Hand Clin 21 (2005) 455–468
Rehabilitation of Distal Radius Fractures: A Biomechanical Guide
David J. Slutsky, MD, FRCS(C)*, Mojca Herman, MA, OTR/L, CHT
3475 Torrance Blvd., Ste. F, Torrance, CA 90503, USA
Watson-Jones pointed out that a fracture is a soft tissue injury that happens to involve the bone . One must keep in mind that the soft tissue envelope greatly inﬂuences the ﬁnal functional result, even though all of the initial attention may be focused on the fracture position. The inﬂammatory cascade that results in edema, pain, and joint stiﬀness must be treated aggressively and concomitantly with the bony injury. Distal radius fractures range from simple extra-articular fractures to daunting complex multi-fragmented fracture dislocations. Extra-articular and minimally displaced intra-articular fractures often can be treated with closed reduction and cast application. Comminuted extra-articular and displaced intraarticular fractures often require more rigid ﬁxation. The basic science behind fracture healing and the inﬂammatory response is reviewed in this article, with a mind to the rehabilitation forces that can be applied during various stages of the healing process. Basic fracture healing The major factors determining the mechanical environment of a healing fracture include the rigidity of the selected ﬁxation device, the fracture conﬁguration, the accuracy of fracture reduction, and the amount and type of loading at the fracture gap . The fracture site stability may be enhanced artiﬁcially by a variety of external or internal means that includes cast treatment, pins, external ﬁxation, and plates. Fracture healing under unstable or ﬂexible ﬁxation typically occurs
by callus formation. This applies to cast treatment with or without supplemental pin ﬁxation and external ﬁxation. The sequence of callus healing can be divided into four stages . The stages overlap and are determined arbitrarily as follows. Inﬂammation (1–7 days) Immediately after a fracture there is hematoma formation and an inﬂammatory exudate from ruptured vessels. The fracture fragments are freely movable at this point. Soft callus (3 weeks) This corresponds roughly to the time that the fragments are no longer freely moving. By the end of this stage there is enough stability to prevent shortening, although angulation at the fracture site still can occur. Hard callus (3–4 months) The soft callus is converted by enchondral ossiﬁcation and intramembranous bone formation into a rigid calciﬁed tissue. This phase lasts until the fragments are united ﬁrmly by new bone. Remodeling This stage begins once the fracture has united solidly and may take from a few months to several years. Four biomechanical stages of fracture healing also have been deﬁned: stage I, failure through original fracture site, with low stiﬀness; stage II, failure through original fracture site, with high stiﬀness; stage III, failure partially through original fracture site and partially through intact
* Corresponding author. E-mail address: [email protected]
0749-0712/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.hcl.2005.01.004
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bone, with high stiﬀness; and stage IV, failure entirely through intact bone, with high stiﬀness. These data help determine the level of activity that is safe for patients with a healing fracture . The distal radius is composed largely of cancellous metaphyseal bone. Bone healing in cortical and cancellous bone is qualitatively similar, but the speed and reliability of healing is generally better in cancellous bone because of the comparatively large fracture surface . Most extra-articular fractures heal by 3–5 weeks after injury . For distal radius fractures, stage I would correspond roughly to the initial 4 weeks or the soft callus phase. Protection of the fracture from excessive force is needed to prevent shortening and angulation. Stage II would coincide with the 4–8-week time period. The period beyond 8 weeks would represent stages III and IV in which the fracture has united clinically and can tolerate progressive loading. Fracture site forces Movement of the bone fragments depends on the amount of external loading, stiﬀness of the ﬁxation device, and stiﬀness of the tissue bridging the fracture. The initial mechanical stability of the bone ﬁxation should be considered an important factor in clinical fracture treatment . The physiologic forces with wrist motion have been estimated to lie between 88–135 Newtons (N) [8,9]. Eighty-two percent of the loads across the wrist are transmitted through the distal radius . Cadaver studies have demonstrated that for every 10 N of grip force, 26 N is transmitted through the distal radius metaphysis. Given that the average male grip force is 463 N  or 105 psi (1 lb of force = 4.48 N), this would imply that