Special Focus Section
119
Stiffness after Total Knee Arthroplasty Miguel M. Gomez, MD1
Javad Parvizi, MD, FRCS1
1 Research Department, Rothman Institute, Philadelphia, Pennsylvania
J Knee Surg 2015;28:119–126.
Abstract
Keywords
► ► ► ► ► ► ►
arthroplasty replacement knee contracture joint deformities acquired reoperation
Address for correspondence Javad Parvizi, MD, FRCS, Rothman Institute at Thomas Jefferson University, 125 S. 9th Street, Philadelphia, PA 19107 (e-mail: [email protected]).
Stiffness after total knee arthroplasty (TKA) adversely affects outcome and impacts patient function. Various risk factors for stiffness after TKA have been identified, including reduced preoperative knee range of motion, history of prior knee surgery, etiology of arthritis, incorrect positioning or oversizing of components, and incorrect gap balancing. Mechanical and associated causes, such as infection, arthrofibrosis, complex regional pain syndrome, and heterotopic ossification, secondary gain issues have also been identified. Management of stiffness following TKA can be challenging. The condition needs to be assessed and treated in a staged manner. A nonsurgical approach is the first step. Manipulation under anesthesia may be considered within the first 3 months after the index TKA, if physical therapy fails to improve the range of motion. Beyond this point, consideration should be given to surgical intervention such as lysis of adhesions, either arthroscopically or by open arthrotomy. If the cause of stiffness is deemed to be surgical error, such as component malpositioning, revision arthroplasty is indicated. The purpose of this article is to evaluate the various aspects of management of stiffness after TKA.
The main objective of total knee arthroplasty (TKA) is to afford pain relief, and restore function to the patient. To achieve adequate postoperative functionality, the joint must be stable and have an adequate range of motion (ROM). Joint stiffness after TKA is fortunately an infrequent complication, with the incidence ranging from 1.3 to 5.3%,1,2 but it can result in severe disability and is the source of frustration for both the patient and the surgeon. Stiffness has been defined as a decrease of postoperative ROM, including flexion contracture, accompanied by persistent pain and/or a clear functional compromise.3 There is a debate as to what degree of motion in the knee is required for daily function. It is known that during push-off of normal gait, 40 degrees of flexion is required to initiate the swing phase (►Fig. 1a). Maximum flexion during walking is 60 degrees, which occurs during the swing phase (►Fig. 1b). Furthermore, a flexion of around 120 degrees is required to climb stairs or rise from a chair without assistance of the arms.4 In certain cultures, much greater flexion, up to 150 degrees, of the knee is required for daily function. Activities such as squatting, sitting at a low-set table, and praying require a
greater degree of flexion of the knee.5 In the Western culture, achievement of ROM ranging from 0 to 110 degrees is considered adequate and generally a measure of success after TKA. There is no consensus in defining stiffness after TKA. Nicholls and Dorr6 stated that stiffness is a flexion contracture greater than 20 degrees or a global ROM of less than 45 degrees. Scranton7 defined a stiff knee as one having a ROM less than 90 degrees. Christensen et al8 defined stiffness as ROM less than 70 degrees of either active or passive flexion. These definitions did not include flexion deficit, thus focusing on either the lack of extension or global ROM as the most important parameter. Kim et al1 defined stiffness as a flexion contracture greater than 15 degrees and/or ROM of less than 75 degrees. Yercan et al2 defined knee stiffness as flexion contracture greater than 10 degrees or flexion less than 95 degrees during the first 6 weeks after TKA, thus adding a temporal component to the definition. Another challenge is the patient’s perception of motion deficit. A patient with preoperative flexion of 70 degrees might consider 90-degree flexion a success, while one with a preoperative flexion of 120 degrees might consider a
received August 26, 2014 accepted after revision October 23, 2014 published online December 16, 2014
Copyright © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI http://dx.doi.org/ 10.1055/s-0034-1396079. ISSN 1538-8506.
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Jorge Manrique, MD1
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postoperative flexion of 90degree a failure. Patient subjectivity might overestimate the problem regardless of objective measures. Postoperative stiffness has been demonstrated to be one of the most common causes of readmission within the first 90 days after surgery and it is one of the common reasons for revision TKA.9 Le et al10 identified stiffness as the third leading cause of TKA revision (18%). In a recent series, stiffness was placed as the fifth leading cause of revision TKA, being responsible for 3% of the revisions.11 Stiffness creates a challenging situation for patients and surgeons. Complete understanding of the etiology, the various treatment options and the expected outcome is paramount for surgeons encountering this complication of TKA.
Natural History of Flexion Contracture after Total Knee Arthroplasty
Fig. 1 (a) Shows the right knee during the push-off phase. (b) Shows the right knee during the swing phase required to prevent contact of the foot with the ground as it comes forward.
When assessing flexion contracture following TKA is important to understand the behavior of this condition through time. The presence of flexion contracture in patients with osteoarthritis (OA) can reach up to 60% preoperatively and 17% postoperatively.12,13 Knee flexion contracture increases quadriceps energy consumption during the stance phase of gait. An extended and more powerful contraction is needed to prevent the flexion collapse. Energy consumption has been directly related to the severity of the contracture. At 15 degrees of flexion contracture, there is a 30% increased energy consumption and up to 50% when the contracture reaches 30 degrees.14 A fixed flexion contracture also affects the contralateral limb, increasing the adductor and extensor moments during gait, thus creating an increase of shearing forces in the contralateral knee.15 About 11% of patients who undergo TKA and have more than 20 degrees of flexion contracture preoperatively experience the persistence of such deformity within the first 6 months postoperatively.16
Obesity has also been associated with diminished ROM after TKA. Shoji et al20 showed that in patients with postoperative ROM greater than 120 degrees, the incidence of obesity was 7%, whereas in patients with ROM with less than 100 degrees, the incidence of obesity was 78%. Patients with a body mass index (BMI) less than 25 kg/m2 had a mean ROM of 125 degrees, whereas patients with a BMI greater than 35 kg/m2 had a mean ROM of 116 degrees.21 It is also known that history of prior knee surgery jeopardizes ROM following TKA.22 van Raaij et al23 showed an average of 10degree loss of ROM in patients with a history of proximal tibial osteotomy who underwent TKA. Springer et al24 found an association between African Americans and age younger than 45 years, demonstrating that this group of patients was twice as likely to undergo manipulation under anesthesia (MUA) after TKA. A multicenter study revealed that 41% of patients younger than 60 years who had TKA had a perception of stiffness postoperatively.25
Patient-Related Risk Factors
Intraoperative Considerations
The most important risk factor for developing postoperative knee stiffness is compromised preoperative ROM.17,18 Among patients with preoperative ROM greater than 90 degrees, 91.3% had a postoperative ROM greater than 90 degrees, and only 71.4% of the patients with less than 90 degrees of ROM preoperatively achieved a ROM over 90 degrees postoperatively.18 The preoperative diagnosis is also considered a risk factor for stiffness. There is a tendency for higher postoperative ROM in patients with rheumatoid arthritis (RA) undergoing TKA compared with those with the diagnosis of OA or posttraumatic arthritis. This is mostly true for RA patients who have not had prior surgery in the affected joint.17 Parsley et al, in a study19 demonstrated that patients with preoperative flexion greater than 105 degrees experience some loss of ROM following TKA. It is believed that improvements in ROM following TKA occur mostly within the first year after index surgery, and beyond this point no significant improvement can occur.18,20
Technical errors at the time of executing the surgery are among the most frequent causes of stiffness after TKA. Technical errors include malpositioned or oversized components, imbalance in flexion and extension gaps, inaccurate bone resection that may alter the joint line, creation of an anterior tibial slope, deficient resection of posterior osteophytes, poor reconstruction of the patellofemoral joint, poor restoration of posterior condylar offset, and under-recession or retraction of the posterior cruciate ligament (PCL). Correct positioning in the sagittal plane of the prosthesis is imperative to achieve satisfactory ROM after TKA. In cases of a hyperflexed femoral component (►Fig. 2a), full extension might be restricted. In cases of a hyperextended femoral component, there is a higher probability of anterior femoral notching and limited flexion of the knee (►Fig. 2b). Inadequate positioning of the tibial component in the sagittal plane can also cause limited ROM. A reverse orientation of the normal tibial slope will lead to a decreased joint space in the posterior aspect, thus reducing postoperative flexion when premature contact
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between the articular surfaces occurs.26 Choosing an oversized femoral component, or creating an overtly thick patella after resurfacing, will alter the kinematics of the patellofemoral joint and decrease deep flexion due to overstuffing.27 The overstuffing is often because of an inadequate resection of the articular surface of the patella or by the anterior placement of the femoral component.26 In cases in which a PCL-retaining prosthesis is used, a tight PCL causes limited flexion, whereas a lax PCL resulting from over-release will cause a paradoxical anterior translation of the distal femur causing impingement of posterior structures and increased tension in the extensor mechanism thus limiting full extension.28 At the time of gap balancing, there are several scenarios that can lead to stiffness in the knee. One such scenario is over-resection of the distal femur that creates a large extension gap, which could lead to an incorrectly chosen larger tibial insert to match the extension to the flexion gap. This will result in a tight flexion gap and a reduction in knee flexion. Another scenario is an excessive soft tissue release for a preoperative flexion deformity or over-resection of the posterior condyles that could lead to a loose flexion gap. If an attempt to correct this by placing a larger tibial insert is made, a tight extension gap will occur that can prevent the knee from achieving full extension. The position of the joint line plays an important role that influences final ROM of the knee. The result of a high joint line is patella baja. Two errors lead to this scenario, anterior placement of the femoral component or selecting an undersized (anterior–posterior) femoral component. On the contrary, lowering the joint line will produce a patella alta. This can result from excessive release of the patellar tendon, a tendon disruption, or a preoperative patella alta that could not be corrected during surgery.29 During TKA posterior tibial and femoral osteophytes must be resected; failing to do so might also result in a decrease in the postoperative ROM.26 Unresected posterior osteophytes create tension in the posterior capsule, resulting in decreased final extension. The mechanical block created by posterior osteophytes may also reduce flexion (►Fig. 3).
