Abstract
Early posttraumatic elbow contractures may be treated with a combination of manipulation with the patient under anesthesia followed by bracing.
Extrinsic contractures of the elbow may be treated with open or arthroscopic release, whereas intrinsic and combined contractures may require tissue release as well as partial or total arthroplasty.
Elbow stiffness commonly occurs following elbow trauma, which may involve substantial bone and soft-tissue injury but may also occur after seemingly trivial trauma. An arc of elbow motion of 100° (from 30° to 130°) is required for most daily activities, with a loss of 50° in the arc of motion causing up to an 80% loss of function1. Posttraumatic elbow stiffness is challenging to treat and often involves young, active patients. In this article, we review the molecular pathogenesis of elbow stiffness, its presentation and means of assessment, and the reported outcomes of open and arthroscopic operative techniques.
Posttraumatic elbow stiffness may be due to soft-tissue contracture (skin, capsule, ligaments, muscles, and tendons) or osseous congruency disruption. The observation of severe elbow stiffness, even with well-reduced stabilized fractures, suggests that soft-tissue contracture is a major contributor. Contractures in immobilized rat knees were mainly capsular rather than myogenic2, and this may be the case in the elbow too. In immobilized fractured rabbit knees, posterior capsular disruption produced more severe, refractory contractures3.
A contracted capsule consists of cellular and extracellular matrix components, showing substantial changes compared with normal controls. Contracted capsules are thicker4 and have increased collagen (type-I, III, and V)4,5 levels, the fibers of which are disorganized4. These fibers demonstrate increased collagen cross-linking, decreased proteoglycan and water content6, an increase in matrix metalloproteinases (MMP-1, 2, 9, 13, and 15), and a reduction in tissue inhibitors of MMP5. Contracted capsules have greater absolute and proportional myofibroblast numbers7.
Role of the Myofibroblast
Myofibroblasts are important cells in the development of posttraumatic elbow stiffness. These cells are tissue fibroblasts that express the intracellular contractile protein alpha-smooth muscle actin (α-SMA)8 that may interact with the extracellular matrix through cell membrane integrins influencing matrix organization9. Myofibroblasts can cause collagen contraction more readily than can normal fibroblasts10.
Myofibroblast number is typically elevated in musculoskeletal fibrosis, such as adhesive capsulitis11 and Dupuytren disease12, but also in cirrhosis and in pulmonary, corneal, and cardiac fibrosis13-15. Hildebrand et al.7 showed that actual and proportional myofibroblast numbers were elevated in elbow capsules that required operative release compared with normal controls. A regional variation was seen with greater increase in the anterior capsule than in the posterior elbow capsule16. This is consistent with the clinical observation that loss of extension is more frequently encountered compared with loss of flexion in elbow stiffness.
Myofibroblast number is inversely related to motion in posttraumatic elbow stiffness16. Rabbit models of acute knee contractures showed that the increase in myofibroblast number occurs early and is similar to that observed in chronic animal and human contractures17.
Differentiation of mesenchymal stem cells and fibroblasts into myofibroblasts and the activity of the myofibroblasts are influenced by a complex system of chemical and mechanical signals (Fig. 1). Chemical regulators of myofibroblast function are elevated in posttraumatic capsules of human elbows and in animal models18. These include transforming growth factor beta (TGF-β1), connective tissue growth factor19, and the domain of fibronectin ED-A (extra domain-A). Myofibroblast contracture can activate latent TGF-β1, providing an interlink between chemical and mechanical signals20. Autocrine production of TGF-β1 may promote myofibroblastic differentiation21. Tumor necrosis factor-alpha (TNF-α) has also been shown to promote myofibroblast proliferation at low doses but inhibit matrix contraction at higher doses22, via the inhibition of α-SMA and collagen type-I gene expression. These regulatory effects of TNF-α were mediated through prostaglandin E2 and inhibited by diclofenac.
Another mechanism contributing to myofibroblast activation is the mast cell-neuropeptide fibrosis axis23, documented in healing skin24. Mast cells occur in joint capsules and contain granules of profibrotic mediators (platelet growth factor A, endothelin 1, basic fibroblast growth factor, and TGF-β125). These can induce myofibroblast differentiation and proliferation. Mast cell degranulation is stimulated by neuropeptide substance-P and calcitonin-G-related peptide released from nerve terminals26 in response to injury and pain27.
