December | 2011 | Hyponatremia and Central Pontine Myelinolysis

31 Dec 2011

What is CPM/EPM?

If you’re reading this, you or someone you love has probably been diagnosed with CPM/EPM. First of all, I’m sorry. My heart goes out to you or your loved one that’s inflicted with this disorder.

Right now, you’re probably confused, angry, depressed, and scared. You have no idea what’s going on, except your body isn’t right. You aren’t right. You might feel crazy because things that you experience can vary so dramatically. Let me offer you this solace; you are not alone.

You want answers, and you can’t find them. You want a support group, but there isn’t one.

Your doctors don’t have many answers either, or you’ll get conflicting information from the different doctors you see.

The information you find online is repetitive, but not very informative. Trust me. I will go through dozens of websites, and the information is verbatim from what was posted by the National Institute of Health.

Right now, you might feel that the answers to your questions are coming from a magic 8 ball.

I hope to give you more depth information, but I want to stress to you that there is no definitive answer with CPM/EPM. It is rare. There are not long term case studies. You will find research papers that have gone through hospital records to study CPM/EPM cases because it is difficult to find more than just a few current cases in a state during a specific period of time.

There is not a lot of research that has been done on it at all, but the long term studies that have been used are done by going through hospital records. I find those studies are vague.

How it impacts you, may not be the same as how it impacts me.

I know it doesn’t sound too promising. I hope to give you more direction, more help, more answers, but I can’t say that you will fit into everything I post. You may. You may not. There is no absolute.

Ok, so what has happened to you or your loved one:

Lesions have developed in your (their) brain. It’s caused extensive neurological and functional damage.

Why has this happened:

The majority of CPM/EPM cases are caused by the too rapid correction of hyponatremia; however, there are a handful of other people that develop it outside of this category. I’m going to try stay focused on the majority and over time, I hope to cover some of the reasons outside of hyponatremia for developing it.

What can you do to fix it:

There is no definitive treatment for CPM/EPM. There have been studies where they have tried steroids to reverse the effects of the damage or prevent new damage from occuring, but this was inconclusive.

Honestly, I would recommend trying it. It can not harm you, and it might help, but again that treatment is inconclusive. Other than that, the treatment is supportive.

What does that mean? It means, they will do everything they can to prevent you from dying, and they will minimize your symptoms.

So, let me explain a little bit more in detail what’s happened to your brain. (I’ve explained a little bit of this previously in my posts on hyponatremia, so if you’re followin my posts, please bear with me).

When a person’s sodium levels drop below normal, certain cells experience a shift in water. The major system effected by this shift is the nervous system. Your brain cells begin to swell from fluid. This type of swelling happens in both acute and chronic hyponatremia.

In acute hyponatremia, the cells swell so quickly that it can lead to rupture of the brain stem and significant cerebral swelling. This type of hyponatremia produces immediate dangers and has a significant risk for death, coma, and/or seizures.

If a person has chronic hyponatremia, the drop in blood sodium happens slowly. Most people will associate chronic as meaning in months or years, but this isn’t what it means in the case of hyponatremia. Chronic in regards to hyponatremia means approximately 48 hours to several weeks.

If a person has the chronic form of hyponatremia, then their brain cells also swell, but the swelling is more gradual, and their body has time to adapt. This is the reason why persons with chronic hyponatremia, despite feeling sick, will be more alert and less severly symptomatic than a person with acute. They are at less risk for immediate death, but they are at greater risk for CPM/EPM if the treatment isn’t performed correctly.

If a person has chronic hyponatremia, they still have brain cell swelling.

If the sodium levels are raised too quickly, the water “rushes” from the brain cells, and this causes the cells that form the myelin sheath and cells that produce myelin to be destroyed or damaged.

This is a very generic description of what happens, and there is debate on how the damage occurs, but this is the most widely used description.

Myelin is a layer of cells that coat the axons of nerve cells. It’s considered a fatty sheath that insulates the nerve cell and allows for rapid conduction of nerve impulses.

Most people will explain myelin as being like the sheath that surrounds electical wires. This is somewhat accurate. I think the most important point regarding that analogy remains true: if the electrical cord wears, the connection becomes bad. The item may or may not work after that or may work intermittently.

Due to the whitish appearance of axons covered in myelin, areas of the brain that contain myelin are called white matter. These specific areas of the brain tend to be damaged with the rapid correction of sodium.

The damage can not be detected through a CT scan. It can be detected by MRI.

