We all know that d50 causes tissue necrosis if it extravasated. Why?? What is the PROCESS at work??
I'm not 100% but I believe the cause is extreme osmolarity of a solution with a solute concentration of 500mg/ml
The massive pull that is exertered by the hypertonicty of such a concentrated substance directly in contact with cells dehydrates the cells resulting in cell death and subsequent necrosis.
Again, not 100% but I think that is it.
That is essentially correct but what I'm looking for is deeper. Why is d50 toxic only if it extravasates? It does not harm your skin or damage the vasculature, so why should it only be toxic in the interstitial space? I can't find this anywhere. Also, yes I fully understand solution solubility.
While we are on the topic, be mindful that D50 isn't the only thing we administer capable of causing local necrosis.
Calcium for example is capable of causing massive necrosis. I've read calcium is actually capable of producing full thickness necrosis.
Even hypo/hypertonic saline can produce necrosis by overhydration/dehydration of cells.
Personally I take a lot of pride in showing up at the hospital with a clean, patent IV site. I know many guys who skip using a lock/flush and just directly attach a drip set but personally I like to always use a saline lock/flush as it provides a detachment point other than the catheter and more importantly it allows me to safely ensure my site is good to go before administering any meds. Unless you extravasate enough normal saline to substantially stretch the connective tissues of the skin you aren't going to cause any adverse effects. Better safe than sorry.
True. But hopefully dopamine is the only pressor you are trying to run through a PIV.
Granted the patient should be in arrest but should they be revived and your infiltrated IV spewed 3amps of epi and 40 of vasopressin into the interstitial space I can imagine it no being pleasant later on.