The Scar Solution Natural Scar Removal

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Shelbourne et al20 developed a classification system of arthrofibrosis based on the motion of the injured knee compared to motion in the uninjured knee. In this classification system, patients with type I arthrofibrosis have an extension loss of 10 degrees or less and normal flexion. Patients with type II arthrofi-brosis have greater than 10 degrees of extension loss and normal flexion. Patients with type III arthrofibrosis have greater than 10 degrees of extension loss, greater than 25 degrees of flexion loss, and decreased patellar mobility. Patients with type IV arthrofi-brosis have greater than 10 degrees of extension loss, greater than 30 degrees of flexion loss, and patella inferna with markedly decreased patellar mobility.

Inflammation in the peripatellar tissues is associated with decreased patellar mobility. Patellar baja may result from the diffuse inflammation because of fibrous hyperplasia of the anterior fat pad. In 1987, Paulos et al21 coined the term infrapatellar contracture syndrome to refer to patients with patellar entrapment associated with loss of extension and flexion despite multiple corrective procedures. The cause of this entrapment is hyperplasia of the anterior fat pad, prolonged immobility, and lack of extension. When the fat pad becomes hyperplastic and adherent to the underlying tibia, the patella has limited excursion, and loss of motion may result.

Capsulitis results in diffuse constant pain and stiffness. The knee is actively inflamed with diffuse swelling and warmth. Both extension and flexion are limited as a result. Patellar mobility is usually limited and, consequently, contraction of the quadriceps fails to create enough tension to actively extend the knee completely. Arthrofibrosis is the end product of capsulitis, and the knee may demonstrate decreased flexion, extension, and patellar mobility, but the swelling and warmth usually subside.


Prevention Preoperative

Preoperative steps are the most important interventions to take to prevent loss of motion. Loss of motion following an injury is usually the result of pain, swelling, quadriceps inhibition, and hamstring spasm. A locked knee from a torn meniscus is relatively rare. Treatment in the preoperative period should be focused on decreasing pain and swelling and improving range of motion. Preoperatively, management consists of the use of ice to reduce pain and swelling, range-of-motion exercises, hamstring and calf stretching, and isometric quadriceps exercises. It is also important to counsel the patient about the possible complication of loss of motion and the importance of appropriate physical therapy.


Some of the important intraoperative considerations to prevent loss of motion postoperatively were discussed earlier in the clinical features section. Accurate surgical technique and meticulous attention to graft placement are necessary to minimize the risk of loss of motion postoperatively. With ACL reconstruction, improper tibial tunnel placement may lead to motion problems. Most commonly, an anterior tibial tunnel may lead to impingement between the graft and the roof of the intercondylar notch with knee extension.17 Ideally, the tibial tunnel should be drilled within the ACL footprint. For less experienced surgeons, or whenever any surgeon is unsure about tunnel location (especially in revision cases where arthroscopic anatomy is potentially distorted), intraoperative lateral radiographs with the knee in extension are critical. A notchplasty should be performed to allow adequate clearance for the graft within the inter-condylar notch. As previously discussed, an inadequate notch-plasty or regrowth and scarring of the notch is one of the commonly identified causes of loss of extension following ACL reconstruction.


An appropriate rehabilitation program that stresses early motion is the most important postoperative measure to take to avoid loss of motion in this period. The goals of the rehabilitation program are to minimize inflammation, restore motion and strength, enhance proprioception and dynamic stability, and return the patient to full function. Our ACL postoperative physical therapy program stresses early motion with passive extension, heel/wall slides, hamstring/calf stretching, and active-assisted range of motion. Straight leg raises, quadriceps sets, half squats/wall slides, standing heel raises, and lateral stepups are important for early postoperative muscle function. It is important to see the patella glide superiorly with the quadriceps sets to prevent infrapatellar contracture syndrome. These exercises may be performed several times daily in the early postop erative period. Modalities such as cold and compression may be helpful to decrease inflammation and swelling.

Postoperative rehabilitation following ACL reconstruction must be done in such a manner that minimizes inflammation, pain, and swelling but stresses early motion to minimize adhesive scar formation. During week 1, we lock the knee brace in extension but allow range-of-motion exercises several times during the day. In most cases, we allow the patient to weight bear as tolerated. Beginning week 2, the brace is unlocked for ambulation. We stress the heel-toe gait to emphasize terminal extension. After week 4, the brace and crutches are discontinued if the patient has reached full extension and 100 degrees of flexion, has no knee extensor lag and minimal swelling, and is able to walk without a bent knee gait. Crutches are critical for successful rehabilitation in the first month postoperatively to achieve and maintain terminal extension without development of a bent knee gait.

Critical milestones for patients to achieve are full passive extension within 1 week, full active extension within 2 weeks, 90 to 100 degrees of flexion within 2 weeks, and full flexion by 6 weeks. The surgeon should recognize that patients who are not meeting these milestones may require more specific and intense treatment for loss of motion.


Recognition of loss of motion must occur as early as possible to allow for immediate initiation of treatment. Although the pre-ventative measures described previously are optimal, treatment of loss of motion must be initiated if these measures fail. The treatment process begins with a systematic approach to identify the cause of loss of motion. Successful treatment of loss of motion depends on early recognition of the cause. Early recognition of loss of motion and appropriate intervention should decrease long-term complications for the patient.

Some patients experience loss of motion because the affected knee continues to be diffusely swollen, painful, and inflamed in the postoperative period. This type of response may be associated with capsulitis and, if left untreated, arthrofibrosis. When identified in the period of active inflammation, the appropriate treatment for the inflamed knee is anti-inflammatory agents, rest, and ice. Patients may continue with pain-free active range-of-motion exercises and strengthening but should avoid forceful manipulation of the knee. Stretching techniques should be gentle to avoid aggravation of pain and swelling.

Efforts toward regaining motion should be focused on reducing the motion deficit in one direction at a time. We address loss of extension first because it tends to cause more functional deficits and patellofemoral pain if left untreated. Patients should be encouraged to perform quadriceps sets and straight leg raises to minimize any knee extensor lag.

A drop-out cast may be used overnight to provide a sustained stretch and prevent further loss of extension. The drop-out cast is constructed by applying a cylindrical long-leg cast with the knee at the end range of extension. Padding is incorporated into the cast anteriorly superior to the patella and posteriorly on the proximal thigh and distal calf to create a three-point pressure system to increase knee extension. After the cast has hardened, a window is cut to expose the anterior aspect of the patella and lower leg. The amount of stretch is then adjusted by incorporating a wedge between the cast and the distal aspect of the calf. The cast is left in place overnight and then removed by splitting it anteriorly over the thigh.

