Arthrofibrosis Nightmares – Prevention & Management Strategies

Abstract

Arthrofibrosis (AF) is an exaggerated immune response to a pro-inflammatory insult leading to pathological periarticular fibrosis and symptomatic joint stiffness. The knee, elbow, and shoulder are particularly susceptible to AF, often in the setting of trauma, surgery, or adhesive capsulitis. Prevention through early physiotherapeutic interventions and anti-inflammatory medications remain fundamental to avoiding motion loss. Reliable non-operative modalities exist and outcomes are improved when etiology, joint involved, and level of dysfunction are considered in the clinical decision making process. Surgical procedures should be reserved for cases recalcitrant to non-operative measures. The purpose of this review is to provide an overview of the current understanding of AF pathophysiology, identify common risk factors, describe prevention strategies, and outline both non-operative and surgical treatment options. This manuscript will focus specifically on sterile AF of the knee, elbow, and shoulder.

INTRODUCTION

Arthrofibrosis (AF) is an exaggerated immune response to a pro-inflammatory insult leading to pathological periarticular fibrosis with subsequent symptomatic limitations in joint range of motion (ROM). Capsular contracture via aberrant extracellular matrix (ECM) deposition is the hallmark of AF and can manifest secondary to periarticular trauma, surgical insult, postinfectious arthritis, or hemarthrosis. Although uncommon, primary (idiopathic) AF occurs in the setting of an unidentifiable trigger.^1-3

AF represents a wide spectrum of disease, occurring in all large diarthrodial synovial joints and ranging from localized to diffuse fibrosis, with varying degrees of intra- and extra-articular extension.^2,4 AF has also been described⁵ as either active or residual, depending on whether the inflammatory and ECM deposition processes remain active or have resolved. Similarly, definitions for AF and classifications for motion loss vary in the literature, often depending on the joint involved, objective ROM measurements, subjective clinical criteria, or associated with specific surgical procedures.^2,6,7 Nonetheless, the functional consequences of joint fibrosis can severely limit patient quality of life and challenge healthcare professionals. The knee, elbow, and shoulder are the most commonly affected joints, usually following musculoskeletal injury or surgery.

The knee is most commonly affected by AF after periarticular trauma, ligament reconstruction or fracture fixation procedures.^6,8 AF is also a major cause of elbow functional impairment due to soft tissue injuries and periarticular fractures.⁹ The glenohumeral joint is a highly mobile articulation with great capacity to compensate for motion losses. However, proximal humerus fractures and adhesive capsulitis can cause joint fibrosis.^10-12 Joint pain, stiffness, and overall dysfunction from AF provides orthopedic surgeons with an opportunity to enhance patient quality of life through prevention, improved diagnosis and more effective treatment strategies. The purpose of this review is to provide an understanding of AF pathophysiology, identify common risk factors, describe prevention strategies, and outline both non-operative and surgical treatment options. This manuscript will focus specifically on sterile AF of the knee, elbow, and shoulder.

PATHOPHYSIOLOGY

AF is a fibrosing disorder characterized by uninhibited periarticular ECM protein deposition leading to symptomatic joint stiffness. Fibrosis represents the final common pathway of numerous chronic inflammatory injuries and is a pathologic feature of disease in virtually all organs.^13,14 Consequently, much of what is known about AF pathophysiology has been guided by extensive research investigating the pathogenic pathways of various organ fibrosing disorders.^14-16 Tissue injury under normal conditions induces the release of local inflammatory cytokines that initiate a complex inflammatory cascade responsible for the infiltration of activated immune cells into the area of tissue injury. Local fibroblasts under the influence of inflammatory cytokines differentiate into myofibroblasts and produce reparative ECM proteins. In the final stages of healing, inflammatory cytokines are downregulated and myofibroblasts either undergo apoptosis or dedifferentiate. The mechanisms that normally terminate the healing process become dysregulated through complex positive feedback networks that are not fully understood.⁵

Transforming growth factor-beta (TGF-β) is a necessary cytokine that exists in most cells to regulate immunity and wound healing.¹⁷ However, ample evidence exists to support the hypothesis that TGF-β is a potent mediator in the pathology of AF and all fibrosing disorders.^18-22 TGF-β is a pro fibrotic cytokine capable of multiple complex interactions with fibroblasts that lead to the activation and proliferation of myofibroblasts, increased production of disorganized ECM, and the inhibition of both myofibroblast apoptosis and collagen degradation.⁵ Other growth factors and pro-inflammatory cytokines believed to be important mediators of AF include tumor necrosis factor-alpha (TNF-α), platelet-derived growth factor (PDGF), and interleukin (IL)-1, IL-6, and IL-17.^2,23