up to 2410 N of force could be applied to the distal radius during power gripping . Previous studies of radius osteotomies showed that plates fail at 830 N . External ﬁxators compress as much as 3 mm under a 729 N load . To prevent a failure of ﬁxation the grip forces during therapy should remain less than 159 N (36 psi) for plates and less than 140 N (31 psi) for external ﬁxators during the initial 4 weeks [13,14]. Gripping and strengthening exercises should be delayed until there is some fracture site healing. When a bone fractures, the stored energy is released. At low loading speeds the energy can dissipate through a single crack. At high loading speed the energy cannot dissipate rapidly enough through a single crack. Comminution
and extensive soft tissue damage occur . Fractures that exhibit multiple fracture lines are thus inherently more unstable because of the greater energy absorption at the time of injury. The diﬀerence in stability between an undisplaced fracture and a displaced fracture with comminution is signiﬁcant and dictates a slower pace of fracture site loading during rehabilitation. Biochemical response to injury The basic response to injury at the tissue level is well known. It consists of overlapping stages, including an inﬂammatory phase (1–5 days), a ﬁbroblastic phase (2–6 weeks), and a maturation phase (6–24 months) . Following a fracture there is bleeding from disrupted vessels, which leads to hematoma formation. Several chemical mediators, including histamine, prostaglandins, and various cytokines are released from damaged cells at the injury site, inciting the inﬂammatory cascade [17,18]. The resultant extravasation of ﬂuid from intact vessels causes tissue swelling . Edema ﬂuid Simple hand edema is a collection of water and electrolytes. It is precipitated by myriad events, such as limb immobilization or paralysis, axillary lymph node disorders, and thoracic outlet compression. Edema restricts ﬁnger motion by increasing the moment arms of skin on the extensor side and by direct obstruction on the ﬂexor side. Since the work that is needed to eﬀect a joint angle change is dependent upon the product of the tissue pressure and the volumetric change during angulation, there is an increase in the muscular force that is necessary to bend a swollen ﬁnger. Compression, repeated ﬁnger ﬂexion, and dynamic splinting redistribute this ﬂuid to areas with lower tissue pressure. This allows the skin to lie closer to the joint axis, which decreases the eﬀort needed for ﬁnger ﬂexion . Inﬂammatory hand edema has the same mechanical eﬀects as simple edema and is treated in a similar fashion. The consequences of neglect, however, are dire. The swelling that occurs after wrist trauma as a part of the inﬂammatory response consists of a highly viscous protein laden exudate. This exudate leaks from capillaries and contains ﬁbrinogen. In many instances the ﬁbrin network is resorbed by approximately 7–10 days. Other times the ﬁbrinogen is polymerized into ﬁbrin, which becomes a lattice work for invading
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ﬁbroblasts. The ﬁbroblasts produce collagen, which, if the part is immobilized, forms a randomly oriented, dense interstitial scar that obliterates the normal gliding surfaces . The excessive ﬁbrosis also impedes the ﬂow of lymphatic ﬂuid , which perpetuates the edema (Box 1). Tendon gliding Much of the work on tendon gliding has been applied to tendon repairs. The information gleaned from this work, however, has therapeutic implications with regard to distal radius fractures (Box 2). The dorsal connective tissue of the thumb and phalanges forms a peritendinous system of collagen lamellae that provides gliding spaces for the extensor apparatus [24–26]. The extensor retinaculum is divided into six to eight separate osteoﬁbrous gliding compartments. Within the tunnels and proximal and distal to it, the extensor tendons are surrounded by a synovial sheath . The ﬂexor tendons are surrounded similarly by a synovial bursa and pass through a clearly deﬁned pulley system. Hyaluronic acid is secreted from cells lining the inner gliding surfaces of the extensor retinaculum and the annular pulleys [28,29]. The hyaluronate serves to decrease the friction force or gliding resistance at the tendon pulley interface through boundary lubrication . This in turn inﬂuences the total work of ﬁnger ﬂexion . Fracture hematoma can interfere with this boundary lubrication. Injury to the gliding surfaces by fracture fragments or surgical hardware can aﬀect tendon excursion and can lead to adhesions. Adhesions also can occur in nonsynovial regions such as the ﬂexor mass of the forearm and can restrict the muscle’s gliding and lengthening properties . Diﬀerential tendon gliding and active ﬁnger ﬂexion are necessary to restore range of motion.
