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JUL
10

 

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The use utilization of packed red blood cell (PRBC) infusions has become a staple in many retrieval services all over the world.

"If a patient is losing blood, we should replace it.”

"I do not want to dilute their clotting factors with isotonic or balance crystalloid's.”

These are the statements that are sung from day one of any trauma-related course. Yet, when one tries to dive into what evidence actually supports the concept of giving pre-hospital blood PRBC transfusions, your eyes open up in the realization of the lack of literature support. 

Let's take a look at what we know for sure.

  1. PRBC's offer zero clotting factors.
  1. PRBC's at the time of use must be kept at a temp from 1-9 degrees Celsius.

Knowing these facts, we can without hesitation draw the conclusion that if we are going to transfuse PRBC's it is with the goal to increase the amount of hemoglobin, and if we initiate this transfusion, the blood must be warmed prior to entering the body. If you are hanging cold blood on trauma patients, you are doing an exponential more amount of harm than good.

Increasing the hemoglobin is our primary reason for administering PRBC's in a trauma patient… right?

The D02(amount of oxygen delivered) equation is D0= Q X [(1.34 X Hgb X SaO2) + PaO2 x 0.003]. When one begins to utilize this equation, you will find that the most efficient way of increasing oxygen delivery is by increasing the hemoglobin concentration. However, the amount of hemoglobin available will not matter if cardiac output is compromised. 

So, does this mean that our exsanguinating patient will benefit from a PRBC infusion?

The initial recommendation of transfusing PRBC's came from a paper by Adam and Lundy in 1941. The paper made the statement "when the concentration of hemoglobin is less than 8-10g/dL of whole blood, it is wise to give a blood transfusion before the operation. This 10/30 trigger was universally accepted without any evidence or clinical trials to support it. To this day there have not been any studies to support a transfusion trigger of 10g/dL. Our threshold more commonly acceptable for transfusion now is 7g/dL. This recommendation comes from the American Blood Bank Association (ABBA) in 2012.

There is very little evidence to support increased oxygen utilization when a transfusion is administered to an individual with a hemoglobin higher than 4 g/dL. The reason is that our oxyhemoglobin disassociation curve shifts to the right during shock. This shift increases oxygen extraction above the normal 25%.  The citrate in PRBC’s actually starts to shift this curve to the left due to the bound 2,3-DPG.  As we all know a left shift means oxygen is bound to hemoglobin very strongly and has a hard time disassociating.  The 2,3 DPG will remain bound until the eight-hour mark after transfusion. At this point, approximately 50% of the 2,3-DPG is now unbound and available for facilitating oxygen offloading from the Hgb molecule.  All the 2,3-DPG will not be available until 24 hours after transfusion. This puts the patient at high-risk for poor tissue oxygen until all bound 2,3-DPG is available and fully unbound from citrate.  Citrate toxicity is usually caused by multiple units of PRBC’s.

How Does Our Body React to Anemia?

A reduction in oxygen carrying capacity of blood is met by two intrinsic compensations.

  1. Increase in cardiac output (Q)
  2. Increase in oxygen extraction from the capillaries. 

Our oxygen consumption is calculated by multiplying the D0by the 0extractions (CvO2). In a normal healthy individual the hemoglobin will leave the left ventricle 100% saturated in oxygen and return to the right atrium 75% saturated with oxygen. This explains the physiological oxygen extraction (O2ER) of 25%. 

As hematocrit drops the blood will become thinner and cardiac output will increase until the hematocrit drops below 10%. This is the point in which the increase in oxygen extraction is no longer able to compensate for a decrease in oxygen delivery. The tissue oxygen consumption will begin to fall, and lactate will begin to rise. This is the point where we reach > 40% O2ER.  It’s important to point out that the increased lactate production is simply a result of the increase in glycolysis seen in the anaerobic state.  Simply put, it is an indication of stress. 

Volume Expansion

One of the benefits I can actually see behind the administration of PRBC’s is the lack of third spacing. When trauma patients are resuscitated with 0.9% saline or balanced crystalloids there is a considerable amount of third spacing that occurs within the first few hours. I believe this to be the only benefit in the trauma patient. Are there better volume expander options with less risk? Stay tuned.

    

References:

      1.  https://www.medscape.com/viewarticle/760919

  1. National Blood Data Resource Center. Comprehensive report on blood collection and transfusion in the United States. http://www.aabb.org/content/program_and_services/data_center/NBCUS/.2001.Acessed15 May 2007
  2. Wells AW, mounter PJ, Chapman CE, et al. Where does the blood go? Prospective observational study of red cell transfusion in north England. Br Med J. 2002; 325:803-6
  3. 4.Creteur J, Neves AP, Vincent JL. Near-infrared spectroscopy technique to evaluate the effects of red blood cell transfusion on tissue oxygenation. Crit Care. 2009; 13 Suppl 5: S11
  1. Marik PE, Corwin HL. Efficacy of RBC transfusion in the critically ill: a systematic review of the literature. Crit Care Med 2008; 36:2667-74
JUN
14

Screen Shot 2018 06 14 at 07.46.19

As I prepare my flight suit for tomorrows shift, I feel uneasy because there is a calm, quiet chatter in our community, free of the intensity after a loss. I have no doubt that I will return home tomorrow night, navigating the same risks, but feel as though I am always waiting for the "other shoe" to drop when things get quiet and comfortable on social media and in the news.

Sometimes that is good. I enjoyed when we went an entire year without a single fatality. If we back away and look at the larger picture, it is a different result. There will be some that prefer me to not tell you what I see.

I have waited to post this to avoid anyone feeling that it is pointed towards any one event. I also become more frustrated over the years as the names (read: empathetic grief and growing anger) pile on, year after year:

There has been three fatal helicopter air ambulance crashes in about six months, nine crew and one patient died. The public response to it seems to be far less of an outrage and outcry than that of the crash of the NYC tour helicopter that claimed five lives and had one survivor, or even far less than the SINGLE passenger killed when Southwest Airlines had their first fatal incident in forever. Why is that? 

Have we come to accept the deaths of our air medical families? I am convinced the industry as a whole has become numb and has fallen into some sort of apathetic acceptance that we are “dying, doing what we love.” I am not pointing fingers at anyone but us, all of us. 94 percent of crashes are due to human decision making, human error* -- not just the pilot, but the entire crew. No loss of life is acceptable for commercial flight -- zero. What number of fatalities is an acceptable one for helicopter air ambulance? Do we not set the bar? C’mon folks. 

I have lost people close to me, have worked with the entire community to achieve the number of ZERO lost in a crash. I still fly/transport full time and being exposed to the same risks. I feel empathetic, sad, frustrated and at times I am angry. This must stop. It cannot ever become OK or normal.

The helicopter air ambulance community is necessary for the fabric of EMS. We must always strive for a healthy, safe and efficient reputation. We must do better, to the point of outrage if that is what is needed.

Vigilance, my friends.

 

Jonathan Godfrey

 

Reference:

Dr. Ira Blumen, OSI HEMS, et al.

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