Knee Dislocation — Vascular Workup

Knee dislocation is a high-energy injury that disrupts multiple ligamentous structures of the knee and carries a significant risk of associated popliteal artery injury (7–35% of all knee dislocations) and peroneal nerve injury (10–40%). Despite its severity, the diagnosis is frequently missed — up to 50% of knee dislocations spontaneously reduce before clinical assessment, and a reduced knee dislocation may appear deceptively normal on plain radiograph. The primary concern following knee dislocation is vascular injury — an unrecognised or delayed popliteal artery injury leads to limb ischaemia, and delays beyond 6–8 hours significantly increase the risk of amputation.

• Mechanism: high-energy (road traffic accidents, falls from height, sporting injuries — particularly hyperextension and contact sports); ultra-low velocity dislocations are increasingly recognised in morbidly obese patients from trivial mechanisms (rising from a chair, low falls) — these carry the SAME risk of vascular injury as high-energy dislocations and must not be underestimated; the combination of high BMI and knee size creates the same force vectors across the popliteal vessels
• Classification (Kennedy): anterior (most common — ~40%; hyperextension mechanism; the tibia dislocates anteriorly relative to the femur; most likely to cause popliteal artery stretch or avulsion injury); posterior (~33%; dashboard mechanism — axial force on the flexed knee; the tibia displaces posteriorly); lateral (~18%); medial (~4%); rotatory (<5% — subluxation with rotational component; `irreducible` due to button-holing of femoral condyle through the capsule); Anterior KD carries the highest popliteal artery injury rate due to the tethering of the artery at the popliteal fossa during hyperextension
• Ligament injuries: true knee dislocation requires disruption of BOTH the ACL AND the PCL (bicruciate injury); additional disruption of the medial collateral ligament (MCL), lateral collateral ligament (LCL), posterolateral corner (PLC — popliteofibular ligament, popliteus tendon), and posteromedial corner (PMC) may occur; the Schenck classification grades knee dislocations by the ligament pattern (KDI–KDIV); the full ligament inventory must be assessed once vascular status is secured

• Popliteal artery anatomy — why it is at risk: the popliteal artery is tethered at two points — proximally at the adductor hiatus (where it emerges from the femoral triangle) and distally as it passes through the fibrous arch of the soleus to become the anterior and posterior tibial arteries; these two fixation points mean that when the knee dislocates, the artery is stretched and cannot move with the displaced tibia; anterior dislocation is particularly dangerous because the tibia moves anteriorly and levers the popliteal artery over the back of the femoral condyle — causing intimal tear, thrombosis, or complete transection
• Types of vascular injury: (1) Intimal tear — the inner lining of the artery is disrupted; the limb may appear well-perfused initially (the artery is patent), but progressive thrombosis develops over hours; initial vascular assessment may appear NORMAL — this is the most dangerous scenario as the clinician may be falsely reassured; (2) Complete transaction or occlusion — limb is immediately ischaemic; easy to diagnose clinically; (3) Intimal flap — acts as a valve that occludes blood flow distally; may be missed on initial Doppler assessment
• Hard signs of vascular injury (immediate vascular surgery involvement): absent or markedly diminished distal pulses; expanding pulsatile haematoma; pulsatile haemorrhage; audible bruit over the popliteal fossa; distal limb ischaemia — the 6 Ps: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold (poikilothermia); presence of ANY hard sign = immediate vascular surgery consultation and operative exploration WITHOUT waiting for CT angiography (time is limb)
• Ankle-Brachial Index (ABI) — the cornerstone of vascular assessment: the ABI (also called the Ankle-Brachial Pressure Index — ABPI) is measured by comparing the systolic blood pressure at the ankle (using a Doppler probe over the posterior tibial or dorsalis pedis artery) to the systolic blood pressure in the arm (brachial artery); ABI = ankle systolic BP / brachial systolic BP; NORMAL ABI = 1.0 ± 0.1; ABI <0.9 = abnormal; ABI <0.9 after knee dislocation = significant vascular injury until proven otherwise and requires urgent CT angiography; ABI ≥0.9 with no hard signs = serial clinical monitoring (ABI re-measured at 2–4 hourly intervals for 24 hours); the major limitation of ABI is that it may be normal (>0.9) in the presence of an intimal tear (which will later thrombose)

