THE KNEE: DIAGNOSIS AND MANAGEMENT Gaetano P. Monteleone, Jr., M.D. Director, Division Sports Medicine Dept Family Medicine West VirginiaUniversity School of Medicine [email protected] I. The KNEE A. Anatomy and Biomechanics
1
from DeLee, Drez, Orthopedic Sports Medicine, 1994
• BONES 1. Femur- The trochlear groove of the femur is the “valley” within which, the patella glides. The lateral femoral condyle in most patients is higher and wider than the medial femoral condyle. The articular cartilage lining the femur is considerably less than that of the patella. The femur transmits forces from the lower leg to the pelvis and L-spine. It also facilitates ambulation. 2. Patella- One of the largest sesamoid bones of the body. It is located within the quadriceps/patellar tendon. There are facets on the posterior surface of the patella (in contact with the femur): medial, lateral and odd. The cartilage overlying these facets are the thickest cartilage in the body (especially the medial facet).
3. Tibia- serves as the distal-most attachment of the extensor mechanism. The patellar tendon inserts onto the tibial tubercle (apophysis).
This apophysis may become inflamed to result in Osgood-Schlatter “disease”. The tibial plateau supports the femur from above and the menisci. • SOFT TISSUE
2 1. Quadriceps- the quadriceps musculature allows knee extension. • Vastus lateralis • Vastus medialis (VMO) • Vastus intermedius • Rectus femoris 2. Quadriceps and patellar tendons-provide superior and inferior stabilizing forces to the patella. 3. Medial and lateral retinacula- primary stabilizers on either side of the patella. 4. Patellofemoral ligaments- other major soft tissue restraints to mobility of the patella. 5. Bursae- multiple bursae, especially the prepatellar bursa. Acute inflammation may lead to anterior knee pain. 6. The hamstring muscles cause flexion of the knee and assist with flexion of the hip. They insert medial and lateral knee and contribute small amount to the stability of the knee to varus and valgus stress. Note- the vastus lateralis and rectus femoris muscles tend to build up preferentially. The result is a relatively weaker vastus medialis obliqus (VMO).
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This allows for lateralization and tilting of the patella. The patella may not sit nicely in the femoral groove, but may ride on top of the lateral femoral condyle, increasing wear-and-tear. Concomitantly, the vector analysis of forces created by the quadriceps and patellar tendons reveals that the mean resultant vector is posteriorly directed (through the patella and femoral condyles).
In fact, the greatest force occurs with the knee flexed to 70-90°. This posteriorly-directed force is magnified if the hamstrings are tight. The above biomechanical factors cause the patella and femur to “grind” together, increasing wear-and-tear, pain, inflammation. The exact etiology for pain in patellofemoral pain syndromes is not known. It is believed to be a combination of mechanical and biochemical factors. • LIGAMENTS 1. ACL is the primary restraint to anterior directed force of the tibia relative to the femur. Secondary restraints to anterior translation include MCL, LCL, iliotibial band and capsule. In fact, in pts with a torn ACL, the MCL provides significant contribution to anterior translation restraint. In addition, ACL provides secondary restraint for valgus stress. 2. MCL is the primary restraint to valgus stress. It is also a secondary restraint to anterior translation. MCL originates from the medial femoral condyle and inserts distal to the tibial
3 plateau. There are superficial and deep components. The superficial component is extra-articular. The deep component is more intra-articular and adherent to the medial meniscus. This explains why there exists the terrible triad: ACL tear, MCL tear and medial meniscus tear. 3. PCL is larger and stronger than the ACL. It is the primary restraint to posterior translation of the tibia relative to the femur. Secondary support to posterior motion is contributed by the LCL, posterolateral capsule (especially with full extension).
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4. LCL primary restraint to varus translation. ACL/PCL are secondary restraints to varus stress. 5. Meniscofemoral ligaments two small ligaments arise from the posterior horn of the lateral meniscus, pass anterior (Humphrey) and posterior (Wrisberg) to the PCL respectively, and insert into the lateral aspect of the medial femoral condyle. • MENISCUS The meniscus is a hydrated fibrocartilage composed of a dense extracellular matrix and a sparse population of fibrochondrocytes. Vascular supply of the menisci are a major determinant of a healing response. Fetal development of the menisci creates vasculature throughout the entire width of the meniscus. By nine months, the inner one third will be avascular. By adulthood, only the thicker periphery will be vascular (10-30%).
Note that the menisci will translate upon the tibial plateau during flexion and extension of the knee. The lateral meniscus translates more than the medial meniscus. This increased mobility is probably one factor in the decreased risk of injury for the lateral meniscus. Functions of the meniscus Joint congruity: the menisci increase the contact area between the femur and tibia Load transmission: The forces acting at the surface of the meniscus are distributed to a larger surface area on the femoral condyles. Load-bearing and the subsequent distribution of force is one of the most important functions of the meniscus. In that regard, meniscectomy has been shown to increase peak stress and decrease contact area, leading to the classic degenerative changes that we see clinically. “Shock transmitters.” Joint lubrication Joint stability- The meniscus lend some support to the overall stability of the knee. Therefore, meniscal tears may present as instability sxs (buckling or giving way).
