Rheumination

Gold Treatment for Sanya Richards

Sanya Richards, american sprinter in the 400 metres, finished short of the gold at the Olympics this week but became a poster girl for a rare rheumatological condition, Behcet's disease.  It's hard to believe that she fought off this disease only last year and was still able to train up for the Olympics.   Painful mouth and genital ulcers, fatigue and a multitude of other possible symptoms make this an ugly and disabling condition which is not always easy to control. Even the treatment, often involving corticosteroids, causes un-sprinter friendly side-effects like weight gain and muscle wasting. We have not heard much about the  actual presentation of the disease in her case (it's quite variable) but she did mention the spots on her legs, suggesting she may have had vasculitis as part of her disease. (It may have been erythema nodosum but those would likely be bumps, not spots)    No matter, any combination of the above symptoms of the disease would knock most of us out of running for the bus, let alone the olympics. So Sanya didn't bring home a gold  medal, but from a rheumatologist's point of view, she should still get the gold treatment.

Cat Scans Easier than People Scans

Today I tried to arrange an MRI for one of my elderly patients. She had foraminal stenosis with bad sciatic pain, as was confirmed by a CT scan that took 3 months to get and an EMG that took 2 months. The orthopod refuses to see her without an MRI in hand, and so onto an MRI waiting list she goes.  She doesn't have insurance nor the $750 it would cost to go privately.  The hospital waiting list for such a non-urgent case will be at least six months, more likely nine.  So she'll wait.

Meanwhile in what must be a universe far, far away, there's a comment on a  veterinarian blog concerning herniated discs in dogs 

I'd just like to add that this can happen to cats too. A few months ago my 13 year old cat threw a disc. Unfortunately she began to go down in the rear so I had no choice but to be aggressive about treatment. My neurologist saw her right away, and my cat went from ultrasound to myleogram to surgery for a hemilaminectomy. I am so happy that she was healthy enough to go through all of that. She regained control over her back legs immediately, but sadly, remains urinary and fecal incontinent to this day. I tried acupuncture but it didn't help. My cat has taken up residence in my rottweiler's old kennel and when I'm home to keep an eye on her, she dons a kitty diaper and gets free run of the home.

# Posted By Robyn W | 12/12/07 5:22 PM

My patient isn't incontinent  yet, but I am certainly starting to feel rather impotent.

The Closer

DB over at DB's Medical Rants is trying to come up with a curriculum of essential bedside clinical skills.  Of the many skills I learned after I started practice, closing the interview is probably the most important.  In rheumatology we often make the diagnosis at the first visit because in our specialty, history and physical rules. A classic example would be a new rheumatoid arthritis patient with multiple swollen joints in a classic distribution.  Early in my career I would make the diagnosis,  pass on my opinion to the patient with a brief course on the natural history of the disease and a treatment plan.  The protocol was fairly standardized and efficient but the results disconcertingly  variable.  Some patients would leave the room with the bouncy gait of renewed optimism that I had hoped to instill, while others left no less anxious than when they came in, others worse.  What I've learned since is that patients come in with a lot of baggage and a diagnosis alone doesn't always lessen the burden.  You have to find where the patient is coming from and try to unload the old stuff while addressing the new.  I was surprised to find that many patients with RA believe they have another more serious disease.  Interestingly, my french patients seem to have a morbid fear of multiple sclerosis, and my english patients tend more to 'bone cancer".  When you tell these patients they have rheumatoid arthritis, that doesn't necessarily take these possibilities out of the picture.  I will now often tell patients directly that they have no cancer or MS, but RA, a treatable disease .

  RA is also a common disease  with a hereditary component so there is a fair chance that the new patient will know somebody who had the disease, often years ago, in the days when there was no effective treatment.  These pre-methotrexate patients suffered horribly and deformed relentlessly.  They became cushingoid because of the corticosteroid treament that was the only thing that gave any relief and then they died, the death more often than not attributed to 'the cortisone'.  So when I come along and tell them that they have RA and will start them on a small dose of prednisone while I get them on a remittive agent, what they actually hear is CORTISONE!  It's important to find out where the patient is coming from and address those concerns. 

