ADHESIVE CAPSULITIS

ADHESIVE CAPSULITIS

Adhesive capsulitis, most commonly referred to as frozen shoulder (FS), is an idiopathic disease with 2 principal characteristics: pain and contracture.

PAIN

Shoulder pain associated with FS is progressive and initially felt mostly at night or when the shoulder is moved close to the end of its range of motion (ROM).

It can be caused by certain combined movements of the shoulder, such as abduction and external rotation (eg, grooming one's hair, reaching for a seatbelt overhead) or extension and internal rotation (eg, reaching for a back pocket or bra strap).

The pain usually progresses to constant pain at rest that is aggravated by all movements of the shoulder and that may be worsened by repetitive movements of the involved upper extremity, psychological stress, exposure to cold or vibration, and changes in the weather.

In approximately 90% of patients with FS, this pain usually lasts 1-2 years before subsiding.

CONTRACTURE

The second principal characteristic of FS is progressive loss of passive ROM (PROM) and active ROM (AROM) of the glenohumeral joint in a capsular pattern.

That is, the movements are usually restricted to a characteristic pattern, with proportionally greater passive loss of external rotation than of abduction and internal rotation.

In 1934, Codman stated, "This entity [FS] is difficult to define, difficult to treat, and difficult to explain from the point of view of pathology." Codman's statement continues to hold true today.

In 1992, the American Shoulder and Elbow Surgeons Society agreed on the following definition of FS by consensus: 

“A condition of uncertain etiology that is characterized by clinically significant restriction of active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder”.

PATHOPHYSIOLOGY

NEUROLOGIC, SURGICAL, AND HISTOLOGIC FINDINGS

The pathophysiology of FS continues to be largely mysterious. However, certain consistent neurologic, surgical, and histologic findings in soft-tissue specimens of patients with FS have been identified and appear to be specific to the pathology of FS.

Evaluation of anatomic, histologic, and surgical specimens from subjects affected by idiopathic FS demonstrates that the glenohumeral joint synovial capsule is often involved in this disease process.

However, most of the notable loss of ROM is caused by disease in structures outside the synovial capsule glenohumeral joint, such as the coracohumeral ligament, soft tissues in the rotator interval, the subscapularis muscle, and the subacromial bursae.

Most authors do not describe clinically significant capsular adhesions as a predominant finding in the chronic phase of this condition.

Instead, pathologic data confirm an active process of hyperplastic fibroplasia and excessive type III collagen secretion that lead to soft-tissue contractures of the aforementioned structures (ie, the coracohumeral ligament, soft tissues of rotator interval, the subscapularis muscle, the subacromial bursae).

However, these findings were observed in surgical patients who had severe and late-phase disease and cannot be applied to early phases of the disease.

From the chromosomal, cytochemical, and histologic points of view, the soft-tissue contractures are identical to those seen in a Dupuytren contracture of the hand.

These contractures result in the classic progressive loss of ROM of the glenohumeral joint, which affects external rotation and abduction, then flexion, adduction, and extension (in descending order of severity).

Despite these histopathologic similarities, the favorable and regressive outcome of adhesive capsulitis differs from the unfavorable and progressive outcome of Dupuytren disease.

GENETIC ABNORMALITIES

Specific genetic abnormalities have been identified with this condition. In particular, frequent trisomy 7 and trisomy 8 in the fibroblasts were confirmed in cultures of tissue samples obtained from glenohumeral joint capsules resected at the time of surgery for FS.

These pathologic findings were observed in studies of tissue specimens that usually were obtained from subjects with chronic FS that did not respond to typical conservative modalities. Little is known about the tissue characteristics of the acute phase of this condition.

FREQUENCY

Shoulder pain is the third most common cause of musculoskeletal disability after low back pain (LBP) and neck pain. The prevalence of FS in the general population is reported to be 2%, with an 11% prevalence in unselected individuals with diabetes.

For patients with type I diabetes, the risk of developing FS in their lifetime is approximately 40%.

FS most frequently occurs in subjects with hyperthyroidism and hypertriglyceridemia.

Most survivors of cerebral vascular accidents (CVAs) that cause hemiplegia develop painful stiffening of their shoulders. However, the painful hemiplegic shoulder has distinct characteristics, which are not discussed in this article.

