Paramagic

Sorry, 'we' being the service I work for. It's a Third Service model that is reasonably well integrated into the health system as a whole (although it could be better), and the research we carry out looks not just at how well we get people to hospital, but the overall, long term outcomes, both in terms of the patient, and the benefit (or cost) to the community at large.

I have no doubt that nothing would be missed in your handover. However, what taking and recording the GCS in this instance will do, is quantify your observations in a manner that is easily transmissable, reproducible and useful to the Docs in determining their course of action. I also personally find it easier to say "GCS 5: 1, 2, 2" than "Eyes closed, groaning incoherently to painful stimuli, with extension of the arms and hyperpronation of the hands" We are encouraged strongly to consider the long-term outcomes of patients when we are devising a treatment plan, and in those we assess as having a poor likelihood of good outcome, we are supported in electing to withhold treatment such as intubation. One of the ways we determine this is obviously the GCS. I realise that this is not the way most EMS approach these things. GCS less than or equal to 9 = GCS less than 10. But I do agree to some extent, GCS is not just a "do we intubate or not" tool. Last week I carried out an RSI in a patient with a GCS of 15, because he needed his airway protected. The week before I elected not to intubate a patient with a GCS of 6. However, Bernards trial was not primarily about managing the airway, it was about mitigating the effects of secondary brain injury through elimination of reflexes and good sedation/pain relief, along with managing EtCO2 to minimize hyper/hypocapnia, and examining whether this improved neurological outcome at 6 months. Your phrases "irked by the pseudo-intellectual smarminess" and "It's usage is interchangable with "I couldn't care less" rendering your correction moot, yet pretentious" not to mention the reference to the Oxford English Dictionary, to me smacks of smarmy, pretentious pseudo-intellectualism.

Well, it helps me understand hypoglycemia, but what I am still having trouble with is how this pathology eliminates the transmission of impulses via the nervous system, to the point where even spinal reflexes are eliminated, thereby rendering hte patient unable to mount a response to noxious stimuli. Please explain, I am struggling with this and would like to understand it better.

Sorry, I'm having a bit of a brain fade today. Can you explain what it is about hypoglycemia that renders the body unable to mount a physiological response to noxious stimuli? It seems counter intuitive given that one only needs intact spinal nerves to mount a response normally. Even patients with spinal cord transection will manifest pain even though they are completely unaware of it themselves thanks to spinal reflexes. But I beg your indulgence, I'm struggling a little today (not enough coffee I think)

Oh sorry, I see there were some posts while I was typing. I'm a bit confused with the last reference you posted from the Annals of Epidemiology. This article is discussing the advantages of IN administration that need to cross into CSF and across the blood/brain barrier to be effective. Midazolam, naloxone and fentanyl are good examples of these drugs. However, I don't see how this applies to glucagon, which of course needs to get to skeletal muscle and the liver to have an effect. Can you explain how this applies as I'm obviously missing something?

Johnboy, it is entirely possible for an unconscious patient to have an adverse physiological repsonse to painful stimuli, whether they are conscious of that stimuli or not. You may not be aware of this, but that is the reason that those of us who carry out RSI give not just sedation but also pain relief following intubation, regardless of why the RSI was carried out. This is also why intensive care units have protocols for assessing and managing pain in the comatose/intubated patients. There is quite a significant volume of literature on this issue, not because pain relief is not warranted, but because it is a vital part of care of the unconscious patient, yet difficult to assess. I think it is entirely appropriate to give lidocaine prior to other drugs via an IO irrespective of the conscious state. The only time I may forgoe this is in the cardiac arrest setting. Might I recommend some texts to read regarding this? Wall's Textbook of Pain is always a good place to start for anything pain related. There is a good little book whose name escapes me at the moment that deals with this sort if thing in the ER. Analgesia and sedation in the emergency department? Something like that. It has a red cover. Damn. It will come to me later no doubt. Oh's Intensive Care Manual is a good resource also. I hope these help. I would love to know if there are any updated references for IN glucagon that you could provide. I'm a big fan of the MAD, would love to hear of more uses for it. Thanks. Paramagic.