1. Medial meniscus: the medial meniscus is semilunar in shape, narrow anteriorly and broadening posteriorly. The medial meniscus is closely adherent to the deep portion of the MCL, a fact that reflects clinical relevance in combination injuries. 2. Lateral meniscus nearly circular and covers a larger portion of the lateral plateau. The width is fairly uniform throughout.
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ACL Injuries in Athletes The Anterior Cruciate Ligament (ACL) attaches the femur, which is the thighbone, and the tibia, which is the shin, together (northstar). A torn ACL is one of the most excruciating experiences in an athlete? s life. It is the first thing that comes to mind when they hurt their knee on the field; for many it is their greatest fear. A torn ACL can sometimes mean the end of an ...
4 B. History Localization of pain or symptomsLocation of Pain Anterior
• • • • • • • • • • • • • • • • •
Differential Diagnosis
Patellofemoral arthralgia (PFA) Patellar/quadriceps tendinitis Osgood-Schlatter disease Sinding-Larsen-Johansson disease Degenerative joint disease (OA) OCD MCL sprain Medial meniscus tear Pes anserine bursitis/tendinitis OA LCL sprain Lateral meniscus tear Iliotibial band syndrome Meniscal tears in the posterior horns PCL tear Baker’s cyst Popliteus tendinitis
Medial
Lateral
Posterior
Mechanism of Injury- pivot injury may cause dislocated patella, ACL tear or meniscus tear. Direct blow may cause fractures or MCL/LCL/PCL sprains (depending upon the direction of the force).
Presence of effusion- large effusions point toward ligamentous and meniscal pathology. Timing of effusion- ACL tear usually first 4-12 hrs; meniscus by 12-36 hrs. Locking? Determine true from pseudo-locking. True locking causes knee to become incapable of further flexion and extension. Pseudo-locking involves clicks and clunks as the patella moves within the femoral groove. Instability- the sensation of knee giving way, buckling or shifting (again, determine true from pseudo-buckling).
True buckling should cause the pt to fall to the ground. This implies ligamentous or meniscal damage. Pseudobuckling (caused by weakness of quadriceps) occurs when the pt does not fall to the ground, and often does not relate to pathology of the ligaments and meniscus. Acute vs Chronic- acute traumatic injuries imply ligamentous, bony and meniscal injuries. Acute injury may be patellar subluxation/dislocation and patellar/quad tendon rupture. Recent treatment- PRICES, NSAID’s, rehab PMHx/PSHx- include diagnoses, meds, rehab. Some poorly controlled medical conditions may inhibit healing potential (DM, hypothyroidism, renal insufficiency).
5 D. Physical Exam Inspection- deformity, effusion, ecchymoses, erythema, muscle asymmetry (atrophy) and Quadriceps angle. a. Q (quadriceps) angle- measure of genu valgus (knock-kneed).
The angle created by two lines: one drawn from the middle of the patella to the tibial tubercle, and the other line from the middle of the patella to the ASIS of the iliac crest. Normal in males is
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... and grade-three tears completely disrupt the ligament. Twisting injuries to the knee put stress on the cartilage or meniscus and can pinch ... cleats, such as football players, are susceptible to ACL injuries. An MCL injury are usually caused by a direct blow to ... plan your procedure, your orthopaedic surgeon may order pre-operative tests. These may include blood counts or an EKG (electrocardiogram). ...
6 flexion: instability (opening) during valgus stress with the knee in complete extension demonstrates both and MCL and ACL tears. e. Lachman’s test for ACL. Knee in 30°of flexion. Outside hand stabilizes the femur, inside hand around the tibia at the tibial tubercle. An anteriorly-directed force is applied. Assess for translation (in mm) and endpoint (good, fair, poor).
This is the most accurate exam maneuver for ACL tears acutely. False negative tests occur when hamstring spasm with tense effusion, bucket-handle tears of meniscus. False positive test with PCL tear.
f. Anterior/posterior drawer tests- for ACL and PCL, respectively. The knee is flexed to 90°, hip at 45° with feet flat on exam table; examiner may sit on foot, apply an anteriorly or posteriorly-directed force. Maintain thumbs at joint line. Assess for translation and quality of endpoint. The anterior drawer is generally not as helpful as the Lachman and pivot shift tests for ACL integrity. In addition, it requires more motion to an acutely injured knee. The posterior drawer test, on the other hand, is the most helpful test for PCL integrity. g. Pivot shift test- for ACL integrity. Start with knee straight and an examining hand under heel of foot. Turn the foot into internal rotation with one hand, place a valgus-directed force at the knee with the other hand. At the same time, bring the knee from extension to flexin. A palpable clunk appreciated at 30° of flexion at the joint line represents the tibia reducing on the femur in ACL-deficient knee. This may be quite uncomfortable for the acutely injured patient. It requires significant relaxation on the part of the patient, and they probably won’t let you do it a second time (so get it right the first time!).
