JBJS | Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Common Complications of Total Knee Arthroplasty*†

The Journal of Bone & Joint Surgery, Volume 79, Issue 2

Instructional Course Lecture | February 01, 1997

Instructional Course Lectures, The American Academy of Orthopaedic Surgeons - Common Complications of Total Knee Arthroplasty*†

DAVID C. AYERS, M.D.‡, SYRACUSE, NEW YORK; DOUGLAS A. DENNIS, M.D.§, DENVER, COLORADO; NORMAN A. JOHANSON, M.D.¶, PHILADELPHIA; VINCENT D. PELLEGRINI, JR., M.D.,#, HERSHEY, PENNSYLVANIA

View Disclosures and Other Information

An Instructional Course Lecture, The American Academy of Orthopaedic Surgeons

The Journal of Bone & Joint Surgery. 1997; 79:278-311

5 Recommendations (Recommend) | 3 Comments | Saved by 3 Users Save Case

text A A A

Introduction

The success of a total joint arthroplasty is contingent on a clear understanding of the potential complications of the procedure. This Instructional Course Lecture presents a review of specific problems related to wound-healing, neurovascular injuries, infections, thromboembolic disease, the extensor mechanism, stiffness, and periprosthetic fractures to provide the reader with a clear understanding of ways to avoid and treat these common complications.

*Printed with permission of The American Academy of Orthopaedic Surgeons. This article will appear in Instructional Course Lectures, Volume 46, The American Academy of Orthopaedic Surgeons, Rosemont, Illinois, March 1997.

†No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

‡Department of Orthopaedic Surgery, State University of New York Health Science Center at Syracuse, 550 Harrison Center, Suite 100, Syracuse, New York 13202. E-mail address for Dr. Ayers: ayersd@vax.cs.hscyr.edu.

§Denver Orthopaedic Specialists, 1601 East 19th Avenue, Suite 5000, Denver, Colorado 80218.

¶Department of Orthopaedic Surgery, Temple University Hospital, 3401 North Broad Street, Philadelphia, Pennsylvania 19140.

#Department of Orthopaedics and Rehabilitation, The Milton S. Hershey Medical Center, The Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033-0850.

§Denver Orthopaedic Specialists, 1601 East 19th Avenue, Suite 5000, Denver, Colorado 80218.

¶Department of Orthopaedic Surgery, Temple University Hospital, 3401 North Broad Street, Philadelphia, Pennsylvania 19140.

#Department of Orthopaedics and Rehabilitation, The Milton S. Hershey Medical Center, The Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033-0850.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 1 The top diagram demonstrates the asymmetrical thickness of the facets of the normal patella. Resection of an equal amount of bone from the medial and lateral facets retains the asymmetry of the patella. The lower diagram demonstrates the recommended level of resection; little bone is removed from the lateral facet.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 2 Diagram demonstrating internal rotation of the femoral component, which moves the trochlear groove medially in relation to the patella.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 3 Diagram demonstrating the correct alignment of the tibia (left) and lateralization of the tibial tubercle due to internal rotation of the tibial component on the proximal part of the tibia (right).

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 4-A and 4-B: Diagrams demonstrating the peripatellar vascular supply. Fig. 4-A: The extraosseous peripatellar anastomotic ring, which is supplied by six main arteries. LSG = lateral superior genicular, MSG = medial superior genicular, MIG = medial inferior genicular, LIG = lateral inferior genicular, SG = supreme genicular, and ATR = anterior tibial recurrent.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 4-B The intraosseous vascular system. QT = quadriceps tendon, MP = mid-patellar, and P = polar.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 5-A and 5-B: Lateral radiographs of a knee that was treated with a metal-backed patellar component. Fig. 5-A: Radiograph demonstrating early angulation of the pegs of the patellar component.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 5-B: Subsequent radiograph demonstrating a peg-plate fracture.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 6-A, 6-B, and 6-C: Patellar clunk syndrome. Fig. 6-A: Diagram demonstrating a suprapatellar fibrous nodule entrapped within the intercondylar notch during flexion of the knee.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 6-B Diagram demonstrating how the fibrous nodule clunks out of the intercondylar notch with extension of the knee.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 6-C Intraoperative photograph demonstrating the suprapatellar fibrous nodule.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 7 Anteroposterior and lateral radiographs of a supracondylar fracture in a patient who had osteopenic bone.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 8-A through 8-D: Anteroposterior and lateral radiographs of an impacted supracondylar fracture proximal to a total knee replacement in a patient who had rheumatoid arthritis.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 8-A and 8-B: Before treatment. The normal alignment of the limb has been maintained.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 8-C After closed treatment, which led to an excellent result.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 8-D After closed treatment, which led to an excellent result.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 9-A through 9-D: Anteroposterior and lateral radiographs of a sixty-eight-year-old patient who sustained a displaced supracondylar fracture of the distal part of the femur two years after a total knee replacement.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 9-A and 9-B: Before treatment.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 9-C Six months after operative stabilization with a locked supracondylar nail.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 9-D Six months after operative stabilization with a locked supracondylar nail.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 10-A Anteroposterior and lateral radiographs made six months after open reduction and internal fixation of a supracondylar fracture of the distal part of the femur with use of a condylar buttress-plate.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 10-B Anteroposterior and lateral radiographs made six months after open reduction and internal fixation of a supracondylar fracture of the distal part of the femur with use of a condylar buttress-plate.

