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Cumulative trauma disorder of the upper extremity from occupational stress
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CASESTUDY~
Cumulative Trauma Disorder of the Upper Extremity from Occupational Stress Barry C. Poole, OTR, eVE Hand Rehabilitation Center of San Diego, Inc. La Mesa, California
INTRODUCTION Pper-extremity cumulative trauma disorders (CTD) provide a fascinating and perplexing U study for the surgeon and therapist alike. Aspects of
the management of these disorders encompass a broad range of professional disciplines. A comprehensive approach is necessary in order to understand the full ramifications of their treatment. These syndromes are not a phenomenon of recent times. Extending back to the 17th century, Ramazini documented and discussed these occupational problems.! However, it does appear that the incidence of these disorders is on the increase as confirmed by the U.S. Bureau of Labor Statistics. 2 The cost and significance of these injuries is far reaching. 1- 3
Upper-extremity cumulative trauma disorders provide a fascinating and perplexing study for the surgeon and therapist alike. Perhaps arising from the limited success rate in the remedial treatment of these problems have been the recent efforts directed toward prevention, utilizBased on a case study written in partial requirement for membership in the American Society of Hand Therapists. Reprint requests to Barry C. Poole, OTR, CVE, Hand Rehabilitation Center of San Diego, Inc., 8881 Fletcher Parkway, Suite 240, La Mesa, CA 92042.
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ABSTRACT: The case presented is of a 33-year-old female with a non-dominant upper-extremity cumulative trauma disorder, which involves multiple soft tissue inflammatory problems sustained as a result of occupational stress. Surgical management has included carpal tunnel release with internal neurolysis, multiple tenosynovectomy, decompression of ulnar nerve into Guyon's canal with internal neurolysis, FCU tenolysis, and ulnar nerve anterior transposition with neurolysis. Additionally, a first dor.sal compartment tenovaginotomy is planned. Hand therapy has included the postoperative management of these procedures, and the case demonstrates a challenging rehabilitative scenario.
ing the applied science of ergonomics. 2,4 A full discussion of the application of ergonomics is beyond the scope of this analysis but deserves mention as it helps in understanding the etiology of CTD. Additionally, it assists in the application of tendon and nerve protection techniques, including tool and job modification. The Patient. PW is a 33-year-old female who presented with a classic case of the "checker syndrome." She is a right-hand dominant grocery checker of 12 years and uses a laser scanning system. On 10/17/85, she was unable to continue working because the gradual onset of left arm pain and numbness worsened this day to the point of intolerance. Upon referral, she presented to the hand surgeon on 10/ 25/85. The surgeon noted subjective complaints of shooting pains into the left thumb, tingling and numbness in the median nerve distribution area, and nocturnal symptomatology. His impression was that of carpal tunnel syndrome (CTS) and conservative treatment was initiated.
BACKGROUND AND CASE HISTORY Regardless of the specific etiology of CTS, it is always related to a volumetric increase in the contents within the carpal tunnel. This may be caused by an actual increase in volume or decrease in dimensions of the tunnel. There are numerous acute and chronic etiologic factors causing CTS.5 Nonspecific flexor tenosynovitis is one inflammatory problem leading to CTS, which in this case was confirmed at the time of surgery. Phalen reported it as the most common cause of CTS, occurring in 203 of 212 of his cases. 6
Accurate diagnosis of CTS is paramount because it may be confused with more proximal nerve compressions and may be associated with systemic disorders. Appropriate studies to rule out these conditions may be necessary, and many times a patient may have a normal physical examination. Phalen reported a 70% incidence of decreased sensibility, 60% positive Tinel's sign and 80% positive Phalen's test in one of his studies. 7 Other tests assist in diagnosing CTS, such as the Allen test, tourniquet test and electrodiagnostic studies. No single exam has been shown to be 100% conclusive. Therefore, each case must be evaluted in its entirety and many times lies in the judgment of the surgeon. 8 Neurological evaluation occurred between 11/ 8/85 and 11 /22/85. Evaluation concluded that blood sugar and thyroid functions were normal, and that there were no proximal nerve compressions. The only quantitative evidence found for left CTS was a prolongation of the distal median sensory latency conduction, which measured 3.7 msec. This was recorded after performance of provocative Phalen's maneuver held for 3 minutes. A reading of 3.45 msec was recorded without the Phalen's maneuver. When negative, electrodiagnosis is of questionable value in determining the diagnosis of CTS. Electrodiagnosis does appear most beneficial in ruling out proximal compressions, systemic disease or generalized neural pathology. The slowing of sensory conduction has proven to be the most sensitive reading. Heckler and Jabaley reported that distal sensory latencies of above 3.5 msec are present in 85% to 95% of surgically confirmed cases. s No correlation has been established between the degree of abnormalities recorded in these tests and the amount of damage noted at surgery.S,8 Conservative treatment was directed toward decreasing edema with oral anti-inflammatories and corticosteroid injection. Neutral wrist splinting positions the median nerve away from the transverse carpal ligament and makes the ligament less tense, This provides for less pressure upon the median nerve,S,8 Satisfactory results were not obtained with conservative treatment and surgery was performed on 1/9/86, This included left carpal tunnel release (CTR) with complete transection of the transverse carpal ligament and internal neurolysis, Tenosynovectomy of the flexor tendons was accomplished after exploration revealed a marked amount of tenosynovitis. Neurolysis separates the epineurium from its scarred bed or removes crossing thrombosed tressels or thickened fascia. 9 One study concluded that in chronic nerve compression, the nerve develops connective tissue changes that create a thickened perineurium and dense intrafascicular epineurium fibrosis. Dissection of the large fasicles from each other is accomplished with careful procedure in order to avoid injury to the nerve fibers themselves. l Extensive internal neurolysis can induce fibrosis throughout the neural layers, The perineurium acts to maintain the normal pressure gradient within the funiculus and is a carrier for the passage of proteins
and other large molecules. Therefore, violating the perineurium with internal neurolysis can be damaging, and many authors recommend aVOiding this if possible.l 9 Since damaging myofibroblasts were found in the epineurium of artificially compressed rat nerves, external neurolysis has been recommended as a possible treatment technique. This procedure involves removal of the epineurium; however, satisfactory expansion of the nerve bundles is frequently obtained with removal of the epineurium from only the volar aspect of the nerve,8 The less a nerve is disturbed, the better it will respond to release of the constriction. Complete removal of the epineurium was not performed in this case.
The less a nerve is disturbed, the better it will respond to release of the constriction. Tenosynovitis is the inflammation of the tendon sheath, Tendonitis is the inflammation of the tendon. Generally, this occurs Simultaneously, and the synovial-lined tendon sheath is usually the site of maximum inflammation. This condition may cause visible swelling due to inflammation and fluid accumulation. The sheaths may also remain relatively dry but irregularly contoured, causing friction upon movement as the tendon glides in its sheathP Tenosynovitis is stenosing when the tendon becomes constricted by its retaining fibrous ligament, which establishes irritation and inflammation,13 Tenosynovectomy involves the excision of the inflamed tendon sheath. Studies have suggested that the repetitiveness and forcefulness of manual work has a significant association in inducing irritative changes of the tendon sheaths, leading to chronic tenosynovitis and nerve compressions. Furthermore, women appear to be at greater risk than men. IUS Hammer reported that human tendons cannot tolerate more than 1500 to 2000 manipulations per hour.16 The pathogenesis of tendon disorders is important to understand as a basis for its treatment. Tendons are subjected to tensile stresses by the contractile force of the muscles. They also have compressive and shearing stresses from the bones and ligaments. The tendons become deformed in their mechanical responses to these forces, which is referred to as elastic strain. Viscous deformation or "creep" is the strain that occurs after the application of load (stress). This is believed to cause cumulative microdamage to the molecular links between the tissue matrix and the filler material. It is suggested that if the time between successive loads is not sufficient, significant "creep" in tendons will occur. IS There are also physiologic responses of tendons to repeated stresses. The results are seen as serous edema, thickening, proliferation of fibrocytes and fibrous connective tissue, destruction of synovial membranes, and adhesions. These are probably related to the breakdown of the nutritional pathway by loss of blood flow. The tendon is bathed by the surJuly-September 1988
