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- Apr 21, 2003
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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.
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.
