Review Article
Adhesive Capsulitis of the Hip: A Review Abstract Colin G. Looney, MD Brett Raynor, MD Rebecca Lowe, PT, COMT
From the Vanderbilt Bone and Joint Clinic, Vanderbilt University Medical Center, Franklin, TN (Dr. Looney), Vanderbilt University Medical Center, Nashville, TN (Dr. Raynor), and Manual Therapy of Nashville, Nashville (Ms. Lowe). Dr. Raynor or an immediate family member has stock or stock options held in Merck. Neither of the following authors nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Looney and Ms. Lowe. J Am Acad Orthop Surg 2013;21: 749-755 http://dx.doi.org/10.5435/ JAAOS-21-12-749 Copyright 2013 by the American Academy of Orthopaedic Surgeons.
December 2013, Vol 21, No 12
Adhesive capsulitis of the hip (ACH) is a rare clinical entity. Similar to adhesive capsulitis of the shoulder, ACH is characterized by a painful decrease in active and passive range of motion as synovial inflammation in the acute stages of the disease progresses to capsular fibrosis in the chronic stages. Once other diagnoses have been ruled out, management of ACH is tailored to reduce inflammation in the acute stages with NSAIDs, intra-articular steroid injections, and targeted physical therapy while biomechanical dysfunction in the spine, hip, sacroiliac joint, or lower limb joints is addressed. In chronic stages of the disease, intervention should focus on decreasing the progression of fibrotic changes and regaining range of motion through aggressive physical therapy. Interventions described for chronic ACH include manipulation under anesthesia; pressure dilatation; and open or arthroscopic synovectomy, lysis of adhesions, and capsular release. Surgical intervention should be considered only after failure of a minimum 3-month course of nonsurgical treatment.
B
yrd and Jones1 describe adhesive capsulitis of the hip (ACH) as a “clearly identifiable entity” that is similar to adhesive capsulitis of the shoulder (ACS). ACH is characterized by a painful decrease in active and passive range of motion (ROM) as synovial inflammation in the acute stages of the disease progresses to capsular fibrosis in the chronic stages. McGrory and Endrizzi2 suggest that ACH is often overlooked because decreased ROM is better tolerated in the hip than in the shoulder. In 1963, Caroit et al3 were the first to report on capsular constriction of the hip. Since then, approximately 12 articles have referenced this condition; most are case reports and case series.1,2,4-13 In this review, we use the term ACH rather than “capsular constriction”3,7 or “frozen hip.”4,9,10 It should be emphasized
that our review is based on a handful of case reports. Diagnosis of ACH in many of these case reports remains questionable secondary to evidence of concomitant pathology, such as osteoarthritis (OA) or femoroacetabular impingement (FAI), on radiography. This further highlights the fact that true ACH is a rare diagnosis; the surgeon must be meticulous about ruling out other pathologies before arriving at a diagnosis of ACH. Because primary research on the condition is lacking, classification schemes and management strategies have been borrowed from the ACS literature. ACH can occur without concomitant pathology. In a study of nine patients with decreased ROM on examination under anesthesia, Byrd and Jones1 found clear arthroscopic evidence of capsular fibrosis on ar-
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Adhesive Capsulitis of the Hip: A Review
throscopy, with no evidence of other concomitant pathology on imaging or arthroscopy. Modesto et al11 demonstrated the progression from capsular inflammation to capsular fibrosis on biopsy analysis in a single patient with no other underlying pathology. The similarities between the disease processes of ACH and ACS in these and the other case series can only be inferred based on these findings.
Pathology The pathology of ACH follows the same process as that of ACS: synovial inflammation progresses to fibrosis of the capsule.11 In a pivotal study of ACS, Rodeo et al14 demonstrated that both synovial hyperplasia and capsular fibrosis are involved in adhesive capsulitis, with cytokines (eg, transforming growth factor-β, platelet-derived growth factor) possibly involved in the inflammatory and fibrotic processes of ACS. The authors found that matrix-bound transforming growth factor-β can act as a persistent stimulus, resulting in capsular fibrosis. In a study of 15 patients with stage 2 ACS, Mullet et al15 examined shoulder aspirate and demonstrated a dose-dependent relationship between concentrations of cytokines in the shoulder joint and the rate of fibroblast proliferation. Hormonal factors such as diabetes mellitus and thyroid dysfunction have been associated with ACS.16 However, no such association has been noted in the ACH literature and can only be assumed given the similarity between the two conditions.4,7,11 Trauma or sports involvement can be a predisposing factor in ACH.1,11,13 Biomechanical influences on the hip from the lumbar spine, sacroiliac joint, and lower limb joints should be considered as possible catalysts for ACH.
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Prevalence and Natural History The incidence of ACH seems to be substantially lower than that of ACS, but the true incidence remains unknown. To date, approximately 30 cases of ACH have been reported in the literature. Of those cases, no significant difference in the prevalence of ACH in men versus women has been reported, and most cases were reported in middle-aged persons, with only one report of ACH in a 10-year-old girl.11 Although surgical or nonsurgical intervention is performed in most cases of ACH, spontaneous resolution of symptoms is possible. Caroit et al3 reported on two separate cases of ACH; one case resolved spontaneously within 8 months and the other resolved within 2 years. Lequesne et al7 reported on seven cases of ACH with spontaneous resolution of symptoms between 5 and 18 months. Chard and Jenner4 described three cases that resolved spontaneously within 1 year. Luukainen and Asikainen9 described a spontaneous resolution 2 months after failed nonsurgical management (physical therapy and injection).
Staging and Differential Diagnosis The symptoms, signs, arthroscopic appearance, biopsy findings, and time frames of the four stages of ACS have been described and correspond with those of ACH17,18 (Table 1). Stages 1 and 2 are acute and stages 3 and 4 are chronic. In a study of the progression of ACH in a single patient during a 1-year period, Mont et al12 described many aspects of the progression from synovial inflammation to capsular fibrosis without describing the stages of ACH. The differential diagnosis is differ-
ent based on the patient’s age. In children and adolescents, the clinician should consider slipped capital femoral epiphysis, acute or chronic infection, congenital abnormalities (eg, developmental dysplasia of the hip), FAI, and complex regional pain syndrome. In adults, differential diagnoses include OA, inflammatory arthritis, posttraumatic arthritis, neoplasm, labral tears, loose bodies, chondral lesions, osteonecrosis, sacroiliac disease, lumbar pathology, FAI, and complex regional pain syndrome. It should be noted, however, that many of the reported cases of ACH in the literature were published before FAI was recognized as a clinical entity that results in hip pain.