FS will undoubtedly become increasingly common as the baby-boom generation ages, because this condition most frequently occurs in the fifth and sixth decades of life.

Patients who present with an idiopathic FS when they are younger than 40 years should definitely be examined to rule out occult diabetes, hyperthyroidism, hypertriglyceridemia, or concomitant neurologic or systemic rheumatologic disorder affecting the upper extremity.

MORTALITY/MORBIDITY

Shoulder pain is the third most common cause of musculoskeletal disability in the workplace after LBP and neck pain.

The degree of pain and disability caused by idiopathic FS is highly variable and depends on the stage of the disease. Retrospective data tend to show that patients cope well with a painless glenohumeral contracture. Therefore, most disabilities occur during the initial, painful phase and the subsequent, freezing phase.

SEX

FS affects women more frequently than men, with a female-to-male ratio of about 1.4:1.

Menopause is often reported as a cause of FS in women, although Lundberg seems to have ruled out this hypothesis by demonstrating that age is the principal predictor. He specifically demonstrated that women with early menopause did not have FS any earlier than their counterparts who undergo late menopause.

AGE

To date, the best data available seem to show that FS affects women somewhat earlier than it does men. The mean ages of onset are 52 years for women and 55 years for men, with a standard deviation of 7.

CLINICAL

HISTORY

CLINICAL PHASES

The following 3 clinical phases typically characterize FS: this disease:

• Phase 1 - The painful phase; the patient describes an insidious onset of predominantly nocturnal pain, usually without a precipitating factor. The pain is not related to activity, although the farthest ROM can increase the pain. As the disease progresses, patients have pain at rest. In this phase, lasts 2-9 months, ROM is not restricted, and the diagnosis may remain unclear.

• Phase 2 - The frozen, or adhesive, phase; the pain from phase 1 can persist, although it may decrease. Progressive limitation in ROM occurs in a capsular pattern (that is, in all directions). Normal daily activities can be severely affected. Hallmarks of this phase are an inability to move at great amplitude and an inability to move on the affected side. Diagnosis is easier in this phase than in phase 1. Although phase 2 is reported to last 3-9 months, it can persist longer than this.

• Phase 3 - The thawing, or regressive, phase; pain progressively decreases, and limitations in ROM progressively increase over 12-24 months. Although approximately 40% of patients have slight, persistent limitations in ROM, only 10% have clinically significant long-term functional limitations.

TRAUMA

FS can result from clinically significant trauma to the shoulder, cervical radiculopathy, and pathology of the brachial plexus, any neurologic insult affecting shoulder function or innervation, or an episode of rotator cuff tendonitis. However, FS usually occurs without any clear precipitating factors.

Most patients with FS have no notable history of trauma. Hence, the clinician must remember that this is an idiopathic disease in which the loss of ROM results from a dystrophic pain syndrome combined with contracture caused by an active process resembling fibromatosis.

Although patients often try to recall minor trauma associated with the onset of their shoulder symptoms, careful history taking on the part of the examiner often reveals subtle symptoms, such as night pain or pain and stiffness at the end of ROM that predated the episode of minor trauma.

In most cases, the minor trauma simply makes the patient conscious of the insidious, underlying disease process.

PAIN

Patients with FS typically describe a progressive onset of pain over several weeks. Patients usually report that the initial pain was night pain or pain associated with involved movements of the shoulder (eg, combing one's hair, reaching overhead for a seat belt, reaching for one's back pocket).

Combing one's hair and reaching overhead for a seat belt require a combined motion of abduction and external rotation, and reaching for one's back pocket requires extension and internal rotation of the shoulder. These combined movements tend to stretch the anterior and posterior glenohumeral capsule, respectively.

The pain of FS then progresses to a constant pain at rest that is often aggravated by any movement of the shoulder, psychological stress, exposure to cold or vibration, and changes in the weather.

Patients report worsening of the pain after they engage in activities that require repetitive movements of the affected shoulder.

In about 90% of patients, the pain associated with this condition usually lasts 1-2 years before subsiding.

