Covid 19 autopsies reveal thrombosis...

[Dave-G]

I saw something the other day about Aspirin can help Covid recovery or words to that effect. Now someone has posted up more about blood thickening/clotting - and it can be found on several Google results - including the dreaded facebook.

I'm no good at wading through real or fake news as we all know so perhaps some of our more capable sleuths can dig into this a bit?

 

https://www.cidrap.umn.edu/news-perspective/2020/05/autopsies-covid-19-patients-reveal-clotting-concerns

Some of us oldies will be on blood thinning medication - which MIGHT bode well for us?

Edited May 17, 2020 by Dave-G

[Raja Clavata]

It's been widely reported as an issue affecting some patients with COVID, just like lots of aspects of the virus not yet very well understood, but it's one I've been following.

[oldypigeonpopper]

hello, Asprin can also have bad side effects if used as a blood clotting agent,

[Medic1281]

here is a little bit of info on it. The other thing that seems really important is vitamin D, most people in the uk are deficient in this vitamin. There is a belief that lack of vitD is the reason for more dark skinned patients dying from covid. 
 

 

https://www.ascopost.com/news/april-2020/hypercoagulability-in-critically-ill-patients-with-covid-19/

[JohnfromUK]

I think it has been a known fact that various prolonged hospital/ill in bed stays can increase the risk of clotting - and I had understood this was (at least in part) due to lack of physical activity (a bit like the long stationary period in long travel journeys can increase clotting risks).  In the Covid instance - I have read that there are possibly additional changes to the blood that make it 'more sticky' and maybe Aspirin isn't the right thing for that?.

17 minutes ago, Medic1281 said:

The other thing that seems really important is vitamin D

This seems another very valid point - again, not well understood in relation to Covid specifically, but vitamin D shortage is already associated with weakened immune system.  Unlike many vitamins which we get through eating a balanced diet, vitamin D is not found in many foods (so not usually diet related), but is made in the body by exposure to sunlight.  Those who get little sunlight (often the elderly who don't get out much and those who dress to cover up fully) risk vitamin D shortages, especially in winter when sun and outside exposure are less.  Dark skin doesn't absorb the suns rays as easily.  Vitamin D can be taken as a supplement where deficiency occurs.

Like all medicines, both anti clotting things (like Aspirin) and additional vitamins can have side effects in some people and if too great a dose is taken, and don't suit everyone.  Proper medical advice should be taken, especially for those on other medications or with medical conditions.  I do take regular Aspirin, but under medical direction and get grilled accordingly at periodic reviews to ensure it is the right thing to take it.

10 hours ago, Dave-G said:

I saw something the other day about Aspirin

As above - it would be wise to seek medical advice before taking as it can have side effects.

Edited May 18, 2020 by JohnfromUK

[Mice!]

Chestnut mushrooms are packed with vitamin D, I eat them raw.

 

[Fatcatsplat]

I knew i'd be gratful to warfarin one day. Makes up for being freezing most of the year!!

[Raja Clavata]

Clots caused by inactivity normally originate in the limbs and move to the heart or lungs once dislodged, whilst inactivity from being bed ridden by COVID may well be a contributing factor, from the material I have read it seemed more likely that in these cases it is localised in the lungs, which is aligned with the hypoxia affects of COVID.

I was "advised", after asking several times, to take aspirin on mountaineering trips at altitude but since I have access to far superior options - tablets in the form of rivaroxaban and clexane injections - I opted for the former. In discussing this with my GP and then a subsequent visit to see a DVT consultant I was flabberghasted at the lack of understanding and lateral thinking displayed by the Consultant around all this, at least my GP acknowledged my query and wasn't sure so referred me to an "expert".

Just now, Fatcatsplat said:

I knew i'd be gratful to warfarin one day. Makes up for being freezing most of the year!!

Get on the rivaroxaban mate, or at least ask about it! 👍

[henry d]

"The other thing that seems really important is vitamin D, most people in the uk are deficient in this vitamin."