Postoperative Considerations Postoperative management of TKA, to prevent stiffness, has been approached in a variety of different ways. Physical therapy (PT) and continuous passive motion (CPM) machines have been used with variable results. Herbold et al30 found in a recent randomized controlled trial, that CPM machines do not provide an additional benefit over the conventional interventions in patients undergoing TKA. This is consistent with most series in the literature regarding the use of CPM.31–33 In a meta-analysis of randomized, controlled trials that evaluated the effectiveness, PT demonstrated no benefit for ROM at 1 year, and minimal effect was seen at 3 months.34
Fig. 3 Lateral right knee radiograph showing a large posterior tibial osteophyte. The Journal of Knee Surgery
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Fig. 2 (a) Lateral right knee radiograph showing an overdimensioned femoral component in a flexed position. (b) Lateral right knee radiograph showing an extended femoral component with notching on the anterior aspect of the femur.
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Etiology Infection Periprosthetic joint infection (PJI) is one of the main complications leading to revision surgery.10,35,36 It is also seen as one of the most frequent causes of readmission to hospital after a joint replacement.9 Symptoms are usually insidious in onset and reaching the diagnosis requires keeping a high index of suspicion. The most common symptoms of PJI are chronic dull pain, but stiffness is a very common finding in patients with PJI. PJI rarely manifests with sepsis or acute illness. It is, therefore, highly recommended to rule out PJI in the setting of stiffness and pain after a TKA. It is necessary to use standardized diagnostic criteria and follow an algorithmic approach for the diagnosis. The definition of PJI as offered by the Musculoskeletal Infection Society and recently modified by the International Consensus Group is the currently accepted definition for PJI.37 Because of the lack of a gold standard to diagnose PJI, the diagnostic algorithm proposed by the American Academy of Orthopaedic Surgeons may also be followed.38
Arthrofibrosis Arthrofibrosis is a well-recognized cause of stiffness following TKA, with an incidence ranging from 1.2 to 17%.3 This is an illdefined condition ranging from a localized process to a generalized involvement that can affect the entire joint and result in the formation of extensive extra-articular fibrous tissue.39 The histopathology findings in arthrofibrosis are characterized by the development of metaplasia that consists of calcified tissue, myofibroblasts, and excessive fibrosis.40 There is in addition hyperplasia of the synovial membrane and an increase number of macrophages and lymphocytes in the periarticular tissue.41 In some cases of arthrofibrosis, chronic inflammatory process may also exist with a pathologic cellular expression of collagen and excessive vascular proliferation within the connective tissue.42 There is no gold standard for the diagnosis of arthrofibrosis beyond the clinical examination. However, recent efforts have been made toward identifying inflammatory markers associated with arthrofibrosis to assist with its diagnosis. It has been shown that transforming grow factor β plays an important role in the pathogenesis of this disease. Within this super family, bone morphogenetic protein 2 (BMP-2) has been recognized to result in an increased inflammatory tissue reaction. Pfitzner et al43 demonstrated an overexpression of BMP-2, with an up to 11-fold increase in patients with arthrofibrosis. BMP-2 is considered a marker to accurately diagnose the symptoms in a potential case of arthrofibrosis. Interventions that block the cellular pathway through which BMP-2 exerts its effects, are being explored as a potential strategy for prevention of arthrofibrosis.44 Arthrofibrosis has also been seen to correlate with a hypoxic-associated oxidative stress. As demonstrated by Freeman et al,40 this process initiates mast cell proliferation with fibroblast growth factor secretion that promotes fibroblast proliferation and fibrous tissue formation followed by heterotopic ossification. Reactive oxygen and nitrogen speThe Journal of Knee Surgery
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cies accumulation and dysregulation play a major role in the initiation and sustaining the arthrofibrotic response. This is because of either the upregulation of myeloperoxidase expression in fibroblast, or a decrease in cellular antioxidant expression. This exposes the imbalance of oxidant/antioxidant homeostasis during the wound-healing process.41 To date, there is no effective method for prevention or treatment of idiopathic arthrofibrosis following TKA, beyond the early and aggressive mobilization, and patient education.45,46
Complex Regional Pain Syndrome As the name implies, complex regional pain syndrome (CRPS) is a condition characterized by constant regional, neuropathic pain, usually associated with sensory alterations, autonomic, motor, and/or trophic skin changes.47 The pain is disproportionate in time and/or intensity to expected postoperative pain. The pathophysiology is multifactorial and remains unclear; however, evidence in the literature suggests that an abnormal response of tissue to trauma is involved.48 The incidence of CRPS after TKA has been reported to be approximately 0.8%.49 The diagnosis is entirely clinical and tests are usually noncontributory. Reaching the diagnosis is difficult due to the variability in symptoms between individuals and even in a given individual over time. The compromised region is usually the distal aspect of the limbs and does not follow a specific dermatome. The clinical features are usually spontaneous pain, vasomotor changes, motor abnormalities, hyperalgesia, and allodynia. Treatment should be initiated immediately and managed by a multidisciplinary pain management team. In patients who develop CRPS, caution should be taken when repeated surgical intervention is required, hence an increase in symptoms might occur.50
Associated Diseases As part of the evaluation of a stiff TKA, symptoms that may derive from the adjacent joints or the spine must be ruled out. A flexion deformity of the hip predisposes the knee to develop a compensatory flexion deformity. Pain originated at the hip radiating to the knee also needs to be considered in the workup of a patient with painful and stiff TKA.51,52 Occult radiculopathy can have very similar negative effects on the knee motion because of referred pain in the knee that worsens with certain activity.53,54
Heterotopic Ossification Heterotopic ossification (HO) has been correlated with the presence of stiffness after TKA. It is usually located around the extensor mechanism or the supracondylar region and manifested as bone spurs (►Fig. 4). The incidence of HO after TKA is estimated to be around 15%.55 Risk factors associated with development of HO are hypertrophic OA and surgical wound problems.56 HO also has been seen as an end result of fibrous tissue formation in an hypoxic environment following surgery.40 HO formation can be asymptomatic and discovered incidentally on radiographs. Treatment is only justified for symptomatic cases. The management of stiffness as a result of HO formation is the same as general stiffness and consists
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Fig. 4 Lateral right knee radiograph showing a formation of anterior bone spur of the femur.