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rounding synovium, which is maintained by circulation. This provides for nutrients by diffusion. When the tendon is compressed against adjacent surfaces or there is a thickening of the tendon sheaths, an occlusion of the blood flow occurs leading to nutritional deprivation. The complete mechanism that causes the results seen from repeated tendon stress is not yet full y understood. 15 Tenosynovectomy is recommended in CTS cases where there is obvious pathological change in the synovium or if the bulk of it is so great that it would still impinge upon the nerve despite the ligament release. This requires careful procedure to avoid postoperative compression of the nerve by hematoma or tendon adhesions limiting range of motion. s Postoperatively, the wrist was immobilized in slight wrist extension but full finger and thumb mobility was ensured. This continued for approximately 2 weeks and then gentle active range of motion was begun. Splinting is required to prevent prolapse of the contents of the carpal canal. Volar bowstringing of the flexor tendons and anterior migration of the median nerve could occur through the open transverse carpal ligament. Scarring during this time secures their position and the splint maintains optimal position for finger and thumb function.s,s Hand therapy began 2/5/86, approximately 4 weeks postoperative, and complications developed early. Tenderness overlying the distal portion of the FCU tendon, as it inserts into the pisiform, was noted, This continued with increasing symptomatology and was conservatively treated with rest, splinting and oral anti-inflammatory medication, Injection therapy finally produced temporary relief. Since complications continued through April (4 months postop), electrodiagnostic studies were requested to be certain that the CTR had indeed relieved pressure on and within the median nerve, Studies were conducted on 5/6/86 on the left median and ulnar nerves, No abnormalities were recorded with the median and ulnar motor or sensory conduction velocities, The electromyographic studies of the left median and ulnar innervated muscles were also entirely normal. The median sensory distal latency was again performed after provative Phalen's maneuver and found to be 3.3 msec. This was a better reading than the 3.7 msec recorded for the same test prior to surgery, On 5/13/86, the surgeon noted that there were no symptoms referable to the median nerve. He did report that other symptoms as noted preoperatively had continued. These symptoms were tenderness in the first and sixth dorsal wrist compartments and the FCU tendon. Also reported was a burning pain that radiated up the ulnar forearm to the ulnar groove area and discomfort in the radial wrist that radiated into the thumb. Examination on 6/6/86 revealed tenderness with palpation to the areas above, but all displayed negative stress tests, No positive Tinel's signs were noted at the wrist or elbow for the ulnar nerve, Conservative treatment continued until July 1986 but was not providing favorable results, An additional neurological exam was requested 174
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because of continued and increasing symptoms. Intermittent pain at the left elbow and ulnar aspect of the left forearm and intermittent paresthesias were now noted in the fourth and fifth digits, On 7/7/86, examination by a different neurologist suggested that there were no signs of a symptomatic CTS. He did feel that the patient had left ulnar nerve irritation at the level of the elbow, but examination of strength and nerve conduction as well as sensibility did not confirm this, Tenderness of the ulnar nerve was noted just proximal to and in the proximal portions of the ulnar groove in the left elbow. There were no impressions of cervical compression, thoracic outlet syndrome, or systemic problems. ' "Visible swelling and tenderness about the ulnar volar aspect of the wrist, and the previously described symptomology and examinations, led the surgeon to suspect an impinging mass possibly affecting the ulnar nerve into Guyon's canal. The mass was believed to be either tenosynovitis or a ganglion. Surgery on 8/13/86 explored this area and confirmed a marked amount of tenosynovitis of the flexor tendons, inflammation, and scarring along the ulnar nerve and the FCU tendon. Decompression of the ulnar nerve into Guyon's canal by neurolysis was performed. Tenolysis of the FCU tendon and tenosynovectomy of the flexor tendons to the fingers was also completed. Ulnar tunnel syndrome refers to the compression of the ulnar nerve into Guyon's canal. The anatomical confines of the ulnar nerve in this area include: the volar carpal ligament on the volar aspect, the hook of the hamate and insertion of the transverse carpal ligament on the lateral aspect, and the pisiform and attachments of the pisohamate ligament on the medial aspect. This is a common site of nerve compression and its etiology is similar in nature to the factors causing CTSP Surgery confirmed this compression and external neurolysis as previously described was the method of decompression, Postoperatively, the wrist was immobilized in slight wrist extension for wound healing. Approximately 2 weeks postoperative, the patient gradually began mobilizing the wrist. About 6 weeks after surgery, the surgeon reported that the symptomatology in the volar ulnar wrist area had dissipated. He further reported that "with increasing activities, the patient's elbow discomfort has reoccurred and is becoming worse," Examination now revealed tenderness overlying the ulnar nerve as it entered the ulnar groove. Additional hypersensitivity at the first carpometacarpal jOint and overlying the first dorsal compartment was reported but produced negative stress tests. Conservative treatment continued for these problems, including injection of the first dorsal compartment. The exam of 10/30/86 now revealed a positive Tinel's sign of the ulnar nerve at the elbow and a "weakly positive" Finklestein's test. Subjective discomfort continued in the forearm, especially in the medial aspect from the elbow into the fourth and fifth fingers. The surgeon made no mention of the elbow flexion test, but this is sometimes helpful in diagnosing ulnar nerve compression at the elbow. The
elbow is held in maximum flexion for 1 minute, which stresses the ulnar nerve as it passes in the sulcus between the medial epicondyle and the olecranon process. If paresthesias are noted upon this maneuver, this indicates a positive test. This is similar in principle to Phalen's test. 17 As the patient increased her level of ADLs these symptoms were exacerbated. The surgical alternative of anterior transposition of the ulnar nerve at the elbow was discussed and recommended, since other treatments had failed and the patient felt it was symptomatically justified. Neurolysis and anterior transposition of the ulnar nerve was performed on 1/14/87. The area of typical compression is between the ulnar and humeral origins of the FCU. This is just distal to the medial epicondyle as the nerve passes through the two heads of the FCU. This is referred to as cubital tunnel syndrome. 9 . 17 The method of this transposition involved excision of the medial intramuscular septum and release of the arcade of Struthers. This is an important procedure in order to prevent an additional entrapment of the nerve at the level of the arcade. 9 The nerve was transposed anteriorly to the medial epicondylar area and held in place by suturing in subcutanous tissue. Careful procedure was followed so that the nerve had enough freedom to be relocated without kinking and slid both proximally and distally. An important consideration in compressive neuropathies is the role of peripheral nerve excursion. Longitudinal sliding of the nerves during limb movement has been observed and measured. In compressive or adhesive conditions, this excursion may lead to further neural damage. With fixed compression of a nerve in one area, the excursion forces during limb movement produce a shearing force on the proximal and distal nerve segments. This longitudinal force causes further internal compressive pressures on the nerve substance. From measurements of the amount of nerve excursion, it suggests that there are greater forces in the proximal direction to the nerve compression site. This may explain why swelling of the nerve is characteristically seen at the proximal end and usually is less defined distally. IS The internal nerve compression pressures induced by nerve excursion represent mini-traction lesions in the nerve. This leads to axonal excitement (irritation) both proximal and distal to the actual compressed site. Clinically, this may be why symptoms often radiate proximally and distally to the area of actual entrapment. This further supports the treatment of splinting. The lack of motion from splinting reduces longitudinal excursion forces and allows the nerve to rest and inflammation to subside.IS This excursion phenomenon is of particular importance in this case because of the "double-crush" of the ulnar nerve. If a nerve has two areas of fixed compression, and the longitudinal forces further add to internal compression pressures on the nerve substance, then damage to the nerve would be intensified in the double~crush case. One study suggested that a proximal compression of a nerve may lessen its ability to withstand further compression in its distal seg-
ment. It was also concluded that if each area of compression in the syndrome is mild, the nerve damage can be greater than suspected because of the double lesion. In this experimental model, an incomplete recovery was observed when only one compression area was released. Release of the distal compression appeared to achieve better results than a proximal release. 19 This supports the method of management utilized in this case.
An important consideration in compressive neuropathies is the role of peripheral nerve excursion. A long-arm splint immobilized the elbow postoperatively. Gentle AROM exercises and the use of a sling were introduced approximately 3 weeks postop. The patient was referred for hand therapy 6 weeks after surgery. At this time, the surgeon noted a lack of 20 degrees of elbow extension with almost fullelbow flexion . The Finklestein's test remained "weakly positive."
CURRENT THERAPY The patient re-initiated hand therapy after ulnar nerve anterior transposition. The focus of this study is upon this most recent therapeutic intervention. In consideration of this, it should be .recognized that therapy was included in the postoperative management of the earlier surgeries. Suffice it to conclude that rehabilitation efforts after the earlier surgeries were successful for the specific problems but limited by the course of symptomatology and treatment, as already explained.
