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.

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

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

DIP, distal interphalangeal; MCP, metacarpophalangeal; PIP, proximal interphalangeal.

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.