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Soft-Tissue Procedures and Osteotomies About the Knee
This chapter discusses the surgical treatment of nontraumatic abnormalities involving the bone, muscles, tendons, tendon sheaths, fascia, and bursae of the knee. The cause of these disorders may be degenerative, developmental, related to repetitive use, or a combination of these factors. Many of these disorders are encountered frequently in office practice, but few require surgery. Most respond favorably to treatment such as rest, application of ice or heat, elevation, and local or systemic antiinflammatory medication.
Muscle Contractures
Contractures can develop in almost any muscle group. The cause can be obscure, as in congenital contractures, or obvious, as in infection, ischemia, trauma, or injection myositis. Injection fibrosis most commonly occurs in the quadriceps muscle but also has been described in the gluteal, deltoid, and triceps muscles. Contractures in infants often follow intramuscular antibiotic injections. We have seen several adults with multiple areas of fibrosis and contracture after the addictive intramuscular use of the opioid pentazocine (Talwin). Oral pentazocine now comes compounded with naloxone (Talwin NX), which will cause opioid withdrawal symptoms if the pills are crushed and injected. Chronic intramuscular use of other opioid analgesics also can induce muscular fibrosis and contracture.
Quadriceps Contracture of Infancy and Childhood
The etiology of quadriceps contracture is divided into congenital and acquired types, and in some cases there is a mixture of both types. The congenital type appears to have a familial component because it can occur in siblings, and it often occurs in patients of central and eastern Asian descent. The acquired type is seen in association with multiple injections or infusions into the thigh soon after birth. The Ad Hoc Committee of the Japanese Orthopaedic Association for Muscular Contractures classified quadriceps contractures into three types ( Table 9.1 ). The exact mechanism causing these contractures is unclear, but suggested causes include compression of the muscle bundles and capillaries by the volume of medication injected and the toxicity of the drug. Whatever the cause, a delay between injection and contracture of several years is common.
TABLE 9.1
Quadriceps Contracture Classification
From Santo S, Kokubun S: Report of the diagnosis and treatment of muscular contracture. The Ad Hoc Committee of the Japanese Orthopaedic Association for Muscular Contracture, J Jpn Orthop Assoc 59(2):223–253, 1985.
| Knee Flexion | When Knee is Forced to Flex in Prone Position | |
|---|---|---|
| Rectus femoris type | Restricted with hip extension | Hip is forced to flex |
| Vastus type | Restricted with hip flexion | Hip remains the same |
| Mixed type | Slightly restricted with hip extension | Hip is forced to flex |
The most common symptom is progressive, painless limitation of knee flexion. Hyperextension and subluxation of the knee may occur with continued growth. Normal skin creases over the knee may be absent, and a characteristic dimple may be present over the area of fibrosis, especially when the knee is flexed. Habitual dislocation of the patella is common.
Radiographic changes are not apparent early, but if left untreated, the muscle contracture can cause changes in the soft tissues and in the articular cartilage of the femur and tibia. Progressive displacement and hypoplasia of the patella can occur with long-standing quadriceps contracture. In older children with early onset of symptoms but delayed treatment, flattening of the femoral condyles, genu recurvatum, anterior dislocation of the tibia, and gross degenerative changes in the joint can be seen.
Early recognition and prevention of quadriceps contracture through passive exercise in children receiving intramuscular injections is crucial. When the scar contracture is well established, however, surgical treatment is indicated to prevent late changes in the femoral condyles and the patella. Surgical treatment is indicated early in patients with habitual dislocation of the patella.
The following may be involved in quadriceps contracture: (1) fibrosis of the vastus intermedius muscle tying down the rectus femoris to the femur in the suprapatellar pouch and proximally, (2) adhesions between the patella and the femoral condyles, (3) fibrosis and shortening of the lateral expansions of the vasti and their adherence to the femoral condyles, and (4) actual shortening of the rectus femoris muscle. To correct the deformity, Thompson devised an operation known as “quadricepsplasty.” Its success depends on (1) whether the rectus femoris muscle has escaped injury, (2) how well this muscle can be isolated from the scarred parts of the quadriceps mechanism, and (3) how well the muscle can be developed by active use.