Evaluation Walker has described an evaluation format specific for soft tissue inflammatory disorders that should include a meticulous interview for obtaining an accurate understanding of the pathology.2o It is important to examine both extremities, because when one extremity is involved, frequently the opposite limb demonstrates pathologic changes as well. In patients where the disorder is greater on the non-dominant side, as in this case, it is usually occupationally specific.2o Gathering baseline information on the "uninvolved" limb assists in monitoring its ,condition for changes, since increased stress is caused by shifting the work load. In the examination of the uninvolved right upper extremity, there were no findings to suspect inflammatory problems, but the work history was indicative of possible CTD. The decrease.d stress associated with being off work for 1% years may have allowed the inflammatory conditions in this extremity to subside. This indeed seemed to be the case, as previous evaluations in therapy showed possible signs of CTS and tenosynovitis. July-September 1988
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Upon evaluation, the patient was no longer using a sling or any splints. She reported little to no use of the arm in most ADLs but was performing AROM exercises at the elbow. She related a burning pain of the intensity "3" rated on an arbitrary pain scale from 1-10 with 10 being the most intolerable pain imaginable. This was located in the posterior portion of the elbow, which was periodically uncomfortable. She was unable to identify the specific times during the day or night it occurred and did not recognize a relationship of this pain to any activity. She noted "tightness" in the elbow when attempting to move it but did not report it as painful. There were subjective complaints of "discomfort" or "aching" overlying the pisiform and in the dorsum of the thumb and first CMC joint, but this was also vague in time of occurrence and in being activity-related. She was somewhat protective of the extremity holding it in approximately 45 degrees of elbow flexion. Upon examination, the skin was warm and dry and showed no discoloration, sympathetic changes, or open wounds. There were well-healed, non-adherent surgical scars about the proximal thenar crease and ulnar volar wrist areas from the previous surgeries. The well-healed surgical scar about the medial elbow was approximately 6 inches in length, minimally hypertrophic and minimally adherent to subcutaneous tissue. No deformities or visible abnormalities were noted except mild generalized atrophy associated with disuse. 21 No edema was noted but the patient was moderately overweight, making edema less obvious. Vascular status is assessed by the Allen test. This is a recommended test in ruling out vascular insufficiency as a cause of symptoms in CTS.8 This test had been performed in prior evaluations and was not deemed necessary as it demonstrated adequate patency. Sensibility testing is a method of establishing how a peripheral nerve is functioning. Clinical tests are divided into two categories, innervation density tests and threshold tests. Innervation density tests (i.e., static and moving two-point discrimination) have been shown to measure multiple overlapping peripheral receptor fields and the density of innervation in the region being tested. 22 These tests are highly dependent on the cortical integration of peripheral impulses. Since the cortex can organize this information if only a few fibers are conducting to their correct cortical end-points, these tests are useful in cases of nerve laceration and regeneration. 23 Threshold tests (i.e., Semmes-Weinstein monofilament pressure discrimination and vibratory d.iscrimination) measure a single nerve fiber innervating a receptor or group of receptor cells. These tests are more likely to show a gradual and progressive change in value as a greater proportion of nerve fibers are lost while others still maintain the proper central connections. Therefore, these tests are appropriately used in evaluation for nerve compression syndromes. 23 Vibratory sensibility was assessed by using the 256 cps tuning fork as outlined by Dellon. 22 The patient was unable to qualify any difference between 176
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sensations experienced in the right verses left hands. Semmes-Weinstein monofilaments were not available for administration in this case but would be recommended for the reasons as previously described. No Tinel's sign was present at the median or ulnar nerves at the wrist. This was not attempted at the elbow since the ulnar nerve had been transposed. Tinel's sign is positive when pain or hypersensitivity is elicited with percussion over the nerve. 24 One study concluded that this indicates that nerve fiber damage has occurred and the nerve is making an attempt to regenerate. Since a positive Tinel's sign remains localized at one area in entrapment syndromes, this sllggests that local changes in nerve fiber pathology must occur before the presence of Tinel's Sign. These damaged fibers may be more mechanically sensitive and respond quicker to percussion at the site of compression.lO Phalen's test is positive when the wrist is held in maximum flexion for at least one minute and pain or paresthesias are elicited. 24 Modified Phalen's test incorporates pinch with wrist flexion and some consider this more likely to strain the median nerve.14 Phalen reported that 80% of his patients with surgically confirmed cases of CTS tested positive. This test was negative on both right and left, but was warranted to help rule out median nerve symptomatology and possible CTS on the right. Attention was now directed to the muscle and tendon structures. Manual muscle testing revealed between 3+ /5 and 4- /5 for the entire upper extremity musculature including the median and ulnar nerve innervated muscles. In soft-tissue inflammatory disorders, stress tests and palpation of the muscles and tendons are important to identify areas of pain, inflammation and tenderness. This identification is accomplished by palpation at rest, with ROM and with resistance at the middle to end of the range. It is important to observe for signs of tenderness, pain, arrhythmic motion or excessive effort. Friction with tendon excursion causing squeaking, popping, cracking or locking may be observed in addition to palpable nodules. 2() Minimal stressing and resistance were applied about the elbow to ensure the integrity of the recent surgery. Pain was reported with resistive elbow flexion and extension, forearm pronation and supination, as well as full-elbow AROM. There was tenderness noted upon palpation overlying the pisiform, the first dorsal compartment containing the APL and EPB, and the medial epicondyle area of the elbow. Resistance to the APL and EPB muscles elicited only slight discomfort as well as stress testing using the Finklestein's test. This test is positive if pain is caused by having the patient grasp the thumb with the fingers and ulnarly deviate the wrist. A positive test is indicative of de Quervain's tenosynovitis, which must be differentiated from CMC arthritis. The axial compression adduction test is sometimes helpful in identifying this condition. This test is positive for CMC arthritis if crepitus, instability and/or pain is elicited with a grinding maneuver produced by the examiner upon the CMC joint. 25
Grip and pinch strength was measured following ASHT and ASSH guidelines. Left grip was 22 Ibs and the right was 42 Ibs. No pain was elicited with these tests. AROM and PROM were entirely within normal limits except a 15 degree lack of full elbow extension. This was probably secondary to protective posturing producing a tightness or slight shortening of the biceps, since disuse and immobilization can produce these results in muscles. 28 ,29 The muscle belly of the biceps was noticeably firm upon full elbow extension, indicating protective muscle splinting. The FDS tendons were carefully examined for full AROM because of the history of chronic tenosynovitis. This condition may lead to adhesions causing less than full tendon excursion. Full AROM was recorded using the pulp to palmar crease measurement. 20 Precision handling and dexterity appeared physically intact upon observation of simple hand functions. Therefore, standardized functional tests were not administered because activity tolerance was of greater significance in this case. This, however, is quantitatively extremely difficult to measure. Because ADL tests are to date nonstandardized, interview and observation appear to provide the best means of assessing current activity levels.27 Ongoing assessment of activity tolerance requires careful grading and monitoring of activities. Monitoring should be done before and after activities and may include tests for edema, sensibility, ROM, strength and palpable tenderness with or without ROM or resistance. Reports of pain during and after activities can indicate changes in the inflammatory process.20 The patient reported no problems associated with ADLs in which she could successfully limit the use of the left upper extremity. Significant pain and difficulty accomplishing tasks were noted with bilateral ADLs. Avocational activities were mostly limited to unilateral tasks. Specifically, pain was associated with the use of the left upper extremity in 5-10 minutes of light function (Le., doing dishes and folding laundry).
Treatment Plan The goals and general treatment plan included the following: (1) reduction and control of inflammation, pain and
swelling; (2) achieve full AROM; (3) achieve functional hand strength and endurance; (4) maximize activity tolerance in ADLs. Home therapy included a graded application of exercises and ADLs that were carefully monitored for exacerbation of symptoms. Gentle AROM of the entire upper extremity was initiated early to prevent joint stiffness in the "uninvolved" areas and to increase elbow extension. In ranging of the elbow to gain extension, it was important to consider what structures were being placed on stretch. As previously mentioned, biceps shortening was suspected, thus resistant to elbow exten-
sion. Since the ulnar nerve had been transposed anteriorly, and it is no longer stressed with elbow flexion, it is now lengthened by elbow extension. Peripheral nerves react to longitudinal stresses by the increased resultant intraneural pressures. These pressures may produce mini-traction lesions causing nerve irritation and excitation. IS Therefore, gentle procedure and monitoring for nerve reaction (changes in sensibility, pain and paresthesias) was important to avoid further neural damage. Paraffin baths and hot packs to the elbow, especially the biceps, in conjunction with therapeutic exercises, were used to induce biceps relaxation and soft tissue extensibility (to increase elbow extension). Heat has a direct effect on the gamma fibers of the muscle spindles. The spindle activity and sensibility to stretch are reduced with heat application. Relaxation may also be induced due to reflexes negotiated through the thermal receptors. The specific mechanism of these reactions is not fully understood. At increased temperatures, tendons are apparently able to withstand greater extensibility when combined with tensile forces .3o Heat also acts on the free nerve endings and peripheral nerve fibers to increase the pain threshold. Exercises were approached cautiously to avoid tissue damage that would be undetectable because of this analgesic effect. The physiological responses to heat and cold modalities are not clearly defined and research is sometimes contradictory, especially concerning the physiological effects of cold. Clinically, however, observations indicate uses for both modalities in certain pathologic conditions. 31 ,35 In the case of chronic inflammatory problems, authors have recommended heat to increase blood flow and metabolism, associated with the simultaneous vasodilation that heat causes. This increases the process of phagocytosis, infiltration of leukocytes, antibodies, flushing of metabolics, and nutrient and oxygen delivery.31,36 Cold therapy or cryotherapy has also been recommended for these problems. Its application is thought to produce a "hunting reaction" or alternating vasoconstriction and vasodilation, which theoretically would slow the inflammatory reaction, then assist in "flushing" the area by the increased blood flow to clear the metabolites. 2o,33 It has not been clearly shown, as of yet, that cold does indeed induce vasodilation.2o•33 Most authors do agree, however, that heat will cause an increase in blood flow (vasodilation). It seems that patient responses to these modalities administered on a trial basis are often the determinant of the best treatment. 3S Conservative treatment for the de Quervain's disease occurred concurrently with the rehabilitation efforts. The pathology of this disease involves inflammation of the tendon sheath and its associated vaginale ligament. Most authorities agree that the tendons present with only slight thickening unless the condition is chronic. With this, the sheath may become 3-4 times its normal size and either brown or red in color. Adhesions may occur between the synovium and the tendon. To prevent this, AROM of the thumb was encourgaged. The tendons may also be July-September 1988
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thin, flattened and have granulation tissue that may produce connecting fibrous bands. In the local inflammation area, the tendons may be constricted but remain normal elsewhereP Heat was used at the proximal upper extremity for the reasons previously addressed. Trial applications of heat and cold were attempted to reduce the inflammatory response of the stenosing de Quervain's tenosynovitis. There were subjective complaints of stiffness and irritation with cold, and heat produced greater relief of pain during AROM.
It has not been clearly shown, as of
yet, that cold does indeed induce vasodilation.
