Frozen shoulder diabetic The natural history of adhesive capsulitis and its clinical course is divided into three stages: the painful stage, the adhesive stage and the recovery stage. The painful stage involves gradually increasing pain and stiffness and lasts between three and eight months. Muscle spasms in the trapezius also commonly occur during this phase. A history of a minor strain or injury before onset may be noted; however, it is unclear whether the initial strain is an independent phenomenon or an early awareness of the pain associated with the onset of adhesive capsulitis. Commonly, patients note a decreased ability to reach behind the back when fastening a garment or removing a wallet from a back trouser pocket. The initial discomfort is described by many patients as a generalized shoulder ache with difficulty pinpointing the exact location of the discomfort. The pain may radiate both proximally and distally, is aggravated by movement and alleviated with rest. Sleep may be interrupted if the patient rolls on the involved shoulder. This condition progresses to one of severe pain accompanied by stiffness and decreased range of motion. The stiffening increases to the point where the natural arm swing that accompanies normal gait is lost. The patient tries to compensate for this loss by using other muscles and increasing scapular rotation to accomplish various activities. This places additional strain on the other muscle groups, leaving them overworked and tender. The physical examination during the painful stage of adhesive capsulitis may reveal muscle spasm and diffuse tenderness about the glenohumeral joint and the deltoid muscle. An area of pinpoint tenderness is seldom found. With disease progression and in long-standing cases, disuse atrophy of the shoulder girdle may result. Passive and active range of motion in all planes of shoulder movement are lost. This global loss of motion is the primary factor distinguishing adhesive capsulitis from many of the conditions associated with secondary adhesive capsulitis. The second stage, the adhesive stage, involves increasing stiffness with diminishing pain. Pain decreases at night, and discomfort occurs only at the extremes of motion, although movement is dramatically decreased. This stage lasts four to six months.
The final stage, called the recovery stage, lasts from one to three months and is characterized by minimal pain but severe restriction of movement. This latter stage is self-limiting, with a gradual and spontaneous increase in range of motion. Complete recovery, however, is infrequent. The external rotation range of motion improves first, followed by abduction and internal rotation. Short recovery periods may have associated bouts of pain before each phase of improvement. Although approximately 7 to 15 percent of patients permanently lose their full range of motion, only a few have a true functional disability. The pathophysiology of primary and secondary adhesive capsulitis remains elusive. It is believed that in patients with diabetes, associated microvascular disease causes abnormal collagen repair, which predisposes them to adhesive capsulitis. Occasionally, fibrous strands are seen traversing the joint space. Patients with diabetes often present with fibrosis elsewhere (i.e., Dupuytren's contracture). Trauma, the associated transient inflammatory state with granulation tissue, and eventual fibrous adhesions and thickening of the capsule may cause adhesive capsulitis. Immobilization is an intriguing possible etiologic factor for adhesive capulitis in patients with stroke or postmyocardial infarction; however, prolonged casting studies have not supported this theory. Neuropathic mechanisms, including suprascapular nerve compression, have been considered, but none accounts for most cases of adhesive capsulitis. Although strong evidence suggests an association among these neuropathic and vascular conditions and adhesive capsulitis, no pathophysiologic mechanisms are convincing. Theories regarding autoimmune reaction to tendon degeneration have led to immunologic investigations. Although random and inconsistent, the inflammatory indexes measured (e.g., erythrocyte sedimentation rate) were partially supported because they were slightly elevated and improved as the disease improved. Synovial fluid offers no clues to the etiology of adhesive capsulitis. Biopsies of the synovial lining have revealed increased fibroblasts and vascular dilatation, but few or no perivascular inflammatory cells.
The diagnosis of adhesive capsulitis is primarily clinical. In general, the scapular rotation occurs at 60 degrees with active abduction of the shoulder. In an unaffected person, the shoulder can be passively abducted to 90 degrees even when the physician holds the scapula. Inability to achieve the 90-degree arc with scapular stabilization is the clue to the diagnosis in both primary and secondary adhesive capsulitis. It is important to assure that the scapula is secured when assessing passive range of motion. Radiographs are important in assessing restricted range of motion in the diagnosis of secondary adhesive capsulitis. Osteoarthritis, fracture, avascular necrosis, crystalline arthropathy, calcific tendinitis and neoplasm may be detected on plain radiographs. Radiographs of patients with early adhesive capsulitis are normal. Later changes sometimes show osteopenia, cyst-like changes in the humeral head and joint-space narrowing. A chest radiograph may be useful in establishing the diagnosis of tuberculosis or malignancy-associated adhesive capsulitis.
Arthrography, although invasive, is useful to document decreased joint volume. The unaffected shoulder will accommodate 20 to 30 mL of contrast material, whereas the shoulder with adhesive capsulitis will only be able to hold 5 to 10 mL. Arthrograms may reveal an irregularity of the capsular insertion at the anatomic humeral neck and a decreased axillary fold. From 10 to 30 percent of patients are found to have a demonstrable rotator cuff tear at arthrography, yet a significant number also have normal findings. Arthrography should be reserved for use in patients whose diagnosis remains uncertain following physical examination and radiography. Arthroscopy may have a limited role in the diagnosis of other diseases that mimic adhesive capsulitis, but it does not aid in the diagnosis of adhesive capsulitis itself and is not used frequently. The usefulness of magnetic resonance imaging (MRI) in the diagnosis of adhesive capsulitis has also been evaluated. Studies revealed that some changes seen on MRI are specific and sensitive for adhesive capsulitis; however, the decrease in joint fluid is not appreciated. MRI may become a useful, noninvasive way to document capsular thickening, but further studies are needed. In most cases, the diagnosis of adhesive capsulitis is clinical; however, if any imaging is necessary, arthrography remains the procedure of choice. If there are no underlying illnesses, laboratory investigations will be unremarkable.