Primary Versus Secondary Adhesive Capsulitis In patients with primary, or idiopathic, adhesive capsulitis, history and physical examination findings that account for the onset of disease are lacking. Secondary adhesive capsulitis develops from known causes such as trauma or surgery.16 If an obvious trauma or structural pathology cannot be found, then dysfunction of the hip, lumbar spine, sacroiliac joint, and lower limb joints should be explored as a microtraumatic cause of ACH. We are careful to differentiate postoperative adhesive capsulitis from primary ACH. Postoperative ACH requires a workup for infection, complex regional pain syndrome, surgical failure, and/or poor rehabilitation. Management of postoperative ACH should be tailored to its underlying cause.
Diagnosis Serology and Imaging In all case reports of ACH, patients were negative for infectious and sys-
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Colin G. Looney, MD, et al
Table 1 Stages of Adhesive Capsulitis Stage 1
2
3
4
Symptoms
Signs
Arthroscopic Appearance
Pain referred to deltoid insertion, pain at night
Capsular pain on deep palpa- Fibrinous synovial inflamtion, empty end feel at exmatory reaction, no adhetremes of motion, full motion sions or capsular contracunder anesthesia ture Severe night pain, stiffness Motion restricted in forward Christmas tree synovitis, flexion, abduction, internal some loss of axillary fold and external rotation, some motion loss under anesthesia Profound stiffness, pain only Significant loss of motion, no Complete loss of axillary at the end range of motion improvements under anesthe- fold, minimal synovitis sia Profound stiffness, pain minimal
Significant motion loss, gradual Fully mature adhesions, improvement in motion identification of intraarticular structures difficult
Biopsy Rare inflammatory cell infiltrate, hypervascular, hypertrophic synovitis, normal capsular tissue Hypertrophic, hypervascular synovitis, perivascular, subsynovial capsular scar Hypercellular, collagenous tissue with a thin synovial layer, similar features to other fibrosing conditions Not reported
Adapted with permission from Neviaser AS, Hannafin JA: Adhesive capsulitis: A review of current treatment. Am J Sports Med 2010;38:23462356.
temic disease. Laboratory tests performed include complete blood count, erythrocyte sedimentation rate, serum uric acid concentration, liver function tests, serum calcium concentration, C-reactive protein level, rheumatoid factor, chemistry panels, and rapid plasma reaction testing as well as Rose-Waaler antibody and other antibody (antinuclear, Chlamydia, Yersinia, and Salmonella) tests.4,6,9-13 Some clinicians have used arthrography to diagnose ACH.3,5,7,13 Lequesne et al7 injected both hips to compare the fluid capacity of the joints. A significant reduction in fluid capacity may indicate ACH; however, a patient may have ACH without a significant reduction in volume.1 In a patient with ACH, standard synovial fluid analysis, including Gram stain, cell count, crystals, and culture, should be normal.4,9,10 Similarly, ultrasound, CT, MRI, and magnetic resonance arthrogram findings can be normal, except in cases with concomitant pathology.1,5-7 In chronic cases (stages 3 or 4) of ACH, MRI can show eviDecember 2013, Vol 21, No 12
dence of capsular fibrosis where there is thickening of the anterior joint capsule.12 Findings on plain radiography and dual-energy x-ray absorptiometry suggest osteopenia or osteoporosis of the femoral head and acetabulum.4,9-11,13 These findings are most likely the result of limb disuse secondary to pain or restriction of motion.
Surgical Appearance In a case report of a single patient with ACH, Mont et al12 reported mild synovitis found during surgical exploration. When the patient underwent capsulectomy 9 months later, no synovial lining was found. Modesto et al11 performed a diagnostic hip arthroscopy in a 10-year-old patient and found that the capsule was tethered to the femoral head and there was no synovial fluid in the joint. In a study of four patients with hip pain who underwent arthrotomy, Griffiths et al5 found a thickened capsule in all patients. Characteristics of adhesive capsulitis (eg, hemorrhagic fibrinous debris in the peri-
capsular recesses and acetabular fossa) have been found in the hip joint during arthroscopy.1
Synovial and Capsular Biopsies Synovial and capsular biopsies are helpful for diagnosis and staging of ACS.17-19 Some studies have reported that the progression from perivascular mononuclear inflammatory infiltrates to reactive capsular fibrosis is clearly demonstrated on biopsy results in patients with stage 1, 2, or 3 ACS.20,21 Because the number of ACH biopsy specimens is limited, insufficient evidence exists to demonstrate the progression from synovial inflammation to capsular fibrosis. However, biopsy results show similarities between ACH and ACS. Mont et al12 reported on biopsy findings in one patient with ACH. The biopsy was obtained during surgical exploration and showed evidence of synovial inflammation. The patient underwent capsulectomy 9 months later; there was evidence of extensive mature fibrosis, and the synovial lin-
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ing was absent. Griffiths et al5 reported similar histologic findings, including a chronic inflammatory reaction in the capsule and evidence of fibroplasia.
Clinical Presentation Presentation of ACH differs based on the stage of disease at the time of examination. The acute stages of ACH are characterized by symptoms and signs of inflammation. Patients often report an insidious onset of pain,1,4-6,8-10,12 microtrauma,5,11 or trauma.1,13 In acute and chronic stages of disease, symptoms can include night pain, difficulty lying on the affected side, and pain with weight-bearing activity. In stages 2 through 4, patients demonstrate decreased active and passive ROM. Pain is the primary cause of limited ROM in the acute stages of ACH. Chronic stages of ACH are characterized by symptoms and signs of fibrosis in the hip.8 Patients describe less pain and more restricted ROM in stages 3 and 4 than in acute stages. Patients also have substantial loss of active and passive ROM, with firm resistance from the capsule at end ROM. Little or no further ROM will be noted on examination under anesthesia compared with that observed on examination without anesthesia.
