Tag Archives: ROTEM

How To Make TEG / ROTEM Useful

A lot of papers have been written on the use of thromboelastography in trauma. And pretty much any meeting or course you may attend has at least one talk on it. And I get it. It can be an important tool in treating trauma patients who have some sort of coagulation disturbance. It helps us figure out what specific part of the coagulation process is out of whack and suggests how we can fix it.

But there are a few problems, as I mentioned yesterday. And the “friction” that those issues cause overall decreases how useful it is. Here’s a partial list of the problems:

  • The equipment costs money, and the disposables that must be used for every patient do, too.
  • Where do you put the machine? Most hospitals can’t put one unit in every possible area it might be used.
  • How to you get the results to a care area if there is no unit there?
  • There is a significant learning curve for interpreting the results
  • How can it be integrated into the massive transfusion protocol?

The main issue is that the current state of TEG and ROTEM are very similar to the state of electrocardiography shortly after it’s discovery. Here’s what you got then:

In order to get the most from an EKG, you need to combine this tracing with that from other leads, do a bunch of measurements, look for abnormal shapes and elevations/depressions, etc.  This is exactly where we are with TEG and ROTEM today. Relatively crude, and it takes a lot of work to use it.

The tracing below shows where we are with EKGs today. A computer program looks at all the tracings, and rapidly applies a complex set of rules to come to a set of diagnoses. Notice in the image below that this reading is “unconfirmed.” But how many times in your career have you seen a cardiologist correct one of these? The machines are actually very good!

Bottom line: The tracing above is where we need to be with TEG and ROTEM. Instead of a clinician staring at a developing tracing and figuring out what products to give, these machines need to be just like an automated EKG machine. Sure, a human can still stare at the trace. But the machine will automatically monitor it, apply rules about what abnormalities are present and what is needed to correct them. Send off your blood specimen, and within minutes instructions like “infuse 2 units of plasma now” or “give 12u cryo now” appear. These may be displayed on a monitor in the treatment area, or be broadcast to the phone or pager of the responsible clinicians.

Current TEG/ROTEM equipment is what I would consider 1st generation. The next generation will reduce or remove much of the “friction” in the current process and allow us to really integrate TEG/ROTEM meaningfully into the massive transfusion protocol for trauma. And for anyone who develops this 2nd generation equipment, don’t forget my royalty checks for this idea! 

Related post:

Does Hemostatic Resuscitation Really Work?

Hemostatic resuscitation (HR) is the new buzzword (buzz phrase?) these days. The new ATLS course touts it as a big change, and quite a few publications are being written about it. But, like many new things (think Factor VII), will it stand the test of time?

It has long been recognized that hemorrhage from trauma is bad. Mortality rates are high, and traditional management with crystalloids and then blood products leads to persistent coagulopathy, troublesome bleeding, tissue injury, and finally death. HR was devised to address the early coagulopathy. It concentrates on early coag correction with plasma and platelets, permissive hypotension, and rapid definitive correction of hemorrhage.

The end result of HR has been measured, and both organ perfusion and coagulopathy can be corrected with it. Unfortunately, these measurements are typically taken once hemorrhage control has been achieved. Is looking at (or beyond) the endpoint really the best way to gauge its effectiveness? 

A robust multicenter study scrutinized looked at coagulopathy correction and organ perfusion during active hemostatic resuscitation. They used ROTEM to gauge the former, and lactate levels for the latter. Values were measured on arrival and after administration of every 4 units of blood. Only patients who received at least 4 units were included (106 subjects).

Here are the factoids:

  • Average admission lactate was 6.2 meq/L, so these patients were sick
  • Patients with a lactate > 5 did not clear it until after hemorrhage was controlled and no further blood was needed
  • 43% of patients were coagulopathic by ROTEM on arrival. 
  • Coagulopathy increased for every 4 units of blood given, despite a plasma infusion ratio of close to 1:1 throughout their resuscitation

Bottom line: This was a well-done study on a relatively large number of patients, although a number of weaknesses and potential improvements are pointed out in the discussion. There’s a lot of data in the paper, and I urge you to read it in depth. But it seems to show that hemostatic resuscitation is not necessarily doing what we want it to do during the acute phase of hemorrhage. Both bleeding AND transfusions must be stopped before it appears to work. And even then, there is a delay before ROTEM and lactate parameters return to normal. For now, rapid control of hemorrhage is of utmost importance. We still need to figure out how tools like ROTEM or TEG and various serum markers will help us while we accomplish it.

Reference: Hemostatic resuscitation is neither hemostatic nor resuscitative in trauma hemorrhage. J Trauma 76(3):561-568, 2014.

Does Hemostatic Resuscitation Really Work?

Hemostatic resuscitation (HR) is the new buzzword (buzz phrase?) these days. The new ATLS course touts it as a big change, and quite a few publications are being written about it. But, like many new things (think Factor VII), will it stand the test of time?

It has long been recognized that hemorrhage from trauma is bad. Mortality rates are high, and traditional management with crystalloids and then blood products leads to persistent coagulopathy, troublesome bleeding, tissue injury, and finally death. HR was devised to address the early coagulopathy. It concentrates on early coag correction with plasma and platelets, permissive hypotension, and rapid definitive correction of hemorrhage.

The end result of HR has been measured, and both organ perfusion and coagulopathy can be corrected with it. Unfortunately, these measurements are typically taken once hemorrhage control has been achieved. Is looking at (or beyond) the endpoint really the best way to gauge its effectiveness? 

A robust multicenter study scrutinized looked at coagulopathy correction and organ perfusion during active hemostatic resuscitation. They used ROTEM to gauge the former, and lactate levels for the latter. Values were measured on arrival and after administration of every 4 units of blood. Only patients who received at least 4 units were included (106 subjects).

Here are the factoids:

  • Average admission lactate was 6.2 meq/L, so these patients were sick
  • Patients with a lactate > 5 did not clear it until after hemorrhage was controlled and no further blood was needed
  • 43% of patients were coagulopathic by ROTEM on arrival. 
  • Coagulopathy increased for every 4 units of blood given, despite a plasma infusion ratio of close to 1:1 throughout their resuscitation

Bottom line: This was a well-done study on a relatively large number of patients, although a number of weaknesses and potential improvements are pointed out in the discussion. There’s a lot of data in the paper, and I urge you to read it in depth. But it seems to show that hemostatic resuscitation is not necessarily doing what we want it to do during the acute phase of hemorrhage. Both bleeding AND transfusions must be stopped before it appears to work. And even then, there is a delay before ROTEM and lactate parameters return to normal. For now, rapid control of hemorrhage is of utmost importance. We still need to figure out how tools like ROTEM or TEG and various serum markers will help us while we accomplish it.

Reference: Hemostatic resuscitation is neither hemostatic nor resuscitative in trauma hemorrhage. J Trauma 76(3):561-568, 2014.