View Larger

TABLE I INTERCONDYLAR DISTANCE OF COMMONLY USED FEMORAL PROSTHESES

Manufacturer	Prosthesis	Intercondylar Distance
		(mm)
Biomet, Warsaw, Indiana	AGC	18
DePuy, Warsaw, Indiana	AMK	20
Howmedica, Rutherford, New Jersey	PCA	18
Johnson and Johnson, New Brunswick, New Jersey	PFC	20
Osteonics, Allendale, New Jersey	Omnifit	19
Smith and Nephew Richards, Memphis, Tennessee	Genesis	20
Zimmer, Warsaw, Indiana	IB-II	15

Add to My JBJS

TABLE I INTERCONDYLAR DISTANCE OF COMMONLY USED FEMORAL PROSTHESES

Manufacturer	Prosthesis	Intercondylar Distance
		(mm)
Biomet, Warsaw, Indiana	AGC	18
DePuy, Warsaw, Indiana	AMK	20
Howmedica, Rutherford, New Jersey	PCA	18
Johnson and Johnson, New Brunswick, New Jersey	PFC	20
Osteonics, Allendale, New Jersey	Omnifit	19
Smith and Nephew Richards, Memphis, Tennessee	Genesis	20
Zimmer, Warsaw, Indiana	IB-II	15

Wound Complications

Primary wound-healing is critical for the success of any total knee arthroplasty. Any delay in wound-healing increases the risk of infection and failure of the arthroplasty^214,216. The prevention of soft-tissue problems through the selection of the proper skin incision, an understanding of the vascular anatomy and patient-related risk factors, and prompt treatment of wound problems (should they arise) are imperative if a good result is to be achieved.

Vascular Anatomy

The blood supply to the soft tissues of the anterior aspect of the knee is completely random, with contributions from multiple vessels^{2,23,43,161,203,258,295}. This blood supply arises predominantly from the terminal branches of the peripatellar anastomotic arterial ring, which has numerous contributing arterial branches, including the medial and lateral superior genicular arteries, the medial and lateral inferior genicular arteries, the supreme genicular artery, the anterior tibial recurrent artery, and a branch of the profunda femoris artery. In contrast to the skin circulation of the thigh proximal to the knee, there is no underlying muscle or intermuscular septum directly anterior to the knee to provide a direct pathway for arterial perforators^43,161. Skin circulation in this area is dependent on the dermal plexus, which originates directly from arterioles traveling within the subcutaneous fascia. Any operative dissection performed superficial to this subcutaneous fascia disrupts the arterial supply to the skin and increases the possibility of skin necrosis. Elevation of skin flaps about the anterior aspect of the knee requires dissection deep to the subcutaneous fascia to preserve the perforating arteriolar network between the subcutaneous fascia and the dermal plexus¹⁶¹.

Choice of Skin Incision

An analysis of the vascular anatomy about the knee suggests that the choice of a midline skin incision is less disruptive to the arterial network¹⁶¹. A medial peripatellar skin incision is undesirable as it creates a large, laterally based skin flap, which has been associated with higher rates of wound complications¹⁶¹. Measurements of transcutaneous oxygen, performed both before and after skin incisions about the knee, have demonstrated reduced oxygenation of the skin in the lateral region^146,150. The farther medially the skin incision is made, the larger the lateral skin flap and the greater the risk of wound complications. Placement of the skin incision slightly lateral to the midline assists in eversion of the patella, particularly in obese patients in whom a large and bulky lateral skin flap resists patellar eversion.

Use of a pre-existing skin incision generally is recommended. Although it usually is safe to ignore previous short medial or lateral peripatellar incisions^64,308, one should be wary of wide scars with thin or absent subcutaneous tissue as damage to the underlying dermal plexus is likely and the risk of wound necrosis therefore is increased¹⁶¹.

If there are long, parallel scars, the lateralmost incision should be used to avoid the creation of a large lateral skin flap containing an operative scar. In complex situations—for example, when there are multiple incisions or areas of previously burned or irradiated skin—it is wise to consult with a plastic surgeon, both with regard to the design of the impending skin incision and for consideration of preoperative muscle-flap procedures if the risk of skin necrosis is substantial. In selected complex situations, the risk of wound problems can be reduced with use of a staged technique. Before the total knee arthroplasty, a skin incision is made to the depth of the subcutaneous fascia and then is closed. If this incision heals without difficulty, the surgeon can proceed with the total knee replacement through this incision with much greater confidence²⁵⁰.

Soft-tissue expansion has been used successfully to treat soft tissues that are contracted because of previous skin incisions, irradiation, or burns^{7,83,186,188,189,220,241}. This procedure involves implantation, usually subcutaneously, of an expandable reservoir into which saline solution is injected intermittently to expand the surface area. Studies have shown that epidermal thickness is maintained when this technique is used^6,298. While some dermal thinning occurs, the synthesis of dermal collagen actually increases. Complications associated with soft-tissue expansion have been minimum but have included hematoma formation, deflation of the reservoir, infection, and skin necrosis due to overly vigorous soft-tissue expansion.

Technical Factors

A thorough preoperative vascular examination of the limb is necessary to minimize the risk of difficulties related to wound-healing. The skin incision should be of adequate length to avoid excessive tension on the wound edges, particularly when the knee is fully flexed. Gentle retraction of the skin edges is necessary to avoid disruption of perforating arterioles originating in the subcutaneous fascia. It is best to avoid undermining large areas of skin. If a flap is to be used, it must be created in the subfascial plane to preserve the blood supply to the skin that originates in the dermal plexus^43,161. Numerous studies have demonstrated that a lateral retinacular release decreases oxygenation of the skin in the lateral region and increases the subsequent risk of wound complications^{37,149,158,270}. If a lateral retinacular release is to be performed, an attempt should be made to preserve the lateral superior genicular artery. Meticulous wound hemostasis is required to avoid the creation of a postoperative hematoma. Routine use of suction drainage in total knee arthroplasty has been questioned^12,238. We have found that increased pain, postoperative ecchymosis, and drainage occur without a drain; therefore, we recommend the routine use of such a device. Finally, a layered wound closure without tension is imperative to minimize the risk of skin necrosis.

