Preventing and Treating Stiffness

38


Preventing and Treating Stiffness


Corey Weston McGee


The inflexible distal upper extremity occurs in many client populations in a variety of rehabilitative settings. The rehabilitation therapist working with clients who are prone to or experiencing distal upper extremity stiffness should be armed with background knowledge in anatomy, soft tissue mechanics, soft tissue healing, the etiology and pathomechanics of conditions predisposing to or resulting in distal upper extremity stiffness, and the medical-surgical management of such conditions. Additionally, the novice therapist should have a fundamental understanding of how to differentially identify the type/location of stiffness. Without a well-executed evaluation, the therapist’s approach toward preventing or remediating stiffness may be misguided and ineffective. Likewise, the therapist must be capable of applying the evaluation results by appropriate planning and administering of interventions that are appropriate to the client, the client’s condition, and, when applicable, their phase of healing. Additionally, in the case of the occupational therapist, his or her intervention planning and interventions should be true to their discipline and be occupation-focused.



Diagnosis


Broadly speaking, the term stiffness implies that there is a mechanical resistance to deformation. In the case of the “stiff” distal upper extremity, this resistance results in a limitation in joint mobility. Let’s now focus on some of the most common sources for limitation in joint mobility. Prior to reducing our clients to a diagnosis, however, it is important to recognize all of the other factors, intrinsic or extrinsic to the client, which may be influencing his or her incorporation of an affected upper extremity into daily occupations. The therapist who recognizes the interaction of person, environment, and task will likely be most successful in helping to restore his or her clients’ upper extremity function.


There are many sources for limitations in joint mobility. These can be psychosomatic (that is, guarding due to pain or in anticipation of pain) or physical in etiology. Physical restrictions of joint mobility may result from collagenous or muscular changes that arise from metabolic disorders, such as diabetic “cheiroarthopathic” hand, or systemic conditions, such as inflammatory arthritis, or nonuse.


Nonuse resulting from pain, denervation, and immobilization triggers a cascade of problems that further perpetuate stiffness. These include muscle atrophy (and further weakness), edema, muscle collagen fiber cross-linkage, and altered motor programs (Fig. 38-1). All of these must be considered when working to undo the effects of upper extremity nonuse.


image
FIGURE 38-1 Cycle of nonuse. (Adapted from Skirven TM, Osterman AL, Fedorczyk JM, et al, editors: Rehabilitation of the hand and upper extremity, ed 6, Philadelphia, 2011, Mosby, p. 896.)

Physical limitation in joint mobility may also result from decreased tendon excursion due to scarring or tenosynovial thickening (for example, from trigger finger or de Quervain’s tenosynovitis). Movement may also be restricted by changes in more superficial structures, such as skin. Limitations in the excursion of skin due to trophic changes that are proximal, peri, or distal to a joint may result in poor joint mobility (for example, scleroderma and burn scarring).


Edema in the distal upper extremity produces a similar effect by making skin taut or “full” to the point where joint mobility is restricted (that is, passive insufficiency). This creates more work for the flexor tendons attempting to move stiff joints, and when uncontrolled or chronic, can lead to subcutaneous hardening (that is, fibrosis), which further restricts joint mobility and can lead to additional complications.


Other soft tissues that may indirectly restrict joint mobility include adhered or taut muscular fascia and taut peripheral nerves. In both cases, these adhered or taut structures can create painful and restricted joint mobility. See Chapters 12 and 24 for additional information on the cause and treatment of these conditions.


Lastly, a joint may be restricted by changes in the joint’s bony architecture. Arthritis; ankylosis (that is, fusion); and bony malalignment resulting from fracture, subluxation, or dislocation may result in structural “blockades” to joint motion. Chapters 25, 27, and 33 explore these conditions and the treatment of resultant physical and occupational performance limitations.



Timelines and Healing


Before discussing why, when, and how to assess and intervene with those who have upper extremity joint mobility limitations, a review of the process by which healing occurs is necessary. As we move through this review, it is important to consider concerns or processes that are unique to that phase in healing. In addition to reviewing the body’s responsiveness to soft-tissue injury, we will identify the primary focus to the therapist working with clients in each of these phases.


