paramatt_

Hey there, new thread!

Just after some anecdotal information on those providers who carry multiple or second-line antiepileptic medications, epscially non benzos. I've had a few cases over the past year or so where pts have responded poorly to treatment, including a couple of pediatric febrile status epilepticus.  (we only carry midaz with weight based dosing).

I've done a bit of research on the topic but just interested to know what others are actually doing/using including how often they get used and indications for use.

Thanks for sharing that Dwayne...never heard of it.

I have come across a couple cases of septic arthritis however...definitley makes you think twice before rolling your eyes at that 2am call for knee pain

Paramedics are prescribing antibiotics? How much pharmacology training do they have to know which ones to prescribe? Or how about checking against current meds? I'm sincerely curious as to what training they're getting before being allowed to go out and be a community paramedic.

Honestly, I'm not 100% certain. The paramedic practioner pathway is still in the infancy stage, though I think a few states have had internally run programs for atleast a few years. Currently, the federal government (this is Australia i'm speaking about) is running a two year trial in selected areas, but in terms of education requirements, I couldn’t tell you what they currently are. There is definitely no registration of any kind (nor as there are with a normal paramedic) and a quickie google search only came up with one university that's currently running a master degree specific course.

I would hazard a guess that most of the staff selected to participate in the trials already have a post-graduate level of education and have a very strong fundamental

understanding of pharmacology, plus whatever additional/specific training they've received prior to commencement . I know of one person who is currently undertaking the trial who is a former RN and also a pharmacist. Nursing to paramedicine down this way is a very common transition...but that's a whole different topic

Anyways, if I speak to someone that has some better insight of the program, I'll findout what the current training and scope of practice is or maybe one of the Aus members can chime in. It does look like the masters level will be the norm as these programs start to expand.

Also wouldn't it be nice to tell the patient who is calling you for a stubbed toe and demands to be treated to go to the pharmacy and get a prescription of Ibuprofen filled!!!!! ;P

Don't you have the ability to refer patients to other providers? Am I wrong to be under the impression that all paramedics are able to give basic advice to patients that may not need transport or can be managed by some other means?

At any rate, the service I work for is currently running a community paramedic trial...not sure what the exact title is, but they're basically functioning like a community nurse. The focus is to do basic hospital based interventions such as changing catheters, basic wound care, and can book patients in to other services, order x-rays, and prescribe some ab's, etc, etc.

I think it’s great to have this sort of service available, but to echo chbare, it shouldn’t take away from other healthcare providers who already have a degree or post-grad education. Granted, coming from someone working in a country with an already high level of paramedic education, this is already looking like the next step forward. Community based paramedicine master degrees have begun to pop up around these parts. Not sure what resistance the nurses’ union have, though in my opinion, it will play out like the way PAs/NPs function in the states….similar level of education, with a different background, serving in different settings, thus different titles.

I've used it a few times. I was able to pick up an SVT where absent P waves were hard to distinguish. With that being said, I've also had just as good, if not better, results in using V1 and turning up the gain. Intresting concept though

Along the lines of what Bushy said...I was a member for a couple of years, but left as I felt it wasn't good value for money. However,
many of my colleagues seem to be affiliated. I will probably re-join at some stage, but can't justify it, espeically living in a reginonal area

Though I was a bit late to join in, I’m really enjoying the scenario.

I was considering two aetiologies, first is the obvious chest infection causing SIRS and ARDS/ALI as described. Second, is the subsequent cardiac failure.

Here’s a decent article: http://circ.ahajournals.org/content/116/7/793.full

As the crackles are throughout the complete respiratory phase, plus the etc02 and waveform you’re describing, fluid overload seems like a less likely suspect, and more in favor of consolidation

As for the steroids, I know they are frowned upon and have been proven to be detrimental early in SIRS, however, the evidence seems to be inconclusive in cases of ARDS. With the amount of pulmonary infiltration present and the long transport time, I would be considering them for this reason. Granted, I would like some additional info if someone with more knowledge and experience than myself has any reason to totally avoid doing so.