Some systemic diseases are known to be associated with adhesive capsulitis and should be considered in patients with restricted shoulder movement. Trauma, avascular necrosis and osteoarthritis may predispose a patient to secondary adhesive capsulitis. Systemic diseases such as diabetes, hyperthyroidism and rheumatoid arthritis are also associated with secondary adhesive capsulitis and must be considered in a patient with limited range of motion of the shoulder. Patients often have referred shoulder pain from the heart, neck, diaphragm, liver or spleen. It is unclear why patients with a history of myocardial infarctions, cerebrovascular accidents and chronic pulmonary diseases, such as tuberculosis and pulmonary cancer, are also predisposed to adhesive capsulitis. Patients with reflex sympathetic dystrophy (related to some of these events) may have restricted range of motion of the shoulder that becomes permanent in the later stages of disease. Some patients may also develop reflex sympathetic dystrophy as a result of primary or secondary adhesive capsulitis.
Although studies comparing various treatment modalities for adhesive capsulitis reveal that no specific treatment method has any long-term advantage, early and accurate diagnosis is imperative. In patients with adhesive capsulitis, the goal of treatment is pain reduction and preservation of shoulder mobility. The first step is preventing secondary adhesive capsulitis by definitively addressing underlying causes. Avoiding prolonged immobilization in patients who may be predisposed to adhesive capsulitis is crucial. Treatment of a shoulder injury of any etiology requires early range of motion therapy to reduce muscle spasm while maintaining full range of motion. Heat, cold and other modalities that relax the muscles may help preserve range of motion. Adequate analgesia is necessary for successful treatment in this phase. Vigorous and forceful exercises are contraindicated because of the pain associated with the rupture of adhesions. Also, the more painful treatment regimens have been found to be associated with a higher level of noncompliance. Constant encouragement is necessary for patients with adhesive capsulitis, since resolution may be slow. Gradually increasing the range of motion of the shoulder will decrease the pain associated with the disease. Physical therapy done at home, including Codman exercises, "climbing the wall" or placing things up higher to encourage reaching, is cost effective but requires a long rehabilitative process.
Nonsteroidal anti-inflammatory drugs (NSAIDs) help to relieve pain and inflammation. Analgesics are indicated when NSAIDs are contraindicated. Muscle relaxants are helpful in the early stages of the disease when spasm is predominant. Low-dose antidepressant medications (e.g., 10 mg of amitriptyline [Elavil] taken at night) may help to avoid a cycle of sleep disturbance leading to a chronic pain syndrome and fibromyalgia. Intra-articular corticosteroid injections are used in affected patients to relieve pain and permit a more vigorous physical therapy routine. The injection site is located 1 cm distal and 1 cm lateral to the coracoid process. Full external rotation of the humerus with the elbow held in a relaxed position at the patient's side helps open up the space, which is difficult to enter if contracted by adhesive capsulitis. The usual dosage is 15 to 40 mg of triamcinolone acetonide (Kenalog) or another depot steroid, such as Depomedrol, with 1 mL of 1 percent lidocaine. Although intra-articular corticosteroids are frequently used, no long-term benefits from this therapy (i.e., shorter time to full recovery) have been proved. Some clinicians advocate simultaneous intra-articular and bursal injections for pain relief before beginning physical therapy. Oral corticosteroids are not helpful. Severe adhesive capsulitis diagnosed in the later stages is more difficult to manage. The above treatments, useful on occasion, are not always successful. Surgical intervention should be considered when physical therapy and injections fail (no improvement after three months of therapy). Manipulation under anesthesia to break up the adhesions is reserved for use in the adhesive stage. During this procedure, the joint capsule and subscapular muscles are ruptured, and aggressive rehabilitation is employed to restore and maintain range of motion of the shoulder. Patients undergoing manipulation may receive an intra-articular corticosteroid injection after the procedure and begin physical therapy the day of the procedure. Icing is often helpful.
Another option is the administration of an interscalene block before the manipulation; this renders the patient pain free and allows for the immediate start of physical therapy. Risks associated with manipulation under anesthesia include humeral fracture, dislocation and rotator cuff rupture. Contraindications to manipulation include severe osteopenia, a history of fracture or dislocation, or recurrence following adequate manipulation. For patients with loss of motion refractory to closed manipulation, arthroscopic capsular release has been shown to improve motion with minimal operative morbidity. In this study, most patients had a marked decrease in pain, and functional improvement. Some investigators demonstrated that arthroscopic release was helpful in patients with diabetes-associated adhesive capsulitis who were refractory to conservative measures. Thirteen of the patients studied had no pain, full range of motion and full function after surgical release. Interestingly, a marked discrepancy exists between the patient's subjective awareness of residual range deficit and the measurable (objective) restrictions. Many patients with range deficits regard their recovery as complete. This difference in subjective and objective assessment of recovery, plus the variation and confusion in the definitions of adhesive capsulitis, may account for the conflicting reports of prognosis and therapy.
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