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Idiopathic

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Short and sweet. Not sure if this breaks any confidentiality rules. Please let me know if it needs to be modified

60-ish y.o. male presents in the AM with acute SOB. Px was dx one year prior with ALS, but that dx was recently changed to "chronic Lyme disease" and px was begun on high dose rocephin via PICC. Px is notably weak, especially in the LE, but after two HHN rx, px is breathing better and ready to go.

Approx. 6 hours later px re-presents with worse SOB, RR about 35, struggling to keep sats above 90. Px agrees to elective intubation and RSI is begun.

After intubation, EKG complex on monitor widens significantly, raising suspicion of new onset LBBB, VTach, or hyperkalemia. Stat K+ shows potassium >9, so it was rerun and shown to be 8.6. Albuterol was administered through the tube as soon as the complex widened, and bicarb was pushed. By the time the second K+ was read, the complex had narrowed back to normal. Px K+ earlier in the day had been 3.9. Px is now stable in the ICU.

SO, an acute increase in K+ of at least 4 and maybe 5 from 150 mg of succinylcholine. The patient had obvious lower extremity muscle weakness and atrophy, will likely turn out to have a clinical diagnosis of ALS, and my question is this: is it likely that the K+ response was solely due to the succ? I argue that it was, but others have a hard time agreeing. I was there, and while I suspected that succ was a bad idea, d/t the muscle weakness, I didnt expect it to be that dramatic, and, of course, I didnt say anything at the time.
 
Jeezy Peezy, really a no brainer. Upper or lower motor neuron Dz-- don't give pt. sux. Just bang him with the Dip and put the tube in, no muscle relaxant needed. ---Zippy
 
It was sux...I've coded someone like that....the K+ does normalize fairly quickly....but if you're doing CPR, it seems like an eternity
 
militarymd said:
It was sux...I've coded someone like that....the K+ does normalize fairly quickly....but if you're doing CPR, it seems like an eternity

Have seen this as well. When I was a resident our chairman and one of the professors came in to "help" myself and a junior resident put a critically ill ICU pt to sleep for an ELAP...coded after sux administration.

Remember the clandestine risk factors when giving sux...everyone knows burns, myopathies, UMN and LMN issues, but dont forget certain catabolic states are risk factors too, like severe abdominal infections (think 2am ELAP on an ICU pt), massive trauma, and bedridden patients....these cases may go awry after getting sux.
 
The patient i coded was a closed head injury patient with no apparent extremity weakness....he was just bed ridden for a while...a young guy too ....that's why it took me a little to figure out what's going on.


On by the way...iv Calcium is one of the quick things that should be given.
 
Idiopathic said:
Short and sweet. Not sure if this breaks any confidentiality rules. Please let me know if it needs to be modified

60-ish y.o. male presents in the AM with acute SOB. Px was dx one year prior with ALS, but that dx was recently changed to "chronic Lyme disease" and px was begun on high dose rocephin via PICC. Px is notably weak, especially in the LE, but after two HHN rx, px is breathing better and ready to go.

Approx. 6 hours later px re-presents with worse SOB, RR about 35, struggling to keep sats above 90. Px agrees to elective intubation and RSI is begun.

After intubation, EKG complex on monitor widens significantly, raising suspicion of new onset LBBB, VTach, or hyperkalemia. Stat K+ shows potassium >9, so it was rerun and shown to be 8.6. Albuterol was administered through the tube as soon as the complex widened, and bicarb was pushed. By the time the second K+ was read, the complex had narrowed back to normal. Px K+ earlier in the day had been 3.9. Px is now stable in the ICU.

SO, an acute increase in K+ of at least 4 and maybe 5 from 150 mg of succinylcholine. The patient had obvious lower extremity muscle weakness and atrophy, will likely turn out to have a clinical diagnosis of ALS, and my question is this: is it likely that the K+ response was solely due to the succ? I argue that it was, but others have a hard time agreeing. I was there, and while I suspected that succ was a bad idea, d/t the muscle weakness, I didnt expect it to be that dramatic, and, of course, I didnt say anything at the time.

Great, learning post, Dude. 👍
 
jetproppilot said:
Remember the clandestine risk factors when giving sux...everyone knows burns, myopathies, UMN and LMN issues, but dont forget certain catabolic states are risk factors too, like severe abdominal infections (think 2am ELAP on an ICU pt), massive trauma, and bedridden patients....these cases may go awry after getting sux.

I think the one contraindication to succ that may be easily forgotten is the bedridden thing... i seem to remember reading that around 1 wk the risk gets significantly higher. I saw a case once when succ was given to a bedridden pt without any other contraindications and the K rose from 3.7 or so to 6.8. Luckily, there was no sequela.
 
I found a great article on medline about this...K+ rose to arrest levels in ALS patients at a ridiculously high rate. Basicly, succ in absolutely contraindicated in people with UMN/LMN disease, and only relatively contraindicated (?) in those with general muscle atrophy.
 
I think you may have helped with the diagnosis in this case.

