Effective rehabilitation of the stiff hand requires that the effects of immobilization be minimized while not overloading healing tissue.
Interosseous muscle tightness frequently contributes to limited finger flexion. One should assume that interosseous muscle tightness contributes to the limited motion until it can be proven otherwise.
In the chronically stiff hand, tissue adherence and stiffness, chronic edema, and maladapted cortical patterning are interdependent problems. To be successful regaining mobility of the stiff hand, all three problems must be altered simultaneously.
The Challenge of the Stiff Hand
Clinical experience confirms certain risk factors for stiffness in the hand. The more tissue traumatized, the greater the likelihood of stiffness. Severe trauma injuring bone and multiple soft tissue layers usually requires longer periods of immobilization because of the need to regain skeletal stability. The decrease in tissue elasticity that accompanies increasing age creates less tolerance for the insult of trauma. Infection that extends the wound beyond its mechanically created boundary creates adherence between multiple remote tissue planes. Although we know these basic facts, many questions about stiffness in the hand remain unanswered: Why do some patients have great difficulty regaining motion long after others have returned to normal function? How can we identify what amount of motion, at what frequency, and with what duration will maximize individual patient results? We do know, as did Sir Charles Bell in 1883, that “the mechanical properties of the living frame, like the endowments of the mind, must not lie idle, or they will suffer deterioration.” Prolonged immobilization is the greatest enemy of hand mobility. Our challenge is to devise a treatment program that provides balanced stimuli to elicit a positive response.
Definition of Stiffness
The term stiff is used commonly when describing the hand lacking full mobility. The word stiff is usually reserved to describe the physical property of matter whose close molecular structure makes it rigid, resisting deformation when an external force is applied. Stiffness of the hand is not an increased rigidity of the tissues themselves but a constraint created by crosslinking of the previously elastic configuration of the collagen fibers.
Collagen provides most of the tensile strength of the tissue in the hand. Collagen fibers themselves are inelastic, but movement between the collagen fibers imparts elasticity to the tissue. Normal hand motion occurs when these strong, dense connective tissue structures glide relative to one another. Stiffness is caused by the fixation of the tissue layers so that the usual elastic relational motion is restricted by crosslinks binding the collagen fibers together.
Peacock and Cohen , provide an excellent analogy for the concomitant strength and elasticity of normal collagen. They compare collagen fibers to the strength of the relatively inelastic nylon thread used to make women’s nylon stockings. Significant elasticity of the stocking fabric is created by the way in which the nylon threads are knitted together. Collagen crosslinking does not change the collagen fibers themselves (analogous to the nylon thread), but it restricts the movement of one fiber (thread) in relation to another ( Fig. 67-1 ).
Stiffness and the Stages of Wound Healing
Tissue injury creates a relatively extended period of heightened collagen synthesis, degradation, and deposition within a wound as compared with the rate of this process within normal uninjured tissue. Healing tissue progresses through three stages: inflammatory, fibroplasia, and remodeling (or maturation). Although these are chronologic stages, they do not follow a precise timeline unless the wound has no complications.
During the inflammatory stage the wound prepares to heal, during the fibroplastic stage the tissue structure is rebuilt, and during the remodeling stage the final tissue configuration develops. In the ideal circumstance a healing wound progresses through these stages in an orderly and timely manner. Wounds with massive tissue injury, infection, absence of wound closure, or delayed healing, or wounds requiring repeated surgery or lacking proper wound hygiene, have extended stages of healing far beyond the ideal time frame. Therapists treating complex injuries cannot follow the chronology of a wound and assume a certain stage; instead they must be able to evaluate the characteristics of the wound or healing scar and determine the appropriate stage to devise appropriate therapy.
In the uncomplicated wound, the initial inflammatory phase of wound healing is completed within a few days. Randomly oriented, matted collagen fibrils unite the injured structures during this early phase of healing, although fibers cannot be visualized through the light microscope until the fourth or fifth day after injury. Because the intercellular forces are weak, wounds may be disrupted with ease during this stage. Most surgical wounds are protected with immobilization until the wound healing has begun.
In the uncomplicated wound the fibroplasia stage begins at the end of the first week of healing, when the fibroblast begins replacing the macrophage as the most common cell type. About 2 days later fibroblasts begin the process of collagen synthesis and outnumber the granulocytes and macrophages in the wound. The fibroblasts evolve into myofibroblasts and are responsible for collagen fiber synthesis and concurrent contraction of the wound edges. Capillaries reestablish within the wound, forming a dense network. Collagen fibers are laid down between the capillaries, forming the scar needed to keep the wound closed. By the end of the second week, the wound is filled with newly synthesized but disorganized collagen fibers invading all areas of the wound. Although the strength of the wound remains diminished (at 3 weeks an incised and sutured wound has less than 15% of its ultimate tensile strength), the random orientation of the collagen fibers limits their movement relative to one another. At this stage the scar is not strong and cannot tolerate excessive stress. If wound circumstances are ideal, the fibroplastic stage (also called the proliferative stage) occurs within the first week after the wound is created. However, in complex wounds or wounds with complications, this period is greatly extended.