Treatment of de Quervain's is designed to control and reduce the inflammatory response through immobilization, anti-inflammatory medication, and corticosteroid injection. This patient was treated in the above fashion, and immobilization was achieved by fabrication of a static thumb spica type splint. The splint was fabricated on 4/17/87,4 weeks into therapy, because with the gradual progression of left upper extremity activity, the de Quervain's symptoms were exacerbated. The splint was designed to specifically immobilize the involved APL and EPB. Care was taken in the fabrication and utilization of this splint to avoid acute compressive neuropathy of the ulnar digital nerve of the thumb. This has been a complication with this splint in two reported cases by Rayan and O'Donoghue. Symptoms include numbness of the ulnar aspect of the thumb and pain at the level of the volar aspect of the first MCP jOint. If detected early, the nerve lesion is reversible and splint adjustments to correct the pressure areas are usually successfu1. 38 Iontophoresis was also administered to introduce dexamethasone sodium phosphate into the inflamed region. This medication is a long-acting synthetic glucocorticoid compound that has a potent anti-inflammatory effect.39 The Phoresor unit was used because of its ease of set up and built-in safety features. It supplies a DC current that is adjustable from 0-5 milliamperes. The built-in safety factor ensures a constant current control, because the unit shuts off when skin impedances are lower than 500 ohms or greater than 100 kilohms.40 Ions in solution are transferred through the intact skin via electrical potential using bipolar electrodes. The positive ions are carried through at the positive treatment electrode. DC current is required because of its continuous, undirectional flow and since it has only one charge. This causes the ions to migrate according to their electrical charge. 4o• 4 1 Heat was used over the treatment area (first dorsal compartment) prior to the iontophoresis in order to reduce the skin impedance. Normal human skin has a high degree of skin impedance, approximately 3000 ohms, primarily due to its relative lack of water 178
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content. Since heat increases blood flow, it hydrates the skin which allows improved conductivity. Glass et a1. have demonstrated that dexamethasone (with 4% lidocaine HCL) was iontophoresed into tissue overlying the elbow, shoulder, hip, knee and ankle joints of Rhesus monkeys. The medication transferred into all tissue layers underlying the electrodes down to and including tendinous and cartilaginous tissues. This effectively delivered a therapeutic dosage at sufficient tissue depthsY In a clinical investigation, Harris reported that 75% of the patients treated with this method of iontophoresis for musculoskeletal inflammation had excellent to good resultS.40 Conservative treatment, including the above procedures, did not yield satisfactory long-term results after 4 months time, and surgical intervention is pending. Surgical correction is often viewed as a simple procedureY Arons has recently emphasized the complexity of this diagnOSis and its correction. In 11 preoperative cases of de Quervain's disease, 6 patients had associated general tendonitis. Of the 5 cases with isolated de Quervain's, 2 responded successfully to conservative treatment using injection, splinting, anti-inflammatories and occupational therapy lasting for 3 months. Of the 6 cases with generalized tendonitis, 3 eventually required surgical releaseY In the elbow, AROM achieved normal status after 2 weeks of therapy. Gentle strengthening, endurance and activity training was tolerated fairly well except at the dorsal thumb area. The splint was used during exercises for tendon protection. Exercises and simulated activities were graded and monitored in time, resistance, and repetitions as measured on the BTE Work Simulator.
Surgical correction is often viewed as a simple procedure. This program and the home program encouraged both anaerobic and aerobic exercises. Biopsies of tissue have revealed a relationship between excess lactic acid and glycogen depletion to tendonitisY Aerobic exercise causes oxygen consumption to increase and accumulation of lactic acid begins at a higher rate of work than before training. Tolerable levels of lactic acid and oxygen debt are raised with anaerobic exercise also, but this is not well understood. 44 ,45 Endurance training is also believed to increase glycogen storage. IO Aerobics were encouraged without the use of the left upper extremity to avoid symptomatic flareups, Heat, AROM and gentle stretching preceded controlled PREs to increase muscle temperature. This increase in temperature is proposed to assist in efficiency, speed and strength of muscle contraction. 46 It should be noted, however, that some authors recommend cold versus heat prior to therapeutic exercises because of its "efficiency effect." This phenomenon is related to the effects of heat and cold on local
metabolism. Heat and exercise both increase metabolism and cold decreases metabolism. With a decrease in metabolism (cold therapy), there is less of a demand on the muscles for nutrients, etc. Therefore, the muscles handle the effects of exercise more efficiently, prolonging the fatigue point. Since heat increases metabolism, as does exercise, the fatigue point is reached sooner because of the higher demands placed upon the muscles. 33 This leads to an interesting question specific to soft tissue inflammatory problems. What is the physiological end result of enhancing the activity tolerance with heat and/or cold? Does this lead to improved strength and endurance without delayed exacerbation of symptoms? Does this lead to further tissue damage because of continued mechanical stresses upon the tendons, nerves, etc.? Regardless of the effects of heat or cold, careful monitoring of the patient's immediate and delayed response to exercise is the only method for determining how to structure therapy. After 3 months of therapy, the patient was tolerating I-hour sessions of slow-rate, low resistance/ repetition activity. Left grip strength increased from 22 lbs to 47 lbs after 3 months of treatment and activity tolerance improved allowing greater functional status. This, however, fluctuated greatly due to generalized complaints of pain resulting from the increased activity.
Regardless of the effects of heat or cold, careful monitoring of the patient's immediate and delayed response to exercise is the only method for determining how to structure therapy. Ergonomic principles were applied to ADLs to increase the patient's functional abilities. Risk factors associated with cumulative trauma are repetitive and forceful exertion, mechanical stresses, certain postures, fibration and low temperatures. Wrist flexion and extension are associated with tenosynovitis of the flexor and extensor tendons and CTS. Ulnar and radial deviation are associated with de Quervain's disease. 47 ,48 Therefore, ADL tasks were modified to maintain the wrist in neutral. The thumb spica splint allowed for performance of most ADLs in this position, but tool and job redesign improved posture and reduced forceful exertions and mechanical stress. Examples of tools that were used are long-handle jar opener, pistol-shaped cutting knife, adapted parring board, and built-up handles for writing instruments.
Treatment Outcome Four months of therapy yielded full AROM and good left upper extremity strength. Activity tolerance remained poor, limited by exacerbations of pain and
tenderness about the first dorsal compartment, ulnar carpal area, and occasionally the lateral epicondyle area of the elbow. The patient appears to have responded to the surgeries and therapy with fair resolution of symptoms. Low-grade problems continued to limit function, and tenovaginotomy of the left first dorsal compartment was imminent. If indeed the patient could be stabilized medically, a work-capacity evaluation would be necessary to determine what the residual functional abilities are. Job and tool modifications would be extremely important in considering any occupational role for this patient. Ergonomically designed check stands have been developed but not yet sufficiently studied.49 Despite this, the prognosis for return to her previous occupation is extremely poor and would seem only to invite further problems.
REFERENCES 1. Louis OS: Cumulative trauma disorders. J Hand Surg 12A:823825,1987, 2. Blair SJ, Bear-Lehman J: Editorial comment: prevention of upper extremity occupational disorders, J Hand Surg 12A:821822, 1987, 3. Kelsey J, Pastides H , Kreiger N, et al: Upper extremity disorders-a survey of their frequency and cost in the United States. St. Louis, the CV Mosby Co, 1980, pp, 1-70, 4. Poole Be, Lacey P: Prevention of industrial injuries. Proceedings of American Society of Hand Therapists annual meeting. J Hand Surg 8:625-627, 1983. 5, Heckler FR, Jabaley ME: Evolving concepts of median nerve decompression in the carpal tunnel. Hand Clin 2:723-736, 1986. 6. Phalen GS: The carpal tunnel syndrome. J Bone Joint Surg 48: 211-228,1966. 7. Phalen GS: The carpal tunnel syndrome: clinical evaluation of 598 hands. Clin Orthop 83:29, 1972. 8, Kessler FB: Complications of the management of carpal tunnel syndrome. Hand Clin 2:401-406, 1986. 9, Spinner M: Nerve lesions in continuity. In Hunter JM, Schneider L, Mackin E, Callahan AD (eds): Rehabilitation of the Hand, 2nd ed. St. Louis, The CV Mosby Co, 370-377, 1984. 10. Mackinnon SE, Dellon AL: Experimental study of chronic nerve compression. Hand Clin 2:639-650,1986, 11. Curtis RM, Eversmann WA: Internal neurolysis as an adjunct to the treatment of carpal tunnel syndrome. Hand Clin 2:641644,1986. 12. Berkow R, Talbott JH: The Merck Manual of Diagnosis and Therapy. New Jersey, Merck Sharp and Dohme Research Laboratories, 1977, p . 1358. 13. Conklin JE, White WL: Stenosing tenosynovitis and its possible relation to the carpal tunnel syndrome, Surg Clin North Am 40:531-540,1960. 14. Smith EM, Sonstegard DA, Anderson WH: Carpal tunnel syndrome: contribution of flexor tendons. Arch Phys Med Rehab 58:379-385,1977. 15. Armstrong TJ, et al: Ergonomics in hand and wrist tendonitis. J Hand Surg 12:832-836, 1987" 16. Hammer AW: Tenosynovitis. Medical Record 140:353-355, 1934. 17. Bayne LG, etal: Regional review course in hand surgery. American Society for Surgery of the Hand. 4:1-10, 1986. 18. Wilgis EF, Murphy R: Significance of longitudinal excursion in peripheral nerves. Hand Clin 2:761-765, 1986. 19. Nemoto K, Matsumoto N, Tazaki K, et al: An experimental study on the "double crush" hypothesis, J Hand Surg 12:552558, 1987. 20. Walker SE: Treatment of soft tissue inflammatory problems of the forearm and hand , Paper presented to American Society of Hand Therapists, 1983. 21, Poland JL, Hobard OJ, Payton 00: The musculoskeletal system, New York, Medical Examination Publishing Co, 76-77, 1977.
