Hyponatremia and Central Pontine Myelinolysis

What is hyponatremia? Information regarding CPM and EPM.

Archive for the tag “Hyponatremia”

Hyponatremia Recent Stats:

I have meant to do this for awhile, and I apologize for it taking so long. I guess, better late than never.

The HCUP website reformulated the way that they record statistics. Now, I did not read why or how, but it did show that the previous stats that they recorded before July of 2014 were across the board higher, than what they are listing now. For 2011, I will include all the data points that I found, ie old and newer stats.

Hyponatremia diagnosis codes: ICD-9: 276.1

ICD-10: E87.1

To obtain the date, I used the ICD-9 code: 276.1

For 2011, hyponatremia was recorded as this:

2011 National statistics – principal diagnosis only (hyponatremia only -from all hospitals in US)

Outcomes by 276.1 Hyposmolality
276.1 Hyposmolality Standard errors
Total number of discharges 100,215 2,333
In-hospital deaths 1,085 (1.08%) 73 (0.07%)

Therefore, there were a total number of patients that had hyponatremia specifically, 101,300 +/- 2406

If you look at all possible combination of hospitalized patients that had hyponatremia AND an additional condition (ie severe burns, cancer, liver transplant, etc):

2011 National statistics – all-listed
You have chosen all-listed diagnoses. The only possible measure for all-listed diagnoses is the number of discharges who received the diagnoses you selected. If you want to see statistics on length of stay or charges, go back and select “principal diagnosis.”

276.1 Hyposmolality
276.1 Hyposmolality Standard errors
Total number of discharges 1,940,211 51,938

Now, these are the NEW reference points, the older version listed for 2011 hyponatremia only diagnosis: 104,744 (discharged), 1,124 people died.

If you include all possible diagnoses with hyponatremia, it is 2, 019, 550 +/- 53,454.

Yeah, that’s a lot of people who are at risk for CPM/EPM if hyponatremia is not diagnosed and managed correctly.

For 2012:

2012 National statistics – principal diagnosis only

Outcomes by 276.1 Hyposmolality
276.1 Hyposmolality Standard errors
Total number of discharges 101,330 1,139
In-hospital deaths 1,160 (1.14%) 75 (0.07%)

There is no older version of documenting with this system.

However, if you look at all hospitalizations that included hyposmolality:

2012 National statistics – all-listed
You have chosen all-listed diagnoses. The only possible measure for all-listed diagnoses is the number of discharges who received the diagnoses you selected. If you want to see statistics on length of stay or charges, go back and select “principal diagnosis.”

276.1 Hyposmolality
276.1 Hyposmolality Standard errors
Total number of discharges 1,934,996 22,563

I love numbers because they don’t lie. What I don’t like with this 2nd break down (all hospitalization that listed 276.1 with another condition), it is impossible to tell if hyponatremia actually killed the person or the other illness.

Regardless, there an extremely HIGH number of people who are diagnosed with hyponatremia each year, even if it is or isn’t with a secondary diagnosis. More people should be aware of the condition, and how it should be treated! Hopefully, you will spread the word on how common it is to get it, and how it should be treated.

Blessings!

(Use the link below to find the statistics above: http://hcupnet.ahrq.gov/HCUPnet.jsp)

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Hyponatremia: What you should really know to prevent CPM and EPM.

Today has been a rough day for me. I knew that my hyponatremia was treated incorrectly when I developed Extra Pontine Myelinolysis. However, I didn’t realize to what extent my treatment of hyponatremia was mismanaged.

It is absolutely a fundamental point of this blog to try to prevent ANYONE from having to live with this injury. There is no reason anyone should.

So, in this post, I am going to try to simplify the steps of how hyponatremia should be treated.

First, it is important for you to recognize the symptoms. *Please see my earlier posts for those*

Once you realize there is a problem, seek treatment. It is an emergency.

A basic metabolic panel should be ordered to determine if your sodium levels are low.

Next, it is important for the doctor to figure out WHY you have hyponatremia, and how LONG you have had it.

If they can’t figure out the time line, then it is better for them to assume that it is chronic because it is more likely that you will develop CPM if they treat chronic hyponatremia too quickly versus acute. (Acute is when sodium has been too low for less than 48 hours. Chronic is when sodium levels have been low for more than 48 hours).

Acute hyponatremia can cause severe symptoms such as seizures, respiratory distress and coma. The severity of symptoms determines how quickly the levels should be raised. However, it is generally accepted that once your symptoms begin to improve, the treatment should be decreased or halted.

According to Dr. Sterns, an expert on hyponatremia, acute hyponatremia should be treated in the following manner, “should be treated immediately with a bolus infusion of 100 mL of 3% NaCl to acutely reduce brain edema, with up to 2 additional 100-mL 3% NaCl bolus infusions that should be given at 10-minute intervals if there is no clinical improvement.10 We believe that this is a reasonable regimen for all symptomatic patients with acute hyponatremia…” (use the link below to find the information).

According to Dr. Sterns, chronic hyponatremia should be treated with “…we suggest a goal of 6 to 8 mmol/L in 24 hours, 12 to 14 mmol/L in 48 hours, and 14 to 16 mmol/L in 72 hours.” (http://www.uphs.upenn.edu/renal/important%20pdf%20III/Sterns%20-%20The%20Treatment%20of%20Hyponatremia.pdf)

The cause of your hyponatremia is extremely important because it absolutely determines what treatment you should receive.

For instance, if a drug has caused your hyponatremia, like a diuretic, then the first course of treatment is to stop taking the diuretic. Sometimes, just discontinuing the medication is enough to reverse the low sodium.

I HIGHLY recommend the following article posted by the Cleveland Clinic that outlines in exact detail which types of treatments based on the cause of the hyponatremia.

There is little question that if you are on a 3% saline solution for treatment, that your sodium levels should be monitored every 1 to 2 HOURS. As soon as your levels start to increase to the point that your symptoms start to resolve, even BEFORE it reaches the 6 to 8 m/mol GOAL, the 3% saline should be halted. This will stop your levels from reaching the “danger zone” which is approximately 8 to 12 m/mol in the first 24 hours with chronic hyponatremia. It is generally accepted that with acute hyponatremia that you can raise the levels a bit faster and not risk CPM or EPM.

ONE OF THE MOST IMPORTANT FACTORS TO REALIZE: IF YOUR LEVELS HAVE BEEN INCREASED TOO QUICKLY, THEN THEY CAN BE DECREASED BACK TO A HYPONATREMIC STATE TO PREVENT CENTRAL PONTINE MYELINOLYSIS. IT IS BELIEVE THAT THIS DROP CAN OCCUR DURING A 5 DAY PERIOD AFTER THE RAPID CORRECTION OCCURRED.

For further information and more detailed description of these steps as well as how to treat certain types of hyponatremia, please access this article: http://www.ccjm.org/content/77/10/715.full

These simple steps could save your life!

Additional symptoms related to CPM:

 

I’ve previously described movement issues like dystonia, Parkinson like tremors, other tremors, and random jerking movements, but this is something I have not heard about previously, choreic.

I had no idea what the word meant or what it is related to before a few days ago, so please feel free to add any input you might have about it.

 

The dictionary definition is: “An involuntary spasmodic twitching or jerking in muscle groups not associated with the production of definite purposeful movements.”

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.
Basically, these movements are involuntary movements and jerks, so I guess in a way, I have discussed this issue before. I have jerks a lot.
If I get really stressed there seems to be this movement that my left leg does. It’s weird, and if I every experience it for a long period, I will upload a video of it. It really feels like I should have control of it. It seems ridiculous that I can’t, but it’s like my body has a mind of its own and this is one thing that I never had an issue with before. It really bugs me, but others don’t seem to notice. I guess some might consider it a  nervous tic.
I believe that the following videos really do what the motions are like for those who have these types of jerks.
This is kind of what I have experienced, so I’m posting it. I don’t have issues with my face so much as I do with kind of a rolling to my left and a rocking of my left leg and rolling of my body. It  really seems like I’m jittery or nervous or can’t sit still.  I don’t experience it very often and the periods that I go through are brief. I believe this is a positive sign.
With the following video, the little girl developed this because of scarlet fever, not huntington’s disease. She was able to recover almost completely so the following videos show her before and after:
Another good example. I believe these kind of show the extremes. Some people just seem fidgety. Others are extremely disabled.
The information that I have found has been sparse when it comes to directly attributing these choreic movements to CPM/EPM. However, it has been documented. It may not be an immediate appearing symptoms. In some cases it did not appear until months after CPM/EPM was first diagnosed. I have read that this in not an uncommon theme regarding EPM. It seems that movement disorders with EPM can appear months after the injury. I really noticed my issue develop at a doctor’s appointment. I was becoming extremely agitated, and I realized that my left kept moving as well as my left shoulder. I kept crossing and uncrossing my leg as well as moving in my chair. I’ve noticed those movements at other times of stress.
Thankfully, I don’t think it is getting worse for me.
The following information is a chart that describes that chorea can be caused by electrolyte issues:
J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

Table 6

Metabolic aetiologies of dystonia and chorea

Hyperthyroidism
Hypocalcaemia (hypoparathyroidism)
Hypoglycaemia
Hyperglycaemia
Hypernatraemia
Hyponatraemia
Hypomagnesaemia
Osmotic demyelination syndrome (central pontine myelinolysis)
Splenorenal shunt

 

Literature also seems to suggest that these reasons that these choreic movements occur is because of injury the putanem or basal ganglia. It suggests that there is a decreased amount of GABA, and there there are issues with Dopamine and glutamate.

Frankly, folks, I simply can’t read through this very detailed information from the following journal link, but it goes into great explanation why both dystonia and chorea are found in a variety of brain damage injuries, including CPM/EPM, Huntington’s disease, and many others.

Here is the quote:

As discussed earlier, dystonia and chorea most commonly result from striatal dysfunction, and hypoxia-ischaemia has been shown to alter several neurotransmitter systems in the striatum. Glutamate is the main neurotransmitter in cortical neurons projecting to the striatum and may contribute excitotoxic injury. Hypoxia-ischaemia has been shown to increase striatal extracellular glutamate, and decrease glutamate transporter concentrations. Direct lesioning of the globus pallidus with excitatory amino acids in monkeys produces cocontraction of opposing muscle groups on reaching, as in dystonia.9Extracellular dopamine concentrations rise and concentrations of dopamine metabolites fall after hypoxia-ischaemia.710Dopamine may also potentiate the excitotoxic properties of glutamate, and depleting the striatum of dopamine before hypoxia-ischaemia decreases the degree of striatal injury. In the neonatal rat model of cerebral hypoxia-ischaemia, striatal D1 and D2 dopamine receptor numbers fluctuate until 9 to 11 weeks after injury, at which time the D1 receptor number has returned to normal but the reduction in D2 receptors persists.11 Hypoxia-ischaemia also results in areas of complete loss of preproenkephalin mRNA in the dorsal striatum of the rat brain.12 Enkephalin, together with GABA, is an inhibitory neurotransmitter in the projections from the putamen to the external pallidum. Hypoxic-ischaemic necrosis of medium sized spiny striatal neurons may be responsible for decreased concentrations of the inhibitory neurotransmitter, GABA. By contrast, the striatal cholinergic system remains relatively preserved or even upregulated after hypoxia-ischaemia, as evidenced by an increase in cholinergic fibres and cell bodies, and an increase in acetylcholine release.13This is interesting in that anticholinergic medications often ameliorate dystonic movements.

http://jnnp.bmj.com/content/65/4/436.full

J Neurol Neurosurg Psychiatry 1998;65:436-445 doi:10.1136/jnnp.65.4.436

  • Review: Neurology and medicine

Dystonia and chorea in acquired systemic disorders

I will try to add more to this post in the future if I can, but right now, I can’t. Please feel free to leave questions or suggestions as you like.

 

Have a great night 🙂

 

Michael’s Story:

I am happy to include Michael’s story. He has been suffering from CPM since 2008. He like others saw initial improvements, but has now experienced a decline.

