The Nerve of THIS NERVE-Failed Amputation-Going for Round 3!

Yesterday I saw my surgeon-the amputation was a fail. The darn median nerve continues to curse my days and sleep. It went five days nonstop. Doc gave me no less than EIGHT lidocaine shots yesterday to shut it down. By the time he was done I couldn't feel any part of my right foot EXCEPT THE NERVE PAIN. I mean, it practically defies nature. The other possibility according to the million dollar nerve conduction equipment is that there are severely damaged small to medium fiber peripheral nerves in the skin that was used to close up the amputation. Anyway, THIS IS WAR (as my BIL used to say)
End of story is I'm going in for another surgery. I'll let you know when it is. He's cutting the median nerve in two new places and ripping out the skin used to cover up where the toe is amputated and stretching what's left to use. He may have to graft later if it doesn't take and I get a wound problem. Ah, another risk I'm willing to take-wound problems. Like I said, "THIS IS WAR" and I'm not backin down until this nerve is gone for good.
I know what your thinking but I'm actually very lucky to have a surgeon willing to go thrice trying to help me. This is his last suggestion, after that-he is outta ideas. You've got to remember I am a complicated case with circulating immune complexes causing inflammation in my blood vessels that press on nerves and damage them. This is my particular present from lupus.
So.......that's whats happening. :)

Toe Amputated-Goodbye Neuroma! Hello Successful SSDI Hearing! Goodbye Lidocaine Overdose!

So much has happened! I’ll break it up in Parts.  Part 1-toe amputation.  Part 2- I WON at my disability appeal hearing for SSDI.  Part 3-My favorite pain doc accidentally hit my vein with lidocaine and I became UNRESPONSIVE! 

 

PART 1 – TOE AMPUTATION
A week ago I had my 4th toe right foot amputated.  It’s still wrapped up.  I have a little phantom pain-but not too much and I think it’s just the nerve remembering-soon to forget.  I had it done in the hospital in the early afternoon and was home by 4pm!
I’ll take a pic of what my foot looks like as soon as I have the bandage wrap taken off.  Here is my right foot-bandage on.

A little bit about Neuroma’s from feetmd.com:  4th toe right foot amputation for neuroma

amputated toe

Morton’s Neuroma

In the foot, there are the long bones (metatarsals) and thin nerves running between them. The nerves split in a Y-shape when they reach the toes. If the metatarsals move abnormally, they can pinch the nerve between them, which causes inflammation and, eventually, permanent nerve damage. Morton’s neuroma is the most common of this type and affects the nerve between the third and fourth toes.

Click here to read more about Morton’s Neuroma»

Other Neuromas

A neuroma is a painful swelling of a nerve, usually in the ball or heel of the foot. Neuromas may occur after a nerve has been injured, either from a traumatic wound or from damage suffered during surgery. Symptoms include sporadic pain; burning, tingling or numbness of one or more toes; and a popping sensation when walking. Pain is often soothed by taking weight off the foot or by massaging the area.

Tarsal Tunnel Syndrome

Tarsal tunnel syndrome is a condition classified by chronic pain in the ankle, foot and toes caused by abnormal pressure on nerve roots. It is similar to carpal tunnel syndrome in the wrist and hand, but is not as common. The specific cause of tarsal tunnel syndrome is not known, but it can be a result of inflamed tissues around the tibial nerve, injury or other conditions that may affect the area.
The main symptom of tarsal tunnel syndrome is tingling or burning pain while standing or walking that starts in the ankle and spreads to the toes. Pain is usually relieved during rest. Doctors diagnose this condition by trying to induce the tingling sensation when tapping the nerve.
Treatment for tarsal tunnel syndrome depends on the cause of the pain but can include anti-inflammatory medication, orthotics, corticosteroid injections or surgery. Surgery is usually used as a last resort to relieve pressure on the nerve.
I had a failed median neurectomy July 12th and this amputation was a last resort for intractable nerve pain.  I’m 52, married 23 years and perfectly willing to take the risk of surgery if it means less pain.  Having several painful conditions, lupus, spondyloarthritis, recurring sacroillitis, osteoarthritis, PN, carpal, tarpal and ulnar neuropathy-this toe was the camel that broke the camel’s back.  That is why I decided on the total solution.  Also between surgeries I have to go off my lupus meds-and THAT is very difficult.  I have experienced a low grade fever almost every day, tons of mouth and nose sores, fatigue, muscle and joint pain, worsening anemia, etc.  This was my third surgery this year.  I am very positive I made a good choice FOR ME. 

PART 2:  I WON AT MY SSDI APPEAL HEARING!

