Orthopedics

Review Article 

The Painful Total Knee Arthroplasty: Diagnosis and Management

Edward C. Brown III, MD; Giles R. Scuderi, MD; Henry D. Clarke, MD

Abstract

Total knee arthroplasty (TKA) is a reliable and reproducible procedure that provides pain relief and improved function for patients with symptomatic knee arthritis. Despite the generally favorable outcomes, with clinical success rates of 95% at 10-year follow-up, some patients experience clinical failure, with symptoms of pain and impaired function.1

Knee pain after TKA can have a broad spectrum of etiologies. It is helpful to divide them into two broad categories: extra-articular and intra-articular causes of pain. When trying to establish the diagnosis, it is important to approach the task in a systematic fashion. Evaluation must begin with a thorough history and physical examination. Laboratory tests and imaging studies can provide additional evidence to support a particular diagnosis. Once the diagnosis has been established the treatment can then be divided into surgical and nonsurgical options. Certainly, one of the most important principles in the management of these patients is to avoid surgical intervention until a diagnosis has been made. A practical approach to the evaluation and treatment of patients with problems after TKA is presented in this article.

Many potential causes can lead to pain after TKA. These can be broadly categorized into extra-articular and intra-articular problems (Tables 1 and 2). Extra-articular etiologies are frequent comorbidities in patients who undergo TKA. Common disorders that can produce knee pain include degenerative joint disease of the hip and neurologic problems, including spinal stenosis, neurogenic claudication, and lumbar radiculopathy. These problems usually are easily confirmed with the appropriate tests, and in many cases it is a simple failure to consider these disorders by the surgeon.

Complex regional pain syndrome type 1, previously known as reflex sympathetic dystrophy, while an uncommon cause, may also be the source of the patient’s complaints.2,3 Pain out of proportion to the physical findings should make the physician suspicious of complex regional pain syndrome type 1. The four cardinal features of complex regional pain syndrome type 1 are pain, swelling, stiffness, and skin changes, but pain is the most notable. The pain often is difficult to localize and is characterized as a burning or deep ache that is exacerbated by motion or cold. Stiffness also is a common problem, and at times loss of motion can be substantial. If long-standing, arthrofibrosis may result. Swelling associated with this condition typically is peri-articular rather than intra-articular. Skin changes include a dusky or cyanotic discoloration about the knee, leg, and foot. This discoloration may increase with exposure to cold. Other changes include decreased skin temperature and skin atrophy.

The list of intra-articular causes is extensive and includes infection, aseptic loosening, polyethylene wear, soft-tissue impingement, and arthrofibrosis. The patella remains an important source of pain after TKA. The diagnosis of infection requires a high index of suspicion. However, other problems such as flexion instability have been poorly understood until recently and may be missed unless specifically excluded by careful examination.

A painful TKA, unexplained by other mechanisms, must be evaluated with a high index of suspicion for infection. Early, acute infection is easily diagnosed but is infrequently encountered. Chronic infections are more common. Persistent, unexplained pain, effusion, erythema, prolonged wound drainage, or failure of primary wound healing should raise suspicions of deep wound infection. The diagnosis of infection should always be in the foreground of the differential diagnosis for patients presenting with pain related to TKA.

A systematic approach helps to improve the efficiency of evaluating patients who often are frustrated by the problems that they encounter after TKA. A complete evaluation includes the history and physical, supported by laboratory tests and imaging studies.

History

The first step in making the diagnosis is to…

Total knee arthroplasty (TKA) is a reliable and reproducible procedure that provides pain relief and improved function for patients with symptomatic knee arthritis. Despite the generally favorable outcomes, with clinical success rates of 95% at 10-year follow-up, some patients experience clinical failure, with symptoms of pain and impaired function.1

Knee pain after TKA can have a broad spectrum of etiologies. It is helpful to divide them into two broad categories: extra-articular and intra-articular causes of pain. When trying to establish the diagnosis, it is important to approach the task in a systematic fashion. Evaluation must begin with a thorough history and physical examination. Laboratory tests and imaging studies can provide additional evidence to support a particular diagnosis. Once the diagnosis has been established the treatment can then be divided into surgical and nonsurgical options. Certainly, one of the most important principles in the management of these patients is to avoid surgical intervention until a diagnosis has been made. A practical approach to the evaluation and treatment of patients with problems after TKA is presented in this article.