Dwayne, no offense taken, and my apologies if I caused any; none was intended. Stephen Bernard and colleagues published in Annals of Surgery in 2010 the only well controlled study into pre-hospital RSI that showed a benefit in functional outcome in patients who recieve pre-hospital as opposed to in hospital RSI. In this study it was patients with a GCS <10 who recieved benefit. So if we want to provide validated scientific treatment to these patients following traumatic brain injury we need to be able to assess GCS in the field. As for it being a prognosticating tool, this is indeed true. Surely we are interested in the prognosis of out patients? It's prognostic value has been demonstrated in many different conditions, not least of which is head injuries. However, with increased intervention for these patients in the field, the prognostic value is clouded if a GCS is not accurately recorded, so again, we need to be able to assess and record GCS accurately so Doctors can provide appropriate treatment with reference to their expected outcomes (Problems with initial Glasgow Coma Scale assessment caused by prehospital treatment of patients with head injuries: results of a national survey. J Trauma, 1994) If a patient has their eyes open (actually open) then their GCS score for eyes is 4. I'm not sure why you would think otherwise. However, no-one has suggest that GCS is taken in isolation; it has to be taken in context, but this doesn't diminsh it's value. Nobody has suggested that it should be used without context, that is just a strawman. I would ask again, if this well studied, well understood (for all it's pros and cons) internationally recognized, reproducible and validated tool is not being used, then what is? Certainly. With regards to the study you have linked to, I am aware of this, hence my comment "there are problems with interrater reliability to begin with, but proper training and education can minimize this" Paramedics should not be the inexperienced or poorly trained providers that confound this. Other references for the validity of the GCS include (but are not limited to): Bishara, S. N., Partridge, F. M., Godfrey, H. P., & Knight, R. G. (1992). Post-traumatic amnesia and Glasgow Coma Scale related to outcome in survivors in a consecutive series of patients with severe closed-head injury. Brain Injury, 6(4), 373380. Bush, B. A., Novack, T. A., Malec, J. F., Stringer, A. Y., Millis, S. R., & Madan, A. (2003). Validation of a model for evaluating outcome after traumatic brain injury. Archives of Physical Medicine and Rehabilitation, 84(12), 18031807. Changaris, D. G., McGraw, C. P., Richardson, J. D., Garretson, H. D., Arpin, E. J., & Shields, C. B. (1987). Correlation of cerebral perfusion pressure and Glasgow Coma Scale to outcome. Journal of Trauma, 27(9), 10071013. Demetriades, D., Kuncir, E., Murray, J., Velmahos, G., Rhee, P., Chan, L. (2004). Mortality prediction of head abbreviated injury score and Glasgow Coma Scale: Analysis of 7,764 head injuries. Journal of the American College of Surgeons, 199(2), 216222. Diringer, M. N., & Edwards, D. F. (1997). Does modification of the Innsbruck and the Glasgow Coma Scales improve their ability to predict functional outcome? Archives of Neurology, 54(5), 606611. Gill, M., Windemuth, R., Steele, R., & Green, S. M. (2005). A comparison of the Glasgow Coma Scale score to simplified alternative scores for the prediction of traumatic brain injury outcomes. Annals of Emergency Medicine, 45(1), 3742. Healey, C., Osler, T. M., Rogers, F. B., Healey, M. A., Glance, L. G., Kilgo, P. D., et al. (2003). Improving the Glasgow Coma Scale score: Motor score alone is a better predictor. Journal of Trauma, 54(4), 671678. Lieberman, J. D., Pasquale, M. D., Garcia, R., Cipolle, M. D., Mark Li, P., & Wasser, T. E. (2003). Use of admission Glasgow Coma Score, pupil size, and pupil reactivity to determine outcome for trauma patients. Journal of Trauma, 55(3), 437442; discussion 442433. Mamelak, A., Pitts, L., & Damron, S. (1996). Predicting survival from head trauma 24 hours after injury: A practical method with therapeutic implications. Journal of Trauma: Injury, Infection, and Critical Care, 41(1), 9199. Meredith, W., Rutledge, R., Hansen, A., Oller, D., Thomason, M., Cunningham, P., et al. (1995). Field triage of trauma patients based upon the ability to follow commands: A study in 29,573 patients. Journal of Trauma, 38, 129135. Novack, T. A., Bush, B. A., Meythaler, J. M., & Canupp, K. (2001). Outcome after traumatic brain injury: Pathway analysis of contributions from premorbid, injury severity, and recovery variables. Archives of Physical Medicine and Rehabilitation, 82(3), 300305. Pal, J., Brown, R., & Fleiszer, D. (1989). The value of the Glasgow Coma Scale and Injury Severity Score: Predicting outcome in multiple trauma patients with head injury. Journal of Trauma, 29(6), 746748. Poon, W. S., Zhu, X. L., Ng, S. C., & Wong, G. K. (2005). Predicting one year clinical outcome in traumatic brain injury at the beginning of rehabilitation. Acta Neurochirurgica, 93 (Suppl.), 207208. Ross, S., Leipold, C., Terregino, C., & O'Malley, K. (1998). Efficacy of the motor component of the Glascow Coma Scale in trauma triage. Journal of Trauma, 45, 4244. Wellons, J., & Tubbs, R. (2003). The management of pediatric traumatic brain injury. Seminars in Neurosurgery, 14(2), 111118. Young, B., Rapp, R. P., Norton, J. A., Haack, D., Tibbs, P. A., & Bean, J. R. (1981). Early prediction of outcome in head-injured patients. Journal of Neurosurgery, 54(3), 300303. Zafonte, R. D., Hammond, F. M., Mann, N. R., Wood, D. L., Black, K. L., & Millis, S. R. (1996). Relationship between Glasgow Coma Scale and functional outcome. American Journal of Physical Medicine & Rehabilitation, 75(5), 364369.