After just over three years I had my day in court for social security disability.  I WON my  case.  I had a wonderful lawyer who did a tip-top job of organizing and preparing my medical files which were over two feet high, lol!  I’m still in shock!  I will talk more about this in another post where I hope I can be helpful for other people like me with lupus who are applying for disability.
Here’s the short list:  One thing is to keep all your medical records.  Have a good repore with your doctors, especially your rheumatologist and GP, neurologist if they are a big part of your case, etc.  Prepare them that you are coming to the end of your working days-and hopefully get their support.  Enough to have them fill out paperwork for your lawyer or to write you a letter describing your inability to work and why.
If you worked and had to stop-get a letter from your previous employers.  Hopefully this letter will reflect that due to no fault of your own you had to stop working-that your condition symptoms, doctor appointments and medication side effects all effected your ability to work but that while you did work you were an exemplory employee!  This is very beneficial to your case.
Of course, find a lawyer who specializes in social security disability, hopefully one that has been doing this type of work for many years-a local attorney is always better because they have dealt with the particular judges that you will be seeing should your case go to a hearing.  Any lawyer you do find should work on contingency-with about a 25 to 33% of your backpay reward as a fee.  There is a cap at $6000, so no worries there.  If a lawyer wants to charge you upfront I would look around for another.

PART 3-MY FAVORITE PAIN DOC HIT A VEIN BY ACCIDENT WITH LIDOCAINE DURING A PROCEDURE!  BIG OOPS!

I was considered unresponsive!  First let me say that I adore this doctor-he has given me back quality of life with radiofrequency ablations, cortisone and alcohol shots, and nerve blocks in addition to effective pain management medications.
I have all procedures in office and without sedation.  I’m good about that.  My theory is if your there for dealing with pain, you can make it through the procedures without being knocked out.  That said, this accident KNOCKED ME OUT COLD!
I woke up in a recovery chair confused and bewildered to say the least.  One of the nurses handed me my purse and coffee cup, which I dumped and spilled all over my lap in a dazed state.  They slid the thingy off my finger and said I was done and to go up front and wait for my scripts.  Huh?  I was really out of it.  I knew I was asleep but not why..really strange feeling.
As I wobbled down the hallway I looked back and my doctor half jogged towards me.  He said he accidentally got a blood vessel with the lidocaine.  I had no idea what that meant but it didn’t sound good.  I asked the one question that mattered.  I said, “AM I OK?”   He said “YES”, so I continued my wobble down the hall to check out and make my next appointment.  Really dazed…
Long story short when I got home I noticed I had bandages around my wrist and that both arms were black and blue.  My right wrist was black and blue-looked a little like dirt, and my left wrist where the bandage had been was bruised also but with puncture marks both on the wrist and then up by the inside of my elbows.
My husband called the docs office after this fiasco to find out exactly what happened.  They told him (they read it off the docs report)  that I was unresponsive and that he accidentally injected the lidocaine into a vein.  I still don’t know what that means exactly.  I know I was unconscious since the last thing I heard was “Julie, your doing great-almost done” and then I WOKE UP in a chair.  Huh?  Was I unresponsive other than unconscious?  Did my heart stop?  Did my breathing stop?  And WHAT DID THEY INJECT that they made all these holes in me?
Why did they not explain to me when I woke up, etc.  I was expecting a call back from my doc but he had a nurse call.  I wasn’t happy about that.  She tried to make it sound like it was all normal and no big deal.  SHE wasn’t the one UNRESPONSIVE.  I told her I want to know what happened exactly.  She spent her time defending why the nurses around me when I woke up didn’t know any better since they deal with people who are sedated waking up all the time.  I recanted with the fact THAT I WAS NOT SEDATED EVER DURING A PROCEDURE, so it certainly wasn’t normal for me!!!!!!!

Here is a pic of my wrists when I got home:  

Thanks for listening!  I read that lidocaine injections accidentally in veins can cause strokes, arrested breathing, severe hypertension, heart attacks, YIKES!

About Lidocaine Accidental Intravascular Overdose from epilepsy.com:

