Post-traumatic elbow stiffness: Pathogenesis and current treatments

Abstract

Post-traumatic elbow stiffness is a major cause of functional impairment after elbow trauma. A stiff elbow limits patients’ ability to position their hand in space for optimal use of their upper extremities, and as such, is a frequent indication for reoperation. This article reviews current concepts on the pathogenesis of post-traumatic elbow stiffness. Current nonoperative treatment options include therapy, bracing, and manipulation under anesthesia, while operative treatment options include arthroscopic and open arthrolysis. The pros and cons of various treatment options are discussed, with a focus on the evidence supporting their use, the expected functional gains, and associated complications. Future directions in post-traumatic elbow stiffness are highlighted.

Introduction

Painless motion at the elbow joint is critically important for normal function, because it allows humans to position the hand in space. After a traumatic insult, a cascade of events may occur that leads to a decrease in passive range of motion from the normal anatomic arc. The resultant post-traumatic stiffness, or arthrofibrosis, at the elbow joint is functionally limiting and adversely affects the quality of life.

Morrey classified the post-traumatic elbow stiffness as intrinsic, extrinsic, or mixed.¹ Intrinsic causes of elbow stiffness, such as articular incongruities, impinging osteophytes, and intra-articular adhesions, arise from the elbow articulation, whereas extrinsic causes of elbow stiffness include capsular contractures, heterotopic ossification, and impinging hardware. In practice, causes of post-traumatic elbow stiffness are frequently mixed. Our understanding of the pathogenesis of post-traumatic elbow stiffness is expanding, yet limited. The incidence of elbow stiffness after trauma is not well-described; however, more severe stiffness is correlated with higher energy trauma and prolonged immobilization.^1,2

Common activities of daily living can be performed with a 100° arc of elbow motion, from 30° of extension to 130° of flexion, and a 100° arc of forearm rotation, from 50° of pronation to 50° of supination.³ The goal of the treatment of post-traumatic elbow stiffness is the restoration of a functional, if not normal, elbow range of motion. Current treatment options range from conservative to surgical, with varying rates of success, invasiveness, and complications. Nonoperative treatment options include therapy, bracing, and manipulation. The operative treatment is arthrolysis, which may be performed via an arthroscopic or open approach. Continued basic science and translational research provide hope of a pharmacological treatment option in the future.

Pathogenesis

The pathogenesis of post-traumatic elbow stiffness is multifactorial, and the etiology of a clinically stiff elbow is often a result of both intrinsic and extrinsic factors. Intrinsic causes of post-traumatic elbow stiffness are inherent to the elbow articulation, and range from articular incongruities from the initial trauma to impinging osteophytes from subsequent arthrosis. Post-traumatic or post-surgical immobilization may result in intra-articular adhesions that limit motion.

Common extrinsic causes of elbow stiffness include heterotopic ossification, retained hardware, and capsular contractures. Heterotopic ossification is a form of dystrophic calcium deposition that results from local tissue damage secondary to trauma, either from injury or from surgery. The ossified deposit serves as a mechanical block to motion and may restrict flexion, extension, or both, depending on its location. While no patient-related risk factors have been identified for the formation of heterotopic ossification after elbow trauma, ulnohumeral dislocation, longer time from injury to surgery, and a greater number of surgical procedures are independent risk factors for heterotopic ossification formation.⁴ Orthopedic hardware is often used for fixation of peri-articular elbow fractures. Retained hardware can also serve as a mechanical block to motion, for instance, a prominent olecranon plate limiting terminal elbow extension by impinging in the olecranon fossa. Moreover, retained hardware may impair gliding of overlying musculotendinous units.

Capsular contracture is the hallmark of arthrofibrosis. The elbow joint capsule comprises of fibroblasts in a collagen-based extracellular matrix; both components are affected in arthrofibrosis. The pathogenesis of arthrofibrosis begins with an inflammatory cascade and progresses to a fibrotic process. With the inflammation of trauma or surgery comes an influx of pro-inflammatory cytokines, including interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF)-α. In the formation of hypertrophic contractures, normal fibroblasts are transformed into myofibroblasts, which express higher levels of the contractile protein α-smooth muscle actin (SMA). This process is largely cytokine mediated through transforming growth factor (TGF)-β.⁵ In vivo gene delivery of TGF-β through an adenovirus vector into rat knee joints has been shown to produce arthrofibrosis.⁶ TNF-α may play a modulatory role in myofibroblast activity—at low levels, it increases myofibroblast viability and proliferation, while at high levels, it reduces myofibroblast contractile forces, and it down-regulates α-SMA and type I collagen expression.⁷

