Major static stabilizers: superficial MCL, deep MCL, and posterior oblique ligament.

Dynamic stabilizers: pes anserinus, semimembranosus, medial head of the gastrocnemius, and vastus medialis.

These structures can be divided into three layers:

Layers II and III conjoin posteriorly to form the posteromedial corner.

The posterior oblique ligament runs from the adductor tubercle of the femur to the tibia and posterior capsule.

The MCL is supplied by the superior medial and inferior medial geniculate arteries.

Separated in three layers:

PLC is made up of the LCL, popliteus tendon, popliteofibular ligament, lateral capsule, arcuate ligament, and the fabellofibular ligament.

The LCL originates on the lateral femoral condyle, proximal and posterior to the popliteus insertion, and inserts on the anterolateral fibular head:

The primary function of the LCL is resisting varus stress with a secondary role of resisting posterolateral rotation when the knee is in less than 50° of flexion.

Because its axis is behind that of the knee axis, it is tight in extension and lax in flexion.

The blood supply is via the superolateral and inferolateral geniculate arteries.

The MCL is a valgus stabilizer.

Commonly injured when the knee is forced into valgus and external rotation.

Commonly seen in combined injuries with the anterior cruciate ligament (ACL) and meniscus.

Usually a direct blow to the lateral knee leads to a more severe injury compared with a noncontact injury.

Rupture more commonly occurs at the femoral insertion which is also the location where the MCL heals best.

Chronic MCL deficiency can lead to calcification of the MCL femoral insertion site and is known as Pellegrini-Stieda syndrome.

Lateral knee injuries most commonly is seen in motor vehicle accidents and athletic injuries and occurs by an excessive varus force, external tibial rotation, or hyperextension.

The lateral collateral ligament (LCL) is the main stabilizer of the lateral knee and is rarely an isolated injury but commonly is seen with posterolateral corner (PLC) injury.

The typical history of MCL injury is hearing a “pop” and medial joint line pain with difficulty ambulating.

On exam, patients are classically tender on the medial knee with an effusion and swelling.

Valgus stress testing at 30° of knee flexion isolates the superficial MCL.

If medial laxity at 0° of knee flexion as well, a posterior medial capsule or cruciate ligament injury is considered.

It is important to evaluate the patient for other ligamentous, meniscal, and chondral lesions.

A neurovascular exam should be performed with special attention to the saphenous nerve distribution.

Symptoms of injury to the LCL is lateral joint line pain, swelling, difficulty ascending and descending stairs, instability with knee extension, and problems with cutting or pivoting.

On exam, patients classically walk in hyperextension or a varus thrust gait and have lateral joint line tenderness.

Isolated LCL injury:

LCL combined with ACL and/or PCL injury:

Dial test—patient prone and applying external rotation stress on tibia:

A complete neurovascular exam is critical as common peroneal nerve injuries do occur.

MCL: AP and lateral X-rays and MRI to identify the location and severity of MCL injury as well as other knee structures.

LCL: similar radiographic analysis is recommended as well as a varus stress view.

Three grades based on the amount of valgus opening:

Injuries of the LCL and PLC are graded by the amount of lateral opening on varus stress:

Grade I and II are partial tears while grade III is a complete tear.

Treatment is based on the grade of injury.

Grade I injuries:

Isolated grade II and III injuries:

Functional knee bracing for prophylactic MCL treatment has been shown to be successful in football.

Operative intervention is utilized with combined ligamentous injuries and grade III injuries with continued instability after nonoperative treatment.

Repairing the MCL is successful in acute avulsion injuries where suture anchors are used.

MCL reconstruction is utilized in chronic instability or if repairing the MCL is not possible.

Graft types include semitendinosus, hamstring autograft, tibialis anterior, or Achilles allograft.

Nonoperative treatment is many times successful in isolated grade I or II LCL injury and includes immobilization and functional rehabilitation.

Return to sports usually possible in 6–8 weeks.

Grade III LCL injuries.

Rotatory instability (combined LCL and PLC).

Posterolateral instability (combined LCL/PCL and ACL/PCL injuries).

The proper order of repair/reconstruction of these combined knee injuries is not well defined and is a source of controversy.

Outcomes are improved when operative intervention occurs in the acute setting.

Avulsed LCL injuries have shown good outcomes with suture anchor fixation and direct suture repair of midsubstance injuries within 2 weeks of injury.

When reconstruction is required in isolated LCL injury, patellar tendon autograft has shown good outcomes.

In combined LCL and popliteofibular ligament reconstruction, the Larson technique can be used where the hamstring graft is passed through a fibular head bone tunnel and is fixed to the lateral femur to create a figure of eight.

