Cumulative Trauma Disorders (CTDs) have become a matter of urgent ergonomic concern in the 1980's and 1990's. They represent nearly half of the occupational illness reported in the annual U.S. Bureau of Labor Statistic survey .

Sufficient evidence from early medical reports show that injuries due to repetitive stresses are not a new phenomenon. Names such as bricklayer's shoulder, carpenters elbow, and stichers wrist represent a sampling of the names used to label symptoms describing CTD.

Today, with the proliferation of assembly-line techniques, the ever-increasing tempo of production, and the widespread use of vibrating and air tools, CTD have become a modern fact of life. Recent reports describe new evidence of CTD among such diverse groups as retail clerks, computer keyboard operators, and assembly-line workers .

Three major occupational risk factors leading to CTD are repetitive motion, forceful exertion with limited opportunity for recovery, and poor or awkward postures. Static loading has also been observed to increase the risk of CTD. Static loading occurs when muscles are required to generate tension without movement. Static work is not very effecient and causes the, muscles to rapidly fatique. Vibration is another variable which has been implicated in the development of CTD. Vibration causes constriction of blood vessels in the fingers as well as numbness and swelling of the hand tissues. In general, these occupational risk factors and their subsequent interactions, can lead to a reduction in grip strength and range of motion. As the differential between task demands and human capacities increases, the associated risk for the development of CTD rises.

The term CTD has been used to refer to those musculosketal impairments that appear to be work-related and tend to be chronic. Upper extremity CTD are categorized in three major groups: tendon disorders, neurovascular disorders, and nerve disorders. Kienbock's disease, on the other hand, has been documented in the workplace, and has a similar etiology, but due to current anatomic classifications cannot be considered a CTD because it does not fit into one of the established categories. With this in mind, the present article makes a critical examination of risk factors, diagnosis and treatment, with the purpose of providing physicians, engineers, and designers with information to reduce the risk of workers developing this potentially debilitating disease. Furthermore, additional support will be accumulated and combined with Part I of this article with the intent of introducing into the literature a new category of upper extremity CTD: Bone Disorders.

RISK FACTORS

Different predisposed risk factors have been implicated in the development of this disease. The most commonly cited factors are the interruption of the blood supply to the lunate, negative ulnar variance, and the workplace environment. These factors, as well as how to minimize the risk for developing this disease will be discussed in the following paragraphs. Stahl believed that in a lunate with an already tenuous blood 5upply, traumatic compression fracture leads to avascular necrosis. Lee found three vascular patterns in lunates from cadavers: a single vessel, either volar or dorsal, supplying the entire bone; several vessels at both volar and dorsal surfaces of the lunate without central anastomosis; and several vessels at both volar and dorsal surfaces of the lunate with central anastomosis. Therefore according to Lee, patients with the former two patterns are at a greater risk for developing Kinbock’s disease.

,In fresh specimens, Gelberman and associates also studied the extraosseous and intraosseous blood supply of the lunate. They found that the intraosseous blood supply consisted of three patterns Y in 59 percent, I in 31 percent, and X in 10 percent, with dorsal and Volar anastomosis just distal to the center of the lunate . Evaluation of the terminal vessels in the lunate allowed Gelberman and associates to conclude that the proximal subchondral bone, adjacent to the radial articular surface, was least vascular. Because of the rich extraosseous blood supply, they discounted the theory held by some that interruption of vessels entering a single pole of the lunate caused avasucularity. Based on the work, Gelberman and coworkers suggested that it is intraosseous disruption of vascularity, owing to repeated trauma with compression fracture, that causes Kienbock's disease.

Negative u1nar variance as a risk factor has received considerable attention from the research community. In 1928, Hulten noted that a short ulnar was present in 78 percent of his patients with Kienbock's disease, whereas only 23 percent of normal patients had a short ulna. He called this condition ulnar minus variant. Since the condition was first discovered, many other authors have confirmed negative ulnar variance in their patients Kienbock's disease.