mostly of nonoperative measures. Surgical resection is only recommended after nonoperative measures are exhausted and in the presence of mechanical problems.57 Recurrence must be prevented aggressively by administration of irradiation and/or anti-inflammatory medications. Prophylaxis should be administered in the high-risk patients, which includes those with positive history of HO requiring surgical excision, or in those who undergo HO resection of the same joint. External beam radiotherapy has been proven successful in preventing HO formation. A single dose of 700 cGy58 should be administered either within 4 hours before surgery or less than 72 hours postoperatively after surgery.57 Nonsteroidal anti-inflammatory drugs (NSAIDs) also have prophylactic properties with the most commonly used drug being indomethacin (25 mg three times a day) given for 5 to 6 weeks postoperatively; however, there is an increased risk of postoperative bleeding, gastrointestinal issues, renal impairment, and bone nonunion.57,59 Celecoxib, a selective COX-2 inhibitor, is another option for HO prophylaxis exerting the same efficacy with lower risk of NSAIDS adverse effects.60
Treatment Initial Assessment The initial evaluation of stiffness following TKA should include a thorough evaluation of the presurgical status of the patient, in particular, the knee ROM. In general, patients with poor motion will experience a moderate improvement in the ROM following TKA and others with great ROM preoperatively may experience some loss of ROM following TKA.61
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Evaluation of the postoperative course should also be done with particular attention to issues such as wound-related complications that can predispose the patient to PJI. As mentioned previously, work up for PJI is critical in patients with stiffness following TKA. Basic laboratory screening tests namely C-reactive protein and erythrocyte sedimentation rate, should be performed. In patients with abnormal serology or in those with high index of suspicion for PJI, the joint should be aspirated and analyzed for synovial neutrophil count, synovial polymorphonuclear percentage, and culture. At our institution, we also utilize leukocyte esterase strips to analyze the synovial tissue.62 On physical examination, the lack of passive motion of the patella might differentiate the underlying cause and point out to arthrofibrosis as a cause of stiffness. When the patella can be mobilized passively the problem might be related to gap balancing or other issues. Radiological examination of the knee is essential in the diagnosis of mechanical causes helping to assess the prosthetic alignment in the sagittal and coronal planes; the axial plane might need additional imaging such as the use of computed tomography when rotational malpositioning is suspected. Plain radiographs aid in determining prosthetic loosening, oversizing, and joint line positioning using the approach proposed by Figgie et al.29 Radiographs will also help to confirm or refute the presence of HO. The origin of symptoms must be clearly defined, ruling out referred pain from the hip or spine. Treatment options can include knee MUA, arthrolysis (arthroscopic or open), quadricepsplasty, or even the need for revision.
Manipulation under Anesthesia Although the role of knee MUA continues to be debated, this treatment option is an effective tool, if used for appropriate indications.63 The main objective of the manipulation is to accelerate the initial rehabilitation process in patients who have fallen behind. Maloney61 found no difference in ROM at 1 year of follow-up between patients who underwent manipulation after TKA and those who did not. Manipulation achieves increased mobility by breaking immature adhesions within the knee. MUA should be performed within the first 6 to 8 weeks post-TKA.63 After this period of time, intra-articular adhesions will mature, and manipulation increases the likelihood of developing complications such as periprosthetic fractures or rupture of the extensor mechanism. In two literature reviews studying time to manipulation, it appears that MUA may be effective up to 12 weeks postoperatively.64,65 This procedure should be performed under general or regional anesthesia with adequate muscle relaxation. After achieving a suitable relaxation, measures of passive knee extension and flexion should be taken with the patient in supine position. Manipulation is performed with application of gentle and constant pressure to the knee forcing it into flexion. With pressure, some of the intra-articular adhesions may break and an improvement in the ROM is experienced. The knee should also be gently forced into full extension. After achieving a full extension, manipulation of the patella should be performed with the knee in extension, bringing the The Journal of Knee Surgery
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patella medially and inferiorly, to break the adhesions in the suprapatellar pouch. This manipulation should be done until a satisfactory ROM is achieved or when no additional improvement in ROM can be achieved.63 Afterward, aggressive rehabilitation should be implemented to avoid formation of new adhesion. The initial postoperative process should include optimal pain control, such as the use of a spinal catheter. After manipulation, plain radiographs are obtained to ensure that iatrogenic periprosthetic fracture has not occurred. The results of manipulation are summarized by Fitzsimmons et al64 in a systematic review in which the average gain in mobility ranged between 30 and 47 degrees. A systematic review performed by Ghani et al65 found an average improvement in the ROM of 38.4 degrees, mean improvement in flexion of 29 degrees, and extension of 5.7 degrees, with a failure rate of 6.7%. The long-term results of manipulation were explored by Pivec et al.66 The aim was to evaluate longterm results (> 10 years) and showed a gain in the ROM of 30, 33, and 33 degrees at 1, 5, and 10 years, respectively. The authors found a 0.2% incidence of iatrogenic periprosthetic fractures.
Arthroscopy Arthroscopy can be a useful tool in the management of a stiff TKA secondary to arthrofibrosis. The surgery is fairly uniform in all reports, with resection of the fibrous tissue in the suprapatellar pouch and medial/lateral gutters as well as in the intercondylar groove.65 Intervention is generally reserved for patients with no progression after 3 months. It is also useful and indicated when a tight PCL release is warranted. This procedure is associated with improved postoperative mobility after 20 months follow-up. Treatment failure has been reported in up to 22% of cases.67 Some surgeons argue that poor access to the posterior structures and the area above the suprapatellar pouch could be a disadvantage. In a systematic review of the literature, the result of arthroscopic release had a mean gain of 36.2 degrees of ROM, with an average gain of 35.2 degrees of flexion and 6.4 degrees of extension. The rate of treatment failure was 3.6%. It should be noted that arthroscopic release must be accompanied by an MUA. When the clinical results of MUA and arthroscopy were compared, there was no difference,64,65 calling into question the value of this technique except in properly chosen candidates.
Open Arthrolysis Open arthrolysis is recommended when ROM is severely compromised. Open arthrolysis may also be considered when severe flexion deformity may preclude the use of arthroscopy. Open procedure is appropriate in patients who have failed nonoperative management and in whom there is no component malpositioning or other causes that require revision TKA to address them. Open arthrolysis should be accompanied by polyethylene liner exchange to allow access to the posterior area of the knee.3 Exposure of the knee can be challenging, due to the presence of severe adhesions. Debridement of the posteromedial corner, posteThe Journal of Knee Surgery
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rior capsule, suprapatellar pouch, and medial and lateral gutters should be performed meticulously. If an adequate exposure cannot be achieved, and the patella cannot be everted, additional maneuvers can be employed such as osteotomy of the tibial tuberosity or a quadriceps snip. At times in more extensive cases, a more formal quadricepsplasty must be performed to free the quadriceps from the underlying anterior femur and the overlying contracted fascia. In a systematic review of the literature by Fitzsimmons et al,64 the average gain in ROM after arthrolysis was 23.6 degrees. A subsequent review by Ghani et al65 that included more studies, found that the results of this procedure was better than previously reported, and more optimal that those obtained by MUA and arthroscopy, having an average gain in the ROM of 39.9 degrees.