The pain is a prominent feature of the initial phase and of the second (frozen) phase of the disease. During the thawing phase, the pain usually is less intense than it is in the other phases.

It is usually felt only if the patient is moving at the end of his/her ROM (particularly in positions of subacromial impingement), if the patient performs repetitive movements of the shoulder, or if the patient is exposed to other important ergonomic stresses of the shoulder.

PHYSICAL

In the early phase of FS, the only physical finding may be pain produced at the end of ROMs in the glenohumeral joint, particularly those that stretch the capsule, such as combined abduction and external rotation (such as combing one's hair) or combined extension and internal rotation (such as reaching to scratch one's midback).

During the initial, painful stage, FS may not be distinguishable from an inflammatory synovitis affecting the glenohumeral joint or from a painful episode of rotator cuff tendinopathy. In the second, or freezing, stage of the disease, contracture of the glenohumeral joint becomes readily apparent. This stage may occur only several months after the onset of symptoms.

As the condition progresses, the clinician should observe progressive limitation of the PROM, characterized by a painful capsular end-feel. The motion affected first and most severely is external rotation, followed by abduction, internal rotation, and flexion.

Extension and horizontal adduction tend to be least affected. PROM of the glenohumeral joint progressively worsens over several months and may result in a loss of up to 80% of the normal movement of glenohumeral joint.

In severe cases, evaluation of AROM may show an inverted scapulothoracic motion (that is, motion of the scapula on the thorax).

Example: The scapulothoracic joint initiates abduction (followed by the glenohumeral joint) to compensate for the loss of ROM in the glenohumeral joint.

On occasion, a sizable calcification of the rotator cuff in its resorptive phase may cause an acute tendinobursitis that may mimic FS. This type of acute tendinobursitis may be extremely painful, and it may result in an antalgic phenomenon, causing a loss of PROM.

The acute and rapidly progressive onset of tendinobursitis over a few hours or days differentiates it from the relatively progressive onset of FS, which occurs over weeks.

Another mimic of FS is severe synovitis or arthritis of the glenohumeral joint caused by an underlying primary rheumatologic inflammatory, degenerative, septic, or metastatic process.

Most patients with a painful FS have pain during resisted contraction of all of the rotator cuff tendons, during specific maneuvers designed to detect subacromial impingement (for example, the Hawkins, Neer, and Yocum maneuvers), and during maneuvers designed to detect tendinopathy of the long portion of the biceps (such as the Yergason and Speeds maneuvers).

This phenomenon results because the pain generators in FS may include all of the extra-articular and intra-articular soft tissues of the glenohumeral joint and humeroscapular-motion interface (eg, subacromial bursa, rotator cuff, biceps tendon).

In the presence of a clinically significant loss of PROM of the glenohumeral joint in the previously described capsular pattern, the clinician should probably be content with retaining the diagnosis of FS while de-emphasizing the aforementioned maneuvers designed to diagnose other specific, painful soft-tissue disorders affecting the shoulder.

CONCOMITANT CONDITIONS

Careful neurologic examination should be conducted in all patients presenting with signs and symptoms associated with FS. Patients who have a history of smoking should undergo chest radiography with apical views to rule out a Pancoast tumor irritating the brachial plexus, which can cause FS.

All patients should receive a thorough neurologic examination of the upper extremities and neck to rule out cervical radiculopathy and brachial plexopathy.

Care also should be taken to look for signs of Parkinson disease, because the prevalence of shoulder pain in patients with this treatable condition is 4-5 times that of the healthy population. Furthermore, shoulder pain often is an early manifestation of Parkinson disease, and it sometimes precedes the tremor by many years.

Proper and complete musculoskeletal and integumentary examination should be performed to rule out concomitant systemic rheumatologic, inflammatory, metastatic, or infectious disorders.

Clinicians should also take the time to properly examine the thyroid gland to rule out concomitant hyperthyroidism. Physicians should remain alert to signs of unsuspected diabetes, which may be present in approximately 25% of subjects presenting with FS.

CAUSES

Early authors pointed to chronic inflammation as the cause of the fibrosis in FS, but objective findings have not supported this suggestion.