Differential Diagnosis

 
Table 1
Differential Diagnosis in
the Failed TKA:
Extra-articular Etiologies
      Etiologies
  1. Neurologic
    1. Spinal stenosis
    2. Lumbar radiculopathy
    3. Neuroma
    4. Complex regional pain syndrome
  2. Vascular claudication
  3. Hip osteoarthritis
  4. Pes bursitis
  5. Tendonitis
    1. Quadriceps
    2. Patellar
  6. Stress fracture
    1. Tibia
    2. Patella
  7. Periprosthetic fracture

Many potential causes can lead to pain after TKA. These can be broadly categorized into extra-articular and intra-articular problems (Tables 1 and 2). Extra-articular etiologies are frequent comorbidities in patients who undergo TKA. Common disorders that can produce knee pain include degenerative joint disease of the hip and neurologic problems, including spinal stenosis, neurogenic claudication, and lumbar radiculopathy. These problems usually are easily confirmed with the appropriate tests, and in many cases it is a simple failure to consider these disorders by the surgeon.

Complex regional pain syndrome type 1, previously known as reflex sympathetic dystrophy, while an uncommon cause, may also be the source of the patient’s complaints.2,3 Pain out of proportion to the physical findings should make the physician suspicious of complex regional pain syndrome type 1. The four cardinal features of complex regional pain syndrome type 1 are pain, swelling, stiffness, and skin changes, but pain is the most notable. The pain often is difficult to localize and is characterized as a burning or deep ache that is exacerbated by motion or cold. Stiffness also is a common problem, and at times loss of motion can be substantial. If long-standing, arthrofibrosis may result. Swelling associated with this condition typically is peri-articular rather than intra-articular. Skin changes include a dusky or cyanotic discoloration about the knee, leg, and foot. This discoloration may increase with exposure to cold. Other changes include decreased skin temperature and skin atrophy.

The list of intra-articular causes is extensive and includes infection, aseptic loosening, polyethylene wear, soft-tissue impingement, and arthrofibrosis. The patella remains an important source of pain after TKA. The diagnosis of infection requires a high index of suspicion. However, other problems such as flexion instability have been poorly understood until recently and may be missed unless specifically excluded by careful examination.

A painful TKA, unexplained by other mechanisms, must be evaluated with a high index of suspicion for infection. Early, acute infection is easily diagnosed but is infrequently encountered. Chronic infections are more common. Persistent, unexplained pain, effusion, erythema, prolonged wound drainage, or failure of primary wound healing should raise suspicions of deep wound infection. The diagnosis of infection should always be in the foreground of the differential diagnosis for patients presenting with pain related to TKA.

Table 2
Differential Diagnosis in
the Failed TKA:
Intra-articular Etiologies
      Etiologies
  1. Infection
  2. Instability
    1. Axial
    2. Flexion
  3. Malalignment
    1. Axial
    2. Rotational
  4. Aseptic loosening
  5. Prosthesis fracture
  6. Polyethylene wear
  7. Osteolysis
  8. Arthrofibrosis
  9. Soft-tissue impingement
    1. Patellar clunk
    2. Popliteus impingement
    3. Component overhang
  10. Extensor mechanism
    1. Patellar maltracking
    2. Patellar fracture
    3. Patellar pain
      1. Unresurfaced patella
      2. Undersized patellar button
        with lateral facet impingement
      3. Baja
      4. Patella-prosthetic construct
        too thick
    4. Rupture
      1. Quadriceps tendon
      2. Patellar tendon

Clinical Evaluation

A systematic approach helps to improve the efficiency of evaluating patients who often are frustrated by the problems that they encounter after TKA. A complete evaluation includes the history and physical, supported by laboratory tests and imaging studies.

History

The first step in making the diagnosis is to establish the chief problem, which may be pain, instability, stiffness, or swelling.4 The most frequent is pain, and this is often the most troubling to the patient.4 A visual analog scale is helpful for classifying the magnitude of the presenting pain and for documenting the response to treatment. The nature, onset, duration, location, and associations with rest or activity also should be explored to establish the characteristics of the pain.

It is important to distinguish between pain that began in the early postoperative period versus pain that occurred after a long period of assymptomatic total knee function. Four frequent causes of early postoperative pain include the four “I’s”; wrong indications for TKA (initial pain was not due to knee pathology), postoperative infection, instability due to inadequate soft-tissue balancing, and soft-tissue impingement. In distinction, delayed onset of pain is more characteristic of prosthesis loosening. A sharp catching pain usually indicates a mechanical etiology such as impingement, whereas pain at rest usually is not mechanical. Pain after activity is characteristic of synovial irritation or tendonitis. Radiating pain may indicate extra-articular sources such as the hip or lumbar spine. The presence of pain at rest or nocturnal pain is an important element of the history and should raise concerns about infection or referred neurogenic pain. Reports of giving-way or instability, recurrent swelling, and stiffness suggest a problem with the knee, rather than symptoms produced by a comorbid condition. Finally, it is important to relate the present problem to the symptoms experienced prior to TKA. Persistence of the preoperative symptoms in the immediate postoperative period suggest an extra-articular source of pain.