If you’re reading this, here’s the thing…there is not enough information available about what’s going to happen. It’s not known. The doctors will tell you: you may get worse; you may get better; you may stay the same. Isn’t that true for EVERYTHING? That’s why I feel it important to get stories from people that HAVE it, and are living with it every day out to you. BUT, I want to stress to you that it doesn’t mean that YOU are going to experience those same issues.

I would compare this blog to making a path in a forest. What they know and understand about CPM/EPM is virgin territory. Most research articles just repeat what other research articles tell them, and it always end with basically, we don’t know. I figure the best way to make a path is by asking the natives. It doesn’t mean it’s the only way, but I figure it’s a good start.

So, here we go, another account from a native:

First thing I need to say is that I am an alcoholic, I was not drinking from 2001 to 2007 then I went back out. From, the first week of 2007 to the first week of 2009, I was drinking. I have not had a drink in over three and a half year and I hope I never have another. With that said, here is my recollection of what happen to me and how I got CPM

The last ten days of 2008 I had been throwing up between 4 and 6 times a day. I didn’t feel bad, I didn’t have the flu or anything like that I just could not keep anything down. For those ten days I didn’t drink alcohol, just small sips of water and orange juice. Well on the second day of January I went to visit my mother and she took one look at me and said get in my car I am taking you to the hospital, I think you have had a “stroke” when I got to the hospital they took one look at me and thought the same thing, “stroke” so they put me in a room in the emergency room and started doing the tests. That’s when they found out my sodium level was 106. So they admitted me and started me on two IV’s to replace the lost sodium. Well looking at my medical records, (which all of this information is coming from) my sodium level went from 106 to 124 in 24 hours. So boys and girl, what happens when one of the very best hospitals in the whole world gives you almost double the amount of sodium that they should in a 24-hour time frame, you get… CPM!!! (Non- diagnosed)

So, I want to point out in Michael’s case, it is difficult to say what caused Michael’s hyponatremia. The most probable cause of the hyponatremia was alcohol. I am guessing that he started to develop hyponatremia after drinking and that caused him to get sick for those ten days where he couldn’t hold anything down. Now, it’s also very possible that he just had a stomach flu and after getting sick for so long, not being able to eat and only drinking water and OJ, caused him to develop hyponatremia, but the important thing here is that he had the chronic form. Because he didn’t develop seizures or go into a coma from the hyponatremia, his brain and brain stem had enough time to adjust to the swelling. That said, when you have chronic hyponatremia, it puts you at higher risk for CPM. Back to his story:

  With that said about 8 days after I was given CPM by the hospital the first signs started to show up. I ended up at a local hospital in basically a coma for six and a half days. They thought it was alcohol induced because there was quite a bit in my system. When I got out of this local hospital for the next 120 days were complete hell. I walked like a 90 year old man; it would take me two hours to walk half a mile. One day I fell in a snow bank and could not get up for over 45 minutes. I needed help to get in and out of chairs. In and out of cars, ect. My speech was awful; it was like English was my second language. Had to wear non-tie shoes in the winter because I could not tie them. I had little control over my bladder, and my hands shook so bad, drinking anything hot was out of the question.

Then after about 120 to 130 days had past I started to get better and things started to clear up. I could walk better and talk and things went back to normal. The company I was working for went out of business and I went and painted houses with a buddy of mine. Then after about 6-8 month I started to notice numbness and a small shake in my left hand and left leg. Not all the time, just now and then. Then I started dropping the paintbrush, which I never did. So I went to see my PCP. He ignored it few times and then finally said ok lets take a look. So on February 25 2011 I was finally diagnosed withCPM.

Sense I started dropping the paintbrush; I am back with the company that I have work for, for 32 years. I am a salesmen, have been for all of the 32 years, but I stutter, shake, have spasms, I am down to calling on one account, can only work till noon, some days English is my second language, have no memory what so ever, and my fine motor skills are gone. With out my wife I would be back to wearing non-tie shoes, tea shirts and sweat pants. So basically I am back to were I was the first 120 days of hell with this disease.

Thank you Michael!!

 

Todd’s Story: CPM

Todd and I have corresponded for the past year, and I find his story also very motivational, so I’m happy to start sharing it here. Todd’s story shows how alcohol can lead to hyponatremia, and being an alcoholic can further increase your chances of developing CPM. It’s a dangerous combination, alcoholism and hyponatremia.

Now, I want to spend time explaining some of the things I’ve hit upon before regarding alcohol.

You are at risk for developing hyponatremia if you have even one drink….however, it is very unlikely for you to develop it after drinking just one drink.

The more you drink, the more likely you are to develop hyponatremia. If you are an alcoholic, you are at great risk for developing it. You can also develop CPM/EPM if you are an alcoholic without developing hyponatremia. In other words, drinking chronically can lead to demyelination of your pontine area, basal ganglia, or other areas of your brain.

I hope Todd’s story will motivate those who are drinkers to think twice about picking up their next drink.

……Unfortunately, I don’t know how to blog, but anything I share with you is free game, my life is an open book now, I don’t hold any secrets about myself anymore. You description of the causes of CPM was explained to me as the perfect storm:

1. I am an alcoholic
2. I pounded scotch and water.
3. I was taking htc for HBP.
4. I got sick on both ends

I am starting to work on my testimony for my recovery group and will share if when I am done.

I try to wake up everyday trying to figure out why God spared my life? Everyday is a great day is I choose to make it one which I suppose about 50/50…..

Hey,
I finished ready your blog today. I know exactly what you mean because sometimes it takes me an hour to write these short little notes because I do not want to offend anyone. I’m in a quandary, I what to forward the blog address to my health care providers but can’t find the right words. There is a long story behind it: They were my clients and they fired me! My work with them was in the med-mal arena.

Hey,
Housekeeping: I was diagnosed with CPM Late December 2007. I am an alcoholic. I haven’t seen a neurologist in 2+ years, they really never wanted o bother with me. My primary care Doc’s are great. I use to go once a week but now it is once a year. The remnants of the CPM are my involuntary grunting, drooling and uncontrolled belching. I also 90% of the time have a “deer” in the headlights expression. Physically, I’m proud to tell you I am in the best condition of my adult life. Over 4 years of sobriety with 3*** and Copenhagen FREE. I’m into biking and spinning. You have to brag when you can: I burned 818 calories in today’s spinning class, a personal best.

My life partner read your Blog and is super impressed with your research. She will be way more useful than me, because she lived the CPM, I only remember certain aspects of my time in prison.

She obviously has permission to correspond with you but is still getting computer literate (I finally bought her and everyone I love a MAC) and is also busy.
We have 5 children, 2 still at home………

Hey,

I forgot to mention that my speech is not perfect. I do stutter when I get excited and my volume increases and I don’t realize it. I also cannot write that well anymore not that I could in the first place. My mother, an RN, who in retirement took me to her continuing education seminars on brain injuries, when I would look down always reminded me, with brain injuries, always give it at least 4 years for recovery.

p.s. Spinning is the best Cardio ever and it is easy on the knees.

My life partner swears that my better days are the ones when I’m active in exercise. I can remember the first time to the gym: 1/11 of a mile was a victory….then a mile…..then two and now 100 mile bike rides.

Keep up the great work.
I’m still encouraging Linda my life partner to write you, I overheard her discussing the Blog with my oldest daughter about their experience with my CPM and the surrounding events. The only things I remember are the peace of the ICU, before being admitted telling my boy to take me out if they cath me, being able to memorize the 8 questions of “Are you an Alcoholic“. Being on the general floor on the Hospital, constantly asking to be walked, because I new something was wrong. I do not remember having headaches. I’ll keep encouraging her because your story sounds familiar to what happened to me except alcoholism was the proximate cause of my low blood sodium.

Hey,
I just got back from a session of speech therapy. I went for a 4 year/50,000 mile tune up. The good news is in their humble opinion and expertise my speech is great. I would admit that normally I feel 95-98% but somethings dip below 90%, I admit the speech problem is all in my head.
One issue that they identified is my facial expressions.
“deer in the headlights” eyebrows always up and my mouth is constantly open. Two things I was not aware of.
So much for my Neurologist’s suggestion for becoming a professional poker player! At the end of the day I can feel some self confidence with my speech.

Hey,
The “deer in the headlights” look is definitely a CPM issue along with my mouth being unconsciously open 24/7 unless I’m thinking about correcting it. The toughest setback of CPM is the mental aspect: Remembering how things were before CPM, then now. Trying your hardest for minuscule gains is a bitch. Don’t be worried about the muscle issue yet. I cannot specifically say that happened to me but I definitely lost strength. Three hunting seasons ago, I could barely carry a 20 gauge and was so pissed off after the season I went directly to the gym. Three years later, I carry what affectionately call “the cannon”–Weatherby O/U 30inch 12 gauge. After this year a buddy told me to “knock off that disabled shit because you can’t fool me, I saw you dropping everything you shot.” He was right. Bottom line–we know when someone is BSing with us or is sincere. Personally I like the BS too because I like to give it out.

SO, as you can see from Todd’s story. There is hope for living with CPM/EPM. He isn’t the same person he was before the injury, but he’s making strides to make the best of his life now. I still have a lot of questions for Todd, so please don’t consider his story complete at this point, but I wanted to get his story out there.

Have a great night.

Hyponatremia: Statistics Updated:

Well, folks, I hate to say that I was right, but I was right. The number of hospitalizations due to hyponatremia increased in 2010. It is an ongoing epidemic, and one that needs to be addressed.

I’m am praying that if you read this post, you will do your part in spreading the word about hyponatremia. PLEASE, share my blog with your friends, family, neighbors, co-workers, ANYONE and EVERYONE that you know. It’s preventable, and it should be a household name.

The following information was obtained from, HCUPnet: http://hcupnet.ahrq.gov/HCUPnet.jsp

2010 National statistics – all-listed
You have chosen all-listed diagnoses. The only possible measure for all-listed diagnoses is the number of discharges who received the diagnoses you selected. If you want to see statistics on length of stay or charges, go back and select “principal diagnosis.”
276.1 Hyposmolality
276.1 Hyposmolality Standard errors
Total number of discharges 1,901,923 48,831

Weighted national estimates from HCUP Nationwide Inpatient Sample (NIS), 2010, Agency for Healthcare Research and Quality (AHRQ), based on data collected by individual States and provided to AHRQ by the States. Total number of weighted discharges in the U.S. based on HCUP NIS = 39,008,298. 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.

This is a table of the people above that are impacted by age:

Patient and hospital characteristics for
ICD-9-CM all-listed diagnosis code
276.1 Hyposmolality

Total number of discharges Standard errors
Total number of discharges
All discharges 1,901,923 (100.00%) 48,831
Age group <1 25,749 (1.35%) 2,251
1-17 25,657 (1.35%) 2,808
18-44 199,628 (10.50%) 7,021
45-64 586,155 (30.82%) 16,448
65-84 777,902 (40.90%) 21,587
85+ 286,523 (15.06%) 8,866
Missing * *

SO, the majority of those who are being treated for hyponatremia are the elderly. This information tends to be true for the majority of illness and disease. The elderly and children tend to be the targets for most health concerns. However, surprisingly, after the elderly between the ages of 65 and older, the next largest group are adults age 45 to 64. So, children are less likely to develop this than other age groups. I thought that was pretty interesting.

The following section of information includes additional statistics, which I found also surprising. Usually, illnesses or disease tends to target those impoverished, but that is not the case for hyponatremia. Women develop it more than men. Please take your time to read the following statistics, and feel free to ask me questions if you need assistance deciphering the figures.

Patient and hospital characteristics for
ICD-9-CM all-listed diagnosis code
276.1 Hyposmolality
Total number of discharges Standard errors
Total number of discharges
All discharges 1,901,923 (100.00%) 48,831
Sex Male 863,661 (45.41%) 22,666
Female 1,038,073 (54.58%) 26,924
Missing * *
Median income for zipcode Low 525,033 (27.61%) 21,741
Not low 1,330,533 (69.96%) 42,237
Missing 46,357 (2.44%) 4,125
Patient residence Large central metro 511,650 (26.90%) 38,083
Large fringe metro (suburbs) 460,735 (24.22%) 35,726
Medium and small metro 534,770 (28.12%) 39,687
Micropolitan and noncore (rural) 357,490 (18.80%) 18,234
Missing 37,278 (1.96%) 9,566

Weighted national estimates from HCUP Nationwide Inpatient Sample (NIS), 2010, Agency for Healthcare Research and Quality (AHRQ), based on data collected by individual States and provided to AHRQ by the States. Total number of weighted discharges in the U.S. based on HCUP NIS = 39,008,298. 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.

