Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, February 11, 2021

Combination of oral corticoid, aspirin, anticoagulant, colchicine and furosemide may improve outcome of hospitalised COVID-19 patients

 I had all but furosemide, direct anti-Xa inhibitor and salicylate already on my list. But this suggests for hospitalized patients, I think that is way too late.

But I'm not medically trained so don't listen to me. Don't tough this out at home. 

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Heparin:

Why I'm getting heparin.  Heparin binds to cells at a site adjacent to ACE2, the portal for SARS-CoV-2 infection, and "potently" blocks the virus, which could open up therapy options.

Anticoagulation Again Shown to Improve Survival in COVID-19 Patients;-Mortality risk about 50% lower

But this research below suggests not due to bleeding risks. I'll take that risk since I've been on warfarin, aspirin and had Lovenox shots. 

COVID-Related Strokes Especially Severe, Result in Worse Outcomes

The paragraph from there:

"On the other hand, in most patients with COVID-19 associated ischaemic stroke, very early anti-coagulation is probably not warranted as a strategy to prevent inpatient stroke recurrence, as this outcome is too uncommon to justify the increased risk of secondary haemorrhage," according to the group.(So you wait until the clots are severe before you do anti-coagulation. OK, not for me.)

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Colchicine:

Colchicine reduces hospitalization, death in COVID-19

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Aspirin:

This Common Medication Could Save You From Deadly COVID Complications

Researchers found that hospitalized COVID patients who took a daily low dose of aspirin had a significantly lower risk of complications and death from the virus. Aspirin users were 43 percent less likely to be put in the intensive care unit (ICU) and 44 percent less likely to be placed on a ventilator. They also had a 47 percent decrease in the risk of dying from their coronavirus infection compared to hospitalized patients who were not taking daily aspirin doses.

But I'm sure your doctor will be more worried about bleeding risks from aspirin. I'm doing 325(low dose is 81) and have been for 15 years.

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The latest here:

Combination of oral corticoid, aspirin, anticoagulant, colchicine and furosemide may improve outcome of hospitalised COVID-19 patients

An early short-course oral regimen combining prednisolone, colchicine, salicylate, direct anti-Xa inhibitor and furosemide may reduce the risk of high flow oxygen need, mechanical ventilation requirement or 28-day mortality in hospitalised non-critically ill coronavirus disease 2019 (COVID-19) patients, according to a study published in the Journal of Infection

“Based on the data [from previous studies] and the pathophysiology of COVID-19 and its complications, i.e. thrombosis, inflammation and congestion, we hypothesised that a five-drug regimen consisting in a 5-day course of 1mg/kg/day prednisone, 80 mg/day furosemide, 75 mg/day salicylate, colchicine (1mg loading dose followed by 0.5 mg one hour later then 0.5 mg every 8h as recommended to treat acute gout) and direct anti-Xa inhibitor such as rivaroxaban or apixaban would optimally mitigate COVID-19-attributed mortality,” wrote Jean-Philippe Kevorkian, Université de Paris, Paris, France and colleagues. 

A total of 68 non-critically ill COVID-19 patients (median age, 66 years) requiring >1L/min-oxygen admitted between January 9 and November 30, 2020 were included in this observational study. Of the patients, 28 (41%) received the five drug-therapy regimen while 40 (59%) in the control group were treated with dexamethasone (6 mg once daily for up to 10 days). The primary composite endpoint was the requirement of high-flow oxygen therapy, non-invasive or invasive mechanical ventilation (corresponding to care escalation from ward to intensive care unit [ICU]) or 28-day mortality).

Among patients receiving the five-drug regimen, study data showed that the incidence of primary composite endpoint was lower than that in the control group (odds ratio [OR], 0.097; 95% confidence interval [CI], 0.001-0.48; P = 0.0009). Multivariate analysis confirmed the significant effect of the five-drug regimen on outcome after adjusting for covariates including age, body-mass index, 4C Mortality Score, high serum brain natriuretic peptide (BNP) level and high white blood cell count (OR, 0.043; 95% CI, 0.0053-0.21; P = 0.0005).

Additionally, the researchers analysed patient subgroups following stratification by age, gender and risk factors including diabetes, elevated BNP (threshold, 100ng/ml) and troponin levels (threshold, 16ng/mL). They found that the five-drug regimen was associated with a significant reduction in primary composite endpoint in males only (OR, 0.059; 95% CI, 0.01-0.45; P = 0.0009). Further, the primary composite endpoint was improved in patients with elevated-BNP compared with low-BNP patients (P = 0.0003).

“The five drugs included in our regimen were given orally for a short course, paving the way for an outpatient treatment,” the authors noted. Nonetheless, they said that these preliminary observational findings should be confirmed in larger cohorts.

SOURCE: Journal of Infection
 
 
 

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