Joint stiffness and tissue adherence palpated during this stage can be described by a soft end-feel at the limitation of passive motion. This tissue responsiveness occurs because the crosslinking of the collagen fibers is weak and stress causes the collagen fibers to align themselves with the direction of stress. The fluctuant end-feel of the passive joint limitation results primarily from edema filling the interstitial spaces and thus limiting full passive mobility. Because of the diminished strength of the healing tissue, excessive force can tear the fibrils, causing more injury and reviving the inflammatory process. Any force must be applied slowly and gently, and be sustained for a brief period of time. During fibroplasia, intermittent active motion is the ideal means of applying stress to the disorganized collagen to encourage realignment. More resistive motions can be coaxed by the application of a gentle sustained force applied using orthotic mobilization. Young scars can be altered morphologically by conditions of stress that are ineffective in older scars.
In the uncomplicated wound the maturation stage usually begins between 3 and 6 weeks after surgery or injury. In the hand with delayed healing, infection, multiple tissue trauma, or multiple surgeries, the beginning of the maturation phase may be prolonged many weeks or months. As the cell population decreases, the number of scar collagen fibers increases. The total collagen accumulation then stabilizes and remains constant. At this stage collagen deposition is accompanied by collagen degradation, creating equilibrium. Alteration in the architecture of scar collagen fibers occurs as the scar matures. The tissue continues to respond to applied stress, but the response is greatly diminished as compared with the earlier stages. Physical changes are caused by changes in the number of covalent bonds between collagen molecules (see Fig. 67-1 ). Scars remain metabolically active for years, slowly changing in size, shape, color, texture, and strength, and ultimately begin to resemble normal tissue.
Wounds that are well into the maturation stage exhibit a hard end-feel when passive joint motion is applied. The joint motion does not yield to gentle force and stops abruptly. This response to palpation requires more consistent application of force to effect change. In the early part of the maturation stage, intermittent serial static or static progressive use of an orthosis can effectively mobilize the stiff hand. More complex injuries and more resistive chronically stiff hands require a more consistent application of gentle force, requiring a different approach. A nonremovable cast is recommended to consistently direct active force across stiff joints. This technique, casting motion to mobilize stiffness (CMMS), is discussed later (see “ Evaluation and Treatment of the Chronically Stiff Hand ”).
Evaluation and Treatment of Early Stiffness
The demarcation line between the early stiff hand and the chronically stiff hand is difficult to pinpoint. In the following sections the early stiff hand is discussed separately from the chronically stiff hand, because the treatment approaches suggested differ greatly. Regardless of the stage of stiffness, manual examination is required to determine exactly which anatomic structures are limiting motion. The early stiff hand that is past the acute stage of healing but continues with edema, joint stiffness, and/or tissue adherence remains relatively immobile. This immobility may result from lack of functional use, pain, fear, or continued protection of healing tissue. A cycle is established in which inactivity leads to stiffness and adherence. This leads to continuing edema, which leads to continued inactivity ( Fig. 67-2 ). In most postsurgical hand patients, changing one of these three factors readily breaks this cycle. For example, reducing edema allows greater potential for movement, which decreases inactivity and in turn decreases stiffness and tissue adherence. As the therapist and patient work together on each of the three factors, the other factors are directly influenced and the mobility of the hand returns.
Treatment of the stiff hand cannot begin without a thorough understanding of the causes of edema and the factors that influence it. Because its presence is a primary cause for immobility of the injured hand, edema reduction to create potential for motion is always a primary component of treating the stiff hand.
The reader is encouraged to review the other chapters about the lymphatic system and treatment for edema in this text (see Chapters 63 and 65 ). Key points are briefly reviewed here to support edema reduction recommendations made later in this chapter. These recommendations may differ from some long-held treatment beliefs.
Edema is excess fluid in the interstitium (the spaces between cells). Because one-sixth of the body consists of spaces between cells, there is significant room for expansion when the spaces are filled with edema. The injured hand normally develops edema as a result of increased capillary permeability, which allows leakage of fluid and protein into the tissue spaces. The presence of mild postoperative edema actually facilitates wound healing by causing a moderate increase in the strength of the healing wound and an increase in macrophages and fibroblasts. , Greater amounts of edema destroy the continuity of the wound, breaking the fibrin seal and the integrity of the sutures.
The lymphatic system is an intricate network of lymphatic conduits that drain excess fluid and other substances, including cells, proteins, lipids, microorganisms, and debris from the tissues to maintain homeostasis. ,
Following an injury, the lymphatic system is often overwhelmed by the rate of capillary filtration and cannot carry the volume of fluid as fast as it is produced. This results in the development of edema. This normal edema production in response to injury is to be clearly differentiated from lymphedema, caused by lymphatic obstruction that causes protein to accumulate in the tissue spaces, which gives rise to osmosis of the fluid out of the capillaries.
Movement of lymph fluid through the lymphatic system is aided greatly by external forces—adjacent muscle contraction, tissue compression (e.g., gentle massage, bandaging), and general stimulation (e.g., arterial pulsations, body movement)—because the lymphatic system itself has no active pump. If wound healing progresses without complication, edema begins to subside and motion is regained. However, injured hands that develop significant stiffness do not follow this path, and inflammation and edema persist.
