INTRODUCTION

A methodologic approach to the rehabilitation that follows distal radius fractures is presented based on knowledge of the biology of fracture healing, tissue healing, biomechanics of fixation, and biomechanics of splinting. Procedure-specific protocols are outlined.

It is important to realize that a distal radius fracture affects more than just the bone. 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 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 that 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 intra-articular fractures often require more rigid fixation.

The basic science behind fracture healing and the inflammatory response is reviewed with consideration of 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 speed, 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 can occur. Fractures that exhibit multiple fracture lines are thus inherently more unstable owing to 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 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 are generally better in cancellous bone because of the comparatively large fracture surface. Most extra-articular fractures heal within 3 to 5 weeks after injury.

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 artificially enhanced by a variety of external or internal means, which include 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, as well as to external fixation. The sequence of callus healing can be divided into four stages. The stages overlap and are determined arbitrarily.

• 1.
  

  Inflammation (1 to 7 days). Immediately after a fracture, hematoma forms and an inflammatory exudate is produced from ruptured vessels. The fracture fragments are freely movable at this point.

  
  
• 2.
  

  Soft callus (3 weeks). This roughly corresponds to the time during which 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 can still occur.

  
  
• 3.
  

  Hard callus (3 to 4 months). The soft callus is converted by endochondral ossification and intramembranous bone formation into a rigid calcified tissue. This phase lasts until the fragments are firmly united by new bone.

  
  
• 4.
  

  Remodeling (a few months to several years). This stage begins once the fracture has solidly united. It may take 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.

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 during which 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.

The physiologic forces with wrist motion have been estimated to lie between 88 and 135 newtons (N). 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 are transmitted through the distal radial metaphysis. Given that the average male grip force is 463 N or 105 psi (1 lb of force = 4.48 N), this implies that up to 2410 N of force could be applied to the distal radius during power gripping.

The biomechanical requirements of external fixation for fractures of the distal radius have not been ascertained until recently. The magnitude and direction of the physiologic loads on the distal radius were dynamic and unknown. However, recent work by Rikli and associates has shed new light on this point. Using a new capacitive pressure-sensory device, his group measured the in vivo dynamic intra-articular pressures in the radioulnocarpal joint of a healthy volunteer under local anesthesia. With the forearm in neutral rotation, the forces ranged from 107 N with wrist flexion to 197 N with wrist extension. The highest forces of up to 245 N were seen with the wrist in radial deviation and the forearm in supination. Presumably, any implant or external fixator would need to be strong enough to neutralize these loads to permit early active wrist motion.

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 under 159 N (36 psi) for plates and less than 140 N (31 psi) for external fixators during the initial 4 weeks. Either type of fixation, however, provides enough stability to institute immediate wrist motion. Gripping and strengthening exercises during rehabilitation should generally 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). After a fracture, the bleeding from disrupted vessels leads to hematoma formation. A number of chemical mediators including histamine, prostaglandins, and various cytokines are released from damaged cells at the injury site, inciting the inflammatory cascade. The resultant extravasation of fluid from intact vessels causes tissue swelling.

TENDON GLIDING

Much of the work on tendon gliding has been applied to tendon repairs. However, the information gleaned from this work has therapeutic implications with regard to distal radius fractures ( Box 13-1 ) .

The dorsal connective tissue of the thumb and phalanges forms a peritendinous system of collagen lamellae that provide gliding spaces for the extensor apparatus. The extensor retinaculum is divided into six to eight separate osteofibrous gliding compartments. Within the tunnels and both proximal and distal to it, the extensor tendons are surrounded by a synovial sheath. 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 both the extensor retinaculum and the annular pulleys. 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 lead to adhesions. Adhesions can also 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.

TISSUE BIOMECHANICS IN RELATION TO SPLINTING

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 when immobilized in a shortened position, leading to clinical joint stiffness. This tissue includes the skin, ligaments, and capsule as well as the neurovascular structures. To restore the length of the shortened tissue, one must hold the tissue in a moderately lengthened position for a significant amount of time so that it will grow. Growth takes a matter of days, and the stimulus (i.e., splinting) needs to be continuous for hours at a time to be most effective.

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. Various materials have an elastic region whereby there is no permanent deformation of the material after the load is removed, as with a rubber band. When the point of no return is exceeded (the yield point), there is permanent deformation of the material, as when 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 are dependent on the loading rate is said to be viscoelastic. Biologic tissue is viscoelastic in that it has elastic properties but demonstrates viscosity at the same time.

Collagen contributes up to 77% of the dry weight of connective tissue. The fibers are brittle and can elongate only 6% to 8% before rupturing. Elastin makes up only 5% of the soft tissue weight, but it can elongate 200% without deformity. 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 the fibers are lined up parallel with the line of pull, the tissue becomes 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 leads to fibrin deposition with secondary interstitial fibrosis, which may result in further contracture. Therefore, knowledge of tissue biomechanics greatly enhances appropriate 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 to 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 physiologic theory that controlled tension applied over a long period of 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.