Physical Examination ROM is tested with the patient in the supine and prone positions so that pain inhibition or resistance from the joint capsule can be assessed. If the patient cannot tolerate these positions, internal and external rotation can be assessed with the patient seated and the hip and knee flexed at 90°. Pain during ROM should be noted. In the acute stages of ACH, pain, which is the limiting factor, precedes restriction of motion. In chronic stages of the condition, mo-
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tion is limited by the fibrotic capsule, and pain will be felt only at the extremes of motion. The ROM of both hips should be assessed and compared, with differences noted. Carvalhais et al22 reported good intra- and interexaminer reliability of clinical tests (for detecting the first position of resistance) used to assess passive stiffness of the hip. However, these findings are nonspecific because pain during ROM is a hallmark of other differential diagnoses, such as OA or FAI. Combined ROM testing can still be useful as a diagnostic adjunct and for documentation of the progression from acute to chronic ACH in a patient already diagnosed with ACH. Pain is taken out of the equation during examination under anesthesia. Byrd and Jones1 examined hip ROM with the patient under anesthesia before manipulation was performed. They measured hip internal rotation and external rotation at 90° of flexion. These measurements are compared to those taken preoperatively and post-intervention. Byrd and Jones1 do not recommend measuring hip flexion and extension because the degree of pelvic flexion cannot be measured reliably.
Management Similar to ACS, many case reports of ACH describe spontaneous resolution of symptoms.3,4,7,9 In cases that do not resolve spontaneously, management methods include pharmacologic intervention, physical therapy, and surgery. In the acute stages of ACH, intervention should focus on decreasing inflammation, addressing concomitant pathology, and correcting any underlying etiologies. In chronic stages, intervention should focus on decreasing the progression of fibrotic changes.
Pharmacology Oral NSAIDs and intra-articular steroid and analgesic injections have been used to manage pain associated with ACH. Injections into the hip joint are helpful for diagnosis. They often offer some pain relief, which suggests that the pain is intraarticular rather than secondary to an extrinsic cause such as the lumbar spine or adjacent musculature; however, this is usually a short-term solution. The patient should be instructed to note how much relief the injection yields. At the time of injection, reduced joint volume is often noted and insertion of the needle may be difficult secondary to capsular fibrosis. Luukkainen et al,10 Mont et al,12 Griffiths et al,5 and Joassin et al6 used injections to manage pain associated with ACH, often with positive results.
Physical Therapy Hannafin and Chiaia17 and Kelley et al23 described a rehabilitation model for management of ACS; this model will likely apply to ACH, as well. The regimen included progression of exercise and manual techniques as tolerated by the patient. The physical therapy regimen should be based on the stage of the disorder. In acute stages of ACH, therapy focuses on decreasing pain and inflammation via anti-inflammatory techniques, functional adaptations, correction of hip and other associated joint mechanics, and correction of muscle imbalances or deficiencies.8 Information on self-treatment and a home therapy program are also provided.8 Aggressive ROM exercises should be avoided in acute stages of ACH because they tend to exacerbate inflammatory symptoms. Chronic ACH requires more aggressive physical therapy techniques to improve joint mechanics and reduce the progression or effects of
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Colin G. Looney, MD, et al
capsular fibrosis. These techniques include increasing ROM through joint mobilization, soft-tissue mobilization, and stretching; strengthening of specific muscles (typically the hip abductors and extensors); and instruction on a home program of aggressive ROM, stretching, strengthening, and self-treatment techniques. The goal of rehabilitation for chronic ACH is a return to prior functional and recreational activities. Evaluation and treatment of joints adjacent to the spine is important. If the mechanics of the hip, lumbar spine, sacroiliac joint, and lower limb joints are not evaluated, treated, and supplemented with ACH stage-appropriate stretching and strengthening exercises and a home physical therapy program, there is little chance for improvement of joint mechanics and reduction in the progression of capsular fibrosis. Physical therapy can reach its maximal benefit during chronic stages of the disease. If no demonstrable improvement is achieved with the use of NSAIDs, corticosteroid injections, and physical therapy, surgery can be considered. Surgery should be avoided in the acute stages of ACH and should be considered only after failure of a 3-month course of nonsurgical measures. This time frame has been extrapolated from common treatment recommendations for ACS described in the literature.17 The definition of failure should also be tailored to the individual patient. The hip tolerates decreased ROM; therefore, restoration of full ROM may not be necessary for nonsurgical management to be considered a success.
Surgery Several surgical options have been described for management of ACS and ACH, including pressure dilatation with joint manipulation December 2013, Vol 21, No 12
performed under anesthesia,10 open synovectomy,11 and arthroscopic surgery.1 Often, saline and a steroid are injected under pressure into the joint in an effort to dilate the constricted capsule. Buchbinder et al24 used this technique to manage ACS and concluded that the technique had shortterm benefits when compared with placebo. If this technique is used, it should be an adjunct to a standard physical therapy protocol. The hip is manipulated under anesthesia in conjunction with pressure dilatation,10 open synovectomy,11 or arthroscopic surgery.1 In a study of nine patients with ACH, Byrd and Jones1 performed the manipulation before arthroscopy. The lower extremity was placed in the figure-offour position, with a downward force directed on the knee. The authors stressed the importance of stabilizing the body with only the weight of the torso to avoid excessive stress and possible fracture of the femoral neck.1 Byrd and Jones1 and Modesto et al11 described feeling and hearing crepitus during manipulation as capsular adhesions were disrupted. Open surgery for management of ACH and concomitant pathology has been well described in the literature.5,7,11,12 Procedures include manipulation, synovectomy, capsulectomy, and total hip arthroplasty (THA). Synovitis is prevalent during the acute stages of ACH, and several studies have described the use of synovectomy in patients with ACH.6,7,13 However, similar to ACS, surgical intervention during acute stages of ACH should be discouraged and nonsurgical measures should be pursued. Nonsurgical measures are meant to maintain motion during the acute, inflammatory stages, and, as with ACS, it is believed that capsular constriction can be exacerbated by operating in the inflammatory environment of stages 1 and 2.25 Mont
et al12 and Lequesne et al7 reported on the use of capsulectomy for ACH. Portions of the fibrotic capsule were removed to improve ROM. However, the results were skewed because many of the patients had evidence of degenerative joint disease on plain radiographs. Several studies reported on the use of THA in patients with ACH and additional hip degeneration to such a degree that THA was required.6,7,13 Although the patients in these studies were said to have ACH, capsular constriction associated with OA of the hip should be considered part of the degenerative disease process. The senior author (C.G.L.) does not feel that these patients had true ACH. Many of the case series that we reviewed included patients with obvious degenerative joint disease, which makes it difficult to extrapolate a treatment strategy based on these articles.
