This is a comments/discussion page for folks to weigh in on how they are managing COVID-19 DIC.
The section in the IBCC discussing this can be found here.
Whenever possible, please cite relevant literature and list your name/affiliation.
Thanks for sharing your insights!
Josh Farkas. How should we manage COVID DIC??. EMCrit Blog. Published on March 29, 2020. Accessed on March 11th 2026. Available at [https://cmefix.emcrit.org/squirt/covid-dic/ ].
The course director, Dr. Scott D. Weingart MD FCCM, reports no relevant financial relationships with ineligible companies. This episode’s speaker(s) report no relevant financial relationships with ineligible companies unless listed above.
Original Release: March 29, 2020
Date of Most Recent Review: Jul 1, 2024
Termination Date: Jul 1, 2027
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A few thoughts, on what might be happening – although I do not know how to treat the clotting:
– Fibrinogen is made mostly in the liver
– SARS-CoV-2 has been shown to invade liver cells
– And very rudely hijack the cells into fused syncytial virus factories:
– Glycoproteins: Fibrinogen has them.
– SARS-CoV-2 seems to love them…?
– What’s going on here?
– See: novel coronavirus preferentially attacking / latching onto glycated hemoglobin
– Series of tweets / research paper
– Probably one reason why diabetics are high risk.
– My dad is a doctor (family medicine) and when I asked him about the hemoglobin, he said:
– “Glycated” just means it’s got a bunch of sugar (moieties) stuck on it. It isn’t functioning very well.
– Makes the outside more “sticky” on a molecular level.
– Causes cloudy vision in diabetics; the glucose sticks to the lens of the eye. It clears when the blood sugar goes down – washes off.
– My take: virus is eating the juicy, sticky stragglers of the cells. A terrifying lion – impala situation.
– Dad also said: Please don’t quote me on this by name until you fact-check it, Sarah.
– (It’s been a while since med school; he did not expect a pop quiz)
– Again – I don’t really have useful advice on clotting, but –
– I do have some wild speculation about bromantane, for ARDS in general?
– Its precursor drug was developed as an antiviral for influenza
– It has been shown “to lower the levels of pro-inflammatory cytokines IL-6, IL-17 and IL-4”
– # 6 of which is involved in cytokine storm, that everybody wants to avoid
– A 1999 paper showed that bromantane raised hemoglobin and white blood cell count, for first 3 months
– And with all the heme-destroying and leukopenia going around – this seems useful
– Bromantane is well-tolerated and used as a nootropic by lots of internet nerds
– Although: it has a bit of an odd side effect, of occasionally making users somewhat sassy?
– (This is probably an OK tradeoff)
– See google doc linked below for more info
– Sarah McManus, @SarahAMcManus on Twitter
Medical background: none
Affiliation / conflicts: none, unless you count EndCoronavirus.org Slack group
(it has plenty of conflicts, let me tell you)
I have been stuck in my room, in self-quarantine
dealing with likely symptoms of neuroinvasive coronavirus
(feeling a bit better, as of yesterday!)
and googling a heck of a lot of research papers.
(I do have an academic background in systems ecology, and some PhD level work
so not unfamiliar with research papers and science communication
– although of course, human medicine is a whole giant thing unto itself, and not my specialty)
Work in progress – gathering these thoughts in simple terms, with extensive citations:
Simple language exploration: How COVID-19 sets off a Rube Goldberg Machine of Death
So: more thoughts, on the whole thing with syncytia and fusion proteins.
I think that:
As I have written in the document I linked above, wondering about what initially causes the lung surfactant dysfunction in ARDS:
– Something around here is sticky; I don’t know quite what it is, and I don’t like it.
With clotting in the middle of the bloodstream:
– Something around here is sticky, it absolutely should not be,
and we need a way to make it stop doing that as soon as possible.
I think it’s very much worth looking into:
Viral fusion proteins on the surface of SARS-CoV-2.
The virus can use these proteins to cause infected cells to fuse with other nearby cells.
It, in a word: is sticky and causing agglomeration.
As SARS-CoV-2 virus exits infected cells it “will leave little bits of S Protein on the surface.” – like little bits of cell velcro?
Here is a direct link to a section with more questions and links that I am collecting about the syncytia and the fusion proteins.
These tweets also have clear diagrams of the syncytia; see previous comment for a paper about syncytia in the liver.