During the active stage of capsulitis, gentle patellar mobilization is also important. Superior excursion of the patella, which is necessary for proper functioning of the extensor mechanism, may be restored by performing quadriceps sets in terminal extension. This mobilization must not be overly aggressive and must be pain free, as further inflammation of the peri-patellar tissues may lead to further delay in restoration of motion.

The surgeon, physical therapist, and the patient must have patience in the management of capsulitis. Overly aggressive stretching, manipulation, or surgical intervention during the period of active inflammation may only further inflame the knee and worsen the problem. Once the active inflammation has subsided, which may be 6 months or longer after reconstruction, surgery or manipulation may be considered if the patient has persistent loss of motion.

Manipulation under anesthesia is a more invasive means of gently flexing and extending the knee under general or regional anesthesia to loosen scar tissue in patients with arthrofibrosis not responsive to standard physical therapy techniques. Manipulation is most effective for mild arthrofibrosis leading to flexion loss, as knees with greater extension deficits have been shown to achieve significantly less final extension than knees with smaller deficits.22 We believe that manipulation is most effective around 3 months postoperatively, after the acute response has subsided, but before the fibrotic response is complete. Manipulation under anesthesia should be performed gently to prevent chondral damage or stimulation of myositis ossificans or ossification of the medial collateral ligament.

When loss of motion appears to be caused by impingement, physical therapy to improve extension should be the focus of the initial management. Gentle stretching techniques that employ a sustained, low-amplitude force should be used. Quadriceps strengthening exercises are stressed to eliminate any quadriceps lag that may be contributing to the loss of extension. A drop-out cast may also be used in this setting to provide a sustained stretch and prevent further loss of extension.

If impingement is the suspected cause of loss of motion and extension fails to improve with physical therapy within 2 or 3 weeks, arthroscopic evaluation and débridement of the intercondylar notch (as described in the following section) may be necessary. Aggressive nonoperative manipulation should not be performed in the setting of a physical impingement. Forceful stretching may result in graft failure and will not be successful unless the physical block to motion is removed.


Surgical management of loss of knee motion is indicated when nonoperative interventions have failed or if a specific, correctable abnormality exists. Several techniques have been described, including open débridement, arthroscopic débridement, and combined open and arthroscopic débridement.

Arthroscopic Débridement

Arthroscopic débridement has been advocated as the first-line surgical treatment for loss of motion. It is often successful and may be performed on an outpatient basis. Loss of extension following ACL reconstruction may be particularly appropriate for arthroscopic intervention, as correction of loss of extension secondary to pathology localized to the notch or scarring may be particularly amenable to this approach.

Prior to undertaking a surgical intervention to address loss of motion, the surgeon should have an idea of the etiology of the loss of motion. Even when the surgeon has a strong suspicion preoperatively of the underlying pathology, it is important to thoroughly visualize all compartments of the knee. We use a diagnostic arthroscopic approach to evaluate the knee in the setting of loss of motion that is similar to the nine-step approach described by Millett et al.23 We create the standard anterolateral and anteromedial portals immediately adjacent to the respective border of the patellar tendon, at previous arthroscopy portal sites if possible. We first evaluate the suprapatellar pouch, the medial gutter, and the lateral gutter, using a motorized shaver to reestablish these spaces if scarring has compromised their visualization (Fig. 61-2).

We then turn our attention to the infrapatellar fat pad, which is debrided and mobilized to reestablish the pretibial recess. Any infrapatellar adhesions between the anterior tibia and the fat pad must be debrided to allow patellar mobilization and superior patellar excursion. The medial and lateral retinaculum are then evaluated and released with a motorized shaver if tight or scarred. If the anterior aspects of the menisci are involved in the scarring, this scarring should be released to allow normal anterior-posterior meniscal translation.

Evaluation of the intercondylar notch is next. When loss of knee extension following ACL reconstruction is a result of impingement, the offending pathology may be visualized in the intercondylar notch. Proliferation of a cyclops lesion from the tibial side of the reconstruction is usually first visualized with any attempt to visualize the intercondylar notch. This nodule should be debrided, and the intercondylar notch should be evaluated for scarring.

Regardless of the presence of a cyclops lesion, intercondylar notch scarring should be debrided to allow the knee to reach as nearly normal extension as possible. Once the excess scarring is excised, the graft should lock into the notch without impinging on it during knee extension. Impingement of the graft in the intercondylar notch may result in failure of the graft to incorporate. The graft insertion should be evaluated for evidence of failure. An inadequate notchplasty may cause impingement and loss of extension following ACL reconstruction. A notchplasty should be performed if there is evidence of continued impingement despite debridement of the notch scarring. In severe cases of intercondylar notch scarring, the ACL and/or posterior cruciate ligament may need to be released. Following intercondylar notch debridement, a drop-out cast may be applied.

An anteriorly placed ACL graft may contribute to the loss of motion following ACL reconstruction. In the case of an anteriorly placed ACL graft causing impingement and loss of extension, an adequate notchplasty must be completed to provide the anterior graft the opportunity to reduce into the notch without impingement. If elimination of the impingement is not feasible through notchplasty, the ACL graft may have to be resected. If necessary, revision reconstruction is performed later as a staged procedure.

The posterior capsule should be evaluated at its tibial and femoral insertions, as tightness of the posterior capsule may contribute to loss of extension. Some authors advocate release of the posterior capsule if tightness is noted.23 This debridement must be performed carefully, with special consideration given to the neurovascular anatomy of the posterior knee. We do not routinely perform a posterior capsule release and have found a drop-out cast in the postoperative period to be effective for relieving posterior knee tightness.

Loss Flexion Penis

Figure 61-2 A, Suprapatellar pouch scarring in a patient with severe arthrofibrosis after a tibial plateau fracture (preoperative flexion <60 degrees). B, Creating a space with the shaver. C, Suprapatellar pouch after nearly completed excision of adhesions. D, Scarring in the lateral gutter in the same patient.

Figure 61-2 A, Suprapatellar pouch scarring in a patient with severe arthrofibrosis after a tibial plateau fracture (preoperative flexion <60 degrees). B, Creating a space with the shaver. C, Suprapatellar pouch after nearly completed excision of adhesions. D, Scarring in the lateral gutter in the same patient.