Another option for this same injury is a transtibial double-bundle technique:

Careful physical exam is critical for quick diagnosis of combined injuries which improves outcomes.

Exertional compartment syndrome is a relatively uncommon cause of leg pain in the athletic population.

It is defined as reversible muscle ischemia within one of the compartments of the leg that is induced by exercise and relieved by rest.

There are no permanent sequelae in the affected tissues.

Exertional compartment syndrome is found most commonly in male in the third decade of life.

Athletes who perform significant amounts of running are frequently affected.

There are four compartments of the leg (anterior, lateral, superficial posterior, and deep posterior):

The anterior compartment is most commonly affected in approximately 70 % of cases.

The lateral compartment is involved in 10 % of cases.

Posterior compartment involvement is rare and has less predictable surgical outcomes.

The exact mechanism by which exertional compartment syndrome induces pain remains unknown.

It is theorized that increasing blood perfusion, muscle hypertrophy, and increased interstitial fluid volume within a confined fascial compartment lead to significantly elevated pressures. Accordingly, there is decreased venous return, leading to impaired tissue oxygenation and ischemia. Individual muscle cells are unable to clear the metabolic waste products at a sufficient rate, and they accumulate within the cell membrane.

Additionally, fascial hernias are suspected to be causal in some cases, with an incidence of 40 % during surgical decompression. The most common location is the intermuscular septum between the anterior and lateral compartments at the exit of the superficial peroneal nerve.

Patients generally present complaining of aching or burning leg pain that is induced by running. It is both predictable and reproducible in nature, often beginning 10 min or so after the onset of exercise, escalating during activity, and slowly resolving after a 30 min period of rest.

The patient may note a recent increase in training intensity that exceeds their threshold for generating symptoms.

There is no history of trauma.

Bilateral involvement is common.

Pain is localized to the involved compartment.

Occasionally, patients will complain of distal neurologic findings in addition to pain, specifically numbness, paresthesias, or weakness in the affected nerve distribution. However, the physical exam is frequently normal.

The diagnosis is commonly confused with medial tibial stress syndrome, colloquially referred to as “shin splints.” However, in medial tibial stress syndrome, pain is worst at the onset of exercise and tends to decrease during training.

Plain film radiographs, magnetic resonance imaging, and bone scan are often normal in patients with exertional compartment syndrome. However, these studies are often helpful in excluding other diagnoses such as tibial stress fracture and medial tibial stress syndrome.

Exertional compartment syndrome is definitively diagnosed by measuring compartment pressures. Measuring compartment pressures during exercise proves difficult and impractical.

Per Pedowitz criteria, three pressures must be measured for each suspected compartment: resting pressure, immediate postexercise pressure, and continuous postexercise pressure for 30 min. Diagnostic criteria are the following: (1) resting pressure >15 mmHg, (2) immediate postexercise pressure >30 mmHg, and (3) continuous postexercise pressure that does not return to resting level or fall below 15 mmHg after 15 min after completing activity.

While the anterior and lateral compartments may be tested fairly reliably, the deep posterior compartment can be challenging.

Alternative methods of diagnosis are being explored. Near-infrared spectroscopy will show increased deoxygenation of muscle during activity with delayed normalization after activity cessation. T2-weighted magnetic resonance imaging during exercise will demonstrate increase signal in the involved compartments when compared to normal surrounding tissue. SPECT bone scan has also demonstrated potential to localize an ischemic compartment.

Nonoperative treatment includes activity modification and antiinflammatory medications but often proves ineffective. Patients generally do not improve unless they completely eliminate the inciting activity.

The mainstay of treatment is surgical decompression fasciotomy of the involved compartments, most commonly anterior and lateral. This can be performed using an open or endoscopic approach with similar results.

The open approach involves a longitudinal incision over the anterolateral leg, identification of the intermuscular septum, and proximal and distal fascial division of both compartments. Careful attention should be paid to localize and protect the superficial peroneal nerve.

Posterior compartments may be accessed through an extensile anterolateral dissection or a separate medial approach. The superficial compartment is easily decompressed, and the deep compartment must be reached by undermining the soleus to access the posterior tibial margin.

Many surgeons advocate an individual release of the tibialis posterior muscle as well.

Most patients are able to return to sports postoperatively within 4 weeks.

Success rates are greater than 80 % when involving anterior and lateral compartments but fall to between 50 and 65 % when involving posterior compartments, particularly the deep.

Patients note a high level of pain relief and satisfaction with the surgical result.

The most common complication is recurrence of symptoms, which has been found in 7–17 % of operative cases. This is often attributed to incomplete fasciotomy and not specifically releasing the tibialis posterior during deep posterior decompression.

Less frequent complications include wound infection, nerve injury (most commonly the superficial peroneal), and deep venous thrombosis.