3.3 Total Knee Arthroplasty (TKA): Indications, Implant Designs & Surgical Techniques

Surgical Indications: UKA vs. Tricompartmental TKA

Total Knee Arthroplasty (TKA) is indicated for severe, end-stage degenerative, post-traumatic, or inflammatory arthritis of the knee refractory to at least 3 to 6 months of comprehensive conservative interventions (including physical therapy, weight loss, NSAIDs, intra-articular corticosteroid, or viscosupplementation injections). Preoperative radiographic evaluation typically demonstrates Kellgren-Lawrence Grade 3 or 4 changes: complete joint space narrowing, subchondral sclerosis, subchondral cysts, and osteophyte formation across one or more anatomical compartments (medial tibiofemoral, lateral tibiofemoral, and patellofemoral).

                      ARTHROPLASTY SELECTION ALGORITHM

    [End-Stage Knee Arthritis]
                |
    +-----------+-----------+
    |                       |
    v                       v
[Isolated Single-Compartment OA]      [Multi-Compartment / Inflammatory OA]
- Intact ACL                          - Incompetent ACL / PCL
- Fixed flexion contracture <10-15°   - Fixed deformity >10° varus / >5° valgus
- Varus <10°, Valgus <5°              - Inflammatory arthritis (RA, Gout)
- Non-inflammatory etiology           - Severe patellofemoral bone loss
    |                                       |
    v                                       v
[Unicompartmental Arthroplasty (UKA)]  [Total Knee Arthroplasty (TKA)]

Unicompartmental Knee Arthroplasty (UKA / Partial Knee)

UKA involves resurfacing only the damaged single compartment of the knee—most frequently the medial tibiofemoral compartment (85%–90%), followed by the lateral tibiofemoral compartment (10%–15%), or isolated patellofemoral joint.

• Strict Indications & Selection Criteria:
  1. End-stage osteoarthritis or avascular necrosis strictly confined to a single compartment.
  2. Intact, functional Anterior Cruciate Ligament (ACL): Without an intact ACL, the tibia subluxates anteriorly during flexion, loading the posterior tibial plateau and causing rapid wear and loosening of the unicompartmental implant.
  3. Correctable, non-fixed angular deformities: Varus deformity <10 degrees or valgus deformity <5 degrees.
  4. Flexion contracture <10 to 15 degrees and pre-existing range of motion of at least 90 degrees.
• Absolute Contraindications to UKA:
  • Inflammatory arthropathy (e.g., Rheumatoid Arthritis, Psoriatic Arthritis, Lupus, Gout)—the autoimmune process invariably attacks the retained compartments.
  • ACL insufficiency or incompetence.
  • Significant arthritic degeneration in the contralateral tibiofemoral or severe bone-on-bone patellofemoral compartment with facet tracking loss.
  • Fixed, uncorrectable varus/valgus deformity.
• Clinical Advantages: Preserves both cruciate ligaments (ACL and PCL) and native joint proprioception, smaller surgical exposure, reduced blood loss, faster functional recovery, lower postoperative infection rate, and kinematics that more closely replicate a "natural knee."

Implant Constraint Hierarchy and Kinematics

TKA implants are engineered across a spectrum of mechanical constraint. As implant constraint increases, more rotational and shear forces are transferred away from the soft tissues directly onto the bone-implant cement interface, increasing the long-term risk of aseptic loosening. Orthopaedic surgeons adhere to the core biomechanical principle: use the least constrained implant that provides absolute joint stability.

                      SPECTRUM OF TKA IMPLANT CONSTRAINT

    Low Constraint -----------------------------------------> High Constraint
    [Cruciate-Retaining]  [Posterior-Stabilized]  [Constrained Condylar]  [Rotating Hinge]
    (Retains PCL)         (Cam-and-Post for PCL)  (Varus/Valgus stability) (Linked central axle)

1. Cruciate-Retaining (CR) Implants

• Mechanism: Retains the patient's native Posterior Cruciate Ligament (PCL). The femoral component features an open, shallow intercondylar groove, and the tibial polyethylene insert has a gentle posterior slope and low anterior lip.
• Biomechanical Function: The retained PCL drives physiological femoral rollback (the femur rolls posteriorly on the tibial plateau during flexion), preventing anterior impingement and maximizing flexion clearance.
• Prerequisites: Requires a structurally intact, competent, well-balanced PCL and minimal baseline coronal deformity.

2. Posterior-Stabilized (PS) Implants

• Mechanism: The native PCL is sacrificed (resected). A tibial polyethylene post (spine) projects upward into an engineered femoral cam box.
• Biomechanical Function: As the knee flexes past 60°, the femoral transverse cam engages the tibial spine, mechanically forcing the femur to roll backward on the tibia, substituting for the PCL.
• Indications: Deficient, ruptured, or attenuated PCL; inflammatory arthritis; prior patellectomy; severe fixed flexion contractures (>15°–20°); or marked preoperative varus/valgus deformities requiring extensive ligamentous release.

3. Constrained Condylar Knee (CCK / Non-Hinged Constrained)

• Mechanism: Features a significantly taller, broader, rectangular tibial polyethylene post that fits snugly inside a deep, reinforced femoral housing box.
• Biomechanical Function: Restricts varus-valgus tilting and axial rotation, providing mechanical coronal stability when collateral ligaments are compromised.
• Indications: Severe collateral ligament deficiency or attenuation (e.g., severe valgus knee with stretched, incompetent medial collateral ligament [MCL]), marked flexion-extension gap mismatch, or substantial bone loss during revision surgery.

