I. Let me clarify….
I have to be transparent and admit, I may not have spoken as clearly as intended. During the last FOAMFrat Open Mic Night, I gave, what I refer to as a “leftfield” talk on how the paradigm of permissive hypotension is flawed. Rather, we should focus more on the approach to hemorrhagic trauma as a normotensive approach. We, as prehospital providers, should balance the avoidance of the lethal trauma triad while maintaining adequate end-organ perfusion.
Permissive hypotension has been in vogue for some time and advocates keeping a systolic BP between 80-90 in order to not “pop the clot”. My concern with this approach is that it grossly under-resuscitates our patients. Not from a fluid standpoint but rather from an end-organ perfusion perspective. Our brain and kidneys require a minimum mean arterial pressure (MAP) of 70 mmHg in order to maintain perfusion and proper autoregulatory features (Marik et al., 2011). A blood pressure of 90/60 gives us a MAP of exactly 70, meaning this should be the very bottom end of our hemodynamic resuscitation goal. Yet, our protocols continue to advocate that permissive hypotension to a systolic of 80-90 is okay. Quite frankly, I just don’t agree.
In addition, a large multi-center study looked at over 47,000 blunt trauma patients. The researchers wanted to see, at what systolic blood pressure did mortality rates sharply increase. The results were astounding – Mortality rates exponentially increased at systolic pressures below 110 mmHg. In fact, they doubled at 100 mmHg, tripled at 90 mmHg, and increased 5-6 fold at 70 mmHg.
(Hasler et al., 2011)
The jury is out whether this is “practice changing” but it did make me question where this permissive hypotension and systolic in the 80-90s came from.
II. So much pressure!!
It took me a little while to figure out all the biophysics associated with shock and perfusion. This is by no means the meat and potatoes of the talk but to put it simply: perfusion is measured in pressure and if we have good pressure then we have good perfusion.
Have you ever thought about why we measure pressure though??
Pressure is a surrogate measure for blood flow. That is what we are really concerned about -- how much blood flow the brain, heart or kidneys are receiving. What we cannot do is measure blood flow to each organ. Maybe in some fancy lab they can but, in the back of the ambulance, in the helicopter or in the ED resus room, I highly doubt we are doing that. Instead, we use blood pressure and MAP to gauge or get an idea of what that flow is based on the pressure we see. For you firefighters and apparatus engineers, this would equate to your discharge pressure on your pump panel. You can see a discharge pressure but cannot immediately see your GPM (aka your flow).
III. Pressure and Shock Trauma
With a greater emphasis on end-organ perfusion, we can appreciate how when faced with an exsanguinating shock trauma patient that a balancing act must take place. We have to balance the perfusion to meet the metabolic demands all the while not tipping the patient into the lethal trauma triad.
The first thing we reach for to increase our patient’s pressure is fluids. This isn’t wrong at all and in fact, is the mainstay treatment for hypovolemic shock – volume replacement. It is difficult to sit here and write a blog and make a “one size fits all” general statement about fluid resuscitation as every patient is hemodynamically unique. Meaning, the approach between the 25-year-old patient with no medical history in an MVA versus the 75-year-old patient on beta-blockers involved in an MVA is going to be very different. Their individual compensatory mechanisms are going to vary and inevitably you will have to change your approach to treating the specific patient in front of you.
Inevitably, you will find yourself in a clinical situation where your exsanguinating patient has hemorrhaged substantial amounts. You may be on your second, or maybe the third liter of fluid and are barely reaching your normotensive resuscitation goals.
My question to the providers reading this is: In the absence of carrying blood, at what point are you willing to consider that more fluid is doing more harm than good?
We have to maintain that perfusion, yet in order to do that, we just push that lethal trauma triad onto the patient. Our fluids dilute clotting factors, they contribute to hypothermia and some degree of acidosis depending on what type of fluid you are using. In my mind, there has to be a middle ground. Something to buy us and the patient more time…
IV. The Misunderstanding
In my talk on open mic night, I postulated that perhaps something like the Trendelenburg, or shock position could augment perfusion pressures as it counts as an “autotransfusion” without contributing to the trauma triad—It was the “bridge” therapy I had in mind. I even mentioned the Levophed assisted transfusion that Tyler argues for. I wanted to clarify some of the points brought up that night.