Cacl, albuterol, and insulin/glucose Don't mess around with these cases. Thay don't all come back so easy. Count your blessings.
 
indulge a newly minted ms1, if you will please...

so succs is a depolarizing nmj blocking agent, right? so is the increase in extracellular K+ due to an inapropiately strong ion flux? abnormally long opening of gated ion channels? or perhaps an inability to renormalize membrane potentials after the flux?

thanks,

dave
 
stoic said:
indulge a newly minted ms1, if you will please...

so succs is a depolarizing nmj blocking agent, right? so is the increase in extracellular K+ due to an inapropiately strong ion flux? abnormally long opening of gated ion channels? or perhaps an inability to renormalize membrane potentials after the flux?

thanks,

dave

Kind of a combination of the above. An upregulation of junctional and extrajunctional cholinergic receptors is the primary mechanism. Receptor upregulation provides more postjunctional sites for Succinylcholine to interact with, causing an increased release of potassium. Patients with upper motor neuron lesions resulting from stroke, brain or spinal cord tumors, other intracerebral or spinal cord mass lesions, closed head injury, or encephalitisun, along with healed third-degree burns, severe intra-abdominal infections, severe metabolic acidosis with hypovolemia, crush injuries, and prolonged nondepolarizing muscle blockade or immobility, all may lead to this type of massive potassium efflux.
 
UT is on the right path... but not quite there... it turns out that the ACh receptors actually change their subunit conformation in pts who are bedridden... if you look at the new edition of Miller (the big version, not baby) there is a whole chapter written by my old buddy Jeeva Martyn on this topic alone. The different subunits actually cause the efflux period of K+ to be consistently longer... hence the huge K+ release in these specific patients... I personally think it is just plain dumb to use Sux unless you have a good reason to use it (oh... and every one says that RSI needs to be done w/ Sux... well show me one paper that shows RSI prevents aspiration?)

The correct treatment is CALCIUM CHLORIDE! Albuterol down the tube is worthless - but good in theory... and Bicarb won't affect the cardiac membranes quickly enough... You are just lucky he didn't arrest... the amazing thing about calcium is that it stabilizes the heart within 30 seconds if pushed centrally! If you ever have somebody on the verge of sinusoidal rhythm from a K (personal record by the way is 10.4), the complex literally snaps tight within seconds of the calcium going in...
 
I had a patient with the "sinusoidal" ECG....Calcium chloride went in....5 minutes later...still sinusoidal.....
 
militarymd said:
I had a patient with the "sinusoidal" ECG....Calcium chloride went in....5 minutes later...still sinusoidal.....

That's because when you asked for CaCl, they thought you said "more KCl!" In certain parts of Parkland, that would happen.
 
UTSouthwestern said:
That's because when you asked for CaCl, they thought you said "more KCl!" In certain parts of Parkland, that would happen.

Damn..you're right!!! Must have been my heavy Asian accent!!!!
 
militarymd said:
Damn..you're right!!! Must have been my heavy Asian accent!!!!

One of the OB dudes had a story that cracked us up for months....one of his buddies from residency used to say frequently:

HORY CRAP! ITS ONE O CROCK!! I GOTTA GET TO CRINIC!!! :laugh:
 
Idiopathic said:
And then you have our case presentation from two weeks ago with a K+ of 7.8 in someone who is dig toxic. Do you rx with calcium then?


From what I can remember, hyperkalemia usually does not happen in the setting of chronic dig toxicity. So it's probably acute dig toxicity. What rhythm is the patient showing? Calcium is contrindicated in this case because intracellular Calcium levels are usually above normal in cases of dig toxicity. Treat with Digibind, Insulin and glucose Control metabolic acidosis follow other ACLS protocols(ABC's). Attempt to normalize other electrolytes especially Mag. Then find underlying causes for the dig toxicity like acute ingestion, MI, ARF, Acute acidosis, and drug interactions.
 
And then you have our case presentation from two weeks ago with a K+ of 7.8 in someone who is dig toxic. Do you rx with calcium then?

Learned a week ago or so when I was on cards gap night and pt. was hyperK with very mild elevated dig levels (2.4). i was treating him and I ordered calcium but i was advised not to by an ER guy. his argument was that there are cases of something call "stiff heart" - mostly seen by pathologiest during an autopsy. i have not had time to find articles for that myself but i beleive him. so he didn't get calcium afterall due to his dig toxicity and hyperkalemic state. now, some of you may aruge that this does not happen but i am not 100% sure about this stiff heart thing myself.
 
Learned a week ago or so when I was on cards gap night and pt. was hyperK with very mild elevated dig levels (2.4). i was treating him and I ordered calcium but i was advised not to by an ER guy. his argument was that there are cases of something call "stiff heart" - mostly seen by pathologiest during an autopsy. i have not had time to find articles for that myself but i beleive him. so he didn't get calcium afterall due to his dig toxicity and hyperkalemic state. now, some of you may aruge that this does not happen but i am not 100% sure about this stiff heart thing myself.

I've heard of it but never seen it. Many people have described it in the heart room when Ca is given to a pt with a hypertrophied ventricle. I always gave it causiously to these pts hence possibly the reason i have never seen it. I'm not sure of its relation to Digoxin. Maybe someone will answer that for us here soon.

See I'm not a "Know it all". LOL
 
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