Arthrofibrosis after Arthroplasty

Arthrofibrosis — the development of excessive intra-articular and periarticular scar tissue leading to restricted joint motion — is one of the most challenging complications after total joint arthroplasty, occurring in approximately 1–5% of TKA patients. It is also seen after THA (rare), shoulder arthroplasty, and following other orthopaedic procedures including ACL reconstruction and fracture surgery. After TKA, arthrofibrosis typically presents as inability to achieve functional knee flexion (target >90° for most activities of daily living) and/or inability to fully extend the knee. The pathophysiology involves an abnormal fibroproliferative response to surgical trauma and possibly implant-related factors, resulting in dense fibrous adhesion formation within and around the joint.

• Pathophysiology: surgical trauma triggers a wound healing response; in most patients this resolves normally; in susceptible individuals, the fibroblastic phase of healing is dysregulated — transforming growth factor-β (TGF-β) and other pro-fibrotic cytokines drive excessive collagen deposition and myofibroblast activation; myofibroblasts contract and consolidate scar tissue; the joint capsule and periarticular soft tissues become thickened, contracted, and inelastic; adhesions form between tissue planes, preventing normal joint motion; the risk is higher in patients with a history of prior surgery, haematoma, infection, inflammatory arthritis, complex regional pain syndrome (CRPS), and poor compliance with early rehabilitation
• Risk factors: pre-operative poor range of motion (ROM) — the most consistent predictor; pre-operative stiffness (ROM <90°) predicts post-operative stiffness; the `tight knee` preoperatively tends to be tight postoperatively; inadequate post-operative analgesia and physiotherapy compliance; obesity; diabetes; prior knee surgery (multiple previous procedures increase scarring); component malposition (particularly flexion gap imbalance or component malrotation — a tight flexion gap will manifest as post-operative stiffness); haematoma formation; infection (early PJI must be excluded in any acutely stiff TKA)
• Infrapatellar contracture syndrome (IPCS): a specific form of arthrofibrosis after TKA characterised by contracture of the infrapatellar fat pad and inferior patellar retinaculum, leading to patella baja (inferior patellar displacement) and restricted patellar mobility; presents with anterior knee pain, patella baja on X-ray (Insall-Salvati ratio <0.8), and inability to achieve full flexion; the patellar tendon is shortened and the inferior pole of the patella is pulled into the tibial plateau during flexion

• Multimodal analgesia for early mobilisation: the most effective prevention strategy is aggressive early mobilisation enabled by adequate analgesia; the goal is active-assisted knee flexion to >90° on the day of surgery (or first post-operative day); adductor canal block + periarticular injection + oral multimodal analgesia (paracetamol + NSAID + gabapentin) allows early physiotherapy without excessive post-operative pain; inadequate analgesia causes guarding and reluctance to flex the knee, allowing scar tissue to consolidate
• Correct component position: femoral component internal rotation is a specific cause of a `tight` flexion gap → post-operative stiffness; the femoral component must be externally rotated (3° from posterior condylar axis or aligned to the transepicondylar axis); a symmetric flexion and extension gap (balanced gaps) is essential for normal post-operative motion; intraoperative gap assessment and balancing prevents post-operative stiffness from component malposition
• Continuous passive motion (CPM): a motorised device that passively flexes and extends the knee post-operatively; once widely used after TKA; Cochrane reviews have failed to show consistent benefit over standard physiotherapy for final ROM or complication rates; CPM is no longer routinely recommended by most guidelines but may still be used in specific cases (slow to mobilise, high-risk patients)