I think we are ok with vit d, we had 10 days in the costas in October, and both spent plenty of time in the garden and have a good base tan already, Scotland eh!

[AVB]

44 minutes ago, henry d said:

"The other thing that seems really important is vitamin D, most people in the uk are deficient in this vitamin."

I think we are ok with vit d, we had 10 days in the costas in October, and both spent plenty of time in the garden and have a good base tan already, Scotland eh!

My tan has never been this good at this time of year. 

[Fatcatsplat]

1 hour ago, Raja Clavata said:

Get on the rivaroxaban mate, or at least ask about it! 👍

Regrettably not for me - It doesn't fit my condition, so monthly testing and varying doses

[Mice!]

42 minutes ago, Fatcatsplat said:

Regrettably not for me - It doesn't fit my condition, so monthly testing and varying doses

Well a relative of mine has just ended up in hospital because of meds being changed, not want you want at the moment,  so if they change anything be sure to question them. 

[7daysinaweek]

1 hour ago, Raja Clavata said:

Clots caused by inactivity normally originate in the limbs and move to the heart or lungs once dislodged, whilst inactivity from being bed ridden by COVID may well be a contributing factor, from the material I have read it seemed more likely that in these cases it is localised in the lungs, which is aligned with the hypoxia affects of COVID.

I was "advised", after asking several times, to take aspirin on mountaineering trips at altitude but since I have access to far superior options - tablets in the form of rivaroxaban and clexane injections - I opted for the former. In discussing this with my GP and then a subsequent visit to see a DVT consultant I was flabberghasted at the lack of understanding and lateral thinking displayed by the Consultant around all this, at least my GP acknowledged my query and wasn't sure so referred me to an "expert".

Get on the rivaroxaban mate, or at least ask about it! 👍

Hi Raja

I suspect what you are making reference to  is the developing picture of thrombosis in relation to Covid is the over production of pro inflammatory cytokine chemicals in the response to the infection. As the inflammation increases it creates a cascade release of blood clotting factors in the initial immune response this leads to further increasing levels of Cytokines chemicals being  produced and these appear to be the cardinal ones. Large levels of cytokines produce an overwhelming inflammatory response which leads to multi organ damage, this results in a homeostatic response from the body and production of increasing amounts of clotting factors which makes the blood more sticky. The clotting cascade is a tightly controlled mechanism, however in the large inflammatory response some anti clotting thrombin factors which inhibit the formation of thrombin clots are disrupted among other anticoagulant factors thus increasing the production of blood clots and microthrombi. The immobility of patients with severe pneumonia, hypoxia, ARDS puts patients at a increase risk of thrombotic events exacerbating incidence. All these factors are associated with poorer outcomes.

The physiology of community acquired  pneumonia (CAP)  of thrombi production at lower levels is well documented and can result in the increased risks associated with higher risk thrombotic events. From the current evidence based and pragmatic observations it would appears that Covid produces are much larger inflammatory response within the lung. The initial pathway of pathology of Covid is primarily a respiratory one. Hypoxia can result in acute respiratory distress syndrome (ARDS) but is also seen in bacterial pneumonia.

At the height of the pandemic the media reported on "problems with equipment", what was becoming evident was increasing numbers of ICU patients with a Covid infection requiring arterial monitoring lines changing much more frequently, it is now more understood this is due to the increase in clotting factors making blood more stickier. This has been increasingly reported across the globe. Giving the increased incidence of thrombotic events supported by several recent high level evidence based studies clinicians are reminded to hold a low diagnostic threshold for patients whose clinical picture does not fit the the diagnostic picture, for example the CXR result does not correlate with hypoxic 02 levels among other factors, though this is not a new, prompting is demonstrating the increasing incidence of these pathological events with covid up and above other pneumonia infections.