The absence of crystals, synovial effusion, systemic symptoms, prodromal illness, and serologic markers of autoimmune or reactive arthropathic disease has limited possible theories of an inflammatory process secondary to crystalline, inflammatory, viral, or autoimmune disease.

FS remains a largely idiopathic disorder. The conditions most commonly associated with idiopathic FS are diabetes, hyperthyroidism, hypertriglyceridemia, CVA with upper-extremity paresis, brachial plexus injury, cervical spinal cord injury, and Parkinson disease. The performance of repetitive movements of the upper extremities also is associated with FS.

Patients who have active glenohumeral synovitis in relation to a systemic inflammatory rheumatologic disorder may develop FS as a complication of this condition. Patients who have undergone surgery to the shoulder area, with postoperative immobilization or with clinically significant pain that causes them to immobilize their shoulder, also are predisposed to develop FS.

DIAGNOSIS

LABORATORY STUDIES

• Whether laboratory investigations should be mandatory in patients presenting with the classic syndrome of idiopathic FS but without symptoms of concomitant systemic rheumatologic, inflammatory, peptic, or metastatic disorders remains unclear.

• The scientific literature shows an elevated incidence of diabetes, hyperthyroidism, and hypertriglyceridemia in patients with FS.

  • Lequesne and colleagues found that 28% of 60 new patients who presented with idiopathic FS had unsuspected diabetes.

  • This association should prompt possible testing of thyroid-stimulating hormone (TSH), serum triglyceride, and fasting blood sugar levels in most patients, particularly those presenting with bilateral disease and patients presenting with FS who are younger than 45 years.

IMAGING STUDIES

• Radiologic studies

  • In general, idiopathic FS is considered a clinical diagnosis that does not require confirmation with radiologic imaging.

  • Current radiologic studies do not seem to confer any useful information, prognostic or otherwise, that changes the way the patient is treated.

  • For the moment, the principal utility of these tests is in ruling out concomitant conditions that may influence the treatment of an individual patient.

• Plain radiography

  • All patients presenting with FS should undergo plain radiography of the shoulder, with the acquisition of soft-tissue views of the rotator cuff to rule out a septic or metastatic process.

  • A plain radiograph may also show evidence of a large calcification of the rotator cuff in the painful resorptive phase, an avascular necrosis of the humeral head (that is, Milwaukee shoulder), or a Charcot joint.

• Gallium nuclear scanning - Patients who are immunocompromised, as well as those who abuse intravenous (IV) drugs, should undergo gallium nuclear scanning to rule out a septic joint.

• Arthrography of the glenohumeral joint

  • Binder and colleagues examined the arthrographic and scintigraphic features of 36 patients who presented with clinically diagnosed FS. They reported no association between uptake on bone scans and arthrographic features (glenohumeral contrast enhancement), and neither finding was useful in predicting the rate or extent of recovery. FS of traumatic onset behaved no differently than did spontaneously arising FS. The authors concluded that arthrography or99m Tc diphosphonate scanning performed at presentation did not contribute to the assessment of a painful, stiff shoulder.

  • The present authors share the opinions of Binder and coauthors on this matter.

  • Of 36 subjects who met strict clinical criteria for FS in the study by Binder and colleagues (ie, loss of >50% of glenohumeral PROM in abduction and external rotation), only 50% had a positive arthrogram. Either arthrography had low sensitivity in diagnosing FS, or the expert physicians tended to overdiagnose FS. The fact that a positive arthrogram had no affect on the clinical outcome in this 4-year prospective study suggests that arthrography of the glenohumeral joint is a poorly sensitive test for diagnosing FS, although a positive glenohumeral arthrogram showing the classic signs of FS confirms the diagnosis beyond any doubt.

  • A study by Mao and coauthors showed a poor correlation between ROM of the glenohumeral joint and its arthrographic appearance in patients with shoulder pain for 2 months or longer. This result once again showed the limited prognostic usefulness of arthrography of the glenohumeral joint.

  • To date, arthrography is used mostly to treat FS, rather than to diagnose the condition.

  • The injection of contrast medium into the glenohumeral joint helps to determine its volume and configuration. The normal volume of the joint is 13 mL. In FS, the volume can be reduced to 5-8 mL.