Theoretically, a short ulnar variance, relative to the distal articular surface of the radius, causes increased shear and compressive loads on the lunate. Elaborate studies by Werner and associates proved that altered load transmission through the radial carpal joint with ulnar minus variance predisposes the radiolunate articulation to increase loads. This is thought to be a contributing factor in the development of Kienbock's disease

Until recently, Hulten's findings have been confirmed by many investigators but has been questioned by others. To date, this controversy has not been resolved. To make matters more complicated accurate measurement of ulnar variance is not simple. As pointed out by Epner et al. and Palmer et al., the apparent variance changes with the position of the arm.

With this in mind, Palmer and associates further standardized the method for determining ulnar variance. They found the position of the distal ulna, in relation to the distal radial surface changes with varying degrees of forearm rotation and that the change in variance was least with the elbow flexed 90 degrees. The standard view recommended is a posteroanterior wrist radiograph obtained with the patient's shoulder abducted 90 degrees, the elbow flexed 90 degrees, and the forearm in neutral rotation. The importance of accurate measurement of ulnar variance is highlighted by the recent gain in popularity of ulnar lengthening and radial shortening techniques to treat Kienbock's disease.

It appears the effect of aging on ulnar variance supports the theory that negative ulnar variance is a predisposed risk factor in the development of this disease. It has been shown by -several researchers that ulnar variance increases with age. The cause of the increase of ulnar variance with aging is unknown, but it might be due to shortening of the radius because the force of the forearm muscle is mainly transferred to the radius. This can offer a reasonable explanation of why the young are more susceptible to developing Kienbock's disease.

Although Kienbock's disease mostly affects young, active males, usually in the 3rd or 4th decade of life, Yoshida et al. reported that of a 127 cases reviewed, 15 patients were found with aged onset. Among these 15 cases women predominated. This is a striking difference from Kienbock's disease in young adults. Other findings reported from that study revealed that symptoms in elderly are usually not so severe and conservative treatment is typically effective. It was also shown that the degree of negative ulnar variance was not as great as in the young effected population. Several other researchers have shown that the degree of negative ulnar variance is greater in males than in females. This supports the findings that males are more susceptible.

Besides the anatomical and biological risk factors, the workplace also has been implicated as a contributing factor to the advancement of this disease. Occupations which require the use of pneumatic tools such as rivet guns and hammers are at particular risk for development of Kienbock's disease. The increased impact loading upon the wrist is thought to be a catalyst for the disruption of the blood supply to the lunate ultimately leading to its demise. As previously mentioned, the etiology of Kienbock's disease is thought to be either repeated minimal trauma or by a single acute epidose. The underlying theme behind the theory of repeated minimal trauma is repetition coupled with force. Both of these established CTD risk factors have been recognized as potentially harmful elements to the musculoskeletal system. The other proposed etiology, a single acute episode, indicates that force may be of greater importance. In either case, ergonomist must evaluate these factors carefully when designing/redesigning the workplace.

Wrist posture has been indirectly implied as another possible risk factor for the development of Kienbock's disease. In two separate studies, individuals with cerebral palsy were evaluated because they have high muscle tone, which is essentially repeated trauma, and the radiocarpal joint is constantly exposed to considerably higher pressure than what is found in normal individuals. Rooker and Goodfellow found five cases of Kienbock's disease in a group of 53 adults with cerebral palsy. An abnormally flexed wrist posture was the common feature in all five cases. This suggested to them that this extreme posture compromised the blood supply to the lunate and was considered a contributing factor to the development of Kienbock's disease. In a more recent study, Joji et al. reported that there is increased pressure between the radius and lunate due to the dynamic conditions of excessive muscle tone characteristics of cerebral palsy. The resting postures of their subjects was predominantly ulnar flexion with one case of' volar (palmar) flexion. Joji and associates went on to conclude that it was unlikely that volar flexion was the cause of Kienbock's disease. However, in both studies a resting deviated wrist posture was observed. It is therefore possible that deviated wrist postures, incorporated with other risk factors could lead to the development of Kienbock's disease.