The history should include a list of the patient’s other medical and psychiatric disorders. Certainly, the presence of vascular or neurologic disorders may be responsible for the knee pain. The presence of psychiatric disorders also may influence or be responsible for some of the patient’s perceptions referable to their knee. Furthermore, psychiatric comorbidities also may influence the patient’s response to treatment and should be carefully considered.

A review of systems may identify important information. Disturbed sleep is not uncommon in fibromyalgia and associated psychiatric disorders that may require ancillary treatment. However, this may represent a response to the primary problem, especially if this is pain. Systemic symptoms such as fever, chills, or lethargy may accompany infection.

It also is important to establish the patient’s use of medications, including nonsteroidal anti-inflammatory drugs, narcotics, antidepressants, and anxiolytics. In some cases use of specific medications may suggest comorbid conditions that the patient initially fails to report. It also is important to enquire about medications that have been used to try to alleviate the symptoms but have been stopped because they failed to provide any benefit.

Physical Examination

Evaluation of the patient’s knee generally begins with inspection. Erythema, swelling, and gross deformity may be noted. Marked erythema or visible discharge should raise concerns about possible infection. Atrophic or dusky skin discoloration over the knee and lower leg may be associated with complex regional pain syndrome type 1 or vascular disease. The presence and location of scars about the knee also should be noted. An assessment of limb alignment is important. Varus or valgus alignment can be noted clinically but is more accurately measured with standing mechanical axis radiographs. Excessive internal or external rotation of the foot may be indicative of suboptimal rotational positioning of the tibial component. However, as discussed in subsequent sections, the rotational position of both the femoral and tibial components is best evaluated with computed tomography (CT) scanning.

Palpation should be systematic and include a careful evaluation of the painful areas identified by the patient. Tenderness along the lateral edge of the patella, along the medial edge of the tibial joint line, or over the pes anserine bursa should be correlated with radiographs to evaluate whether lateral patellar facet impingement or component overhang is the cause of pain. Patellofemoral compression and general patellar mobility also should be evaluated. Occasionally, peripheral neuromas are identified by careful palpation and a positive Tinel’s sign.

Joint stability and range of motion (ROM) of the knee also should be noted. The presence of medial or lateral soft-tissue laxity, significant hyperextension, flexion contractures, or extensor lag are all pathologic following TKA. Joint stability must be thoroughly evaluated. Axial instability, which is primarily due to incompetence of one of the collateral ligaments, may occur after trauma but usually represents a failure of intraoperative soft-tissue balancing. Medial or lateral joint opening under valgus or varus stress should be noted with the knee in full extension. Occasionally, asymmetric medial and lateral collateral ligament tension is best noted with the knee in flexion. However, what has now become widely known as flexion instability primarily refers to a knee replacement with excessive anteroposterior (AP) laxity.

Flexion instability may occur in cruciate retaining knees where late postoperative rupture of the posterior cruciate ligament (PCL) occurs. However, flexion instability usually represents an intraoperative failure to create symmetric flexion and extension gaps. In a posterior stabilized knee, flexion instability may present with an acute dislocation of the knee with the femoral cam displaced anterior to the tibial post.5 In these cases, the patient will report sudden pain and that the knee will not extend. A recent misconception is that an acute dislocation is the only manifestation of flexion instability in a posterior stabilized knee. However, chronic flexion instability also can occur with a posterior stabilized knee. The presentation is very similar to flexion instability in a knee with a cruciate-retaining prosthesis. Patients may report pain, swelling, and difficulties climbing stairs and arising from a sitting position.6,7 In a posterior stabilized knee with flexion instability, because the interaction of the cam and post mechanism limits posterior translation, the most noticeable finding on physical examination is an exaggerated anterior draw test. Excessive anterior translation also can be evaluated with the knee at 90° of flexion, such as with the patient sitting and dangling their leg over the side of the examination table. In a cruciate-retaining knee with flexion instability, as there is no cam and post mechanism to limit posterior translation, in addition to noting a positive anterior draw test, a posterior sag or positive posterior draw also will occur. In many cases of flexion instability, a recurrent effusion also will be noted.

