NCCEd: Neurocritical Care Education for Residents

(Hoang 2020)

(Anderson et al. 2014)

There's a lot here, so let's go through this systematically. Note that the Deranged Physiology page referenced below gives excellent examples of this systematic process of reviewing ROTEM data. The EMRA page on a simplified approach to TEG and ROTEM also provides a nice algorithm for it. The system for reviewing the results is echoed from both of these sites. The ROTEM graphics were adapted from that page, which in turn were adapted from the official ROTEM documentation. Reference ranges given are from our institution's labs and the results are presented in the same overall appearance that we'd see in our own institutional practice.

First, the clotting times (CT) are all normal based on the reference ranges given, which tells us that the coagulation factors are all functioning well. (Fresh frozen plasma (FFP) and prothrombin complex concentration (PCC) have most of the coagulation factors.) Similarly, the clot formation times (CFT) are all normal, which is reassuring as to the process of clot propagation. (If this wasn't the case, thrombocytopenia, poor platelet function, or hypofibrinogenemia would be the problem.)

Next, we can see that the alpha angles are normal. The speed of clot formation/propagation is thus normal.

Finally, we can see that for EXTEM, INTEM, and FIBTEM, the amplitudes (A10, A20) are all low. This indicates poor clot stability, and could be attributed to thrombocytopenia, poor platelet function, hypofibrinogenemia, or hyperfibrinolysis. However, in APTEM-- a test in which fibrinolytic proteins are inhibited-- the amplitudes and mean clot formation (MCF) are preserved. Thus, hyperfibrinolysis is the problem here.

IV tranexamic acid 1g.