Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Hyponatremia”

Getting a diagnosis:

Please bear with me tonight, I had my wisdom teeth removed today, so I’m taking pain killers. Let’s just say, I’m a bit off my game.

Most people who are treated for hyponatremia are already in the hospital for a secondary issue, like burns or liver transplants, etc. I believe persons who are being treated for other conditions are at a higher risk for a delay in diagnosis for hyponatremia. This would make it most likely for them to develop chronic hyponatremia (chronic, meaning longer than 48 hours, up to a few weeks). This will put them at higher risk for developing CPM/EPM.

That said, it is harder to diagnose these individuals with CPM/EPM because they are already ill. Most will be experiencing issues with nausea, headaches, vomiting, etc. They may even already be in a coma, so the symptoms will be attributed to other issues.

If you’re already in the hospital with a major disease, injury, or disorder and then develop hyponatremia followed by CPM/EPM, you will probably have significant damage. To be honest, you probably won’t make it.

If you do live through those major health issues, you will be lucky to get a diagnosis of CPM/EPM. Here’s why: in most cases, if you are already in the hospital for something like severe burns, to help manage the pain, the hospital will sometimes put you into a medically induced coma. If you are in a coma, it is difficult for the hospital to know if you are experiencing neurological issues.

When they awaken you from the coma, they might deduce that the issues you are having are due to the induced coma. If you have cancer, they might believe the issues (nausea, headache, balance issues) are due to the cancer especially if you have something like a brain tumor and especially if you are having chemotherapy treatments.

Depending on your doctor’s expertise and the symptoms you present with, you may not get a diagnosis of CPM/EPM right away.

CPM/EPM can appear on a MRI as early as two to three days; however, it may not appear on a MRI for up to two to four weeks. In less severe cases of CPM/EPM, your symptoms can begin to improve within a week after the injury. This makes it even more difficult to detect because doctors are even more likely to attribute the symptoms to the primary reason for hospitalization, so they don’t look for it.

To complicate things further, most individuals will begin to experience a disappearance of the lesions on the MRI as early as 4 to 6 weeks. In most cases, the lesions can completely disappear in 4 to 6 months. Despite the healing of the lesions, symptoms may or may not approve accordingly. In most research papers that I read, most lesions will disappear but a person will have ongoing issues with dystonia, speech issues, cognitive and learning issues, tremors, etc. Generally, the symptoms that remain after the lesions have disappeared are related to motor functions and cognitive functions. There can also be on going issues with behavioral and psychological deficits.

This leads to a misdiagnosis, or you may not ever get a diagnosis.

So, what do you do?

Get your medical records. Look for hyponatremia (keep in mind that CPM/EPM does not always occur with hyponatremia), but it is most common with it.

You can also request a MRI. A really good neurologist and/or radiologist can see something called sequelae. Basically, this is, for lack for better words, scar tissue. It is usually very difficult to see in our current scans. So, if you really believe CPM/EPM is responsible for your issues, you might have to see several neurologists or radiologists.

Some doctors will diagnose you based on symptoms and your clinical history alone.

For arguments sake, let’s say you really don’t have CPM/EPM. If you have symptoms that aren’t typical for the disorders or diseases that you experienced, you should pursue getting answers anyway.

I’ve been a patient for more than 8 years. I’ve been diagnosed with other health issues/ disorders before I was injured from CPM/EPM. From past experience, it is common for doctors to attribute any new symptoms that you may have to the previous diagnosis. Basically, they think that since you have one disease or disorder that you will not be unlucky enough to develop another. They might also attribute these new symptoms to being a psychological issue. They will state that this new issue is due to the stress of having a previous illness.

Follow your gut instinct! Only you know what you are going through. If you keep getting the run around from one doctor, find a new one…BUT whatever you do, do NOT tell this new doctor that he is your second opinion. Trust me, I know. It is hard to find a doctor who will go against what another doctor has diagnosed.

It shouldn’t be that way, but it is. You may be very blessed and have a doctor whom you do trust, if that’s the case, level with them.  If he’s a great doctor, he will look into new possibilities.

In the end, you should find a diagnosis that answers ALL the questions, fits ALL the symptoms. In your situation, look at the symptoms of your initial disorder/disease, and check out CPM/EPM symptoms. You have to a detective. You also have to be your own advocate.

If you’re able, look for information online. We are in a fantastic technological age where information is just a few key strokes away. Take advantage of it, but try not to be consumed by it. Easier said than done, I know.