If you want to test whether apparent differences are significant, use the Z-Test Calculator. A p-value of less than 0.05 is generally considered statistically significant.

Here is the statistics for those who developed hyponatremia in 2009:

2009 National statistics – all-listed
You have chosen all-listed diagnoses. The only possible measure for all-listed diagnoses is the number of discharges who received the diagnoses you selected. If you want to see statistics on length of stay or charges, go back and select “principal diagnosis.”
276.1 Hyposmolality
276.1 Hyposmolality Standard errors
Total number of discharges 1,735,847 52,458

Weighted national estimates from HCUP Nationwide Inpatient Sample (NIS), 2009, Agency for Healthcare Research and Quality (AHRQ), based on data collected by individual States and provided to AHRQ by the States. Total number of weighted discharges in the U.S. based on HCUP NIS = 39,434,956. 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.

NOW, I HAVE TO SAY THIS: I NOTICED THAT THERE WAS A DISCREPANCY, A SIGNIFICANT DISCREPANCY, IN THOSE LISTED AS TO HAVE HYPONATREMIA IN 2009, AS THE ONLY DIAGNOSIS IN 2009 VS THE DATA LISTED IN 2010. WHEN I SELECTED HYPOSMOLALITY AS THE ONLY DIAGNOSIS CODE IN 2009, THE STATISTICS DROPPED TO ~90,000 PEOPLE. HOWEVER, WHEN I SELECTED HYPOSMOLALITY AS BEING A DIAGNOSIS WITH OTHER MEDICAL CONDITIONS, THERE WERE OVER 1.7 MILLION. WHEN I FUNNELED THE SAME SEARCH OPTIONS INTO THE 2010 DATA, THE NUMBER WAS THE SAME FOR BOTH SEARCHES.

WHAT DOES THIS MEAN?

I think the information was coded incorrectly in previous years, or in 2010, but it’s difficult to say which information is correct. It is accurate to say that there are millions being treated for hyponatremia each year, but it is apparently difficult to determine if they are developing hyponatremia while being treated in the hospital for other conditions or whether or not they are being hospitalized because they have hyponatremia on its own.

I hope that makes sense, but it’s important to keep that in mind when reviewing the statistics.

I hope to obtain the same information for CPM/EPM, but it’s more difficult because it is rare, and I don’t believe there is an actual single diagnosis code for it. In other words, they include CPM/EPM, in a blanket diagnosis code for central nervous system injury, which can include numerous other injuries.

Well, there you go folks. I am completely exhausted, so I am going to leave it there right now. Please, if you read my blog, and feel that I dropped the ball on a topic or think there should be expansion on a topic, PLEASE, PLEASE, let me know. I do not remember the things I’ve posted about before, and it’s difficult for me to go back and read through my other posts, so I am relying on you to keep me on track.

Thank you!

 

Deb’s Story:

 

Deb has helped provide insights into symptoms that are related to CPM/EPM. She’s suffered from the condition for four years, and I am including excerpts from comments that she’s left me in my comments section to help journal some of the symptoms that aren’t recorded in the medical literature.

In the beginning:

I had the headache for about a month before my collapse into a coma. I kept going to the Chiropractor thinking there was something wrong with my neck, but as it turned out it was my sodium.

She further describes her experience:

My initial symptoms were severe. I was in a coma for 4 weeks. Went into cardiac arrest twice. When I woke I was paralized from the neck down, unable to speak or swallow. I had a feeding tube thru my nose while in my coma, but when I woke and they realized I wasnt able to swallow they put one in my stomache. I was then sent to a nursing home where I did 5 hours of phsyical, occupational, and speach therapy daily. I was in a wheel chair for quite a while. I had horrible pain, sharp shooting pains, and alot of cramping. When I woke from my coma my left foot and leg were cramped up, my foot was up to my knee. My hands, were curled up in balls. To make you understand my mind set, when I saw my neurologist for the first time after I left the hospital, he told me I may be in a wheelchair for the rest of my life. My very first words were “F*** you”. They were faint, and hard to get out, but he had to know what I was thinking. Over the next few months I continued my therapy daily. Eventually I was walking with a wlaker. Then my therapy was cut from 5 days a week to 3. And again over many, many months I began to walk with a cane. My tremers are bad in the AM before my meds, my muscles feels like they are constantly being torn. But now I am duing therapy on my own, I can still only lift 2lbs, I have lost over half of my muscle tissue. They say I may never get that back, also eventually I WILL be back in a wheelchair. I can type with 2 fingers, I used to type 80wpm. I have trouble with my vision, My left eye is now considered a “lazy eye”. When I am tired, or look at the computor for too long it gets a mind of its own. My ligaments in every joint are kinda like broken rubber bands, my joints are what they call “free floating”. So, beginning in Sept I am going to start a series of surgeries on them to tighten the ligaments. I have constant pain, never letting up. Not even for a minute. I go once a week to a Chiropractor because my muscles pull my bones out of place. I also have a massage once a week to help keep me limber. Mind you, I am a former swimmer, loved to run, play volleyball, softball, or pretty much any outdoor sport. Now I have the body of a 80 year old (according to all my docs) and the life of one too. CPM/EPM has stolen everything from me. The only thing I enjoy now is watching my kids screw around in the yard and watching birds. My hands are so weak I can’t even enjoy baking or cooking. Hope this helps, I appreciate your site because I don’t have to say all this stuff on facebook, or even inspire. Sick, just sick to death of this disease. Deb

The following describes her experiences with tremors, a problem that I’ve described in previous posts:

The tremors, Mine are really bad in the AM before my meds. After my meds, they get better. If I am doing anything with my hands for too long they will get bad. I have to have an easy hairstyle because I don’t have the control to “do” my hair. If I hold the hairdryer for too long They will start to shake and cramp. I have an experiment for you; Take your thumb and 1st finger and make a “o” with them. Your thumb should point out at the joint closest to your hand. If it doesn’t you have significant muscle loss. Mine is completely flat, my “o” is more the shape of an egg. Give it a whirl. let me know what you find.

In regards to her experience with how she experienced improvements, but over time, she experienced a decline in her health:

Yes, I have had a decline in my health where things initially improved. I have the same issue with recall, I get so pissed at myself! I can remember things that make me angry or upset just fine, but any happy memories just fade away…… My thumbs face a weird way too when I try to make my “o”. My occupational therapist was the first to notcie it. Also, every morning I cry when getting up, all my joints and muscle are so tight it is rediculous! That’s why I do yoga, it help stretch things back out. What is happening is when you sleep your spasticty is causing your joints and muscles to tighten. So, when you wake in the AM, your body needs to move, if you didn’t move would become “stuck” . I have the reading issues as well, haven’t read a book in almost 4 years. All for now. Deb

………I have been pretty lucky as far as docs go. Since they don’t know much about my disease they take my word for pretty much most of the time. My new issues are my thyroid. I now have hypothryoidism. Never had any issues ever before in my life. My memory sucks as well. I have issues with concentration and my spelling. I could spell anything before, now I have to think thru a word, and sometimes I still get it wrong. I am very spastic, my movements are almost robot like. They have gotten better in some ways, and worse in some ways………

You can read more about spasticity through the blog post I made that included the information that Deb provided.

In regards to the emotional issues related to CPM/EPM, which I touched upon in my previous posts:

….. I know exactly what you are talking about. I still struggle with these things and my cpm/epm happened 3 1/2 years ago. And your right, I never feel truly happy. I can feel good about things that happen to other people. I have lost all of my family (mom, dad, brother, sister) because I just tell it like it is. Things I kept bottled up for 30 years just came flying out of my mouth, I had no control. It was like I was another person. Most of my husbands family has walked away too. They just can’t handle my brutile honesty. Things just blurt right out. I have no control. Before I know what I am saying people are standing there with their mouthes hanging open, just stairing at me. Whatever I am thinking just fly’s out of my mouth! I am almost always so close to tears all it takes is one weird look from someone, anyone and I am crying. In fact yesterday, I told my husband I think I need to find someone to talk to. Someone who justs listens and has no judgement. Since this happened I have felt useless. I have tried every kind of “hobby” you can imagine. Most I can’t do because of my hands, and the rest I just don’t have the patience for. I have been reading your blog on a regular basis, and I think it;s great!……..

Deb has also left several comments on the importance of using sea salt. There is a growing recognition on how sea salt is the better type of salt to use, but I haven’t researched it myself, so I don’t know where the difference is.

…….Also, I have seizures when my sodium gets down to 128. That is the “magic number”. Since my incident, my sodium has been pretty well controlled. I read an article that if you eat sea salt on everything it won’t raise your blood pressure, but also give you what you need. I eat it on everything!!! ……

…….I have been writing to Dr. OZ for 3 years. Also Dr nancy from the Today show. But they don’t want this info out. It would ruin their “salt is bad” campain. They are right, table salt is bad, but sea salt couldn’t be any better for you………..

I hope to post more regarding how CPM/EPM has impacted others, so please feel free to leave me comments, etc if you would like to participate. I really believe this is the only way we”ll ever be able to express our stories in their fullest. Medical journals do not research symptoms or experiences that we suffer from long term. There’s just not enough information regarding our experiences, so we will have to document them ourselves.

THANKS, DEB!!! Hopefully, you will be the first of many 😉

A large number of case reports regarding CPM/EPM:

This post is going to list a website that I found regarding dozens of case reports regarding CPM/EPM.

I was really surprised that these case reports, though brief, do correlate to many of my previous descriptions of symptoms associated with CPM/EPM. I do not know where these case reports were cited from, and I wish that there were more detailed accounts, but we have to work with what we have. The following information comes from this link: http://www.lookfordiagnosis.com/cases.php?term=Myelinolysis%2C+Central+Pontine&lang=1&from=10

11/105. immunoglobulins are effective in pontine myelinolysis.

Although the exact pathogenesis of central pontine myelinolysis (CPM) is unknown, correction of hyponatremia, thyreotropin releasing hormone, plasmapheresis, and corticosteroids seem to be effective. Assuming intravenous immunoglobulins (IVIG) to also be effective in CPM, 0.4 g/kg body weight/d immunoglobulins were applied to a 48-year-old patient who developed CPM with double visiondysarthria, dysphagia, and left-sided hemiparesis 3 weeks after spontaneous normalization of hyponatremia. After 5 days of IVIG, his symptoms markedly improved, confirmed by improvement in the Norris score (42%), Frenchay score (19%), Kurtzke score (20%), Disability score (54%), vital capacity(26%), and peak torque (69%). The promising clinical effect of IVIG was assumed to be caused by the reduction of myelinotoxic substances, the development of antimyelinantibodies, and the promotion of remyelination. In conclusion, IVIG appear to be a promising therapeutic option in CPM. (+info)

12/105. Parkinsonism after correction of hyponatremia with radiological central pontine myelinolysis and changes in the basal ganglia.

Parkinsonism has been rarely described following central pontine and extrapontine myelinolysis. We report a case of parkinsonism developing following rapid correction ofhyponatremia with radiological evidence of central pontine myelinolysis and changes in the basal ganglia. A 56-year-old man developed drooling and bilateral hand tremors 3 weeks after correction of hyponatremia from 103 to 125 mmol/L over 14 h. He had a prominent 6 Hz resting tremor which worsened with action and mild cogwheel rigidity.magnetic resonance imaging (MRI) showed changes consistent with central pontine myelinolysis and increased signal on T1-weighted images in the putamen bilaterally. Histremor responded well to L-dopa therapy. There have been several other cases of parkinsonism developing after central pontine/extrapontine myelinolysis. Increased signal in the basal ganglia on T1-weighted images has been described in another case of central pontine myelinolysis imaged about the same time after sodium correction as our case.(+info)

13/105. Central pontine myelinolysis: association with parenteral magnesium administration.

