Genu Valgum (Valgus): Physical Signs of Knock-Knees.   If there is an abnormal space between the malleoli when the knees are touching when the patient is standing with the kneecaps straight ahead, a degree of genu valgum is present that may be more marked on one side than the other. There will also be (1) excessive internal rotation of the femur and external rotation restriction, (2) excessive external rotation of the tibia and internal rotation restriction, (3) medial patella deviation due to femur rotation, and (4) foot pronation.

Valgum results in a short leg producing pelvic imbalance if the condition is unilateral. Be aware, however, that people with a large degree of joint flexibility (especially females) can hyperextend their knees along with femoral rotation to give a false appearance of structural deformity. Bilateral valgus is common in late childhood but typically corrects before the age of 8 or 9 years. Acquired causes include postural dysfunction and metabolic diseases.

Genu Varum (Varus): Physical Signs of Bowed-Leg.   If the medial malleoli are touching and the knees are not when the patient is standing, the space between the knees determines the degree of genu varum. There will also be (1) excessive external rotation of the femur and internal rotation restriction, (2) excessive internal rotation of the tibia and external rotation restriction, (3) lateral patella deviation due to femur rotation, (4) anteversion of the femoral neck, and (5) an in-toeing gait.

As with genu valgum, bilateral genu varum is common in early childhood. It spontaneously corrects itself 95% of the time, states Mercier, during further growth and maturation. Nontraumatic causes include rickets, Paget's disease, scurvy, fibroid dysplasia, Blount's disease, and various other bone diseases. Other significant causes are postural dysfunction and degenerative arthritis.

Genu Recurvatum.   Genu recurvatum refers to exaggerated hyperextensibility. It is usually associated with a joint disorder that produces A-P instability of the knee. Contact sports, high jumping, or any activity that may induce anterior leg trauma or strenuous "take-offs" from a locked knee would be contraindicated for severe injury is predisposed.

Tibial Rotation and Torsion.   If the patient's kneecaps are facing straight ahead and the feet point distinctly outward, a positive sign of tibial lateral rotation on the femur exists. This sign is usually more pronounced on one side than the other. If the feet appear normally positioned but the patellae appear rolled medially inward, it is a positive sign of tibial torsion.   Various causes have been shown to be at the root of tibial rotation or torsion. A common cause is tibial subluxation. Other causes are attributed to a congenital defect or predisposition, spastic paralysis, poliomyelitis, scurvy, or a consequence of tibial fracture.

Mikulicz's Roentgenographic Line.   In the frontal view of the adult lower extremity (from hip to ankle) in the standing position, Mikulicz's line connects the middle of the inguinal ligament to the center of the talocrural joint, passing through the head of the femur and the center of the patella. If the center of the knee joint is found medial to this line, genu valgum (knock knee) exists. When the center of the knee joint is lateral to Mikulicz's line, genu varum (bowleg) presents.

Q-Angle Sign.   The patient is placed in the supine position with the knees extended in a relaxed position. The quadriceps (Q) angle of the knee is then measured. The Q-angle is formed by a visualized line drawn along the long axis of the femur that is intersected by a line drawn through the center of the patella and the tibial tubercle. To record, a goniometer is centered on its side over the patella with one arm aimed at the ipsilateral ASIS and the other arm placed in line with the center of the patellar tendon. This angle is normally 10° in men and 15° in women. In external tibial rotation and/or genu varus, however, the Q-angle can be markedly increased; ie, the angle increases as the tibial tubercle is displaced laterally or when the distal femur and proximal tibia are angled toward the midline.

Management.   Little can be accomplished once bone remodeling has occurred. However, much can be done in preventing further malformation by a long-term regimen of soft-tissue therapy, strengthening muscles showing weakness, stretching muscles and ligaments exhibiting shortening, maintaining fixation-free motion, nutritional concern, and assuring adequate innervation. Surgical reconstruction is rarely considered except in extreme cases.

Instability

The normal knee is provided with strong ligaments, a large joint capsule, and adjacent muscles and tendons that offer great stability. Severe sprain, especially that in hyperextension, readily leads to functional instability with chronic "giving way." A large degree of proprioception loss and loss of quadriceps power will undoubtedly be involved. In mild ligament tears, sprain symptoms are more pronounced but there is little or no instability involved. Severe tears exhibit marked laxity on stress tests.


External Rotation-Recurvatum Test

Coupling.   Because of its design, the leg cannot be fully extended without a degree of external tibial rotation on the femur. A maximal rotation of 6° lateral rotation occurs during the last 10° of extension, and the reverse occurs during the first 10° of flexion. This is called the "screw-home" mechanism. A simple test described later, the Helfet test, determines the integrity of the knee relative to the presence of this normal motion.

Technique.   To screen for external rotation-recurvatum, place the patient supine. Grasp the heel with one hand, and support the calf with the other hand. Allow the knee to pass from about 10° flexion into full extension. A positive sign occurs when the knee assumes a position of slight recurvatum, the tibia rotates externally, and there is increased tibia vara. The sign indicates injury to the arcuate complex, lateral half of the posterior capsule, or posterior cruciate ligament.

Anterolateral Rotary Instability Tests

McIntosh's Test.   The patient is placed supine, the lower extremity is supported at the heel with one hand, and the other hand is placed laterally over the proximal tibia just distal to the patella. The caudad hand applies valgus stress and internally rotates the tibia as the knee is gradually moved from full extension into flexion. During knee flexion, the lateral tibial plateau can be felt to subluxate anteriorly relative to the lateral condyle. Lateral crepitation may be felt, and a slight resistance to flexion may be perceived. When the knee is flexed about 35° , the iliotibial band tightens, and the tibial plateau is suddenly reduced, often with a "clunking" sensation that can often be both felt and heard.

Houghston's Jerk Sign.   This is a modification of McIntosh's test. With the patient supine, grasp the patient's foot with one hand while your other hand rests over the proximal lateral aspect of the leg just distal to the patella. The knee is flexed to 90° , and valgus stress is applied as the tibia is rotated internally. The knee is then gradually extended. The lateral tibial plateau is initially in a reduced position to the femoral condyle. However, as the knee is moved to about 35° of flexion, the lateral tibial plateau suddenly subluxates forward in relation to the femoral condyle with a jerking sensation. The lateral plateau slowly obtains its reduced position, which completes on full extension as the knee is extended.

Slocum's Test.   This is another modification of McIntosh's test. The patient is placed in the lateral recumbent position with the involved knee uppermost. The under extremity is flexed at 90° at both the hip and knee. The pelvis is rotated slightly posterior about 30° , and the weight of the extremity is supported by the inner aspect of the foot and heel. This position causes valgus stress at the knee and a slight internal rotation of the leg. With the patient in this position, grip the patient's distal thigh with one hand and the proximal leg with your other hand and press back of the fibula and femoral condyle with your thumbs. The knee is then gently pushed from extension into flexion and, as the iliotibial tract passes behind the transverse axis of rotation at about 35° , the lateral tibial plateau, which has subluxated forward, is reduced with a palpable "clunk" or "giving way" sensation.

Anterior-Posterior Instability Tests

Anterior Drawer Sign.   The anterior and posterior cruciate ligaments provide A-P stability to the knee joint. These intracapsular ligaments originate from the tibia and insert onto the inner aspects of the femoral condyles. To evaluate anterior stability, place the patient supine and flex the knees to 90° so that the feet are flat on the table. Sit sideways so your hip can stabilize the patient's feet from moving during the tests. Grasp your hands around the knee being examined, with your thumbs pointing superiorly over the lateral and medial joint lines and fingers wrapped around the lateral and medial insertions of the hamstrings. In this position, pull the tibia forward. If a distinct sliding forward of the tibia from under the femur is felt, it indicates a torn anterior cruciate ligament. Slight anterior sliding, however, is often normal. A positive sign should be confirmed by repeating the maneuver with the patient's leg internally rotated 30° and again with the leg externally rotated 15° . The reason for this is that even if the anterior cruciate ligament is torn, external rotation should reduce forward movement of the tibia. If it does not, both the anterior cruciate and the anteromedial aspect of the joint capsule are likely torn. The medial collateral ligaments may also be involved in loss of A-P stability.

Posterior Drawer Sign.   With the patient supine and the knees flexed, the stability of the posterior cruciate ligament is tested in the same manner as the anterior cruciate except the tibia of the flexed knee is pushed backward rather than pulled forward. Thus, both tests can be done in one continuous maneuver. When a distinct sliding backward of the tibia from under the femur is felt, a torn posterior cruciate ligament is indicated. A positive drawer sign is less common than its anterior counterpart.

Bounce-Home Test.   With the patient supine, cup one hand under the patient's heel and slightly flex the patient's knee with your other hand. While the patient's heel is held, the patient's knee is allowed to passively drop gently toward the top of the table in full extension, normally with an abrupt stop. If this full extension is not achieved and passive pressure elicits a "rubbery" resistance to extension, a motion block is indicated. This lack of full extension points to a torn meniscus, intracapsular swelling, or a loose fragment within the knee joint.

Knee Hyperextension Stress Test.   The patient is placed prone with the knees extended in the relaxed position. Place a fist under the distal thigh of the involved side, flex the patient's knee to about 30° with your other hand, and then allow the leg to drop without assistance when the muscles are relaxed. Most knee lesions limit extension to some degree. Thus, if extension is limited or the rebound is abnormal during this "leg drop" test (as compared to the contralateral knee), some type of knee disorder should be suspected and possibly be localized. This test, essentially, is the same as the bounce-home test except that the patient is prone.

Knee Hyperflexion Stress Test.   With the patient in the supine position, place one hand on the involved knee and your other hand on the patient's ipsilateral ankle. The patient's knee is moderately flexed, the thigh is brought toward the patient's abdomen, and the patient's heel is slowly pushed toward the patient's buttock. Unless the patient is very obese, the normal knee can be flexed without pain so it closely approaches the buttock. If knee pain or severe discomfort is induced by this maneuver, a subtle localized knee lesion may be brought out.

Management.   Injuries resulting in anterior or posterior instability may be treated conservatively if a complete rupture has not occurred. Initial cryotherapy and pressure support followed by a carefully supervised regimen of articular correction, interferential therapy, massage, crutch walking, guarded weight bearing with the knee in 30° flexion, other inducement's to enhance circulation and promote healing, and strengthening exercises (quadriceps after posterior cruciate injury, hamstrings after anterior cruciate injury) are often successful in returning an athlete to competition in 3 6 weeks. Many cases challenge the doctor's expertise.

Posterolateral Rotary Instability

Posterolateral rotary instability arises from a posterior subluxation of the lateral tibial plateau, relative to the lateral femoral condyle, accompanied by abnormal external tibial rotation. This type of instability usually results from trauma on a weak (lax) arcuate complex and lateral half of the posterior capsule, and a degree of failure of the posterior cruciate ligament.

Posterolateral Rotary Instability Test.   To test for posterolateral rotary instability, the external rotation-recurvatum and a posterior drawer test are performed. Excessive posterior sag of the lateral tibial plateau with external tibial rotation are noted.

Lateral and A-P views are the standard views of the knee. Anthrography is more helpful in the diagnosis of acute ligament or meniscus injury and synovial cysts than are standard views.

Weight-bearing views, a tangential view of the patella, and a tunnel view of the intercondylar notch to show articular margin defects (eg, condyle compression fracture) are often helpful. Stress views of the knee are beneficial in gaining evidence of fracture or ligament ruptures by expressing abnormal hinging that is not evident on standard views. Local anesthesia may be required.

Effusion

The most common traumatic soft-tissue disorder of the knee area is the result of effusion at the suprapatellar joint space where adjacent fat pads are displaced. Lateral views are best for determining effusion if it can be viewed at all. Fat above the patella, anterior to the femur, and posterior to the quadriceps tendon near the superior aspect of the patella is somewhat lucent in the normal knee. If effusion exists, fatty areas are replaced by fluids matching the density of thigh muscles and normal signs of fat are obliterated.

Knee effusion may be shown in an A-P view by soft-tissue density medial to the tibia below the joint line. This is usually attributed to paratibial synovial cysts progressing posteriorly and medially that may extend via bursae connections to the popliteal space or to the posterior aspect of the upper calf. Rarely is extension to the posterior thigh.


Fragmentation

The residual epiphyseal cartilage of the distal femur should be fairly uniform in thickness. Displacement of its margins should be noted. The articular margins of the femoral condyles are normally smooth, but fragmentation will appear in osteochondritis dissecans and osteochondral fractures. Swelling at the insertion of the quadriceps tendon at the apophysis of the tibial tubercle suggests Osgood-Schlatter's disease.

Strong sudden muscle contractions may cause fracture avulsions in the lateral knee area. Small bone fragments may also be found in an A-P view at the lateral edge of the proximal tibia on iliotibial band injury.


Ossification

Signs of ossification may appear in the patellar tendon following hemorrhage produced by partial tendon tears. If dislocation has occurred, such signs may also be found in the soft tissues. After blunt trauma to a limb, soft tissues may show evidence of heterotopic bone formation. Such ossification involves not only muscle tissue but also occurs within the fascial planes. The typical history reveals trauma, muscle pain and soreness, and hemorrhage into the soft tissues. Signs of poorly defined ossification develop in 2–5 weeks.


Fractures

If knee fracture is suspected, special care must be made to avoid soft-tissue damage during movement. Supracondylar or intracondylar fractures are rare in the young and during athletics but are quite frequent in the elderly with minimal trauma. The fracture site may be stable, displaced, or comminuted. The mechanism of injury is usually a sideways blow just above the knee or a direct anterior blow when the knee is fully flexed (eg, hard-surface fall on the knee).

Football helmet "spearing" to stop a runner frequently occurs by hitting laterally and anteriorly at the junction of the fibula, tibia, and femur articulations. "This osseous impact (clip) is so traumatic that it frequently immobilizes the player –possibly to the extent of a fractured extremity, ruptured collateral ligament and meniscus, or severe contusions and hemorrhaging of infra- and supra-patellar synovial sacs and tendinous attachments." Yet, according to statistics, knee fractures are rare in sports.

Distal Femur Fractures.   Comminuted lower femoral osteochondral fractures can result from jumping compression forces producing bony fragments difficult to view on film. On axial or tangential views, ossicles of the tibial tubercle may project over the femoral margins or patella and be confused with an osteochondral fracture or a loose body of bone.

Proximal Leg Fractures.   After violent twisting of the knee with pain localized near the proximal fibula, fracture and/or upper fibula dislocation should be the first suspicions. Chronic subluxations and posttraumatic arthritis of the proximal tibiofibular joint are frequent complications. As in the forearm, leg fractures often involve both bones. Sometimes, however, these bones do not fracture at the same level. When an x-ray film of the leg does not include the entire length of the bones, there is a possibility that a fracture may be missed. When a fracture is seen in only one of the paired bones at a given level, one must seek other levels for fracture of the other bone. Tibial fractures rarely occur; when they do, they are usually the result of running into an obstacle (eg, a bench).

Fatigue (Stress) Fractures

With repeated, forceful contractions of leg muscles, lower leg stress fractures are sometimes seen as the result of tibia or fibula "wobble." This sign is commonly related to track and field injuries but can occur whenever a force exceeds the bone's structural strength. Progressive pain during physical activity is the primary complaint.