• Common peroneal nerve (CPN) injury: occurs in 10–40% of knee dislocations; the CPN wraps around the fibular neck and is tethered here — making it particularly susceptible to traction injury when the knee dislocates posterolaterally or laterally; CPN injury causes foot drop (weakness of dorsiflexion and eversion), loss of sensation over the dorsum of the foot and first web space; the CPN is injured by traction (neuropraxia or axonotmesis) rather than sharp transection — complete recovery in 30–50%; surgical decompression or repair is indicated for complete nerve transection discovered at the time of vascular surgery; nerve exploration and repair if no recovery at 3–6 months
• Assessment: test dorsiflexion strength (tibialis anterior, EHL), eversion (peroneus longus/brevis), toe extension; test sensation on the dorsum of the foot; document pre- and post-reduction neurological status; improvement after reduction may indicate traction neuropraxia

• Reduction: immediate closed reduction under procedural sedation (ED) or GA; counter-traction on the thigh + longitudinal traction on the leg + gentle correction of the displacement; for anterior dislocation — flex the knee while applying posterior pressure to the tibia; assess stability after reduction; document neurovascular status before and after reduction; post-reduction X-rays confirm reduction; do NOT manipulate if there are hard vascular signs — proceed directly to OR; `irreducible` dislocation (posterolateral rotatory — femoral condyle through capsule) requires urgent surgical open reduction
• Acute stabilisation: after reduction, the knee is placed in a long leg backslab or brace in approximately 15–20° of flexion; spanning external fixator (ExFix) is applied if the knee is grossly unstable, if vascular repair has been performed (protects the repair), or if the patient requires multiple theatre trips; the ExFix stabilises the knee, protects vascular and nerve repairs, and allows wound and soft tissue management; definitive ligament reconstruction is deferred for 3–6 weeks to allow acute swelling to settle

• Knee dislocation: bicruciate (ACL + PCL) injury mandatory for true dislocation; popliteal artery injury in 7–35%; peroneal nerve injury in 10–40%; 50% self-reduce before assessment — a `reduced` knee with bicruciate disruption on MRI = knee dislocation until proven otherwise
• Popliteal artery tethering: fixed at adductor hiatus proximally and soleus arch distally; anterior dislocation = highest arterial injury risk (artery levered over femoral condyle); intimal tear may present with normal pulses initially → delayed thrombosis → late ischaemia
• Hard signs of vascular injury: absent pulses, ischaemia (6 Ps), expanding haematoma, pulsatile haemorrhage, bruit → immediate vascular surgery, no waiting for CTA; ischaemia time <6–8 hours → amputation risk rises dramatically after 8 hours
• ABI: normal ≥0.9; ABI <0.9 after knee dislocation = urgent CTA; ABI ≥0.9 = serial monitoring every 2–4 hours for 24 hours; ABI can be FALSELY NORMAL with intimal tear (delayed thrombosis risk)
• Liberal CTA policy: many centres now perform CTA for ALL knee dislocations regardless of ABI; the risk of missed intimal injury (leading to delayed thrombosis and amputation) outweighs CTA risks; widely adopted at major trauma centres
• Sequence for vascular injury + knee dislocation: (1) reduce the knee (may restore perfusion); (2) temporary ExFix for stabilisation; (3) temporary intravascular shunt if ischaemia confirmed; (4) definitive vascular repair (bypass); (5) fasciotomy of the leg (4-compartment) prophylactically after revascularisation
• CPN injury: 10–40%; tethered at fibular neck; foot drop + dorsal foot anaesthesia; mostly neuropraxia/axonotmesis — 30–50% recovery; surgical exploration at 3–6 months if no recovery; AFO (ankle-foot orthosis) for foot drop
• Irreducible dislocation: posterolateral rotatory — femoral condyle buttons through the anteromedial capsule; `dimple sign` = skin puckering medially; requires open surgical reduction; do NOT force closed reduction — risk of neurovascular injury
• Morbidly obese patients: ultra-low velocity knee dislocation from trivial injury; SAME vascular risk as high-energy dislocation; do NOT underestimate due to mechanism; full vascular workup mandatory