Adhesive Capsulitis (Frozen Shoulder)

                                Dr. KS Dhillon

Introduction

The two terms that have been used to describe a painful and stiff shoulder are adhesive capsulitis and frozen shoulder syndrome (FSS). The consensus definition of a frozen shoulder by the American Shoulder and Elbow Surgeons is "a condition of uncertain etiology characterized by significant restriction of both active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder" [1].  The American Academy of Orthopaedic Surgeons has defined this condition as: "A condition of varying severity characterized by the gradual development of global limitation of active and passive shoulder motion where radiographic findings other than osteopenia are absent."

In frozen shoulder there is a loss of passive range of motion (ROM). This passive loss of motion is a critical element in establishing the diagnosis of a true frozen shoulder. Conditions such as subacromial bursitis, calcifying tendinitis, and partial rotator cuff tears can be associated with significant pain and loss of active ROM, passive ROM is usually preserved. 

Lundberg divided patients with frozen shoulder into two groups: primary and secondary [2]. In patients with primary frozen shoulder there is no known cause for motion loss and pain. Patients with secondary FSS describe an event that preceded the onset of shoulder symptoms. Symptoms of primary frozen shoulder have been divided into three phases: namely freezing (painful), frozen (stiffening), and thawing.

The initial painful phase is marked by a gradual onset of diffuse shoulder pain lasting 9 months. The stiffening phase is characterized by a progressive loss of ROM that may last from 4 months to 20 months. Most of the patients lose glenohumeral external rotation, internal rotation, and abduction during this phase. The final, thawing phase is from 5 months to 26 months. It constitutes a period of gradual motion improvement. Once in this phase, the patient may require up to 9 months to regain a functional shoulder ROM [3-6].

Younger patients and patients with diabetes may be more likely to develop contralateral idiopathic adhesive capsulitis [7].

Unlike patients with primary FSS, patients with secondary FSS describe an event that preceded the onset of shoulder symptoms. These include:

• Upper extremity trauma (eg, proximal humerus fracture, shoulder surgery, rotator cuff tear)

• Immobilization (eg, neurosurgery, cardiothoracic surgery)

•  Metabolic/endocrine (eg, diabetics, thyroid disease, autoimmune disease, hyperlipidemia)

• Neurologic (eg, Parkinson disease, stroke)

• Cardiac disease (eg, hypertension, ischemic heart disease) 

• Drugs (eg, antiretrovirals, immunizations, protease inhibitors, fluoroquinolones)

• Malignancy

Etiology

Duplay was the first physician to present the concept of periarticular tissue pathology rather than periarticular arthritis as the cause of frozen shoulder [8]. There is no evidence linking frozen shoulder to any specific etiology.  However, various triggers that may predispose patients to FSS appear to exist. Some of these etiologic agents include:

• Trauma

• Inflammatory disease

• Diabetes

• Regional surgery 

• Regional conditions

• Various shoulder maladies

An autoimmune theory has been postulated, with elevated levels of C-reactive protein and an increased incidence of HLA-B27 histocompatibility antigen reported in patients with frozen shoulder as compared to controls [9,10]. DePalma was of the opinion that muscular inactivity was a major etiologic factor [11]. Bridgman identified an increased incidence of FSS in patients with diabetes mellitus [12]. Frozen shoulder  has been associated with the following disorders:

• Parkinson disease [13]

• Hyperthyroidism [14]

• Hypothyroidism

• Cervical spine disease

• Ischemic heart disease

Most patients with FSS have undergone a period of shoulder immobilization for various reasons. Reasons for immobilization can be diverse. The common finding in all of these patients is a period of restricted shoulder motion. Bruckner in a study of neurosurgery patients who immobilized their shoulder for varying periods found that the incidence of frozen shoulder was 5 to 9 times greater than that found in the general population [15].

Epidemiology

Frozen shoulder syndrome (FSS) usually affects patients aged between 40 to 60 years. Although the precise incidence of FSS is not known, it is estimated that 2% to 5% of the general population develops the disease during their lifetime [16]. Men are usually less affected than women, and there is no predilection for race. Bilateral shoulder involvement is rarely simultaneous. It occurs sequentially.

