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Coagulopathy and Trauma

Who here loves trauma? Now, who loves talking about coagulopathy related to trauma?

*** crickets and awkward silence***


Today we are going to be talking about the big, the bad, the misunderstood and confusing portion of trauma..... COAGULOPATHY. The issue with trying to tackle this subject is that coagulation is a dynamic process and add multi-system trauma into the mix… plain and simple, it’s just F***ing confusing. I won’t be here to give you a 100% understanding on the complexity of the clotting cascade, but we are also not going to dumb things down either. 🤓

Today we are going to grasp the simple understanding of coagulation and the clotting cascade, issues with coagulopathy and trauma, and interventions that can be both harmful and helpful in treating our multi-system trauma patients.

Cellular Effects of Coagulopathy

Hemostasis is a multistep process to regulate the control of blood clotting. This complex process not only localizes blood clotting to damaged vessels while blood continues to perfuse all other areas, but it also balances blood clotting actions with anti-clotting actions. Three processes occur with blood clotting: primary hemostatic plug, the blood clotting cascade, and formation of a complete fibrin clot.

When bleeding occurs, there is a disruption in the endothelial layer of our blood vessels. This disruption exposes collagen which allows the first function of hemostasis to occur, the formation of the primary hemostatic plug. The undisrupted endothelium cells secrete Von Willebrand Factor (VWF) which lays down in the wound. A layer of platelets cling to the VWF and the platelets begin attracting other platelets causing aggregation. The platelets clump together with fibrinogen, which is important for the last step in the clotting cascade.

The clotting cascade is triggered by platelet aggregation and collagen exposure. The platelets clumping together is a temporary solution and are the “pre-game” to getting the hemostatic process started. The clotting cascade is the real OG. This guy’s end result is a complete, stable fibrin clot. Activation of the intrinsic and extrinsic pathways lead to the common pathway and the formation of a complete fibrin clot.

  • Intrinsic pathway is activated when Factor XII is exposed to damaged endothelial collagen. The end result is factor X activation.

  • Extrinsic pathway is activated by tissue factor during cell damage. The endothelial cells release tissue factor which activates factor VII. The end result is factor X activation.

  • Common pathway: Anyone see a common theme there? Factor X is the end goal “factor” activation of the intrinsic and extrinsic pathway. Factor X is the start of the Common pathway. With the help of Factor V, Ca++, and Lipids, Factor X activates Prothrombin, which activates Thrombin, which activates fibrinogen into fibrin. The fibrin strands then come together to form a fibrin mesh. The fibrin mesh is there to help stabilize the platelet plug.


Essentially, when two pathways love each other, they come together to make a common pathway and they name it “Fibrin Clot”.

❤️ A love story like no other. ❤️

On a typical day, our body is not only pro-clotting, but also providing anti-clotting mechanisms. The endothelium is very important in the prevention of clot formation. When intact, the endothelium provides a smooth surface that prevents platelets from sticking to it. It secretes heparin molecules that help neutralize certain clotting factors. Synthesized prostacyclin promotes vasodilation and decreases platelet aggregation.

We also have plasminogen that is converted to Plasmin by tPA. Plasmin plays a vital role in clot destruction or fibrinolysis. This YouTube video Anti-clotting Mechanisms does a great job of further in-depth describing the anti-clotting mechanisms.

Coagulopathy in Relation to Trauma

Coagulopathy is defined as the derangement of hemostasis that results in either excessive bleeding or excessive clotting. Trauma-induced coagulopathy (TIC) is an abnormal clotting process that may be the result of exsanguination, acidosis, hypothermia, hemodilution in relationship to fluid or blood administration, or a combination of any of the above. TIC has many effects on the trauma patient including longer ICU stays, higher transfusion requirements, mechanically ventilated for a longer period of time and multi-organ dysfunction.

We have to remember that the body is smart. The body is constantly balancing pro-coagulation with anti-coagulation. Sometimes the body is too smart. During trauma, tissue damage stimulates endothelial cells, immune response, platelet activation, and the clotting cascade. In the early phases of TIC bleeding is present. Our body is in full effect activating and exhausting all efforts to compensate for acute blood loss. Later as TIC progresses, we get abnormal clotting, thrombosis, and multi-organ failure.

Coagulopathy in Relation to Hypothermia

Normal hemostasis is dependent on normothermic conditions. Our ideal core body temperature is 37 C (98 F). The body’s ability to regulate appropriate platelet function, clotting factor activation and appropriate breakdown of clots can compensate at mild hypothermic conditions. It is when the body’s core temperature drops to moderate or severe hypothermic conditions that the system begins to fail drastically. Hypothermia impairs tissue factor, platelet aggregation, and platelet adhesion. For a full in-depth look at trauma related to hypothermia, check out my blog, Hypothermia and Trauma I recently posted, here. 🥶

Coagulopathy in Relation to Acidosis

Our body’s normal pH ranges from 7.35 to 7.45. Acidosis is defined at an arterial pH < 7.35. The major contributor to acidosis in the trauma patient is poor perfusion to the tissues resulting in lactic acid accumulation from anaerobic metabolism. Respiratory depression (hypoventilation) resulting in hypercapnia can also lead to respiratory acidosis. Common causes include: pain control and giving narcotics, alcohol use, traumatic brain injuries and flail chest to name a few.