Open Debridement

Open debridement procedures are indicated in patients in whom nonsurgical and arthroscopic surgical procedures have been unsuccessful for resolving the motion deficit or for patients with severe motion deficits and patellar baja. Most patients respond to the less invasive means previously described. Open procedures are usually salvage interventions that involve an extended hospital stay, analgesia, and prolonged rehabilitation.

Open debridement may be indicated in patients with diffuse periarticular and intra-articular scarring who have failed arthro-scopic intervention or in whom arthroscopic intervention is not feasible. Patients with arthrofibrosis and no localizable lesion may benefit from this approach. When performing an open approach, it is important to completely remove all scar tissue encountered. A systematic approach to the knee is important to ensure complete debridement. We also place all patients who undergo open debridement in a drop-out cast postoperatively.

Our technique is similar to that described by Millett et al.24 We approach the knee through a medial parapatellar arthrotomy. The knee is inspected to identify any areas of particular involvement. A release of the medial soft tissues over the medial tibial cortex is first performed if medial scarring is identified. These areas deep to the medial collateral ligament overlying the tibial plateau and femoral condyle are particularly important to release. The infrapatellar fat pad is then debrided, and a lateral peripatellar release may be performed if additional exposure or mobilization is needed. The undersurface of the extensor mechanism is then debrided to allow full mobilization of the patella. We then address any intra-articular adhesions, paying particular attention to the intercondylar notch and the posterior capsule.

Once all identifiable impediments to motion are addressed, the knee is closed and adequate analgesia ensured.


The postoperative rehabilitation following surgery to address loss of motion is structured according to the intervention undertaken. Patients undergoing limited arthroscopic debridement to address impingement, such as with cyclops lesion excision, may more aggressively rehabilitate. These patients may continue with the previously described exercises for regaining extension. Following open debridement, patients may benefit from cry-otherapy, early bracing in extension, and early active and active-assisted range-of-motion exercises. In patients being treated for more severe deficits with loss of flexion and extension, we focus our postoperative rehabilitation on regaining extension first, as full extension may be more difficult to achieve and lack of extension may cause more functional deficits.


We use the same criteria for return to sports following treatment for knee loss of motion as we would following any knee injury or reconstruction. Following an ACL reconstruction, our patients begin running at an average of 4.3 months postoperatively, light sports at 5 months, moderate sports at 5.8 months, jumping at 6.5 months, and strenuous sports at 8.1 months. We use the following criteria to guide this return: absence of pain and swelling, laxity, quadriceps strength greater than 80% to 90%, hop test, and proprioception and neuromuscular control. Following treatment of loss of motion, we use these same criteria to guide the patient's return to sports. If the patient's loss of motion was due to intercondylar notch scarring that was treated with an arthroscopy, the patient may advance very quickly to meet these criteria and return to sports. However, if the patient required open debridement following loss of motion after a knee dislocation and multiligament reconstruction, the return to sports will be significantly delayed. Usually a patient will need a deficit of less than 3 degrees of extension to return to full athletic activity. Loss of flexion is more forgiving and usually does not interfere with activity unless the patient has a loss of flexion to approximately 125 degrees.


Several authors have reported outcomes following treatment of the knee with loss of motion. Sprague et al25 were the first to describe the arthroscopic treatment of patients with limited knee motion following open knee surgery. They described 24 patients whose mean total range of motion increased from 70 degrees preoperatively to 115 degrees at final follow-up. They found that the morbidity associated with the procedure was low and complications were infrequent and mild.

Shelbourne et al20 reported the results of 72 patients who sustained loss of motion following ACL reconstruction. These patients were classified by their staging system and treated arthroscopically. They classified and recorded passive motion as a/b/c with "a" representing the degree of hyperextension, "b" representing the degree of flexion that is short of 0 degrees of extension, and "c" as the degree of flexion present. The patients underwent arthroscopic scar resection at an average of 12.5 months following the initial ACL reconstruction and were exam ined at a mean follow-up of 35 months. Patients with type I arthrofibrosis improved from a preoperative mean of 0/3/140 degrees to a postoperative mean of 4/0/140 degrees. Patients with type II arthrofibrosis improved from 0/11/135 degrees to 3/0/137 degrees, while patients with type III arthrofibrosis improved from 0/10/111 degrees to 3/0/139 degrees. Patients with type IV arthrofibrosis improved from 0/15/103 degrees to 3/0/130 degrees. The authors also noted a considerable improvement in mean modified Noyes knee score, stiffness score, self-evaluation score, and functional activity for patients in all groups.

Jackson and Schaefer19 reported on a series of 13 patients who were found to have cyclops nodules anterolateral to the tibial tunnel placement of the ACL graft following reconstruction. They noted improvement in mean extension following arthroscopic excision of the nodule and knee manipulation from 16 degrees preoperatively to 3.8 degrees at final follow-up. Loss of motion secondary to a discrete cyclops nodule carries a more favorable prognosis for recovery than does recovery from diffuse arthrofibrosis.

We recently reported the results of a series of 229 patients undergoing ACL reconstruction.10 Twenty-eight patients underwent an arthroscopic procedure to improve loss of motion. The majority of the patients (25 of 28) were found to have inter-condylar notch scarring, resulting in graft impingement and a physical block to extension. Following arthroscopy and debride-ment, 4 patients, or 1.7% of the original series, continued to have passive motion deficits between 6 and 10 degrees, while no patients had a deficit greater than 10 degrees.

Millett et al24 recently reported on the outcomes of eight patients who underwent open debridement for severe loss of knee motion. In this series, mean extension was 18.8 degrees and mean flexion was 81 degrees preoperatively. Following debridement, mean extension improved to 1.25 degrees and mean flexion improved to 125 degrees. They noted improvement in function, patient satisfaction, and Lysholm II scores, but a high incidence of patellofemoral arthritis and patellar tendon shortening at follow-up.


The complications of loss of knee motion are more obvious with loss of extension than flexion, as patients usually experience greater functional deficits. Patients with loss as little as 3 degrees of extension may walk with a bent knee gait, which places increased strain on the quadriceps and increases contact forces in the patellofemoral joint.6 As a result, patients may experience quadriceps weakness, patellofemoral pain, and fatigue.7 Loss of flexion rarely causes functional difficulties unless the knee fails to flex at least 120 degrees. This degree of deficit may interfere with functional activities such as sitting, squatting, stair climbing, or running.

