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#52.... Much More Than Meets The Eye...


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#181 TexRNmedic

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Posted 27 April 2010 - 05:06 PM

I "over stocked" the rig with some ICU meds just for the teaching points.
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Wes Seale
Houston , TX

#182 DartmouthDave

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Posted 27 April 2010 - 05:55 PM

Hello,

According to the London Health Science Centre`s Momograph a risk of Octreotide is hyper- or hypoglycemia.

London Health Science Ctr - Octreotide

All the times that I have seen it used it works quite well. The loading dose and infusion dose is outlined in the Momograph. I think the risk of a rise in BGL might be worth it to control bleeding quickly. Also, I think Panto 80 mg IV plus an infusion may be beneficial as well.

I have never seen the Varcies Dose of Vassopressin used. Nor have I read much about it. It has been added to my never ending list of things to research. So, I can not comment on it.

Have to run....

Cheers
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#183 SerendepitySaki

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Posted 29 April 2010 - 06:22 PM

looks good to me Dave...(and good look out working it on "other" forums!... hopefully you won't be dropping a combitube! B))

here's one more ref for y'all...
http://www.sovegastr...iceal agudo.pdf

... take us home Dave... we've got other cases to get up! ABCs and diesel.... and i think we'll be ready for the wrap up....

oh! and guys, plenty of folks have provided feedback and criticism either within the thread itself or via PMs/e-mails... if you haven't, PLEASE do! good "bad" or indifferent... we're all about the process improvement....we're here to serve YOU, so let us know what we can do to make it better....

Hello,

According to the London Health Science Centre`s Momograph a risk of Octreotide is hyper- or hypoglycemia.

London Health Science Ctr - Octreotide

All the times that I have seen it used it works quite well. The loading dose and infusion dose is outlined in the Momograph. I think the risk of a rise in BGL might be worth it to control bleeding quickly. Also, I think Panto 80 mg IV plus an infusion may be beneficial as well.

I have never seen the Varcies Dose of Vassopressin used. Nor have I read much about it. It has been added to my never ending list of things to research. So, I can not comment on it.

Have to run....

Cheers


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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#184 DartmouthDave

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Posted 29 April 2010 - 09:28 PM

Hello,

No combitubes here...LOL

I will take it from the top so I don't miss anything.

Airway:

Failed airway. It would be nice to clear the obstruction somehow. Try and pass the tube once more while my partner get the surgical airway ready. I do not relish the thought of surgical airway on a liver failure patient. Odds are the INR and PTT are elevated. Low platelets.

Breathing:

Once some type of airway is established (ET or trach) I would hook up the vent. This lady is frail to say the least. So I would go with AC, FiO2 100%, Vt 6-8 cc/kg PEEP +5 to start with. See how that plays out and make adjustment accordingly. I would be concerned with a possible aspiration of blood. I also would keep an close eye the airway pressures and on the ETCo2 as well.

Circulation:

Goal SBP of 100 and a MAP of 60 (see HOCM for rationale). I would also give some fluid because she may be dry intravascular (emesis, bleeding, third spacing, ect....). Again, see below for my rationale.

Summary of Treatment:

--> Upper GI bleed - I would load with Panto 80mg plus an 8mg/hr infusion. I would add to this (as noted above) Octrotide 50mcg IV loading dose and a 50mcg/hr infusion. According to the London Health Sciences site there is a risk of messing with serum glucose levels. But, we have little option I think. I am picking Octreotide over Vasopressin because I know it and have seen it work quite well. Also, here is some evidence pulled from Serendepity's link: "When compared with other vasoactive drugs, octreotide was better than vasopressin and equivalent to terlipressin.....


--> HCM -"Treatment of symptoms of obstructive HCM is directed towards decreasing the left ventricular outflow tract gradient and symptoms of dyspnea" (Wikipedia..lazy I know). So, this is why an I going for a SBP of 100. More push so to speak. As for vasopressors.....I would want and see how things play out.


