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Permissive Hypotension/ Low-Volume Resus In Peds


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#21 TexRNmedic

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Posted 02 May 2011 - 03:10 AM

Yep. I received a PM. I still need to read the references and I'll post up some stuff tomorrow. From a 2007 med student presentation.

Still off deep in the weeds writing papers tonight. I'll post some of the articles Brian sent me as well as my thoughts regarding HR, MAP, pulse pressure, trending pleth and arterial waveforms, STO2, SVO2 etc as soon as I can.
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#22 SerendepitySaki

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Posted 02 May 2011 - 03:22 AM

don't forget DO2, "TBV", hemodilution, and coagulopathies...B)
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#23 TexRNmedic

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Posted 02 May 2011 - 03:31 AM

don't forget DO2, "TBV", hemodilution, and coagulopathies...B)

Sure that too. I was thinking of how I would assess the effects of resuscitation in the prehospital setting and what would be my hemodynamic endpoint or goal. No fancy fiberoptic PA cath or continuous ABG machine when picking up a 6 year old ATV accident victim out in the middle of the woods.
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#24 BrianACNP

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Posted 02 May 2011 - 04:05 AM

1. oh, trust me... if Matt is NOT well familiar with basic calculus and integrating the area under a curve and its application to atrial fibrillation, etc..., he WILL be... B)


Not only A-fib.......also those not on full mechanical ventilation w/ 8ml/kg tidal volume........no literature that supports SVV in PSV or spontaneous breathing patients either....no available literature at the moment anyway.


Brian
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#25 SerendepitySaki

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Posted 02 May 2011 - 04:33 AM

Not only A-fib.......also those not on full mechanical ventilation w/ 8ml/kg tidal volume........no literature that supports SVV in PSV or spontaneous breathing patients either....no available literature at the moment anyway.


Brian


yep. that would be covered in my comment under "etc"....

in my mind, whether or not we used the actual end technology in trauma resus wasn't relevant to the conversation at hand....

my point was for him to understand the basic calculus behind the principle of SVV and PPV and apply THAT principle to the bigger picture... along with the relevance of CVP, etc...and of course, that is only PART of the picture....

and in the meantime, we are almost but not quite, completely off the topic of the rationales for permissive hypotension in adults, much less, their applicability to pedes...
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#26 SerendepitySaki

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Posted 02 May 2011 - 04:39 AM

therein lies an argument for hypertonics vs colloids vs isotonics...

how much does each change intravascular volume for how long?

and is that long enough to cause coagulopathy before you can get blood products on board and diurese excess volume? etc etc?

is the cost:benefit ratio of priming the pump worth the hemodilution, etc? can you stop the bleed?

i.e. is your DO2 relatively stable?

what % of little red trucks, etc are soaked into the forest floor, if critical, how quickly can they be replaced, etc?

Sure that too. I was thinking of how I would assess the effects of resuscitation in the prehospital setting and what would be my hemodynamic endpoint or goal. No fancy fiberoptic PA cath or continuous ABG machine when picking up a 6 year old ATV accident victim out in the middle of the woods.


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#27 SerendepitySaki

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Posted 02 May 2011 - 04:51 AM

Sure that too. I was thinking of how I would assess the effects of resuscitation in the prehospital setting and what would be my hemodynamic endpoint or goal. No fancy fiberoptic PA cath or continuous ABG machine when picking up a 6 year old ATV accident victim out in the middle of the woods.



and without fancy labs, etc., once you stop the bleed, how do you currently assess end organ perfusion in the field?

specifically, how do you think applying "permissive hypotension" might change that?
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#28 SerendepitySaki

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Posted 02 May 2011 - 04:54 AM

oh... and i used my own pet peeve...

should have read "is your DO2 relatively stable/SUFFICIENT?"

after all, asystole is a very stable "rhythm"... B)
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#29 TexRNmedic

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Posted 03 May 2011 - 06:46 AM

[quote name='TexRNmedic' date='01 May 2011 - 10:31 PM' timestamp='1304307069' post='25969']
Sure that too. I was thinking of how I would assess the effects of resuscitation in the prehospital setting and what would be my hemodynamic endpoint or goal. No fancy fiberoptic PA cath or continuous ABG machine when picking up a 6 year old ATV accident victim out in the middle of the woods.
[/quote]

Did a little lit review to get started. I've come across quite a bit more, but this should be a good start to spark a few conversations.

