Tag Archives: TEG

General

EAST 2015: What If You Don’t Have TEG For Trauma?

Leave a comment

The new hot items in trauma care are thromboelastography (TEG) and ROTEM (thromboelastometry), a new spin on TEG from the TEM Corporation. These tools allow for in-depth assessment of factors that influence clotting. We know that rapidly recognizing and treating coagulopathy in major trauma patients can reduce mortality. So many trauma centers are clamoring to buy this technology, citing improved patient care as the reason.

But new technology is always expensive, and isn’t always all it’s cracked up to be. TEG and ROTEM require an expensive machine and a never-ending supply of disposable cartridges for use. Some hospitals are reluctant to provide the funds unless there is a compelling clinical need.

Surgeons at the University of Cincinnati compared the use of TEG with good, old-fashioned point-of-care (POC) INR testing in a series of major trauma patients seen at their Level I center.

Here are the factoids:

  • This was a retrospective review of 628 major trauma patients who received both TEG and POC INR testing using an iSTAT device over a 1.5 year period
  • Median ISS was 13, and there were many sick patients (20% in shock, 21% received blood, 11% died)
  • INR correlated with all TEG values, with better correlation in patients in shock
  • Both INR and TEG correlated well with treatment with blood, plasma, and cryoprecipitate
  • Processing time was 2 minutes for POC INR vs about 30 minutes for TEG
  • Charges for POC INR were $22,000 vs $397,000 for TEG(!!)

Bottom line: Point of care INR testing and TEG both correlate well with the need for blood products in major trauma patients. But POC INR is much cheaper and faster. Granted, the TEG gurus will say that you can tailor the products administered to meet the exact needs of the patient. But in all my travels, I have never visited a center that has fully and effectively incorporated TEG or ROTEM into their massive transfusion protocol. Before you make the financial leap to buy these new toys, make sure that you have a very good clinical reason to do so.

Related posts:

Reference: All the bang without the bucks: defining essential point-of-care testing for traumatic coagulopathy. Presented at EAST 2015, Paper 30.

General

Does Hemostatic Resuscitation Really Work?

Leave a comment

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.

General

Does Hemostatic Resuscitation Really Work?

Leave a comment

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.