After hemostasis has been achieved, our body responds during the first 2 to 12 days after a soft tissue injury through local vasodilatation and infiltration of white blood cells that clean up dead cells and, in the case of a wound, help to fight off infection. This phase is referred to as the inflammatory stage. Late in this phase, early bonding of the injured tissue begins via the migration of disorganized collagen fibers. A primary repair (that is, via suture) of injured soft tissue will typically require some amount of immobilization until the end of this phase to help facilitate healing. It is at this time that edema is prevalent and should be treated (see Chapter 3 for interventions). Edema control is often the emphasis at this time. The therapist works to facilitate prompt healing so that mobilization can be initiated. When inflammation is well controlled, the fibroblasts are signaled to begin their job of strengthening the repair of the damaged tissue. This is the fibroblastic stage and lasts from 3 days to about 3 weeks post injury in ideal conditions. Evolved fibroblasts soon begin laying down disorganized collagen fibers that cross-link with one another to stabilize the injury. This cross-linkage does not permit these fibers to efficiently move relative to one another and thus are an early source of stiffness.1 Edema continues throughout much of this phase as the wound environment continues to be hyperemic. Additionally, disuse leads to weakness of muscles that are antagonistic to this early stiffness. Stiffness early in this phase typically has a soft end feel but can feel firm as healing progresses. During this phase the therapist continues to focus on controlling edema and begins looking for critical opportunities to introduce appropriate controlled-stress to these healing structures to maintain soft tissue elasticity by promoting more functional organization of the collagen fibers.2 In the maturation phase, the process of laying down collagen normalizes and strong cross-linkages between collagen fibers form. Stiffness early in this phase feels firm in nature; however if pervasive for long periods, may feel hard. By this time, the therapist’s options become fewer.



image Clinical Pearl


Stiffness perpetuates nonuse, which perpetuates weakness and alterations in motor programs. Although inflammation related to the initial injury is controlled at this point, nonuse further enables edema and the cycle persists (see Fig. 38-1).


Although stiffness can result from the cascade of processes that occur following traumatic injury, it can also occur in those who have systemic conditions that create inflammatory responses in a number of soft tissues (for example, rheumatoid arthritis, and scleroderma) or in those with conditions of the central nervous system (for example, brain and spinal cord injury), the peripheral nervous system (for example, peripheral nerve injury), muscle (for example, muscular dystrophy) and the neuromuscular junction (for example, myasthenia gravis). In the inflammatory conditions, the role of the therapist, when possible, is to control inflammation and control or prevent stiffness. For those with conditions affecting the nervous system, muscle, or neuromuscular junction, the therapist must focus on preventing stiffness that results from heightened or lessened tone, nonuse, and muscle changes. Remediating or preventing stiffness and subsequent deformity is done to promote occupational performance and participation. The therapist, however, must recognize that these approaches alone will not guarantee such and must consider other barriers, such as inadequate social supports, and conflicting habits, roles, and routines, as well as other approaches that may also enable participation (for example, adaptation, prevention, and health promotion). This top-down approach makes participation and performance central and does not assume that impairments in joint mobility are the only barriers to optimal function. The focus of this chapter is on correcting or preventing stiffness, but as therapists we do not treat stiffness alone; we work with a client to enable engagement in occupations and participation. This perspective deserves attention in the rehabilitation therapies.



Evaluation Tips


The evaluation of the client with a stiff hand begins as it should with any client. This first step involves seeking background information on the client’s medical condition(s), date of onset of medical condition or surgery, orders, and precautions. This is accomplished via a chart review, communications with referral sources, and interview of the client. This data will guide the therapist’s reasoning through the evaluation and intervention processes.


The therapist then gathers an occupational profile. This is achieved by interview and survey (for example, Canadian Occupational Performance Measure [COPM]3) and entails seeking information on your client’s:



Your interview will also yield information about:





Observation of Hand Use in Manual Occupations


When a source of joint stiffness is unknown, it may be beneficial to first observe the client’s use of his hand when performing various occupations that are manual in nature.



image Clinical Pearl


If MP extension precedes wrist extension during reaching tasks, then your client either has weakness of the prime movers of the wrist (that is, extensor carpi radialis brevis and longus) or altered motor programming. If wrist extension overtly precedes MP and PIP flexion during grasp, then your client is likely experiencing some long finger flexor weakness or impaired differential flexor tendon gliding. Conversely, if wrist flexion precedes MP extension then long finger extensors may be weak or there may be an exaggerated imbalance of wrist stabilizer strength (that is, flexors > extensor ).5