I was trying to get into med school before I developed CPM/EPM. It happens to the best of us that the more we read about disorders or diseases, you start to believe you have every disorder that you read about.

To keep this from happening, I would recommend with coming up with your list of symptoms and the dates that they began BEFORE you start doing any research. Take your time in coming up with this list. It’s easy to forget little things, and you don’t want to begin adding things after you start researching because you’ll end up in the same position where you start thinking you have every disease imaginable.

Things to look for on the MRI. Previously, I mentioned that T1 and T2 MRI‘s showed high signal intensity; however, only T2 shows high signal intensity, but T1 shows low signal intensity. This means in T2 MR images, the areas of damage are bright, and in T1 the same areas of damage are darker than surrounding areas. This information might come in handy when you get your medical records. If you review your radiology reports, you might find these things defined, and this is what it means.

Sequelae: an abnormal condition that results from a previous injury or disease. If you are reading it on your radiology report, then it means that there was a previous injury that has caused an abnormality on your MRI.

An EEG may or may not show abnormalities. If there are abnormalities, than it is usually present in theta and delta activity. Usually these abnormalities will also improve in the following months.

J Neurol Neurosurg Psychiatry1998;65:119-121 doi:10.1136/jnnp.65.1.1, Parkinsonism and dystonia in central pontine and extrapontine myelinolysis: 

…….bilateral hyperintense areas within the putamen, caput nuclei caudati, and lateral thalamus (figure). Subsequent control images made up to six months after the onset of the condition showed a marked decrease of these signal intensities. An EEG disclosed diffuse slow background activity and bilateral theta and delta activity which improved gradually during the subsequent months.

Next article:J Neurol Neurosurg Psychiatry2011;82:326-331 doi:10.1136/jnnp.2009.201764 Clinical and functional outcome and factors predicting prognosis in osmotic demyelination syndrome (central pontine and/or extrapontine myelinolysis) in 25 patients

The higher incidence of extrapontine lesions in recent series and ours may be due to the availability of better-quality MRI picking up subtle lesions. Also, the extent of involvement in the imaging depends on the interval at which imaging is done after the onset of ODS.2 21 The MRI done early (1–6 days) in six (24%) of our patients failed to show any abnormality. However, in all these patients, a repeat MRI done 1–2 weeks later showed positive findings. Therefore, we concur with the other authors that a repeat MRI after 1–2 weeks in all clinically suspected cases of ODS is very helpful.2 Also, diffusion MRI can pick up early lesions when conventional MRI is still negative.

CT was done in seven cases and was positive in two (28.5%). All had MRI-detectable lesions (n=23). Six required repeat MRI as the initial one did not reveal any lesion. The mean interval between the first and repeat imaging was 10.6 days in these patients (range 9–17 days). There were T1W hypointense and T2W and FLAIR sequence hyperintense lesions involving pons (76%), basal ganglia (76%) and thalamus (20%) (figures 1 and 2). Contrast enhancement was not seen in any of the cases. Diffusion-weighted imaging (n=3) showed a restricted diffusion in two cases. The radiological findings are summarised in table 3.

Figure 1

Okay, so since I’ve gone on a bit. Please trust me when I say, that this information comes up in pretty much every research paper. This is also a few more types of imaging that have been used to detect CPM/EPM that I wasn’t aware of previously. I do not know anything about what this means, so I will have to get back to you when I know for sure what it refers to, but TcTrodat-1 and 1-IBZM spect images show higher correlations with the severity of clinical features in EPM than MRI alone. (Annals of Nuclear Medicine 2009 23, 409-412.

In summary: MRI is the best method to diagnose CPM/EPM. It usually may not show the lesions until 1 to 4 weeks after injury. The CT scan is the worst at detecting damage. The spect images mentioned above might be a better way showing the damage that correlates to symptoms. The MRI signals usually detect the injury for a few months, but then shows improvements that do not necessarily correlate with the severity in symptoms. This is also true for EEG abnormalities. You may have an abnormal EEG, but improvements usually show within months but do not necessarily correlate to the symptoms you experience. Finally, trust your symptoms. If you had issues with hyponatremia while being hospitalized for a different condition, be sure to access your medical records and consult with one or more neurologists or radiologists to try to determine whether or not CPM/EPM is responsible for issues that seem unrelated to your original conditions.

