Multi-ligament Knee Injury

Multi-ligament knee injury (MLKI) represents one of the most complex and potentially limb-threatening injuries in orthopaedics. It involves disruption of two or more major ligamentous complexes of the knee and often implies true or spontaneously reduced knee dislocation. The priorities of management are: identify and treat vascular injury, assess neurological status, and plan timely ligamentous reconstruction to restore knee stability and prevent long-term arthritis.

• Knee dislocation (KD) may be defined as displacement of the tibiofemoral joint requiring disruption of at least two major ligamentous complexes; spontaneous reduction before assessment is common and underrepresentation in the literature means the true incidence is unknown
• Schenck classification of knee dislocation: KD I — one cruciate torn + collateral intact; KD II — both cruciates torn, collaterals intact; KD III — both cruciates + one collateral (KD IIIM medial, KD IIIL lateral); KD IV — all four ligaments torn; KD V — fracture-dislocation; the most common pattern is KD III and KD IV
• Mechanisms: high-energy (motor vehicle collision, pedestrian vs vehicle, fall from height, sports); low-energy dislocation increasingly recognised in obese patients (BMI-related knee dislocation) — may occur with a simple fall or twist
• Popliteal artery injury: the most feared complication of knee dislocation — occurs in 20–40% of true dislocations; the popliteal artery is tethered proximally at the adductor hiatus and distally at the soleus arch, rendering it vulnerable to traction injury in tibial displacement; intimal tear (not always apparent externally) can thrombose and cause limb ischaemia hours after reduction; time to revascularisation <6 hours is critical to limb salvage
• Common peroneal nerve injury: 16–40% of knee dislocations; most commonly from posterolateral corner (PLC) disruption; often a traction neuropraxia; recovery is unpredictable; complete motor and sensory loss at presentation warrants MRI nerve assessment

• Immediate management: gentle reduction under sedation if dislocated; splint after reduction; assess distal neurovascular status before and after reduction; document pulse character, capillary refill, Doppler signals, and neurological examination before any further management
• Ankle-brachial index (ABI): measured after reduction; normal ABI ≥0.9; ABI <0.9 = significant vascular injury — proceed to CT angiography urgently; hard signs of vascular injury (absent pulse, expanding haematoma, bruit, pulsatile bleeding, distal ischaemia) mandate immediate vascular surgical referral without waiting for ABI
• Serial vascular assessment: even with normal ABI at presentation, the risk of delayed intimal tear thrombosis means that serial vascular assessment every 4–6 hours for 24–48 hours is recommended; any deterioration = CT angiography
• CT angiography vs conventional angiography: CT angiography (CTA) is now the investigation of choice — fast, widely available, high sensitivity and specificity; conventional angiography reserved for cases requiring intervention (endovascular stenting or open vascular repair)
• Fasciotomy: four-compartment lower leg fasciotomy performed at the time of vascular repair to prevent compartment syndrome from ischaemia-reperfusion injury; also indicated prophylactically in prolonged ischaemia time
• Limb salvage: revascularisation within 6 hours is the key determinant of limb salvage; amputation rate increases significantly with prolonged ischaemia; early vascular surgery involvement is mandatory in all suspected vascular injuries

• Common peroneal nerve (CPN): assess ankle dorsiflexion (deep peroneal — L4/5), foot eversion (superficial peroneal — L5/S1), and sensation over the dorsum of the foot and first web space; CPN most commonly injured in PLC disruption (stretch injury at the fibular neck)
• CPN injury management: expectant management with serial neurological examination; splinting in the neutral position (ankle-foot orthosis, AFO) to prevent equinus contracture; EMG/NCS at 6 weeks to assess severity; recovery of neuropraxia typically within 3 months; axonotmesis may take 12–18 months; neurotmesis (complete disruption) — poor prognosis for spontaneous recovery; exploration and nerve grafting considered for complete lesions not recovering
• Tibial nerve: less commonly injured; assess plantar flexion and intrinsic foot muscles; injury associated with worse prognosis than CPN

• Clinical examination: full ligamentous assessment under adequate analgesia; Lachman (ACL), posterior drawer and posterior sag (PCL), valgus stress 0° and 30° (MCL and PMC), varus stress 0° and 30° (LCL and PLC), reverse pivot shift (PLC), dial test (PLC)
• Dial test (tibial external rotation test): performed at 30° and 90° of knee flexion; examiner externally rotates both feet simultaneously and compares external rotation bilaterally; >10° side-to-side difference at 30° but not 90° = isolated PLC injury; >10° difference at both 30° and 90° = combined PCL + PLC injury
• MRI knee: essential after neurovascular clearance; documents all ligamentous injuries; assesses menisci and articular cartilage; guides surgical planning; whole-leg alignment assessment (standing long-leg X-ray) important — pre-existing or injury-related malalignment affects ligament reconstruction planning
• Standing long-leg alignment X-ray: assess mechanical axis deviation; significant varus malalignment must be corrected (HTO) before or simultaneously with LCL/PLC reconstruction — lateral side reconstruction fails in a varus knee