One recent high level evidence based study  of 80 ICU patients with a severe covid disease noted that  25% had a lower leg deep vein thrombosis (DVT) and none of these 25% had been on prophylactic anticoagulant medication for management of dvt prior to admission so it is extremely likely that the patients developed the thrombosis from a covid infection. Another ICU study demonstrated that patients with severe covid infections were at around 6 times risk of pulmonary embolism (PE) and 2.5 times risk associated thrombotic events, VTE, (dvt)

I have seen in the other threads posters stating about the death rates in the uk, my own assumption is that the Uk has "the" highest rate of all cause respiratory disease in the eu, north America and Australia, only one exception to this is lung cancer which we are not the highest. There are approximately 12 million people in the uk with a underlying respiratory condition. We have some of the highest rates of auto immune inflammatory disease in the world, approx 5 million, the EU has slightly more at around 6.5 million. Approx 7.5 million people with circulatory/heart disease and around 4 million with diabetes, the two latter can be found at lower and increased levels in other countries with in the eu ,these conditions increase the incidence for worse outcomes in severe disease cumulatively. As I have previously stated "Covid pathology is primarily a respiratory one" which can lead to further complications and worse outcomes. Hopefully time will give us the  data and a improved insight into this pandemic in relation to societal disease burden. 

I do not wish to spread fear ,I am just highlighting the current evidence and some of my thoughts. Again like I have said in my other threads that not all patients who are admitted end up with severe pneumonia, sepsis or ARDS, many are admitted to lower level dependency Covid wards and not icu and  not all will  not require ventilation. There are millions of people in the UK living with long term conditions every day who are "health optimised" through their gp and nhs services and in the current climate we can see that we have not had millions of referrals into hospital which puts things into a somewhat sensible perspective. 

Regarding the use of rivaroxaban that is a NOAC , it has many benefits over traditional oral anticoagulants such as non plasma monitoring (inr checks) reduced bleed risks among a few others. However its has a short half life and it is not suitable for patients who have a history of reduced pharmacological concordance (taking medication at infrequent times ) as the risk of increased thrombotic events. Like many medications it is contraindicated in some thrombotic risk conditions.

3 hours ago, Mice! said:

Well a relative of mine has just ended up in hospital because of meds being changed, not want you want at the moment,  so if they change anything be sure to question them. 

I hope they be on the mend very soon K

atb

7diaw

 

 

[Raja Clavata]

19 minutes ago, 7daysinaweek said:

Hi Raja

I suspect what you are making reference to  is the developing picture of thrombosis in relation to Covid is the over production of pro inflammatory cytokine chemicals in the response to the infection. As the inflammation increases it creates a cascade release of blood clotting factors in the initial immune response this leads to further increasing levels of Cytokines chemicals being  produced and these appear to be the cardinal ones. Large levels of cytokines produce an overwhelming inflammatory response which leads to multi organ damage, this results in a homeostatic response from the body and production of increasing amounts of clotting factors which makes the blood more sticky. The clotting cascade is a tightly controlled mechanism, however in the large inflammatory response some anti clotting thrombin factors which inhibit the formation of thrombin clots are disrupted among other anticoagulant factors thus increasing the production of blood clots and microthrombi. The immobility of patients with severe pneumonia, hypoxia, ARDS puts patients at a increase risk of thrombotic events exacerbating incidence. All these factors are associated with poorer outcomes.

The physiology of community acquired  pneumonia (CAP)  of thrombi production at lower levels is well documented and can result in the increased risks associated with higher risk thrombotic events. From the current evidence based and pragmatic observations it would appears that Covid produces are much larger inflammatory response within the lung. The initial pathway of pathology of Covid is primarily a respiratory one. Hypoxia can result in acute respiratory distress syndrome (ARDS) but is also seen in bacterial pneumonia.