Patient-Related Risk Factors

Numerous reports have suggested that chronic use of corticosteroids increases the prevalence of difficulties related to wound-healing^{42,102,161,185,206,213,271,294,301}. Use of corticosteroids has been shown to decrease fibroblast proliferation, which is necessary for proper wound-healing¹⁰², and to reduce collagenase clearance from the healing wound^294,301. This results in diminished accumulation of collagen, and a subsequent decrease in tensile strength, at the site of wound-healing^42,294,301. An increased prevalence of wound complications among patients who have rheumatoid arthritis has been well documented. Although the specific cause of this association is not known, it may be related to the increased long-term use of corticosteroids by many of these patients^{48,90,104,216,284,306,311}.

An increased prevalence of wound complications also has been noted among obese patients^{45,63,206,306}. Extreme obesity can create difficulties with exposure during total knee arthroplasty, thereby necessitating more vigorous retraction of skin flaps. Additionally, in heavier patients, who have a thick layer of adipose tissue, the skin is less adherent to its underlying vascular supply, and this increases the chances that the dermis will separate from the subcutaneous layer during skin retraction¹⁶¹.

Malnutrition, represented by an albumin level of less than 3.5 grams per deciliter (thirty-five grams per liter) and a total lymphocyte count of less than 1500 cells per cubic millimeter, has been associated with poor healing of the stump after a Syme amputation and may play a role in wound-healing after a total knee arthroplasty^54,63. The damaging effects of cigarette-smoking have been well documented and probably are related to systemic vasoconstriction resulting from the use of nicotine^{17,44,157,202,236}. While the exact relationship is unclear, the increased frequency of wound problems in patients who have diabetes mellitus may be secondary to delayed collagen synthesis and decreased tensile strength at the site of the wound. Early capillary growth into the healing wound also is reduced^{63,97,98,161,184}. High-dose non-steroidal anti-inflammatory drugs inhibit the acute inflammatory response, which is an important step in the early phases of wound-healing¹⁸⁰. Patients managed with chemotherapy similarly may be at risk for delayed wound-healing. The routine need to discontinue methotrexate preoperatively for patients who have rheumatoid arthritis is unclear. Bridges et al.²⁹ found a slight increase in the prevalence of infection in ten patients managed with methotrexate perioperatively compared with the prevalence in patients who had stopped using methotrexate more than one month preoperatively. Other, larger comparison studies have demonstrated no increase in the prevalence of complications related to wound-healing in association with the continued perioperative administration of methotrexate in patients who have rheumatoid arthritis^154,213.

Normovolemic vascular status is necessary for satisfactory wound-healing. Hypovolemia can delay wound-healing because of reduced delivery of oxygen to the healing soft tissues^42,44,161. Reduction in the level of transcutaneous oxygen has been found to increase the prevalence of wound-healing complications in patients managed with lateral retinacular release during total knee arthroplasty¹⁴⁹ and to decrease the rate of wound-healing after soft-tissue-flap transfers³. With use of continuous passive motion, flexion of the knee to 40 degrees or more reduces oxygen tension in the healing wound edges, especially during the initial three days after a total knee arthroplasty. Continuous passive motion should be limited to less than 40 degrees in the early postoperative period^95,147.

Treatment of Wound Complications

Various types of wound complications can occur, including prolonged postoperative drainage; superficial soft-tissue necrosis; and full-thickness soft-tissue necrosis, which usually results in exposure of the prosthetic components. All three types of wound problems require immediate attention, as any delay in treatment increases the risk of deep infection and subsequent failure of the total knee arthroplasty.

Prolonged Serous Drainage

If the wound is chronically draining but does not exhibit substantial erythema or purulence, immobilization and local wound care can be attempted. In our experience, drainage that persists for more than five to seven days despite immobilization and local wound care is unlikely to cease spontaneously and is an indication for open débridement. Subcutaneous hematomas or large intra-articular hemarthroses commonly are encountered in association with such persistent wound drainage. Hematomas threaten the wound because they increase soft-tissue tension, release toxic products of hemoglobin breakdown, and serve as a favorable medium for bacterial growth¹⁶¹. We are aware of no scientific data that clearly support open drainage rather than observation of a non-draining hematoma; therefore, we recommend that a non-draining hematoma be treated non-operatively with close observation as long as there are no signs of impending skin necrosis due to excessive soft-tissue tension. An additional indication for open drainage is a large hematoma that is contributing to a substantial limitation of the range of motion of the knee. Drainage procedures should be performed in the operating theater with perioperative antibiotic prophylaxis.

The prevalence of prolonged drainage among patients in whom a culture-proved infection eventually developed at the site of a total knee arthroplasty has ranged from 17 to 50 per cent^{15,104,110,136,172,299}; in the study by Bengtson et al.¹⁵, for example, persistent drainage was noted in twenty-six (51 per cent) of fifty-one knees. Weiss and Krackow²⁹⁹, in a retrospective review of the results of 597 total knee arthroplasties, reported that eight (1.3 per cent) were followed by persistent wound drainage. All eight patients were managed with open irrigation and débridement and parenteral administration of antibiotics, and all had healing without infection despite the fact that two had a positive culture at the time of irrigation and débridement. Bengtson et al.¹⁵ suggested that prompt operative intervention may prevent chronic drainage from becoming an established infection.

Superficial Soft-Tissue Necrosis

Although small necrotic areas that are less than three centimeters in diameter may heal with local wound care or delayed secondary closure²⁷¹, necrotic tissue generally necessitates operative débridement. Larger areas of superficial necrosis should be debrided and covered with a split-thickness skin graft or a fasciocutaneous flap^110,172.