During the early stage of contracture, when no significant joint changes have occurred, proximal release has been recommended to eliminate extensor lag and hemarthrosis of the knee. When more extensive changes are apparent, a Thompson type of quadricepsplasty is indicated. When genu recurvatum has developed, a supracondylar femoral osteotomy (see Chapter 22 ) can restore some flexion if severe degenerative changes have occurred. Arthrodesis may be indicated if symptoms are severe.
Sasaki et al. found that best results were obtained using a longitudinal skin incision over the rectus muscle through which the fibrotic muscle was released with a transverse incision. After surgery, the leg was positioned with the knee in 90 degrees of flexion and the hip in full extension but a cast was not used. Active exercises were begun at 2 days. Results were found to deteriorate with time, and surgery was recommended at age 6 years or older. An isolated contracture of the rectus femoris can be treated in this manner.
Moderate contractures, before significant bony changes have occurred, are treated best with a proximal release of the quadriceps ( Fig. 9.1 ).
Proximal Release of Quadriceps
Technique 9.1
(Sengupta)
- ▪
Make a curved incision along the base of the greater trochanter and vertically downward along the lateral aspect of the thigh for a variable distance, depending on the extent of fibrosis ( Fig. 9.1A ).
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Through the upper part of the incision, section the iliotibial band transversely. Often the iliotibial band is thickened and fibrotic, contributing to the contracture.
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Expose the upper attachment of the vastus lateralis below the greater trochanter ( Fig. 9.1B ). Detach the origin of the vastus lateralis from the trochanteric line and distally along the lateral intermuscular septum ( Fig. 9.1C ).
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As the vastus lateralis retracts to expose the vastus intermedius, use a periosteal elevator to release the vastus intermedius from the femoral surface.
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Flex the knee, and release any remaining adhesions.
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If the rectus component also is contracted, expose its origin at the upper part of the incision and detach it, after identifying and retracting the femoral nerve ( Fig. 9.1D ).
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Full knee flexion should be possible; release of the joint capsule usually is unnecessary in children.
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Close the wound in routine fashion, and apply a posterior splint with the knee in maximal flexion.
Postoperative Care
The splint is worn until all tenderness has disappeared, usually 3 to 4 weeks, and then vigorous quadriceps exercises are begun. Extension lag improves rapidly, and the child usually can walk in 4 weeks and stand up from a squatting position in 3 months. Knee stretching exercises should be continued throughout growth to prevent recurrence of the contracture.
Quadricepsplasty for Posttraumatic Contracture of the Knee
Hahn et al. achieved 90% good to excellent results in 20 patients with a mean active flexion arc of approximately 115 degrees with this release technique. Liu et al. described successful release of extension knee contracture in 12 patients using a combination of manipulation and percutaneous pie-crusting of the distal and lateral quadriceps with an 18-gauge needle with the knee in flexion. An average of 70 degrees of increased flexion was achieved at 8 months. There was a positive correlation between the number of punctures and knee flexion achieved. Birjandinejad et al. achieved good to excellent results in 87% of 64 patients at a mean of 36 months. Preoperative range of motion, number of previous surgeries, duration of extension contracture, and body mass index influenced the final flexion achieved.
Technique 9.2
(Modified Thompson Quadricepsplasty as Described by Hahn et al.)
- ▪
Perform the procedure using a tourniquet.
- ▪
Make medial and lateral parapatellar incisions for arthro-lysis ( Fig. 9.2A ).
- ▪
Flex the knee, and if adequate flexion is not obtained, make an anterolateral or lateral incision in the distal two thirds of the thigh and release adhesions around the quadriceps muscle.
- ▪
Divide the tensor fascia lata transversely in the distal thigh. Isolate the vastus lateralis from the rectus femoris, and release it close to its patellar insertion. Release the vastus medialis from the rectus femoris by blunt dissection ( Fig. 9.2B ).
- ▪
Free the rectus femoris from the vastus intermedius, the anterior surface of the femur, and the upper pole of the patella ( Fig. 9.2C ).
- ▪
Perform a Z-plasty lengthening of the rectus femoris tendon if satisfactory flexion has not been achieved ( Fig. 9.2D ).