At the height of the pandemic the media reported on "problems with equipment", what was becoming evident was increasing numbers of ICU patients with a Covid infection requiring arterial monitoring lines changing much more frequently, it is now more understood this is due to the increase in clotting factors making blood more stickier. This has been increasingly reported across the globe. Giving the increased incidence of thrombotic events supported by several recent high level evidence based studies clinicians are reminded to hold a low diagnostic threshold for patients whose clinical picture does not fit the the diagnostic picture, for example the CXR result does not correlate with hypoxic 02 levels among other factors, though this is not a new, prompting is demonstrating the increasing incidence of these pathological events with covid up and above other pneumonia infections.

One recent high level evidence based study  of 80 ICU patients with a severe covid disease noted that  25% had a lower leg deep vein thrombosis (DVT) and none of these 25% had been on prophylactic anticoagulant medication for management of dvt prior to admission so it is extremely likely that the patients developed the thrombosis from a covid infection. Another ICU study demonstrated that patients with severe covid infections were at around 6 times risk of pulmonary embolism (PE) and 2.5 times risk associated thrombotic events, VTE, (dvt)

I have seen in the other threads posters stating about the death rates in the uk, my own assumption is that the Uk has "the" highest rate of all cause respiratory disease in the eu, north America and Australia, only one exception to this is lung cancer which we are not the highest. There are approximately 12 million people in the uk with a underlying respiratory condition. We have some of the highest rates of auto immune inflammatory disease in the world, approx 5 million, the EU has slightly more at around 6.5 million. Approx 7.5 million people with circulatory/heart disease and around 4 million with diabetes, the two latter can be found at lower and increased levels in other countries with in the eu ,these conditions increase the incidence for worse outcomes in severe disease cumulatively. As I have previously stated "Covid pathology is primarily a respiratory one" which can lead to further complications and worse outcomes. Hopefully time will give us the  data and a improved insight into this pandemic in relation to societal disease burden. 

I do not wish to spread fear ,I am just highlighting the current evidence and some of my thoughts. Again like I have said in my other threads that not all patients who are admitted end up with severe pneumonia, sepsis or ARDS, many are admitted to lower level dependency Covid wards and not icu and  not all will  not require ventilation. There are millions of people in the UK living with long term conditions every day who are "health optimised" through their gp and nhs services and in the current climate we can see that we have not had millions of referrals into hospital which puts things into a somewhat sensible perspective. 

Regarding the use of rivaroxaban that is a NOAC , it has many benefits over traditional oral anticoagulants such as non plasma monitoring (inr checks) reduced bleed risks among a few others. However its has a short half life and it is not suitable for patients who have a history of reduced pharmacological concordance (taking medication at infrequent times ) as the risk of increased thrombotic events. Like many medications it is contraindicated in some thrombotic risk conditions.

 

Fantastic insight, thank-you!

I'd assume the classic D-dimer test is of no real use in COVID patients as the increased level of inflammation would be expected irrespective of presence or absence of a clot?

[7daysinaweek]

1 hour ago, Raja Clavata said:

Fantastic insight, thank-you!

I'd assume the classic D-dimer test is of no real use in COVID patients as the increased level of inflammation would be expected irrespective of presence or absence of a clot?

Yes you are correct to a greater extent.

A raised d dimer does not always indicate a  thrombus, ultrasound of the limb is the gold standard for dvt (VTE). d dimer can be raised in other inflammatory conditions, liver disease, heart failure ,sepsis among many others. Some recent Covid studies have shown individuals with mid range d dimer and confirmed dvt,  others conversely had a raised d dimer and no dvt. d dimer alone does not  always confirm or refute a thrombus and should be used to guide the clinical picture, diagnostics ,risk benefits and treatments.If a thrombus is present the larger the thrombus the likelihood more d dimer levels are produced.

d dimer is a non specific protein which is commonly elevated in pneumonia because of the inflammatory response so it is not possible to establish if raised levels are the result of a thrombus alone.

Pulmonary embolism (PE) cannot be seen directly on a plain film xray and diagnostics for pe can range from raised d dimer with ct scanning to inform/confirm diagnosis.