Static splints are rigid splints used for immobilization while providing stabilization, protection, and support. They are the most common splints fabricated, since they restrict unwanted arcs of motion ( Fig. 13-1 A–C) .

Static splints . A, Custom circumferential below-elbow splint. B, Custom below-elbow wrist splint. C, Noncustom wrist splint.

Serial static splints can be a serial application of splints or plaster casts. They are applied with the tissue at its maximum length and are worn for long periods of time to accommodate elongation of the soft tissue in the desired direction of correction. They can be constructed to be nonremovable to provide for greater patient compliance.

Dynamic splints allow for continuous controlled mobilizing loads applied through dynamic (elastic) components, that is, rubber bands, springs, or wrapped elastic cord. This type of splinting relies on the principle of creep that results from stretching the tissue under a constant load. By applying the stretching force slowly, the collagen fibers have time to slide past one another, allowing the polymer chains to recoil. The dynamic force continues as long as the elastic component can contract, even when the shortened tissue reaches the end of its elastic limit. Dynamic splints are traditionally advocated when the passive end range of a joint has a “soft end feel.” They are fabricated with a static base for ease of outrigger attachments ( Fig. 13-2 A–E) .

Dynamic splints using elastic components for mobilization . A, Dynamic pronation splint. B, Dynamic wrist extension splint. C, Dynamic wrist flexion splint. D, Dynamic proximal interphalangeal/distal interphalangeal flexion straps. E, Dynamic metacarpophalangeal flexion splint.

Static progressive splinting achieves mobilization by applying a unidirectional, low-load force to the tissue’s maximum end range of motion until the tissue accommodates. This splinting approach relies on the principle of stress-relaxation that occurs over time when tissues are stretched and held at a constant length. By holding the tissue 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. The construction is similar to dynamic splints except that these splints use nonelastic components such as strapping materials (Velcro hook and loop), screws, hinges, nonelastic tape, nylon fishing line, turnbuckles, and splint tuners ( Fig. 13-3 A–D) . Once the joint position and tension are set, the force continues until the tissue accommodates; the splint does not continue to stress the tissue beyond its elastic limit. The force is modified only through progressive splint adjustments. As a general guideline, the splint positions the joint 5 degrees beyond the readily available end range—the range of motion that is easily achieved without dramatically increasing joint torque. As the tissue lengthens, the wearer adjusts the joint position to the new maximum tolerable length. Static progressive splints are traditionally advocated when the passive end range of a joint has a “hard end feel.”

Static progressive splints utilizing nonelastic components for mobilization . A, Static progressive wrist extension splint with Velcro hook-and-loop attachment. B, Static progressive wrist extension splint using splint tuner. C, Static progressive proximal interphalangeal joint (PIP) flexion splint. D, Static progressive PIP extension splint.

Wrist splinting with elbow strap . Add a posterior elbow strap to prevent distal migration of a dynamic or static progressive wrist splint.

According to Schultz-Johnson’s clinical experience, 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, whereas the tissue readily accommodates to the tension and is less subject to the influences of gravity and motion.

Schultz-Johnson also advocates wearing a static progressive splint during sleep, thus 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. In essence, the more time the tissue spends at end range, the more quickly passive range of motion will improve.

FRACTURE REHABILITATION

It is essential to communicate with the surgeon regarding the stability of the fixation and the type of fixation in order to guide the loads placed across the fracture site. Implementing the expected forces associated with wrist motion, splinting, strengthening, and functional activities in an accurate and specified timeline minimizes fracture site deformity and optimizes therapeutic intervention (see Fracture Site Forces).

For purposes of rehabilitation, it is useful to consider the stability of the distal radius fracture site in three phases, which in turn guide the therapist as to the loads that can be placed across the fracture site.

SOUTH BAY HAND SURGERY CENTER PROTOCOL

Controlled and progressive joint mobilization after 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 13-2 ) . Tendon gliding exercises and passive finger motion with the wrist neutral are started immediately, since there are no biomechanical concerns regarding phalangeal stability. Dynamic and static progressive finger splinting is instituted early, based on the observation that the total active finger motion typically plateaus by 3 months. With resistant cases, dynamic splinting is initiated for 30- to 60-minute intervals two or three times per day, and then static progressive splinting is continued for 4 to 8 hours during sleep. Schultz-Johnson stresses that wearing the static progressive splint should be pain free and that too much tension does not increase passive range of motion any faster.

The therapy protocol for regaining wrist motion is initiated at different times based on fracture site stability and the type of fixation ( Box 13-3 ) . Synergistic wrist and finger motion for tendon excursion are started in tandem with wrist motion (see Box 3-1 ), and forceful gripping is delayed until there is some fracture site healing. Patient factors such as age, bone density, pain tolerance, and systemic disease may significantly influence the pace of therapy, thus requiring adjustments to intervention accordingly.

PROCEDURE-SPECIFIC TREATMENT