Month: August 2017

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Device Solutions for Difficult Problems
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[av_heading heading=’Collapse deformities of the thumb secondary to CMC joint disease’ tag=’h2′ style=” size=” subheading_active=” subheading_size=’15’ padding=’10’ color=’custom-color-heading’ custom_font=’#403393′ admin_preview_bg=”][/av_heading]

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When the thumb CMC gets in trouble, whether it is from osteoarthritis, Bennett’s fracture or Rheumatoid disease, it does the same mechanical “dance”. As the CMC progressively subluxes on the trapezium, the extrinsic FPL and essentially all the thenar muscles increase their moment arm that each uses to FLEX the CMC. Over the months and years, the entire thumb progressively tends to collapse into a claw or “intrinsic minus” position in which the MP joint tends to extend or hyperextend and the IP joint progressively tends to flex…all as the CMC subluxes.

These elements of deformity manifest as a function of:

• The degree of CMC subluxation.
• The degree of hypermobility of the MP joint.

The poor little IP joint is forced by the mechanics of the two proximal joints to just go along for the ride, and, assuming its flexor and extensor tendons are intact, it will collapse opposite the direction in which the MP does.

With time, the patient’s thumb begins to look “intrinsic minus,” at rest and worsens with pinch activities. (Envision the Grandma/Grandpa zig zag collapse) This is similar to what is seen with weakness or paralysis of the ulnar nerve innervated thumb muscles, but the collapse itself is secondary to the shifting moment arms of the muscles, particularly those that flex the CMC, as opposed to other mechanical ills.

Now, an occasional patient will demonstrate significant CMC subluxation and even dislocation without the MP and IP joints following suit. These thumbs have other assets, such as an MP that is reluctant to stretch out the palm side soft tissues. In fact, if the FPL can keep the MP in slight flexion, its fibro-osseous tunnel will continue to pull the capsular ligaments in a palmar direction and keep the MP joint reaction force where it belongs…even with advanced CMC disease. Said differently, if the whole thumb pinch mechanism, in spite of CMC disease, remains mechanically healthy enough to favor pinch with some degree of MP flexion, the IP joint will often be stable in neutral or even a hint of extension…a much better thumb for most daily activities.

There are precious little median and ulnar nerve innervated thumb muscles generating high tension but not much excursion as they oppose, extend, flex and circumduct our thumbs. Added to those, the APL (named for the thumb but the most powerful radial deviator of the wrist) helps sublux the CMC joint and has little or no ability to extend the CMC once that joint is subluxed or dislocated. This powerful extrinsic, the APL, can’t do squat for positioning the thumb (as a unit) once the MP joint collapses into neutral and then into hyperextension. By this, I mean that the APL and EPB have no useful moment arms to effect CMC extension and therefore no lever arm to “save” the MP joint from its eventual fate of collapsing into hyperextension.

Mother Nature’s solution is what we hand guys and the x-ray docs call osteoarthritis of the CMC joint. The end game in which osteophytes create a broad base to an arthritic CMC joint that eventually stiffens, stabilizes and, thereby, frequently quits hurting. Serial steroid injections during the degenerative-subluxation phase relieves pain and may actually accelerate the subluxation as these steroids have a direct deleterious effect on the remaining bone, hyaline cartilage and capsular ligament mechanical integrity. In addition, when the steroid injection takes away the pain, the patient, who feels for a month or so that their thumb is born again, imposes higher cyclical loads with increased hand use and accelerates the time to each OA thumb’s end stage collapse. Not that I am promoting this, but many of the weak and painful thumbs we see will eventually end up looking very arthritic and the CMC very collapsed, but their 70 year old owners are quite happy with their thumbs natural state once the pain goes away.

Surgery….CMC resection arthroplasty is a great operation. Both the patient and the surgeon find it rewarding. We actually get the opportunity to do something that works, is fun and makes sense…anatomically and biomechanically. Even with a few wrists that get in trouble with a little carpal collapse or scaphoids that are symptomatic at their joint with the trapezoid, this remains a good to great operation.

To some degree, the outcome of the collapse deformity following CMC arthroplasty depends on a few issues:

• Whether or not the MP joint is collapsing into extension or hyperextension with each cycle of pinch.
• Whether or not the MP joint is moving further into hyperextension at the expense of flexion, including passive flexion. (i.e. capsular contracture)
• Whether or not, at the time of CMC arthroplasty, we are technically good enough to create a new ligament that will hold the base of the metacarpal “in place” such that the moment arms of the flexors are returned closer to normal.

