We are all aware of the intimate relationship between hemorrhage and trauma mortality. In our initial education we also find out how much influence we have on mortality, as the “pre-hospital period” in which we operate is so crucial to survival. However, did you know there are physiologic first responders that arrive on scene well in advance of the 911 call? A multi-step process is happening immediately at the site of injury)
Step 1: Vasoconstriction commences and small cells called platelets arrive first (they are always on patrol anyway) – the objectives are simple:
Recruit more platelets through chemical signaling.
Form a relatively unstable platelet plug (a temporizing stop gap).
Step 2: Platelets invite the liver to share clotting factors (backup/reinforcement) – the objectives are simple:
Activate fibrin thru a cascade of events (positive feedback mechanism).
Stabilize and reinforce the initial platelet plug with fibrin mesh (think rebar + concrete).
Step 3: Fibrinolysis (the cleanup crew) – the objectives are heavily regulated by proteins, but simple:
Keep clot controlled to the site of injury (checks/balances).
Breakdown and clear the fibrin clot once the crisis is over (we have to be able to shut off the system) – tPA can play a part in this.
Throughout the process traffics cops (more regulatory proteins) are always present and help ensure blood viscosity remains stable. Some proteins are allowed to move unimpeded (green light), other proteins proceed with caution (yellow light), while other proteins are ordered to stop (red light).
As first responders, it’s not necessarily required to know the pathophysiology of every disease state – quite frankly that’s impossible and unrealistic. However, we should have some familiarity with disease states that are highly prevalent in the population. These diseases alter one or many parts of the events we mentioned above. In short, they cause the pendulum to swing one way or another and the traffic cops lose control of the situation.
Diseases associated with Thrombosis (clotting)
Protein C/S deficiency (treat with heparin (UFH/LMWH) or Dabigatran (Pradaxa))
Factor V Leiden (treat with short term anticoagulants)
Lupus Anticoagulation Syndrome – its an enigma (causes clotting in vivo, but has anticoagulant properties in vitro)
DIC (treat underlying causes)
Atrial Fibrillation (anticoagulated with Apixaban (Eliquis) or Rivaroxaban (Xarelto))
Diseases associated with Bleeding
Hemophilia A, B, C (treat with Factor replacement therapy or Hemlibra)
Von Willebrand Disease (VWD) (treat with synthetic hormones - desmopressin (DDAVP))
Factor deficiencies (can be brought on by liver disease) (treat with factor concentrates, FFP)
As first responders, we can’t forget we have some tools in our arsenal to help these patients as well. Whether they are external devices or pharmacologic agents, they are centered on evidence-based practice and save countless lives every year. Be familiar with your protocols and don’t hesitate to use the following items if the situation at hand warrants it (after all they all promote homeostasis):
Keep the patient warm – BLS matters (cold patients continue to bleed)
Pack the wounds
Promote the STOP THE BLEED campaigns in your community
Place the tourniquet (we needlessly lose too many patients to extremity hemorrhage)
Pull out the TXA
Infuse the blood products, FFP (if dictated by local protocol)
December 11, 2022
Author: Joshua Ishmael, MBA, MLS(ASCP)CM, NRP
Pass with PASS, LLC