• Timing is critical: the management approach differs significantly based on the time since TKA; early stiffness (within 6–12 weeks) is more amenable to aggressive physiotherapy and manipulation before the scar consolidates; late stiffness (>3–6 months) is more likely to require surgical intervention; the `window of opportunity` for manipulation under anaesthesia (MUA) is generally considered to be within the first 3–6 months post-operatively — after this point, the scar is mature and MUA has lower success rates and higher complication risk
• Physiotherapy: first line; intensive physiotherapy (daily sessions) with a specialist musculoskeletal physiotherapist; passive stretching, active-assisted exercises, extension splinting; adequate analgesia is essential to allow participation
• Manipulation under anaesthesia (MUA): performed when physiotherapy fails to achieve adequate ROM and the patient is within the window of opportunity (typically 6 weeks – 3 months post-TKA); the patient is placed under general or regional anaesthesia (allowing complete muscle relaxation); the knee is forcibly flexed (gentle sustained force — NOT sharp jerking) to break adhesions; a `pop` may be heard/felt as adhesions release; the target is to achieve >90–100° of flexion; complications — patellar tendon avulsion, patellar fracture, periprosthetic femoral fracture, wound dehiscence (rare); after MUA, continuous passive motion and aggressive physiotherapy are commenced immediately to maintain the gained motion; MUA is most effective when performed early and loses efficacy with time
• Arthroscopic lysis of adhesions (arthroscopic arthrolysis): when MUA fails or when stiffness persists beyond 3–6 months, arthroscopic lysis of adhesions is performed; the arthroscope is inserted and adhesions are divided with an electrocautery device (arthroscopic shaver and radiofrequency probe); the posterior capsule (the most common site of extension contracture) and the parapatellar gutters (commonly filled with adhesions) are released; CPM is commenced immediately post-operatively; arthroscopic arthrolysis is more precise than MUA and allows visualisation of the adhesion pattern; however, it requires an experienced arthroscopist as the anatomy may be distorted by previous surgery and adhesions
• Open arthrolysis and revision TKA: reserved for severe refractory cases where arthroscopic arthrolysis has failed; open release of all periarticular soft tissue contractures; if component malposition is identified as a contributing cause (particularly femoral/tibial internal rotation — verified on pre-operative CT with MARS sequences), revision of the malpositioned component is performed at the same time; revision for stiffness alone (without malposition) rarely produces reliable improvement and is associated with high complication rates; the decision to revise must be made carefully

• Arthrofibrosis after THA is rare compared to TKA; the most common cause of restricted motion after THA is heterotopic ossification (HO) rather than soft tissue fibrosis; HO (ectopic bone formation in the periarticular soft tissues) occurs in approximately 5–15% of THA cases; significant HO restricts hip flexion and abduction; prophylaxis — indomethacin 25 mg TDS for 6 weeks, or single-fraction radiotherapy (7 Gy within 72 hours of surgery); established significant HO causing functional limitation — surgical excision (after the HO has matured on bone scan — typically 12–18 months); excision before maturity leads to recurrence

• Arthrofibrosis after TKA: 1–5% incidence; excessive fibroproliferative response; TGF-β + myofibroblast activation → dense scar; restricted flexion (target >90°) and/or extension deficit
• Strongest risk factor: pre-operative poor ROM (<90° flexion predicts post-operative stiffness); tight pre-op knee = tight post-op knee
• Prevention: multimodal analgesia enabling early physiotherapy (flexion >90° day 0–1); correct component position (femoral external rotation 3° from PC axis); balanced flexion-extension gaps; exclude PJI in any acutely stiff TKA
• Infrapatellar contracture syndrome (IPCS): fat pad contracture → patella baja (Insall-Salvati <0.8); anterior knee pain; restricted flexion; specific form of arthrofibrosis after TKA
• MUA window: 6 weeks – 3 months post-TKA; general/regional anaesthesia; forcible gentle sustained flexion (not sharp jerk); complications — PT avulsion, patellar fracture, periprosthetic fracture; commence CPM + physio immediately after MUA
• Arthroscopic arthrolysis: for failed MUA or stiffness >3–6 months; posterior capsule release + parapatellar gutter clearance; more precise than MUA; CPM immediately post-op
• Revision for stiffness: only if component malposition proven (CT with MARS confirms internal rotation); revision for stiffness alone rarely effective; high complication rate
• CPM: passive flexion-extension machine; Cochrane reviews — no consistent benefit over standard physiotherapy for final ROM; not routinely recommended by most guidelines
• HO after THA (not TKA): 5–15%; restricts hip flexion/abduction; prophylaxis — indomethacin 6 weeks or 7 Gy single-fraction RT; excision after maturity (12–18 months) on bone scan; early excision = recurrence
• Femoral component malrotation → stiffness: internal rotation of femoral component → tight flexion gap → post-op stiffness; confirm on CT (transepicondylar axis reference); revision required if confirmed