Delaying Fluid Resuscitation

Sasha

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I found this on trauma.org while looking up permissive hypotension. I thought it was pretty interesting since it seems to contradict the quick, agressive fluid resucitation therapy I've been taught and seen in the field. Thoughts, opinions?

Effects of delaying fluid resuscitation on an injury to the systemic arterial vasculature.

Holmes JF, Sakles JC, Lewis G, Wisner DH.
Division of Emergency Medicine, University of California, Davis, School of Medicine,
Sacramento, CA 95817-2282, USA.


Academic Emergency Medicine 2002 Apr;9(4):267-74.

OBJECTIVES: To determine the effects of delaying fluid on the rate of hemorrhage and hemodynamic parameters in an injury involving the arterial system.

METHODS: Twenty-one adult, anesthetized, sheep underwent left anterior thoracotomy and transection of the left internal mammary artery. A chest tube was inserted into the thoracic cavity to provide a continuous measurement of blood loss. The animals were randomly assigned to one of three resuscitation protocols: 1) no fluid resuscitation (NR), 2) standard fluid resuscitation (SR) begun 15 minutes after injury, or 3) delayed fluid resuscitation (DR) begun 30 minutes after injury. All of the animals in the two resuscitation groups received 60 mL/kg of lactated Ringer's solution over 30 minutes. Blood loss and hemodynamic parameters were measured throughout the experiment.

RESULTS: Total hemorrhage volume (mean SD) at the end of the experiment was significantly lower (p = 0.006) in the NR group (1,499 311 mL) than in the SR group (3,435 721 mL) or the DR group (2,839 1549 mL). Rate of hemorrhage followed changes in mean arterial pressure in all groups. Hemorrhage spontaneously ceased significantly sooner (p = 0.007) in the NR group (21 14 minutes) and the DR group (20 15 minutes) than in the SR group (54 4 minutes). In the DR group, after initial cessation of hemorrhage, hemorrhage recurred in five of six animals (83%) with initiation of fluid resuscitation. Maximum oxygen (O2) delivery in each group after injury was as follows: 101 34 mL O2/kg/min at 45 minutes in the DR group, 51 20 mL O2/kg/min at 30 minutes in the SR group, and 35 8 mL O2/kg/min at 60 minutes in the NR group.

CONCLUSIONS: Rates of hemorrhage from an arterial injury are related to changes in mean arterial pressure. In this animal model, early aggressive fluid resuscitation in penetrating thoracic trauma exacerbates total hemorrhage volume. Despite resumption of hemorrhage from the site of injury, delaying fluid resuscitation results in the best hemodynamic parameters.
 

Flight-LP

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Too many providers are needlessly flooding their patients. Very few people require aggresive fluid resuscitation. As long as you have a perfusing MAP, permissive hypotension is acceptable. Why are we hemodiluting and increasing MAP with saline or LR? What benefit will it provide?


According to many trauma surgeons, none. In fact we are causing further harm as evidenced by this particular study. I rarely hang fluids on my trauma patients, most just get a saline lock or two. When I was flying, they would get NS TKO until we started blood.

This logic is at a very basic level, why complicate it? If it ain't broke, don't try to fix it, you may break something else......................
 
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Sasha

Sasha

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In fact we are causing further harm as evidenced by this particular study. I rarely hang fluids on my trauma patients, most just get a saline lock or two.

That makes sense. Increasing BP on an active bleed, wouldn't that just make it bleed faster and prevent platelets from aggregating?
 

MSDeltaFlt

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Actually. yes. You will. Usually the amount of fluid given before surgery is enough to be counterproductive but not necessarily enough to kill. Usually. Sometimes it can.
 

medic417

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This has been known for years. Sadly many in EMS have not stayed up.
 

NebraskanPrincess

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We were just talking about this in class the other night. Protocols around here usually say two initiate two 14 gauge IVs and open 'em up full bore, but with the problem of platelets what ought we do? We discussed keeping the patients pressure at around 90 and using that as a gauge for decision-making. I may not be a -P yet (FAR from it), but I'd feel uncomfortable not initiating lines and running fluids into my trauma patients ESPECIALLY when you talk about hypovolemia. And I know our local ER docs would kill us if we didn't.

Our instructor told us still to adhere to the 2 to 1 philosophy of fluid resuscitation and to watch our BPs. 90 is the golden aim.
 

Veneficus

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finally a thread about trauma and not that cardio nonsense

When the 8th edition ATLS comes out it is supposed to address permissive hypotension. Unfortunately not many field providers are involved in that and instead get the watered down phtls or itls. (not that ATLS is definitive trauma care, but it is way ahead of the others named) The book is for sale to the public at the American College of Surgeons website so even if you don’t take the class it is not time/money wasted.

Anyway, according to all the experts at the last trauma conference I went to this fall.(name dropping removed) Summary for everyone not there: Permissive hypotension seems to work better for penetrating trauma. So it is recommended for that. If you weren’t following the ectopic thread, withholding fluid for blunt injuries seems to make no difference in outcome. <2% if my memory serves but definitely <3%. Pressors have shown not to be effective, hypertonic fluids cause harm, and colloids are the same as LR except more expensive and you need less.