Diabetes mellitus is a risk factor for FSS. Diabetic patients are 5 times more likely to develop adhesive capsulitis as compared to non-diabetic controls. There is a 13.4% overall mean prevalence of adhesive capsulitis in patients with diabetes and there is a 30% mean prevalence of diabetes in a population with adhesive capsulitis. There is no significant difference in the prevalence of the disorder with type 1 versus type 2 diabetes or between patients on insulin therapy and those on oral hypoglycemic agents [17].

Pathophysiology

In frozen shoulders, there is fibrotic and inflammatory contracture of the rotator interval, capsule, and ligaments. The development of adhesive capsulitis (AC) remains poorly understood. Although there are disagreements, the most recognized pathology is cytokine-mediated synovial inflammation with fibroblastic proliferation. In addition, there are adhesions around the rotator interval caused by increased collagen and nodular band formation.

The structure that is usually first affected is the coracohumeral ligament which forms the roof of the rotator cuff interval. Contraction of this ligament limits external rotation of the arm, which is usually first affected in early AC. In later stages, thickening and contraction of the glenohumeral joint capsule occurs which further limits the range of motion in all directions [18].

Histopathology

Histopathology studies have shown a significant increase in fibroblasts, myofibroblasts, and inflammatory cells, like B-lymphocytes, mast cells, and macrophages in the glenohumeral capsule.

History and Physical Examination

Patients having early AC usually present with a sudden onset of unilateral anterior shoulder pain. The typical symptoms include limitation of both passive and active range of motion. First external rotation and later abduction of the shoulder is affected. In general, depending on the stage and severity, the condition is self-limiting. It interferes with activities of daily living, work, as well as leisure activities. Functional impairments caused by a frozen shoulder consist of limiting reach, particularly during overhead or to-the-side activities. 

Patients also have restricted shoulder rotations, resulting in difficulties in personal hygiene, brushing their hair, and wearing their clothes. Patients with frozen shoulder often have neck pain because of overuse of cervical muscles to compensate for the loss of shoulder motion.

A physical examination is essential for the diagnosis of a frozen shoulder. 

Two physical examinations are commonly used for diagnosing AC. These include tests of combined motion, such as touching the scapula from behind the back and from behind the neck. The most pathognomonic feature of AC is the loss of passive ROM. 

Generally, patients with frozen shoulder usually demonstrate significant restriction in active and passive range of motion, especially external rotation and abduction movement. On palpation, there is diffuse tenderness. Resisted movements of the shoulder produces pain and marked limitation in movement mimicking a rotator cuff tear.

Evaluation

The diagnosis of a frozen shoulder is clinical. The diagnosis is made by taking a history and doing a physical examination. Imaging modalities are not needed to make a diagnosis. Imaging modalities are used to rule out other conditions. No specific laboratory test or imaging provides definitive confirmation of the diagnosis of AC [19-21].

Imaging is of not much value in the diagnosis of AC. Radiographs, ultrasound, plain magnetic resonance imaging, and computed tomography are usually unremarkable. Imaging is limited to ruling out concurrent pathologies such as rotator cuff tears and glenohumeral osteoarthritis. The imaging tool most often used in patients with AC is high-resolution musculoskeletal ultrasonography (MUS). There is, however, a lack of specific ultrasound findings for the diagnosis of AC. In patients with AC, several investigators have reported thickening of the coracohumeral ligament to be a sonographic characteristic. Another ultrasound finding is the presence of fluid accumulation around the long head of the biceps tendon. Biceps peritendinous effusion can be seen in other shoulder pathologies such as rotator cuff disorders or biceps tenosynovitis. Plain shoulder X-rays are useful to rule out other pathologies such as tumors, and acromioclavicular and glenohumeral osteoarthritis. MRI may show a thickening of the glenohumeral joint capsule and coracohumeral ligament. MRI arthrography may show a reduction of the joint space.

Treatment

There is no consistent consensus about the management of AC. The majority of treatment options for AC are non-operative. They include physical and pharmacological therapy [22-24].

Early Frozen Shoulder

The aim of treatment in the early stage should focus on pain control, reduction of inflammation, and patient education. The pain is treated with acetaminophen or NSAIDs. Severe pain may require the use of opioid analgesics.