Full-Thickness Soft-Tissue Necrosis

Full-thickness soft-tissue necrosis usually is associated with the exposure of prosthetic components and necessitates immediate, extensive débridement. Simple secondary closure often is unsuccessful, and reconstruction with some type of flap usually is necessary. Various types of flaps—including cutaneous¹⁷³, fasciocutaneous^110,172, and myocutaneous flaps^{16,62,91,103,114,173,253,255}—have been used. Bengtson et al.¹⁶ reported on the treatment of full-thickness skin loss that had resulted in exposure of the prosthetic components after ten total knee arthroplasties. Delayed closure failed in all six knees in which it was attempted, and split-thickness skin-grafting failed in both of the knees in which it was utilized. In contrast, coverage with a gastrocnemius myocutaneous flap proved to be successful and was recommended as the treatment of choice. Gerwin et al.⁹¹ reviewed the records of twelve patients who had had full-thickness skin necrosis and an exposed prosthesis, six of whom had had a positive culture of deep tissue. All twelve patients were managed with extensive débridement and closure with a medial gastrocnemius myocutaneous flap. Eleven patients had an excellent result, and ten of them retained the prosthetic components or had a successful reimplantation.

The medial gastrocnemius muscle flap is often the preferred type of flap. It is larger and two to three centimeters longer than the lateral gastrocnemius flap. Furthermore, it does not have to traverse the fibula and, therefore, it has a larger arc of rotation. It provides excellent soft-tissue coverage in the region of the patella and the tibial tubercle, where skin necrosis occurs most commonly. A free myocutaneous flap also may be used^99,161, but it should be reserved for patients who have full-thickness necrosis that cannot be covered with a local flap.

Parenterally administered antibiotics often are necessary for patients who have persistent drainage and wound necrosis, but they should not be used indiscriminately. Unnecessary use of antibiotics increases the risk of altering the bacterial flora of a deep infection¹⁶¹. Aspiration of the joint should be done before antibiotic therapy is initiated in order to maximize the results of the culture. Cultures of superficial drainage often are spurious, with little relationship between the organisms grown and those causing deep infection^139,161,271.

In summary, wound problems are a dreaded complication of total knee arthroplasty and ideally are avoided. Preventive measures include the proper choice of the skin incision, gentle handling of the soft tissues, meticulous hemostasis, and wound closure without excessive tension. Should persistent wound drainage or soft-tissue necrosis occur, early intervention is imperative as delay increases the risk of deep infection and failure of the arthroplasty. Full-thickness soft-tissue necrosis often necessitates the transfer of well vascularized tissue such as a medial gastrocnemius myocutaneous flap.

Neurovascular Complications

Total knee replacement generally is considered to be a safe and effective procedure. Although neurovascular complications are rare, they are serious, particularly for patients who have complex deformities or who have multiple scars around the knee from previous operative procedures. An awareness of the risk of various neurovascular injuries facilitates the development of preventive strategies and also allows the physician to provide the patient with valuable information regarding this elective procedure before it is performed.

Peroneal Nerve Palsy

Mont et al.¹⁹⁸ found that the cumulative prevalence of peroneal nerve palsy after total knee arthroplasty was 0.58 per cent (seventy-four of 12,784 procedures) as reported in the literature. Variations in prevalence probably are related to the case mix for a given surgeon or institution^132,164,248. Possible mechanisms of nerve injury include traction during correction of a deformity, ischemia when stretching of the surrounding soft tissue causes occlusion of small vessels, and compression by a tight dressing or splint²⁴⁸.

Conditions that have been associated with an increased prevalence of peroneal nerve injury have included a valgus deformity or flexion contracture of more than 20 degrees and a complex biplanar (flexion and valgus) deformity^164,248. Factors that have been found not to be associated with peroneal nerve palsy have included age, type of arthritis, gender, and duration that a tourniquet was used²⁴⁸.

Peroneal nerve palsy most commonly is diagnosed within two days after the total knee replacement. In a study of twenty-two patients (twenty-three knees) who had a peroneal nerve palsy, all were found to have a motor deficit in both the extensor hallucis longus and the tibialis anterior; nine knees (39 per cent) were in patients who had weakness of the peroneus longus and twenty (87 per cent), in patients who had a sensory deficit in the first web space between the great and second toes²⁴⁸. While the prognostic effectiveness of electromyograms and nerve-conduction studies remains unclear¹⁶⁴, confirmatory electrophysiological tests should be done at least three weeks after the operation. The primary purpose of these tests is to document the extent and location of the nerve lesion.

Early treatment of peroneal nerve injury is directed primarily at preventing additional injury. As soon as the injury is diagnosed, all dressings should be loosened and the knee should be allowed to flex to 20 to 30 degrees²⁴⁸. In the study by Rose et al.²⁴⁸, these measures resulted in partial recovery of sensory and motor function in two of eight patients in whom the injury had been recognized early. The role of early open exploration and decompression of the peroneal nerve has not been established; therefore, patients should be managed only with observation unless there is clear evidence of a compressive hematoma, which should be drained operatively.

The chronic treatment of peroneal nerve palsy consists of the use of a dropfoot brace and passive stretching exercises to prevent an equinus deformity. Complete recovery from this injury is rare^164,248. If a dense neurological deficit persists for three months postoperatively, operative decompression of the peroneal nerve may be of some benefit. Krackow et al.¹⁶⁴ reported complete or nearly complete resolution of neurological deficits in five patients who had been managed with decompression five to forty-five months after total knee replacement. In a later study, after twelve to seventy-two months of additional follow-up, thirty of thirty-one patients who had been managed with operative decompression of the peroneal nerve had some degree of functional and neurological recovery, compared with only three of nine patients who had been managed non-operatively¹⁹⁸. The latter study underscores the need for close postoperative follow-up of patients who have peroneal nerve palsy and strongly suggests that operative intervention should be considered if no improvement is noted after three months of non-operative treatment.

A number of strategies can be used in an attempt to prevent peroneal nerve injury in patients who are at high risk. Specifically, an adequate amount of bone should be resected, especially when flexion or valgus deformities are treated, to prevent excessive bow-stringing of the peroneal nerve; tight dressings and plaster splints should be avoided; and flexion of the knee should be allowed in the recovery room. There has been no demonstrated advantage to exploring and prophylactically releasing the peroneal nerve at the time of the total knee arthroplasty in high-risk patients²⁴⁸.