Despite treatment of loss of motion through nonoperative or operative means, continued loss of motion may persist. This finding is the most frequent complication of attempted treatment. Other complications of treatment are less frequent. Manipulation may cause chondral damage, stimulation of myosi-tis ossificans, ossification of the medial collateral ligament, or femoral or tibial fracture. Arthroscopic debridement places a patient at risk of all complications associated with knee arthroscopy, such as neurovascular injury, chondral damage, numbness, and deep vein thrombosis. Open debridement also carries the risk of postoperative hematoma or hemarthrosis.


Loss of motion is a potentially debilitating problem following knee ligament injury or knee surgery. Multiple risk factors for diffuse joint inflammation and scarring or a mechanical block leading to loss of motion have been identified. Preventive strategies and early recognition of loss of motion are the most important means of combating loss of motion. Loss of motion often may be treated with appropriate range-of-motion and strengthening exercises. Arthroscopic treatment of loss of motion is an effective and safe alternative when less invasive therapies fail.


1. DeCarlo MS, Sell K: Normative data for range of motion and single leg hop in high school athletes. J Sport Rehabil 1997;6:246-255.

2. Shelbourne KD, Gray T: Anterior cruciate ligament reconstruction with autogenous patellar tendon graft followed by accelerated rehabilitation. A two- to nine-year followup. Am J Sports Med 1997;25:786-795.

3. Harner CD, Irrgang JJ, Paul J, et al: Loss of motion after anterior cruciate ligament reconstruction. Am J Sports Med 1992;20:499-506.

4. Irrgang JJ, Anderson AF, Boland AL, et al: Development and validation of the international knee documentation committee subjective knee form. Am J Sports Med 2001;29:600-613.

5. Hefti F, Muller W, Jakob RP, Staubli HU: Evaluation of knee ligament injuries with the IKDC form. Knee Surg Sports Traumatol Arthrosc 1993;1:226-234.

6. Perry J, Antonelli D, Ford W: Analysis of knee-joint forces during flexed-knee stance. J Bone Joint Surg Am 1975;57:961-967.

7. Sachs RA, Daniel DM, Stone ML, Garfein RF: Patellofemoral problems after anterior cruciate ligament reconstruction. Am J Sports Med 1989;17:760-765.

8. Johnson RJ, Eriksson E, Haggmark T, Pope MH: Five- to ten-year follow-up evaluation after reconstruction of the anterior cruciate ligament. Clin Orthop 1984;122-140.

9. Shelbourne KD, Wilckens JH, Mollabashy A, DeCarlo M: Arthrofibro-sis in acute anterior cruciate ligament reconstruction. The effect of timing of reconstruction and rehabilitation. Am J Sports Med 1991;19:332-336.

10. Mauro CS, Herrera MF, Irrgang JJ, et al: Loss of extension following ACL reconstruction: Analysis of incidence and etiology using new IKDC criteria. Presented at the annual meeting of the American Orthopaedic Society for Sports Medicine, Quebec City, 2004.

11. Noyes FR, Barber-Westin SD: Reconstruction of the anterior and posterior cruciate ligaments after knee dislocation. Use of early protected postoperative motion to decrease arthrofibrosis. Am J Sports Med 1997;25:769-778.

12. Harner CD, Waltrip RL, Bennett CH, et al: Surgical management of knee dislocations. J Bone Joint Surg Am 2004;86:262-273.

13. Shelbourne KD, Johnson G: Evaluation of knee extension following anterior cruciate ligament reconstruction. Orthopedics 1994; 17: 205-206.

14. Sterett WI, Hutton KS, Briggs KK, Steadman JR: Decreased range of motion following acute versus chronic anterior cruciate ligament reconstruction. Orthopedics 2003;26:151-154.

15. Hunter RE, Mastrangelo J, Freeman JR, et al: The impact of surgical timing on postoperative motion and stability following anterior cruciate ligament reconstruction. Arthroscopy 1996;12:667-674.

16. Bach BR Jr, Jones GT, Sweet FA, Hager CA: Arthroscopy-assisted anterior cruciate ligament reconstruction using patellar tendon substitution. Two- to four-year follow-up results. Am J Sports Med 1994;22: 758-767.

17. Howell SM, Barad SJ: Knee extension and its relationship to the slope of the intercondylar roof. Implications for positioning the tibial tunnel in anterior cruciate ligament reconstructions. Am J Sports Med 1995;23:288-294.

18. McMahon PJ, Dettling JR, Yocum LA, Glousman RE: The cyclops lesion: A cause of diminished knee extension after rupture of the anterior cruciate ligament. Arthroscopy 1999;15:757-761.

19. Jackson DW, Schaefer RK: Cyclops syndrome: Loss of extension following intra-articular anterior cruciate ligament reconstruction. Arthroscopy 1990;6:171-178.

20. Shelbourne KD, Patel DV Martini DJ: Classification and management of arthrofibrosis of the knee after anterior cruciate ligament reconstruction. Am J Sports Med 1996;24:857-862.

21. Paulos LE, Rosenberg TD, Drawbert J, et al: Infrapatellar contracture syndrome. An unrecognized cause of knee stiffness with patella entrapment and patella inferna. Am J Sports Med 1987; 15:331341.

22. Dodds JA, Keene JS, Graf BK, Lange RH: Results of knee manipulations after anterior cruciate ligament reconstructions. Am J Sports Med 1991;19:283-287.

23. Millett PJ, Wickiewicz TL, Warren RF: Motion loss after ligament injuries to the knee. Part II: Prevention and treatment. Am J Sports Med 2001;29:822-828.

24. Millett PJ, Williams RJ 3rd, Wickiewicz TL: Open debridement and soft tissue release as a salvage procedure for the severely arthrofibrotic knee. Am J Sports Med 1999;27:552-561.

25. Sprague NF 3rd, O'Connor RL, Fox JM: Arthroscopic treatment of postoperative knee fibroarthrosis. Clin Orthop 1982;165-172.


Pediatric Knee

Nathalee S. Belser and Craig S. Roberts

In This Chapter

Osteochondritis dissecans (OCD) Osgood-Schlatter disease (OSD) Intercondylar eminence fractures Salter-Harris fractures


The term OCD appears to have originated with Konig, who in 1888 postulated that spontaneous necrosis of the subchondral bone and the overlying cartilage was caused by loose bodies and inflammation.1 Fairbanks in 19332 suggested that OCD stemmed from a violent internal rotation of the tibia that caused impingement of the tibia spine on the femoral condyle.3

OCD is an epiphyseal disorder in which a localized segment of subchondral bone undergoes necrosis and demarcation from the surrounding normal bone.4 Fracture and failure of healing can result in the bone becoming separated partially or completely from the joint surface, forming an osteocartilaginous loose body. Although OCD can also involve the medial or lateral femoral condyle or patella,5 the lateral side of the medial femoral condyle is the most frequent site of involvement, seen in 75% of the cases.