I’m sorry for the length of this post. I hope it doesn’t ramble too much and that you find the information useful.

Many blessings!


UPDATE: 04/20/12….I just wanted to leave a little bit more information regarding imaging. I mentioned above the FLAIR imaging, and I wanted to explain exactly what that is.

Fluid-attenuated inversion recovery (FLAIR) Magnetic Resonance images stands for FLAIR MRI. It can be used in a two dimensional form or 3D form.  This type of imaging can produce an image without showing the fluid in the brain. This type of imaging is used to detect lesions in the brain, and is very useful in diagnosing demyelinating lesions. It is supposed to be a great way to determine lesions caused by MS. I do not have a lot of information regarding CPM/EPM lesions, but it is being used in diagnosing it along with standard MRI’s.

A Lovely Chart for Who is at Risk for Hyponatremia:

Hello, my friends and followers….

I know it has been several days since I’ve last posted, but it’s not because I’m losing interest, I swear. Please be patient with me. I am truly inflicted with EPM, and one of my biggest issues is with concentration and memory (which is EXTREMELY frustrating for a person who used to be able to open a 1400 page textbook and find a sentence in a matter of minutes).

Now, I read through a few research articles and I literally can’t remember what exactly it is that I read or where I read it 😦 However, in my ambition, I still believe I can read through 8 to 10 articles in a night and be able to keep it all straight, but I CAN’T.

I can’t remember what it is I read, and if I do remember something I read, I can’t find the article it was in, so I’m having to experiment with  methods to keep everything organized.

It’s not working very well. I never had to do it before, so I’m finding that my ability to do it SUCKS or maybe it’s not so much ability as the disability of  having EPM.

SO, here’s the thing. I have found tons of new information (or at least I think it’s new..can’t quite remember if I’ve added these things or not, and I tried to go back through previous posts, but can’t keep those straight either 😦 ) . Ok, so I hope it’s new, but if it’s not..PLEASE let me know!

Anyway, I have a lot of information that I want to add to these posts and updates. I will try to add information to older posts where I believe it fits, but I also don’t those who have read the previous posts to have to keep going back to find out about the new information, so I’m going to have to think about a way to keep updates easy to find. Maybe have an updates category/ post section.

Well, for now, here is a really helpful table that shows several categories for those who are at risk for developing hyponatremia. It’s something I just found, and I was surprised that it contained some additional at risk groups that I didn’t mention (didn’t think that was possible).

Normally, I would love to post a link to this, but I can’t. It’s a PDF, and I’m just not that PC savy, so if you would like to find out more, please research the article below:

Diagnosis and management of hyponatraemia
in hospitalised patients
P. Reddy, A. D. Mooradian

This was found in the International Journal of Clinical Practice,  October 2009, 63, 10, 1494–1508

(Okay, I lied: here is the link to the free article: http://onlinelibrary.wiley.com/doi/10.1111/j.1742-1241.2009.02103.x/abstract )

The information taken directly from the link above:

Table 4.   Drug-induced hyponatraemia
  1. SSRI, selective serotonin reuptake inhibitor; TCA, tricyclic antidepressant; MAOI, monoaminooxidase inhibitor; MDMA, methylenedioxymethamphetamine; NSAID, non-steroidal anti-inflammatory drugs; ACE, angiotensin converting enzyme.

Anti-psychotics Phenothiazines Haloperidol Anti-depressantsSSRI’s TCA’s MAOI’s Bupropion Anti-convulsants Carbamazepine, Oxcarbazepine, Sodium valproate Analgesics & Recreational drugs Morphine (high doses), Tramadol, MDMA (Ecstasy), NSAID’s, Colchicine, Venlafaxine, Cymbalta (duloxetine)
Cardiac drugs Thiazides, clonidine, ACE inhibitors, Aldosterone antagonists, Amiloride, Loop diuretics, Methyldopa, Amlodipine, Amiodarone, lorcainide, Propafenone, Theophylline, Terlipressin, Unfractionated heparin (aldosterone antagonist) Anti-diabeticsChlorpropamide, Tolbutamide, Glipizide Lipid lowering agentsClofibrate Anti-neoplastic agentsCyclophosphamide Vincristine Vinblastine Cisplatin, Hydroxyurea, Melphalan Immunosuppressive drugs Tacrolimus, Methotrexate, interferon α and γ, levamisole, Monoclonal antibodies Antibiotics Azithromycin Trimethoprim-sulfamethoxazole, ciprofloxacin, cefoperazone/sulbactam, rifabutinGastrointestinal drugsSomatostatin analogs, Omeprazole OthersBromocriptine
Table 5.   Non-drug induced causes of the syndrome of inappropriate ADH secretion (SIADH)
Non-osmotic stimuli CNS lesions Malignancies Increased intrathoracic pressure
  1. CVA, cerebrovascular accident; HIV, human immunodeficiency virus; TB, tuberculosis; CHF, congestive heart failure.