Postoperative Care
The extremity is immobilized in a splint in about 50 degrees less than the maximal flexion obtained during surgery; this is maintained for 2 to 3 days. The extremity is then placed in a continuous passive motion machine, range of motion is begun, and the patient remains hospitalized until 90 degrees of passive flexion is achieved. Passive and active exercises for the quadriceps and hamstrings continue and are crucial to the success of this procedure. The knee is kept in full extension during the night and is exercised during the day with active and active-assisted exercises. If 90 degrees of flexion is not obtained after 3 months, gentle manipulation with the patient under anesthesia may be required. The patient should expect slow return of active quadriceps extension. Most patients can expect improvement in range of motion of the knee after quadricepsplasty but should expect severe quadriceps weakness for many months. If the patient is not skeletally mature, some of the improvement in flexion may be lost as growth occurs.
Flexion, Extension, and Combined Contractures
Posttraumatic stiffness can be caused by intraarticular adhesions, fibrosis of the surrounding soft tissues, or both. Flexion contractures can be caused by anterior bony impingement or posterior periarticular adhesions. Extension contractures can be the result of posterior bony impingement or anterior periarticular adhesions. Bony impingements need to be treated first followed by soft-tissue releases. Pujol et al. stated that the exact cause(s) of contracture should be determined before surgery. Any complex regional pain syndrome should be controlled and surgery delayed if the patient is in the active phase. Associated fractures must be healed. A thorough workup is necessary and may include a computed tomography (CT) arthrogram, magnetic resonance imaging (MRI), bone scan, and plain radiographs. A combination of open and arthroscopic procedures may be necessary for success ( Fig. 9.3 ). For more information, see the extensive review by Pujol et al.
Snapping Syndromes
It is common for a patient to hear or feel snapping or popping of joints. Disability or pain sufficient to justify surgery for this is rare. Most patients respond favorably to reassurance and avoidance of the specific activity that produces the snapping sensation.
Snapping symptoms are rare in the knee. True snapping of the knee is extraarticular. Intraarticular catching or locking in the knee usually is caused by meniscal tears, meniscal cysts, loose bodies, patellofemoral disorders, or arthritic joint changes.
Snapping of the knee can occur in patients with an abnormal anterior insertion of the biceps femoris tendon on the fibular head. This can be treated by reinsertion of the tendon ( Fig. 9.4 ) or resection of the fibular head with reattachment of the tendon if conservative treatment fails. Biceps femoris snapping caused by a fibular exostosis has been reported, as well as snapping from a direct injury to the tendon. Snapping caused by direct injury can be treated by rerouting the tendon insertion through a tunnel in the fibular head.
The popliteus tendon can cause snapping of the knee, which usually is palpable midway between the lateral epicondyle and lateral joint line. If conservative treatment fails, a popliteus release or tenodesis of the popliteus tendon to the fibular collateral ligament can be done.
Knee snapping also can be caused by abnormal insertion of the semitendinosus tendon, causing it to snap over a prominence on the medial tibial condyle. This can be treated by dividing the semitendinosus tendon at its insertion and transferring it to the semimembranosus tendon. A hamstring tendon sliding over an osteochondroma of the femur likewise can cause snapping, and excision of this generally benign lesion is indicated if it is severe. Shapiro et al. recommend using dynamic ultrasonography to diagnose the cause of mechanical snapping.
Painful Paraarticular Calcifications
Painful paraarticular calcifications similar to those found within the rotator cuff of the shoulder also develop around the knee. These calcific deposits may be located within a tendon or the soft tissues adjacent to a tendon or ligament near its attachment to bone ( Fig. 9.5 ). The calcification most probably is located in an area of focal necrosis or degeneration.
Although most paraarticular calcifications occur without direct trauma, calcification within tendons or ligaments may be a response to degenerative changes within the structures as a result of chronic use or subclinical injury.
The presence of calcification in the tibial collateral ligament, as in Pellegrini-Stieda disease, usually is more directly related to trauma, such as a sprain or tear of the tibial collateral ligament. The treatment is the same as that for a calcification around the shoulder (see Chapter 46 ).
Spontaneous recovery may occur without treatment, and the deposit may partially or completely disappear in time. Infiltration with a local anesthetic agent, supplemented, if desired, by injection of 40 mg of methylprednisolone (Depo-Medrol) or its equivalent, produces immediate relief and can be curative. Ultrasound and extracorporeal shock wave therapy also have been reported to be of benefit. The calcific deposit should be excised if response to nonoperative measures is unsatisfactory.