Lidocaine hydrochloride has proconvulsant and anticonvulsant effects, with CNS effects related to blood concentrations. Low doses (2–3 mg/kg) can terminate status epilepticus.
With increasing blood levels, CNS symptoms and signs of toxicity occur, from perioral numbness, lightheadedness, dizziness, tinnitus, and fine tremors to generalized seizures and coma. In animals, lidocaine produces epileptiform activity that is limited to the amygdala and hippocampus.86
Lidocaine doses that are commonly used for local anesthesia can cause CNS toxicity if they are inadvertently administered intravenously. For example, when administering epidural anesthesia, total doses of 5–8 mg/kg are commonly injected into the epidural space.84 Accidental intravascular injection of this dose can cause epileptic seizures.
In addition to direct intravascular injection and immediate toxicity, systemic lidocaine levels can rise to toxic levels by rapid systemic absorption from the area of injection. This can occur 10 to 20 minutes after injection. Anesthesiologists often add 5 mg/mL of epinephrine to the local anesthetic to decrease systemic absorption and peak serum lidocaine levels. When a regional anesthesia block is successful, early reinjection of local anesthesia can cause toxicity (including seizures), because peak absorption of the first injection occurs while additional medication is injected.
Efforts should be made to deliver minimum amounts of lidocaine to the lower respiratory tract in airway anesthesia (e.g., for bronchoscopy), because its pharmacokinetics at that site are similar to those with intravenous administration.87
High doses of lidocaine cause sedation. Increasing the arterial partial pressure of carbon dioxide (PaCO2) decreases the dose of lidocaine needed to produce a generalized electrical seizure.88 Higher PaCO2 levels increase cerebral blood flow, thus increasing the amount of anesthetic reaching the brain, and may directly excite the amygdala. In contrast to the usual pattern, in which hyperventilation activates seizure activity, hyperventilation may prevent seizures from occurring in patients with lidocaine overdose by decreasing cerebral blood flow.
Lidocaine is injected intravenously to provide local anesthesia (intravenous regional anesthesia or Bier blocks). In this technique, after an extremity is exsanguinated, and the blood supply is arrested by a tourniquet, lidocaine is injected into a vein to provide anesthesia. Doses of lidocaine up to 3 mg/kg of 0.5% solution without preservatives or epinephrine are used. Premature tourniquet release (less than 20 minutes) can result in high systemic lidocaine levels and possible seizure activity. Release after 20 minutes can also be associated with toxicity. Some physicians cycle the deflation of the tourniquet with an intermittent inflation-deflation-inflation cycle in an attempt to decrease rapid absorption of lidocaine from the extremity.
Seizures induced by lidocaine can be terminated with barbiturates.
Etidocaine hydrochloride, a long-acting derivative of lidocaine, as well as mepivacaine and prilocaine hydrochloride, share common pharmacologic properties with lidocaine hydrochloride.
Adapted from: Najjar S, Devinsky O, Rosenberg AD, et al. Procedures in epilepsy patients. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;499–513. With permission from Elsevier (www.elsevier.com).
Reviewed and revised April 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
This conversation is from ExpertLaw.com about the exact subject of a lidocaine overdose by vein during a pain procedure:

1. Lidocaine Reaction

   Yesterday I received lidocaine as a local anesthetic while getting a steriod epidural for bulging disc problems in lower spine. During procedure I began to have a severe allergic reaction that required I be taken by ambulance from the clinic to the ER. I was released after 4 hours of observation (and benedryl), but still not feeling very well today.
   The ER doc (not me) raised the possibility of an overdose, but said he asked the doctor who adminstered the lidocaine who said I got the right dose. I suppose there is also the chance the lidocaine was injected directly into a vein by mistake.
   How do I figure out what happened and if there is any fault here? I’m clearly not allergic to lidocaine or the steriod at normal levels since I’ve received both many times before.

2. Re: Lidocaine Reaction

   What kind of severe allergic reaction? Cardiac or itching/swelling?
   You could always get a copy of your medical record since the procedure, your reaction, and the fact that they had to call an ambulance should be documented.

3. Re: Lidocaine Reaction

   Thank you for your response.
   The reaction began on the table as really bad hot flash and nausea after the lidocaine injection. The doctor told me to hold on while he finished the ESI. It got worse when I got up.
   After moving to a chair post-procedure, symptoms of strong dull pain in chest/upper body and difficulty breathing began, and continued to get worse. Doctor initially said this was “normal” and would go away in 10 minutes or so. My BP was high and O2 level was low (based on the finger clamp thing?). When it didn’t go away, I was moved to a laying position, and after another 10 minutes, the uncontrollable, severe shaking started. I think that’s when they called an ambulance and took me to the hospital.
   In the ambulance they gave me a IV dose of benedryl. I also had tingling/itchy hands and blotchy skin.
   After getting to hospital, shaking and chest pain stopped and breathing seemed to return to normal.
   Also, isn’t the fact that they are billing my insurance company for the ambulance documentation enough that I needed that?

4. Re: Lidocaine Reaction

   First, the informed consent you signed before the procedure listed the side effects/risks of the epidural, as well as the medications given during the procedure.
   The fact that you did not have a previous reaction to Lidocaine doesn’t mean you’ll never have a reaction to it. It also does not mean the reaction you had was necessarily caused by Lidocaine.
   The ambulance company billing your insurance is not he kind of documentation you need. You’ll need a copy of the office notes from the procedure, which should contain notation of your reaction and the fact that 911 was necessary. You’ll also need a copy of the hospital ER record.