Traditional beliefs about the causes of OCD such as trauma, ischemia, and genetics have proven to be wrong.3 In addition, studies concerning familial incidence of OCD document an autosomal dominant pattern of heredity with a high degree of


Clinical Features and Evaluation

Early symptoms of OCD are vague (Box 62-1). As the fragment begins to separate, the patient experiences catching, locking and joint effusion and may limp on ambulation.6 Patients complain of medial knee pain and partial giving way after strenuous physical activity.7 Physical findings include local tenderness over the site of the fragment and quadriceps weakness.

The patient may present with Wilson's sign, which is based on the fact that tibial spines may impinge against the femoral condyle when the OCD is located at the classic site at the lateral side of the medial femoral condyle6 (Box 62-2). The patient is placed in a supine position and the knee is flexed to a right angle. The leg is internally rotated and is gradually extended. The test is positive when pain is felt at 25 to 30 degrees of knee flexion and the tibia is internally rotated. Pain is relieved when the tibia is externally rotated. However, the validity of Wilson's sign has recently been questioned by Conrad and Stanitski,8 who, in a series of 32 patients, found that Wilson's sign was of minimal clinical diagnostic value.

OCD is usually divided into three stages. Stage I is a well-demarcated prominence of the articular surface; the cartilage covers the elevation that is continuous with the rest of the cartilage surface but is a different color.4 The prominence can be easily separated, and beneath it there is an excavation of bone and chondral portion of the articular end of the bone.

In stage II, the fragment is distinctly separated but still lies within its anatomic bed on the articular surface. In stage III, the fragment is displaced out of its anatomic bed into the joint.

Diagnostic Imaging

Imaging recommendations for OCD include anteroposterior, lateral, tunnel, and merchant views.9 Magnetic resonance imaging (MRI) can assess lesion size and the status of cartilage and subchondral bone and subsequent healing of the lesion (Fig. 62-1).9 Luhmann et al10 noted that routine review of MRI scans for pediatric knee disorders such as OCD increased the diagnostic accuracy of the MRI.

Treatment Options

Treatment decisions are based mainly on the stability of the lesion (Box 62-3). Stable lesions are treated with conservative measures in skeletally immature patients. A debate exists regarding therapeutic or detrimental effects of immobilization, which centers on which tissue the treating physician considers most important in healing.9 Advocates who focus on the sub-chondral bone believe that OCD should be treated like a fracture, with a cast or knee immobilizer. In contrast, those who focus on the cartilaginous component of OCD recommend early knee motion.

The conservative management protocol can be divided into three phases. First, the knee is immobilized in a long-leg cast for 6 weeks with toe touch (10 pounds) weight bearing with crutches and regular straight leg raise exercises. In the second


• There is a gamut of knee disorders in the skeletally immature knee.

• Disorders range from repetitive overuse injuries to growth plate fractures.

• This chapter covers OCD, OSD, intercondylar eminence fractures, distal femoral physeal/epiphyseal fractures, proximal tibial physeal/epiphyseal fractures, distal pole patellar sleeve fractures, and tibial tubercle fractures.

Catching, locking, knee effusion, limping Quadriceps atrophy

Presenting complaint of knee giving away while walking in a straight line or during strenuous activity

Wilson's sign: if the knee is flexed to a right angle and the tibia is internally rotated, pain is experienced as the knee is extended. Pain is relieved by external rotation.

Catching, locking, knee effusion, limping Quadriceps atrophy

Presenting complaint of knee giving away while walking in a straight line or during strenuous activity

Wilson's sign: if the knee is flexed to a right angle and the tibia is internally rotated, pain is experienced as the knee is extended. Pain is relieved by external rotation.

Avascular area with overlying articular cartilage that becomes loose and detaches

Typically occurs on lateral aspect of medial femoral condyle

Avascular area with overlying articular cartilage that becomes loose and detaches

Typically occurs on lateral aspect of medial femoral condyle

If lesion is intact, a period of observation is recommended with avoidance of sports. Close follow-up with imaging such as radiographs or magnetic resonance imaging is recommended over the next year to demonstrate healing of the lesion. If symptoms persist or the fragment is detached, knee arthroscopy with fixation of the fragment or excision.

Operative treatment is indicated on a semiurgent basis for detached or unstable lesions.

If lesion is intact, a period of observation is recommended with avoidance of sports. Close follow-up with imaging such as radiographs or magnetic resonance imaging is recommended over the next year to demonstrate healing of the lesion. If symptoms persist or the fragment is detached, knee arthroscopy with fixation of the fragment or excision.

Operative treatment is indicated on a semiurgent basis for detached or unstable lesions.

Figure 62-1 Magnetic resonance imaging of a loose osteochondritis dissecans fragment of the lateral femoral condyle, an atypical location, in a nearly skeletally mature individual.

phase (weeks 6 to 12), weight bearing is permitted without immobilization. A rehabilitation program is initiated emphasizing knee range of motion and low-impact quadriceps and hamstring strengthening exercises. If the patient remains pain free, phase three begins at 3 months after diagnosis. This phase includes running, jumping, and sports readiness activities, but high-impact and shear activities are restricted until the child has had several months of pain free, low-impact conditioning and radiographs document healing. MRI can be repeated if clinically indicated in phase three to assess healing.

Operative treatment is indicated for patients who have detached or unstable lesions, who are approaching epiphyseal closure, or when nonoperative management fails to alleviate symptoms. The goals of operative treatment include rigid internal fixation of unstable fragments and repair of osteochondral defects. Surgical options include drilling, bone grafting, internal fixation in situ, open or arthroscopic reduction with internal fixation, fragment excision, autologous osteochondral grafting, and allogenic osteochondral grafting.11 For patients who fail nonoperative treatment but have a stable lesion and intact articular surface, arthroscopic drilling of the lesion creates channels for potential revascularization and healing. The drilling may either pass through the epiphysis without articular penetration or continue transarticularly. While drilling through the epiphysis avoids articular surface violation, it is associated with the technical challenges of maintaining drill depth and placement accuracy.