Active and passive ROM also should be carefully evaluated. After TKA, ROM is dependent on many factors, including implant design and preoperative motion. Broadly speaking, either a flexion contracture >5° or flexion limited to <95° is poorly tolerated. Active extension also should be confirmed, and any lag should raise concern about the integrity of the extensor mechanism or patellar maltracking. Arthrofibrosis may occur as an isolated condition but may represent a component of complex regional pain syndrome type 1. As the presence of complex regional pain syndrome type 1 complicates treatment of the stiff knee, this syndrome, as previously discussed, should be considered. Significant hyperextension beyond approximately 5° is also pathologic in a TKA. In particular, most designs of posterior stabilized knees do not allow for this extent of hyperextension, as pathologic impingement of the cam on the anterior aspect of the tibial post will occur. This impingement has been associated with accelerated wear of the polyethylene post.8

Patellar tracking also should be evaluated for gross abnormalities as well as for palpable clunks and crepitus that may suggest soft-tissue impingement. The so-called patellar clunk syndrome is primarily noted in early designs of posterior stabilized prostheses and is produced by impingement of a mobile nodule of fibrous tissue that displaces out of the prosthesis notch as the knee is extended producing a palpable, painful catch.9 Other forms of soft-tissue impingement also may be identified on physical examination. Popliteal tendon impingement, which is caused by the tendon catching on the posterolateral aspect of the femoral component, is identified by a snapping at the posterolateral corner of the knee.10,11

The physical examination also should include the evaluation of gait as well as adjacent joints and lumbar spine. It is not uncommon for patients with hip pathology to present without significant hip or groin pain but instead to report significant distal thigh or knee pain. Careful evaluation of hip motion, particularly limitations of internal rotation and any associated discomfort, always should be performed in patients with knee pain. Similarly, the lumbar spine should be examined. Other ipsilateral disorders of the limb also may produce knee symptoms. Significant foot or ankle deformity may affect the knee. In most cases, significant valgus or pes planus deformity may shift the ground reaction force to the lateral aspect of the knee and result in a significant valgus or abduction moment at the knee. If this deformity is of sufficient duration and extent, it may produce pain and eventually medial ligamentous laxity and valgus instability of the knee.

Imaging Studies

Diagnostic imaging plays a central role in the evaluation of painful TKA. Following a thorough clinical evaluation, a tailored approach to imaging these patients begins with conventional radiographs of the knee. In many cases, problems related to the prosthesis will be identified based on these images alone. Additional imaging studies are dependent on the specific diagnosis in question, and may include radionuclear and CT scans of the knee. Also, when extra-articular causes of the patient’s symptoms are suspected, additional studies such as radiographs of the hip or spine and magnetic resonance images (MRI) of the lumbar spine may be required.

Radiographs

In all cases high quality radiographs should be the first imaging study obtained. The standard radiographic series should include weight-bearing AP, lateral, and tangential axial (Merchant) views of the knee. The Merchant view should not be ignored because problems with the patellofemoral joint account for the majority of painful TKAs, comprising half of all TKA complications.12 Impingement due to patellar baja, as well as lateral facet impingement due to use of an undersized button or patellar malalignment can both be identified on routine radiographs. The Merchant view also is helpful for identifying an unresurfaced patella in patients with anterior knee pain after TKA.

If standard radiographs are inadequate, fluoroscopically positioned radiographs can ensure optimal visualization of the prosthesis-bone interface, and are particularly helpful in evaluating uncemented prostheses. In addition, the value of serial radiographs taken over time cannot be over-emphasized. Therefore, whenever possible, old radiographs should be obtained by the patient or treating orthopedist for comparison purposes. A weight-bearing 3-joint radiograph of the entire extremity also is helpful for evaluating overall hip-knee-ankle alignment and component positioning in the coronal plane.

The radiographs should be evaluated for component size and positioning, as well as for signs of peri-prosthetic fracture, loosening, lucencies, osteolysis, polyethylene wear, component fracture, and infection.

“Over-stuffing” of the knee caused by anterior translation of the femoral component, over-sizing of the femoral component, or creation of a patellar composite thicker than the contralateral side all can be readily identified. Any of these errors can result in poor flexion and pain. Similarly, use of components that are too big or inaccurate component positioning can create overhang in the coronal plane that can cause pain. In particular, overhang of the medial edge of the tibial component with impingement on the pes anserine or medial collateral ligament should be avoided. Again, these errors usually are easily noted on routine radiographs.

Radiographic signs of loosening include progressive increases in radiolucent lines, changes in component position including subsidence on serial radiographs, fracture of the cement mantle, and reaction about the tip of stemmed components. Prosthetic loosening most commonly involves the tibial component and often is identified by a shift into varus alignment. Femoral component loosening typically results in a shift of the femoral component into flexion on the lateral view. A characteristic lucency also may be noted on the lateral view, but visualization of the interface may be obscured by the posterior condyles of the femoral component. This is one circumstance where fluoroscopically positioned radiographs can be particularly helpful. The clinical significance of thin radiolucent lines at the prosthesis-bone interface is controversial.13,14

Asymptomatic TKAs often display this finding, however, it also may be abnormal and sometimes is the only sign of a symptomatic loose prosthesis.