 

👍

 

Edited May 18, 2020 by 7daysinaweek

[stumfelter]

1 hour ago, 7daysinaweek said:

Hi Raja

I suspect what you are making reference to  is the developing picture of thrombosis in relation to Covid is the over production of pro inflammatory cytokine chemicals in the response to the infection. As the inflammation increases it creates a cascade release of blood clotting factors in the initial immune response this leads to further increasing levels of Cytokines chemicals being  produced and these appear to be the cardinal ones. Large levels of cytokines produce an overwhelming inflammatory response which leads to multi organ damage, this results in a homeostatic response from the body and production of increasing amounts of clotting factors which makes the blood more sticky. The clotting cascade is a tightly controlled mechanism, however in the large inflammatory response some anti clotting thrombin factors which inhibit the formation of thrombin clots are disrupted among other anticoagulant factors thus increasing the production of blood clots and microthrombi. The immobility of patients with severe pneumonia, hypoxia, ARDS puts patients at a increase risk of thrombotic events exacerbating incidence. All these factors are associated with poorer outcomes.

The physiology of community acquired  pneumonia (CAP)  of thrombi production at lower levels is well documented and can result in the increased risks associated with higher risk thrombotic events. From the current evidence based and pragmatic observations it would appears that Covid produces are much larger inflammatory response within the lung. The initial pathway of pathology of Covid is primarily a respiratory one. Hypoxia can result in acute respiratory distress syndrome (ARDS) but is also seen in bacterial pneumonia.

At the height of the pandemic the media reported on "problems with equipment", what was becoming evident was increasing numbers of ICU patients with a Covid infection requiring arterial monitoring lines changing much more frequently, it is now more understood this is due to the increase in clotting factors making blood more stickier. This has been increasingly reported across the globe. Giving the increased incidence of thrombotic events supported by several recent high level evidence based studies clinicians are reminded to hold a low diagnostic threshold for patients whose clinical picture does not fit the the diagnostic picture, for example the CXR result does not correlate with hypoxic 02 levels among other factors, though this is not a new, prompting is demonstrating the increasing incidence of these pathological events with covid up and above other pneumonia infections.

One recent high level evidence based study  of 80 ICU patients with a severe covid disease noted that  25% had a lower leg deep vein thrombosis (DVT) and none of these 25% had been on prophylactic anticoagulant medication for management of dvt prior to admission so it is extremely likely that the patients developed the thrombosis from a covid infection. Another ICU study demonstrated that patients with severe covid infections were at around 6 times risk of pulmonary embolism (PE) and 2.5 times risk associated thrombotic events, VTE, (dvt)

I have seen in the other threads posters stating about the death rates in the uk, my own assumption is that the Uk has "the" highest rate of all cause respiratory disease in the eu, north America and Australia, only one exception to this is lung cancer which we are not the highest. There are approximately 12 million people in the uk with a underlying respiratory condition. We have some of the highest rates of auto immune inflammatory disease in the world, approx 5 million, the EU has slightly more at around 6.5 million. Approx 7.5 million people with circulatory/heart disease and around 4 million with diabetes, the two latter can be found at lower and increased levels in other countries with in the eu ,these conditions increase the incidence for worse outcomes in severe disease cumulatively. As I have previously stated "Covid pathology is primarily a respiratory one" which can lead to further complications and worse outcomes. Hopefully time will give us the  data and a improved insight into this pandemic in relation to societal disease burden. 

I do not wish to spread fear ,I am just highlighting the current evidence and some of my thoughts. Again like I have said in my other threads that not all patients who are admitted end up with severe pneumonia, sepsis or ARDS, many are admitted to lower level dependency Covid wards and not icu and  not all will  not require ventilation. There are millions of people in the UK living with long term conditions every day who are "health optimised" through their gp and nhs services and in the current climate we can see that we have not had millions of referrals into hospital which puts things into a somewhat sensible perspective. 