 A clinician also has to stay in the present.  When I see a new RA patient I feel pretty confident that I will get it under control in the near future.  Since the arrival of the biologic meds I feel almost cocky about my treatment options.  I'm not worried.  That's all great but the patient still has hugely swollen joints today and can't see much beyond trying to get out of the too-deep chair that I have in my office. Address today and tomorrow and then we can talk about the coming months and years.

Doctor-patient communication.  I'm sure that's what most will comment about on DB's blog.  Just remember, for the internal medicine clinician, making the diagnosis is just a good place to start.  

Carpal Tunnel and Metabolic Disease

It's common knowledge that carpal tunnel syndrome (CTS) is significantly more frequent among patients with diabetes, hypothyroidism, and connective tissue disease (CTD). For this reason, we're all taught to screen CTS patients for these diseases, especially if the condition is bilateral. A recent study in the Journal of Neurology Neurosurgery and Psychiatry asked whether this approach is really justified. Rijk et al. studied 516 CTS patients retrospectively to see if any of the abovementioned diseases was diagnosed by blood testing done at the time of CTS diagnosis.
Of 432 patients with no prior history of diabetes, 10 patients had raised glucose, but subsequent testing confirmed the diagnosis in only 2 patients. Of 468 patients with no history of thyroid disease, 9 patients had an abnormal TSH, but only 2 actual cases were confirmed. In 472 patients with no history of CTD, 40 patients were found to have an elevated ESR but no cases of any CTD were made.
The PPV of CTS for diabetes was .5%, and 216 patients had to be tested for each diagnosis made. For hypothyroidism the PPV was .4%, and 234 patients were tested for each case found.
Overall a rather meagre success rate given that the prevalence of the diseases in the general population is about 4% for diabetes and 9% for hypothyroidism. The false positive rate was rather high as well which ran up the costs because of follow-up testing. The authors put it at about 1400 Euros to make a single diagnosis of hypothyroidism and about 350 Euros per case of diabetes. They didn't do any further calculations on CTD because none were found and because they probably realized how dumb it was in the first place to look for them based on an ESR.

Tendinitis or Tendonitis. Acute Vowel Obstruction

Seriously  now, how hard can it be to decide on the spelling of this common medical condition.  Both terms are used interchangeably in the medical and lay literature which would suggest that both are okay, but really, should we really be tossing vowels about willy-nilly as if it doesn't matter.  I can't think of any other inflammatory diseases that have two spellings, and for good reason.  If proctitis was spelled prictitis we might be scoping the wrong organ.  Gingovitis sounds like a hip hopper with gum disease.  Rhinitis becomes rhonitis and now we're talking about two different river systems altogether aren't we.  It makes no sense.  I suggest we decide once and for all, here and now.  But which way is best.

tendon+itis=tendonitis. Logical right?

But logic isn't everything in language so what do the dictionaries say?  Both the Oxford and Webster dictionaries say both are okay.  Cop out.

Wickipedia calls it tendinitis, but in the same article refers to common tendonitis injuries.  Confused.

My spell-check prefers tendinitis, but it doesn't accept rheumatology as a word so how much credibility can I give it?

A google search of tendonitis finds 1,810,000 hits while tendinitis falls short at 1,580,000.  The masses have spoken.

A google scholar search finds 10,500 for tendonitis and 17,200 for tendinitis.  The braniacs rebut.

So consensus is unlikely in the near future, but there might be a way out.  Research shows that there is, in fact, very little inflammation involved in what we call tendinitis/tendonitis and therefore the 'itis' should be dropped altogether.  It is suggested that it should be called tendinopathy instead.

Or should that be tendonopathy.

Fluoroquinolones, Tendons and the FDA

Some months ago I considered posting about the strange association between quinolone antibiotic use and tendon rupture.  I had seen a case of achilles tendon rupture with a tenuous link to previous antibiotics and wanted to get a better handle on the numbers.  The literature on the subject was, however,  sketchy at best.  I  did come away with the vague notion that the risk with quinolones of tendon rupture was about four to five times the norm, about 10-15/100,000 treated.  This risk increased significantly in patients over sixty, and even more so in corticosteroid treated patients. The whole endeavour was rather unsatisfying though because, aside from the dubious numbers, the  pathophysiology question remained a  complete mystery.  Pathology shows nothing exceptional, no different from your run-of-the-mill tendon damage.  How could an antibiotic snap a tendon within days of treatment.  Anyway, I canned the idea of blogging on the subject until more illuminating data surfaced.