• 99m Tc methylene diphosphonate (MDP) bone scanning

  • Binder and colleagues also examined the utility of nuclear bone scanning in the diagnosis and treatment of patients with FS. They again found that these studies had little prognostic value, although they were considerably more sensitive, with 92% of the study subjects having a positive scan.

  • In general, the problem with bone scans in the practice of musculoskeletal medicine is that they are highly sensitive but not specific. The pilot work by Clunie and colleagues showed that abnormalities on posterior99 Tc MDP shoulder studies of patients with shoulder pain did tend to be specific for FS. However, this work must be reproduced on a large scale to be considered conclusive.

• Other studies - Computed tomography (CT) scanning, CT arthrography, ultrasonography, and magnetic resonance imaging (MRI) are sensitive imaging modalities that depict specific signs for FS. However, use of these modalities is rarely indicated.

TREATMENT

PHYSICAL THERAPY

Although studies have shown the efficacy of physical therapy, no current evidence has suggested that physical therapy alone improves function in the treatment of FS.

However, physical therapy associated with an intra-articular injection of corticosteroid improves function and ROM more rapidly than does intra-articular corticosteroid injection alone.

THERAPEUTIC EXERCISES

Although many therapeutic exercises are described, few have been evaluated in the treatment of FS. Therapeutic exercises that have been studied include articular stretching and pulley therapy.

Passive articular stretching exercises improve ROM. The superiority of supervised versus home exercise programs has yet to be demonstrated.

MANUAL THERAPY

Data from 2 studies support the use of manual therapy to improve ROM in the short term. One study showed that passive mobilization in the end-range position of the glenohumeral joint was more effective for improving ROM and function than was passive mobilization in the pain-free zone.

However, the overall difference between the interventions was small. In addition, patients appeared to achieve greatest improvement in ROM when treatment was administered early.

In summary, the findings indicated that patients with FS improve with physical therapy regardless of when it is administered after the onset of FS but that they achieve the greatest improvement in their ROM when treatment is administered early.

PHYSICAL MODALITIES

Many electroanalgesic and thermoanalgesic modalities are often used in physical therapy.

Prospective, randomized, placebo-controlled clinical trials have demonstrated the inefficacy of bipolar interferential electrotherapy, TENS (transcutaneous electrical nerve stimulation) pulsed ultrasound therapy, laser therapy, and magnetotherapy with electromagnetic fields in the treatment of painful shoulder disorders.

In summary, physical therapy alone has not been shown to improve function. However, when associated with an intra-articular corticosteroid injection, physical therapy improves ROM and function more rapidly than does intra-articular corticosteroid injection alone. The effectiveness of physical modalities has not been demonstrated. However, therapeutic exercises and manual therapy do improve ROM (see above).

OCCUPATIONAL THERAPY

Patients with severe FS may benefit from a referral to an occupational therapist for assistance and instruction in performing activities of daily living (ADLs).

The occupational therapist helps the patient learn how to use adaptive equipment and suggest home and workplace modifications that may be necessary and beneficial for completing professional activities and routine daily tasks (eg, dressing, bathing, grooming).

However, the effectiveness of these interventions has yet to be demonstrated. Researchers who performed a systematic review concluded that evidence supporting the effectiveness of rehabilitation in the workplace is lacking.

SURGICAL INTERVENTION

Duplay, the first person to describe the syndrome of FS, in 1872, proposed treating this condition with manipulation of the glenohumeral joint, with the patient under general anesthesia.

Although some orthopedic surgeons continue to practice this technique, the benefits of this approach have not been demonstrated in controlled clinical trials.

Various improvements in surgical techniques, such as the advent of controlled capsular release by using arthroscopic access to the anterior glenohumeral joint capsule and the coracohumeral ligament, appear to offer promising treatments.

OTHER TREATMENT

Studies of intra-articular and intrabursal injections, glenohumeral distention arthrography, and nerve blocks have been conducted, as described in the following text.

INTRA-ARTICULAR AND INTRABURSAL INJECTIONS

Intra-articular injections of steroid derivatives are the second most common medical intervention for treating painful joint conditions. (The most common intervention is the administration of nonsteroidal anti-inflammatory drugs [NSAIDs]).