I It appears that the dominate hand of the worker is at the greatest risk for developing Kienbock's disease. This finding is consistent with the proposed etiology. In fact, the majority of the time Kienbock's disease is unilateral .

Like many other CTD, Kienbock's disease can be treated by various medical interventions. Many of these interventions will relieve symptoms but if the individual is returned to similar activities it is possible to see a reoccurrence of Kienbock's disease.

DIAGNOSIS

Kienbock's disease is an isolated disorder of the lunate diagnosed from characteristic roentgenographic density changes, often accompanied by fracture lines, fragmentations, and progressive collapse. It should be distinguished from other causes of wrist pain and swelling, particularly in the early stages, when the roentgenograms may be negative. Disorders to be ruled out include rheumatoid arthritis, post-traumatic arthritis, synovial-based inflammatory disease, acute fracture, carpal instability, and ulnar abutment syndromes. The radiographic hallmark of increased density typically seen in Kienbock's disease should be distinguished from transient vascular compromise.

In more severe Kienbock's disease, as the lunate collapses, there is proximal migration of the capitate, widening of the proximal carpal row, and, frequently, rotation of the scaphoid, causing it to appear foreshortened on anteroposterior radiographs. The fore shortening has been referred to as the "ring". Tomograms may be helpful to identify linear fractures or localized area of sclerosis not readily apparent on plain radiographs. Scintigraphic imaging may be of benefit in patients who have otherwise negative radiographs.

Rarely has Kienbock's disease been reported in association with other conditions. There are case reports of Kienbock's disease in sickle cell disease , carpal coalition and gout. One article identified streptococcal infection in several cases and attempted to cite this as the causative organism.

Due to the classic CTD symptoms (wrist pain, limited range of motion and decreased grip strength) Kienbock's disease exhibits, it is not uncommon, in its early stages (Stage 1), to see a diagnosis of Carpal Tunnel Syndrome (CTS). The erroneous diagnosis may be largely due to the normal appearance of the screening x-rays as well as the notoriety and frequency of CTS among the working population. This problem could be possibly avoided by obtaining an MRI or bone scan to check for density changes typically seen in Kienbock's disease. Diagnosis of CTS is made through obtaining medical history, physical examination (range of motion, grip strength), and substantiated by clinical test (electromyography, nerve conduction velocity, vibration threshold, and cold provocation testing). Since a decrease in range of motion and grip strength associated 'With wrist pain are common to both diseases and the substantial cost to administer a MRI or bone scan, it is understandable how errors are made. However, careful evaluation of the injured's medical and work history may provide additional information needed to make the correct diagnosis while keeping the costs to a minimum.

STAGES OF KIENBOCK'S DISEASE

Once the diagnosis'- of Kienbock's disease is established, determination of the degree of involvement should be made in order to assist in guiding one through the maze of treatment options. Plaster immobilization for two to three weeks in uncertain cases will usually bring out the diagnosis by relative diffuse osteoporosis of the adjacent carpal bones.

Stahl's original classification has been modified by Lichtman and coworkers and consists of four stages of Kienbock's disease.

Stage 1. Roentgenograms are normal except for the possibility of either a linear or a compression fracture. Unless a compression fracture is visible, this stage is clinically indistinguishable from a wrist sprain. Scintigraphic and magnetic resonance imaging (MRI) may be helpful.

Stage IL There are defined density changes apparent in the lunate relative to the other carpal bones; however, the size, shape, and anatomic relationship of the, bones are not significantly altered. Fracture lines may be noted. Later in this stage, anteroposterior roentgenograms show loss of height on the radial side of the lunate. The patient exhibits symptoms of recurrent pain, swelling, tenderness in the wrist.