In cases of flap lesions, fibrous tissue found between fragments should be removed. Débridement of significant portions of bone from the fragment and subchondral base of the lesion should be avoided. Wright et al12 reported that only six of 17 patients (35%) had a good result from fragment excision, an average of 8.9 years postoperatively, and recommended "aggressive attempts to preserve the articular cartilage and avoid excision of the fragments when possible." In patients who have unstable lesions with subchondral bone attached that can be anatomically reduced, fixation can be performed by a variety of arthroscopic or open methods. These options include metallic, cannulated, partially threaded small fragment screws; metallic self-compressing screws; bioabsorbable pins; and bioabsorbable screws.

Unique situations include bone and cartilage defects when osteochondral fragments cannot be saved. Newer surgical options include autologous chondrocyte implantation, which involves the transplantation of cloned cartilage cells under a periosteal cover and cylindrical osteochondral autograph transfer. Yoshizumi et al13 treated three cases of OCD in patients with closed growth plates with a 10-mm diameter osteochon-dral autograph transfer with excellent clinical and radiographic results, but areas of signal intensity remained on MRI scans at short-term follow-up.

Recent reports on juvenile OCD have noted a significant number of poor results at follow-up.3 To date, there have been no controlled prospective studies on OCD that accurately measured the effect of different treatments.3


Knee arthroscopy is performed in order to evaluate the size and reducibility of the osteochondral fragment. The bony bed of the lesion is débrided, the fragment is anatomically reduced, and provisionally fixed with a percutaneously inserted guide wire. The guide wire is then overreamed with a cannulated reamer. A partially threaded, cannulated screw is inserted percutaneously; the fragment is compressed, and the guide wire is removed. The

Figure 62-2 Arthroscopic view of the loose osteochondritis dissecans fragment of the lateral femoral condyle.

screw is subsequently removed arthroscopically at 10 to 12 weeks after insertion in a similar manner (Figs. 62-2 through 62-5).


OSD is an overuse injury or traction apophysitis of the tibial tubercle that commonly occurs in boys 13 to 14 years of age and in girls 10 to 11 years of age. Inflammation and new bone formation at the patellar tendon insertion are characteristic. The differential diagnosis includes patellar tendonitis, Sinding-Larsen-Johansson syndrome, avulsion fracture of the tibial

Figure 62-3 Arthroscopic view of provisional fixation after reduction of the osteochondritis dissecans fragment.
Osteochondritis Dissecans Screw
Figure 62-4 Arthroscopic view of the seated cannulated screw that has been used to fix the osteochondritis dissecans fragment.

tuberosity, tumor, and infection. The association of patella alta with OSD has been reported.14,15

The precise cause of OSD is unknown.14 The most common theory is that repeated contractions of the quadriceps mechanism result in an extra-articular osteochondral stress fracture of the apophysis.16 Tension forces produce fracture separation of an osteochondral fragment that includes a segment of the secondary ossification center of the tibial tubercle and the cartilage anterior to it. With healing, new bone forms in the gap between the separated osteochondral fragment and the tibial tubercle, which is deviated and prominent. OSD is usually unilateral but has been reported to occur bilaterally in 20% to 30% of cases.14 Ross and Villard17 reported that subjects with a 7-year history of OSD had significantly lower scores than subjects in a control

Bladder Wall
Figure 62-5 Follow-up arthroscopic view of the healed osteochondritis dissecans lesion at the time of implant removal.

Complaints of pain in anterior aspect of the knee in the region of the proximal tubercle, which is swollen, prominent, and tender. Vague and intermittent onset of symptoms.

Running and jumping aggravate symptoms, while rest relieves them. Physical examination reveals swelling and localized tenderness over tibial tubercle without other abnormalities.

Complaints of pain in anterior aspect of the knee in the region of the proximal tubercle, which is swollen, prominent, and tender. Vague and intermittent onset of symptoms.

Running and jumping aggravate symptoms, while rest relieves them. Physical examination reveals swelling and localized tenderness over tibial tubercle without other abnormalities.

Proximal Tibial Swelling

Figure 62-6 This lateral radiograph of the knee is from a mild case of Osgood-Schlatter disease with ossification over the tibial tubercle.

group on both the Knee Outcome Activities of Daily Living Scale and Sports Activity Scale. Browner-Elhanan et al18 noted a lack of flexibility and strength imbalance of the leg muscles associated with OSD in nine patients who were an average of 11.8 years old.

Clinical Features and Evaluation

Patients present with complaint of pain in the anterior aspect of the knee in the region of the proximal tubercle, which is swollen, prominent, and tender. The onset of symptoms is vague and intermittent.16 Running and jumping aggravate the severity of pain, while rest relieves symptoms. Physical examination reveals swelling and localized tenderness over the tibial tubercle without other abnormalities. Boys are frequently more affected than girls, and about a half of the patients have a history of precipitating trauma. Pain is reproduced by extension against forced resistance. In addition, there may be quadriceps atrophy (Boxes 62-4 and 62-5).

Diagnostic Imaging

The lateral radiograph is the most useful view and shows soft-tissue swelling and a separate ossicle over the tubercle (Fig. 62-6).14 In addition, there may be bilateral accessory ossification centers. MRI can be useful in detecting partial avulsion or an avulsion fracture of the apophyseal cartilage with fragmentation of the accessory centers.

Treatment Options

OSD is generally a self-limited condition.19 Treatment of acute avulsion of the tubercle depends on the size of the fragment and the degree of displacement (Box 62-6). The condition usually resolves within 1 to 2 years, but in about 10% of patients, the formation of a discrete ossicle and bursa results in persistent pain and tenderness.

OSD is managed by modification of activities, nonsteroidal anti-inflammatory drugs, and a knee pad to control discomfort. If OSD is severe or persistent, a knee immobilizer may be effec-

Figure 62-6 This lateral radiograph of the knee is from a mild case of Osgood-Schlatter disease with ossification over the tibial tubercle.

tive. Duri et al14 warned, "The ossicle can be easily enucleated from the patellar tendon by way of a longitudinal fiber-splitting incision. The patient and the family should be forewarned that some residual soft tissue and bony prominence may remain." Operative treatment is reserved for nonunited ossicles and persistent symptoms after the physes have closed. Excision is performed through a short incision by splitting the distal fibers of the patellar tendon. Postoperative casting for 6 weeks may be necessary if more dissection is performed. Excellent results have been reported with surgical excision. Flowers and Bhadreshwar20 reported that 88% of patients reported complete relief of pain an average of 13.5 months after surgical excision of the ossicle after a trial of conservative treatment failed. Overall, the prognosis for OSD is excellent as patients usually are able to return to full activity and participate in athletics.