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22. Dellon At: Evaluation of Sensibility and Re-education of Sensation in 'the Hand. Baltimore, Williams and Wilkins, 1981. 23. Gelberman RH, et al: Sensibility testing in peripheral nerve compression syndromes. J Bone Joint Surg 633-637, 1983. 24. Hoppenfeld S: Physical Examination of the Spine and Extremities. New York, Appleton-Century Crofts, 1976. 25. American Society for Surgery of the Hand: The Hand-Examination and Diagnosis. Aurora, Colorado, ASSH, 1978. 26. Fess EE: A method for checking Jamar Dynamometer calibration. J Hand Therapy 1:28-32, 1987. 27. Fess EE: Documentation: essential elements of an upper extremity assessment battery. In Hunter JM, Schneider L, Mackin E, Callahan AD (eds): Rehabilitation Qf the Hand, 2nd ed. St. Louis, The CV Mosby Co, 1984, pp. 57-78. 28. Evans EB, et al: Experimental immobilization and remobilization of rat knee joints. J Bone Joint Surg 42:737-758, 1960. 29. Poland Jt, Hobard DJ, Payton OD: The Musculoskeletal System. New York, Medical Examination Publishing Co, 1977, pp. 76-77. 30. Warren C, Lehmann JF, Koblanski IN : Elongation of rat tail tendon: effect of load and temperature. Arch Phys Med 29:583, 1948. 31. Lehmann JF, Warren CG, Scham SM: Therapeutic heat and cold. Clin Orthop 99:207-237, 1974. 32. Cannon NM, Mullins PT: Modalities in upper extremity rehabilitation. In Malick MH, Kasch MC (eds.): Manual on Management of Specific Hand Problems. Pittsburgh, Aren-Publications, 1984, p. 78. 33. Moore R: Cold therapy in the rehabilitation of athlete, recent advances. Paper presented to the nineteenth A.M.A. national conference on the aspects of sports. Sail Francisco, 1977. 34. Lehman JF: Therapeutic Heat and Cold. Baltimore, Williams and Wilkins Co, 1982. 35. Burchfield J: The use of cold hyperstimulation analgesia for relief of pain. Occupational Therapy Forum 12-13, 1986. 36. Kirwan LA, Boswick JA: Comprehensive rehabilitation of the diseased and injured upper extremity. In Boswick JA (ed): Advances in Upper Extremity Surgery and Rehabilitation. Rockville, MD, Aspen Publishers, 1986, pp. 257-277.
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37. McGuirre C: Tendonitis related injuries in the workplace: treatment and prevention. Occupational Therapy Forum 2:No. 12, 1986. 38. Rayan GM, O'Donoghnue DH: Ulnar digital compression and neuropathy of the thumb caused by splinting. Clin Orthop 175:170-172, 1983. 39. Facts and Comparisons, St. Louis, J.B. Lippincott Co. July 1984, pp. 119-126. 40. Harris PR: Iontophoresis: Clinical research in musculoskeletal inflammatory conditions. J Orthop Sports Phys Ther 109-112, 1982. 41. Glass JM, Stephen Rt, Jacobson SC: The quantity and distribution of radio-labeled dexamethasone delivered to tissue by iontophoresis. Int J Derm 19:519-525, 1980. 42. Arons MS: De QueJ;'vain's release in working women: A report of failures complications and associated diagnosis. J Hand Surg 12A:540-544, 1987. 43. H\~nter D: The Diseases of Occupations. London, Hodder and Stoughton, 1978. 44. de Lateur B: Exercise for strength and endurance. In Basmajian JV (ed): Therapeutic Exercise, 3rd ed. Baltimore/London, Williams and Wilkins, 1978, pp. 86-92. 45. Wolf S: The morphological and functional basis of therapeutic exercise. In Basmajian JV (ed): Therapeutic Exercise, 3rd ed. Baltimore / London, Williams and Wilkins, 1978, pp. 43-85. 46. Allman F: Exercise in sports medicine. In Basmajian JV (ed): Therapeutic Exercise, 3rd ed. Baltimore/London, Williams and Wilkins, 1978, pp. 450-474. 47. Armstrong TJ: Ergonomics and cumulative trauma disorders. Hand Clin 2:553-564, 1986. 48. Armstrong TJ, Radwin RG, Hansen DJ: Repetitive trauma disorders: job evaluation and design. Hum Factors 28:325-334, 1986. 49. Wallersteiner UC, Stoffman LD, Robertson GE, Smith TJ: Development of a new workstation for cashiers in supermarkets. Vancouver, B.C., Labour Canada-Technology Impact Research Fund. Presented at the Cumulative Trauma Program, San Francisco, CA, Dec. 4-5, 1986.
CASESTUDY~
Cumulative Trauma Disorder of the Upper Extremity from Occupational Stress Barry C. Poole, OTR, eVE Hand Rehabilitation Center of San Diego, Inc. La Mesa, California
INTRODUCTION Pper-extremity cumulative trauma disorders (CTD) provide a fascinating and perplexing U study for the surgeon and therapist alike. Aspects of
the management of these disorders encompass a broad range of professional disciplines. A comprehensive approach is necessary in order to understand the full ramifications of their treatment. These syndromes are not a phenomenon of recent times. Extending back to the 17th century, Ramazini documented and discussed these occupational problems.! However, it does appear that the incidence of these disorders is on the increase as confirmed by the U.S. Bureau of Labor Statistics. 2 The cost and significance of these injuries is far reaching. 1- 3
Upper-extremity cumulative trauma disorders provide a fascinating and perplexing study for the surgeon and therapist alike. Perhaps arising from the limited success rate in the remedial treatment of these problems have been the recent efforts directed toward prevention, utilizBased on a case study written in partial requirement for membership in the American Society of Hand Therapists. Reprint requests to Barry C. Poole, OTR, CVE, Hand Rehabilitation Center of San Diego, Inc., 8881 Fletcher Parkway, Suite 240, La Mesa, CA 92042.
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ABSTRACT: The case presented is of a 33-year-old female with a non-dominant upper-extremity cumulative trauma disorder, which involves multiple soft tissue inflammatory problems sustained as a result of occupational stress. Surgical management has included carpal tunnel release with internal neurolysis, multiple tenosynovectomy, decompression of ulnar nerve into Guyon's canal with internal neurolysis, FCU tenolysis, and ulnar nerve anterior transposition with neurolysis. Additionally, a first dor.sal compartment tenovaginotomy is planned. Hand therapy has included the postoperative management of these procedures, and the case demonstrates a challenging rehabilitative scenario.
ing the applied science of ergonomics. 2,4 A full discussion of the application of ergonomics is beyond the scope of this analysis but deserves mention as it helps in understanding the etiology of CTD. Additionally, it assists in the application of tendon and nerve protection techniques, including tool and job modification. The Patient. PW is a 33-year-old female who presented with a classic case of the "checker syndrome." She is a right-hand dominant grocery checker of 12 years and uses a laser scanning system. On 10/17/85, she was unable to continue working because the gradual onset of left arm pain and numbness worsened this day to the point of intolerance. Upon referral, she presented to the hand surgeon on 10/ 25/85. The surgeon noted subjective complaints of shooting pains into the left thumb, tingling and numbness in the median nerve distribution area, and nocturnal symptomatology. His impression was that of carpal tunnel syndrome (CTS) and conservative treatment was initiated.
BACKGROUND AND CASE HISTORY Regardless of the specific etiology of CTS, it is always related to a volumetric increase in the contents within the carpal tunnel. This may be caused by an actual increase in volume or decrease in dimensions of the tunnel. There are numerous acute and chronic etiologic factors causing CTS.5 Nonspecific flexor tenosynovitis is one inflammatory problem leading to CTS, which in this case was confirmed at the time of surgery. Phalen reported it as the most common cause of CTS, occurring in 203 of 212 of his cases. 6
Accurate diagnosis of CTS is paramount because it may be confused with more proximal nerve compressions and may be associated with systemic disorders. Appropriate studies to rule out these conditions may be necessary, and many times a patient may have a normal physical examination. Phalen reported a 70% incidence of decreased sensibility, 60% positive Tinel's sign and 80% positive Phalen's test in one of his studies. 7 Other tests assist in diagnosing CTS, such as the Allen test, tourniquet test and electrodiagnostic studies. No single exam has been shown to be 100% conclusive. Therefore, each case must be evaluted in its entirety and many times lies in the judgment of the surgeon. 8 Neurological evaluation occurred between 11/ 8/85 and 11 /22/85. Evaluation concluded that blood sugar and thyroid functions were normal, and that there were no proximal nerve compressions. The only quantitative evidence found for left CTS was a prolongation of the distal median sensory latency conduction, which measured 3.7 msec. This was recorded after performance of provocative Phalen's maneuver held for 3 minutes. A reading of 3.45 msec was recorded without the Phalen's maneuver. When negative, electrodiagnosis is of questionable value in determining the diagnosis of CTS. Electrodiagnosis does appear most beneficial in ruling out proximal compressions, systemic disease or generalized neural pathology. The slowing of sensory conduction has proven to be the most sensitive reading. Heckler and Jabaley reported that distal sensory latencies of above 3.5 msec are present in 85% to 95% of surgically confirmed cases. s No correlation has been established between the degree of abnormalities recorded in these tests and the amount of damage noted at surgery.S,8 Conservative treatment was directed toward decreasing edema with oral anti-inflammatories and corticosteroid injection. Neutral wrist splinting positions the median nerve away from the transverse carpal ligament and makes the ligament less tense, This provides for less pressure upon the median nerve,S,8 Satisfactory results were not obtained with conservative treatment and surgery was performed on 1/9/86, This included left carpal tunnel release (CTR) with complete transection of the transverse carpal ligament and internal neurolysis, Tenosynovectomy of the flexor tendons was accomplished after exploration revealed a marked amount of tenosynovitis. Neurolysis separates the epineurium from its scarred bed or removes crossing thrombosed tressels or thickened fascia. 9 One study concluded that in chronic nerve compression, the nerve develops connective tissue changes that create a thickened perineurium and dense intrafascicular epineurium fibrosis. Dissection of the large fasicles from each other is accomplished with careful procedure in order to avoid injury to the nerve fibers themselves. l Extensive internal neurolysis can induce fibrosis throughout the neural layers, The perineurium acts to maintain the normal pressure gradient within the funiculus and is a carrier for the passage of proteins
and other large molecules. Therefore, violating the perineurium with internal neurolysis can be damaging, and many authors recommend aVOiding this if possible.l 9 Since damaging myofibroblasts were found in the epineurium of artificially compressed rat nerves, external neurolysis has been recommended as a possible treatment technique. This procedure involves removal of the epineurium; however, satisfactory expansion of the nerve bundles is frequently obtained with removal of the epineurium from only the volar aspect of the nerve,8 The less a nerve is disturbed, the better it will respond to release of the constriction. Complete removal of the epineurium was not performed in this case.