Box 2. Tendon gliding exercises Immobilized wrist Straight position (MP, PIP, and DIP joints extended) Platform position (MP joints ﬂexed, PIP and DIP joints extended) Straight ﬁst (MP and PIP joints ﬂexed, DIP joints extended) Hook ﬁst (MP joints extended, PIP and DIP joints ﬂexed) Full ﬁst (MP, PIP, and DIP joints ﬂexed) Mobile wrist Synergistic wrist ﬂexion and ﬁnger extension Synergistic wrist extension and ﬁnger ﬂexion Active and passive ﬁnger extension with wrist extended >21( Active and passive thumb extension with wrist neutral in ulnar deviation
Tendon excursion Wehbe and Hunter studied the in vivo ﬂexor tendon excursion in the hand. With the wrist in neutral, the superﬁcialis tendon achieved an excursion of 24 mm and the profundus tendon 32 mm. The ﬂexor pollicis longus excursion was 27 mm. When wrist motion was added, the amplitude of the superﬁcialis became 49 mm, the profundus tendon, 50 mm, and the ﬂexor pollicis longus tendon, 35 mm [33,34]. Passive proximal interphalangeal (PIP) ﬂexion results in more ﬂexor tendon excursion than distal interphalangeal (DIP) ﬂexion . This knowledge formed the basis for an exercise program including three basic ﬁst positions: hook, ﬁst, and straight ﬁst, which allows the ﬂexor tendons to glide to their maximum potential . Synergistic wrist extension and ﬁnger ﬂexion increase passive ﬂexor tendon excursion by generating forces that pull the tendon through the pulley system . Extensor tendon gliding can be facilitated by extending the wrist more than 21(. This allows the extensor tendons to glide with little or no tension in zones 5 and 6 . Similarly, positioning the wrist close to neutral with some ulnar deviation minimizes friction in the extensor pollicis longus sheath .
Box 1. Edema management Acute edema Compression, elevation Active/passive ﬁnger motion Icing Retrograde massage Chronic edema Jobst intermittent compression unit (Jobst Co.; Toledo, OH); ratio of inﬂation to deﬂation time is 3:1 
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Immobilization There is a constant turnover and remodeling of tissue components. Collagen in particular is absorbed and then laid down again with updated length, strength, and new bonding patterns in response to stress. The periarticular tissue adaptively shortens if immobilized in a shortened position, which leads to clinical joint stiﬀness . This tissue includes the skin, ligaments, capsule, and the neurovascular structures . To restore the length of the shortened tissue, one must hold the tissue in a moderately lengthened position for signiﬁcant time so that it grows. Growth takes a matter of days, and the stimulus (ie, splinting) needs to be continuous for hours at a time to be most eﬀective.