Note:   The phrase stress fracture is a misnomer that is common in use. The term fatigue fracture is more accurate biomechanically as all fractures are the result of overstress.

Roentgenography.   An early sign, if any, is that of a linear periosteal reaction that rarely exceeds a centimeter in length, This may be associated with local bony tenderness, but tenderness is not common. In time, resorption of the fracture margin reveals a lucent linear defect on film. Fatigue fractures of the legs are usually horizontal but occasionally longitudinal. The initial signs are (1) a minute radiolucent tunneling of the cortex as a result of osteoclastic resorption, followed by cortical resorption in a fracture line of one cortex, and (2) a localized haze on the bone surface representing callus or periosteal new bone development. Within the endosteal bony surface, a line of condensation may be seen. Later, an abundant callus may be confused with a neoplasm. Soft-tissue views and bone scanning are sometimes necessary to determine fatigue fractures.

Management.   Most fatigue fractures do not require splinting or casting unless extensive or if the patient is unreliable in providing the necessary rest and protection of the area involved.

Dislocations

Knee dislocations rarely occur except in vehicular accidents or falls from great heights. A few cases have been reported in football and from missteps. The diagnosis is usually obvious.

Because of the severe pain involved and the probability of associated ligament and capsule tears, popliteal artery damage, and/or peroneal nerve injury, the patient with a dislocated knee should be referred to an orthopedic surgeon immediately for reduction under anesthesia and continuous evaluation of vascular and nerve status. Vascular repair is often unsuccessful if delayed for more than 8 hours. According to orthopedists Sisto/Warren, only in rare cases will a completely dislocated knee regain normal A-P motion.


Lower Leg Fractures and Dislocations

Displacement of lower tibia or fibula fractures is usually posteromedial because of the strength of the gastrocnemius and soleus.

Lower Tibia Fracture-Dislocation.   Because the tibial epiphysis does not ossify until the early twenties, epiphyseal fractures are not uncommon in adolescent contact sports. Fatigue fractures feature a dull gnawing pain following a run that increases in severity with time and weight bearing. Special care must be taken not to mistake an incomplete fracture of the distal-medial tibia (Pott's fracture) for a severely inversion-sprained ankle.

Lower Fibula Fracture-Dislocation.   Most fibula injuries occur at its distal portion. Minor fractures are sometimes missed because symptoms may resemble a bruise or mild sprain. As the fibula does not carry direct body weight, a player may continue activity long after fracture occurs and thus complicate the original injury. Uncomplicated fractures infrequently require more than support followed by progressive therapeutic exercise unless the medial ligaments of the ankle or tibiofibular supports are ruptured.

In the normal erect relaxed posture, the support of body weight and stability of the knee joint are provided strictly through the bony design and ligaments of the joint. No muscle action is involved.

The Knee Joint

The major osseous structures of the knee joint are the lateral and medial condyles of the distal femur and the superior articular surfaces of the tibia. The head of the fibula at the upper leg can be considered a part of the knee joint complex. On rare occasions, the simple synovial joint of the tibia-fibula articulation communicates with the knee joint proper. The major ligaments of the knee are the collaterals, the cruciates, and coronarys, along with the capsule and menisci.

Collateral Ligaments.   The broad medial (tibial) collateral ligament spans from the medial epicondyle of the femur to the medial aspect of the superior tibia, supporting the posterior aspect of the capsule. These fibers relax on knee flexion and tighten on extension, rotation, and lateral motions. The lateral (fibula) collateral ligament extends from the lateral epicondyle of the femur to the head of the fibula, offering no support to the capsule. These fibers relax on knee flexion and tighten on extension, rotation, and lateral movement.

Cruciate Ligaments.   The cross-shaped anterior and posterior cruciate ligaments lie within the joint capsule but are separated from the joint cavity by synovial tissue. They attach between the menisci in the intercondylar valley. The anterior cruciate spans between the anterior tibial condyle and the back of the medial surface of the lateral condyle of the femur. The posterior cruciate extends from the posterior intercondylar area to the lateral side of the medial condyle of the femur. Both ligaments are tense in all positions but are especially so during extreme flexion, extension, and rotation. Their main function is to restrict shear forces across the joint.

The Coronary Ligaments.   The medial and lateral coronary ligaments are extensions of the capsule. They attach the borders of the menisci to the tibia and femur.

Joint Capsule.   The synovial joint capsule of the knee is supported laterally to the patella by the inferior fibers of the fascia lata and quadriceps. The posterior capsule is supported by the semimembranosus tendon and the oblique popliteal ligament. The popliteus muscle pierces the capsule but is separated from the cavity by a synovial membrane.

The Menisci.   The two wedged-shaped internal and external menisci communicate only anteriorly. These articular crescents deepen the joint, cushion axial forces between the femur and tibia, and help to smooth the distribution of synovial fluid.

The Patella

The triangular knee cap has its apex directed caudally. Its posterior surface is smooth for articulation with the femur. The patella is the largest sesamoid bone in the body. It lies within the tendon of the quadriceps, tending to hold the tendon anterior from the femur. This improves quadriceps extension ability about 30%. In this sense, the patella can be compared with a movable pulley.


Knee Motion Evaluation

Basic knee movements are flexion, extension, internal rotation, and external rotation. See Table 1. Flexion and extension occur essentially between the femur and tibia. Rotation during slight flexion, internal and external, occurs between the tibia and femur and from menisci shifting.


Table 1.   Knee Motion

Joint Motion	Prime Movers	Accessories
Flexion	Hamstrings	Sartorius
	Semimembranosus	Gracilis
	Semitendinosus	Gastrocnemius
	Biceps femoris	Plantaris
		Popliteus
Extension	Quadriceps
	Rectus femoris
	Vastus lateralis
	Vastus medialis
	Vastus intermedius
External rotation	Biceps femoris	Tensor fascia latae
Internal rotation	Semimembranosus
	Semitendinosus
	Gracilis
	Popliteus
	Sartorius

Flexion-Extension Screening.   Test active flexion (135° ) by having the youthful patient carefully squat in a painless knee-bent position. Active extension (0° ) is tested by having the patient arise from this position to the standing position. Note dominance of one knee over the other and the smoothness of movement, especially of the last 10° of extension. Test flexion and extension passively if necessary with the patient prone. Stabilize the popliteal space with one hand, and grasp the patient's ankle with the other hand. Flex the leg as far as possible on the femur, noting the distance from the heel to the buttock. The leg should normally extend to 0° in a smooth arc.

Lateral Stability Screening.   To test sideward stability, place the patient supine and flex the knee just enough to free it from extension. To test the integrity of the medial ligament, apply valgus stress to open the knee joint on the medial side. Test the lateral ligament by applying pressure to open the knee joint on the lateral side. In these maneuvers, secure the ankle with one hand, place the other hand on the opposite side of the knee of the ligament being tested, and apply pressure toward the ligament being tested. More knowledge can be gained, however, if you lock the patient's ankle between your arm and chest and use this hand to palpate the ligaments in question and the underlying joint gap during the test.

Internal and External Rotation Screening.   To test active knee rotation, the patient is asked to slightly flex the knee and rotate the foot laterally and medially. About 10° either way is normal. Passive rotation is tested with the patient supine. Place a stabilizing hand just above the patient's knee, and rotate the tibia internally and externally with your active hand. It is helpful to have your stabilizing hand simultaneously palpate the tibial tubercle to note the amount of movement.

Kinesiology of the Knee

The muscles of the knee, their major functions, and the spinal segment of their nerve supply are shown in Table 2.


Table 2.   Muscles of the Knee

Note: Spinal innervation varies somewhat in different people. The spinal nerves listed here are averages and may differ in a particular patient; thus, an allowance of a segment above and below those listed should be considered.

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1. Stage of Acute Inflammation and Active Congestion

The major goals are to control pain and reduce swelling by vasoconstriction, compression, and elevation; to prevent further irritation, inflammation, and secondary infection by disinfection, protection, and rest; and to enhance healing mechanisms. Common electives include:


Disinfection of open skin (eg, scratches, abrasions, etc)
Cryotherapy
Cold packs
Ice massage
Vapocoolant spray
Compression
Pressure bandage
Aircast
Protection (padding)
Elevation
Indirect therapy (reflex therapy)
Iontophoresis/phonophoresis
Auriculotherapy
Meridian therapy
Spondylotherapy
Mild pulsed ultrasound
Mild pulsed alternating current
Rest
Bedrest
Cane
Crutches
Foam/padded appliance
Immobilization
Brace
Rigid appliance
Strap
Plaster cast
Indicated diet modification and nutritional supplementation.


2. Stage of Passive Congestion

The major goals are to control residual pain and swelling, provide rest and protection, prevent stasis, disperse coagulates and gels, enhance circulation and drainage, maintain muscle tone, and discourage adhesion formation. Common electives include:

Indirect articular therapy (reflex therapy)
Alternating superficial heat and cold
Pressure bandage
Protect lesion (padding)
Light nonpercussion vibrotherapy
Passive exercise of adjacent joints
Mild surging alternating current
Mild pulsed ultrasound
Phonophoresis
Cryokinetics (passive exercise)
Meridian therapy
Spondylotherapy
Rest
Bedrest
Cane
Crutches
Foam/padded appliance
Immobilization
Brace
Rigid appliance
Strap
Plaster cast
Indicated diet modification and nutritional supplementation.


3. Stage of Consolidation and/or Formation of Fibrinous Coagulant

The major goals are the same as in Stage 2 plus enhancing muscle tone and involved tissue integrity and stimulating healing processes. Common electives include:

Mild articular adjustment technics
Moist superficial heat
Thermowraps
Spray-and-stretch
Cryokinetics (active exercise)
Moderate active range-of-motion exercises
Meridian therapy
Sinusoidal current
Ultrasound, continuous
Phonophoresis
Vibromassage
Stretching distraction
High-volt therapy
Interferential current
Spondylotherapy
Mild transverse friction massage
Mild proprioceptive neuromuscular facilitation techniques
Rest
Bedrest
Cane
Crutches
Foam/padded appliance
Immobilization
Brace
Semirigid appliance
Indicated diet modification and nutritional supplementation.


4. Stage of Fibroblastic Activity and Potential Fibrosis

At this stage, causes for pain should be corrected but some local tenderness likely remains. The major goals are to defeat any tendency for the formation of adhesions, taut scar tissue, and area fibrosis and to prevent atrophy. Common electives are:

Deep heat
Articular adjustment technics
Spondylotherapy
Local vigorous vibromassage
Transverse friction massage
Spray-and-stretch
Active range-of-motion exercises without weight bearing
Negative galvanism
Ultrasound, continuous
Phonophoresis
Sinusoidal and pulsed muscle stimulation
High-volt therapy
Interferential current
Meridian therapy
Proprioceptive neuromuscular facilitation techniques
Rest
Bedrest
Cane
Crutches
Foam/padded appliance
Immobilization
Semirigid appliance
Support
Indicated diet modification and nutritional supplementation.


5. Stage of Reconditioning

Direct articular therapy for chronic fixations
Progressive remedial exercise
Passive stretching
Isometric static resistance
Isotonics with static resistance
Isotonics with varied resistance
Plyometrics
Aerobics
Indicated diet modification and nutritional supplementation.

Knee injuries in football have the highest injury incidence (60%). Field physicians should remember that just because a player can walk off the field after injury is no sign that severe injury has not occurred. Athletes are drilled to be stoic.

Skiing also has a high incidence of knee sprains, fractures (usually of the medial collateral ligament), and ankle injuries, but the incidence has lowered with the popularity of release-type bindings. The common fracture in skiing has changed from that of the ankle to that of the lower third of the tibia.

Patellar Bruises

A blow to the prepatellar bursa may quickly lead to a ballooning hemorrhage, which may extend several inches above the patella. This can be quite alarming to the inexperienced physician. Intricate examination must be made to differentiate the effects of contusion about the knee from a low quadriceps strain with suprapatellar bursal hemorrhage. Bone bruises are not difficult to differentiate as there is no effusion, motion restriction, joint instability, locking, ligament tenderness, or joint line tenderness.


Popliteal Aneurysm

When direct trauma affects major vessels and hematoma develops, aneurysmal dilation or a fistula may be produced as a complication. These are most often seen in the popliteal region following injury. The lesion must be differentiated from a pulsating hematoma, which is not a true aneurysm. A pulsating hematoma is fed by a ruptured arteriole and requires the skill of a vascular surgeon for correction. Discomfort behind the knee or upper calf on forced dorsiflexion of the foot is often a sign of thrombosis in the leg (Homan's sign).

      KNEE SPRAINS

When examining joint motion in the knee, special care must be taken that normal motion is not confused with the exaggerated motion resulting from joint instability.


Capsule Sprains

As the knee is a superficial joint and the largest joint in the body, symptoms after severe trauma are readily apparent. Any forced movement beyond the normal range of movement can produce symptoms and signs. Tenderness may be immediate, but effusion and stiffness are usually slow in development. Fluctuation and ballotement of the patella from joint distention may occur, and hemarthrosis may be associated. Pain and motion limitation are constant.

Management.   After mild injuries, cold, corrective manipulation, and strapping may be sufficient. When effusion into the joint is extremely severe, referral for aspiration may be necessary that is followed by compression bandages. Physiotherapy should be employed daily, and a knee support is advisable until full functional power is achieved. During the acute stage, structural alignment, cold, compression, positive galvanism, and possibly elevation are indicated. Ultrasound is especially effective. Hyaluronidase is helpful to reduce tissue swelling and edema if it is "driven in" with iontophoresis or phonophoresis. Complete rest is usually contraindicated in mild or moderate sprains; thus, use of a cane or crutch may be helpful. Therapy must consider rapid quadriceps atrophy, especially that of the vastus medialis.

After 48 hours, passive congestion can be managed by contrast baths, sinusoidal stimulation, ultrasound, light massage, gentle passive manipulation, and a mild range of active exercise. During the stage of consolidation, local moderate heat, moderate active exercise, moderate range of motion manipulation, and ultrasound are beneficial. Supplementation with 140 mg of manganese glycerophosphate six times daily throughout care appears to speed healing. In the stage of fibroblastic activity, deep heat and massage, carefully monitored active exercise, negative galvanism, ultrasound, and active joint manipulation speed recovery and inhibit postinjury effects.

Vapocoolant Technique in Grade I Knee Sprains.   Place the patient supine with a pillow under the involved knee. Spray the painful and tender areas, and gently assist and resist the patient in knee flexion-extension, with emphasis on extension. As the pain shifts position, spray the affected area. Have the patient attempt to walk. Youthful patients may be asked to carefully semisquat and kneel. Spray any painful area. If possible, have the patient stand on his toes and bend forward with his heels on the floor. Once relief is obtained, strap the joint, and instruct the patient in home exercises for 1 or 2 minutes each half hour during the waking hours. Full weight bearing should be restricted until the quadriceps indicate adequate strength. Begin resistance, stretching, and weight-bearing exercises as soon as logical.

Collateral Ligament Injuries

The collateral ligaments provide critical medial and lateral stability to the knee joint. Tears are caused by violent adduction or abduction and sometimes are associated with knee dislocation.

