The Vitals: Trauma-Induced Coagulopathy

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Shyam Murali
Fellow in Trauma and Surgical Critical Care - University of Pennsylvania, Senior Editor -, Writer -, Saxophonist, EDM remixer, husband, puppy father, and new human father
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Sam Epstein

Aspiring Medical Student and current Critical Care RN. Enjoys everything outdoors but can also be found inside nerding out on her medical education artwork.

The Pre-brief

Ever had a trauma patient that just would not stop bleeding despite all of your best resuscitation skills and damage control surgery? As most of us are aware, trauma is the leading cause of death and disability worldwide, and hemorrhage is the leading cause of preventable death due to trauma. At the time that a trauma patient hits the ED doors, they have a one in four chance of being coagulopathic. This disorder has been identified as an independent predictor of mortality (4- to 5-fold increase compared to those without coagulopathy). In the traditional understanding of post-traumatic coagulopathy, the Lethal Triad of Trauma (consisting of hypothermia, acidosis, and coagulopathy) complicates the physiology of multisystem trauma patients and makes resuscitation extremely challenging (actually, check out Ruben Santiago’s post on the Lethal Diamond of Trauma). However, there is now an evolved understanding of the complex mechanisms of trauma-induced coagulopathy and its multifactorial nature.

So what is Trauma-Induced Coagulopathy?

Abnormal blood clotting results in difficult hemorrhage control, increases transfusion requirements, and increases mortality. You may have heard of the terms Acute Coagulopathy of Trauma Shock (ACoTS) or acute traumatic coagulopathy, which refer to the same general phenomenon. This phenomenon occurs through a variety of mechanisms as discussed in the next section.

What factors contribute to coagulopathy in trauma?

  • Shock with tissue hypoperfusion appears to be the driver of ACoTS; virtually all patients with ACoTS have some degree of tissue hypoperfusion as evidenced by an elevated base deficit (usually greater than 6 mmol/L)
  • Acidosis affects coagulation protease activity
  • Hypothermia (below 34oC) also affects coagulation protease activity
  • Hypocalcemia also affects coagulation protease activity as they are required for complete activation of several coagulation factors
  • Dilution of blood by the administration of large volumes of non-blood products
  • Severe tissue injury activates coagulation and hyperfibrinolysis by various mechanisms. When these processes become unbalanced, coagulopathy results.
  • Loss of coagulation factors due to bleeding or consumption
  • Lower Protein C levels are associated with elevated PT, PTT, D-Dimer and mortality
  • Elevated thrombomodulin levels are also associated with increased mortality

As evidenced by normal platelet levels (and in some studies, normal fibrinogen and clotting proteases), ACoTS seems to be due to systemic anticoagulation and hyperfibrinolysis, rather than a consumptive coagulopathy.

Reproduced from Dries 2010, SJTREM

How can we identify and treat it?

Pretty much the same way as always: PT and PTT provide a good starting point. While not yet available at all hospitals, viscoelastic tests of clotting, such as thromboelastometry and thromboelastography (TEG and ROTEM) can provide more directed  information about exactly what aspect of the clotting cascade the patient is lacking and therefore what the patient needs to have replaced. Whether these devices improve patient outcomes is controversial and still remains to be seen. Unfortunately, conventional fibrinogen and platelet assays don’t give us much information about their functional activity.

Consider balanced resuscitation with blood products and aggressive repletion of calcium. The importance of damage control resuscitation (aggressive and early bleeding control, permissive hypotension, blood product [perhaps whole blood] resuscitation, rewarming, correction of acidosis, etc.) cannot be overstated. Early blood-component transfusion, permissive hypotension, and minimum dose crystalloid administration should be used. Also consider using TXA and/or recombinant factor VIIa. Resolving shock and improving tissue hypoperfusion should be the first priority in addressing trauma-induced coagulopathy.

The Debrief

  • Trauma-Induced Coagulopathy is a multifactorial process and a significant cohort of critically-injured patients have this condition as they enter our emergency departments.
  • Suspect this disorder in patients with systemic hypoperfusion (base deficit over 6 mmol/L), particularly in combination with high magnitude of injury.
  • Consider addressing and reversing some specific factors that may contribute to the coagulopathy, including temperature control, correcting acidosis, and repleting calcium


  1. Frith D, Brohi K. The acute coagulopathy of trauma shock: clinical relevance. Surgeon. 2010 Jun;8(3):159-63. doi: 10.1016/j.surge.2009.10.022. Epub 2010 Feb 6. PMID: 20400026.
  2. Li B, Sun H. Research progress of acute coagulopathy of trauma-shock. Chin J Traumatol. 2015;18(2):95-7. doi: 10.1016/j.cjtee.2015.01.003. PMID: 26511301.
  3. Hess JR, Brohi K, Dutton RP, Hauser CJ, Holcomb JB, Kluger Y, Mackway-Jones K, Parr MJ, Rizoli SB, Yukioka T, Hoyt DB, Bouillon B. The coagulopathy of trauma: a review of mechanisms. J Trauma. 2008 Oct;65(4):748-54. doi: 10.1097/TA.0b013e3181877a9c. PMID: 18849786.


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