Pitting versus Nonpitting Edema
Before the development of externally visible pitting edema, the interstitial spaces must first become filled with fluid. This filling of the interstitium with lymphatic fluid increases the internal pressure, eliminating the ease of movement before edema is visible externally. Although this interstitial edema cannot be visually appreciated or measured as easily as pitting edema, it plays a significant role in preventing full motion of the hand.
Most of the interstitial fluid is trapped within the interstitial tissue gel. When edema exists in pockets of free fluid outside the interstitial spaces, it “pits” with pressure. These pockets of free fluid can hold more than half of the volume of the interstitial fluid. One common location of pitting edema is on the dorsum of the hand, where the loose dorsal skin pocket provides ample space for pockets of free fluid to accumulate. Manual pressure placed on the dorsal pocket causes the fluid to move, leaving an indentation (or pit)—thus the term pitting edema ( Fig. 67-3 ).
Evaluation of Edema
External pitting edema can be measured accurately via water displacement. , Measurement of pressure created by interstitial edema is impossible to accurately measure. A precise observational examination is far more useful in appreciating the level of interstitial edema.
Careful inspection of both hands ( Fig. 67-4 ), comparing the general appearance, gives an insightful view of the presence of interstitial edema. Loss or diminution of normal small skin wrinkles, tautness or obliteration of the dorsal finger joint creases, and obscurity of metacarpal head definition and of the dorsal finger extensor tendons are recordable observations of the presence of interstitial edema.
The presence of interstitial edema can be felt if the examiner palpates both hands simultaneously with eyes closed. Comparable fullness of the tissues is palpable, creating diminished tissue mobility in the injured hand. (In contrast, pitting edema is felt as fluctuant.) Active and passive joint motion is limited by a tangible fullness of the space, creating a soft feel to the end-range of joint motion. An experienced clinician can discern by palpation whether edema is the primary cause for limited passive joint motion.
Unfortunately, such palpation does not allow objective, quantifiable measurement, so that accurate comparison examinations and documentation of edema reduction are impossible. Some therapists use circumferential measurements of a digit, palm, or wrist, but the lack of reliability makes such measurements useful only as an approximate indicator of progress. If such measurements are used, the anatomic location of the measuring tape must be recorded and a repeatable amount of force applied to the measuring tape at each examination.
Edema Control Techniques
Minimizing the negative effects of immobilization caused by edema is the most useful initial treatment for the injured hand. Elevation, active muscle contraction, external pressure from various sources, and stimulation via gentle light massage can prevent the accumulation of excessive edema. Understanding which edema reduction technique to use when and the optimal type of force or pressure to use throughout the stages of healing is key to successful prevention of the stiff hand. Readers are urged to review the chapters on edema in this book ( Chapters 63 and 65 ).
Immediately following injury and/or surgery, immobilization of the tissues is usually necessary to allow completion of the inflammatory phase of healing without disrupting the healing wound.
Interstitial fluids tend to accumulate in dependent parts because the increased intravascular pressure increases capillary filtration. , Even a normal hand can develop edema if it is immobile and dependent. Thus, elevation of the immobilized hand minimizes edema. The postcapillary blood pressure that facilitates venous return is less than 15 mm Hg of hydrostatic pressure. If the hand is in a dependent position, the pressure opposing the venous return is approximately 35 mm Hg of hydrostatic pressure.
Elevation of the extremity, i.e., hand above the elbow, elbow above the heart, is the single most useful postoperative instruction to decrease the hydrostatic pressure in the vessels. Patients must be instructed carefully on the precise definition of elevation. The concept of a drop of water being able to run downhill to the heart without ever encountering an uphill run helps patients visualize adequate elevation.
Maintaining the arm in a sling is not adequate elevation and encourages the extremity to become quiescent. It is far more productive to instruct the patient to maintain elevation during the day by using pillows or books and reserve the use of a sling for brief periods of ambulation. During this time, intermittent active motion of the proximal joints should be encouraged to ensure that joint motion is maintained and large proximal muscle groups are recruited to assist venous and lymphatic flow.
When the surgical dressing is removed and intermittent active motion of the injured part is begun, intermittent elevation is still necessary to assist edema reduction. There is often a practical quandary. The hand is edematous and active motion is encouraged, but the patient is also instructed to elevate the hand, which is in an inactive position for the extremity. A balance can be achieved by instructing the patient to do active pumping exercises intermittently with the hand and arm elevated and to elevate the hand when not using it actively. Prolonged periods of using the hand in a dependent position with minimal active motion are to be avoided at this stage because of the difficulty maintaining the pumping balance.
Active Motion: Pumping versus Gliding Motion
Active muscle pumping near the site of edema is the single most important stimulus for increasing lymphatic flow. However, active motion across the site of injury immediately after surgery may disrupt healing and often cannot be immediately employed. Because there are no muscles within the digits, skin movement and tissue compression from active flexion is the stimulus required for increased lymphatic flow in the digits. When digital motion must be limited to protect healing structures, gentle pressure to the digit, elevation, and active muscle contraction in adjacent uninjured areas must substitute for active motion of the digit itself. With many digital injuries, the metacarpophalangeal (MCP) joint may safely be allowed full motion. This permits the patient to perform pumping exercises of digital adduction and abduction, and MCP joint flexion and extension, which contracts the adjacent proximal intrinsic muscles. Conversely, blocking the MCP joints in extension assures active flexion forces are directed to the interphalangeal (IP) joints to effectively mobilize the digital edema. If a well-conformed orthosis is applied to stabilize the MCP joints in extension, the molded volar orthosis surface provides appropriate pressure to the dense lymphatic network in the palm. This palmar pressure further assists in the reduction of digital edema.