Nausea Tumours (neuroblastoma) Lymphoma, leukaemia, and Hodgkin disease Mediastinal tumours (thymoma, sarcoma)
Pain CVA Carcinoma of the uterus positive pressure ventilation
Stress Meningitis Ureteral, prostate, bladder carcinoma Infections (pneumonia, TB, aspergillosis, lung abscess)
HIV Encephalitis Carcinoma of duodenum and pancreas Bronchogenic carcinoma, mesothelioma
Acute psychosis Abscess Ectopic production of vasopressin by tumours (small cell lung ca, carcinoids Bronchiectasis
Surgery Guillain–Barré syndrome Cancers of the head and neck and nasopharynx Empyema
Pregnancy (physiological) Hydrocephalus Renal cell carcinoma Chronic obstructive pulmonary disease
Hypokalaemia Pituitary stalk lesion Osteosarcoma Pneumothorax
CHF exacerbation Delirium tremens
Demyelinating disease
Acute porphyria

I really found this article to be extremely detailed and informative regarding hyponatremia!! I really recommend it. However, it should be digested in small quantities because there is a LOT of medical lingo, etc. I consider it one of the top research articles for hyponatremia. I give it 5 stars 🙂

Anyway, please bear with me. There will be tons more to come. It will just take some time.

CPM/EPM: Count your blessings:

I realize that if you are reading this, then you have most likely been impacted by hyponatremia and/or CPM/EPM. For that, I am sorry. With the information I have found in the months since I was injured from it, I am absolutely certain that this can be avoided!

If you haven’t been impacted by it yet, thank you for being proactive in learning about it. As you age, you are more at risk for it, and it becomes more likely that you will have a more difficult time recovering from it. To put it bluntly, you are at an extremely high risk of perishing from it, the older you are.

I guess that’s true of everything, but if you have knowledge of what this is and how it should be prevented you have a better chance of surviving.

One day, I hope that awareness will become so universal that hyponatremia and CPM/EPM will be prevented from ever happening. Please make this one of your missions too. It takes just a few seconds to hit the “like” button or to send this link to your friends or family members. Getting the word out is what will save lives!

So, if you have been impacted by hyponatremia, I hope you aren’t facing CPM/EPM. In my previous posts, I listed the symptoms that impact most people who are injured.

I also touched briefly on the widely unknown measures that can be used to reverse the consequences of having your sodium levels raised too quickly and the widely unknown treatment options.

If you are not one of the ones fortunate to escape the devastating harm of the brain injury, I want to stress to you; you are not alone! As long as I’m able, I will try to help you.

I find one of the hardest things to do when you’ve been inflicted with CPM/EPM is to count your blessings. When I was diagnosed with it, I felt vindicated. I had returned to the hospital that had treated me 3 times to try to get help. I won’t go into great detail here regarding my story, but I was basically looked at as if I was on fire. I was turned away from the ER twice with the diagnosis of a migraine, and the third time I went back to the same hospital (with significant impairment), they wouldn’t do the MRI that I needed and requested. Instead, they wanted to admit me to the  hospital for further observation.

As I mentioned previously, CPM/EPM can be life threatening. I was demonstrating obvious problems, something akin to having a stroke, and they weren’t taking immediate action. I decided to go to a different hospital at that point. I hoped the bigger more prestigious hospital would be more equipped to handling the situation, as well since they didn’t cause the problem, so they would be more likely to diagnosis a problem they didn’t create. I was right.

When I found that I had CPM/EPM, I was terrified. When I had started to develop my first symptoms, swallowing issues and speech problems, I knew what was wrong, but I didn’t know very much about it at all.

I had just read the generic stuff online, and it was pretty scary. It said that I could go into a coma, die, or develop locked in syndrome. Once I knew I had EPM, each day that I woke up, I felt more and more grateful.

I’m alive and I’m not a vegetable. At the same time, I was absolutely terrified because these new changes were significant.

