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My wife feels cold


brock8024

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In my medic refresher course Bob Page the instructor ran us thru a whole plethora of cases and one of them was Myxedema coma. He also required us to look it up in a text or google to find the info on myxdema coma. It was a eye opening class to say the least.

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Look it up to make sure I am not wrong but that is pretty much what the book says.

You aren't wrong. By default you must be right!

As far as sedation goes, I don't believe we carry anything that would be appropriate for this pt given her vital signs, namely midazolam, morphine, or valium. What do you think? Also since she already has a decreased LOC sedation is not of paramount importance. Why not try some atropine first?

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As far as sedation you might consider Nalbuphine (Nubain). It's similar to morphine without the effect on BP. Or at least the effect isn't as bad. Like I said though I'd really try and manage that Hypotention/Bradycardia before bothering with sedation for TCP.

However you also said to push 1mg of epi? Your internet treatment skills appear to be lacking...Find me where you give a 1mg bolus of epi to an unstable brady patient with a pulse...

This is basically the definition of an unstable brady patient. And your first thoughts IMHO is why is this person hypotensive and not compensating? +/- hypothermia...

LOC - Poorly roused

A - stertorous resp

B - 6 and ineffective

C - 40 weak to absent...

Place 1 or 2 nasals +/- OPA and begin ventilations.

Get vitals, EKG, and a SUGAR...

Why is this person hypotensive and not compensating? Meds issue? Nope Drugs? Doesn't appear Cold? Yes... Sepsis? Meh MI? Meh

Intubate patient...Note changes...

IV access and trial fluid bolus (I'd say 500ml NS) and note changes...

Atropine is relatively contraindicated in hypothermia and with ventricular based blocks/rhythms, but normally you'd likely want to trial 0.5mg first if possible.

Dopamine sure, but...

Pacing is actually your number one concern and this patient is an unstable brady patient (no EKG given and multiple "unstable" factors).

The point is I hope that most people (in Ontario they would be anyway) would be patching following initiation of a fluid bolus and after securing the airway.

If you talk to a doctor and given the scenario outlined here convinced them it was myxedema coma, then kudos. I don't know what prehospital tx is for this, or if they would just say secure the airway and go to hospital. If you wrote that their likely final primary problem was myxedema coma (and were right) then kudos.

Think horses not zebras. I'm all for differentials (and I pride myself on them) but there are alot more differentials that are likely first then myxedema coma.

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Epi wasn't my drug of choice, but I see no reason why it's contraindicated or not desired. The patient is hypotensive and bradycardic. Assuming it's a sinus brady and not a large degree block, Epi would probably be 3-4th on my list. So if you can tell me why Epi is not appropriate here..

You said "1mg epi IVP" which means bolus and I assume you are talking about the preload 1mg in 10ml (1:10,000).

Epi when given to a patient with a pulse is used primary I believe as a pressor in this situation (though with obvious fallout of beta effects). This would be (and we generally don't hang epi here) is 1 or 2 mg (1:1000) ADDED to 250ml of fluid (NS? I dunno). This gives a concentration of 4-8 micrograms per ml and is then TITRATED TO EFFECT. You will soon notice this phrase, which often applies to pain relief and vasoactive medications.

When epi is given as a bolus (as in cardiac arrest), I believe (and correct me if I'm wrong) it is due to the inconsistent/unknown absorption,distribution,biotransformation and excretion of the drug (or any) in such a poorly perfused state. Epi also has a short halflife. 1mg I suppose has been shown to offer the most balanced therapeutic dose in such a situation. High dose epi, say in peds, has been shown to be ineffective and potentially detrimental.

But anyway...From brief reading of myxedema coma that securing the airway and starting fluids (without obvious overload) is the best start. Patching is next.

If you come across a patient such as this, do that.

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So, here is a brief synopsis for the treatment of myxedema from Emedicine (with some highlights based on the discussion here). If you want to read the full story, here is the link: http://www.emedicine.com/emerg/topic280.htm

Prehospital Care: Stabilize acute life-threatening conditions, and initiate supportive therapy (that helps clear it up, doesn't it).

Emergency Department Care: Patients with myxedema coma may present in extremis; implement initial resuscitative measures, including intravenous (IV) access, cardiac monitoring, and oxygen therapy, as indicated. Mechanical ventilation is indicated for patients with diminished respiratory drive or obtundation.

Evaluate for life-threatening causes of altered mental status (eg, bedside glucose, pulse oximetry).

If myxedema coma is suspected on clinical impression, start IV thyroid hormone treatment.

Confirmatory tests often are not available to an ED physician.

With a diagnosis of myxedema coma, initiate hormonal therapy.

Investigate immediately for inciting events such as infection.

Treat respiratory failure with appropriate ventilatory support.

The condition often requires mechanical ventilation.

Treat underlying pulmonary infection.

Hypotension may respond to crystalloid infusion.

Occasionally, vasopressive agents are required.

In refractory cases, hypotension may resolve with thyroid hormone replacement.

Treat hypothermia.

Most patients with myxedema coma respond to passive rewarming measures such as blankets and removal of cold or wet clothing; aggressive rewarming may lead to peripheral vasodilatation and hypotension. However, hemodynamically unstable patients with profound hypothermia require active rewarming measures.

Treat hyponatremia initially with water restriction; however, if sodium levels are less than 120 mEq/L or any seizures occur, hypertonic saline is indicated.

Avoid medications such as sedatives, narcotics, and anesthetics. Metabolism of these agents may be slowed significantly, causing prolonged effects.

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