Background.   Minor sprains usually have a history of a sudden or unexpected movement, especially when the knee is in valgus position from an internally rotated thigh, a pronated or flat foot, or abduction during foot strike in gait. The mechanism is usually a combination of partial flexion, varus position, and sudden internal rotation overstress such as produced during stumbling, misstepping off a curb or stair, stepping into a hole, or onto a small object. Such sprains are common to cross-country runners, joggers, and jumpers who land with the knee in a valgus position.

Severe rupture of the lateral ligaments is produced by trauma where the internal lateral ligament is ruptured by overabduction of the leg or the external ligament is torn by overadduction. Excessive lateral motion during complete extension indicates laceration of lateral ligaments. Thus, the internal lateral ligament is impaired if abduction is excessive; the external ligament, if adduction is excessive.

Clinical Features.   Collateral ligament sprain presents with the same symptoms of localized pain, tenderness, and swelling as does capsule sprain. In minor lateral-ligament sprains, signs of effusion are not common. Stress tests help in differentiation. Pain is progressively severe and aggravated by the motion of injury, swelling is localized, point tenderness is demonstrable, muscles are spastic, and hemarthrosis may be present. Drawer signs are negative. Postinjury x-ray films may show elongated amorphous shadows near the affected femoral condyle, evidence of hematoma resolution, and possible displacement of the fibula or tibia.

Testing Collateral Ligament Stability.   The medial and lateral ligaments provide stability to the knee joint. To examine sideward stability, place the patient supine and flex the knee just enough to free it from extension. To test the integrity of the medial ligament, apply valgus stress to open the joint on the medial side. Test the lateral ligament by applying pressure to open the joint on the lateral side. In these maneuvers, secure the ankle with one hand, place the other hand on the opposite side of the knee of the ligaments being tested, and apply pressure toward the ligaments being tested. More knowledge can be gained, however, if the examiner locks the patient's ankle between his arm and chest and uses this hand to palpate the ligaments in question and the underlying joint gap during the test.

Medial (Tibial) Collateral Ligament Sprain.   Twisting overstress with the valgus knee in partial flexion often produces partial tearing of the long anterior fibers. Complete rupture may occur from violent abduction while the knee is extended or in external rotation and abduction while the knee is partially flexed. Hematoma usually develops, especially if the mechanism of injury is a severe blow. In minor sprains, effusion is slight and rapidly disappears during rehabilitation. In severe sprains, pain and swelling are severe and the meniscus will undoubtedly be involved. Adhesive taping will rarely be strong enough to prevent irritation during weight bearing. An early brace is helpful.

Lateral (Fibular) Collateral Ligament Sprain.   These ligament tears are caused by violent adduction, often associated with knee dislocation. The mechanism of injury is usually partial flexion in a varus position with internal rotation overstress. In minor lateral-ligament sprains, signs of effusion are rare.

Management.   The knee should be strapped in complete extension and treated as a severe sprain. Hirata warns that early aspiration or local anesthesia is contraindicated as they both obscure important signs of progress. Straight-leg lifts should be started 36 hours after injury. Effusion developing the first day after injury that subsides 50% or more the second day is an encouraging sign. However, if the swelling reduces and then returns on ambulation, a related meniscus tear should be suspected.

Early ligament or cartilage tenderness is often obscured by effusion. Once tenderness subsides, graduated resistance exercises may be begun. Once strapping is removed, a brace may be applied that allows flexion but limits lateral motion and full extension. In severe rupture, referral for surgery is usually required, but there are few miracles in knee surgery.

Taping Technique.   The patient should stand with a 1-1/2 to 2-inch wedge under the heel. Shave the knee, and spray with pretaping adherent or apply underwrap. (1) Using 3-inch tape, start the first strip at about midcalf on the medial aspect of the leg, bringing it around the back of the calf so that it angles upward on the inside of the leg and crosses the shin just below the patella. Extend it up the medial side of the leg about 10 inches. The second strip is applied on the same angle, overlapping the first strip by a third. (2) The third strip starts at the same point as the first two but runs upward on the leg and above the top of the patella to end on the lateral side of the leg. The fourth strip begins on the lateral aspect of the calf and angles under the patella to the medial side of the thigh. The fifth strip begins at the same spot as the first three but angles across the shin at the bottom of the patella, ending on the lateral thigh. Strips one, three, four, and five are then repeated, with the new strips overlapping the original strips by about a third. (3) To anchor, a continuous 3-inch-wide strip can then be applied, again leaving the patella free and being sure that the tape is not applied too tightly around the leg to restrict circulation. This is done by pulling the tape to its full elastic extension and then laying it in place. (4) A piece of 3-inch tape about 10 inches long (unstretched) is applied to the popliteal space. If the fossa is not covered by underwrap, pre-cover with cotton or gauze padding. Split the free ends of the tape, and carry the tails above and below the patella. (5) The final strip is applied over the first strip in the same manner. These last two strips, states Christensen, further stabilize the knee and help to prevent cartilage slippage.

Menisci Injury: General Considerations

The design of the knee joint predisposes it to attacks of impingement or instability. Many pathologic factors can produce mechanical derangement within a joint, but none exceeds the incidence of trauma. Symptoms of a meniscus injury closely resemble knee sprain such as sudden localized pain aggravated by motion, disability, and swelling. However, swelling develops gradually in contrast to that of knee sprain and locking is common in meniscus injury and absent in pure sprain. Injury to either semilunar cartilage may occur in either gender at any age but because trauma received during contact sports is the common cause, males are more frequently affected than females.

Menisci Malpositions.   Dislocation of the anterior horn is the most common menisci injury because this part of the meniscus is loosely bound to the internal lateral ligament. After displacement, the anterior border is caught between the articulations and may be rolled posteriorly within the joint to cause further displacement or tear. The posterior horn may be dislodged and nipped between the back part of the articular surfaces in flexion, thus preventing full flexion of the knee. The central portion of the cartilage may be pulled into the joint when its peripheral attachments are torn. In rare situations, the whole cartilage may be detached and avulsed within the joint.

Menisci Fractures.   Knee cartilage fractures may be longitudinal, transverse, oblique, or irregular. Bifurcation of the cartilage's anterior border makes this portion particularly easy to split. When the anterior horn is ripped loose and retracted within the joint, the transverse ligament locks the outer edge of the meniscus while traction on the displaced horn tears the cartilage. The central portion of the meniscus may be jammed between the articulations causing a longitudinal split and displacement of the inner half of the cartilage within the joint (buckethandle type). A similar tear of the posterior horn (posterior tag) may be caused by the same mechanism as dislocation. Transverse fractures are common where the anterior third of the meniscus joins with the posterior two-thirds. A horizontal "T" or oblique fracture may occur at this point by the cartilage bending without detachment.

Almost any sprain involving forced rotation will injure the menisci and one or both central cruciate ligaments. However, studies show that the majority of knee injuries do not involve severe cartilage damage as once supposed. Fractured menisci can be helped by conservative treatment, but recurrent locking is common. Surgery is the alternative, but it too is not always successful. Prognosis must always be carefully guarded.

Signs and Tests of Menisci Integrity

Steinmann's Sign.   In meniscus disorders, tenderness moves posteriorly when the knee is flexed and anteriorly when the knee is extended. This displacement of tenderness is not generally thought to occur in degenerative osteoarthrosis.

Payr's Sign.   The patient is asked to sit flat with the legs crossed and folded inward so that the femurs are internally rotated. The involved knee is flexed and abducted, and the foot is plantar flexed. If pain occurs on the medial side of a knee when downward (valgus) pressure is applied on the knee, a lesion at the posterior horn of the medial meniscus is suggested.

Apley's Compression Test.   The patient is placed prone with one leg flexed to 90° . Stabilize the patient's thigh with a knee and grasp the patient's foot. Apply downward pressure to the patient's foot to compress the medial and lateral menisci between the tibia and femur. Next, rotate the tibia internally and externally on the femur, holding downward pressure. Pain during this maneuver indicates probable meniscal or collateral damage. Medial knee pain suggests medial meniscus damage; lateral pain, lateral meniscus injury.

Apley's Distraction Test.   Apley designed this test to follow the compression test as an aid in differentiating meniscal from ligamentous knee problems. With the patient and the examiner in the same position as in the compression test, apply traction (rather than compression) while the leg is rotated internally and externally. This maneuver reduces pressure on the menisci but stretches the medial and lateral ligaments of the knee.

McMurray's Test.   In this two-part test, the patient is placed supine with the thigh and leg flexed until the heel approaches the buttock. Place one hand on the patient's knee, the other hand on the patient's ankle. Internally rotate the patient's leg, then slowly extend the leg. Next, externally rotate the leg and slowly extend the leg. The test is positive if at some point in the arc a painful click or snap is heard, which is significant of meniscus injury. The point in the arc where the snap is heard locates the site of injury in the meniscus. If noted with internal rotation, for example, the lateral meniscus will be involved. The higher the leg is raised when the snap is heard, the more posterior the lesion is in the meniscus. If noted with external rotation, the medial meniscus will be involved. Unfortunately, false positive and false negative signs are not uncommon with this test.

Childress' Test.   This is a two-phase test for the young: (1) The patient is asked to stand with the feet separated about 12–18 inches apart, assume a "knock-kneed" position by rotating the thighs inward, and then attempt to carefully squat as low as possible. Pain, joint restriction, or a clicking sensation suggests a lesion of the medial meniscus. (2) The test is then conducted with the patient assuming a "bowed-leg" position by rotating the thighs outward before squatting. Pain, joint restriction, or a clicking sensation when attempting to squat suggests a lesion of the lateral meniscus.

Specific Internal Semilunar Cartilage Injury

Cartilage damage medially is most often seen in young adults. Various pathologic factors can produce mechanical derangement within a joint, but trauma is the most common causes.

Incidence.   The internal semilunar cartilage is injured 15 times more frequently than the external meniscus. This is because the internal semilunar cartilage is longer than the external, crescentic in shape, and bifurcates, with the anterior portion of the bifurcation passing across to attach to the external semilunar cartilage. The coronary ligaments holding the meniscus to the tibia are much shorter medially than those of its lateral mate and do not permit free play.

Injury Forces and Effects.   The mechanism of injury causing internal semilunar stress is more common than that for injury to the external cartilage –a sudden inward twist of the femur on the fixed tibia. This produces severe tension and torsion on the anterior border of the meniscus, which may be ruptured or stretched. Tibial abduction is often associated with torsion and, when present, the mid part of the cartilage may be sucked outward and caught between the femur's inner condyle and tibial tuberosity. Also, abduction widens the medial aspect of the articulation, allowing nipping of the internal meniscus. The posterior border of the internal cartilage may be pinched between the articular surfaces by outward rotation of the femur when the tibia is fixed in extreme flexion (eg, the squatting position). During injury, the meniscus may be contused, subluxated, dislocated, or fractured. Fractures and luxations may be combined during the initial injury or occur after cartilage impingement.

Other Clinical Features.   Symptoms usually reflect the amount of damage and impingement. The joint may be locked, swollen, and extremely painful. There is frequently inability to fully extend the knee, indicating joint locking. The infrapatellar fat pad may be hot and enlarged. Either or both side strapings may be stretched or ruptured. Sometimes swelling does not develop for several hours, upon which tenderness increases over the involved ligaments. Diagnosis is arrived at by the history along with physical and roentgenographic findings to differentiate arthritis, anomalies, and other causes for the internal derangement and clinical picture.

Recurring Displacements.   After recurrent dislocation, the picture is not so acute except on rare occasions. A low-grade inflammatory process is related to recurrent displacements and associated with proliferative changes in the synovial membrane. The common protective mechanisms can be expected.

Reduction.   If impingement is mild, first flex the knee over your fist placed in the patient's popliteal fossa for counterleverage. Rock the limb gently in this position to loosen the jammed meniscus. The leg is then grasped at the ankle, and the tibia is laterally rocked on the femur to widen the space between the medial condyle of the femur and the tibia's articular surface, thus further freeing the cartilage. The leg is then rotated inwardly while the patient actively kicks his leg forward and upward. Severe force should never be used. An audible snap is usually heard as the meniscus is repositioned.

The test for reduction is the patient's ability to completely extend the knee without assistance. Reduction must be made within 24 hours after injury; if not, effusion produces a loss in meniscus elasticity preventing it from springing back to its normal seat.

Management.   After reduction, treat the injury as a severe sprain. Painless full weight bearing should be allowed as soon as possible, but excessive motion should be restricted by strapping. The taping procedure is the same as for collateral ligaments. Later, a brace with lateral stays may be applied that allows flexion but not rotation. A sole lift is helpful for several weeks until full strength and stability returns. Competitive activity should never be resumed until all symptoms have subsided and quadriceps strength and tone have returned to normal. Management should also consider strengthening the rotators of the knee.

Triad of O'Donahue

This is a clinical complex consisting of injury to the medial meniscus, medial collateral sprain, and anterior cruciate sprain. All signs and symptoms pertinent to these three injuries will be positive. This complex is also called the "unhappy triad" by many professional athletes.


Specific External Semilunar Cartilage Injury

The external semilunar cartilage is more circular and thicker than the internal. It is strapped to the tibia by coronary ligaments, as is the internal, but lateral fibers are much longer and permit more free play than allowed for the internal cartilage. The external cartilage conforms to the articular surface of the tibia when the knee is extended. The internal meniscus does not fit snugly in any joint position.

Injury Forces and Effects.   The mechanism of injury to the external semilunar cartilage is the reverse of that producing internal cartilage damage. In this type of injury, the foot has usually been fixed on the ground by body weight, the femur is rotated outwardly on the tibia, and the knee is simultaneously adducted. The posterior border of the lateral meniscus ruptures, and the cartilage is avulsed within the anterior compartment. The external lateral ligament may also be stretched or torn. The same type of lesions common to internal malpositions are found, but here the whole cartilage is usually displaced because it is thicker and heavier than its medial counterpart.

Other Clinical Features.   Symptoms are similar to but usually milder than those of medial injury except they are located at the lateral aspect; viz, locking, local tenderness, and inability to make full extension. Sometimes pain and tenderness are referred medially if the lateral ligament is severely stretched.

Reduction.   The reduction maneuver is the opposite of that used for internal meniscus impingement. The knee is acutely flexed, adducted to open the joint laterally, and the leg is rotated outwardly while the patient quickly extends the knee. Again, the test for reposition is active full extension of the knee. Postadjustment management is similar to that for internal meniscus damage.

The Crucial Ligaments

Sprain of the cruciates is often involved in "the unhappy triad" (cruciates and miniscus) because the straps may be ruptured by the same mechanisms producing meniscus displacement. The anterior cruciate restricts backward shifting of the femur and hyperextension. The posterior cruciate ligament restricts forward displacement of the femur or backward displacement of the tibia. Both the anterior and the posterior crucial ligaments may be torn. Because knee twisting disrupts the meniscus, the coincidence of meniscus and anterior ligament sprain is often seen.

Injury Forces and Effects.   Pure A-P shearing overstress of the cruciates is rare. The anterior cruciate ligament is commonly disrupted when internal rotation of the femur with the knee slightly flexed produces a relaxation of the cruciate ligaments as they untwist. The cruciates re-tense with forced external rotation of the femur, and the anterior cruciate gives way because it is weaker than the posterior. Laxity of the anterior cruciate is especially common, but it is unimportant if functional stability is to be maintained. There will be no lateral instability unless the collateral ligaments are also functional.