A 29-year-old woman with diabetes mellitus and nephrotic syndrome was given 30 g ofmagnesium sulfate over 14 hours after a cesarian section. Her serum magnesium level increased to 7.4 mg/dl. Five days later, she became quadriplegic with inability to speak or swallow. Cranial magnetic resonance imaging demonstrated central pontine myelinolysis (CPM). Initial serum sodium was not measured. Although CPM is usually associated with a rapid increase in serum osmolality, most patients who experience a rapid increase inserum osmolality do not develop the clinical syndrome of CPM. Consequently, additional factors may also be important in the pathogenesis of CPM. Parenteral magnesium administration may be a potential contributing factor in the pathogenesis of some cases of CPM. (+info)

14/105. Central pontine myelinolysis: delayed changes on neuroimaging.

The authors report two cases, a 44-year-old woman and a 6-year-old girl who had mental status changes and hyponatremiaserum sodium levels in both of these cases were corrected quickly with further decline in their mental status, and the patients became quadriparetic. magnetic resonance imaging (MRI) studies performed then did not reveal any abnormalities, whereas a repeat imaging study performed 10-14 days after the shift inserum sodium revealed evidence for central pontine myelinolysis and extrapontine demyelination. The clinical manifestations and distribution of lesions seen on the imaging studies demonstrated that the above presentation of neurologic illness is the result ofhyponatremia and its correction. The authors conclude that imaging studies performed early during the illness may be unremarkable, but still a diagnosis of central pontine myelinolysis should be suspected and, most importantly, a repeat imaging study might be required in 10-14 days to establish the diagnosis of central pontine myelinolysis. (+info)

15/105. methylphenidate treatment of neuropsychiatric symptoms of central and extrapontine myelinolysis.

OBJECTIVE: Previous reports describe the presentation and course of theneurobehavioral manifestations of central and extrapontine myelinolysis; as of yet, however, there are no specific recommendations for treatment of these problems. We offer the first report of successful treatment. METHOD: We describe a 55-year-old man with chronic alcoholism who developed central and extrapontine myelinolysis following an episode of heavy drinking and rapid correction of hyponatremia. The patient acutely developed motor, cognitive, emotional and behavioral problems best accounted for by central pontine and bilateral striatal myelinolysis. These neuropsychiatric symptoms were treated with methylphenidate over the course of 1 month in an off-on-off-on fashion. The Neuropsychiatric Inventory and other tests were used to assess treatment response. RESULTS: Marked improvements in the patient’s neuropsychiatric status were noted only during treatment with methylphenidate. CONCLUSIONS: methylphenidate effectively reversed the neuropsychiatric symptoms associated with the patient’s demyelinating lesions. We discuss possible underlying mechanisms of both symptom formation and treatment effect. (+info)

16/105. Slowly progressive dystonia following central pontine and extrapontine myelinolysis.

A 28-year-old woman was hospitalized with dysarthria and oro-mandibular and upper limb dystonia. Approximately 8 years prior to the current admission, the woman became severely hyponatremic due to traumatic subarachnoid hemorrhage-related SIADH. brainMRIs showed a signal increase in the central ponsthalamus and striatum on T2 weighted images compatible with central pontine and extrapontine myelinolysis. From a few months after that event, dystonia progressed slowly over the subsequent 8 years. We speculate that the particular damage chiefly to the myelin structures by myelinolytic process may have caused an extremely slow plastic reorganization of the neural structures, giving rise to progressive dystonia. (+info)

17/105. Central and extrapontine myelinolysis in a patient in spite of a careful correction of hyponatremia.

We report the case of a 54-year-old alcoholic female patient who was hospitalized for neurologic alterations along with a severe hyponatremia (plasma Na+: 97 mEq/l). She suffered from potomania and was given, a few days before admission, a thiazide diuretic for hypertension. A careful correction of plasma Na+ levels was initiated over a 48-hour period (rate of correction < 10 mEq/l/24h) in order to avoid brain demyelination. After a 2-day period of clinical improvement, her neurologic condition started to deteriorate. By the 5th day of admission, she became tetraplegic, presented pseudobulbar palsyataxia, strabism, extrapyramidal stiffness and clouding of consciousness. Scintigraphic and MRI investigations demonstrated pontine and extrapontine lesions associated with Gayet-wernicke encephalopathy. After correction of ionic disorders (hyponatremia, hypokaliemia) and vitamin B (thiamine) deficiency, the patient almost completely recovered without notable disabilities. This case illustrates that profound hyponatremia, in a paradigm of slow onset, can be compatible with life. It also demonstrates that demyelinating lesions, usually considered as a consequence of a too fast correction ofhyponatremia, may occur despite the strict observance of recent guidelines. There is increasing evidence to suggest that pontine swelling and dysfunction may sometimes occur in alcoholic patients even in absence of disturbance in plasma Na+ levels. It is therefore of importance, while managing a hyponatremic alcoholic patient, to identify additional risk factors (hypokaliemia, hypophosphoremia, seizure-induced hypoxemia,malnutrition with vitamin b deficiency) for brain demyelination and to correct them appropriately. (+info)

18/105. Central pontine myelinolysis.

Central pontine myelinolysis (CPM), a neurologic disorder caused most frequently by rapid correction of hyponatremia, is characterized by demyelination that affects the central portion of the base of the pons. There are no inflammatory changes, and blood vesselsare normal. Clinical features usually reflect damage to the descending motor tracts and include spastic tetraparesis, pseudobulbar paralysis, and the locked-in syndrome.magnetic resonance imaging of the brain, the imaging procedure of choice, shows an area of prolonged T1 and T2 relaxation in the central pons, which may have a characteristic shape. Recovery varies, ranging from no improvement to substantial improvement. To avoid CPM, correction of serum sodium in patients with hyponatremia should not exceed 12 mEq/24 h. We describe a case of CPM in a hyponatremic patient who presented with a cerebellar syndrome with no pyramidal tract involvement and in whom the rate of correction of serum sodium was within the recommended limits. (+info)

19/105. Reversible central pontine and extrapontine myelinolysis in a 16-year-old girl.

A rare case of an osmotic demyelination syndrome in a 16-year-old girl is presented. MRI in the acute stage revealed a focal abnormal signal within the basis pontis and both caudate nuclei and putamina. Two years later brain lesions had disappeared on T1- and T2-weighted imaging, indicating that central pontine and extrapontine myelinolysis may be completely reversible. (+info)

20/105. Decreased diffusion in central pontine myelinolysis.

Two patients with central pontine myelinolysis (CPM) were studied with diffusion-weighted MR imaging 1 week after onset of tetraplegia. In both patients, affected white matter showed hyperintensity on diffusion-weighted images associated with a decrease in apparent diffusion coefficient (ADC) values. In one patient studied serially, ADC values normalized by 3 weeks after tetraplegia. Early in the clinical course, diagnosis of CPM can sometimes be difficult. Hyperintensity on diffusion-weighted images may therefore have diagnostic utility. Decreased lesional ADC values support the notion that CPM is a consequence of relative intracellular hypotonicity. (+info)

What’s wrong with me: psychological impact of CPM/EPM:

A few days ago I posted regarding how CPM/EPM has impacted my emotional abilities as well as my cognitive abilities. At that time, I didn’t have a lot of information regarding if this is a typical symptom of CPM/EPM.

Now, I have to stress what I’m sure I’ve mentioned previously; CPM/EPM is RARE. Hyponatremia is not rare, but developing CPM/EPM after it does not happen very often.

It is because it is so rare, there is not very much information, especially detailed information or studies that diagnose the symptoms. So, if  you approach a doctor to get answers, you might very well be given a blank stare. Let’s face it, if we had heart disease or cancer, we would get more information as to what to expect, but CPM isn’t widely seen by the medical profession, and even more importantly there aren’t long term studies or follow up of these patients. You’ll also find a lot of discrepancy in the research articles that are written.

I’ve been to several doctors who have never seen a patient with it.

What does this mean for us?

Don’t set high expectations for doctors who treat you, and as I’ve said before with CPM/EPM, ANYTHING GOES. NO one can tell you with absolution what is happening to you or things that have changed after you developed CPM/EPM isn’t normal or typical, because they DON’T KNOW. They really don’t.

I hope that over time, more research will be done for us who suffer from it, but in the mean time, I hope you find that my blog provides the most detailed information on what to expect.

SO, here’s what I found:

There is a link to emotional issues after CPM/EPM. There’s also a very solid link to cognitive issues. I’m also still trying to find links to the impulsiveness.

The following two links provide brief descriptions in their abstracts about having behavioral changes as well as cognitive changes. Now, here’s the thing; these articles require you to pay for access. I am citing their links, but I will only be able to post them after I gain access to them when I go to my local university, which is what I recommend if you don’t want to pay for them. Simply write down the name of the article, the publication date, etc and go to your local or major university library to access them, usually for free.

http://www.ncbi.nlm.nih.gov/pubmed/10514953

The following link provides information on the cognitive deficits a person experienced after developing CPM/EPM (but again to access full article requires payment):

http://www.tandfonline.com/doi/abs/10.1080/13554799808410619#preview

The following research article gives a fantastic description of how the damage occurs, but I will post that under the information regarding hyponatremia and the CPM section that describes how the damage occurs. The following quotes, I’m including gives an example of why I believe articles are pretty vague, but does give a more detailed account of the cognitive symptoms that we may experience:

A more recent study examined 12 individuals with CPEPM related to a variety of medical causes. In this more diverse population, four patients died in the acute  phase, and two were lost to follow-up. The remaining six were reported to have “good motor and cerebellar recovery.” However, all five of the patients who received neuropsychological testing had evidence of subcortical/frontal dysfunction, and most of these (4/5) were unable to return to work.

The next quote also describes another study that was researched:

Almost half (12/25) died either during the acute phase (2) or after hospital discharge (10). One was lost to follow-up. At final follow-up (mean 2.2 years; median: 1 year; range: 0 – 8 years), 29% (7/24) were normal; 17% (4/24) had mild cognitive or extrapyramidal deficits; and 54% (13/24) had a poor outcome (died or were dependent).

To clarify the above study: 2 people died immediately, 10 died after hospital discharge (but it doesn’t say from what); one died but not sure from what; 7 were “normal”, but it doesn’t clarify what that means; and 4 had deficits. Now, if you do the math these numbers don’t add up to 25…so what does that mean? There must be a mistake or error somewhere, and I think that helps to emphasize my point. The research articles on CPM/EPM are vague.

The next quote provides information from this research article on some of the cognitive impairments experienced:

A patient with only EPM (lesions in
the basal ganglia) had severely impaired attention, verbal and visual memory, visuospatial function, frontal
executive function, recognition memory, free recall
memory, and naming, with preservation of other language-related functions.
29
All these deficits are consistent with previous reports in patients with basal ganglia
lesions. In the other case, the patient had CPEPM (lesions in the pons, caudate, lentiform nucleus, thalamus,
and internal capsules).
28
At 1 week, the patient had
prominent deficits in attention and concentration (e.g.,
high distractibility, slow visual scanning), memory (immediate verbal recall and memory for daily events),
visuomotor functioning, and fine motor speed.

The above information really defines what I’ve been experiencing. My lesions were in the basal ganglia, so I have to say it’s pretty accurate in my regards.

The study goes on to explain that there were additional cognitive dysfunctions that occurred after the initial damage occurred and resulted in “pathological crying and laughter at 6 months after symptom onset, all consistent with a brainstem process.”

Doesn’t that sound a bit familiar. I’m not sure exactly what the pathological crying means. I’m guessing they mean it was inappropriate.

THE ABOVE QUOTES COME FROM THIS ARTICLE: http://neuro.psychiatryonline.org/data/Journals/NP/4399/jnp00411000369.pdf

It is very insightful, but I recommend breaking it up into sections because it can become a bit overwhelming.