Oral corticosteroids can be prescribed in lieu of NSAIDs. They provide a stronger anti-inflammatory effect, however, they should not be given routinely due to their potential adverse effects. Low-dose oral corticosteroids are recommended only in cases of severe refractory frozen shoulder that has either been present for an extended period i.e. longer than 2 months or is causing significant pain. Although oral corticosteroids provide significant short-term benefits, the effect may not be maintained after 6 weeks.

Physical therapy is important for pain control and restoration of shoulder movements. Physical therapy includes soft tissue mobilization and gentle stretching exercises. Therapeutic ultrasound, cryotherapy, or transcutaneous electrical nerve stimulation (TENS) can also be used. A home exercise program should be provided to the patients. Exercises are done at home on a daily basis. In patients with moderate to severe pain who are not responding to non-operative treatments, intra-articular injection of corticosteroid can be done. The injection can be performed under ultrasonographic or fluoroscopic guidance. 

Developed Frozen Shoulder

Once the inflammation-related painful period subsides, the condition progresses to a frozen and then into a thawing phase. Treatment objectives in the advanced stages are to regain movements. Intensive mobilization exercises are provided to restore joint mobility. In patients who do not respond well to non-operative treatments, a more invasive therapy is provided. A suprascapular nerve or interscalene brachial plexus blockage may provide further improvement. In patients who do not improve after 6 months of non-operative treatment, more aggressive treatments are needed. Capsular hydrodilatation i.e. stretching the joint capsule by the saline injection pressure, manipulation of the shoulder under anesthesia, and arthroscopic capsular release, particularly in the rotator interval can be done.

Differential Diagnosis

Adhesive capsulitis especially in the early stage might be a diagnostic challenge. It can mimic subacromial pathology and rotator cuff tendinopathy. Patients with shoulder impingement and rotator cuff pathology usually report predominantly pain with less pronounced loss of passive range of motion. Several facets help to distinguish a frozen shoulder from other shoulder disorders. In patients with other shoulder disorders there often is a history of lifting a heavy object or performing repetitive overhead movements. In patients with frozen shoulder, there is spontaneous onset without an apparent cause or a history of overuse activity. 

Conditions that can mimic early adhesive capsulitis include:

• Post-stroke shoulder subluxation

• Subacromial pathology and rotator cuff tendinopathy

• Referred pain from the cervical spine or malignancy such as Pancoast tumor.

Glenohumeral joint arthritis should also be considered. It can be ruled out by free shoulder movement following lidocaine injection to the shoulder joint.

Age of onset provides clues to diagnose AC. Frozen shoulder is unlikely in patients younger than 40 years and patients older than 70 years are more likely to develop rotator cuff tears or glenohumeral osteoarthritis.

Staging

The natural course of AC is a gradual restriction of passive shoulder motion. The development progresses through 3 overlapping phases. A 4 stages classification can also be found in the literature. From a practical point of view, a  2-stage scheme i.e. early and developed frozen shoulder is used. The three overlapping phases include:

• Freezing (2 to 9 months): Early

• Frozen (4 to 12 months): Developed

• Thawing (12 to 42 months): Developed

Freezing

The early phase is known as the freezing phase. It is a painful phase with predominant pain that is worse at night. There is a gradual increase in glenohumeral joint movement restriction.

Frozen

The second phase is the frozen phase with stiffness and persistent glenohumeral joint motion limitation. The pain, however, is less than that in the “Freezing” stage. 

Thawing

The third phase is the thawing phase. Here there is a gradual return of the range of motion.

Prognosis

Adhesive capsulitis lasts from 1 to 3.5 years with a mean of 30 months.  The contra-lateral shoulder becomes affected within 5 years in about 15% of the patients.

Complications

In patients with adhesive capsulitis, there can be several complications. These include:

• Residual stiffness

• Residual pain

• Fracture of the humerus

• Rupture of the biceps tendon during shoulder manipulation

Outcomes

Frozen shoulder recovers in most people. The recovery, however, may take 1 to 3 years. Physical therapy and shoulder exercises will gradually result in diminishing symptoms in most patients. There is no data to show that diabetics have worse outcomes as compared to non-diabetics. There will be residual shoulder stiffness and disability in about 10% of the patients. After arthroscopic surgery, there is a gradual improvement in symptoms but the recovery is slow. Postoperative physical therapy is a must after surgery to ensure a good recovery [7,22].