In a randomized study of patients who started shoulder range of motion (ROM) immediately versus 7 days after axillary dissection for cancer, those waiting 7 days had less wound drainage, fewer days of drainage, and earlier postoperative discharge than patients who started immediately following surgery. There was no difference in the outcome of ROM in the two groups. This study suggests that active motion should appropriately be delayed when tissue injury or surgical dissection is extensive.
The muscles proximal to the wrist are larger than the intrinsic muscles of the hand and thus more effective stimulators of the lymphatic system. As long as the vascular status of the hand is stable, intermittent active motion of proximal muscles is begun as early as possible following surgery. Waste products that are evacuated from the injured hand are more effectively moved through the lymphatic system with this intermittent active motion. Passive ROM does not stimulate muscle contraction and, for that reason, cannot be substituted for active motion to reduce edema.
When active motion of the injured part is allowed, elevation and proximal pumping must be continued until enough motion is present at the injury site to allow local pumping sufficient for adequate lymphatic flow. Patients who exercise the injured part of the hand while elevated see a dramatic edema reduction as they gain motion at the site of injury.
In addition to active muscle contraction providing intermittent internal compression to the lymphatic conduits, gentle external pressure also aids in lymphatic flow. Excessive pressure restricts lymphatic flow. For this reason, large compressive bandages are applied postoperatively to maintain gentle pressure to the hand. As one would expect, the use of external pressure alone, in the absence of active pumping, provides little long-term change. However, the use of external pressure as an adjunct to active motion often can interrupt the edema cycle, allowing potential for full active motion.
External wraps or elastic garments, external orthoses or bandages, or gentle external massage provide external pressure treatment. In the past, recommendations have been made for firm retrograde pressure to “push” the edema out of the hand. This concept should be abandoned and a concept of gentle external pressure should be adopted to facilitate lymphatic flow. See Chapters 63 and 65 on edema treatment for additional treatment suggestions.
Surgical dressings and other forms of immobilization are used to provide necessary rest so newly injured tissues are protected from external forces and can begin the healing process. When a wound has delayed healing, some form of bandaging that continues to supply gentle compression is advisable. When a patient presents with significant pitting edema (regardless of the stage of healing), the quantity of edema present in the tissues is so great that mobilization of the joints is futile until the edema is reduced. Although the foremost goal is mobilization of the hand, a brief period of partial immobilization in a bulky compressive dressing that distributes pressure to all tissues is a wise initial treatment ( Fig. 67-5 ). The fingers are gently wrapped with a self-adherent elastic bandage before multiple layers of fluffed gauze squares are placed between the digits and also applied dorsally and volarly. A gauze wrap around the hand and wrist compresses the fluffed gauze squares. The fingers are left free to flex and extend at the IP joints, but the motion of the MCP joints is limited temporarily by the bandage. Elastic bandages and/or plaster of Paris slabs may be added to the exterior of the dressing for more specific support and compression. In significant pitting edema, the consistency of pressure provided by such a nonremovable overnight dressing can assist in dramatic edema reduction.
If edema is a result of excessive manipulation of the hand causing a prolonged inflammatory response, a short period of rest and immobilization in a compressive bandage reduces both edema and inflammation. This approach allows a better starting point for upgrading motion and the use of other gentle edema reduction techniques. It may seem contradictory to immobilize a stiff swollen hand. The immobilization is necessary, because it is the most effective way to provide conformed pressure that will reduce the edema to a level at which productive active motion is possible.
Immobilization decreases initial edema, reduces pain, and permits tissue repair without the stress of external forces. The use of immobilization orthoses during the acute stages of wound healing can provide effective rest and compression in addition to accurate positioning to protect healing structures or to maintain a balanced position. If orthoses are applied with straps, the lymphatic vessels can be occluded by the pressure of the strap. Pitting edema distal or proximal to a strap is a sign that strap pressure is impeding lymphatic flow. A safer alternative is the use of a wide elastic wrap or a molded thermoplastic piece that covers both dorsally and volarly. This distributes pressure rather than localizing it to a strap. When applying a hand-resting orthosis to an edematous hand, it is best to hold it in place by wrapping a wide elastic bandage at an angle along the full length of the orthosis. Later, when the edema has subsided, straps may be applied. This application technique is also effective for orthotic fabrications on the edematous elbow.
A removable immobilization orthosis made from dorsal and volar plaster of Paris slabs provides the most precise positioning, intimate fit, and even distribution of pressure possible ( Fig. 67-6 ). As edema subsides, this plaster of Paris splint is serially changed to safely gain new joint positions. Either a plaster of Paris or thermoplastic immobilization orthosis can assist in optimal positioning and provide gentle distributed pressure while still protecting healing tissues from stress.
Self-adherent elastic wraps are commonly used to control edema in the hand and especially in the digits. Any self-adherent elastic wrap must be applied lightly with particular caution so that it does not constrict blood flow or restrict active motion. It is the consistency of light pressure, not the intensity of pressure that is important. It is particularly important to explain this concept to patients and have them demonstrate independent light application of the self-adherent elastic wrap before leaving the clinic.