gains in length. Further attempts at rapid lengthening exceed the ﬁber’s elastic limit, causing microscopic tearing, bleeding, and inﬂammation. This leads to ﬁbrin deposition with secondary interstitial ﬁbrosis, which may result in further contracture . If the stretching force is applied slowly, the collagen microﬁbrils have time to slide past one another. This slippage (or creep) allows the polymer chains to recoil. The tissue now has been lengthened permanently (plastic behavior) together with lessening of the tension over time (stress relaxation). If the same tissue is held in a slightly lengthened position for a period of hours or days, the collagen ﬁbers are absorbed then laid down again with modiﬁed bonding patterns, without creep or inﬂammation. Brand refers to this as growth rather than stretch . Types of splints The principles of splinting exploit the biomechanical properties of tissue to overcome contracture and regain joint motion following injury. The types of splints may be grouped as follows: Static: Rigid splints used for immobilization. Restrict unwanted arcs of motion (Fig. 1A,B). Serial static: Serial application of plaster casts. Relies on tissue growth . Dynamic: Continuous load applied through elastic bands or springs. Relies on timedependent material property creep. The dynamic force continues as long as the elastic component can contract, even beyond the elastic limit of the tissue (Fig. 2A,B). Static-progressive: Static progressive stretch. Relies on the principle of stress-relaxation . Construction is similar to dynamic splints except these splints use nonelastic components, such as nylon ﬁshing line, turnbuckles, and splint tuners. Once the joint position and tension are set, the splint does not continue to stress the tissue beyond its elastic limit . As the tissue lengthens, the wearer adjusts the joint position to the new maximum tolerable length (Fig. 3A–C). Fracture rehabilitation For the purposes of rehabilitation it is useful to consider the stability of the distal radius fracture site in three phases, which in turn guides the therapist as to the loads that can be placed across the fracture site. When internal or external ﬁxation is used, the loads placed on the fracture site
Tissue biomechanics Stress is the load per unit area that develops in a structure in response to an externally applied load. Strain is the deformation or change in length that occurs at a point in a structure under loading . Various materials have an elastic region whereby there is no permanent deformation of the material after the load is removed, eg, a rubber band. When the point of no return is exceeded (the yield point), there is permanent deformation of the material, eg, bending a paper clip until it deforms. Collagen contributes up to 77% of the dry weight of connective tissue. The ﬁbers are brittle and can elongate only 6%–8% before rupturing . Elastin comprises only 5% of the soft tissue weight, but it can elongate 200% without deformity . Viscosity is the property of a material that causes it to resist motion in an amount proportional to the rate of deformation. Slower lengthening generates less resistance. Any tissue whose mechanical properties depend on the loading rate is said to be viscoelastic. Biologic tissue is viscoelastic in that it has elastic properties but also demonstrates viscosity at the same time. Skin and connective tissue is a polymer of loosely woven strands of elastin and coiled collagen chains. With the initial application of tension, little force is needed for skin elongation. The elastin and the collagen chains are unfolding and aligning with the direction of the stress rather than stretching per se. When all of the ﬁbers are lined up parallel to the line of pull, the tissue becomes stiﬀ. Each ﬁber is uncoiled and can elongate only 6%–8%. A much greater force now produces minimal additional
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Fig. 1. Restrictive splint. (A) Above elbow splint restricts wrist motion and forearm pronation and supination. (B) Splint does allow elbow ﬂexion and extension.
may be adjusted accordingly. A rough knowledge of the intrinsic or augmented fracture site stability and the expected forces that are generated during therapy are necessary to minimize fracture site deformity (see section on fracture site forces). Phase I This phase is deﬁned by low fracture site stiﬀness (stage I; see section on basic fracture healing). The wrist splints used at this stage are static and are used for immobilization to limit unwanted motion, to prevent displacement at the fracture site, and to prevent or correct joint contractures. Protected wrist motion is initiated in this phase. Phase II This phase is characterized by increasing fracture site stiﬀness that should be able to withstand the forces generated with light strengthening and dynamic/static progressive wrist splinting (stage II).
Phase III In this phase there is suﬃcient fracture site stability to tolerate the loads generated during gripping and lifting (stages III and IV). Dynamic/ static progressive wrist splinting continues until motion plateaus. South Bay Hand Surgery Center protocol Controlled and progressive joint mobilization following trauma has been shown to give superior results to immobilization . The biochemical and biomechanical events that occur during fracture healing provide the underlying foundation for the rehabilitation program following a distal radius fracture. The therapy protocol for regaining ﬁnger motion is tiered and instituted immediately in all patients (Box 3). Tendon gliding exercises and passive ﬁnger motion with the wrist neutral are started immediately, because there are no
Fig. 2. Dynamic splints. (A) Dynamic supination splint relies on elastic band tension. (From Kleinman WB, Graham TJ. The distal radioulnar joint capsule: clinical anatomy and role in posttraumatic limitation of forearm rotation. J Hand Surg [Am] 1998;23:588–99; with permission.) (B) Dynamic PIP ﬂexion splint added to allow simultaneous ﬁnger and forearm splinting.