Scarring


The therapist will also inspect for incisional scars, scarring that spans joints, or scarring that is proximal/distal to the stiff joint (see Chapter 34). Along with this, the observation of scar blanching (turning a white hue) or migration of surface scarring during joint movement may indicate that scar tissue is restricting mobility.



image Clinical Pearl


In the case of incisional scarring, expect to observe distal movement of an adhered scar when the affixed musculotendinous unit is elongated (for example, a dorsal hand incisional scar moving distally when a fist is made and long finger extensors are put on stretch) and expect to see proximal movement of that same scar when the musculotendinous unit is shortened (for example, the same dorsal hand incisional scar moving proximally when the fingers are brought into extension and the long finger extensors are shortened).



Goniometry


ROM assessment determines the nature and extent of stiffness in a given joint and is the most commonly used measure of change in joint mobility. To determine whether weakness or soft tissue/bony restrictions are sources of limited joint mobility, the therapist will take both active and passive measurements. Generally speaking, a goniometric measurement of the hand is subject to a 5° measurement error,5 and because of this, goniometric measurements need to have a discrepancy of greater than 5° for there to be a “real difference.”6 This is true for all of the following circumstances:



The first step is to compare active measurements to normative measures. If a “real difference” exists that is impeding function, then compare the findings to a passive measurement of the same joint. If the passive measurement is 5° more than the active measurement, weakness or adherence is likely contributing to joint motion limitations. If active movement and passive movement are within 5° of one another yet are different from the norms, then a passive restriction is present. To further complicate things, it is possible to have both weakness and passive restrictions affecting the same joint. In these cases you would expect to have passive measures more than 5° below the norm and active measures more than 5° below passive measurements. When a passive limitation has been confirmed, a firm or hard end feel is experienced. The firm end feel indicates a soft tissue restriction, whereas the hard end feel indicates a boney block to movement.7 True boney blocks to movement are not responsive to stretching and for clients with such limitations, the focus should shift to an adaptation approach.8 If soft tissue is impeding joint motion, a series of differential tests will help to further explain the origin of the impediment.



Proximal Interphalangeal Joint Stiffness


These tests are most commonly used when proximal interphalengeal (PIP) joint passive flexion is limited and the therapist wants to determine if extrinsic finger extensor, intrinsic (lumbrical), or joint capsule tightness are responsible. If posturing in metacarpophalangeal (MP) flexion lessens available passive PIP flexion, there is extrinsic extensor tightness (Fig. 38-2) whereas when a posture of MP extension lessens passive PIP flexion, there is intrinsic (lumbrical) tightness.8 Fig. 38-3 illustrates the testing procedure for this. If the posture of the MP joint does not at all influence passive PIP joint flexion yet passive PIP motion is still limited, a contracted joint capsule is likely the problem. A similar process can be followed when attempting to determine the source of PIP extension contractures. In this case, the therapist measures the available passive PIP extension with MP extension and compares to MP flexion. If the values remain unchanged, capsular tightness is likely responsible;9 if there is greater than 5° difference in PIP passive extension, extrinsic finger extensor tightness is likely responsible. Extrinsic tightness is commonly experienced by those with spasticity, forearm fractures, or those who have had immobilized wrists or elbows. Intrinsic tightness is commonly experienced by those who have sustained hand crush injuries, metacarpal fractures, and those with rheumatoid arthritis. In addition to the reduced grasp associated with intrinsic tightness, there is evidence to support that this tightness may, at times, be partially responsible for the development of carpal tunnel syndrome.10


image
FIGURE 38-2 Test for extrinsic extensor tightness.
Position: Place MP joint in maximal flexion. Test: Passively flex the PIP joint. Rule out PIP joint contracture by repeating with the MP joint extended. Interpret: Extrinsic extensor muscle tightness is present if PIP joint motion is greater when MP is extended than when is flexed. PIP joint contracture is present if position of MP does not influence PIP flexion.

image
FIGURE 38-3 Test for intrinsic tightness.
Position: Place MP joint in full extension. Test: Passively flex the PIP joint. Rule out PIP joint contracture by repeating with the MP joint flexed. Interpret: Intrinsic muscle tightness is present if PIP joint motion is greater when MP is flexed than when is extended. PIP joint contracture is present if position of MP does not influence PIP flexion.