In the pro-inflammatory milieu, matrix metalloproteinases (MMPs) decrease⁵ while tissue inhibitors of matrix metalloproteinase (TIMPs) increase,⁸ resulting in decreased scar remodeling. The pro-inflammatory milieu down-regulates lubricin, an important lubricating and anti-adhesive glycoprotein responsible for the low-friction gliding of musculoskeletal tissues.⁷ Prolonged immobilization and lack of mechanical stress further predisposes the joint to increase in collagen cross-linking and subsequent scarring.^9,10 The contractile effects of myofibroblasts mediated by α-SMA are thought to cause capsular contraction, while increased collagen cross-linking and decreased matrix turnover lead to scar consolidation.

Nonoperative management

The goal of any treatment of post-traumatic elbow stiffness is the restoration of a functional arc of motion. Depending on the severity and time course of the arthrofibrosis, the functional impact to the patient, and prior attempted treatments, nonoperative management may be a viable option. Since there is no universally accepted treatment algorithm, treatment must be individualized and agreed upon through a shared decision-making process with each patient.

Therapy

Physiotherapy is a frequently utilized tool of the surgeon, both to prevent post-traumatic elbow stiffness and to gain motion after the onset of stiffness.¹¹ In the initial phase of elbow trauma, physiotherapy focuses on pain, edema, and inflammation control. Local application of ice packs or cooling systems helps to reduce pain and inflammation. Compressive bandages and elevation of the elbow above heart level help control pain and swelling.¹² In the early phase of elbow trauma, physiotherapists encourage active mobilization in so far as the injury or surgery allows. In theory, early active mobilization aids edema control and prevents adhesion formation; however, there is currently a paucity of evidence for the effects of timing of mobilization on final elbow range of motion and function after trauma.¹³

Passive range of motion exercises may be added to the rehabilitation regimen after sufficient healing of the injured bones and soft tissues, usually 6 to 12 weeks from the time of injury.¹² Supervised passive range of motion with a home exercise program may be effective for some patients to regain a functional range of motion and avoid more invasive interventions.

In the setting of longstanding elbow contractures, the utility of physiotherapy reaches diminishing returns. There is little evidence to support the effectiveness of accessory techniques such as passive mobilizations with movement for post-traumatic elbow stiffness.¹¹ Communication between the surgeon and physiotherapist is important in all stages of rehabilitation, as inappropriate therapy can elicit pain, aggravate inflammation, discourage the patient, and hinder the rehabilitation process. Finally, the treating surgeon must be mindful that the success of any physiotherapy regimen depends both on the motivation and compliance of the patient and the nature of the underlying disease.

Bracing

Bracing has long been employed as a primary or an adjunct therapy for post-traumatic elbow stiffness. There are three main categories of bracing for elbow stiffness: static, static progressive, and dynamic. Static bracing places the elbow in an orthosis at a fixed angle with no additional forces applied across the joint. Static bracing is used to maintain the range of motion and prevent recurrent contracture during resting. Static progressive bracing utilizes a static brace with the ability to adjust the angle of the orthosis (Figure 1). Consequently, static progressive bracing allows patients to affect incremental gains in range of motion and can be used to restore the range of motion over time. An advantage of static progressive bracing is the ability to load the tissue staggered with rest, which allows for intermittent stretching but prevents an exuberant inflammatory response. Dynamic bracing utilizes an orthosis that applies a constant force across the joint in an effort to increase the range of motion. Early forms of dynamic bracing used reverse dynamic slings in balanced suspension traction.¹⁴ Modern dynamic braces are self-contained and no more cumbersome than their static counterparts.

Figure 1.

Clinical photograph showing an example of static progressive bracing.

Static progressive bracing for post-traumatic elbow stiffness has proven successful in multiple case series.^15–17 Substantial improvements in range of motion can be expected after four to six weeks of static progressive bracing. Mean improvements in flexion-extension arc of motion range from 31° to 43° after the bracing course, and improvements in range of motion have been maintained one year after discontinuation of bracing. In most cases, static progressive bracing is initiated within months after injury or surgery; however, clinical improvement in range of motion has been demonstrated even for chronic contractures of many years.¹⁵ In a series of 29 patients with post-traumatic elbow stiffness, Doornberg et al.¹⁶ showed that only 10% of patients who underwent a course of static progressive bracing required subsequent surgery to address stiffness.