5. Re: Lidocaine Reaction

   Thanks. I guess one final question, and I don’t mean this to sound cavalier. If I signed the informed consent assuming all responsibility and risks, why do I “need” a copy of anything at this point?

6. Re: Lidocaine Reaction

   You originally asked:
   

   How do I figure out what happened and if there is any fault here?

   The answer may be in your medical record.

   Thanks. I guess one final question, and I don’t mean this to sound cavalier. If I signed the informed consent assuming all responsibility and risks, why do I “need” a copy of anything at this point?

7. you don’t assume all responsibility nor waive all rights to seek redress. You signed consent based on known risks and complications. That doesn’t mean if a doctor is negligent you have no redress available (not suggesting there were in this case, simply as explanation of what would not be waived by your consent form)

   THANKS FOR LISTENING EVERYONE!   ((((((((HUGS))))))))                Julie

Reactive Arthritis-WHAT? “React THIS-Arthritis”!

For me it took 3 bouts of sacroillitis (one was VERY bad-oy vay- couldn't walk, sleep, lay) that comes accompanied with it's pal uveitis and pinkeye. 
My rheumatologist calls with the results of my genetic testing-the gene HLA-B27 locked up the dx after the MRI of lower lumbar and si joint showed inflammation only and no bone fusing-had there been bone fusing a diagnosis of anklylosing spondylitis would have been appropriate.  Thank goodness it wasn't that-well isn't so far-  My grandmother had AS and she was in great pain and hunched over.  She also had undiagnosed lupus, which attacked her nerves, blood and skin the most-just like ME. 
The pain radiating on one side above my butt and under lower back-now known as the si joint is warm to the touch, swollen looking and varies in intensity when it acts up and is painful.  At it's worst I would not hesitate to clobber ya for getting in touching distance, lol.  Sometimes it's one side, sometimes its both and last December, the worst flare I ever had with it, it was both, it also included the pelvic area and I could not MOVE without pain.  Its horrendous.  It comes with uveitis and/or pinkeye.  And what the two have to do with each other, BEATS ME!  But here's the idea the doctors have:

Fast facts

• Reactive arthritis can affect the heels, toes, fingers, low back, and joints, especially of the knees or ankles.
• The infection that causes reactive arthritis usually presents (shows up) as diarrhea or as a sexually transmitted disease. But, it can have no symptoms (called asymptomatic).
• Though it often goes away on its own, reactive arthritis can be prolonged and severe enough to require seeing a specialist.

This figure shows the areas of the body that reactive arthritis might affect.

What is reactive arthritis?

Reactive arthritis is a painful form of inflammatory arthritis (joint disease due to inflammation). It occurs in reaction to an infection by certain bacteria. Most often, these bacteria are in the genitals (Chlamydia trachomatis) or the bowel (Campylobacter, Salmonella, Shigella and Yersinia). Chlamydia most often transmits by sex. It often has no symptoms, but can cause a pus-like or watery discharge from the genitals. The bowel bacteria can cause diarrhea.
Reactive arthritis can have any or all of these features:

• Pain and swelling of certain joints, often the knees and/or ankles
• Swelling and pain at the heels
• Extensive swelling of the toes or fingers
• Persistent low back pain, which tends to be worse at night or in the morning

Some patients with this type of arthritis also have eye redness and irritation. Still other signs and symptoms include burning with urination and a rash on the palms or the soles of the feet.

What causes reactive arthritis?

The bacteria induce (cause) arthritis by distorting your body's defense against infections, as well as your genetic environment.
How exactly each of these factors plays a role in the disease likely varies from patient to patient. This is a focus of research.

Who gets reactive arthritis?

The bacteria that cause reactive arthritis are very common. In theory, anyone who becomes infected with these germs might develop reactive arthritis. Yet very few people with bacterial diarrhea actually go on to have serious reactive arthritis.
Musculoskeletal
Signs and symptoms that affect your bones and muscles may include:

• Joint pain, usually in your knees, ankles and feet
• Heel pain
• Pain and swelling at the back of your ankle
• Swollen toes or fingers, which may look like sausages
• Pain in your low back or buttocks

Reproductive and urinary
Possible signs and symptoms of your reproductive and urinary systems include:

• Pain or burning during urination
• Increased frequency of urination
• Inflammation of the prostate gland (prostatitis)
• Inflammation of the cervix (cervicitis)

Eyes, mouth and skin
Signs and symptoms that affect your eyes, mouth and skin may include:

• Eye inflammation (conjunctivitis)
• Inflammation of your inner eye (uveitis)
• Mouth ulcers
• Skin rashes

Reactive arthritis develops in reaction to an infection in another part of your body, often in your intestines, genitals or urinary tract. You may not be aware of the triggering infection because it may cause only mild symptoms or none at all.
Numerous bacteria can cause reactive arthritis. The most common ones include:

