W5 Rehabilitation after Distal Radius Fractures
A methodological approach to the rehabilitation of distal radius fractures is proposed based on knowledge of fracture healing, tissue healing, biomechanics of fixation, and biomechanics of splinting. A distal radius fracture affects more than just the bone. Watson-Jones1 pointed out that a fracture is a soft tissue injury that happens to involve the bone. 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. There are a multitude of types of distal radius fractures ranging from simple extra-articular fractures to daunting complex, multifragmented fracture-dislocations. Extra-articular and minimally displaced intra-articular fractures can often be treated with closed reduction and cast application. Comminuted extra-articular and displaced intra-articular fractures often require more rigid fixation. This chapter reviews the basic science behind fracture healing and the inflammatory response with a focus on the rehabilitation forces that can be applied during various stages of the healing process. Special considerations for each type of fixation are outlined to assist in maximizing therapeutic intervention and outcomes.
Basic Fracture 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.2 Fractures that exhibit multiple fracture lines are 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.
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.3 The fracture site stability may be artificially enhanced by various external or internal means, including 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.4 The stages overlap and are determined arbitrarily.
Inflammation (1 to 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 stage roughly corresponds 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 to 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 firmly united by new bone.
Remodeling
This stage begins when the fracture has solidly united and may take a few months to several years. Four biomechanical stages of fracture healing 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 bone, with high stiffness; and stage IV, failure entirely through intact bone, with high stiffness. These data help to determine the level of activity that is safe for patients with a healing fracture.5
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.6 Most extra-articular fractures heal by 3 to 5 weeks after injury.7
For distal radius fractures, stage I would roughly correspond to the initial 4 weeks, or the soft callus phase. Protection of the fracture from excessive forces is needed to prevent shortening and angulation. Stage II would coincide with the 4- to 8-week time period. The period beyond 8 weeks would represent stages III and IV, where the fracture has clinically united and can tolerate progressive loading.
Fracture Site Forces
Movement of the bone fragments depends on the amount of external loading, the stiffness of the fixation device, and the 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.8
The physiological forces with wrist motion have been estimated to be 88 N to 135 N.9,10 Eighty-two percent of the loads across the wrist are transmitted through the distal radius.11 Cadaver studies have shown 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 N12 or 105 psi (1 lb of force = 4.48 N), this would imply that 2410 N of force could be applied to the distal radius during power gripping.13 Previous studies of radius osteotomies showed that plates fail at 830 N.14 External fixators compress 3 mm under a 729 N load.15 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.14,15 Either type of fixation provides enough stability to institute immediate wrist motion. Gripping and strengthening exercises during rehabilitation generally should be delayed until there is some fracture site healing.
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 to 5 days), a fibroblastic phase (2 to 6 weeks), and a maturation phase (6 to 24 months).16 Following a fracture, there is bleeding from disrupted vessels, which leads to hematoma formation. Numerous 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.19
Edema Fluid
Simple Hand Edema
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. The work needed to effect a joint angle change depends on the product of the tissue pressure and the volumetric change during angulation. This requires 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 redistribution allows the skin to lie closer to the joint axis, which decreases the effort needed for finger flexion.20
Inflammatory Hand Edema
Inflammatory hand edema has the same mechanical effects as simple edema and is treated in a similar fashion. The consequences of neglect are dire, however. 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 reabsorbed by about 7 to 10 days. Other times, the fibrinogen is polymerized into fibrin, which becomes a lattice work for invading fibroblasts. The fibroblasts produce collagen, which, if the part is immobilized, forms a randomly oriented, dense interstitial scar that obliterates the normal gliding surfaces.21 The excessive fibrosis also impedes the flow of lymphatic fluid,22 which perpetuates the edema.
Management of Edema and Pain
Treatment for acute edema begins immediately. Initial therapy comprises elevation, ice, and compressive dressings and garments. Coban wrap is used to reduce digital edema, and compression stockinettes can be applied to the hand, wrist, and elbow. Edema that persists for greater than 2 to 3 weeks is even more important to control. Persistent edema increases stiffness in the joints and may lead to adhesions, which interfere with the normal gliding of the tendons and nerves.