This “return of moment arms” toward normal for the MP joint is difficult to do in a really destroyed CMC of long standing. As the CMC progressively subluxes, the moment arms that affect the MP with each pinch or grasp tends to progressively favor extension. The snow-ball effect happens when the MP “breaks” into slight hyperextension. At this point, the FPL can no longer displace its MP pulley in a palmar direction, the collateral ligaments become lax and/or contract, and the FPL shifts dorsally toward the metacarpal head. Flexion moments across the MP deteriorate and the force imbalance then starts to favor MP hyperextension. The IP follows suit and starts to lose extension.

As the CMC subluxes, the fiber lengths of the opponens may lengthen and the remaining thenar muscles (FPB and APB mainly) will be allowed to shorten. This shift in the length of the muscles changes their ability to generate tension as defined by each muscle’s length-tension curve. (See Brand’s book on Clinical Mechanics of the Hand.)

So…back to the practice of fixing thumbs…what does this all mean?

• If the patient isn’t willing to wait and see if Mother Nature will “cure” their pain with time (no guarantee, but frequent enough if the patient is willing to wait…years…perhaps even a decade or more) then a resection arthroplasty is my best option.
• If the surgery is done BEFORE the MP collapses into extension with pinch and preferably before the MP gets stuck in some degree of hyperextension, then resection of the trapezium combined with a nice snug ligament reconstruction that favors holding the base of the metacarpal close to where it started out in youth has the best chance of both pain relief and a pinch that is:
  1. Relatively strong and
  2. Without a collapse that will cause the IP joint to go into flexion each time the patient pinches.

Said differently, the thumb that has a stable pinch “mechanical geometry” will stay that way if the ligament reconstruction is very effective at holding the base of the metacarpal in place at 6 to 12 months post-op and beyond.

If the MP is collapsing into hyperextension pre-operatively, play your best reconstructive hand at creating flexion moments that will hold the MP in some degree of flexion during pinch and grasp. How best to do that is another story.

This remains my favorite operation.
John Agee
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Device Solutions for Difficult Problems
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[av_heading heading=’Carpal Tunnel Pressure – Our Thoughts on Its Surprising Dynamic Behavior’ tag=’h2′ link=” link_target=” style=” size=” subheading_active=” subheading_size=’15’ margin=” padding=’10’ color=’custom-color-heading’ custom_font=’#403393′ custom_class=” id=” admin_preview_bg=” av-desktop-hide=” av-medium-hide=” av-small-hide=” av-mini-hide=” av-medium-font-size-title=” av-small-font-size-title=” av-mini-font-size-title=” av-medium-font-size=” av-small-font-size=” av-mini-font-size=”][/av_heading]

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Ben Goss, MS and John Agee, MD.

Recently, we published a study that looked a bit closer at pressures in the carpal tunnels of 12 patients with idiopathic carpal tunnel syndrome (CTS) while they actively used their hands; “Dynamics of Intracarpal Tunnel Pressure in Patients With Carpal Tunnel Syndrome” (J Hand Surg 2010; 35A:197-206).  While our research helped us better understand just how dynamic these pressures are during hand use, we questioned whether there might be more going on than we originally thought.  Following are a few of the questions we pondered and our thoughts on what we think may be going on with these pressures in the carpal tunnel.  If you’re interested in what we actually know, then please read our publication.  If you’re curious about what we think may be going on, but don’t know for sure, continue reading.  Maybe you’ll have some questions of your own.

The highest pressures we recorded were about 8 times greater than what had been previously reported.

What could cause these higher than expected pressures?

We believe that forceful contraction of the lumbrical muscles within the carpal tunnel may be the primary contributor.  When any hand is used actively (like gripping a golf club or a hammer) and the fingers are flexed, the lumbrical muscles migrate proximally into the carpal tunnel.  We saw a slight increase in pressure in the carpal tunnel when the patients just flexed their fingers, but this didn’t cause the really high pressures we recorded.  The more forcefully patients used their hand (either gripping or pinching a dynamometer), the greater the pressure spiked. The highest pressures we measured were when the patients gripped a dynamometer with maximum force.

To get these maximum pressures, the fingers had to be flexed enough so that the lumbrical muscles moved proximally into the tightest part of the carpal tunnel and then the hand had to be used forcefully enough so the lumbricals contracted, “in synergy” with the finger flexor muscle-tendon units.  When the lumbrical muscles move into the carpal tunnel, their additional volume raises the pressure some.  But, it seems to be something else, like when the lumbricals actively contract and expand further, that causes the pressure to really soar.  Only when the patients in our study, who were fully awake, used their hands forcefully by gripping a dynamometer in the operating room, did the pressures peak.  When the patient’s hands were relaxed with their fingers extended and a force was applied to the palm of the hand, the pressures were only about half of what they were when the patients actively gripped with the same force.

