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Triangle or Diamond? Calcium in Trauma

You respond to the report of a motor vehicle crash with a person entrapped. As you arrive the fire department has just accessed the victim and they are ready to be extricated. You quickly move a middle-aged female patient to your ambulance for further intervention. You have also requested aeromedical evacuation as the trauma center is almost a hour by ground. You begin treating and assessing your patient who is responsive only to pain with vitals that are trending down. You administer IV fluids and continue to assess. As the flight crew arrives they find a somnolent patient with rapidly falling blood pressure and decreasing ventilatory rate and depth. The unstable pelvis and ecchymosis over her abdomen point to hypovolemia as the likely culprit. They begin infusing blood products prior to intubation. The flight paramedic reminds his partner, “don’t forget we are giving calcium with the blood now”. All of this is done and the patient is quickly airlifted to the trauma center.

You return to your base after the call and are completing your chart and ask your partner if they know why the flight crew would have given calcium to the patient and they are unsure. Your conversation leads into discussion of the Trauma Triad which encompasses hypothermia, acidosis, and coagulopathy. There is no mention of calcium. Could this have been left out or does the triad have a side you haven't seen? This uncertainty does not sit well with you and you decide that later you will do some research. For now the dispatcher has other plans and you are off to a chest pain call, the research will need to wait.

It was not that long ago that I myself had this same curiosity as to the reason why some services had begun concomitant administration of calcium with blood products and decided to put together a class to teach as a part of the FOAMfrat Refresher. This took me to not only a greater understanding of the need for calcium in trauma but also a much greater respect for the importance of proper calcium homeostasis in all patients. I hope this information can be beneficial to each of you.

Let’s start by exploring where calcium is found. The above representation gives a basic breakdown of the places we find calcium. An average adult will have about 1-1.3 KG of calcium in their body. The majority of which is found in teeth and bones. Calcium is also found in body fluids and is present in the highest amounts as an intracellular cation. These locations and amounts of calcium are however difficult to measure and therefore not of great clinical utility.

We zoom further in to the calcium found in the blood plasma. It is in this space that we find the calcium available for use, but only about half of it. The ionized calcium (iCal) is the portion here that we have available for use, and we definitely need it. We will explore later the very important roles calcium takes on. The next largest amount can be found bound to albumin. Think about derangements of albumin and the big impact that could have on available calcium. That could be a blog of it’s own! The other important component here is what’s referred to as “complexed”. This simply means it is in use with other anions. Like bicarbonate, lactate, and phosphate. Don’t forget about the lactate, that will be coming up later too!

Next a quick peek at how we regulate it. There are hopefully 4 small glands found behind the thyroid, called the parathyroid glands. These have calcium sensing receptors that secrete parathyroid hormone (PTH) in the presence of decreased calcium levels. The PTH sets it’s sights on the bone and kidneys. The bones represent a huge calcium reservoir but we can’t use it all! Osteoclasts help to liberate some calcium from the bones. PTH also works in the kidneys by causing greater reabsorption of calcium so we don’t pee out as much. The kidneys also release calcitriol which targets the GI tract causing greater absorption of dietary calcium. Cool fact though, the kidneys also need Vitamin D to produce calcitriol. Spring is here, so make sure you get some of that sun!

At this point many of you may be in the same place that I was. "Mike, what is the big deal?" The short answer is calcium is very important for proper compensation, but it is about more than compensation. There is a reason we don’t give our trauma patients calcium channel blockers. Remember that muscular contraction is dependent on an influx of calcium, so without this our vessels can’t use smooth muscle contraction to get smaller. Hypocalcemia further complicates the response by decreasing the strength of myocardial muscle contraction and slows the heart rate. Think of how that impacts cardiac output! Calcium is vital for neurotransmitter release. If calcium is inadequate or channels are blocked this can inhibit the release of neurotransmitters and slows speed of depolarization (dromotropy). Oh yeah, multiple points in the clotting cascade need calcium. Hopefully you are now gaining a respect for calcium!

Ok, so at this point in my research I understood the issue, but why does hypocalcemia potentially have such a profound effect on trauma patients, particularly those receiving blood products? First, please understand that citrate is added to these products to keep them from clotting. This occurs through special binding of the calcium called chelation which keeps the calcium from being available to aid in clot formation. Now under normal conditions our liver will metabolize citrate but these are normal times. Cardiac output is falling and this metabolism is slowed with any hypothermia.

We catch a break on the acidosis side of the house. Increased numbers of those bully hydrogen ions displace some calcium from albumin, making it bioavailable. Don’t get too excited though, this is short lived. That calcium is quickly used up and the acidosis leads to more production of lactate. Bad news, this lactate is also a chelating agent that binds more calcium.

Finally, we know that calcium is integral in clot formation. When we clot less, we bleed more. More bleeding leads to more hypothermia from radiant heat loss, this leads to more bleeding, now more acidosis, more clotting disorder, more bleeding, and born is the bloody, vicious cycle. Hopefully this helps you see the big problem here. This demonstrates how hypocalcemia forms the trauma diamond of death. A side note, almost every step of this decompensation is worsened with normal saline. Think about that during your next wide open bolus.

As we close this out, remember we are not powerless here. Initiate thoughtful, intelligent conversations with your medical directors. There will be more to follow this blog on potential prophylactic treatment, or you could join the FOAMfrat refresher and we could talk about this live! Hope to see you soon.

Peer Review - By Jake Good

When a patient presents in shock, we always say they "compensate". They do so by producing a sympathetic response that results in vasoconstriction to increase mean arterial pressure and increased chronotropy and inotropy to improve overall cardiac output. But how exactly does this all happen? Well at the very molecular level the answer is: Calcium!

Our body responds to shock by releasing catecholamines from the adrenal gland. These catecholamines (collectively, Epi, norepi, & Dopamine) travel around our body and attach to our adrenergic receptors -- Alpha 1, Beta 1, and Beta 2. Once attached to these receptors on the outside of our cells (alpha 1 for blood vessels, beta 1 for our heart tissue, & beta 2 for bronchioles) a cascade of events occurs inside the cell that ultimately produces our desired result. For alpha 1 it's vasoconstriction and beta 1 increased chronotropy and inotropy and beta 2 bronchial dilation.

This cascade inside our cells that is activated by our adrenergic receptor ultimately produces calcium! Calcium is the fuel that allows our cells to undergo the changes of vasoconstriction in our blood vessels, or increased contractility, or broncho-dilation during states of shock. This entire cascade is known as our G-coupled protein receptor second messenger system! It all culminates in the production of calcium to maintain compensation in shock! During states of shock trauma, we rely excessively on this system to compensate -- as Mike elegantly elaborated in this blog!


Higgins, C. (2007, July). Ionized calcium. Retrieved February 30, 2021, from

Farkas, J. (2016, November). Internet Book of Critical Care. Retrieved February 30, 2021, from

Ditzel, Ricky & Anderson, Justin & Eisenhart, William & Rankin, Cody & DeFeo, Devin & Oak, Sangki & Siegler, Jeffrey. (2019). A review of transfusion- And trauma-induced hypocalcemia: Is it time to change the lethal triad to the lethal diamond?. Journal of Trauma and Acute Care Surgery.


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