And there it was.  While I was on holiday the FDA announced that all quinolones will now have a boxed warning about the hazards  of tendon damage.  Serious stuff.  Must finally have some solid figures, Cochrane-level evidence,  systematic review or at a minimum, a segment on Oprah...  Nope.  Not a word about new evidence, just ongoing reports. Quite the let-down.  I was rather miffed at this seeming heavy hand with no goods to back it up..  After all, the association is well known.  Why the drama? 

 As I mulled it over, however, I realized that in my own practice, which as a rheumatologist includes many tendon problems, many patients over sixty and many on corticosteroids, I may not have actually given it the concern it deserves.  I've never actually suggested to a 60 year old rheumatoid patient taking steroids that they should take another antibiotic, given a choice.  Maybe I should. Maybe I should discuss it with the microbiologists and respirologists as well. 

So maybe the boxed warning has done it's job, at least on one clinician.  I still don't know though, if this is the way for the FDA to proceed.  Will including tendonitis as a boxed warning issue dilute the  value of this level of concern?  Can they give boxed warnings for any definite, but hardly life-threatening side-effect?  What would be the point.  Maybe a simple FDA statement or warning would suffice.  Maybe repeated warnings over time, with press releases.  Even better, how about a spot on Oprah.

Spitting Mad

I recently sent one of my patients for an evaluation at the pain clinic of one of our university hospitals. Apparently the interview did not go well.  The consultation letter sent back to me included the following paragraph:

              ...our psychologist was present during part of this interview and when the patient finally left the room, she turned around and spat in my direction...

    Now it's not clear from the letter whether it was the patient or the psychologist who did the spitting, but either way, I think it's fair to conclude that there won't be a follow-up appointment any time soon.

  

    

Joints In Motion: Tim Jackson

Growing Pains

I'm waiting for it to all fall apart.  I know it's going to happen some day.  

When I was an internal medicine resident, drifting through the many subspecialty departments, I was struck by how many were hopelessly mired in political intrigue, infighting and general dysfunction.  Even departments that seemed outwardly to be highly effective were often broiling just below the surface. When I got into rheumatology, I discovered that the group of mellow, type-B clinicians and researchers that I had learned to love, transformed during departmental meetings into rabid hair-pulling maniacs.  Well almost.  In fact, after masochistically joining said department we managed over the next five years to completely destroy it, with the  final result that I and several others left the hospital, the city, or even the province. Landing in a community hospital with a single other rheumatologist proved to be the salve.  Sure it was hectic and there were some serious problems with patient care, but the political side of things were a snap.  "I'm going away this weekend, can you take call?"

 "Okay"

Call schedule complete.

Looking around, however, I saw that not all was well in non-academia.  Many departments were involved in constant inter and intra-departmental battles, not unlike the ugliness of the university setting.

So now the big question.  Why does it all go wrong.  Our own department is now growing quickly and soon we will become at least partially academic. I need to know what the critical factors are that make all departments go wonky in the long term.  A diagnosis now may lead me to some preventative administration.  I have several theories:

Academia:  In academic hospitals there is a toxic mix of clinicians and researchers.  Clinicians gripe about carrying the load and researchers moan about pay inequity.  Researchers compete amongst themselves for status, and believe that clinicians should have none. 

Leadership selection: In a university setting department head selection is particularly warped.  It almost always falls to the most successful grant earner over time, whether or not he/she has any administrative talents or interpersonal skills.  In the community hospital the department head is often chosen by who loses the vote.  An unpaid job with no attached prestige does not have people scrambling for the post. In both settings, there is a built-in self-destruct mechanism.

Critical mass.  It is possible that shear numbers are the root cause.  Insignificant hassles amongst a few colleagues are multiplied many fold with new members, to a point where the system becomes a quagmire despite the best intentions of the individuals.

One bad apple.  With increased numbers comes the likelihood of admitting that one malignant character that kills off the whole department. I've seen it happen and it's odd because you would think that a solid group could fend off one or two poisonous persons. It isn't always so.

Our own department may well be a classic study.  I wonder whether I should apply for a grant.  We've increased our staff and will likely to continue to do so.  We have begun a hesitant dance with the local university and will become progressively more academic.  We are also looking to bring on a research oriented rheumatologist in the near future.  So far no implosion, but can it last.  Experience tells me otherwise.