How would I be able to survive as this new me?

My doctors and my friends and family were incredibly optimistic, but as they saw improvements, I saw the differences, the changes, the difficulties.

I have to say with 110% conviction, IT IS EASIER FOR THEM TO SAY IT!

You are LIVING it. That said, I AM living with it too, and I can tell you with absolute certainty, unless you die, you will see improvements. It’s a matter of degree.

I can not guarantee that if you were in a coma for 3 weeks or suffered from locked in syndrome for 6 weeks, that you will ever be running marathons or even doing basic math in your head, but you are here and you are important and you can expect improvements.

Give yourself time, and continue to do what you’re doing, making an effort to get yourself help and to find support. Contact me if you need me.

There are online support groups that can help you. You can find people, normal people, struggling every day with the same problems you are, and there is nothing better than to know you are not alone.

Your friends and family probably don’t get it, and frankly, most of them don’t want to hear about it. Don’t judge them for that. In most cases, they just don’t know what to do or say. Seriously, before you became ill, would you act any differently?

That said, I know a few people who have it. I consider you part of my family if you have it. You have a private pass to my club. 🙂 And I will do anything I can to help you.

So, now you have one more  blessing to add to your list.

Here’s the thing, if you do have this, and you are like me. You’ll feel better knowing that there is at least one more person out there who has it. You aren’t completely alone, but that only goes so far. It doesn’t take the sting out of not knowing how YOU will be impacted by CPM/EPM.

Frankly, it’s depressing. It’s scary. It’s hard. I was diagnosed six months ago, and I’m still having issues. TRUST ME, my symptoms have improved greatly from where I was, but not being 100% back to my former self is difficult.

Trust me, there are days when I do cry. There are days when I want to go back to the hospital that treated me, and I want to SCREAM at the doctors.

I’m giving you permission to be angry, upset, cry, yell. It’s a benefit of being a member of my club, BUT what I refuse to let you do, is give up. You are not allowed to give up or give in, NO MATTER, how desperately you want to.

Further more, if you ever feel the urge that you just can’t handle it another day. You’ve had all the twitches and stutters you can take, I want you to promise me that you will get help!

You have to promise me that if one day becomes just too difficult to take that you will go to an ER, call a friend, and/or click on the link below:


You can actually seek help via online chat:


You can always reach out to me as well. I’m here for you, and I KNOW how it feels.

With my next post, I promise to bring more information regarding CPM/EPM…like maybe how the symptoms can impact you or the doctors that you can reach for more help, experts if you can consider them that (they have at least heard of it).

Many blessings!


Ok folks, I’m really hoping to keep this post short and sweet.

My last post had information regarding treatments for CPM/EPM. Guess what, I have found new information suggesting there are treatment options for CPM/EPM.

I was shocked to discover that once your sodium levels have been corrected too quickly, you are not destined to CPM/EPM. You doctor has the ability to PREVENT CPM/EPM AFTER your levels have been corrected too quickly. Research has shown that there is an approximate 5 DAY window in which your doctors can LOWER your sodium levels back to abnormal, approximately 120. If they do this after your levels were raised too quickly, within 5 days, CPM/EPM can be avoided!!!

The above information was discussed as early as 2005 and 2007: http://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/pdf/104/6/56.pdf and again in :  http://www.ccjm.org/content/74/5/377.full.pdf and again in:

This type of treatment has been extremely successful in preventing CPM/EPM. I DO NOT UNDERSTAND WHY DOCTORS DON’T KNOW THIS or DO NOT PRACTICE THIS. I’m really at a loss over why my doctors, who admitted to me that they raised my levels too quickly, did not have the knowledge to do this. It turns my stomach to think that this might not be COMMON knowledge among doctors. WOW.

Since this might not be common knowledge among doctors, PLEASE take it upon yourself to inform them if you are in this situation. You might be able to prevent your brain damage after all!

That said, I also found additional treatment options! I went to one of the major teaching hospitals in this country for treatment of my CPM/EPM, and they DID NOT offer this! They told me that there were NO TREATMENT OPTIONS. Imagine my shock and dismay at finding research to the contrary. It really makes me sick to my stomach to think not only could this have been COMPLETELY PREVENTED, it could have been TREATED. 😦

That said, these treatments have not been clinically proven to work. There haven’t been any control group studies.