The less a nerve is disturbed, the better it will respond to release of the constriction. Tenosynovitis is the inflammation of the tendon sheath, Tendonitis is the inflammation of the tendon. Generally, this occurs Simultaneously, and the synovial-lined tendon sheath is usually the site of maximum inflammation. This condition may cause visible swelling due to inflammation and fluid accumulation. The sheaths may also remain relatively dry but irregularly contoured, causing friction upon movement as the tendon glides in its sheathP Tenosynovitis is stenosing when the tendon becomes constricted by its retaining fibrous ligament, which establishes irritation and inflammation,13 Tenosynovectomy involves the excision of the inflamed tendon sheath. Studies have suggested that the repetitiveness and forcefulness of manual work has a significant association in inducing irritative changes of the tendon sheaths, leading to chronic tenosynovitis and nerve compressions. Furthermore, women appear to be at greater risk than men. IUS Hammer reported that human tendons cannot tolerate more than 1500 to 2000 manipulations per hour.16 The pathogenesis of tendon disorders is important to understand as a basis for its treatment. Tendons are subjected to tensile stresses by the contractile force of the muscles. They also have compressive and shearing stresses from the bones and ligaments. The tendons become deformed in their mechanical responses to these forces, which is referred to as elastic strain. Viscous deformation or "creep" is the strain that occurs after the application of load (stress). This is believed to cause cumulative microdamage to the molecular links between the tissue matrix and the filler material. It is suggested that if the time between successive loads is not sufficient, significant "creep" in tendons will occur. IS There are also physiologic responses of tendons to repeated stresses. The results are seen as serous edema, thickening, proliferation of fibrocytes and fibrous connective tissue, destruction of synovial membranes, and adhesions. These are probably related to the breakdown of the nutritional pathway by loss of blood flow. The tendon is bathed by the surJuly-September 1988
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rounding synovium, which is maintained by circulation. This provides for nutrients by diffusion. When the tendon is compressed against adjacent surfaces or there is a thickening of the tendon sheaths, an occlusion of the blood flow occurs leading to nutritional deprivation. The complete mechanism that causes the results seen from repeated tendon stress is not yet full y understood. 15 Tenosynovectomy is recommended in CTS cases where there is obvious pathological change in the synovium or if the bulk of it is so great that it would still impinge upon the nerve despite the ligament release. This requires careful procedure to avoid postoperative compression of the nerve by hematoma or tendon adhesions limiting range of motion. s Postoperatively, the wrist was immobilized in slight wrist extension but full finger and thumb mobility was ensured. This continued for approximately 2 weeks and then gentle active range of motion was begun. Splinting is required to prevent prolapse of the contents of the carpal canal. Volar bowstringing of the flexor tendons and anterior migration of the median nerve could occur through the open transverse carpal ligament. Scarring during this time secures their position and the splint maintains optimal position for finger and thumb function.s,s Hand therapy began 2/5/86, approximately 4 weeks postoperative, and complications developed early. Tenderness overlying the distal portion of the FCU tendon, as it inserts into the pisiform, was noted, This continued with increasing symptomatology and was conservatively treated with rest, splinting and oral anti-inflammatory medication, Injection therapy finally produced temporary relief. Since complications continued through April (4 months postop), electrodiagnostic studies were requested to be certain that the CTR had indeed relieved pressure on and within the median nerve, Studies were conducted on 5/6/86 on the left median and ulnar nerves, No abnormalities were recorded with the median and ulnar motor or sensory conduction velocities, The electromyographic studies of the left median and ulnar innervated muscles were also entirely normal. The median sensory distal latency was again performed after provative Phalen's maneuver and found to be 3.3 msec. This was a better reading than the 3.7 msec recorded for the same test prior to surgery, On 5/13/86, the surgeon noted that there were no symptoms referable to the median nerve. He did report that other symptoms as noted preoperatively had continued. These symptoms were tenderness in the first and sixth dorsal wrist compartments and the FCU tendon. Also reported was a burning pain that radiated up the ulnar forearm to the ulnar groove area and discomfort in the radial wrist that radiated into the thumb. Examination on 6/6/86 revealed tenderness with palpation to the areas above, but all displayed negative stress tests, No positive Tinel's signs were noted at the wrist or elbow for the ulnar nerve, Conservative treatment continued until July 1986 but was not providing favorable results, An additional neurological exam was requested 174
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because of continued and increasing symptoms. Intermittent pain at the left elbow and ulnar aspect of the left forearm and intermittent paresthesias were now noted in the fourth and fifth digits, On 7/7/86, examination by a different neurologist suggested that there were no signs of a symptomatic CTS. He did feel that the patient had left ulnar nerve irritation at the level of the elbow, but examination of strength and nerve conduction as well as sensibility did not confirm this, Tenderness of the ulnar nerve was noted just proximal to and in the proximal portions of the ulnar groove in the left elbow. There were no impressions of cervical compression, thoracic outlet syndrome, or systemic problems. ' "Visible swelling and tenderness about the ulnar volar aspect of the wrist, and the previously described symptomology and examinations, led the surgeon to suspect an impinging mass possibly affecting the ulnar nerve into Guyon's canal. The mass was believed to be either tenosynovitis or a ganglion. Surgery on 8/13/86 explored this area and confirmed a marked amount of tenosynovitis of the flexor tendons, inflammation, and scarring along the ulnar nerve and the FCU tendon. Decompression of the ulnar nerve into Guyon's canal by neurolysis was performed. Tenolysis of the FCU tendon and tenosynovectomy of the flexor tendons to the fingers was also completed. Ulnar tunnel syndrome refers to the compression of the ulnar nerve into Guyon's canal. The anatomical confines of the ulnar nerve in this area include: the volar carpal ligament on the volar aspect, the hook of the hamate and insertion of the transverse carpal ligament on the lateral aspect, and the pisiform and attachments of the pisohamate ligament on the medial aspect. This is a common site of nerve compression and its etiology is similar in nature to the factors causing CTSP Surgery confirmed this compression and external neurolysis as previously described was the method of decompression, Postoperatively, the wrist was immobilized in slight wrist extension for wound healing. Approximately 2 weeks postoperative, the patient gradually began mobilizing the wrist. About 6 weeks after surgery, the surgeon reported that the symptomatology in the volar ulnar wrist area had dissipated. He further reported that "with increasing activities, the patient's elbow discomfort has reoccurred and is becoming worse," Examination now revealed tenderness overlying the ulnar nerve as it entered the ulnar groove. Additional hypersensitivity at the first carpometacarpal jOint and overlying the first dorsal compartment was reported but produced negative stress tests. Conservative treatment continued for these problems, including injection of the first dorsal compartment. The exam of 10/30/86 now revealed a positive Tinel's sign of the ulnar nerve at the elbow and a "weakly positive" Finklestein's test. Subjective discomfort continued in the forearm, especially in the medial aspect from the elbow into the fourth and fifth fingers. The surgeon made no mention of the elbow flexion test, but this is sometimes helpful in diagnosing ulnar nerve compression at the elbow. The
elbow is held in maximum flexion for 1 minute, which stresses the ulnar nerve as it passes in the sulcus between the medial epicondyle and the olecranon process. If paresthesias are noted upon this maneuver, this indicates a positive test. This is similar in principle to Phalen's test. 17 As the patient increased her level of ADLs these symptoms were exacerbated. The surgical alternative of anterior transposition of the ulnar nerve at the elbow was discussed and recommended, since other treatments had failed and the patient felt it was symptomatically justified. Neurolysis and anterior transposition of the ulnar nerve was performed on 1/14/87. The area of typical compression is between the ulnar and humeral origins of the FCU. This is just distal to the medial epicondyle as the nerve passes through the two heads of the FCU. This is referred to as cubital tunnel syndrome. 9 . 17 The method of this transposition involved excision of the medial intramuscular septum and release of the arcade of Struthers. This is an important procedure in order to prevent an additional entrapment of the nerve at the level of the arcade. 9 The nerve was transposed anteriorly to the medial epicondylar area and held in place by suturing in subcutanous tissue. Careful procedure was followed so that the nerve had enough freedom to be relocated without kinking and slid both proximally and distally. An important consideration in compressive neuropathies is the role of peripheral nerve excursion. Longitudinal sliding of the nerves during limb movement has been observed and measured. In compressive or adhesive conditions, this excursion may lead to further neural damage. With fixed compression of a nerve in one area, the excursion forces during limb movement produce a shearing force on the proximal and distal nerve segments. This longitudinal force causes further internal compressive pressures on the nerve substance. From measurements of the amount of nerve excursion, it suggests that there are greater forces in the proximal direction to the nerve compression site. This may explain why swelling of the nerve is characteristically seen at the proximal end and usually is less defined distally. IS The internal nerve compression pressures induced by nerve excursion represent mini-traction lesions in the nerve. This leads to axonal excitement (irritation) both proximal and distal to the actual compressed site. Clinically, this may be why symptoms often radiate proximally and distally to the area of actual entrapment. This further supports the treatment of splinting. The lack of motion from splinting reduces longitudinal excursion forces and allows the nerve to rest and inflammation to subside.IS This excursion phenomenon is of particular importance in this case because of the "double-crush" of the ulnar nerve. If a nerve has two areas of fixed compression, and the longitudinal forces further add to internal compression pressures on the nerve substance, then damage to the nerve would be intensified in the double~crush case. One study suggested that a proximal compression of a nerve may lessen its ability to withstand further compression in its distal seg-
ment. It was also concluded that if each area of compression in the syndrome is mild, the nerve damage can be greater than suspected because of the double lesion. In this experimental model, an incomplete recovery was observed when only one compression area was released. Release of the distal compression appeared to achieve better results than a proximal release. 19 This supports the method of management utilized in this case.