Myofibroblasts are considered the key effector cell in joint fibrosis and have been found to play a significant role in pathological tissue contracture that occurs during organ fibrosis and wound healing.^24,25 Under the influence of TGF-β, myofibroblasts produce a dense ECM, composed mainly of the non-elastic type I collagen that forms numerous connections to adjacent tissue. The disease process remains uninhibited and the focal adhesions become more complex with abundant cross linking, altering the ECM into a contractile unit.^5,26 The contractile properties of myofibroblasts stems from the expression of α-smooth muscle actin (ASMA). Interestingly, activated myofibroblasts are able to potentiate and prolong the fibrotic cascade by producing TGF-β, inducing a positive feedback mechanism.¹³ Immunohistochemical analysis revealed a tenfold higher amount of ASMA containing myofibroblasts in patients with AF undergoing revision anterior cruciate ligament reconstruction (ACLR) compared to patients with primary ACLR.²⁴ Similarly, investigations utilizing a rabbit model of surgically induced knee joint contracture to identify the timeline of myofibroblast proliferation documented significantly elevated levels of myofibroblasts in the operated limbs compared to the control limbs at 2 weeks and not at later time points, suggesting interventions aimed at preventing AF need to be implemented early.³ Subsequent investigation defined the temporal expression of 380 genes during contracture genesis with a microarray analysis, highlighting an early onset imbalance between pro-and anti-fibrotic expression that occurs concomitantly with the development of contractures.²¹

In terms of genetic risk factors, a recent twin study showed an association between various musculoskeletal fibrotic conditions and suggested there may be a common disease process that is genetically mediated.²⁷ As such, considerable research attention has been directed toward describing the genetic basis for pathologic fibrosis of solid organ systems, and recent research has been conducted to determine if there is a genetic predisposition to musculoskeletal tissues.²⁸ Identifying genetic variants in musculoskeletal fibrosis could improve outcomes by implementing early targeted interventions.

PREVENTION

The etiology of joint stiffness is multifactorial comprising both mechanical and biological factors. Accordingly, the development of AF is influenced by modifiable and non-modifiable risk factors. Modifiable risk factors include surgical technique, concomitant or multiple procedures, pain management, BMI, rehabilitation, and prolonged immobilization.^29-33 Non-modifiable risk factors include the severity of trauma, pre-existing stiffness and/or inflammation, heterotopic ossification, infection, early-onset osteoarthritis, sex, and genetic predisposition.^9,28,34 Risk factors are often dependent on the joint involved and the etiology of stiffness. Addressing modifiable predictors of AF is paramount in establishing a predictable postoperative return of motion.

Prevention of AF has been extensively documented within the context of various conditions encountered in orthopedic practice. In primary ACLR, timing of surgery has been heavily debated in the literature; earlier studies have typically recommended delaying reconstruction for a minimum of 3 weeks to reduce the risk of postoperative knee stiffness, while more recent investigations have implemented accelerated protocols with good results.^35,36 While optimal timing of ACLR is controversial, surgical technique may have a more clear role in the development of postoperative AF. Concomitant procedures, such as a meniscus repair with ACLR, have been reported to increase the odds of subsequent arthroscopic arthrolysis. One recent study reported that concomitant meniscal repair at index surgery was associated with an increased risk of subsequent arthroscopic arthrolysis; however, this finding may be secondary to a more restrictive rehabilitation protocol due to meniscal repair.³⁷ Additionally, graft type and tunnel position may influence the risk of subsequent AF after ACLR.³⁸ An increase in graft diameter, particularly in younger patients undergoing primary ACLR, has been associated with increased risk of developing postoperative AF.³⁹ Careful consideration must be taken during preoperative planning to mitigate the risk of developing postoperative stiffness.

There is no consensus regarding the timing of surgical intervention, but a focus on patient-specific factors affecting knee motion is necessary. Reduced preoperative ROM predicts postoperative stiffness.⁴⁰ Subsequent investigations have elucidated predictors of reduced preoperative ROM to optimize functional outcomes in the postoperative period. In patients undergoing ACLR, bone bruising of the lateral femoral condyle on MRI has been demonstrated as a risk factor for a delayed time to achieving full extension preoperatively, which in turn can increase the risk of postoperative loss of motion.^34,41 It is less clear whether perioperative pain levels directly affect ROM in the postoperative period.⁴²

The role of rehabilitation and exercise programs on postoperative outcomes has also been investigated in recent studies. Patients who utilized a combined preoperative and postoperative rehabilitation program reported significant and clinically relevant (>10 points) increases across all KOOS subscale scores at two years following ACLR.⁴³ Many risk factors for the development of AF are outside of control by both the patient and surgeon; therefore, early postoperative motion should be encouraged whenever possible.

