To Bleed or Not to Bleed
Written by: Victor Bernal, DO; Edited by: Timothy Khowong, MD
Introduction:
“Let’s get a TEG”: the trauma surgeon says during a trauma notification resuscitation that encompassed hypotension and a positive FAST. As the nurse starts a Massive Transfusion Protocol, all you can think to yourself is...
Did they mean a Tegaderm to hold down the flimsy IV catheter? Absolutely not…
In Trauma, we are taught that hypotension equals hemorrhage shock until proven otherwise. The cognitive unloading in the Emergency Room results in blood product administration, such as MTP or TXA. Do I give blood only? Platelets? TXA? VK? These are valid questions that can be answered through the use of Thromboelastograms. Thromboelastogram, also known as TEG, is a diagnostic modality for coagulation that has been gaining traction and popularity, especially in recent years at Trauma Centers.
Background: How Does it Work?
First described by Dr. Hellmut Hartert in 1948 at the University of Heidelberg (Germany), TEG was first clinically used to guide transfusions of blood components in injured soldiers during the Vietnam War. TEG is an assay that shows the clotting properties of a specific blood sample. It creates a schematic illustration demonstrating the interaction of platelets with the coagulation cascade. It measures the physical properties of a clot via a pin suspended in a cup from a torsion wire connected with a mechanical-electrical transducer. It is heated to 37 degrees Celsius to mimic human bodies and is then oscillated, eventually forming a clot to the pin. The elasticity and strength of a clot changes the rotation of the pin, which is converted into electrical signals to create a graphical and numerical output. The movement of the pin is proportional to the clot strength. As the clot grows, the pin moves more and vice versa (ie fibrinolysis). TEG is a graphical image of the recorded amplitude of movement over time. Over time, the blood creates a clot and eventually breaks down. The TEG represents a “lifestyle” of the clot.
Basic Learning Point: Stronger Clot = More Movement = Further Along the Y Axis
The Clot Life Cycle: ~60 Minutes
X axis = TIme, Y axis = Motion (remember the larger the Y-axis, the more movement, the stronger the clot)
COAGULATION
R (Reaction Time): As one may note, a clot does not form right away. Hence, the first part represents a straight line and no movement. This represents the time to start forming a clot.
Normal Time: 5-10 Minutes
Analogous to intrinsic pathway/PTT
Depends on clotting factors that activate thrombin
Decreased R indicates hypercoagulable state → risk for VTE
Increased R indicates hypocoagulable state → increased risk for bleeding
Treat with FFP (Contains fibrinogen, coagulation factors including protein C/S) or PCC, Protamine (Heparin Reversal)
K (Kinetics): Measures time to reach 20 mm of clot strength
Normal: 1-3 Minutes
Depends on Fibrinogen
Increase K indicates hypocoagulable state → increased risk for bleeding
Treat with Cryoprecipitate (Contains Fibrinogen)
Alpha Angle: Rate of Clot Formation/Fibrin Cross Linking
Normal: 50-70 Degrees
Decreased Angle indicates hypocoagulable states → increased risk for bleeding
Treat with Cryo
MA (Maximal Amplitude): Correlates with the highest strength
Normal: 55-73 mm
Decreased MA notes weakness in clot, may be secondary to low platelets or fibrinogen
Treat with Platelets or DDAVP (encourages expression of vWF and platelet aggregation)
LY30: Represents how much of the clot has lysed after 30 minutes MA
Normal: 0-8%
Increased LY30 indicates hemorrhage
Treat with TXA or Amicar
As stated before, TEG offers a schematic illustration for the coagulation cascade. Understanding how TEG works can ultimately alter patient dispositions including, answering questions about administering blood products. Figure 2 represents a normal TEG. Figure 3 demonstrates the extremes of hemostasis, hemorrhage and thrombosis.
Why Use it?
MOST HELPFUL in complex coagulopathies where multiple coagulation abnormalities are occurring
Cirrhosis, DIC, CT Sx, Liver Tx, ECMO
Pros
Faster, evaluation in real-time (Future POC testing)
Evaluates platelets function
Evaluates thrombolysis
Avoids repetitive INR-based treatment
Cons
Does not take into account coagulopathies including von Willebrand disease, deficiencies in antithrombin-III, protein C, S, or factor V Leiden.
Insensitive to effects of hypothermia
Conclusion:
The use of TEG in trauma continues to grow. The cost effectiveness and timely value it brings to the Emergency Room and OR have , its value in trauma makes learning and understanding TEG crucial.
Yes, I know it is something that you may or not see during your training due to resources and finances. However, I believe this blog post can give you an appreciation for its use in the Emergency Room and OR. Think of these measurements like an ECG for blood. A STEMI = Cath. A long reaction time = platelets. Take some time to appreciate how these diagrams look and you can save a bleeder!
References
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http://www.emdocs.net/thromboelastogram-teg-five-minute-primer-emergency-physician/
Gilbert BW, Bissell BD, Santiago RD, Rech MA. Tracing the Lines: A Review of Viscoelastography for Emergency Medicine Clinicians. J Emerg Med. 2020 Aug;59(2):201-215. doi: 10.1016/j.jemermed.2020.04.009. Epub 2020 May 14. PMID: 32418869.
https://rebelem.com/rebel-review/rebel-review-54-thromboelastogram-teg/thromboelastogram-teg/
Sharp G, Young CJ. Point-of-care viscoelastic assay devices (rotational thromboelastometry and thromboelastography): a primer for surgeons. ANZ J Surg. 2019 Apr;89(4):291-295. doi: 10.1111/ans.14836. Epub 2018 Sep 25. PMID: 30253452.
Teodoro da Luz L, Nascimento B, Rizoli S. Thromboelastography (TEG): practical considerations on its clinical use in trauma resuscitation. Scand J Trauma Resusc Emerg Med. 2013; 21:29.