Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Vasopressin”

Hyponatremia: More treatment information.

Ok, so I’ve been researching like crazy. I have a friend who has CPM. He was recovering in the hospital from alcoholism. He possibly developed acute hyponatremia, and I have been doing research to find out as much possible about the differences between acute hyponatremia and chronic hyponatremia.

Hyponatremia is really an ugly beast when you try to break it down. It’s complex.

So there are different types of hyponatremia based on how it is induced. There are five different types (classifications) for hyponatremia. (who knew):

1.) Hypovalemic hyponatremia: body water, body sodium and extracellular fluid volume decrease.

2.) Euvolemic hyponatremia: Body water increases but sodium levels remain normal; to put it simply, dilution.  There is no edema but extracellular fluid increases slightly.

3.) Hypervolemic hyponatremia: Blood sodium increases, but body water increases more. There is a great increase in extracellular fluid. There is a presence of edema.

4.) Redistributive hyponatremia: This is related to the administration of mannitol, as well as with hyperglycemia. There is no change in body water or blood sodium, but there is a shift from intracellular fluid to extracellular. (Water moves from inside the cell to outside the cell.)

5.) Pseudohyponatremia: The blood sodium and body water are unchanged, but there is an abundance of lipids and proteins in the blood. Two conditions that cause this are hypertriglyceridemia and multiple myeloma.

This information was found from the following website:


I found the above website very informative in drugs that can cause hyponatremia. It also had a lot of important regarding how it should be treated.

For instance, there is chronic hyponatremia in which a person has below normal sodium levels for more than 48 hours. Then, there is acute hyponatremia in which a person has sodium levels lower than normal for less than 24 to 48 hours.

Now the key with acute hyponatremia is the rate at which it decreases over 24 to 48 hours. For instance, a person may be diagnosed with hyponatremia on day 1 with a level of 130, but by day 2 have a level of 118, and by day 3 have a level of 110. Would this be considered chronic or acute? If sodium levels continue to fall over a period of time, a few days to a few weeks, it is considered chronic, despite where it started or how quickly it initially dropped.  It is the overall period of time it has continued to drop.

This goes back to one of my earlier posts. It is actually believed that the longer it stays low the safer it is medically for the person. What I mean by that, it is less likely for a person to go into a coma or for a person to have their brain stem herniate due to swelling directly caused by a rapid drop in sodium.

There is a fine line between low and too low and how long it should stay that low. There is a large number of studies that say if you can stabilize the hyponatremic state, it is safer long term for the person. However, at that point, it becomes critical that the person’s sodium levels be raised to normal at an extremely slow rate (.5mmol/hr or less and no more than 8 mmol/24 hours)!!!

If a person develops acute hyponatremia, their sodium levels drop extremely low the first 24 to 48 hours. This is most common in persons who drink an excessive amount of water. This is also common in infants when parents water down their formula.

What do I mean by extremely low? The levels go from 135 to 110 or lower in the first 24 to 48 hours.

In persons who have their sodium levels drop this significantly, in this short of a period, they have an extremely high risk of developing brainstem herniation and/or cerebral swelling, and/or coma. Their functions are extremely impaired very quickly.

In persons who develop chronic hyponatremia, their initial physical symptoms are far less significant than those who develop acute hyponatremia. If a person, is conscious and can talk coherently, chances are they have chronic hyponatremia. If the person is unconscious, having seizures, thinks they’re a monkey, they probably have acute hyponatremia.

The difference of how to treat these patients vary greatly based on which type of hyponatremia they have. The chronic hyponatremic patient must have their sodium levels raised slowly.  The acute hyponatremic patient must have their levels raised rapidly, at least initially.

*****The acute hyponatremic patient has a greater risk for developing brainsterm herniation, coma, and cerebral swelling, so they must have their levels raised quickly to control this swelling. As I mentioned previously, raising the sodium levels, decrease the swelling in the brain. That said, the levels can’t be raised too quickly!