--> DKA (or HNNK) - BGL is high (40 mmol or 800 mg\dl....if I recall correctly) I would give some .9 NS 500cc x 2. With careful assessment between. The VBG had a pH of 7.1. I would give HCO3 (3 amp in 1000cc NS) at 200 cc\hr. The Na was normal. If it was high .45 NS may be better.


--> Elevated CL - It was elevated if I recall correctly (Time is tight.....can not go looking). This is due to low HCO3. I would be ok with NS for this initial management.


--> The hyperkalemia - K was 8.2. But, where will it be as the DKA/HNNK is corrected!! Or, as the pH is corrected. We usually add KCL if the K is less than 3.5. So, I would just try and displace the K for now with CaCl amp, and HCO3 amp as well. Skip the D50W and give Humulin `R`` 5 units IV.


--> Hypocalcemia - I can not remember if it was corrected (with the albuim) or not. So, I think the one amp of CaCl will be ok for now.


--> Renal Failure - Lets pop in a Foley. My partner can do that special job!! See what (if any) urine output we have and its quality.


--> Anemia from renal failure and bleeding - Giving this patient some blood if we have it would be helpful.


--> Hypotension - As noted above I would go with blood (if we have it) and NS. The HCM perplexes me some. Maybe go with some Dobutaime (if HR comes down)......not sure. Help!


--> Toxic Alcohol OD - Supportive care as listed above plus Thiamine 100mg IV.


--> Sedation - I would go with Morphine and Versed infusion (0-10mghr) with a goal RAAS of -3. I am picking the Morph because it will, in theory, drop some of the preload and help manage the HCM.

LINK----->Richmond Agitation & Sedation Scale (RAAS)


--> Call a smart person!


--> Flushed Skin - Not sure what is going on here.

Well, that is it, I guess. A little unsure of the HCM management. Get this patient to the ED asap.....

Cheers......




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#185 TexRNmedic

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Posted 29 April 2010 - 09:43 PM

Looks good Dave. Safe play all the way around. Octreotide has an inhibitory effect of glucagon and insulin among other things. It is usually mixed in D5W. I haven't seen any huge swings in glucose using octreotide, but in the unit we are checking BGL and covering Q4 anyways. We'll start wrapping this up. I'm sure Sean will be around in a minute or two to comment. I'll start working on tying up the loose ends. Y'all did great digging through a complex patient and treating what you could with what you had. Great assessment skills!
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Wes Seale
Houston , TX

#186 SerendepitySaki

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Posted 29 April 2010 - 10:44 PM

well done sir! well done!!!!! very well thought out! nice big picture integration!


some specific feedback from the top down ABCs, then RoS that impact them, then the rest...(especially HOCM, number one, because you specifically asked for it in your post, and number two, because from the various answers to date, i've obviously done a crappy job of explaining it.....)

A
1. excellent thought on bleeding concerns and airway....
lightwand (or jury - rigged equivalent) and accurate targeting of the relatively avascular cricothyroid membrane might help with that...

2. as far as the obstruction:
what is it? laryngospasm possibly secondary to hypo calcemia...
you're replacing Ca++, and hopefully dropping a tube, IF yu can get the spasm to break.... cric/trach if not....

a few ways to break... sustained PPV, paralytic, amongst others...(if you wanted to get into trivia, you could argue Succs vs NDMR, due to K+ release in pre-existing hyperkalemia - easy answer....you're putting her on a vent, AND she's NOT coming off anytime soon..... use a NDMR)


excellent thoughts on managing the OTHER potential Airway obstruction/aspiration risk... (varices)

B
good thoughts all.... she will require a LOT of ongoing reassessment.... ACV or SIMV would go well with your specified sedation goal.....

C
1. excellent thoughts on varices mgt.
2. ABSOLUTELY give fluid... WITH ALBUMIN!

that was one of my MAJOR teaching points... with HOCM, as Tex explained, you've got sh*it for Left End Diastolic Volume... (and with her liver dysfx, she MUST have the EXOGENOUS colloids to keep the fluids intravascular,

decreased LEDV, + zero, zip, zilch, nada PRELOAD = one dead train wreck of a patient....


