Posted on 01/01/2021 7:24:16 AM PST by zeestephen
Louisiana Rep.-elect Luke Letlow, who died of COVID-19 complications, was operated on for a blood clot before he succumbed to a heart attack, according to a new report. The 41-year-old Republican underwent two procedures to treat a blood clot that he developed while he battled the coronavirus...The second operation appeared to be successful on Tuesday but he died later that day from a heart attack at Ochsner LSU Health in Shreveport...
(Excerpt) Read more at dnyuz.com ...
Totally agree. I have a niece in charge of hospital management in Miami FL. She was totally freaked out about the cases in the hospitals. I asked her how many cases of Flu were they having. She point blank said no cases of flu at all. Go figure...
What protocol was used to treat the COVID? Did he know he had a heart condition? Or was it 1 of the drugs used in the protocol treatment causing the blood clot?
BTW Why is a BACTERIAL ANTIBIOTIC being used on a Virus?
Dexamethasone reduces immune system weird, as COVID ATTACKS WEAKEN INMUNE SYSTEMS. https://www.webmd.com/drugs/2/drug-1027-5021/dexamethasone-oral/dexamethasone-oral/details
Azithromycin, It is for BACTERIAL INFECTIONS. Azithromycin is used to treat a wide variety of bacterial infections. It is a macrolide-type antibiotic. It works by stopping the growth of BACTERIA. This medication will NOT work for viral infections (such as common cold, flu) ALL CRONAVIRUSES. .https://www.healthwarehouse.com/azithromycin-250mg-tablets-6-tablet-pack.html#:~:text=USES%3A%20Azithromycin%20is%20used%20to,as%20common%20cold%2C%20flu).
Mostly eat chicken salad on Triscuits (fiber)
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I’m a big label reader. Triscuits seem to be one of the healhiest snacks out there. And the new flavors taste great. High fiber, protein, and low in sugar, fat , and salt.
...but you might want to revisit the 25 mph for 20 min. unless your last name is Bolt or you are a Cheetah.
Thanks, Mom...I’ve been given heparin since Wednesday evening, so hopefully that’ll do the trick. All my labs look good, I didn’t really have any of the serious Covid symptoms; the doctor seems pretty positive about things. (Famous last words?)
“Blood clots are an increased risk for flu as well.”
That is nice. But THIS time, the blood clots were COVID related, not flue related.
Re: Why is a BACTERIAL ANTIBIOTIC being used on a Virus?
I can make a guess.
Trying to prevent bacterial pneumonia?
I’m no doctor, but it’s not at all unusual to prescribe a Z-Pac or other antibacterial for common flu, as bacterial lung infections often follow a flu-weakened immune system.
Covid DOES cause clotting in some people.
Shit happens. It doesn’t happen often, but it happens.
You should do well. Hopefully you are home soon!
Blood clots are a much higher risk with covid than with flu.
Because people who walk around don’t get life threatening pulmonary embolus
If you hear hoof beats it’s not a zebra
The presentation of any other prothrombotic disease as a saddle PE is so rare as to be reportable.
It is clear as a bell to those of us who treat this disease. But If you need to believe that this is a conspiracy have at it
Take care, and I truly wish you well!
That is changing as we discuss this:(last updated December 24, 2020). Like everything else we have been told about Covid~19.
COVID-19 and VTE/Anticoagulation: Frequently Asked Questions
(Version 5.1; last updated December 24, 2020)
Input from Drs. Lisa Baumann Kreuziger, Agnes Lee, David Garcia, Adam Cuker, Mary Cushman, Maria DeSancho, and Jean M. Connors
Note: Please review ASH’s disclaimer regarding the use of the following information.
Is COVID-19 associated with an increased risk for venous thromboembolism (VTE)?
The incidence of VTE in COVID-19 patients varies depending on the patient population. Reports have ranged from 1.1% in non-ICU hospital wards to 69% in ICU patients screened with lower extremity ultrasound.
Small sample sizes, retrospective design and differences in patient characteristics, co-morbidities, hospital and ICU admission criteria, criteria for diagnostic imaging, and COVID-19 therapies likely contribute to this wide range of estimates.