Arthrography can provide objective evidence that this lucency represents loosening. Any flow of iodinated contrast material into the lucency at this interval signifies loosening. However, failure to demonstrate this finding does not exclude loosening. Component loosening also may be associated with zones of osteolysis. These focal areas of lucency often are seen on conventional radiographs but CT, as discussed below, can be helpful for accurately delineating the extent of zones of osteolysis.

Polyethylene wear of the tibial and patellar components is manifested radiographically and best appreciated on weight-bearing views with asymmetrically narrowed prosthetic joint spaces or an interval decrease in the space on sequential views. The particulate debris caused by wear also may result in osteolysis as previously discussed. In many cases it is difficult to isolate a single cause of failure as polyethylene wear, osteolysis, loosening, and component malalignment often are identified in the same scenario. Also, without serial radiographs it may be impossible to identify the primary etiology of the aseptic failure.

Early infection during the first two to three weeks postoperatively is most likely due to operative site contamination; whereas late infection following TKA occurs after months of assymptomatic functioning and usually is due to hematogenous seeding from a distant source. The overall incidence of deep infection with modern knee replacement is reported to be about 1%-2%.15 The incidence is greater in revision than in primary cases and is increased in patients with rheumatoid or psoriatic arthritis and diabetes mellitus.15 Differentiation of mechanical loosening from septic loosening cannot be solely made on the conventional radiograph appearance. Also, an infected TKA may present with normal radiographs. Radiographic findings that may indicate chronic TKA infection include bone resorption at the interfaces, periosteal reaction, soft-tissue or intra-articular gas, and early component loosening. The use of radionuclide scans, as detailed below, can be helpful in these cases for differentiating between infection and aseptic loosening.

Radionuclide Scans

Radionuclide scans also are an essential component of the diagnostic imaging. Three-phase Technetium bone scans, indium-labeled white blood cell bone scans, and sulfur-colloid marrow scans should be ordered together. The combination of these radionuclide scans allows the differentiation of infection, aseptic loosening, complex regional pain syndrome type 1, and stress fractures near the prosthesis.

Three-phase Technetium bone scans sometimes can be helpful in evaluating for suspected component loosening in TKA. Unlike after total hip arthroplasty, in which activity typically returns to normal 6-12 months postoperatively, increased peri-prosthetic uptake can persist on the 3-phase bone scan indefinitely after TKA.16,17 This significantly limits the usefulness of this test when performed alone in the evaluation of painful TKAs. Rosenthal et al16 reported increased peri-prosthetic uptake around 89% of tibial components and 63% of femoral components >1 year after surgery. In distinction, when used together, the radionuclide scans have been reported to be highly accurate for the diagnosis of chronic infection after TKA. For example, when used alone the accuracy of Indium-111–labeled leukocyte scans has been reported to be approximately 78%.18 When Indium-111–labeled leukocyte scans are used in conjunction with sulphur-colloid marrow scans to compare areas of incongruent uptake, the combined accuracy for diagnosing infection is reported to be 95% (Figure 1).18

Figure 1AFigure 1B
Figure 1: Technetium 99 methylene diphosphonate bone marrow scan demonstrating increased uptake about the femoral and tibial components of a TKA (A). The Indium 111-labelled leukocyte scan of the same patient shows discordant uptake, with relatively greater uptake in the popliteal fossa (arrow), distal femur, and proximal tibia consistent with an infected TKA (B).

Computed Tomography

 

Figure 2
Figure 2: Coronal CT slice of the tibia with osteolysis about the medial aspect of the tibial component (arrow).

Computed tomography scans can help determine the extent of osteolytic areas and component rotational position better than conventional radiograhs.19 The size and extent of osteolytic lesions, the proximity of the lytic areas to the prosthesis, and the involvement of the cortical bone can all be determined about the tibial component (Figure 2). However, with current CT scanners, visualization of the patellar and femoral component interfaces remains more limited. New MRI software and imaging techniques that suppress metal artifact caused by the prosthesis may prove superior to CT for evaluating osteolytic defects about total knee prostheses, but these technical upgrades are not yet in widespread clinical use.20

The rotational positioning of the components also can be accurately determined using CT.21 The most common mistakes in component rotational positioning are excessive internal rotation of the femoral and the tibial components. The femoral component rotation should be determined with respect to the transepicondylar axis.22 Optimal positioning is parallel to this transepicondylar axis and has been shown to be associated with optimal in-vivo kinematics.23 Tibial component rotation relative to the medial third of the tibial tubercle also can be established. Internal rotation of the femoral and tibial components is a major contributor to patellar maltracking and instability.