Authors’ Preferred Technique Similar to ACS, open surgery for capsular release will likely be replaced by less invasive arthroscopic techniques.16 We recommend combined gentle manipulation under anesthesia with an arthroscopic capsular release. The release of adhesions is felt with the characteristic crepitus that is often noted with shoulder manipulation. Following the manipulation, an arthroscopic capsular release can be performed, using a two- or three-portal technique. Release of the adherent capsule is performed using an arthroscopic banana or beaver blade in combination with a radiofrequency device (Figure 1). The radiofrequency device should be used to lyse only the capsule, not the articular cartilage, and it should not be used for capsular shrinkage. In the senior author’s (C.G.L.) experience, release of the capsule from the
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Adhesive Capsulitis of the Hip: A Review
Figure 1
Arthroscopic image of the left hip demonstrating capsular labral adhesions viewed from the mid anterior portal. The arthroscopic shaver is adjacent to the adhesions with the femoral head below.
labral-capsular junction is believed to diminish the risk of recurrent adhesions. Concomitant intra-articular pathology (eg, labral tears, loose bodies, synovitis, abnormal osseous morphology from FAI) can be addressed; however, when substantial soft-tissue labral repair and bony contouring (osteoplasty) are required, we prefer to avoid ACH surgery to prevent further adhesion formation. After a central compartment capsular release is performed, a thorough evaluation of the peripheral compartment is undertaken, releasing the adhesions encountered. Postoperatively, limited weight bearing is suggested for 7 to 14 days until the patient’s gait is normalized. We prefer to use a block or epidural so that therapy can commence the day of surgery or shortly thereafter. Functional exercises are begun as the patient’s progress dictates, typically at 6 to 12 weeks after surgery.
pathology, this condition can be detected in the setting of painful, restricted hip ROM with no systemic disease or local infection. Diagnostic tests for other pathologies may be negative. Staging of ACH is based on symptoms, signs, the arthroscopic appearance of the hip joint, and biopsy results. Stages 1 and 2 represent acute disease, and stages 3 and 4 represent chronic ACH. However, more studies are needed to determine effective treatment strategies associated with these identifiable stages. Thorough clinical evaluation, including assessment and management of biomechanical dysfunction of the hip, lumbar spine, sacroiliac joint, and lower limb joints, and referral to an experienced manual physical therapist are crucial for effective management of ACH. Pharmacologic measures, physical therapy, and surgical management should be tailored to the stage of ACH. Nonsurgical management is often successful but can take a protracted amount of time and requires patient compliance. In recalcitrant cases of chronic ACH, surgical intervention can be beneficial, but surgery should be avoided in acute stages of the disease.
Byrd and Jones describe ACH as a “clearly identifiable entity” and, whether alone or with concomitant
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Caroit M, Djian A, Hubault A, Normandin C, De Seze S: 2 cases of retractile capsulitis of the hip [French]. Rev Rhum Mal Osteoartic 1963;30:784789.
4.
Chard MD, Jenner JR: The frozen hip: An underdiagnosed condition. BMJ 1988;297(6648):596-597.
5.
Griffiths HJ, Utz R, Burke J, Bonfiglio T: Adhesive capsulitis of the hip and ankle. AJR Am J Roentgenol 1985;144(1):101105.
6.
Joassin R, Vandemeulebroucke M, Nisolle JF, Hanson P, Deltombe T: Adhesive capsulitis of the hip: Three case reports. Ann Readapt Med Phys 2008; 51(4):301-314.
7.
Lequesne M, Becker J, Bard M, Witvoet J, Postel M: Capsular constriction of the hip: Arthrographic and clinical considerations. Skeletal Radiol 1981; 6(1):1-10.
8.
Lowe R: Adhesive capsulitis of the hip: A case report. An entity in question. Man Ther 2012; Sep 20, [Epub ahead of print].
9.
Luukkainen R, Asikainen E: Frozen hip. Scand J Rheumatol 1992;21(2):97.
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Luukkainen R, Sipola E, Varjo P: Successful treatment of frozen hip with manipulation and pressure dilatation. Open Rheumatol J 2008;2:31-32.
11.
Modesto C, Crespo E, Villas C, Aquerreta D: Adhesive capsulitis. Is it possible in childhood? Scand J Rheumatol 1995;24(4):255-256.
12.
Mont MA, Lindsey JM, Hungerford DS: Adhesive capsulitis of the hip. Orthopedics 1999;22(3):343-345.
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Murphy WA, Siegel MJ, Gilula LA: Arthrography in the diagnosis of unexplained chronic hip pain with regional osteopenia. AJR Am J Roentgenol 1977;129(2):283-287.
14.
Rodeo SA, Hannafin JA, Tom J, Warren RF, Wickiewicz TL: Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder. J Orthop Res 1997;15(3):427-436.
15.
Mullett H, Byrne D, Colville J: Adhesive capsulitis: Human fibroblast response to shoulder joint aspirate from patients with stage II disease. J Shoulder Elbow Surg 2007;16(3):290-294.
16.
Hsu JE, Anakwenze OA, Warrender WJ, Abboud JA: Current review of adhesive capsulitis. J Shoulder Elbow Surg 2011; 20(3):502-514.