So this is the information that I have found up to this point, but I’m sure there will be further information to come. There’s so much to go through..dud links…search results that don’t have anything to do with what you want, etc. Consider this post, like all of mine, a work in progress.

I hope it helps, and if you find something, message me with the link so I can add it. I REALLY appreciate your feedback. Truly the only way we can find out what is happening with CPM/EPM is through your feedback of what’s happening to you, so LEAVE comments, and details, etc. You’ll be helping other people!!

UPDATED: 04/20/12….Ok, so folks, so I have been trying to find more references to the psychological impacts of CPM/EPM.  The following link is in reference to a man who developed CPM/EPM after quitting drinking. They performed an MRI that showed lesions in his brain correlating to CPM. His behavior and symptoms progressed, and he began to develop angry outbursts, etc. They performed another MRI that showed demeylination was spreading further in the basal ganglia and the pons.

Two days after the admission, he showed violent behavior, agitation and irritability, getting angry on the slightest provocation without any mental changes or Parkinson symptoms or aggravation of his dysarthria. At first, we considered his symptoms to be alcohol withdrawal psychosis and started antipsychotics to control him, but his symptoms worsened. We performed MRI again 5 days after he developed psychiatric symptoms. The second MRI showed extended lesions in the bilateral basal ganglia and pons, as compared with the previous MRI.

The previous quote and information comes from: http://alcalc.oxfordjournals.org/content/43/6/647.full

This research article states that damage specifically associated with the basal ganglia areas are documented to cause behavioral and cognitive changes:

Abnormality of the basal ganglia is known to cause various cognitive dysfunctions and abnormal behavior via the involvement of the corticostriatothalamic or cortical–subcortical circuit through the basal ganglia (Carlsson,1988), while the role of pontine pathology for cognitive function and personality remains unclear.

UPDATE: 11/14/12

I have found this great research article that sites long term effects of brain injuries. In subsequent posts, I have decided that is safe to draw correlations between all brain injuries, so the following article describes what may happen psychologically after developing a brain injury. I have found that I have experienced a number of these issues, especially with distancing myself emotionally from people. There seems to be an emotional disconnect on a personal level, but I have the ability to cry over anything I experience regarding my brain injury. I don’t have all the answers for what is happening on a psychological level, but the following article does describe a lot:

http://apt.rcpsych.org/content/5/4/250.full.pdf —Psychiatric Sequelae of Acquired Brain Injury-Ken Barrett, APT 1999, 5:250-258

 

I am adding this quote from another research article that I found:

A patient with central pontine myelinolysis (CPM) underwent neurological and mental status examination, as well as neuropsychological testing, during the acute stage of the disease. After correction of the hyponatremia, a gross change in his neuropsychiatric status was observed. The patient underwent extensive neurological, psychiatric, and neuropsychological testing during the acute phase of the disease and at follow-up 4 months later. All major neurological and neuropsychiatric symptoms present at onset were fully reversible. Neuropsychological examination revealed deficits in the domains of attention and concentration, short-term memory and memory consolidation, visual motor and fine motor speeds, and learning ability. Although improved, neuropsychological testing still revealed remarkable deficits at follow-up. We conclude that neuropsychological deficits can accompany CPM, and that these deficits do not necessarily diminish simultaneously with the radiological or clinical neurological findings but may persist for a longer period of time, or even become permanent. In his recovery the patient started to manifest new neurological symptoms consisting of a mild resting tremor of both hands and slow choreoathetotic movements of the trunk and the head, which we considered to be late neurological sequelae of CPM. The significance of CPM in the differential diagnosis of acute behavioral changes after correction of hyponatremia is stressed, even if correction is achieved slowly and carefully.

This really explains the problems that I’ve experienced, and even mentions that you can have late onset symptoms related to CPM/EPM. The above quote comes from http://www.ncbi.nlm.nih.gov/pubmed/10514953

 

Savannah Hardin: Murder or Medical Malpractice

Let me start by saying, Savannah’s death is a tragedy, and I pray for her family and her friends. I hope this post might help shed light upon what caused her death.

A friend of mine posted comments regarding a blog she read about a 9 year old girl who was run to death by her grandmother (Joyce Garrard) and step mother (Jessica Hardin). When I read the title, I reacted immediately like I’m sure everybody did. I believed that these abusive people needed to pay for their crime,  then I read further.

The girl was forced to run for three hours because she had eaten a candy bar! Wow, this was definitely abusive. After running for three hours, she apparently went into a seizure. At this point, the step mother (who was 9 months pregnant) and paternal grandmother called 911.

This happened on a Friday afternoon and evening, and the girl died on the following Monday while in the hospital.

The autopsy revealed that she was dehydrated and had low sodium at the time of her death.

The report also stated that Savannah had a medical condition that involved her urinary system that required her to have monthly doctor’s visits. Apparently, eating chocolate could cause her serious complications which provoked the paternal grandmother into punishing her with running.

The step mother and  grandmother are being charged with murder. The grandmother is being charged with capital murder, so if she is convicted, she will face the death penalty.

Most of the information I’ve cited comes from the following article:

http://news.yahoo.com/2-charged-death-ala-girl-forced-run-082216169.html

My question is: what really happened to Savannah Hardin?

I have very limited information regarding her personal story, but I have a lot of information regarding hyponatremia. (Please see all of my posts regarding hyponatremia to find out more about this very common metabolic condition, and its life threatening consequences).

I really believe that her death was caused by or contributed to by medical malpractice or at the very least lack of appropriate medical care.

When I read the article regarding Savannah, so many questions come to mind. Did the women give the child water while she ran?

It is commonly believed that a person can exercise for long periods of time if they are provided water. (This is the case with many school athletic programs who push children to the extreme every year as long as they provide water breaks every 20 minutes.

Most people don’t realize how dangerous water is when exercising. When a person sweats, they release large amounts of salt through their sweat. If they proceed to drink large amounts of water, this will further dilute their blood sodium levels. It is so dangerous.

If Savannah’s guardians provided her water instead of an electrolyte based refreshment, like Gatorade, then this could have caused her sodium levels to drop dangerously low.

To further complicate her condition, Savannah had a urinary disorder/disease. Depending on what type of disease she had, this might have contributed to her ability to develop low sodium.

The basic symptoms of  severe dehydration and hyponatremia are the same: headache, nausea, vomiting, muscle cramps, seizures, dizziness, delirium and unconsciousness. Some of these symptoms may occur or all of these symptoms may occur. A big differentiation regarding those with dehydration is that they stop sweating.

Dehydration rarely causes seizures though, so I believe that when Savannah experienced seizures after running, it was because she was hyponatremic not dehydrated. It would be extremely difficult to determine without reviewing all of her medical records and questioning her family.

If her family was providing her with water, in combination with her physical condition and intense exercise, this would have been the perfect storm leading to her developing hyponatremia.

Why do I think there could have been medical malpractice?

It has been recognized that the standard treatment at the time of hospitalization for dehydration is IV fluids. These fluids tend to not contain sodium at all. If a person is treated with these nonsaline fluids and they actually have hyponatremia, then this treatment can be fatal.

It dilutes already diluted blood sodium levels. This would cause brain stem and cerebral swelling, further seizures, coma and brain death.

By the time the hospital receives the lab work showing low blood sodium levels, it is already too late to change the IV fluids to a low sodium based fluid, especially in children.

Please read the following information regarding the susceptibility of children for hyponatremia and how it is supposed that it is being caused mostly by hospital malpractice:

 It has now become apparent that the majority of hospital-acquired hyponatremia in children is iatrogenic and due in large part to the administration of hypotonic fluids to patients with elevated arginine vasopressin levels. Recent prospective studies have demonstrated that administration of 0.9% sodium chloride in maintenance fluids can prevent the development of hyponatremia. Risk factors, such as hypoxia and central nervous system (CNS) involvement, have been identified for the development of hyponatremic encephalopathy, which can lead to neurologic injury at mildly hyponatremic values. It has also become apparent that both children and adult patients are dying from symptomatic hyponatremia due to inadequate therapy. We have proposed the use of intermittent intravenous bolus therapy with 3% sodium chloride, 2 cc/kg with a maximum of 100 cc, to rapidly reverse CNS symptoms and at the same time avoid the possibility of overcorrection of hyponatremia.

This same research paper also recognizes that most children that develop it are inflicted by an underlying urinary condition:

 In order for hyponatremia to develop, there must typically be a relative excess of free water in conjunction with an underlying condition that impairs the kidney’s ability to excrete free water (see Table 2). Excretion of free water will be impaired when there is either (1) a marked reduction in glomerular filtration rate, (2) renal hypoperfusion, or (3) arginine vasopressin (AVP) excess. Most cases of hyponatremia are the result of increased AVP production.

The paper discusses what I mentioned above regarding how the symptoms for the cerebral edema in relation to hyponatremia can easily be diagnosed as other conditions, such as dehydration:

Hyponatremic encephalopathy can be difficult to recognize, as the presenting symptoms are variable and can be nonspecific (see Table 3). The only universal presenting features of hyponatremic encephalopathy are headache, nausea, vomiting, and lethargy. These symptoms can easily be overlooked, as they occur in a variety of conditions. There must be a high index of suspicion for diagnosing hyponatremic encephalopathy, as the progression from mild to advanced symptoms can be abrupt and does not follow a consistent progression.

The information that is quoted above comes from:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874061/

Now, here’s the take home message from the above article: if your child is being treated for ANYTHING in the hospital be sure they receive  .9% saline IV fluids.

I believe the hospital will be determined at least partially responsible for Savannah’s death. If the hospital had treated her for hyponatremia instead of dehydration in the beginning, Savannah might still be alive, and the reason I believe that they did not treat her for hyponatremia was because her autopsy showed that she was hyponatremic after being in the hospital for three days.  The media also implied that she was hospitalized for dehydration.

Please do not mistake that I condone the punishment the girl received: I DON’T. I really believe her punishment was harsh, but I am almost positive that her grandmother and step mother did not intend to cause her death, and I further believe that having the girl run that long did not DIRECTLY cause her death. It was a series of unfortunate events complicated by common ignorance, a medical condition, and the hospital incorrectly treating Savnnah for dehydration instead of hyponatremia.

 I hope that over the next few weeks or  months, more information becomes available so that people will better understand what happened to her.

We live in a democratic society, in which a person is presumed innocent until proven guilty. In our country, this has changed. We now get our information from the press, and we are quick to become the jury and the judge in such cases. I wonder if it will be a matter of time before we regress to a time where we will prosecute a person without a trial. This seems especially true in cases that involve children.

Who needs a judge or a jury, we have the press!

It is easy for me to sit back and criticize people for this type of reaction, but I am the same way. I read a story about a woman who microwaved her baby to death while in a drugged stupor, and my first reaction is that woman deserves to die a horrific death.

However, I refuse to read what the press publishes and believe that it is the whole story.

I may have several ideas as to what happened to Savannah, but it’s based on my very limited information. In order to know exactly what happened to her, a person needs to know: how long she ran; if she was provided fluids and what kind while she ran; what the treatment was that she received when she was transported in the ambulance and at the hospital; did the hospital recognize that she was hyponatremic and/or how long did it take for them to figure it out; what type of medical condition did she have and what was her urine osmolity?

If you are reading this, I pray that you pass this information along. It’s important that people know and understand the dangers involved with hyponatremia, especially regarding children. The more people realize the threat, the more pressure there is on a hospital to change their procedures for dehydration, and the fewer the number of children who will die or be forever brain damaged from hyponatremia.

UPDATE: According to news sources like the Huffington Post and ABC news, Jessica Hardin (Savannah’s Step-mother) is in the process of working out a deal with the prosecutors. Hopefully, the charges will be reduced, or her bail will be dropped to $500,000.

I do believe that there was a medical condition that caused Savannah to suffer from hyponatremia and that led to her death. I am hopeful that the charges will be dropped completely if it was, but unfortunately, innocence comes with a price.

http://www.cbsnews.com/8301-504083_162-57517645-504083/jessica-mae-hardin-ala-stepmom-accused-of-savannah-hardins-running-death-seeks-lower-bond/

02/17/2012

This week I had yet another appointment, and this appointment has stuck with me the rest of this week.