Another contributor to these high pressures might be a change in the rigidity of the soft tissues that border and help constrain the contents of the carpal tunnel when the hand is used forcefully.  When a hand goes from being relaxed to being used forcefully, the elastic ligaments and muscles that border the carpal tunnel tighten up.  Part of the increase in stiffness occurs as the intrinsic and extrinsic muscles contract.  Another part of the increase in stiffness is the hardness of the object being forcefully grasped by the hand.  Both of these combined tend to cause a more rigid boundary for the contents of the carpal tunnel to come in contact with.  Both a more rigid boundary and forceful hand use that causes proximal migration of the lumbricals into the tunnel and active contraction of the lumbricals while in the tight part of the carpal tunnel are how we like to think that these high carpal tunnel pressures are generated.

In our study, we didn’t report that we also measured carpal tunnel pressures in two subjects without CTS.  We saw higher than expected pressures in those two subjects too, comparable with the patients with CTS.  This led us to believe that the dynamic behavior of carpal tunnel pressure is not unique to patients with CTS.  While we have data from only two subjects, we now believe that it occurs in everyone, and it happens for a reason.

Previous studies did not identify that the maximum pressure occurs adjacent the hook of the hamate.  Why was this consistently the location of maximum pressure in every subject we tested?

This may be a combination of the pressure sensor we used, the position of the pressure sensor within the tunnel, and the structural anatomy of the carpal tunnel.  In our study, we used a pressure sensor that measured both hydrostatic pressure (like the pressure you feel when you’re underwater) and contact pressure (like the pressure you feel against the palm of your hand when you hold something).  Then we positioned that pressure sensor between the contents of the carpal tunnel (flexor tendons, median nerve, synovium, lumbrical muscles) and the dorsal surface of the flexor retinaculum.   When the hand was relaxed, the pressure sensor measured the resting hydrostatic pressure.  When the hand was active (pinching and gripping dynamometers) the sensor was pressed against the dorsal surface of the flexor retinaculum as the lumbrical muscles pistoned from distal to proximal, into and out of the carpal tunnel.  By being sandwiched between the contents of the carpal tunnel and the flexor retinaculum, our pressure sensor measured the dynamic behavior of the contact pressure as the hand was used.

The type pressure sensor and its positioning weren’t the only reasons.  The pressure sensor had to be in the correct proximal-to-distal location.  The transverse carpal ligament (TCL) is the segment of the flexor retinaculum that attaches to the pisiform, hook of the hamate, tuberosity of the scaphoid, and ridge of the trapezium.  Because of its structural attachments, it is the stiffest segment of the flexor retinaculum.  Because the TCL provides the real restraining force that stops the contents of the carpal tunnel from moving in a palmar direction, it makes sense that the greatest contact pressure…and therefore greatest ischemia producing compression on the median nerve…would occur where the ligament is the most stiff.

Based on the combination of the type pressure sensor we used, its location between the contents of the carpal tunnel and the dorsal surface of the TCL, and the anatomic configuration of the flexor retinaculum, it made sense to us that the maximum pressure would occur adjacent the hook of the hamate.  Peak pressure adjacent the hook of the hamate also correlates with where the constricted part of the median nerve is found in patients with CTS, squeezing the life’s blood out of the patient’s precious median nerve.

The combination of these higher than expected pressures and their concentration along the stiff part of the TCL may not be coincidental.  Could there be some functional significance to this dynamic behavior of carpal tunnel pressure?

Remember, this is only what we think.  Our research didn’t actually produce any direct evidence that these dynamic pressures, those that cycle up and down as we use our hands, play a functional role.  In fact, a lot of the previous research might lead you to conclude that doing anything that increases pressure in the carpal tunnel might contribute to CTS.  But, a closer look at the research shows that it’s only an increase in the resting, or hydrostatic, carpal tunnel pressure beyond a threshold (most accept 30 mm Hg as the threshold) that contributes to CTS.  The role of these dynamic pressures, those that occur during active hand use, remains unknown.  We think that there may be a purpose for these dynamic pressures.  So, we proposed a new theory to help explain one possibility for these dynamic pressures in the etiology of CTS.

We propose that these higher than ever before seen pressures may actually be normal and needed on a regular basis.  Think of the pressure in the carpal tunnel as acting like a balloon trying to expand against the anatomic boundaries of the carpal tunnel.  The structures that form these boundaries are the carpal bones and ligaments, with the TCL being the most obvious.  These structures may need a regular dose of some serious stress to maintain the optimum shape and size of the carpal tunnel.  Providing this stress may be the functional role of these dynamic pressures.  There have been a few clues in the literature that relate to our theory.