MANAGEMENT STRATEGIES

The initial step in the treatment of AF is establishing the etiology of ROM limitations, such as graft malposition following ACLR or capsular fibrosis and contraction. Adequate follow-up is imperative to diagnose AF in a timely manner and to initiate treatment to ensure optimal clinical outcomes. Early identification of motion deficiency and the adoption of a step-wise treatment approach may obviate the need for surgical intervention. Targeted strategies include physiotherapy, splinting or bracing, and oral corticosteroids before progressing to arthroscopic arthrolysis.⁶

A painful and stiff joint despite adequate conservative management may warrant surgical management. There is no consensus on the physical findings and duration of AF that warrant surgery. Much of the decision making for surgical intervention is based on patient progress. For example, joint stiffness of 8 weeks duration is more worrisome in a patient whose ROM has been plateaued for 4 weeks versus a patient with similar ROM restrictions but has been steadily gaining 10 degrees/week with close physical therapy. However, the risks of isolated manipulation under anesthesia (MUA) highly increase when joint stiffness persists beyond 6 weeks in nonarthroplasty patients.⁴⁴ Adequate diagnosis is essential before suggesting a surgical management in this complex population.^29,45,46 Patient related factors must be considered in the treatment of AF, as duration and severity of motion restriction, sex, smoking, and diabetes might be related to increased risks of residual stiffness.⁴⁷ The goal of surgical management is to maximize long term ROM and optimize function. Surgical management of AF requires identification and correction of any extra-articular causes of joint mobility restrictions. Heterotopic ossification, myositis ossificans, soft tissue calcifications, and retained hardware can all be contributors to loss of joint mobility.⁴⁴ For surgically addressing intra-articular scar tissue and hypertrophied synovium related to AF, arthroscopic or open lysis of adhesions (LOA) is the treatment of choice.^11,48 MUA may be done following LOA to maximize ROM. Careful arthroscopic management prior to MUA allows for focal areas of scarring to be addressed and limits the potential for catastrophic complications of manipulation.^11,48,49 These complications include hemarthrosis, tendon tear, chondral injuries, labral tears or periarticular fractures. Contraindications to MUA include significant osteopenia, fracture non-union, or neurovascular injury.

Knee

Csintalan et al. reviewed joint registry data from 14,522 primary ACLR procedures and found female sex (HR, 2.48; 95% CI, 1.66-3.71) and prior surgery (HR, 3.02; 95% CI, 1.39-6.53) to be risk factors for AF requiring subsequent surgery. AF was the second most common reason for reoperations in their series.⁵⁰ Furthermore, graft type, infection, concomitant meniscal repair, and primary reconstruction have been suggested as significant risk factors for undergoing MUA or LOA after ACLR.³⁸ The true incidence of AF is difficult to ascertain as reporting is often limited to patients who undergo a surgical procedure after seeking treatment.^4,6 An additional factor contributing to incidence variability is the lack of an agreed AF definition, ranging from early pathoanatomic classifications⁵¹ to more objective measures of motion loss.⁵² Recent efforts have been made to develop an international consensus on the definition of knee AF with a reported incidence of 2-35% following ACLR.^6-8 Sanders et al. conducted a large population based series with over 20 year follow up and 2% of the patients in their cohort had postoperative stiffness following ACLR that required intervention.⁸ The multi-center ACL revision study (MARS) reviewed the rate of reoperations in 1112 patients following revision ACLR and reported a 9% reoperation rate for AF.⁵³ The incidence of AF remains the highest after high energy, multiligament injuries.³³

The physiologic motion of the knee is 0 to 140 degrees, and the majority of activities of daily living (ADLs) can be executed with an arc of active function from 10 degrees extension to 120 degrees flexion (gait, sitting, stair climbing). Although the arc of terminal extension, defined from 10 degrees flexion to 5 degrees hyperextension, is not utilized during gait, it provides the important “screw home” mechanism that allows deactivation of the quadriceps during stance phase. Consequently, loss of extension is poorly tolerated and more challenging to manage.^4,54 Understanding the pathoanatomy of motion loss is critical to the treatment of AF as certain motion deficits often correlate with specific areas of intraarticular pathology. In general, flexion loss can be the result of suprapatellar adhesions, as well as medial and lateral gutter adhesions. Notch impingement, posterior capsule stiffness, and ACL nodules often contribute to limitations in extension.⁵⁵

Physiotherapy

The goal of physiotherapy is to address pain, edema, and inflammation control. Mobilization of the affected joint can aid edema control and prevent adhesion formation, and early motion should be promoted whenever possible. Passive ROM exercises should be employed after sufficient healing has occurred. There are, however, associated risks of physiotherapy, particularly when patient’s limits are exceeded. Overly aggressive motion in these cases may increase inflammation and fibrosis of the affected joint.

