7

Frozen shoulder

PETER NASH BRIAN L. H A Z L E M A N

Despite initial descriptions of 'periarthrite scapulohumerale' by Duplay (1872) and 'painful periarthritis of the shoulder' by Putnam (1882), this enigmatic rheumatological condition remains as 'difficult to define, difficult to treat and difficult to explain from the point of view of pathology' as Codman observed in 1934. It would appear that the diagnosis is often misapplied and confusion is fostered by the variety of labels given to the same syndrome. Examples include 'frozen shoulder', 'adhesive capsulitis', 'adherent subacromial bursitis', 'shoulder periarthritis', 'shoulder peri- capsulitis' and 'obliterative bursitis of the shoulder'. Some American authors add to this confusion by classifying patients with this syndrome into those with 'adhesive capsulitis' and those with 'painful and stiff shoulder', the latter being a heterogeneous collection of shoulder pathologies differen- tiated predominantly by the presence or absence of classical arthrographic findings (Neviaser and Neviaser, 1987). However, the label used is less important than a clear notion of what is meant by the term when it is applied.

DEFINITION

Primary frozen shoulder is a condition of unknown aetiology distinguished by painful restriction of all shoulder movements, both active and passive, characterized by prominent reduction in the glenohumeral range of movement and in shoulder external rotation. Three phases are recognized: (1) painful, (2) adhesive, and (3) resolution, each of variable duration. Exclusion of a variety of other shoulder disorders which mimic this condition is important (Table 1).

Secondary frozen shoulder is an identical clinical syndrome but an identifiable disorder, such as diabetes mellitus, or readily recognizable precipitating event, e.g. recent cardiac surgery, is discernible. Distinguish- ing a 'secondary' group prompts a search for, and may allow early inter- vention in the treatment of underlying disease. Table 2 lists the disorders associated with secondary frozen shoulder (Rizk and Pinals, 1982).

Baillidre's ClinicalRheumatology--Vol. 3, No. 3, December 1989 551

552 P. NASH AND B. L. HAZLEMAN

Table 1. Causes of shoulder pain mimicking frozen shoulder.

A. Rheumatological conditions 1. Soft-tissue rheumatic disorders

a. Rotator cuff tendinitis, cuff tears b. Subacromial bursitis, bicipital tenosynovitis, acromioclavicular osteoarthritis

2. Inflammatory arthritides manifesting with shoulder arthritis a. Rheumatoid arthritis, spondyloarthropathies b. Crystal arthropathies (gout, pseudogout, apatite associated arthropathy) c. Neuroarthropathy d. Infectious arthritis (tuberculous, bacterial, fungal, etc.)

3. Polymyalgia rheumatica

B. Neurological conditions 1. Intradurallesions (syringomyelia, intramedullary tumours) 2. Preforaminal lesions (extradural neoplasms, cervical disc pathology) 3. Foraminal lesions (neurofibromata, cervical disc pathology) 4. Post-foraminal lesions (brachial plexus lesions, e.g. brachial amyotrophy)

(neurovascular syndromes--cervical rib, scalenus anticus syndrome; Pancoast's turnout)

C. Referred pain to shoulder (subdiaphragmatic lesions, pleural disease, phrenic nerve lesions)

D. Reflex sympathetic dystrophy (shoulder-hand syndrome)

E. Bone lesions (primary and metastatic tumours, Paget's disease)

Table 2. Disorders associated with frozen shoulder.

Shoulder trauma Diabetes mellitus Thyroid disease (hyper- and hypothyroidism) Cardiac disease and cardiac surgery Neurological disorders with impaired consciousness or hemiplegia Pulmonary disease (tuberculosis, antituberculous drugs, carcinoma)

EPIDEMIOLOGY

The annual cumulative risk for the development of frozen shoulder has been estimated at 2% in an 'at risk' Scandinavian population (Lundberg, 1969). Women are slightly more commonly affected than men and, although the evidence is conflicting, the consensus favours involvement of the non- dominant shoulder (Rizk and Pinals, 1982; Lundberg, 1969). The mean age of onset occurs in the sixth decade, with onset before the age of 40 being rare. Proposed associations with the menopause have been shown to be the consequence of increased age (Lundberg, 1969). Occupation does not appear to play a significant role. A history of minor shoulder trauma or 'strain' is common, as is associated ipsilateral cervical and trapezius pain. In 6-17% of patients, the contralateral shoulder develops frozen shoulder during the subsequent 5 years (Rizk and Pinals, 1982).