This is the most accurate test for chronic tear of the ACL (> 6 months).
h. Posterior sag sign- have patient lying relaxed and supine, with knees in position similar to the anterior/posterior drawer tests. In patients with a PCL tear, the tibial tubercle will sag posteriorly relative to the other tibial tuberosity. The quadriceps active test- for PCL integrity involves the same position. Active contraction of the quadriceps will shift the tibial tubercle anteriorly (back to neutral) in a patient with a PCL tear.
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Nursing care after a total knee replacement is very essential in promoting a speedy and safe recovery for a patient. In an attempt to replicate the knee’s natural ability to roll and glide as it bends by cutting away damaged bone and cartilage and replacing it with an artificial joint, acute pain following the procedure can be unbearable. In assisting the patient in controlling the pain would only ...
7 i. McMurray test- positive test indicated by a palpable or audible clunk. Pain is not diagnostic. This test performed by palpating bilateral joint lines with the pt supine. The examiner produces internal/external tibial rotation while flexing the knee. The examiner then extends the knee while simultaneously, the examiner produces a valgus or varus-directed force. The value of this and other clinical exam tests has been questioned. The positive predictive value approximates 85%, for audible/palpable click. The positive predictive value is higher in the medial meniscus than the lateral meniscus. j. Apley’s distraction test- patient lying prone, knee flexed to 90°, examiner stabilizes posterior femur in one hand and distracts the foot upward. At the same time, the foot should be rotated internally and externally. Reproduction of patients pain may indicate MCL/LCL sprain or tear. A variation to this is Apley’s compression test. Performed similarly to the distraction test, the examiner produces a compression force from the heel directed into the exam table. Again, reproduction of pain with internal/external rotation of the foot is a positive test. This may indicate possible meniscal pathology. Note: in patients with open growth plates, positive Lachman’s test, valgus/varus tests may actually represent opening of tibial or femoral growth plate fracture. Grading system for most ligament sprains/tears: Grade 1 2 3 Histology/Translation Fibers stretched, no laxity Few fibers torn, some laxity Many fibers torn, much laxity Endpoint Good Fair Poor, soft
D. Diagnosis 1. The Use of Arthrocentesis Arthrocentesis is aspiration of synovial fluid from a joint. Lipoarthrosis usually indicates a fracture. Hemarthrosis usually indicates ACL tear. 75-80% of all acute hemarthroses represents an ACL tear. Other pathology presenting as hemarthrosis includes osteochondral fracture (often seen with patellar dislocation) and a peripheral meniscus tear. There are risks with this procedure. Possible introduction of bacteria into the joint progressing to septic joint is the primary risk. Consider the indications for surgery and the timing of ligament surgery (relative to the injury date) in the decision-making process. Many surgeons will wait at least 2-3 weeks after ACL injury to allow for decreased inflammation, effusion, increased ROM. Performing serial exams may yield more diagnostic information than arthrocentesis, with less risk. 2. Plain radiographsMy usual knee series for acute trauma includes AP, lateral and Merchant (sunrise) views. Some authors include oblique views (X2).
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I do not believe these views help in the diagnosis of most acute knee injuries. The patient is exposed to more radiation and they add to the cost of diagnosis. Occasionally, you may visualize patellar fractures more readily with the oblique
8 views. Consider notch view if osteochondral fracture of a femoral condyle is considered (including osteochondritis dessicans, bony infarcts).
The use of xray for the diagnosis of acute fractures of the knee with trauma has been evaluated. The tests should have very high sensitivity and negative predictive value and the highest possible specificity and positive predictive value. Meaning, we want to diagnose all fractures that exist (high true positive), not miss fractures (low false negative rate).
Seaberg (1994) evaluated the accuracy and utility of obtaining knee xrays in an ER dept with all traumatic injuries. Over 200 pts were included in the study. The fracture rate was 6%. A decision rule analysis similar to the Ottawa ankle rules for xray utilization was proposed and studied. Factors important in the accurate diagnosis of clinically significant knee fractures included inability to weight-bear (four steps) after the injury or in the ER age 50 yrs mechanism of injury = fall or blunt trauma The sensitivity and specificity of these decision rules in diagnosing clinically significant knee fractures was 100% and 79%, respectively. Their data suggest that 78% of acute knee xrays in the ER can be avoided by addressing these simple clinical characteristics. 3. MRI MRI can effectively and accurately diagnose ligamentous abnormalities of the knee. Cost of this test ranges from $600-1200. The issue, however, is whether MRI can contribute to or change the treatment of these internal derangements of the knee. A number of articles have demonstrated that MRI is better than “diagnostic” arthroscopy in evaluating knee injuries and assisting with treatment options. But only a few studies to date have compared the ability of MRI to the ability of clinical examination (history, physical exam and xrays).