Laboratory Tests

Joint Aspiration

The evaluation of a suspected acute or chronic infection also should involve aspiration of joint fluid for white cell count with differential as well as aerobic and anaerobic cultures. Historically, the presence of >25,000 leukocytes per cubic mm or >75% polymorphonuclear leukocytes was considered highly suggestive of infection.24 However, recent data by Mason et al25 suggests that a much lower limit should be concerning. In a series of 440 revision TKAs, when the cell count was >2500 per cubic mm, and the percentage of polymorphonuclear leukocytes was >60% and the sensitivity and specificity for infection were 98% and 95%, respectively.25 False-negative results may be due to recent antibiotic treatment; therefore, all antibiotics should be discontinued two weeks prior to an aspiration attempt. If the initial culture results are negative, but the clinical scenario is concerning for infection, re-aspiration after a two-week antibiotic-free period should be attempted as a four-week interval without antibiotic treatment has been shown to significantly improve sensitivity and specificity.26

Hematologic Tests

The value of the erythrocyte sedimentation rate (ESR) and C-reactive protein are controversial.27 These parameters often are elevated, but are relatively nonspecific for infection. Levitsky et al28 reported a low sensitivity (60%) and specificity (65%) for infection when a preoperative ESR >30 was used as a cutoff in patients with infected total joints. In distinction, Barrack et al26 found that an ESR >30 had a sensitivity of 80% and a specificity of 62.5% for infection. Furthermore, results may be difficult to interpret in patients with rheumatoid arthritis or other systemic disease.

Clinical Algorithims

A practical algorithm based on the authors’ clinical practices is detailed in Figure 3. These suggestions represent a systematic approach to the evaluation and management of patients with pain after TKA.

Figure 3
Figure 3: Algorithm for the clinical evaluation of a painful TKA.

Treatment

Once the diagnosis has been made, treatment can be initiated and will be dependent on the nature of the diagnosis.

Extra-articular Etiology

Appropriate management of the disorder will be based on the specific etiology and may include nonsurgical or surgical interventions. In most cases, referral to the appropriate consulting physician is the preliminary step. Occasionally the knee must be re-evaluated if the initial concerns regarding an extra-articular problem are excluded after further testing or consultations have been obtained.

Intra-articular Etiology

Arthroscopy in TKA. Indications for arthroscopic intervention after TKA are limited, but this tool can be quite useful in select cases. For the patient with a stiff TKA due to arthrofibrosis, early postoperative manipulation of the knee under anesthesia should be considered. However, beyond approximately 3 months postoperatively, arthroscopic debridement combined with manipulation may be helpful in restoring motion.29 Another potential cause of the stiff knee with a cruciate-retaining prosthesis is when the PCL has been left too tight. If the component size, alignment, and positioning are acceptable, arthroscopic release of the tight PCL has been successful in improving postoperative motion.30 Arthroscopic debridement also has proven helpful in patients where soft-tissue impingement, such as patellar clunk and popliteal tendon impingement, is suspected.10,11 In these circumstances, a diagnostic lidocaine injection can be used to identify those patients in whom arthroscopic intervention may be successful.5

Revision TKA. Establishment of a definitive diagnosis after a systematic evaluation is a necessary prerequisite prior to contemplation of revision TKA. Successful revision is possible to treat a painful TKA when a diagnosis is established.31,32 The outcome of revision arthroplasty is dependent on the etiology of failure. In particular, the surgeon must exercise caution in cases of unexplained pain.32 Mont et al32 reported very poor results when revision TKA was undertaken in patients with unexplained pain. In their review of 27 patients with unexplained pain after TKA, only 11 (41%) patients obtained good or excellent results. Other circumstances that must be approached with caution include cases where isolated patellar or tibial polyethylene insert revision is considered.33-36

High failure rates likely reflected a failure to identify associated problems, such as femoral and tibial component malpositioning. Prior to isolated patellar revision, a comprehensive evaluation of these patients should be conducted to ensure that more extensive revision is not required.33 Isolated polyethylene insert exchange in a modular tibial component for cases of polyethylene wear or arthrofibrosis after TKA is another situation that must also be approached with caution.35,36 In these cases, as in cases where isolated patellar component revision is considered, a comprehensive evaluation of the entire prosthesis should be undertaken, including alignment and rotation, to identify underlying problems that may have contributed to the failure.

