. 2003;89:875–878. Maher KO, Reed H, Cuadrado A et al. , B-Type Natriuretic Peptide in the Emergency Diagnosis of Critical Heart Disease in Children. Pediatrics. 2008;121:e1484–e1488. Mir TS, Marohn S, Laeer S, Eistelt M. Plasma Concentrations of N-Terminal Pro-Brain Natriuretic Peptide in Control Children From the Neonatal to Adolescent Period and in Children With Congestive Heart Failure. Pediatrics. 2002;110(6)1:6. Mir TS, Laux R, Hellwege HH et al. Plasma Concentrations of Aminoterminal Pro Atrial Natriuretic Peptide and Aminoterminal Pro Brain Natriuretic Peptide in Healthy Neonates: Marked and Rapid Increase After Birth. Pediatrics. 2003;112:896–899. D-Dimer Goldenberg NA, Knapp-Clevenger RA, Manco-Johnson MJ. Elevated Plasma Factor VIII and d-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children for the Mountain States Regional Thrombophilia Group. Pediatrics. 2003;112:896–899. Manco-Johnson MJ. How I treat venous thrombosis in children. Blood. 2006; 107(1)21-31. Naqvi M, Miller P, Feldman L, Shore BJ. Pediatric orthopaedic lower extremity trauma and venous thromboembolism. J Child Orthop. 015;9:381–384. Parasuraman S, Goldhaber SZ. Venous Thromboembolism in Children. Circulation. 2006;113:e12-e16. Strouse JJ, Tamma P, Kickler TS et al. D-Dimer for the Diagnosis of Venous Thromboembolism in Children. N Engl J Med. 2004;351:1081-8. Lactate Andersen LW, Mackenhauer J, Roberts JC et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013; 88(10): 1127–1140. Bai et al. Effectiveness of predicting in-hospital mortality in critically ill children by assessing blood lactate levels at admission. BMC Pediatrics. 2014; 14:83. Scott HF, Donoghue AJ, Gaieski DF et al. The Utility of Early Lactate Testing in Undifferentiated Pediatric Systemic Inflammatory Response Syndrome. Acad Emerg Med. 2012; 19:1276–1280. Shah A, Guyette F, Suffoletto B et al. Diagnostic Accuracy of a Single Point-of-Care Prehospital Serum Lactate for Predicting Outcomes in Pediatric Trauma Patients. Pediatr Emer Care. 2013; 29:715-719. Topjian AA, Clark AE, Casper TC et al. for the Pediatric Emergency Care Applied Research Network. Early Lactate Elevations Following Resuscitation From Pediatric Cardiac Arrest Are Associated With Increased Mortality. Pediatr Crit Care Med. 2013; 14(8): e380–e387. This post and podcast are dedicated to Daniel Cabrera, MD for his vision and his leadership in thinking 'outside the box'. Troponin | BNP | D-Dimer | Lactate Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Episode 15.0 – Adrenal Crises + D-dimer in Aortic Dissection

Core EM Podcast

Play Episode Listen Later Sep 28, 2015

Pearls from a core content talk on adrenal emergencies, a journal update looking at D-dimer in aortic dissection and some acid/base cases. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_15_0_Final.m4a Download Leave a Comment Tags: Acid Base, Adrenal Gland, Adrenal Insufficiency, Aortic Dissection, Congenital Adrenal Hyperplasia, D-dimer Show Notes Shownotes Asha SE, Miers JW. A systematic review and meta-analysis of D-dimer as a rule-out test for suspected acute aortic dissection. Ann Emerg Med 2015. PMID: 25805111 Dierks DB et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med 2015; 65: 32-42. PMID: 25529153 Acid-Base Cases Quick questions & answers: For acute respiratory acidosis or alkalosis, how much does the pH change for every 10mm change of PCO2? What is the Winter's formula? For stable chronic respiratory acidosis, for every 10 mm increase in PCO2, how much should the pH decrease by? For each of the following cases, please analyze the acid-base status (i.e. anion gap metabolic acidosis, respiratory alkalosis,

clinical crises pearls adrenal pmid adrenal glands acid base aortic dissection adrenal insufficiency ann emerg med d dimer pco2 congenital adrenal hyperplasia

Episode 15.0 – Adrenal Crises + D-dimer in Aortic Dissection

Core EM Podcast

Play Episode Listen Later Sep 28, 2015

clinical crises pearls adrenal pmid adrenal glands acid base aortic dissection adrenal insufficiency ann emerg med d dimer pco2 congenital adrenal hyperplasia