The areas of damage will show up as a brighter white area on the MRI scan in a T2 scan. Contrast dye does not really make the lesions more distinguishable, but most doctors will order the MRI with contrast. In a T1 scan, the lesions show as hypotense. These are the same lesions, it just shows up differently depending on the scan that was used.

If the pontine area is abnormal, the condition is called central pontine myelinolysis. If areas outside of the pontine area are affected, the condition is called extrapontine myelinolysis.

The injury may be limited to only the pontine area. It may be limited to areas outside the pontine only, or you may have both pontine and extrapontine injuries.

Let me stress, these are very generic descriptions and in the following posts, I will go into great detail regarding what all of this means, and what the research I’ve found says regarding these topics.

Please consider this post as a savory smell of the roast that is in the oven. It’s not even a taste of the information that will be exposed in future posts.

I hope this post finds you in good health.

Posted in Central Pontine Myelinolysis/ Extrapontine Myelinolysis

31 Dec 2011

To summarize:

Ok, I know I’ve covered a LOT of information over the past few weeks regarding hyponatremia.

There is so much information and it is very complex that it’s hard to not get confused and lost in reading it, so I’m going to try to summarize what I’ve discussed so far.

There at least five categories of hyponatremia: Hypovalemic, Euvolemic, Hypervolemic, Redistributive, and Pseudohyponatrmia.

The most commonly impacted people:

Infants due to diluted formula

Alcoholics

athletes (especially marathon runners)

Those who have liver cancer, liver damage, chirossis of the liver.

The elderly (usually due to malnutrition and dehydration)

Brain injuries, brain tumors

Transplant patients

Burn patients

Person’s who are receiving chemotherapy

Person’s with kidney disease and those who receive dialysis

Person’s who take certain medications like diuretics and anti depressants.

AID’s patients

Person’s who have pneumonia or flu

Anorexics and bulemics.

I’m sure I’m leaving about a dozen other groups affected, but you get the picture. It’s pretty common. Approximately, 1.5 million people are treated for it each year, and that’s probably a low number because I do not believe it includes persons who develop it while being treated for other conditions and develop hyponatremia as a secondary illness. I’ll try to find more information on that in the future.

Hyponatremia is extremely dangerous. If your blood sodium levels drop very quickly in a 24 to 48 hour period (acute hyponatremia), your brainstem can herniate and/or your brain swells. This can lead to seizures, comas, and of course death.

If you develop chronic hyponatremia, (when your sodium levels drop over a period of 2 days to several weeks) you are less likely to have brain swelling or brainstem herniation, but you become at extremely great risk for developing Central Pontine Myelinolysis or Extrapontine myelinolysis.

The proper treatment is an absolute must. General IV fluids should be avoided if hyponatremia is suspected. Instead, an IV of saline solution ranging from .9% to 3% saline should be used. In some cases, fluid restriction will correct hyponatremia.

A person should have their sodium levels checked a minimum of every 2 to 4 hours.

If they are uncertain of the type of hyponatremia you have, then an MRI should be used to determine if there is cerebral swelling (swelling of the brain) or brainstem swelling. If there’s swelling present on the MRI, then you most likely have an acute form of hyponatremia.

If you have an acute form of hyponatremia, you are at a high risk of dying from immediate brain injury. Because of the risk, it is necessary to raise your blood sodium levels quickly to a safe level. It should be raised 2 to 4 mmol/L in 1 to 2 hours. However, once symptoms improve, the treatment should be halted for at least 24 to 48 hours. No matter what, levels should not be raised more than 15 mmol in 24 hours, in regards to acute hyponatremia.

If a person has chronic hyponatremia, they do not usually display the same severe symptoms. They usually feel sick. They might experience fatigue, nausea, have a severe headache, dizziness, loss of consciousness, delirium, etc. They do not usually have seizures, coma, or death. They are usually more alert compared to a person with acute hyponatremia.

The treatment for someone with chronic hyponatremia is signficantly different from acute hyponatremia because their sodium level MUST be raised slowly. It should be raised no more than .5 to 1 mmol/ L per hour. It should not be raised more than 8 to 10 mmol in a 24 hour period. Some even caution that it should be raised no more than 6 to 8 mmol per 24 hours. If it is raised faster than this, a person can develop Central Pontine Myelinolysis or Extrapontine Myelinolysis.

Expect to be in the ICU for 4 to 5 days at the very least if the treatment is being done correctly.