No well documented case of recurrence of the condition in the same shoulder has been described, although Rowe and Leiffert (1988) briefly describe a patient who appeared to suffer a recurrence in the same shoulder,

FROZEN SHOULDER 553

2 years after undefined 'successful treatment and resolution of the problem'. This patient was found to have an underlying seizure disorder resulting from cerebral meningioma.

Bruckner and Nye (1981) prospectively studied a high-risk group of neurosurgical in-patients and found 25.3% of patients developed frozen shoulder within a mean postoperative interval of 2.5 months. Significant associations with its development included increased age, impairment of consciousness, side of hemiparesis, duration of postoperative intravenous infusion and depressive personality. No autonomic disturbance was demon- strable in the affected limb. Postoperative therapy with high-dose cortico- steroids did not inhibit the development of the condition.

NATURAL HISTORY

Table 3 summarizes those studies that have addressed the natural history of frozen shoulder. Reeves (1966) prospectively studied 41 patients, treated with sling, analgesics and exercises alone over a 5-10 year follow-up period. He demonstrated that the painful phase lasted 10-36 weeks, the adhesive phase 4-12 months and the resolution phase 5-26 months. The total duration of symptoms lasted 12-42 months (with a mean disease duration of 30.1 months).

These and other studies confirm that frozen shoulder is a protracted painful illness. Significant numbers of patients have residual, clinically detectable limitation of shoulder movement. A smaller number have residual functional shoulder disability. Disability is associated with a prolongation of the painful and restrictive phases.

CLINICAL FEATURES

Painful phase

Classically, an otherwise-well patient insidiously develops a generally pain- ful aching shoulder. Increasing stiffness and limitation of shoulder movement becomes apparent. Persistence despite general anaesthesia argues against this limitation being the consequence of muscle spasm alone. Pain is constant, dull, nagging, felt at rest, with movement and prominently at night. There is inability to lie on the affected shoulder. Non-steroidal anti-inflammatory drugs and simple analgesia provide little relief. The arm is held splinted to the side, adducted and internally rotated. Splinting the ipsilateral side of the shoulder girdle often results in localized muscle pain and tenderness at girdle musculotendinous insertions.

Adhesive and resolution phases

Over subsequent weeks the pain eases to become chiefly apparent with shoulder movement rather than at rest and at night. Limitation of shoulder

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FROZEN SHOULDER 555

movement reaches its extreme. This lasts a variable period until spon- taneous and gradual improvement of range is seen.

Examination

Physical signs may include minor deltoid and supraspinatus atrophy. There is diffuse tenderness over the glenohumeral joint. Shoulder motion, both passive and active, is restricted in all directions with prominent reduction in external rotation and the glenohumeral range of movement. There is a sense of mechanical blockage due to tethering rather than resistance due to pain. Pain is reproduced on extremes of permitted range of all movements. It is often not possible to test for a 'painful arc of abduction' due to gross restriction in forward flexion and abduction. Pain on resisted shoulder movement is less marked and muscle power is generally unimpaired or pain restricted.

Other 'frozen' joints

It has been considered that the shoulder is unique in its development of this clinical syndrome. However, using arthrographic diagnostic criteria of (1) raised intracapsular pressure. (2) reduction in joint volume, and (3) obliteration of normal capsular recesses, 'adhesive capsulitis' of the hip (Lequesne et al, 1981; Chard and Jenner, 1988), ankle (Griffiths et al, 1985) and wrist (Maloney et al, 1988) have been described. These cases tend, however, to follow significant joint trauma or be associated with synovial osteochondromatosis or intra-articular loose bodies complicating advanced osteoarthritis--quite dissimilar to frozen shoulder. Available biopsy material from these joints show capsular fibroplasia and oedematous synovium with scanty focal mononuclear infiltration comparable to that described in frozen shoulder.