I'm not sure why you think I'm moody or defensive, something must have come across in my post that was not intended. I'm also not sure why you think that my first post was directed at you. I agree entirely with your first post that just using one number is meaningless without a breakdown and a context, but if that is how it has been taught, then that represents a deficiency in the teaching of using the GCS. The post that prompted me to reply was the "Honestly I could care less" post, partly because I think that is a sad indictment on EMS education and to some extent attitudes, and also because that comment is non-sensical given the context. It should be "I couldn't care less." But that is a discussion for another time. Nonetheless, you asked for my justification of why I think the GCS is important, and I gave it. I stand by the fact that although there are flaws in the GCS it is still a valuable tool for assessing, monitoring and prognosticating when used properly.

That certainly is putting words in my mouth,but you are clearly already aware of that. I'm interested that the question of justifying the exclusion of GCS has not been asked. On what basis do provides decide that a long-standing, clinical useful, reproducible, standardized scale to determine level of consciousness, degree and to some extent, location of neurological dysfunction and prognosis from neurosurgical events like trauma or hemorrhage? If GCS isn't used, what is? GCS is not perfect; there are problems with interrater reliability to begin with, but proper training and education can minimize this. This is important given the increasing level of prehospital management of neurosurgical emergencies as initial GCS is an important in determining prognosis. Change in GCS from the prehospital situation to in-hospital (assuming it has been obtained) is strongly predictive of outcome. GCS was initially and is still fundamentally, designed for use in patients with traumatic brain injuries, but it has been widely used and is accepted as appropriate for the se in any patient with an acute neurosurgical issue. However there are more accurate methods of determining outcome, using age, presence of hypoxia or hypotension and pupil response and so on, but GCS, and in particular the motor score (which is less susceptible to being confounded) is still an important part of these other systems. GCS is most accurate when it is at either extreme (which stands to reason) but still has value in the entire range. Understanding the pros and cons of the GCS lets us realise that GCS isn't just a random number, or collection of random numbers put together so people can parrot "GCS less than 8, intubate" at every opportunity. It is an important part of assessment and monitoring of range of patient presentation, and an important predictor of outcome in head injured patients.

I read the original post and had a little chuckle, thinking to myself "Who uses the GCS? LOL! That's like asking who takes a pulse, or who takes a blood pressure! Everyone does, silly!" Then I read the rest of the "Don't know/Don't care" posts and became sad, scared and angry in equal measures at the abysmal education that must be reqired that people not only don't understand, but don't care to understand about fundamental patient assessment.