• Chlamydia
• Salmonella
• Shigella
• Yersinia
• Campylobacter

Reactive arthritis isn't contagious. However, the bacteria that cause it can be transmitted sexually or in contaminated food. But only a few of the people who are exposed to these bacteria develop reactive arthritis.
Also called Reiter's Syndrome-here is more info:
https://www.mayoclinic.com/health/reactive-arthritis/DS00486
http://www.rheumatology.org/Practice/Clinical/Patients/Diseases_And_Conditions/Reactive_Arthritis/

 

for·ti·tude

/ˈfôrtiˌto͞od/

Noun

Courage in pain or adversity: “she endured her illness with great fortitude”.

I was writing an email to my father and out popped the word “fortitude”.  “Wish I had the fortitude” I wrote.  I know what it means but I looked it up anyway. Its definition pops out AT ME.  (see above)  And I can’t help thinking it’s not a coincidence.  I’m not enduring my illness with any for·ti·tude  at all and I should be.  I am more of an unorganized mess-lately hit with that dreaded brain fog forgetting what I’m doing and what I’m saying, names, places, faces, details.  Not enough of a help to my family.  I need to step up higher.  My husband is tired.  My son needs my help.  

Disability hearing is coming up in September.  The board of education kicked back my dismissed Sallie Mae school loans because my GP is a DO.  Go figure.  Alot going on and alot coming up.  My foot surgery seems failed and I will likely need two more, one to kill the other side of the nerve and one to take the toe.  The familiar pain has returned along with my unsettledness & has run off with my for·ti·tude.
Tomorrow is another day.  Tally Ho!

The EYES have it! Uveitis, that is!

ps.  Does the inflammation highway ever run out of track?  I don’t think so!  Todays stop boys and girls will be recurring anterior uveitis.  You-vee itis?  Me-vee-itis?  We all you-me-itis!

This is my second round of pretty bad uveitis-bad enough for the men in white to give me an iv of steroids and a shot in the eyes of the same.  YES, I said a Shot In The Eyes.
My last bout-December 2012 came accompanied with sacroiliitis, alias inflammatory arthritis, alias “are you kidding me” kind of pain.  So far it’s starting about the same.  While uveitis can come to the inflammation party on its own-there are alot of conditions that also can cause it.  In my case docs just blamed the L-Word although my grandmother had ankylosing spondylitis-and she may have set a genetic trap for me.  lol.  There’s a genetic marker-it is called HLA-B27 tissue type and testing is appropriate if you have both sacroiliitis and chronic recurring anterior uveitis.
Here’s what to look for in the inflammation of the eye: 
And here’s my eyes:  Of course the uveitis highjacked a malar rash and low grade fever  on it’s way to rain on my surgery recovery parade.  Just when I thought it was safe to start dibbling and dabbling with projects and posts.  It’s getting better now by leaps and bounds thanks to the evil but wonderful prednisone and steroid drops.  All the white floaters are gone (I CAN SEE AGAIN) and the pressure and inflammatory pain is down!  Yippeee!  I don’t know about you-but lupus might be the great imitator-however I am the great procrastinator-and that trumps lupus. 
Here is some info about Uveitis (there is more than one kind) and also while playing around I found a new medicine in trial stages for eye inflammation.  This is potentially sight-saving.  And unfortunately-once lupus stops at the door of the eyes, it comes back often to the party.
From Mayo.com:
The signs, symptoms and characteristics of uveitis include:

• Eye redness
• Eye pain
• Light sensitivity
• Blurred vision
• Dark, floating spots in your field of vision (floaters)
• Decreased vision
• Whitish area (hypopyon) inside the eye in front of the lower part of the colored area of the eye (iris)

The site of uveitis varies and is described by where in the eye it occurs.

• Anterior uveitis affects the front of your eye (also called iritis).
• Posterior uveitis affects the back of your eye (also called choroiditis).
• Intermediary uveitis affects the ciliary body (also called cyclitis).
• Panuveitis occurs when all layers of the uvea are inflamed.