An important consideration in compressive neuropathies is the role of peripheral nerve excursion. A long-arm splint immobilized the elbow postoperatively. Gentle AROM exercises and the use of a sling were introduced approximately 3 weeks postop. The patient was referred for hand therapy 6 weeks after surgery. At this time, the surgeon noted a lack of 20 degrees of elbow extension with almost fullelbow flexion . The Finklestein's test remained "weakly positive."
CURRENT THERAPY The patient re-initiated hand therapy after ulnar nerve anterior transposition. The focus of this study is upon this most recent therapeutic intervention. In consideration of this, it should be .recognized that therapy was included in the postoperative management of the earlier surgeries. Suffice it to conclude that rehabilitation efforts after the earlier surgeries were successful for the specific problems but limited by the course of symptomatology and treatment, as already explained.
Evaluation Walker has described an evaluation format specific for soft tissue inflammatory disorders that should include a meticulous interview for obtaining an accurate understanding of the pathology.2o It is important to examine both extremities, because when one extremity is involved, frequently the opposite limb demonstrates pathologic changes as well. In patients where the disorder is greater on the non-dominant side, as in this case, it is usually occupationally specific.2o Gathering baseline information on the "uninvolved" limb assists in monitoring its ,condition for changes, since increased stress is caused by shifting the work load. In the examination of the uninvolved right upper extremity, there were no findings to suspect inflammatory problems, but the work history was indicative of possible CTD. The decrease.d stress associated with being off work for 1% years may have allowed the inflammatory conditions in this extremity to subside. This indeed seemed to be the case, as previous evaluations in therapy showed possible signs of CTS and tenosynovitis. July-September 1988
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Upon evaluation, the patient was no longer using a sling or any splints. She reported little to no use of the arm in most ADLs but was performing AROM exercises at the elbow. She related a burning pain of the intensity "3" rated on an arbitrary pain scale from 1-10 with 10 being the most intolerable pain imaginable. This was located in the posterior portion of the elbow, which was periodically uncomfortable. She was unable to identify the specific times during the day or night it occurred and did not recognize a relationship of this pain to any activity. She noted "tightness" in the elbow when attempting to move it but did not report it as painful. There were subjective complaints of "discomfort" or "aching" overlying the pisiform and in the dorsum of the thumb and first CMC joint, but this was also vague in time of occurrence and in being activity-related. She was somewhat protective of the extremity holding it in approximately 45 degrees of elbow flexion. Upon examination, the skin was warm and dry and showed no discoloration, sympathetic changes, or open wounds. There were well-healed, non-adherent surgical scars about the proximal thenar crease and ulnar volar wrist areas from the previous surgeries. The well-healed surgical scar about the medial elbow was approximately 6 inches in length, minimally hypertrophic and minimally adherent to subcutaneous tissue. No deformities or visible abnormalities were noted except mild generalized atrophy associated with disuse. 21 No edema was noted but the patient was moderately overweight, making edema less obvious. Vascular status is assessed by the Allen test. This is a recommended test in ruling out vascular insufficiency as a cause of symptoms in CTS.8 This test had been performed in prior evaluations and was not deemed necessary as it demonstrated adequate patency. Sensibility testing is a method of establishing how a peripheral nerve is functioning. Clinical tests are divided into two categories, innervation density tests and threshold tests. Innervation density tests (i.e., static and moving two-point discrimination) have been shown to measure multiple overlapping peripheral receptor fields and the density of innervation in the region being tested. 22 These tests are highly dependent on the cortical integration of peripheral impulses. Since the cortex can organize this information if only a few fibers are conducting to their correct cortical end-points, these tests are useful in cases of nerve laceration and regeneration. 23 Threshold tests (i.e., Semmes-Weinstein monofilament pressure discrimination and vibratory d.iscrimination) measure a single nerve fiber innervating a receptor or group of receptor cells. These tests are more likely to show a gradual and progressive change in value as a greater proportion of nerve fibers are lost while others still maintain the proper central connections. Therefore, these tests are appropriately used in evaluation for nerve compression syndromes. 23 Vibratory sensibility was assessed by using the 256 cps tuning fork as outlined by Dellon. 22 The patient was unable to qualify any difference between 176
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sensations experienced in the right verses left hands. Semmes-Weinstein monofilaments were not available for administration in this case but would be recommended for the reasons as previously described. No Tinel's sign was present at the median or ulnar nerves at the wrist. This was not attempted at the elbow since the ulnar nerve had been transposed. Tinel's sign is positive when pain or hypersensitivity is elicited with percussion over the nerve. 24 One study concluded that this indicates that nerve fiber damage has occurred and the nerve is making an attempt to regenerate. Since a positive Tinel's sign remains localized at one area in entrapment syndromes, this sllggests that local changes in nerve fiber pathology must occur before the presence of Tinel's Sign. These damaged fibers may be more mechanically sensitive and respond quicker to percussion at the site of compression.lO Phalen's test is positive when the wrist is held in maximum flexion for at least one minute and pain or paresthesias are elicited. 24 Modified Phalen's test incorporates pinch with wrist flexion and some consider this more likely to strain the median nerve.14 Phalen reported that 80% of his patients with surgically confirmed cases of CTS tested positive. This test was negative on both right and left, but was warranted to help rule out median nerve symptomatology and possible CTS on the right. Attention was now directed to the muscle and tendon structures. Manual muscle testing revealed between 3+ /5 and 4- /5 for the entire upper extremity musculature including the median and ulnar nerve innervated muscles. In soft-tissue inflammatory disorders, stress tests and palpation of the muscles and tendons are important to identify areas of pain, inflammation and tenderness. This identification is accomplished by palpation at rest, with ROM and with resistance at the middle to end of the range. It is important to observe for signs of tenderness, pain, arrhythmic motion or excessive effort. Friction with tendon excursion causing squeaking, popping, cracking or locking may be observed in addition to palpable nodules. 2() Minimal stressing and resistance were applied about the elbow to ensure the integrity of the recent surgery. Pain was reported with resistive elbow flexion and extension, forearm pronation and supination, as well as full-elbow AROM. There was tenderness noted upon palpation overlying the pisiform, the first dorsal compartment containing the APL and EPB, and the medial epicondyle area of the elbow. Resistance to the APL and EPB muscles elicited only slight discomfort as well as stress testing using the Finklestein's test. This test is positive if pain is caused by having the patient grasp the thumb with the fingers and ulnarly deviate the wrist. A positive test is indicative of de Quervain's tenosynovitis, which must be differentiated from CMC arthritis. The axial compression adduction test is sometimes helpful in identifying this condition. This test is positive for CMC arthritis if crepitus, instability and/or pain is elicited with a grinding maneuver produced by the examiner upon the CMC joint. 25
Grip and pinch strength was measured following ASHT and ASSH guidelines. Left grip was 22 Ibs and the right was 42 Ibs. No pain was elicited with these tests. AROM and PROM were entirely within normal limits except a 15 degree lack of full elbow extension. This was probably secondary to protective posturing producing a tightness or slight shortening of the biceps, since disuse and immobilization can produce these results in muscles. 28 ,29 The muscle belly of the biceps was noticeably firm upon full elbow extension, indicating protective muscle splinting. The FDS tendons were carefully examined for full AROM because of the history of chronic tenosynovitis. This condition may lead to adhesions causing less than full tendon excursion. Full AROM was recorded using the pulp to palmar crease measurement. 20 Precision handling and dexterity appeared physically intact upon observation of simple hand functions. Therefore, standardized functional tests were not administered because activity tolerance was of greater significance in this case. This, however, is quantitatively extremely difficult to measure. Because ADL tests are to date nonstandardized, interview and observation appear to provide the best means of assessing current activity levels.27 Ongoing assessment of activity tolerance requires careful grading and monitoring of activities. Monitoring should be done before and after activities and may include tests for edema, sensibility, ROM, strength and palpable tenderness with or without ROM or resistance. Reports of pain during and after activities can indicate changes in the inflammatory process.20 The patient reported no problems associated with ADLs in which she could successfully limit the use of the left upper extremity. Significant pain and difficulty accomplishing tasks were noted with bilateral ADLs. Avocational activities were mostly limited to unilateral tasks. Specifically, pain was associated with the use of the left upper extremity in 5-10 minutes of light function (Le., doing dishes and folding laundry).