Boluyt, N., Bollen, C., Bos, A., Kok, J., & Offringa, M. (2006). Fluid resuscitation in neonatal and pediatric hypovolemic shock: a Dutch Pediatric Society evidence-based clinical practice guideline. Intensive Care Medicine, 32(7), 995-1003. DOI 10.1007/s00134-006-0188-4

Abstract:
Objective: To develop a clinical practice guideline that provides recommendations for the fluid,i.e. colloid or crystalloid, used for resuscitation in critically ill neonates
and children up to the age of 18 years with hypovolemia. Methods: The guideline was developed through a comprehensive search and analysis of the pediatric literature. Recommendations were formulated by a national multidisciplinary committee involving all stakeholders in neonatal and pediatric intensive care and were based on research evidence from the literature and, in areas where the evidence was insufficient or lacking,on consensus after discussions in the committee. Results: Because of the lack of evidence in neonates and children, trials conducted in adults were considered. We found several recent meta-analyses that show excess mortality in albumin-treated groups, compared with crystalloid-treated groups, and one recent large randomized controlled trial that found evidence of no mortality difference. We found no evidence that synthetic colloids are superior to crystalloid solutions. Conclusions: Given the state of the evidence and taking all other considerations into account, the guideline-developing group and the multidisciplinary committee recommend that in neonates and children with hypovolemia the first-choice fluid for resuscitation should be isotonic saline.

Mecham, N. (2006). Early recognition and treatment of shock in the pediatric patient. Journal of Trauma Nursing, 13(1), 17-21: http://search.ebscoh...9&site=nrc-live

Abstract:
Pediatric cardiopulmonary arrest is frequently a terminal event of an unrecognized progressive shock state. This article describes predisposing factors and classifications of shock as they relate to pediatric patients. It assists the experienced pediatric nurse as well as the nurse who is less experienced in caring for children in identifying early shock in this population and provides practical advice on the assessment of children. In addition, management and intervention techniques are addressed.

[quote]
Infants and children have a higher cardiac output than adults (200 mlVkg/min vs 100 mL/kg/min).' This higher cardiac output is imperative because the pediatric patient has a higher oxygen demand due to a higher metabolic rate. The higher cardiac output also provides for a child's higher oxygen consumption (6-8 ml./kg/min compared to 3-4 mL/kg/min in adults...Because tachycardia is a nonspecific sign of circulatory compromise and hypotension can be a late sign, it is important to look for other signs of adequate cardiac output and endorgan perfusion. Pulses, skin perfusion, brain perfusion, and renal blood flow are all part of the systemic perfusion assessment.(Mecham, 2006).[/quote]

Patanwala, A., Amini, A., & Erstad, B. (2010). Use of hypertonic saline injection in trauma. American Journal Of Health-System Pharmacy: AJHP: Official Journal Of The American Society Of Health-System Pharmacists, 67(22), 1920-1928: DOI 10.2146/ajhp090523