Total Knee Arthroplasty Revision Surgery Revision TKA is indicated for patients whose stiffness is because of technical errors that need to be corrected. The outcome of revision TKA for stiffness may not meet the full expectations of the patients and their needs to be discussed thoroughly and before surgery. Specific surgical goals must be set and a clear preoperative plan must be created. The skin incision should follow the previous scar and if multiple scars are present the most lateral one may need to be used. Resection of the scar on the skin is not recommended, as this can lead to tension on the wound closure. Almost always a quadriceps snip needs to be performed to improve the exposure and in some cases more extensile approach such as the tibial tubercle osteotomy may be needed. Meticulous debridement of the scar tissue, in particular, in the lateral and medial gutters, needs to be performed. The tracking of the patella also needs to be assessed. The orientation and fixation of all components then need to be scrutinized and any malpositioned and/or loose component removed. The patellar thickness should be measured and in cases of thickness being > 26 mm in men and > 24 mm in women, additional resection is indicated.3,63 Flexion and extension gaps should be evaluated for symmetry and, considering the very high recurrence rate of postoperative stiffness, 5 degrees of hyperextension as the ultimate goal is desired during surgery.68 Kim et al69 found that patients who undergo revision TKA have an incidence of stiffness around 4%, similar to primary TKA cases. It was also seen that poor preoperative ROM, stiffness as the primary indication for revision, younger age, shorter interval between index primary and revision TKA, presence of well-fixed components at the time of revision, postoperative wound drainage, and lower Charlson index, demonstrated to be additional risk factors for postoperative stiff knee among this patient population. The outcome of revision TKA for stiffness has not been optimal. The average improvement in ROM degrees after surgery has been reported to be between 21.8 and 27.6 degrees, with flexion improving from 12 to 19.6 degrees and extension from 8.1 to 10.5 degrees1,70 with an overall clinical and functional improvement of 69.6%.70
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Management of stiffness following TKA is truly challenging. Any patient with this condition needs to be evaluated thoroughly. Management of these patients includes a work up for PJI. Majority of patients with stiff TKA should be subjected to nonoperative methods that involve aggressive PT. Other pathologies, such as hip arthritis or spine disease, that may masquerade as stiff TKA should be ruled out. The preoperative radiograph of all patients presenting with painful TKA needs to be evaluated to ensure that the indication for TKA was appropriate. Evaluation of patients with stiff TKA must also include scrutiny of the component positioning with regard to restoration of joint line, proper slopes, and sizing. For patients in whom component malpositioning is suspected, revision TKA is indicated. MUA is a viable option for patients without component malpositioning or severe arthrofibrosis. The procedure is likely to provide better results if performed close to the index arthroplasty. In patients with arthrofibrosis or sever heterotopic bone formation who are more than 3 months from the index arthroplasty and have failed nonoperative management either arthroscopic or open arthrolysis is indicated. During open arthrolysis, further scrutiny of the component positioning and sizing should be performed and components revised if indicated. The thickness of patella also needs to be measured and additional resection performed for those with overstuffed patellofemoral joints. Regardless of the treatment modality chosen, the outcome of interventions for management of stiff TKA is generally unrewarding. This needs to be discussed with the patient and surgical intervention avoided if at all possible except in cases of stiff TKA where the cause is a proven technical error.
10 Le DH, Goodman SB, Maloney WJ, Huddleston JI. Current modes of
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failure in TKA: infection, instability, and stiffness predominate. Clin Orthop Relat Res 2014;472(7):2197–2200 Koh IJ, Cho W-S, Choi NY, Kim TK; Kleos Korea Research Group. Causes, risk factors, and trends in failures after TKA in Korea over the past 5 years: a multicenter study. Clin Orthop Relat Res 2014; 472(1):316–326 Su EP. Fixed flexion deformity and total knee arthroplasty. J Bone Joint Surg Br 2012;94(11, Suppl A ):112–115 Tew M, Forster IW. Effect of knee replacement on flexion deformity. J Bone Joint Surg Br 1987;69(3):395–399 Perry J, Antonelli D, Ford W. Analysis of knee-joint forces during flexed-knee stance. J Bone Joint Surg Am 1975;57(7):961–967 Harato K, Nagura T, Matsumoto H, Otani T, Toyama Y, Suda Y. Knee flexion contracture will lead to mechanical overload in both limbs: a simulation study using gait analysis. Knee 2008;15(6):467–472 Aderinto J, Brenkel IJ, Chan P. Natural history of fixed flexion deformity following total knee replacement: a prospective fiveyear study. J Bone Joint Surg Br 2005;87(7):934–936 Harvey IA, Barry K, Kirby SP, Johnson R, Elloy MA. Factors affecting the range of movement of total knee arthroplasty. J Bone Joint Surg Br 1993;75(6):950–955 Lizaur A, Marco L, Cebrian R. Preoperative factors influencing the range of movement after total knee arthroplasty for severe osteoarthritis. J Bone Joint Surg Br 1997;79(4):626–629 Parsley BS, Engh GA, Dwyer KA. Preoperative flexion. Does it influence postoperative flexion after posterior-cruciate-retaining total knee arthroplasty? Clin Orthop Relat Res 1992;(275): 204–210 Shoji H, Solomonow M, Yoshino S, D’Ambrosia R, Dabezies E. Factors affecting postoperative flexion in total knee arthroplasty. Orthopedics 1990;13(6):643–649 Gadinsky NE, Ehrhardt JK, Urband C, Westrich GH. Effect of body mass index on range of motion and manipulation after total knee arthroplasty. J Arthroplasty 2011;26(8):1194–1197 Efe T, Heyse TJ, Boese C, et al. TKA following high tibial osteotomy versus primary TKA—a matched pair analysis. BMC Musculoskelet Disord 2010;11:207 van Raaij TM, Reijman M, Furlan AD, Verhaar JA. Total knee arthroplasty after high tibial osteotomy. A systematic review. BMC Musculoskelet Disord 2009;10:88 Springer BD, Odum SM, Nagpal VS, et al. Is socioeconomic status a risk factor for stiffness after total knee arthroplasty? A multicenter case-control study. Orthop Clin North Am 2012;43(5):e1–e7 Parvizi J, Nunley RM, Berend KR, et al. High level of residual symptoms in young patients after total knee arthroplasty. Clin Orthop Relat Res 2014;472(1):133–137 Laskin RS, Beksac B. Stiffness after total knee arthroplasty. J Arthroplasty 2004;19(4, Suppl 1):41–46 Lo CS, Wang SJ, Wu SS. Knee stiffness on extension caused by an oversized femoral component after total knee arthroplasty: a report of two cases and a review of the literature. J Arthroplasty 2003;18(6):804–808 Dennis DA. The stiff total knee arthroplasty: causes and cures. Orthopedics 2001;24(9):901–902 Figgie HE III, Goldberg VM, Heiple KG, Moller HS III, Gordon NH. The influence of tibial-patellofemoral location on function of the knee in patients with the posterior stabilized condylar knee prosthesis. J Bone Joint Surg Am 1986;68(7):1035–1040 Herbold JA, Bonistall K, Blackburn M, et al. Randomized controlled trial of the effectiveness of continuous passive motion after total knee replacement. Arch Phys Med Rehabil 2014;95(7): 1240–1245 Alkire MR, Swank ML. Use of inpatient continuous passive motion versus no CPM in computer-assisted total knee arthroplasty. Orthop Nurs 2010;29(1):36–40 Maniar RN, Baviskar JV, Singhi T, Rathi SS. To use or not to use continuous passive motion post-total knee arthroplasty The Journal of Knee Surgery