Posterior tears are caused by sudden external rotation of the femur with the foot fixed while the knee is forced into abduction, flexion, or by forceful displacement of the tibia backward on the femur with the knee flexed. Another mechanism is a fall on the knee with the force received on the proximal tibia.

Lachman's Test.   With the patient supine, the examiner slightly flexes the involved knee (about 20° ), cups a palm against the proximal calf, and attempts to pull the tibia forward. Excessive anterior translation of the tibia from the femur (anterior drawer sign) and lack of a definite end point suggest a rupture of the anterior cruciate ligament. If the anterior crucial ligament is torn, the tibia can be glided forward on the femur (drawer sign) and the knee can be hyperextended. Again, this sign must be elicited early before reflex hamstring spasm obscures a possibly positive sign. If the posterior crucial ligament is torn, the tibia can be glided posteriorly on the femur.

Other Clinical Features.   After rupture of either portion, the subject is apprehensive and insecure. The history reveals the knee "giving way" with slight locking, similar to that seen with stretching of a lateral ligament. In full rupture, severe avulsion or fracture of the bony attachment is usually associated. Stress films reveal excessive joint motion.

Classes of Injury.   (1) Mild: pain is elicited by passive stress, and point tenderness and local swelling develop. The joint is stable, and there is no locking or effusion. (2) Moderate: there is local swelling, some effusion, constant pain aggravated by passive stress, and locking if a meniscus rupture is related. There may be hemarthrosis. (3) Severe: With complete tear with or without avulsion, there is overt disability, instability, extensive swelling, agonizing pain, protective spasm, locking if a meniscus is involved, and probable hemarthrosis. Referral for surgery must be decided within 24 hours.

Taping Procedure for Moderate Sprain.   (1) The heel should sit on a 2-inch wedge to place the knee in approximately 20° flexion. Apply underwrap, leaving the patella free. (2) Apply 2-inch-wide strips in a diagonal basketweave fashion from midcalf to midthigh. Extension is restricted by placing three vertical strips from the posterior thigh to the calf. Pad the popliteal space. (3) Strapping is anchored by 3-inch-wide strips to cover the entire basketweave but not covering the patella. This technique can be combined with that described for collateral ligament sprain to give additional support.

Management.   In mild cases, treat by activity restriction, cold packs, compression, elevation, support, and muscle therapy. Heat is helpful in the late stages. In moderate to severe cases, the limb should be elevated and cold packs applied for 36–72 hours. When effusion completely subsides, mild heat may be applied. The knee is often pressure-dressed, casted in extension and treated as a severe sprain until the ruptured ligament(s) is repaired by fibrosis. Early weight bearing should be limited, and ultimately a program of muscle re-education can be initiated. A brace may be applied that allows flexion but firmly inhibits lateral motion. Rehabilitation must emphasize strengthening the extensors in the last 10° –15° . Management should also consider strengthening the rotators of the knee. In severe rupture, referral for surgery may be required, especially if there is evidence of bone damage.

Knee Joint Locking

While meniscus tears and lax coronary ligaments may be exhibited in joint locking, there can be other causes such as free bodies within the joint that produce a motion block. Transient locking is often the result of recurrent nipping of the alar folds to produce pedunculated tags that are easily caught. Hemarthrosis is typically associated.

It was described earlier that because of its design, the leg cannot be extended without a degree of external tibial rotation on the femur. A maximal rotation of 6° of lateral rotation occurs during the last 10° of extension and the reverse during the first 10° of flexion. This is called the "screw-home" mechanism. Helfet's test determines the integrity of the knee relative to the presence of this normal motion.

Helfet's Test.   This test is designed to detect the presence of an intra-articular "loose body" disturbing the normal biomechanics of the joint. To test normal knee locking, a dot is made with a skin pencil in the center of the patella and another is made over the tibial tubercle when the knee is flexed. The knee is then passively extended, and the motion of the dot relative to the patella is observed. A positive sign occurs when there is lack of full lateral movement of the dot.

Palpation of the tibial tubercle during this test allows for subtle determination of disturbed joint mechanics. Apart from intra-articular bodies, a lack of rotational joint play at the tibiofemoral articulation and imbalance in the tone of the internal and external rotators of the tibia could promote the pathomechanics observed during the test. It should also be noted that all but two of these muscles find their origin in the pelvis.

Osteochondromatosis

Osteochondromatosis is a noninflammatory condition in which pedunculated or loose bodies form from the synovial membrane within the joint cavity or within bursae and/or tendon sheaths. Traumatic, infectious, and neoplastic etiologies have been put forth. The exact cause is controversial, but the facts tend toward trauma being the primary precipitating agent.

Pathology.   The disorder features villous hypertrophy of the synovial membrane with bony or fibrous bodies forming in the villi. One large cauliflower-like displaced body or several hundred small round or kidney-shaped bodies, closely packed, may be revealed floating free within the joint on x-ray examination. There is some progressive growth after development. Each body contains a cancellous core with fat cells surrounded by a hyaline-like exterior. With time and pressure, large bodies may develop smooth convex facets.

Associated False Locking.   While true joint locking can occur from a displaced fragmented cartilage, a false locking may occur where there is stiffening on extension that gives way with persistence. It is more like a painful arc than a true block.

Osgood-Schlatter Disease

The most likely form of osteochondrosis met with in young athletics is that of the tibial tubercle. It is seen quite frequently in young male football backs and runners of either sex. The disorder is misnamed, however, in that it is not a disease. The exact cause is unknown, but it is thought to be a form of osteochondrosis with intrinsic trauma as the inciting factor; eg, sudden contractions of quadriceps femoris concentrated on a portion of an incompletely developed tibial tubercle resulting in an avulsion fracture. The disorder is not usually severely disabling and is milder in girls than boys. The disorder can be bilateral.

Roentgenography.   Findings of the A-P view are usually negative. In a lateral film, the epiphysis of the tibia is seen fragmented and irregular in outline and density during the advanced stage. The patellar ligament becomes thickened at its insertion early. This is usually evident before osseous changes occur. Williams/Sperryn believe the anterior tibial tubercle becomes infarcted because of excessive pull from the patella tendon. The primary trauma is followed by numerous lesser injuries that constantly give rise to new interruptions of continuity during the growth period.

Clinical Features.   Symptoms depend on the extent of involvement of the synovial membrane and the mechanical interference of the loose bodies. The typical complaint is pain at the anterior knee, inferior to the patella, especially when the knee is flexed. Repeated attacks of "catching" are common. A hot, red, tender swelling develops over the tibial tubercle when the disorder is active. The patient reports pain during activity and the inability to kneel. There is also pain on running and climbing stairs. An enlarged tubercle may be palpable. While joint motion may be only slightly affected, crepitation on active and passive motion is typical. Pain is increased by any activity that produces active knee extension against resistance.

Management.   Immediate rest of the part is indicated. Normalize any vertebral motion-unit abnormality if possible, especially those found in the hip, lumbar, or sacroiliac areas. Normalize muscle tone in the lower back, pelvis, and thigh. A plaster cast, brace, or other means to restrict joint flexion may be necessary to allow the tubercle to fuse. Some authorities say this should always be done, others say it is never necessary. Ultrasonic therapy helps in increasing vascularization at the appropriate stage. Weight-bearing is permitted after the acute stage, but knee flexion is restricted until overt symptoms subside. Afterwards, weakened muscles must be strengthened. Never overlook a possible aggravating balance defect in the foot or pelvis. Patients responding poorly to conservative measures or who are subject to frequent attacks should be referred for surgical appraisal.

Traumatic Arthritis

Osteoarthritis of the knee is not always a sequel of aging degeneration; it is sometimes seen in the young athlete. Trauma usually initiates symptoms that began, often subclinically, after earlier trauma that was improperly managed or neglected (eg, inadequate mobilization and/or muscle re-education). Heavy weight bearing superimposed on a joint with microcirculation impairment, possibly of a reflex nature, and congenital defects are two other common predisposing factors. When seen in the elderly very obese patient, the articular cartilages may be too far destroyed to offer much help.


Traumatic Synovitis

Even mild trauma can produce extensive knee swelling if the alar folds of the synovial fringes are pinched between the tibial and femoral condyles. Movement quickly becomes limited and maintained in about 20° flexion (position of rest), pain is severe, and tenderness is acute. Swelling is less severe in complete rupture because the fluid is able to escape through the tear. Uncommon tears of the posterior capsule, characterized by extension instability, may produce painful swelling and bleeding into the popliteal fossa.


Knee Pain in Athletes from Ankle Distortion

Runners with a hyperpronated ankle (ipsilateral or bilateral) frequently report nonspecific medial knee pain. Weight bearing medially shifts the pronated foot, and these stresses transmit up the leg medially to the knee. Thus, internal tibial rotation is commonly associated with both hyperpronation and medial knee pain.

In contrast, lateral knee pain may result from iliotibial band or popliteal tendinitis. Ankle hyperpronation may predispose runners to these conditions. Internal tibial rotation related to overpronation excessively stretches involved fiber attachments. The result is iliotibial band tendinitis, popliteal tendinitis, or both. In addition, ankle hyperpronation often leads to a valgus deformity of the knee. This angulation results in an increased lateral pull of the patella during quadriceps contraction.


Cyst Development

Synovial cysts are frequent complications of knee trauma and various arthritides (especially rheumatoid). Long-standing posttraumatic effusion may be great enough to distend the semimembranosus gastrocnemius bursal complex in the popliteal area to produce Baker's cyst. A firm, mildly tender meniscal cyst may also occur, usually occurring on the anterolateral aspect of the knee and is nonfluctuating.


Intracapsular Pinches

Intracapsular pinches are common in sports than cartilage injuries. Sudden joint stress, usually rotational, may cause some soft tissue to be pinched within articular structures during jumping, defensive running, kicking, etc. This is frequently seen in the knee where the infrapatellar fat pad is nipped, resulting in some effusion and possibly hemorrhage.

Clinical Features.   Diagnosis is essentially by exclusion. There is no history of external trauma, nor are there signs of joint line tenderness or instability. Discomfort is felt directly behind the patella. A slight effusion may be found that is associated with a slight loss in full extension. The sides of the patella and its tendon will feel thick and firm. This mass will be tender, and it will be the sole site of tenderness if ligament and fibrocartilage involvement are excluded.

Management.   Treatment is the same as that for sprain, but active movement is slightly delayed because injured fat is slow to heal. In forming a prognosis, keep in mind that damaged fat is frequently replaced by inelastic fibrous tissue that is readily irritated by further stress. Cold packs, compression, and elevation should be continued as long as there is palpable thickening near the patella and any degree of extension restriction. Despite patient objections, no forceful activity should be permitted for 6–10 days.

Referral for surgery may be necessary if the superior portion of the tibia severs a large portion of the infrapatellar pad or if a tag later becomes calcified and causes trouble. Surgery is mandated in cases where a pedunculated part may become strangled by adhesions resulting in joint locking, hemarthrosis, and torsion gangrene.

Acute Bursitis

The term "housemaid's knee" refers to prepatellar bursitis. Fluctuation, with or without heat and tenderness, limited to the prepatellar space is usually diagnostic. Management of an acutely swollen bursa is not difficult if undertaken immediately. Cold packs, rest, some elevation, and a pressure bandage are usually adequate. On rare occasions, referral for aspiration and steroids may be necessary if swelling does not begin to subside within 24 hours. Graduated activity may start as soon as the acute phase has resolved.

Knee Effusion Test.   If a joint is greatly swollen from major effusion, place the patient in a relaxed supine position. With the limb relaxed, slowly extend the involved knee. The patella is then pushed into the trochlear groove and released quickly. This forces fluid under the patella to the sides of the joint and then to return under the patella. This rebound effect is referred to as a ballottable patella.   Minimal effusion, however, will not ballot the patella. In cases of mild effusion, it is necessary to "milk" the fluid from the suprapatellar pouch and lateral side to the medial side of the joint. Once the fluid has been moved medially, tapping over the fluid will return it to the lateral side. This is confirmatory.

Chronic Effusion

In chronic "water on the knee," the original trauma may not be remembered. The effect is from an inflamed synovial membrane of the knee with escape of fluid into a synovial sac. Causes include sharp trauma, repeated minor blunt or intrinsic trauma, lymphatic congestion, and atherosclerosis that may be associated with flat feet and/or genu valgum. The cause can sometimes be traced to psoas dysfunction from an anterior pelvic tilt and everted feet producing an increased torque at the knee. This disorder is not as common today as it was in past years when people scubbed floors or did other chores when on their knees.

Clinical Features.   The presenting picture consists of prepatellar or infrapatellar bursitis with a locally inflamed knee. There is little pain except on motion, mild-to-extensive swelling, and obvious low quadriceps atrophy. Knee instability tests may not be strongly positive. There may be signs of inhibitions of the neuromuscular mechanisms of the knee and features of recurrent subluxation of the patella over the lateral condyle

Management.   Standard regimens for chronic strain/sprain management and muscle re-education are usually sufficient. If not, referral for aspiration of fluid, steroids, and possibly antibiotics may be advisable. In competitive sports, there is no absolute cure as reaggravation can be anticipated. Swimming is beneficial during recuperation. Protection and compression must be provided during competitive activity until healing is secure. The duration is approximately one month. For the hypersensitive knee, standard padding is usually inadequate in contact sports.

Peripheral Nerve Lesions of the Knee Area

Peroneal Nerve Contusion.   The peroneal nerve, a terminal branch of the sciatic nerve, is exposed to injury at the knee especially as it winds about the neck of the fibula. In addition to laceration, it is frequently injured in fracture of the neck of the fibula and occasionally by pressure of poorly padded athletic supports. A typical "foot drop" results.

Lust's Sign.   When the external branch of the sciatic nerve (the peroneus communis) is struck with a percussion hammer, the reflex produces dorsal flexion and abduction of the foot. This is best accomplished by following the nerve below the bifurcation of the great sciatic nerve, especially in an oblique position outwardly along the outer portion of the popliteal space. This pathologic reflex indicates peroneal spasmophilia.

Pellegrini Stieda

Pellegrini stieda is a chronic disorder characterized by posttraumatic calcification and ossification of the medial collateral ligament of the knee. The physical features mimic chronic ligament overstress; eg, severe pain localized on the medial aspect of the knee, tenderness over the medial condyle of the distal femur, mild swelling, restricted range of knee motion, and difficulty ascending stairs.


Osteochondritis Dissecans (Osteochondral Fracture)

A bony defect of the articular margin of the femur at the lateral aspect of the medial condyle is called osteochondritis dissecans. This is, however, a misnomer in that it represents a form of compression fracture rather than a dissecting inflammatory lesion. It is frequently related to a history of sports-related trauma. It is essentially an affection of adolescence and young adults, rarely seen in middle age, and almost unknown in later life. It occurs frequently between the ages of 12 and 25, and males are more often affected than females in a ratio of 15:1. Usually one joint is affected, sometimes bilaterally; and 90% of the time it occurs in the knee. Elbow involvement is next in frequency.