Stage III The entire lunate has collapsed in the frontal plane and is elongated in the sagittal plane. The capitate migrates proximally. Scapholunate dissociation, rotation of the scaphoid (the ring sign), and ulnar deviation of the triquetrum. may be seen on the anteroposterior roentgenograms. To better assess the degree of collapse in Stage III, it is helpful to establish the carpal height ratio. Carpal height is the distance between the base of the third metacarpal and the distal radial articular surface, as determined on a posteroanterior roentgenogram of the wrist; the carpal height ratio is defined as the carpal height divided by the length of the third metacarpal. in normal persons, this ratio is 0.54+0.03, outside of this range is considered not normal. Knowledge of the carpal height ratio is becoming more important, since the factors determining results of treatment in Stage III appear to be tied to the degree of collapse. Stage III into Stage IIIA (lunate collapse without fixed scaphoid rotation) and stage IIIB (lunate collapse with fixed scaphoid rotation and other secondary derangements). Clinically, patients in these stages have the same symptoms as those in Stage 11 but with an increased level of wrist stiffness.

Stage IV. All findings characteristic of stage III are present as well as generalized degenerative changes in the carpus.
TREATMENT

One problem in devising effective treatment for patients with Kienbock's disease is that by the time the diagnosis has been made as determined by plain radiographs, there is usually irreversible damage to the lunate. Current methods of treatment include immobilization, revascularization, ulnar lengthening or radial shortening, simple excision, silicone replacement arthroplasty (SRA), soft tissue replacement arthroplasty, limited intercarpal fusion, or salvage procedures. Table 1 list the various treatment modalities for Kienbock's disease, along with the stage for which the procedure is recommended.

Table 1. Treatment modalities recommended for stages of Kienbock's disease

Treatment        Stage
Immobilization        I
Revascularization        II, IIIA
Ulnar lengthening or radial shortening        II, IIIA
Silicone replacement arthroplasty (SRA)*        IIIA
Excision + autogenous tendon graft       IIIA
Capitohamate fusion + SRA       IIIA, B
Triscaphe fusion + SRA        IIIB
Limited intercarpal fusion       IIIB, IV
Salvage (proximal row carpectomy, wrist arthrodesis)       IV

*Presently this method has fallen out of favour: Titanium implant options are being explored.

Impairment ratings for Kienbock's disease and for other upper extremity injuries are based on criteria established by the American Medical Association (AMA). Although a 4th edition of Guides to the Evaluation of Permanent Impairment has been released, Kansas state law accepts the 3rd edition as its method of determining impairment ratings. The methods for evaluating impairments of the upper extremity may be considered anatomic, cosmetic, or functional. A combination of these methods is necessary to show an accurate profile of the injured. Impairment ratings for Kienbock's disease can range from 0 (if successfully diagnosed and treated in its early stage) to 88% of total impairment of the upper extremity or 53% impairment of the whole person (AMA, 1988). Although there are no current studies to determine the cost of this injury in terms of lost work time, lost productivity, and worker compensation expenditures, it is interesting to note that CTS, by comparison, has been documented to cost a large mid-western manufacturing facility $15,000 and $18,000 (15) in worker compensation expenditures alone. Impairment ratings for CTS generally can range from 1 to 30% of the upper extremity or 18% impairment of the whole person (AMA, 1988). All of these numbers assume that maximum medical improvement has been achieved and there are no coexisting conditions. The potential for loss productivity, loss work time and worker compensation expenditures appears to warrant further investigations into the area of risk factor identification and prevention.

ERGONOMIC INTERVENTION

With the difficulties in identifying Kienbock's disease, as well as the potential cost associated with it, ergonomic intervention could be an advantageous. tool in minimizing the risk of workers developing this potentially debilitating disease. In the past, ergonomic intervention for other CTD has been shown to increase productivity, improve safety and health, increase job satisfaction, increase work quality, lower worker turn over, lower lost time at work, lower worker compensation claims, and decrease the risk of OSHA fines. It is believed that intervention for protection of workers developing Kienbock's disease will yield similar results. A three pronged intervention in the form of engineering controls, administration controls, and personal protection equipment is recommended.