I mean, here’s the thing, CPM/EPM is uncommon. It’s not like heart disease or cancer where people can enroll in studies to test therapies, so your doctor may or may not know about these treatments. If they know about them, they are not going to suggest you forgo the treatment since it hasn’t been studied in a controlled study. They will suggest to do the treatment. If you don’t do the treatment, you have an approximate 67%  probability of having some type of neurological deficit for the rest of your life.

The research studies did not report ANY side effects (I’m sure there are), so proceeding with these unstudied/ unproven treatments would be the best thing. Furthermore, all of the case studies that were listed had a 100% recovery when given the treatments.

In other words, there needs to be more research regarding CPM/EPM, but in the mean time, if you are facing permanent neurological issues, try these treatments that have shown effective in treating the brain damage. What do you have to lose???!

Here are the additional treatments that I did not mention previously:

1.) plasmaphoresis

2.) TRH  (thyrotropin releasing hormone)

3.) immunoglobulins

4.) methylprednisolone (the cleveland clinic journal also listed dexamethasone, but it did not provide information regarding its effectiveness.)

This information comes from :http://www.wisconsinmedicalsociety.org/_WMS/publications/wmj/pdf/104/6/56.pdf

It has also been reported in several additional journals.

There are also natural remedies that have been recommended. I will post more information on possible natural treatments as well.

Please feel free to post any information you have in regards to treatments you might have been given for CPM/EPM.

Thank you for reading!

CPM/EPM–What to expect:

English: Central pontine myelinolysis, MRI FLAIR

English: Central pontine myelinolysis, MRI FLAIR (Photo credit: Wikipedia)

I hope for those who are reading this, you are in good health or your loved one is.

If you developed a chronic form of hyponatremia, you are at risk for CPM if your sodium levels were raised too quickly.

Too quickly is not an absolute term. There are person’s who disagree on what “too quickly” means in regards to the treatment of hyponatremia.

Some specialists believe that too quickly is greater than 8 mmol in a 24 hour period. Other specialists would consider “too quickly” as 12 mmol in a 24 hour period.

I would recommend the safer the better no more than 8 mmol in a 24 hour period.

Bottom line, if your levels were raised more than 8 mmol in a 24 hour period, and you started to experience symptoms of CPM/EPM in a period of 3 to 10 days after your treatment for hyponatremia, it was raised “too quickly” for your system.

If it is raised more than 8 mmol in a 24 hour period, you are at risk for CPM/EPM. It doesn’t mean you will absolutely develop it.

I caution you to watch for symptoms during the next 3 to 10 days after treatment if you know your levels were raised at this rate or faster.

When you first start to develop CPM/EPM, your symptoms can vary, but will usually begin with muscle weakness, possible fatigue, headache, muscle stiffness, twitches/spasms/ jerks, trouble swallowing, issues with balance and coordination, visual issues, speech issues (stuttering, slurring or inability to form words), cognitive difficulties, issues with understanding speech, reading, and/or writing. Most importantly, a person can develop complete paralysis (locked-in syndrome), coma, and/or death.

I know, that’s enough to make your heart skip beats. Try to stay calm. This is a huge list of symptoms, and it does not mean that you will develop each one. You are at risk for them.

It is a serious condition, and you need to go to a well equipped hospital immediately, if you were recently released after receiving treatment for hyponatremia and have started to develop any of these symptoms.

It is not worth risking your life. If you are not certain if you are really experiencing these symptoms or not, but were recently treated for hyponatremia and “feel” as if something isn’t quite right, go and get it checked out.

The best way to determine if you have CPM/EPM is to have a T1 and T2 weighted MRI with contrast performed. It must be done with contrast.


Yeah, I know, this makes it really difficult to diagnose. By the time you begin to develop symptoms, they might not be able to see the damage on the MRI. If your doctor waits too long to take an MRI, the lesions can heal. JUST BECAUSE THE LESIONS HEAL DOES NOT MEAN THAT YOUR INJURY IMPROVES.

This can lead to a misdiagnosis of Parkinsons. Some of the longest lasting symptoms a person may experience are movement issues (tremors, jerks, spasms, etc). So, it is not uncommon for a person to be misdiagnosed as having Parkinsons.

It is also not uncommon for a person to be incorrectly diagnosed as having a stroke, especially in the elderly.

So, what does this mean?

It means that you should spread the word regarding CPM/EPM. The more the public becomes aware of CPM/EPM, the less it will occur. In this case, prevention is the best way of defeating this disorder.