In any of these conditions, the jelly-like material in the center of your eye (vitreous) can also become inflamed and infiltrated with inflammatory cells.
Symptoms may occur suddenly and get worse quickly, though in some cases, symptoms develop gradually. Symptoms may be noticeable in one or both eyes.
When to see a doctor
Contact your doctor if you think you may have symptoms of uveitis. Your doctor may refer you to an eye specialist (ophthalmologist). If you’re having significant eye pain and new vision problems, seek prompt medical attention.
If uveitis is caused by an underlying condition, treatment will focus on that specific condition. The goal of treatment is to reduce the inflammation in your eye.
Treatment of uveitis may include:

• Anti-inflammatory medication. Your doctor may prescribe anti-inflammatory medication, such as a corticosteroid, to treat your uveitis. This medication may be given as eyedrops. Or, you may be given corticosteroid pills or an injection into the eye. For people with difficult-to-treat posterior uveitis, a device that’s implanted in your eye may be an option. This device slowly releases corticosteroid medication into your eye for about 2 1/2 years.
• Antibiotic or antiviral medication. If uveitis is caused by an infection, antibiotics, antiviral medications or other medicines may be given with or without corticosteroids to bring the infection under control.
• Immunosuppressive or cell-destroying (cytotoxic) medication. Immunosuppressive or cytotoxic agents may be necessary if your uveitis doesn’t respond well to corticosteroids or becomes severe enough to threaten your vision.
• Surgery. Vitrectomy — surgery to remove some of the jelly-like material in your eye (vitreous) — may be necessary both for diagnosis and management of your uveitis. A small sample of the vitreous can help identify a specific cause of eye inflammation, such as a virus, bacterium or lymphoma. The procedure may also be used to remove developing scar tissue in the vitreous.

The part of your eye affected by uveitis — either the front (anterior) or back (posterior) of the uvea — may determine how quickly your eye heals. Uveitis affecting the back of your eye tends to heal more slowly than uveitis in the front of the eye. Severe inflammation takes longer to clear up than mild inflammation does.
Uveitis can come back. Make an appointment with your doctor if any of your symptoms reappear after successful treatment.

Eye Disease: Preliminary Findings On Uveitis Drug

Aug. 22, 2012 — Shree Kurup, M.D., director of research in the ophthalmology department at Wake Forest Baptist Medical Center, will present the preliminary findings of a Phase 3 clinical trial on a new drug for the treatment of uveitis, a serious inflammatory condition of the uvea, the middle layer of the eye that provides most of the blood supply to the retina.
Link to Clinical Trials for NEW uveitis medication! 

L for LUPUS, N for Neurectomy & No More Pain??

I had what is called a median nerve neurectomy.  My orthopedic surgeon snipped the median nerve in my right foot that leads to the bottom of the fourth toe (on the left side of the toe) with the hopes and intentions of killing the nerve dead!  That toe has certainly been the bane of my existence for the last five years.  Sometimes something so small can turn into something so big and painful.  They call it a Morton's Neuroma.  Likely mine was caused by inflammation in the connective tissue of my feet-plantar fasciitis.  At one time my PF was so bad I couldn't walk.  Cortisone shots right into the plantar gave me back my mobility but the shots into that toe and median nerve stopped working and the zapping and stinging and sharp pains continued. 

I was lucky.  I found an orthopedic surgeon that specializes in FEET.  He went in through the top of the foot and snipped the median nerve right down the middle to the back of the fourth toe right foot.  Here's a better explanation of what a Morton's Neuroma is and a short video animation I found.
Lupus is different in every patient.  Mine likes to attack my peripheral and cranial nerves, skin and blood.  This is just one example of what lupus can do.

From myfootshop.com: 

Morton's Neuroma is a painful condition of the forefoot that is caused by the entrapment of the common intermetatarsal nerve as it passes through the forefoot to the toes. This condition was first described by Dr. Morton, a Viennese physician, in 1876. The most common location for Morton's neuroma is between the third and fourth toes. The second most common location is between the second and third toes.

To help understand this condition a bit better, let's break down the word neuroma into its' root form. Neuro relates to the nervous system and in this case, we are describing a portion of the peripheral nervous system. The suffix 'oma' is the Latin term that defines a tumor or swelling that is of primary origin. Put the terms together and what is described is a tumor or swelling of a peripheral nerve. Interestingly, a Morton's neuroma is not truly a tumor, but more accurately, a nerve entrapment. Although the term neuroma is somewhat inaccurate in describing this condition, the term neuroma is still used today to describe this unique nerve entrapment.  Other terms may be used to describe Morton's neuroma.  These terms include intermetatarsal neuroma, Morton's metatarsalgia, Morton's neuralgia, plantar neuroma, intermetatarsal perineural fibroma or intermetatarsal nerve entrapment. 

What causes Morton's Neuroma? Why does the intermetatarsal nerve become entrapped? Clinicians and surgeons recognize a number of factors that may aggravate Morton's neuroma, but the primary cause of Morton's neuroma remains elusive. Shoes that are tight in the forefoot will contribute to the symptoms of Morton's Neuroma by binding the forefoot and compressing the common intermetatarsal nerve. High heels will also act to increase the ground reactive forces. Ground reactive force is the amount of force generated as the foot pushes against a fixed surface like the floor. With high heels, the amount and focus of ground reactive force increases since weight bearing is focused in a smaller area (just the forefoot). A higher heel also puts the common intermetatarsal nerve under tension, making it more prone to injury. Activities such as squatting will increase the ground reactive force applied to the plantar foot and aggravate the symptoms of Morton's neuroma. And finally, clinician also agree that hypermobility of the forefoot can contribute to the formation of Morton's neuroma.