Abstract:
Purpose. The use of hypertonic saline injection in trauma patients is discussed.
Summary. Patients with hemorrhage, burns, and traumatic brain injury (TBI) may develop hypovolemic shock and require resuscitation. Compared with conventional isotonic crystalloids, hypertonic saline has several advantages, including hemodynamic, immune-modulating, and antiinflammatory effects, for use in trauma patients for resuscitation. In addition, hypertonic saline is also used in patients with TBI to reduce intracranial pressure (ICP). Overall, studies have not shown a difference in mortality or other clinically important outcomes with the use of hypertonic saline for resuscitation in trauma patients; however, most of these studies were not adequately powered to show significant differences. A recent Cochrane review concluded that there is no evidence that hypertonic crystalloids are better than isotonic or near-isotonic crystalloids for fluid resuscitation in trauma patients. Two recent trials that were adequately powered to investigate a mortality endpoint were halted for futility. A few small randomized controlled studies found that hypertonic saline was more effective than mannitol as a hyperosmolar agent for ICP reduction. Recent guidelines from the American Burn Association have suggested that hypertonic saline may be used for burn shock resuscitation by experienced providers with close monitoring to avoid excessive hypernatremia. One of the main concerns with the use of hypertonic saline is its potential to cause central pontine myelinolysis due to a rapid increase in serum sodium levels.
Conclusion. There is no evidence that hypertonic saline provides any additional benefit over isotonic crystalloid solutions for trauma resuscitation. Hypertonic saline may be more effective than mannitol at reducing ICP in patients with TBI.

[quote]
Fluid resuscitation with crystalloids is one of the first pharmacologic interventions in advanced trauma life support(ATLS), though overaggressive fluid resuscitation may be detrimental with regard to hemorrhage control and neuronal injury...Until bleeding is controlled through surgical hemostasis, overaggressive fluid administration may increase blood loss through clot destabilization and hemodilution of clotting factors. Currently, the aim of fluid resuscitation before definitive hemostasis is permissive hypotension in which fluids are administered to achieve a palpable pulse or below-normal blood pressure measurement (e.g., systolic blood pressure of approximately 80mm Hg). This may be achieved with isotonic crystalloid solutions such as 0.9% sodium chloride injection, but several liters may be required in patients with more-severe hemorrhage, since only about 25% of the infused volume remains in the intravascular space. The substantially increased osmolarity of hypertonic saline compared with isotonic crystalloids allows the use of a much lower volume to achieve the same degree of plasma expansion. The degree of plasma or intravascular expansion is dependent on several factors in addition to osmolarity, such as volume and rate of fluid administration, vascular permeability to water and electrolytes, time when plasma expansion is measured, and the technique used to measure plasma expansion (Patanwala, A., et.al, 2010).[/quote]
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#30 JLP

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Posted 04 May 2011 - 07:49 PM

just to bring it back...obviously you all know this, but: Adult may get hypotensive from shock and still warrant cautious resuscitation, because adults cannot generally mount as powerful a vasoconstrictive response as kids and generally tolerate moderate hypotension better than kids. Due to their vastly better ability to vasoconstrict and shunt blood distribution, kids generally don't get hypotensive until this compensatory mechanism has outright failed and they are on the steep slope to irreversible circulatory collapse. Given this physiological difference, I would be suspect that permissive hypotension should be used very carefully, if at all, in kids with suspected hypovolemic shock.
Personally, if I have a kid who is post-trauma, showing hypotension and signs of organ compromise, I would not hesitate to give a fluid bolus unless there is another treatable cause for shock (hypoxia, arrhythmia, tension pneumo, vagal stimulus, toxicity, etc). I don't mind titrating the bolus, say splitting it into small aliquots and looking for a response, but not holding it off altogether until the pressure changes. That's like waiting until the bus starts moving before you run after it - you ain't gonna catch it (as my son is finally learning).

My own experience is that unlike adults, kids tend to be UNDER-resuscitated and given too LITTLE fluid too LATE, rather than the other way around - I have seen too many examples of medical staff being hesitant to aggressively resuscitate a tachy, compromised kid with poor/no urine output, and waiting until the pressure started to drop. By then the child has usually gone into refractory shock and things get really ugly. Perhaps other people here have a different experience; I would like to hear from them for a counterpoint.