To be honest, I'm not sure how much it would matter. The problem with head injured patients and their raise in ICP is loss of autoregulation. So where you would normally have a spike in ICP from a stimulus that would then subside, with the head inured patient that spike becomes a plateau. The Australians have shown us that careful and appropriate pre-hospital RSI in head injured patients, with consideration for reduction or elimination of reflexes using ongoing paralysis and good sedation, will actually lead to a favourable outcomes. So I would recommend properly performed RSI over anything else in this cohort of patients. If you cannot RSI and the patient needs their airway manged, then use whatever it is that you have available.

Sad that these absurdities continue to hang around. Personally for the shocked patient I prefer using ketamine, both for analgesia, and (if it's necessary) induction for RSI (with the larger dose of roc or sux). It's a pity that there is not more use of ketamine, it is a wonderful drug.

Head injuries I can understand (although I don't necessarily agree with it), but no pain relief for polytrauma? Huh?

You do realise that the typical (studied) dose of morphine is 0.1mg/kg? 2-4mg to a max of 10mg is almost placebo, unless you are talking about 20-40kg pediatric patients. If you don't use fentanyl, on what grounds do you feel qualified to "prefer" morphine over fentanyl? Even if you prefer morphine, what about your patients who are suffering from oligoanalgesia? Do they get a say? And as for "routinely" causing nausea, no study I have ever read places the incidence of nausea/vomiting secondary to morphine adminstration over 28%, with most ranging from 5-25%. Why give another drug that is not going to be indicated in 3/4s of the patients recieving morphine? Finally, vasodilation is often something we want to avoid, whilst still be able to give pain relief, so the histamine release associated with morphine administration in some people can be detrimental, not beneficial.

Nasty stuff. I presume he has a ruptured diaphragm as well as his flail segments and contusions. He needs intubated and ventilated now. Agents of your choice for RSI: I like ketamine with some more fentanyl given his tenuous BP and falling MAP (are you sure there is nothing wrong with his heart? That's a very narrow pulse pressure). Long term paralysis is indicated with adequate ongoing sedation to reduce O2 demand, and to enable adequate ventilation given his very high (and inadequate) respirations which would very much get in the way of a SIMV setting I think. More fluids are in order, but we need to replace red stuff with red stuff, not water. Now he really needs to be somewhere where they can fix him. Get him out!

He needs to be in this hospital for as short a time as possible. Arrange urgent transfer to highest level trauma service immediately. Get another line in him (large bore) and get some blood and products up from the bank. Get some decent pain relief on board, see what happens with his respirations following that. I prefer ketamine, but whatever floats your boat. Once he's breathing easier, reassess, he may have low sats purely from poor effort secondary to pain. Low sats in the setting of a pneumothorax would normally be expected later in the evolution of the injury rather than earlier. He could also have lung contusions of course. Regardless, he needs pain relief and plenty of it. If there is going to be any imaging done, it's a toss up between portable x-ray and a FAST. On one hand, portable chest (AP and lateral) may show us a pneumo, but as he is supine it will be difficult to tell. A FAST will show us the free fluid in the abdomen, but lets face it, we can be reasonably certain he has blood in his belly, so is it really going to change anything we do now? I'm glad there is no CT, the last thing he needs to be is a VOMIT. Splint his pelvis, it is quite possible he has a fractured pelvis and subsequent bladder injury which is a nasty, nasty thing to have. Align and splint the leg to regain pulses, it doesn't really matter how it is done, the orthopods are sharpening their chisels even as we speak. It may not be worth the time putting a traction splint on if we can get good pulses back with anatomical splinting, and being worried about a pelvic fracture would make you worry about tractioning off that. Finally: get him the hell out of there!