Continuous Passive Motion

Some clinicians advocate for the use of continuous passive motion (CPM) protocols; however, the literature investigating the utility of CPM has yielded mixed results regarding its efficacy on increasing long-term ROM ⁵⁶. It is unclear whether there is a direct benefit of CPM on functional outcomes including pain and ROM after ACLR.⁵⁷ A recent study using an animal model of ACL rupture has demonstrated a chondroprotective effect of immediate CPM therapy, creating a superior in situ microenvironment for reducing posttraumatic osteoarthritis.⁵⁸ Further research into potential utility of CPM in cartilage protection and long-term clinical outcomes is warranted.

Manipulation Under Anesthesia

MUA has been shown to improve ROM in stiff knees after ligament reconstruction. Traditionally, MUA is performed by applying progressive flexion to the affected joint in order to disrupt the scar tissue. The amount of applied force is influenced by multiple factors, including the patient’s bone quality and the presence of hardware or stress risers in the bone.¹⁰ It is estimated that up to 8% develop AF after knee arthroscopic procedures and these patients require a secondary procedure to regain full knee motion.⁵⁹ In this patient population, it is common for MUA to be performed concurrently with arthroscopic LOA. Typically, an MUA is attempted, and if the surgeon feels the risk is too high to push more firmly then a knee arthroscopy with releases is done first followed by the MUA. That said, at times a fairly gentle manipulation is all that is needed to break through adhesions and regain ROM. MUA is accepted as a safe, non-surgical procedure for loss of motion. While complications of MUA are rare, they can be devastating. These include loss of motion or need for revision surgery, fracture, cartilage damage, hemarthrosis, and extensor mechanism injury.⁶⁰

Mayo Clinic Institutional AF Protocol Following MUA

In select cases of severe AF, patients receive an adductor canal indwelling nerve catheter preoperatively to maximize aggressive CPM and physiotherapy in the early post-operative period. Patients receive a dose of dexamethasone (8mg IV) once intraoperatively and again the morning following surgery. If renal function permits, patients are also given 24 hours of ketorolac (15mg IV q6 hrs). CPM begins as soon as patients arrive on the floor and continues in the outpatient setting for six weeks. Additionally, dedicated physical therapy sessions are initiated the day after surgery and continue five days per week for six weeks. Celecoxib is prescribed for a total of four weeks.

Arthroscopic Lysis of Adhesions

Combined arthroscopic LOA and MUA for the treatment of knee AF has shown great results (Fig. 1).^44,48,61 Access to the arthrofibrotic knee can be difficult. Initial joint distention may therefore be helpful prior to arthroscopy. A standardized approach to the knee allows the surgeon to address specific areas responsible for loss of motion (Fig. 2).^62,63 To address flexion deficits, attention should be drawn to the suprapatellar pouch, the patella-femoral joint, and the anterior interval. Scarring at the intercondylar notch may be associated with flexion and extension deficit. For extension deficits, the surgeon should draw attention to the medial and lateral gutters as well as the posterior joint space. Given the inflammatory nature of the disease, the use of a radiofrequency wand and a tourniquet is usually necessary. All abnormal scar tissue should be removed with a shaver. After LOA is complete, the capsular release should be extended proximally from the anteromedial and anterolateral portals to the suprapatellar pouch. The anterior interval of the knee should also be released to allow for adequate tendon excursion, starting with anterior fat pad release, then developing the interval between the anterior tibia and the patellar tendon, all the way to the tibia tubercle (Fig. 3).^63,64 Several authors have reported significant improvement in knee ROM following arthroscopic LOA with sustained increase in knee flexion ranging from 45 to 68 degrees in posttraumatic injuries.^63,65-67 Duration of preoperative stiffness and degree of deficits negatively correlate with post-operative ROM.⁶⁶

Figure 1.

Preoperative clinical photos of right knee showing (A) −10 degrees extension and (B) 45 degrees flexion. Postoperative range of motion (ROM) assessment under anesthesia shows (C) full extension and (D) complete flexion after lysis of adhesions (LOA) followed by manipulation under anesthesia (MUA).

Figure 2.

The arthroscope is placed in the anterolateral portal of the left knee. (A) View of the suprapatellar pouch prior to release demonstrating restricted patellofemoral space. (B) Following release of adhesions and complete capsulotomy using radioablation device. (C) View of the intercondylar notch showing dense adhesions surrounding the anterior cruciate ligament (ACL). (D) ACL is preserved following complete release of scar tissue. (E) Arthroscopic field of view prior to posteromedial release. (F) Following complete posteromedial capsulotomy. The posteromedial knee is accessed through the intercondylar notch using the Gillquist maneuver.

Figure 3.

Right knee LOA. (A) The arthroscope is placed in the anterolateral portal and the shaving device is accessing the knee from the anteromedial portal with the knee in flexion demonstrating abundant adhesions of the anterior aspect of the knee limiting access to the suprapatellar pouch. (B) View of the suprapatellar pouch from the anteromedial portal. Note the adhesion which can contribute to patellar mobility restriction. (C) The anterior interval is viewed from the anteromedial portal with the knee in flexion. Notice the patellar tendon attaching to the tibial tubercle, indicating complete release of the anterior interval.