A person should NOT be given oral prescription medications along with IV saline solutions. The treatment should be fluid restriction if the hyponatremia is not severe or if it is a chronic form. If the fluid restriction does not work (with the chronic form), than a .9% solution should be started. If they have the acute form, then the 3% solution should be used first. Again, if the sodium levels begin to rise to a point where the symptoms begin to subside, then the treatments should be discontinued to see how the body responds.

If a person’s body is not responding to fluid restriction or IV saline solutions, then a person should be given the oral prescription medications. THEY SHOULD NOT BE GIVEN AT THE SAME TIME AS IV SALINE SOLUTIONS. IT SHOULD BE ONE OR THE OTHER–NOT BOTH.

I really think these are the most important aspects to hyponatremia. Please feel free to contact me if you have any questions or want more information over any of the topics I’ve posted so far. If you find out any relevant information regarding hyponatremia that you think I should include, PLEASE contact me or leave a message here. I REALLY appreciate your help.

Thank you for your support!

Posted in What is Hyponatremia?, Your Hyponatremia/CPM story: and tagged Central pontine myelinolysis, Hyponatremia

26 Dec 2011

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:

http://emedicine.medscape.com/article/767624-overview

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.

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Hyponatremia, Vasopressin

23 Dec 2011

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:

http://pubs.niaaa.nih.gov/publications/arh21-1/84.pdf

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

http://alcalc.oxfordjournals.org/content/35/6/612.full

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.

Posted in What is Hyponatremia? and tagged Alcoholism, Hyponatremia, Hypovolemia, Syndrome of inappropriate antidiuretic hormone hypersecretion, Vasopressin

23 Dec 2011

Hyponatremia: Other’s personal accounts and blogs

I want to encourage you to post your experience or notify me of blogs that you might find in regards to hyponatremia.

There is not much research regarding hyponatremia, especially when you compare it to other diseases and disorders. There is far fewer studies in regards to CPM/EPM. In order to get a better idea how CPM/EPM impacts people, both short term and long term. Your personal testimony is essential in getting awarness for this cause.

Ironically, I am including the link of a research scientist who was afflicted with CPM after a bought of hyponatremia. She developed hyponatremia after running the Vermont 100.

http://www.wvmtr.org/hyponatremia.htm

Please post them or email them to me, or if you have a problem getting them to post here, let me know. I am truly a blogging novice, so I am learning as I go. If you want to share your story here, I will do everything I can to make that happen.

Posted in Your Hyponatremia/CPM story: and tagged Central pontine myelinolysis, Hyponatremia

21 Dec 2011

Hyponatremia: more on treatment

***I wanted to emphasize that this post contains a lot of my non professional opinion. I am not completely ignorant regarding human physiology, but I am not a medical doctor or physiology professor. I do not recommend that my opinion be used as a professional opinion, but please feel free to discuss them with your doctor or other medical professional.*****

At times, it’s hard to figure out exactly how to start the next topic. It’s kind of like when you’re about to enter a lake in which you know the water is icy cold. Do you jump in head first? Do you walk in and try to slowly adjust? Do you just change your mind altogether and wait for warmer water?

I don’t think there’s a right answer.

Writing a blog is kind of like that. It’s hard to know how to approach the next topic. I guess with time, it will become easier.

I really wanted to address how important it is once you’ve developed hyponatremia that the correction be made unbelievably slowly.

Every doctor and every nurse that cared for me in the ICU made this abundantly clear. They all had the same consensus, if we raise your sodium levels too quickly, you can die, go into a coma, develop brain damage.

I have an Aunt who is a doctor, and she emphasized the importance that it be raised slowly. It seemed like it was pretty universal that it was going to take a long time, and if they didn’t do it correctly, I could be universally screwed.

So, how is it that everyone knew how important it was, warned against its rapid correction, but it still happened?

For me, it was a series of errors. I hope these posts prevent anyone from going through the same fate.

However, I have read over the course of weeks that there is a division between some on how the treatment should progress.

There are some that believe once your sodium drops, your life is in danger and corrections need to be made to adjust your levels to a safe zone, slowly but as quickly as possible. In other words, they should raise your levels the maximum amount allowed per every 24 hours.

However, others believe that it is safer to let a person stay in a hyponatremic state, as long as the person isn’t dying. Now, that’s a tricky situation because if your sodium levels are below 135, you risk going into a coma and dying. There’s no guarantee.

