High LDH

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MicA

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Oops not high LDH, but high CK.

This is just a test question that I am struggling with. Basic history is that a person with anaemia runs a marathon and then collapses dehydrated. Test results show:

[Na] = 155 mmol/l
[K] = 7.3 mmol/l
ALT = 25 U/l
CK = 1050 U/l
Albumin = 52 g/l
Urea = 8 mmol/l
Glucose = 5 mmol/l
Lactate = 10 mmol/l

The next question asks if the patient has liver damage.

Albumin is normal and so is ALT, but what I am confused by is the high CK. What can cause such a high CK? Muscle damage?

And another thing, would the high [Na] be evidence that RAAS is in effect especially since the patient is dehydrated?

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Okay, so I've got no formal training in this type of test question being that I'm only an MS1, so I'm throwing this out just for fun: rhabdomyolysis. I'd think that low O2 availability to an exercising body could lead to muscle damage and high CK levels.
 
High CK is probably due to the marathon he/she just ran.

Also, to show proof of RAAS activation you would most likely have to have urine data (to see if the urine is dilute or concentrated) . Since the K is elevated along with the Na, it is just saying that the patient is dehydrated and you can assume that the RAAS is activated.
 
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Anemia + extreme exercise + dehydration(signified by the hypernatremia and hyperalbuminemia) --> ischemia and damage to muscle fibers --> elevated CK and potassium (CK and K+ are intracellular contents of dying cells spilling out into the serum). His albumin is through the roof, another sign of severe dehydration. He is in metabolic acidosis (lactic acidosis = high lactate) due to an increased muscle demand of O2 > supply of O2. The acidosis is also contributing to the hyperkalemia due to the intracellular/extracellular shift of H+/K+.

You can't call this rhabdo without myoglobinuria or a CK of at least 10,000-20,000.

Either way, his liver is fine.
 
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Ah, cool. If 2nd year is more like this, then I'm sure I'll like it a lot more than 1st year. MS1 is soooooooo freeaaaaaaakin boring!
 
Doesn't MS1 have questions like that?

I would honestly love to have a table that indicated which values meant what, we were given normal value tables but it still doesn't tell you how high values need to be before they are something in particular. I would also have guessed Rhabdo but that is only because I am not sure of the values.

Thanks a lot for the help.
 
Doesn't MS1 have questions like that?

I would honestly love to have a table that indicated which values meant what, we were given normal value tables but it still doesn't tell you how high values need to be before they are something in particular. I would also have guessed Rhabdo but that is only because I am not sure of the values.

Thanks a lot for the help.
Some of my professors will give questions like that. But, often it's useless trivia that really pisses me off thrown in with some boring regurgitation answers.
 
Anemia + extreme exercise + dehydration(signified by the hypernatremia and hyperalbuminemia) --> ischemia and damage to muscle fibers --> elevated CK and potassium (CK and K+ are intracellular contents of dying cells spilling out into the serum). His albumin is through the roof, another sign of severe dehydration. He is in metabolic acidosis (lactic acidosis = high lactate) due to an increased muscle demand of O2 > supply of O2. The acidosis is also contributing to the hyperkalemia due to the intracellular/extracellular shift of H+/K+.

You can't call this rhabdo without myoglobinuria or a CK of at least 10,000-20,000.

Either way, his liver is fine.

There are no "official" cut off numbers for rhabdo. Just FYI.
 
Some of my professors will give questions like that. But, often it's useless trivia that really pisses me off thrown in with some boring regurgitation answers.

It seems like useless trivia, but it's kind of the way you'll first approach patients, especially one too sick to talk . . . through the labs. You have to learn to sift through the information.

What I often see is some gorked patient, and we run a Complete Metabolic Panel (CMP), which includes the "liver function tests" (LFTs), and you'll see an eleavtion in AST and ALT and be like, "Whoa!! This guy's liver is angry!", but when you look at the rest of the liver tests like the Alk Phos or the Bilirubin, you'll see these are normal, and that's when you'll check a CK, especially in a patient you think may have been laying in one place too long.
 
So, when do you start calling it rhabdo?

You tell me Doctor :D

Medicine is an art as well as a science, and any doc that can be replaced by a computer algorithim, should be.

I call it rhabo when it is - muscle breakdown either either from a history of extreme physical stress (a marathon), crush trauma, or laying in one place too long. If the CK is elevated within given the clinical history, it's rhabdo, you make the call. Purists will make sure their is myoglobin in the urine, but this is often unecessary for diagnosis. Remember we're trying to protect the beans here, so fluids, Fluids, FLUIDS is the correct answer.