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presenting functional assessment results in early recovery. J Arthroplasty 2012;27(2):193–200.e1 Leach W, Reid J, Murphy F. Continuous passive motion following total knee replacement: a prospective randomized trial with follow-up to 1 year. Knee Surg Sports Traumatol Arthrosc 2006; 14(10):922–926 Minns Lowe CJ, Barker KL, Dewey M, Sackley CM. Effectiveness of physiotherapy exercise after knee arthroplasty for osteoarthritis: systematic review and meta-analysis of randomised controlled trials. BMJ 2007;335(7624):812 Dalury DF, Pomeroy DL, Gorab RS, Adams MJ. Why are total knee arthroplasties being revised? J Arthroplasty 2013;28(8, Suppl): 120–121 Sharkey PF, Hozack WJ, Rothman RH, Shastri S, Jacoby SM. Insall Award paper. Why are total knee arthroplasties failing today? Clin Orthop Relat Res 2002;(404):7–13 Parvizi J, Gehrke T; International Consensus Group on Periprosthetic Joint Infection. Definition of periprosthetic joint infection. J Arthroplasty 2014;29(7):1331 Della Valle C, Parvizi J, Bauer TW, et al; American Academy of Orthopaedic Surgeons. American Academy of Orthopaedic Surgeons clinical practice guideline on: the diagnosis of periprosthetic joint infections of the hip and knee. J Bone Joint Surg Am 2011;93(14):1355–1357 Sprague NF III, O’Connor RL, Fox JM. Arthroscopic treatment of postoperative knee fibroarthrosis. Clin Orthop Relat Res 1982;(166):165–172 Freeman TA, Parvizi J, Dela Valle CJ, Steinbeck MJ. Mast cells and hypoxia drive tissue metaplasia and heterotopic ossification in idiopathic arthrofibrosis after total knee arthroplasty. Fibrogenesis Tissue Repair 2010;3:17 Freeman TA, Parvizi J, Della Valle CJ, Steinbeck MJ. Reactive oxygen and nitrogen species induce protein and DNA modifications driving arthrofibrosis following total knee arthroplasty. Fibrogenesis Tissue Repair 2009;2(1):5 Gollwitzer H, Burgkart R, Diehl P, Gradinger R, Bühren V. Therapy of arthrofibrosis after total knee arthroplasty [in German]. Orthopade 2006;35(2):143–152 Pfitzner T, Geissler S, Duda G, Perka C, Matziolis G. Increased BMP expression in arthrofibrosis after TKA. Knee Surg Sports Traumatol Arthrosc 2012;20(9):1803–1808 Pfitzner T, Röhner E, Krenn V, Perka C, Matziolis G. BMP-2 dependent increase of soft tissue density in arthrofibrotic TKA. Open Orthop J 2012;6:199–203 Pua Y-H, Ong P-H. Association of early ambulation with length of stay and costs in total knee arthroplasty: retrospective cohort study. Am J Phys Med Rehabil 2014;93(11):962–970 Livbjerg AE, Froekjaer S, Simonsen O, Rathleff MS. Pre-operative patient education is associated with decreased risk of arthrofibrosis after total knee arthroplasty: a case control study. J Arthroplasty 2013;28(8):1282–1285 Fukushima FB, Bezerra DM, Villas Boas PJF, Valle AP, Vidal EIO. Complex regional pain syndrome. BMJ 2014;348(June):g3683 Marinus J, Moseley GL, Birklein F, et al. Clinical features and pathophysiology of complex regional pain syndrome. Lancet Neurol 2011;10(7):637–648 Katz MM, Hungerford DS. Reflex sympathetic dystrophy affecting the knee. J Bone Joint Surg Br 1987;69(5):797–803
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Am Acad Orthop Surg 1994;2(2):79–86 51 Dittrich RJ. Disability of the knee due to referred pain and related
phenomena. J Am Geriatr Soc 1955;3(10):800–803 52 Vince KG. The stiff total knee arthroplasty: causes and cures. J Bone
Joint Surg Br 2012;94(11, Suppl A):103–111 53 Miller KJ. Physical assessment of lower extremity radiculopathy
and sciatica. J Chiropr Med 2007;6(2):75–82 54 Westbrook A, Tambe A, Subramanian K, Monk J, Calthorpe D. The
mannequin sign. Spine 2005;30(5):E115–E117 55 Dalury DF, Jiranek WA. The incidence of heterotopic ossification
after total knee arthroplasty. J Arthroplasty 2004;19(4):447–452 56 Roth KE, Salzmann G, Maier GS, Schmidtmann I, Rompe JD, Babin
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K. Risk factors for heterotopic ossification and spur formation after total knee arthroplasty. Arch Orthop Trauma Surg 2014;134(7): 991–996 Board TN, Karva A, Board RE, Gambhir AK, Porter ML. The prophylaxis and treatment of heterotopic ossification following lower limb arthroplasty. J Bone Joint Surg Br 2007;89(4):434–440 Popovic M, Agarwal A, Zhang L, et al. Radiotherapy for the prophylaxis of heterotopic ossification: A systematic review and meta-analysis of published data. Radiother Oncol 2014;113(1): 10–17 Burd TA, Hughes MS, Anglen JO. Heterotopic ossification prophylaxis with indomethacin increases the risk of long-bone nonunion. J Bone Joint Surg Br 2003;85(5):700–705 Romanò CL, Duci D, Romanò D, Mazza M, Meani E. Celecoxib versus indomethacin in the prevention of heterotopic ossification after total hip arthroplasty. J Arthroplasty 2004;19(1):14–18 Maloney WJ. The stiff total knee arthroplasty: evaluation and management. J Arthroplasty 2002;17(4, Suppl 1):71–73 Wetters NG, Berend KR, Lombardi AV, Morris MJ, Tucker TL, Della Valle CJ. Leukocyte esterase reagent strips for the rapid diagnosis of periprosthetic joint infection. J Arthroplasty 2012;27(8, Suppl):8–11 Van P, Stamos JB. Management of the stiff total knee arthroplasty. In: Bono JV, Scott RD, eds. Revision Total Knee Arthroplasty. New York, NY: Springer-Verlag; 2005:251–257 Fitzsimmons SE, Vazquez EA, Bronson MJ. How to treat the stiff total knee arthroplasty?: a systematic review Clin Orthop Relat Res 2010;468(4):1096–1106 Ghani H, Maffulli N, Khanduja V. Management of stiffness following total knee arthroplasty: a systematic review. Knee 2012;19(6): 751–759 Pivec R, Issa K, Kester M, Harwin SF, Mont MA. Long-term outcomes of MUA for stiffness in primary TKA. J Knee Surg 2013; 26(6):405–410 Williams RJ III, Westrich GH, Siegel J, Windsor RE. Arthroscopic release of the posterior cruciate ligament for stiff total knee arthroplasty. Clin Orthop Relat Res 1996;(331):185–191 Ries MD, Badalamente M. Arthrofibrosis after total knee arthroplasty. Clin Orthop Relat Res 2000;(380):177–183 Kim GK, Mortazavi SMJ, Purtill JJ, Sharkey PF, Hozack WJ, Parvizi J. Stiffness after revision total knee arthroplasty. J Arthroplasty 2010;25(6):844–850 Keeney JA, Clohisy JC, Curry M, Maloney WJ. Revision total knee arthroplasty for restricted motion. Clin Orthop Relat Res 2005; 440:135–140
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Stiffness after Total Knee Arthroplasty Miguel M. Gomez, MD1
Javad Parvizi, MD, FRCS1
1 Research Department, Rothman Institute, Philadelphia, Pennsylvania
J Knee Surg 2015;28:119–126.
Abstract
Keywords
► ► ► ► ► ► ►
arthroplasty replacement knee contracture joint deformities acquired reoperation
Address for correspondence Javad Parvizi, MD, FRCS, Rothman Institute at Thomas Jefferson University, 125 S. 9th Street, Philadelphia, PA 19107 (e-mail: [email protected]).
Stiffness after total knee arthroplasty (TKA) adversely affects outcome and impacts patient function. Various risk factors for stiffness after TKA have been identified, including reduced preoperative knee range of motion, history of prior knee surgery, etiology of arthritis, incorrect positioning or oversizing of components, and incorrect gap balancing. Mechanical and associated causes, such as infection, arthrofibrosis, complex regional pain syndrome, and heterotopic ossification, secondary gain issues have also been identified. Management of stiffness following TKA can be challenging. The condition needs to be assessed and treated in a staged manner. A nonsurgical approach is the first step. Manipulation under anesthesia may be considered within the first 3 months after the index TKA, if physical therapy fails to improve the range of motion. Beyond this point, consideration should be given to surgical intervention such as lysis of adhesions, either arthroscopically or by open arthrotomy. If the cause of stiffness is deemed to be surgical error, such as component malpositioning, revision arthroplasty is indicated. The purpose of this article is to evaluate the various aspects of management of stiffness after TKA.