Persistent knee extension deficits are difficult to manage and can be addressed with arthroscopic posterior compartment LOA and posterior capsular release. Anterior adhesions and medial and lateral gutter releases should be completed before addressing posterior capsular releases, as anterior adhesions can contribute to loss of knee extension. Additionally, knee flexion to 90 degrees is necessary for safe posterior portal placement and posterior capsular release secondary to the intrinsic proximity of neurovascular structures. Through a standard approach, a posterior medial portal is established under direct visualization and LOA is completed in the posterior medial compartment. Releases are completed until the medial gastrocnemius tendon can be visualized (Fig. 4). A standard approach to the posterolateral compartment is conducted with partial lateral capsular release completed in a similar fashion. The use of a trans-septal portal can also be useful to complete posterior releases.^68,69 Wierer et al. reported excellent results following an all arthroscopic approach and posterior capsulotomy in 10 patients with knee flexion contractures after ACLR. No complications were observed in their cohort and the median extension deficit improved from 15 degrees preoperatively to 1 degree at 2 year follow-up (median, 25 months).⁷⁰

Figure 4.

Right knee posterior release. Arthroscopic field of view (A) before and (B) after posterior medial capsule release. The release is continued until the medial gastrocnemius tendon is visualized.

Careful hemostasis should be achieved after releasing the tourniquet and lowering the water inflow pressure. MUA is then performed for completion of the releases and maximizing ROM. Careful manipulation is carried by minimizing the lever arm and therefore the risk of iatrogenic fractures. Once ROM is maximized, radiographic imaging is recommended to rule out any acute complications.⁶⁴

Open Surgical Release

Although rarely necessary with the development of less invasive arthroscopic techniques that allow great intraarticular visualization in the anterior and posterior compartments of the knee, open surgical management of knee AF should be considered when arthroscopic LOA does not allow for adequate and functional ROM. This approach should be performed through a parapatellar approach with fat pad excision and residual scar excision. Of 207 knees treated for postoperative stiffness, 202 responded to conservative management or arthroscopic surgical LOA in a series published by Noyes et al.⁷¹

Salvage procedures may be necessary in refractory cases where adequate knee flexion cannot be achieved. Combined arthroscopic release and open quadricepsplasty has been described with good results by Wang et al. However they did report persistent extensor lag in 1 of the 22 patients.⁷² Proximal sliding tibial tubercle osteotomy for persistent patella baja is also a recognized salvage technique in refractory cases.⁴⁴ Use of these techniques should be reserved for severe flexion mobility restrictions after arthroscopic LOA and careful manipulation and should be done by experienced surgeons given the high complexity of this patient population.

Elbow

AF in the form of post traumatic elbow stiffness following soft tissue injuries, chondral damage, instability and periarticular fractures is a major cause of functional impairment at the elbow.⁹ The elbow joint contains three articulations and nearby musculature and ligaments that are surrounded by a capsule predisposed to the inflammatory cascade, making it highly susceptible to AF.⁷³ Although normal elbow ROM is from 0 to 140 degrees along the flexion/extension axis, most ADLs involving the elbow can be completed with an arc of active function from 30 to 130 degrees.⁷⁴ Elbow stiffness is commonly defined as <120 degrees flexion and loss of extension >30 degrees. Clinically, loss of flexion is often a greater functional problem than loss of extension as it inhibits a person’s ability to reach their mouth, face, and back of the head.⁷⁵ In fact, 80% elbow function is sacrificed with a 50% reduction in elbow ROM.⁷⁶ The incidence of post traumatic elbow stiffness increases with higher energy trauma and extended immobilization.⁷⁵

Physiotherapy

Physiotherapy is commonly utilized both to help prevent stiffness following elbow trauma and to reverse motion loss after the onset of fibrosis. The primary focus of early therapy regimens should be to control inflammation, edema, and pain with conservative measures such as ice, compression, elevation, and the initiation of early active mobilization.⁹ Patients can begin implementing passive ROM exercises after the injured bone and soft tissues demonstrate adequate healing, typically 6 to 12 weeks from the date of injury. Physiotherapy regimens should be started promptly following injury and continue for duration of at least 6 months before cases are considered recalcitrant.⁷⁷ It is important for the treating surgeon to establish effective communication with the physiotherapist to prevent unfortunate complications associated with inappropriate therapy such as increased pain and inflammation and patient discouragement. Physiotherapy is less effective in the setting of chronic contractures, often requiring more invasive techniques.