Episode 15.0 – Adrenal Crises + D-dimer in Aortic Dissection

Core EM Podcast

Play Episode Listen Later Sep 28, 2015

Pearls from a core content talk on adrenal emergencies, a journal update looking at D-dimer in aortic dissection and some acid/base cases. https://media.blubrry.com/coreem/content.blubrry.com/coreem/Podcast_Episode_15_0_Final.m4a Download Leave a Comment Tags: Acid Base, Adrenal Gland, Adrenal Insufficiency, Aortic Dissection, Congenital Adrenal Hyperplasia, D-dimer Show Notes Shownotes Asha SE, Miers JW. A systematic review and meta-analysis of D-dimer as a rule-out test for suspected acute aortic dissection. Ann Emerg Med 2015. PMID: 25805111 Dierks DB et al. Clinical policy: critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection. Ann Emerg Med 2015; 65: 32-42. PMID: 25529153 Acid-Base Cases Quick questions & answers: For acute respiratory acidosis or alkalosis, how much does the pH change for every 10mm change of PCO2? What is the Winter’s formula? For stable chronic respiratory acidosis, for every 10 mm increase in PCO2, how much should the pH decrease by? For each of the following cases, please analyze the acid-base status (i.e. anion gap metabolic acidosis, respiratory alkalosis,

clinical crises pearls adrenal pmid adrenal glands acid base aortic dissection adrenal insufficiency ann emerg med d dimer pco2 congenital adrenal hyperplasia

Episode 33 - Hemoptysis

FOAMcast - Emergency Medicine Core Content

Play Episode Listen Later Aug 30, 2015 19:13

This week we cover Dr. Ryan Radecki's post on Gestational Age Adjusted D-Dimer covering an article by Murphy et al. Then we review the differential diagnosis and workup of hemoptysis using Rosen's Emergency Medicine and Tintinalli as a guide. We have Rosh Review questions and more available on our website, FOAMcast.org. Thanks y'all! -Jeremy Faust and Lauren Westafer

pe foam adjusted pulmonary gestational embolism hemoptysis d dimer jeremy faust rosh review tintinalli lauren westafer rosen's emergency medicine

Episode 04 - English - D-Dimer Dilemma

NursEM - Nursing in Emergency

Play Episode Listen Later Apr 30, 2015 11:14

In this episode we discuss what the D-Dimer is and why we shouldn't be ordering them willy-nilly!Support the show (https://nursem.org/en/home/)

english dilemma d dimer

Journal Jam 1: Age Adjusted D-dimer with Jeff Kline and Jonathan Kirschner

Play Episode Listen Later Sep 15, 2014 34:29

In this first ever episode of the Journal Jam podcast, a collaboration between EM Cases, Academic Life in EM and The Annals of Emergency Medicine's Global Emergency Medicine Journal Club, Teresa Chan and I, along with Jeff Kline, Jonathan Kirschner, Anand Swaminathan, Salim Rezaie and Sam Shaikh from ALiEM, discuss the potential for Age Adjusted D-dimer to rule out pulmonary embolism in low risk patients over the age of 50. We discuss 4 key questions about the ADJUST-PE Study from JAMA in March 2014 including: Would you order a CTPA on a 60 year old woman with an age adjusted D-dimer of 590 ng/L? The problem until now has been that the older the patient, the more likely the D-dimer is to be positive whether they have a PE or not, so many of us have thrown the D-dimer out the window in older patients and go straight to CTPA, even in low risk patients. If you are a risk averse doc, this strategy will lead to over-utilization of resources, huge costs, length of stay, radiation effects etc; and if you're not so risk averse, then you might decide not to work up the low risk older patient at all and miss clinically important PEs. expert peer reviewFor all the questions discussed on this podcast, the original Google Hangout interview from which this podcast was based, and the crowd sourced opinions from around world, visit the ALiEM website. Many thanks to all the talented people who made this podcast possible. Together, we're smarter! The post Journal Jam 1: Age Adjusted D-dimer with Jeff Kline and Jonathan Kirschner appeared first on Emergency Medicine Cases.

journal pe emergency medicine jama google hangouts pes annals adjusted kirschner academic life d dimer jeff kline salim rezaie anand swaminathan teresa chan aliem ctpa em cases

Journal Jam 1: Age Adjusted D-dimer with Jeff Kline and Jonathan Kirschner