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Fig. 3. Static progressive splints. (A) Static progressive wrist ﬂexion splint. (B) Static progressive PIP extension splint. (C) PIP and DIP ﬂexion strap used to regain DIP motion. Note that it cannot increase PIP motion beyond 90( because of its vector force.
biomechanical concerns regarding phalangeal stability. Dynamic and static progressive splinting are instituted early if necessary, based on the observation that the total active ﬁnger motion typically plateaus by 3 months . In the authors’ experience, static progressive splinting of the ﬁngers is more painful and hence is instituted only after no further gains are seen with dynamic splinting. Wrist motion is initiated at diﬀerent times depending on the fracture site stability and the type of splinting or ﬁxation (Box 4). Patient factors, such as age, bone density, pain tolerance, and systemic disease may inﬂuence signiﬁcantly the pace of therapy, which should be adjusted accordingly. Synergistic wrist and ﬁnger motion for tendon excursion are started in tandem with wrist motion (see Box 2). Forceful gripping is delayed until there is some fracture site healing.
because of the intervening soft tissue. A cast relies on three-point ﬁxation to maintain the fracture position. If the wrist is casted in a ﬂexed and ulnar deviated position, a component of ligamentotaxis is also in play. The initial focus of therapy is directed toward reestablishing ﬁnger motion. Active ﬁnger motion should be gentle and not pushed early on, because the ﬂexed and ulnar deviated wrist position relaxes the ﬂexor tendons and tightens the extensors, making it painful to make a ﬁst. Displaced fractures often are associated with more soft tissue trauma, which leads to more swelling and slower healing. The loss of the immobilizing soft tissue envelope around the bones also leads to greater fracture site instability. In these cases it may be necessary to delay strengthening exercise as well as dynamic splinting of the wrist. Rehabilitation Week 1–6: ﬁnger rehabilitation protocol Week 6–8 (after cast removal): phase I wrist exercises Week 8–10: phase II wrist exercise >10 weeks: phase III wrist exercises
Procedure-speciﬁc treatment Cast treatment Cast treatment is nonrigid ﬁxation: it reduces fracture site mobility but does not abolish it
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Box 3. Finger rehabilitation protocol Day 1–7 Individual passive and active ﬁnger and thumb motion Thumb opposition exercises Intrinsic muscle stretching exercises Aggressive edema management (see Box 1) Tendon gliding exercises (see Box 2) Week 2–4 Dynamic PIP ﬂexion splint if passive PIP ﬂexion <60( Switch to PIP ﬂexion strap after >80( of passive PIP ﬂexion achieved Dynamic MP ﬂexion splint if passive MP ﬂexion <40( Dynamic PIP and DIP ﬂexion strap if passive DIP ﬂexion <40( Intrinsic muscle tightness: dynamic PIP ﬂexion splint with MP blocked in full extension Week 4–8 Switch to static progressive PIP splint if ﬂexion is still <60( Switch to static progressive MP splint if ﬂexion is still <40( Dynamic/static progressive PIP extension splint if PIP ﬂexion contracture >30( Dynamic MP extension splint if MP ﬂexion contracture >30( Dynamic/static progressive thumb opposition splint if opposition >2 cm from ﬁfth MPJ After week 8 Home splinting until motion plateaus
Box 4. Wrist rehabilitation protocol Phase I: low fracture site rigidity Custom or noncustom below-elbow splint Gentle active and passive wrist ﬂexion/ extension, pronation/supination Phase II: intermediate fracture site rigidity Add dynamic/static progressive splinting if wrist ﬂexion <30( Add dynamic/static progressive splinting if wrist extension <30( Dynamic/static progressive supination splinting if <60( Dynamic/static progressive pronation splinting if <60( Address functional activities, light strengthening Phase III: high fracture site rigidity Progressive strengthening exercises Home splinting until motion plateaus
static progressive elbow extension splints if elbow ﬂexion contracture is >30( at 8 weeks. Satisfactory results can be achieved with a home program in uncomplicated Colles fractures . Intrafocal pinning Intrafocal pinning is indicated in unstable extra-articular distal radius fractures. Intrafocal pinning, however, does not provide rigid ﬁxation. Supplemental cast or splint immobilization is necessary for 4–6 weeks; otherwise, early wrist motion may produce pain and dystrophy. The therapy protocol diﬀers little from cast treatment alone, but there are added requirements for pin site care. Typically K-wires are introduced through the snuﬀbox, where injury and irritation of the superﬁcial radial nerve branches (SRN) are common . Pin site interference with thumb or ﬁnger extensors requires added emphasis on thumb opposition and extensor tendon gliding exercises (see Box 2). If comminution involves more than two cortices or if the patient is older than 55 years of age, there is a high likelihood of subsequent fracture collapse . In these cases supplemental external ﬁxation or a spanning bridge plate may be used. Wrist motion therefore is delayed until after ﬁxator/plate removal.