Tendinitis and Bursitis
In the evaluation of patients with tendinitis of the lower extremity, a careful history of work conditions and exercise routines is necessary. Overuse (repetitive activity) or overload (sudden increase in activity) often accentuates tendinitis. Tendinitis from these causes usually responds to relative rest, ice, the use of a Neoprene sleeve, antiinflammatory medications, and alterations in work or exercise habits. Mechanical abnormalities, leg-length inequality, and leg malalignment may respond to the use of a properly fitted shoe orthosis. Muscle imbalance should be treated with appropriate flexibility and strengthening exercise programs.
Bursae are sacs lined with a membrane similar to synovium; they usually are located around joints or where skin, tendon, or muscle moves over a bony prominence, and they may or may not communicate with a joint. Their function is to reduce friction and to protect delicate structures from pressure. Bursae are similar to tendon sheaths and the synovial membranes of joints and are subject to the same disturbances: (1) acute or chronic trauma; (2) acute or chronic pyogenic infection; and (3) low-grade inflammatory conditions such as gout, syphilis, tuberculosis, or rheumatoid arthritis. There are more than 140 bursae in the human body; bursae consist of two types: those normally present (e.g., over the patella and olecranon) and adventitious ones (e.g., develop over a bunion, an osteochondroma, or kyphosis of the spine). Adventitious bursae are produced by repeated trauma or constant friction or pressure.
Treatment is determined primarily by the cause of the bursitis and only secondarily by the pathologic change in the bursa. Surgery is not required in most instances. Systemic causes, such as gout or syphilis, and local trauma or irritants should be eliminated, and, when necessary, the patient’s occupation or posture should be changed. One or more of the following local measures usually are helpful: rest, moist heat, elevation, protective padding, and, if necessary, immobilization of the affected part. Surgical procedures useful in treating bursitis are (1) aspiration and injection of an appropriate steroid preparation or antibiotic, (2) incision and drainage when an acute suppurative bursitis fails to respond to nonsurgical treatment, (3) excision of chronically infected and thickened bursae, and (4) removal of an underlying bony prominence.
The usual principles of treating general infections are employed in treating infected bursae. The responsible organisms should be identified if feasible, and the infection should be treated with appropriate systemic antibiotics. Aspiration of the bursa and injection of the appropriate antibiotic may be indicated in addition to the supportive measures just described; a compression dressing should be applied after aspiration. Surgical drainage occasionally is necessary.
Traumatic bursitis often responds favorably to nonoperative treatment, consisting of ice, rest, antiinflammatory medication, and protection with external padding. Occasionally, aspiration and injection of an appropriate steroid preparation are required if symptoms do not respond to the usual nonoperative treatment.
Adventitious bursae that develop as a result of repeated trauma usually have a much thicker fibrous wall than do normal bursae and are more susceptible to inflammatory changes. This type of bursa is treated by removing the cause (e.g., excising an osteochondroma of the distal femur; Fig. 9.6 ); at the time of operation, the bursal sac usually is excised. Only bursae that most often require surgical drainage or excision are described.
Prepatellar Bursitis
Traumatic prepatellar bursitis ( Fig. 9.7 ) can be caused by an acute injury, such as a fall directly onto the patella, or by recurrent minor injuries, such as those that produce “housemaid’s knee.” Either type usually responds to conservative treatment. If fibrosis or synovial thickening with painful nodules fails to respond to such treatment, however, excision of the bursa is indicated.
Pyogenic prepatellar bursitis is common, especially in children. If the bursa is unusually large, the swelling may be so pronounced that a diagnosis of pyogenic arthritis of the knee joint can be made by mistake. A careful physical examination should lead to the correct diagnosis. This septic prepatellar bursitis often responds to one or two daily aspirations, appropriate immobilization, and antibiotic coverage. If symptoms have not improved significantly in 36 to 48 hours, incision and drainage should be done. Smason reported a patient in whom a posttraumatic fistula connected the prepatellar bursa with the knee joint. This could present a problem in diagnosis and treatment, especially in a pyogenic bursitis. The bursa is easily drained as follows.
Drainage of Bursa
Technique 9.3
- ▪
Approach the bursa through two longitudinal incisions, one medial and one lateral, or through a single transverse incision.
- ▪
Open the bursa, evacuate its contents, and pack it loosely with petrolatum gauze, or close it loosely over a drain as seems appropriate.
