| In this
issue : Spring 2000
|
|
Spring 2000
(This is the second in a series of 2 presentations on
repetitive strain disorders involving the upper extremities).
"I wake up in the middle
of the night with numbness and tingling in my thumb, forefinger and part of the middle
finger. I have to get out of bed and shake my hands and wrists to get relief. My hands
feel clumsy and I have a great deal of difficulty buttoning my shirt. The longer I
sit at my computer, the worse it gets, and sometimes it seems to radiate up my arm into my
shoulder and even into my neck."
Thus, some of the classic
complaints of the patient suffering from the "repetitive strain syndrome"
frequently labeled "carpal tunnel". The phenomenon is much more common in women
than in men and is mostly seen between the ages of 30 and 60. For many years the
cause was assumed to be repetitive work, particularly heavy manual labor and computer
usage, and recreational traumata. However, recent nerve conduction studies show no
consistent relationship between the prevalence of CTS and the type and level of
occupational hand activity. We are no longer convinced of the significance of the
ergonomic factors in causation of CTS. Diabetes, hypothyroid disorders, pregnancy
and other disorders of the neuromusculoskeletal and endocrine system can cause or
perpetuate the clinical picture of CTS. (see below)
[In light of this
information, recent proposals by OSHA to classify CTS and other repetitive strain
disorders as occupational may result in the imposition of onerous ergonomic regulations.
These proposals should be rigorously opposed by employers and employees alike as they
would probably result in higher taxes, increased insurance premiums and decreased quality
of medical care.]
What is the mechanism?
Essentially CTS is the result of compression of the median nerve as it passes
through a fibro-osseous canal over the wrist bones called the carpal tunnel.
Swelling is produced in tissue lining the nerve and its smaller subdivisions (think very
fine telephone cable) and as a result of that injury, protein leaks out into the fluid
around the nerve, the amount of fluid within and around increases, initiating a vicious
cycle.
Diagnosis is based on
the symptom history and on physical findings, including provocative tests. These include
Tinel’s sign, which is obtained by percussing over the median nerve at the transverse
carpal ligament and by Phalen’s sign which is obtained by allowing the wrist to flex
with gravity with the forearms perpendicular and the elbows resting on the table. However,
these signs are both inconsistent. Both may be present in normal subjects, and neither may
be found in those with proven CTS. There are several other sophisticated tests involving
such elements as 2 point discrimination, vibratory sense, tourniquet compression, etc. The
evidence is that the most elaborate and expensive tests, including electro diagnostics are
not statistically strong enough to be accepted as definitive standards. As we discussed in
the last issue, other clinical syndromes resulting in nerve compression at higher levels
may mimic or coexist with CTS. These include cervical disc compression, compression at the
thoracic outlet, the forearm or at the elbow. Arthritis at the base of the thumb,
“trigger fingers” and deQuervain’s tendonitis may be associated with or
mimic CTS and must be distinguished and treated.
Treatment of CTS is
directed initially toward relieving pressure on the median nerve at the wrist. Night pain
may be related to habitual maintenance of the wrist in flexion during sleep. A night
splint, maintaining the wrist in a neutral position is usually effective. Avoidance of
possible ergonomic and postural factors such as vibratory and repetitive flexion movements
may be helpful. Some early cases of CTS are completely relieved by these methods alone.
Osteopathic manipulative therapy, in the form of myofascial release and physical therapy
using soft tissue mobilization, ultrasound and infrared laser have been shown anecdotally
to be beneficial. Nonsteroid anti-inflammatory medication may be used, although it has
never been verified that an inflammatory process is involved in the causation of CTS.
Steroid injection into the carpal tunnel, underneath the transverse carpal ligament,
around (not into) the median nerve may decrease the swelling and relieve the condition for
varying time periods. The success of such injection is also considered to be a positive
indicator should surgery be contemplated.
Concurrent and perpetuating
conditions such as cervical disc disease, thoracic outlet syndrome, myofascial pain
syndromes, diabetes, thyroid imbalance, gout and rheumatoid and osteoarthritis must also
be addressed. Pregnancy is another condition also associated with CTS, possibly related to
fluid retention and consequent edema around the median nerve. That, of course, usually
takes care of itself in due time.
