There are many causes of residual pain after total knee arthroplasty (TKA). Evaluation and management begins with a comprehensive history and physical examination, followed by radiographic evaluation of the replaced and adjacent joints, as well as previous films of the replaced joint. Further workup includes laboratory analysis, along with a synovial fluid aspirate to evaluate the white blood cell count with differential as well as culture. Advanced imaging modalities may be beneficial when the diagnosis remains unclear. Revision surgery is not advisable without a clear diagnosis, as it may be associated with poor results.
Key points
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Pain after total knee arthroplasty can be caused by numerous factors, and a systematic evaluation that includes a thorough history, physical, radiographic and laboratory evaluation, and understanding of the differential diagnosis is essential.
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Intra-articular, peri-articular, and extra-articular pathology may cause pain after total knee arthroplasty.
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Revision total knee arthroplasty performed without a firm diagnosis has a high chance of failure.
Introduction
Total knee arthroplasty (TKA) has been shown to produce good clinical results in approximately 80% of patients at long-term follow-up, but the 20% of patients who continue to experience pain following TKA often present a diagnostic challenge to orthopedic surgeons. The evaluation and treatment of these patients relies on a thorough understanding of the differential diagnosis of a painful TKA, and a systematic approach is instrumental to efficiently and effectively resolve their pain.
Introduction
Total knee arthroplasty (TKA) has been shown to produce good clinical results in approximately 80% of patients at long-term follow-up, but the 20% of patients who continue to experience pain following TKA often present a diagnostic challenge to orthopedic surgeons. The evaluation and treatment of these patients relies on a thorough understanding of the differential diagnosis of a painful TKA, and a systematic approach is instrumental to efficiently and effectively resolve their pain.
Definition and mechanism of pain
Pain can serve as a protective mechanism by inducing a reaction to eliminate a harmful stimulus. Excessive pain after a TKA often diminishes one’s quality of life. Pain has been defined as “what the patient says it is.” This simplistic definition emphasizes that pain is a subjective experience with no reliable objective measures. Thus the patient’s self-report is the most reliable indicator of pain and should not be discredited. The International Association for the Study of Pain (IASP) defines pain as an “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” This definition emphasizes that pain is a complex, multifactorial experience that involves multiple organ systems. To better understand this complex problem, 2 basic types of pain have been described: nociceptive and neuropathic pain.
Nociceptive Pain
Nociceptive pain is caused by the ongoing activation of sensory neurons in response to a noxious stimulus, such as injury, disease, or inflammation, and it is indicative of real or potential tissue damage. There is generally a close correlation between pain perception and stimulus intensity. Nociceptive pain may be described as visceral or somatic. Somatic pain arises from tissues such as skin, muscle, joint capsules, and bone and is further categorized as superficial and deep somatic pain. Superficial somatic pain presents with a well-localized, sharp, pricking, or burning sensation, whereas deep somatic pain presents as a diffuse, dull, or aching sensation. Deep somatic pain has also been described as a cramping sensation that may be referred to or from other sites (ie, referred pain).
Neuropathic Pain
Neuropathic pain is caused by aberrant signal processing in the peripheral or central nervous system and is broadly categorized as peripheral or central in origin. Animal studies suggest that several changes likely contribute to neuropathic pain:
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Generation of spontaneous ectopic activity,
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Loss of normal inhibitory mechanisms in the dorsal horn,
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Altered primary afferent neuron phenotypes, and
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Sprouting of nerve fibers leading to altered neural connections.
These changes result in abnormal nerve firing and/or abnormal signal amplification. Common causes of neuropathic pain include nerve transection, inflammation, tumors, toxins, metabolic diseases, infections, and primary neurologic diseases. Neuropathic pain is sometimes called “pathologic” pain because it serves no purpose. A chronic pain state may occur when pathophysiologic changes become independent of the inciting event. Neuropathic pain may be continuous or episodic and is perceived as a variety of different sensations (eg, burning, tingling, prickling, shooting, electric shock–like, jabbing, squeezing, deep aching, spasm, or cold). In contrast to nociceptive pain, neuropathic pain is often unresponsive or poorly responsive to nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids. However, neuropathic pain may respond to antiepileptic drugs, antidepressants, or local anesthetics.