Also:
There are a bunch of things floating around in the bloodstream that can also become sticky, and they can probably stick together into giant rafts of cellular detritus, that are showing up as little tiny drifting clots?
Immune cells: can be sticky.
Antibodies: can be sticky
Platelets: can be sticky.
Thrombin activates fibrinogen into crosslinked fibrin mesh: Sticky.
These viral fusion proteins: definitely sticky.
Glycated hemoglobin: more sticky than usual, more vulnerable to getting stuck?
Glycoproteins likely involved in a number of the sticky interactions.
Here are some references, many of which you all likely already know and I am putting them here for myself too:
– An absolutely top notch 2 minute video of how platelets aggregate with fibrin and thrombin. Really shows each cell receptor clearly, dynamically, and in an engaging way.
https://socratic.org/questions/what-is-the-difference-between-fibrinogen-fibrin-and-platelets
– Wikipedia on viruses that form syncytia and different ways they do this – mentions the fusion proteins and immune cell aggregations:
https://en.wikipedia.org/wiki/Syncytium#Viral_infection
–
Surfactant polymorphisms?
https://www.ncbi.nlm.nih.gov/pubmed/11076040
Close
https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.25887
COVID coagulopathy appears to be a form of thrombotic DIC. I know clinicians that have used tPA in critical patients; but the half-life of tPA is only 72 minutes. The DIC lasts much longer; this is not trying to open a coronary artery or lyse a clot in the pulmonary artery; this is an ongoing thrombotic coagulopathy that is causing organ failure. Of the 300+ studies listed at clinicaltrials.gov, there is only ONE trial listed that employs any anticoagulation at all, and there are no planned studies on thrombolytic/fibrinolytic therapy! For critically ill patients with elevated d-dimer, low fibrinogen and low platelets, we need a low-dose streptokinase infusion study… I’d propose a bolus of 125,000 units followed by a continuous infusion of 60,000 units per hour… what do you think???
We’ve been starting therapeutic anticoagulation on patients with elevated D-Dimer (>3.0 mg/L) + an elevated SIC score (>4) and using UFH primarily with a goal PTT 40-60.
We have changed our anticoagulation protocol and most of our critically ill patients are now on therapeutic bemiparin doses. We’ve been wondering about ADAMTS13 (and we’ve recently started measuring it) and if there is a role for plasma exchange in some of these patients. What’s your take on this?
Alexander Schult
re PLEX:
https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-2836-4
Quick question, I don’t have experience with TEG (Mexico, low resource hospital). Does the fact that heparin seems to not be working a peculiarity of COVID19? Is this something unique and different from other causes of severe sepsis?
You may have seen: onlinelibrary.wiley.com/doi/epdf/10.1111/jth14810
I believe the hypercoagulable state can be explained by covid19s downregulation of ACE2-> Increased Angiotensin II->
“High levels of angiotensin II cause arterial hypertension by a complex vascular
inflammatory pathway that requires leukocyte recruitment and reactive oxygen species production and is followed
by vascular dysfunction”
See the research article “Platelet-localized FXI promotes a vascular coagulation-
inflammatory circuit in arterial hypertension”
“platelet-localized thrombin generation was amplified in an FXI-dependent manner in
patients with uncontrolled arterial hypertension, suggesting that platelet-localized thrombin generation may serve
as an inflammatory marker of high blood pressure. Our results outline a coagulation-inflammation circuit that
promotes vascular dysfunction, and highlight the possible utility of FXI-targeted anticoagulants in treating hyper-
tension, beyond their application as antithrombotic agents in cardiovascular disease.”
https://stm.sciencemag.org/content/9/375/eaah4923.full
DOI: 10.1126/scitranslmed.aah4923
I’ve thought about this. We know based on the ATHOS-III trial that angiotensin use can promote thrombosis. Chronic hypertension with imbalance in the RAAS can promote macro and microthrombosis ( PMC3023299). Again, with everything COVID related, this is hypothesis inducing but could there be a role for inhibition of the system??
epoprostenol helpful?
