15018752330
发表时间:2015-12-09 浏览次数:556次
Introduction
The practice of hand surgery requires an understanding of the anatomy,
the intimate relationships between collagen and synovium, and the
ultimate function of the hand. This is critical to the performance of
surgery ranging from skin coverage following a crush injury to tendon or
toe transfers in congenital hand cases. We present a series of surgical
procedures based on this understanding.
Pathologic conditions
resulting in synovial irritation or inflammation involve an array of
molecular pathways, which can lead to the pathologic deposition of
collagen in the hand and wrist. Chronically inflamed synovium will
thicken adjacent collagen and create these phenomena (the "collasyn
theory"). In the hand, collagen and synovial tissue are anatomically
closely associated. The support structures, mostly made up of collagen
(bones, tendons, ligaments), are lined with synovial tissue in areas
where tissue motion requires a reduction in the coefficient of friction.
Surgical
procedures must address the inflamed synovium, which, by virtue of its
close anatomic proximity, "communicates" with the adjacent collagen
structures and may cause collagen thickening and multiple symptomatic
changes. Surgery may be needed to: (1) remove inflamed synovium; (2)
increase space around affected structures and (3) remove abnormal
tissues (such as osteophytes) that occur secondary to the effects of the
inflamed synovium on adjacent collagen structures. This surgical
approach decreases symptoms and may enhance joint longevity.
Surgical Series
Rheumatoid arthritis
The deformities in the hand in
rheumatoid arthritis often follow a predictable pattern. The formula is
destructive synovitis plus load equals deformity. If viewed through the
lens of the collasyn theory, synovitis will rupture tendons at the
distal edge (load area) of the extensor retinaculum. Synovitis also
stimulates protective over-activity of the intrinsics, creating abnormal
loads in the fingers. These loads most often create pressure on the
dorsoradial capsule and ligaments of the metacarpophalangeal (MP) joint
resulting in volar and ulnar subluxation of the proximal phalanx. If
there is insufficient synovitis in the MP joint, the MP joints will not
subluxate. The intrinsic loads then are transmitted to the fingers,
resulting in swan necks, boutonnieres, dislocations or even
interphalangeal fusion. Applying this concept allows prediction of
expected deformity on clinical examination. Tight intrinsics (positive
Bunnell test) should be released early, removing the load component of
the destructive formula. The ulnar drift and deformities of the wrist
are the result of the "downslope" loads created by the anatomy of the
articular surface of the distal radius.
Stenosing tenosynovitis or trigger finger
The
effects of the interaction between synovium and collagen can be seen in
trigger fingers. In stenosing tenosynovitis of the finger flexors,
there is a thickened retinaculum or pulley that constricts the
osseofibrous tunnel through which the tendon runs. [1]
Chronic synovial irritation affects collagen deposition in the A1
pulley and leads to a progressive thickening and sometimes metaplasia of
the pulley [1],[2],[3] [Figure 1].
During sleep, edema collects in the tendon proximal and distal to the
pulley. The symptomatic sequelae include stiffness in the mornings as
patients open and close their fingers to "milk" the fluid back into the
natural shape of the tendons, or "locking" of the fingers if a nodule is
too big to pass through the pulley. Conservative treatment may include
steroid injections, splinting and activity modification. If this fail,
surgery is indicated. [4]
A release of the A1 pulley increases space to allow normal tendon
gliding. Surgery has been shown to be more successful in the absence of
diabetes. [5]
The collasyn theory explains why there is an increased incidence of
stenosing tenosynovitis (trigger finger) in the thumb and little finger
following carpal tunnel surgery. Infection can move from thumb to little
finger through the common synovial lining between the thumb, the carpal
tunnel and the fibro-osseous sheath of the little finger flexors.
Surgery on the carpal tunnel produces inflammation of this communicating
synovium, which then has its hypertrophic effect on the collagen of the
A1 pulleys.
Fourth extensor compartment synovitis
Collasyn
pathology is also seen in the extensor retinaculum. Patients with
fourth extensor compartment stenosing tenosynovitis develop a thickened
retinaculum. In performing ultrasound evaluation, Zhou et al. [6]
found that with increased extension of the wrist, the contact area
between the extensor retinaculum and the extensor tendons decreased,
causing increased friction. We have found that a release of the septa
between the fourth and fifth extensor compartments without releasing the
external retinaculum is all that is needed to provide sufficient room
for the tendons. [7]
Check reins
Treatment of proximal interphalangeal (PIP) joint contractures is often reported to be less than optimal. [8]
The volar plate at the PIP joint is a unique structure that prevents
hyperextension at the PIP joint and absorbs enormous compression loads.
