Predicting massive transfusion

Do you have access to thromboelastometry in your Emergency Department? Further research by some of the first discoverers of acute traumatic coagulopathy involved using this tool to identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion. Measures of coagulopathy more familiar to ED staff such as the INR took longer or (when point-of-care testing was employed) were less accurate.

OBJECTIVE: To identify an appropriate diagnostic tool for the early diagnosis of acute traumatic coagulopathy and validate this modality through prediction of transfusion requirements in trauma hemorrhage.

DESIGN: Prospective observational cohort study.

SETTING: Level 1 trauma center.

PATIENTS: Adult trauma patients who met the local criteria for full trauma team activation. Exclusion criteria included emergency department arrival >2 hrs after injury, >2000 mL of intravenous fluid before emergency department arrival, or transfer from another hospital.


MEASUREMENTS: Blood was collected on arrival in the emergency department and analyzed with laboratory prothrombin time, point-of-care prothrombin time, and rotational thromboelastometry. Prothrombin time ratio was calculated and acute traumatic coagulopathy defined as laboratory prothrombin time ratio >1.2. Transfusion requirements were recorded for the first 12 hrs following admission.

MAIN RESULTS: Three hundred patients were included in the study. Laboratory prothrombin time results were available at a median of 78 (62-103) mins. Point-of-care prothrombin time ratio had reduced agreement with laboratory prothrombin time ratio in patients with acute traumatic coagulopathy, with 29% false-negative results. In acute traumatic coagulopathy, the rotational thromboelastometry clot amplitude at 5 mins was diminished by 42%, and this persisted throughout clot maturation. Rotational thromboelastometry clotting time was not significantly prolonged. Clot amplitude at a 5-min threshold of ≤35 mm had a detection rate of 77% for acute traumatic coagulopathy with a false-positive rate of 13%. Patients with clot amplitude at 5 mins ≤35 mm were more likely to receive red cell (46% vs. 17%, p < .001) and plasma (37% vs. 11%, p < .001) transfusions. The clot amplitude at 5 mins could identify patients who would require massive transfusion (detection rate of 71%, vs. 43% for prothrombin time ratio >1.2, p < .001).

CONCLUSIONS: In trauma hemorrhage, prothrombin time ratio is not rapidly available from the laboratory and point-of-care devices can be inaccurate. Acute traumatic coagulopathy is functionally characterized by a reduction in clot strength. With a threshold of clot amplitude at 5 mins of ≤35 mm, rotational thromboelastometry can identify acute traumatic coagulopathy at 5 mins and predict the need for massive transfusion.

Functional definition and characterization of acute traumatic coagulopathy.
Crit Care Med. 2011 Dec;39(12):2652-2658

8 thoughts on “Predicting massive transfusion”

  1. TEGs seems way to go…although I (like many) don’t have it available in the ED.

    My understanding is that POC INR is affected by patient’s albumin and haematocrit, so not terribly iseful in bleeding or the sick ICU patient who drops their bundle. And lab turnarounds can be depressingly long.

    Are you guys all transfusing in 1:1 ratios?

  2. I think this paper has great implications, however, I think the technology is still lacking. Having used TEG quite extensively in a swine haemorrhage model I know how sensitive the machines are. In an ED resuscitation room situation I think the current technology would not last and would produce inconsistent results.
    Unless you have a specific, dedicated, trained user in more of a lab situation, using TEG as bedside point-of-care to me does not seem feasible.

    It would be interesting to see what device this team used to get thromboelastometry (possibly Rotem?), where they used it, and similarly how they managed to get results in 5mins.
    Even doing a fast TEG takes around 10-15mins sometimes.

  3. I believe this work was done at the Royal London, where they use the ROTEM. I understand it is a little bit quicker and less operator dependent then older TEG machines. Interestingly it is currently only used at The Royal London as a research tool and not to individualise massive transfusions, although I believe this will be changing soon. Currently for unstable/bleeding trauma pts (code red traumas) blood packs are issued similar to the shock packs in military medicine. Initially a pack A (6u prbc and 4u FFP) followed by pack B (6u PRBC, 4u FFP, Cryo and platelets) for all further bleeding and transfusion requirements. Although there is a mortality benefit when higher plasma to prbc ratio transfusions are utilised, from my understanding the exact ratio has not been established i.e. 1:1 versus 1:1.5?