The professionals that believe your levels should be maintained at the hyponatremic state, argue that the brain cells are already swollen. If you raise the sodium at this point, it is believed that rapid fluctuations in sodium cause the myelin damage in CPM/EPM, so if you keep it at a hyponatremic state for an extended period (maybe a few days), then the brain cells have time to adjust naturally.Fluid flows out of the cells, and it becomes less of an issue with demyelination when the sodium levels are corrected.

That said, there aren’t studies being done to prove or disprove these ideas. It really is kind of like playing Russian roulette, but there’s no one who wants to risk pulling that trigger with the stakes literally being a person’s life. There’s also not a lot of funding going towards animal studies for this disorder.

My idea (which has absolutely no medical validity): put the person into a medically induced coma, lower their body temperature to hypothermia for several days. Then, slowly raise the sodium, and then their body temperature.

Here’s my reasoning: the body does not respond well to rapid fluctuations of any kind. In patients who have experienced brain trauma, the patients have been placed in medically induced comas and their body temperature has been lowered. This has had success in reducing the amount of brain damage a person experiences.

I believe these principles can be applied to brain damage that is caused by fluctuations in sodium. The body’s system all slow in a hypothermic state. This includes the reactions experienced in the brain. If you raise the sodium levels before returning the body to a normal rate, you might be able to prevent the rapid fluctuations in cells.

My ideas are probably improbable, so I would side with the professionals who recommend keeping a person in a state of hyponatremia for several days before attempting to raise their sodium levels to normal.

In order to do this in a more safe manner, I would recommend placing the person in a medically induced coma vs. hoping the person does fall into a coma because of the hyponatremia.

The studies that have shown a person who has a stabilized blood sodium level (their levels aren’t dropping lower, but aren’t rising steadily), is less likely to develop CPM/EPM.

I think this post might raise more questions than answers, but that tends to happen in medicine. I hope you will be able to make an informed decision on how your care for hyponatremia is managed.

(Addendum: This is extremely important, so I will post it again on a separate page of it’s own. It’s actually been reported in several case studies that there has been a huge success in preventing CPM/EPM, AFTER the sodium levels have been raised too QUICKLY, then the sodium levels should be dropped back to the 120 mmol/L level(hyponatremic state) within 5 days of the rapid increase. This has been shown extremely successful in preventing CPM/EPM. However, it means that you or your caregiver need to be aware of the rises in your sodium levels because your doctor might not admit to incorrectly raising the levels).

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Hyponatremia

19 Dec 2011

Back to treatments:

I hope you found the statistics in the previous post as unbelievable as I did. I really need to explore the website in depth to figure out what it all means. The information on its own is mind blowing, but the information isn’t entirely clear.

For instance, is the data for all people who are hospitalized for hyponatremia, as well as those who develop it while in the hospital for other issues. If you’ve read my previous posts, you understand that there is a high incidence for people to develop hyponatremia if they are hospitalized for longer than a day. It is also extremely common for patients who are hospitalized for burns, complications of chemotherapy, recovering from brain surgery, etc. The statistics I found did not acknowledge how comprehensive it is. If I am correct and it only includes people being hospitalized for hyponatremia on arrival, then there could be as many as 3 million people per year that develop it.

The statistics that I have at this time are only for US hospitals, and if I am correct, then close to 10% of the US populations develops hyponatremia each year. WOW!

So, I believe this makes it even more important to spread the word regarding hyponatremia and how to treat it.

That leads me back to this post.

The treatment plans that I explained in the previous post is fundamental for everyone who develops hyponatremia, but I will go into more detail about why and how specific types of disorders lead to hyponatremia.

Athletes have a high incidence of developing hyponatremia, especially those who experience long lasting, strenuous activities, like marathon runners, dancers, tri-athletes. Now, this really hits home for me. My son (15) has been playing football since he was in first grade. Every year, he goes out on the field in the unbearable summer heat and runs at least a mile per practice. The first 2 weeks is called conditioning, and they spend most of their time running.

I have always “pushed” him to drink water both before and after his practices. When the summer reaches its hottest days, my son is wearing about 5lbs in pads and running for several hours. He is always drenched in sweat.

Sweat is comprised of a considerable amount of sodium. In your bodies, effort to lower its core temperature, it produces a significant amount of sweat. After significant sweating, its not uncommon for a person to develop a thin layer of salt over their body. It’s the reason why sweat stings your eyes and why it tastes so salty.