Here's your mission, if you choose to accept it . . . do we alkalize the urine with sodium biacarb or not? What's the evidence?
 
It seems like useless trivia, but it's kind of the way you'll first approach patients, especially one too sick to talk . . . through the labs. You have to learn to sift through the information.

What I often see is some gorked patient, and we run a Complete Metabolic Panel (CMP), which includes the "liver function tests" (LFTs), and you'll see an eleavtion in AST and ALT and be like, "Whoa!! This guy's liver is angry!", but when you look at the rest of the liver tests like the Alk Phos or the Bilirubin, you'll see these are normal, and that's when you'll check a CK, especially in a patient you think may have been laying in one place too long.
Ha, ha... no, I mean I "really" get useless trivia sometimes. Like, what type of receptor is the LH Receptor: G-protein coupled receptor, tyrosine kinase, nuclear, etc? Or, What is the likelihood that a randomly chosen neonate will have be born with ________? I swear to God most of my classmates pass exams because they sit and memorize every old exam they can get their hands on. It's ridiculous.

Only a minority of our exams are providing questions with history and lab data. I'm starting to wonder how our students do so well on the boards... *sigh*

Thanks for the input, though!
 
Ha, ha... no, I mean I "really" get useless trivia sometimes. Like, what type of receptor is the LH Receptor: G-protein coupled receptor, tyrosine kinase, nuclear, etc? Or, What is the likelihood that a randomly chosen neonate will have be born with ________? I swear to God most of my classmates pass exams because they sit and memorize every old exam they can get their hands on. It's ridiculous.

Only a minority of our exams are providing questions with history and lab data. I'm starting to wonder how our students do so well on the boards... *sigh*

Thanks for the input, though!

I appreciate your frustration. M1 and M2 are a bit of a game. But it all does build an important foundation, even if it doesn't seem like it. I to thought it was BS, but it's the BS that allows for faster connections later IMHO. And you should be memorizing those old tests too - yeah much of it is BS, but the best grades possible afford the most choices.
 
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You tell me Doctor :D

Medicine is an art as well as a science, and any doc that can be replaced by a computer algorithim, should be.

I call it rhabo when it is - muscle breakdown either either from a history of extreme physical stress (a marathon), crush trauma, or laying in one place too long. If the CK is elevated within given the clinical history, it's rhabdo, you make the call. Purists will make sure their is myoglobin in the urine, but this is often unecessary for diagnosis. Remember we're trying to protect the beans here, so fluids, Fluids, FLUIDS is the correct answer.

Here's your mission, if you choose to accept it . . . do we alkalize the urine with sodium biacarb or not? What's the evidence?

Ha, ha... okay, I'll give it a shot, but don't expect much considering I don't even know what ALT stands for :oops:

K+ is high and Na+ is high, but I think hyperkalemia would be my major concern since it's raised proportionally higher than Na+ and could lead to some dangerous arrythmia.
[EDIT: I believe alkalosis should cause an increase K+ excretion via both a transcellular shift of intracellular H+ for plasma K+ and by high alkalized urine increasing the transluminal potential and increasing K+ secretion as a result. So NaHCO3- wouldn't hurt in that regard]

Okay, take it easy one me :) haha
 
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Ha, ha... okay, I'll give it a shot, but don't expect much considering I don't even know what ALT stands for :oops:

K+ is high and Na+ is high, but I think hyperkalemia would be my major concern since it's raised proportionally higher than Na+ and could lead to some dangerous arrythmia. I believe alkalizing the blood / urine should lead to K+ reabsorption, and if I'm correct in that I'm pretty sure it'd be a bad thing.

So, I guess I'd refrain from administering NaHCO3.

Okay, take it easy one me :) haha

Look it up when you get a chance. Send me a PM.

Good to see you're thinking. :D
 
I appreciate your frustration. M1 and M2 are a bit of a game. But it all does build an important foundation, even if it doesn't seem like it. I to thought it was BS, but it's the BS that allows for faster connections later IMHO. And you should be memorizing those old tests too - yeah much of it is BS, but the best grades possible afford the most choices.
Yeah, I know I "should". But, my first year is pass fail and I started out the school year totally burned out, so I'm trying to recuperate my brain. (I had switched majors and been in undergrad for a length of time, while taking full time units, that should have earned me two bachelors. On top of it, my summer was SUPER intense, right up to the week before school started. I really need this summer break to get my head on straight. Ha, ha. I know I need to kick it up a notch in the future, but for now, I'm doing fine on my exams and I'm going to give myself this Pass/Fail year to recuperate a bit.
 