Direct Injury of Vascular Structures about the Knee

Direct injury of vascular structures about the knee can be prevented when a thorough knowledge of the anatomy of the knee is combined with careful operative technique²⁵¹. The locations of the critical vascular structures can be likened to the points on the face of a clock. In the left knee, at the level of the joint line, the popliteal vein is directly posterior (twelve o'clock), with the tibial nerve lying medial to the vein (eleven o'clock) and the popliteal artery lying lateral to the vein (one o'clock). All three of these structures are vulnerable to penetrating injury through the posterior portion of the capsule during meniscal resection, removal of the posterior cruciate ligament, or capsular release. Distal to the joint line, the popliteal artery bifurcates to form the posterior and anterior tibial arteries at the two o'clock position. The common peroneal nerve lies against the fibula, distal to the joint line, at the three o'clock position. Damage of any of these structures between the eleven o'clock and three o'clock positions may occur when excessively long screws are used in this zone for fixation of tibial components inserted without cement²⁵¹.

Any suspicion of intraoperative vascular injury should be evaluated after deflation of the tourniquet and before implantation of the components. The joint and the popliteal region should be inspected carefully, and the return of distal arterial pulses should be confirmed. An expanding popliteal mass, copious posterior bleeding into the joint, and the loss of distal pulses are indications for intraoperative arteriography and an immediate vascular surgery consultation. A small vascular perforation may be treated with simple sutures. Transection of a vessel may be repaired directly if there is no tension on the anastomosis with the knee in full extension¹⁹⁰. Vascular grafting may be necessary when there is tension at the site of the direct repair or extensive vessel damage.

During the resection of the medial and lateral menisci, there is a risk of penetrating injury of the popliteal vessels. Therefore, it is helpful to perform as much of the resection as possible with the scalpel blade parallel to the posterior part of the tibia, pulling the meniscus anteriorly during this procedure. Laterally, the popliteal artery is protected by the belly of the popliteus muscle. The lateral meniscus is more mobile and usually is easily retracted anteriorly.

When the notch for a cruciate-substituting prosthesis is cut, extensive resection of the posterior cruciate ligament may result in entry into the popliteal fossa, where the popliteal vein lies directly behind the capsule in the midline. Leaving a stump of posterior cruciate ligament behind reduces the risk of vascular injury in this situation.

The division of the posterior portion of the capsule at the joint line during the correction of a flexion contracture requires special care to avoid injury of the popliteal vessels and the tibial nerve. A safer approach is to elevate the capsule from the posterior aspect of the tibia and the distal part of the femur while making sure that the scalpel or the elevator stays on the bone.

As pointed out earlier, wound-healing can be affected by the blood supply to the area. The preoperative vascular evaluation should include a thorough inspection of the skin of the lower extremity. The location of operative or traumatic scars, skin color, temperature variations, capillary refill, and the presence of ulcerations should be noted. The strength of the dorsalis pedis and posterior tibial pulses should be documented by palpation or, if necessary, with use of Doppler ultrasound. The ankle-brachial pressure index has been a valuable indicator of the extent of peripheral vascular disease²⁹¹. The measurement of transcutaneous oxygen tension has been reported to be an objective indicator of skin viability and has been used clinically to select the level of amputation for patients who have ischemic disease⁵⁹. Normal volunteers were found to have oxygen pressures of between forty-five and ninety-three millimeters of mercury (6.00 and 12.40 kilopascals) while patients who had peripheral vascular disease were found to have decreasing levels, depending on the severity of the disease⁵⁹.

Preoperative arteriography should be reserved for patients who may be candidates for vascular bypass before total knee replacement or who are having the reconstruction because of a severe post-traumatic condition or a tumor.

Absolute vascular contraindications to total knee replacement include verified vascular claudication with slight or no activity, active skin ulcerations secondary to arterial insufficiency or venous stasis, and ischemia or frank necrosis of the toes¹⁸⁷. If the peripheral pulses are not palpable and there is no potential for vascular bypass, the total knee arthroplasty should be done without use of a tourniquet as a tourniquet may cause thrombosis of the atherosclerotic femoral artery²⁵².

Infection

While successful total joint replacement offers dramatic and lasting improvement in the quality of life, deep infection is the most feared complication of this procedure as it threatens the function of the joint, the preservation of the limb, and occasionally even the life of the patient. Since the inception of prosthetic joint replacement, total knee arthroplasty has been associated with a greater rate of infection than total hip replacement. The reason for this difference may be related to the fact that the knee lies superficially beneath the skin and the fascial envelope and is covered by only a limited amount of well vascularized muscle as well as by a watershed area of vascular supply to the skin, which lies directly anteriorly in the position of the typical skin incision. While many advances (such as the routine use of antibiotics perioperatively) have led to a decrease in the rate of infection, anatomical risk factors inherent to the knee contribute to a rate of infection that probably always will be higher than the rate associated with total hip arthroplasty.

Prevalence

The reported rate of deep infection after contemporary total knee replacement has been about 2 per cent (sixty-seven infections were noted after 4171 procedures in one study³⁰⁶ ), with a greater risk of infection associated with implants that have more mechanical constraint between the components^214,304,306. In contrast, no meaningful difference in the rate of infection has been noted between implants inserted with cement and those inserted without it³⁰⁶. The most prevalent organisms, as reported in two series of sixty-seven and twenty-seven knees, were gram-positive: Staphylococcus aureus accounted for 50 to 65 per cent of the infections; Staphylococcus epidermidis, for 25 to 30 per cent; and other bacteria, fungi, and mycobacteria, for 10 to 15 per cent^261,306. Other authors have observed a trend toward an increasing prevalence of Staphylococcus epidermidis as the pathogenic organism for infections about prosthetic joints^14,230.

