Total knee arthroplasty (TKA) has been demonstrated to be an efficacious and cost-effective solution for end-stage osteoarthritis (OA) of the knee. One of the most common complications within the early postoperative period is reduced knee range of motion (ROM). Stiffness following TKA is a challenge for patients and surgeons alike and occurs in approximately 5% of patients post surgery.¹,² The definition of what constitutes a stiff knee and the overall severity varies across studies.²,³,⁴,⁵,⁶,⁷,⁸,⁹ A recent classification system provided by the International consensus of the definition and classification of fibrosis categorizes knee stiffness according to loss of movement based on the deviation from full flexion or extension as mild, moderate, and severe extension restriction (5° to 10°, 11° to 20°, >20°) or flexion range (90° to 100°, 70° to 89°, <70°).¹⁰ However, what is considered as total stiffness is probably best related to the preoperative knee ROM. Flexion of 90° is considered unsatisfactory when presented with an initial preoperative flexion of 120°. Yet, in a patient presenting with a preoperative flexion of 60°, reaching 90° can be considered a promising outcome. The evaluation of the stiff knee after TKA must be approached in a systematic fashion as the underlying etiology may be biologic, psychosocial, or mechanical, and the treatment plan must be modified based on these data. Further, several potential reasons for knee stiffness include primary arthrofibrosis, component malrotation, component overstuffing, instability, coronal malalignment, pain catastrophizing, and kinesophobia.¹⁰ In addition, severe preoperative knee stiffness and prior open surgical procedures increase the risk of reduced ROM post TKA.

Developing stiffness can be frustrating for the patient: walking requires 65° of flexion, rising from a chair requires 70°, and descending stairs around 100° depending on the stair height. When a patient has severe stiffness, almost every activity of daily living is negatively impacted, with the most basic tasks requiring a minimum of 60° of flexion.⁸,¹¹ For this reason, stiffness after TKA leads to inferior patient-reported outcomes scores and inferior general health scores. Proper patient education and evaluation are integral in optimizing patient satisfaction following TKA.¹² To date, the best predictors of ROM post TKA are preoperative motion and the passive motion achieved at time of surgery.²,⁹ The aim of this chapter is to outline the specific causes of stiffness in the setting of TKA and provide surgical management tailored to the underlying etiology.

The prevalence of stiffness post TKA ranges from 1.3% to 14%.⁶,⁷,⁹,¹³ However, the definition of stiffness is variable among these studies. Gandhi et al reported an incidence of 3.7%, using a definition of stiffness as flexion less than 90°,⁶ while Yercan reported an incidence of 5.3% with a definition of 10° or more of extension and/or less than 95° of flexion.⁷ Le et al showed stiffness as the third most common reason for TKA failure, behind infection and instability.¹³ Zmistowski et al further demonstrated that postoperative stiffness following TKA is one of the most common causes of readmission within the first 90 days after surgery and for revision TKA.¹⁴ Regardless of the selected study, stiffness post TKA is one of the more commonly encountered early complications requiring conservative and possibly operative management.

Knee stiffness can be categorized as intrinsic (anatomically localized in the knee) or extrinsic (outside of the knee joint). Intrinsic etiologies include severe reduction in preoperative ROM, low-grade infection, aseptic loosening, or poor surgical technique.⁹ Extrinsic etiologies include hip or spine disease, neurologic injury, abnormal inflammatory response, complex regional pain syndrome (CPRS), patient motivation, and improper indication for the TKA.⁹ Among these, perhaps the most significant risk factor is a preoperative reduction in ROM, as a stiff knee is more likely to yield postoperative stiffness after a knee replacement. Vince further categorized etiologies of stiffness into five groups: pathology, patient, rehab, surgical technique, and implant design.¹⁷ Among those five, some etiologies are more commonly associated with early stiffness after TKA, while others have a strong affinity with late-onset stiffness. Etiologies more commonly associated with early stiffness after TKA include component malposition, arthrofibrosis, and CPRS. Etiologies seen in late stiffness include synovitis, tendinitis, aseptic loosening, or prosthetic breakage. Periprosthetic joint infections (PJIs) have been known to cause both early and late reductions in ROM.

Knee stiffness can arise due to extrinsic causes outside of the knee joint as well. Patient factors (including preoperative ROM), body habitus, and patient personality have all previously been implicated with stiffness.¹⁵ Patients that are obese may have limited ROM secondary to posterior soft-tissue impingement as the knee flexes,¹⁵ and some studies have shown a direct relationship between BMI and reduced ROM.²⁶ Interestingly, patients with low BMI may be at increased risk for reduced ROM as well.¹⁷

Demographic risk factors that have been reported in the literature include age and ethnicity. Younger age at time of TKA has been associated with increased risk of stiffness post TKA.¹⁷ Springer et al reported that patients younger than 45 years and of African-American ethnicity were twice as likely to undergo a manipulation under anesthesia (MUA).²⁷ Patient comorbidities may also contribute to the risk of developing stiffness. For example, the diagnosis of diabetes mellitus has been associated with reduced ROM and risk for arthrofibrosis. Other patient factors that may limit ROM include poor patient motivation which may compromise postoperative rehabilitation protocols and overall compliance with postoperative exercises.⁶ In addition, previous open surgical procedures on the affected knee have been suggested as a risk factor for arthrofibrosis after TKA.⁵,²⁸

Other extrinsic causes that can lead to knee stiffness include any muscular or nervous system disorder that prevents normal knee motion. Central or peripheral nervous system disorders that may lead to spasticity might negatively influence final ROM. Parkinson disease, not well pharmacologically controlled, results in increased spasticity, cogwheel rigidity, and knee stiffness. Additionally, tight quadriceps or hamstring muscles secondary to muscle injury, heterotopic ossification (HO), or long-standing juvenile inflammatory conditions limiting knee ROM prior to the completion of skeletal growth may be an extrinsic source of knee stiffness.⁹ Problems affecting other joints can influence TKA outcome. Pain originated at the hip radiating to the knee should be evaluated such as radiculopathy. Moreover, flexion deformity of the ipsilateral hip can develop into a compensatory flexion deformity of the knee. A patient with severe valgus or varus OA of both knees who undergo a TKA in one of the affected joints, after the surgery, would have a leg length discrepancy resulting in longer operated limb versus the nonoperated one. The patient may balance the leg length discrepancy by bending the operated knee resulting in a potential flexion contracture. The two possible solutions are the use of a shoe lift on the nonoperated limb or to perform a simultaneous bilateral TKA. In addition, spine deformity, such as dorsal or lumbar kyphosis, can lead to knee flexion.¹² Finally, improper surgical indications for TKA might lead to a painful and/or stiff TKA. Evaluation of preoperative radiographs may confirm this suspicion, and caution must be taken when considering surgery for patients with severe pain but minimal preoperative radiographic degenerative changes.²⁹