covid binds ACE2 and depletes it, leading to high ANG2 levels- which is very bad causing clots, lung injury. We need ACE2- it counterregs RAS. produces ang 1-7, ang 1-9, ang 1-5 all beneficial for lung, heart, kidney…. until recombinant ACE2 available we can drop Ang2 and increase ang 1-7 via NEP pathway by giving an ace inhibitor ( enalaprit)
OVERVIEW:
https://blogs.sciencemag.org/pipeline/archives/2020/03/17/angiotensin-and-the-coronavirus
https://www.the-scientist.com/news-opinion/possible-biological-explanations-for-kids-escape-from-covid-19-67273
ace in sars- https://www.nature.com/articles/nm1267
higher ace2 levels in patients- the better they do-
https://www.preprints.org/manuscript/202003.0191/v1/download
https://pubmed.ncbi.nlm.nih.gov/32221983/
HIGH ANG2 causes lung injury- and portends worse prognosis in COVID-
https://link.springer.com/content/pdf/10.1007/s11427-020-1643-8.pdf#page8
https://www.ncbi.nlm.nih.gov/pubmed/12754187
high ang2 leads to clots –
https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.110.158220
https://cmefix.emcrit.org/pulmcrit/angiotensin-ii/
https://pubmed.ncbi.nlm.nih.gov/23414567/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023299/
http://europepmc.org/article/med/16391415
give aceI improved lung injury- https://thorax.bmj.com/content/62/6/527
https://europepmc.org/article/med/19748795
ACE2 produces ang 1-7. But covid decrease the ability to do this. Giving an ACE inhibitor will decrease negative effects of high Ang2 and increase ang 1-7 via NEP.
https://icm-experimental.springeropen.com/articles/10.1186/s40635-015-0044-3
recomb ACE- will bind virus and also give beneficial effects of Ace2 like production of ang 1-7 and ang1-5
https://pipelinereview.com/index.php/2020022673884/Proteins-and-Peptides/APEIRONs-respiratory-drug-product-to-start-pilot-clinical-trial-to-treat-coronavirus-diseaseCOVID-19-in-China.html
Ok. Here me out. The H1N1 epidemic had ARDS and autopsy specimen had microthrombi in the lungs. We put all of those patients on activated protein C. Any chance that drug and it’s 96 hour infusion might work for COVID-19? Theory seems good and patients are quite ill.
Has anyone had COVID patients with genetic thrombophilias (ie Factor V Leiden)? Was the disease course any different compared to someone without a genetic predisposition to clot?
Thank you so much for asking this question as I have a double factor of Factor V. I have found no information on the effects of covid 19 on Factor V. I am currently on warfarin. I am fairly healthy 53 year old female. I live in Denver area and so far have been spared the covid19 threat through social distancing. But I am extremely nervous as when they open schools up next fall. I feel we could be exposed to Covid 19 at that time. Well anyway Thank you for your selfless acts of saving lives at the risk of your own lives.
M Marrs
I’m in the exact same boat. I’m terrified of the implications of clotting with Covid-19 because Factor V already increases our likelihood of DVTs or PEs. I have homozygous (got it from both parents – according to my dr it’s like hitting the genetic lottery in terms of odds – lucky me ) so that means both my children also have it. I’m so unbelievably anxious about any of us catching this damn virus now.
You have my empathy. I’ve only got one marker, but my mother (who I inherited it from) had problems with clots during the 70s when I was a wee one so I’m very nervous too.
Unrelated to covid, have you ever had other symptoms that may be related to Factor V? I keep being told by my Dr that it won’t cause issues, but I think I have had baby clots throughout my body that have caused significant issues. I think this may not be well studied either because it is so rare and possibly because the techniques are not there to detect.
Yes, I would also like to hear about an experiences around COVID patients with genetic thrombophilias. Our family is deeply affected by Factor V and have years of collective experience with DVTs and PEs.
I too would like to know more about the increased Covid19 risks, if any, for those of us with Factor V Leiden. Has anyone found any studies addressing this issue?
I have yet to find any articles or data about Covid-19 and FVL. I read the clotting in the lungs was from excess coughing but that didn’t make sense to me. Hopefully it doesn’t have anything to do with Factor V
I’d be interested too. I’m heterozygous Factor V Leiden and I work in an essential job. I’m currently on LoA due to being high-risk, but am freaked about going back and have no idea when it would be ‘safe’ to do so. I’ve heard enough scary stuff about how COVID affects clotting and enough family background with clots that I’m nervous. I don’t mind going back to work, but I *do* mind the very real possibility of a perfect storm in my lungs. Thank you for all your help in this time.
I am also heterozygous, are we considered high risk?