First, the TCL has certain mechanical properties (i.e. its strength and stiffness) that are partially determined by both the size and number of collagen fibrils that it’s made of.  In patients with CTS, both the size and number of collagen fibrils in the TCL are different than the fibrils in subjects without CTS.  This alteration in mechanical properties may be a factor in the etiology of CTS [1].  Second, myofibroblasts have been found in the TCL’s of patients with CTS, suggesting that the TCL may be constantly trying to shorten [2].  Third, using hand exercises to create stress in the TCL has been promoted as necessary to maintain its length and reduce the signs and symptoms of CTS [3,4].  These findings all help support our idea that the fibrils of the TCL may be changing their morphology because of a lack of regular and sufficient mechanical stress.

This shouldn’t be any surprise; ligaments all over the body try to shorten if they are not regularly stressed.  The same occurs with the TCL.  If there’s not enough regular mechanical stress, the TCL starts to shorten.  It transitions from being just the right compliance to be both a competent pulley and permit adequate perfusion of the median nerve to being this rigid constraint.  If the TCL becomes too constraining, the contents of the carpal tunnel can’t expand as they need to, causing the resting pressure to creep up.  If the TCL isn’t being stressed enough, it may be because it’s not getting enough cycles of this increased pressure.

So, how do you get the pressure in the carpal tunnel high enough and regularly enough to stress the TCL, preserve its elastic properties, and resist contraction?  Using your hands forcefully.  As we discussed above, forceful hand use delivers the lumbrical muscles into the carpal tunnel and then, with their active contraction, releases a cyclic force that acts against the TCL to dilate the tunnel.  This may be the key to achieving the level of stress that the TCL needs, as well as the other ligaments that form the structural boundary of the carpal tunnel.  It may be a completely normal physiologic function that one day we will accept that it’s only when the hand is doing real work that you can reach these stress levels.  So, does a sedentary hand contribute to the onset of CTS?  We’re not sure, but we do believe there is something significant about the dynamic behavior of carpal tunnel pressures that, if better understood, might help us better understand not only CTS, but also other symptoms that often present clinically along with CTS, such as trigger finger.

We hope you enjoyed our thoughts and if you have any constructive criticism, we would appreciate hearing from you.

References:

1.    Stransky G, Wenger E, Dimitrov L.  Collagen dysplasia in idiopathic carpal tunnel syndrome.  Path Res Pract  1989;185:795-798.

2.   Allampallam K, Chakraborty J, Bose K, Robinson J.  Explant culture, immunofluorescence and electron-microscopic study of flexor retinaculum in carpal tunnel syndrome.  J Occup Environ Med  1996;38:264-271.

3.   Sucher B.  Myofascial manipulative release of carpal tunnel syndrome: documentation with magnetic resonance imaging.  JAOA  1993;93:1273-1278.

4.   Sucher B.  Palpatory diagnosis and manipulative management of carpal tunnel syndrome.  JAOA  1994;94:647-663.
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Device Solutions for Difficult Problems
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[av_heading tag=’h2′ padding=’10’ heading=’The MP and PIP Joints… how they influence each other’ color=’custom-color-heading’ style=” custom_font=’#403393′ size=” subheading_active=” subheading_size=’15’ custom_class=” admin_preview_bg=”][/av_heading]

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The following was written in response to a surgeon user of the Digit Widget asking about MP joint hyperextension when using the Digit Widget. He noted it was most troublesome in the little finger.

One of the main barriers to rebalancing the PIP joint resides in the reciprocal deformity the PIP contracture imposes on the MP joint. Let me explain:  in any PIP contracture involving any finger, the PIP contracture itself imposes a force imbalance on its MP joint. This is similar, but not identical, to the engineer’s explanation of an intercalated beam collapse pattern. PIP flexion pulls the central slip of its extensor mechanism distally and thereby increases the tension available to extend the MP joint.  In addition, PIP flexion “relaxes” the tension on the sublimus and profundus tendons at the MP joint, thereby decreasing flexor torque at the MP joint. In a patient where the primary problem is at the PIP joint, then the force imbalance we see at the MP joint is secondary to the pathology at the PIP.

The ulnar two fingers, with their mobile CMC joints, have more pronounced collapse deformities of their entire “ray” (all four joints…CMC to DIP) driven by any force imbalance. These include:

1.     Ulnar nerve palsy…low ulnar palsy more so than high.

2.     An apex palmar, malunited proximal phalangeal fracture with shortening of the dorsal length of the bone that creates an impotent extensor at the PIP joint and secondary MP torque imbalance favoring hyperextension.