17.
Hannafin JA, Chiaia TA: Adhesive capsulitis: A treatment approach. Clin Orthop Relat Res 2000;(372):95-109.
18.
Neviaser AS, Hannafin JA: Adhesive capsulitis: A review of current treatment.
References Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, reference 24 is a level I study. References 1-13, 16, 17, and 22 are level IV studies. Reference 23 is level V expert opinion. References printed in bold type are those published within the past 5 years. 1.
Byrd JW, Jones KS: Adhesive capsulitis of the hip. Arthroscopy 2006;22(1):8994.
2.
McGrory BJ, Endrizzi DP: Adhesive capsulitis of the hip after bilateral adhesive capsulitis of the shoulder. Am J Orthop (Belle Mead NJ) 2000;29(6): 457-460.
Summary 1
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Colin G. Looney, MD, et al Am J Sports Med 2010;38(11):23462356. 19.
20.
21.
Neviaser AS, Neviaser RJ: Adhesive capsulitis of the shoulder. J Am Acad Orthop Surg 2011;19(9):536-542. Hannafin JA, Dicarlo EF, Wickiewicz TL, Warren RF: Adhesive capsulitis: Capsular fibroplasia of the glenohumeral joint. J Shoulder Elbow Surg 1994;3(5): 435. Nago M, Mitsui Y, Gotoh M, et al: Hyaluronan modulates cell proliferation
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22.
23.
and mRNA expression of adhesionrelated procollagens and cytokines in glenohumeral synovial/capsular fibroblasts in adhesive capsulitis. J Orthop Res 2010;28(6):726-731.
24.
Carvalhais VO, de Araújo VL, Souza TR, Gonçalves GG, Ocarino Jde M, Fonseca ST: Validity and reliability of clinical tests for assessing hip passive stiffness. Man Ther 2011;16(3):240-245.
Buchbinder R, Green S, Youd JM, Johnston RV, Cumpston M: Arthrographic distension for adhesive capsulitis (frozen shoulder). Cochrane Database Syst Rev 2008;(1):CD007005.
25.
Neviaser RJ, Neviaser TJ: The frozen shoulder: Diagnosis and management. Clin Orthop Relat Res 1987;223:59-64.
Kelley MJ, McClure PW, Leggin BG: Frozen shoulder: Evidence and a
proposed model guiding rehabilitation. J Orthop Sports Phys Ther 2009;39(2): 135-148.
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Adhesive Capsulitis of the Hip: A Review Abstract Colin G. Looney, MD Brett Raynor, MD Rebecca Lowe, PT, COMT
From the Vanderbilt Bone and Joint Clinic, Vanderbilt University Medical Center, Franklin, TN (Dr. Looney), Vanderbilt University Medical Center, Nashville, TN (Dr. Raynor), and Manual Therapy of Nashville, Nashville (Ms. Lowe). Dr. Raynor or an immediate family member has stock or stock options held in Merck. Neither of the following authors nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this article: Dr. Looney and Ms. Lowe. J Am Acad Orthop Surg 2013;21: 749-755 http://dx.doi.org/10.5435/ JAAOS-21-12-749 Copyright 2013 by the American Academy of Orthopaedic Surgeons.
December 2013, Vol 21, No 12
Adhesive capsulitis of the hip (ACH) is a rare clinical entity. Similar to adhesive capsulitis of the shoulder, ACH is characterized by a painful decrease in active and passive range of motion as synovial inflammation in the acute stages of the disease progresses to capsular fibrosis in the chronic stages. Once other diagnoses have been ruled out, management of ACH is tailored to reduce inflammation in the acute stages with NSAIDs, intra-articular steroid injections, and targeted physical therapy while biomechanical dysfunction in the spine, hip, sacroiliac joint, or lower limb joints is addressed. In chronic stages of the disease, intervention should focus on decreasing the progression of fibrotic changes and regaining range of motion through aggressive physical therapy. Interventions described for chronic ACH include manipulation under anesthesia; pressure dilatation; and open or arthroscopic synovectomy, lysis of adhesions, and capsular release. Surgical intervention should be considered only after failure of a minimum 3-month course of nonsurgical treatment.
B
yrd and Jones1 describe adhesive capsulitis of the hip (ACH) as a “clearly identifiable entity” that is similar to adhesive capsulitis of the shoulder (ACS). ACH is characterized by a painful decrease in active and passive range of motion (ROM) as synovial inflammation in the acute stages of the disease progresses to capsular fibrosis in the chronic stages. McGrory and Endrizzi2 suggest that ACH is often overlooked because decreased ROM is better tolerated in the hip than in the shoulder. In 1963, Caroit et al3 were the first to report on capsular constriction of the hip. Since then, approximately 12 articles have referenced this condition; most are case reports and case series.1,2,4-13 In this review, we use the term ACH rather than “capsular constriction”3,7 or “frozen hip.”4,9,10 It should be emphasized
that our review is based on a handful of case reports. Diagnosis of ACH in many of these case reports remains questionable secondary to evidence of concomitant pathology, such as osteoarthritis (OA) or femoroacetabular impingement (FAI), on radiography. This further highlights the fact that true ACH is a rare diagnosis; the surgeon must be meticulous about ruling out other pathologies before arriving at a diagnosis of ACH. Because primary research on the condition is lacking, classification schemes and management strategies have been borrowed from the ACS literature. ACH can occur without concomitant pathology. In a study of nine patients with decreased ROM on examination under anesthesia, Byrd and Jones1 found clear arthroscopic evidence of capsular fibrosis on ar-
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Adhesive Capsulitis of the Hip: A Review
throscopy, with no evidence of other concomitant pathology on imaging or arthroscopy. Modesto et al11 demonstrated the progression from capsular inflammation to capsular fibrosis on biopsy analysis in a single patient with no other underlying pathology. The similarities between the disease processes of ACH and ACS in these and the other case series can only be inferred based on these findings.