My husband and son and many family members have Factor V as well. We are very concerned about the clotting reports as well. Trying to make decisions about returning to work/school and if the risks are greater for them. Any info would be helpful!
Apparently so far no one has actually had an answer to this but I am in the same boat as all the other people who have replied. So hoping someone answers this.
I also have Factor V Leiden and I’ve had a DVT in the past. I’m a teacher and I’d like to know if this condition puts me at risk of complications with CV19? I have asthma but it has only put me on the clinically vulnerable list. I’m not on anticoagulants. I cannot socially distance at school. Any help would be appreciated.
I have factor v Leiden and am heterogeneous. My father had it also but they caught his clots sooner. I have a calcified clot from foot to belly button. I have been concerned about coronavirus and the possibility that it will cause clots. I have an essential job and I haven’t taken a loa yet as there are only 9 cases in our county. I am also in the county where the infamous pool party at the lake of the ozarks photo was taken. I am very concerned, I don’t know if our blood thinners would be enough to help. I’m on warfarin.
I am also a teacher with Factor V and we haven’t been told yet about our district plans for next school year. I’m paranoid because I’m a single mother and I’m all my daughter has.
I’m in the same boat: I have factor v Leiden, I’ve already had a DVT, I’m a school teacher and my district is going back f2f 5 days a week not reducing class sizes, so around 40 per class. I have the same question and concerns as you, and it’s hard because they haven’t added blood clotting disorders to the high risk category.
I also have factor V Leiden and asthma. I am a teacher too. I worry about going back to school with 33-36 students, plus we have about 42 teachers and a huge support staff. I am wondering if I should be on blood thinners or something
This is only on case, but my sister-in-law has heterozygous FVL and got COVID and had a mild case. I would of course still love to see data on how people are faring with this condition.
I also have fvl and am currently on elliquis. How old is your sister-in-law that had Covid? Was she on a blood thinner? My school is going back to face to face instruction with no mandated masks. I am 43 and have taught for 21 years. There is no way to socially distance with 39 kids in a small classroom so I am terrified.
I’m lucky enough to be Factor V Leiden negative, but both my parents were heterozygous and my sister was unfortunate enough to inherit both genes and is homozygous. I’ve been concerned about her during the pandemic and like all of you responding below, have found virtually no info on the relationship between Factor V Leiden and Covid-19. I DID, however, recently find this (somewhat old given the evolution of other learnings about Covid-19) video posted by a doctor specializing in genetics related to cardiovascular disease. https://www.youtube.com/watch?v=VMeW0PVOmKU
It seems as though as of end-of-April, there was little-to-no consolidated clinical information/reports about the relationship between genetic clotting disorders and Covid-19, and I still can’t find any. However, this doctor seems to me to posit a ‘best guess’ based on extremely limited, ever-evolving covid-specific info that the relationship might not be multiplicative (yay!), but likely IS additive, meaning that…
(Keep in mind I’m VERY roughly estimating the “let’s say” assumption numbers if not almost making them up entirely.)
Keep in mind that with increased age and other risk factors (obesity, hormonal birth control, etc.), this doctor suggests that EVERYTHING is additive. So according to this expert’s opinion (based on very little available clinical Covid info), those with ANY previous risk factor for clotting, including Factor V AND other risks, should assume that their clotting risk factors are additive and they are at SOME increased risk compared with those with no clotting risk factors.
I know it’s not much but I hope this helps!
I have symptoms now and factor v Leiden. I had virtual dr visit last night and she said people with factor v Leiden ARE high risk! She also told me to get second test because first one was negative and I have same symptoms worse.
How are you doing?
I’m assuming there isn’t anything conclusive regarding this issue? I’m homozygous for FVL and heterozygous for 4 other clotting mutations, yay me! I’ve gone back to work, I sit in an office by myself and rarely come in contact with people, however, the cases in my city are still rising dramatically. I spoke to an ICU doctor about this and he said they are hoping our anticoagulants keep us safe, but that was months ago and things seem to have changed. If anyone finds something conclusive, I’d love to know. Y’all stay safe!
I’m a teacher with heterozygous Leiden Factor 5. I’m worried about my possible increased risk because I have the MTFKR gene. Hoping there’s some research soon that sheds some light on these kinds of genetic mutations and the likelihood of worse outcomes if we contract COVID.
I’m also following this thread hoping for more information. Also an educator. Also heterozygous for FVL.
