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Cool, thanks for the link! I did a whole bunch of Googling and couldn't find an answer.

I've always thought that with a plasma transfusion, blood type is critical, just as with PRBC's, and that therefore a Type A patient, for example, must get only Type A or AB plasma. However, someone told me that in an emergency, a Type A plasma can be given to a Type B patient, and vice versa. Is this correct? The explanation I was told is that although the Type A plasma donated to the Type B patient has antibodies that will attack the recipient's Type B red cells, those antibodies will be so diluted by the recipient's blood that it the transfusion will not harm them.

I know that the recommendation for treating hypertension in a subarachnoid bleed is to keep the BP below 140, but is there any accepted recommendation for traumatic subarachnoid bleeds? Would you treat a BP of 230/120 in a patient with a traumatic brain bleed (not subarachnoid) if you did not know the ICP?

I'm wondering what protocols/decisions strategies the neurologists in your ICU/ER use for deciding to use Keppra prophylacticaly for seizures, and mannitol/hypertonic saline? I ask the question because I don't seem to see uniformity in how certain patients are treated. FYI I'm not a neuro ICU nurse, so perhaps I'm ignorant about something basic. 1) Patient has extensive subarachnoid bleed showing on CT. There is no signs of herniation yet. Is it standard of care to give an anti-epileptic prohylactically? Is there evidence that it really will prevent seizures? Would you give mannitol/hypertonic saline, again prophylacticly for expected clinical course? 2) A patient with an extensive intraparenchymal bleed, again with no signs of herniation yet. Do you give Keppra and mannitol/hypertonic saline? 3) A patient who is ALOC, combative with an obvious traumatic head injury, but no CT has been done. Would you give these treatments? If they were posturing, you would give the mannitol/hypertonic saline, correct?

Thanks for your responses! What do you guys think is the best way to monitor tube placement during transport of a neonate? In adults waveform capnography is great because you get an immediate alert if the tube is dislodged (i.e., into the hypopharanx). With little babies, it is obviously so much easier to dislodge an ET tube and not realize it. What do neonate transport teams use for monitoring?

For a neonate, can waveform capnography be used for ET tube confirmation (post intubation and during transport)? I guess I don't see why it shouldn't be, but I don't see any reference to waveform capnography in my NRP book.

I get that, but my understand is that an arterial occlusion of the leg is going to happen in the femoral artery, or in the popliteal artery proximal to the knee. In either case, you'd have no circulation to the lower leg, and thus neither a pedal pulse nor a posterior tibial pulse.

Thanks for the reply. My understanding is that we are mainly checking pedal or posterior tibial pulses to make sure the patient hasn't developed an arterial clot higher up in the leg, in which case we would find neither pulse. So, as long as we are finding one pulse, it is safe practice to not bother checking for the other pulse, correct? On my unit everyone automatically documents both, and I'm quite sure hardly anyone consistently checks both pulses. It is awfully time consuming when you can feel one of the pulses but can't feel the other, and then have to spend time trying to find it when you already know that there is good circulation.

If you can feel or Doppler a pedal pulse, is there really any need to find a posterior tibial pulse? Likewise, if you can get a posterior tibial pulse, any need to feel for a pedal pulse?

Thanks for your replies. I didn't realize I had gotten any messages, hence this late reply. I've worked in the ER for many years, but I've never seen a seizure due to hyponatremia. We're always ready to treat for this whenever the L.A. marathon comes around.? I'm mostly curious to hear experiences in treating these seizures, and also in how they present. Are these people usually in status? Will they respond to benzos? Of course I understand you want to correct their sodium a bit with hypertonic saline, but I wonder if initially giving them Versed or Ativan will suppress their seizure until you can confirm their sodium level, or until you get that hypertonic saline from the pharmacy since many ER's won't have it immediately available.

Has anyone ever seen a hyponatremic seizure in the ER? I'm just curious on how the patient presented, how long the seizure lasted, if you saw immediate relief from treatments, etc. details.

Taking a two-week paramedic course may certify you on paper, but it will not make you a competent paramedic. You need a bunch of experience working as a medic, not just a little bit of classroom time. I understand that flight programs look more favorably on applicants who have a medic cert, but is it really that important? By the way, I took the online Creighton master's in EMS a few years ago. Maybe you should look into that program. You won't get a paramedic cert out of it, but you will have a master's in EMS, which will look good on your resume.

Thanks for your responses. We didn't want to do amio because she wasn't anticoagulated yet. The obvious thing to me was to do rate control, but I wasn't sure if Cardizem was the right thing to use since it would antagonize the Levophed. The doc didn't want to use it for that reason, though one of my experienced co-workers said she'd seen Cardizem and Levo used together and believed that that was the right thing to do. What do you guys think?

How would you treat this patient in regards to rate control: Pt has been going in AF for a few days, and now they are in AF RVR with a rate of 130. The patient is also on Levophed at 5 mcg/min. BP is 100/60.

I recently heard of a case (if I remember it was the EmCrit podcast, but it may have been another) where a patient with asymptomatic HTN was given hydralazine IVP for a BP of 175/90 in the ED. The patient was admitted for an unrelated complaint (cellulitis) and after the medication his BP was 130 systolic. He was doing fine prior to being sent up stairs, but when he arrived on the med-surg unit, he had developed hemiplegia, so the floor nurse called the doc, who called the neurologist, and after a CT (negative for a bleed), he was given TPA. The neurologist was unaware that the patient had received the hydralazine. The following morning, the patient was unresponsive and was found to have a bleed, likely due to the TPA. The hemiplegia was thought to have been due to the rapid reduction in BP. So my question is, has anyone seen this before? A rapid lowering of BP causing stroke-like symptoms? I have heard of this but never seen it, and it is very common in our ER to lower patient's blood pressures with IV antihypertensives. My second question is why is it such a widespread practice--to give IV antihypertensives even when the patient is asymptomatic---when the current practice guidelines say not to?