A single layer of the self-adherent elastic wrap can be applied by wrapping either a 3- or 4-inch width around the digit and gently pinching it together on the dorsum of the finger and trimming to a narrow seam ( Fig. 67-7 ). This application allows easier adjustment of the tension with the one hand the patient has available than does the wrapping of multiple overlapping layers. One or two layers of tubular stockinette sized to fit the finger and applied underneath the self-adherent elastic wrap will offer a more gentle contact with the skin during movement of the digit.
Elastic gloves are a convenient and inexpensive means of providing external pressure. Since one glove does not fit all patients and there is a lack of direct contact of the glove in the palm, the fit of the glove should be carefully assessed. The glove should fit like a loose second skin, providing a very gentle traction to the skin when the hand is moved within it. U.S. suppliers now market various brands of inexpensive edema gloves that are appropriate for use with the edematous hand. Tight constrictive gloves should be avoided.
Gentle External Massage
All hand therapists should become thoroughly familiar with the gentle-massage approach of manual lymphatic therapy techniques (see Chapter 63 , Chapter 64 , Chapter 65 ). Originally developed as a means of facilitating lymphatic flow in patients with chronic lymphedema, this gentle facilitatory massage can be helpful with many hand trauma patients, most of whom have normal lymphatic anatomy.
After the acute healing phase has subsided, patients with isolated injuries may require only a short period of gentle massage. Patients with extensive crush injuries or large wound areas where the lymphatic anatomy is altered are ideal candidates for longer-term manual edema mobilization techniques (see Chapter 63 , Chapter 64 , Chapter 65 ) to facilitate lymphatic flow around injury areas to reestablish lymphatic flow. Above all else, vigorous, forceful massage as recommended by many in the past should be abandoned. Superficial lymphatic vessels are thin, fragile structures that may be further destroyed by vigorous therapy.
Mobilizing the Early Stiff Hand
Although many treatment techniques have been developed to mobilize the stiff hand, no basic research supports any particular exercise treatment regimen to regain mobility. , Two basic principles for postoperative rehabilitation are imperative: The effects of immobilization must be minimized, and healing tissue must not be overloaded.
Benefits of Early Motion
After injury, limited early movement reestablishes tissue homeostasis, increases venous and lymphatic flow, increases tensile strength of the wound, and directs the alignment and orientation of collagen fibers.
In the early postoperative period, the beneficial effects of motion can be provided either by active or continuous passive motion (CPM), but active motion must quickly assume the dominant role if the patient is to resume functional use. The challenge is to allow enough motion to nullify the negative effects of immobilization but prevent excessive motion that will impede normal healing.
Beginning with Arem and Madden, many studies have validated the concept of controlled stress to promote favorable collagen orientation and to increase tensile strength of the healing tissue. Unknown, however, is how much, how many repetitions, how often, how long, and to what extent motion should be carried out for optimal stress application to influence tissue. If we knew how to precisely apply stress, postoperative therapy would be more efficient and productive. At this time, the guideline for the parameters of stress application must be the observation of a positive influence on the tissue and the absence of a renewed inflammatory response.
Early active motion should be precise, preventing substitution motions of the uninjured looser joints. For active motion to be productive in the stiff hand, it is usually necessary to block the looser joints. Active motion should be to the easy maximum end-range and should be repeated intermittently throughout the day. Frequent repetitions during each exercise period or extremely frequent exercise periods are not indicated early in rehabilitation. As a general guideline, the more acute the injury and the more inflamed the tissues, the more intermittent the active motion should be. As edema subsides and active motion is tolerated without an increasing inflammatory response, more frequent motion is indicated. The schedule for the balance between rest and motion depends on the tolerance of the tissue for increased frequency of motion, which can be determined only by a gentle trial-and-error method.
Importance of Preventing or Resolving Interosseous Muscle Tightness
A discussion of the stiff hand is incomplete without a focus on the most frequent cause of finger stiffness: Interosseous muscle tightness (commonly, but incorrectly, called “intrinsic tightness”). The interosseous muscles reside within a tight fascial compartment between the metacarpal bones. These small interosseous muscles have limited excursion, making them relatively intolerant to the adaptive shortening that occurs as a result of immobilization. Direct trauma to the metacarpal area may also create injury or ischemia to these muscles, causing potential for an even greater severity of interosseous muscle tightness.
Full finger flexion demands elongation of the interosseous muscles. If the interosseous muscles are tight, full finger flexion is limited by the tightness. Since the line of pull of the interosseous muscles is volar to the MCP joint and dorsal to the IP joints, interosseous muscle tightness is determined by defining the amount of passive proximal interphalangeal (PIP) joint flexion when the MCP joint is flexed and then determining if this amount of PIP joint flexion is less when the MCP joint is simultaneously brought into passive hyperextension. This is the position of maximum elongation of the interosseous muscles.
Lack of full finger flexion is often assumed to be caused only by joint stiffness and/or lack of full glide of the extrinsic flexor tendons, and testing for interosseous muscle tightness is overlooked. Since interosseous muscle tightness from either direct injury or adaptive shortening frequently contributes to limited finger flexion, one should always assume this is contributing to the limited motion until it can be proven otherwise.