INVESTIGATIONS

General

Systemic markers of inflammation, such as elevations in erythrocyte sedimentation rate and acute phase reactants, are absent in frozen shoulder. Similarly, serum levels of globulins, calcium, phosphate and bone alkaline phosphatase are generally within normal limits. Plain radiographs show either no abnormality, minor periarticular osteoporosis or minor degener- ative changes in the shoulder and acromioclavicular joints, present in the same frequency as on the unaffected side.

Arthrography

Characteristically, there is difficulty in needling the shoulder joint for arthro- graphic purposes because of joint contracture and restricted range of

556 e . N A S H A N D B. L. H A Z L E M A N

movement. Classical features include limitation of joint capacity, a small or non-existent dependent axillary fold and irregularity about capsular insertion on to the anatomical neck of the humerus. The insistence of the presence of these characteristic findings by some American authors before a diagnosis of frozen shoulder is made may result in missing 'early' disease; a point when the study of aetiological agents is more likely to be fruitful. Between 10 and 30% of patients with the disorder undergoing arthrographic examination prior to any joint manipulation demonstrate rotator cuff perforation with free flow of contrast into the subacromial space (Lundberg, 1969; Binder et al, 1984b).

Binder et al (1984b) studied a strictly defined group of patients with frozen shoulder and delineated three discrete subgroups arthrographically. Evi- dence of rotator cuff perforation was present in one third, 50% had classical arthrographic findings as described above, and a further 20% had a normal examination. The contribution of rotator cuff disease to the development of frozen shoulder warrants reassessment. Binder's patients with normal arthrograms had a longer duration of illness at presentation, no difference in shoulder restriction and no difference in rate and extent of recovery.

Postmanipulation arthrography demonstrates capsular rupture, usually inferiorly, suggesting that this is the mechanism for recovery of shoulder range with this procedure. Normalization of arthrograms is seen in the resolution phase when shoulder range has recovered (Reeves, 1966).

Arthroscopy

Arthroscopic evaluation of frozen shoulder patients has revealed four stages of involvement (Neviaser and Neviaser, 1987).

Stage 1

Minimal or no limitation of shoulder range is seen and a fibrinous synovitis is present. Symptoms mimic the impingement syndrome.

Stage 2

An acute proliferative synovitis with early adhesion formation is present. This predominates in the dependent fold. There is loss of the normal interval between humeral head and glenoid. Severe loss of movement occurs in all planes, with pain on all motion.

Stage 3

Synovitis lessens as capsular contracture and loss of the axillary fold occurs.

Stage 4

With chronicity, synovitis is no longer present, marked and adhesions are fully developed.

capsular restriction is

FROZEN SHOULDER

Table 4. Shoulder arthroscopic and surgical findings.

557

No. of Duration Study patients of symptoms Findings

Ogilvie-Harris and 81 > 6 months Wiley (1986)

Neviaser and Neviaser (1987)

Ha'eft and Maitland 24 Mean 8 months (1981)

Cofield (1983) 3 3 years

Nevaiser (1945) 10

Simmonds (1979) 4

Lundberg (1969) 20

De Palma (1973) 42 'Long and protracted'

Small joint capacity, mild synovitis no adhesions. 17 partial rotator cuff tear

Stages 1-4 (as described in text). Synovitis and adhesions in varying degrees

No adhesions. 1 rotator cuff tear; 2 biceps tendon tear; 5 chronic synovitis; 8 normal axillary fold

Synovitis, chondromalacia and capsular scarring

Adhesive capsule to humeral head capsule thickened and tense. Axillary fold adhesions. Chronic inflammatory changes in capsule with fibrosis. No synovitis

Vascular thickened cuff. Chronic inflammatory changes subacromial bursa. No adhesions

No adhesions. Thickened capsule. Periarticular inflammatory changes in rotator cuff

Low grade inflammatory process in capsule and periarticular structures

The synovitis seen in f rozen shoulder is poor ly character ized and the presence of adhesions a mat te r of controversy. Table 4 lists the findings at a r th roscopy and open a r th ro tomy in a number of studies. It would appear that these studies have assessed the shoulder joint and capsule in well advanced disease, such that early inf lammatory events are missed and a bland fibrotic capsule found. In our hands, investigation within 12 weeks of the onset of symptoms has demons t ra t ed a mild non-specific synovitis that is negat ive for crystals (calcium pyrophospha te and urate) and iron (such as following haemarthros is ) and is culture negative. Elec t ron microscopy shows no viral inclusions (unpubl ished observations) . Sur rounding soft tissues show fibrosis, are friable and hypervascular . The subacromial bursa is of ten th ickened and obl i terated by adhesions.