Special considerations Ensure the cast does not block thumb and ﬁnger metacarpophalangeal (MP) ﬂexion creases to minimize collateral ligament contracture/intrinsic tightness. Avoid wrist hyperﬂexion in the cast. Bivalve/ remove cast with any signs of acute carpal tunnel syndrome (may require additional ﬁxation). If an above-elbow cast is used, regaining forearm rotation is more diﬃcult. Institute
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Rehabilitation Week 1–6: ﬁnger rehabilitation protocol Week 6–8 (after pin removal): phase I exercises Week 8–10: phase II exercises >10 weeks: phase III wrist exercises Special considerations Pin site care After pin removal Superﬁcial radial nerve (SRN) desensitization Ulnar deviation exercises (with radial sided pins) External ﬁxation External ﬁxation may provide improved wrist motion through less interference with the soft tissue envelope . External ﬁxation is considered ﬂexible ﬁxation. Regardless of the type of external ﬁxator, callus development is the overriding element providing the rigidity of the ﬁxator–bone system . The stability of ﬁxation can be enhanced signiﬁcantly through the addition of 0.62 percutaneous K-wires, which approaches the rigidity of a 3.5-mm dorsal AO plate (Synthes, Inc.; Paoli, PA) [54,55]. With intra-articular fractures, increasing the rigidity of the ﬁxator does not increase appreciably the rigidity of ﬁxation of the individual fragments . Augmentation with percutaneous K-wire ﬁxation reduces the dependence on ligamentotaxis to position the fragment and signiﬁcantly increases the stability of the construct, especially when the K-wire is attached to an outrigger . Pitfalls of ligamentotaxis External ﬁxators may be applied in a bridging or nonbridging manner. Bridging external ﬁxation relies on ligamentotaxis. Wrist distraction combined with hand swelling predisposes toward extensor tightness, which mandates an emphasis on MP to DIP ﬂexion exercises. If necessary a dynamic MP ﬂexion splint is applied while the ﬁxator is still in place (Fig. 4). Added extensor tendon stretch is accomplished by strapping the PIP and DIP joints in full ﬂexion while using the dynamic MP ﬂexion splint. Overdistraction of the wrist leads to intrinsic tightness and subsequent clawing of the ﬁngers . The index ﬁnger extensor tendons are especially sensitive to this and act as an early sentinel warning device. Patients with external ﬁxators often keep their forearms in pronation, which may lead to contractures of the distal radioulnar joint . Distraction, ﬂexion, and locked ulnar deviation of the external ﬁxator should be avoided, because they encourage pronation contractures and may predispose to acute carpal tunnel syndrome (Fig. 5A). Ideally the wrist should be positioned in mild extension, which relaxes the extensor tendons and facilitates ﬁnger ﬂexion . This often requires augmentation with percutaneous K-wire ﬁxation of the fracture (Fig. 5B). Dynamic or static progressive supination splinting can be eﬀective and should be instituted soon after ﬁxator removal . Because ligaments are viscoelastic, there is a gradual loss of the initial distraction force applied to the fracture site. The initial immediate improvement in radial height, inclination, and volar tilt are decreased signiﬁcantly by the time of ﬁxator removal . For this reason, light gripping exercises or using the hand for activities of daily living (ADL) should not be encouraged in the initial 4 weeks, with fracture site loading being limited to <31 psi . Nonbridging ﬁxators allow the institution of early wrist motion (Fig. 6A,B). In these cases therapy includes the addition of early wrist ﬂexion and extension in addition to the ﬁnger exercises. Radial deviation usually is blocked by the ﬁxator itself, and ulnar deviation exerts traction on the ﬁxator pin sites, which is painful. Simple extraarticular fractures can tolerate the earlier onset of loading as compared with comminuted extraarticular fractures. When nonbridging external ﬁxation is used for complex intra-articular
Fig. 4. Dynamic MP ﬂexion splint. This splint is converted easily to a static progressive splint by using a nonelastic nylon line and substituting a splint tuner for the post.