Etiology.   Osteochondritis dissecans occurs in the knee (or elbow) at the point of greatest impact; ie, the lateral portion of the surface of the internal condyle adjacent to the intercondylar notch. The exact cause is unknown, but there are many theories: traumatic, embolic, and constitutional. Most authorities feel that trauma is at least a predisposing agent if not the cause. Knee trauma may occur in three ways: (1) by direct force at the point of greatest contact; (2) by direct pull on the anterior attachment of the posterior ligament; and (3) by injury to the arterial supply. Fat embolism or bacterial embolism may also be involved. Aseptic necrosis due to embolism, low-grade bacterial infection, and congenital predisposition of the femoral epiphysis are other factors to be weighed.

Symptoms.   The chief complaint is intermittent mild joint disability. There is usually a low-grade inflammatory process associated with slight effusion, swelling, and joint clicking or locking. Before fragment separation, the associated pain is dull and aching.

Wilson's Sign.   The patient is placed supine with the legs in an extended, relaxed position. The knee of the involved side is flexed to a right angle, the leg is firmly rotated internally, and then the knee is slowly extended while maintaining the leg in internal rotation. If osteochondritis of the knee exists, the patient will complain of pain in front of the medial condyle of the distal femur. If the leg is then externally rotated, the pain will subside.

Roentgenography.   Routine A-P and lateral films plus a tunnel-view projection are recommended. Whatever the cause, a somewhat crater-like, rarefied, and conical-shaped depression on the border of the condyle involving subchondral bone is characteristic. This may require months or years to develop. Giammarino reports the most frequent site of the lesion is in the medial femoral condyle near the intercondylar notch. On the surface of the condyle, a punched-out irregular triangular notch of varying size appears. The loose body or sequestra may be seen in the crater or within the joint space. If the body is not completely detached, it may be seen lying in the cavity and separated from the underlying bone by a clear line of demarcation. If detached, it appears as an oval shadow in the joint. If it is cartilaginous, it may not be visible. As a line of cleavage is formed, the cavity and loose body are covered with fibrocartilage, becoming rough and irregular. It later releases and falls into the joint cavity where it is ground into small fragments by body weight. The fragments may be small or large, round, oval, or irregular, and each fragment usually continues to increase in size.

Management.   Mild mobilizing manipulation, traction, and various forms of physiotherapy to improve circulation, reduce pain and swelling, and enhance healing will usually ameliorate the symptoms. Mechanical traumatic arthrosis may result if a joint "mouse" repeatedly sets up irritation. As in Perthe's disease, revascularization of an undisplaced fragment in osteochondrosis dissecans of the knee in children appears to progress with reasonable rapidity in some cases provided the joint is protected from bearing injurious weight for about 6 months.

If a fragment is caught and unable to be dislodged or if a loose body is within the joint, surgical consultation should be considered. In spite of symptom absence, some authorities advise surgery to prevent osteoarthritis. Surgery is normally reserved only for those cases in which clinical and roentgenographic improvement cannot be demonstrated or if displacement occurs repeatedly.

Femorotibial Fixations

Releasing Restricted Distraction (Joint Separation).   With the patient prone, stand perpendicular to the involved knee. Flex the patient's knee to a right angle, place your cephalad knee gently in the patient's popliteal space to stabilize the patient's femur, grasp the patient's leg distally (above the ankle) with both hands, and apply a short, sharp upward pulling force directed through the vertical axis of the tibia.

Evaluating A-P Glide.   To judge A-P motion glide of the knee, sit at the foot of the table obliquely facing the supine patient, flex the involved knee to approximately 45° , grasp the proximal aspect of the patient's leg with both hands (thumbs pointing upward and fingers interlocking at the posterior), and apply pressure posteriorly and anteriorly in a rocking motion. This is the same position used to elicit a drawer sign.   It usually helps to stabilize the patient's leg by placing the toes of the foot of the involved limb slightly under your cephalad thigh. Normal joint play will be perceived as a slight but distinct motion (about 1/8 inch) and is best felt when the knee is in midflexion. Weak or torn tissues should be suspected if A-P glide is felt during full flexion or extension.

Releasing Restricted Posterior Glide.   If the posterior glide of the femur on the tibia is restricted, place the patient supine. Insert about 2 inches of toweling under the distal aspect of the patient's femur. On the side of involvement, stand perpendicular to the patient's knee, grasp the anterior surface of the patient's thigh just above the patella with your cephalad hand, place the heel of your caudad (active) hand on the anterior surface of the patient's tibia (just below the patella), apply pressure, and administer a short moderate thrust.

Releasing Restricted Anterior Glide.   With the patient supine, flex the involved hip and knee so the plantar surface of the foot rests firmly on the table. Sit on the table, obliquely facing the patient, so your cephalad thigh rests lightly against the patient's foot for stabilization. Grasp the patient's knee (proximal tibia and fibula) with both hands as to elicit a drawer sign, apply a pulling force directed toward your sternum, hold the traction for several seconds, and conclude by administering a short dynamic pull.

Another method to release anterior glide restriction is the reverse of the technic described above to release posterior glide restrictions. With the patient prone, insert about 2 inches of toweling under the distal aspect of the patient's femur. On the side of involvement, stand perpendicular to the patient's knee, grasp the posterior surface of the patient's thigh just above the popliteal space with your cephalad hand, place the heel of your caudad (active) hand on the posterior surface of the patient's tibia (just below the popliteal space), apply pressure and administer a short moderate thrust.

A common home therapy is to have the sitting or supine patient bring the involved flexed knee toward the abdomen after inserting a rolled towel against the popliteal space, grasp the anterior surface of the leg distally with both hands, and apply firm painless pressure (directed toward the buttock) several times.

Evaluating Restricted Rotation.   To appraise the rotory ability of the knee, place the patient supine, stand perpendicular to the involved limb, and flex the patient's knee and hip to approximately 45° . Grasp the patient's knee with your cephalad (stabilizing) hand and just above the patient's ankle with your caudad (active) hand. In this position with the patient fully relaxed, rotate the patient's leg clockwise and counterclockwise with your active hand by supinating and pronating your forearm. Slight motion should be felt that will normally be absent in full knee flexion or extension if the integrity of the ligaments of the knee and tendons of the quadriceps is intact.

Releasing Restricted Rotation.   With the doctor-patient positions the same as during evaluation, apply clockwise or counterclockwise pressure (according to the restriction), hold the pressure for several seconds, and conclude with a firm shallow twist to free the motion.

Evaluating Restricted Lateral Tilt.   To test lateral tilt (outside opening) of the knee, the doctor-patient positions remain the same as described above but pressure of the contact hand is applied from the medial to the lateral to open the lateral aspect of the femorotibial joint. If joint motion is restricted at its lateral aspect, normal lateral tilt will be lost. If the lateral ligaments are torn, exaggerated motion will be perceived. It will also be felt when the knee is fully extended.

Releasing Restricted Lateral Tilt.   Place the patient supine, stand on the side of involvement obliquely facing the patient so that you can flex the patient's hip and knee to a right angle. Place your stabilizing cephalad hand on the patient's flexed knee, and reach around and under the patient's leg so your caudad palm can support the proximal aspect of the patient's leg. The patient's leg should rest on your caudad forearm and hip. While holding the patient's leg distally by elbow pressure, slowly adduct the patient's leg by shifting your trunk medially over the table. This will place a lateral stretch on the patient's knee. Once tension is achieved, apply a shallow thrust with your caudad hand directed laterally. The application of a temporary wedge (1/8–1/4 inch) to the patient's shoe medially may be helpful in stretching chronic lateral restrictions.

Evaluating Restricted Medial Tilt.   To evaluate medial tilt (inside opening) of the knee, stand perpendicular on the side of involvement of the supine patient. Grasp the anterior surface of the patient's leg distally on the involved side for stabilization with your caudad hand, and place the supinated heel of your cephalad hand against the lateral aspect of the patient's knee, just above the joint line (over the lateral femoral condyle). The fingers of your active hand (cephalad) should be curled under the knee against the popliteal space. As there is almost no perceptible femorotibial sideward tilt or rotational joint play when the knee is fully extended (locked) and the ligaments are intact, flex the patient's knee slightly by raising it 3–4 inches with your contact hand, and apply lateral to medial pressure. This should elicit slight opening (about 1/8 inch) of the medial aspect of the femorotibial joint. If joint motion is restricted medially, medial tilt will be nonexistent. If the medial ligaments are torn or the vastus medialis muscle is extremely weak, exaggerated motion will be perceived. This will also be felt when the knee is fully extended. Atrophy of the vastus medialis is an early sign in many knee disorders and articular derangements.

Releasing Restricted Medial Tilt.   Place the patient supine, stand on the side of involvement obliquely facing the patient so that you can flex the patient's hip and knee to a right angle. Place your stabilizing cephalad hand on the patient's flexed knee, and reach around and under the patient's leg so your caudad palm can support the proximal aspect of the patient's leg. The patient's leg should rest on your caudad forearm and hip. While holding the patient's leg distally by elbow pressure, slowly abduct the patient's leg by shifting your trunk laterally away from the table. This will place a medial stretch upon the patient's knee. Once tension is achieved, apply a shallow thrust with your caudad hand directed medially. The application of a temporary wedge (1/8–1/4 inch) to the patient's shoe laterally may be helpful in stretching medial restriction.

Proximal Tibiofibular Fixations

Mennell states that the only joint-play movement at the tibiofibular joint is A-P glide: maximum at knee midflexion, minimal at full knee extension. Gillet reported that superior tibiofibular fixation is quite common. The joint between the proximal heads of the tibia and fibula normally opens slightly when the foot is inverted. This gap can be palpated just inferolateral to the patellar tendon. In addition, the head of the fibula will shift slightly cephalad when the foot is actively dorsiflexed. These movements will not be felt if the joint is locked. Gillet believed fixation at this joint is often linked to an L5 or sacral subluxation.

Evaluating Tibiofibular A-P Glide.   To judge this motion, sit at the foot of the table obliquely facing the supine patient as if you were to evaluate A-P glide of the femorotibial joint. With your lateral active hand, grasp the head of the patient's fibula between your thumb anteriorly and the tips of your index and middle fingers posteriorly. Your medial hand can be used to stabilize the proximal aspect of the patient's tibia. In this position, use your active hand contact to pull the head of the patient's fibula forward and then push it backward to appraise A-P glide motion.

Releasing Restricted Tibiofibular A-P Glide.   With doctor and patient remaining in the examination position, mobilization is made by applying pressure for several seconds and then a slight thrust against the resistance.

      TIBIAL SUBLUXATIONS

All signs of tibial and fibular subluxations are usually subtle. They require a trained kinesthetic sense during dynamic and static palpation to determine.

When a subluxation exists between the distal femur and the proximal tibia, the malpositioning may be attributed to either the femur or the tibia. The tibia has been elected in the following descriptions, but the reader should realize that this has been an arbitrary decision. Thus, a listing for an externally rotated tibia may be described by another writer as an internally rotated femur, for example. A lateral tibia subluxation may be rightfully described as a medial femur subluxation. Keep in mind that bones do not subluxate, articulations do.

Because the articulation between the femur and tibia is so complex, an array of subluxation possibilities exists. The tibia may be translated solely in one direction; eg, medially, laterally, posteriorly, anteriorly, or diagonally relative to the femur. In addition, rotary instability may produce a displacement in the anteromedial, anterolateral, posteromedial, or posterolateral direction. Therefore, astute evaluation of these displacement possibilities and the integrity of the associated soft tissues must be made before an efficient corrective adjustment can be applied.


Anterior Tibia Subluxation

The major features of anterior tibial subluxation include patellar tendon tenderness, an anterior drawer sign, anterior cruciate tenderness, patellar tendon hypertonicity or tendinitis, and restricted posterior tibial motion. The history often reveals a blow to the back of the upper leg or falling backward over a low obstacle.

Adjustment.   Place the patient supine, and stand on the side of involvement. Apply contact with your cephalad hand against the proximal anterior aspect of the patient's tibia. Place your caudad hand under the patient's calf to support the weight of the leg and to apply traction during the adjustment. As traction is applied, simultaneously make a short A-P thrust to correct the malposition.

Posterior Tibia Subluxation

Physical indications include popliteal fossa tenderness, posterior cruciate ligament tenderness, posterior drawer sign, patella tendon hypotonicity and depression, and restricted anterior tibia motion. A history of high anterior tibial trauma is usually involved.

Adjustment.   Place the patient prone with the involved knee flexed 70° . Squat at the end of the table, and place the patient's involved leg against your medial shoulder. Interlock both hands on the posterior aspect of the tibial condyles. Apply traction and simultaneously deliver a fairly strong thrust directed to bring the tibia anteriorly, correcting the malposition.

Lateral Tibia Subluxation

Lateral tibia subluxation is often consequent to lateral collateral ligament sprain with restricted medial motion. A history of trauma to the medial aspect of the upper tibia is frequently associated.

Adjustment.   Place the patient supine with the involved knee extended and the ipsilateral hip flexed about 40° . Stand on the side of involvement, and place your cephalad contact palm against the upper-lateral aspect of the patient's tibia. A pisiform contact is applied against the lateral aspect of the tibial condyle. Wrap your caudad hand under the patient's calf to support the weight of the patient's leg. Slightly flex the patient's knee, apply traction to the leg, and simultaneously make a short thrust directed from the lateral to the medial to correct the malposition.

Medial Tibia Subluxation

Medial tibial subluxation is frequently consequent to medial collateral ligament sprain with restricted lateral motion. A history of trauma to the lateral upper aspect of the tibia is usually reported.

Adjustment.   Place the patient supine with the involved knee extended and the ipsilateral hip flexed about 45° . Stand on the side opposite to involvement, and place your cephalad contact palm against the upper medial aspect of the patient's tibia. A pisiform contact is applied against the medial aspect of the tibial condyle. Wrap your caudad hand under the patient's calf to support the weight of the patient's leg. Slightly flex the patient's knee, apply traction to the leg, and simultaneously make a short thrust directed from the medial to the lateral to correct the malposition.

Externally Rotated Tibia Subluxation

The physical features of an externally rotated tibia are medial capsular pain and tenderness, genu valgum, a prominent medial tibial condyle and plateau, tightness of the pes anserine tendons, chondromalacia patellae, and restricted internal tibial rotation.

Patient Prone Adjustment.   Place the patient prone with the involved knee flexed about 70° . Stand at the side of the involved tibia, and set your cephalad knee on the distal aspect of the patient's femur to stabilize the patient's knee against the table. Grasp the patient's distal tibia and fibula with your fingers interlocking on the anterior aspect. Apply upward traction to the leg, and then make a firm but gentle internal rotation maneuver of the leg to correct the malposition.

Patient Supine Adjustment.   Place the patient supine, and stand on the side of involvement facing the patient. Place your medial foot upon the table. It sometimes helps to place your knee against a pad in the patient's popliteal space for countertraction. Next, place the patient's leg against your hip for stabilization. Your medial hand grasps the anterior surface of the patient's leg just above the ankle, and your lateral hand is moved under the patient's leg so you can grasp your medial forearm. The patient's leg rests within your cubital fossa for support. Apply traction to the leg while simultaneously manipulating the leg into internal rotation to correct the malposition.

Alternative Patient Supine Adjustment Procedure.   Stand on the side of involvement of the supine patient. The patient's hip should be flexed about 60° with the knee flexed about 110° . Grasp the patient's lower leg with your medial contact hand, and place your lateral hand on the patient's knee to stabilize the patella. The adjustment is made in this position by flexing and internally rotating the patient's leg to correct the malposition.