Bone densitometry

Bone densi tometr ic studies of the affected humera l head show an average 50% reduct ion in bone mineral content compared to the unaffec ted side. This finding was independent of age, did not increase with ex tended durat ion of illness and did not restore with t ime (Lundberg , 1969).

5 5 8 P. NASH AND B. L. HAZLEMAN

Bone scintigraphy

An increased uptake of [99mTc]pertechnetate in the affected shoulder region of frozen shoulder patients is demonstrable when comparisons are made with the contralateral side and controls. A small study by Wright and Haq (1976) suggested increased uptake may identify steroid responsiveness. However, Binder et al (1984a), in a prospective study of 38 patients found no correlation with therapeutic response to steroid, duration of symptoms, initial disease severity or ultimate recovery. Scintigraphy does not appear to be useful in predicting outcome and is not of value in routine assessment.

Histocompatibility antigen studies

Four controlled studies have addressed the prevalence of HLA B27 antigen carriage in patients with the condition. The consensus, independent of race, favours no increase in prevalence (Bulgen et al, 1976; Noy et al, 1981; Seignalet et al, 1981; Rizk and Pinals, 1984).

Immunological studies

Controlled studies of 25 frozen shoulder patients by Bulgen et al (1978) have shown no significant differences in the presence of rheumatoid or anti- nuclear factors, immunoglobulin quantification and immunoelectrophoresis, lymphocyte transformability and DNA synthesis in response to mitogens. A small depression in serum IgA was noted and awaits further evaluation. Kessel et al (1981) screened 50 frozen shoulder patients for autoantibodies to smooth muscle, collagen and cartilage, as well as quantitating complement and circulating immune complexes. No immunological disturbance was demonstrable.

Macnab (1973), studying avascular rabbit tendon implants into viable achilles tendon, postulates that the capsulitis of this condition results from a type 4 autoimmune response targeted against damaged or infarcted supra- spinatous tendon.

Histological and histochemical studies

Lundberg (1969) examined shoulder capsules from 14 frozen shoulder patients and found increased fibrous tissue, increased fibroblast numbers and increased vaseularity but an unchanged synovial lining and no inflam- matory cell infiltrate. A similarity to the morphology seen in Dupuytren's contracture was noted. No structural changes were apparent in collagen fbres on electron microscopic examination. Increased levels of sulphated glycosaminoglycans (particularly dermatan sulphate) and reduction in levels of glycoprotein were noted. These changes are suggestive of a repair reaction. The duration of the disorder prior to histological examination was not defined in these studies but may well have been late in the disease process.

FROZEN SHOULDER 559

PATHOGENESIS

The aetiopathogenesis is not known; however, those diseases associated with secondary frozen shoulder may provide pointers. Controlled studies have shown an increased prevalence of frozen shoulder in patients with diabetes (Bridgman, 1972; Lequesne et al, 1977). Disease in diabetics occurs at a younger age, may be less painful, is more often bilateral and is associated with prolonged duration of diabetes, the development of limited joint mobility syndrome and widespread microvascular disease.

Kay and Slater (1981) examined shoulder capsular tissue from a diabetic with frozen shoulder and found an appearance identical to that seen in the fibromatosis of Dupuytren's disease (fibroblast and myofibroblast prolifer- ation), with vascular changes suggestive of diabetic microangiopathy. They postulate that platelet derived growth factor released from abnormal or ischaemic blood vessels may act as a stimulus to local myofibroblast proliferation. Microvascular disease, abnormalities of collagen repair and predisposition to infection may link diabetes with frozen shoulder.