In these studies, clinical exam was found to be as good as MRI in evaluating knee derangements and assisting with their treatment. The reported overall sensitivity and specificity of MRI in the diagnosis of internal derangements of the knee are 88% and 94%, respectively. In general, the MRI does much better with diagnosis of ligament injuries, and does fairly well with meniscal tears. These results are very institution and radiologist specific. Diagnosis: MRI Medial meniscus Lateral meniscus ACL Diagnosis: Clinical Exam Medial meniscus Lateral meniscus Sensitivity 73-100% 55-90 92-100 Sensitivity 92 % 67 Specificity 55-97 94-98 99-100 Specificity 60 90 + PV 81-98 90-95 93-100 + PV 86 84
– PV
86-100 70-97 99-100
– PV
75 77
9 ACL
from Rose, et al. Arthroscopy. 1996.
100
100
100
100
More physicians are incorporating serial exams over a short period of time, radiographs and response to physical therapy in the evaluation of knee injuries. Further, the ability of clinical exam to diagnose ligament injuries of the knee is generally considered very good. It’s the ability of clinical exam to diagnose associated injuries (meniscal tears) which is considered less reliable. Many clinicians now assess the patient’s response to pharmacologic and rehabilitative treatment options in the decision to surgerize or not. If the patient continues to have recurrent effusions, episodes of instability or pain after a reasonable nonsurgical treatment plan, referral to surgery is appropriate. The MRI may not always assist with this treatment plan, though it does add greatly to the cost of diagnosis and treatment. E. Specific Injuries and Treatment 1. Anterior Knee Pain Disorders- there is no consensus on the definition or classification of anterior knee pain, making literature comparisons difficult. a. Patellofemoral arthralgia (PFA)- also known as patellofemoral dysfunction, patellofemoral pain syndrome, chondromalacia patella…. HxPain in the anterior, peripatellar areas Pain with prolonged sitting (“movie theater sign”), driving distances Pain with stairs, ascension and descension A subset will have symptoms of instability, pseudolocking and quad weakness (patellar subluxation/dislocation).
Pseudolocking (feeling of a catch) is evident with patellar tracking disorders and synovial plica entrapment. PE- pain with palpation of medial facet,+ patellar compression, ↑ Q angle, Inspection – “Grasshopper eyes,” patella alta (high-riding patella), genu valgus, high Q angle. Usually little or no effusion. Palpation- Peripatellar pain, pain to palpation of the medial facet of the patella. Range of motion- normal Special tests- + patellar compression/grind, + hamstring tightness, VMO atrophy (or dysplasia).
Normal ligament/meniscus exams. XrayAnteroposterior view • ? patella alta- inferior pole of the patella seen greater than 2 cm above a line drawn to connect the two femoral condyles assess for other causes of anterior knee pain (patellar fx, OCD) • • medial or lateral joint space narrowing, spurs (arthritis) Lateral view • apophysitis of inferior pole of the patella = Sinding-Larsen-Johansson disease; tibial tubercle = Osgood-Schlatter disease.
• •
OA, spurs patella alta- Inferior pole of the patella witnessed above Blumensaat’s line (this method more accurate if the lateral is taken at 30° knee flexion).
Another method that is not dependent upon the amount of knee flexion is the ratio method, described by Insall and Salvati. The ratio is a/b where a is the length of patellar tendon and b is the length of the patella diagonally. A normal ratio is 1.00-1.20. Greater than 1.20 ratio demonstrates patella alta.
Tangential (axial) views. Also known as the Merchant, Hughston, Laurin and sunrise views. Different views require varied amounts of knee flexion. This is particularly important with acutely painful knees. Different indices have been described to reflect objective evidence for risk of patellofemoral disorders. Congruence angle, lateral patellofemoral angle, sulcus angle, etc. Again strict adherence to exact numbers is not prudent. • Patellofemoral joint space • Lateralization/Tilt • Spur formation (OA) • Depth of the trochlear groove, height of the lateral femoral condyle Rx- Paramount in treatment of patellofemoral disorders is the strengthening of the VMO and the improved flexibility of the hamstrings. PRICES NSAID’s or analgesics Bracing- include lateral support (donut or “U”) with patellar cutout VMO strengthening Hamstring flexibility Correct leg length inequality (heel lift- not pad or cushion) ? McConnell patellar taping VMO strengthening- see ExerciseXpress exercises at the end of this handout. Hamstring flexibility- see ExerciseXpress exercises at the end of this handout. Note- chondromalacia patella should be reserved for visualized cartilage defects and fibrillation (arthroscopy vs. MRI).
b. Patellar subluxation and dislocation Hx- acute traumatic dislocation occurs mostly with flexion and concomitant pivot. Acute, immediate swelling (possibly hemarthrosis).