Several steps can be taken to minimize the risk of infection. Chief among these is the prophylactic use of antibiotics. The most important dose appears to be that administered immediately preoperatively so that adequate levels of antibiotics are present in the hematoma that accumulates after the operation. There are good data only to support the use of prophylactic antibiotics for twenty-four hours after the operation, beginning with an immediate preoperative dose of a first-generation cephalosporin that provides excellent coverage against staphylococcal organisms^89,117,193. There is some additional evidence that the use of adjunctive measures, such as ultraviolet light^18,19 and closed-air exhaust suits^36,174, may substantially reduce the rate of infection even more. The use of clean-air systems remains controversial. There is increasing evidence that horizontal laminar airflow systems actually increase the rate of infection in patients managed with total knee replacement because of the frequent interposition of operating-room personnel between the source of air and the open operative wound^80,254; therefore, vertical laminar airflow systems are preferable.

Various factors increase the risk of infection after total knee replacement; some are inherent to the host and cannot be altered while others may be reduced or eliminated by meticulous preoperative screening of the patient. Rheumatoid disease (independent of the associated use of steroids) (p <0.001), open skin lesions on the affected extremity (p = 0.002), a previous operation about the knee (p < 0.007), and a history of infection (p < 0.01) all have been associated with a significant increase in the rate of deep infection^228,306,307. While three of these factors cannot be altered by the surgeon, open skin lesions should be noted and treated before the elective operation is performed. We prefer a three-month interval of intact dermis over a previous ulceration, such as a venous stasis ulcer, before an elective total knee replacement is performed. The greatest risk of infection is associated with a previous infection of the knee. Wilson et al.³⁰⁶ reported a rate of infection of 3.1 per cent in a study of 1857 osteoarthrotic knees that had had a revision total knee arthroplasty because of an infection around the previous implant. Wilson et al.³⁰⁶ also reported that recurrent urinary-tract infection, diabetes mellitus, systemic use of steroids, and obesity appeared to be associated with an increased rate of infection after total knee replacement but noted that the relationships were not significant. A recurrent urinary-tract infection certainly can be identified and treated preoperatively. When a structural cause of recurrent urinary-tract infection is identified, it should be corrected before a total knee replacement is performed; patients who have chronic, uncorrectable urinary-tract infection should be managed with lifelong antibiotic suppression to minimize the risk of immediate postoperative infection as well as late hematogenous seeding of the site of the prosthesis. Rheumatoid disease, in addition to being associated with the risk of acute infection, also is associated with a risk of late infection secondary to hematogenous bacterial seeding of the site of the prosthesis. The risk of late infection is high; late infections accounted for forty-five (67 per cent) of the sixty-seven infections in the series of 4171 total knee arthroplasties reported by Wilson et al.³⁰⁶.

Routine dental cleaning and extraction produces bacteremia in nearly all patients. Conventional wisdom suggests that antibiotic prophylaxis is appropriate at the time of dental manipulation, but the topic remains controversial³⁴. We believe that the guidelines developed by the American Heart Association¹³³ for prophylaxis against infection around prosthetic heart valves are both sound and sensible and that they may reasonably be extended to prophylaxis against infection in patients who have a prosthetic joint replacement.

Diagnosis

A patient who has an infection at the site of a prosthetic device in the knee usually has a painful, warm, stiff, swollen, and tender joint. The differential diagnosis of pain at the site of a knee replacement in the absence of mechanical loosening includes reflex sympathetic dystrophy, heterotopic ossification, and arthrofibrosis. A patient in whom such an infection is suspected should be evaluated with a physical examination as well as plain radiographs; the latter often demonstrate no abnormal findings initially but later reveal evidence of marginal osseous resorption, erosion, and loosening of the prosthetic components. The keystone of diagnosis, however, is aspiration of the joint and analysis of the fluid with gram-staining as well as complete and differential cell counts. The joint should be aspirated under meticulously sterile conditions with operative preparation of the skin to minimize the risk of contamination of the specimen with skin flora. An erythrocyte sedimentation rate provides a baseline for serial follow-up analysis of the response to treatment. Various nuclear-medicine techniques, ranging from the traditional technetium bone scan to the indium-labeled white-blood-cell scan, have received a great deal of attention. Sequential and differential application of these two techniques reportedly yielded an 84 per cent rate of accuracy in a series of thirty-eight patients²²⁹, but accuracy remains highly dependent on both the technique and the institution in which it is used. Occasionally, all efforts at definitive identification of an infecting organism are fruitless despite a very suspicious and often convincing clinical course characterized by pain as well as loosening of the components. In this situation, staged reconstruction commonly is performed, and it is only with direct culture of the tissue membrane beneath the implant, material obtained by swabbing of the device, or cement fragments that an organism is identified.

Management

Once the presence of a deep-seated infection has been established, the greatest challenge to the physician is related to the conflict between management of the patient and treatment of the infection at the site of the prosthesis. It is important to manage the patient rather than an isolated knee joint, and the physician must balance the anticipated quality and longevity of life and function against the desire to eradicate the infection. Important factors to consider include the chronological and physiological ages of the patient, the concurrent medical illnesses (particularly insulin-dependent diabetes mellitus and rheumatoid arthritis), and the functional demands of the patient. Local conditions that influence the decision are the nature of the infecting organism and its sensitivity to available antibiotics, the integrity of the extensor mechanism, the adequacy and integrity of the skin and the soft-tissue envelope, and the adequacy of adjacent bone stock. It is clear that if eradication of the infection is the primary goal of treatment the entire prosthetic joint should be removed to optimize the chance of the infection resolving^230,310. In an elderly and infirm patient who has a mechanically secure knee replacement, however, the morbidity associated with removal of the prosthesis is often considerably greater than that associated with chronic antibiotic suppression with preservation of the knee joint. Therefore, in placing the priority of management of the patient above that of intensive treatment of the knee infection, retention of a secure prosthesis in conjunction with chronic antibiotic suppression often offers greater function to the elderly patient. When an infection contributes to mechanical loosening and symptoms in the knee joint, operative removal is a more practical and functional, and a less destructive, treatment course.