Instead of working on active and passive end-range composite finger flexion, the most appropriate approach to resolving stiffness of the fingers may be to block the MCP joints in extension while allowing full IP joint flexion. An exercise orthosis that blocks the MCP joints in extension is appropriate for the newly injured hand. For more severe and long standing interosseous muscle tightness a nonremovable cast may be required. (See “ Dominant Interosseous Flexion Pattern ”.)
The complex subject of interosseous muscle tightness versus lumbrical muscle tightness, and methods for testing, quantifying, and resolving interosseous muscle tightness are beyond the scope of this chapter, and the reader is referred to other sources.
Unlike most of the large joints in the body, the small joints of the hand are moved by muscles crossing multiple joints. Because muscle pull results in the movement of the joints with the least resistance, muscle excursion will affect proximal mobile joints before affecting stiffer distal joints. Manual blocking transfers the muscle force to the targeted stiff joint, enabling the patient to experience glide at the site of restriction. For example, when the MCP joint is blocked during finger flexion, extrinsic flexor glide is directed across the IP joints rather than allowing MCP flexion directed by the interosseous muscles ( Fig. 67-8 ). If blocking is an early part of treatment, many patients require only intermittent manual blocking exercises to regain balanced motion. If joint stiffness and/or tissue adherence is persistent, a blocking orthosis offers a longer period of sustained redirected active motion across the stiff joints to regain balanced motion (see Fig. 67-8 ).
Balance of Exercise and Rest
The primary guideline for exercise progression should be the status of the hand after exercise. If edema, pain, and stiffness increase after exercise (or any treatment), the hand is not yet ready for that level of stress. Conversely, if the patient experiences sustained increased comfort and mobility, the amount of exercise is appropriate for the stage of recovery and may be slowly upgraded. Most patients can sense a positive tissue response versus a negative one and modify their exercise regimen accordingly to maintain the positive response.
When working to regain finger flexion, proprioceptive feedback is essential. Providing resistance to finger flexion to increase the patient’s proprioceptive sense of digital motion is beneficial. This is particularly critical in the presence of diminished sensibility. This type of feedback can be accomplished by the patient holding an object slightly smaller than the available range of finger flexion. Use of a padded handle that demands some effort to be held firmly will allow use of the hand for eating and self-care activities while demanding slightly more finger flexion than is readily available. The size of the handle is decreased as the patient gains flexion range.
Muscle Isolation and Pattern of Motion
Patients who experience stiffness of the hand following injury invariably feel that a strong muscle pull is required to overcome the stiffness. Unfortunately, this excessive effort recruits the strongest muscles and overpowers the weaker muscles ( Fig. 67-9 ). Co-contraction of muscles is a common result of excessive effort. The patient must first be taught that a gentle pull isolates the desired muscle and that exercise for strengthening comes later in therapy. The patient learns a clear difference between a strong global pull that is ineffectual and a gentle but sustained precise pull that reestablishes muscle balance. Understanding this difference between the “right” and the “wrong” way to exercise ensures that the patient repeats the exercise correctly at home. It may be helpful to have the patient pull intensely and let the stronger muscles overpower to appreciate the contrast with the gentler isolation exercises.
Patients whose limbs have been immobilized in a cast following a distal radius fracture provide a practical example. The weakened wrist extensor muscles cannot adequately stabilize the wrist in extension to allow the finger flexor muscles to flex the digits. When the patient is asked to extend the wrist, the finger extensor muscles substitute for the wrist extensor muscles because they have been unrestrained in the cast and are stronger (see Fig. 67-9 ). If edema and finger stiffness are accompanying complications, little progress can be made with finger motion until the patient can stabilize the wrist with the wrist extensor muscles.
Low-Load, Prolonged Stress
It is often stated that therapy should apply a low-load, prolonged stress to accomplish plastic deformation of the tissues. Early in the fibroplasia stage of healing, before collagen crosslinking is well established, intermittent active motion is usually enough stress to favorably alter the crosslinking. Later in healing, when excess collagen crosslinking limits motion, low-load, prolonged stress favorably modifies the crosslinks and the collagen fibrils slip over each other. This slippage is accomplished by active exercises that provide a concentrated force application to achieve maximum joint motion and soft tissue glide, which allows slippage of the crosslinks. This may be gained in a number of ways. If the tissues do not mobilize in response to blocked active exercise, orthotic mobilization that provides a gentle force for a longer period may be indicated. If the stiffness is persistent, a nonremovable cast promotes cyclic motion directed to the stiffer joints. This concentration of active force across stiff joints can mobilize even the most resistant of joints. (See “ Evaluation and Treatment of the Chronically Stiff Hand ” section.)
Passive Range of Motion
Although joint motion can be maintained by either active or passive motion, passive motion provides limited glide of the tissue planes other than the periarticular structures. Increasing passive motion does not necessarily increase active motion.