Inability to continue play, work, etc. The dislocation usually relocates with the first knee extension. Therefore, swift and accurate diagnosis requires a high index of suspicion.
PE- acute swelling, pain to palpation throughout: inferiorly (patellar tendon), superiorly (quad tendon), medially (medial retinaculum), and laterally (lateral femoral condyle).
+ patellar apprehension test. See figure at right. Xray-patella lateral to the trochlear groove. If patella relocated, effusion may be only radiographic clue to dislocation. Look for small avulsion fx on medial patella on the sunrise view (pathognomonic for dislocation).
Rx- knee extension immobilizer for ~ 4 weeks. Start early isometric quad contraction exercises (quad setting) to improve muscular function and decrease intra-articular effusion. At 4 weeks, start PRE’s to sx tolerance. Progress activity with bracing (patellar support).
Return to sport when full, painless ROM, normal strength, adequate aerobic fitness. c. Patellar tendon rupture, Quad tendon rupture-may be the end-stage of inflamed extensor mechanism Hx- acute onset of pain, sudden “pop,” with or without significant force, + recent steroid injections PE- Defect or lack of palpable tendons, inability to actively extend the knee or greatly decreased strength, ecchymosis, effusion; patella alta (patellar tendon rupture) or patella baja (quad tendon rupture) Xray- Normal or: avulsions, patella alta/baja, as above Rx- Partial patellar tendon rupture = extension immobilizer for 4-6 weeks, gradual increased ROM, PRE’s with bracing. Full patellar tendon rupture and all quad tendon ruptures should undergo early surgical reattachment. d. Patellar tendinitis, Quadriceps tendinitis, Osgood-Schlatter disease, SindingLarsen-Johansson syndrome Hx- insidious onset anterior knee pain, especially with overuse (jumping, running, etc.).
PE- point tender on tendon or tibial tubercle (Osgood-Schlatter Disease).
Also, may see deformity or bony irregularity with Osgood-Schlatter disease (tibial tubercle) and Sinding-Larsen-Johansson syndrome (inferior pole of the patella).
Tightness of the hamstring, quadriceps and heel cord musculature. Xrays- most often, normal. May see calcification at one of the poles of the patella. May also see fragmentation or avulsion fracture at the tibial tubercle. At times xray is advocated to rule out tumor. Rx- as described in the rehabilitation section. A Chopat strap may be used to provide comfort. This may also be accomplished with taping or other braces. Note: Osgood-Schlatter disease and Sinding-Larsen-Johansson syndrome are common in the patient undergoing a growth spurt (ie: 11-15 yrs old).
e. Synovial plica syndrome- normal embryologic synovial folds. Most patients with plicae never experience symptoms. The most common location of plicae is in the superior or superomedial patella region. They may become inflamed and create pain. If chronically inflamed, may become fibrotic and more easily palpable. They may also become impinged or entrapped, further exacerbating pain. Other symptoms include snapping, especially with knee flexion. f. Multipartite patella- again, not necessarily causative of pain. May be incidental on xray. There is a male preponderance with a male:female of 9:1. Bilateral in up to 40% of the cases. The most common location of multipartite patella is laterally (see figure).
• Type I 5% • Type II20% • Type III 75% Note- type I may be variant of apophysitis (SindingLarsen-Johansson disease).
Hx- insidious onset of pain. Acute trauma may indicate fracture. PE- when symptoms are present, pain can occur at the junction of the main body and the fragment. Xray- superolateral fragment of the patella. The fragment may not “fit like a puzzle” Rx- supportive 2. Ligamentous injuries a. ACL tears- complete vs partial Natural History- ACL contributes significant stability to the knee. ACL provides primary stability to anterior motion and secondary role in preventing valgus stress and rotatory instability. Acute ACL tears associated with some other injury 67% of time (MCL tears, meniscal tears, osteochondral fractures).
Hx- Mechanism usually planted foot with pivot or hyperextension. Knee effusions usually early, first 4-12 hours. Usually cannot continue working, playing. Pt may describe a significant “pop.” Pts may also experience shifting, buckling episodes resulting in falls. PE- ⇓’d ROM, effusion (+ hemarthrosis), + Lachman’s/Anterior drawer/Pivot shift tests. Absolute pt relaxation is key to accurate ligamentous assessment. Also, consider serial exams for improved diagnostic acumen. With decreased swelling, increased ROM, the exam will yield more information. The Lachman test is the most accurate assessment of the acutely injured ACL. Dx- Xray with effusion, + lateral capsular sign on AP (“Segond fracture”) at the lateral tibial plateau. Typical segond fragment is 10 x 2 mm located up to 10 mm from the lateral joint line. Also, ? depression > 2 mm on the lateral femoral condyle. Arthrocentesis should be reserved for tense or painful effusions, ? of
infectious or metabolic disease. The use of serial exams can give good diagnostic information without the invasiveness and risk of this procedure. RxMost active people require surgical reconstruction to decrease shifting (instability) episodes, further trauma to supporting structures. Results of simple repair (suture of the two ends) has been disappointing. Indications for surgery include recurrent shifting episodes and effusions, combined injuries (ACL, meniscus).
