Applied Lower Limb Anatomy

Common in elderly osteoporotic patients after a low-energy fall; classified as intracapsular (subcapital, transcervical) or extracapsular (intertrochanteric, subtrochanteric).

• Intracapsular, displaced fractures disrupt the retinacular vessels (medial circumflex femoral artery branches) running along the neck, threatening femoral head viability.
• Classic presentation: shortened, externally rotated limb.

• Posterior dislocation (~90%) typically from a high-energy axial force through a flexed hip/knee (classic dashboard injury); limb appears shortened, flexed, adducted, internally rotated.
• Risks the sciatic nerve and disrupts the posterior retinacular blood supply.
• Anterior dislocation is rarer; limb appears abducted and externally rotated.

• Follows disruption of the retinacular blood supply, most commonly after displaced intracapsular femoral neck fracture or hip dislocation.
• Femoral head collapse may occur months to years later, given delayed ischaemic bone death and subsequent structural failure.
• Other causes include corticosteroid use, alcohol excess, and sickle cell disease, all via microvascular compromise of the same retinacular supply.

• Tests gluteus medius/minimus function (superior gluteal nerve).
• On single-limb stance on the affected side, the contralateral pelvis drops due to failed pelvic stabilisation, a positive sign.
• Causes include superior gluteal nerve injury, hip abductor tear, and chronic hip pathology.

• Occurs with poorly placed intramuscular injections placed too high/medial, or during the anterolateral (Hardinge) approach to hip surgery.
• Paralyses gluteus medius, minimus, and tensor fasciae latae.
• Produces the Trendelenburg gait: a compensatory trunk lean toward the affected side.

• Vulnerable to posterior hip dislocation, pelvic fracture, misplaced gluteal injection, and piriformis entrapment.
• Complete lesions cause loss of knee flexion and total motor/sensory loss below the knee, sparing only the medial strip supplied by the saphenous nerve.
• The safe IM injection zone (upper outer quadrant of the buttock) exists specifically to avoid this nerve.

• Occurs with pelvic/retroperitoneal haematoma (psoas compartment), hip surgery, prolonged lithotomy positioning, or diabetic femoral neuropathy.
• Causes weak knee extension (quadriceps) and an absent patellar reflex.
• Functionally significant given the reliance on quadriceps for standing, walking, and stair climbing.

• Vulnerable during pelvic surgery (especially gynaecological/lymph node dissection near the pelvic sidewall) and obturator hernia entrapment.
• Causes weak hip adduction, often with minimal functional impact in isolation.
• The nerve's dual hip/knee joint innervation explains referred knee pain from hip pathology.

• Herniation through the femoral canal, below the inguinal ligament and lateral to the pubic tubercle.
• The canal's rigid boundaries (inguinal, lacunar, and pectineal ligaments, femoral vein) give it a narrow, unforgiving neck, carrying a high risk of strangulation.
• More common in women, related to a wider pelvis and femoral canal dimensions.

• Raised pressure within a closed fascial compartment (most classically the anterior leg compartment) exceeds capillary perfusion pressure.
• Follows fractures, crush injury, or reperfusion after vascular repair; the tibia's subcutaneous position and the leg's tight fascial boundaries make this region particularly vulnerable.
• Pain out of proportion to injury and pain on passive stretch are cardinal features; a surgical emergency requiring fasciotomy.

• Common in sports with sudden deceleration, pivoting, or landing: classically a non-contact mechanism.
• Produces anterior tibial instability, tested by the anterior drawer and Lachman tests.
• Often accompanied by rapid haemarthrosis from the rich synovial vascularity surrounding the (poorly vascularised) ligament itself.

• Classic mechanism: direct blow to the anterior tibia with the knee flexed (dashboard injury) or hyperflexion.
• Produces posterior tibial instability, tested by the posterior drawer test and posterior tibial sag.
• Generally better intrinsic healing potential than the ACL, given greater size and vascularity.

• Typically from a twisting force on a flexed, weight-bearing knee.
• Medial meniscus is more commonly injured, due to its firm MCL attachment and reduced mobility.
• Peripheral ("red zone") tears have better healing potential than central ("white zone," avascular) tears.

• Vulnerable at the fibular neck, where it lies directly subcutaneous against bone.
• Causes include fibular neck fracture, prolonged compression (leg crossing, tight casts, lithotomy positioning), and penetrating trauma.
• Produces combined loss of dorsiflexion and eversion (foot drop), since both deep and superficial fibular territories are affected before the common trunk divides.