We have to be very careful when we apply concepts from adult resuscitation to kids. As smarter folks than I have said, they aren't little adults.
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#31 Ectopy

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Posted 05 May 2011 - 02:10 AM

Going back a few posts above, my understanding of SVV is that it is an indication of preload by taking the pressure difference between the increased arterial pressure during mechanical inspiration and the pressure during a mechanical expiration. Once again, this is just what's floating around in my head, so may be completely wrong.

The goal of SVV is to get it down to a relatively lwo percentage difference (less than 10%?) which indicates a good preload/afterload balance (?). Thus the problem with SVV with someone who is irregular is that the area under the waveform curve is not consistent, whereas your inspiratory/expiratory cycles will be relatively consistent. Is that where you were going with the curve differentiation Sean?

How exactly does this differ from PPV besides PPV not requiring an A-Line, or does it?

-Padawan
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#32 Ectopy

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Posted 05 May 2011 - 03:05 AM

therein lies an argument for hypertonics vs colloids vs isotonics...

how much does each change intravascular volume for how long?

and is that long enough to cause coagulopathy before you can get blood products on board and diurese excess volume? etc etc?

is the cost:benefit ratio of priming the pump worth the hemodilution, etc? can you stop the bleed?

i.e. is your DO2 relatively stable?

what % of little red trucks, etc are soaked into the forest floor, if critical, how quickly can they be replaced, etc?


OK here we go:

Hypertonics
: Questionable use for neuro patients but has been pretty panned in the latest round of papers to come out. HUGE study:
http://www.medicalsc...n_surg_2011.pdf

Colloids: Once again, good in theory. Provide some "stuff" in the fluid to prevent intravascular fluid leakage to the surrounding tissue, especially in the case of aggressive fluid managment. Kool Aid blood tends to not hold fluid, concentrations gradients will get you every time.
http://www.bmj.com/c...6/961/suppl/DC1

isotonics: Seem to be where everyone is finally agreeing on. Isotonics of course dilute, but so do the others. Unless you can provide more little red trucks, all of these non oxygen carrying fluids will eventually lead to the same set of issues. Even though isotonic fluid hasn't been proven to be "better" than the other two, the other two havent been proven to be "better" than isotonic. Isotonic is crazy cheap, the other two are not.

Anyone have any evidence that can prove my fling with isotonics invalid?

As for the "time" issue, I'm not really sure where you're going. Colloids are retained a bit longer as some of the solutions are hard to renally excrete? Hmmm....

Bringin' it all back....
Sean's point about priming the pump vs. dilution is something that I think is critically important, but perhaps overlooked at times. This brings us back to the point as to how we should be targeting our fluids. If we go with the SVV argument, you're adequately priming the pump. We've shown a few examples of how that isn't a reliable indicator.

Increasing right atrial pressure increases cardiac output per our good friends Mr. Frank and Mr. Starling. If we can target a good RAP, then we can be sure to increase one of the criteria inherent in Starlings law.

Bringing this back again to SVV, what about keeping someone at slightly below optimal preload. This makes sense right? If we keep them slightly below a great preload, we'll keep them alive, keep their kidneys and brain perfusing, but won't have to use tons of fluids to dilute their "little red trucks" or to cause a concentration induced fluid shift. This is essentially the permissive hypotension argument.

The argument that I've heard AGAINST permissive hypotension is the need for blood volume expansion. Hespan, the great starch expander, has had a ton of papers revoked on its use. No one can reliably point to advantageous outcomes. Is volume expansion really that important? I think the jury is still out.

