Biologic Basis for Hand and Upper Extremity Splinting

JAMES W. STRICKLAND, MD

Splints are used to put all or part of the hand at rest so that diseased, injured, or surgically violated tissues can undergo orderly, uninterrupted healing. They are also used to favorably influence tissue healing and minimize the development of restrictive scar tissue, which has a detrimental effect on normal joint and tendon movement. In many clinical situations, there is an appropriate time for the use of immobilizing, mobilizing, restriction, and torque transmission splints to control the essential events of repair. A strong appreciation for the biologic state of the involved tissues will aid in making decisions as to whether the injured part should be managed by rest or stress and the best timing for the use of each type of splint. This chapter provides insight into the nature of normal and abnormal tissue healing in the human hand and upper extremity, and the biologic basis for the use of splints as part of a treatment program designed to restore maximum functional recovery.

Whether secondary to intra-articular destruction, capsular fibrosis, tendon adhesion, or skin and soft tissue scarring, the reduction or cessation of function of the shoulder, elbow, forearm, wrist, or digital joints is profoundly detrimental to hand and upper extremity performance. To proceed with effective therapy to restore function in the involved joints, one must have a thorough understanding of the biologic basis for the underlying pathology. Why is the joint stiffened? Are the articular surfaces damaged? Are the capsular and ligamentous tissues thickened, scarred, or shortened? Are adherent flexor, extensor, or intrinsic tendons preventing motion by a tenodesis checkrein phenomenon? Is the skin, fascia, or subcutaneous tissue scarred or fibrotic? Are there many factors involved in combination to limit joint movement?

Armed with an understanding of the pertinent pathology, one must define the goals of splinting for a particular situation. Is the splint to be used to allow healing, to biologically modify contracted and scarred skin, subcutaneous tissue, fascia, or ligamentous tissues, or is it meant to lengthen tendon adhesions that have become fixed to bone or surrounding tissues? What dangers exist with regard to joint injury or tendon rupture?

Finally, when the pathologic process and the goals of splinting have been defined, consideration is given to the method of splinting that can most effectively impart the desired biologic alteration of the affected tissues. What is the most desirable vector for the appli cation of force to a given joint? How much force should be imparted? For how long a period should the force be applied? Through how wide a surface? On what anatomical structures is the force being placed? What measurements will ensure the most effective application of the splint?

To answer these questions and proceed with the design, construction, and application of an effective splint, one must know the necessary sequence of biologic events involved in normal tissue healing and the aberrations in this process that may result in the loss of joint motion. Splinting methods can then be selected to alter and control these events to restore maximum function.

I TISSUE HEALING

Normal upper extremity function depends on the smooth, friction-free gliding of small cartilaginous articular surfaces and the excursion of stout collage-nous tendons unimpeded by restrictive scars and adhesions. The biologic response of tissues to injury results in an alteration of their physical properties and the replacement of normal structures with scar tissue. Therefore a thorough understanding of wound healing and scar formation provides a foundation for the recognition and treatment of problems related to the successful restoration of function following upper extremity injury and surgery.

It must be recognized that scar formation is nonspecific in the sense that the biologic processes and the sequence in which they occur are virtually identical in all organs and tissues. However, the final appearance of the healed scar and the effect it has on function may differ with respect to the specific organ or tissue involved. In the upper extremity and especially the hand, any alteration in the physical characteristics or anatomic arrangement of tissues may prevent relative gliding and reduce function significantly. Although the functional effect varies, the common denominator for the healing of all tissues is scar. The components of the process of tissue healing sequentially include inflammation, fibroplasia, and scar maturation, along with concomitant wound contracture (Fig. 3-1). In the upper extremity, it is particularly relevant that the presence of scar in specialized tissues such as tendon, bone, and joint can result in severe impairment of function. It should also be remembered that the process of wound healing results not only from accidental injury, but also from surgical intervention.

I INFLAMMATION

Following wounding, the initial biologic response is inflammation (Fig. 3-1, A-C). The open wound,

Scab
Epithelial scar

Fig. 3-1 Stages of wound healing. A, Initial injury: lacerating object producing injury to the epidermis, dermis, and subcutaneous tissues. B, Skin wound repair, inflammatory phase (early). The wound is filled with blood and cellular debris. Clotted blood unites the wound edges. Epithelial cells mobilize and begin migrating across the defect. Serum, plasma, proteins, and leukocytes escape from the venules and enter the wound area. Undifferentiated mesenchymal cells begin transformation to mature fibroblasts. C, Late migratory phase. Epithelial cells continue to migrate and proliferate. Debris is removed by leukocytes, and fibroblasts migrate into the wound area along fibrin strands. Capillaries begin regrowth by budding, and the open wound is recognizable as granulation tissue. D, Fibroplasia (proliferative phase). Epithelium increases in thickness beneath the scab and forms irregular projections into the dermis. Collagen fibers are laid down in a random pattern. Capillaries continue to invade the wound and fibrin strands, debris, and leukocytes disappear. E, Maturation phase. Scab sloughs completely as epithelium resumes normal stratification. Collagen remodels in bulk and form and becomes organized. Wound strength increases and fibroblasts begin to disappear. Vascularity is restored.

containing injured tissues and hemorrhage, is easily contaminated by bacteria and foreign substances. Inflammation is a vascular and cellular response that serves several purposes, including the removal of microorganisms, foreign material, and necrotic tissue in preparation for repair. This inflammatory response is the same regardless of the cause of the injury and is characterized by a transient vasoconstriction, which is followed by vasodilation of local small blood vessels resulting in increased blood flow to the injured area. This phenomenon is associated with local edema and the migration of white blood cells through the walls of the blood vessels.