Treatment Plan The goals and general treatment plan included the following: (1) reduction and control of inflammation, pain and
swelling; (2) achieve full AROM; (3) achieve functional hand strength and endurance; (4) maximize activity tolerance in ADLs. Home therapy included a graded application of exercises and ADLs that were carefully monitored for exacerbation of symptoms. Gentle AROM of the entire upper extremity was initiated early to prevent joint stiffness in the "uninvolved" areas and to increase elbow extension. In ranging of the elbow to gain extension, it was important to consider what structures were being placed on stretch. As previously mentioned, biceps shortening was suspected, thus resistant to elbow exten-
sion. Since the ulnar nerve had been transposed anteriorly, and it is no longer stressed with elbow flexion, it is now lengthened by elbow extension. Peripheral nerves react to longitudinal stresses by the increased resultant intraneural pressures. These pressures may produce mini-traction lesions causing nerve irritation and excitation. IS Therefore, gentle procedure and monitoring for nerve reaction (changes in sensibility, pain and paresthesias) was important to avoid further neural damage. Paraffin baths and hot packs to the elbow, especially the biceps, in conjunction with therapeutic exercises, were used to induce biceps relaxation and soft tissue extensibility (to increase elbow extension). Heat has a direct effect on the gamma fibers of the muscle spindles. The spindle activity and sensibility to stretch are reduced with heat application. Relaxation may also be induced due to reflexes negotiated through the thermal receptors. The specific mechanism of these reactions is not fully understood. At increased temperatures, tendons are apparently able to withstand greater extensibility when combined with tensile forces .3o Heat also acts on the free nerve endings and peripheral nerve fibers to increase the pain threshold. Exercises were approached cautiously to avoid tissue damage that would be undetectable because of this analgesic effect. The physiological responses to heat and cold modalities are not clearly defined and research is sometimes contradictory, especially concerning the physiological effects of cold. Clinically, however, observations indicate uses for both modalities in certain pathologic conditions. 31 ,35 In the case of chronic inflammatory problems, authors have recommended heat to increase blood flow and metabolism, associated with the simultaneous vasodilation that heat causes. This increases the process of phagocytosis, infiltration of leukocytes, antibodies, flushing of metabolics, and nutrient and oxygen delivery.31,36 Cold therapy or cryotherapy has also been recommended for these problems. Its application is thought to produce a "hunting reaction" or alternating vasoconstriction and vasodilation, which theoretically would slow the inflammatory reaction, then assist in "flushing" the area by the increased blood flow to clear the metabolites. 2o,33 It has not been clearly shown, as of yet, that cold does indeed induce vasodilation.2o•33 Most authors do agree, however, that heat will cause an increase in blood flow (vasodilation). It seems that patient responses to these modalities administered on a trial basis are often the determinant of the best treatment. 3S Conservative treatment for the de Quervain's disease occurred concurrently with the rehabilitation efforts. The pathology of this disease involves inflammation of the tendon sheath and its associated vaginale ligament. Most authorities agree that the tendons present with only slight thickening unless the condition is chronic. With this, the sheath may become 3-4 times its normal size and either brown or red in color. Adhesions may occur between the synovium and the tendon. To prevent this, AROM of the thumb was encourgaged. The tendons may also be July-September 1988
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thin, flattened and have granulation tissue that may produce connecting fibrous bands. In the local inflammation area, the tendons may be constricted but remain normal elsewhereP Heat was used at the proximal upper extremity for the reasons previously addressed. Trial applications of heat and cold were attempted to reduce the inflammatory response of the stenosing de Quervain's tenosynovitis. There were subjective complaints of stiffness and irritation with cold, and heat produced greater relief of pain during AROM.
It has not been clearly shown, as of
yet, that cold does indeed induce vasodilation.
Treatment of de Quervain's is designed to control and reduce the inflammatory response through immobilization, anti-inflammatory medication, and corticosteroid injection. This patient was treated in the above fashion, and immobilization was achieved by fabrication of a static thumb spica type splint. The splint was fabricated on 4/17/87,4 weeks into therapy, because with the gradual progression of left upper extremity activity, the de Quervain's symptoms were exacerbated. The splint was designed to specifically immobilize the involved APL and EPB. Care was taken in the fabrication and utilization of this splint to avoid acute compressive neuropathy of the ulnar digital nerve of the thumb. This has been a complication with this splint in two reported cases by Rayan and O'Donoghue. Symptoms include numbness of the ulnar aspect of the thumb and pain at the level of the volar aspect of the first MCP jOint. If detected early, the nerve lesion is reversible and splint adjustments to correct the pressure areas are usually successfu1. 38 Iontophoresis was also administered to introduce dexamethasone sodium phosphate into the inflamed region. This medication is a long-acting synthetic glucocorticoid compound that has a potent anti-inflammatory effect.39 The Phoresor unit was used because of its ease of set up and built-in safety features. It supplies a DC current that is adjustable from 0-5 milliamperes. The built-in safety factor ensures a constant current control, because the unit shuts off when skin impedances are lower than 500 ohms or greater than 100 kilohms.40 Ions in solution are transferred through the intact skin via electrical potential using bipolar electrodes. The positive ions are carried through at the positive treatment electrode. DC current is required because of its continuous, undirectional flow and since it has only one charge. This causes the ions to migrate according to their electrical charge. 4o• 4 1 Heat was used over the treatment area (first dorsal compartment) prior to the iontophoresis in order to reduce the skin impedance. Normal human skin has a high degree of skin impedance, approximately 3000 ohms, primarily due to its relative lack of water 178
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content. Since heat increases blood flow, it hydrates the skin which allows improved conductivity. Glass et a1. have demonstrated that dexamethasone (with 4% lidocaine HCL) was iontophoresed into tissue overlying the elbow, shoulder, hip, knee and ankle joints of Rhesus monkeys. The medication transferred into all tissue layers underlying the electrodes down to and including tendinous and cartilaginous tissues. This effectively delivered a therapeutic dosage at sufficient tissue depthsY In a clinical investigation, Harris reported that 75% of the patients treated with this method of iontophoresis for musculoskeletal inflammation had excellent to good resultS.40 Conservative treatment, including the above procedures, did not yield satisfactory long-term results after 4 months time, and surgical intervention is pending. Surgical correction is often viewed as a simple procedureY Arons has recently emphasized the complexity of this diagnOSis and its correction. In 11 preoperative cases of de Quervain's disease, 6 patients had associated general tendonitis. Of the 5 cases with isolated de Quervain's, 2 responded successfully to conservative treatment using injection, splinting, anti-inflammatories and occupational therapy lasting for 3 months. Of the 6 cases with generalized tendonitis, 3 eventually required surgical releaseY In the elbow, AROM achieved normal status after 2 weeks of therapy. Gentle strengthening, endurance and activity training was tolerated fairly well except at the dorsal thumb area. The splint was used during exercises for tendon protection. Exercises and simulated activities were graded and monitored in time, resistance, and repetitions as measured on the BTE Work Simulator.
Surgical correction is often viewed as a simple procedure. This program and the home program encouraged both anaerobic and aerobic exercises. Biopsies of tissue have revealed a relationship between excess lactic acid and glycogen depletion to tendonitisY Aerobic exercise causes oxygen consumption to increase and accumulation of lactic acid begins at a higher rate of work than before training. Tolerable levels of lactic acid and oxygen debt are raised with anaerobic exercise also, but this is not well understood. 44 ,45 Endurance training is also believed to increase glycogen storage. IO Aerobics were encouraged without the use of the left upper extremity to avoid symptomatic flareups, Heat, AROM and gentle stretching preceded controlled PREs to increase muscle temperature. This increase in temperature is proposed to assist in efficiency, speed and strength of muscle contraction. 46 It should be noted, however, that some authors recommend cold versus heat prior to therapeutic exercises because of its "efficiency effect." This phenomenon is related to the effects of heat and cold on local
metabolism. Heat and exercise both increase metabolism and cold decreases metabolism. With a decrease in metabolism (cold therapy), there is less of a demand on the muscles for nutrients, etc. Therefore, the muscles handle the effects of exercise more efficiently, prolonging the fatigue point. Since heat increases metabolism, as does exercise, the fatigue point is reached sooner because of the higher demands placed upon the muscles. 33 This leads to an interesting question specific to soft tissue inflammatory problems. What is the physiological end result of enhancing the activity tolerance with heat and/or cold? Does this lead to improved strength and endurance without delayed exacerbation of symptoms? Does this lead to further tissue damage because of continued mechanical stresses upon the tendons, nerves, etc.? Regardless of the effects of heat or cold, careful monitoring of the patient's immediate and delayed response to exercise is the only method for determining how to structure therapy. After 3 months of therapy, the patient was tolerating I-hour sessions of slow-rate, low resistance/ repetition activity. Left grip strength increased from 22 lbs to 47 lbs after 3 months of treatment and activity tolerance improved allowing greater functional status. This, however, fluctuated greatly due to generalized complaints of pain resulting from the increased activity.
Regardless of the effects of heat or cold, careful monitoring of the patient's immediate and delayed response to exercise is the only method for determining how to structure therapy. Ergonomic principles were applied to ADLs to increase the patient's functional abilities. Risk factors associated with cumulative trauma are repetitive and forceful exertion, mechanical stresses, certain postures, fibration and low temperatures. Wrist flexion and extension are associated with tenosynovitis of the flexor and extensor tendons and CTS. Ulnar and radial deviation are associated with de Quervain's disease. 47 ,48 Therefore, ADL tasks were modified to maintain the wrist in neutral. The thumb spica splint allowed for performance of most ADLs in this position, but tool and job redesign improved posture and reduced forceful exertions and mechanical stress. Examples of tools that were used are long-handle jar opener, pistol-shaped cutting knife, adapted parring board, and built-up handles for writing instruments.
Treatment Outcome Four months of therapy yielded full AROM and good left upper extremity strength. Activity tolerance remained poor, limited by exacerbations of pain and
tenderness about the first dorsal compartment, ulnar carpal area, and occasionally the lateral epicondyle area of the elbow. The patient appears to have responded to the surgeries and therapy with fair resolution of symptoms. Low-grade problems continued to limit function, and tenovaginotomy of the left first dorsal compartment was imminent. If indeed the patient could be stabilized medically, a work-capacity evaluation would be necessary to determine what the residual functional abilities are. Job and tool modifications would be extremely important in considering any occupational role for this patient. Ergonomically designed check stands have been developed but not yet sufficiently studied.49 Despite this, the prognosis for return to her previous occupation is extremely poor and would seem only to invite further problems.
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