The PIP volar plate is a thick, strong fibrocartilaginous structure,
lined on the volar surface by peritendinous synovium of the
fibro-osseous sheath and on the dorsal surface by joint synovium. These
two layers of synovium lie on either side of the thin joint capsule at
the lateral sides of the volar plate. [9]
Inflammation of these two different synovial surfaces influence each
other and produce the unusual abnormal collagen hypertrophy termed the
checkrein ligaments. These do not exist in the normal state but are
produced under the influence of this "synovial sandwich." When treating
contractures of the PIP joints, one must release these pathological
structures in order to increase the movement in the joint. Results of a
study using this technique indicated full intraoperative extension in
110 of 115 joints, with 2 joints requiring a collateral ligament
release. Three of the 115 digits required a second checkrein release
after intraoperative gains were not maintained. [9]
Peripheral arthritis
Peripheral
arthritis is secondary to synovial traction and inflammation.
Osteophytes and abnormal cartilage build up on the joint periphery. It
is hypothesized that the areas of synovial attachment are responsible
for the synovitic influence on collagen and bone formation. With chronic
synovial inflammation, the mechanical traction at the synovial
attachment point may play a part but the inflamed synovium communicates
with the bone collagen resulting in osteophyte formation. Resecting
these bone areas along with excision of involved synovium results in
clearing of the patient's symptoms and significantly extending joint
longevity. This occurs without having altered joint mechanics at the
time of surgery.
Distal radioulnar joint
This
approach has been used in the treatment of arthritis in the distal
radioulnar joint (DRUJ). The treatment of DRUJ degenerative arthritis
following failure of conservative treatment such as splinting and
antiinflammatory medication includes complete elimination of the
arthritic joint, as popularized by Darrach, [10] a hemiresection-interposition technique, [11] the matched distal ulna resection [12] or the Sauvι-Kapandji procedure, as well as ulnar head or total joint replacement. [13]
A modified DRUJ arthritis technique based on the concept of proximal to
distal progression of degenerative joint disease at the DRUJ has been
described [14] [Figure 2].
The proximal one-third to one-half of the articular surface is
typically resected around the entire circumference of the joint. In one
published study, all patients noted significant improvement in symptoms. [14]
One patient went on to have a matched ulna arthroplasty. In another
report on results of 29 patients, 5 (17%) had additional surgery after
the DRUJ arthroplasty specific to the ulno-carpal/DRUJ complex (four
patients matched ulna arthroplasty, one patient triquetral impingement
ligament tear [TILT] and ulna styloidectomy). [15]
Dorsal wrist syndrome
Another example of peripheral
arthritis is the dorsal wrist syndrome (DWS). This common diagnosis of
wrist pathology results from scaphoid instability after ligament tears,
extreme loading of the wrist or a physiologically inadequate ligament
system. The most common problem in the human wrist is the tendency for
the proximal scaphoid pole to escape from beneath the capitate. Under
load, this displacing scaphoid produces stretch and insult to the
synovium. In its mildest form, acute wrist trauma produces scapholunate
(SL) synovitis and ligamentous strain without a SL ligament tear. A more
substantial ligament tear may result in a displacing scaphoid
accompanied by chronic synovitis. These wrists are painful and will not
tolerate loading. Conservative treatment consists of splinting and other
types of activity modification. [16]
Surgical management of DWS after 6 months of conservative care involves
exploration of the SL joint with excision of the soft tissue synovial
mass and any associated ganglia. Bony ridging and osteophytes form on
the dorsum of the scaphoid and occasionally the lunate and are present
in every case to some extent [Figure 3].
The dorsal ridging is believed to be the synovial attachment point
responsible for molecular remodeling of collagen and bone due to the
synovial inflammation. No change in scaphoid stability is accomplished.
One hundred and fifty-one cases of surgically treated DWS were evaluated
and <10% of these wrists required subsequent scaphoid stabilization
(scaphoid-trapezium-trapezoid (STT) fusion). Wollstein et al. [17]
presented results on 80 patients surgically treated for DWS, with 25%
requiring some form of further surgery, including 9 STT fusions and 2
proximal row carpectomies. It is hypothesized that the resection of this
synovitic attachment point is responsible for the relatively low rates
of progression to arthritis despite continued abnormal scaphoid
migration under load. A second group with a similar surgical procedure
has been described with 86% of their patients having good to excellent
results. [18]
In conclusion, inflamed synovium influences adjacent collagen. This
fundamental relationship is the basis for many of the pathologic
conditions of the hand, from capsular and ligament collagen to bone
collagen (the "collasyn theory"). Viewing pathology of the hand in this
manner may enhance our understanding and consequent treatment of hand
conditions. The synovial cells produce a multitude of molecules and
mediators involved in normal joint function as well as inflammatory
mediators such as cytokines in response to osteoarthritis. [19],[20]
Lubricin and hyaluronic acid are two important lubricant molecules
produced by synovium. Recent evidence has shown that these molecules are
important in articular cartilage maintenance and loss of these
substances can lead to osteoarthritic degeneration. [21],[22],[23] A reactive synovium produces factors related to inflammation through participation in multiple pathways. [24],[25],[26],[27]
Synovium includes mesenchymal stem cells capable of differentiating
into various tissue types including cartilage, muscle and bone. [28],[29],[30]
Thus, synovium plays a key role in the repair of injured connective
tissue components, but may also create the environment in which further
pathology occurs. [19]
Further
study in this area may allow us to understand and address this synovial
influence before it exerts its effect on surrounding collagen.
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