Pathology The pathology of ACH follows the same process as that of ACS: synovial inflammation progresses to fibrosis of the capsule.11 In a pivotal study of ACS, Rodeo et al14 demonstrated that both synovial hyperplasia and capsular fibrosis are involved in adhesive capsulitis, with cytokines (eg, transforming growth factor-β, platelet-derived growth factor) possibly involved in the inflammatory and fibrotic processes of ACS. The authors found that matrix-bound transforming growth factor-β can act as a persistent stimulus, resulting in capsular fibrosis. In a study of 15 patients with stage 2 ACS, Mullet et al15 examined shoulder aspirate and demonstrated a dose-dependent relationship between concentrations of cytokines in the shoulder joint and the rate of fibroblast proliferation. Hormonal factors such as diabetes mellitus and thyroid dysfunction have been associated with ACS.16 However, no such association has been noted in the ACH literature and can only be assumed given the similarity between the two conditions.4,7,11 Trauma or sports involvement can be a predisposing factor in ACH.1,11,13 Biomechanical influences on the hip from the lumbar spine, sacroiliac joint, and lower limb joints should be considered as possible catalysts for ACH.
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Prevalence and Natural History The incidence of ACH seems to be substantially lower than that of ACS, but the true incidence remains unknown. To date, approximately 30 cases of ACH have been reported in the literature. Of those cases, no significant difference in the prevalence of ACH in men versus women has been reported, and most cases were reported in middle-aged persons, with only one report of ACH in a 10-year-old girl.11 Although surgical or nonsurgical intervention is performed in most cases of ACH, spontaneous resolution of symptoms is possible. Caroit et al3 reported on two separate cases of ACH; one case resolved spontaneously within 8 months and the other resolved within 2 years. Lequesne et al7 reported on seven cases of ACH with spontaneous resolution of symptoms between 5 and 18 months. Chard and Jenner4 described three cases that resolved spontaneously within 1 year. Luukainen and Asikainen9 described a spontaneous resolution 2 months after failed nonsurgical management (physical therapy and injection).
Staging and Differential Diagnosis The symptoms, signs, arthroscopic appearance, biopsy findings, and time frames of the four stages of ACS have been described and correspond with those of ACH17,18 (Table 1). Stages 1 and 2 are acute and stages 3 and 4 are chronic. In a study of the progression of ACH in a single patient during a 1-year period, Mont et al12 described many aspects of the progression from synovial inflammation to capsular fibrosis without describing the stages of ACH. The differential diagnosis is differ-
ent based on the patient’s age. In children and adolescents, the clinician should consider slipped capital femoral epiphysis, acute or chronic infection, congenital abnormalities (eg, developmental dysplasia of the hip), FAI, and complex regional pain syndrome. In adults, differential diagnoses include OA, inflammatory arthritis, posttraumatic arthritis, neoplasm, labral tears, loose bodies, chondral lesions, osteonecrosis, sacroiliac disease, lumbar pathology, FAI, and complex regional pain syndrome. It should be noted, however, that many of the reported cases of ACH in the literature were published before FAI was recognized as a clinical entity that results in hip pain.
Primary Versus Secondary Adhesive Capsulitis In patients with primary, or idiopathic, adhesive capsulitis, history and physical examination findings that account for the onset of disease are lacking. Secondary adhesive capsulitis develops from known causes such as trauma or surgery.16 If an obvious trauma or structural pathology cannot be found, then dysfunction of the hip, lumbar spine, sacroiliac joint, and lower limb joints should be explored as a microtraumatic cause of ACH. We are careful to differentiate postoperative adhesive capsulitis from primary ACH. Postoperative ACH requires a workup for infection, complex regional pain syndrome, surgical failure, and/or poor rehabilitation. Management of postoperative ACH should be tailored to its underlying cause.
Diagnosis Serology and Imaging In all case reports of ACH, patients were negative for infectious and sys-
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Colin G. Looney, MD, et al
Table 1 Stages of Adhesive Capsulitis Stage 1
2
3
4
Symptoms
Signs
Arthroscopic Appearance
Pain referred to deltoid insertion, pain at night
Capsular pain on deep palpa- Fibrinous synovial inflamtion, empty end feel at exmatory reaction, no adhetremes of motion, full motion sions or capsular contracunder anesthesia ture Severe night pain, stiffness Motion restricted in forward Christmas tree synovitis, flexion, abduction, internal some loss of axillary fold and external rotation, some motion loss under anesthesia Profound stiffness, pain only Significant loss of motion, no Complete loss of axillary at the end range of motion improvements under anesthe- fold, minimal synovitis sia Profound stiffness, pain minimal
Significant motion loss, gradual Fully mature adhesions, improvement in motion identification of intraarticular structures difficult
Biopsy Rare inflammatory cell infiltrate, hypervascular, hypertrophic synovitis, normal capsular tissue Hypertrophic, hypervascular synovitis, perivascular, subsynovial capsular scar Hypercellular, collagenous tissue with a thin synovial layer, similar features to other fibrosing conditions Not reported
Adapted with permission from Neviaser AS, Hannafin JA: Adhesive capsulitis: A review of current treatment. Am J Sports Med 2010;38:23462356.
temic disease. Laboratory tests performed include complete blood count, erythrocyte sedimentation rate, serum uric acid concentration, liver function tests, serum calcium concentration, C-reactive protein level, rheumatoid factor, chemistry panels, and rapid plasma reaction testing as well as Rose-Waaler antibody and other antibody (antinuclear, Chlamydia, Yersinia, and Salmonella) tests.4,6,9-13 Some clinicians have used arthrography to diagnose ACH.3,5,7,13 Lequesne et al7 injected both hips to compare the fluid capacity of the joints. A significant reduction in fluid capacity may indicate ACH; however, a patient may have ACH without a significant reduction in volume.1 In a patient with ACH, standard synovial fluid analysis, including Gram stain, cell count, crystals, and culture, should be normal.4,9,10 Similarly, ultrasound, CT, MRI, and magnetic resonance arthrogram findings can be normal, except in cases with concomitant pathology.1,5-7 In chronic cases (stages 3 or 4) of ACH, MRI can show eviDecember 2013, Vol 21, No 12
dence of capsular fibrosis where there is thickening of the anterior joint capsule.12 Findings on plain radiography and dual-energy x-ray absorptiometry suggest osteopenia or osteoporosis of the femoral head and acetabulum.4,9-11,13 These findings are most likely the result of limb disuse secondary to pain or restriction of motion.