In animals and human elbows showing posttraumatic contracture, the proportional numbers of myofibroblasts, mast cells, and neuropeptide-containing nerve fibers are greater in contracted capsules than in normal capsules23.
The mast cell may thus be the link between acute inflammation and subsequent contracture, and could be an intervention target. Red Duroc pigs show greater wound contraction than Yorkshire pigs28. Ketotifen, an inhibitor of mast cell degranulation, reduced wound contraction in red Duroc pigs to a level seen in Yorkshire pigs. Similarly, ketotifen reduced mast cell and myofibroblast numbers and the degree of flexion contractures by 42% to 52% in rabbit knees immobilized for fractures29.
Role of Female Sex Hormones
Female sex hormones may act on extracellular matrix and myofibroblasts to influence joint laxity and fibrosis. Joint hypermobility is more common in females, and increased laxity occurs in pregnancy30. Estrogen, progesterone, and relaxin receptors occur in the anterior cruciate ligament (ACL)31-33. Increased ACL laxity correlates with menstrual cycle estrogen and progesterone peaks34,35. Estrogen reduces collagen synthesis, whereas relaxin may decrease collagen formation and increase the expression of MMP36,37. Knee contractures were created in rats38. After two weeks of immobilization, there was a trend toward reduced contractures in pregnant rats. The connective tissue sensitivity to sex hormones may be modulated by injury. Pregnancy increased the laxity of the medial collateral ligament (MCL) in uninjured but not in injured rabbit knees39. Sex hormone receptors are found in myofibroblasts of normal and pathological tissues. Estrogen prevented cardiac fibrosis via activation of the myofibroblast estrogen receptor beta40. Relaxin decreased myofibroblast proliferation and downregulated α-SMA expression in cell cultures41. Relaxin therapy in vivo enhanced muscle regeneration and reduced fibrosis after skeletal muscle injury42.
Role of Mechanical Factors
Differentiation of fibroblasts into myofibroblasts requires a mechanically stiff substrate. Progenitor stem cells growing on a substrate whose stiffness corresponds to bone, muscle, or brain develop into the corresponding cell lineages43. Even in the presence of TGF-β1, lack of stress inhibits myofibroblast differentiation with TGF-β1 upregulating α-SMA only in fibroblasts grown on stiff but not compliant collagen44.
Individuals with similar elbow injuries show varying degrees of contractures, raising the possibility of genetic predisposition to stiffness. Nesterenko et al.45 reviewed the cases of 116 patients with posttraumatic stiffness and identified a subgroup of four patients who, following a trivial insult, had developed severe elbow contractures, refractory to multiple operative and nonoperative interventions. This predisposition is supported by animal studies. Forty rats from four inbred rat strains had knee immobilization. The mean contracture observed in two of these strains was significantly greater than that in the other two (p < 0.05), supporting intrinsic genetic factors influencing the severity of joint contractures46.
Understanding the molecular pathogenesis of posttraumatic stiffness can allow molecular targeting interventions to prevent stiffness following elbow injury or its recurrence following operative release of established contractures. Understanding the genetic influence may shed light on the molecular pathogenesis but also offer the exciting opportunity of identifying individuals with an inherent susceptibility to stiffness and allow early selective targeting.
Posttraumatic elbow stiffness may be classified as occurring early or late in relation to the time of the injury. Early presentation, within six months of injury, may be more amenable to operative intervention. Classification according to the structures involved (soft tissue, osseous, or combined) is described47. Classification of posttraumatic elbow stiffness into intrinsic, extrinsic, or combined48 allows better understanding of the cause of stiffness and provides more logical guidance to management. Intrinsic contractures are secondary to involvement of the articular surface, whereas extrinsic are those not involving the articulation. In reality, most are a combination of both (Table I).
Establishing the exact injury mechanism and subsequent treatment of a patient presenting with elbow stiffness after trauma is important. It is essential to examine elbow flexion-extension and pronation-supination actively and passively. The functional limitations and patient’s expectations of treatment need to be established. Typical posttraumatic elbow stiffness is painless. Pain at mid-motion suggests an intrinsic component to stiffness. Pain at the extremes of motion is consistent with impingement between the olecranon or coronoid process and the distal end of the humerus, usually due to osteophyte formation. With previous operative treatment and internal fixation, the possibility of infection should be considered. Neurological signs such as ulnar nerve involvement must also be considered48.