Now, here is the danger. I’ve always pushed water and lots of it. During the hottest days of summer, the football players stop every fifteen minutes for water breaks. These players are already releasing a large amount of sodium through their sweat, and when they consume large sums of water in addition, it further dilutes the sodium in their blood!

They symptoms for hyponatremia are the same for heat stroke: nausea, vomiting, headache, passing out, cramps, fatigue, etc. Most hospitals will assume that a person has heat stroke if they have been participating in sports. They will start treatment with IV fluids, and this could kill the person rapidly. It wouldn’t be until the ER gets the patient’s electrolyte panel back before they realize the error; by that time, the IV fluids have already depleted the blood sodium levels further. This has a disasterous impact. Ultimately, it could cause death.

In one study I found, the paper urged that doctors NOT administer IV fluids, until after the blood work is reviewed. However, this creates the ultimate dilemma: if the patient actually has heat stroke, then IV fluids are essential to prevent the person from dying. If the person, has hyponatremia then the IV fluids could kill the person.

So, what does this mean? It seems it’s a 50/50 shot. The answer is in prevention! It should be made mandatory that all children participating in highschool activities be provided a sports drink, like Gatorade/Poweraide, Vitamin Water, etc. Secondly, the sports drink that’s provided should contain sodium.

If there isn’t access to sports drinks, then the person should consume salt tablets over the counter. The product I have located is Thermotabs. They are available at Drugdepot.com. I would highly recommend that athletes etc. use these, especially prior to and during intense workouts.

People have developed a caution regarding salt. They consume low salt/no salt products. I can only wonder if this is part of the reason of why hyponatremia cases continue to rise. There has been a steady increase since 1999.

In conclusion, I believe that a person should listen to their body and to quote a famous sports drink company, “Obey your thirst”. If you are thirsty, drink. If you aren’t, then don’t. However, be careful of what you drink. Don’t consume large sums of water while working out. It could kill you.

Posted in What is Hyponatremia? and tagged Hyponatremia

16 Dec 2011

Hyponatremia: YOU’LL WANT TO READ THIS. Statistics.

I have been trying to locate statistics for hyponatremia for months. I have searched hundreds of websites. I have tried contacting local hospitals. FINALLY, I’ve had a breakthrough, and it’s a HUGE breakthrough.

There is a research tool funded by the government and due to the Freedom of Information Act hospitals must post their annual diagnostic statistics.

I’m a novice at researching facts on this website, so as I am able to locate more information, I will be certain to post it. Without further adieu, here is the golden nugget for hyponatremia.

First, let me explain that hyponatremia is coded as hyponatremia/and or Hyposmolality. The ICD-9-CM code for this is 276.1. This is the medical billing code used by doctors and hospitals to receive payment from insurance companies or medicaid/medicare. Please use the following link to confirm the diagnositc codes:

http://www.icd9data.com/2011/Volume1/240-279/270-279/276/default.htm

To make this a little more accesible, I will simply copy and paste the essential information from the above site:

2011 ICD-9-CM Diagnosis Code 276.1convert to ICD-10-CM

Hyposmolality and/or hyponatremia

abnormally low sodium levels in the blood; salt depletion.
Abnormally low blood sodium level.
Hypernatremia; lower than normal levels of sodium in the circulating blood.

Let me point out that the above information, contains an error. Hypernatremia is not LOWER than normal sodium levels. I believe this is simply an editing error and that the above description should read: Hyponatremia; lower than normal levels of sodium in the circulating blood. I believe this is a logical deduction considering the title of the code is a description of hyposmolality and/or hyponatremia, not hypernatremia. I would also like to reassure you that hyposmolality is another way to describe hyponatremia.

There are further codes that describe other electrolytic disorders, like hyperkalemia (high potassium), etc.

That said, check out the following information from this link:

http://hcupnet.ahrq.gov/HCUPnet.jsp

This link has the motherload for statistics for hyponatremia, and it is astounding!

The following is taken directly from the above link:

HCUPnet provides trend information for the 17 year period: 1993-2009

Number of discharges

ICD-9-CM all-listed diagnosis code and name		1993	1994	1995	1996	1997	1998	1999	2000	2001	2002	2003	2004	2005	2006	2007	2008	2009
276.1	Hyposmolality	1,035,284	1,114,170	1,100,355	1,011,519	975,253	922,323	773,223	753,530	905,743	923,473	1,005,420	1,105,431	1,239,144	1,265,353	1,362,216	1,602,836	1,735,847

YES, you are reading that right. In most years, more than a MILLION people per year are diagnosed with hyponatremia. WOW! I would also like to point out that the incidence of hyponatremia has been STEADILY increasing since 1999! I think this speaks volumes for why hyponatremia/CPM and EPM should be a household name.