1. Trendelenburg or modified Trendelenburg?
The real Trendelenburg position is where the head is below the level of the heart and the legs are tilted up. In EMS, this is not possible as the patient’s head cannot go below parallel on our cots. Just the legs get tilted up, this is considered the modified Trendelenburg (Castiglione & Landry, 2015). In the hospital setting, I can see the true Trendelenburg being utilized but in EMS, that would be tough or there are some acrobatic stretchers or cots out there. Now, this is very much my fault because I failed to recognize the nomenclature. But, it did prompt some pretty awesome, academic discussion amongst pre-hospital clinicians!!
Now the literature is pretty sparse and inconsistent when it comes to evaluating the use of Trendelenburg position. Between 2005-2015 there were 5 review articles reviewing a number of small studies. Unfortunately, most of the sample sizes were very small. Three RCT’s were released but they were for healthy patients undergoing anesthesia. And in all of these studies, the degree of tilt varied amongst studies, as well as the duration and several other factors (Castiglione & Landry, 2015).
From a theoretical standpoint, I can understand how a fluid shift using Trendelenburg can acutely increase afterload making it harder for the heart to pump against, displacing the diaphragm upwards and reducing functional residual capacity, and increasing ICP in a patient who may have suspected TBI with concomitant multi-system trauma.
2. Exit Trendelenburg and enter............. The Passive Leg Raise
Several mentioned the Passive Leg Raise (PLR) and this is essentially a method for measuring volume responsiveness in patients who are “preload responsive”. This is accomplished by starting the patient at a 45-degree semi-recumbent position, then lying them supine and tilting their legs up 45 degrees (Nickson, 2019). Other studies have altered that and even kept the patient in a 45-degree semi-fowlers position and elevated the legs (Monnet & Teboul, 2015).
Anyways, remember that Frank-Starling curve? Patients who benefit from the PLR are those that live here on the curve:
And by giving more volume you can “stretch” the cardiac myofibrils and get a better squeeze. If the patient has a transient increase in blood pressure by 10% then they are considered “preload responsive” and may benefit from fluid therapy.
I understand, however, that we cannot exactly measure cardiac output in the field, but one study looked at the correlation of the PLR to end-tidal CO2. They found that a PLR induced increase in EtCO2 by 5% from baseline corresponded to an increase in Cardiac Index by 15% (Monnet et al., 2013). Monitoring your end-tidal CO2 with a passive leg raise could potentially tell you if the patient is preload responsive and could benefit from fluids. Now bear in mind this study was conducted on mechanically ventilated patients as well.
Here is where I may ruffle some feathers… if EMS is utilizing the modified Trendelenburg by lying patients supine and tilting their legs up, how is this any different than the passive leg raise? How is that any different than volume redistribution via a "levophed assisted transfusion"? I think we were just arguing about nomenclature when at the end of the day we were doing the passive leg raise, to begin with.
3. PLR and Shock Trauma (Bringing it all Together)
A PLR can theoretically autotransfuse approximately 300 cc’s of blood from the patient’s lower extremities into their intrathoracic space, thereby augmenting preload (Monnet & Teboul, 2015). I theorized that in situations as I spoke about above when you have given 2-3 Liters of fluid, have no blood, or ran out, could you buy yourself and the patient more time by utilizing a Passive Leg Raise (not the true Trendelenburg)? Thereby giving the patient 300 cc’s of oxygen-carrying capacity blood of their own instead of diluting them down with more crystalloids?
In no way am I running on every hemorrhaging trauma patient and flipping their legs up first thing no matter what. But in situations where more fluid can start to become harmful than helpful, is something like a PLR not completely out of the question? A levophed assisted transfusion functions the same way by redistributing the unstressed volume into stressed volume to augment pressure and preload, right?
Trauma resuscitation is a balancing act between end-organ perfusion and the trauma triad. We should be diligent about reaching those pressures for end-organ perfusion while utilizing the least amount of fluid as possible. Sometimes, we may need to think outside the box and use certain “bridge” therapies in austere situations. Maybe a modified trendelenburg/passive leg raise? Maybe a levophed assisted transfusion?
The reality is, much of this is theoretical. Limited evidence exists on the subject that is worthy of being practice-changing. But our protocols don't perfectly fit every situation, and when those moments sneak up on us we are forced to think outside of our black and white box we call protocols and force us to think in the gray area.
I apologize if I confused anyone the other night! This is very a theoretical approach to a hypothetical situation. It sparked significant and elegant conversation amongst providers, even without our FOAMFrat cohort! I hope this sparks some conversation at your local base, or station while on a coffee break!