The main objective of total knee arthroplasty (TKA) is to afford pain relief, and restore function to the patient. To achieve adequate postoperative functionality, the joint must be stable and have an adequate range of motion (ROM). Joint stiffness after TKA is fortunately an infrequent complication, with the incidence ranging from 1.3 to 5.3%,1,2 but it can result in severe disability and is the source of frustration for both the patient and the surgeon. Stiffness has been defined as a decrease of postoperative ROM, including flexion contracture, accompanied by persistent pain and/or a clear functional compromise.3 There is a debate as to what degree of motion in the knee is required for daily function. It is known that during push-off of normal gait, 40 degrees of flexion is required to initiate the swing phase (►Fig. 1a). Maximum flexion during walking is 60 degrees, which occurs during the swing phase (►Fig. 1b). Furthermore, a flexion of around 120 degrees is required to climb stairs or rise from a chair without assistance of the arms.4 In certain cultures, much greater flexion, up to 150 degrees, of the knee is required for daily function. Activities such as squatting, sitting at a low-set table, and praying require a
greater degree of flexion of the knee.5 In the Western culture, achievement of ROM ranging from 0 to 110 degrees is considered adequate and generally a measure of success after TKA. There is no consensus in defining stiffness after TKA. Nicholls and Dorr6 stated that stiffness is a flexion contracture greater than 20 degrees or a global ROM of less than 45 degrees. Scranton7 defined a stiff knee as one having a ROM less than 90 degrees. Christensen et al8 defined stiffness as ROM less than 70 degrees of either active or passive flexion. These definitions did not include flexion deficit, thus focusing on either the lack of extension or global ROM as the most important parameter. Kim et al1 defined stiffness as a flexion contracture greater than 15 degrees and/or ROM of less than 75 degrees. Yercan et al2 defined knee stiffness as flexion contracture greater than 10 degrees or flexion less than 95 degrees during the first 6 weeks after TKA, thus adding a temporal component to the definition. Another challenge is the patient’s perception of motion deficit. A patient with preoperative flexion of 70 degrees might consider 90-degree flexion a success, while one with a preoperative flexion of 120 degrees might consider a
received August 26, 2014 accepted after revision October 23, 2014 published online December 16, 2014
Copyright © 2015 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662.
DOI http://dx.doi.org/ 10.1055/s-0034-1396079. ISSN 1538-8506.
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postoperative flexion of 90degree a failure. Patient subjectivity might overestimate the problem regardless of objective measures. Postoperative stiffness has been demonstrated to be one of the most common causes of readmission within the first 90 days after surgery and it is one of the common reasons for revision TKA.9 Le et al10 identified stiffness as the third leading cause of TKA revision (18%). In a recent series, stiffness was placed as the fifth leading cause of revision TKA, being responsible for 3% of the revisions.11 Stiffness creates a challenging situation for patients and surgeons. Complete understanding of the etiology, the various treatment options and the expected outcome is paramount for surgeons encountering this complication of TKA.
Natural History of Flexion Contracture after Total Knee Arthroplasty
Fig. 1 (a) Shows the right knee during the push-off phase. (b) Shows the right knee during the swing phase required to prevent contact of the foot with the ground as it comes forward.
When assessing flexion contracture following TKA is important to understand the behavior of this condition through time. The presence of flexion contracture in patients with osteoarthritis (OA) can reach up to 60% preoperatively and 17% postoperatively.12,13 Knee flexion contracture increases quadriceps energy consumption during the stance phase of gait. An extended and more powerful contraction is needed to prevent the flexion collapse. Energy consumption has been directly related to the severity of the contracture. At 15 degrees of flexion contracture, there is a 30% increased energy consumption and up to 50% when the contracture reaches 30 degrees.14 A fixed flexion contracture also affects the contralateral limb, increasing the adductor and extensor moments during gait, thus creating an increase of shearing forces in the contralateral knee.15 About 11% of patients who undergo TKA and have more than 20 degrees of flexion contracture preoperatively experience the persistence of such deformity within the first 6 months postoperatively.16
Obesity has also been associated with diminished ROM after TKA. Shoji et al20 showed that in patients with postoperative ROM greater than 120 degrees, the incidence of obesity was 7%, whereas in patients with ROM with less than 100 degrees, the incidence of obesity was 78%. Patients with a body mass index (BMI) less than 25 kg/m2 had a mean ROM of 125 degrees, whereas patients with a BMI greater than 35 kg/m2 had a mean ROM of 116 degrees.21 It is also known that history of prior knee surgery jeopardizes ROM following TKA.22 van Raaij et al23 showed an average of 10degree loss of ROM in patients with a history of proximal tibial osteotomy who underwent TKA. Springer et al24 found an association between African Americans and age younger than 45 years, demonstrating that this group of patients was twice as likely to undergo manipulation under anesthesia (MUA) after TKA. A multicenter study revealed that 41% of patients younger than 60 years who had TKA had a perception of stiffness postoperatively.25
Patient-Related Risk Factors
Intraoperative Considerations
The most important risk factor for developing postoperative knee stiffness is compromised preoperative ROM.17,18 Among patients with preoperative ROM greater than 90 degrees, 91.3% had a postoperative ROM greater than 90 degrees, and only 71.4% of the patients with less than 90 degrees of ROM preoperatively achieved a ROM over 90 degrees postoperatively.18 The preoperative diagnosis is also considered a risk factor for stiffness. There is a tendency for higher postoperative ROM in patients with rheumatoid arthritis (RA) undergoing TKA compared with those with the diagnosis of OA or posttraumatic arthritis. This is mostly true for RA patients who have not had prior surgery in the affected joint.17 Parsley et al, in a study19 demonstrated that patients with preoperative flexion greater than 105 degrees experience some loss of ROM following TKA. It is believed that improvements in ROM following TKA occur mostly within the first year after index surgery, and beyond this point no significant improvement can occur.18,20
Technical errors at the time of executing the surgery are among the most frequent causes of stiffness after TKA. Technical errors include malpositioned or oversized components, imbalance in flexion and extension gaps, inaccurate bone resection that may alter the joint line, creation of an anterior tibial slope, deficient resection of posterior osteophytes, poor reconstruction of the patellofemoral joint, poor restoration of posterior condylar offset, and under-recession or retraction of the posterior cruciate ligament (PCL). Correct positioning in the sagittal plane of the prosthesis is imperative to achieve satisfactory ROM after TKA. In cases of a hyperflexed femoral component (►Fig. 2a), full extension might be restricted. In cases of a hyperextended femoral component, there is a higher probability of anterior femoral notching and limited flexion of the knee (►Fig. 2b). Inadequate positioning of the tibial component in the sagittal plane can also cause limited ROM. A reverse orientation of the normal tibial slope will lead to a decreased joint space in the posterior aspect, thus reducing postoperative flexion when premature contact
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between the articular surfaces occurs.26 Choosing an oversized femoral component, or creating an overtly thick patella after resurfacing, will alter the kinematics of the patellofemoral joint and decrease deep flexion due to overstuffing.27 The overstuffing is often because of an inadequate resection of the articular surface of the patella or by the anterior placement of the femoral component.26 In cases in which a PCL-retaining prosthesis is used, a tight PCL causes limited flexion, whereas a lax PCL resulting from over-release will cause a paradoxical anterior translation of the distal femur causing impingement of posterior structures and increased tension in the extensor mechanism thus limiting full extension.28 At the time of gap balancing, there are several scenarios that can lead to stiffness in the knee. One such scenario is over-resection of the distal femur that creates a large extension gap, which could lead to an incorrectly chosen larger tibial insert to match the extension to the flexion gap. This will result in a tight flexion gap and a reduction in knee flexion. Another scenario is an excessive soft tissue release for a preoperative flexion deformity or over-resection of the posterior condyles that could lead to a loose flexion gap. If an attempt to correct this by placing a larger tibial insert is made, a tight extension gap will occur that can prevent the knee from achieving full extension. The position of the joint line plays an important role that influences final ROM of the knee. The result of a high joint line is patella baja. Two errors lead to this scenario, anterior placement of the femoral component or selecting an undersized (anterior–posterior) femoral component. On the contrary, lowering the joint line will produce a patella alta. This can result from excessive release of the patellar tendon, a tendon disruption, or a preoperative patella alta that could not be corrected during surgery.29 During TKA posterior tibial and femoral osteophytes must be resected; failing to do so might also result in a decrease in the postoperative ROM.26 Unresected posterior osteophytes create tension in the posterior capsule, resulting in decreased final extension. The mechanical block created by posterior osteophytes may also reduce flexion (►Fig. 3).