Postoperative Care
Because cellulitis is always present, the extremity is immobilized in a posterior splint, and appropriate antibiotics are given. If gauze has been used to pack the bursa, it is changed at least twice weekly. Despite sufficient drainage, sinuses often persist for a time on one or both sides of the knee. Immobilization is continued until the sinus has closed.
Excision of Bursa
The patient should be informed when first seen that complete excision of the bursa may be necessary if healing fails to occur after simple drainage. If the walls of the bursa are thickened from chronic inflammation, resecting the entire bursa usually is easy, but if the lesion is acute and the effusion is serous, excising the bursa completely may be impossible; however, enough can be excised to relieve symptoms.
Technique 9.4
- ▪
Make a transverse incision of appropriate length centered over the bursa.
- ▪
Dissect the bursal sac from the overlying skin and subcutaneous tissue and from the patellar aponeurosis beneath it.
- ▪
If possible, excise the bursa without rupturing or perforating it.
- ▪
Trim away the redundant skin, obtain complete hemostasis, and close the wound primarily.
- ▪
Because the most common complication after excising a superficial bursa is a large hematoma, obliteration of the dead space by inserting one or more mattress sutures through the skin and deeper tissues on each side of the incision is recommended. After the skin edges have been apposed with interrupted sutures, the mattress sutures are tied over large buttons.
Postoperative Care
A moderately large compression dressing is applied, and the extremity is immobilized from groin to ankle for at least 2 weeks until the wound has healed completely. Alternatively, suction drainage can be used to obliterate the dead space. Quadriceps-setting exercises are begun the day after surgery. Antibiotics are indicated if an infection is present or is possible.
Dillon et al. reported excellent results with no complications in eight patients who had endoscopic excision of septic prepatellar bursae. Huang and Yeh described endoscopic excision of posttraumatic prepatellar bursae in 60 patients in whom conservative treatment failed. The procedures were done through two or three small portals. There were no recurrences.
Tibial Collateral Ligament Fibrositis and Bursitis
Voshell and Brantigan observed bursae between the longitudinal part of the tibial collateral ligament and the capsule of the knee ( Fig. 9.8 ); these bursae can be located in five different positions, and three have been found beneath the ligament in a single knee. These authors also reported instances of calcification in one or more of these bursae and suggested that this may be identical to Pellegrini-Stieda disease. We consider most disorders that cause pain and tenderness beneath the tibial collateral ligament (not directly opposite the knee joint) to be fibrositis of the ligament; most have responded favorably to the injection of an appropriate steroid preparation and to other nonoperative measures.
Tibial collateral ligament bursitis should be included in the differential diagnoses in patients with medial joint line pain and no history of mechanical symptoms of instability or laxity. Tenderness usually is localized to just below the joint line. This can be treated with local steroid injection followed by early exercise. If symptoms do not respond to one or two injections, MRI or arthroscopy should be considered for evaluation of possible intraarticular derangement or stress fracture of the medial tibial plateau. Tibial collateral ligament bursitis has a characteristic MRI appearance of fluid deep to the tibial collateral ligament in the shape of an inverted “U.” We have seen several patients who were unresponsive to one or two local steroid injections and had stress fractures visible only by MRI or bone scan.
Fibular Collateral Ligament Bursitis
Bursitis beneath the fibular collateral ligament causes localized, tender swelling on the lateral side of the knee and often is confused with a cyst of the lateral meniscus. The distended bursa varies from 0.6 to 2.5 cm or more in diameter, is extrasynovial, and lies beneath or just anterior or posterior to the fibular collateral ligament. Varus strain of the knee is painful, but typical signs and symptoms of an internal derangement of the knee are absent. Other lesions that should be considered include biceps tendinitis, partial biceps avulsion with pain and popping at 30 to 45 degrees of flexion, and posterolateral popping caused by a previous injury to the posterolateral corner or by a bony tubercle that causes popping of the popliteus tendon.
If a mass is not evident, injections of a local anesthetic agent or a steroid preparation into the area of tenderness, together with support and rest, usually relieve the symptoms. When a mass is palpable, excision is curative.