Historically, surgeons have been less inclined to reconstruct pts over 40 yrs. Surgical candidacy now depends more upon physiologic age than chronological age. Goal is to supply normal function and stability. Surgery cannot duplicate the natural structure and function of intact ACL. A special consideration is the care of ACL-deficient adolescent. Early physeal fracture data indicated that altered growth patterns occurred when fractures crossed the growth plates (Salter III-VI).
The concern was that during reconstructive surgery, placing a screw across a growth plate may alter growth response. Subsequent data has not supported these theories, however. Currently, younger children with wide-open physes, nonoperative approach may be more appropriate. However, in children nearing closure of growth plates, more surgeons are treating with intra-articular reconstruction. Timing of ACL surgery is important. Most authors agree, surgical reconstruction is associated with a higher rate of arthrofibrosis in those pts undergoing surgery during the acute, inflammatory stage (effusion, hemarthrosis).
A common waiting period of three weeks after injury is considered a reasonable wait.
There is no indication that reconstruction does anything to alter a patient’s risk for accelerated degenerative joint disease down the road.
Nonsurgical approach with rigorous rehab (especially hamstrings and gastrocnemius) is another option. This may be a better option for an older active person who is willing to modify his or her activity, or if supporting structures are not damaged. The use of functional knee braces to prevent further shifting episodes in nonsurgically treated pts does not have scientific basis. The forces at the knee generated in today’s athletic events are considered higher than the braces can withstand. This practice is considered controversial. What about the partial ACL rupture? Rupture of > 40% of the total ACL behaves pathophysiologically as a total rupture in terms of significant AP translation and risk for supporting structures, subsequent OA. In addition, there is some data to suggest that many partial tears will eventually progress to a full tear. There are no current means of identifying those partial tears at risk for propagation. The treatment options of partial tears of the ACL are similar to full tears. The data is inconclusive comparing nonsurgical and surgical treatment. b. MCL tearsHx- Mechanism = valgus stress (a lineman falling on the outside of another lineman’s
14 leg).
Patient c/o medial knee pain, pain that may be along the joint line. Possibly small effusion, but not like the large effusion seen with ACL. They may have difficulty with weight-bearing, depending on the grade of injury. PE- Tender to palpation MCL anywhere along the length of the ligament (origin to insertion).
Usually not a large intra-articular effusion. May see localized edema along the length of the ligament. Pain, pain, pain (+) opening with valgus stress with knee at 30° of knee flexion. If opening at full extension, then concomitant ACL tear. Apley’s distraction test will produce pain at MCL (Apley’s compression test negative).
Dx- H&P, plain films help r/o acute bony pathology. Remember in young pt (with open growth plates) “opening” with valgus stress may indicate physeal injury and not MCL tear. Rx- most MCL tears treated nonoperatively. Early functional ROM exercises combined with support for valgus stress at the knee (lateral hinged knee brace) are the mainstays of treatment for MCL tears. After the pt obtains 90° of flexion, resistive exercises can begin, strengthening the quads and hamstrings. Note that few authors suggest cast or extension brace immobilization, even for isolated grade 3 (full-thickness) tears. Histologic scar formation occurs whether immobilization or early functional rehab is the mode of treatment. The early rehab knees, however, demonstrate fibroblasts and connective tissue that is oriented in a more functional way. However, grade 3 MCL tears may have concomitant ACL or meniscal tear, then treatment is consistent with individual treatment plans of these injuries. Natural Hx- interestingly enough, unlike long-term follow-up of ACL and meniscus tears (regardless of specific treatment), follow-up of MCL tears has not demonstrated significant degenerative changes/symptoms up to 10 years7,8, 11. c. PCL tears-isolated vs combined Hx- Mechanism = sports-related and motor vehicle accidents are the most common causes of injury. In athletics, a fall on a flexed (~ 90°) with the foot plantarflexed is the most common mechanism for PCL injuries. In MVA’s, direct force applied to the tibial tubercle by the dashboard creates a PCL injury. PE- effusion (smaller than ACL).
+ Posterior drawer. This translation will decrease with internal rotation of the tibia, probably because of the meniscofemoral ligaments (of Humphrey and Wrisberg).
+ posterior sag sign, + quadriceps active test. The exam may demonstrate a false positive Lachman and anterior drawer tests. The patient’s knee may exhibit increased flexion during gait (esp at mid-stance phase of gait).