Surgical release of the
transcarpal ligament compressing the median nerve is a last resort but has a rather high
rate of success, but is reserved for those intractable cases.
In summary, this is another of those things that may not be what it seems
to be. CTS has many interrelated diagnostic and therapeutic facets, all of which must be
explored and corrected if therapy is to be successful. back to top
In June of 1987, I had been practicing medicine for 32 years. During that time, I had missed exactly no
day’s work because of sickness or injury. I had just moved my office from 41st Street
to 42nd Street and Madison Avenue, increasing my office space from 3200 to approximately
10,000 feet square, of course proportionately increasing our overhead. The insurance
picture was still manageable. The majority of
my practice ranged from almost totally impecunious dancers to mid- to upper level
executives, young captains of industry earning what, in our naïveté, were considered
spectacular incomes in banking or in the stock market.
On Saturdays and Sundays, just as fiercely competitive, they were
“weekend” athletes. But things change, and by October of 1987, you could contact
one of my yuppy patients by raising your right arm in a restaurant and calling:
“Waiter”!
Shortly after the market had bottomed out, I went
to the office one Monday morning feeling somewhat less than prepared to begin the week of
attending to other people's ills. As the day
progressed, I became aware of an unfamiliar state of being which soon evolved into:
"how come I am so hot and sweaty and freezing and shaking and I can't see and I can't
stand up anymore? Why, can it be that I am
what regular human beings term, sick"?
Shortly it became clear to even my fever-clouded mind that my physical, mental and
emotional state was not compatible with any activity more strenuous than turning over in
bed, if I could handle even that much.
I have no really clear
recollection of the immediate succeeding events however I assume that some person or
persons in my employ succeeded in delivering me to my bed.
From that time, my body temperature ebbed and flowed like a tide caught by time
lapse photography. My fever reached the
unlikely levels of 103 to 104 degrees Fahrenheit, interrupted only by chills which
threatened to shake from my body all manner of insulation, tenderly and lovingly applied
by my dear wife: blankets, sweaters, overcoats, my recently departed mother’s mink. All of little avail. As a physician, of course, I
had no family doctor, internist, or what is now referred to as a Primary-Care Physician,
or PCP.
(Which, by the way, was the acronym in the 60s
and 70s for a drug that, when smoked or snorted, was capable of producing alterations of
consciousness, hallucinations, severe pain, or even death. Nothing changes).
I called my brother-in-law
the cardiologist and asked his advice. He
strongly advised me to hike myself off to the nearest emergency room. Naturally, being a doctor and knowing a few things
about emergency rooms, I ignored his advice.
After two days of this,
showing no signs of improvement, I allowed my wife to bring me to an infectious disease
specialist. (How she managed that task shall be forever her secret). The doctor made the
observation that I seemed to have discovered a new treatment for hypertension: toxic
shock. My blood pressure, which previously
had hovered unhealthily about robust levels such as 160/90, had now dropped to 90/50. With great skill she managed to tap practically
nonexistent veins and obtain about a gallon of blood, which she dispatched for analysis. She strongly urged me to allow her to admit me to
the hospital. I declined, preferring, since I
was obviously going to die, to do so at home where my wife could prepare tremendous
volumes of fresh chicken soup, with noodles and perhaps if I got strong enough to eat
them, matzoth balls, the consumption of which would certainly be the only way to
deliverance.
Somehow, my wife got me home
and into our own bed. Chickens all over the country died like flies, and were efficiently
transformed into chicken soup which could only have been consumed faster and in greater
quantity were it administered via intravenous infusion. I watched W. C. Fields and Marx
Brothers movies in an attempt to laugh myself into recovery a la Norman Cousins. My
infectious disease doctor maintained telephone contact with me. She knew only that I had an overwhelming
infection, the specific nature of which was still unidentified. I had an FUO (fever of
unknown origin). If things did not turnaround quickly, either I would enter a hospital, or
she would wash her hands of the entire issue. That threat seemed to work. Three or four
days later my condition gradually and erratically took a turn for the better. The chills and fever subsided, and I was actually
able to sit up and take nourishment. By the fifth day I was able to sit up the edge of my
bed, and subsequently to take a few assisted steps around the bedroom. Without doubt, whatever it was, was relinquishing
its hold on me.