Surgical Appearance In a case report of a single patient with ACH, Mont et al12 reported mild synovitis found during surgical exploration. When the patient underwent capsulectomy 9 months later, no synovial lining was found. Modesto et al11 performed a diagnostic hip arthroscopy in a 10-year-old patient and found that the capsule was tethered to the femoral head and there was no synovial fluid in the joint. In a study of four patients with hip pain who underwent arthrotomy, Griffiths et al5 found a thickened capsule in all patients. Characteristics of adhesive capsulitis (eg, hemorrhagic fibrinous debris in the peri-
capsular recesses and acetabular fossa) have been found in the hip joint during arthroscopy.1
Synovial and Capsular Biopsies Synovial and capsular biopsies are helpful for diagnosis and staging of ACS.17-19 Some studies have reported that the progression from perivascular mononuclear inflammatory infiltrates to reactive capsular fibrosis is clearly demonstrated on biopsy results in patients with stage 1, 2, or 3 ACS.20,21 Because the number of ACH biopsy specimens is limited, insufficient evidence exists to demonstrate the progression from synovial inflammation to capsular fibrosis. However, biopsy results show similarities between ACH and ACS. Mont et al12 reported on biopsy findings in one patient with ACH. The biopsy was obtained during surgical exploration and showed evidence of synovial inflammation. The patient underwent capsulectomy 9 months later; there was evidence of extensive mature fibrosis, and the synovial lin-
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Adhesive Capsulitis of the Hip: A Review
ing was absent. Griffiths et al5 reported similar histologic findings, including a chronic inflammatory reaction in the capsule and evidence of fibroplasia.
Clinical Presentation Presentation of ACH differs based on the stage of disease at the time of examination. The acute stages of ACH are characterized by symptoms and signs of inflammation. Patients often report an insidious onset of pain,1,4-6,8-10,12 microtrauma,5,11 or trauma.1,13 In acute and chronic stages of disease, symptoms can include night pain, difficulty lying on the affected side, and pain with weight-bearing activity. In stages 2 through 4, patients demonstrate decreased active and passive ROM. Pain is the primary cause of limited ROM in the acute stages of ACH. Chronic stages of ACH are characterized by symptoms and signs of fibrosis in the hip.8 Patients describe less pain and more restricted ROM in stages 3 and 4 than in acute stages. Patients also have substantial loss of active and passive ROM, with firm resistance from the capsule at end ROM. Little or no further ROM will be noted on examination under anesthesia compared with that observed on examination without anesthesia.
Physical Examination ROM is tested with the patient in the supine and prone positions so that pain inhibition or resistance from the joint capsule can be assessed. If the patient cannot tolerate these positions, internal and external rotation can be assessed with the patient seated and the hip and knee flexed at 90°. Pain during ROM should be noted. In the acute stages of ACH, pain, which is the limiting factor, precedes restriction of motion. In chronic stages of the condition, mo-
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tion is limited by the fibrotic capsule, and pain will be felt only at the extremes of motion. The ROM of both hips should be assessed and compared, with differences noted. Carvalhais et al22 reported good intra- and interexaminer reliability of clinical tests (for detecting the first position of resistance) used to assess passive stiffness of the hip. However, these findings are nonspecific because pain during ROM is a hallmark of other differential diagnoses, such as OA or FAI. Combined ROM testing can still be useful as a diagnostic adjunct and for documentation of the progression from acute to chronic ACH in a patient already diagnosed with ACH. Pain is taken out of the equation during examination under anesthesia. Byrd and Jones1 examined hip ROM with the patient under anesthesia before manipulation was performed. They measured hip internal rotation and external rotation at 90° of flexion. These measurements are compared to those taken preoperatively and post-intervention. Byrd and Jones1 do not recommend measuring hip flexion and extension because the degree of pelvic flexion cannot be measured reliably.
Management Similar to ACS, many case reports of ACH describe spontaneous resolution of symptoms.3,4,7,9 In cases that do not resolve spontaneously, management methods include pharmacologic intervention, physical therapy, and surgery. In the acute stages of ACH, intervention should focus on decreasing inflammation, addressing concomitant pathology, and correcting any underlying etiologies. In chronic stages, intervention should focus on decreasing the progression of fibrotic changes.
Pharmacology Oral NSAIDs and intra-articular steroid and analgesic injections have been used to manage pain associated with ACH. Injections into the hip joint are helpful for diagnosis. They often offer some pain relief, which suggests that the pain is intraarticular rather than secondary to an extrinsic cause such as the lumbar spine or adjacent musculature; however, this is usually a short-term solution. The patient should be instructed to note how much relief the injection yields. At the time of injection, reduced joint volume is often noted and insertion of the needle may be difficult secondary to capsular fibrosis. Luukkainen et al,10 Mont et al,12 Griffiths et al,5 and Joassin et al6 used injections to manage pain associated with ACH, often with positive results.