First, I want to apologize for not posting more recently than this. If you have CPM/EPM, you will find that your life seems to be full of the unexpected. You will find that there are days that seem normal and days that you wonder how will you be able to live the rest of your life in this manner.

It’s exhausting. It’s frustrating. It’s unfair.

It seems like everyday is chaotic and for someone who used to be so focused and moderately organized, this is driving me freaking crazy!!!

IT’S STRESSFUL!

SO, now I’m starting yet another category for my blog, but I still have to go back and add to hyponatremia, to CPM/EPM, and to my story!!! However, what I experienced this week needs to be addressed before I forget it, and it has really consumed me, so I feel I have to write about it.

C’est la vie!

This week I traveled 4 hours to meet with a neurologist who is a movement disorder specialist. I also had a MRI and something else….what was it. For real!! Another five minutes gone to trying to figure out what it was that I actually did while I was there. I only had three appointments. Oh, yes, the skin biopsy.

I thought I was going to go to the neurologist to get a TREATMENT for my tremors, jerks, shakes, twitches, spasms, etc. In other words, my neurological problems with movement.

I guess this is where I made my mistake. I had already met with a neurologist who is treating me for EPM, and she was sending me to get treatment for my EPM movement issues. She told me that she was sending me to a movement specialist neurologist for this purpose. I assumed that this was going to be the reason for the appointment: I was going to get medicine for my neurological issues related to EPM.

If I thought that I was going to be examined to determine on whether or not my movement issues were related to EPM, I would have been more prepared. I would have brought materials on EPM.

Here’s the thing: EPM IS RARE. CPM IS RARE. MOST DOCTORS HAVE NEVER TREATED A PATIENT WITH THIS INJURY, and it’s not that they are stupid or trying to be judgmental, they are purely ignorant!

This doctor was the same way.

I had no idea what the true intention for this appointment was, and this set me up for disaster.

This doctor did a complete neurological exam. He was pretty thorough.

After the examination, he told me: Well, you have an essential tremor and it is not related to your EPM. It’s fairly mild, but I can give you medication to treat it. I would also like you to test for Wilson’s disease. You don’t have any of the symptoms for Wilson’s, but it is a cause for tremors in a person who is younger. I don’t think you have it, but we’ll do the test as a precaution.

Before, having EPM, I would have just nodded my head and left. I would have spent the rest of the day biting my lip and waiting to say the things I wanted to say.

I don’t know what would have been better. I really don’t.

I literally started arguing with the doctor. He told me that because my MRI images were normal that the tremors weren’t caused by EPM.

Ok, folks, you know I’ve done research. I’ve spent the past 8 MONTHS researching this injury, and my first question to the doctor was: how many patients have you treated with this? His answer: ONE!!!

I then went on to say: My MRI still shows the injury (and it does). This is what my other neurologist has told me. However, if you were more familiar with EPM/CPM, you would understand that there is no correlation to the findings on an MRI and a person’s symptoms.

The doctor didn’t cotton to my pointing this out to him.

We literally started to ARGUE.

He basically told me that he wasn’t going to have me lecture him on this, but then I explained to him that I wasn’t pulling this information from WebMD. My information comes from credible medical research documents, and that I was preparing to go to medical school.

He warmed up a little bit at that point.

He tried to explain to me that the ONE patient that he’s treated with this disorder had the Parkinson’s like tremor that is associated with EPM/CPM. He told me that he had a video that he took on that patient. This particular person had both significant injury to the pontine region as well as the extra pontine regions AND that this person’s MRI still showed the injury.

He believed that my movement issues have nothing to do with EPM. He thought they were random.

He told me that I did not have Parkinson’s, and I did not have a Parkinson’s tremor.

Okay, so what’s wrong with what he was telling me, and how could I have better handled it? How could have this appointment gone better? What should I have done?

First, I should have been prepared. Really. I’ve been to hundreds of appointments. When you have something rare or not clearly understood, you need to come ready for everything. You need to have any research that you’ve found regarding your disorder. Make copies of your labs, of your reports, of research that you have found.

I had no idea what a Parkinson’s tremor was and how it was different from the tremors that I have. I will make a separate post on tremors and how they differ. Of course, with everything that is medical, there is disagreements on what is and isn’t a Parkinson’s tremor.

Basically, if you have a tremor or movements that impact one side of the body (at least in the beginning stages) that are present when you ARE NOT moving, they suspect Parkinson’s.

The tremor that the movement neurologist suspected is something called essential tremor. This type of tremor is usually found in both sides of the body. It generally becomes worse when you are moving. For instance, if you are trying to get food to your mouth or trying to get a cup to your mouth, but your hands shake so severely that your food falls off your fork or you spill liquids from your cup, they suspect essential tremors.

Now, I had no CLUE what the difference was. I had no idea that there was a difference. All I knew was that this issue became extreme when I developed EPM.

If I was prepared for this appointment, then I would have been able to produce information regarding my tremors. I would have also been able to represent the different types of tremors that are associated with EPM.

I did not know until after the appointment that this doctor really did not know what he was talking about: EPM/ CPM can have both, either, or neither…Parkinson-like or bilateral tremors.

In other words, my “essential” tremors, are probably caused by the EPM.

Furthermore, the doctor told me that there were no reasons to think that these tremors would not be long lasting if they were indeed caused by EPM. He believed that because the MRI images were improving then my symptoms would also improve.

I can not say whether or not this is true. I would have to point out to anyone who states that because your MRI images get better does NOT mean that your symptoms will improve. Further, if your MRI images DO NOT improve, that does NOT mean that you will not improve. The MRI, at this time, WILL NOT show anything more than that you had this injury.

The doctor also tried to state that symptoms will NOT get worse after the injury has happened. THIS IS TOTALLY NOT TRUE. DOCTORS DO NOT KNOW WHAT WILL HAPPEN WITH CPM/EPM!!! They do NOT KNOW.  People do see a progression in their symptoms even AFTER 8 and 9 months.

There has not been enough research in this area to know with any certainty what will happen. I know of 4 individuals with CPM/EPM that had improvements, but after a period of 1 to 2 years, their symptoms worsened. I really believe that this is related to just normal aging.

I would compare it to my cell phone that I dropped in the toilet. (It was an unused toilet at the time). I made the mistake of turning it on as soon as I fished it out. Now, anyone who is familiar with electronics knows this was a mistake. It basically fried it. However, I did not want to go out and buy a new phone. So, I took it apart. I sprayed it down with electronic cleaner. I let completely dry out and put it back together. IT WORKED! 🙂 BUT, there were certain keys that did not work, the pound and star button. I was perfectly fine with that because I didn’t really use those buttons that much any way.

So, I was happy, but several months later, other keys started not working properly. Some numbers would repeat a dozen times when I pushed them once. Sometimes, letters wouldn’t show up.

And this is my point, truly the brain works in a fairly similar way. We don’t understand how it works completely. Medicine is really archaic in this field. However, we know as we age the body breaks down. They don’t work as well. This is true for the brain. So, if you already have an injury in the brain, yes, you are likely to see improvements, but it’s like my cell phone, you just don’t know how long those improvements will last, and you are most likely to see these areas degrade over time as your brain ages.

Getting back to my appointment:

I tried to explain that the delay in new symptoms is believed to be caused NOT BY CPM/EPM INJURY directly, BUT BECAUSE YOUR BRAIN TRIES TO REBUILD CONNECTIONS, and it is believed that these new pathways can cause the new symptoms.

Therefore, people have seen NEW symptoms months and EVEN years after the injury. The doctor I saw agree with this, but he felt that new symptoms would not be seen after 1 or 2 months after injury.

See this article for a description on how this isn’t true:

Journal of Clinical Neuroscience 19 (2012) 179–180

And this one:

Journal of  Neurology (1995) 242:450-454
© Springer-Verlag 1995

Regarding the types of tremors that are experienced in CPM/EPM injuries, most are considered Parkinson’s like, resting tremors; however there are also studies that show that both types of tremors can be present, parkinson’s and tremors that worsen with movements.

Here is information from Wikipedia http://en.wikipedia.org/wiki/Central_pontine_myelinolysis:

 Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis andlocked-in syndrome.[14]

Okay, the following is what I have. I do have a bilateral resting tremor that gets worse with movement:

A 56-year-old man developed drooling and bilateral hand tremors 3 weeks after correction of hyponatremia from 103 to 125 mmol/L over 14 h. He had a prominent 6 Hz resting tremor which worsened with action and mild cogwheel rigidity. Magnetic resonance imaging (MRI) showed changes consistent with central pontine myelinolysis and increased signal on T1-weighted images in the putamen bilaterally. His tremor responded well to L-dopa therapy.

(http://www.ncbi.nlm.nih.gov/pubmed/10833626)

I could go on all day quoting journals regarding tremors and EPM/CPM. Here’s another:

Rigidity was present in all four limbs, with orofacial dystonia and dystonic posture of hands and feet and with tremor in both hands.

http://dmc.academia.edu/MahmudurSiddiqui/Papers/893372/Selective_Extrapontine_Myelinolysis_in_Osmotic_Demyelination_Syndrome_in_a_Case_of_Previously_Undiagnosed_Sheehans_Syndrome_with_Recurrent_Hyponatraemia_-_A_Rare_Association

If I had been better prepared, I would have been able to bring these things to his attention.

More importantly, I showed him two videos of my tremors. He believed these videos demonstrated that I indeed have essential tremors. And I cannot disagree with this statement. I don’t know. I’m not an expert in tremors.

That said, I only recently started recording my tremors, and more importantly, I have spasms and jerks in certain fingers, in my legs, or feet, but these jerks are fleeting. So, I will have three or four twitches in my finger and there’s no way that I can record those particular movements without making a video diary of my every waking moment. I never know when these movements will occur.

This is extremely frustrating because by this point in my appointment, there was no trying to communicate with the doctor. I was too emotionally involved and so was he.

His take away message was: you’re going to be fine. You aren’t going to get worse. You are going to get better. You should try this medication to help with the essential tremor that you have, and I am almost positive that your tremors are not related to EPM. Even if they are, the medicine should help them. You do not have Parkinson’s.

Now, this seemed to be a crux in the conversation that I haven’t hit upon previously. He kept stressing that I did not have Parkinson’s. He stated that he was an expert for Parkinson’s.

I really did not understand why he kept bringing up Parkinson’s disease. I DO NOT HAVE PARKINSON’s. I did not think that I had Parkinson’s. I believe that I have Parkinsonism. Now, I’ve previously discussed Parkinsonism. From the knowledge that I have, it is any tremor that a person has, along with dystonia, and dyskinesia, and possible issues with your voice. I am not an expert on this. I know what I’ve read, and I promise to research this further and try to post on this more when I post specifically on tremors.

What’s wrong with his message:

HE HAS ONE FREAKING PATIENT WHO HAS HAD CPM/EPM. He certainly hasn’t spent the past 8 months researching every possible thing you can find on it.

He made incorrect comparison’s: Parkinson’s and EPM. People with EPM/CPM DO NOT HAVE PARKINSON’s. They have a Parkinson’s like tremor, and that isn’t even true for everyone with EPM/CPM. He did not understand that there IS NO SET STANDARD for CPM/EPM. It’s like saying someone who has colon cancer will have the same symptoms and issues as someone with esophageal cancer. It’s like saying there is only one cause for heart disease.

He was unwilling to say: I DON’T KNOW. I will need to evaluate you further. Please spend time making more videos of your issues and feel free to contact me when your symptoms change or if you have a video of something different. He didn’t even ask me when I took the videos I made.

I tried to explain that my symptoms vary in severity from day to day. Truthfully, they vary from hour to hour. Right now, I barely have any tremor at all. However, an hour ago, I did. I have twitches and spasms even at night when I’m trying to go to sleep, at rest. They make it difficult to fall asleep. I don’t have this problem EVERY night, but probably three or four times a week.

So, what could I have done?