Subacute and long-term management techniques include active and passive range of motion exercises, manual edema mobilization such as retrograde massage, compression dressings and garments, contrast baths, electrical stimulation, high-voltage galvanic stimulation, and the use of a Jobst intermittent compression unit as appropriate.23 The pressure generated by these techniques must be low to prevent obstruction of lymphatic flow, which plays a primary role in the absorption of larger plasma proteins associated with chronic edema and fibrosis.
Electrical stimulation has been shown to assist in the reduction of the amount of edema formed with an acute injury and inflammation.24 Explanatory theories include the idea that the negative charge of cathodal stimulation repels the negatively charged serum proteins, blocking their movement out of the blood vessels. It also is thought that the current decreases blood flow by reducing the microvessel diameter.25 A reduction in the pore size in the microvessel walls occurs, preventing large plasma protein leakage through the pores.26
Transcutaneous electrical nerve stimulation, based on the modified gate control theory, can be used for pain modulation by inhibiting the activation of pain and closing off the pain pathways.27 Electrical stimulation used on a conventional transcutaneous electrical nerve stimulator setting can interrupt the pain-spasm-pain cycle, resulting in some reduction of pain after the stimulation stops.26 Ice can be used in conjunction with the electrical stimulation to allow the patient to benefit from edema management and pain relief. Cold seems to increase the pain threshold by desensitizing the pain receptors and by reducing the chemical mediators of inflammation, which can stimulate the pain receptors.28 These modalities assist with the management of pain and edema, enabling the patient to participate more effectively in important therapeutic activities.
Tendon Gliding
Much of the work on tendon gliding has been applied to tendon repairs. The information gleaned from this work has therapeutic implications, however, with regards to distal radius fractures (Table W5-1). The dorsal connective tissue of the thumb and phalanges forms a peritendinous system of collagen lamellae that provide gliding spaces for the extensor apparatus.29–31 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.32 The flexor tendons are similarly surrounded 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.33,34 The hyaluronate serves to decrease the friction force or gliding resistance at the tendon-pulley interface through boundary lubrication35; this influences the total work of finger flexion.36 Fracture hematoma can interfere with this boundary lubrication. Injury to the gliding surfaces by fracture fragments or surgical hardware can affect tendon excursion and lead to adhesions. Adhesions also can occur in nonsynovial regions, such as the flexor mass of the forearm, and restrict the muscle’s gliding and lengthening properties.37 Differential tendon gliding and active finger flexion are necessary to restore range of motion.
TABLE W5-1 Tendon Gliding Exercises
| Immobilized Wrist |
| Straight position (MCP, PIP, and DIP joints extended) |
| Hook fist (MCP joints extended, PIP and DIP joints flexed) |
| Full fist (MCP, PIP, and DIP joints flexed) |
| Straight fist (MCP and PIP joints flexed, DIP joints extended) |
| Platform position (MCP joints flexed, PIP and DIP joints extended) |
| Mobile Wrist |
| Synergistic wrist flexion and finger extension |
| Synergistic wrist extension and finger flexion |
| Active and passive finger extension with wrist extended >21 degrees |
| Active and passive thumb extension with wrist neutral in ulnar deviation |
DIP, distal interphalangeal; MCP, metacarpophalangeal; PIP, proximal interphalangeal.
Tendon Excursion
Wehbe and Hunter38,39 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 achieved an excursion of 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. Passive proximal interphalangeal (PIP) flexion results in more flexor tendon excursion than distal interphalangeal (DIP) flexion.40
To allow flexor tendons to glide to their maximal potential, the three basic fist positions are performed as part of a tendon gliding exercise program: straight fist, full fist, and hook fist.41 The straight fist (metacarpophalangeal [MCP] and PIP joints flexed, DIP joints extended) elicits maximal flexor digitorum superficialis glide in relation to surrounding structures. The full fist (MCP, PIP, and DIP joints flexed) elicits maximal flexor digitorum profundus glide. The hook fist (MCP joints extended, PIP and DIP joints flexed) elicits maximal differential gliding between the two tendons.42 Synergistic wrist and finger motion increases passive flexor tendon excursion by generating forces that pull the tendon through the pulley system.43
Extensor tendon gliding can be facilitated by extending the wrist more than 21 degrees. This extension allows the extensor tendons to glide with little or no tension in zones 5 and 6.44 Similarly, positioning the wrist close to neutral with some ulnar deviation minimizes friction in the extensor pollicis longus sheath.45
Tissue Biomechanics
There is a constant turnover and remodeling of tissue components. Collagen in particular is being 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, leading to clinical joint stiffness.46 This tissue includes the skin, ligaments, and capsule as well as the neurovascular structures.47 To restore the length of the shortened tissue, one must hold the tissue in a moderately lengthened position for a significant time so that it grows. Growth takes days, and the stimulus (i.e., splinting) needs to be continuous for hours at a time to be most effective.