Treatment of Morton's neuroma

It's interesting to note that until the early 1990's, we treated Morton's neuroma in same way as described by Dr. Morton some 100 years ago. But over the past ten years, our understanding and treatment of neuromas has changed dramatically. Our understanding of Morton's neuroma as an entrapment and not a tumor can be attributed to the work of Steve Barrett, DPM. Dr. Barrett was the first to take a critical look at Morton's neuroma and describe it as an entrapment rather than a tumor.

What Dr. Barrett recognized was that the common intermetatarsal nerve is sometimes prone to becoming entrapped as it passes beneath the intermetatarsal ligament. This was a new concept for us in light of the fact that we had considered Morton's neuroma a tumor. In fact, Dr. Barrett's findings enabled us to recognize Morton's Neuroma to be similar to other nerve entrapments such as carpal tunnel syndrome or tarsal tunnel syndrome. Subsequently, the treatment of Morton's Neuroma has been slowly changing over the last ten years as the result of a new endoscopic surgical procedure first described by Dr. Barrett.

Diagnostic testing to evaluate Morton's neuroma includes plain x-rays, diagnostic ultrasound and MRI. Plain x-rays are not actually used to visualize the nerve, but are use rather to screen for bone and joint pathology adjacent to the nerve. Metatarsal fractures, Freiberg's infraction and osteoarthritis are common conditions that can influence the behavior of Morton's neuroma and need to be evaluated with x-ray.

Several authors have suggested that the efficacy of MRI and ultrasound as diagnostic tools are comparable when evaluating patients for Morton's neuroma. Diagnostic ultrasound is significantly less expensive and much more readily available compared to MRI. Kankanala et. al described a 91.48% pre-op predictive value for diagnostic ultrasound when screening for Morton's neuroma.

Conservative care of Morton's neuroma can be quite successful. 70% or more of new Morton's neuroma patients respond to simple changes in shoes such as a wider toe box. Shoe padding can also help treat Morton's neuroma. Metatarsal pads are an important tool for patients with Morton's neuroma symptoms. A metatarsal pad is a small lift that is positioned in the shoe just proximal (behind) the weight bearing surface of the metatarsal bones. A metatarsal pad lifts and separates the metatarsal bones thereby decreasing the pressure on the intermetatarsal nerve. Some prefabricated arch supports come with a metatarsal pad already seated in the correct position. Using inserts with a metatarsal pad is sometimes the easier way to use a met pad because they can be easily moved from shoe to shoe. Also, by using an insert with a fixed metatarsal pad, the position of the met pad is always in the correct location.

Other non-surgical methods of treating Morton's neuroma include injectable cortisone and chemical sclerosis of the intermetatarsal nerve. Cortisone has been used successfully for years in treating Morton's neuroma. Although the use of cortisone does not actually treat or change the entrapment of the intermetatarsal nerve, cortisone can decrease inflammation and swelling of the nerve, resulting in a decrease in pain. Care should be exercised when using cortisone injections noting that excessive cortisone injections can thin the plantar fat pad of the foot.

Sclerosis of the nerve (also called chemical neuro-ablation or chemical neurolysis) can be performed in the office using a number of different solutions, most commonly dilute (4%) alcohol. Multiple sclerosing injections are used to destroy the contents of the peripheral nerve. A series of injections are employed, each injection separated by a period of 7-10 days. The total number of injections may vary from 3 to 7. The success rates of injectable sclerosing solutions have been reported to be as high as 60-90%. Chemical neurolysis is also a great tool for failed neuroma surgeries where a stump neuroma has formed.

The intent of chemical neurolysis is to destroy the internal contents while preserving the external sheath of the nerve. This would be a bit like removing the copper wire in an electrical wire while preserving the plastic outer insulation or cover of the wire. The reason that this is important is due to the fact that peripheral nerve will regenerate over time. With the nerve sheath intact, regeneration of the nerve is possible in a controlled manner utilizing the existing sheath. By contrast, removal of the nerve by surgery results in the nerve regenerating and the formation of a mass of scar tissue called a stump neuroma. Knowing that peripheral nerve may regenerate also means that sclerosing injections may need to be repeated at some point in the future. The percentage of repeat sclerosing injections varies but is overall quite low.