It is recommended that sodium levels be increased by 4-6 mmol/L during the first 1 to 2 hours. (http://emedicine.medscape.com/article/767624-treatment#a1126). ONCE SYMPTOMS BEGIN TO IMPROVE THIS THERAPY SHOULD BE SLOWED OR CEASE!!! In other words, once a person has stabilized there should be a reduction to this high dose treatment to prevent CNS abnormalities. It is further recommended that a person should not have their levels increased more than 12 to 15 mmol during that first 24 hours. Once it has reached that point, it should not be increased further for a total of 48 hours.*****

It is extremely difficult for a medical professional to determine which type of hyponatremia you or your loved one might have. You can help them determine this by letting them know if there were any issues the day or so before you were brought to the hospital. Were you feeling sick or experiencing headaches, fatigue or cramps in the 24 to 48 hours before you made it to the hospital?

Most people experience unexplained cramps in their hands or feet as the one of the first symptoms of hyponatremia; however, they don’t realize it, so they delay seeking treatment until the symptoms progress.

IF your doctor is unable to determine what type of hyponatremia you have by your symptoms or time frame alone, then they should perform an MRI or CT scan to check for swelling in the brain or brainstem!!! Please, be aware of this crucial step. If a person shows brainstem or brain swelling, then they should be treated for acute hyponatremia. This type of injury is less common in persons who have the chronic form!

There is so much to this puzzle, and it becomes more complex the more I research. It also leaves questions. For instance, it is known that alcoholics are more likely to develop CPM; however, I have not been able to determine what type of hyponatremia alcoholics develop most often, chronic or acute. If the develop chronic, then that is in accord with the research I have found thus far because those with chronic hyponatremia have the highest risk for developing CPM. If alcoholics develop acute hyponatremia, this would go against research that says those with acute hyponatremia rarely develop CPM.

So, the more I research, the more questions I have.

Please be patient as I learn more and pass the information to you. Please leave any questions or point out any inconsistencies you might find in my posts.  No matter what, please continue to pass the information forward. It will be nearly impossible to protect people from this threat without your help.


Hyponatremia: Alcohol relation

It’s been a few days since I last posted. My excuses: it’s the Christmas season. My son just had his tonsils out a week ago 😦 I’ve been horribly upset because I had cognitive testing to see how CPM/EPM has impacted my cognitive abilities.

My issues are with memory, concentration, communication. Anyway to make the longest story short, the neuropsychologist that administered the test decided I was faking and/or my issues weren’t related to CPM/EPM, but were being caused by stress and fatigue, because my results on things like memory, etc were way below normal, but my tests that test intelligence show I’m way above normal.

Most of you don’t know that much about me, so you might not understand why this really ticks me off. I wasn’t faking. I’m an A type personality. It’s not in my blood to do badly on a test, definitely not on purpose!!

I was hoping to take the MCAT before this all happened. I’m still hoping to take it, but it will literally take an hour or two to write these brief posts, so it will be difficult to take something like the MCAT.  Thank God, I can catch my mistakes, but it takes me an hour or two of constantly reading and re-reading my post before I get it right.  You can’t do this on a MCAT.

I’m not the same person I was a year ago. A lot of my CPM/EPM issues have improved, but one of the areas I’m experiencing the greatest frustration is with my cognitive abilities. I have a hard time remembering simple things.

Ok, see. I’m going off on a rant. I’m already way off the topic I wanted to discuss. So, I’m going to just leave it at that. At one point, hopefully soon, I will discuss my story, how this all happened, but right now, I want to discuss how alcohol impacts blood sodium.

Some of this information might have been posted about in previous blogs, but I honestly don’t remember. So forgive me if this is a bit redundant.

I was extremely surprised to find out that you do NOT have to be an alcoholic to develop hyponatremia or CPM! You have a higher chance of developing hyponatremia even if you have just one drink.

You have a much greater chance of developing CPM if you are an alcoholic or a recovering alcoholic than a person who has just consumed one drink.

Reasons why alcoholics develop hyponatremia:

A.) They vomit due to excessive alcohol intake.

B.) hypovolaemia is decreased blood volume/ blood plasma. This occurs in alcoholics because of vomiting.  This also leads to secretion of ADH (helps control urine output) which causes a person to urinate less and leads to fluid retention.  Also, it stimulates thirst mechanisms. This leads to an increase of fluid consumption and a decrease of urine output which essentially dilutes your blood and lowers your blood sodium level.