Yeah, I know I "should". But, my first year is pass fail and I started out the school year totally burned out, so I'm trying to recuperate my brain. (I had switched majors and been in undergrad for a length of time, while taking full time units, that should have earned me two bachelors. On top of it, my summer was SUPER intense, right up to the week before school started. I really need this summer break to get my head on straight. Ha, ha. I know I need to kick it up a notch in the future, but for now, I'm doing fine on my exams and I'm going to give myself this Pass/Fail year to recuperate a bit.

I promise I understand. No need to explain anything. Just saying sometimes I look back and wish I'd studied an extra hour a day. It wouldn't have killed me. :D
 
True, true! I think that to myself every day. When I first started school, I really doubted my "cognitive abilities". But, after 8 or 9 months I'm kicking myself because now I know I have what it takes to be at the top 5-10% of the class, yet my laziness is keeping me down. (Well, that and I'm married and choose to spend lots of time with my wife--I'm ridiculously attached at the hip and have been for 8 yrs :))

*sigh* I'll try to get things into gear for year 2. lol
 
You tell me Doctor :D



muscle breakdown either either from a history of extreme physical stress (a marathon), crush trauma, or laying in one place too long. .

I'd throw statin use in the differential too
 
There are no "official" cut off numbers for rhabdo. Just FYI.

Agreed. With that said, ask most nephrologists and they will tell you they need to see CKs well above 10,000 before they call it true rhabdo. All the cases I've seen in my somewhat short medical career have been well above that (30,000, 50-55,000). I suppose if you want to get technical, since there are no diagnostic criteria, a CK of 500 post exercise could be considered rhabdo to some.

To the medical students reading, anyone who runs a marathon or lifts heavily at the gym and is otherwise healthy will see a harmless bump in their CK that requires no treatment except with perhaps some fluids PO for dehydration.

To tncekm: JDH mentioned a somewhat controversial treatment consisting of alkalizing the urine in the sense of protecting a certain organ that may be damaged during severe rhabdomyolysis. The theorized mechanism behind said toxicity/treatment is actually pretty interesting but it may be just that - a theory.
 
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To tncekm: JDH mentioned a somewhat controversial treatment consisting of alkalizing the urine in the sense of protecting a certain organ that may be damaged during severe rhabdomyolysis. The theorized mechanism behind said toxicity/treatment is actually pretty interesting but it may be just that - a theory.

Yeah, I'm planning on looking into it deeper, but after a brief internet search I saw that there is some controversy. I guess lot of people think that the alkalized urine (via NaHCO3) is getting credit for improvement that's simply a result of the high fluid volumes given for rhabdo cases. Sounds interesting, so I'm going to keep looking into it for sure.

Thanks for the heads-up.
 
Yeah, I'm planning on looking into it deeper, but after a brief internet search I saw that there is some controversy. I guess lot of people think that the alkalized urine (via NaHCO3) is getting credit for improvement that's simply a result of the high fluid volumes given for rhabdo cases. Sounds interesting, so I'm going to keep looking into it for sure.

Thanks for the heads-up.

yeah, the alkalinizing the urine is questionable in efficacy but still often done; it's probably hydration itself rather than the pH of the saline that helps the kidneys clear the CK (ie, either give them lots of saline with NaHCO3 or just lots of saline).

as an aside, the question stem probably didn't give AST because it could quite possibly be elevated in this pt. AST can be released by muscle damage (it used to be a heart attack marker). it's kind of like how bone can release alk phos. even if they told you his AST is 200, you still don't suspect liver damage in this scenerio.

either way, the most concerning finding is his K+, which is at a level that could kill him. he needs a stat EKG, insulin/amp of dextrose/amp of bicarb, kayexalate PO, and probably some calcium IV. cheers :).
 
yeah, the alkalinizing the urine is questionable in efficacy but still often done; it's probably hydration itself rather than the pH of the saline that helps the kidneys clear the CK (ie, either give them lots of saline with NaHCO3 or just lots of saline).

either way, the most concerning finding is his K+, which is at a level that could kill him. he needs a stat EKG, insulin/amp of dextrose/amp of bicarb, kayexalate PO, and probably some calcium IV. cheers :).
Ah, cool. Thanks for the info!
 