Retention of the Prosthesis

In the setting of acute infection (onset, within ten to twenty-one days after the operation) with susceptible gram-positive bacteria and no evidence of mechanical loosening of the components, antibiotic therapy instituted within forty-eight hours of onset has been associated with a success rate of 6 to 10 per cent in several large studies^{14,148,228,261,307}. The likelihood of successful retention of the prosthesis in a patient who has an acute infection may be increased by open débridement and radical synovectomy. Success rates of 18 per cent (seven of thirty-nine knees³² ) to 23 per cent (seven of thirty-one knees²⁶¹ ) have been reported with this approach, which necessitates lifelong antibiotic suppression in an effort to contain the infection indefinitely. In the setting of late infection (onset, more than twenty-one days after the initial implantation), this approach has been associated with a lower rate of success^32,228,261. Operative débridement followed by short-term parenteral administration of antibiotics and then indefinite oral antibiotic suppression led to successful retention of the implant at five years in thirty (26 per cent) of 114 patients in three studies^32,261,306. Recent reports concerning the use of rifampin in combination with a fluorquinone antibiotic for suppression of infection around a prosthetic joint have been encouraging⁶⁰, and this technique may be useful when removal of the prosthesis is not thought to be in the over-all best interest of the patient.

Removal of the Prosthesis

It is widely accepted that removal of the prosthesis is a mandatory part of the over-all treatment plan when eradication of the infection is the primary goal. Although resection arthroplasty infrequently is selected as the definitive treatment, it remains a viable option for patients who have involvement of multiple joints (such as those who have rheumatoid disease), limited functional goals and a prospect for walking only with assistance of a walker, or local risk factors precluding a reoperation about the knee⁷³. In such patients, modest motion, often in the range of 45 degrees, is preserved for activities of daily living. Usually, a brace is needed for walking. In the study by Falahee et al.⁷³, over-all patient satisfaction approached 80 per cent and most patients had good or excellent relief of pain despite the persistence of a draining sinus in three (11 per cent) of twenty-eight knees.

Alternatively, arthrodesis of the knee provides a more durable lower extremity. After an arthrodesis, the ability to walk independently depends on good function of the neighboring joints of the lower extremity. This procedure, however, has been complicated by a rate of non-union of as low as two of eighteen knees⁶⁷ and as high as 30 per cent^228,307. Intramedullary nailing has become the preferred method of knee arthrodesis; when this procedure was performed in a staged fashion, with removal of the prosthesis and débridement of the infected area followed at a later date by placement of an intramedullary nail, solid fusion was achieved in seventy-four (89 per cent) of eighty-three patients^{55,67,218,304}. Staging of the débridement and reconstruction portions of the procedure reduces but does not eliminate the risk of spreading the infection into the medullary canals. The mean time to osseous union is six months, but the rate of complications associated with this technique has been as high as ten complications in eighteen patients⁶⁷. Alternatively, Rand et al.²³² reported that arthrodesis with use of an external fixation technique led to a successful fusion in nineteen (68 per cent) of twenty-eight patients. This method is indicated in the setting of a particularly virulent organism, in which the risk of intramedullary metastasis of the infection is considerable, or when there is an osteoarthrotic hip or an ipsilateral total hip replacement proximal to the infected knee that precludes the use of the intramedullary device. Arthrodesis with the external fixator can be accomplished in a single operative setting and permits delayed skin coverage for the treatment of a deficient soft-tissue envelope. Rand et al.²³² reported that ten (36 per cent) of twenty-eight patients who were managed with this technique had a total of seventeen different complications, largely consisting of pin-track infections that resolved with removal and replacement of the offending pin.

In the setting of a particularly virulent or resistant organism, amputation may be considered. While fortunately it is only infrequently required to treat a life-threatening infection that is refractory to antibiotic therapy, gross bone deficiency, or an irretrievably incompetent soft-tissue envelope, amputation may provide the most expeditious resolution of a very difficult problem. Unfortunately, a poor functional result is the rule, with only one-third of patients retaining the ability to walk (even with assistive devices) and the other two-thirds remaining confined to a wheelchair²¹⁷.

Exchange of the Prosthesis

Single-stage exchange currently is done only rarely. Historically, the success rate of this procedure has ranged from 50 to 75 per cent^{228,230,307,310}, with a good or excellent result noted in twenty-four of thirty-eight knees in one series³¹⁰ and successful reimplantation with clearing of infection observed in eight of fourteen patients in another series²³⁰. It is now commonly accepted that if the treatment goal is a durable and functional prosthetic knee joint that is free of infection, débridement followed at a later date by reimplantation is the preferred treatment plan^230,307,310. Several conditions must be met in order for such a staged reimplantation to be successful. Skin coverage must be adequate as the presence of multiple old incisions or myofascial flaps increases the risk of subsequent failure of the soft-tissue envelope. An intact extensor mechanism-patellar ligament complex is essential for independent function of the knee. Adequate bone stock to support the revision implant also is required, and the use of allografts to reconstruct osseous defects is associated with an increased risk of infection and failure. The antibiotic sensitivity of the infecting organism must be such that several antibiotics are therapeutic options. Finally, the patient must have a competent immune system that is not compromised by the presence of diabetes mellitus, rheumatoid disease, or any other such disorder. We have found that problems in any two of these five critical areas considerably increase the likelihood of failure of reimplantation of a prosthetic knee joint, and we do not perform prosthetic reimplantation in patients who have deficiencies in three of these critical areas.