Multiple meta-analyses have shown similar efficaciousness of static progressive bracing and dynamic bracing for post-traumatic elbow stiffness.^18,19 Static progressive bracing and dynamic bracing achieve similar gains in range of motion with comparable rates of adverse events. Both outperform static bracing in improvements in motion. Therefore, the choice between static progressive bracing and dynamic bracing is based on the experience and preference of the treating surgeon and the patient.

Surgeons and patients should be aware of potential complications of bracing. With all forms of bracing, skin complications have been reported, including pressure ulcers and contact dermatitis. In both static progressive splinting and dynamic splinting, new cases of heterotopic ossification and ulnar neuropathy have been observed.^18,19 Treating surgeons must be wary in chronic contractures in which significant flexion is gained through bracing, because ulnar nerve symptoms may develop and often require surgical decompression.

Ideal candidates for bracing are motivated patients with mild or moderate elbow stiffness, who are within attainable reach of a functional arc of motion, without external blocks to motion such as impinging heterotopic ossification. In this cohort, a trial of static progressive bracing or dynamic bracing until clinical improvement plateaus is appropriate and can be met with excellent results.

Manipulation under anesthesia

A paucity of evidence exists for manipulation under anesthesia for the post-traumatic stiff elbow. Duke et al.²⁰ report a series of 11 patients who underwent manipulation under general anesthesia for elbow stiffness failing supervised therapy. Six patients (55%) had improved motion after manipulation; however, two patients (18%) had lost motion after manipulation and two patients (18%) experienced transient ulnar sensory neuropathy. The current indications for manipulation of the stiff elbow are unclear.

Operative management

Surgical treatment of post-traumatic elbow stiffness is often able to restore functional elbow range of motion where nonoperative treatments have failed. The ability of surgery to restore motion is balanced against its invasiveness and inherent risks. The decision for surgery is best made after a thorough discussion of risks, benefits, and alternative treatment options. Patients with severe contractures or near ankylosis stand to gain the most from surgical release. However, depending on patients’ preferences and expectations, even those with relatively mild contractures may be appropriate surgical candidates, because what is considered functional elbow range of motion must be individualized for each patient’s vocation and avocations. Surgical treatment of post-traumatic elbow stiffness consists of arthroscopic and open arthrolyses.

Arthroscopic arthrolysis

It is our preference to perform arthroscopic arthrolysis in the lateral decubitus position. The elbow joint is insufflated with saline at the posterolateral soft spot. The posterolateral viewing portal and the straight posterior trans-tricipital working portal are established. Loose bodies in the posterior elbow are removed with arthroscopic graspers. The medial and lateral gutters, which may contain loose bodies, are examined, with special care taken in the medial gutter due to its proximity to the ulnar nerve. Bony osteophytes are debrided with the arthroscopic burr, particularly on the olecranon process and olecranon fossa. After the bony debridement, the posterior capsule is released arthroscopically.

The anterolateral viewing portal and the anteromedial working portal are established next. Loose bodies in the anterior elbow are removed with arthroscopic graspers. Bony osteophytes are debrided with the arthroscopic burr, particularly on the coronoid process and coronoid fossa. After the bony debridement, the anterior capsule is released with an arthroscopic shaver or biter, with special care taken due to the proximity of the radial nerve to the anterior joint capsule.

A separate open approach for ulnar nerve decompression and anterior transposition should be considered in patients with preoperative flexion limited to 90°, in order to prevent traction neuropathy secondary to increased postoperative flexion. Anterior transposition of the ulnar nerve may preclude future elbow arthroscopy.

Open arthrolysis

Open arthrolysis allows for the release of capsular adhesions as well as the removal of loose bodies, osteophytes, heterotopic ossification, and retained hardware. Open arthrolysis was initially described as an anterior capsulotomy,^21–23 which did not provide access to the posterior compartment of the elbow and required careful dissection of the neurovascular bundle. The lateral approach has gained popularity, because it provides access to both the anterior and posterior compartments of the elbow while staying further from major neurovascular structures.^24,25 Mansat and Morrey²⁶ named this procedure the column procedure, because capsular adhesives are released along the lateral column of the distal humerus. An isolated medial approach may be utilized when there is medial contracture with sparing of the lateral collateral ligament.²⁷ In cases where flexion is limited preoperatively, concurrent release or transposition of the ulnar nerve can be performed through the medial approach. An extensile posterior skin incision provides a utilitarian approach to access both the lateral and medial column and is helpful in cases of severe stiffness.