Summary

The results of TKA during the past two decades have been reliable and favorable. While success rates are high, some patients experience pain and impaired function. This clinical scenario can be frustrating to both the patient and the surgeon who is accustomed to good outcomes. A systematic evaluation of the patient and arthroplasty can lead to a definitive diagnosis of the cause of the patient’s symptoms.

Problems can be caused by a broad spectrum of possible etiologies. It is helpful to divide the differential diagnosis into two broad categories: extra-articular and intra-articular etiologies. When trying to establish the diagnosis, it is important to approach the task in a systematic fashion. Evaluation must begin with a thorough history and physical examination. Laboratory tests and imaging studies can provide additional evidence supporting a particular diagnosis. Once the etiology has been established, symptomatic relief may be achieved with appropriate treatment including revision TKA. However, revision TKA that is performed for unexplained pain is associated with a low probability of success.

References

  1. Diduch DR, Insall JN, Scott WN, Scuderi GR, Font-Rodriguez D. Total knee replacement in young, active patients. Long-term follow-up and functional outcome. J Bone Joint Surg Am. 1997; 79:575-582.
  2. Lindenfeld TN, Bach BR Jr, Wojtys EM. Reflex sympathetic dystrophy and pain dysfunction in the lower extremity. Instr Course Lect 1997; 46:261-268.
  3. Wasner G, Backonja MM, Baron R. Traumatic neuralgias: complex regional pain syndromes (reflex sympathetic dystrophy and causalgia): clinical characteristics, pathophysiological mechanisms and therapy. Neurol Clin. 1998; 16:851-868.
  4. Lonner JH, Siliski JM, Scott RD. Prodromes of failure in total knee arthroplasty. J Arthroplasty. 1999; 14:488-492.
  5. Sharkey PF, Hozack WJ, Booth RE Jr, Balderston RA, Rothman RH. Posterior dislocation of total knee arthroplasty. Clin Orthop. 1992; 278:128-133.
  6. Pagnano MW, Hanssen AD, Lewallen DG, Stuart MJ. Flexion instability after primary posterior cruciate retaining total knee arthroplasty. Clin Orthop. 1998; 356:39-46.
  7. Waslewski GL, Marson BM, Benjamin JB. Early, incapacitating instability of posterior cruciate ligament- retaining total knee arthroplasty. J Arthroplasty. 1998; 13:763-767.
  8. Callaghan JJ, O’Rourke MR, Goetz DD, Schmalzried TP, Campbell PA, Johnston RC: Tibial post impingement in posterior-stabilized total knee arthroplasty. Clin Orthop. 2002; 404:83-88.
  9. Beight JL, Yao B, Hozack WJ, Hearn SL, Booth RE Jr. The patellar “clunk” syndrome after posterior stabilized total knee arthroplasty. Clin Orthop. 1994; 299:139-142.
  10. Allardyce TJ, Scuderi GR, Insall JN. Arthroscopic treatment of popliteus tendon dysfunction following total knee arthroplasty. J Arthroplasty. 1997; 12:353-355.
  11. Barnes CL, Scott RD. Popliteus tendon dysfunction following total knee arthroplasty. J Arthroplasty. 1995; 10:543-545.
  12. Johnson DP, Eastwood DM. Patellar complications after knee arthroplasty. A prospective study of 56 cases using the Kinematic prosthesis. Acta Orthop Scand. 1992; 63:74-79.
  13. Hendrix RW, Anderson TM. Arthrographic and radiologic evaluation of prosthetic joints. Radiol Clin North Am. 1981; 19:349-364.
  14. Gelman MI, Dunn HK. Radiology of knee joint replacement. AJR Am J Roentgenol. 1976; 127:447-455.
  15. Hanssen AD, Rand JA. Evaluation and treatment of infection at the site of a total hip or knee arthroplasty. Instr Course Lect. 1999; 48:111-122.
  16. Rosenthall L, Lisbona R, Hernandez M, Hadjipavlou A. 99mTc-PP and 67Ga imaging following insertion of orthopedic devices. Radiology. 1979; 133:717-721.
  17. Rosenthall L, Lepanto L, Raymond F. Radiophosphate uptake in asymptomatic knee arthroplasty. J Nucl Med. 1987; 28:1546-1549.
  18. Palestro CJ, Swyer AJ, Kim CK, Goldsmith SJ. Infected knee prosthesis: diagnosis with In-111 leukocyte, Tc-99m sulfur colloid, and Tc-99m MDP imaging. Radiology. 1991; 179:645-648.