As with other therapeutic techniques, there are no research data to dictate the ideal force, speed, and duration of passive motion. Although passive joint motion often is prescribed to overcome post-traumatic joint stiffness, no research supports the efficacy of either intermittent passive motion or CPM to reduce joint stiffness. Aggressive passive motion of the hand is detrimental and should be avoided. ,
Passive motion in the injured hand should be defined as the gentle encouragement of tissues to reach a maximum available length. The amount of force should respect the resistance of the tissues, and the position should be increased only when the tissues relax and decreased resistance is felt. When edema is diminished, any gentle passive joint motion should be done with accompanying gentle traction to the joint to allow room for one joint surface to glide over the other without compression. One gentle, prolonged hold will allow the motion to be repeated actively more effectively than many repeated quick sudden passive stretches. Quick, forceful stretches result in tissue damage and should be avoided at all times.
In the hand with more mature stiffness caused by increased collagen crosslinking, the brief intermittent nature of passive motion is ineffective and should be avoided. This seems contradictory, because one assumes that the stiffer the joint the more force is required to mobilize it. Rather than increased force, it is the increased duration of a low-level force that best creates change. When patients with significantly stiff hand joints undergo passive ROM during a therapy session, there is an immediate response of tissue mobilization. However, when the patient returns, the progress gained in the previous session has not been retained. A study of stiffness in rabbits after tibia fracture compared ankle stiffness between joints undergoing CPM and joints that remained immobile in a cast. The ankles receiving CPM demonstrated immediate reduced stiffness, but over time the stiffness in the CPM group was progressively and significantly greater than the group immobilized. This study suggests that further investigation is warranted regarding the long-term effects of passive ROM on stiff joints.
Active Range of Motion
Active ROM has multiple advantages over passive ROM. Active motion stimulates the lymphatic system, diminishing edema, and more quickly returns the hand to a state of homeostasis. Active motion also requires normal reciprocal glide of soft tissue structures such as tendons and ligaments. Another advantage of active motion is the continued association of the motor cortex to the active muscle contraction. Patients sustaining injury who are unable to use normal muscle recruitment patterns move in maladapted patterns. If maladapted movement continues, the motor cortex learns the maladapted motion and defines it as normal. A period of only 9 weeks will alter the motor cortex patterning. The earlier the patient is able to recruit the appropriate muscle pattern, the greater the patient’s potential to recapture full mobility.
Although manual joint mobilization is advocated by many for the treatment of stiff joints of the hand, manual mobilization of the small joints of the hand is best reserved for specific capsular tightness with no accompanying inflammation. When motion is limited as a result of edema, manual joint mobilization may be ineffective and can lead to an increased inflammatory response. Joint mobilization without accompanying edema reduction does not increase the available room for movement. There are no published data on the effectiveness of joint mobilization in reducing joint stiffness. Nor are there any data that suggest harm.
Benefits of CPM
Because joint motion is needed to preserve joint lubrication, , CPM often is used postoperatively to treat joint pathology. Neither laboratory nor clinical studies have shown that CPM is useful for treating joint stiffness once it has occurred. , Therefore, CPM is appropriately reserved for the immediate postoperative period to prevent complications rather than to resolve stiffness. Readers are referred to the archives on the companion Website for the chapter Continuous Passive Motion for the Upper Extremity: Why, When, and How by LaStayo and Cass from the 5th edition.
Pathologic Patterns of Motion in the Early Stiff Hand
Loss of Wrist Tenodesis Pattern
The exquisite balance of muscle forces crossing the wrist and fingers creates a reciprocal motion called tenodesis. Finger extension occurs with wrist flexion as a result of the increased tension on the extrinsic extensor muscles when the wrist flexes. Conversely, when the wrist extends, tension is increased in the extrinsic flexor muscles that flex the fingers. This reciprocal action establishes the normal grasp and release pattern of the hand.
With stiffness, the tenodesis balance in the hand is frequently affected. In a minor injury, tenodesis is regained as motion at the injury site improves. In more severe injuries requiring long periods of immobilization, many joints may become stiff and the muscles crossing them become weak, altering the reciprocal balanced motion.
The wrist is the key joint to reestablishing the tenodesis balance in the hand. Without the ability to stabilize the wrist in extension, the finger flexor muscles cannot transfer enough power to regain finger flexion. Usually the primary goal is to regain digital flexion for grasp and manipulation of objects. However, when the fingers and the wrist all have limited motion, active finger flexion is not possible without first gaining some wrist extension ( Fig. 67-10 ).
During normal finger flexion, IP joint flexion dominates before significant MCP joint flexion begins. If the hand is edematous and extrinsic flexor glide is limited (commonly seen after immobilization of wrist fractures or flexor tendon repair), the patient will initiate finger flexion with MCP joint flexion, and little IP joint flexion occurs. In this pattern of motion the interosseous and lumbrical muscles are never elongated to their maximum length, and they adaptively shorten, making the mobilization of the IP joints even more difficult.
Early treatment—consisting of activities, exercises, and/or orthoses that block MCP joint flexion and require IP joint flexion (unless contraindicated by surgical repairs)—can convert global finger flexion into specific glide across the IP joints (see Fig. 67-8 ). In the chronically stiff hand, longer periods of intervention may be necessary to change the pattern of motion. (See section on “ Evaluation and Treatment of the Chronically Stiff Hand .”)