Word. 72/40 = a MAP of 50

With 3l of fluid in and a chest like that, sounds like she's fluid overloaded as well.

+1 for the adrenaline infusion.

To go alone with Kiwi's ceftiraxone, I'd be reaching for a steroid as well..8mg of dexamethasone should suffice

Also, have you done a BGL recently? Probably not the most pressing thing at this moment, but if you have a couple seconds

This continues to be problem where I work. No free beds in the wards, and things get gridlocked in emergency. Or more frequently its just busy and we’ll have a patient who is not suitable for the waiting room and not sick enough to go through to the resus area thus we end up looking after them.

We’ll continue to provide care, on occasion we’ll assist by taking bloods, go with the patient to x-ray, etc. Not an ideal situation by any means. Once in a while a patient will be seen by a specialist team and get admitted while still in our care, or more commonly, be assessed by an ED doc a sent home.

I recently attended an 89 year old patient in bed at home presenting with palpitations with associated with chest discomfort. The onset of symptoms woke him up.

History of bypass surgery some 20+ years prior, AF, hypertension. Had once instance of rapid AF about a year prior that was medically managed. Recently well and reasonably healthy otherwise

Meds were metoprolol, a dihydropyridine ca channel blocker, and was warfarinized. Also had a nitrate spray that was “hardly ever used”

ECG showed rapid AF (ventricular rate between 130-160), hemodynamically stable and well perfused…initial SBP was 160 or so, GCS 15, no evidence of failure/pulmonary oedema, etc etc.

My partner, who was treating, began treating the patient with nitrates as he had chest pain. Aside from dropping his blood pressure over the next to 10-15 minutes, he still remained adequately perfused. The pain marginally decreased.

The obvious concern was that he was at risk of losing his pre-load and was in obvious need of some rate control, but what really surprised me was that the hospital emerg staff continued the nitrate regime.

It never fails to amaze me how the chest pain = nitrate mentality is so strongly engrained into the mind of so many health care workers, both EMSers and non, that it’s almost primeval. I’ve lost count how many times I’ve attended a doctor surgery for a chest pain patient who has received nitrates but no aspirin. More worrying is that one of the most dangerous drugs we carry (in my opinion) can be administered by someone with 115hrs training and is host of a whole cascade of adverse reactions, whilst anti-platelet agents which have a proven benefit in ACS are not in the basic scope.

Note: I work in an upsidedown non-US system with volunteers that can give aspirin but not nitriates

I don’t want to turn this into a ALS vs BLS medication discussion, but just felt like ranting a bit on the topic. Other observations are most welcome

I'm replying as someone who has done both pathways. First, was a semester each general anatomy then physiology class both with labs. A few years after completing those I undertook a non-US based paramedic degree that had combined elements of A&P over two semesters with very limited lab time. Topics covered were almost identical as were exams and marking criteria. I performed equally in both.

As both classes met their objectives I wouldn’t think that there would be much different solely based upon being integrated or not. The only thing that comes to mind would be with the integrated class, is that if students are covering other topics simultaneously, while someone may choose to solely do an independent class thus having more focused time.

At the end of the day, as stated in the first post, I think you are still going to have good performers and poor performers independent on what the layout is like. Like some of the others have pointed out, the hard thing is the ability of to measure both the betterness and the long term effects of both pathways (i.e. differences in retaining and applying knowledge, who makes a better practitioner, etc)

Interesting topic nevertheless

Very poor prognosis if we are talking about a rupture as Kaisu stated....which dose fit with the tamponade. My inital thinking was along the lines of conservative fluid management as not to aggravate the dissection, however, it seems like we've past this point and are in need of bolus fluids.

And lets go for 100mcg fentanyl...no harm making her comfortable.

How would you support that BP?