Conclusion

The two terms that have been used to describe a painful and stiff shoulder are adhesive capsulitis and frozen shoulder syndrome. It is a condition of uncertain etiology characterized by significant restriction of both active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder. A frozen shoulder can be primary or secondary to trauma, inflammatory disease, etc. Patients having early AC usually present with a sudden onset of unilateral anterior shoulder pain. The typical symptoms include limitation of both passive and active range of motion. The diagnosis of a frozen shoulder is clinical. X-rays are used to exclude other pathologies.

There is no consistent consensus about the management of AC. The majority of treatment options for AC are non-operative. They include physical and pharmacological therapy. In patients who do not respond well to non-operative treatments, a more invasive therapy is provided including 

nerve blocks, capsular hydrodilatation i.e. stretching the joint capsule by the saline injection pressure, manipulation of the shoulder under anesthesia, and arthroscopic capsular release.

Frozen shoulder recovers in most people. The recovery, however, may take 1 to 3 years. There will be residual shoulder stiffness and disability in about 10% of the patients.

References

1. Zuckerman JD, Rokito A. Frozen shoulder: a consensus definition. J Shoulder Elbow Surg. 2011 Mar. 20 (2):322-5.

2. Lundberg BJ. The frozen shoulder. Clinical and radiographical observations. The effect of manipulation under general anesthesia. Structure and glycosaminoglycan content of the joint capsule. Local bone metabolism. Acta Orthop Scand Suppl. 1969. 119:1-59.

3. Tveita EK, Sandvik L, Ekeberg OM, Juel NG, Bautz-Holter E. Factor structure of the Shoulder Pain and Disability Index in patients with adhesive capsulitis. BMC Musculoskelet Disord. 2008 Jul 17. 9:103. 

4. Tasto JP, Elias DW. Adhesive capsulitis. Sports Med Arthrosc. 2007 Dec. 15(4):216-21.

5. Hand C, Clipsham K, Rees JL, Carr AJ. Long-term outcome of frozen shoulder. J Shoulder Elbow Surg. 2008 Mar-Apr. 17(2):231-6. 

6. Hand GC, Athanasou NA, Matthews T, Carr AJ. The pathology of frozen shoulder. J Bone Joint Surg Br. 2007 Jul. 89(7):928-32.

7. Lamplot JD, Lillegraven O, Brophy RH. Outcomes From Conservative Treatment of Shoulder Idiopathic Adhesive Capsulitis and Factors Associated With Developing Contralateral Disease. Orthop J Sports Med. 2018 Jul 12.

8. Duplay ES. De la periarthritis scapulohumerale et des raiderus de l'epaule qui en son la consequence. Arch Gen Med. 1872. 20:513-42.

9. Bulgen DY, Binder A, Hazleman BL, et al. Immunological studies in frozen shoulder. J Rheumatol. 1982 Nov-Dec. 9(6):893-8. 

10. Bulgen DY, Hazleman BL, Voak D. HLA-B27 and frozen shoulder. Lancet. 1976 May 15. 1(7968):1042-4.

11. DePalma AF. Loss of scapulohumeral motion (frozen shoulder). Ann Surg. 1952. 135:193-204.

12. Bridgman JF. Periarthritis of the shoulder and diabetes mellitus. Ann Rheum Dis. 1972 Jan. 31(1):69-71.

13. Chang YT, Chang WN, Tsai NW, Cheng KY, Huang CC, Kung CT, et al. Clinical Features Associated with Frozen Shoulder Syndrome in Parkinson's Disease. Parkinsons Dis. 2015. 2015:232958. 

14. Wohlgethan JR. Frozen shoulder in hyperthyroidism. Arthritis Rheum. 1987 Aug. 30(8):936-9. 

15. Bruckner FE, Nye CJ. A prospective study of adhesive capsulitis of the shoulder ("frozen shoulder'') in a high risk population. Q J Med. 1981 Spring. 50(198):191-204.