Regarding the use of rivaroxaban that is a NOAC , it has many benefits over traditional oral anticoagulants such as non plasma monitoring (inr checks) reduced bleed risks among a few others. However its has a short half life and it is not suitable for patients who have a history of reduced pharmacological concordance (taking medication at infrequent times ) as the risk of increased thrombotic events. Like many medications it is contraindicated in some thrombotic risk conditions.

I hope they be on the mend very soon K

atb

7diaw

 

 

I was just going to post the very same thing but you beat me to it.  😁😁

[mel b3]

13 minutes ago, stumfelter said:

I was just going to post the very same thing but you beat me to it.  😁😁

you beat me to it 

[Dave-G]

Well despite the seriously well informed replies being well above my comprehension grade, I'm glad I asked - thank you all.

As I have a stent fitted I guess I ought to continue shielding myself a little more than most and will raise this issue with doctor - online consultations seem to work quite well ATM.

[Raja Clavata]

2 hours ago, 7daysinaweek said:

Yes you are correct to a greater extent.

A raised d dimer does not always indicate a  thrombus, ultrasound of the limb is the gold standard for dvt (VTE). d dimer can be raised in other inflammatory conditions, liver disease, heart failure ,sepsis among many others. Some recent Covid studies have shown individuals with mid range d dimer and confirmed dvt,  others conversely had a raised d dimer and no dvt. d dimer alone does not  always confirm or refute a thrombus and should be used to guide the clinical picture, diagnostics ,risk benefits and treatments.If a thrombus is present the larger the thrombus the likelihood more d dimer levels are produced.

d dimer is a non specific protein which is commonly elevated in pneumonia because of the inflammatory response so it is not possible to establish if raised levels are the result of a thrombus alone.

Pulmonary embolism (PE) cannot be seen directly on a plain film xray and diagnostics for pe can range from raised d dimer with ct scanning to inform/confirm diagnosis.

 

👍

 

Cheers for that. Without going too far off topic - in 2014, when I was probably the fittest I've ever been in my life (45bpm resting HR, Vo2Max > 50 etc.) I was diagnosed with a small DVT in my lower left calf after an over-night return flight from Nairobi following a particularly stressful and traumatic two weeks abroad. The d dimer test suggested my complaints of discomfort were not phantom and the ultrasound confirmed it.

In 2017 I had changed jobs and was working in the Midlands during the week, returning home at weekends, after a month of working stupidly long hours (a bit like now, sigh) I felt the same issue in the calf. Took myself off to the local A&E and after a night waiting there had the d dimer test then later in the morning an ultrasound. Whilst the d dimer was high there was no sign of a clot so they immediately discharged me.

Returning home on the Friday, I awoke Saturday morning with discomfort in the calf slightly elevated, despite feeling like I was being a bit OCD, I took myself back to my local A&E. Couple hours later and 30 seconds on the ultrasound with the same technician as back in 2014 and bingo, small DVT in exactly the same place.

My point for sharing this relates to the notion of the gold standard for DVT, which I'm aware of in principle, but have first hand experience to suggest it's dependent on the machine used and / or the diligence of the technician. What would have happened if I wasn't such a PITA or if I was physically or mentally compromised to the point that I couldn't present myself to A&E twice in those couple days...

[Raja Clavata]

51 minutes ago, Dave-G said:

Well despite the seriously well informed replies being well above my comprehension grade, I'm glad I asked - thank you all.

As I have a stent fitted I guess I ought to continue shielding myself a little more than most and will raise this issue with doctor - online consultations seem to work quite well ATM.

Dave - I think the take-away from this is, if you've ever had any issues with clotting and are unfortunate enough to get COVID bad then ensure that the medical folks looking after you are aware of the fact from day one! ATB

[Dave-G]

1 minute ago, Raja Clavata said:

Dave - I think the take-away from this is, if you've ever had any issues with clotting and are unfortunate enough to get COVID bad then ensure that the medical folks looking after you are aware of the fact from day one! ATB

Thanks for that advice. I've queried this with the online medication request facility at our clinic.