Granted that the MAP has much to be desired, however, I would still be wary about fluid administration. OP stated we have radials…I would be content with this for the time being. Maybe start off with legs elevated as long as it’s tolerated and some 02 via mask if not already done.

Anything we can do for the pain/anxiety? Opioids would be out due to the poor perfusion…anything else at your disposal?

I agree with fakingpatience and the tamponade but there seems to be something much larger at play.

I'd be initating a prompt transport, IV access but no fluid...

Maybe thoracic aneurysm/disection?

Bilateral radials present?

I agree 100% that calcium is the best treatment option, however, I don’t think I’ll get much love if I propose its use as the current time. We’ve just had a major overhaul of our guidelines including some additional medications, though calcium wasn’t one of them. Being realistic, I don’t see any new medication being added anytime soon, especially without any data on cost vs potential usage I really don’t know how I’d be able justify it. Maybe a clinical trial could be beneficial, but coming up with data to support that is another story.

We do carry bicarb it as an alkalising agent. The evidence I’ve come across for its use as a mono-therapy for hyper-K however isn’t flattering

Thanks for the replies.

Looking at the research, calcium glutonate seems to be the preferred treatment, though not possible as we don't carry it. Same goes for the insulin/glucose. Though beta-2 agonists can take 30mins+ to take effect, it’s all we really have to work with. Also our transport times that can be well over an hour, so I suppose it is possible to see a change in patient condition if implemented in the field.

What criteria were you going to use for justifying intervention?

That's what I was wondering...what criteria is being used, as obviously all we have to work with is a patient's history and ECG changes. I'll I'm doing is proposing the use of beta-2 agonists for hyper-K, including the research, patient's likely to be at risk (crush injury, renal failure, burns, etc), suggestive ECG changes, and potential doses.

It will be the higher-ups that will go through the proposal, see if it’s worth implementing, make a decision, tweak accordingly, and come out with a final guideline if they see it as appropriate. As there is lots of literature on the subject and we already carry both IV and nebulized beta-2 agonists I don't see any reason why a guideline wouldn't be formulated.

What's the odds for potential harm from the hyperkalemia vs. beta agonist effects?

In terms of risk vs benefit, some transient sympathetic stimulation will occur, and granted, some patients will have a greater predisposition to adverse reactions. At the end of the day the benefit is high. The ability to prevent/correct any of the 4 H's and T's prehospitally isn’t always possible, but when it is, I'd say that's a pretty strong step in the right direction.

Hello all,

My employer recently came up with a new policy that enables us to suggest changes or new interventions to our guidelines. I’ve been looking at the use of (s)albuterol for hyperkalemia both in the context of crush injury as well as other etiologies. Now I’ve done the research…there’s lots out there on the topic, but was wondering if anyone uses beta-2 agonists for suspected hyperkalemia. And if so, what is the implementation of the protocol/guidline based upon (all crush injury pateints, EGC changes, etc). Anyways, I'm just curious to see what others out there are doing...any feedback appreciated

Unless you carry vasopressors there's probably not a whole lot you're going to be able to do. AV in Australia carries metarminol, an alpha 1specific agonist, specifically for this...can't tell you how effective it is, but as Dwayne said, epi would be a second best due to the unwanted beta effects. If that's all you have, then it sounds like you did you best.

Just out of curiosity, what doses of epi were you using and what was the inital BP and any improvement at all?

I ask that because I have been told when the bronchi is severely constricted, it can be so severe that wheezing may be difficult or impossible to detect with stethoscope. Granted I would imagine that would be a 1 in a million extreme case. But I just wanted to throw something in the mix.

Definitely can occur, but you would probably be more likely to see this in cases of asthma (extremis) where there is significant air trapping and hyperinflation of the lungs.

To answer your original question, no airway involvement what so ever. No facial edema, no complaints of being short of breath/chest tightness, etc, and was able to swallow and verbalize that everything felt normal. I probably auscultated her lungs 5 or 6 different times as well…quite decent respiratory status overall.