If the volume expansion argument is thrown out, than the permissive hypotension argument is certainly in. But how do we determine that threshold? :D
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#33 Ectopy

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Posted 05 May 2011 - 03:44 AM

Hit the submit button too soon? The above is meant to present my understanding of the issues brought up. However, my understanding has been known to be flawed, and I would love to see a further discussion on this - but don't be shy in pointing out where I may have gone astray.
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#34 SerendepitySaki

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Posted 05 May 2011 - 11:36 AM

IMHO, my 2 cents, etc...and please bear in mind, this is BEFORE morning espresso is on board....this is an inherently limited communication modality and i frequently fail to make my point, even when i am firing on all four cylinders....B)

don't sweat the small stuff...titrating resus efforts to SVV/PPV not necessarily that clinically significant at this stage of its development... and apologies if i led anyone to believe that that is where i was going.....

was trying to get folks to revisit the basic concept of stroke volume itself ... CO = SV x HR.... and what ITS components are... which ultimately brings us back to supply and demand... DO2 and MVO2/etc....balancing end organ perfusion with its cost ...

as far as where i was going with time...each of the IVFs expands intravascular volume for a different amount of time...

and DOES increase DO2, even though they themselves do not carry appreciable oxygen content...by increasing stroke volume... CO = HR x SV...

so, if you must have little red trucks, but don't have any, you can use volume expansion* as a temporary measure to increase the perfusion of the few Oxygen carrying units you DO have until you can get some PRBCs, FFP, & Platelets on board ...then diurese the IVF off, PRN....

PROVIDED you are NOT doing more harm than good by disturbing hemostasis/etc... disrupting clots in the short term OR negatively affecting clot formation,etc by dilutional coagulapathies...

very roughly, that's my take on the whole theory of Permissive Hypotension in a nutshell...

* the THEORY behind WHICH IVF is based on two things...how hard is it to carry (tactical medicine) and how long it stays on board...(when are you getting to more little red trucks?)...

outside tactical /"trauma" situations, because CO = HR x SV, you will sometimes see IVFs given post operatively to boost SV UNTIL the heart recovers, myocardial contractility improves and SV improves...thereby increasing DO2 w/ out PRBCs

the next question is then:

Given their developmental differences in compensating for hypotension, different TBV, etc....to what extent,if any is the above applicable in neos and pedes?

be curious to hear what comes out of Wes' conference/etc.....
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#35 SerendepitySaki

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Posted 09 May 2011 - 09:21 PM

this was alluded to earlier, but i can't recall if there was a good link posted...

After Retractions in Boldt Case, Experts Ponder the Fate Of Hetastarch

http://www.anesthesi...=17099&ses=ogst
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#36 TexRNmedic

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Posted 17 May 2011 - 10:23 AM

Heading to the symposium this morning. I hope to have more information to post here soon.
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Wes Seale
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#37 TexRNmedic

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Posted 18 May 2011 - 10:55 PM

I got a boat load of good info and will post it soon. Short version is the pedi trauma docs say low volume resus may have a place in penetrating trauma but no place in blunt. Concurrent TBI is too common in pedi blunt trauma and one epidsode of hypoxia or hypotension has significant impact on outcomes. He also said little issue with resus up to 40cc/kg isotonics, but need to consider blood products beyond that. Will post references and more details soon.
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#38 SerendepitySaki

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Posted 27 May 2011 - 02:44 AM

Mortality after Fluid Bolus in African Children with Severe Infection: http://www.nejm.org/...101549?query=OF

Fluid Resuscitation in Acute Illness Time to Reappraise the Basics: http://www.nejm.org/...105490?query=OF
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#39 Gila

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Posted 27 May 2011 - 05:04 AM

I think the paradigm is bound to shift around a bit; however, my suspicion is that at some point we may be looking at personalised resuscitation. As we begin to better understand the body in a "shock" state and better define inflammatory mediators and response to hypoperfusion and ischaemia, I wouldn't be surprised to find genetic connections to certain responses. I've already seen certain therapies become more personalised, but my intuition is that we will not have a one size fits all algorithm in the future. I don't have much to add and what I've added is simply musing.
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#40 SerendepitySaki

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Posted 28 May 2011 - 01:45 AM

and while i'm stirring the pot.... y'all might want to search the following:


"FAST Is Specific but Not Sensitive in Pediatric Blunt Abdominal Trauma"
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Sean G. Smith, RN-Alphabet Soup