The rationale for injection of an intra-articular steroid derivative is to allow direct delivery of a modest dose of concentrated drug with analgesic and anti-inflammatory properties to the targeted site of pathology.

INTRABURSAL CORTICOSTEROID INJECTIONS

Many authors have shown that the pathology of FS is in the extra-articular structures, such as the coracohumeral ligament, the interval of the rotator cuff, the subacromial space, and the articular capsule. From a pathophysiologic point of view, a rationale supports the use of corticosteroid injection in the subacromiodeltoidian bursa to treat FS.

INTRA-ARTICULAR INJECTION OF SODIUM HYALURONATE

Sodium hyaluronate has a metabolic effect on the articular cartilage, synovial tissues, and liquid. Few studies on the effect of sodium hyaluronate have been reported.

The present authors are aware of only 1 controlled study of the effectiveness of sodium hyaluronate as a sole treatment of FS. At 3 months, sodium hyaluronate was as effective as an intra-articular corticosteroid injection or physical therapy in improving function, but it was less effective than the comparators in improving ROM.

Although additional studies are needed before conclusions about efficacy can be drawn, intra-articular injections of sodium hyaluronate may be an alternative treatment for FS, mainly in patients in whom corticosteroid injections are contraindicated.

GLENOHUMERAL DISTENTION ARTHROGRAPHY

One controlled study showed no benefit to distention arthrography over intra-articular corticosteroid injection without distention. Another controlled study showed a significant increase in ROM and a significant decrease in the use of analgesics after distention arthrography, compared with the use of intra-articular corticosteroid injection alone.

The benefit of performing distention arthrography until the capsule ruptures must be demonstrated.

One uncontrolled study that was designed to examine the optimal number of distention arthrography procedures that should be performed showed that 2 procedures administered within 3 weeks, when combined with home exercises, significantly improved function. However, a third procedure offered no benefit.

Another unknown factor is the stage at which infiltration should be performed. To the authors' knowledge, only 1 uncontrolled study on this question has been completed.

The researchers concluded that distention arthrography should be done in the second stage of disease that is not progressing, despite the patient's participation in physical therapy.

NERVE BLOCKS

SUPRASCAPULAR NERVE BLOCK

The suprascapular nerve block is a simple procedure but is not well known by most clinicians.

Dangoisse's technique for suprascapular nerve block was modified to render it steroid free and accessible to most physicians who practice musculoskeletal medicine in ambulatory-care facilities and private offices.

A 3.75-cm, 25-gauge needle is directed in the plane of the scapula toward the center of the floor of the supraspinous fossa. The needle-insertion point is 2 cm above the bisection point of the upper border of the spine of the scapula.

After aspiration is performed to rule out intravascular needle placement, 10 mL of bupivacaine 0.5 is slowly injected into the floor of the supraspinous fossa to fill the fascial contents of this fossa and to produce an indirect suprascapular nerve block.

The highly concentrated bupivacaine bathes the suprascapular nerve as it enters the fossa through the suprascapular notch.

STELLATE BLOCK

An uncontrolled study of the combined effect of electropuncture, stellate block, and suprascapular nerve block showed that the combination improved pain control and increased ROM more than electropuncture or nerve block alone.

MEDICATION

The goal of pharmacologic intervention in FS is uniquely the control of pain in the 2 first stages of the disease because no drug affects the underlying disease process.

Medication does not affect the duration of disease or the severity or duration of glenohumeral joint contracture. Most of the time, patients with FS can manage their pain with analgesics, such as acetaminophen, as needed.

However, during the most painful months of the condition, when rest pain and night pain are most bothersome, appropriate use of narcotic agents is warranted.

Pain control should be aimed at relieving pain in the following order of priority:

1.      Rest pain and night pain: The preferred agent should be a long-acting, centrally acting agent (eg, calcitonin) or a sustained-release narcotic preparation (eg, low-dose oxycodone HCl [OxyContin]).

2.      Activity-related pain: Some physicians advocate the use of short-acting analgesic agents, such as oxycodone, before sessions of physical therapy to improve shoulder mobilization. The authors' opinion is that this regimen should be used with care because of the risk of causing a flare-up after physiotherapeutic mobilization due to an excessively vigorous mobilization session.