3. and dobutamine would totally be MY choice, IF i wanted to layer something else on top (with this particular patient)

4. have some issues w/ HCO3, but what are you gonna do? not only do you not have it, but THAM isn't right for this lady, and
YOU ARE GIVING CaCl2, which will stabilize her various poor little heart membranes... (Ca++ will definitely help with the high K+, and the possibly the prodysrythmic irritability caused by HCO3...will also, of course, help with any potential occult BB OD this lady may have...) kind of like the Octreotide... good with HCO3 good FAR outweighs the bad....

RoS

1. much addressed above.

LYTES

(you done good ...IMHO.... Ca and HCO3 are best and most appropriate for this lady prehospital..
i'd add some albuterol down the ETT ... another double whammy....helps with both respiratory AND hyper K+...
2. her Cl- is actually on the low side... not relevant to short term mgt, and should correct... MOST of her lytes INCLUDING THE HYPERKALEMIA will get corrected post admission on HD, when they spin her get the rest of the Ethylene Glycol off....

obviously don't give yer HCO3 and CaCl2 in the same line or make sure you flush well in between, otherwise they will precipitate out...

Ca does NOT displace K... it only stabilizes the membranes... ask me why off-line, if you REALLY want a lesson in basic electronic theory that will make your eyes glaze over....

bazillion points... does HCO3 itself actually directly redistribute Ca2+?

Foley, yeah, whatever... she could very well be anuric.... ESRD.....

ANEMIA.... good call for the short term... long term, she will need some more EPO and nutrition (B vits and Iron) she actually has MULTIPLE anemias...

and i'd DEFINITELY consider getting the dobutamine up for a LONG xport...! more of an inotrope than a chronotrope... you can find refs that both support and refute use in HOCM... dobutamine a preferred agent in HOCM.... short x-sport, unless you can bill for it, i wouldn't worry.... the albumin and IVFs are the MOST important and the ED's just gonna throw your GTTs away, once they get theirs up....

i'd go for fentanyl over morphine.... more hemodynamically stable... your choice to cautiously bolus or mix up a GTT either in a bag of NS or a syringe, depending on what dosage you wanted to be able to give, what sort of pumps/tubing you have, yadda yadda....


AGAIN, you do NOT want to drop pre-load in this lady with HOCM! BAD! if i've been as clear as mud why, just let me know and i'll run thru again.....

WELL DONE!!!!!!!

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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#187 Speed

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Posted 30 April 2010 - 02:19 AM

Foley, yeah, whatever... she could very well be anuric.... ESRD.....


I was wanting to use the Foley as a Blakemore. I understand we're in a well stocked CCT, but a Blakemore tube stocked on board I thought would be a tall order. I'm assuming this is a varices based on her liver.
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Mike Williams CCEMT-P/FP-C

#188 SerendepitySaki

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Posted 30 April 2010 - 02:32 AM

speed, my apologies,
i was referring to Dave's post where he was specifically talking about cathing her...
i missed your mention... i've picked up a thing or three from your posts since i started reading this board, ...teach me something new... it sounds AWESOME! sort of.... as i understand it, the blakemore balloon runs the length of the shaft, while the foley is only at the end....

I was wanting to use the Foley as a Blakemore. I understand we're in a well stocked CCT, but a Blakemore tube stocked on board I thought would be a tall order. I'm assuming this is a varices based on her liver.


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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#189 TexRNmedic

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Posted 30 April 2010 - 03:53 AM

I've only seen a B/S tube a couple of times. Gastric ballon and esophageal ballon. It requires cephalad traction to seat the ballon in the gastric cardia. We keep an old field-kicker football helmet to tie it off on. I'm not a big fan of using foleys unless it truly is a last ditch effort as it can cause rapid necrosis or trauma to already extremely sensitive tissue as it applies pressure to such a small surface area.