Postoperative Considerations Postoperative management of TKA, to prevent stiffness, has been approached in a variety of different ways. Physical therapy (PT) and continuous passive motion (CPM) machines have been used with variable results. Herbold et al30 found in a recent randomized controlled trial, that CPM machines do not provide an additional benefit over the conventional interventions in patients undergoing TKA. This is consistent with most series in the literature regarding the use of CPM.31–33 In a meta-analysis of randomized, controlled trials that evaluated the effectiveness, PT demonstrated no benefit for ROM at 1 year, and minimal effect was seen at 3 months.34
Fig. 3 Lateral right knee radiograph showing a large posterior tibial osteophyte. The Journal of Knee Surgery
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Fig. 2 (a) Lateral right knee radiograph showing an overdimensioned femoral component in a flexed position. (b) Lateral right knee radiograph showing an extended femoral component with notching on the anterior aspect of the femur.
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Etiology Infection Periprosthetic joint infection (PJI) is one of the main complications leading to revision surgery.10,35,36 It is also seen as one of the most frequent causes of readmission to hospital after a joint replacement.9 Symptoms are usually insidious in onset and reaching the diagnosis requires keeping a high index of suspicion. The most common symptoms of PJI are chronic dull pain, but stiffness is a very common finding in patients with PJI. PJI rarely manifests with sepsis or acute illness. It is, therefore, highly recommended to rule out PJI in the setting of stiffness and pain after a TKA. It is necessary to use standardized diagnostic criteria and follow an algorithmic approach for the diagnosis. The definition of PJI as offered by the Musculoskeletal Infection Society and recently modified by the International Consensus Group is the currently accepted definition for PJI.37 Because of the lack of a gold standard to diagnose PJI, the diagnostic algorithm proposed by the American Academy of Orthopaedic Surgeons may also be followed.38
Arthrofibrosis Arthrofibrosis is a well-recognized cause of stiffness following TKA, with an incidence ranging from 1.2 to 17%.3 This is an illdefined condition ranging from a localized process to a generalized involvement that can affect the entire joint and result in the formation of extensive extra-articular fibrous tissue.39 The histopathology findings in arthrofibrosis are characterized by the development of metaplasia that consists of calcified tissue, myofibroblasts, and excessive fibrosis.40 There is in addition hyperplasia of the synovial membrane and an increase number of macrophages and lymphocytes in the periarticular tissue.41 In some cases of arthrofibrosis, chronic inflammatory process may also exist with a pathologic cellular expression of collagen and excessive vascular proliferation within the connective tissue.42 There is no gold standard for the diagnosis of arthrofibrosis beyond the clinical examination. However, recent efforts have been made toward identifying inflammatory markers associated with arthrofibrosis to assist with its diagnosis. It has been shown that transforming grow factor β plays an important role in the pathogenesis of this disease. Within this super family, bone morphogenetic protein 2 (BMP-2) has been recognized to result in an increased inflammatory tissue reaction. Pfitzner et al43 demonstrated an overexpression of BMP-2, with an up to 11-fold increase in patients with arthrofibrosis. BMP-2 is considered a marker to accurately diagnose the symptoms in a potential case of arthrofibrosis. Interventions that block the cellular pathway through which BMP-2 exerts its effects, are being explored as a potential strategy for prevention of arthrofibrosis.44 Arthrofibrosis has also been seen to correlate with a hypoxic-associated oxidative stress. As demonstrated by Freeman et al,40 this process initiates mast cell proliferation with fibroblast growth factor secretion that promotes fibroblast proliferation and fibrous tissue formation followed by heterotopic ossification. Reactive oxygen and nitrogen speThe Journal of Knee Surgery
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cies accumulation and dysregulation play a major role in the initiation and sustaining the arthrofibrotic response. This is because of either the upregulation of myeloperoxidase expression in fibroblast, or a decrease in cellular antioxidant expression. This exposes the imbalance of oxidant/antioxidant homeostasis during the wound-healing process.41 To date, there is no effective method for prevention or treatment of idiopathic arthrofibrosis following TKA, beyond the early and aggressive mobilization, and patient education.45,46
Complex Regional Pain Syndrome As the name implies, complex regional pain syndrome (CRPS) is a condition characterized by constant regional, neuropathic pain, usually associated with sensory alterations, autonomic, motor, and/or trophic skin changes.47 The pain is disproportionate in time and/or intensity to expected postoperative pain. The pathophysiology is multifactorial and remains unclear; however, evidence in the literature suggests that an abnormal response of tissue to trauma is involved.48 The incidence of CRPS after TKA has been reported to be approximately 0.8%.49 The diagnosis is entirely clinical and tests are usually noncontributory. Reaching the diagnosis is difficult due to the variability in symptoms between individuals and even in a given individual over time. The compromised region is usually the distal aspect of the limbs and does not follow a specific dermatome. The clinical features are usually spontaneous pain, vasomotor changes, motor abnormalities, hyperalgesia, and allodynia. Treatment should be initiated immediately and managed by a multidisciplinary pain management team. In patients who develop CRPS, caution should be taken when repeated surgical intervention is required, hence an increase in symptoms might occur.50
Associated Diseases As part of the evaluation of a stiff TKA, symptoms that may derive from the adjacent joints or the spine must be ruled out. A flexion deformity of the hip predisposes the knee to develop a compensatory flexion deformity. Pain originated at the hip radiating to the knee also needs to be considered in the workup of a patient with painful and stiff TKA.51,52 Occult radiculopathy can have very similar negative effects on the knee motion because of referred pain in the knee that worsens with certain activity.53,54
Heterotopic Ossification Heterotopic ossification (HO) has been correlated with the presence of stiffness after TKA. It is usually located around the extensor mechanism or the supracondylar region and manifested as bone spurs (►Fig. 4). The incidence of HO after TKA is estimated to be around 15%.55 Risk factors associated with development of HO are hypertrophic OA and surgical wound problems.56 HO also has been seen as an end result of fibrous tissue formation in an hypoxic environment following surgery.40 HO formation can be asymptomatic and discovered incidentally on radiographs. Treatment is only justified for symptomatic cases. The management of stiffness as a result of HO formation is the same as general stiffness and consists
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Fig. 4 Lateral right knee radiograph showing a formation of anterior bone spur of the femur.
mostly of nonoperative measures. Surgical resection is only recommended after nonoperative measures are exhausted and in the presence of mechanical problems.57 Recurrence must be prevented aggressively by administration of irradiation and/or anti-inflammatory medications. Prophylaxis should be administered in the high-risk patients, which includes those with positive history of HO requiring surgical excision, or in those who undergo HO resection of the same joint. External beam radiotherapy has been proven successful in preventing HO formation. A single dose of 700 cGy58 should be administered either within 4 hours before surgery or less than 72 hours postoperatively after surgery.57 Nonsteroidal anti-inflammatory drugs (NSAIDs) also have prophylactic properties with the most commonly used drug being indomethacin (25 mg three times a day) given for 5 to 6 weeks postoperatively; however, there is an increased risk of postoperative bleeding, gastrointestinal issues, renal impairment, and bone nonunion.57,59 Celecoxib, a selective COX-2 inhibitor, is another option for HO prophylaxis exerting the same efficacy with lower risk of NSAIDS adverse effects.60
Treatment Initial Assessment The initial evaluation of stiffness following TKA should include a thorough evaluation of the presurgical status of the patient, in particular, the knee ROM. In general, patients with poor motion will experience a moderate improvement in the ROM following TKA and others with great ROM preoperatively may experience some loss of ROM following TKA.61
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Evaluation of the postoperative course should also be done with particular attention to issues such as wound-related complications that can predispose the patient to PJI. As mentioned previously, work up for PJI is critical in patients with stiffness following TKA. Basic laboratory screening tests namely C-reactive protein and erythrocyte sedimentation rate, should be performed. In patients with abnormal serology or in those with high index of suspicion for PJI, the joint should be aspirated and analyzed for synovial neutrophil count, synovial polymorphonuclear percentage, and culture. At our institution, we also utilize leukocyte esterase strips to analyze the synovial tissue.62 On physical examination, the lack of passive motion of the patella might differentiate the underlying cause and point out to arthrofibrosis as a cause of stiffness. When the patella can be mobilized passively the problem might be related to gap balancing or other issues. Radiological examination of the knee is essential in the diagnosis of mechanical causes helping to assess the prosthetic alignment in the sagittal and coronal planes; the axial plane might need additional imaging such as the use of computed tomography when rotational malpositioning is suspected. Plain radiographs aid in determining prosthetic loosening, oversizing, and joint line positioning using the approach proposed by Figgie et al.29 Radiographs will also help to confirm or refute the presence of HO. The origin of symptoms must be clearly defined, ruling out referred pain from the hip or spine. Treatment options can include knee MUA, arthrolysis (arthroscopic or open), quadricepsplasty, or even the need for revision.