Sensitization has a vital role in the etiology of neuropathic pain. With intense, repeated, or prolonged exposure to inflammatory mediators, nociceptors exhibit a lowered threshold for activation and an increased rate of firing. Peripheral sensitization in turn plays a vital role in central sensitization and clinical pain states such as hyperalgesia and allodynia. Central sensitization refers to a state of spinal neuron hyperexcitability. Dysregulated activation of certain N-methyl- d -aspartate (NMDA) receptors is responsible for this process. Central sensitization is associated with a reduction in central inhibition, spontaneous dorsal horn neuron activity, the recruitment of responses from neurons that normally only respond to low-intensity stimuli (ie, altered neural connections), and expansion of dorsal horn neuron receptive fields. Clinically, these changes may manifest as (1) hyperalgesia, (2) allodynia, (3) prolonged pain after a transient stimulus (persistent pain), and (4) the spread of pain to uninjured tissue (ie, referred pain).
Sensitization is likely responsible for most of the continuing pain and hyperalgesia after an injury or surgery. This may be due to noxious stimuli from injured and inflamed tissue or “abnormal” input from injured nerves. Sensitization may serve an adaptive purpose to encourage protection of the injured area during the healing phase; however, these processes may persist long after healing of the injury and lead to chronic pain. Furthermore, sensitization may be why neuropathic pain often exceeds the provoking stimulus, both spatially and temporally. Finally, central sensitization may explain why chronic pain is more difficult to treat than acute pain.
Evaluation of painful total knee arthroplasty
The management of a painful TKA requires a multidisciplinary team approach that involves orthopedic surgeons, physical therapists, pain management physicians, and primary medical doctors. A full assessment of both the surgical and nonsurgical factors that can cause pain after TKA is often time-consuming, but timely management of the pain is essential and should be approached irrespective of the origin of the pain and whether or not it may be addressed surgically. Depending on the acuity and necessity of surgical intervention, this evaluation may best be done by a pain management specialist, which in itself may help to alleviate anxiety. As a result, the emphasis may be focused on a nonsurgical resolution of the problem.
The use of appropriate analgesics may help to alleviate pain, reduce the sense of urgency for further intervention, and decrease the desperation often felt by patients and their families. Most patients report low pain scores in the first 3 months after TKA, but some report continued pain or even increasing pain as time passes. This often correlates with the cessation of regular pain medications by patients who feel that these medications are not required for such a long period postoperatively. The pain may lead to a reduction in the range of motion, with subsequent stiffness and increased sensitivity around the joint. Patients should be encouraged to take analgesics if warranted, and these should be prescribed according to the World Health Organization (WHO) analgesic ladder ( Fig. 1 ). However, medical management of pain should not delay the diagnosis and targeted treatment of the source of the pain by the orthopedic surgeon.
Differential Diagnosis
Laskin categorized etiologies of pain after TKA based on their temporal associations: start-up pain, pain on weight bearing, early postoperative pain, pain associated with full flexion, pain with stair climbing or descent, rest pain, and continuous postoperative pain. For example, start-up pain can indicate loosening of TKA components, whereas pain with stair climbing can be caused by extensor mechanism pathology. Furthermore, the differential diagnosis may be organized according to the anatomic source: intra-articular, peri-articular, and extra-articular ( Box 1 ). Pain that was present preoperatively that then persisted without change following TKA suggests an extra-articular etiology. Extra-articular sources of knee pain include lumbar spine and hip conditions, vascular insufficiency, and complex regional pain syndrome (CRPS). With regard to intra-articular pathology, pain that began within the first year after the surgery suggests infection, instability, malpositioned components, or soft tissue impingement. In contrast, pain that began more than 1 year postoperatively suggests wear, osteolysis, aseptic loosening, or infection. A patient’s pain trajectory, describing change in magnitude over time, may also be considered when attempting to make the diagnosis within the first 12 months.
Intra-articular
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Infection
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Aseptic loosening
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Instability
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Axial
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Flexion
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Midflexion
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Malalignment
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Polyethylene wear
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Osteolysis
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Component overhang
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Implant failure
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Arthrofibrosis
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Implant fracture
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Recurrent hemarthrosis
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Loose cement
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Extensor mechanism dysfunction
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Unsurfaced patella
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Undersized/oversized patella
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Patellar baja
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Lateral facet impingement
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Patellar clunk
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Osteonecrosis
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Peri-articular
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Periprosthetic fractures
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Traumatic fracture
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Tibial stress fracture
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Patellar stress fracture
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Popliteal tendon impingement
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Biceps tendonitis
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Pes bursitis
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Quadriceps tendonitis/rupture
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Patellar tendonitis/rupture
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Neuroma
Extra-articular
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Hip pathology
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Lumbar spine pathology
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Vascular claudication
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Complex regional pain syndrome
Pain that is activity related may indicate a mechanical etiology, whereas pain that is constant and does not abate with rest and activity modifications should raise suspicion of underlying periprosthetic joint infection. Pain associated with constitutional symptoms such as fevers and chills should also raise suspicion for infection. Activity-related pain associated with recurrent swelling suggests instability. Pain described as burning, tingling, prickling, shooting, electric shock–like, jabbing, squeezing, spasm, or cold may indicate a neuropathic origin. Pain that radiates to the thigh or down to the foot may be referred from the lumbar spine or ipsilateral hip.