Internally Rotated Tibia Subluxation

The typical physical features of an internally rotated tibia are lateral capsular pain and tenderness, genu varum, a prominent lateral tibial condyle and plateau, tightness of the iliotibial band and lateral hamstring tendons, chondromalacia patellae, and restricted external tibial rotation.

Patient Prone Adjustment Procedure.   Place the patient prone with the involved knee flexed about 70° . Stand facing away from the patient at the side of the table, opposite to the involved tibia, and place your medial knee on the distal aspect of the patient's involved femur for stabilization. Grasp the distal aspect of the patient's tibia and fibula, with your fingers interlocking on the anterior aspect. Apply upward traction to the leg, and make the adjustment by externally rotating the patient's leg to correct the malposition.

Patient Supine Adjustment Procedure.   Place the patient supine, and stand on the side of involvement facing the patient. Place your medial foot on the table, and put the patient's ankle in your axilla. Your lateral hand should grasp the anterior surface of the patient's leg just above the ankle. Your medial hand is moved under the patient's leg so you can grasp your arm laterally. The patient's leg rests within your cubital fossa medially for support. Apply traction to the leg while simultaneously manipulating the leg into external rotation to correct the malposition.

      FIBULAR SUBLUXATIONS

Superior Fibula Subluxation

A superior fibula subluxation often follows eversion sprain of the ankle. Typical features include tenderness about the fibular collateral ligament due to jamming, restricted inferior fibula joint play, and possibly a slight foot-drop sign.

Adjustment.   Place the patient supine with knee extended and hip flexed at about 45° . Stand at the end of the table with the patient's foot placed on the anterior aspect of your thigh. Grasp the patient's ankle with your lateral hand, and take a web or capitate contact at the proximal aspect of the lateral malleolus. With your medial hand, overlap the wrist of your contact hand for stability. Apply traction, and simultaneously make a short inferiorly directed thrust to correct the malposition.

Inferior Fibula Subluxation

An inferior fibula subluxation can be the result of inversion ankle sprain and is often associated with tenderness about the collateral ligament of the fibula and restricted superior fibula joint play.

Adjustment.   Place the patient in the lateral recumbent position with the affected side upward and the medial aspect of the affected foot resting relaxed on the table. Stand at the foot of the table in line with the longitudinal axis of the patient's affected leg. Apply a capitate contact with your medial hand against the inferior aspect of the lateral malleolus, with your lateral hand grasping your contact wrist for stability. Apply pressure, and simultaneously make a short thrust directed superiorly along the vertical axis of the fibula to correct the malposition.

Anterolateral Fibula Subluxation

An anterolateral fibula subluxation is often the result of lateral hamstring strain, eversion ankle sprain, or trauma to the posterolateral aspect of the knee. It is characterized by lateral hamstring tendon tenderness, genu varum, excessive ankle pronation, and restricted posteromedial fibula motion.

Adjustment.   Place the patient prone with the involved knee flexed. Squat at the end of the table (facing the patient) so that the patient's leg can rest on your shoulder for stability. Grasp the involved leg and interlace your fingers around the posterior aspect of the patient's leg proximally. Direct a pisiform contact with your cephalad hand against the anterolateral aspect of the fibular head. Apply traction, and simultaneously rotate the fibula posteromedially to correct the malposition.

Posteromedial Fibula Subluxation

A posteromedial subluxation of the fibula often follows inversion ankle sprain, violent hamstring pull, trauma to the anterolateral knee, and genu valgum. Abnormal anterolateral fibula joint play is usually associated.

Adjustment.   Place the patient prone with the involved leg flexed. Squat at the end of the table (facing the patient) so that the patient's leg rests on your shoulder for stability. Grasp the involved leg and interlace your fingers around the posterior aspect of the patient's leg proximally. Apply a specific pisiform contact with your lateral hand against the medial aspect of the involved fibular head. Apply traction, and simultaneously rotate the fibula impulsively anterolaterally to correct the malposition.

Posteroinferior Fibula Subluxation

The typical physical features of a posteroinferior subluxation of the fibula include pain at the fibula head, lateral collateral ligament pain at the ankle, lateral hamstring complaints, and restricted anterosuperior fibula joint play. This subluxation is often the result of inversion ankle sprain.

Adjustment.   Place the patient supine with the affected knee flexed. Stand lateral to the involved limb with your cephalad hand within the popliteal fossa. Apply a thenar-pad contact against the fibular head. For leverage, grasp the anterior aspect of the patient's lower leg with your caudad hand. Apply oblique pressure with your stabilizing hand to flex the knee and push the leg superiorly, while simultaneously briskly lifting the fibular head anteriorly with your contact hand to make the correction.

      PATELLA DISORDERS

Patella Dysfunction

Rupture or inflammation of the patella tendon, quadriceps rupture or tendinitis, and fatigue fracture of the tibia have a high incidence of injury. In tendinitis, the pain may be perceived either during and shortly after activity or be chronic. Forceful jumping may result in an avulsion fracture of the patella.

Patella Apprehension Sign.   The patella normally displaces laterally with vigorous quadriceps contraction. When a person strongly extends the knee with the leg externally rotated, the patella may dislocate and lock if its attachments are weak. In testing, place the patient in the relaxed neutral supine position and apply increasing pressure against the patella. If a chronic weakness exists, the patient will become increasingly apprehensive as the patella begins to dislocate.

Dreyer's Sign.   Place the patient supine with the legs extended in the relaxed position, then ask the patient to raise the involved thigh while keeping the knee extended. If the patient is unable to do this, grasp the large quadriceps tendon just above the knee to anchor it against the femur and ask the patient to try to lift the limb again. If the patient is able to lift the limb when the quadriceps tendon is stabilized, a fractured patella should be suspected because the rectus femoris (a primary hip flexor) tendon attaches to the patella.

Patella Tendon Strain

The patella tendon is subject to partial tears, complete rupture (rare), peritendinitis, and focal degeneration. Partial tears are often misdiagnosed as simple strain. The clinical picture is pain on forced knee extension and during activity, point tenderness, possible extension block and weakness, thickened adjacent tissues, and roentgenographic soft-tissue changes. Differentiation from peritendinitis is likely only made during surgery. Treat as a severe acute or chronic sprain according to the history, with emphasis on rest, heel pads, ultrasound or deep heat.

Posttraumatic Ossification.   Ossification may be found in the patellar tendon during roentgenography following hemorrhage in partial tendon tears. The typical clinical picture is traumatic muscle pain and soreness and hemorrhage into adjacent soft tissues. Poorly defined ossification develops in 3–5 weeks. If a reduced dislocation has occurred, signs of ossification may be found in the soft tissues. After blunt trauma, the soft tissues may show evidence of heterotopic bone formation. Such ossification involves muscle tissue and fascial planes.

Chrondromalacia Patellae

Anything adversely affecting the normal movement of the patella within its track in the femoral groove can be the cause of knee pain. Chondromalacia is such a condition. It features rapid erosion and fragmentation of the cartilage of the patella. Incidence is highest in the young adult, and genu recurvatum is the typical exciting agent; ie, hyperextension during single-leg stance and the push-off phase of gait. The exact cause of the syndrome is unknown, but trauma is associated in two-thirds of the cases.

It is known that chondromalacia patella is invariably secondary to malposition; eg, direct trauma, recurrent patella subluxation, short lateral ligaments accompanying a weak vastus medialis, increased Q angle (20° +), genu valgum, external tibial torsion, pronated or flat feet, Morton's syndrome, and lower extremity postural instability. It is sometimes seen associated with a short-leg syndrome.

Pathology.   During the degeneration process, the cartilage thins, softens, cracks, and fissures appear. This causes underlying bone to become sclerotic.

Clinical Features.   In extreme flexion, subpatella pressure may rise to 20 times that of body weight. Thus it is not surprising that the pain is severely aggravated by walking steep stairs or running hilly terrain. Prolonged sitting with the knee flexed leads to stiffness relieved by extension. Pain rises from the posterior aspect of the patella that is increased by patellar compression against the femoral condyles and by strong quadriceps contraction. Tenderness is found at the posteromedial and posterolateral aspects of the patella. A sensation of "giving way," locking, or chronic joint clicking is typical. Squatting is aggravating. During active knee motion but not passive motion, grating is palpable, and usually audible, and accentuated with patella compression. Joint effusion and quadriceps atrophy are typical findings. Early x-ray films are negative, but the inner aspect of the patella shows sclerosis, roughening, irregularity, a narrowed patellofemoral space, and spurring in the late stage. Clarke's sign is positive.

Clarke's Sign.   The supine patient is asked to extend the knee and relax the quadriceps. Place the web of your hand against the superior aspect of the patella and depress it distally. The patient is then asked to actively contract the quadriceps as you compress the patella against the condyles of the distal femur. The sign is positive if the patient cannot maintain contraction without producing pain.

Perkin's Tests.   Place the patient in a relaxed supine position. Lock the top of the patella between your thumb and first finger and apply pressure toward the patient's foot. Ask the patient to tighten the quadriceps by hyperextending the knee. As the patella moves proximally, its movement should be smooth and gliding. An alternative method is to place a firm double-hand contact over the anterior knee, lean over the limb, and displace the patella from side to side while simultaneously applying pressure from the anterior to the posterior. Induced pain, grating, or crepitation (palpable or audible) during this maneuver is a positive sign, suggesting roughening as in chondromalacia patellae, osteochondral defects, or degenerative changes within the trochlear groove (eg, retropatella arthritis).

Management.   Treatment is similar to that for chronic sprain. Strapping is made to restrict excessive motion such as that for sprained collateral ligaments. Important to healing is restoring normal vastus medialis function through straight-leg quadriceps re-education with or without galvanic help. Rehabilitative exercises should include internal and external rotation exercises of the tibia, short-arc quadriceps exercises, and static quadriceps contractions. Special C-pads with a brace are helpful during early rehabilitation.

Sinding-Larsen-Johannson Disease

A complaint of knee pain and joint tenderness at the lower pole (rare at the upper pole) of the patella can be attributed to Sinding-Larsen-Johannson disease. Necrosis within the poles of the patella is the direct cause, and point tenderness is the main feature. Characteristics mimic chondromalacia; eg, pain on kneeling, insidious onset, a history of trauma, peripatellar edema, motion limitation, and lower pole thickening and tenderness. It is a self-limited condition, benign, and only temporarily disabling. Associated focal tendinitis is seen more often in boys than girls. It is apparently the pathologic result of traction irritation of the tendon at its patella attachment.


Infrapatellar Fat Pad Hypertrophy

Repeated stress to the knee joint may cause the infrapatellar fat pad or the synovial villi to become hypertrophied. The symptoms are joint weakness or definite locking, joint effusion when acute, pain on the medial aspect of the knee, and tenderness below and medial to the patella. However, positive diagnosis is likely only made by exploratory surgery. Conservative care is the same as that for severe sprain.

Patella Wobble Sign.   A patient in the sitting position is asked to extend the involved knee while you cup a palm over the patella. If erratic patellar motion is felt during the last phase of extension, an irregular retropatellar growth or some type of incomplete obstruction is indicated (eg, hardened fat pad, hypertrophied infrapatellar synovial folds).

Bipartite Patella

Bipartite patella is a congenital deformity characterized by development of the patella as two or more fragments. Two fragments are seen in films, usually bilateral. The condition may be discovered incidentally during knee roentgenography. It is usually asymptomatic unless the components are disrupted.


      SUBLUXATION-FIXATIONS OF THE PATELLA

In athletic knee injuries, the incidence of patella subluxation is second only to collateral ligament and meniscus injuries

Inferior Patella Subluxation

An inferior subluxation of the patella is typically associated with a patella that appears low during rest in the recumbent position, chondromalacia of the patella, blocked superior joint play, suprapatellar tendinitis, and restricted extension of the knee.

Adjustment.   The patient is placed supine with the involved knee extended. If full extension cannot be made comfortably, the popliteal space should be supported by one or more rolled towels. Stand on the side of involvement. Apply a web contact with your caudad hand against the inferior aspect of the patella, deep against the patella tendon. Your cephalad hand should grasp the wrist of your contact hand for support and added strength. Apply slow progressive pressure superiorly until all joint play is removed, then make a short thrust to stretch the patella tendon and normalize the position of the patella.

Superior Patella Subluxation

The major features of superior subluxation of the patella are upward displacement during rest in the recumbent position, patellar tendinitis, quadriceps spasm, chondromalacia patellae, and restricted inferior patella motion.

Adjustment.   Place the patient supine with the affected knee extended. Stand on the side of involvement. Apply a web contact with your cephalad hand against the superior aspect of the involved patella. Stabilize the patient's leg by your caudad hand grasping the patient's shin. Apply progressive pressure with your contact, and make a short thrust directed inferiorly to correct the malposition.

Superomedial and Superolateral Patella Subluxations

The physical features of these subluxations include unusual position during rest in the recumbent position, patellar tendinitis, quadriceps spasm, and chondromalacia patellae. Genu varum and restricted inferolateral patella motion are often associated with superomedial subluxations. Genu valgum and restricted inferomedial patella motion are associated with superolateral subluxations.

Adjustment.   Place the patient supine with the affected knee extended. Stand on the side of involvement. Apply a web contact with your cephalad hand against the pertinent superomedial or superolateral aspect of the involved patella. Stabilize the patient's leg by your caudad hand grasping the upper shin. Apply progressive pressure with your contact, and make a short thrust directed obliquely (ie, inferomedially or inferolaterally) to correct the displacement.

The lower leg, ankle, and foot work as a functional unit. Total body weight above is transmitted to the leg, ankle hinge, and foot in the upright position, and this force is greatly multiplied during gait. Thus the ankle and foot are uniquely affected by trauma and static deformities infrequently seen in other areas of the body. Common injuries are bruises, strains, tendon lesions, postural stress, compression syndromes, and tibia and fibula fractures. Bruises of the lower leg are less frequent than those of the thigh or knee, but the incidence of intrinsic strain and fatigue fractures is much greater.

A continual program of running and jogging is typical of most sports. A common result is strengthening of the antigravity muscles at the expense of others to produce a dynamic imbalance unless all muscles of the leg are developed simultaneously. An anatomical or physiologic short leg as little as an eighth of an inch can affect a stride and produce an overstrain in long-distance runners.


General Leg Bruises and Contusions

The most common bruise of the lower extremity is that of the shin where disability may be great because the poorly protected tibial periosteum is usually involved. Skin splits in this area can be difficult to heal. Signs of developing suppuration signal referral to guard against periostitis and osteomyelitis.

Management.   Treat as any skin-bone bruise with cold packs and antibacterial procedures, and shield the area with padding during activity. When long socks are worn, the incidence of shinbone injuries is reduced. An old but effective protective method in professional football that does not add weight is to place four or five sheets of slick magazine pages around the shin secured by a cotton sock covered by a conventional wool sock. A blow to the shin is reduced to about a third of its force as the paper slips laterally on impact.

Gastrocnemius Contusions

This highly debilitating injury is characterized by severe calf tenderness, abnormal muscle firmness of the engorged muscle, and an inability to raise the heel during weight bearing.