Question for the group: what could be a foreseeable problem with using a King LT-D with this patient(hint-does it have a distal esophageal opening)?
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Wes Seale
Houston , TX

#190 DartmouthDave

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Posted 30 April 2010 - 07:56 AM

Hello,

There was a discussion on an other web site that I post on that suggested a Combitube (...or any supraglotic airway...) to stop bleeding. This, of course, is very bad due the risk of an esophageal rupture. Plus, it simply won't work. Not a bad discussion:

EMT City

How dose NaHCO3 effect Ca++ levels.........Not a clue. Need to look it up. I have a few books on the topic.

As for the Ca and membrane potential. Phase 2 o f the cardiac action potential is depended on an influx of Ca and an efflux of K. Maybe, a derangement of K and Ca would shorten this? Or, maybe, low Ca will mess up the Pacemaker Action Potential? Again, I need to look this up again. I am sure I knew this years ago...sigh.

Or, maybe, there will be a nice answer online later.....LOL!!!!!!


Here is a question for the group:

I have seen Milrinone used a few rare times over the years. Last time was 6 years ago for a 22 year-old SAH (Hunt & Hess Grade III) with a `stunned myocardium`. Any use with HOCM?

Cheers......
<br style=""> <br style="">
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#191 SerendepitySaki

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Posted 30 April 2010 - 12:51 PM

and i've lost track...: did anyone consider controlling nausea and vomiting before pushing evomidate? what might vomiting do to the pressure in her esophagus and her bleeding? something to think about.....(not the biggest deal, but possible style points)

lots of good stuff at this website: shameless plug... Carol was one of my earliest inspirations in cardiac nursing... have attended many of her lectures, etc...
if you folks ever get the chance, do so....

http://www.cardionursing.com/

specifically, she has a good BASIC lecture on cardiac drugs here:


http://www.cardionur...for-website.pdf

hey Dave!
love your hunger! it may be a week or two until the next case is up, but I hope you come to play... and bring some friends!

yes, you can use milrinone in HOCM... like anything else, it becomes a balancing act... always working to minimize myocardial oxygen consumption, while maximizing output....

it's nice, because it gives you more squeeze AND first and foremost, reduces afterload....all with minimal effects on rate... you can see where in disorder like HOCM, where you have an outflow gradient and usually significant regurg, where reducing afterload might be a good idea... in this instance, you would almost certainly see it being used post-op after surgical correction of her HOCM to ease the workload on the freshly traumatized heart...not generally a pre-hospital drug, might see on an IFT...

I misspoke on the bicarb and calcium.... i MEANT bicarb and Potassium
.... bicarb does not directly effect calcium.... bet it makes more sense now.. . B) sorry about that... if y'all are still stuck, for starters, reread Will's ACE-SAT notes on how serum potassium and hydrogen ion move, relative to each other....(if serum K goes up, pH goes.....___________) then, i think he has a few lines about bicarb and where hydrogen ion comes from...that should get things clicking......

with regards to Ca2+ and "stabilizing" the myocardium.... i was trying to keep it "street level...NEED to know" and stay away from too much "pie in the sky....NICE to know"... let's see....short version...

for all you neurosurgeons and electronic engineers in the audience, i am deliberately leaving out resting membrane potential, capacitance, "all or none", action potential, sarcoplastic reticulum, etc..... if you know enough to know those terms, but don't understand how it works, just drop a note off line with a specific question and i'll answer... yes, dave, you're on the right track....for everyone else, more than i really want to go into here...already baffled with enough bullsh*t for one case. here's the short version....