The procedure is performed with the patient supine. Under tourniquet, the proximal portion of the Kocher interval is used to approach the lateral column of the distal humerus. Alternatively, if an extensive release or ulnar nerve decompression is expected, a posterior skin incision is preferred for the ability to develop lateral and medial skin flaps to gain access to both the lateral and medial sides of the joint. Regardless of skin incision, the lateral side is usually approached first, exposing the thickened capsule of the radiohumeral joint. Brachialis muscle is separated from the anterior capsule with a periosteal elevator. The anterior capsule is excised as medially as safely reachable from the lateral approach, taking care to protect the neurovascular bundle. It is often difficult to reach the anteromedial capsule from the lateral approach, but one can usually reach at least the level of the coronoid. Loose bodies and osteophytes may also be excised at this stage. If extension is still limited, a medial column approach should be undertaken to finish resection of the anteromedial capsule.

In cases of significant limitation of flexion, it is often necessary to release thickened adhesions of the posterior capsule. The triceps muscle is elevated off of the posterior capsule with a periosteal elevator, and the posterior capsule is excised. Loose bodies and osteophytes may be excised from the posterior compartment as well. Similarly, the posterior compartment may be approached both laterally and medially as needed. The medial collateral ligament may be sequentially released from its posterior bundle through its transverse bundle until flexion is restored; the anterior bundle is preserved to ensure stability. Ulnar nerve decompression and anterior transposition are performed in patients with limited preoperative flexion. Once the capsular release is adequate, it is important to document the final intraoperative passive range of motion and elbow stability. It is our practice to take an intraoperative video of the final passive range of motion, so that the patients have an objective goal to work towards postoperatively. In rare circumstances, where the elbow is unstable after open arthrolysis, a hinged external fixator or internal joint stabilizer may be applied to prevent instability while allowing for early motion.^28,29 A closed suction drain is used in the minority of cases with a particularly vascular wound bed, and this drain can be safely removed within 24 h.

Outcomes

Good restoration of elbow range of motion is achieved with arthroscopic arthrolysis. Published mean improvements in flexion-extension arc of motion range from 18° to 66°.^30–35 Functional outcomes are good to excellent,^32–35 and over 85% of patients are able to return to their previous level of work.³⁴

Open arthrolysis reliably improves arc of motion in the post-traumatic stiff elbow, with reported improvements in arc of motion ranging from 45° to 59°.^{24–27,35–39} Gains in range of motion are observed regardless of operative approach and are maintained nearly a decade after surgery.³⁸ Good or excellent functional outcomes are generally achieved.

Arthroscopic and open arthrolysis are both viable options for post-traumatic elbow stiffness. Insufficient evidence currently exists to recommend one procedure over the other,⁴⁰ and therefore, the choice largely depends on the experience and preference of the treating surgeon. When open arthrolysis is performed within 10 months from time of injury, better final range of motion is achieved with fewer complications.⁴¹ Patients with significant existing post-traumatic elbow arthrosis achieve less improvement in range of motion from open arthrolysis than those without significant arthrosis.²² Patients with motion-restricting heterotopic ossification achieve better range of motion than patients without heterotopic ossification, once the block to motion is removed as a part of surgery.⁴² Current evidence does not support the use of continuous passive motion following elbow arthrolysis.^43,44

Complications

The complication rate of open arthrolysis is approximately 10%.⁴⁴ Common complications include superficial wound infections and nerve palsies.^{26,37,39,45,46} Ulnar sensory neuropathy is the most common nerve complication after open arthrolysis, approximately 25% of which will require operative decompression.⁴⁷ Prophylactic ulnar nerve decompression and transposition are indicated in cases of severe preoperative flexion deficiency to prevent this complication. Hematomas and seromas can occur secondary to flap elevation in a vascular wound bed. Reflex sympathetic dystrophy has been reported after open arthrolysis.³⁹ Elbow instability is a rare but challenging complication of contracture release. If a hinged external fixator is used to facilitate early motion after arthrolysis, pin site complications are frequently encountered.