Management.   Treat with cold packs, compression, and elevation for 24–48 hours. Follow with mild heat or contrast baths and interferential therapy. Massage early is contraindicated as it might disturb muscle repair. The danger of ossification is less in the calf than in the thigh, but management must incorporate precautions against it and adhesion formation.

Nerve Contusions

Peripheral nerve injury in the leg features palsy, paresthesia, or anesthesia. Trauma behind the knee to the external popliteal nerve is characterized by the inability to extend the foot. Trauma to the peroneal nerve along the lateral aspect of the lower third of the leg may result in a palsy characterized by inability to flex the foot (foot drop). Peroneal symptoms are sometimes associated with asymptomatic loose tibiofibular ligaments. The excessive mobile fibula head, with demonstrated false motion, sometimes "clicks" during gait and tends to irritate the peroneal nerve as it winds around the neck of the fibula.

Management.   Treat as any peripheral nerve contusion with emphasis on ice massage or cold packs, rest, and firm support, followed later by a choice of vibrotherapy, contrast baths, high-volt therapy, alternating current stimulation, and graduated exercises. Temporary bilateral heel lifts are helpful in relieving tension on the injured nerve. A loose tibiofibular head can be aided by a sponge pad placed over the area and secured by an elastic bandage. Any case exhibiting a degree of atrophy or sensation loss over a few days deserves specialized neurologic consultation.

Seddon's General Classification of Nerve Injury

1.     Axonotmesis.   This type of nerve injury involves loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve (the encapsulating tissue, the epineurium and perineurium, are preserved). Because axonal continuity is lost, Wallerian degeneration occurs. Electromyography (EMG) performed 2 to 3 weeks later shows fibrillations and denervation potentials in musculature distal to the injury site. Loss in both motor and sensory spleens is more complete with axonotmesis than with neuropraxia, and recovery occurs only through regeneration of the axons, a process requiring time. Axonotmesis is usually the result of a more severe crush or contusion than neuropraxia. There is usually an element of retrograde proximal degeneration of the axon, and for regeneration to occur, this loss must first be overcome. The regeneration fibers must cross the injury site, and regeneration through the proximal or retrograde area of degeneration may require several weeks. Then the neuritis tip progresses down the distal site. The proximal lesion may grow distally as fast as 2 to 3 mm per day and the distal lesion as slowly as 1.5 mm/day. Thus, regeneration requires a number of weeks.

2.     Neuropraxia.   In this event, there is an interruption in conduction of the impulse down the nerve fiber, and recovery takes place without Wallerian degeneration. This is the mildest of nerve injuries, and is probably a biochemical lesion caused by concussion or shock-like injuries to the fiber. Neuropraxia is brought about by compression or relatively mind, blunt blows, including some low-velocity missile injuries close to the nerve. There is a temporary loss of function that is reversible, within hours to months, of the injury (the average is 6–8 weeks). There is frequently greater involvement of motor than sensory function. Autonomic function is usually retained.

3.     Neurotmesis.   This is the most severe lesion with a potential of recovering. It occurs on severe contusion, stretch, and in lacerations. Both the axon and the encapsulating connective tissue lose their continuity. The last (extreme) degree of neurotmesis is transsection, but most neurotmetic injuries do not produce gross loss of continuity of the nerve. Rather, internal disruption of the architecture of the nerve occurs sufficient to involve perineurium and endoneurium as well as axons and their covering. Denervation changes recorded by EMG are the same as those seen with axonotmetic injury. There is a complete loss of motor, sensory and autonomic function. If the nerve loss has been completely divided, axonal regeneration produces a neuroma in the proximal stump.

Common Peroneal Nerve Compression

This is an entrapment syndrome of the common peroneal nerve near the head of the fibula or as the nerve enters the anterior compartment. There is usually a history of recurrent ankle and/or foot injury. The major complaint is pain on the lateral aspect of the leg and foot initiated or aggravated by direct pressure over the trunk of the common peroneal nerve. This pressure pain usually radiates into the sensory distribution of the nerve.

Neurologic tests indicate motor loss characterized by weak ankle and toe dorsiflexion and weak foot eversion. Foot drop and tenderness at the head of the fibula are the most dramatic signs. As in any case of nerve compression, the cause must be determined and corrected. If conservative therapy fails, referral for surgical exploration should be considered.


      LEG STRAIN: GENERAL CONSIDERATIONS

Two of the most common injuries of the leg are calf strain and shin splints. Subtle stress fractures may be associated. A tear of the musculotendinous junction of the medial belly of the gastrocnemius sometimes occurs. At the site of tenderness, a palpable gap in the muscle is usually found.

Muscle Rehabilitation.   When mechanical elasticity is impaired, muscle tissue does not yield to passive stretch. After injury, this "Contracture Tiegel" is frequently the effect of spasm or prolonged immobilization, or both. For this reason, it is helpful to conduct goniometry in the weight-bearing position. For example, an ankle or knee may record a full range of motion while supine but be severely restricted in the squatting or kneeling position due to residual muscle shortening without actual fibrous contracture.

In most sports, a player should not be allowed to return to competition until the injured muscle becomes as strong as its uninjured contralateral mate. Strength-building exercises should be given just below the fatigue level, keeping in mind that injured muscles fatigue rapidly.

Muscle Fatigue.   Muscle elasticity, its ability to release tension, is essential for normal movement. A tired muscle loses some ability to relax, thus affecting its elasticity and endurance. A muscle with good endurance readily assumes its maximum length after repeated prolonged contractions, but a tired muscle does not return to its maximum length.

Frequent leg fatigue may lead to posttraumatic contractures and produce pain. Fatigue spasms are treated biomechanically by (1) warming the muscle with limbering movements; (2) stretching the muscle by resistance to the tightened muscle and its antagonist; (3) active stretching in an attempt to fulfill the possible range of motion; and then by (4) passive stretching to fulfill the possible range of motion. The stretching force must be a careful balance between that of easy performance and that of excessive misuse.

Toe Walk Test.   Walking for several steps on the base of the toes with the heels raised will normally produce no discomfort to the patient. With the exception of a localized forefoot disorder (eg, plantar wart, neuroma) or an anterior leg syndrome (eg, shin splints), an inability to do this because of associated low back pain or weakness can suggest a lumbosacral or sacroiliac lesion.

Management.   Heat is helpful to relieve muscle spasm, but cold and vapocoolant sprays have shown to be as effective in some studies. Compression and elevation during the early period are helpful to minimize the possibility of further bleeding. Later, mild passive stretch is an excellent method of reducing spasm in the long muscles. For example, standing on an incline (eg, Flex Wedge) relaxes a spasm through passive stretching. As a general use, spasms in a leg can be treated by warming and stretching as described above for fatigue spasms.

Peripheral inhibitory afferent impulses can be generated to partially close the presynaptic gate by acupressure, acupuncture, or transcutaneous nerve stimulation (TENS). Isotonic exercises benefit by improving circulation and inducing the stretch reflex when done supine to reduce exteroceptive influences on the central nervous system. An acid-base imbalance from muscle hypoxia or acidosis may be prevented by alkalinization with supplements.

Once the focal cause has been found and relieved, which may be as high as the lower back or as low as the foot, treat locally as a strain. Primary upper cervical subluxation has not been found to be a factor in the author's experience. After the acute stage, emphasis should be on structural alignment along with choices of deep heat, interferential therapy, analgesic pack, passive massage, heel pad, and good strapping support. Taping should continue for a month after full activity is resumed. No regimen has proved ideal, and modalities offer unencouraging benefit. Prevention through properly graduated conditioning and interval training is the best advice. If conservative measures are unsuccessful, surgical decompression must be considered.

An anatomical short leg is often involved that requires a permanent heel lift that should be prescribed moderately under actual need. A weak longitudinal arch is sometimes implicated. A 2 X 2-inch pad of 1/4-inch gauze can be secured on the plantar surface of the foot to cover the arch and the anterior third of the heel. Heavy patients may require a double pad.

Strapping.   Good support requires taping high up the lateral and medial leg, and applied with considerable force. Unyielding tape should never be used. However, the more modern and simpler method is to place a 2 X 6-inch piece of 1/2-inch-thick foam rubber over the involved shin or calf and secure it with an elastic bandage.

Gastrocnemius Strain (Tennis Leg)

Gastrocnemius overstress leads to a common strain of the leg that is sometimes misdiagnosed as a ruptured plantaris tendon. The onset usually features immediate calf cramping, generalized calf spasm, and extreme tenderness at the site of strain. Strain near the Achilles tendon is usually attributed to excessive running on the balls of the feet. Calf strain occasionally occurs at the gastrocnemius heads and is confused with knee injury after a snapping overextension. If this is the situation, tenderness will be found deep in the popliteal fossa when the knee is flexed.

Heel Walk Test.   A patient should normally be able to walk several steps on the heels with each forefoot flexed. With the exception of a localized heel disorder (eg, calcaneal spur) or contracted calf muscles, an inability to do this because of associated low back pain or weakness can suggest an L5 lesion.

Repetitive Heel Raise Test.   The standing patient is asked to raise the heels (ie, toe stand) repetitively several times. If this induces ankle pain, instability, a posterior compartment syndrome, or a subluxation complex should be suspected. If this exercise cannot be done because of weakness and ankle pain is absent, a gastrocnemius or neurologic deficit should be suspected.

Management.   Treat as any severe strain, but be forewarned that rehabilitation is slow. Heat enhances relaxation and aids circulatory flow but increases swelling and pain. Cold reduces swelling but increases cramping. Thus, structural normalization, rest, muscle techniques, interferential therapy, acupuncture, and a gradual program of progressive locomotion appear to be the best approach.

Popliteus Tendon Rupture

This accident occurs most often in the middle aged. An individual makes a jump, lands abruptly, feels a "pop" in the calf, a sudden sharp pain develops, and incapacity ensues. This typical history of popliteus tendon rupture is sometimes confused with meniscal injury, phlebitis, or Achilles rupture or tendinitis.

Management.   Ice, compression, elevation, and rest appear to be the treatment of choice during the early stage, followed by appropriate physiotherapeutic measures. A careful check should be made for associated lower spine, pelvic, or lower extremity subluxations or fixations.

Soleus Strain

Soleus strain independent of the gastrocnemius strain is rare, but it does occur. It is characterized by a palpably tight and tender soleus but relaxed and nontender gastrocnemius.

Ankle Dorsiflexion Test.   Limitation of the gastrocnemius or soleus muscles restricting ankle dorsiflexion can be differentiated by this test. Have the patient sit on the examining table with the knees flexed and relaxed. Grasp the foot and flex the knee to slacken the calf, then dorsiflex the ankle. If this can be achieved, the gastrocnemius is the cause of the restriction. If the soleus is at fault, it will not be affected by knee flexion; ie, it will be the same in either knee flexion or extension.

Management.   As with gastrocnemius strain, healing is often slow and frustrating. Rest, related structural correction, muscle techniques, interferential therapy, acupuncture, and a slowly graduated program of foot dorsiflexion and stretching exercises are usually recommended. It often takes 2 weeks or more before full competitive strength returns.

Plantaris Rupture

Although frequently called "tennis leg" because of its frequent association with overstress during serving, this disorder can be related to many physical activities. Some authorities, however, define tennis leg as a Grade III tear of the medial aspect of the gastrocnemius.

Plantaris rupture is sometimes confused with and often accompanies soleus or gastrocnemius strain because the function of the plantaris muscle is to assist the soleus and gastrocnemius muscles. In isolated plantaris strain, which is not common, there is sharp calf pain with an explosive onset, tenderness, and an area of indurated tissues located deep at midcalf and lateral to this site when palpating (thumb) from the popliteal space to the heel. Pain is increased by dorsiflexing the foot against resistance. Bleeding and a deep thrombophlebitis are often associated. Signs of ecchymosis on each side of the Achilles tendon usually appear in a few days. Quite frequently, an Achilles strain and separation of calf fascia are associated. There is always a danger of tendinitis ossificans, and recurring symptoms can often be traced to a degree of myositis ossificans.

Management.   General strain therapy should include initial cold packs and compression for 36–48 hours; elevation for 24 hours. An analgesic pack of menthol salicylate (buttered and covered under the strapping), deep heat, interferential therapy, heel pads, cane support while walking, progressive passive stretching, and whirlpool or shower hydrotherapy at 108° F are helpful. Full activity is rarely assumed before 3–4 weeks. If sports activity is resumed, it should be preceded by deep massage and stretching exercises for 3–5 months after injury.

Fascial Hernia and Tears

Fascial tears can occur most anywhere, but they are usually found in the leg following blunt trauma near the tibial crests. Bleeding is more persistent here than in other contusions of the leg. After swelling reduces, palpation reveals the muscle herniating through the fascial defect.

Management.   Symptoms are usually present only during activity when the muscle swells and impinges at the hole. This can be prevented simply by an overlaid sponge pad secured by an elastic bandage. While the method may be crude, it is often the choice of the patient over that of surgery requiring a second donor-site incision.

Shin Splints (Tibialis Anterior or Posterior Tendinitis)

Leg pain and local tenderness after unaccustomed running or stressful walking characterize this syndrome. It is associated with an aseptic inflammation of one or more injured muscle-tendon units. The anterior shin muscles warm slowly and cool rapidly because they are squeezed tightly between bone and skin by fascia. The blood supply of the interosseous membrane is quite limited.

The undiagnostic term "shin splints" is a general phrase for any overuse discomfort in the anterior leg following exercise. The common cause may be better classified as tibialis anterior or posterior tendinitis or myositis syndrome, tendoperiostosis, or stress fracture. Differentiation is made by mode of onset, site of tenderness, and late signs in roentgenography. Tenderness is often acute over the posterior tibialis muscle attached along the medial border of the tibia, but it is just as frequently found at the attachment of the anterior tibial muscle to the lateral border of the tibia.

Intramuscular tension from engorgement is exaggerated in this syndrome by the unyielding surrounding tissues to a degree that local infarction may occur. It can easily lead to local massive necrosis or Volkmann's contracture. Alternately raised muscle fiber tension so alters the muscle's internal frictional resistance that rapid movements are impossible and muscle tearing develops if the whole muscle does not go into spasm. The engorged muscle becomes trapped within its fascial compartment and tends to strip from its attachments to bone. Circulation of the anterior tibial artery becomes impaired.

Most authorities do not attribute any part of the disorder to a local accumulation of lactic acid. Prolonged overuse may produce muscle hypertrophy of the lower fibers of the tibialis anterior causing blocking of the upper extensor retinaculum of the ankle. This "space-occupying" lesion effect produces local symptoms. A blow to the lower leg will have the same effect.

Shin splints frequently results from posterior tibial muscle overstress occurring when hyperpronation produces traumatic traction on the tendon, tibial periosteum, or interosseous membrane. Pain arises along the tendon or at the medial and distal two-thirds of the tibial border, or both. Periostitis resulting from acute or recurring posterior tibial muscle strain may progress to tibial fatigue fractures. Symptomatology, case history, and signs from diagnostic imaging are useful in differentiation.