• Results from common fibular nerve injury (most common cause) or, less commonly, sciatic nerve injury or L5 radiculopathy.
• Loss of dorsiflexion causes the foot to catch during swing phase, compensated by a steppage gait (exaggerated hip/knee flexion).
• Distinguishing a peripheral nerve lesion from L5 radiculopathy: an isolated common fibular lesion spares hip abduction (gluteus medius), while an L5 lesion often weakens it too.

• Vulnerable in the popliteal fossa (where it is the most superficial structure) and within the tarsal tunnel.
• Causes loss of plantarflexion and toe flexion, with an absent Achilles reflex.
• Sensory loss over the sole and heel is functionally significant, predisposing to unnoticed plantar trauma/ulceration.

• Compression of the tibial nerve within the tarsal tunnel, posterior to the medial malleolus, beneath the flexor retinaculum.
• Causes include space-occupying lesions, tenosynovitis, and ankle deformity altering tunnel geometry.
• Produces sensory symptoms and pain in the sole/heel, with a positive Tinel sign over the tunnel, the lower-limb analogue of carpal tunnel syndrome.

• Most commonly an inversion injury with the foot plantarflexed, injuring the lateral ligament complex.
• Order of injury frequency: ATFL > CFL > PTFL: ATFL is taut in this position and fails first.
• The stronger medial (deltoid) ligament means eversion injuries more often fracture the fibula before the ligament itself fails.

• Typically occurs during forceful, eccentric loading of a plantarflexed ankle (e.g., pushing off during sprinting or jumping) in middle-aged, intermittently active individuals ("weekend warriors").
• The tendon has a relative watershed zone of poor vascularity approximately 2–6 cm above its calcaneal insertion, predisposing to rupture at this level.
• Presents with sudden posterior calf pain, a palpable gap, and a positive Simmonds-Thompson (calf squeeze) test: absent plantarflexion on calf compression.

• Chronic microtears and degeneration at the calcaneal origin of the plantar aponeurosis, from repetitive tensile overload.
• Associated with the windlass mechanism: pain classically worst with the first steps in the morning or after rest, as the fascia is re-stretched.
• Risk factors include prolonged standing, obesity, and abnormal foot biomechanics affecting arch support (both flat and high-arched feet can predispose).

• Loss or reduction of the medial longitudinal arch, which normally rests on the calcaneus posteriorly and the metatarsal heads anteriorly, supported by the plantar aponeurosis, spring (plantar calcaneonavicular) ligament, and tibialis posterior tendon.
• Can be flexible (arch restores on tiptoe/non-weight-bearing, common and often asymptomatic, especially in children) or rigid (structural, may indicate tarsal coalition or other pathology).
• Tibialis posterior tendon dysfunction is a common acquired cause in adults, given its key role supporting the arch.

• Abnormally elevated longitudinal arch, reducing the foot's normal shock-absorbing flexibility.
• Can be idiopathic or associated with underlying neuromuscular conditions (e.g., Charcot-Marie-Tooth disease, spina bifida) affecting the balance of intrinsic/extrinsic muscle forces on the arch.
• Predisposes to excessive lateral foot loading, ankle instability, and metatarsalgia.

• The great saphenous vein at the ankle, anterior to the medial malleolus, is a classic, reliable site for emergency venous cutdown, given its consistent anatomical position even when collapsed (e.g., hypovolaemic shock).
• Its long, relatively straight course also makes it a common site for harvesting as a bypass conduit (e.g., coronary artery bypass grafting) and for varicose vein intervention.
• The vein's proximity to the saphenous nerve at the ankle means procedures here carry a risk of nerve injury/numbness.

• Dilated, tortuous superficial veins, most often involving the great saphenous vein and its tributaries, from valvular incompetence.
• Saphenofemoral junction incompetence is a common underlying cause, allowing reflux down the entire length of the vein.
• Risk factors include prolonged standing, pregnancy, obesity, and a family history of venous insufficiency.

• Deep vein thrombosis most commonly originates in the calf deep veins (soleal sinuses classically), where blood flow stasis is greatest.
• Can propagate proximally into the popliteal and femoral veins: proximal (above-knee) propagation carries the greatest pulmonary embolism risk, given larger vessel calibre and clot burden.
• Follows Virchow's triad (stasis, hypercoagulability, endothelial injury), immobility, surgery, malignancy, and pregnancy are classic risk factors.