Infrapatellar Bursitis
A small, deep, subpatellar or infrapatellar bursa is located between the tuberosity of the tibia and the patellar tendon and is separated from the synovium of the knee by a pad of fat. When distended, this bursa causes a fluctuant swelling that obliterates the depression on each side of the ligament. Infrapatellar bursal infection should be considered when symptoms resemble septic arthritis or osteomyelitis of the proximal tibia, such as loss of full extension of the knee, resistance to full flexion, and maximal tenderness near the patellar ligament. The infrapatellar bursa should be aspirated, taking care not to enter the knee joint. If infection is found, immediate drainage is recommended in addition to evaluation of the proximal tibial metaphysis for evidence of osteomyelitis. A sterile effusion of the knee joint, which may accompany an infrapatellar bursitis, should not be confused with infection. The bursa can be drained through a small medial parapatellar incision without entering the knee joint. A knee immobilizer is used after surgery until acute symptoms have resolved, and then range-of-motion exercises are begun.
Popliteal Cyst (Baker Cyst)
A Baker cyst, described by Baker in 1877, has since borne his name even though it had been described previously by Adams in 1840. In most instances, a Baker, or popliteal, cyst is a distended bursa. Numerous bursae are located in the popliteal space between the hamstring tendons and the collateral ligaments or condyles of the tibia; a bursa also is located deep to each head of the gastrocnemius muscle. Symptoms develop most often in the bursa beneath the medial head of the gastrocnemius or in the semimembranosus bursa; the latter is a double bursa located between the semimembranosus tendon and the medial tibial condyle and between the semimembranosus tendon and the medial head of the gastrocnemius.
A popliteal cyst can be produced by herniation of the synovial membrane through the posterior part of the capsule of the knee or by the escape of fluid through the normal communication of a bursa with the knee, that is, the semimembranosus or the medial gastrocnemius bursa. Kim et al. described the arthroscopic anatomy of the posteromedial capsule and found an association between the presence of capsular folds and holes in the capsule and the incidence of popliteal cysts in 194 knees treated arthroscopically for a variety of knee problems.
Diagnosing a popliteal cyst usually is not difficult. One third to one half of patients with these cysts are children. The cyst must be distinguished from a lipoma, xanthoma, vascular tumor, fibrosarcoma, and other tumors; occasionally, the cyst may be confused with an aneurysm. A pyogenic abscess may sometimes be located in the popliteal space, but this can be diagnosed easily. Usually, the diagnosis can be made by transilluminating the cyst. Other diagnostic techniques, such as arthrography, MRI, and ultrasound, can be helpful in establishing the diagnosis. MRI is the preferred modality because it also can show intraarticular pathology. In children, the cyst infrequently communicates with the joint, and intraarticular pathologic findings are rare. Rarely, a popliteal cyst can dissect down into the calf in an intramuscular path. Fang et al. reported three cases involving the medial head of the gastrocnemius. These were confirmed with MRI. It was hypothesized that the dissection took the path of least resistance through a weakness in the medial gastrocnemius fascia.
Giant synovial cysts of the calf often are associated with rheumatoid arthritis. They arise from and communicate with the knee in the popliteal area, as can be shown by arthrography or MRI. If a popliteal cyst is suspected, arthrography or MRI of the knee or ultrasound examination of the calf is done, and the popliteal cyst is excised. In patients with rheumatoid arthritis who have a giant synovial cyst removed, a synovectomy should be performed later to prevent recurrence of the cyst. Development of acute compartment syndrome as a result of a ruptured Baker cyst and spontaneous venous bleeding have been reported. We have seen several patients on strong anticoagulants bleed into popliteal cysts, leading to dissection into the calf. Popliteal vein thrombosis can occur, and a dissecting popliteal cyst can occur concurrently. Venous thrombosis should be excluded as part of the evaluation of suspected pseudothrombophlebitis caused by a dissecting or ruptured popliteal cyst.
The results of simple excision usually are excellent even if incomplete. In our experience with a large series of children, these cysts generally resolve with benign neglect. Occasionally, aspiration may be attempted, provided that the diagnosis is certain. In adults, intraarticular pathologic findings are common, and the cyst can recur if the intraarticular pathologic condition is not corrected. Most involve the posterior horn of the medial meniscus. Saylik and Gökkus reported 103 knees treated with posterior open cystectomy with valve and posterior capsule repair and arthroscopic treatment of intraarticular lesions. Cyst recurrence was seen in fewer than 2% of patients. Ko and Ahn recommended removal of the capsular fold of the valvular mechanism of the popliteal cyst with a motorized shaver arthroscopically. Takahashi and Nagano reported success using posterior portals to arthroscopically resect the popliteal cyst origin. Yang et al. found significantly better outcomes in patients treated with arthroscopic cystectomy compared with patients who underwent arthroscopy followed by open cystectomy or those who had open cystectomy alone. The open cystectomy alone group had a 40% recurrence rate.