Splinting/Bracing

Elbow bracing remains a fundamental component in the treatment of posttraumatic elbow stiffness, utilized both as a primary non-operative treatment modality and as an adjunct in postoperative protocols. Current studies support the notion that elbow bracing can be effective for increasing ROM when heterotopic ossification is not present.⁷⁵ A prospective randomized trial comparing dynamic and static progressive (turnbuckle) splints reported that both are equally efficacious in posttraumatic elbow stiffness.⁷⁸ Both types of splints function to gradually lengthen scar tissue. Dynamic splinting works by applying a constant force, typically through a spring-loaded mechanism, to gradually stretch tissue. On the other hand, static progressive splinting maintains a fixed angle that can be advanced in a step-wise fashion to apply progressive stretching forces. Typically, the dynamic splint is worn for several hours continuously each day, while the static progressive splint is worn several times per day in thirty-minute intervals.

Manipulation Under Anesthesia

Limited evidence exists for MUA in the setting of posttraumatic elbow stiffness. Duke et al. retrospectively reviewed eleven patients who had isolated elbow MUA to improve dysfunctional ROM. The authors reported that 6 (55%) patients improved their motion while 5 (45%) patients had either no change in motion or a loss of motion. Two (18%) patient experienced transient ulnar sensory neuropathy.⁷⁹ Periarticular fractures and heterotopic ossification are additional complications commonly associated with isolated elbow MUA.⁸⁰ However, better results have been reported when MUA is utilized as an adjunct procedure following surgical contracture release.⁸¹

Arthroscopic Lysis of Adhesions

Arthroscopic arthrolysis can be integrated as a first step in the management of post traumatic elbow stiffness, allowing the surgeon to remove loose bodies, osteophytes, and the capsule. The posterolateral and trans-tricipital portals are useful for posterior arthrolysis. The medial and lateral gutters are exposed, with care taken to protect the ulnar nerve medially, before moving to the anterior release through the standard anteromedial and anterolateral portals (Fig. 5). In addition to removing synovitis and adhesions, the capsule is generally released and resected in a near circumferential fashion (depending on the severity and direction of the contracture). During this process, it is critical that great care is taken to ensure neurovascular structures are protected. In cases of significant pre-operative contracture, consideration should be given to performing an open ulnar nerve decompression to prevent ulnar neuropathy as the nerve experiences increased stretch when flexion is increased after surgery.⁸²

Figure 5.

Right elbow LOA. (A) Arthroscopic field of view from the proximal anteromedial portal demonstrating extensive adhesions limiting view of the elbow joint. (B) Same view following progressive lysis of anterior adhesions proximal to the capitellum, using the electrocautery device from the midlateral portal. (C) LOA has been completed and viewed from the proximal anteromedial portal and the (D) midlateral portal.

Open Surgical Release

Although some controversy exists, open surgical release of the elbow is typically best accomplished through a standard lateral column approach. If needed, a separate medial exposure can be performed as well. On the lateral side, a safe interval between the brachialis and the anterior capsule should be developed. With care to protect the anterior neurovascular bundle, the anterior thickened capsule is resected as medially as possible. Osteophytes and loose bodies should then be excised as needed. If extension deficits persist, the medial column should be exposed for complete capsular excision. To address flexion deficits, posterior releases should be performed. First, elevate the triceps from the posterior capsule before excising the posterior capsule and any loose bodies or osteophytes. Ligament releases can further be performed if needed.⁸² The balance between a mobile and stable elbow should be considered before performing more extensile releases.

Outcomes of elbow arthrolysis do not show definitive clinical superiority of open vs arthroscopic releases, with reported average movement arc increases between 18 and 66 degrees.^82-84 Complication rates of elbow arthrolysis is approximately 10%, with ulnar neuropathy being the most common.⁸⁵ Ulnar nerve decompression and transposition should therefore be considered when preoperative elbow flexion is under 90 degrees.⁸² Recurrence of elbow stiffness after arthrolysis ranges from 10-34%. Heterotopic ossification is one of the leading causes of stiffness recurrence.⁸⁵

Shoulder

The glenohumeral joint is a highly mobile articulation with great capacity to compensate for motion losses through the thoracic spine and scapulothoracic interface. However, AF of the shoulder, commonly referred to as adhesive capsulitis, can cause significant pain and dysfunction secondary to joint fibrosis. Normal shoulder motion has been described as 170 degrees forward flexion (sagittal plane), 180 degrees abduction (coronal plane), and 100 degrees external rotation (with the arm abducted at 90 degrees). Functional ROM at the shoulder requires 120 degrees forward flexion, 130 degrees abduction and 60 degrees of external rotation, allowing a deficit of at least 40 degrees in any plane before significantly interfering with ADLs.^10,86 The incidence of adhesive capsulitis in the general population is estimated at 3% - 5% and as high as 20% in the diabetic population.¹¹ It is often accompanied by disabling pain in addition to the restricted motion. Although it commonly resolves with comprehensive non-operative treatment, complete resolution can take up to 1-2 years making this a significant source of disability for patients.

