# opa or npa?



## emt brando (Feb 7, 2012)

which is better overall


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## tssemt2010 (Feb 7, 2012)

emt brando said:


> which is better overall



thats kind of situational, on a patient with a gag reflex, npa, if theyre unconscious and/or dont have a gag reflex, an opa would be the better option


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## DesertMedic66 (Feb 7, 2012)

tssemt2010 said:


> thats kind of situational, on a patient with a gag reflex, npa, if theyre unconscious and/or dont have a gag reflex, an opa would be the better option



Agreed. Even tho my protocols say that the NPA is the preferred airway adjunct.


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## emt brando (Feb 7, 2012)

i agree, protocol goes with npa, but i think it is more of a situational thing


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## FeatherWeight (Mar 2, 2012)

Say a PT has a skull fracture and still has a gag reflex but has an obstructed airway that couldnt be suctioned what would you do then?


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## DesertMedic66 (Mar 2, 2012)

FeatherWeight said:


> Say a PT has a skull fracture and still has a gag reflex but has an obstructed airway that couldnt be suctioned what would you do then?



No NPA and no OPA. Suction might still be able to be done. If the hard suction cath won't fit in the patients mouth use a soft suction cath that can be inserted in extremely small areas. BVM if needed.

ALS in my area can't RSI so no intubation. ALS in my area won't be able to do anything for airway that BLS can't do for this scenario, at least that I can think of.


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## FeatherWeight (Mar 2, 2012)

Cricothyrotomy?


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## Veneficus (Mar 2, 2012)

FeatherWeight said:


> Say a PT has a skull fracture and still has a gag reflex but has an obstructed airway that couldnt be suctioned what would you do then?



cut


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## DesertMedic66 (Mar 2, 2012)

FeatherWeight said:


> Cricothyrotomy?



If I remember correctly that skill is being taken out of our medics scope of practice on April 1st.


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## adamjh3 (Mar 2, 2012)

FeatherWeight said:


> Say a PT has a skull fracture and still has a gag reflex but has an obstructed airway that couldnt be suctioned what would you do then?



Get orders to _properly_ insert an NPA.  Working als, since we don't have RSI, I'd see if I can't get an order for high dose versed or morphine to knock out that gag reflex, suction, and try an OPA. 
How far off is my thinking?


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## STXmedic (Mar 2, 2012)

FeatherWeight said:


> Say a PT has a skull fracture and still has a gag reflex but has an obstructed airway that couldnt be suctioned what would you do then?



They won't have a gag reflex for long...  Or you could beat 'em to it with a little pharmacology


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## FeatherWeight (Mar 2, 2012)

firefite said:


> If I remember correctly that skill is being taken out of our medics scope of practice on April 1st.



Everywhere?


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## NomadicMedic (Mar 2, 2012)

Interesting. NPA is not allowed to be used by BLS in King County Washington.


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## DesertMedic66 (Mar 2, 2012)

FeatherWeight said:


> Everywhere?



Just RivCo I believe.


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## thisgirlisamedic (Mar 2, 2012)

Wouldn't rsi be a little risky to icp in a the pt with a skull fx, depending on drugs u have available. I'd consider phenergen for the gag reflex, yes it does work no your girlfriends won't do that more lol but i would think that bls airway would, be better at that time dependent on pts response to that get more aggressive


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## Veneficus (Mar 2, 2012)

thisgirlisamedic said:


> Wouldn't rsi be a little risky to icp in a the pt with a skull fx, depending on drugs u have available. I'd consider phenergen for the gag reflex, yes it does work no your girlfriends won't do that more lol but i would think that bls airway would, be better at that time dependent on pts response to that get more aggressive



"_A consensus panel has addressed the question of poorer outcomes in prehospital patients with TBI who have been intubated. This panel found no prospective controlled trials to adequately address the efficacy of paramedic RSI for severe TBI.[35] _"

http://www.medscape.com/viewarticle/585165


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## thisgirlisamedic (Mar 2, 2012)

Wow hadn't seen that cool, our med director needs to check that out we still have to  bolous steroids with rsi on an skull fx, i hate having to do all the extra if i don't have to, but like I said if it condition demands it or shows like it will ill do it, don't wanna be behind the game then it sucks to try to catch up lol


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## Veneficus (Mar 2, 2012)

thisgirlisamedic said:


> Wow hadn't seen that cool, our med director needs to check that out we still have to  bolous steroids with rsi on an skull fx, i hate having to do all the extra if i don't have to, but like I said if it condition demands it or shows like it will ill do it, don't wanna be behind the game then it sucks to try to catch up lol



Your med director may want to consider this one too then:

Corticosteroid Administration

"The main indication for the use of steroids is for the treatment of vasogenic edema associated with brain tu mors or accompanying brain irradiation and surgical manipulation.[71] Although the precise mechanisms of the beneficial effects of steroids in this paradigm are un known, steroids decrease tight-junction permeability and, in turn, stabilize the disrupted BBB.[61,91] Gluco cor ticoids, especially dexamethasone, are the preferred ster oidal agents, due to their low mineralocorticoid activity. *The ther apeutic role of steroids in TBI and stroke has been studied extensively. In TBI, steroids failed to control elevations in ICP or to show any benefit in outcome, and they may even be harmful.[17,72]* In stroke, steroids have failed to show any substantial benefit[64]* despite some success in animal models.[93] Given the deleterious side effects of steroid use (peptic ulcers, hyperglycemia, impairment of wound healing, psychosis, and immunosuppression), until further studies are published, caution is advised in the use of steroids for cerebral edema unless absolutely indicated.* The role of steroids in the treatment of bacterial meningitis and postinfectious encephalitis is beyond the scope of this article."