Stay safe out there! :)
References:
Castiglione, S., & Landry, T. (2015). Rapid Review-Evidence Summary: Use of Trendelenburg for Hypotension October 2015-Rapid Review Evidence Summary. https://www.muhclibraries.ca/Documents/RR_Final-Report_Trendelenburg-Hypotension_OCT2015.pdf
Hasler, R. M., Nuesch, E., Jüni, P., Bouamra, O., Exadaktylos, A. K., & Lecky, F. (2011). Systolic blood pressure below 110mmHg is associated with increased mortality in blunt major trauma patients: Multicentre cohort study. Resuscitation, 82(9), 1202–1207. https://doi.org/10.1016/j.resuscitation.2011.04.021 Marik, P. E., Monnet, X., & Teboul, J.-L. (2011). Hemodynamic parameters to guide fluid therapy. Annals of Intensive Care, 1(1). https://doi.org/10.1186/2110-5820-1-1
Monnet, X., Bataille, A., Magalhaes, E., Barrois, J., Le Corre, M., Gosset, C., Guerin, L., Richard, C., & Teboul, J.-L. (2013). End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Medicine, 39(1), 93–100. https://doi.org/10.1007/s00134-012-2693-y
Monnet, X., & Teboul, J.-L. (2015). Passive leg raising: five rules, not a drop of fluid! Critical Care, 19(1), 18. https://doi.org/10.1186/s13054-014-0708-5
Nickson, C. (2019, January 12). Passive Leg Raise • LITFL • CCC Resuscitation. Life in the Fast Lane • LITFL. https://litfl.com/passive-leg-raise/
Peer Review by Tyler Christifulli, FP-C
Jake presents an intriguing post that challenges the concept of permissive hypotension in trauma patients. I would like to address several points and see if you agree.
1. While a MAP below 65 has been burnt into our heads as a critical "stop and intervene" point. We all have likely seen patients creating urine and mentating with MAP's much lower.
2. When we discuss permissive hypotension, we are specifically talking about non-compressible hemorrhage (blunt or penetrating).
3. Blood product should be used to replace blood loss when it is available.
4. Pressure is a poor surrogate of perfusion because it can exist in the absence of flow.
I am cautious with studies that show a higher mortality rate associated with a poor vital sign. It would make sense that patients with a lower blood pressure end up being the sicker cohort in a retrospective analysis. In a prospective trial that resuscitates to various MAP goals, data may be useful in determining a mortality benefit. In addition, systolic pressure while largely used in trauma literature, may not be the best parameter to resuscitate to. A 2011 study evaluating the use of systolic blood pressure to predict ongoing bleeding in patients with torso trauma, concluded by stating that systolic pressure was a poor surrogate for on-going bleeding (Kassavin, 2011).
The transient leg raise theory that Jake discusses makes a lot of sense to me as long as intervention such as blood product is not withheld due to an improvement in vital signs. In transport we may be discussing at most 20 minutes in which lower extremities are elevated to auto transfuse whole blood blood from the patient's legs to their heart. Consequences may include an increase in abdominal pressure and decrease in functional residual capacity. These risks/benefits will need to be weighed by the clinician at time of resuscitation.
Kassavin, D. S., Kuo, Y. H., & Ahmed, N. (2011). Initial systolic blood pressure and ongoing internal bleeding following torso trauma. Journal of emergencies, trauma, and shock, 4(1), 37–41. https://doi.org/10.4103/0974-2700.76833
Peer Review by Brian King
Jake eloquently brings up a number of thought provoking points as it relates to the resuscitation of hemorrhagic shock by using some unconventional methods. Tyler brings up a number of excellent points, so I am not going to beat a proverbial deal horse. But what I will bring up is that the use of "protocols" in the management of hemorrhagic shock can be somewhat flawed. While making protocols and practice guidelines for the management of these patients make it easy for providers to decide if they are going to pull the trigger and start a specific intervention wether it be blood or something else. It may result in us missing some patients or not intervening on them earlier during their clinical course.
It's important to approach each patient individually and tailor their treatment specifically to them. For example; some patients in hemorrhagic shock get hypotensive with a normal pulse, while others are profoundly tachycardic with a normal blood pressure, all while maintaining their mean arterial pressure yet still being in shock.
This is why its imperative that we look at all the information that we have at our disposal wether it be traditional vital signs (HR, RR, BP, Cap Refill, etc), mental status, shock index, the use of point of care testing (BD, Lactate), point of care ultrasound or even some emerging diagnostic tools such as the use of microcirculation monitoring and tailor each patient's treatment to the information that we have available.