16. Hsu JE, Anakwenze OA, Warrender WJ, Abboud JA. Current review of adhesive capsulitis. J Shoulder Elbow Surg. 2011 Apr. 20(3):502-14.

17. Zreik NH, Malik RA, Charalambous CP. Adhesive capsulitis of the shoulder and diabetes: a meta-analysis of prevalence. Muscles Ligaments Tendons J. 2016 May 19. 6 (1):26-34.

18. Cho CH, Song KS, Kim BS, Kim DH, Lho YM. Biological Aspect of Pathophysiology for Frozen Shoulder. Biomed Res Int. 2018; 2018: 7274517.

19. Hubbard MJ, Hildebrand BA, Battafarano MM, Battafarano DF. Common Soft Tissue Musculoskeletal Pain Disorders. Prim Care. 2018 Jun;45(2):289-303. 

20. Xiao RC, DeAngelis JP, Smith CC, Ramappa AJ. Evaluating Nonoperative Treatments for Adhesive Capsulitis. 2017 WINTERJ Surg Orthop Adv. 26(4):193-199.

21. Wu F, Kachooei AR, Ebrahimzadeh MH, Bagheri F, Hakimi E, Shojaie B, Nazarian A. Bilateral Arm-Abduction Shoulder Radiography to Determine the Involvement of the Scapulothoracic Motion in Frozen Shoulder. Arch Bone Jt Surg. 2018 May;6(3): 225-232.

22. Oderuth E, Ali M, Atchia I, Malviya A. A double blind randomised control trial investigating the efficacy of platelet rich plasma versus placebo for the treatment of greater trochanteric pain syndrome (the HIPPO trial): a protocol for a randomised clinical trial. Trials. 2018 Sep 21;19(1):517. 

23. Wong CK, Strang BL, Schram GA, Mercer EA, Kesting RS, Deo KS. A pragmatic regional interdependence approach to primary frozen shoulder: a retrospective case series. J Man Manip Ther. 2018 May;26(2):109-118.

24. Chen Y, Yang J, Wang L, Wu Y, Qu J. [Explanation on Evidence-based Guidelines of Clinical Practice with Acupuncture and Moxibustion: Periarthritis of Shoulder]. Zhongguo Zhen Jiu. 2017 Sep 12;37(9):991-4.

           Synovial Impingement in the Ankle

                     Dr. KS Dhillon

Introduction

Abnormal entrapment or contact of structures resulting in pain or restricted motion is referred to as impingement. Impingement syndromes are seen in many areas, notably subacromial impingement in the shoulder and femoroacetabular impingement in the hip. Impingement syndromes are an increasingly recognized source of pain and disability in the ankle.

Impingement syndromes in the ankle have a broad spectrum of pathology with varying etiologies, anatomic features, and presentations. There is no official classification for the impingement syndromes. These syndromes are generally defined by the particular anatomic area involved. These include anterior, anterolateral, anteromedial, posterior, posteromedial, posterolateral, and syndesmotic impingements [1,2]. These pathologies are generally grouped into anterior and posterior impingement syndromes for simplicity.

Anterior ankle impingement syndrome occurs due to compression of structures at the anterior margin of the tibiotalar joint during dorsiflexion. It has long been recognized as a cause of pain in athletes. McMurray in 1949 described the “footballer’s ankle” which is a commonly observed condition in professional soccer players. It involves anterior osteophytes of the dorsal talar neck and distal tibia. The term was later changed to “impingement exostoses” in 1957 by O’Donoghue to include other patient populations [3].

The posterior impingement syndrome is characterized by compression between the posterior tibia and calcaneus during plantar flexion. Anatomists and surgeons have long recognized structures at risk for posterior compression, such as the os trigonum. The operative treatment for posterior impingement was first described by Howse in 1982. He treated a “posterior block of the ankle joint” in a population of elite dancers [4]. The condition was later termed “talar compression syndrome” [5].

Etiology

Anterior impingement

Anterior ankle impingement occurs when there is entrapment of structures along the anterior margin of the tibiotalar joint in full dorsiflexion. It is secondary to multiple osseous and soft tissue anatomic abnormalities. 