It is important for people to be aware of the symptoms associated with CPM/EPM. It is important for you to obtain your medical records if you developed any of the previously mentioned symptoms after your treatment to determine how quickly your sodium was raised.

If you experienced any of the above symptoms and your sodium level was raised faster than 8 mmol in a 24 hour period, it is very possible that you developed CPM/EPM.

If you’re making this discovery long after your treatment, you will still want to contact your doctor to request an MRI.

I would highly recommend contacting a neurologist who is experienced in treating CPM/EPM. Trust me, this is easier said than done. I will post information on some of the doctors who are associated with treating CPM/EPM, but please be aware that these doctors are few and far between.

That’s because there are approximately only 2000 cases “documented” each year. Now this number is under dispute. I received this number from the website I reported in my earlier post for hyponatremia. (I will insert it again in the near future). However, my friend, Jeffrey, who was trying to develop a CPM awareness support group, received information from the National Institute of Health that this number could be as high as 30,000 to 50,000.

WOW! That’s a huge difference. How could this be possible?

Well, it’s possible because CPM/EPM is almost 100% caused by medical malpractice, and more than half of those who develop it, die. Those who develop hyponatremia and CPM/EPM are usually being treated for other disorders, such as traumatic brain injury or major burns, etc. In other words, hyponatremia is common as a secondary illness.

To protect the hospital and doctors from a malpractice lawsuits, it is believed that in cases where hyponatremia is a secondary condition that leads to CPM/EPM, the hospital and doctor will list the cause of death as being from the burn, the brain injury, cancer, etc.

For those people who do not die, it is suspected that the hospital/ doctor will tell the patient or their families that the reason they are experiencing these new physical symptoms is because they are having side effects or reactions to the illness or treatments.

Even if there are 30,000 to 50,000 people who develop CPM each year, that is not a huge number of people. Consider the reported fact that at least 1.5 to 1.7 million people develop hyponatremia each year, this means that less than 5% of those will develop CPM/EPM. The reported statistical data suggests that only .03% to .15% of those who develop hyponatremia will develop CPM/EPM. According to recent statistics (which again can be very vague), approximately 500 to 2500 were reported in 2010-2011. I believe that these statistics aren’t extremely accurate due to the drastic variations that were reported from one year to the next.

It is extremely difficult to know for sure what is accurate and what isn’t. I will try to resume the research Jeffrey was uncovering, but his unexpected death due to complications from CPM has made it difficult.

I will report it and update my blog accordingly.

So, what does this mean? YOU need to be your own advocate. You need to access your medical records and determine if your levels were raised too quickly. If you are currently in the hospital, track your sodium levels as they raise it. Be sure you question your doctors regarding your treatment. If you are conscious and able, access information regarding the medicines that you are being given.

If you were recently released from the hospital, TRACK your symptoms. If you start experiencing any subtle changes, go to a DIFFERENT hospital from where you were treated for hyponatremia and demand that they do a MRI.

I literally had to drive to a different city and a major hospital. No one believed that I could have CPM/EPM.

Be adamant. It is also helpful if you provide the new hospital with the records for your treatment.

In most cases, you won’t have issues with being admitted for the problems you are experiencing because it is painfully obvious that there is an issue. Be sure that you have a representative who can speak for you, such as a friend or family member. Make sure you have your living will and/or power of attorney up to date.

It is not uncommon for a person to experience a temporary recovery from their HYPONATREMIA symptoms once their sodium levels are corrected. It is a brief window of relief before you begin to experience different neurological symptoms from CPM/EPM.

The window, as mentioned previously, is approximately 3 to 10 days after your sodium levels have been stabilized. It is the quiet before the storm.

I would use this time frame to prepare if your levels were corrected too quickly. It’s better to be safe than sorry. Try to get as many of your affairs in order as possible, and obtain your medical records from the hospital.

Remember, there are only a very few who experience issues with CPM/EPM, but if your sodium levels were raised too quickly then you are at a greater risk for it.

This is by far, one of my longest posts to date. I understand I’ve repeated some of the information over and over again, but you will only have this opportunity once. It’s absolutely necessary for you to do everything right from the start because there is no room for errors once you start down this road.

I hope this finds you in good health, but if you are one of those being impacted by CPM/EPM, please take comfort in that you are not alone. I hope my message can help you or your family cope with this road bump.

Many blessings!

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


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!

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.


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.


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.


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).


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.


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:


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:


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.


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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