Hypovolaemia is not the same as dehydration. Dehydration is due to excess fluid loss, but hypovolaemia is characterized by a loss of sodium..which leads to hyponatremia.

C.) Excessive consumption of large amounts of alcohol, which is low in salt, along with being malnourished. This is called “beer potomania”.

D.) The less common cause is because of SIADH, syndrome of inappropriate antidiuretic hormone secretion.  The body secretes too much ADH. This again leads to dilution of the sodium in the blood.

Ok, folks. Here’s the thing. Earlier, I posted that ADH is inhibited when you drink alcohol. Now, I’m saying it is produced in excess. I’m totally aware of this contradiction, but this is a contradiction that is published in the literature.

According to the NIH, it is inhibited. Check out this link below:


According to this published article, ADH is produced in excess. Check out this link below:


SO WTF?? I really don’t know. I’m going to say that with everything in the body there has to be balance, so I’m going to say that if a person starts to consume alcohol, ADH is inhibited. However, as alcohol consumption increases, ADH begins to be released excessively because the body has dumped a large amount of nutrients, etc due to the frequent urination and possible vomiting.

Let me see if this makes a bit more sense. If you consume a large amount of fluids, you pee more (less ADH is released)…what goes in, must come out. At some point, you can push that balance to the other extreme. At some point your body realizes that you’ve lost a lot of your nutrients and fluids (have become dehydrated), so your pituitary releases large amounts of ADH to try to maintain that balance. If you continue to consume liquids, at the same time you are releasing more ADH, then you dilute the system even more quickly.

So, that’s my opinion, and I’m guessing that’s why there’s a contradiction in how ADH is impacted when you consume alcohol…but this is just my opinion. I will try to find some more clarifying information regarding it.

I hope you find it helpful or at least inspiring to do your own research.


Research and Links:

Technology is a magnificent thing, when it works. Today, I’m using my cellphone to start this post. It most definitely will need to be edited from my home PC. The reason: my laptop won’t allow me to connect to the internet. Frustratingly, I have no idea why, and I have spent most of last night and this afternoon trying to figure it out. Obviously, I haven’t, and after so much time fruitlessly invested, I’m at the moment restraining myself from stomping, throwing, and crushing it into 300-$1.00 pieces.

I should have realized that spending less on a laptop than a cellphone won’t buy you the best laptop on the market, but I really thought I would at least be able get online and write papers. Lesson learned.

Before I started the laptop rant, I was prepared to describe how long it takes me to write these brief posts. Before developing CPM, I could write approximately 3 full pages in 45 minutes. Now, I’m lucky if I can write 8 paragraphs in 2 to 3 hours. Now, that is frustrating!

Since developing CPM, my ability to communicate what I think clearly is significantly compromised. Some hours are better than others, but that also adds to my complete frustration. In this world,  you can’t call your employer and say, “I’m sorry. I’m not able to think through anything today. I won’t be coming to work. Maybe tomorrow.” Obviously, the world doesn’t work that way. It can’t.

Let me stress that, I don’t believe my intelligence has been impacted but my ability to recall information but the ability to communicate my thoughts have. It’s extremely stressful when you can’t say what you feel. At times, when I am under significant stress, I have been reduced to monotone grunts and sputters.  That’s not an exaggeration. I make absolutely no sense.

Ok, so I’ve gone on several rants and haven’t relayed any facts, and that’s really what I want to focus on right now.

I want to start posting some of the links that you can access some of the information I have. I am attaching links for the Toronto study from PubMedhttp://www.ncbi.nlm.nih.gov/pubmed/20142578.  This study is pretty recent, Feb. of 2010.

At this time, I still haven’t received any word from any of the local hospitals from which I requested their hyponatremia statistics. I’m not really surprised, but I will try again tomorrow.

Regarding sports athletes:


The following link is in regards to a study performed on the 2002 Boston Marathon Runners.  Thirteen percent of 488 participants developed severe hyponatremia. Wow, right?!!