I’m also a teacher with a school population of 3,000 kids and we are headed back in October. I have multiple clotting mutations, including FVL and survived two major clots so far. My little brother died of a PE at age 41. I am 49 and an avid runner/cyclist — but I’m terrified. Called my hematologist today to explore FMLA.
I have a COVID patient whose D-Dimer came back >22,000 (repeated multiple times and by two different labs to verify). His fibrinogen level was moderately elevated and I made the decision to start a heparin drip. His other labs such as LDH, CRP, etc. are improving. And his overall clinical picture is improving as well. Now I’m tasked with the decision of how long do I leave him on full anticoagulation. Any thoughts?
Hi David, I was hoping for a little advice. My dad is in the hospital for Covid with elevated D-Dimers (17,000) He is on day 23 of mechanical ventilation, and day 30 since symptom onset.
His vent settings are at 40% FIO2, Peep of 5. No organ damage. Normal blood pressure and heart rate. Although the virus has probably left his system by now, his D-Dimers continue to rise.
His doc refused to give him heparin IV, but then another doctor was brought in, who started him on Heparin therapy two days ago. (And since starting Heparin therapy, my dad’s unexplained consistent low-grade fever has gone away)
The original doctor is still insisting on discontinuing Heparin, but we think it’s necessary to prevent a future clot/heart attack.
I just wanted to ask, what did you end up doing for this patient? We are also confused on how long the heparin therapy should last,.
Thank you for your help
Hi to anyone reading — I just wanted to give an update. My dad survived his severe bout with Covid. He spent 31 days intubated, with another extra 7 days on ventilator with a trach. He is now home, and is doing well! Still weak, but improving every day.
Stay safe, everyone!
Eastern Virginia Medical School (EVMS) has some of the best treatment protocols for Covid I have seen. In their Critical Care COVID-19 Management Protocol (updated late Nov. 2020) here is what they list for Essential Treatment (dampening the STORM). Item 3. Full anticoagulation: Unless contraindicated we suggest FULL anticoagulation (on admission to the ICU) with enoxaparin, ie 1 mg kg s/c q 12 hourly (dose adjust with CrCl <30mls/min). Heparin is suggested with CrCl <15 ml/min. There are also 1., 2. and a Note. Suggest you look for EVMS site(s) on line.
Has anyone looked at complement levels in these patients?
Does anyone know if there are currently any studies looking to see if there is any correlation with those Covid patients who are having blood clotting complications and Factor V Leiden? There are six of us in our family who are heterozygous, Three adult siblings (ages 57-51) and three out of four of our children (Ages 20-22). Any information is appreciated. Like the others writing in this forum, we are afraid. It has been recommended by my hematologist to start a low dose of Xarelto at the earliest sign of Covid. Any thoughts on this?
My husband has Factor V Leiden and we are worried about his risk with covid. If anyone has any info on this it would be greatly appreciated! Thanks so much! He’s on Warfarin
Like everyone else, I’m nervous. I’m heterozygous and 42. I’m a professor whose school has chosen to open in the fall. I’m trying to decide if I should request to teach all online.
I am also concerned and trying to find out info on how patients with covid and Leiden Factor are being treated so I have some info if I do contract it. It seems like a lot of doctors don’t know much about it so I’m worried.
Posted above but here is again what I found.
I’m lucky enough to be Factor V Leiden negative, but both my parents were heterozygous and my sister was unfortunate enough to inherit both genes and is homozygous. I’ve been concerned about her during the pandemic and like all of you posting above, have found virtually no info on the relationship between Factor V Leiden and Covid-19. I DID, however, recently find this (somewhat old given the evolution of other learnings about Covid-19) video posted by a doctor specializing in genetics related to cardiovascular disease. https://www.youtube.com/watch?v=VMeW0PVOmKU
It seems as though as of end-of-April, there was little-to-no consolidated clinical information/reports about the relationship between genetic clotting disorders and Covid-19, and I still can’t find any. However, this doctor seems to me to posit a ‘best guess’ based on extremely limited, ever-evolving covid-specific info that the relationship might not be multiplicative (yay!), but likely IS additive, meaning that…
(Keep in mind I’m VERY roughly estimating the “let’s say” assumption numbers if not almost making them up entirely.)