I should have made a journal of these things. I should be keeping a daily record of my symptoms, the times, places, how much caffeine have I consumed, etc. Doctors really like data. They like it when you have detailed information for them to look at.

I really haven’t documented my symptoms and when I have them. I should be keeping more videos. I feel embarrassed to pull out my cell phone or video recorder to make these videos in public places when I’m experiencing these problems. I believe that those localized spasms that I get in my fingers or feet don’t last long, so I shouldn’t bother trying to record them.

I AM MY ONLY ADVOCATE. NO ONE ELSE IS GOING TO DO IT. You really need to take this to heart if you are reading my posts.

No one else is going to go to bat for you, and if you are willing and able, you need to make as many records as you can regarding your situation. It can and will help you out. It might help your doctor more fully understand your situation. More importantly, you can post it here on my blog and help others with CPM/EPM.

I also shouldn’t have bothered correcting this doctor when I didn’t have access to the medical journals or very good videos of my symptoms. Now, this doctor has formerly based his opinion. He isn’t going to bother to do anything else with me. If I ever need to go back to him, I will have to have a huge collection of evidence proving him wrong.

Let me stress, it’s not important to prove him wrong for the sake of being right, but because I will not get help from him unless that happens. I also won’t get the correct medications for the types of neurological issues that I have.

It’s also important to realize that it’s important to realize when you’ve lost a battle. It’s your choice on whether or not you are going to waste your precious time and health on trying to bring this person up to speed on CPM/EPM.

As more and more records become easier to access, hospitals will become able to share information on your medical history. This means that this doctor may be able to pollute the opinions of future doctors that I see, even at different hospitals, in different cities or states.

So, you really need to make a decision on whether or not you are going to spend your time and resources on “educating” a doctor on your condition.

If you choose to, I think it’s really important to “educate” him on the first appointment. First impressions make the biggest impact, and this is most certainly true for your doctors.

In other words, you need to be prepared for EVERYTHING on that first appointment. You have to have research articles on the types of symptoms and issues that you have, especially when those symptoms are rare. You need to have videos and if at all possible, personal testimony from family and friends (hopefully someone can go with you for your appointment that can attest to your issues and their severity). It’s great if you have a journal of your symptoms from each day.

You need to ask your doctors questions like: how many patients have you treated or seen with CPM/EPM? And it’s important for you to make a decision on whether or not you are going to continue to see this person if the appointment does not go well. Be prepared. Don’t be afraid to ask questions.

I’m sorry if this post was a bit repetitive. I believe that when I have something that I feel especially strongly about, I tend to repeat it. I will try to edit in the future for those type of repetitions.

For now, I’m going to retire. and as always, please feel free to write me with any questions or your personal story.

Hyponatremia: Children

I know I’ve mentioned that children are at risk for hyponatremia, but this is a growing epidemic.

Here’s the thing: children can be at great risk because when they go to a hospital for treatment they receive a general IV which is usually lacking in sodium. When this happens, a child’s blood sodium level becomes diluted to point of hyponatremia.

At this point the child’s brain begins to swell and their brain is larger at this point compared to the size of their skull VS that of an adult. In other words, a child’s brain is fully developed at 6, but their skull doesn’t become fully developed until around age of 16. This gives a child’s brain less room to expand, and so they are more likely to develop injury.

Use the following link to find out more:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874061/

It is suggested in this article that a child should be given IV fluids containing .9% saline whenever treated in the hospital. This includes ER visits.

Because the early symptoms of brain swelling are common symptoms of nausea, headache, vomiting and lethargy. This article suggests that their blood sodium levels be checked at the presentation of these symptoms.

I’m not sure what it is with me tonight, but I’m at a point of loss right now. I just can’t concentrate fully. The article I have cited above contains extremely pertinent information for the treatment and prevention of hyponatremia in children. It is also a recent article from 2010.

I highly recommend if you have a child who is in the hospital who is being treated for any disorder, make a copy of this article and go over it with your pediatrician or your treating physician.

At some point in the future, I will attempt to edit the post to a more complete form, but I really find that the information itself is important enough to publish even in this rough draft form.

May you never need to use it personally.

 

My EPM story: the diagnosis:

Up to this point, I have talked about how I developed hyponatremia, how it was treated incorrectly, and how I tried return to the local hospital (the place that treated my hyponatremia) THREE times to get treatment for my developing issues with EPM.

The last trip to my local ER, I asked  for a MRI because I was almost positive that I had developed EPM. Instead, they attempted to admit me for observation because of the reaction I had from their doctors, I decided it would be better for me to travel to meet with my ENT and endocrinologist.

After hearing about my issues, they were also determined to get me into to see a neurologist, despite it was the Thursday before the Fourth of July. Trust me, despite going to a HUGE hospital with hundreds of doctors, trying to get an appointment with one of their 50 or more neurologists was a big deal.

Tom and I had no idea what was going to happen next.

I left my local ER around 7pm. I was pumped full of narcotics and was almost dead to the world. I mean, I really did not know what was going on.

I got home, and I think it was at some point around 3 or 4 am, we started our oddessy. We had our three year old with us, and this trip was unexpected. We had no idea how long we would be gone, or what we would need.

I guess we planned for the worse because we didn’t run out of clothing, etc. Granted, I spent my time in a hospital gown.

So, our trip up to the hospital was awful. I had a splitting headache. I didn’t feel well. My daughter was acting like all three year olds. At first, she slept but around 9am, we stopped to get breakfast.

It became absolutely clear there was a problem when I tried to order breakfast for us. Tom had gone to do something, find a table, I don’t know what, so I was left at the counter alone to order.

I knew what we needed, but I was having trouble understanding what the girl was saying. I was extremely frustrated. All I had to do was give the girl the numbers and tell her what drink we needed with each. Tom’s order was easy. Izabel is a picky eater, so I had to make adjustments with her order, and I had a hard time asking if they had pancakes or cereal. I had a hard time explaining that I needed milk with her meal not coffee. The most frustrating thing was when I wanted to change the kind of cheese on my order. I didn’t want Swiss cheese that normally came on the sandwich, I wanted American cheese.

I kept telling the cashier: I don’t want cheese. I want cheese.

Of course, she looked at me like I was retarded because I was.

I tried to explain further: Not cheese. Yellow cheese.

My entire order was like that; I couldn’t express the changes I wanted to make. I had a hard time asking for coffee with Tom’s meal. I had a hard time finding out if they had cereal, and by the time it came to my order, I was left to pointing irrationally at the pictures on the wall. Number 6, no cheese, cheese. I don’t want cheese. I want cheese.

Yeah.

I KNEW what I wanted. I couldn’t say it. AND, these episodes kept skipping. It wasn’t continuous issues with communicating. Talk about feeling like you’re going completely nuts.

Shortly after we left Arby’s, I started experiencing the crippling stomach pains which I no longer was considering as an issue for porphyria but for my adrenal glands.

With all the physical and mental stress I was having, it isn’t difficult to believe that my adrenal glands were becoming stressed. Maybe it’s not my adrenals, maybe it is AIP, maybe it’s both…I really think only God truly knows, but all I did know is that sugar/glucose would stop the pains.

So, Tom and I went off track to find a CVS or other drug store to pick up a bottle of glucose tabs. This delayed our getting to the hospital, but trust me I don’t think I could survive an attack of crippling abdominal pain.

After a shot of liquid glucose and about 1000mg of glucose via tabs, the pain subsided a bit. I was feeling more nausea, but the painful cramps weren’t as bad.

I swear this trip was CRAZY. I think it took four hours longer than it normally does, and I can not explain WHY it took so long. I mean, there was the stop for breakfast. There was the stop for glucose. We did hit road construction at some point, and then there were at least three potty breaks for Izabel.

During the drive, we were also working with an awesome receptionist for the neurology department to try to get an appointment with a neurologist. All of the neurologists were booked or gone already for the 4th of July weekend.

They could only make the appointment for about a WEEK from that date.

At this point, I still had no true clue as to what having EPM or CPM meant. I really didn’t understand that I was in a life threatening situation.

I believe I had read about it, but it didn’t sink in that this was really what was going on with me.

I was relieved when I got to my first appointment with my ENT. I really thought that he must have left packing in my sinuses and that this was going to be the reason I was having such a horrible headache.

I remember sitting in the waiting room, extremely calm. My little girl was striking up a conversation with another little girl. Tom was looking up the newspaper on his laptop, and I was just waiting.

I tell you. I was still experiencing difficulties speaking. Then they did the torturous search of my nasal cavity and sinuses. They spray your throat and nose with a numbing spray, and I was getting extremely ill from the spray. It’s supposed to taste like bananas. It doesn’t. Some people don’t have any issues with it, but other people, like me, the numbness triggers your gag reflex and you because extremely ill.

Then they slowly insert this 1/4 inch diameter, flexible, rubber hose with a scope on the end up your nose.

It doesn’t seem like they should be able to get that much of the hose up your nose (ha, that rhymes), but they did, and I can’t imagine having an alien abduction be more painful or uncomfortable. Just saying.

The ENT reassured me that things looked good. He assured me that there was no packing in my sinuses. He assured me that the surgical site was looking great. However, he was concerned with my neurological issues. He was glad that I was going to see my endocrinologist. He thought I should be hospitalized, but he wanted me to see the endocrinologist first.

So, by this point, I needed a wheelchair to get around. I was truly nauseous, dizzy. I was having issues with my balance. I had the horrible headache.

My endocrinologist is the most awesome doctor in the world, with a close second for my neurosurgeon and an even closer third with my ENT. Truly, I’ve been to hundreds of doctors, or at least a hundred. I’m not sure if that’s an exaggeration. I’ve seen a lot of doctors, so please believe me when I say, these doctors are amazing.

My endocrinologist was disturbed at my neurological issues. She was concerned at how long they had been going on. I told her that I thought I had CPM. I explained why I thought I had CPM. She didn’t arch her eyebrows. She didn’t give me a smirk or a shrug.

She told me that it would be unlikely for me to have CPM because I was 34. She believed that only babies and old people developed CPM. I became concerned that she wasn’t going to do anything.

She left the room to try to get an emergency consult with a neurologist. She checked back with us in about 10 minutes to let us know that the neurology department had not gotten back with her at that point.

She came back five minutes later to tell me that there weren’t any neurology appointments available, and so she was going to admit me. She felt I needed to have a MRI, NOW, not a day from now, not a week from now, NOW.

I was checked into the hospital and in my room in about an hour.

I was seeing the neurology residents in about 15 minutes after that. I was seeing another neurologist about an hour after that.

I was given another IV, pain medications, and because my endocrinologist totally believes me, she also requested the IV glucose to help with whatever it was, adrenal crisis or porphyria. (Even though my endocrinologist ordered it, the neurology department-unbeknownst to me- did not want me to have the glucose treatment, so that wasn’t started. This caused my abdominal pains to become unrelenting.

By 11pm that night, I was being wheeled down for the MRI. Trust me, even though my endocrinologist and ENT believed that I was experiencing a major problem, this belief was not as well received by the neurology department. I got arched eyebrows. I got the smirks.

I was desperate that they find something on the MRI. I KNOW that sounds funny. I KNOW that sounds crazy, but when you’re in that much pain, when you have that significant of a problem, the last thing you want is for them NOT to find anything. Trust me, when you have that many arched eyebrows and funny looks, if they came back with there’s NOTHING on your MRI, the next place you’ll be heading to is the psych ward.

My relief became absolute. My confidence in myself became iron clad, when the neurology resident came rushing into my room.

Resident: You were right. You were right. You have myelinolysis. THEY DID THIS TO YOU. THEY ARE 100% responsible.

I think I was on the verge of tears. I can’t remember exactly what he said after that. This injury was out of his league, and he assured me that the fellow in neurology would be in to see me in a very short while. He stressed that this was a serious issue and that the fellow was actually coming in from home to see me.

I had my answer. I had my reason. I wasn’t crazy. I didn’t have a stroke. I was right. I WAS RIGHT.

I wish that I could say, that’s it. That’s all that happened, but it’s not. The story does continue. Maybe, now, you’ll see why I’ve chosen to write about this later. It’s easy to become distracted and angry about what happened.