I would venture a guess that in this particular case there was no respiratory involvement; from a physiologic point of view it seems kind off doesn't it?

Respiratory features and bronchospasm always pop into mind straight away when considering anaphylaxis, though it seems such symptoms occur more often in children than adults.

http://www.ncbi.nlm....les/PMC2082667/

http://apjai.digital...viewArticle/370

Thanks for all the replies. Our guidelines outline the use of both IM and IV adrenaline, although IM is generally preferred. We are getting pumps shortly, which will obviously have its benefits.

In a patient that has extremely poor perfusion with brochospasm I would be more inclined to go the IV route, however, then comes the increased likelihood of the adverse B-1 effects, so I suppose a bit of risk vs benefit vs being able to manage the appropriate infusion rate all play into the discussion as well.

And Bushy, for what its worth I had a look at Therapeutic Guidelines (eTG), metaraminol is advocated in anaphylaxis with persistent hypotension. Not to say you guys will ever use it as such, but something worth noting

Now I have done a little research on this topic, but was wondering if anyone out there in ambulance land has the ability to use alpha agonists in anaphylaxis that’s refractory to /in combination with adrenaline.

I recently had a patient in anaphylactic shock, I can’t remember all of the vitals, but she was poorly perfused, tachy, BP 65/50, decreased conscious state, mottled skin, urticarial, GIT upset, but no broncho spasm. She received IM adrenaline, 02, fluids, supine legs elevated, etc. Upon reassessment somewhere after the five minute mark, she still remained hypotensive and had a marginal increase in heart rate, though no ectopics. She got a second dose of IM adrenaline and dexamethasone. After this, she became increasingly tachy and began having multiple PVCs, developed a bit of a tremor, though still was hypotensive. All in all, it took a good 25 minutes and close to a 1000mls of pressure infused saline to get her stabilized....minus the tremor and anxiety

Aside from the potential use of an adrenaline infusion, there wasn’t much else we could offer this patient and I don’t think it would have been possible to avoid the cardiac effects anyways. With this being said, however, I kept thinking how a solely alpha-1 agonist such as phenylephrine or metaraminol might have been handy. I like to hear from anyone who has experience with these meds in similar situations

Many thanks

We also have Compazine, but its hardly ever used.

We also have prochlorperazine which dosesn't seem to get used all that often. With that being said however, I have very good results when used for vertigo/Merniere attacks as well as migraies.

Good links WH, I vaugely remember learning SPIKES. Here's another link that explains it out a bit more

http://theoncologist.alphamedpress.org/content/5/4/302.full

People have a very incomplete understanding of what a heart attack or stroke, or any other acute condition is, even if they recognize the name. They will recognize it's serious, but beyond that, they might have no idea what that means. Avoid false assurances, but let them know that there is a plan for their care and it's happening right now.

It's really strange what people will remember, which is why I thought discussing how we communicate with patients can really change things not only in the short term (reducing fear and anxiety), but also to the long term. The few thank you cards I've recieved in my short career weren't thanks for driving fast to hospital, or for any technical skill, but rather for being thoughtful and professional.

Not trying to get off track here, but an example from personal experiance from when my granpa died (I was 4 or 5). One of the few things I can remember 20-something years later is how the nurse held my hand and gave me a 7up. I'll be my bottom dollar, it's the little things like that patients and thier families are going to remeber. I would really hate that if the only lasting memory of the patient or family in the case I originally presented left them feeling lost, confused, or scared if we didn't bothered to take into account their feelings/emotions at the said time. Not sure, maybe that makes some sence

To reply to ERDoc: Bascially, what WolfmanHarris posted. I ended up explaining to the patient and family why were suspecting he was having a heart attack, and what was going to happen (in terms of our treatment and what might happen at hospital), which is what the student failed to do.

When we talked about it after, the issue seemed to revolve around his mindset which was focused treatment side of things without giving much thought to how his rapport with the patient might effect the situation.