  19. Seitz P, Ruegsegger P, Gschwend N, Dubs L. Changes in local bone density after knee arthroplasty. The use of quantitative computed tomography. J Bone Joint Surg Br. 1987; 69:407-411.
  20. Sofka CM, Potter HG, Figgie M, Laskin R. Magnetic resonance imaging of total knee arthroplasty. Clin Orthop. 2003; 406:129-135.
  21. Berger RA, Crossett LS, Jacobs JJ, Rubash HE. Malrotation causing patellofemoral complications after total knee arthroplasty. Clin Orthop. 1998; 356:144-153.
  22. Miller MC, Berger RA, Petrella AJ, Karmas A, Rubash HE. Optimizing femoral component rotation in total knee arthroplasty. Clin Orthop. 2001; 392:38-45.
  23. Scuderi GR, Komistek RD, Dennis DA, Insall JN. The impact of femoral component rotational alignment on condylar lift-off. Clin Orthop. 2003; 410:148-154.
  24. Windsor RE, Bono JV. Infected Total Knee Replacements. J Am Acad Orthop Surg. 1994; 2:44-53.
  25. Mason JB, Fehring TK, Odum SM, Griffin WL, Nussman DS. The value of white blood cell counts before revision total knee arthroplasty. J Arthroplasty. 2003; 18:1038-1043.
  26. Barrack RL, Jennings RW, Wolfe MW, Bertot AJ. The Coventry Award. The value of preoperative aspiration before total knee revision. Clin Orthop. 1997; 345:8-16.
  27. Duff GP, Lachiewicz PF, Kelley SS. Aspiration of the knee joint before revision arthroplasty. Clin Orthop. 1996; 331:132-139.
  28. Levitsky KA, Hozack WJ, Balderston RA, et al. Evaluation of the painful prosthetic joint: relative value of bone scan, sedimentation rate, and joint aspiration. J Arthroplasty. 1991; 6:237-244.
  29. Diduch DR, Scuderi GR, Scott WN, Insall JN, Kelly MA. The efficacy of arthroscopy following total knee replacement. Arthroscopy. 1997; 13:166-171.
  30. Williams RJ III, Westrich GH, Siegel J, Windsor RE. Arthroscopic release of the posterior cruciate ligament for stiff total knee arthroplasty. Clin Orthop. 1996; 331:185-191.
  31. Haas SB, Insall JN, Montgomery W III, Windsor RE. Revision total knee arthroplasty with use of modular components with stems inserted without cement. J Bone Joint Surg Am. 1995; 77:1700-1707.
  32. Mont MA, Serna FK, Krackow KA, Hungerford DS. Exploration of radiographically normal total knee replacements for unexplained pain. Clin Orthop. 1996; 331:216-220.
  33. Berry DJ, Rand JA. Isolated patellar component revision of total knee arthroplasty. Clin Orthop. 1993; 286:110-115.
  34. Leopold SS, Silverton CD, Barden RM, Rosenberg AG. Isolated revision of the patellar component in total knee arthroplasty. J Bone Joint Surg Am. 2003; 85:41-47.
  35. Babis GC, Trousdale RT, Pagnano MW, Morrey BF. Poor outcomes of isolated tibial insert exchange and arthrolysis for the management of stiffness following total knee arthroplasty. J Bone Joint Surg Am. 2001; 83:1534-1536.
  36. Engh GA, Koralewicz LM, Pereles TR. Clinical results of modular polyethylene insert exchange with retention of total knee arthroplasty components. J Bone Joint Surg Am. 2000; 82:516-23.

Authors

Dr Brown is from the Department of Orthopedic Surgery, National Naval Medical Center, Bethesda, Md; Dr Clarke is from the Mayo Clinic, Scottsdale, Ariz; and Dr Scuderi is from Insall Scott Kelly Institute for Orthopaedics and Sports Medicine, Beth Israel Medical Center, New York, NY.

Drs Brown and Scuderi have no industry relationships to declare. Dr Clarke is a consultant to Zimmer Inc.

The material presented in any Vindico Medical Education continuing education activity does not necessarily reflect the views and opinions of Vindico Medical Education or Slack Incorporated. Neither Vindico Medical Education or SLACK Incorporated nor the authors endorse or recommend any techniques, commercial products, or manufacturers. The authors may discuss the use of materials and/or products that have not yet been approved by the US Food and Drug Administration. All readers and continuing education participants should verify all information before treating patients or using any product.

Reprint requests: Henry D. Clarke, MD, Mayo Clinic, 13400 E Shea Blvd, Scottsdale, AZ 85259.

10.3928/01477447-20060201-14

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