4. Hinged Knee Implants (Rotating Hinge Prostheses)

• Mechanism: The femoral and tibial components are physically linked together by a central metallic rotating axle or hinge pin mechanism.
• Biomechanical Function: Provides complete, absolute stability against varus, valgus, and anteroposterior translation while allowing axial rotation to dissipate torsional stresses.
• Indications: Gross multidirectional instability with complete loss of both collateral ligaments (MCL and LCL); catastrophic bone defect/loss (oncologic resections or massive revision bone loss); severe neuromuscular conditions (e.g., neuropathic Charcot arthropathy, polio, severe post-stroke flaccidity).

Pneumatic Tourniquet Kinetics and Tranexamic Acid (TXA) Protocols

Intraoperative blood management and field visualization during TKA heavily rely on pneumatic thigh tourniquets and antifibrinolytic pharmacotherapy.

Tourniquet Physiology, Pressure Limits, and Reperfusion Kinetics

A pneumatic tourniquet is applied around the proximal operative thigh over protective cast padding:

                      TOURNIQUET SAFETY & KINETICS TIMELINE

    [Inflation Phase: 0 - 90 min]            [Critical Threshold: 120 min]     [Deflation / Reperfusion]
    - Pressure: SBP + 100-150 mmHg           - Mandatory 15-20 min holiday     - Sudden drop in SVR & MAP
    - Cellular hypoxia & anaerobic           - Risk: Post-tourniquet syndrome, - Spike in end-tidal CO2
      metabolism (lactic acid, K+)             permanent nerve palsy & rhabdo  - Transient metabolic acidosis

• Pressure Settings: Pressure should be calibrated to the minimum effective pressure required to occlude arterial inflow, typically 100 to 150 mmHg above the patient's baseline systolic blood pressure (or calculated via automated Limb Occlusion Pressure [LOP] sensors; usually 200–250 mmHg in adults).
• Ischemia Time Thresholds:
  • Continuous tourniquet inflation time must never exceed 120 minutes (2 hours); current best practice targets <90 minutes.
  • If surgical time exceeds 120 minutes, the tourniquet must be completely deflated for a minimum 15 to 20-minute "breathing period" (tourniquet holiday) to allow tissue reperfusion and cellular oxygenation before re-inflation.
  • Prolonged tourniquet times (>120 minutes) induce severe tissue ischemia, rhabdomyolysis with myoglobinuria, compressive neuropathy of the femoral/sciatic nerves, and post-tourniquet syndrome (characterized by severe postoperative limb edema, stiffness, pallor, and delayed quadriceps recovery).
• Reperfusion Kinetics (Tourniquet Deflation Dynamics):
  • Deflating the tourniquet washes accumulated anaerobic metabolites (lactic acid, potassium, hydrogen ions, carbon dioxide) into the systemic venous circulation.
  • Systemic Hemodynamic Response: Rapid vasodilation causes a transient drop in systemic vascular resistance (SVR) and mean arterial pressure (MAP; reperfusion hypotension), a transient spike in end-tidal CO2 (EtCO2) on capnography, and a mild, transient metabolic acidosis. The perioperative nurse must anticipate these hemodynamic shifts and ensure adequate volume resuscitation.

Tranexamic Acid (TXA) Antifibrinolytic Protocols

Tranexamic Acid (TXA) is a synthetic lysine analogue that revolutionized blood conservation in total joint arthroplasty:

                       TRANEXAMIC ACID (TXA) MECHANISM

    [Tissue Trauma & Surgical Fibrinolysis]
                     |
    [Plasminogen] ===(Blocked by TXA binding to lysine sites)===> [Plasmin]
                     |
    [Fibrin Clot Breakdown Prevented]  ---> [Preserved Clot Stability & Hemostasis]

• Mechanism of Action: TXA competitively blocks the lysine-binding sites on plasminogen molecules, preventing plasminogen from binding to fibrin and converting into active plasmin. By inhibiting fibrinolysis, TXA stabilizes existing physiological blood clots at the surgical site.
• Dosing Protocols:
  • Intravenous (IV) Administration: Typically 1 g (or 10–15 mg/kg) IV administered within 15 to 30 minutes prior to surgical incision / tourniquet inflation, followed by a second 1 g IV dose during wound closure or 3 to 6 hours postoperatively.
  • Topical / Intra-Articular Administration: 1 to 3 g of TXA diluted in 50 to 100 mL of normal saline instilled directly into the joint cavity prior to wound closure and allowed to dwell (often with drain clamped for 1–2 hours if a drain is used).
  • Combined / Oral Routes: Oral TXA (1,950 mg PO preoperatively) demonstrates equivalent clinical efficacy to IV formulations.
• Efficacy and Safety: High-level evidence confirms TXA reduces perioperative blood loss by 300 to 600 mL and decreases allogeneic blood transfusion rates from >20% to <2%, without increasing the risk of Deep Vein Thrombosis (DVT), Pulmonary Embolism (PE), ischemic stroke, or myocardial infarction in standard-risk patients.
• Relative Precautions: Active thromboembolic disease (acute DVT/PE within 3–6 months), active coronary stent thrombosis, severe subarachnoid hemorrhage, or severe chronic kidney disease (requires renal dose adjustments).