  • you gotta have a separation of charge, or potential difference to conduct electricity...
  • in other words, a "pool" of positively charged stuff, separated from a pool of negatively charged stuff
  • the electricity won't flow unless you have big enough pools
  • electric flow can be altered by changing the sizes of the various normal pools...
  • it can be made to flow faster or more slowly...(either of which you may have heard described as "irritability")
  • various cells in the heart conduct electricity (nerve and muscle)
  • the cardiac cell membranes separate the cell contents from the environment...They also separate pools of charges, which allows then allows the cell membrane to conduct electricity.
  • Hyperkalemia is a large pool of positively charged stuff and alters electrical flow down the various membranes
  • Calcium helps restore the natural "set point" between your pools of positive and negatively charged stuff, which "stabilizes" the membrane, or soothes it's "irritability", and makes it more likely to conduct electricity normally....
apologies if that's too basic... if you want a specifc hard copy reference, you can check out Dale Dubin's "Ion Adventures into the Heartland" .... he wrote a 12 lead interpretation book I'm sure many of you are familiar with..... lots of links to other good cardiac stuff with free downloads here: http://www.ionadventure.com/

all right folks... BREAK! enough theory! as Oldschool says, let's bring it on in for the real thing!

GREAT audience.... you guys did AWESOME

wes and i will be posting round up soon....if you have something specific you want to see, shoot us a line

and seriously, Speed, i really do want to hear your ideas... teach me something new... how would you handle this lady?

Cheers!
Sean


Hello,

There was a discussion on an other web site that I post on that suggested a Combitube (...or any supraglotic airway...) to stop bleeding. This, of course, is very bad due the risk of an esophageal rupture. Plus, it simply won't work. Not a bad discussion:

EMT City

How dose NaHCO3 effect Ca++ levels.........Not a clue. Need to look it up. I have a few books on the topic.

As for the Ca and membrane potential. Phase 2 o f the cardiac action potential is depended on an influx of Ca and an efflux of K. Maybe, a derangement of K and Ca would shorten this? Or, maybe, low Ca will mess up the Pacemaker Action Potential? Again, I need to look this up again. I am sure I knew this years ago...sigh.

Or, maybe, there will be a nice answer online later.....LOL!!!!!!


Here is a question for the group:

I have seen Milrinone used a few rare times over the years. Last time was 6 years ago for a 22 year-old SAH (Hunt & Hess Grade III) with a `stunned myocardium`. Any use with HOCM?

Cheers......
<br style=""> <br style="">


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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#192 TexRNmedic

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Posted 30 April 2010 - 01:25 PM

Sean you had me stumped with the NaHCO3 vs Ca++ relationship. I was waiting to see where you were going with that. Beautiful run down here. Thanks for taking the time to put it together. BTW someone mentioned Zofran along the way.

For those wanting an easy answer re: K and bicarb. For a 0.1 change in pH expect a reciprocal 0.6 change in K. 7.1 and 4.6 to 7.2 and 4.0 to 7.3 and 3.4 etc.

...And to wrap up the case a bit. I'd continue with the RSI including the NDMB of choice (I prefer roc) and give the calcium a little quicker. Try BLS airway management including PPV with the BVM. If the laryngospams don't break pretty quick than cut her neck. Set the vent for high minute volumes. The King LTD doesn't have an esophageal port so everything will end in up in the stomach with no way to suction it off, if you end up using that.

NS boluses and 25 gram/100cc of albumin(if available) to start with. Octreotide, vasopressin or levophed in that order if available. If anyone has a different plan, please feel free to share and if you have any unresolved questions, feel free to ask them here or PM Sean or I behind the scenes.

Best regards everyone!
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Wes Seale
Houston , TX

#193 Speed

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Posted 30 April 2010 - 02:46 PM