History
A comprehensive history is the first step in identifying the etiology of a painful TKA, and it is crucial to use a systematic approach when taking a focused history. The patient’s primary symptom should be clearly identified and described in terms of pain, instability, swelling, or stiffness. Information about the initial surgery, including the date, surgeon, approach, implant records, operative reports, and preoperative radiographs and notes regarding physical examination, should be obtained. The nature and extent of the pain is important. Bates’ Guide to Physical Examination and History Taking suggests 2 mnemonics that can be used to help the physician better clarify pain: OLD CARTS (Onset, Location, Duration, Character, Aggravating/Alleviating Factors, Radiation, and Timing) and OPQRST (Onset, Palliating/Provoking Factors, Quality, Radiation, Site, and Timing).
In addition to clarifying the predominant complaint, details regarding the postoperative course of the index procedure should be obtained. Such examples would include prolonged postoperative wound drainage, delayed wound healing, return trips to the operating room, and treatment with antibiotics following surgery. Comorbid conditions also should be considered. These conditions include diabetes, renal failure, peripheral vascular disease, lumbar spondylosis and stenosis, and adjacent hip pathology.
Physical Examination
A thorough physical examination must be performed on every patient complaining of continued pain after TKA. The patient should be appropriately disrobed to allow for full evaluation of the limb. Examination should include vital signs, height, weight, general appearance, and gait. A detailed inspection is performed of the skin looking for lesions, erythema, warmth, effusion, vascular changes, and draining sinus tracts. The surgical scar may show evidence of prior wound dehiscence, which may lead one to further consider an infectious etiology. Gait should specifically be analyzed for evidence of antalgia, varus or valgus thrust, and presence of a Trendelenburg sign.
A focused musculoskeletal examination of the knee should include the measurement of active and passive range of motion and the ability to actively maintain full extension without extensor lag. The stability of the knee may be evaluated with varus and valgus forces at 0° and 30°. Stability in the sagittal plane may be assessed with posterior drawer testing at 60° and 90° of flexion to assess for flexion stability. Manual strength testing as well as evaluation for muscle atrophy should be noted. The knee should be palpated to evaluate for swelling, effusion, and focal tenderness. The knee should be assessed for point tenderness along the iliotibial band and pes anserine bursa, which may be indicative of flexion instability or bursitis.
Patellar tracking should be assessed closely, as the patellofemoral compartment is a common source of continued pain following TKA. Numerous factors have been associated with painful patellar crepitus, which include previous knee surgery, patellar clunk syndrome, decreased patellar component size, decreased patellar composite thickness, shorter patellar tendon length, increased posterior femoral condylar offset, use of smaller femoral components, thicker tibial polyethylene inserts, and increased flexion of the femoral component. These factors are postulated to increase quadriceps tendon contact forces against the superior aspect of the intercondylar box subsequently increasing the risk of fibrosynovial proliferation.
A neurovascular examination should be performed and the quality and symmetry of the peripheral pulses should be assessed. The strength of the quadriceps and vastus medialis obliquus should be evaluated. Finally, examination of the spine, hip, foot, and ankle should always be undertaken to elucidate extra-articular causes of pain, such as lumbar radiculopathy, referred pain from hip arthritis, and vascular claudication.
Imaging
A comprehensive series of plain radiographs includes standing anteroposterior, lateral, posteroanterior flexed, full-length mechanical axis, and Merchant view radiographs. When possible, serial radiographs may be useful. The anterior-posterior images should be closely evaluated for component size, position, polyethylene gap symmetry, component overhang, bony impingement, osteolysis, progressive radiolucent lines, subsidence, and fracture ( Fig. 2 ). The lateral images should be evaluated for femoral component size, posterior femoral offset, patellar height and thickness, and tibial component slope. Osteolysis is typically evident on lateral radiographs along the posterior condyles. High-quality films are important in assessing the prosthesis-bone interface in cementless implants and the bone-cement-implant interface in cemented prostheses. Fluoroscopic examination may be useful in the evaluation of these interfaces as well as assessing varus and valgus stability. The Merchant view should be evaluated for patellar tilt, patellar malalignment, femoral component overhang, component thickness, and patellar facet impingement ( Fig. 3 ). Mechanical axis films should be evaluated to assess overall alignment and may provide some additional information on the condition of the hips and spine ( Fig. 4 ).