yeah, the alkalinizing the urine is questionable in efficacy but still often done; it's probably hydration itself rather than the pH of the saline that helps the kidneys clear the CK (ie, either give them lots of saline with NaHCO3 or just lots of saline).

as an aside, the question stem probably didn't give AST because it could quite possibly be elevated in this pt. AST can be released by muscle damage (it used to be a heart attack marker). it's kind of like how bone can release alk phos. even if they told you his AST is 200, you still don't suspect liver damage in this scenerio.

either way, the most concerning finding is his K+, which is at a level that could kill him. he needs a stat EKG, insulin/amp of dextrose/amp of bicarb, kayexalate PO, and probably some calcium IV. cheers :).

Not "probably" the calcium. He definitely needs the calcium, which is the only hyperK treatment which may help prevent arrhythmia - the insulin and bicarb temporarily put the K into the cells. Kayexcelate is a matter of some controversy at this time . . . but most still give it. Big dose of lasix can also be given, provided the kidneys are working. The gut and kidneys are the only way to get rid of the K.
 
Would you be standing by with amiodarone for this patient until the K+ came back down Earth?

I wouldn't order it to the bedside. It's in the crash carts.

Plus the important thing to remember is this patient doesn't have an amiodarone deficiency :D he has too much extracellular K. He needs the K treated.

But that's a good thought.

Amio is more that is more helpful in v-tachs associated with ischemia or structural issues, in other words more "fixed" type of defects. The high K can give you v-tach, and you would probably end up giving the patient shocks and amiodarone if they went into v-tach because that is the current ACLS protocol, but this type of v-tach is of a different sort, and the problem is the K.
 
Plus the important thing to remember is this patient doesn't have an amiodarone deficiency :D he has too much extracellular K.
:laugh:

He needs the K treated.

Assuming you load 'em up with NS and maybe furosemide, how long would you expect his/her K+ to be elevated, assuming the kidneys are working like they should?
 
Assuming you load 'em up with NS and maybe furosemide, how long would you expect his/her K+ to be elevated, assuming the kidneys are working like they should?

Should be reasonable by morning.

Of course you'll pull all of the other tricks too - insulin, bicarb, calcium, kayexcelate, albuterol, etc.

But if that patient's creatinine is elevated, which wouldn't be out of the question in dehydration and rhabdo, "Houston, we have a problem" . . . what would you think we should do if the kidneys are acutely not working? :D
 
Should be reasonable by morning.

Of course you'll pull all of the other tricks too - insulin, bicarb, calcium, kayexcelate, albuterol, etc.

But if that patient's creatinine is elevated, which wouldn't be out of the question in dehydration and rhabdo, "Houston, we have a problem" . . . what would you think we should do if the kidneys are acutely not working? :D


I'm going to guess here, so without looking it up say give dopamine. It'll dilate the vascular beds in the kidneys and increase filtration, hopefully moving some of that excess K+ on out. It could help with BP if the patient is dehydrated as well.
 
I'm going to guess here, so without looking it up say give dopamine. It'll dilate the vascular beds in the kidneys and increase filtration, hopefully moving some of that excess K+ on out. It could help with BP if the patient is dehydrated as well.

Good to see you are thinking, but if the beans aint workin' and the K is high, you need dialysis.

What are the indications for dialysis? HINT: A, E, I, O, U
 
Ha, ha... no, I mean I "really" get useless trivia sometimes. Like, what type of receptor is the LH Receptor: G-protein coupled receptor, tyrosine kinase, nuclear, etc?

You'll probably see a few of these type of questions on the step... or at least there were kaplan questions that asked "useless trivia" similar to this.
 
Per a quick Google search:

Mneumonic for indications of Dialysis: AEIOU
1. Acidosis
2. Electrolyte abnormalities-hyperkalemia
3. Ingestion of substances like barbiturates, salicylates, lithium, methanlo, etc
4. Overload fluid (unresponsive to diuretics)
5. Uremia symptoms (pericarditis, encephalopathy)



^ This came from a site called prep4usmle.com. I'm assuming this is the correct mnemonic.
 
You'll probably see a few of these type of questions on the step... or at least there were kaplan questions that asked "useless trivia" similar to this.
Ah, lame. I really don't think knowing stupid trivia like, exact efficacy of using condoms, is worth memorizing. Oh well, hoops to jump... such is life.
 
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