As it happens my stent was fitted after getting chest pains that were diagnosed as angina. After having the stent placed into an artery beneath my heart from a small tube pushed into a vein in my wrist I have had no further issues. Amazing procedure that was - all done while I watched it on a monitor. 

[7daysinaweek]

16 hours ago, Raja Clavata said:

Cheers for that. Without going too far off topic - in 2014, when I was probably the fittest I've ever been in my life (45bpm resting HR, Vo2Max > 50 etc.) I was diagnosed with a small DVT in my lower left calf after an over-night return flight from Nairobi following a particularly stressful and traumatic two weeks abroad. The d dimer test suggested my complaints of discomfort were not phantom and the ultrasound confirmed it.

In 2017 I had changed jobs and was working in the Midlands during the week, returning home at weekends, after a month of working stupidly long hours (a bit like now, sigh) I felt the same issue in the calf. Took myself off to the local A&E and after a night waiting there had the d dimer test then later in the morning an ultrasound. Whilst the d dimer was high there was no sign of a clot so they immediately discharged me.

Returning home on the Friday, I awoke Saturday morning with discomfort in the calf slightly elevated, despite feeling like I was being a bit OCD, I took myself back to my local A&E. Couple hours later and 30 seconds on the ultrasound with the same technician as back in 2014 and bingo, small DVT in exactly the same place.

My point for sharing this relates to the notion of the gold standard for DVT, which I'm aware of in principle, but have first hand experience to suggest it's dependent on the machine used and / or the diligence of the technician. What would have happened if I wasn't such a PITA or if I was physically or mentally compromised to the point that I couldn't present myself to A&E twice in those couple days...

Hi Raja

From the raised d dimer and initial non finding of the clot it may have been so small it was not picked up or not fully formed and the blood flow distal of the developing thrombus was still within adequate parameters. However,it is possible it was missed, I think around 1 in a 600 venous thrombolitic embolus are "missed" on doppler scanning. (my old boss was a VTE specialist) I can recall him telling me the rates a few years ago.

If you had a "Wells score" of greater than 2 or more?, given what you say from a raised d dimer and a negative initial scan and your history of previous vte a clinical decision to interim anticoagulate would have been appropriate then re d dimer and doppler scan 6-8 days later.

I take it they gave you the "red flag symptoms" safety netting advice of worsening symptom concerns and to return/review without delay and any onset of chest pain onset, sob, haemoptysis (coughing up blood) to ring 999 ? This gives the patient informed decision accountability.

atb

7diaw

 

Edited May 19, 2020 by 7daysinaweek

[Vince Green]

I thought the blood clots and thickening of the blood was a known problem from the very earliest days? 

[Dave-G]

1 hour ago, Vince Green said:

I thought the blood clots and thickening of the blood was a known problem from the very earliest days? 

I hadn't seen or heard anything about that. 

[7daysinaweek]

33 minutes ago, Vince Green said:

I thought the blood clots and thickening of the blood was a known problem from the very earliest days? 

I think I know what you are saying Vince. What I was trying to say and should have worded better was that as the infection spread  globally and throughout the duration of the pandemic has shown an ever increasing prevalence of clotting complications as the disease has transmitted to different populations. When I speak of multi organ damage, this can be detected early on in patients admitted to higher dependence area and this cascade can be set off in some people quite early on resulting in thrombus production. In ICU patient with covid commonly present with a degree of single organ failure, e.g., the lungs and micro organ damage to one or more other organs from the immune response. Covid also produces an inflammatory response in many areas of the body resulting in increased inflammatory responses which is damaging at a micro level, it does not always mean that it will lead to multi organ failure. The process of response, damage and repair happens all the time there are just different levels of it. The awareness of the clotting disorders has been known since early stages as more of the data comes in, it is the wider awareness of the mechanisms and higher incidences that are being more reported and raised.

atb

7diaw