Concerns have been raised about safety of harvesting a bone-patellar tendon-bone autograft for anterior cruciate ligament (ACL) reconstruction in patients with an ossicle associated with OSD. However, Di Gennaro et al21 noted that an autogenous bone-patellar tendon-bone graft can be safely harvested in ath-

Extra-articular osteochondral stress fracture of the apophysis caused by repeated contractions of the quadriceps Tension forces produce fracture separation of an osteochondral fragment.

Fragment can include a segment of the secondary ossification center of the tibial tubercle and the cartilage anterior to it.

The condition usually resolves within 1 to 2 years. Manage by modification of activities. Nonsteroidal anti-inflammatory drugs. Knee pad to control discomfort. Knee immobilizer may relieve inflammation.

Extra-articular osteochondral stress fracture of the apophysis caused by repeated contractions of the quadriceps Tension forces produce fracture separation of an osteochondral fragment.

Fragment can include a segment of the secondary ossification center of the tibial tubercle and the cartilage anterior to it.

The condition usually resolves within 1 to 2 years. Manage by modification of activities. Nonsteroidal anti-inflammatory drugs. Knee pad to control discomfort. Knee immobilizer may relieve inflammation.

Box 62-7 Intercondylar Eminence Fractures: Signs and Symptoms

• Inability to bear weight

• Hemarthrosis

• Knee held in a flexed position letes who have an ossicle associated with OSD. McCarroll et al22 noted the importance of recognizing the OSD ossicle preoperatively, so that it is not mistaken for the tibial tubercle intraoperatively. The surgeon can safely excise the ossicle intraoperatively with a small surgical knife blade after graft harvest.


Intercondylar eminence fractures are the children's equivalent of an ACL tear in the adult.23,24 The reported mechanisms of injury in the child are similar to those in the adult and include motor vehicle accidents, falls, and sports activities.23,25 Because the collagenous portion of the ACL is stronger than the bony attachments in the skeletally immature individual, bony avulsion occurs at the tibial ACL insertion site (the intercondylar eminences), usually as a result of an athletic, noncontact, twisting injury. Although the bony avulsion appears to be the primary pathology, interstitial tearing of the ACL also occurs in most cases.

Clinical Features and Evaluation

Patients present with knee pain and limited knee motion and are unable to bear weight. An effusion caused by the hemarthrosis is present (Boxes 62-7 and 62-8). Patients hold the knee in a fixed position, once pain is controlled. The presence of a locked knee (usually determined on examination under anesthesia) is indicative of concomitant knee pathology or that the fracture is not fully reduced due to an interposed meniscus or a transverse intermeniscal ligament. Neurovascular status should not be affected and the skin should be intact.

These injuries have traditionally been classified into three types according to the system first described by Meyers and McKeever26 in 1959. Type I injuries are nondisplaced or minimally displaced fractures of the intercondylar eminence. Type II injuries have partial displacement of the eminence fracture prox-imally and anteriorly with a "beaklike" deformity on the lateral radiograph.27 In type III injuries, the eminence is completely displaced from its tibial attachment, and in type IV injuries, a displaced, comminuted fracture is present.28

Diagnostic Imaging

Standard anteroposterior and lateral radiographs are obtained. The lateral radiograph is the most helpful because it can demonstrate the degree of displacement.29 Alternatively, MRI can be used to assess for displacement, possible interposition of the meniscus, ACL injury, and other concomitant bony and soft-tissue injuries.

Treatment Options

Nonoperative treatment of type I injuries is generally accepted. Historically, conservative treatment has also been recommended for type II injuries (Box 62-9). However, authors have reported that 26% of type II injuries involve entrapment of either the anterior horn of the medial meniscus, transverse meniscal ligament, or the anterior horn of the lateral meniscus.30 Hunter and Willis27 reported on arthroscopic fixation of type II and III eminence fractures in a series of 17 patients who were an average of 26.6 years old. Eight of the 17 subjects were 16 years of age or younger, and these patients had better outcomes as measured by the International Knee Documentation Committee functional and overall rating scores. These authors noted the phenomenon of interposition of the meniscal ligament between the avulsed fragments in 17 patients (59%). They equated the intermeniscal ligament with the Stener lesion (interposed adductor pollicis tendon), associated with ulnar collateral ligament of the thumb tears where the lesion prevents the tendon or bony avulsion from returning to its anatomic position.27 Kocher et al30 reported on arthroscopic reduction and cannulated screw fixation of six patients with type III injuries and reported persistent laxity but excellent functional outcome.30 The use of bioabsorbable fixation of the fracture has been used in a small number of patients.31 A metallic screw shorter than 25 mm can be used to avoid the proximal tibial growth plate. Alternatively, Lubowitz et al32 recommended repair using nonabsorbable suture fixation, citing the advantages of eliminating the risks of comminution of the fracture fragment, vascular injury, and future hardware removal. Patients and parents should be counseled that persistent laxity is normal even after the surgical treatment of intercondylar eminence fractures. Persistent laxity is nonetheless still associated with an excellent clinical outcome. Future surgical procedures will most likely be necessary for removal of implants and possible ACL reconstruction in athletically active patients or those who subsequently experience symptoms of knee instability.


Knee arthroscopy is performed and may require the use of a pump for inflow or a tourniquet. The knee joint is inspected. Particular attention is paid to visualization of the avulsed fragment. The anterior infrapatellar fat pad may prevent adequate visualization and may require debridement. The fracture bed is inspected for possible incarceration of the anterior horn of the

Box 62-8 Intercondylar Eminence Fractures: Anatomic Lesions

• Fracture of the intercondylar eminence

• Variable amount of fracture displacement

• Possible entrapment of the meniscus

• Interstitial tearing of the anterior cruciate ligament

Box 62-9 Intercondylar Eminence Fractures: Treatment Options

• Type I injuries: nonoperative treatment (immobilization)

• Type II injuries: treatment is controversial (recent trend toward operative treatment)