The following are the maximum amount of error that’s possible each year with this diagnosis. What does that mean?

It means that the statistics, for example, in 2009 has a possible range in error of being a maximum of 1,788,305 and a minimum of
1,683,389. Each year, there is a maximum number of errors that can positively or negatively impact the reported data. The following table documents the number of possible errors. Please feel free to post any questions associated with this.

Number of discharges – Standard Errors

ICD-9-CM all-listed diagnosis code and name		1993	1994	1995	1996	1997	1998	1999	2000	2001	2002	2003	2004	2005	2006	2007	2008	2009
276.1	Hyposmolality	35,104	36,817	37,056	36,746	36,207	35,803	20,986	19,120	21,021	22,157	23,650	27,058	34,350	34,636	31,387	44,683	52,458

The next description is the how they determined the above chart regarding possible errors.

Weighted national estimates from HCUP Nationwide Inpatient Sample (NIS), Agency for Healthcare Research and Quality (AHRQ), based on data collected by individual States and provided to AHRQ by the States. Statistics based on estimates with a relative standard error (standard error / weighted estimate) greater than 0.30 or with standard error = 0 in the nationwide statistics (NIS, NEDS, and KID) are not reliable. These statistics are suppressed and are designated with an asterisk (*). The estimates of standard errors in HCUPnet were calculated using SUDAAN software. These estimates may differ slightly if other software packages are used to calculate variances.

Bottom Line:

There are an extremely large number of people being hospitalized each year for hyponatremia. This number is on the rise, and it is of the utmost importance to spread the facts about hyponatremia, the proper treatment and what occurs if it is not treated properly (CPM/EPM).

Please continue to read this blog. Forward the information to friends and family. Post links to your FaceBook pages, Twitter, etc. Please, help spread the word and save people’s lives.

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Freedom of information legislation, Hyponatremia, International Statistical Classification of Diseases and Related Health Problems

15 Dec 2011

Hyponatremia: treatments

This topic might take several days to compose because there is so so much to discuss regarding this.

I’m sure it’s not surprising to most that each type of cause of low sodium is unique, so the treatments will be unique as well. This is true to an extent, but I have a few universal key facts for everyone who is being treated for low sodium.

Please take note of these KEY Treatment facts, and then look at your specific cause of low sodium for additional treatment information.

1.) It is absolutely imperative that you limit your intake of water once you develop low sodium. Increasing your water levels while you are experiencing low blood sodium will further DECREASE/DILUTE your blood sodium. If your sodium levels increase with just fluid restriction, then there should be no further treatment needed.

I believe it is absolutely necessary to listen to your body while being treated for low sodium, so if you are on a fluid restriction, but at some point start to develop extreme thirst (not dry mouth but thirst), then you should listen to your body and consume more fluids. However, in some cases, there is a psychological disorder that makes a person drink extreme amounts of water, so in some cases, this would not be logical.

Fluid restrictions are common when being treated for hyponatremia, but my suggestion is to listen to your body if you develop thirst is my opinion. It’s not a medical fact or medical suggestion. You will probably find the medical community does not agree.

Let me stress that fluids that do not contain sodium are extremely dangerous during this period, but consuming higher sodium fluids are fine, i.e. chicken or beef broths.

My opinion:

Might I even suggest diluting something like a fleet laxative. Fleet oral laxatives work because they are extremely high in sodium. Your body dumps EXCESS sodium through urine and the GI tract, and where sodium goes water follows. Typically, this causes the liquid stools that GI doctors require for a colonoscopy. However, if your body needs sodium, it will absorb the sodium through the GI tract and release the sodium it doesn’t need.

I have no medical research to back up my idea that using fleet or other sodium solutions will increase your sodium levels more effectively than IV saline solution. I will try to research this more and contact my GI doctors for their opinions in the future.

2.) IV saline of 3% is the typical starting treatment for hyponatremia. This is typically done in conjunction with water restriction. However, in some medical circles, it is believed that ONLY fluid restriction should be used. This is dependent upon the type of hyponatremia you have, as well as your starting sodium.