Another new technique used to treat Morton's neuroma is called cryogenic neuroablation. Cryo surgery is surgery that uses extremely cold instrumentation to selectively destroy tissue. Cryosurgery has been used commonly to destroy superficial skin lesions such as warts and moles.  The technique uses what is referred to as the Joule-Thompson effect. The Joule-Thompson effect occurs when a gas is passed through an area where it may expand. As the gas expands, it cools to approximately -70 degrees centigrade . In the case of cryogenic neuroablation, the expansion of the gas is controlled in a 5.5 mm probe that freezes and subsequently destroys the nerve tissue.

In the cryogenic ablation study carried out by Drs. Caporusso, Fallet and Savoy-Moore, thirty one neuromas were treated in 20 patients. All procedures were performed in an office setting. The procedure used a small amount of local anesthetic to numb the skin to allow the passage of a 12-gauge cannula through the skin. A nerve stimulator was passed through the cannula to locate the nerve. Once the position of the nerve was established, two three minute freeze sessions were utilized to destroy the nerve tissue. A sterile dressing was applied to the site and the patient was dismissed without the need for pain medication. The study cites a 65% success rate.

Dr. Morton's original treatment plan as described in 1876 included changes in shoes, multiple injections of cortisone and if necessary, complete excision of the common intermetatarsal nerve. We've mentioned before that Morton's neuroma is a nerve entrapment much like carpal tunnel. Now let's see if we can apply Dr. Morton's treatment plan to any other nerve entrapment such as carpal tunnel syndrome. Perhaps we'd splint the wrist, try some injectable cortisone, but completely excise the nerve? No way. But that's what's been done for the past 100 years for Morton's Neuroma. Post-op complications were common and included thinning of the plantar fat pad and loss of sensation in the 3rd and 4th toes.

The introduction of Dr. Barrett's EDIN procedure has revolutionized the treatment of Morton's Neuroma and really represents the first unique contribution to treating this condition in over 100 years. The EDIN procedure stands for endoscopic decompression of the common intermetatarsal nerve. Interestingly enough, Steve describes first thinking about this procedure as he watched another surgeon perform an endoscopic carpal tunnel surgery. Steve recognized the problem to be the ligament and not the nerve. The EDIN procedure selectively releases the ligament and leaves the nerve intact.

The EDIN procedure provides us with a new alternative. In the past we knew that the traditional surgery used to treat Morton's Neuroma, called a neurectomy, was destructive and carried with it a number of post-op complications. Therefore, we would tend to use excessive amounts of cortisone to avoid surgery. The EDIN procedure provides a new alternative using non-invasive endoscopic techniques that usually return patients to activities much sooner than the traditional surgery. And, what I find most helpful is the fact that it enables us to use less cortisone, thereby avoiding fat pad atrophy. The question remains; was the common complication of fat pad atrophy due to the neurectomy itself or did it result from the overuse of cortisone? The EDIN procedure shows none of the traditional post-op complications that were so commonly seen in the neurectomy, therefore we can assume that fat pad atrophy was in part due to overuse of cortisone.

The EDIN procedure has been used for at least ten years and has shown promising results. It can be technically challenging for some who are not familiar with endoscopic techniques. As with other surgical procedures there are pros, cons and possible complication that need to be discussed thoroughly with your physician prior to surgery. The following pictures show the technique used to perform an EDIN procedure. Image 1 shows pre-operative markings identifying the 3rd and 4th metatarsal heads. Image 2 shows placement of the cannula through an interdigital incision. The cannula is much like a small 4mm drinking straw with a slot cut in one side. The slot or open side of the cannula is placed adjacent to the intermetatarsal ligament. The cannula passes from between the toes to a second incision on the plantar aspect of the foot just proximal to the weight bearing surface. The endoscope and knife are used within the slotted cannula to identify and transect the intermetatarsal ligament. Image 3 show the use of a blunt probe without the cannula to verify a complete release of the intermetatarsal ligament. In the bottom of image 3, a metatarsal spreader can be seen. The spreader is used to separate the 3rd and 4th metatarsals subsequently putting pressure on the intermetatarsal ligament. The procedure takes about 20 minutes and is completed in a hospital or surgery center. Local anesthesia with sedation is used. Patients return to regular shoes in two days with just a band-aid on the incisions.

Traditional neurectomy, or removal of the nerve for the treatment of Morton's neuroma, is used less often due to the success of sclerosing injections and the EDIN procedure. Neurectomy can be performed from a dorsal or plantar approach. The advantage of a dorsal approach is that patients are able to walk immediately following the surgery. The disadvantage of the dorsal approach is that it requires more dissections and possible tissue trauma. The plantar approach results in less tissue trauma but requires that patients are non-weight bearing on the surgery foot for 3 weeks post-op.  Traditional neurectomy for the treatment of Morton's neuroma is performed on an out-patient basis at a surgery center or hospital using a local or general anesthetic.  The procedure is completed in less than 30 minutes.

from youtube: 

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