Interestingly enough, despite the obvious benefits of therapeutic hypothermia in the post arrest patient, there is no evidence that starting cooling in the field confers any added benefit. I would like to see a decent study where cooling with large volume cold fluid is started prior to ROSC, this would seem intuitively to be useful (intuition being no substitute for evidence)

The treatment he received in hospital is somewhat of a moot point. As has been pointed out (with accompanying head smashing ) acute cardiogenic pulmonary edema is a problem of fluid in the wrong place, not too much fluid in total. The treatment should be nitrates and CPAP. However, depending on how long the patient required positive pressure ventilation, it is entirely possible that they did receive furosemide in hospital. This is not necessarily because they were fluid overloaded in the inital stages, but because positive pressure ventialtion is known to cause SIADH after 24 hours or so, making diuresis necessary. Furosemide in the early stages of a sympathetic mediated acute cardiogenic pulmonary edema is an evil, evil drug.

What a great opportunity! You will have a hard time finding a lot of research specific to out-of-hospital care, but search long and hard and present a compelling case for everything you can. In some cases you won't necessarily find any research, so it pays to think long and hard about why you may want to include certain drugs/interventions and to be able to present a clear and rational case for their inclusion when the RCTs don't exist. With regards to specific stuff mentioned (and based on not much more than my personal preferences!) : Morphine/Fentanyl: Have both, there is no real reason not to. Some people like one, others like the other, give them (and the patient) the choice. It also allows opiod coverage when someone is allergic to morphine. Consider ketamine if you can. It is an absolutely wonderful drug; safe, effective, can be given IV, IO, IM, Oral, won't knock off respiratory drive or airway reflexes and can be used as part of an induction for RSI as well (especially useful in patients with tenuous perfusion) On RSI, if you are going to include a protocol, take a look at the Ambulance Victoria (Australia) protocol for this. To date they are the only people to carry out a high quality intention to treat study and show a benefit. RSI is a wonderful tool, but it has to be done perfectly or not at all. To my knowledge they do not include ketamine as an induction agent, but this can be included in yours (really, ketamine rocks!) If you really wantt to be cutting edge, DON'T include heparin, plavix or beta-blockers for ACS. They cause nothing but harm (discussed briefy here by DP Gumby and I) Good luck!

Yep. Use them routinely, especially in children nice and early, but they are good in adults too, for the reasons Doc posted. I typically go OG as well for trauma patients, will use NG for non-traumatic cases occassionally, but mostly I'm in the habit of going OG. Never had charcoal.

Sorry, but I'm a bit lost. What exactly does this rambling have to do with this thread? Maybe you could start your own thread on reimbursement rather than clutter up other conversations with unrelated stuff.

I've done my best to be polite, respectful and helpful, but I seem to be coming up against a wall here. I would like to think that is true, but a really have my doubts. If you were really interested in obtaining data I would have thought that you might like to know where I source my statements from. I'd be happy to furnish you with references, but it does not appear to be important to you, and while you are happy to agree with me without question when my statements correspond to your desires, you are also happy to dismiss out of hand any contrary position. It seems to me that you are interested in getting more "toys" rather than improving patient care. Improving patient care has little to do with how many drugs you carry, and even less to do with what other services carry, but everything to do with the judicious application of best available evidence by well educated and experienced providers as an integrated part of the health system at large. I hope you come to this realization sooner rather than later.

Ok, I'll try again. It is admirable to want to change your practice or the practice of your service for the benefit of the patient. However, there is little that you have put forward that is of benefit to the patient. Continuous nebulized albuterol probably is, and in some situations (such as your seizure example) it may be useful to have further options for seizure management. But, as I tried to point out, it is not necessarily just a matter of everyone getting all the new toys. If you look at the big picture (as you ask us to do) the service has to train everyone in the use of these treatment modalities, have continuing education on them and supply the drugs or equipment (and possibly thow away a large amount of what they supply if it is something that doesn't get used often). All of this costs money; sometimes a lot of money. A sad reality of the world we live in is that we have to consider the cost versus the benefits in anything we would like to see instituted, as there is nevere (particularly for EMS) a bottomless pool of money to spend. When it comes to things like nitrates for ACS, which have been shown to have no impact on mortality and morbidity, or furosemide for acute cardiogenic pulmonary edema which has been shown to be bad for patients, it would seem pointless to lobby for spending more money on things that don't help. Hell, we are currently lobbying to have furosemide removed from our formulary because it never gets used any more! Now, when we start looking at things like RSI (as an extreme example, although this holds true for all interventions) we have to start looking at not just the cost to implement and continue with the treatment modality, but also the risk involved versus the potential benefits. With RSI the risk is enormous, and thus far (certainly until the publication of Bernard's trial last month) there has been no benefit to the patient demonstrated. I would have thought that as an ambulance manager this would be something that you would have a good grasp of. Now, with reference to your letter to the medical director: Not withstanding any issues there are with grammar, there is certainly nothing in this letter that would make me even consider changing any protocols. The sole reference you have provided that comes from a medical journal is from the Indian Journal of Anaesthetics, which does not rate very highly on impact factor. The article also doesn't actually address in any relevant way the issues you have put forward, so I'm not even sure why it is there. The rest of the references that are accessible are from websites dedicated to providing largely generic information to lay-people. Providing such links to your medical director is unlikely to impress him/her. You need to provide some decent references from peer reviewed medical journals to be able to support your requests, not consumer health advice from the internet. It really isn't relevant what other services are doing, what is relevant is what is the best for the patient that can be sustained by the service. If you really want to effect change you need to be prepared to support it with evidence and clear rationales.