http://www.medscape.com/viewarticle/559004


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## Veneficus (Mar 2, 2012)

or this one:

http://www.ncbi.nlm.nih.gov/pubmed/21262204

"The CII of MP treated rats was comparable to that of saline treated control rats before injury but was significantly decreased in injured rats receiving high-dose MP on post-injury day 7. Similarly, the incidence of acute CIRCI was significantly higher in the high-dose MP group on post-injury day 7. Furthermore, the CII of rats that did not survive post-injury was significantly lower compared to that of survival and was indicative of acute CIRCI. We also examined apoptosis in the paraventricular nucleus (PVN) of the hypothalamus and the adenohypophysis of the pituitary, using a TUNEL assay and transmission electron microscopy (TEM). The number of TUNEL-positive cells was significantly higher in injured rats treated with high-dose MP. No TUNEL-positive cells were detected in the adenohypophysis across experimental groups at either 7 or 14days after TBI. However, autopsies performed on rats that did not survive post-injury revealed obvious apoptotic cells in the adenohypophysis. Moreover, TEM revealed morphological changes characteristic of apoptosis in both the PVN and adenohypophysis of high-dose MP treated rats. *These data suggest that MP therapy for TBI could increase neuronal apoptosis in both the hypothalamus and pituitary and consequently exacerbate acute CIRCI and mortality induced by TBI."*


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## thisgirlisamedic (Mar 2, 2012)

I had heard this and was talking to the neurologist at the university hospital about this, only thing we could figure out is that our med. Director is a little behind, or backwoods in his terms not mine, I have brought up concerns multiple times about many of our meds. But I never get anywhere, maybe that's why I'm looking for other employment, lol but thanks for the info I really enjoy these studies , and learning new things, it can really make a difference if u know what i mean, I don't think I could ever know enough, by the way what have u heard about the role of " prils" meds on the ability to recover from shock/ trauma


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## Veneficus (Mar 2, 2012)

thisgirlisamedic said:


> by the way what have u heard about the role of " prils" meds on the ability to recover from shock/ trauma



Does this have a technical name, not only have I never heard of it (which is extremely rare in trauma), but both a medscape and pubmed search brings up nothing.


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## thisgirlisamedic (Mar 2, 2012)

Prils are gonna be the class of ace inhibiters aka hypertension meds.


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## Veneficus (Mar 2, 2012)

thisgirlisamedic said:


> Prils are gonna be the class of ace inhibiters aka hypertension meds.



I have heard captopril is being tried as a renal protective therapy in addition to erythropoietin in the ICU. 

I haven't heard anything about its use in the EMS or emergent trauma setting.


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## thisgirlisamedic (Mar 2, 2012)

I don't think it'd a use as much as it a life threat, someone said something about since it works on the kidneys production of the receptors that it would cause the body to not be able to respond to shock? I'm trying to find information about this because I had a call that still bothers me and I think his meds, were part of the reason that he died


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## Veneficus (Mar 3, 2012)

*There is nothing simple about trauma*



thisgirlisamedic said:


> I don't think it'd a use as much as it a life threat, someone said something about since it works on the kidneys production of the receptors that it would cause the body to not be able to respond to shock? I'm trying to find information about this because I had a call that still bothers me and I think his meds, were part of the reason that he died



I think the idea behind using the ace inhibitor is to stop constriction of the afferent renal arterioloes. 

In hypovolemia, renal arteriole constriction (starting with efferent) for maintaining GFR is a physiologic reaction. With a high enouugh level of stimulation can be pathologic by reducing or eliminating glomular blood flow.

If the mechanism is identified and treatment begun early enough, AKI is treatable. The kidney can actually last days in some cases.

I can see where in resuscitation, in the effort to mitigate catecholamine response and preserve renal blood flow, the ace inhibitor would be a logical choice.

It may (theorhetically) also have some residual effects in the pulmonay vascular circuit too, which may secondarily inhibit neutrophil activation in the lungs. (haven't found anything that states it actually works though)

The erythropoeitin is still in early research stages, but it is being shown to have an antiapoptotic effect in not only the kidney but on many other cells. (This would offer molecular support to the clinical observation that the loss of the kidneys plays a larger role in the development of MODS than just a single organ would suggest. Particularly with the availability of dialysis.)

Progesterone and pregnenolone are being shown to have antiapoptotic effects as well, particularly in TBI, but I have yet to figure out if it acts conjunctively,  synergistically, or not at all with the erythro.  

People on chronic medications present increased challenges in trauma care. Especially elderly patients who have not only physiologic and pathologic changes, but may be on multiple meds too. ( I once silenced a M&M meeting at a major hospital I was visiting when I suggested that perhaps resuscitating to the normal textbook respiratory end points of the elderly chronic smoker, post car vs. ped, whos death was attributed to respiratory failure by pathology, was probably a predictable outcome of the efforts.)

Recently I ran across some information on endorphins causing endocardial capilary constriction resulting in Q wave infarctions. (an MI while in hypovolemic shock would be bad) There is no reason to think that synthetic opioids would not have the same or potentiate the effect.

Additionally, several anesthesia studies show that overresuscitation increases mortality, particularly with over fuild resus. So not only does what you are doing, but how much. 

did your dead person have an autopsy?


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