• Type III and IV injuries: operative management lateral meniscus. If present, the meniscus must be retracted and preserved and the fragment reduced. Reduction maneuvers include decreasing the amount of knee flexion and manual manipulation of the fragment with a nerve hook. The ACL should also be carefully assessed for interstitial stretching, partial tearing, and loss of function. Optimal viewing of the ACL from the anteromedial portal will usually be required. Decision making for choice of fixation of the fragment is based on the operative pathology. If the fragment is not comminuted (type II or III), then cannulated screw fixation can be used. Guide wire insertion often requires placing an arthroscopic portal somewhat higher than usual. Positioning the knee in less flexion also helps reduce the fragment. The portal location can be precisely localized using a percutaneously inserted spinal needle. Oftentimes, three anterior portals are required: one for the arthroscope, one for the nerve hook to maintain reduction, and one to insert the cannulated screw over a guide wire. Small fragment, partially threaded screws about 25 mm long are usually used. If the fragment is comminuted (type IV), options include one or two can-nulated screws and washers (Figs. 62-7 and 62-8) or suture methods that pass sutures through the base of the ACL using arthroscopic suture passers. Sutures can be tied over an anterior tibial bone bridge.


Fractures of the growth plates around the knee occur in skele-tally immature individuals. These injuries can be thought of in terms of "3s": the three major physes or growth plates (femur, tibia, and fibula), the three major epiphyses (femur, tibia, and fibula), and three traction sites (patella, tibial tubercle, and tibial intercondylar spines). Although many of these injuries occur by mechanisms that would cause a ligamentous injury in an adult, the determining factor of which injury occurs is a function of the rate and magnitude of the injuring force.33 High-magnitude forces at a low rate of application result in physeal fractures, whereas low-magnitude forces applied at a high rate produce lig-

Figure 62-7 Lateral radiograph of a displaced intercondylar eminence fracture (type IV).
Spines Intercondylar Eminence

Figure 62-8 Postoperative anteroposterior (A) and lateral (B) radiographs after fixation of an intercondylar spine fracture.

Figure 62-8 Postoperative anteroposterior (A) and lateral (B) radiographs after fixation of an intercondylar spine fracture.

ament injuries. Physeal fractures are generally classified according to the Salter-Harris classification, which divides injuries into types I through V A Salter type I injury is an epiphyseal separation.34 A Salter type II fracture is also an epiphyseal plate injury, but after the fracture line continues a variable distance across the physis, it then extends out into the metaphysis producing the characteristic Thurston-Holland fragment. The Salter type III fracture is intra-articular and extends from the joint surface to the physis and then out perpendicularly across the physis. A Salter IV fracture is also intra-articular. The fracture line extends from the joint surface through the physis and then through the metaphysis producing a complete split. A Salter type V fracture is a rare occurrence and involves a crush-

Box 62-10 Fractures about the Knee: Signs and Symptoms

• Tenderness over the growth plate (physis) or epiphysis

• Hemarthrosis

• Crepitation

• Inability to move knee ing injury to the epiphysis and physis. This section includes the following fractures: distal femoral physeal fracture, proximal tibial physeal fracture, patellar sleeve fracture, and tibial tubercle avulsion fracture (Boxes 62-10 and 62-11).

The knee physes are immature tissues and vulnerable to injury. Effects on future growth from these fractures may occur. As a general rule, the femur has more remodeling capacity than the tibia. Although the prognosis of these injuries traditionally has been assumed to be favorable, these injuries can cause future problems. Careful follow-up is important.

Clinical Features and Evaluation Distal Femoral Physeal Fractures

Although knee ligament ruptures can occur in children, most prepubescents and adolescents suffer growth plate injuries rather than ligamentous injuries. The distal femoral physis is the largest in the body. The epiphysis is the first to ossify and provides 70% of the overall growth of the femur.

Proximal Tibial Physeal Fractures

About 50% of proximal tibial fractures occur in sports. These fractures are about one fourth as common as distal femoral physeal fractures. The mechanism of injury is usually hyperextension and valgus stress. The most important part of the initial treatment of these fractures is the recognition that these injuries can be the pediatric equivalent of an adult dislocation of the knee. Associated vascular injuries, compartment syndromes, or neurologic deficits may be present and must be recognized. Arte-riograms are necessary if there is any question about the vascular status. Metaphyseal injuries are more common than tibial plateau fractures (epiphyseal injuries). Proximal tibial metaphyseal injuries commonly occur between the ages of 2 and 8. Patients and parents need to be counseled about the unpredictability of possible valgus deformity from medial overgrowth after fracture or subsequent hyperextension deformity secondary to anterior growth plate arrest. Salter type II fractures are the most common tibial epiphyseal injuries.35 Physical examination demonstrates severe tenderness and swelling over the proximal tibial physis for epiphyseal injuries.

Patella Sleeve Fractures

Patella sleeve fractures are commonly misdiagnosed and usually involve the distal rather than the proximal pole of the patella.

Clinical findings include an extensor lag and patella alta. Differential diagnosis includes Sinding-Larsen-Johansson syndrome and bipartite patella.

Tibial Tubercle Avulsion Fractures

These injuries tend to occur in the robust athlete, near skeletal maturity, usually as a result of a jump or fall.36 There is a possible association with OSD.36 Fractures of the tibial tuberosity are classified according to the system of Ogden et al.37 Associated injuries are uncommon but must be ruled out. These include tears to the menisci, medial collateral ligament, lateral collateral ligament, and ACL as well as compartment syndromes and neu-rovascular injuries.

Diagnostic Imaging

As a general rule, nondisplaced fractures may not be visible on plain radiographs. Subtle radiographic findings such as a small fleck of bone at the periphery of the metaphysis may be the only radiographic finding of a proximal tibial epiphyseal fracture.35 Stress views for the diagnosis of radiographically occult fractures in the skeletally immature patient were previously thought to be of value but have fallen out of vogue since the advent of MRI. The Thurston-Holland sign is a metaphyseal, wedgelike component of a physeal fracture. It is the sine qua non of a Salter type II fracture. Patella sleeve fracture radiographic findings include a small avulsion or "chip" about the distal pole of the patella.

Treatment Options

Distal Femoral Physeal Fractures

All fractures of the distal femoral physis usually require surgical stabilization38 (Box 62-12). Surgical options include crossed Kirschner wires, wires/screws parallel to the growth plate for a Salter type II, and a transepiphyseal screw for a Salter type IV. Salter type I fractures are usually treated with smooth pins. Salter type II fractures with large metaphyseal fragments can often be treated with 4.5 or 7.3mm screws. Salter type III or IV fractures can be treated with percutaneous screws

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