Spurs or “exostoses” at the anterior distal tibia and dorsal talar neck have been observed in athletes with anterior ankle pain and limited motion. Talofibular lesions have also been described [6]. The morphology of anterior tibiotalar exostoses has been studied. Cadaveric dissections have found that these lesions are intra-articular within the distal tibial and dorsal talar capsular attachments [7,8]. These tibial and talar spurs often do not actually overlap and abut. CT scans have shown that talar spurs usually lie medial to the midline of the talar dome and tibial spurs are generally located laterally [9]. There is a trough in the articular talar dome that often “accepts” the tibial osteophyte during dorsiflexion. Kim et al [10] referred to the trough as a “tram-track lesion” [10], and Raikin et al [11] termed it a “divot sign” [11]. Several studies have found a high rate of corresponding talar cartilage lesions (80.7 %) and loose bodies in patients with distal tibial lesions [12].

In addition to bony impingement, anterior intra-articular soft tissues may also contribute to impingement. There is a triangular soft tissue mass composed primarily of adipose and synovial tissues in the anterior joint space. These tissues are compressed after 15° of dorsiflexion in individuals who are asymptomatic [7]. Anterior osteophytes can limit the space available for these soft tissue and that can exacerbate its entrapment, resulting in synovitis, chronic inflammation, and capsuloligamentous hypertrophy. Fibrous bands from trauma [13], thickened anterior tibiofibular ligaments [14,15], and synovial plica [16], can also cause the impingement.

The impinging anatomic lesions have been well described but their exact etiology is not well understood. Spurs are enthesophytes that are produced by traction to the anterior capsule during repetitive plantar flexion of the ankle [3]. However, studies have shown that the chondral margins and lesions are deep to the joint capsule rather than at its attachment. This disproves the traction theory [7–9]. Now it is believed that the pathology occurs due to repetitive impaction injury to the anterior chondral margin from hyper-dorsiflexion or direct impact from an external object [17,18].

It has been hypothesized that chronic lateral ankle instability also contributes to the development of both bony and soft tissue lesions associated with anterior impingement due to abnormal repetitive micromotion [14,19]. Several studies have examined the prevalence of anterior impingement lesions at the time of arthroscopy of the ankle in patients undergoing stabilization procedures for lateral ankle instability. Soft tissue lesions, such as synovitis in the anterior compartment or anterior lateral gutter, have been observed in 63–100 % of the patients. Anterior tibial osteophytes have often been found in 12–26.4 % of the patients [20–22]. In a study by Scranton et al [23], patients undergoing a Brostrom procedure had 3.37 times the incidence of bone spurs than matched asymptomatic controls.

Posterior impingement

Posterior ankle impingement occurs due to compression of structures posterior to the tibiotalar and talocalcaneal joints during full plantar flexion. This can be caused by multiple osseous and soft tissue etiologies. Posterior impingement most commonly occurs due to pathology associated with the lateral/trigonal process of the posterior talus. There are anatomic variants of this structure. An elongated tubercle is referred to as a Stieda process. An os trigonum represents the failure of fusion of a posterior secondary ossification center to the talar body. Posterior impingement related to the trigonal process can result from chronic injury due to repetitive microtrauma, acute fracture, or mechanical irritation of the surrounding soft tissues [24].

Less often, posterior impingement symptoms can result from tibiotalar or subtalar osteoarthritis due to osteophyte impingement or associated hypertrophic capsule and synovium. Symptoms can also occur from post-traumatic sequelae from fracture malunion of the posterior malleolus, talus, or calcaneus [25]. Talar osteonecrosis causing posterior impingement has also been reported [26].

There are various soft tissue structures that can cause posterior impingement symptoms. Posterior capsuloligamentous injury due to repetitive or acute hyperflexion can produce inflammation, scarring, and thickening of the capsule leading to posterior impingement. The posterior inferior tibiofibular ligament and posterior fibers of the deltoid ligament can also produce posterior impingement symptoms [27–29]. The flexor hallucis longus tendon which runs between the medial and lateral posterior processes of the talus, is commonly affected by tenosynovitis and tendinosis. The tendinopathy can result from overuse or irritation from surrounding abnormal bony anatomy. Other sources of impingement include soft tissue variants, such as the posterior intermalleolar ligament and several anomalous muscles [30–34].

