KCl in hyponatremia -> risk of pontine myelinolysis?

[Tuloste]

Do I have the mechanism figured out correctly? If not, please explain!

Patient who is hyponatremic and hypokalemic is given potassium chloride. Potassium enters cells to replace sodium which enters ECF and plasma. Because the BBB blocks potassium chloride from entering the brain, the increased tonicity of plasma draws water from the brain resulting in myelinolysis. [I read that potassium also takes the place of some intracellular hydrogen ions that are buffered in the ECF, essentially pulling some water and chloride into the cells with it. This should counteract the dehydration behind the myelinolysis if it also took place in the brain? So is potassium chloride basically entering the ICF compartment minus the brain and thus raising the tonicity of ICF - brain and ECF resulting in a net water movement out of the brain?]

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[Doctor Bob]

Maybe

 

[Nephroexp]

You're making it too complicated. Essentially the potassium goes inside the cell on sodium comes out this is through sodium potassium atpase


That is no blood brain bad barrier for potassium

 

[Tuloste]

Thanks for the reply Nephroexp. I don't question your knowledge on the subject, but do have a few follow up questions as the subject remains incompletely clear to me.

Firstly, Miller's Anaesthesia states that the BBB reflects sodium chloride effectively enough to make fluid filtration across it dependent more on hydrostatic pressure and total osmolarity as opposed to oncotic pressure. Could this mean that the charged electrolyte potassium from KCl would be unable to cross as well?

Secondly. If potassium did indeed cross into the brain and drive out sodium, then wouldn't the tonicity of the brain equal that of plasma already before any net movement of water out of the brain had taken place?

 

[Nephroexp]

I am no neurologist or anesthesiologist, but having read enough about sodium/potassium - I di not come across this BBB for electrolytes like sodium - will review and get back to you.

 

[jdh71]

wtf is this nerd ****?

 

[Hernandez]

wtf is this nerd ****?

Lots of over thinking for a condition that's only been reported a handful of times.

 

[Nephroexp]

May be rare but when it happens it is devastating bit for patient and physician(lawsuit to follow) .when you correct sodium , remember that k is same as sodium as it gets exchanged.


Please have some respect for intellectual curiosity and patient care. Don't be dismissive.

 

[jdh71]

May be rare but when it happens it is devastating bit for patient and physician(lawsuit to follow) .when you correct sodium , remember that k is same as sodium as it gets exchanged.


Please have some respect for intellectual curiosity and patient care. Don't be dismissive.

Going to pull the condescension card. Classic.

PROVE you have ANY real clue what you are talking about and that it matters.

I'll patiently wait.

 

[Hernandez]

May be rare but when it happens it is devastating bit for patient and physician(lawsuit to follow) .when you correct sodium , remember that k is same as sodium as it gets exchanged.


Please have some respect for intellectual curiosity and patient care. Don't be dismissive.

Lawsuit perhaps, but not one that would have an easy chance of winning. It would be very easy to find someone on the other side that would rightfully state that severe hypokalemia can and will kill you and not treating it based off of fear of something that is case report level occurrence is malpractice.

Don't spend time worrying or studying esoteric bs until you have the basics down.

 

[Nephroexp]

Hernandez you have no clue !! Ignorance is a bliss. Stay there

 

[Hernandez]

Hernandez you have no clue !! Ignorance is a bliss. Stay there

Then by all means...please enlighten me on how this isn't exceedingly rare.

 

[deleted171991]

Do I have the mechanism figured out correctly? If not, please explain!

Patient who is hyponatremic and hypokalemic is given potassium chloride. Potassium enters cells to replace sodium which enters ECF and plasma. Because the BBB blocks potassium chloride from entering the brain, the increased tonicity of plasma draws water from the brain resulting in myelinolysis. [I read that potassium also takes the place of some intracellular hydrogen ions that are buffered in the ECF, essentially pulling some water and chloride into the cells with it. This should counteract the dehydration behind the myelinolysis if it also took place in the brain? So is potassium chloride basically entering the ICF compartment minus the brain and thus raising the tonicity of ICF - brain and ECF resulting in a net water movement out of the brain?]

Suppose we are giving the patient 200 mEq of KCl to a 100 kg patient (60L of water, 40 L ICF, 20 L ECF). Almost 100% of the K+ should end up intracellularly, where it will raise the K concentration by 200 mEq/40 L = 5 mEq/L. Thus it will increase intracellular osmolarity by 5 mOsm.

In exchange, suppose that we get 200 mEq of Na+, by the way of the Na-K-ATP-ase, that will end up in the ECF, raising the ECF osmolarity by 200/20 L = 10 mOsm. That will create an osmotic gradient of 5 mOsm (slowly, over the 5+ hours it takes the KCl to be administered, 40 mEq/h max), or 1 mOsm/h.

Are you scared by how that 1 mOsm/h increase in osmotic gradient will drain all that water from the brain? (For 70 kg patient it's 1.4 mOsm/h.)

Disclaimer: I am not an intensivist.

 

[Nephroexp]

Sodium and potassium are not the only osmoles moving around !