Tag Archives: clotting

General

Central Line Insertion Causes Hypercoagulability?

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Again, I’m not a fan of animal studies. But this one, presented at EAST 2012 and now published, involves both pigs and humans and is so intriguing I just have to share it. The authors have a track record of studying coagulation issues with thromboelastography (TEG) in both animals and people. They previously showed that hypercoagulability detectable by TEG occurs after insertion of pulmonary artery catheters in swine and critically ill humans.

In this follow-on study, they looked at TEG profiles in 16 healthy swine and 8 critically ill humans after insertion of a central venous catheter (CVC). They found that CVC insertion induced the same type of hypercoagulable state. TEG clotting time and initial clot formation time decreased, and fibrin cross-linking accelerated. The changes were somewhat less in humans, but were still significant in both groups. All coag tests (PT, PTT, INR) and measured coag factors (von Willebrand, AT III) were unchanged.

Interestingly, in the animal group the hypercoagulable state persisted for at least 3 hours after CVC removal. And the hypercoagulability could be prevented with enoxaparin, but not heparin.

Bottom line: The idea that hypercoagulability could be induced by central arterial or venous catheter placement is intriguing, although this work has not been replicated by others yet. What if hypercoagulability occurs with any invasion of the vascular system? We may eventually discover that the increased incidence of DVT we have been fighting in the hospital setting is in part due to our ubiquitous use of IVs and routine blood draws.

Reference: Insertion of central venous catheters induces a hypercoagulable state. J Trauma 73(2):385-390, 2012.

General

Papers To Change Our Practice 1: Tranexamic Acid

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The first paper I’ll be presenting on Friday at the Penn Reunion deals with tranexamic acid (TXA). This drug works differently than the quick clotting agents out there. It’s an antifibrinolytic, so it actually prevents clot breakdown. It has been approved by the FDA for use in hemophiliacs undergoing dental work and for menorrhagia. Thrombotic complications have been described, so it cannot be used with prothrombin complex concentrate or recombinant activated factor VII.

The most recent and best known study on TXA is the CRASH-2 study. It was extremely well designed and included over 20,000 patients in hospitals spanning 40 countries. The study design has survived serious scrutiny. They found that TXA use in trauma patients reduced the relative risk of death by 9% (from 16% to 14.5%). The risk of death specifically from bleeding was reduced by 15%. And use of TXA in the most severely injured patients, those who would die of bleeding on the day of randomization, was reduced by 20%. CRASH-2 suggested that TXA was of most benefit when given within 3 hours of injury and in patients with a systolic pressure less than or equal to 75 torr. There were no adverse events or differences in thrombotic events, including deep venous thrombosis.

Bottom line: TXA has been shown to be effective, safe and inexpensive (about $200 for treatment using retail pricing). It is the only drug that has been shown to reduce all-cause mortality from bleeding in a high quality trial. And it only needs to be used in 67 major trauma patients before one life will be saved. It has already been adopted by some hospitals in both the US and the UK. Trauma centers should begin to think about incorporating this important drug into their initial treatment protocols now. HOWEVER: Since it is not FDA approved in the US, we may have to wait a little longer here to start using it in earnest. And think about the possibilities when EMS can start giving it in the field!

Reference: Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2): a randomised, placebo-controlled trial. Lancet. 2010;376:23–32.

General

Central Line Insertion Causes Hypercoagulability?

Leave a comment

Again, I’m not a fan of animal studies. But this one, presented at EAST 2012, involves both pigs and humans and is so intriguing I just have to share it. The authors have a track record of studying coagulation issues with thromboelastography (TEG) in both animals and people. They previously showed that hypercoagulability detectable by TEG occurs after insertion of pulmonary artery catheters in swine and critically ill humans.

In this follow-on study, they looked at TEG profiles in 16 healthy swine and 8 critically ill humans after insertion of a central venous catheter (CVC). They found that CVC insertion induced the same type of hypercoagulable state. TEG clotting time and initial clot formation time decreased, and fibrin cross-linking accelerated. The changes were somewhat less in humans, but were still significant in both groups. All coag tests (PT, PTT, INR) and measured coag factors (von Willebrand, AT III) were unchanged.

Interestingly, in the animal group the hypercoagulable state persisted for at least 3 hours after CVC removal. And the hypercoagulability could be prevented with enoxaparin, but not heparin.

Bottom line: The idea that hypercoagulability could be induced by central arterial or venous catheter placement is intriguing, although this work has not been replicated by others yet. What if hypercoagulability occurs with any invasion of the vascular system? We may eventually discover that the increased incidence of DVT we have been fighting in the hospital setting is in part due to our ubiquitous use of IVs and routine blood draws.

Reference: Insertion of central venous catheters induces a hypercoagulable state. Presented at the 25th Annual Scientific Assembly of EAST, Orlando FL, 2012.