Keep in mind that with increased age and other risk factors (obesity, hormonal birth control, etc.), this doctor suggests that EVERYTHING is additive. So according to this expert’s opinion (based on very little available clinical Covid info), those with ANY previous risk factor for clotting, including Factor V AND other risks, should assume that their clotting risk factors are additive and they are at SOME increased risk compared with those with no or even a subset of clotting risk factors.
I know it’s not much but I hope this helps!
Hi Sarah, I’m also a homozygote. My hematologist told me today that he would immediately put me on blood thinners if I get COVID, because he’s considering me high risk. He’s part of a large university study on the topic of coagulation and COVID. I’m taking great precautions not to get it. I hope this helps your sister. I’m also healthy, 47 years old, and have never had a major clot.
I was wondering if a doctor would suggest blood thinners now, but it sounds like not until you get Covid. I have FVL and asthma. I am a teacher that will eventually go back to teaching 33-36 students. Did your doctor suggest any other precautions? Just wondering..take care
Thank you Sarah for your post. I wish you and your sister well. Best, Kim
Recent research notes that Von Willebrand’s factor, when elevated, is predictive of severe COVID-19. It is causally associated with Blood Type A and high load of ACE-2 receptors, which have been identified in numerous articles as causally (?) associated with severe COVID-19. https://medicalxpress.com/news/2020-07-complications-covid-von-willebrand-factor.html
I am happy to see the underpinnings of coagulopathy being investigated. Since platelets are first responders to vascular injury and ride, after shear force unrolls WP particles exposing vWF surface to platelet aggregation in a FVIII environment, a perfect storm of hypercoagulation arises with the suppression of ADAMTS13. The situation cries for ASA addition to anticoagulation.l To guidelines even mention platelets.
Sorry Donald, this was not meant to be a reply just to your post, but I can’t figure out how to delete it and repost to the larger discussion. Anyway….
Now that some time has gone by, I wonder if any connections have been made between thrombofilias and Covid-19? My father, myself, and both of my children are heterozygous for FVL and FII (prothrombin gene mutation G20210A), and my father and I have histories of clotting; he is on warfarin and I am xarelto. We have been taking extra precautions on social distancing and wearing masks when out, and we kept my daughter virtual for school, as 87% of her school is back face to face. The worry and constant state of hermitage is taking its toll on all of us, but are we better safe than sorry? I feel like clotting issues definitely put us at higher risk, but to what extent? Are those of us on blood thinners better off than those that aren’t? Are children with clotting factors at an increased risk also, even though those factors don’t tend to be problematic until later in life? There seems to still be so many unanswered questions months and months into this virus.
In late March/early April I had a mild case of Covid with all of the standard symptoms, including slight fever, sore throat, shortness of breath, and fatigue – all of which resolved within 2 weeks. At the time of symptoms I noted some bowel discomfort and minor bowel changes. Late in May I awoke to intense abdominal pain and took myself to the ER where C-T scan showed significant large bowel changes, resulting in a right hemicolectomy. Apparently, a blood clot was noted to have blocked the mesenteric artery. After 10 days in hospital I was discharged. Follow up hematologic study revealed the presence of Factor 5 Leiden which, it was hypothesized, was activated by Covid. At the age of 66, this was my first blood clot. Cardiology installed a LINQ monitor to determine if AFib was present; after 4 months no episodes of AFib are noted. Complications are limited to scar tissue and one episode of stricture in the large intestine causing pain; a liquid and, later, soft diet (i.e., low fiber) is now in progress to help relax the large bowel and hopefully prevent future strictures and/or scar tissue difficulties.
Consider taking Vitamin C and Vitamin E to reduce scar tissue formation. Found this in Adelle Davis, “Let’s Eat Right to Keep Fit” or “Let’s Get Well” 50 years ago. Fixed a painful episiotomy scar in a week or 2, and softened a nickle sized 30 year old hard scar.
Streptokinase would theoretically be the most effective anticoagulant. It activates plasminogen, which attacks and dismembers the insoluble fibrin polymer into fibrin split products. It should dissolve both the strands of insoluble fibrin that form in arterial lumens and the “microemboli” that obstruct capillary flow. It was regarded as a “miracle drug” for treating heart attacks and ischemic strokes in the 1980’s. It has been extensively tested for safety and effectiveness, and has an excellent therapeutic record. Like many excellent drugs, it is no longer supported by pharmaceutical companies in North America because it its patent has expired, but it is available from its manufacturer in Germany. The second best alternatives would be urokinase and TPAccc