Physiotherapy

Of the various modalities available for management of shoulder AF, non-operative treatment with physical therapy is the initial approach in most patients. Patients who present with shoulder stiffness typically have pain associated with functional impairment. Medical therapy with NSAIDs or other anti-inflammatories are helpful in reducing symptoms and allowing patients to participate in physical therapy. It is important to emphasize that medication alone does not improve functional status of the shoulder, but rather allows patients to effectively participate in physical therapy. In general, physical therapy is combined with additional treatment modalities including medications, corticosteroid injections, ultrasound therapy, or hydrodilatation.¹¹

Corticosteroid Injections

Intraarticular corticosteroid injections have been reported to decrease the amount of fibrosis and presence of fibroblasts in patients with adhesive capsulitis.⁸⁷ Particularly in the early stages of adhesive capsulitis, corticosteroid injections have utility in pain reduction. A double-blind, randomized trial comparing intraarticular and rotator interval corticosteroid injections to placebo in 122 patients reported significant pain improvements at 12 weeks; however, at 26 weeks these significant differences were not maintained. Of note, no difference was seen between patients who received either intraarticular or combined intraarticular and rotator interval injections.⁸⁸ The combination of intraarticular corticosteroid injections with physical therapy may be more beneficial than each modality alone, particularly in regards to ROM and patient reported outcomes.⁸⁹

Hydrodilatation

Hydrodilatation of the glenohumeral joint capsule under fluoroscopy and local anesthetic has been shown to be effective in improving pain in the short term; however, long-term relief or improvements in ROM are less clear. A prospective randomized trial comparing hydrodilatation with joint manipulation to intraarticular corticosteroid injections in 121 patients reported improvements in patient satisfaction and ROM at 6 weeks, but these differences were no longer apparent at 12 months.⁹⁰ While patients did achieve rapid declines in pain and early ROM recovery, these differences lasted only for a short period. In addition, the hydrodilatation procedure itself can be a painful experience, and thus the authors relied on interscalene blocks to allow patients to tolerate the procedure. Furthermore, a randomized, controlled trial compared hydrodilatation plus corticosteroid to intraarticular corticosteroid injection alone and reported no significant differences between the two groups.⁹¹

Manipulation Under Anesthesia

The efficacy of MUA for the treatment of shoulder AF remains unclear. A recent systematic review of 22 studies including 989 patients comparing MUA instead of, or in addition to, arthroscopic capsular release reported minimal difference in median changes in abduction, flexion, and external rotation between the groups.⁹² Of note, 21 of the included studies provided level IV evidence, and the authors suggest that high quality evidence is required to definitively evaluate the relative efficacy of these procedures. On the other hand, reports of good long-term outcomes following MUA have been documented in the shoulder literature. Theodorides et al. sought to determine factors affecting clinical outcomes following MUA in a retrospective analysis of 315 shoulders.⁹³ The authors reported that significant improvements in Oxford Shoulder Scores and ROM were achievable, and that secondary adhesive capsulitis significantly reduced the efficacy of MUA in terms of ROM.⁹³ This highlights the necessity of tailored treatment regimens for achieving clinically significant improvements for patients with shoulder AF.

Arthroscopic Lysis of Adhesions

Arthroscopic LOS and capsular release is a recognized safe and effective method for the treatment of AF (Fig. 6).^94,95 Unlike isolated MUA and hydrodilatation, this technique allows confirmation of the diagnosis and assessment of other potential reasons for a painful and stiff shoulder.¹¹ Capsular release addressing the thickened CHL and rotator interval is the standard treatment for shoulder AF (Fig. 7). The anteroinferior release allows for external rotation improvements in both adduction and abduction positions. Posterior capsular release remains controversial. If deemed necessary, it should be conducted through an anterior viewing portal, with a capsular release of the thickened capsule from the posterior margin of the biceps tendon, and extended inferiorly with care taken to the neurovascular structures distally.^11,49 The posterior release is complete when the infraspinatus muscle is visible. Favorable outcomes have been described with arthroscopic capsular release for shoulder AF. El Hassan has recently reported outcomes after arthroscopic release for shoulder AF in 115 patients with 46 month follow-up. All patients showed improvements in pain and ROM. Patients with postoperative related AF showed less improvement compared to post traumatic or idiopathic AF.⁹⁵ Other studies have shown uniform improvement amongst different groups in shoulder function and pain after arthroscopic capsular release.^96,97 A recent systematic review and meta-analysis of randomized controlled trials investigating management of shoulder AF further supports the efficacy of arthroscopic capsular release for improvements in ROM.⁸⁹ The authors noted that the effect difference of surgery was at least double that of other treatment modalities for all ranges of motion, and that surgery was the only treatment modality to significantly improve forward flexion.⁸⁹

Figure 6.