Rx- isolated, complete PCL injuries do well nonoperatively. PCL tears that are combined with meniscal tears or other associated injuries are generally treated operatively. Again, goal is to decrease instability and improve function. The ability of surgery to decrease risk of degenerative process over the years has not been demonstrated.
d. LCL tears-much less common. Hx-Mechanism = varus stress. Rare isolated LCL. Look for ACL, PCL tears. PE- + varus stress test (with or without laxity).
+ effusion. May have associated ITB and
15 popliteus tendon injuries. Dx- xrays will r/o bony abnormalities if appropriate. Rx- grade 1 and 2 injuries usually treated nonsurgically. PRICES, functional bracing and rehab are the mainstays of treatment. Isolated grade 3 tears of the LCL may be treated as above. If associated injuries (ACL, PCL, meniscus), better treated surgically per the specific injury. 3. Meniscal Tears a. Epidemiology Most meniscal tears are medial 70-90%. Meniscal injuries account for 45-50% of acute hemarthrosis in adolescents (as opposed to adults where 75% of acute hemarthroses represent ACL tears).
Assess for concomitant ACL tears (associated ≈ 15-35%).
Meniscal tears may be acute or degenerative. b. History- recurrent effusions, locking or sensation of giving way. c. Physical Exam• Decreased ROM (especially extension).
May represent a tear that flips up and blocks full extension, AKA “locked knee.” • Joint line tenderness- posterior joint line tenderness more sensitive for meniscal injury than anterior. Anterior joint line tenderness may reflect anterior knee pain syndromes, osteochondritis dessicans, etc. In addition, joint line tenderness is most sensitive if not associated with an ACL tear. N.B. When palpating joint line, internal tibial rotation renders the lateral meniscus more palpable, external tibial rotation renders the medial meniscus more palpable. • McMurray’s test produces a palpable (audible) clunk. This test attempts to catch a meniscal flap in between the tibia and femur. Apley’s compression test for meniscal pathology = positive for pain. Pt • prone. Knee flexed to 90°. The examiner produces a compression force directed toward the exam table. Pain may indicate a meniscal tear. The distraction test may stretch the collateral ligaments and create pain. This may help distinguish MCL vs meniscus injury. d. Diagnosis Hx of recurrent effusions, instability; PE of + McMurray’s, Apley’s compression tests Xrays- more useful for ruling out other causes of pain, locking or effusion. DDx = loose bodies, OCD, OA, ligament tears MRI- useful in confirming diagnosis; its utility improves if the reason for the MRI is to assess if associated injuries that may change the course of treatment (ACL, PCL, etc.).
There are a significant number of changes on MRI in totally asymptomatic individuals, however! Types of tears I. Longitudinal
16 II. III. IV. Horizontal Oblique Radial CT/arthrogram- largely supplanted by MRI. Useful in patients with intra-articular hardware.
•
• • • •
e. Treatment Nonoperative Acute rehab- ROM, Quad setting (isometric contraction of the quadriceps- no flexion/extension of the knee) Subacute rehab- ROM, PRE’s Bracing- early mobilization with hinged knee brace when tolerable Continue with functional drills, sport-specific drills, etc. Current data demonstrate symptomatic/clinical healing in about six weeks for many pts (especially younger athletes).
Therefore, if continued Sxs at this time I would recommend surgical options. Operative- note there is no literature support that arthroscopic partial menisectomy decreases the likelihood of degenerative arthritis at a later date. This fact has supported increased attempts at nonoperative treatment. I tend to recommend surgery for failed nonoperative treatment (≈ 6 weeks), continued pain or extension block, recurrent effusions, loose body Sxs. In addition, if there are associated injuries (ACL/PCL) I would be more likely to recommend surgery. 1. Partial menisectomy 2. Meniscal repair- attempt at suturing the torn pieces together. More applicable in younger patients with smaller tears, especially in the periphery. 3. Total menisectomy- not much indication today for total menisectomy, due to progressive degenerative changes. Basic science studies have shown that peak local articular contact stresses increase by approximately 65% with partial meniscectomy and as much as 235% with total meniscectomy.
N.B. Rates of meniscal retear or failure to heal following meniscal repair range from 5% to 30% in the literature. These figures are somewhat misleading, however, since failure can be defined clinically (based solely on sxs), based on imaging studies, or based on arthroscopic findings. 4. Osteoarthritis a. Epidemiology: OA is one of the most common disorders requiring medical attention in a family physician’s office. In men, the predominant joint is the knee, with
17 the first MTP and DIP joints affecting women. Radiographic evidence of OA can be seen in up to 40 million Americans. Approximately 25 million will actually experience symptoms or dysfunction. Reports of prevalence range from 65-85% of patients over the age of 65 years will be affected by OA. Multiple risk factors for OA have been proposed. The lack of prospective, wellcontrolled human studies, however, make definitive assessment of risk difficult. Proposed risk factors include: • • • • Age Previous injury/internal derangement Obesity Gender – women may demonstrate a higher prevalence of OA.