I'm afraid I have to agree with Rock_Shoes: When the written form is the only means of communication you have, it is important that it is clear. Please remember that this board is accessed by health care professionals from all over the world, so "standard" abbreviations may not, in fact, be standard to them. You may not want to hear it, but it is clearly making it difficult for people to understanyd you, so you are hamstringing your own efforts by not observing proper grammar. As to your questions, there are a number of things that need to be addressed when looking to change protocol. As fiznat has pointed out, you need ot be able to provide good evidence that the change you have mooted is going to be beneficial to the patient, and that the benefits will outweigh the risk. However, it doesn't end there. You also need to demonstrate that the treatment will be both clinically effective and cost effective. No EMS agency will institute change to protocol if you have a drug with NNT=5000 and a high cost to buy, store and maybe throw away. Now, as for the specifics: Nitrates for Acute Coronary Syndrome (ACS) or Acute Cardiogenic Pulmonary Edema (ACPE) - You will probably find this one difficult for ACS, but maybe easier to get in for ACPE. As has been pointed out, there is no benefit in terms of morbidity or mortality when using nitrates for ACS. That said, I disagree with RomeViking: Whilst an IV infusion is definitely easier to titrate, it is more costly to equip and run, and has no added benefit. In the scenario given, I would simply not give more nitrates. Just because you have it, doesn't mean you have to give it. Now, personally I can give as much SL nitrate as I feel is necessary, and I often do go above 3, especially in those Killip I ACS patients with big blood pressures, as we think it is probably important to reduce myocardial workload by reducing pre-load (with the understanding that evidence is lacking, as above) I certainly don't give morphine to vasodilate as morphine's vasodilatory effects are unpredictable. However, for ACPE, nitrates and CPAP are the treatments of choice, and I think you could mount a much stronger case to continue with SL nitrates in these patients. Albuterol/Atrovent. I thnk you could mount a reasonable case for continuous nebulized albuterol in moderate to severely unwell asthmatic patients, as it has been shown to be slightly more effective than intermittent nebulized albuterol and to have a good safety profile. Atrovent has a very long duration of action and you do not get much, if any added effect, so a single dose, or maybe two doses is ample. Benzodiazepines for status epilepticus: If a patient does not respond to appropriate doses of benzodiazepines, it may be that they are not going to, and that a second line agent should be used. However, if you were to be giving repeated or large doses, I would suggest that some definitve airway care (such as Rapid Sequence Induction and intubation) may be required to be able to continue with treatment without needing to worry about airway/breathing. This obviously introduces a whole new level of potential complication. You might need to do a patient care record review to see how often your agency attends status epilepticus patients who do not respond to the doses of benzo that you have already. If it is a large number, it may be worth pursuing, if not, then I would expect the risk would outweigh the benefit. Thiamine: Sorry, can't really get excited about this, maybe you can find some evidence somewhere that it is useful. I have my doubts though. Finally, I don't think that physical distance to hospital is an excuse for not providing appropriate patient care. It's not mandatory to finish a protocol before getting to the ER, but you should always have to options, even for day to day business, not just extremes as we have been seeing lately.