Female patients and patients with less preoperative range of motion are at greater risk for complications after open arthrolysis.⁴⁴ Patients with higher body mass index have more postoperative pain and less improvement in motion after open arthrolysis compared with patients with normal weight.⁴⁸ Patients with diabetes mellitus can expect less improvement in motion and poorer functional outcome compared with normoglycemic patients.⁴⁹ Application of vancomycin powder into the wound prior to closure may have a role in preventing postoperative infections after open elbow arthrolysis.⁵⁰

The most common complications following arthroscopic arthrolysis are nerve palsies, which are uncommon and usually transient. Radial nerve or posterior interosseous nerve injuries can occur during arthroscopic release of the anterior capsular, as this structure can be within 1 to 2 mm from the anterior joint capsule.³ The ulnar nerve is vulnerable to injury during arthroscopy in the medial gutter. Wound infections are exceeding rare after arthroscopy. One case of synovial fistula has been reported in the literature.³³

Recurrent elbow stiffness can be problematic after arthrolysis; the reported rate of reoperation for stiffness ranges from 10% to 34%.^45,46 Recurrent heterotopic ossification, occurring in 6% to 17% of cases,^45,46 is a major cause of recurrent stiffness. There is no difference in heterotopic ossification recurrence rate in patients who received indomethacin prophylaxis, radiation therapy prophylaxis, or no prophylaxis.⁴⁵

Future directions

Current treatments of post-traumatic elbow stiffness focus on stretching or excising hypertrophic scar tissue and adhesions in and around the elbow joint. Although multiple animal models of arthrofibrosis exist,^51,52 a pharmacologic treatment specifically targeting pathologic, contracted tissue is still lacking. The role of intraoperative injection of botulinum toxin A has been explored.¹¹ Botulinum toxin prevents the release of acetylcholine at the neuromuscular junction, and local botulinum toxin injection is used to treat muscle spasticity. In theory, botulinum toxin would only be effective against post-traumatic elbow stiffness insofar as the stiffness is a result of increased muscle activity. No evidence currently exists for its use.

There is interest in the use of Clostridium histolyticum collagenase for arthrofibrosis. Collagenase isolated from C. histolyticum has revolutionized the treatment of Dupuytren’s contractures of the hand. Local injection of collagenase into the fibrotic palmar cords of Dupuytren’s disease followed by manipulation has been met with excellent results.⁵³ Collagenase has not been studied for arthrofibrosis of the elbow. Further research on the safety profile of peri-articular collagenase injections and its effect on nearby musculoskeletal structures is needed.

Immunomodulatory agents may play a role in the future treatment of post-traumatic elbow stiffness. The inflammatory cascade that precedes arthrofibrosis is cytokine mediated. One such cytokine is TNF-α, which increases myofibroblast viability and proliferation. Infliximab, a chimeric monoclonal antibody against TNF-α, currently used to treat a number of autoimmune diseases, has been shown in vitro to inhibit the effects of TNF-α on myofibroblasts.⁵⁴ A possible future direction for the treatment of arthrofibrosis is intra-articular injection of immunomodulatory agents to interrupt the inflammatory cascade that leads to myofibroblast proliferation and scar consolidation at the cytokine level.

Mast cells have been recently implicated in the pathogenesis of joint contractures through the myofibroblast–mast cell–neuropeptide axis of fibrosis.⁵⁵ Increased numbers of mast cells have been observed in arthrofibrotic joint capsules, and their granules contain pro-fibrotic cytokines. Release of substance P from local nerve endings may trigger mast cell degranulation and subsequent activation of myofibroblasts. A randomized controlled trial is underway on the effects of ketotifen, a mast cell stabilizer, on post-traumatic elbow arthrofibrosis.⁵⁵

Gene delivery provides hope of interrupting the inflammatory cycle by altering the cytokine expression profile at the genetic level.⁷ Xue et al. published on the successful treatment of joint stiffness in a rat model using RNA interference. In their experiments, short hairpin RNA was delivered through a lentivirus vector to silence expression of the Smad4 gene, which encodes a key downstream mediator of the TGF-β signaling pathway. Smad4 gene silencing resulted in decreased levels of α-SMA, type I collagen, type III collagen, TNF-α, IL-1, IL-6, IL-10, and MMP, while motion and synovial intima length increased.⁵⁶ Continued refinement of gene delivery methods may one day allow control of the inflammatory cascade and fibrosis process through preferential gene expression.

Local delivery of antifibrotic proteins into arthrofibrotic joints has shown promise. Relaxin-2 is an antifibrotic protein hormone excreted by the placenta, associated with increased tissue laxity during pregnancy. Relaxin-2 acts by inhibiting fibrogenesis and collagen overexpression. Multiple intra-articular injections of recombinant relaxin-2 have been demonstrated to reverse range of motion deficits on biomechanical measurements in rat models of joint stiffness. Rats that received multiple intra-articular injections of relaxin-2 were found histologically to have a return to normal capsular thickness.⁵⁷ Future studies should focus on pharmacologic agents that prevent or reverse the motion-limiting effects of arthrofibrosis.

Declaration of Conflicting Interests

The author(s) declare that there is no conflict of interest with respect to the research, authorship, and publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.