Phagocytic cells carry out the removal of dead tissue and foreign bodies, including bacteria; when some of the white cells die, their intracellular enzymes and debris are released and become part of the wound exudate. Some of these enzymes facilitate the breakdown of necrotic debris and others dissolve connective tissue. The acute inflammatory response usually subsides within several days except in those wounds that become contaminated with bacteria or retain foreign material; in these cases the wounds continue to have a persistent inflammatory response and remain unhealed for quite some time. A wall of collagen may ultimately be laid down, resulting in the formation of a granuloma.

I FIBROPLASIA

At the end of the inflammatory phase, migratory fibroblasts enter the wound depths and begin synthesizing scar tissue. This period of scar tissue formation is known as fibroplasia (Fig. 3-1, D). It usually begins at the wound site on the fourth or fifth day after injury and continues for 2 to 4 weeks. During this period the wound area becomes recognizable microscopically as granulation tissue with the formation of capillaries or endothelial budding, which results in a characteristic vascularity and redness of the involved tissues.

From the third to the sixth week after injury the number of fibroblasts and blood vessels within the wound slowly diminishes. As the cell population decreases, scar collagen fibers increase and the wound changes from a predominantly cellular structure to predominantly extracellular tissue. It is during this phase that fibroblasts manufacture collagen by a poorly understood mechanism. The collagen molecule is a complex helical structure whose mechanical properties are largely responsible for the strength and rigidity of scar tissue.

Tensile strength is defined as the load per cross-sectional area that can be supported by the wound, and it increases at a rate proportional to the rate of collagen synthesis. During the period of fibroplasia the tensile strength of the wound increases rapidly. As collagen is produced, the fibroblasts in the wound diminish. The disappearance of fibroblasts marks the end of the fibroblastic phase and the beginning of the maturation phase of wound healing.

I SCAR MATURATION

The scar tissue formed during the fibroblastic phase is a dense structure of randomly oriented collagen fibers. During the maturation phase of wound healing (Fig. 3-1, E), changes in the form, bulk, and strength of the scar occur. Microscopically the weave or architecture of the collagen fibers changes to a more organized pattern, and the strength of the wound continues to increase despite the disappearance of fibroblasts and the reduction in the rate of collagen synthesis. Remodeling is a spontaneous process, and scars may remain metabolically active for years, slowly changing in size, shape, color, texture, and strength. It is during this phase that there is continuous and simultaneous collagen production and breakdown. If the rate of breakdown exceeds the rate of production, the scar becomes softer and less bulky. If the rate of production exceeds the rate of breakdown, then a keloid or hypertrophic scar may result.

Through an unknown mechanism, the surfaces against which scar tissue is deposited influence the nature of the remodeling process. Scar deposited in the presence of cut tendon ends remodels to mimic the organization of tendon bundles. Scar adjacent to an uninjured tendon surface tends to remodel to resemble peritendon. The rate and extent to which a scar remodels vary among individuals and also within the same individual depending on age at the time of injury. Younger animals have been shown to remodel scar tissues more effectively than older animals. In the young, remodeling is rapid and effective and this increased rate of metabolic turnover may be responsible for the excellent restoration of gliding seen in younger patients following injury to bone or tendon. The quantity of scar deposited is directly related to the amount of injured tissue; the larger the scar, the less likely the effective restoration of joint or tendon function.

Because wounds remain metabolically reactive for long periods of time, surgery or a second injury may further increase scar collagen synthesis and lead to more scarring. It may be many months before a wound is sufficiently healed to allow one to proceed with further reconstructive surgical procedures. The physical characteristics of the injured tissues may provide important clues as to the metabolic state of the wound. This prolonged period of metabolic activity may also explain the need for long-term splinting to prevent and overcome joint contractures resulting from wound scar formation.

I WOUND CONTRACTURE

Open wounds with or without tissue loss undergo wound contraction with dramatic changes in size and shape. The process of contraction begins after a 2- or 3-day latent period, and by 2 to 3 weeks the wounds are often less than 20% of their original area. The forces of contraction will continue to close the wound until balanced by equal tension in the surrounding skin. In the hand this contraction may produce significant functional impairment. Contracture is, of course, beneficial to healing wounds but in the hand it may be functionally detrimental when it involves mobile tissues around or over joints. Splints may be an effective method of minimizing the deleterious effects of wound contracture.

I SPECIFIC TISSUE HEALING

Although this general scheme is applicable to almost all tissues, hand and upper extremity injuries often involve complex wounding to the deep structures such as bone, joint, tendon, and nerve that must heal so that the unique function of each tissue will be restored. A brief discussion of the unique features of wound healing for each of these tissues is provided next.

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