I took a liter bag of saline and placed it within a pressure bag in front of my class. As the students watched in expectation, I pumped it up to somewhere around 70 mmHg. I released the roller clamp and let the fluid drain into the garbage can. I asked them what blood pressure they would feel comfortable maintaining a patient with a pelvic fracture at. Most said 100 to 120. So I pumped up my pressure bag until I was somewhere around that. The saline increased in evacuation rate. At this point they realized what the point of this illustration was.
It has become a staple in HEMS to carry and deliver blood products to trauma patients who need them. Some agencies will carry plasma, packed red blood cells, and platelets. The majority will only carry packed red blood cells (PRBC's). From the curb this makes sense. If a patient is losing blood, we should replace it. However there is heterogeneous views on when this should be done and how.
I once had a trauma physician tell me "the decision to transfuse blood is not benign and should be viewed as an organ transplant." While maybe a hyperbole, I understood his point. The majority of clinicians I speak with will relate their own anecdotal experiences of when they decide to pull the trigger on blood. Some will cite studies, pathophysiology, and gestalt's. In my opinion a procedure that is not without risk to execute, should be done with the most informed best practices in accordance to evidence. This is how we base out decisions to do pretty much everything in emergency medicine. Once while teaching a ACLS class I had a clinician tell me they understood that we were not suppose to put high flow oxygen on ischemic chest pain patients if saturation was above 90%, however they would continue to do so because of personal experiences with these patients crashing. Is this acceptable? Are evidence based stop signs, merely suggestions?
Popping Clots Up In This Joint
In 1982 during the Falkland war, British military developed a concept they referred to as "popping the clot." As soldiers were found with significant injuries on the battlefield. They discovered them often hours after the initial injury. The bleeding had seemed to have stopped or clotted off, until they were evacuated to the medical center and aggressively fluid resuscitated. The increase in hydrostatic pressure had disrupted the clot formation, and bleeding would begin again. While seemingly small evidence, this concept is the basis behind damage control resuscitation. The Anesthesia Trauma & Critical Care (ATACC) guidelines recommend the following in regards to resuscitation during active bleeding.
Avoid crystalloid/colloid resuscitation unless there is no other option.
Transfuse blood if systolic is < 80 mmHg or the MAP is <50 (unless there is evidence of head injury target MAP of 80)
Try and avoid raising the MAP >60mmHg
Keep the patient in this hypotensive state for the shortest possible time, with control of bleeding achieved in less than 1 hour.
What About Tachycardia As A Trigger?
I will commonly hear of situations where a provider pulls the trigger on starting blood based on an elevated heart rate. The first sign of shock is tachycardia, and I could completely see the thought process behind this. However there are multiple things that cause tachycardia in a trauma patient (pain, nerves, etc.). While we are trained to suspect zebras amongst the hoof beats, sometimes it's just a damn horse.
Is the point of the thresholds above mentioned by ATACC too low? I believe this has to do with your logistics of resuscitation. My current program spikes a bag of 0.9% on blood tubing for every trauma call. This tubing is placed in a Buddy Lite and warmed up while responding. The cooler with blood is inches from my feet, and can be started within 60 seconds if needed. This is rather different in some situations where just getting the blood to your patients bedside can take 10-15 minutes. In that situation I believe it makes sense to begin the process of ordering blood based on tachycardia and significant trauma. However an elevated heart rate for someone in a helicopter (including mine) is very normal. I would use this sign as part of a larger puzzle in which the decision for transfusing is made. It is also worth mentioning that the typical formula for MAP does not really apply in patients with tachycardia. This is because that formula is based on your patient spending 2/3's of their time in diastole. This obviously changes when the heart rate becomes tachycardic. They will spend the majority of their time in systole. That is why you will commonly see a systolic pressure goal as opposed to a MAP goal in trauma literature. If you want to go full geek on this one, check out this article.
"They are going to get blood at the hospital, why not start it now?"
This is another argument I commonly hear from clinicians all around the world. This is typically used in the context of a patient who has a strong potential/suspicion of bleed, but doesn't quite meet the criteria for transfusion. I could completely get behind this thought process if whole blood was an option. While some research shows PRBC's may play a passive role in clot development, this is not well established. The problem with just infusing PRBC's, is there is almost a complete lack of evidence that it is doing anything to improve outcomes within the traumatic exsanguination context.
Oxygen carrying capacity is poor as a result of low 2,3, DPG levels.
Oxygen delivery is poor because stored red cells start to become stiff and move poorly through capillary beds.
The endothelial walls have a coating of glycoprotein/glycolipid film called the glycocalyx. This coating serves multiple purposes in regards to maintaining the durability of the vessel, and assisting in clot formation. When the hydrostatic pressures are increased, this layer can be disrupted and begin to loose its integrity. This finding is typically in the latter stages of care, and causes third spacing of plasma into the interstitial compartment. This is part of the reason we refrain from utilizing pressors in trauma if possible. The constriction of peripheral vessels will exaggerate parabolic flow as seen below.
As fluid moves through a lumen, the fluid in the middle will move faster than than the fluid that is in contact with the endothelial lining. When the pressure of this flow is increased, and the vasculature is constricted, shearing of the glycocalyx can occur. Sudden increases in preload will cause the release of atrial natriuretic peptide (ANP). This has been shown to break down and injure the glycocalyx, and is well documented in sepsis as part of the reason to be judicious with fluid resuscitation.
Sydney HEMS Protocol