Hyponatremia and Central Pontine Myelinolysis

Thanks to the Ninjadoc, I have been made aware of another way that a person can develop hyponatremia, which increases their risk for CPM.

Ketoacidosis can be caused by several factors:  Diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketosis and hypoglycaemic ketoacidosis. (http://qjmed.oxfordjournals.org/content/97/6/365.full)

Type 1 diabetics have an increased likelihood of developing ketoacidosis. It can also occur in those who have eating disorders, such as anorexia. Those with type 2 diabetes can also develop it, but it is not as common as in type-1 diabetes (http://www.ucdenver.edu/academics/colleges/medicalschool/centers/BarbaraDavis/Documents/book-understandingdiabetes/ud15.pdf).

So, what is ketoacidosis and how does this lead to hyponatremia?

This is a bit complicated, but I’ll try to make it so understandable that even I can comprehend what I’m talking about 😉

Ok. Everyone has a pancreas, and the pancreas has MANY jobs, but one of it’s most important jobs is to produce hormones that regulate your blood sugar. Insulin is one of the most important hormones that the pancreas produces. After you eat, your body starts to break down food and liquids into glucose. As more and more glucose is absorbed into your blood stream, your blood glucose levels increase, and your body triggers a release of insulin from your pancreas. The insulin causes glucose to be transported from the blood into muscle cells, liver cells, and other types of cells.

Insulin also prevents the break down of fats in the body.

In type 1 diabetics, there is a dysfunction in the pancreas that prevents a release of insulin or the pancreas does not make insulin. This means that when a person eats and glucose floods the blood stream, it stays in the blood stream.

Also, because there is a lack of insulin in the body, cells miss that signal that tells them to NOT break down fats.

Now, I’m not an expert on ketoacidosis, but basically because the cells are unable to use the glucose in the blood, they start to break down fatty acids into glucose in the cells. It’s kind of like having an on sight manufacturing plant of glucose using fatty acids. Also because insulin is not being produced or when a diabetic person does not take their insulin, the cells do not receive that message to stop or not break down fats/ fatty acids. As more and more fats and fatty acids are broken down, more ketones are produced as a by-product.

Ketones are acidic in nature and the build up of ketones in the blood lead to an acidic PH.

So,  ketoacidosis will usually occur when a person does not get enough insulin, which means that their cells are not getting the energy that is needed to maintain function. Those cells are also missing the signal to stop breaking down fats, so that inner cellular factory is breaking down fats in high gear.  At this point in the reaction, a person will have a very high blood sugar level (in regards to those who develop it in type 1 or type 2 diabetes), and they will also have high ketone levels. This lowers their blood PH, and is termed as ketoacidosis.

I hope that makes perfect sense 🙂 If not, please don’t hesitate to ask questions, and I will try to find the best answers for you.

A person has to go to the hospital to receive treatment for the ketoacidosis, and the treatment is a decrease in blood sugar and a restoration of the proper electrolytes.

So, at the point that the blood sugar is reaching high levels and ketones are reaching toxic levels, the body starts to try to regulate the system by flushing these toxins through the kidneys. This increases a person’s thirst and urine output which leads to dehydration. Also because there is a high concentration of glucose in the blood, the body tries to correct this imbalance by shifting water from inside the cell to the blood. It is trying to dilute the high levels of glucose by adding water. However, because sodium levels do not change this gives an impression that a person has hyponatremia. They may indeed have hyponatremia or it may just be a fluctuation of the fluid balance from in the cell to the blood.

Now according to the University of Texas Medical Branch, lab work can be misleading in cases of diabetic ketoacidosis. It can show that a person has hyponatremia, but in fact, they just have these shifts in sodium and potassium due to the high glucose levels in the blood (known as pseudohyponatremia), but they also acknowledge that in some cases, a person might  in fact develop true hyponatremia as well. Now if that seems complicated to you, don’t worry because it is. It seems in regards to ketoacidosis, you definitely have to have an expert in endocrinology oversee your care. I’m not an expert, but if you are interested in finding out more about how you can develop false hyponatremia (pseudo hyponatremia) and want to know more about it, use the following link: http://www.utmb.edu/pedi_ed/CORE/Endocrine/page_27.htm.

Now this is where things get tricky, I believe that because the causes behind the development of hyponatremia (real or pseudo) are so complex, this can lead to an inappropriate treatment of it. For instance, if a person has pseudo hyponatremia because of the high glucose levels, it is believed that once the glucose levels are corrected then the sodium levels will correct naturally as well too. This means that the water shift from the blood back to the cells will occur naturally, however, if treatment is administered in the form of saline iv solution, this fluctuation could happen too quickly and cause CPM/EPM.

It’s something to be aware of if you have diabetes or if you have another cause of hyponatremia. In other words, it is important to understand the root cause behind why a person has developed hyponatremia and make a logical and educated basis of correction from that cause or there will be a great risk of correcting the sodium levels too quickly and an increased chance of myelinolysis.

I hope that makes sense.

For more information on ketoacidosis related to diabetics, please use the following links:

http://emedicine.medscape.com/article/118361-overview

http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html

http://www.ucdenver.edu/academics/colleges/medicalschool/centers/BarbaraDavis/Documents/book-understandingdiabetes/ud15.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770770/

Have a great night!

(I also want to call out a special call out to my helpers on this article, Ninja doc and Dr. R. They both gave me great insight and helped direct me in areas that were a bit off the mark. THANKS guys 😉 )