    What would be interesting would be to look at is clinical outcomes and blood use in trauma related massive transfusions guided by protocols vs whole blood near pt. testing. Although the use of near pt. testing may not be particularly practical in patients in extremis!

    I haven’t had a chance to read the whole paper, but in the abstract I note it was the clot amplitude at 5 mins that was significant, with no mention of the reaction and clot time/alpha angle/Max amplitude/Ly30. I assume the clot amplitude at 5 mins is indirectly a measure of the reaction, clot time and the alpha angle? Would be interested if the presence of hyperfibrinolysis and low MA where useful predictors of massive transfusion/mortality as well.

    Thanks again for all the hard work and interesting posts,


  4. Hi Cliff,

    Just a further query to the above post. Given that a large proportion of trauma patients with haemorrhagic shock will develop an early acute traumatic coagulopathy, along with the acidosis/hypothermia/dilutional coagulopathy, will there be a place in a pre-hospital service (such as your own, who carry prbc and tranexamic acid I understand) to have available to them prothrombin complex concentrate or freeze dried plasma if a massive transfusion seems likely? Beyond warfarin reversal, I know the evidence is not extensive for PCC and FDP in the setting of trauma and massive transfusion, but animal models and case series (below) certainly do look promising and it would certainly overcomes the obvious logistical issues of carrying pre-thawed AB or low titre O FFP.

    Thanks again for your posts and work,


  5. Hi Cliff
    This is a recent obsession of mine
    Have tried to produce a rational real world protocol
    Now up at Broome Docs
    Live to hear your crtitique

  6. ROTEM is embedded into UK military massive transfusion medicine and has been for some time, however its use is not in deciding initial resuscitation empirical products, rather the ongoing specific product needs individualised to that patient once initial resuscitation is ongoing. There is no role for prothrombin concentrates or DDAVP that we can see nor evidence for in haemorrhagic shock. Current modalities include recombinant Epo, THAM for buffering acidosis, and a novel hybrid resuscitation protocol in blast injury. One of the biggest challenges remains hypothermia mitigation especially prehospital and delivering warmed blood products (not crystalloids) prehospital through central subclavian access (not jugular or femoral). We steadfastly avoid the use of vasopressors and non blood products at least until surgical haemostasis is achieved and base deficit cleared. Calcium and Tranexamic acid are used heavily in our system.


  7. Hi Rob,

    Completely agree about the role of ROTEM in massive transfusion medicine. As for PCC and FDP, I disagree that it doesn’t have a role. I think it is inevitable that in the future, particularly in austere environments, we will be using a non-ABO related/lower volume/lower immune priming clotting product in haemostatic resuscitation. Even though PCC already has all of these advantages over FFP, it has also been shown to be faster and more effective at normalising clotting parameters. It is already been used some European trauma centres with great results (See below 1-4). It just needs a good RCT. As for FDP, John Holcomb’s group (5) is particularly interested in its potential application in the American military. I was very interested to hear from a colleague about the armed forces use of alkalising agents such as THAM. It clearly makes very good physiological sense in massive transfusion and trauma related acidosis, but from my understanding it is unproven as yet with no good level of evidence. A lack of evidence does not obviously mean a lack of effect or benefit and I look forward to emerging evidence for all of the aforementioned therapeutic interventions.

    The placement of trauma lines or PA sheaths via the subclavian vein for massive transfusion is well established, as long as the time to definitive surgical management is not delayed.

    Certainly agree that hypothermia is an on going problem, particularly in anaesthetised polytrauma pts. Use of a Level 1or Belmont and bair hugger will only go so far when the chest and abdo are open. Having recently worked in a burns centre there is certainly a number of techniques that would cross over well, such as powerful overhead radiant heaters.

    Kindest regards,


  8. In relation to my comments above, it seems that the ‘Rapid TEG’ or r-TEG could have potential in assessing traumatic coagulopathy, giving results in minutes.

    Whether we can fully rely on the ACT, k-time or r-value to guide initial transfusion requirements at time zero remains to be seen.

    It is clear however, that thromboelastometry is more of a useful tool at looking at a patients coagulation profile than relying on the INR. Especially with the introduction of the lethal dabigatran

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