3.) A person’s blood sodium levels should be evaluated every 2 to 4 hours to prevent a rapid rise in sodium. (This should be done regardless of your starting sodium levels).

A rapid in rise of blood sodium levels can be catastrophic and lead to CPM/EPM, or death. I will discuss this topic in the future.

4.) If a person’s sodium level stabilizes while being treated with an IV saline solution of 3%, no further treatment should be administered. In this case, stabilizing means that the levels do not decrease further, but remains the same or increases slightly over a 24 hour period.

5.) Prescription drugs like Samsca (tolvaptan) should NOT be used at the same time IV saline solutions are being administered. It is ABSOLUTELY dangerous to use IV saline solutions and most prescription drugs TOGETHER to treat hyponatremia. If a person you know or you are being treated for hyponatremia, be certain that you check the medications you are being given. The contradictions for these medications are typically found online.

A few of the oral prescription drugs used to treat hyponatremia:

Samsca Oral

sodium chloride Oral

tolvaptan Oral

5.) A 6 to 8 mmol/L increase in blood sodium concentration per every 24 hour period is the MOST a person’s sodium should be raised during a 24 hour period. ANYTHING greater than 6 to 8 mmol/L in a 24 hour consecutive frame is considered DANGEROUS!!! Let me stress that it is a 24 hour consecutive time frame that needs to be considered. Do not consider a CALENDAR day as the 24 hour period. (Some studies suggested that an 10 to 12 mmol/L increase was acceptable, but most doctors now agree that 6 to 8 is the highest it should rise.) Let me stress: THE MOST your sodium level should rise is 6 to 8 mmol/L in a 24 hour period. Consider this point the RED zone. That means it is at this point that you are on the borderline of causing brain injury. The goal should be NOT to reach this RED zone because once your surpass these levels (which can be VERY difficult to control), you will be at high risk for brain injury.

Let me define how to classify a 24 hour period; if your levels were checked between 12 am, Jan 1st and 12 am Jan 2nd and your levels were only raised 5mmol/L, that is fine, but between 2pm Jan. 1st and Jan 2nd, your levels were raised 10 mmol/L, your levels were raised TOO much for a 24 hour consecutive period. A rapid correction of blood sodium levels can cause brain damage and/or death.

I cannot think of any additional absolutes for the treatment for hyponatremia. These are the key treatment facts.

Please be on guard if you are being treated for this condition. I will post tomorrow more on what I think are important ideas on the treatments for hyponatremia that are opinion based, but I will include additional facts regarding specific treatments for the different causes of hyponatremia.

Please, pass this information forward. It might save your life or someone else’s.

Posted in What is Hyponatremia? and tagged low sodium, sodium levels

15 Dec 2011

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 PubMed, http://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:

http://www.ux1.eiu.edu/~cfje/4900EN/GSSI-88-hyponatremia.pdf

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?!!

http://www.nejm.org/doi/full/10.1056/NEJMoa043901

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

http://www.ncbi.nlm.nih.gov/pubmed/11828223

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.

http://www.psychweekly.com/aspx/article/articledetail.aspx?articleid=1302

The risk in the Elderly:

http://www.inaactamedica.org/archives/2011/21979280.pdf

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

http://mdmag.hcplive.com/publications/hospital-medicine/2011/August-2011/Hyponatremia-A-Hospitalists-Perspective

Hyponatremia and it’s impact on children:

http://www.indianpediatrics.net/dec2000/dec-1348-1353.htm

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

http://alcalc.oxfordjournals.org/content/35/6/612.full

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

http://findarticles.com/p/articles/mi_m0847/is_n3_v13/ai_8193360/

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

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Hyponatremia, PubMed, Tufts University School of Medicine, University of Pittsburgh, Vasopressin

13 Dec 2011

2 Comments

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!!

Posted in What is Hyponatremia? and tagged Diabetes mellitus, Hyponatremia, Pituitary gland, Vasopressin

12 Dec 2011

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.

Posted in What is Hyponatremia? and tagged Central pontine myelinolysis, Hyponatremia, Vasopressin, Water intoxication

11 Dec 2011

Hyponatremia: More Facts

Hyponatremia is the most common metabolic disorder. This fact comes from PubMed and other research articles.

What is Hyponatremia? It is blood sodium levels of 135 mEq/L or less. The normal range for blood sodium is 135 to 145 mEq/L.

It sounds pretty innocent in nature. Just consume a little more salt, and you should be fine, right?