It can consume you.

Plus, it’s a hell of a long story. I mean, these are by far the longest posts that I’ve made, and they take the longest to write. It’s really exhausting, but I really feel, you need to know. You deserve to know. You need to learn to trust what you feel and to fight for what you’re going through. You need to understand that even the most prestigious hospitals in the country are fallible. You need to ask questions and push for answers, even when you meet resistance.

I hope this helps you with your struggles or helps to push you forward when you feel like giving up. You aren’t alone.

My story: The middle….

So, if you’re the random physician, you might have read my beginning story and thought, “hypochondriac”. You might think that if you aren’t a physician. Trust me that crossed my mind over and over again in the past 8 years.

Really…are you really feeling what you’re feeling? Try just sucking it up for a few weeks. Try concentrating on other things. Try the 20th antidepressant because your doctor believes it’s all in your head.

I even went to a psychologist not just once, but for dozens of appointments. I didn’t want to be sick any more than I wanted to have a broken bone.

Being sick robs you of life! You want to take your 6 year old son to the zoo, but every bone,muscle, joint in your body hurts. You want to go on vacation, but you’ve spent every day of your sick and vacation time at home or recovering from surgery. You’ve spent THOUSANDS of dollars on medical treatment, so you can’t afford to send your kid to camp or get a newer car.

To all of those people who believe that I was making it up, that it was all in my head or that I wanted to be sick, this is all I have to say to you: F*** You! Walk a day in my shoes and you would fall to the ground and would never get up.

(I would have totally left the proper cuss word in, however, I was told by Tom it might be a touch dramatic. I guess he didn’t read the rest of my post ;0)

I GET UP! Every time. It’s not easy, and I do struggle with it. I am extremely lucky to have great friends and family in my life that help carry me when everything becomes way too much for me to handle.

I have not given up, not yet. There are days when I want to. Yes, living a life with illness has caused me to make sacrifices. I’ve had to work on days that I could barely move. I’ve missed my son’s football games. I have scrimped to get by and have had to max out credit cards to make sure that I had food and clothes for my kids and me.

Being ill for this many years has PUSHED me to be a better person.

I started back to school while working full time, so that I could become a doctor because I had NO DOUBT that I can make a difference in the lives of other people. Money wasn’t a motivator. Trust me. It would be easier for me to work for less and not go to school than get up each day go to school, then go to work, and then come home and do laundry or homework.

I PUSHED myself to work 40 hours or more a week, while going to school full time, while taking care of my family, while being PREGNANT, while being SICK because of my absolution to help people, because I have been there. I have faced the struggle that 99.9% of the doctors have never faced.

It’s not enough to have an arrogant ass in a white coat tell you they are sorry or they don’t know. You need to have someone who has drunk the foul tasting barium, who has had a half dozen colonoscopies, who has gone years being ill with no answers; that is a person who you want to hold your hand or tell you they don’t know.

I am that person, and that’s why I have pushed myself to do what I have done.

YES, I AM EVERY WOMAN. I AM STRONG. I AM INDEPENDENT, but that doesn’t mean that I’m invincible.

Being told that I had a pituitary tumor gave me an answer, and it gave me a solution. No, I wouldn’t be able to put the toothpaste back in the tube. There were certain things that are irreversible, the auto immune issues, but I knew I could handle those things. I wasn’t going to continue to get worse, at least not from the pituitary tumor. IT was fixable, stoppable, and most importantly I had my answer.

My pituitary surgery happened June 10th. Everything went well with the surgery. There was an issue after the surgery where they thought I might have developed diabetes insipidus (see my earlier posts in hyponatremia for an explanation of what the difference between diabetes mellitus and insipidus are). It was pretty inconclusive. They thought I might have been just drinking too much water. I don’t think this was the case, but I honestly don’t know.

I know I was peeing a lot. I didn’t think there was much of an issue. Diabetes insipidus is when you pee more than you drink. So if you drink 8oz of water but excrete 16oz, then you probably have diabetes insipidus. They continuously measured my input and output, and this is what they felt was my issue.

I was kept in the hospital for 6 days after the pituitary surgery with all normal labs and normal vitals. That was a Wednesday.

Finally, I felt my exodus was over. There was a light at the end of the tunnel.

Friday morning, I woke up. I had a headache, but I really felt it was from the pituitary surgery. Then, I noticed my feet were cramping.

I’ve had muscle spasms in my feet since I was a kid, so I really didn’t believe this was anything new.

I had to go to the grocery store, so Tom and I went. It was there that my feet started cramping again. Now, this was unusual. The cramping felt different from when I get the spasms in my feet, but I didn’t think too much about it.

When I got home, I just felt-blah. I felt weak and tired. I ate some watermelon, drank some tea, and went to bed.

I woke up, went to the bathroom, ate some watermelon, drank some tea, and went back to bed.

I really felt off.

The next time I woke up, I felt really bad. I knew there was something radically wrong. The headache was just not going away. It was starting at the base of my neck and radiated through my brain. I felt sick to my stomach. My feet cramped when I stood up. I couldn’t tell if I was going to pass out or vomit.

I told Tom, he had to take me to the ER. I didn’t think I was going to live. (Yeah, I know, but there was this strange feeling, different from times in the past when I felt really sick. Can’t truly explain it, but you’ll know it if you’ve gone through it.)  I thought I was going to have to call an ambulance. (Tom was picking up our son, Zack, from a friend’s house, so he wasn’t home when I made the decision that this was really bad.

It seemed like an eternity for him to make it home and for me to get to the ER. I don’t remember much when I got there. This was around 11pm to midnight Friday night.

I remember going in and out of consciousness. I remember asking for pain medications. I remember at one point they did a CT scan, but I don’t remember getting back and forth from the room or having it done.

I remember a doctor coming in and telling me that my CT was normal. I thought, oh my God, they are going to send me home, but part of me didn’t care. The other part of me wanted to fight.

I was really lucky that they didn’t.

I think he came back later and he told me that my sodium levels were too low and that I would need to be transferred to the main hospital. I had a sodium level of 118.

They actually repeated the test to make sure it wasn’t a lab error. It came back 117.

I felt horrible.

I asked for pain and nausea medications over and over again because I couldn’t remember them giving me any. I just kept going in and out of consciousness. I want to stress this is not like falling asleep. Falling asleep you can generally fight. This I had NO control over.

I remember at one point I got up to go to the bathroom. The nurse asked me if he needed to assist me. My stubbornness and humility was still prevailing at this time, and I refused his help. I was really, really, lucky I didn’t pass out on the way to the bathroom.

Around 5 or 6 am I got transferred. I felt a huge moment of relief because I really thought this meant that I would get relief. I felt once I got there I was going to be better.

I remember being loaded onto an ambulance. I don’t remember the ride there. I remember staring at lights as they wheeled me down the hallway.

I remember being pushed through the doors of the ICU room where I was going to stay.

The next thing, I remember was waking up and it was morning, but I had NO idea what day it was. I didn’t know if I was out for a few hours or if days had passed. I knew where I was. I knew I had to go to the bathroom.

I know the nurse asked me questions. I thought it was Sunday. However, I don’t think it really was now. I think the nurse misinformed me.

I never went into an actual coma. I was in and out of consciousness the first day.

I believe I was still able to text my friends and family that morning to let them know what was happening.

Tom had left me the night before at the ER. He didn’t realize what serious condition I was in, and he went home to be with the kids.

I’m going to leave it here at this point because I wrote notes to myself about what I experienced a long time ago. My memory fails me now. I have to go back through my notes to know for certain what actually happened next.

I hope you find strength in this so far. I hope you understand that just because you have been sick or have faced issues, doesn’t mean that this is the end of the story. It’s just the middle. You’ve got a lot more ahead of you both good and bad, but it’s definitely not over.

Have faith.

Doctors:

I was finished with all of my pre-med classes and was seated to take the MCAT in June of 2011. That was before being told that I was going to have to have surgery for Cushing’s Disease.

I was actually relieved to find out that I had Cushing’s Disease because suddenly everything  made sense. The years of illness made sense.

Doctors try to find an answer that fits everything, but I kept having problems that didn’t fit the diagnosis. It started with endometriosis (and of course irritable bowel and fibromyalgia), but that didn’t make sense. Yes, I had pain with my menses, and I had heavy periods, but endometriosis didn’t really explain weight gain, fatigue, low grade fevers, hair loss, aches and pains, etc. I would also have crippling abdominal pain, nausea, vomiting, and blood in my stools.

I will try not to go into all the details, but over the years, I also developed hypertension. They found high uroporphyrins in my urine and blood, so my doctors believed I had acute intermittent porphyria.

Antiphospholipid syndrome explained the several miscarriage, and my elevations in cardiolipins, etc.

Bottom line, Cushing’s Disease explained everything (elevated uroporphyrins and autoimmune issues), so I was excited. I wouldn’t be cured from the autoimmune issues, but removing the pituitary tumor would take care of the Cushing’s disease, and I would feel better and there would be nothing stopping me from becoming a doctor.

I’m still hopeful that I will get into med school, but I’ve had another set back. After the pituitary surgery, I developed hyponatremia. The hospital corrected my sodium levels too quickly and that led to EPM. That was six months ago.

I’m better than where I was, but I’m a long way from MCAT ready. The MCAT is a thinking test. I not only can’t member what I need to remember, but I can’t think as quickly as I once did.

Because I’ve seen many sides of health care (that of the doctors as well as a patient), I feel conflicted regarding what I’ve been through. Life is not black and white.

I am extremely angry at the doctor’s who treated me, but I also feel an understanding about what’s happened.

I think people expect their doctors to be perfect. They get paid a huge amount of money to know what they are doing. Is it too much to expect that they do?

If you every look at a physician’s desk reference, it’s about 8 inches thick, in a font that’s similar to that used in a Bible, on paper that’s practically see through. It’s been said that about 5000 new diseases are discovered EVERY year.

If that’s the case then why do we feel that a single doctor will know and understand every disease and disorder that we might have?

Is it too much to expect?

That said, hyponatremia is a COMMON metabolic disorder. It is the MOST common metabolic disorder. Over 1.5 million people are treated for hyponatremia each year!

So now I feel caught in the middle. Yes, I do expect doctors to know more than the common person. They get paid to know it. At the same time, how will I feel if I’m on the other side of the clipboard, trying to figure out what this person’s tapestry of symptoms means?

Yes, life is not black or white.

Okay, now let me give you some more important information. Let me direct you to a group of doctors that are supposed to know more than most doctors in regards to CPM/EPM. Keep in mind, as I’ve stated before, there aren’t any “true” experts in the field because CPM/EPM is really rare, but these are doctors that have at least heard of it.

My neurologist, Dr. Noor Pirzada. I was referred to him by Jeffrey Amitin. I had the expectation that Dr. Pirzada had treated several patients with CPM/EPM. However, when I’ve questioned him regarding how many patients he’s treated, he won’t give me a direct answer, but will tell me that it’s very rare. I don’t know what that means exactly, but he’s understanding.

Dr. Noor Pirzada, University of Toledo Medical Center,

3120 Glendale Ave
Ruppert Health Center
Suite 1500 Door F
Toledo Ohio 43614
Phone: 419-383-3760
Fax: 419-383-3364
The following names come from GARD. They may or may not treat patients, but they have at least heard of it.
  • Dr. Richard Sterns: University of Rochester School of Medicine, Rochester, NY. (He is an expert in the treatment of hyponatremia and knows a lot about CPM/EPM.
  • Dr. Amyn Rojiani: University of South Florida, Tampa, FL.
  • Dr. Yeong-Hau Lien: University of Arizona, Tucson, AX

Yeah, I know, that list is really disappointing. If you’ve been treated by an “expert” in CPM/EPM, post it in the comments section.

I will also update it with doctors that I am in the process of contacting. Right now, I have contacted a handful of doctors that have written research papers on CPM/EPM, but I haven’t gotten a lot of information from them as of yet.

Thank you for putting up with my rant on doctors, and I hope this information helps a little bit.

 

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