Attaining the favorable prognosis requires patience on the part of the physician and the patient.

ENDOCRINE METABOLIC AGENTS

Agents in this class may have analgesic effects. 

CALCITONIN (Miacalcin, Osteocalcin)

Can relieve some back pain associated with adhesive capsulitis. A prospective, randomized study was conducted to compare calcitonin SC for 3 wk with manual therapy and physical therapy with physical therapy alone.

Pain decreased more in patients with posttraumatic capsulitis who were receiving calcitonin, manual therapy, and physical therapy than it did in others. The speed of recovery was comparable in both groups.

Adult: 200 IU/d intranasally

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypocalcemia may occur; examine urine sediment during prolonged therapy

NSAIDS

Given the absence of histopathologic evidence of capsular inflammation, NSAIDs must be used for their analgesic effects. To our knowledge, no researchers have compared the efficacy of NSAIDs with that of placebo in adhesive capsulitis.

Comparisons of the efficacy of different NSAIDs in the treatment of adhesive capsulitis show a positive effect regardless of the NSAID used.

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase (COX) activity and prostaglandin synthesis.

Other mechanisms may exist as well; examples are inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

COX-2 – selective NSAIDs are recommended in cases of FS. Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeds is clearly less with COX-2 inhibitors than it is with traditional NSAIDs.

Ongoing analysis of the cost of preventing GI bleeds will help in further defining the patient populations who are most likely to benefit from COX-2 inhibitors.

PO corticosteroid therapy is significantly less effective than intra-articular corticosteroid injection in the short term.

Given the systemic adverse effects, one should question the indication for PO corticosteroids in the treatment of FS. Other drugs with fewer adverse effects are available; alternatively, corticosteroids can be administered intra-articularly with fewer adverse effects. 

CELECOXIB (Celebrex)

Inhibits primarily COX-2, an isoenzyme induced during pain and by inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; therefore, GI toxicity may be decreased. Seek the lowest dose for each patient.

Adult: 200 mg/d PO qd; alternatively, 100 mg PO bid 

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Category D in third trimester of pregnancy; may cause fluid retention and peripheral edema; caution in compromised cardiac function, hypertension, or conditions predisposing patient to fluid retention; may cause circulatory hemodynamics to deteriorate, leading to severe heart failure and hyponatremia; NSAIDs may mask usual signs of infection; caution in existing controlled infections; evaluate symptoms and signs of liver dysfunction

ANALGESIC AGENTS

In rare cases, narcotic analgesia may be needed for adequate pain control if the patient's condition is refractory to the judicious use of bupivacaine or bupivacaine suprascapular nerve blocks or in situations in which these nerve-block procedures and/or steroid injections (which are most often performed with fluoroscopic guidance) are not readily available.

When combined with anti-inflammatory agents and physical modalities, analgesics should result in good pain control.

In the occasional patient whose condition does not respond to the aforementioned therapies, the use of a long-acting narcotic agent, such as codeine, morphine sulfate (MS Contin), oxycodone HCl (OxyContin), or hydromorphone, should be considered, along with rescue doses of short-acting drugs every 4-6 hours. 

ACETAMINOPHEN (Tylenol, Tempra, Aspirin Free Anacin)

Should be first-line drug of choice. In most patients, 3 g/d suffices to control the pain of FS during all but the most painful months. Narcotics and NSAIDs should be used only if the regular use of acetaminophen 1 g tid fails to adequately control pain. The authors prefer to be conservative and limit the prescription to 75% of the maximal daily dosage because patients may be prone to liver toxicity if they take the maximal dosage for many consecutive months.

Adult: 1 g PO q8h

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatotoxicity possible at various dosage levels in chronic alcoholism; severe or recurrent pain or severe or continued fever may indicate serious illness; many over-the-counter (OTC) products contain acetaminophen, and their combined use may result in cumulative dose exceeding recommended maximum dose 

OXYCODONE (OxyContin, OxyIR, Roxicodone)

Indicated for relief of moderate to severe pain.

Adult:

10 mg PO 2 h hs (or ideally 12 h before waking up); may give 5 mg q4h during daytime to patients with severe rest pain during day.