Careful arthroscopic evaluation should be performed before excision of a popliteal cyst. Intraarticular pathologic conditions, such as patellofemoral chondromalacia or a degenerative tear of the posterior horn of the medial meniscus, can be identified and treated by debridement of loose cartilaginous fragments or partial meniscectomy. Significant intraarticular pathologic conditions are present in more than 50% of adults with popliteal cysts. Kp et al. recommended careful study of prearthroscopic cystectomy MR images because these cysts can be predictive of potential popliteal artery injury. When the popliteal artery is close to the cyst, the lateral wall of the cyst should not be removed. Zhou et al. performed a systematic review and meta-analysis of the surgical treatment of popliteal cysts. They concluded that arthroscopic excision of the cyst wall, enlarging the communication between the articular cavity and the cyst, and arthroscopic management of intraarticular lesions produce the best results.
Froelich and Hillard-Sembell demonstrated that loose bodies can intermittently travel between the intraarticular space and an extraarticular popliteal cyst. If a known posteromedial loose body cannot be found, a capsular opening into the cyst should be sought. The loose body can then be removed through an accessory posteromedial portal.
If the cyst does not appear to communicate with the joint or if significant changes cannot be treated arthroscopically, an open procedure is indicated. Most cysts can be approached by a posteromedial (Henderson) incision. Very large or midline lesions can be approached through a posterior incision.
Popliteal Cyst Excision
For a popliteal cyst that requires excision, Hughston et al. described a posteromedial approach made through a medial hockey-stick incision. The procedure can be performed with the patient supine. If an arthroscopic evaluation is part of the procedure, the leg does not have to be rescrubbed or redraped and the patient does not need to be turned prone for open excision of the cyst.
Technique 9.5
(Hughston, Baker, and Mello)
- ▪
With the patient supine, externally rotate the hip fully and flex the knee to 90 degrees. Make a medial hockey-stick incision at the joint line ( Fig. 9.9A ).
- ▪
Use only the posteromedial portion of the incision if an arthroscopic examination already has been performed. Otherwise, inspect the joint through an anteromedial retinacular incision ( Fig. 9.9B ).
- ▪
Make a posteromedial capsular incision beginning between the medial epicondyle and adductor tubercle along the posterior border of the tibial collateral ligament ( Fig. 9.9B ).
- ▪
Retract the posterior oblique ligament posteriorly and inspect the posteromedial compartment. Identify the popliteal cyst; it is usually in the area between the medial head of the gastrocnemius and semimembranosus tendon ( Fig. 9.9B ).
- ▪
Inspect the posteromedial joint and cyst lining for an intraarticular communication ( Fig. 9.9C ).
- ▪
Separate the adherent cyst lining from the surrounding soft tissues, and trace it to the posterior capsule.
- ▪
Excise the cyst at the base of its stalk on the capsule.
- ▪
Close the orifice if possible with one or two nonabsorbable sutures.
- ▪
At closure, the posterior oblique ligament may be lax because of pressure from the cyst beneath it. If it is lax, advance it onto the medial epicondyle and tibial collateral ligament to restore tension to the posteromedial capsular ligaments and semimembranosus capsular aponeurosis. Close the wound in layers.
Postoperative Care
The limb is placed in a knee immobilizer, and weight bearing to tolerance is allowed. Straight leg raising and quadriceps-setting exercises are begun on the first day after surgery. The immobilizer is discontinued, and active range-of-motion exercises are begun when acute inflammation has resolved. Mild prophylactic anticoagulation is recommended for 6 weeks. If the patient develops a synovial fistula, reapply the knee immobilizer until the fistula closes.
Medial Gastrocnemius Bursitis
If the medial gastrocnemius bursa is involved, a palpable mass is located in the midline of the popliteal space or extends beneath the head of the gastrocnemius and manifests between the medial head of the muscle and the semimembranosus tendon, simulating an enlarged semimembranosus bursa. In the latter instance, the bursa is excised through a posteromedial incision after arthroscopy with the patient supine, as described for semimembranosus bursitis; when in the midline of the popliteal space, it is excised as follows.
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