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Fig. 5. External ﬁxation. (A) Note the marked wrist ﬂexion, which should be avoided. (B) Augmentation with K-wires allows external ﬁxation with mild wrist extension.
fractures, articular incongruity is common . This may be prevented by use of custom designed ﬁxators with dorsal outriggers (Fig. 7). Rehabilitation Bridging external ﬁxator Week 1–6: ﬁnger rehabilitation protocol Week 6–8 (after ﬁxator removal): phase I wrist exercises Week 8–10: phase II wrist exercises >10 weeks: phase III wrist exercises
Special considerations Pin site care Aggressive MP ﬂexion; add dynamic MP ﬂexion splint if MP ﬂexion <40( by 2 weeks Intrinsic tightness stretching; add dynamic intrinsic tightness splint as needed (MP extended, PIP/DIP ﬂexed) After pin removal SRN desensitization Ulnar deviation exercises (with radial sided pins)
Fig. 6. Nonbridging external ﬁxator. (A) Nonbridging application of an external ﬁxator. (B) Fracture position is maintained without spanning the joint.
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Initially the plate bears all the stress; hence, the rehabilitation forces must not exceed their tolerance. As healing progresses the plate load shares until the fracture is healed and bears almost the entire stress . Feedback from the operating surgeon is necessary as to the stability of ﬁxation before instituting wrist motion and gripping, especially when there is signiﬁcant intra-articular comminution. Dorsal plating
Fig. 7. Custom nonbridging external ﬁxator with dorsal outrigger bar.
Nonbridging external ﬁxator Week 1–6: ﬁnger rehabilitation protocol; phase I wrist exercises Week 6–10 (after ﬁxator removal): phase II wrist exercises >10 weeks: phase III exercises
Newer low proﬁle dorsal plate designs were greeted with much enthusiasm [67,68]. Extensor tendon irritation is still a problem [69,70]. Rapid tendon acceleration through preload has been proposed as one method to maximize extensor tendon excursion . Rehabilitation Week 1–4: ﬁnger rehabilitation protocol; phase I wrist exercises Week 4–8: phase II wrist exercises >8 weeks: phase III exercises Special considerations Emphasize extensor tendon gliding (see Box 2) Emphasize wrist ﬂexion Suspect extensor pollicus longus (EPL) impingement/entrapment with resistant thumb extensor tightness Volar plating Volar ﬁxed angle plating is currently in vogue . Proponents of this procedure cite improved fracture stability and better soft tissue coverage of the implant. Normal wrist extension may be diﬃcult to regain, which has led some to recommend splinting the patient’s wrist in 30( of extension between therapy sessions . Dynamic or static progressive splints may be used if needed. Flexor tendon tightness may occur. This should be treated with dynamic MP extension splinting combined with static extension splinting of the PIP and DIP joints, while the wrist is incrementally brought from neutral to extension. Rehabilitation Week 1–4: ﬁnger rehabilitation protocol; phase I wrist exercises Week 4–8: phase II wrist exercises Late (>8 weeks): phase III exercises
Plate ﬁxation Rigid ﬁxation of fractures by plating alters the biology of fracture healing. When motion is abolished completely between fracture fragments, no callus forms . This has been termed direct healing, whereby osteons directly bridge the fracture gap to regenerate bone, and the fracture heals by remodeling . Conventional plate ﬁxation relies on friction between the plate and bone interface for stability and the dynamic compression properties of the plate, which preload the fracture site . In general, plate ﬁxation allows earlier loading of the fracture site. Newer locking plates act by splinting the fracture site without compression, resulting in ﬂexible elastic