Manipulation under Anesthesia Although the role of knee MUA continues to be debated, this treatment option is an effective tool, if used for appropriate indications.63 The main objective of the manipulation is to accelerate the initial rehabilitation process in patients who have fallen behind. Maloney61 found no difference in ROM at 1 year of follow-up between patients who underwent manipulation after TKA and those who did not. Manipulation achieves increased mobility by breaking immature adhesions within the knee. MUA should be performed within the first 6 to 8 weeks post-TKA.63 After this period of time, intra-articular adhesions will mature, and manipulation increases the likelihood of developing complications such as periprosthetic fractures or rupture of the extensor mechanism. In two literature reviews studying time to manipulation, it appears that MUA may be effective up to 12 weeks postoperatively.64,65 This procedure should be performed under general or regional anesthesia with adequate muscle relaxation. After achieving a suitable relaxation, measures of passive knee extension and flexion should be taken with the patient in supine position. Manipulation is performed with application of gentle and constant pressure to the knee forcing it into flexion. With pressure, some of the intra-articular adhesions may break and an improvement in the ROM is experienced. The knee should also be gently forced into full extension. After achieving a full extension, manipulation of the patella should be performed with the knee in extension, bringing the The Journal of Knee Surgery
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Stiffness after Total Knee Arthroplasty
Manrique et al.
patella medially and inferiorly, to break the adhesions in the suprapatellar pouch. This manipulation should be done until a satisfactory ROM is achieved or when no additional improvement in ROM can be achieved.63 Afterward, aggressive rehabilitation should be implemented to avoid formation of new adhesion. The initial postoperative process should include optimal pain control, such as the use of a spinal catheter. After manipulation, plain radiographs are obtained to ensure that iatrogenic periprosthetic fracture has not occurred. The results of manipulation are summarized by Fitzsimmons et al64 in a systematic review in which the average gain in mobility ranged between 30 and 47 degrees. A systematic review performed by Ghani et al65 found an average improvement in the ROM of 38.4 degrees, mean improvement in flexion of 29 degrees, and extension of 5.7 degrees, with a failure rate of 6.7%. The long-term results of manipulation were explored by Pivec et al.66 The aim was to evaluate longterm results (> 10 years) and showed a gain in the ROM of 30, 33, and 33 degrees at 1, 5, and 10 years, respectively. The authors found a 0.2% incidence of iatrogenic periprosthetic fractures.
Arthroscopy Arthroscopy can be a useful tool in the management of a stiff TKA secondary to arthrofibrosis. The surgery is fairly uniform in all reports, with resection of the fibrous tissue in the suprapatellar pouch and medial/lateral gutters as well as in the intercondylar groove.65 Intervention is generally reserved for patients with no progression after 3 months. It is also useful and indicated when a tight PCL release is warranted. This procedure is associated with improved postoperative mobility after 20 months follow-up. Treatment failure has been reported in up to 22% of cases.67 Some surgeons argue that poor access to the posterior structures and the area above the suprapatellar pouch could be a disadvantage. In a systematic review of the literature, the result of arthroscopic release had a mean gain of 36.2 degrees of ROM, with an average gain of 35.2 degrees of flexion and 6.4 degrees of extension. The rate of treatment failure was 3.6%. It should be noted that arthroscopic release must be accompanied by an MUA. When the clinical results of MUA and arthroscopy were compared, there was no difference,64,65 calling into question the value of this technique except in properly chosen candidates.
Open Arthrolysis Open arthrolysis is recommended when ROM is severely compromised. Open arthrolysis may also be considered when severe flexion deformity may preclude the use of arthroscopy. Open procedure is appropriate in patients who have failed nonoperative management and in whom there is no component malpositioning or other causes that require revision TKA to address them. Open arthrolysis should be accompanied by polyethylene liner exchange to allow access to the posterior area of the knee.3 Exposure of the knee can be challenging, due to the presence of severe adhesions. Debridement of the posteromedial corner, posteThe Journal of Knee Surgery
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rior capsule, suprapatellar pouch, and medial and lateral gutters should be performed meticulously. If an adequate exposure cannot be achieved, and the patella cannot be everted, additional maneuvers can be employed such as osteotomy of the tibial tuberosity or a quadriceps snip. At times in more extensive cases, a more formal quadricepsplasty must be performed to free the quadriceps from the underlying anterior femur and the overlying contracted fascia. In a systematic review of the literature by Fitzsimmons et al,64 the average gain in ROM after arthrolysis was 23.6 degrees. A subsequent review by Ghani et al65 that included more studies, found that the results of this procedure was better than previously reported, and more optimal that those obtained by MUA and arthroscopy, having an average gain in the ROM of 39.9 degrees.
Total Knee Arthroplasty Revision Surgery Revision TKA is indicated for patients whose stiffness is because of technical errors that need to be corrected. The outcome of revision TKA for stiffness may not meet the full expectations of the patients and their needs to be discussed thoroughly and before surgery. Specific surgical goals must be set and a clear preoperative plan must be created. The skin incision should follow the previous scar and if multiple scars are present the most lateral one may need to be used. Resection of the scar on the skin is not recommended, as this can lead to tension on the wound closure. Almost always a quadriceps snip needs to be performed to improve the exposure and in some cases more extensile approach such as the tibial tubercle osteotomy may be needed. Meticulous debridement of the scar tissue, in particular, in the lateral and medial gutters, needs to be performed. The tracking of the patella also needs to be assessed. The orientation and fixation of all components then need to be scrutinized and any malpositioned and/or loose component removed. The patellar thickness should be measured and in cases of thickness being > 26 mm in men and > 24 mm in women, additional resection is indicated.3,63 Flexion and extension gaps should be evaluated for symmetry and, considering the very high recurrence rate of postoperative stiffness, 5 degrees of hyperextension as the ultimate goal is desired during surgery.68 Kim et al69 found that patients who undergo revision TKA have an incidence of stiffness around 4%, similar to primary TKA cases. It was also seen that poor preoperative ROM, stiffness as the primary indication for revision, younger age, shorter interval between index primary and revision TKA, presence of well-fixed components at the time of revision, postoperative wound drainage, and lower Charlson index, demonstrated to be additional risk factors for postoperative stiff knee among this patient population. The outcome of revision TKA for stiffness has not been optimal. The average improvement in ROM degrees after surgery has been reported to be between 21.8 and 27.6 degrees, with flexion improving from 12 to 19.6 degrees and extension from 8.1 to 10.5 degrees1,70 with an overall clinical and functional improvement of 69.6%.70
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Stiffness after Total Knee Arthroplasty
Management of stiffness following TKA is truly challenging. Any patient with this condition needs to be evaluated thoroughly. Management of these patients includes a work up for PJI. Majority of patients with stiff TKA should be subjected to nonoperative methods that involve aggressive PT. Other pathologies, such as hip arthritis or spine disease, that may masquerade as stiff TKA should be ruled out. The preoperative radiograph of all patients presenting with painful TKA needs to be evaluated to ensure that the indication for TKA was appropriate. Evaluation of patients with stiff TKA must also include scrutiny of the component positioning with regard to restoration of joint line, proper slopes, and sizing. For patients in whom component malpositioning is suspected, revision TKA is indicated. MUA is a viable option for patients without component malpositioning or severe arthrofibrosis. The procedure is likely to provide better results if performed close to the index arthroplasty. In patients with arthrofibrosis or sever heterotopic bone formation who are more than 3 months from the index arthroplasty and have failed nonoperative management either arthroscopic or open arthrolysis is indicated. During open arthrolysis, further scrutiny of the component positioning and sizing should be performed and components revised if indicated. The thickness of patella also needs to be measured and additional resection performed for those with overstuffed patellofemoral joints. Regardless of the treatment modality chosen, the outcome of interventions for management of stiff TKA is generally unrewarding. This needs to be discussed with the patient and surgical intervention avoided if at all possible except in cases of stiff TKA where the cause is a proven technical error.
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