Radiographs are often sufficient to image the stiff elbow. Computed tomography with three-dimensional reconstruction may accurately localize loose bodies and/or impinging osteophytes, assisting in planning arthroscopic debridement49. Checking inflammatory markers (C-reactive protein level and erythrocyte sedimentation rate) helps in excluding infection or inflammatory conditions. Examination with the patient under anesthesia may differentiate an apparent loss of elbow motion due to pain and apprehension from true mechanical stiffness.
Management options involve nonoperative (serial bracing, examination under anesthesia, and splinting) or operative treatment in the form of open or arthroscopic release, interposition arthroplasty, or partial (radial head excision and replacement and capitellar resurfacing) or total elbow arthroplasty. Treatment is guided by the timing of presentation, the symptoms and expectation of the patient, functional level, and the underlying cause of contracture.
Intervening for loss of the functional arc of elbow motion (30° to 130°) seems appropriate. However, intervention for the loss of a lesser amount of motion may be needed in individuals such as professional athletes or musicians for whom motion beyond the average functional arc is important.
For patients seen within six months of injury, nonoperative treatment with serial bracing and/or examination under anesthesia is preferable.
Braces for improving elbow motion are either dynamic or static progressive types50. Dynamic splints have an adjustable spring exerting a constant stretching load, set to an extent not producing pain. In static splinting, the maximum load that can be tolerated comfortably is applied. As the tissue stretches, the load required to maintain this stretched state reduces, and the load becomes better tolerated; the splint is readjusted so that more load is applied and further stretching achieved. Biological tissues show viscoelastic properties including creep and stress relaxation. Dynamic splinting is based on creep (an increase in length with the application of a constant load for prolonged time50) and static progressive splinting on stress relaxation (a decrease in load required to maintain a certain length over time).
Successful results have been reported with both dynamic and static splinting, but a controlled comparison awaits. Table II summarizes several studies51-59 that have described serial elbow splinting. We favor static progressive splitting because it is better tolerated, and shorter utilization periods may increase compliance. The exact protocol for bracing is based on the degree of contracture, splint tolerance, personal circumstances, compliance, and rate of deformity correction.
Examination under anesthesia may be used for elbow contractures presenting early. It involves assessing the passive range of motion; evaluating for crepitus, surface irregularity, and stability; and manipulation to improve motion. The presence of crepitus and surface irregularity may signify an intrinsic component to the stiffness. Manipulation is attempted only when there is radiographic evidence of osseous fracture union and should be avoided with fractures that have not healed. Regaining elbow flexion is easier to achieve than is elbow extension. Examination with the patient under anesthesia is followed by serial bracing. The value of examination under anesthesia in treating stiffness comes mainly from reports of its use following operative treatment60,61 rather than following trauma.
Operative treatment is guided by the type of contracture present. Extrinsic contractures are usually managed with open or arthroscopic release. Those with a large intrinsic component are managed with arthroplasty. In combined contracture, both methods of treatment may be used.
Open Release
Open release has been the standard treatment for managing extrinsic contractures. Several open approaches have been described, and they have been guided by the cause, anatomical location, and goals of the treatment.
Lateral Column Procedure
The lateral column procedure62 consists of an arthrotomy, capsular release, and osteophyte excision. It allows release of the anterior and posterior capsule. The incision is centered over the lateral humeral epicondyle, elevating the brachioradialis muscle from the humerus, the common extensor origin from the lateral collateral ligament (LCL), and the brachialis muscle off the anterior elbow capsule. The capsule is entered at the level of the radiocapitellar articulation, the lateral capsule is excised, and the medial capsule is incised. Intra-articular adhesions and coronoid osteophytes are removed. Elevation of the triceps and anconeus muscles from the distal end of the humerus and proximal part of the olecranon allows posterior capsular release and olecranon fossa debridement. The LCL is preserved but, if released, it is reattached via drill-holes or suture anchors. The lateral approach may not give adequate exposure to the far medial part of the joint.