Just to put into perspective how much acidosis affects normal clotting function: calcium, factor X, factor V, and prothrombin are impaired by 70% at a pH of 7.0 and 90% at a pH of 6.8. Ooof. 🤯The Journal of Emergencies, Trauma, and Shock published a research paper, “Characterization of Acidosis in Trauma Patient” in 2020 stating that a pH < 7.2 and < 7.0 have a 4- 25 times greater likely hood of mortality and went on to state that acidosis in the presence of coagulopathy (INR > 1.6) further increases the risk of mortality.

Seriously, acidosis is way under appreciated.

Interventions to Mitigate Coagulopathy

This is where we (mostly me) get excited. What can we do to help our patients when it comes to coagulopathy? Our biggest intervention is, STOP THE BLEED. 🩸🩸🩸 If we bleed out, not only are we losing all of our precious clotting factors and platelets, but we are also decreasing our oxygen-carrying capabilities putting us in an acidotic and hypothermic state. Stop the bleed by holding direct pressure, pack the wound, apply a tourniquet or bind the pelvis.

I know you guys have been eagerly waiting for me to specifically talk about normal saline administration. So before you pick me apart, take a chill pill, pour a shot of tequila and take this with a grain of salt. 🧂🍋🥃. Patients with uncontrolled hemorrhage and shock have typically lost 30-40% of their blood volume. It’s pretty simple when you add NOT blood to blood, you decrease or dilute the blood you have. Restated in medical terms, resuscitation with crystalloids can lead to dilution of clotting factors and platelets. I know a lot of EMS do not carry blood and have guidelines/protocols that call for a normal saline bolus in trauma patients. Numerous EMS providers have told me that this is all they have. To that, I say give judiciously and provide rapid transport to the closest, most appropriate facility.

A metabolic derangement can also be acquired by administering normal saline boluses. With a pH of 5.5 and high chloride content, normal saline only serves to compound the existing acidosis that occurs with poor tissue perfusion.

I’m going to start with this next intervention to preface the following intervention. Blood product administration. Blood product administration should be a 1:1:1 ratio of PRBCs, platelets, and plasma OR whole blood. PRBCs contain the red blood cells for oxygen-carrying capabilities. Platelets of course replenish our stores that we have exhausted either by bleeding out or use of in clot formation. Plasma makes up 55% of our overall blood content and most importantly, contains 65% of our clotting factors.

Whole blood has many benefits to the trauma patient. Not only does whole blood offer all the components, it offers peak performance of these components with an HCT count of 38-50%, a platelet count of 150,000+, and 100% of coagulation factors are present.

This leads me to my next intervention. The drawback to blood administration is in the storage. To help preserve and keep our blood product as fresh as possible, we use citrate as a preservative. Citrate chelates to the calcium in the blood to help decrease the clotting and clumping of our stored blood. In doing so, we decrease the amount of calcium available. Calcium is a very valuable electrolyte and most importantly related to this blog, serves an important role in the clotting cascade. Calcium works with vitamin K and fibrinogen in the clotting cascade. The Solution is to administer calcium gluconate or calcium chloride with blood product administration.

Temperature management seems basic, but boy does it pack a punch. In my last blog, Hypothermia and Trauma, we went into detail about how to rewarm our trauma patients. As a quick overview interventions include: covering our patients after exposure, administering warmed fluids, cranking the heat up in the ambulance, and remembering that RSI takes away our biggest ability to shiver which is our biggest compensator for hypothermia.

And last but not least, Tranexamic Acid (TXA). TXA works by binding to receptors on plasminogen which prevents plasminogen from activating plasmin. Plasmin is responsible for fibrinolysis, which breaks down the fibrin clot. The earlier TXA can be administered, the better the outcome. TXA should be given within 3 hours of injury to be most effective.


Coagulopathy is very problematic in our trauma patients. We have to be diligent in our assessments to provide the right interventions for our patients. Whether it be stopping the bleed, reaching in your fanny pack for the foil blanket, blood product administration, tiering with an ALSs provider, and/or rapid transport to the closet appropriate facility. Time is of the essence with our trauma patients and our end goal should be definitive treatment as soon as possible. I really hope you enjoyed this complex and confusing topic of trauma-induced coagulopathy.

Thanks for reading. Peace out! ✌️

Brittany Grandfield, Flight Nurse. 🚁


Chaudhry, Raheel. “Physiology, Coagulation Pathways.” StatPearls [Internet]., U.S. National Library of Medicine, 3 Sept. 2020,

Gerecht, Ryan, et al. “Trauma's Lethal Triad of Hypothermia, Acidosis & Coagulopathy Create a Deadly Cycle for Trauma Patients.” JEMS, 10 Dec. 2020,

Ignatavicius, Donna D., and M. Linda Workman. Medical-Surgical Nursing: Patient-Centered Collaborative Care. Elsevier, 2016.

Kutcher, Mathew. “Coagulopathy in Trauma Patients.” Uptodate,

Leung, Lawrence. “Overview of Hemostasis.” Uptodate,

Moore, Ernest E., et al. “Trauma-Induced Coagulopathy.” Nature News, Nature Publishing Group, 29 Apr. 2021,

RL;, Johnston TD;Chen Y;Reed. “Functional Equivalence of Hypothermia to Specific Clotting Factor Deficiencies.” The Journal of Trauma, U.S. National Library of Medicine,

Van Poucke, Sven, et al. “Hypothermia: Effects on Platelet Function and Hemostasis.” Thrombosis Journal, BioMed Central, 9 Dec. 2014,

Wells, Jack C, and James J Stevermer. “Purls: Trauma Care--Don't Delay with Txa.” The Journal of Family Practice, Quadrant HealthCom Inc., May 2013,,needed%20to%20harm%20%3D%2077).

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