The question of whether exercise (such as jogging, etc.) increases the risk of OA of the knees, hips and lumbar spine has not been fully answered. While anecdotal and retrospective studies imply an associated risk, the available prospective, controlled human studies do not support this. There does appear to be an increased risk of OA in joints with prior injury, internal derangement or biomechanical abnormalities. b. Clinical presentation: Osteoarthritis (OA) is a slowly progressive degeneration of the articular cartilage of the body. At the same time, hypertrophy of the underlying bone may contribute to irregularities such as subchondral sclerosis and osteophytes. The arthropathy is typically devoid of inflammation, though adjacent synovitis may exist. Common symptoms include pain, brief (
18 d. Diagnostic tests: The typical historical and physical examination features assist with the diagnosis. Recall that severity of symptoms does NOT correlate well with radiographic findings. A number of grading systems have been proposed for different joints. One commonly accepted grading system is proposed by Kellgren and Lawrence. Standard OA xrays include AP pelvis (hip), PA of hand, AP and lateral (knee) and AP and lateral (L-spine).
Kellgren and Lawrence Grading System for the Knee GRADE 1 2 3 4 RADIOGRAPHIC FINDINGS Possible osteophytes; no joint space narrowing. Definite osteophytes; possible narrowing of joint space. Moderate multiple osteophytes; definite joint space narrowing; some sclerosis and possible deformity of bone ends. Large osteophytes; marked joint space narrowing; severe sclerosis and definite deformity of bone ends.
Radiographic evidence of OA includes: • Subchondral sclerosis and cysts • Osteophyte formation • Narrowing of joint space • Deformity and malalignment Laboratory testing is helpful more in ruling out other differential diagnoses rather than specifically diagnosing OA. The complete blood count (CBC), chemistry profile and urinalysis are usually normal. Markers for inflammation (ESR, C-reactive protein) are usually normal, though may be slightly elevated during the acute phase of erosive OA. Rheumatoid factor and antinuclear antibody titers are normal. Occasionally, small intra-articular effusions may be present. If the diagnosis is still in question, a joint aspiration may be considered. Synovial fluid analysis may demonstrate clear-to-yellow color, few WBC’s (
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Nonpharmacologic management • Weight reduction techniques – a loss of just 5 kg may significantly decrease symptoms • Aerobic conditioning (low impact) • Joint specific rehabilitation (including, range of motion, stretching and strengthening exercises).
• Thermal and cryotherapy • Emotional and social support • Physical support (braces, canes, walkers).
Also, since many of these patients have severe varus deformity, shoe inserts (lateral heel and sole wedges) may correct biomechanical abnormalities that greatly contribute to symptoms. Pharmacologic management • Acetaminophen- should be drug of first choice. It has a good safety profile and increasing support for efficacy in noninflammatory pain. • NSAID’s- use lowest effective dose. Consider pulse therapy, drug holidays, etc. Significant risk for gastric, renal and hepatic toxicity with long-term use. • Nonacetylated salicylates- (such as salsalate and choline-magnesium-trisalicylate) often overlooked but provide good analgesia. In addition, these medications do not inhibit prostaglandins that are protective to gastric mucosa. • Opiates- may be a short-term alternative for severe pain. Keep in mind that they may be sedating and increase the risk for falls. • Corticosteroids- intra-articular injections may offer modest benefit and should be used sparingly. Optimal dosing and frequency are not known, but many authors suggest no more than 2-3 injections per year. • Cyclo-oxygenase 2 inhibitors- new class of medications to hit the market. They are “NSAID’s” without the GI, renal or hepatic toxicities. They selectively inhibit COX 2; COX 1 enzyme is primarily responsible for the side effects. These meds should be considered for breakthrough pain, unresponsive to tylenol. • Hyalgan/Synvisc- intra-articular injection of hyaluronic acid. Receiving alot of press at this time. Multiple injections (Hyalgan = 1 q week x 5; Synvisc = 1 q week x 3) of these substances may improve pain and function. ? May temporize the pt’s need for surgical procedures (debridement, total knee replacement, etc.).
Early data looks promising (especially for Synvisc), better designed clinical trials needed for more definitive recommendations.
Surgical Management • Indications for surgery- consider surgery when ADL’s are affected, pain is severe and recalcitrant, medical management has been maximized. Older patients may undergo total joint replacement. In younger patients, a high tibial osteotomy may be required. This involves resection of a wedge of the tibia to decrease the severe varus deformity. Another
20 • surgical option is arthrodesis, where the joint is rendered immobile. Autogenous transplantation- newer surgical technique attempting to transplant the patient’s own normal articular cartilage and insert this into a cartilaginous defect. Not standard of care, yet. Clinical trials pending.
21 REFERENCES
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