Medial Approach
A skin incision is made over the medial humeral epicondyle, and while the ulnar nerve is protected, the pronator teres muscle is elevated from the common flexor mass, exposing and releasing the anterior capsule. The triceps muscle is elevated off the humerus and olecranon, allowing release of the posterior band of the MCL and posterior capsule and removal of the olecranon osteophytes. The anterior band of the MCL is preserved for stability. This approach is limited, not giving sufficient exposure to the lateral part of the joint48.
Anterior Approach
This approach accesses the anterior capsule to better manage flexion contractures63. An anterior bayonet incision is made across the elbow flexion crease. The medial and lateral antebrachial cutaneous nerves; brachial artery; and median, radial, and musculocutaneous nerves are protected. Medially, the interval between the common flexor origin and biceps tendon and, laterally, the interval between biceps and brachioradialis muscle are developed. The brachialis muscle is dissected from the anterior capsule medially to laterally, exposing the capsule, which is released and excised.
Posterior Approach
This approach allows extensive medial and lateral releases and can be used to perform interpositional arthroplasty when indicated. A midline posterior incision is utilized. The triceps and anconeus muscles are reflected from the ulna. The common extensor origin is elevated from the anterior capsule, which is released. The ulnar nerve is decompressed and the posterior part of the MCL is released. If greater exposure is necessary, further release of the triceps and anconeus muscles from the olecranon is performed laterally to medially. The triceps is reattached to the olecranon via drill-holes64.
Other descriptions of open releases include isolated MCL division65, and the transolecranon osteotomy approach66. We favor the lateral column procedure for most cases of open release, reserving the posterior approach when lateral and extensive medial releases are needed or when the ulnar nerve must be decompressed. The isolated medial release has limited indications, whereas an anterior approach is used for isolated anterior ectopic bone excision.
Arthroscopic Surgical Release
Arthroscopic osteocapsular release involves the removal of osseous components, such as osteophytes and ectopic bone, and capsular release. Various arthroscopic portals provide access to the olecranon fossa and elbow joint. Capsular retractors facilitate exposure and protect neurovascular structures. Shavers are used in free-flow mode with suction avoided. Arthroscopic release is a challenging procedure because of the close proximity of the neurovascular structures. Although arthroscopic release has been used for the most difficult and challenging posttraumatic elbow stiffness by experienced surgeons, it is a procedure with a steep learning curve, associated with serious complications67-70. For most surgeons, particularly those who perform few arthroscopic elbow procedures, it is a procedure to be undertaken with care and is reserved for the less severe spectrum of posttraumatic contractures.
We reviewed the English-language literature to identify clinical studies examining the outcome of open and arthroscopic release for posttraumatic elbow stiffness. These are summarized in Tables III and IV63,71-99. These studies describe primarily Level-IV evidence involving case series, with no randomized trials identified. Although there has been a variation in the approaches utilized and in postoperative rehabilitation protocols, both open and arthroscopic procedures can reliably increase elbow flexion and extension (Tables III and IV). The results of open arthrolysis are durable over time. Sharma and Rymaszewski71 reviewed the cases of twenty-five patients treated by open arthrolysis. The improvement in mean elbow motion from 55° preoperatively to 105° at one year postoperatively was maintained over a mean follow-up interval of 7.8 years.
Management of the Ulnar Nerve
Regardless of the surgical technique used, understanding the status of the ulnar nerve is critical. With a large flexion loss, or if ulnar nerve symptoms are present prior to operative release, nerve decompression is performed at the time of surgery, as motion gain can initiate or exacerbate ulnar nerve symptoms100. If there is nerve instability, it is transposed.
Continuous Passive Motion
Continuous passive motion is used to reduce stiffness following operative treatment or trauma. Joint stiffness occurs in four stages (bleeding, edema, granulation tissue formation, and fibrosis). The first two occur early, whereas granulation tissue and fibrosis occur over days to months. Continuous passive motion aims to reduce intra-articular bleeding and periarticular edema through a sinusoidal change in intra-articular and periarticular pressure. Continuous passive motion is effective if applied early and has very little role to play once granulation tissue and fibrosis are established101.