Left shoulder ROM examination under anesthesia. Preoperative assessment showing restricted (A) abduction, (B) external rotation at 90 degrees abduction, and (C) forward flexion. Significant improvements attained in (D) abduction, (E) external rotation at 90 degrees abduction, and (F) forward flexion following capsular release and MUA.

Figure 7.

Left shoulder arthroscopic images. (A) View of the rotator interval and anterior capsule through the posterior portal. (B) The rotator interval is released to the upper border of the subscapularis and the (C) middle glenohumeral ligament is identified prior to release. View of the posterior capsule from the anterior portal (D) before and (E) after capsulotomy is completed.

Open Surgical Release

Open surgical release of the shoulder is indicated in the presence of extra-articular adhesions, or in the event of failed arthroscopic release and MUA. An open approach may also be considered in cases when significant arthritis and excessively large inferior humeral head osteophytes need to be resected. The use of an open technique may result in increased post-operative pain due to extensive dissection. A thorough surgical technique addressing extra-articular (subdeltoid, subacromial and subcoracoid spaces) and intra-articular capsular adhesions and rotator interval thickening is necessary. A delto-pectoral approach is preferred with a careful dissection in the context of a distorted anatomy. Subdeltoid adhesions should be released with abduction and internal rotation of the shoulder for easier access. When releasing adhesions, location of the axillary nerve should be considered as it travels 3-5cm distally to the acromion edge, on the deep portion of the deltoid. The dissection is continued to the subpectoral space, followed by the subacromial space. Before performing a release of the rotator interval, careful dissection of the interval between the conjoined tendon and the subscapularis is performed, protecting the axillary nerve which travels inferiorly to the subscapularis. Subscapularis scarring and adhesions may limit ER significantly and warrant Z-plasty lengthening in some circumstances.^11,49

Postoperative Care and Pain Control

Prior to surgical management, adequate pain control strategies should be discussed with the patient and pain management specialists in order to maximize postoperative rehabilitation. Regional anesthesia in the immediate post-operative period allows for early rehabilitation and preserved ROM gains. Pharmacological strategies, such as cyclooxygenase (COX) inhibition may limit the release of cytokines contributing to the initial pathological process of AF.⁹⁸

For the shoulder, interscalene pain catheters allow for better pain control and maintained ROM in the post-operative period. The literature does not support the use of continuous passive motion after elbow arthrolysis.⁸² For the knee, indwelling femoral nerve blocks give great pain relief and allow patients to maximize aggressive CPM and physiotherapy in the early post-operative period. This should be initiated right away and continued for at least the first 6 weeks in order to limit any residual loss of mobility.

Novel Approaches and Future Directions

Novel therapies for the prevention of AF have generated much interest. At-risk patients could receive anti-fibrotic therapies and intensive monitoring to control inflammation. The development of a minimally invasive diagnostic tool kit which assesses the levels of pro-inflammatory cytokines, collagen fragments, or other mediators of fibrosis may help determine which patients are at high-risk for developing postoperative AF.⁵ Anti-fibrotic coatings on surgical implants may also prove beneficial in prevention of AF.⁹⁹

Research in the prevention of AF and joint contracture continues to evolve, which opens potential avenues for therapeutics and novel approaches for non-surgical management. Studies investigating the genetic predisposition of fibrosis in musculoskeletal tissue have expanded our fundamental understanding of this pathologic cascade, however the specific genes that activate these cellular pathways remains unclear.²⁸ Validated animal models of joint contracture provide insight into potential novel therapies for AF. The use of intraarticular COX-2 inhibition with celecoxib has shown significant decreases in posterior capsular stiffness along with decreased expression of inflammatory and pro-fibrotic cell surface markers.⁹⁸ Furthermore, the authors demonstrated that celecoxib delivery through drug-eluting implanted collagen membranes has an even more robust effect in decreasing contracture severity.¹⁰⁰

SUMMARY

AF is an exaggerated inflammatory response causing pathologic periarticular fibrosis and symptomatic limitations in joint motion. The knee, elbow, and shoulder are particularly susceptible to AF, often in the setting of ligament reconstruction surgery, periarticular fracture fixation, or adhesive capsulitis. Although challenging, the significant pain, stiffness, and overall dysfunction associated with AF provide orthopedic surgeons an opportunity to enhance patient quality of life through improved diagnosis, prevention, and treatment strategies. Prevention through early physiotherapeutic interventions and anti-inflammatory medications remain fundamental to avoiding motion loss. Reliable non-operative modalities exist and outcomes are improved when etiology, joint involved, and level of dysfunction are considered in the clinical decision making process. Surgical procedures should be reserved for cases recalcitrant to non-operative measures. Contemporary research efforts are showing promise in the identification of biomarkers and therapeutic targets to aid in the creation of novel diagnostic, preventative, and treatment strategies.