Like other medical patients, those with more severe disease, especially if they have additional risk factors (e.g. older, male, obesity, cancer, history of VTE, comorbid diseases, ICU care), have a higher risk of VTE than those with mild or asymptomatic disease. The risk of VTE following hospital discharge appears low and similar to other patients following a medical admission. VTE rate in those who do not require hospitalization has not been reported. The benefit of thromboprophylaxis in these patients is being investigated in a placebo-controlled randomized controlled trial.
What is the recommended VTE prophylaxis in patients with COVID-19?
All hospitalized adults with COVID-19 should receive pharmacologic thromboprophylaxis with LMWH over unfractionated heparin to reduce contact, unless the risk of bleeding outweighs the risk of thrombosis. In the setting of heparin-induced thrombocytopenia, fondaparinux is recommended. Dose adjustment for obesity may be used per institutional guidance. In patients where anticoagulants are contraindicated or unavailable, use mechanical thromboprophylaxis (e.g. pneumatic compression devices). Combined pharmacologic and mechanical prophylaxis is not generally recommended.
Optimal anticoagulant dosing to reduce thrombotic complications is being actively investigated. The ASH guideline panel suggests using prophylactic-intensity over intermediate-intensity or therapeutic-intensity anticoagulation in patients with COVID-19 related critical illness who do not have suspected or confirmed VTE. We encourage participation in ongoing clinical trials and epidemiologic studies.
Should therapeutic dose anticoagulation be empirically used in COVID-19 patients requiring ICU level care (i.e., in the absence of confirmed or suspected VTE)?
Microvascular thrombosis is hypothesized to be involved in hypoxemic respiratory failure in some patients with COVID-19. Autopsy studies show large vessel and microvascular thrombosis, pulmonary hemorrhage and high prevalence of VTE.
Although retrospective cohort studies of patients treated or not treated with therapeutic anticoagulation have been published, such observational data should not be used to support changes in practice due to survivor bias, confounding by indication, and lack of adjustment for important patient comorbidities and other treatments.
Recently, enrollment of patients requiring ICU level of care in the 3 ongoing multiplatform trials (REMAP-CAP, ATTACC and ACTIV-4A) was paused (as of December 21, 2020) due to an interim pooled analysis demonstrating futility of therapeutic-intensity anticoagulation in reducing the need for organ support over the first 21 days compared with standard-intensity prophylaxis in this specific subgroup. ICU level of care and organ support were defined as requiring high flow nasal oxygen, invasive or noninvasive mechanical ventilation, vasopressor therapy, or ECMO support.
Additional outcomes have not yet been reported. This FAQ will be updated as more information becomes available. Enrollment in these three trials is continuing for patients who require hospitalization but do not require an ICU level of care at time of enrollment. Patients who require therapeutic anticoagulation for other indications are not enrolled in these trials.
Consequently, we discourage the empiric use of therapeutic-intensity heparin or LMWH in COVID-19 patients with no other indication for therapeutic anticoagulation, outside a clinical trial. Patients should be given therapeutic anticoagulation only as otherwise indicated. We recommend participation in ongoing clinical trials and epidemiologic studies.
How should we manage COVID-19 patients who experience recurrent clotting of access devices (e.g., central venous catheters, arterial lines) or extracorporeal circuits (e.g., CRRT, ECMO) despite prophylactic anticoagulation?
Although of unproven benefit, it may be reasonable to increase the intensity of anticoagulation (i.e., from standard-intensity prophylaxis to intermediate-intensity prophylaxis or from intermediate-intensity prophylaxis to therapeutic-intensity) or switch anticoagulants in these settings. Any decision to increase the intensity of anticoagulation should take into account the individual patient’s bleeding risk.
Should COVID-19 patients receive post-discharge thromboprophylaxis?
Patients hospitalized for acute medical illness are at increased risk for VTE for up to 90 days after discharge. A symptomatic VTE incidence between 0-0.6% at 30-42 days post discharge has been reported in patients with COVID-19. Whether post-discharge thromboprophylaxis is warranted is being investigated in clinical trials and enrollment is encouraged.
Any decision to use post-discharge thromboprophylaxis should consider the individual patient’s VTE risk factors at the time of discharge, including reduced mobility and bleeding risk, as well as feasibility. For example, COVID-19 patients who are discharged early to free up inpatient beds (“home hospital” approach) might still have significantly reduced mobility.