Lindenhovius et al.102 reported a case-control study assessing continuous passive motion following open elbow release. The case group had continuous passive motion immediately set at the level of flexion-extension achieved intraoperatively. Continuous passive motion was used at home for two weeks as tolerated. There was no difference between the continuous passive motion and control groups with regard to motion gain and functional scores. However, this was a retrospective study with no guidelines for treatment allocation, inconsistencies in the protocol for the use of continuous passive motion, and no formal compliance assessment. The numbers of patients were small (twelve in the continuous passive motion group and ten in the control group). Gates et al.103 prospectively studied continuous passive motion following anterior capsulotomy for elbow flexion contracture. There was no difference in extension gain between the continuous passive motion and control groups; however, continuous passive motion significantly increased flexion gain (p = 0.0036). The mean gain in total arc of motion was greater in the continuous passive motion group (48° preoperatively to 96° postoperatively) compared with controls (69° preoperatively to 94° postoperatively).
Postoperatively, continuous passive motion may be used in the hospital, under a nerve block to control pain, and then continued at home. The continuous passive motion machine is set to allow maximal motion within pain limits. The use of continuous passive motion requires careful patient monitoring to avoid neurological injury or wound breakdown. Tight, circumferential dressings are avoided. Once the patient is able to actively maintain most of the motion achieved intraoperatively, continuous passive motion is changed to a program of splinting, usually for three months. Nighttime splinting is continued for up to six months.
If an external fixator was utilized at the time of operative release to protect ligamentous repair, it is removed approximately three weeks postoperatively with the patient under anesthesia. This allows examination under anesthesia and, if needed, further manipulation61.
The role of physiotherapy in managing the stiff elbow is uncertain. To our knowledge, there is no comparative study evaluating the role of therapy in this context. We believe that uncontrolled therapy may exacerbate pain and inflammation and inhibit rather than facilitate mobilization. Therapy, if given, should be done in a controlled manner in close communication with the surgical team, guiding rather than forcing motion gains.
Managing intrinsic posttraumatic stiffness is challenging, as patients are often young and functionally demanding. The options in these patients are release of extrinsic contractures alongside interposition, total, or partial arthroplasty if there is substantial articular cartilage damage. Resection arthroplasty and arthrodesis are poorly tolerated options and should be avoided.
Total elbow arthroplasty or partial arthroplasty will likely lead to the need for additional operative treatment in young patients because of wear or loosening, and interposition arthroplasty may offer a more durable solution. Several interposition materials have been described. Larson and Morrey104 reported interposition arthroplasty with fresh-frozen Achilles tendon allograft in posttraumatic and inflammatory arthritis in forty-five elbows in patients with a mean age of thirty-nine years. Operative treatment was for pain, stiffness, and instability, with >50% involvement of the articular surface of the trochlea and capitellum. At a mean follow-up interval of six years, seven elbows required revision. In those with surviving allografts, the mean flexion-extension arc improved from 51° preoperatively to 97° postoperatively. The mean Mayo elbow performance score (MEPS) increased from 41 to 65 points. Thirteen patients had a good or excellent result; fourteen, a fair result; and eleven, a poor result. Although improvement in the pain score was only 4 of 45 points on the MEPS pain component, patients were subjectively highly satisfied, with nineteen rating their elbow as much better and twelve, as somewhat better following interposition arthroplasty.
Interposition arthroplasty can be converted to total elbow arthroplasty with results comparable with those of total elbow arthroplasty performed for other indications. Blaine et al.105 reported on twelve total elbow arthroplasties following interposition arthroplasty (average patient age at the time of total elbow arthroplasty was fifty years, and the average interval from interposition to total elbow arthroplasty was 9.9 years). There were no intraoperative or perioperative complications. Pain was mild or none, and the result was satisfactory in ten. The mean MEPS improved from 32.1 preoperatively to 80.4 postoperatively. This study supports the potential benefit of interposition arthroplasty in buying time until the patient is older before undergoing total elbow arthroplasty.