Another marathon study for hyponatermia. This was also a 2002 study done by University of Pittsburgh:


A recent study, June 2011, regarding hyponatremia and antidepressants. I really didn’t know that antidepressants would cause hyponatremia, so this study took me by surprise. I know A LOT of people who take antidepressants. It’s actually the most commonly prescribed class of drugs. This is really scary.


The risk in the Elderly:


I found this article, EXTREMELY interesting. It’s a September 2011 interview with the vice president (a doctor) of a hospital consulting company:


Hyponatremia and it’s impact on children:


Hyponatremia and Alcoholics. I also wanted to let you know, it frequently occurs in drug addicts as well:


I am going to pull important information from the following link. I think it really puts into perspective, how alcohol impacts blood sodium levels:


Alcohol consumption can have pharmacological effects on water and sodium metabolism. The effects of alcohol on sodium and water balance may differ with acute alcohol intake, chronic alcohol intake, or acute withdrawal from chronic alcohol abuse.

As the blood alcohol level rises with acute alcohol intake, a transitory increase in the elimination of “free water” (water without salts) by the kidney occurs (Rubini et al. 1955), resulting from inhibition of the release of antidiuretic hormone (ADH). As the plasma alcohol level decreases, urinary flow is reduced (Nicholson and Taylor 1938). Concomitant stimulation of water intake (Sargent et al. 1978) causes significant water gain. This water retention occurs together with sodium retention (Nicholson and Taylor 1938; Sargent et al. 1978) due to increases in the reabsorption of sodium by the kidney.

Animal studies involving chronic alcohol intake have shown significant retention of water, sodium, potassium, and chloride after the first week of daily alcohol ingestion (Beard and Knott 1968). Urine output does not decrease, but fluid ingestion is stimulated.

During acute withdrawal following chronic alcohol abuse, urinary elimination of sodium, chloride, and water increases (Beard and Knott 1968). The augmented urinary flow eliminates the fluid and electrolytes that were retained in excess during alcohol abuse.

I hope this post emphasizes the fact that at some point nearly EVERYONE will develop hyponatremia. I hope that listing these links, you may realize, I am not over exaggerating anything.

I believe it is absolutely fundamental that everyone is educated on the risk factors and what the proper treatment is. Tomorrow, I promise, I will explain everything I know about how hyponatremia should be treated. I will also provide my best insights on how some treatments may induce CPM, and what I believe would be extremely important considerations to discuss with your doctor if you are being treated for it.


UPDATE: 04/20/12—-I just wanted to include this link. It’s a link for Tufts Medical School. It outlines what happens in hyponatremia. It gives a great explanation for the medical aspects of hyponatremia. I would consider this a really great condensed version of things I’ve written about so far: http://ocw.tufts.edu/data/33/497472.pdf

More to the Story:

Last night, I couldn’t sleep. For some reason, I thought thinking about what I would post today would allow me to fall into slumber. Not that I think my posts are boring ;), but I thought concentrating on something I was going to do would soothe me. Ha, I was so wrong!!

Normally, I don’t have a problem falling asleep, but I have a horrible time staying asleep. I wake up about 10 to 13 times a night! Really, I don’t know what the purpose of my trying to sleep is. It doesn’t work. But, in an effort to fix this problem and to relieve my utter exhaustion, I started using Ambien last week.

Anyone who has used Ambien will tell you, its effectiveness doesn’t last long. After a few peaceful nights of only waking 3 or 4 times per night, I feel more rested, but I only get that effect for the first 2 or 3 days. After that, I start waking up more and more again, so I try to use it for short periods. I will use it for a few days, maybe a week and then stop. I know if I keep using it, it won’t do any good at all after two weeks or so, but if I use it, then stop, in a week or so, I can use it again and have it work for a few nights or so. At least, I’ll have a few “good” nights of sleep.

So, last night, I had an Ambien free night, and that led to insomnia, which is a problem that I don’t have very often. I simply could not fall asleep, and when I did, I had horrible dreams along with waking up every 20 to 45 minutes.

Getting back to my point, I thought thinking about my hyponatremia story would soothe me into slumber. Of course, it didn’t. I became so upset with how my treatment was handled, and how I developed EPM because of it that I had to concentrate on not thinking about it.