3.     An apex dorsal, malunited metacarpal fracture, such as a boxer’s fracture, that creates an “intrinsic minus” type of finger deformity. This develops not entirely from weakness of the interosseous muscles, but from the mechanical imbalance of both intrinsic and extrinsic forces.

We hand surgeons and our patients are fortunate if long-standing PIP contractures have not created MP hyperextension. A hyper-extended MP joint is the enemy of reversing PIP contractures AND of restoring active force balance to all three joints of the problem finger.

1.     MP hyperextension has concomitant bow stringing of the central extensor tendon at MP level, thereby increasing the tendon’s moment for joint hyperextension.

2.     MP hyperextension pulls the transverse fibers of the extensor mechanism straight, thereby decreasing the longitudinal excursion of the extensor hood over the proximal phalanx. This decreases excursion of the central slip in a proximal direction. This proximal excursion is necessary for restoration of a competent extensor for the PIP.

3.     Impaired extensor excursion limits the ability of the extensor mechanism to return its lateral bands dorsal to the axis of rotation of the PIP joint. Restoration of mechanical health to the PIP joint requires both proximal & distal as well as dorsal and palmar forces on the lateral bands during active finger motion. Scar from prior injury or surgery that involves the lateral bands and/or Landsmeer’s ligamentous attachments to the same are the kiss of death for restoring active PIP extension.

Dupuytren’s contracture isolated to the PIP joint will slowly pull the PIP joint into flexion. Interestingly, if the patient has just enough Dupuytren’s in the palm to prevent MP hyperextension, the disease will actually prevent the acceleration of the force imbalance and secondary contracture of the PIP joint.  I am currently caring for a patient that has both advanced intrinsic muscle atrophy and weakness from a low ulnar nerve palsy and Dupuytren’s contracture at MP level that is preventing MP hyperextension. His MP level Dupuytren’s is serving as the perfect “built-in splint” to hold his MP’s in neutral or slight flexion so that the full tension and excursion of the extrinsic extensors can be transmitted across the MP joints distally to the IP joints. If the disease advances to the PIP joint, then the surgical treatment should be designed to reverse the PIP contracture but leave enough MP “contracture” to retain this hand’s built in splint.

Successful restoration and post-treatment maintenance of active PIP joint extension requires concomitant analysis of forces at the MP joint. If MP joint hyperextension shares a common etiology to PIP joint flexion (e.g., weak or paralyzed interosseous muscles), then restoration of the PIP to health requires not only reversal of its joint contracture, but concomitant rebalance of tendon forces at MP level. These type problems are far more common and troublesome on the little and ring fingers.

Look for and address every force imbalance that can either cause a primary MP hyperextension or MP hyperextension secondary to the PIP’s troubles. Do this and you will have the best opportunity to maintain the reversal of a given PIP contracture. The best place to start is to look proximal. If there is significant dorsal edema in the hand, the elastic skin gets lifted off the metacarpals and MP’s to create an MP extension torque. In addition, wrists that collapse into flexion with grasp cause or aggravate all claw type deformities of the fingers.

And finally, don’t forget to examine what is going on with the profundus and sublimus tendons from their entry into the A-1 pulley all the way to their phalangeal insertions. Lack of normal tendon excursion, whether primary or secondary, combined with moment arm shift favoring increased flexion torque across the PIP joint, are the second “kisses of death” for reversal of PIP contractures.

Now, let’s examine the value of skeletal extension torque (i.e., the Digit Widget) as a tool in reversing a PIP contracture. For extensor torque to be of value, it needs to focus its effect on PIP joint extension. The counter force for the Widget’s rubber band motor for PIP extension torque is a lever arm that attaches to the dorsal side of the hand (Fig. 1)

If the lever’s Velcro tab (the counter force or “anchor” for the device’s effect at the PIP) pulls dorsally at or distal to the MP joint, then the device will create only PIP extension. If the Velcro tab of the device pulls up proximal to the metacarpal head, then the distance from that dorsal pull to the MP joint axis defines the moment arm for the device to hyperextend the MP joint  (Fig. 2). If the Velcro tab can remain at the MP joint, then this negative effect is minimized.

Because it is difficult to keep the hand cuff of the Digit Widget kit situated in the optimal location, preventing MP hyperextension by a separate splint or strap will optimize reversal of the PIP contracture. It is not necessary to hold the MP joint in advanced flexion, but just enough to prevent joint hyperextension (Fig. 3). An MP Flexion Strap is now included in every kit.

John Agee

Sacramento, CA
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