Distal Interphalangeal Joint Stiffness


Extrinsic finger flexor tightness (tested by comparing passive distal interphalangeal [DIP] extension with wrist in flexion to passive DIP flexion with wrist in neutral) or capsular (joint) tightness can restrict DIP passive extension. Conversely, DIP passive flexion is typically hindered by either a contracted joint capsule or oblique retinacular ligament (ORL) tightness (Fig. 38-4) An ORL tightness test (Fig. 38-5) determines the source of limited passive flexion. If by placing the PIP in extension your client’s passive DIP flexion measurements become more impaired, then ORL tightness is present. If changing the posture of the PIP joint does not alter your DIP flexion measurements, then the joint capsule is likely contracted. A tight ORL often accompanies a boutonnière deformity and, along with the management of a PIP flexion contracture, requires therapeutic attention.


image
FIGURE 38-4 Anatomy of oblique retinacular ligament (ORL).
The ORL originates from the volar surface of the A2/C1 pulleys of the proximal phalanx and travels “obliquely” toward the dorsum of the distal phalanx where it inserts into extensor mechanism. (Adapted from Skirven TM, Osterman AL, Fedorczyk JM, et al, editors: Rehabilitation of the hand and upper extremity, ed 6, Philadelphia, 2011, Mosby).

image
FIGURE 38-5 Test for oblique retinacular ligament (ORL) tightness.
Position: Place PIP joint in full extension. Test: Passively flex the DIP joint. Rule out PIP joint contracture by repeating with the PIP joint flexed. Interpret: ORL tightness is present if DIP joint motion is greater when PIP is flexed than when extended. DIP joint contracture is present if position of PIP does not influence DIP flexion.

In all cases of intrinsic or extrinsic tightness, there may also be capsular and ORL tightness. Case Study 38-1 illustrates this.



CASE STUDY 38-1


Sandy recently sustained a crush injury to her dominant right hand that required pinning of her ring finger PIP joint. She is now 6 weeks out and ready for passive stretching of all affected joints. Your ROM assessment reveals the following:









Your Interpretation


There is no discrepancy in active and passive PIP measurements; therefore weakness or adherence does not explain the loss of motion. MP posture did not change the available passive PIP extension; therefore capsular tightness is limiting PIP extension. MP posture did, however, alter PIP flexion passive range of motion (PROM); thus, extensor extrinsic tightness (not intrinsic) is in part responsible for passive PIP flexion limitations. But there is still a 40° discrepancy between passive flexion, so capsular tightness is also limiting PIP flexion. In summary, there is likely PIP capsular tightness restricting flexion and extension, as well as extrinsic extensor tightness restricting flexion. Additionally, the DIP joint’s flexion limitation is a result of ORL tightness as well as some weakness in or difficulty recruiting the flexor digitorum profundus (FDP). Greater than 2 cm discrepancy in circumferential measures compared to the unaffected extremity, although not empirically validated, is often accepted to indicate clinically significant edema. Fortunately, the firm end feel would indicate that there are no bony blocks to movement. We’ll revisit Sandy’s case later when we begin discussing intervention planning.



Wrist Stiffness


Extrinsic tightness can also impact wrist motion. Differential testing is useful to determine the origin of wrist stiffness. The follow reasoning can be followed when determining the cause of wrist stiffness:



• Passive wrist extension that is not impaired with fingers in flexion but is impaired when adding finger extension indicates extrinsic finger flexor tightness


• Passive wrist flexion that is not impaired with fingers in extension but is impaired when adding finger flexion indicates extrinsic finger extensor tightness


• Passive wrist movement that is impaired but not impacted by the posture of the digits is likely capsular in origin or due to tightness of the prime movers (for example, extensor carpi radialis brevis, or flexor carpi radialis). If the posture of the elbow (flexed versus extended) influences wrist movement, the prime wrist movers may be tight; if not, capsular tightness is likely responsible


• Passive wrist flexion less than the unaffected side regardless of finger or elbow posturing and further impaired by finger or elbow posturing in extension or flexion indicates both capsular tightness and muscular tightness