Saki,

The use of a Blakemore is now really like a last ditch effort to prevent irretractable bleeding and exanguanation. It's use doesn't have great stats on morbidity and it can be dangerous to use without experience, but not as dangerous as a large Foley. You really need a big one, at least a 30 ml balloon. Football helmets, oversized c-collar "chin ridge", tongue blades, or a et tube holder would work to pull traction. Varices are usually at the point where the esophagus meets the stomach; hence it's effectiveness in applying direct pressure. The antifreeze pretty much painted the picture. Now a days the best thing for someone like this is a fast as transport as possible to the closest team who could band her, have them fully informed and ready, instantly when she hits the door. The patients that I've seen like this usually die from the old triad of hypothermia, DIC, and acidosis; those I would think would be your major targets, plus airway, fluid/colloid resuscitation, renal function, liver transplant... In reality I wouldn't have sando, but I'd definitely start an infusion of vasopressin, and put some Levo down into her belly to apply "topical hemostasis" to the tissue down there. Really I'd call this a load and go situation, no messing around. Definitive tx in my mind after resuscitation/banding would probably be transplant, and she doesn't sound like a candidate. Right now her chances of surviving are very slim. you guys are doign a really good job with the cases; I would have burnt out on it after about three or four posts; A.D.D., wish I had the H.D.
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Mike Williams CCEMT-P/FP-C

#194 SerendepitySaki

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Posted 30 April 2010 - 02:56 PM

thanks Mike! i KNEW you'd bring up something i forgot...

folks, this is much like a STEMI or stroke scenario.... my semi-flippant remarks about txing w/ diesel are NOT enough.... you must verbalize the following....

i know it sounds obvious, but you MUST get the ER to start calling in the specialty team to the hospital ASAP!




Saki,

The use of a Blakemore is now really like a last ditch effort to prevent irretractable bleeding and exanguanation. It's use doesn't have great stats on morbidity and it can be dangerous to use without experience, but not as dangerous as a large Foley. You really need a big one, at least a 30 ml balloon. Football helmets, oversized c-collar "chin ridge", tongue blades, or a et tube holder would work to pull traction. Varices are usually at the point where the esophagus meets the stomach; hence it's effectiveness in applying direct pressure. The antifreeze pretty much painted the picture. Now a days the best thing for someone like this is a fast as transport as possible to the closest team who could band her, have them fully informed and ready, instantly when she hits the door. The patients that I've seen like this usually die from the old triad of hypothermia, DIC, and acidosis; those I would think would be your major targets, plus airway, fluid/colloid resuscitation, renal function, liver transplant...


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LET THE WILD RUMPUS BEGIN !!!!!!
Sean G. Smith, RN-Alphabet Soup

#195 TexRNmedic

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Posted 07 May 2010 - 03:00 AM

Ok. Time to start the long overdue wrap up-

With PPV, NDMB paralytic and aggressive suctioning you are able to secure an ETT. High dose vasopressin, albumin and crystaloid boluses stabilize hemodynamic and minimize esophageal blood loss. A timely call to the receiving facility has uncross-matched O neg and the endoscopy team ready on arrival. The EG ingestion is treated with emergent HD and ethanol. The patient has an extended stay in the ICU for stabilization of H&H, electrolytes, optimization of cardiac output and treatment of aspiration chemical pneumonitis. About 2 months later you make a call on her again for AMS. At least this time you know what to expect.

Although the patient looks as if she is in her 50's, she is a 34 year-old female with a history of bipolar disorder, NIDDM, HOCM, methamphetamine and ETOH abuse, with renal failure requiring hemodialysis secondary to previous ethelyne glycol ingestion and hepatic failure secondary to Hep C and ETOH induced cirrhosis. The patient is well known at "County Hospital" trauma center and is known for referring to the ED every week or two for emergent hemodialysis as the patient does not regularly attend scheduled HD.

This patient has a mix of compounding comorbidities, but thanks to a systematic approach to patient assessment and treatment, we were able to successfully identify emergent conditions and manage the patient from the scene to definitive care. As they say, when over your head go back to the basics and what you know.

Here are a couple of journal articles RE: HOCM and EG ingestion.
http://www.ncbi.nlm....part=hyper-card
http://journals.lww....e_Glycol.5.aspx

I'll post this and see what Sean has to add.
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Wes Seale
Houston , TX

#196 VolandoP

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Posted 12 July 2015 - 01:09 AM

There is not much to form for a .35 Whelen. I would load it and shoot it with normal loads. If you compare a .303 Brit factory round to a fired case you will find there is more fire forming going on with factory .303 ammo than many of the cases we reform.
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