The following is an overview of specific mechanical properties and tissue composition that establish the foundation for splinting intervention in distal radius fracture management. 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.48 Various materials have an elastic region whereby there is no permanent deformation of the material after the load is removed (e.g., a rubber band). When the point of no return is exceeded (the yield point), there is permanent deformation of the material (e.g., bending a paper clip until it deforms).
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. Biological tissue is viscoelastic in that it has elastic properties, but also shows viscosity at the same time.
Collagen contributes 77% of the dry weight of connective tissue. The fibers are brittle and can elongate only 6% to 8% before rupturing.49 Elastin comprises only 5% of the soft tissue weight, but it can elongate 200% without deformity.50 Skin and connective tissues are a polymer of loosely woven strands of elastin and coiled collagen chains. With the initial application of tension, very 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 quite stiff. Each fiber is uncoiled and can elongate only 6% to 8%. A much greater force now produces minimal additional gains in length.
Further attempts at rapid lengthening exceed the fiber’s elastic limit, causing microscopic tearing, bleeding, and inflammation. This situation leads to fibrin deposition with secondary interstitial fibrosis, which may result in further contracture.20 Knowledge of tissue biomechanics greatly enhances decision making and application of splinting during the rehabilitative process.
Types of Splints
The principles of splinting exploit the biomechanical properties of tissue to overcome contracture and regain joint motion after injury. The types of splints may be grouped as follows: static, serial static, dynamic, and static progressive. Dynamic, static progressive, and serial static splinting are considered mobilization splints. The rationale of mobilization splinting is based on a physiological theory that controlled tension applied over a long time alters cell proliferation. The effectiveness is not based on the concept of stretching tissue, but relies on actual cell growth. The target tissue lengthens when the living cells of the contracted tissues are stimulated to grow. The stimulation occurs when consistent external tension is applied through the splint over time.51
FIGURE W5-1 Static splints. A, Custom circumferential below-elbow splint. B, Custom below-elbow wrist splint. C, Noncustom wrist splint.
FIGURE W5-2 Dynamic splints using elastic components for mobilization. A, Dynamic supination splint. B, Dynamic wrist extension splint. C, Dynamic proximal interphalangeal/distal interphalangeal flexion strap. D, Dynamic metacarpophalangeal extension splint.
FIGURE W5-3 Static progressive splints using nonelastic components for mobilization. A, Static progressive wrist extension splint. B, Static progressive metacarpophalangeal flexion splint. C, Static progressive proximal interphalangeal flexion splint. D, Static progressive proximal interphalangeal flexion strap.
According to Schultz-Johnson’s clinical experience,55 static progressive approaches to passive range of motion limitations for “soft end feel” joints offer faster results without additional tissue trauma. Some patients may tolerate static progressive splinting better than dynamic splinting, perhaps because the joint position is constant while the tissue readily accommodates to the tension and is less subject to the influences of gravity and motion.53,56
Schultz-Johnson55 also advocates wearing a static progressive splint during sleep, obtaining up to 8 hours of end range time that does not take away from function and movement during the day. She states that gains at a joint of 5 to 10 degrees per week indicate splint success. The more time the tissue spends at end range, the more quickly passive range of motion improves.57
Fracture Rehabilitation
It is essential to communicate with the surgeon regarding the stability of the fixation and the type of fixation to guide the loads placed across the fracture site. Implementing wrist motion, splinting, and strengthening in an accurate and specified timeline minimizes fracture site deformity and optimizes therapeutic intervention.