Clinical Presentation

Anterior impingement

The anterior impingement syndrome presents as anterior ankle pain on full dorsiflexion. Activities such as climbing stairs, running, walking up hills, ascending ladders, and deep squatting usually exacerbate the pain. The classic association of anterior impingement with competitive soccer players has long been recognized, but the reason that this subset of athletes are commonly affected is not very clear [10,17,18]. In the later stages of anterior impingement, dorsiflexion of the ankle may be limited secondary to mechanical block or pain. This creates a cycle of progressive joint stiffness and loss of function. When there are isolated soft tissue lesions, the patient may experience subjective popping or snapping sensation.

Posterior impingement

The posterior impingement syndrome usually presents with pain deep to the Achilles tendon. Symptoms are often worsened by activities involving plantar flexion and repetitive push-off maneuvers, including downhill running and walking, descending stairs, and wearing high-heeled shoes. Posterior impingement classically presents in dancers, especially those participating in classic ballet. The impingement is due to repetitive weight bearing in the plantar-flexed en-pointe and demi-pointe positions [35–38]. In a recent systematic review by Ribbans et al [39], dancers represented 61% of patients undergoing surgery for posterior impingement. It has also been reported in fast-bowlers in cricket [40].

Physical examination

When assessing for impingement syndrome a comprehensive physical examination of the foot and ankle is carried out. The ankle and foot are inspected for joint effusion, soft tissue edema, and abnormal alignment. In patients with anterior impingement, there will be anterolateral ankle tenderness. Posterior impingement signs can be more difficult to elicit and localize since the structures are deeper. Posterolateral ankle tenderness with forced ankle plantar flexion is most likely to involve pathology associated with the trigonal process. Posteromedial ankle tenderness with resisted plantar flexion of the first metatarsophalangeal joint is most likely due to flexor hallucis longus pathology. 

The active and passive range of motion of the joints is measured. This includes plantarflexion, dorsiflexion, subtalar, and midfoot movements. On the lateral side, the peroneal tendon is assessed for tenderness, deformity, or subluxation. The sural nerve is evaluated for hypersensitivity. The Achilles tendon is assessed for fusiform enlargement or retrocalcaneal bursitis. On the medial side, the tibial nerve is evaluated for tarsal tunnel syndrome, and the posterior tibial tendon’s function is also assessed. The anterior drawer and talar tilt tests of the tibiotalar joint are performed to detect ankle instability. A straight leg raise test can be done to exclude L5 or S1 radiculopathy.

Imaging

X-rays of the ankle are done if impingement is suspected. Weight-bearing AP, lateral, and mortise view xrays are done. The lateral view x-ray can show exostoses on the distal anterior tibia and dorsal talar neck as well as posterior bony abnormalities, including a Stieda process or os trigonum.

Oblique views have been described for both anterior and posterior impingement lesions to better assess for bony abnormalities. For anteromedial lesions, the beam is aimed 45° craniocaudally with the leg externally rotated at 30° [41]. The oblique anteromedial impingement view has been confirmed to have a higher sensitivity in detecting both tibial and talar osteophytes when added to a standard lateral radiograph [42]. For lesions associated with the trigonal process, a 25° external rotation-lateral view is useful [43]. Dynamic hyper-plantar-flexed or dorsiflexed laterals can be done to demonstrate abnormal bony contact.

When the diagnosis remains inconclusive an MRI can be done. The MRI can show effusion, synovitis, bone edema, tenosynovitis, and chondral injury. In anterior soft tissue impingement there may be hypertrophic synovium or fibrosis in the anterolateral gutter. Increased marrow signal intensity at the trigonal process or os trigonum may be due to an acute injury or chronic stress fracture [44]. The efficacy of MRI in evaluating soft tissue impingement lesions is variable. The reported sensitivity is 42–89 % and specificity is 75–100 % [45–50]. Computed tomography has been used to define the morphology of bony lesions for planning surgical resections [51]. More recently, ultrasound has also gained popularity as a reliable and inexpensive modality in evaluating impingement lesions as well as for administering therapeutic injections [52,53].