A number of reports describe associations between hypo- and hyper- thyroidism and frozen shoulder (Wohlgethan, 1987; Bowman et al, 1988). Resistance to any form of treatment is described until control of the thyroid disease occurs. Again, the underlying anomalies may be abnormal connective tissue proliferation in articular capsule, abnormal collagen repair, tissue deposition of mucopolysaccharides, or regulatory hormone imbalance at a cellular level.

Immobilization of the affected limb appears to be a common risk factor in the development of frozen shoulder. This alone is not sufficient explanation for its development, as shoulder stiffness is generally brief after prolonged shoulder casting in the majority of patients.

A number of studies propose an association between pulmonary disease and frozen shoulder (Johnson, 1959; Saha, 1966). Johnson noted an average incidence of 14.7% per hospital year in a tuberculosis sanatorium. Reflex neurohumeral mechanisms may be of aetiological importance.

There is little to support a crucial role for an autoimmune process in frozen shoulder. Acute phase reactants, complement, immunoglobulins (apart from IgA), immune complexes and autoantibodies to a variety of connective tissues are normal or absent. High-dose corticosteroids are ineffective in preventing its development and do not have a marked effect on established disease. Histological studies show an absence of inflammatory cell infiltrates, granulomas or vasculitis in synovium, capsule or rotator cuff. The musculoskeletal system outside the shoulder is otherwise unaffected and frozen shoulder does not appear to recur in the same joint.

HLA-B27 negativity, the lack of other systemic features of a spondylo- arthropathy, normal acute phase reactants and the absence of inflammatory synovial fluid argue against the condition being a reactive arthropathy.

Blood is particularly irritant to synovium and features of trauma, immobility and synovitis may suggest frozen shoulder follows a haem- arthrosis in a predisposed individual. The lack of recurrence, the absence of synovial cell hyperplasia with erythrophagocytosis, haemosiderin granules

560 P. N A S H A N D B. L. H A Z L E M A N

or subsynovial inflammatory cell exudates, do not support this proposition. Patients with coagulopathies do not have an increased incidence of frozen shoulder.

The shoulder is a common site of calcium pyrophosphate or hydroxy- apatite induced crystal arthropathy. The presence of crystals has not been described. The lesion does not recur; there is an absence of an acute phase response, inflammatory synovial fluid, or cartilage and bone destruction.

There is little to support an infective aetiology. Patients with frozen shoulder lack systemic symptoms, do not have a prodromal illness, inflam- matory synovial fluid or cartilage or bone destruction. No other joint is infected.

Features against frozen shoulder being a forme fruste of algodystrophy include the absence of upper limb oedema and vasospasm, lack of prominent bone demineralization, absence of demonstrable autonomic disturbance in the affected limb, and arguable benefit of corticosteroids and stellate ganglion blockade. The possibility that it is due to a suprascapular nerve entrapment (Kopell and Thompson, 1959) requires further substantiation.

De Palma (1973) considered the degenerative rotator cuff of shoulders immobilized by the pain of bicipital tenosynovitis to be the setting for the development of frozen shoulder. Duplay (1872) implicated the subacromial bursa, Lippman (1943) the biceps tendon, Codman (1934) the supraspinatus tendon and Neviaser (1945) the inferior capsule. As mentioned previously, the aetiological role of rotator cuff disease warrants reconsideration.

FS is an inflammatory process commencing in the joint capsule or rotator cuff, resulting in capsular contracture and fibrosis. Individuals with abnor- malities of connective tissue repair such as diabetics, are predisposed to its development. Abnormalities at a cellular level, with malfunction in fibro- blast recruitment, cytokine or growth factor production and release, may be incriminated in the initiation of frozen shoulder. Abnormalities of platelet derived growth factor release from alveolar macrophages have been demon- strated to occur in the fibrosis developing in idiopathic pulmonary fibrosis. Platelet derived growth factor, a most potent mitogenic polypeptide for mesenchymal cells, has a similar structure and function to the gene product of simian sarcoma virus: the first possible link between infection and the development of fibrosis. It will be necessary to obtain capsular and synovial tissue early in the course of the disease, to characterize infiltrating cell types and cytokine profiles when acute events are underway and to further investigate events at a cellular level to advance our knowledge about the aetiopathogenesis of this disease.