Engineering controls typically focus on redesigning workstations, jobs/tasks, and tools. In the case of Kienbock's disease, force and repetition are of particular concern. Mechanization and/or automatization of tasks requiring constant impact loading could decrease the risk of the disease developing. Redesigning tools and handles to reduce impact loading such as incorporating damping devices, as well as decrease the over all weight of the tool may also help reduce the risk. Providing employees with appropriate worksurfaces to minimize deviated wrist postures and appropriate hand tools to match the employees capacities will also help reduce the risk.

Administrative controls refer to those actions taken by the management or medical staff to limit the potential harmful effects of a physically stressful job on individual workers. In this case, limiting the workers exposure time to high frequency, impact loading task *on the wrist will aid in the reduction of risk. This might be accomplished by job rotation. The principle of job rotation is to alleviate physical fatigue and stress of a particular set of muscles and tendons by rotating employees among other jobs that use different muscles-tendon groups (OSHA, 1990). In fact it is suggested that restructuring of the job sequence be performed instead of arbitiary job rotation. Work rest cycles should be structured to provide adequate rest for the hand arm system to recover from the highly stressful situation. Another method used is training employees to perform task correctly as well as recognize symptoms can also aid in the reduction of risk.

Providing personal protective equipment (PPE) can also help aid in the reduction of risk. Since the reduction of repetitive blows to the hand is an important objective in the reduction of Kienbock's disease, it seems reasonable that providing workers with padded glove will help. This should not be done blindly for the parameters of coupling (the interface between the hand and tool handle) will be changed and must therefore be checked to be sure no anthropometric mismatches occur.

Ergonomic intervention in the past has aided many companies in increasing their product quality and productivity while reducing their worker compensation cost and the same is expected in the case of Kienbock's disease.

SUMMARY

In summary acute fracture repeated minor trauma have all been implicated in the etiology of Kienbock's disease. The symptoms include wrist pain, limited range of motion, and decreased grip strength.

Potential anatomical and biological risk factors for this disease include negative ulnar variance, prejudice blood supply to the lunate, age, and gender. Possible risk factors associated with the workplace include deviated wrist posture, repetition and force. The diagnosis is made from characteristic changes seen in the lunate on radiographs of the wrist. The severity of the disease can be categorized by staging the degree of involvement. Carefully scrutinized work histories could possible aid physicians in a reduction in the misdiagnosis of Kienbock's disease as CTD. The treatment of Kienbock's disease begins with conservative measures that include immobilization and analgesics or anti-inflammatory medication or both. If symptoms are not relieved, then, based on the degree of involvement, several surgical options exists that can provide relief. It is possible however, for symptoms to return if work structure is not modified. If progression of Kienbock's disease is not terminated and treated, it is possible for individuals to receive impairment ratings as high as 88% of the upper extremity. This could translate to a considerable amount of lost work time, lost productivity and worker compensation expense. Since ergonomic intervention has decreased the risk of development of other CTD, it is believed that a well structured ergonomic intervention program will have similar success with Kienbock's disease.

It is evident by the etiology and the risk factors, that Kienbock's disease should be included in the realm of CTD. Since this disease does not fit into one of the classification of CTD it is evident a new category should be introduced: bone disorders. As the workplace environment continues to change it is possible to see other bone disorders arise in the future. Epidemiological studies need to be conducted to identify other work related risk factors as 'well as the projected proportion of the population exposed to this disease. Early identification and recognition of the symptoms of Kienbock's disease can aid in the protection of Workers as well as decrease worker compensation expenditures. This means an enhancement in the quality of life of the worker and improvement in the productivity of the organization.

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