If I start talking about what happened to me that will be the end of my spreading the word of how to prevent it. I will, at some point in the near future, start discussing what happened to me and how it’s impacted my life. I definitely encourage anyone who is experiencing their own incidence of hyponatremia to post their stories. Please post your story! Post any information you might feel that I have missed because I know I am missing things, which leads me to what I am going to focus on right now.

In my post yesterday, I forgot to mention a few important groups of people that are susceptible to hyponatremia.

I can’t believe I didn’t include this yesterday, but persons who have brain tumors (especially those of the pituitary gland), and those persons who have had brain surgery have an increased chance of developing hyponatremia. (I really can’t believe I forgot this group yesterday because this is the group that I am in!!)

So, the pituitary gland (located in the brain) is the master gland. It produces hormones that control additional hormones through out the body. I don’t want to delve into a tremendous amount of detail about the pituitary gland. The most important thing to know is that it is responsible for the hormone, ADH.

ADH, is one of the hormones that controls the amount of fluid the body holds on to. If ADH is not produced or too little is produced, a person will pee constantly. This leads to an issue known as diabetes insipidus.

Okay, so most people will think…wait, diabetes has to do with blood sugar, and I’ve never had that problem. This isn’t entirely correct.

Diabetes by definition is a metabolic disorder that causes excessive thirst and excessive urination. There are several types of diabetes. The most commonly known type of  diabetes is diabetes mellitus.

Mellitus is Latin for sweet. So, diabetes mellitus is translated to mean “Sweet Urine”. This is because doctors used to taste the urine of patients to determine whether or not they had an issue with their pancreas. (Now, you know why they were paid so much money. You would have to pay me A LOT to drink someone’s urine. Just saying.) They knew that the issue was with the pancreas if the urine was sweet because the excess  sugar would be dumped from the body through the urine.

The type of diabetes that leads to hyponatremia is usually diabetes inspidus. Insipidus means tasteless in Latin. So a person with diabetes insipidus would produce a large amount of  dilute tasteless urine. This issue is most commonly caused by an issue with the pituitary gland.  The pituitary gland stops producing the hormone, ADH, so a person releases a large amount of urine.

I hope that all makes sense.

Moving forward, another important group I didn’t mention yesterday, are people who are starting antidepressants. During the first few weeks of starting an antidepressant, a person has a high incidence of developing hyponatremia. I’m guessing since antidepressants impact brain chemistry (usually seratonin uptake inhibitors), in some people it impacts pituitary function as well. This is totally a guess, so don’t quote me on that.

A few additional groups that frequently develop it: persons with AIDS, pneumonia (or severe respiratory issues), and burn victims.

Finally, I mentioned that liver disease increases hyponatremia, but I wanted to specify that cirrhosis of the liver increases your chance of developing hyponatremia.

I think this really emphasizes the point of it’s not a matter of who, but WHEN will you develop hyponatremia, and the seriousness of hyponatremia should be addressed. It’s extremely dangerous. It’s not uncommon and most people have never even heard of it. The more scary part is: if your doctor doesn’t treat it properly, you can die, end up a living vegetable, or with brain damage.

I hope that I can prevent that from happening to someone, and I greatly appreciate if you are reading this that you will help spread the word by posting this information to your Facebook page, or sending the information directly to your friends. You really might save a life!!


The Facts Continued: Who is impacted

Even though it is 1pm, my hours are so screwy that this is like 8am to me. So, if my thoughts are a bit jumbled this is why.

Today, I wanted to discuss WHO gets hyponatremia. This information was startling when I first read about it because it really isn’t a matter of who will get it but WHEN.

I already posted previously a research study regarding a Toronto, Canada hospital that found 38% of patients were admitted for hyponatremia and another 38% develop hyponatremia if they are hospitalized longer than a day. Shocking.

I am currently trying to obtain information from my local hospitals about the number of patients that are admitted or develop hyponatremia each year. Of course, I’m meeting obstacles in obtaining this information. No one seems to know who to contact, but if I ever receive the information, I will be certain to post it.

So who is impacted by hyponatremia, who are the people most at risk?

It can occur in persons who have the flu due to vomiting and diarrhea (also with bulimics).