The pain is usually throbbing, deep seated, relieved slightly with rest, but increased at night. A poorly responding case of shin splints with pain even on rest suggests a compartment syndrome or fatigue fractures. Other features include gradually increasing swelling and restricted motion. Keep in mind, however, that all muscles swell after exercise, and this is particularly true of unconditioned muscles. Flat feet, tight calves producing plantar flexion, and imbalance between the anterior and posterior muscle groups are commonly associated. That is, the anterior leg muscles are often weaker than the posterior group, and this produces a biodynamic imbalance requiring special consideration in rehabilitation.


Periostitis

Tibial Periostitis.   Anterior tibial periostitis is a frequent complication of leg strain that results from traumatic microelevation of the periosteum by fascial overstress. Severe pain localized at the medial tibial border occurs during activity. A small tender area may be palpable. If extremely severe, conservative measures are rarely helpful. If pain cannot be relieved within 1–-2 days, referral should be considered (eg, local anesthesia and steroids).

Fibula Periostitis.   Fibula periostitis is a frequent complication of blows to the lateral leg, especially at the lower third of the bone. There is persistent soreness aggravated by activity, shaft tenderness, and shaft thickening demonstrated by roentgenography. Crepitus may or may not be present. Management should include 1–2 weeks of rest followed by graduated active exercise.

1. INIITIAL REHABILITATION FOLLOWING PRIMARY CARE (RICE) 
   a.  Postexercise ice, pulsed ultrasound, alternating-current muscle stimulation
   b.  Compressionette for residual effusion
   c.  Passive knee and hip ROM stretches to tolerance
   d.  Aquatic therapy
   e.  Isometrics
   f.  Cryokinetics or cryostretch following:
       1.  Straight leg raises (active)
       2.  Quadriceps sets
       3.  Terminal knee extensions (active)
       4.  Cocontractions
       5.  Heel slides (supine and sitting)

2. INTERMEDIATE PHASE
   a.  Stationary bicycling
   b.  Moist heat, continuous ultrasound
   c.  Passive knee and hip ROM stretches to tolerance, quadriceps stretching
   d.  Increased demand in aquatic therapy
   e.  Active exercises:
       1.  Proprioception exercises
       2.  Knee extensions, no resistance
       3.  Terminal knee extensions against mild resistance
       4.  Knee flexion against mild resistance
       5.  Lateral step-ups
       6.  PNF patterns
       7.  Heel walking
       8.  Stationary bicycling

3. ADVANCED PHASE
   a.  Protective wrapping or Orthoplast
   b.  Eccentric knee extensions
   c.  Rapid isokinetics, nonweight-bearing
   d.  Theraband hip extension, flexion, abduction, adduction
   e.  Moderate-speed walking, long steps
   f.  Postexercise cryotherapy

4. CRITERIA FOR RETURN TO STRESSFUL ACTIVITY
   a.  Adequate hip/knee muscle strength, endurance, power for lifestyle
   b.  Quadriceps tenderness absent or minimal
   c.  Quadriceps flexibility at least 80% and equal bilaterally
   d.  Asymptomatic after maximum function

      CIRCULATORY AND VASCULAR DISORDERS

Low back pain is one of the most common entering complaints in a chiropractic office. Because of this, Wiehe points out the importance of recognizing associated problems of neurovascular stenosis in the large arteries of the leg due to L4–L5 irritation and differentiating them from other factors that can produce circulatory insufficiency. For example, thrombosis of the femoral artery can induce the same symptomatic picture as sciatic neuritis. Thus, diagnostic procedures might include, when indicated, unilateral-vertical and bilateral-horizontal blood pressure comparisons, Doppler ultrasound readings, plethysmography, and reactive hyperemia tests in addition to common clinical tests.

Screening Lower Extremity Circulatory Insufficiencies

Lymphatic obstruction, venous disease, or acute arterial occlusion may result in ankle edema. Venous disease is the most common cause of pitting on pressure. Trauma or local disease is the usual cause for unilateral swelling, while cardiac or lymphatic disorders produce bilateral swelling.

When pulses are absent in a limb, the examiner should return to the most distal palpable pulse and auscultate for an audible bruit suggesting the site of obstruction. Next, finger pressure is applied to the medial dorsal area of the foot and the time noted for the white spot to disappear. Then the patient's weight can be rotated to the outer border of the foot and the test repeated. Blanching time is delayed in cases of pronation and arch weakness due to circulatory compromise. To evaluate the capillary filling time of the toes, a selected toe is compressed until it blanches white, and then the pressure is released quickly. Normal color should return within 6–-10 seconds.

Skin color of the lower extremities normally darkens in the weight-bearing position. An elevated pink foot that markedly deepens in color in the standing position suggests arterial insufficiency or vascular disease. Venous filling time on the dorsum of the foot should be noted at the same time. Collapsed veins should fill within 12 seconds on standing.

The pulse of the posterior tibial artery is often difficult to locate, even when the ankle is relaxed. This artery lies between the tendons of the flexor digitorum longus and the flexor hallucis longus muscles. When the pulse is found, it should be compared bilaterally. The tibial nerve follows the course of the posterior tibial artery and is located just behind and lateral to the artery. A ligament binds the neurovascular bundle to the tibia creating the tarsal tunnel, which has the same implications as the carpal tunnel of the wrist.

Intermittent claudication and cramps from insufficient circulation through the arteries of the legs may cause a sudden "giving way" of one or both legs during running or walking. Leg strength returns after a short rest. The frequent recurrence of painful cramps at rest may be the only manifestation of the disorder. In other cases, there are various forms of paresthesia such as numbness, prickling, and "hot feet" at night. Obliteration of the dorsalis pedis (or larger arteries) by arteriosclerosis is sometimes found in the older patient, but there is reason to believe that local anemia due to vasomotor disturbance (vasospasm) or other causes may produce similar cramps such as those seen in athletes after a hard run and in pregnancy. Rarely is Buerger's or Renault's disease found to be the cause.

Buerger's Test.   The patient is placed supine with the knees extended in a relaxed position. Lift the patient's involved leg with the knee extended so the lower limb is flexed on the hip to about a 45° angle. Then ask the patient to move the ankle up and down (dorsiflex and plantar flex the foot) for a minimum of 2 minutes. The limb is then lowered, the patient is asked to sit up, the legs are allowed to hang down loosely over the edge of the table, and the color of the exercised foot is noted. Positive signs of arterial insufficiency are found if (1) the skin of the foot blanches and the superficial veins collapse when the leg is in the raised position and/or (2) it takes more than 1 minute for the veins of the foot to fill and for the foot to turn a reddish cyanotic color when the limb is lowered.

Moskowicz's Test.   The patient is placed supine with the knees extended in a relaxed position. Elevate the straight limb to about 45° , wrap an elastic bandage around the limb in an overlapping fashion from the ankle to the midthigh, and support the elevated limb in this position for 5 minutes. At the end of this time, quickly untwirl the bandage from above downward and note how rapidly the skin blushes when the obstruction to the collateral circulation has been removed. If the normal blush is absent or lags far behind the unbandaged area, something (eg, an arteriovenous fistula) interfering with the collateral circulation should be suspected.

Treadmill Claudication Test.   If lower extremity claudication is suspected, the patient is asked to walk on a treadmill at a rate of 120 steps/minute. If cramping, and sometimes a skin color change, occurs, the approximate level of the local lesion can be identified. The time span between the beginning of the test and the occurrence of symptoms is used to record the "claudication time," which is usually recorded in seconds.

Compartment Syndrome

There are four compartments within the leg (anterior, lateral, superficial posterior, and deep posterior), and any one of them can develop an acute or chronic syndrome of swelling and mild ischemia following vigorous exercise. See Table 3. Two common causes are local arterial spasm (vasospasm) and muscle swelling increasing intracompartmental pressure that, in turn, inhibits local circulation, which leads to ischemia. Less frequently, the cause can be traced to a crushing injury, a severe burn, or a vascular defect. If severe or recurring (eg, in long-distance runners), muscles become fibrotic and nerve damage occurs. The initial symptoms are similar to those of a shin-splint syndrome or a crushing injury.


Table 3.   Lower Extremity Compartment Syndromes

SIGN	Anterior	Lateral		Posterior Superficial	Posterior Deep
Pain on passive movement	Toe flexion	Foot inversion		Foot dorsi-flexion	Toe extension
Site of tissue tenseness	Between fibula and tibia, anteriorly		Lateral fibula area	Bulk of calf	Between tibia and Achilles tendon in posteromedial lowere leg
Weakened muscles	Tibialis anterior, toe extensors, foot dorsiflexors	Peroneals		Gastrocnemius, soleus	Tibialis anterior, toe flexors
Specific sign of weakness	Drop foot	Eversion		Plantar flexion	Inversion
Sensory change distribution	First dorsal web space (deep peroneal)	Anterolateral leg; dorsum of foot (deep and superficial peroneal)		No signs or sural nerve distribution	Posterior plantar surface, medial arch

Local cramps, entrapped swelling, and sometimes numbness can be severely debilitating. The onset may be sudden or gradual. The engorged muscle becomes trapped within its fascial compartment and tends to strip from its attachments to bone. The overlying skin becomes red, warm, and possesses a stony hardness. Signs of tendinitis behind the medial malleolus or along the tibia, deep calf myositis, tenderness in the posteromedial angle of the tibia, pain during use, and foot pronation are usually related. Mild weakness may develop.

Being surrounded by bone, tendons, and fascia, the compartment has difficulty in expanding and this leads to necrosis of vessels, muscles, and nerves, creating foot-drop and other complications. A difficult complication to treat is widespread tendoperiosteitis tending to terminate in severe scars and adhesions. Referral for surgical decompression is often required.

Anterior Compartment Syndrome.   An anterior compartment syndrome is the most common of the leg. Acute cases are often mistaken for shin splints, and chronic cases must be differentiated from chronic tendinitis and tibial fatigue fractures. Tissues of the anterior compartment should normally feel soft and yielding; tautness suggests a pathologic condition increasing intracompartmental pressure. The sinus tarsi area is often involved in ankle sprains wherein its normal concavity is swollen and tender. Deep tenderness may suggest concomitant arthritis, myositis, fracture, or spastic-foot syndrome. The ankle pulse is absent or greatly diminished, and passive stretch increases the pain. The pulse of the dorsal pedal artery can be felt between the extensor hallucis longus and extensor digitorum longus tendons of the dorsum of the foot.

Management.   Relax taut muscles and fascia, and free any fixations found in the lumbar, pelvic, hip, knee, and ankle areas. Treat during the early stage as an acute strain/sprain with circulatory interference (eg, cold, rest, acupuncture, or microcurrents as indicated), and enhance venous and lymphatic return (eg, elevation, mild vibromassage, remote superficial heat). Do not apply compression as one might normally do to minimize bleeding. Once acute symptoms subside, local deep warmth, stretching, passive exercise, and nutritional supplementation are commonly used. Until healing is well established, athletes should be warned against poor shoes, running on unlevel surfaces, running at high speed, and running uphill. Bilateral heel lifts may help during rehabilitation to reduce the tension on the Achilles tendon, but prolonged use leads to contraindicated shortening.

Varicosities

Perthe's test is an excellent procedure to use in differentiating the extent of superficial and deep lower limb varicosities. A variation of this is Pratt's tourniquet test, which can be used to evaluate the integrity of specific communicating veins. If a suspicion arises that something is interfering with the collateral circulation, Moskowicz's tourniquet test (described previously) is helpful. Homan's sign offers a strong indication that thrombophlebitis exists, and Kelly's test will help in general differential diagnosis.

Perthe's Tourniquet Test.   An elastic bandage is applied to the upper thigh of a standing patient, sufficient to compress the long saphenous vein. The patient is then asked to walk around briskly for a couple minutes. The varicosities are then examined. This exercise with the thigh under pressure should cause the blood in the superficial (long saphenous) system to empty into the deep system via the communicating veins. Thus: (1) If the varicosities increase in their distention (become more prominent) and possibly become painful, it indicates the deep veins are obstructed and the valves of the communicating veins are incompetent. (2) If the superficial varicosities remain unchanged, the valves of both the long saphenous and communicating veins are incompetent. (3) If the superficial varicosities disappear, the valves of the long saphenous and the communicating veins are normal.

Pratt's Test.   This variation of Perthe's test is used to evaluate the integrity of specific communicating veins. The patient is placed in the supine position with the knees extended. The involved limb is raised about 45° to empty the veins, placed on the examiner's shoulder or held by an assistant, and an elastic bandage is applied to the upper thigh sufficient to compress the long saphenous vein. A second elastic bandage is wrapped about the limb from the foot to the tourniquet on the thigh. The patient is then asked to stand, and the examiner carefully observes the varicosities of the leg as the lower bandage is slowly unwrapped from above downward. The tourniquet on the thigh is left in place. As the lower bandage is untwined, the site of an incompetent communicating vein is shown by the appearance of a prominently bulging varicosity (blowout). When the first blowout is found, the spot is marked, and the upper bandage is extended to that point. Another bandage is then applied from that site downward, and the test is repeated again and again until all blowouts have been marked. Caution should be taken in this test because severe pain and swelling may arise in the calf if the deep veins are obstructed.

Homan's Sign.   The patient is placed supine with the knees extended in a relaxed position. The examiner, facing the patient from the involved side, raises the involved leg, sharply dorsiflexes the ankle with one hand, and firmly squeezes the calf with the other hand. If this induces a deep-seated pain in the calf, a strong indication of thrombophlebitis is found.

Trendelenburg's Vein Test.   This simple test helps to decide which valves are incompetent when varicose veins appear with standing. Raise the affected leg of the patient in the supine position until the veins drain completely. Next, apply a tourniquet about the upper thigh and have the patient stand upright. The perforators are incompetent if the varicosities now fill partially from below, allowing blood to flow from the deep to the superficial system. However, if the veins remain collapsed on standing, remove the tourniquet and observe the reaction. Rapid filling from above indicates the saphenous valves are faulty.

Kelly's Test.   To differentiate between saphenous varix and femoral hernia, compress the veins below the knee with one hand applied to the calf. With the other hand, squeeze the inner side of the thigh firmly just above the knee. The blood will be returned through the internal saphenous vein and make the swelling in the groin quiver.

Mild Traumatic Phlebitis

Contusion to the greater saphenous vein may lead to rupture resulting in extensive swelling, ecchymosis, redness, and other signs of local phlebitis. Tenderness will be found along the course of the vascular channel.

Bruising of the inner leg or thigh may present superficial venous thrombophlebitis as a complication. Fortunately, the lesion is usually well localized and emboli are rare in mild cases. Phlebitis with thrombosis of a vein, usually the saphenous, is a common cause for a swollen thigh and leg with pain and tenderness, especially over the inflamed vein where a cordy induration may be felt. Secondary bacterial infection is the usual cause, yet sometimes the cause cannot be found. Diagnosis depends on eliminating the presence of another cause.

Note:   Severe phlebitis should be referred for specialized care for the danger of embolism is great. Referral should be made on the first sign of thrombosis regardless of other signs.

Management.   Management of mild cases is by rest, cold, compression by an elastic bandage, and elevation for at least 24 hours. Later, progressive ambulation, mild heat, and contrast baths can be used. Progressive exercises may begin in 4–6 days. If physically demanding work or competitive activity is resumed, the area should be provided extra protection. Anticoagulants are considered by Williams/Sperryn to be unnecessary unless the thrombotic process is actively spreading.