Extrinsic Tendon Adherence and Muscular Tightness


Tendon-incisional scar adherence may be a source of passive joint limitations. In such cases, adherence of extrinsic tendons presents slightly differently than does muscular shortening. Extrinsic tightness will likely influence the mobility of all joints crossed by the muscle-tendon unit; however scar adherence impacts only joint mobility distal to the site of adhesion. This is because there is muscular elasticity proximal to the site of adherence yet, because a tendon has little elasticity, there is minimal motion from the point of tendon adherence distally. Likewise, tendon-tendon adherence may occur; particularly in the case of the extrinsic flexors. In this situation, the passive excursion of these tendons would be unaffected yet active composite fisting would be challenging because the adhered FDP and flexor digitorum superficialis (FDS) tendons are less capable of differentially gliding relative to one another.11 Differential gliding may be compromised after flexor tendon repairs, with carpal tunnel syndrome, or following carpal tunnel release surgery. Active tendon gliding exercises (Fig. 38-6) are often prescribed, when not contraindicated, to prevent or remediate problems with differential gliding in such cases. Differential tests for joint motion are very detailed and typically involve modifying the posture of joints that are proximal or distal to the joint of interest. Therapists need to be intentional and consistent in positioning the joints proximal and distal to those that are measured. If therapists are not consistent in their goniometric assessment, interrater reliability suffers and so does our ability to document the effectiveness of our interventions.


image
FIGURE 38-6 Differential flexor tendon gliding exercises. (From Skirven TM, Osterman AL, Fedorczyk JM, et al, editors: Rehabilitation of the hand and upper extremity, ed 6, Philadelphia, 2011, Mosby.)


image Clinical Pearl


Extrinsic tightness will likely impact wrist and digital mobility, whereas with adhesions, joint mobility is limited only distal to the site of adhesion.



Edema Evaluation


With any client who has stiffness resulting from trauma, an inflammatory condition, dependency, weakness, or nonuse, an evaluation for the presence of edema is critical. See Chapter 3 for a more details on the process of edema assessment and intervention. Early attention to edema when present or when expected is crucial.




Hand Therapy (Non-Operative) Interventions


The first steps are to work with the client to identify barriers to performance, prioritize which barriers to address, and collaborate to formulate client centered goals. The client’s priorities and the therapist’s clinical knowledge and reasoning skills allow priorities to be established.



Soft Tissue Mechanics


While each form of soft tissue has its own unique properties, the mechanics of soft tissue are generally applicable to all types. The therapist’s ability to stretch or prevent tightness relies heavily on the relationship between stress and strain (Fig. 38-7). Stress is the amount of force per unit area (that is, pressure) applied to soft tissue. Strain is a result of stress and is expressed mathematically as the change in length of soft tissue/original length × 100. Most biological materials have elastic and plastic properties. Materials that are elastic return to their original form when stress is removed, whereas material that is plastic undergoes a change in composition that remains stable when stress is eliminated. To safely elongate or maintain the length of a soft tissue, strain must occur only in the elastic range. Stress that results in elongation of soft tissue into its plastic range will lead to microtearing, inflammation, and fibrosis. It has been suggested that 200 g (1/2 lb) of force12 is sufficient to adequately stress the PIP joint. However, these types of torque measurements are seldom performed clinically and thus therapists typically rely on subjective report from the client and changes in objective measures (for example, goniometry) to determine if the “just right” force administered by, for example, an orthotic intervention has been achieved. Ideally, your client should report the sensation of stretching but not pain while wearing a mobilizing orthosis.8 This brings us to the next important concept, strain rate, or the amount of tissue elongation per unit of time. Although the amount of stress is critical, so is the duration that this stress is longer than the total end range time (TERT) or amount of time a contracted joint is placed at its maximal length, the better the results.13 This combined low stress, long TERT or low load, long duration (LLLD) approach is believed to be best practice when attempting to resolve soft tissue contracture, because it promotes reorganization of collagen fibers within their elastic range without undue strain.13 (Table 38-1) highlights intervention options that are specific to a given impairment as well as a given phase of healing.



TABLE 38-1


Intervention Highlights across Phases of Healing and Physiological Barriers














Healing Phase Physiologic Barriers Therapist Interventions Orthotic Option(s)
Inflammatory
(2 to 5 days post-injury in optimal circumstances)		 Edema
Get Clinical Tree app for offline access