TREATMENT

The list of suggested therapies (Table 5) emphasizes the unsatisfactory nature of treatment in this disorder. Assessment of trial data is fraught with difficulties. Adequate patient numbers are often lacking and few studies are blinded or controlled. Patient selection is often poor, with inadequate disease definition, and treatment comparisons are made on groups of patients at differing stages of the disease process.

FROZEN SHOULDER 561

Table 5. Suggested therapies for frozen shoulder.

Analgesics Non-steroidal anti-inflammatory drugs Heat and ultrasound Physiotherapy and graded exercises Corticosteroids (oral and intra-articular) Stellate ganglion blockade Magnetic necklace Dimethyl sulphnxide (topical) Arthrographic distension Joint irradiation Manipulation under anaesthetic (early/late)

Tables 6-8 summarize the results from a number of studies examining popular methods of therapy.

Prophylaxis

Patients at high risk can be identified (see Table 2). Shoulder immobilization should be actively discouraged and active and passive shoulder exercise programmes instituted in high-risk situations, e.g. post-cardiac surgery. Simple analgesia and non-steroidal anti-inflammatory drugs are generally inadequate to control symptoms; other modalities are employed.

Corticosteroids

Oral corticosteroids in two blinded and controlled trials (Blockley et al, 1954; Binder et al, 1984a) have been shown to improve pain without altering the rate of recovery. A number of studies (Murnaghan and Macintosh, 1955; Quin, 1965; Lee et al, 1974; Bulgen et al, 1984) have demonstrated that the use of intra-articular corticosteroid injections results in improve- ment in pain and range of movement but no long-term benefit has been demonstrated.

Manipulation

Manipulation under anaesthetic has been demonstrated to improve shoulder range by causing rupture of the inferior capsule close to the glenoid margin and of the subscapularis tendon at its insertion. Although uncom- mon, complications of this procedure include capsular bleeding, humeral fracture and shoulder dislocation. Good, controlled studies are lacking but improvements in pain and range of movement are claimed (Table 8). Total recovery time appears to be unchanged. The timing of manipulation is also contentious. Charnley (1959) claims manipulation in the acutely painful phase is futile as capsular contraction recurs but that good results are obtained during the adhesive phase. Kessel et al (1981) have shown improvements in pain and range of movement following manipulation during the adhesive phase. Postoperative rehabilitation, particularly main-

562 P. N A S H A N D B . L . H A Z L E M A N

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ta in ing the a f fec ted l imb fully a b d u c t e d and ex te rna l ly r o t a t e d , a p p e a r s to be i m p o r t a n t for a successful o u t c o m e .

S y m p a t h e t i c b l o c k a d e

In con t ro l l ed s tudies , cervical sympa the t i c gangl ion b l o c k a d e has no t b e e n d e m o n s t r a t e d to give m o r e than t e m p o r a r y re l ie f (Cal l ie t , 1966; T u r e k , 1967).

C O N C L U S I O N

This cond i t i on r ema ins an en igma . F u r t h e r advances in our u n d e r s t a n d i n g of d isease p a t h o g e n e s i s will r equ i r e t issue s tudy at ear ly s tages of the d i so rde r ut i l iz ing c o n t e m p o r a r y m e t h o d s , such as in situ hybr id i za t ion to def ine cy tok ine and g rowth fac tor prof i les , and monoc lona l s and t issue cul ture to def ine cell types . T h e d e v e l o p m e n t of effect ive t h e r a p y will r equ i re b l i nde d and con t ro l l ed s tudies of well se l ec ted pa t i en t g roups at s imi lar s tages of this synd rome . G i v e n tha t ou r u n d e r s t a n d i n g has a d v a n c e d l i t t le s ince C o d m a n ' s wri t ings in 1934, at p r e sen t we do l i t t le m o r e than prac t i se the art of med ic ine which, as V o l t a i r e wou ld suggest , 'is to keep the pa t i en t occup ied whils t the d i sease runs its inev i t ab le course ' .

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FROZEN SHOULDER 565

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