When the intrinsic muscles are not actively participating in digital flexion, isolated MCP joint flexion is absent. Flexion occurs first at the IP joints, and only after full IP joint flexion do the extrinsic flexors pull the MCP joint into flexion. This may result from denervation of the intrinsic muscles, but in the stiff hand it is more commonly a result of isolated capsular tightness of the MCP joints or the restraint created by adherence of the extensor tendons on the dorsum of the hand. Blocking the wrist so that flexion forces from the extrinsic flexors can be directed to the MCP joints is required to actively mobilize the MCP joints. Without MCP joint flexion the intrinsic hand muscles cannot participate in the digital flexion.
Evaluation and Treatment of Joint Stiffness and Decreased Tissue Glide
Joint tightness is identified by manually examining the passive ROM of a joint to determine whether the passive ROM changes as proximal and distal joint positions are altered. If the joint ROM does not change, isolated joint tightness is present ( Fig. 67-11 ).
Clinical reality usually provides a combination of joint tightness and other external constraints, such as muscle–tendon unit tightness or tendon adherence. An experienced therapist can determine the balance and mix of the many tissues that are limiting motion. Accurate appraisal may be limited until certain joint motions have been regained. For example, PIP joint flexion must be gained before the full extent of interosseous muscle tightness can be determined.
Accurate, repeated ROM measurements must be the means of monitoring improvement. If there is a large discrepancy between the active and passive ROM, the emphasis should lie on active pull-through. If the active and passive ROM are equal, it may be appropriate to gain passive motion via mobilization orthotic positioning. Increased passive motion can also be achieved by blocking the more flexible joints, allowing active motion to reduce joint stiffness, which in turn increases passive ROM.
The degree of trauma to the joint capsule and the stage of healing determine whether the palpated resistance to full-joint motion is the expected amount of joint stiffness. When joint tightness is evaluated, a distinction should be made between a joint with a soft end-feel and one with a hard end-feel. A soft end-feel refers to a joint whose stiffness is characterized by a soft and springy end to the passive joint motion. This soft end-feel joint tightness results from edema within the joint capsule and the early stages of collagen crosslinking. With active motion and an intermittent low-load stress, the capsular joint structures can regain independent glide. Hard end-feel joint tightness has less edema present and is primarily a result of more mature collagen crosslinking. When moved to its maximum ROM, there is an abrupt and well-defined end point to the passive test. The hard end-feel joint requires more prolonged periods of mobilization in an orthosis to gain motion or more sustained periods of cyclical active motion. (See the section on “ Evaluation and Treatment of the Chronically Stiff Hand ”.)
It is appropriate to apply manual gentle passive ROM to joints with a soft end-feel. If the joint edema is minimal, gentle prolonged passive stretching to soft end-feel joints can allow more active motion to be transmitted across the stiff joint. In many cases this is enough influence to resolve joint stiffness. In the joint sustaining minor trauma, early intermittent gentle passive motion may produce full active motion without further intervention.
Joint Mobilization via Use of an Orthosis
If active and passive mobilization techniques are not successful or if the joint resistance is significant when initially evaluated, mobilization orthotic positioning to regain capsular length in one direction may be essential to regain joint motion. The motion with the greatest resistance is the least likely motion to be regained with only active and intermittent passive stretching, and this motion should be the target of mobilization via use of an orthosis. Wrist joint extension, MCP joint flexion, and IP joint extension are often the most resistant joint motions, and must be given orthotic priority to balance the strength of the more powerful opposing muscles.
Mobilizing orthoses directed toward isolated joint tightness requires that only the involved joint be included in the orthosis ( Fig. 67-12A ). Orthoses may be applied that provide a dynamic, serial static, or static progressive force. Dynamic force applied by rubber band or spring traction is a soft application of force appropriate for joints with a soft end-feel. If joint edema is present, serial static orthoses can gain joint motion concurrent to providing edema reduction via gentle joint compression. Joints with greater resistance respond favorably to prolonged application of serial static orthoses, or may respond to static progressive orthoses. Serial static or static progressive orthoses should be reserved for extension mobilization positioning, since compression of the joint in the maximally flexed position is poorly tolerated. A dynamic force may be more comfortable for the patient at the end-range of joint flexion than an unyielding static progressive force, because flexion dramatically increases intra-articular pressure ( Fig. 67-12B ). (See Chapters 123 through 125 for further discussion regarding use of orthoses for mobilization of joints.)
Muscle–Tendon Unit Tightness
Muscle–tendon unit tightness is shortening of the muscle–tendon unit from origin to insertion, limiting full simultaneous motion of all joints crossed by the muscle–tendon unit. The muscle is the elastic part of this unit, which shortens with disuse. This tightness commonly occurs as a result of immobilization or restricted motion following injury or surgery. If a muscle–tendon unit is left in a short position in the presence of tissue inflammation, the tendon will also become adherent along its entire path, even if there is no direct trauma to the tendon or tendon bed. Specific trauma to the tendon or tendon bed, however, creates distinct adherence at the site of injury. Tendon adherence thus may be isolated to the point of trauma or extend over a larger area of more extensive trauma or immobilization in the presence of inflammation. Tendon adherence affects movement only of the joint(s) distal to the point of adherence. Although both muscle–tendon unit tightness and tendon adherence may have similar clinical presentations, careful examination identifies the exact location of the problem.
Both tendon adherence and muscle–tendon unit tightness are demonstrated by a distinct difference between the passive distal joint motion when the proximal joints are positioned in flexion versus extension ( Fig. 67-13 ).