Nonsurgical treatment

The anterior and posterior impingement syndromes are initially treated without surgery. Acute symptoms are treated with rest and avoidance of provocative activities. This can be supplemented with ice and NSAIDs.  For severe cases cast immobilization can be done. Heel lift orthoses to prevent dorsiflexion can be used in chronic cases. Physical therapy is done to improve ankle stability and optimize proprioception. Some authors have reported successful symptom relief with ultrasound-guided corticosteroid injections [54,55].

Surgical treatment

Surgical intervention is indicated for patients with persistent symptoms that have not responded to non-operative treatment, affected activities of daily living, or athletic performance. The surgical approach and technique will vary by the anatomic region involved and the pathology involved.

Anterior impingement

During surgery for anterior impingement, the offending pathologic lesion contributing to the symptoms is removed. This usually involves resection or debridement of bony lesions and soft tissue lesions. In earlier studies, open anterior or lateral arthrotomy was done for the surgery [3]. A lateral arthrotomy is often still used if a lateral ligamentous procedure is being performed concurrently. Now, however, most open approaches have largely been replaced by arthroscopic techniques [56–80].

Hawkins was the first in 1988 to use an arthroscope for the treatment of bony anterior ankle impingement. He stated that visualization was better and the approach was less invasive [81]. Anterolateral and anteromedial portals are utilized and may be extended with conversion to open arthrotomy if the need arises. An arthroscopic burr is used for the debridement of bony lesions. A shaver and an electrothermal device are used to debride hypertrophic or inflamed synovium and fibrotic tissue. Intraoperative fluoroscopy can be used to confirm adequate resection of the spurs. 

Zwiers et al [75] conducted a systematic review to examine the outcome of the arthroscopic treatment of anterior impingement. The review included 19 studies and 905 patients. The average age of the patients was 32.7 years. At a mean follow-up of 35.3 months, 74–100 % of patients were satisfied with the results of the procedure. AOFAS scores improved, ranging from 34–75 preoperatively and increasing to 83.5–92 postoperatively. There was a 5.1 % overall complication rate. One point two percent were considered as major complications. This is similar to a 4 % complication rate in a previous review by Simonson et al [82].

Posterior impingement

Treating posterior impingement involves resection of the anatomical structures that are causing the symptoms. Usually, relief of symptoms is obtained by excision of a painful trigonal process or os trigonum, with debridement of surrounding inflammatory or hypertrophic soft tissues.

Posterior pathology can be approached through an open lateral, open medial, or endoscopic approach. The lateral approach allows a more direct access to the trigonal process and there is less risk of injury to the medial neurovascular bundle. A medial approach allows for access to flexor hallucis longus pathology. Since 2000, posterior endoscopic approaches have gained popularity. With an endoscopic approach, there is potential for faster return to sport and lower complication rates [31,83–97]. The patient is positioned prone and the posteromedial and posterolateral hindfoot portals adjacent to the Achilles tendon provide excellent access to extra-articular posterior structures.

Ribbans et al [39] reviewed 47 papers consisting of 905 patients who were treated surgically with both open and endoscopic approaches for posterior impingement. Eighty-one percent of symptoms were due to osseous pathology. Good to excellent outcomes were seen in 67–100 % of patients. Zwiers et al [98] conducted a similar systematic review. The review included 16 studies. They found significantly lower complication rates (7.2 vs. 15.9 %) and earlier return to full activity (11.3 vs. 16 weeks) with endoscopic surgery.

Conclusions

Ankle impingement occurs due to a broad spectrum of anterior and posterior pathology that involves both osseous and soft tissue abnormalities. Anterior impingement produces symptoms with terminal dorsiflexion of the ankle. Posterior impingement is exacerbated by activities that involve hyper-plantarflexion. The diagnosis is made by taking a good history and doing a proper physical examination. Imaging studies and diagnostic injections contribute to the accurate diagnosis of the conditions. Many patients respond favorably to non-operative treatment modalities. Those not responding to non-operative treatment would need surgery. Both open and arthroscopic techniques have evolved to address chronic symptoms with successful and predictable outcomes.

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