Then, on the following
morning, a Saturday, I awoke with the most unbelievable pain in my right knee. There was no position that would assuage it. Ice did not work.
Warm compresses did not work. Screaming,
principally foul epithets, had no effect, nor did prayer.
There was nothing for it but to call my good friend the orthopedic surgeon, Bill
Hamilton who would, hopefully, make a house call and there in my bedroom, sever the
connection between my thigh bone and my shin bone by extracting my knee. He declined the opportunity for this
groundbreaking surgery and after a few minutes gentle examination quickly made the
diagnosis that I was suffering from gout! This, brought on by the consumption of epic
amounts of purine-rich Jewish penicillin in combination with rapid weight loss and
dehydration, caused by my FUO.
Now,
fully on the way to complete recovery with the administration of the appropriate
anti-inflammatory medication and clear fluids, I am able to segue into today's lesson:
Gout.
Hamilton & Bachrach in Rio de
Janeiro 1987, not talking Gout
back to top
Gout
is an acute or chronic metabolic disorder characterized by the in-born inability of
the body to metabolize and/or excrete in the urine, purines, an end product of protein
digestion. This results in the accumulation of the purine degradation product, uric acid,
in the blood stream and the consequent deposition into body tissues, tendons, joints,
earlobes, etc. of sodium monourate crystals where a painful inflammatory reaction may be
set up. The joints usually affected are the great toe or bunion joint, the ankle, the
knee. Almost any joint may be affected. Men, usually those between the ages of 30 and 60
are the most frequent sufferers. Less than 5% of gout victims are female.
An acute gouty
episode may be triggered by excessive inhibition of alcoholic drinks, excessive protein
intake, (see above), excessive fluid depletion, rapid weight loss, or even emotional
crisis. Predisposition is through obesity, hypertension, renal insufficiency and chronic
ingestion of foods high in purines such as herring, anchovies, caviar, chicken soup,
gravy, beef extracts, consommé or other protein concentrates, liver, sweetbreads or other
organ meats. Legumes such as dried beans, soy beans, etc., mushrooms, spinach, cauliflower
and asparagus have also been indicted.
Gouty tophi
are depositions of urate crystals in the earlobes or under the skin. Aspiration of these
crystals from the skin or an inflamed joint and subsequent examination under a microscope
can confirm the diagnosis. The blood uric acid level is usually found to be elevated in
gout patients, but not always.
Gout is treated best,
like anything else, preventively. Maintenance therapy with colchicine is an old standby.
Agents are available, such as allopurinol, that will reduce the blood uric acid level.
Other medications (probenecid and others) will increase the rate of excretion of uric acid
by the kidneys.
The
acute attacks can be quickly treated with non-steroid anti-inflammatory agents (NSAIDs)
and the old reliable, colchicine, although that method may be quite unpleasant.
It is often said that the pain of a kidney stone is the worst a human can
experience outside the old matches under the fingernails trick. Don’t try telling
that to me or to anyone else who has experienced an attack of gouty arthritis.
IMPORTANT
NOTICE
The old doc is finally catching up.
Beginning with this issue, the CSOM Kwarterly Klarion will come your way thru cyberspace.
The newsletters will be available on my website:
www.bonesdoctor.com
By the way, a good way of communicating NON-EMERGENCY
stuff is through Email. If you have an Email address, please give it to us by faxing or
copying, then Emailing this form to:
FAX: 212-697 4541
Email: here.
Your name _____________________________
Your Email address ___________________________
For those of you who don’t have access to Email, hard copies of the
newsletter will be available upon request, by direct mail or fax, or, you can pick them up
at the office. back to top
|
