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Lots of things can cause hypoglycemia, and lots of things can cause hypokalemia. Treatment is aimed at correcting the cause. We can temporarily give dextrose for the hypoglycemia, and temporarily give potassium replacement for the hypokalemia, but ultimately the workup should reveal the underlying condition so that it can be addressed.
Some causes of hypoglycemia are:
*
- Hepatic disease: (eg, hepatic failure, cirrhosis, galactose intolerance, fructose intolerance, glycogen storage diseases)
- Transient ischemic attacks
- Cardiac dysrhythmia
- Endocrine disorders (eg, pheochromocytoma, Addison disease, glucagon deficiency, carcinomas, extrahepatic tumors)
- Substance abuse (eg, cocaine, ethanol, salicylates, beta-blockers, pentamidine)
- Hypoglycemic agents (eg, insulin, oral hypoglycemic agents)
- Nutritional disorders (eg, prolonged starvation before anesthesia, protein calorie malnutrition, L-leucine-sensitive hypoglycemic defect in children, low-calorie ketogenic diet, renal disease)
- Autoimmune disorders (eg, Graves disease)
- Central nervous system (CNS) disorders
- Psychogenic
*In most cases, the cause of hypokalemia is apparent from the history and physical examination. However, measurement of urine potassium is of vital importance because it establishes the pathophysiologic mechanism behind hypokalemia and, thus, aids in formulating the differential diagnosis.
Since insulin increases potassium uptake, I think insulinoma is a fair guess, but the workup should exclude other things such as liver disease, infection, autoimmune issues, etc. I'm a little confused by your statement that the interventions weren't drastic enough. What do you think should have been done that wasn't?
*Source: Medscape
Wow, great answer AF. I would guess OP was surprised that at least 1 amp of D50 wasn't pushed, I am.
You know, I was surprised not too long ago when that wasn't done in the field for a hypoglycemic patient that came to the ER.
But then, when I did a little research, I learned a lot.
Pushing an amp of D50 is old school. Evidence based practice these days shows that there are many advantages to giving D10 in measured doses instead.
Thanks again, Anna. It seems like I've heard that before also. Is OP stating BG in mmol/l or mg/dL? 3 mmol/l is 54 mg/dL, which makes more sense to me. I can't imagine someone being alert with a BG of 2-3 mg/dL.
Yes, I'm assuming mmol/l also. Normal range is 4-6. 2-3 would be 36-54 mg/dL.
Sounds as if her pancreas is not working properly....and perhaps even pancreatic ca.
However, these 2 can both be low when a person is severely dehydrated and have had multiple bouts of diarrhea, vomiting that kind of thing.
There are newer standards in blood glucose that have near 70 as a "normal". Some will show signs of low blood sugar then, others will not. So the blood glucose was perhaps not really horribly low. The K has to be given slowly as to not upset the cardiac function of the patient.
All of these things are bandaids, however, unless the cause is discovered. Whether that be an acute episode or a chronic condition. And I would think that if it is the result of an acute episode, it can work itself out as normal function (eating and drinking) returns.
I would also think about if this patient is an ETOH abuser with acute pancreatitis, anorexic/bulimic--an underlying cause for this.
Interesting case. Let us know how it goes.
seks
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Had a pt where she was hypoglycemic (below 2-3) and hypokalemic (2.2) simultaneously. She was still alert and talking.
We hung dextrose 50% 25g and 10mmol K+ minibags...quite a # of them. Those were resident's order which I feel wasn't an enough drastic intervention.
I'm not sure what came out of it since when I left, bgm still 2.9 and k+ 2.4 after 4 K+ minibags and 5 dextrose bags.
So what's the relationship between those two conditions?
I know that insulin is given during hyperkalemia to stimulate the Na+K pump. Could it be her pancreas was producing lots of insulin?????????????