• Temporary external fixation: used when soft tissue swelling and wound conditions prevent immediate definitive surgery; stabilises the knee after reduction; allows time for vascular repair, skin monitoring, and swelling to reduce before ligamentous reconstruction; spanning external fixator across the knee in slight flexion is standard

• PLC reconstruction (Laprade technique): figure-of-eight graft around the fibular head recreating the FCL and popliteofibular ligament; a separate limb can reconstruct the popliteus tendon if required; fibular head is the key landmark; graft tensioned and fixed at 20–30° of knee flexion with internal rotation of the tibia (neutral rotation); primary repair acceptable in acute injuries within 2–3 weeks
• PCL reconstruction in MLKI: single-bundle AL reconstruction or double-bundle; tibial inlay technique avoids the "killer turn"; tensioned at 70–90° of flexion with an anterior tibial force applied; most critical: do not overtighten the PCL (limits flexion)
• ACL reconstruction: standard anatomical single-bundle technique; BPTB or hamstring; tensioned and fixed at 30° of flexion with tibia in neutral
• Order of fixation in combined reconstruction: PCL first (fixes posterior tibial translation), then PLC (fixes rotational and varus laxity), then ACL last (fixes residual anterior translation); this sequence avoids overtensioning one structure while another is slack
• Allografts: commonly used in MLKI reconstruction when multiple grafts are required and autograft supply is limited; acceptable in this context — the overall injury severity and recovery time outweigh the graft biological properties argument; reduces total autograft harvest morbidity

• Obesity-related knee dislocation: low-energy knee dislocation in morbidly obese patients is increasingly common; the clinical examination may be unreliable due to body habitus; vascular injury risk is comparable to high-energy dislocation; skin condition (ulceration, poor healing) may preclude early surgery; temporary external fixation and staged reconstruction after weight optimisation or bariatric surgery may be the best strategy; all patients require ABI assessment regardless of energy of injury
• Varus malalignment and PLC reconstruction failure: PLC reconstruction in a varus knee will fail — the varus moment arm places the lateral structures under constant tension; a high tibial osteotomy (HTO — valgus producing) should be performed either simultaneously with or before PLC reconstruction to unload the lateral side; failure to address malalignment is the most common cause of PLC reconstruction failure
• Arthrofibrosis after MLKI: the single most common complication after MLKI surgery; risk factors include early reconstruction (before ROM has recovered), prolonged immobilisation, excessive bleeding, and infection; prevention: delay definitive ligament reconstruction until ROM is improving (ideally close to full extension and at least 90° flexion); post-operative continuous passive motion and early physiotherapy; manipulation under anaesthesia (MUA) if stiffness develops at 6–12 weeks; arthroscopic lysis of adhesions for established arthrofibrosis
• Long-term outcomes of MLKI: even with optimal management, MLKI has high rates of residual laxity, stiffness, and OA; approximately 50% of patients return to pre-injury sport level; OA prevalence at 10–15 years is approximately 50–75%; meniscal and chondral injury at the time of dislocation are the primary drivers; prophylactic meniscal preservation is essential

• Schenck classification: KD I (one cruciate); KD II (both cruciates); KD III (both cruciates + one collateral — M or L); KD IV (all four); KD V (fracture-dislocation)
• Popliteal artery injury: 20–40% of knee dislocations; intimal tear can thrombose hours later; revascularisation within 6 hours critical
• ABI <0.9 after reduction → CT angiography urgently; hard signs of vascular injury → immediate vascular surgery without waiting for ABI
• CPN injury: 16–40%; AFO to prevent equinus; serial EMG/NCS; recovery unpredictable
• Dial test: >10° at 30° only = isolated PLC; >10° at both 30° and 90° = combined PCL + PLC
• PLC must be repaired within 2–3 weeks — delay causes retraction; primary repair not possible after this
• Order of graft fixation: PCL first → PLC → ACL last
• Varus knee + PLC injury: HTO required before or with PLC reconstruction; failure to correct varus = PLC reconstruction failure
• Arthrofibrosis: most common complication; prevent by delaying surgery until ROM recovering; early post-op physio essential
• Low-energy obesity-related KD: increasing incidence; equal vascular risk; ABI mandatory regardless of energy