Peden and Morrey106 reported on thirteen patients who underwent total elbow arthroplasty with use of the Coonrad-Morrey107 total elbow prosthesis (Zimmer, Warsaw, Indiana) for spontaneous ankylosis. The position of ankylosis ranged from 35° to 95° of flexion and was posttraumatic in ten patients and inflammatory in three. Surgery was challenging, with a mean operating time of 182 minutes and a high rate of complications (component malposition, humeral epicondylar fracture, wound necrosis, skin breakdown, and ulnar loosening in one patient each; deep infections in three; and heterotopic ossification in five). However, the mean arc of motion achieved was 37° of extension to 118° of flexion. The mean MEPS for ten patients was 74 points at a mean of approximately ten years, with good to excellent outcomes in seven of the thirteen patients. Preoperatively, only three of thirteen patients were able to complete any of the MEPS activities of daily living; however, postoperatively, all were able to complete some activities and seven, all activities, with varying degrees of difficulty. Figgie et al.108 reported on nineteen total elbow arthroplasties performed for complete ankylosis that had been present for an average of five years. A 26% complication rate occurred. Five patients required further manipulation to increase motion. The elbows achieved a mean arc of motion of 80° (range, 35° to 115°) that was maintained at mean follow-up interval of 5.75 years. The mean Hospital for Special Surgery Score increased from 23 to 84 points, with four excellent, eleven good, and three fair results and one failure108. The duration of ankylosis before total elbow arthroplasty was not related to postoperative motion.
In patients with articular cartilage destruction of the radiocapitellar articulation but preservation of the ulnohumeral articulation, partial elbow arthroplasty may be utilized109. This is an attractive option in young patients as it is bone-preserving and could avoid total elbow arthroplasty complications. Isolated radial head, capitellar, or total radiocapitellar replacement may be performed along with open capsular release.
Heijink et al.110 reported on three patients who underwent radiocapitellar hemiarthroplasty for arthritis. At a mean follow-up of eighty-seven months, the MEPS was 80 points for one patient and 100 points for two patients, and all patients were satisfied. Pooley111 described lateral elbow resurfacing and presented his early results112. Fifty-five elbows had lateral elbow resurfacing (hemiarthroplasty or total) for osteoarthritis, rheumatoid arthritis, or posttraumatic arthritis. The mean MEPS increased from 46 points preoperatively to 90 points postoperatively, and mean flexion-extension increased from 79° to 110° by twenty-four months. Forty-eight patients had satisfactory results, but five with isolated capitellar resurfacing required conversion to a total lateral elbow resurfacing. Longer results are pending.
Distraction arthroplasty is used for instability following contracture release and reattachment of the collateral ligaments and following interposition arthroplasty to protect the graft113. Gausepohl et al.114 reported on fourteen children or adolescents treated with isolated distraction using dynamic external fixation. Intraoperative distraction was followed by a six-day relaxation phase and then by elbow mobilization and distraction for seven weeks. Impinging ectopic bone was removed in four patients, but no formal arthrolysis was performed. At a mean follow-up of thirty-four months, the mean flexion-extension had increased from 37° preoperatively to 108°.
It is difficult to treat elbow stiffness occurring secondary to immobilization for instability, such as after a missed radial head dislocation with associated ulnotrochlear subluxation. One option is to address the instability and stiffness at the same setting with open reduction, arthrolysis, and ligament reconstruction followed by mobilization with an external fixator to protect the ligamentous repair. The alternative is a staged procedure in which the joint congruity is first established and the ligaments are repaired or reconstructed and, at the second stage, the stiffness is addressed in an open or arthroscopic procedure.
Recently, there has been an increase in our understanding of the molecular pathogenesis of posttraumatic contractures. The myofibroblast and its regulators—in particular, the mast cell-neuropeptide fibrosis axis—may have a pivotal role in stiffness development, providing specific molecular treatment targets by existing or yet to be developed pharmacological agents. Regulators, such as substance P, may provide the link between clinical interventions and the molecular pathogenesis of stiffness. The recognition that some individuals may be inherently predisposed to joint contractures suggests that there may be specific phenotypes in which patients are more likely to develop stiffness after injury. The ability to identify high-risk groups could be an important advance in the treatment of this condition.
Although satisfactory outcomes are reported with both open and arthroscopic surgical techniques, a direct prospective comparison of the two has not been performed. There is a paucity of high-quality clinical evidence on the role of physiotherapy, continuous passive motion, and splinting in the treatment of elbow stiffness.
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