ﬁxation and stimulation of callus formation. Locking plates do not require friction to secure the plate to the bone. Comminuted diaphyseal or metaphyseal fractures are suited particularly to bridging ﬁxation using locked plates . Fragment-speciﬁc ﬁxation (TriMed, Inc.; Valencia, CA) relies on a combination of low proﬁle pin plates with a variety of ﬂexible wire form buttress plates. The pin plates usually are applied dorsoradially underneath the ﬁrst extensor compartment and dorsoulnarly between the ﬁnger extensors and the extensor digiti minimi, although volar applications are not uncommon.
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Fig. 8. Volar perspective, 3-D CT reconstruction of a right distal radius malunion. (A) The distal fragment is pronated (arrow) at the fracture site (*), which blocks supination at the distal radioulnar joint. S, scaphoid; L, lunate; T, triquetrum. (B) Clinical photograph showing attempted supination on the right.
Special considerations Suspect FPL entrapment with resistant thumb ﬂexor tightness Fragment-speciﬁc ﬁxation Same as for dorsal and volar plate ﬁxation: hardware irritation of the ﬁrst extensor compartment tendons and the ﬁnger extensors may occur from pins backing out. Emphasize thumb/ﬁnger extension with dynamic splinting as necessary. Combined ﬁxation Some intra-articular fractures are so inherently unstable that combined internal and external ﬁxation is necessary for the initial 6 weeks. In these instances strengthening exercises may need to be delayed longer than usual because of the risk for displacing the articular fragments. Combined volar and dorsal plating may devascularize bone fragments, which also may contribute to these delays. In these complex fractures it is important to have frequent communication with the treating surgeon together with a review of the radiographs before loading the fracture site. Rehabilitation Same as for plate or external ﬁxation, although fracture site loading may be delayed as necessary Combined radius and scaphoid ﬁxation Same as for plate or external ﬁxation Special considerations Variable delay in implementing wrist motion with carpal fracture–dislocation
Delay strengthening until there is evidence of scaphoid union by CT scan
Causes of treatment failures There are a large number of extrinsic tendons crossing the fracture site. Dorsal angulation of >30( and radial angulation >10( greatly aﬀects the moment arms and subsequently the excursion and strength of these tendons . If joint malalignment is the etiology of loss of forearm rotation, then continued therapy is of no beneﬁt (Fig. 8A,B). Biomechanical studies have demonstrated that radial shortening 10 mm caused a 47% pronation loss and a 27% supination loss . More than 10( of dorsal tilt leads to a dorsal carpal shift with compressive forces. This leads to feelings of pain and insecurity with gripping and diﬃculties with ADL . More
Fig. 9. Malunited Colle’s fracture. Note the marked dorsal tilt of the joint surface with dorsal migration of the carpus resulting in a secondary dorsal intercalated segmental instability pattern.
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severe dorsal tilt leads to a dynamic dorsal intercalated segmental instability (Fig. 9) .
Summary Fracture healing and surgical decision making are not always predictable. The suggested protocols are intended to be ﬂexible rather than rigid to be responsive to patient progress and the fracture site stability. A methodologic approach to the rehabilitation following a distal radius fracture, based on a knowledge of the biology of fracture healing and biomechanics of ﬁxation, may preempt some of the pitfalls associated with distal radius fracture healing. References
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