Those who are athletes (esp. marathon runners). I want to stress that it is not uncommon for athletes to be misdiagnosed with heat stroke or dehydration when it is actually hyponatremia. This is really scary because the hospitals will treat these patients with fluids and the increase of fluids will actually drop their sodium levels further!!!! Please if you are ever in a situation in which you have just completed vigorous, long lasting activities, and you develop the symptoms of hyponatremia, be certain they check your sodium levels before they administer fluids!!!

Chemotherapy recipients are also at an additional risk. Now, this information comes from my ICU nurse that treated me. I honestly can’t remember her name, but she explained to me that they will get chemotherapy patients who develop low sodium levels because they are not able to handle eating or drinking without vomiting. She said it happened frequently.

Alcoholics who are quitting “cold turkey” are at extremely high risk for developing hyponatremia, and further more they are at even greater risk for developing CPM. I know several people who developed CPM that were former alcoholics. It seems to be that it isn’t when they consume large amounts of alcohol that causes the problem, but when they are “drying out”.

I really think more research needs to be done on this.It would be interesting to find out if developing hangovers have anything to do with hyponatremia.

Alcohol impacts the hormone, ADH (anti-diuretic hormone) which is released from your pituitary. ADH controls your fluid out put, i.e. how much you pee. Alcohol decreases the amount of ADH released from the pituitary which signals to the kidney’s that you are going to release more sodium from your system. Where sodium goes, water follows. Drinking alcohol causes you to pee a lot. I’ve been told that this causes your brain to shrink due to dehydration and you develop headaches. However, this would contradict what is known to happen when sodium levels drop. When blood sodium levels drop, your brain cells swell, and one of the major symptoms of hyponatremia is severe headache. Interesting, right?

Obviously, research really needs to be done to understand why people get hangovers but also the relationship between low sodium and persons who consume vast amounts of alcohol.

Moving on…

Persons who drink large volumes of water are also at an extremely high risk for hyponatremia. Let me stress that water is dangerous if you consume too much. I think, it’s called water toxicity. You dilute your blood electrolyte levels to a non-functioning capacity. This is why if you participate in vigorous training, exercise, running, swimming, etc, you should consume a product like Gatorade or even sodas (but I highly recommend sports drinks because they not only have sodium but other electrolytes like potassium). There is a certain type of psychological disorder where people consume large amounts of water. These persons are at frequent risk for hyponatremia.

It can also be caused by certain blood pressure medications (diuretics) can induce hyponatremia. Here’s the really scary thing regarding this, you might be on the diuretic for Years and never have an issue, but then one day, with no warning, it causes you to develop hyponatremia.

My GP described an incidence of this with one of his older patients. The person had been taking a certain diuretic blood pressure medication for over TEN years, and then one day developed severe hyponatremia!!! The only determined cause was her BP medication.

There is strong incidence of persons who have heart failure, kidney disease, and liver disease to develop low sodium.

The elderly and the very young are also at great risk. Isn’t that the case with everything?

(Addendum: I recently found out from my local children’s hospital that it is pretty common and devastating for infants. They develop hyponatremia because in this depressed economy families are watering down formula to conserve costs. The watering down effects impacts the electrolyte balances in infants and leads to hyponatremia. It was mentioned that this is a huge issues in Kentucky. I’ve raised two children. One of which received infants formula, I had no idea that this was potential threat. I am so relieved that I was never in the position where I had to dilute formula to save money, but I am certain this occurs a lot. The representative also warned that if an infant or child developed hyponatremia, they were at greater risk for death or brain damage. It was not stated if this was because of CPM/EPM or hyponatremia itself. If you or someone you loved is in this situation, please inform them of this risk! ).

So, at this point, you might be wondering who DOESN’T have a high risk for hyponatremia? That is precisely my point. Hyponatermia is very common, and it is absolutely necessary for people to become more aware of this condition and the proper treatment.

If you are in one of the higher risk categories, take a few minutes to read about the symptoms, how it should be treated, and then pass it on. Make other people aware of it, and SAVE A LIFE 🙂

Some basic symptoms of hyponatremia: Muscle cramps, severe headache, nausea, fatigue, vomiting, confusion, delirium, hallucinations, and coma.

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