Physical Therapy Hannafin and Chiaia17 and Kelley et al23 described a rehabilitation model for management of ACS; this model will likely apply to ACH, as well. The regimen included progression of exercise and manual techniques as tolerated by the patient. The physical therapy regimen should be based on the stage of the disorder. In acute stages of ACH, therapy focuses on decreasing pain and inflammation via anti-inflammatory techniques, functional adaptations, correction of hip and other associated joint mechanics, and correction of muscle imbalances or deficiencies.8 Information on self-treatment and a home therapy program are also provided.8 Aggressive ROM exercises should be avoided in acute stages of ACH because they tend to exacerbate inflammatory symptoms. Chronic ACH requires more aggressive physical therapy techniques to improve joint mechanics and reduce the progression or effects of
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Colin G. Looney, MD, et al
capsular fibrosis. These techniques include increasing ROM through joint mobilization, soft-tissue mobilization, and stretching; strengthening of specific muscles (typically the hip abductors and extensors); and instruction on a home program of aggressive ROM, stretching, strengthening, and self-treatment techniques. The goal of rehabilitation for chronic ACH is a return to prior functional and recreational activities. Evaluation and treatment of joints adjacent to the spine is important. If the mechanics of the hip, lumbar spine, sacroiliac joint, and lower limb joints are not evaluated, treated, and supplemented with ACH stage-appropriate stretching and strengthening exercises and a home physical therapy program, there is little chance for improvement of joint mechanics and reduction in the progression of capsular fibrosis. Physical therapy can reach its maximal benefit during chronic stages of the disease. If no demonstrable improvement is achieved with the use of NSAIDs, corticosteroid injections, and physical therapy, surgery can be considered. Surgery should be avoided in the acute stages of ACH and should be considered only after failure of a 3-month course of nonsurgical measures. This time frame has been extrapolated from common treatment recommendations for ACS described in the literature.17 The definition of failure should also be tailored to the individual patient. The hip tolerates decreased ROM; therefore, restoration of full ROM may not be necessary for nonsurgical management to be considered a success.
Surgery Several surgical options have been described for management of ACS and ACH, including pressure dilatation with joint manipulation December 2013, Vol 21, No 12
performed under anesthesia,10 open synovectomy,11 and arthroscopic surgery.1 Often, saline and a steroid are injected under pressure into the joint in an effort to dilate the constricted capsule. Buchbinder et al24 used this technique to manage ACS and concluded that the technique had shortterm benefits when compared with placebo. If this technique is used, it should be an adjunct to a standard physical therapy protocol. The hip is manipulated under anesthesia in conjunction with pressure dilatation,10 open synovectomy,11 or arthroscopic surgery.1 In a study of nine patients with ACH, Byrd and Jones1 performed the manipulation before arthroscopy. The lower extremity was placed in the figure-offour position, with a downward force directed on the knee. The authors stressed the importance of stabilizing the body with only the weight of the torso to avoid excessive stress and possible fracture of the femoral neck.1 Byrd and Jones1 and Modesto et al11 described feeling and hearing crepitus during manipulation as capsular adhesions were disrupted. Open surgery for management of ACH and concomitant pathology has been well described in the literature.5,7,11,12 Procedures include manipulation, synovectomy, capsulectomy, and total hip arthroplasty (THA). Synovitis is prevalent during the acute stages of ACH, and several studies have described the use of synovectomy in patients with ACH.6,7,13 However, similar to ACS, surgical intervention during acute stages of ACH should be discouraged and nonsurgical measures should be pursued. Nonsurgical measures are meant to maintain motion during the acute, inflammatory stages, and, as with ACS, it is believed that capsular constriction can be exacerbated by operating in the inflammatory environment of stages 1 and 2.25 Mont
et al12 and Lequesne et al7 reported on the use of capsulectomy for ACH. Portions of the fibrotic capsule were removed to improve ROM. However, the results were skewed because many of the patients had evidence of degenerative joint disease on plain radiographs. Several studies reported on the use of THA in patients with ACH and additional hip degeneration to such a degree that THA was required.6,7,13 Although the patients in these studies were said to have ACH, capsular constriction associated with OA of the hip should be considered part of the degenerative disease process. The senior author (C.G.L.) does not feel that these patients had true ACH. Many of the case series that we reviewed included patients with obvious degenerative joint disease, which makes it difficult to extrapolate a treatment strategy based on these articles.
Authors’ Preferred Technique Similar to ACS, open surgery for capsular release will likely be replaced by less invasive arthroscopic techniques.16 We recommend combined gentle manipulation under anesthesia with an arthroscopic capsular release. The release of adhesions is felt with the characteristic crepitus that is often noted with shoulder manipulation. Following the manipulation, an arthroscopic capsular release can be performed, using a two- or three-portal technique. Release of the adherent capsule is performed using an arthroscopic banana or beaver blade in combination with a radiofrequency device (Figure 1). The radiofrequency device should be used to lyse only the capsule, not the articular cartilage, and it should not be used for capsular shrinkage. In the senior author’s (C.G.L.) experience, release of the capsule from the
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Adhesive Capsulitis of the Hip: A Review
Figure 1
Arthroscopic image of the left hip demonstrating capsular labral adhesions viewed from the mid anterior portal. The arthroscopic shaver is adjacent to the adhesions with the femoral head below.
labral-capsular junction is believed to diminish the risk of recurrent adhesions. Concomitant intra-articular pathology (eg, labral tears, loose bodies, synovitis, abnormal osseous morphology from FAI) can be addressed; however, when substantial soft-tissue labral repair and bony contouring (osteoplasty) are required, we prefer to avoid ACH surgery to prevent further adhesion formation. After a central compartment capsular release is performed, a thorough evaluation of the peripheral compartment is undertaken, releasing the adhesions encountered. Postoperatively, limited weight bearing is suggested for 7 to 14 days until the patient’s gait is normalized. We prefer to use a block or epidural so that therapy can commence the day of surgery or shortly thereafter. Functional exercises are begun as the patient’s progress dictates, typically at 6 to 12 weeks after surgery.
pathology, this condition can be detected in the setting of painful, restricted hip ROM with no systemic disease or local infection. Diagnostic tests for other pathologies may be negative. Staging of ACH is based on symptoms, signs, the arthroscopic appearance of the hip joint, and biopsy results. Stages 1 and 2 represent acute disease, and stages 3 and 4 represent chronic ACH. However, more studies are needed to determine effective treatment strategies associated with these identifiable stages. Thorough clinical evaluation, including assessment and management of biomechanical dysfunction of the hip, lumbar spine, sacroiliac joint, and lower limb joints, and referral to an experienced manual physical therapist are crucial for effective management of ACH. Pharmacologic measures, physical therapy, and surgical management should be tailored to the stage of ACH. Nonsurgical management is often successful but can take a protracted amount of time and requires patient compliance. In recalcitrant cases of chronic ACH, surgical intervention can be beneficial, but surgery should be avoided in acute stages of the disease.
Byrd and Jones describe ACH as a “clearly identifiable entity” and, whether alone or with concomitant
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