It really isn’t that simple. Once your sodium levels drops below 135mEq/L, your brain cells begin to swell with fluid. The swelling of your brain cells causes severe headache, nausea, fatigue, vomiting, confusion, delirium, hallucinations, and coma. Of course, it can also lead to death. One of the other symptoms it causes is cramping. Sodium is an important electrolyte in the regulation of muscle contraction, so when it drops below normal your muscles experience hyper contractility.

So that sounds a little bit more scary, right? No one wants brain swelling.

That’s true, but the really scary thing is how frequently it occurs and who it effects.

One study showed that 38% of hospital admissions were due to hyponatremia. You might not be great with math, but that’s almost half. That figure was the number of people being sent to the hospital due to hyponatremia. An even scarier number, is that 38% of patients who were hospitalized experienced hyponatremia if their hospital stay was longer than ONE day. This study was found on PubMed and was done at St. Michael’s Hospital in Toronto, Canada. The study was performed by the University of Toledo.

In the United States, there are by far, fewer studies being performed for hyponatremia, and the consequences of improper treatment. The main reason, in my opinion, is because the consequences of improper treatment can be significant brain damage, coma, death and/or a permanent paralyzed state known as, locked-in syndrome. This injury is known as CPM/EPM, and it is 100% caused by medical malpractice. (Okay, I have to add an addendum to this. In most cases, CPM/EPM is caused by the error of raising sodium levels too quickly; however, there have been additional studies that suggest that CPM/EPM can be associated with disorders other than hyponatremia. It is known to happen without hyponatremia in cases of alcoholism, liver transplants, certain lung cancer treatments, leukemia, brain injuries and other transplants. The information regarding these other causes of CPM/EPM are fairly uncommon (except in the case of alcoholics which can be as high as 30% incidence of spontaneous causal).

CPM/EPM is caused when a person’s sodium levels are raised too quickly. This drastic increase causes the previous swollen brain cells to rapidly shrink. The shrinking causes neurons (nerve cells) to be stripped of their myelin.

So, this is the second post that I’ve mentioned myelin, and you may or may not understand the significance of it, so let me explain a little more about it.

Myelin is a fatty white sheath surrounding the axons of nerve cells. It coats the cells. Compare it to an electrical cord. Because my parent’s had an ancient vacuum cleaner, I’m going to use it in this description.

My parent’s Kirby vacuum cleaner was purchased when they were first married. Being the devious and creative children that my brothers and I were, we played extensively with the vacuum cleaner. We would unwind the cord and pretend that it was a rope which we used to cross canyons. We used it as a whip, as a lasso, as a tightrope, a jump rope. The possibilities were endless. Is it any real big surprise then, that this poor cord began to fray and wear. In certain places, the plastic coating surrounding the conducting wires became completely worn away. I actually think my older brother would use the vacuum cord as a chew “toy”. Of course, this happened only when it was unplugged, but you get the idea.

Eventually, the frays in the cord made it difficult (probably even a bit dangerous) to operate. In order to get a current from the electrical outlet to the vacuum motor, the cord would have to be kinked in certain ways. Some times this was effective and the vacuum would work. Other times, the only thing that would happen is you would receive a healthy shock.

Myelin is the in much regards comparable to the sheath that insulates the wires to the vacuum. It allows the current in the wires to travel unmolested from the electrical outlet to the motor. When the cord became damaged, the current could travel to the motor or it could take an alternate path to the hand of the user. Myelin allows the current from the cell body (consider it the electrical outlet) of a neuron to the terminal ends (called axon terminals) rapidly and in the correct direction. There are millions of cells in your brain that don’t have myelin (grey matter). These cells function perfectly fine without this coating. However, the signals that travel these cells move at a considerably slower rate.

If a nerve cell has a myelin sheath, the transmission of signals is more rapid than those without myelin. This might explain why when the myelin sheath is injured, such as in Parkinson’s Disease and CPM/EPM, a person can experience halted, jerky movements.

In closing for today, CPM/EPM is the disorder that is demyelination caused by the rapid swelling and shrinking of brain cells. The rapid swelling occurs because the sodium drops below normal. The rapid shrinking occurs when the blood sodium levels are increased too quickly. The impact this has is hundreds of thousands of short circuits in the wiring of the brain.

I hope this is understandable. Please leave posts with questions, and I will try my best to answer them.

Posted in What is Hyponatremia? and tagged Hyponatremia, Myelin, PubMed, University of Toledo

Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the month “December, 2011”