Another important thing to consider is that SBP does not easily correlate to CVP which was the point of the theory fluid resuscitation. There was a French surgeon as far back as WWI who noticed it was better to let patients get hypotensive. Most of the European countries have already adopted the knowledge learned from Iraq and Afghanistan, but it is slow to reach US EMS. I think because it is more knowledge based and less procedure or gadgets.
Obviously US EMS cannot adopt massive transfusions. I have seen hypotension guidelines for SBP as low as 70 prior to surgery. If your agency is looking for guidelines I would suggest getting in touch with some of the trauma surg people working on this instead of the local ED docs. (they are easily found on trauma.org)

If you are really interested in trauma there is also a book from the Army available from the government printing office. It can be found here:

http://bookstore.gpo.gov/actions/GeneralSearch.do

War Surgery in Afghanistan and Iraq: A Series of Cases, 2003-2007

Ok, I know this is long and not specific but I really hope providers on this forum will expand their knowledge on trauma past what little is taught in EMS classes. I also have no idea where to begin to talk about this here because of the complexity of trauma care. (whoever says trauma is simple is a fool or a liar)
 

mycrofft

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Veneficus and Sasha, thanks!

Sasha, coincidentally I stumbled across the Sacramento COUNTY EMS prehospital protocols online. They specifically prohibit starting and running an IV "just to make sure we have a line".
 

jochi1543

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Sasha, coincidentally I stumbled across the Sacramento COUNTY EMS prehospital protocols online. They specifically prohibit starting and running an IV "just to make sure we have a line".

What's so bad about starting an IV and putting a saline lock in?
 
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Sasha

Sasha

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What's so bad about starting an IV and putting a saline lock in?

I think he means "running an IV" like running NS TKO, not a saline locked IV.
 
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Sasha

Sasha

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We were just talking about this in class the other night. Protocols around here usually say two initiate two 14 gauge IVs and open 'em up full bore, but with the problem of platelets what ought we do? We discussed keeping the patients pressure at around 90 and using that as a gauge for decision-making. I may not be a -P yet (FAR from it), but I'd feel uncomfortable not initiating lines and running fluids into my trauma patients ESPECIALLY when you talk about hypovolemia. And I know our local ER docs would kill us if we didn't.

Our instructor told us still to adhere to the 2 to 1 philosophy of fluid resuscitation and to watch our BPs. 90 is the golden aim.

I found an article about permissive hypotension and trauma patients that made a lot of sense. The article is too big to post in it's entirety but here's the main point:

If maintaining blood pressure is the goal, fluid resuscitation is the treatment. Keeping in mind the definition of shock, our immediate goals clearly are to arrest hemorrhage and maintain oxygen delivery. Although acellular fluid resuscitation may increase cardiac preload, it also may disrupt the formation of thrombus, increase bleeding time, and hemodilute the existing hemoglobin, platelet, and coagulation factors. Although essential, blood product administration is often beyond the scope of prehospital providers and, therefore, this article.

Because oxygen delivery is paramount, our challenge is to set goals and define measurable responses to treatment. Traditionally, we have relied on normalized blood pressure, heart rate, and urine output to gauge response to treatment of hemorrhagic shock. However, recent research has revealed that 80% of severely traumatized patients who are maintaining normal vitals and urine output still suffer subnormal oxygen delivery, evidenced by increased lactate.4 It appears both the treatment and assessment tools are missing the mark of measuring oxygen delivery.

An ideological shift has occurred in the past 10 years toward limiting prehospital fluid resuscitation. This idea is certainly not new and was originally proposed by Cannon in 1918 while studying shock in casualties of World War I.10 This challenge to the long-held dogma that acellular fluid resuscitation improves outcomes remains controversial, but evidence is mounting in its defense.

As hemorrhagic shock begins, the hypotension that ensues actually helps the patient meet 2 goals: arrest of exsanguination and maintenance of existing oxygen delivery. This is accomplished by sparring forming thrombus and maintaining coagulation factor and hemoglobin levels. Once aggressive fluid resuscitation is instituted, increasing blood pressure dislodges thrombus and hemodilutes hemoglobin, platelets, and clotting factors, therefore decreasing overall oxygen delivery

The full article can be found here:
http://www.nursingconsult.com/das/j...sn=1067991X&ja=494000&ANCHOR=text&PAGE=1.html
 
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Veneficus

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lactate has long been the measure of trauma experts. It was the gold standard back when I was doing my paramedic clinicals. (a long long time ago.)

It is quite distressing that this topic is just now gaining popularity in EMS circles. it might be time for a poll.
 

Aidey

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When I was in my Basic class 5+ years ago I remember my instructor talking about permissive hypotension. He was a flight medic though, with a very good MD sponsor, which may be why they were using it. Anyway, I've never been taught to go for aggressive fluid resuscitation in trauma. If I remember right in P school we were taught 20cc/kg bolus, max 500cc at once to sustain a systolic BP between 80-90mmHg with a slow TKO between boluses.
 

BossyCow

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If I remember right in P school we were taught 20cc/kg bolus, max 500cc at once to sustain a systolic BP between 80-90mmHg with a slow TKO between boluses.

This is our current protocol.
 

Aidey

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Sweet! At least I remember something that is right somewhere. ^_^
 

Ridryder911

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Let me ask all the Paragod students. What is a side effect of shock (cellular level) and what is the pH of Saline and then what fluid is most EMS using and why?

R/r 911
 
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Sasha

Sasha

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Let me ask all the Paragod students. What is a side effect of shock (cellular level) and what is the pH of Saline and then what fluid is most EMS using and why?

R/r 911

At the cellular level, don't the cells shift into anaerobic metabolism once perfusion becomes inadequate, which sends the body into acidosis, which causes cell damage and death?
 

Ridryder911

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At the cellular level, don't the cells shift into anaerobic metabolism once perfusion becomes inadequate, which sends the body into acidosis, which causes cell damage and death?

+1 point, true into acidosis (what type of acidosis is produced as by product ?)

R/r 911
 
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Sasha

Sasha

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+1 point, true into acidosis (what type of acidosis is produced as by product ?)

R/r 911

Metabolic acidosis, due to the build up of lactic acid?
 
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