Aspirin has been studied for VTE prophylaxis in low-risk patients after hip or knee arthroplasty and is currently being investigated for COVID-19 post-discharge thromboprophylaxis.
Patients should be educated on the signs and symptoms of VTE at hospital discharge and advised to seek urgent medical attention should these develop.
If a patient with COVID-19 requires therapeutic anticoagulation for VTE or AFIB stroke prevention, are there any special considerations?
Multiple medications are being used for COVID-19 treatment. Dexamethasone is an inducer of CYP3A4 and the extent of the drug interaction with direct oral anticoagulants is unknown. Sarilumab (KEVZARA) and tocilizumab (ACTEMRA) can increase cytochrome P450 enzyme activity and so they should not be used together with apixaban (Eliquis®) or rivaroxaban (Xarelto®) and may also increase the doses of warfarin required. Atazanavir and lopinavir/ritonavir will increase drug concentrations of apixaban and rivaroxaban and decrease the active metabolite of clopidogrel and prasugrel.
The University of Liverpool has collated a list of drug interactions (Link: http://covid19-druginteractions.org/). LMWH or UFH in hospitalized critically ill patients is preferred because of the shorter half-life and fewer drug-drug interactions compared with direct oral anticoagulants.
Regular warfarin users who are unable to get INR monitoring during isolation may be candidates for direct oral anticoagulant therapy (add link), but patients with mechanical heart valves, ventricular assist devices, valvular atrial fibrillation, antiphospholipid antibody syndrome, or lactation should continue treatment with warfarin therapy. LMWH or UFH remain the anticoagulants of choice in pregnancy.
For additional information, see:
2018 ASH VTE guidelines – prevention in medical patients
2018 ASH VTE guidelines – anticoagulation therapy
COVID-19 drug interactions
Transitioning to DOAC from Coumadin, British Columbia Ministry of Health, BC
https://docs.google.com/document/d/1sPM98LodBHoNPtriu0Bm94SXEYuq0fFwdSUEPXlRkMU/edit
I’m sure it was a typo doc. I think the original question used there language.
The Covid came first
Yes ‘they’ can say what ‘they’ want BUT the breakdown has to be
Died FROM BeerFlu
or
Died WITH BeerFlu.
To throw out EVERY other cause of death because the person showed symptoms of or even had the BeerFlu is potentially criminal....It should not be the ONLY cause of death listed.
One would think Hospitals and Funeral Homes could charge more for tending to one with the BeerFlu....(SARC)
FOLLOW THE MONEY
Well, you are just...wrong
Thank you for your medical opinion. I just researched blood clot (platelets sticking together), which can be caused by many reasons. What special Scooby-Do process does Covid create more blood clots? I suspect laying in a hospital bed or genetic predisposition in this case. I can't imagine the cardio specialists didn't have this man on anti-coagulants. My guess is he had a bad heart after all they did. And no, I've not even stayed at a Holiday Inn.
It is not easy to tell what goes wrong. I had an irregular heart beat so they suggested blood thinners and aspirin. Then I had a procedure (ablation) where a microwave probe is inserted in an artery and run up inside the heart. Because of the action of trying to fuse heart beat tissue, they add additional blood thinner, (In my case I was on heperin and plavix). Somehow my brain started leaking and developing pressure (subdural hematoma). This lasted for weeks without me understanding that something was wrong. (I was stronger on my left side, so walked in circles when trying to walk straight lines.) When they eventually discovered this I was so far gone that they had to open my skull and clean and drain. I am OK, but this actually happened a second time on a different set of blood thinners. Now I live blood thinner free and have a clamp on part of my heart where blood clots form (Lower Atrial Appendage). I have a permanent a-fib condition and lung problems because I also had blood clots that went into the lung.
The message is that modern medicine is not able to cope with everything, And yet we do the best we can.
So this is the problem with people who think that they can read internet and have expertise
Azithromycin is a macrolide antibiotic that has bacteriostatic properties. It also has demonstrable anti-inflammatory and anti viral activity. If you advocate for ivermectin guess what. Ivermectin is also a macrolide
It is usually wise to know what you are talking about before spouting off. But we seem to have lost that here at free republic.
Your anti knowledge and clear lack of understanding of anything medical combined with your attempts to sound as if you have any idea what the f*ck you are talking about is really getting tedious.
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