All foreign material, including the implant and all methylmethacrylate, must be removed at the time of the initial débridement. The bone is cleaned meticulously, and an antibiotic-impregnated methylmethacrylate spacer-block is interposed between the femur and the tibia, both to preserve the joint space for later reimplantation and to permit stability with weight-bearing across the resected knee joint. Vancomycin (500 milligrams) and tobramycin powder (1.2 grams) usually are added to each forty-gram bag of methylmethacrylate. Often, two to three packs of cement are necessary to create a block of sufficient size to fill a large defect. Parenteral administration of appropriate antibiotics is continued for six weeks, and then we prefer to continue oral administration of antibiotics for an additional six weeks, for a total of three months of systemic antimicrobial therapy. The administration of antibiotics is discontinued at least six weeks before the pseudarthrosis is reaspirated. Reimplantation can be considered if the culture of aspirate is negative. It is critically important to assess the readiness of the soft-tissue envelope to undergo an additional operative procedure; continued induration and dermal edema are relative contraindications to the reimplantation of a knee prosthesis. It is best to perform the delayed reimplantation when the wound is soft, supple, and free of edema and induration. Reimplantation is therefore carried out between twelve weeks and one year after the initial débridement. While a negative culture of fluid aspirated from the pseudarthrosis does not guarantee that the infection will not recur after reimplantation, a confirmed positive culture is a contraindication to reimplantation of a prosthetic device. A posterior-cruciate-replacing implant always is used in this setting, and patellectomy occasionally is helpful to obtain skin closure in difficult situations in which the soft-tissue envelope is marginal. Antibiotic-impregnated methylmethacrylate (prepared as described) is routinely used for prosthetic fixation, with the antibiotic agents selected according to the sensitivity profile of the organism or organisms previously grown on culture. Antibiotics generally are not used chronically but rather such treatment is discontinued after all cultures are negative. While staged reimplantation is fraught with numerous potential problems and is dependent on meticulous management of the patient and operative technique, the reported rate of success (defined as freedom from the original infection and a functioning prosthetic knee joint) has been as high as 97 per cent (sixty-one of sixty-three knees)^26,310.

Thromboembolic Disease

Historical data from large series of patients managed with a total of 638 total knee replacements have demonstrated a prevalence of deep-vein thrombosis of 70 to 80 per cent in the absence of prophylaxis²⁸². Additionally, while the prevalence of subsequent pulmonary embolism following total knee replacement is considerably less than that following total hip replacement, the risk is real; moreover, this complication often escapes the attention of the surgeon as it most frequently occurs weeks after discharge^{178,209,211,273,282}. Thromboembolic disease following total knee arthroplasty has been studied less systematically than that following total hip arthroplasty and remains an important area for organized prospective clinical investigation.

Thromboembolic disease following total knee replacement has a considerably different profile than that following total hip arthroplasty. There is a strong propensity for deep-vein thrombosis in the vessels of the calf, with 85 to 90 per cent of thrombi after total knee replacement occurring distal to the trifurcation of the popliteal vein^84,178,282. In contrast to the situation after total hip replacement, only 10 to 15 per cent of patients have thrombosis of the femoral or popliteal vein after knee arthroplasty, and when proximal thrombosis is present it is most frequently a continuous extension of concurrent thrombosis in the calf^{84,101,178,209}. Segmental, discontinuous femoral thrombosis rarely is noted after total knee replacement, which again is quite distinct from the situation after total hip arthroplasty. Bilateral deep-vein thrombosis is noted in 10 to 15 per cent of patients who have had a total knee replacement; more specifically, deep-vein thrombosis has been identified in the normal, contralateral lower extremity of 10 to 15 per cent of patients who have had unilateral total knee arthroplasty^84,282.

The effect of the use of a pneumatic tourniquet on the development of deep-vein thrombosis has been difficult to characterize definitively. Previous authors have identified both beneficial and detrimental effects of this device^72,165,167. Beyond the obvious detrimental effect of the promotion of venous stasis distal to the tourniquet, stimulation of the fibrinolytic system by the vascular endothelium has been observed following release of the tourniquet^72,167. This latter effect may contribute to a reduction in the risk of venous thrombosis, but it clearly is not the predominant effect in view of the high prevalence of thrombi in patients managed without prophylaxis.

The benefit of adjunctive non-pharmacological measures is supported by circumstantial evidence. Perhaps most interesting among these measures is the use of regional anesthesia, specifically continuous epidural anesthesia, which has been associated with a decreased frequency of deep-vein thrombosis⁴⁷. The effects of regional anesthesia on the hemodynamics of the lower extremity are better understood than is the direct impact of such anesthesia on thromboembolic disease. Most evident is an increase in venous flow and blood return to the central circulation secondary to a sympathectomy effect and decreased resistance in the capacitance vessels of the lower extremity following the epidural administration of an anesthetic. Additionally, there is evidence of increased fibrinolysis secondary to activity of the vascular endothelium as well as of decreased platelet adhesiveness as a possible direct effect of the local anesthetic agent. The net clinical effect of a regional anesthetic has been reported to be a decrease in the frequency of deep-vein thrombosis^{47,152,208,286}. Additional analysis has suggested that regional anesthesia has a selective effect in that it reduces thrombosis in the veins of the calf but has relatively little impact on thrombosis in the larger, more proximal (femoral and popliteal) vessels⁴⁷. Unfortunately, the true effect of regional anesthesia on deep-vein thrombosis is not entirely clear because of differences in the literature with regard to the exact type of anesthetic used (spinal or epidural), whether the anesthetic was used for the operation only or whether epidural analgesia was maintained postoperatively for pain control, the patient population, the presence or absence of hip fracture, the type of operation (hip or knee replacement), and whether the local anesthetic was used alone or in combination with narcotics or even general anesthesia. Therefore, the true beneficial effect of regional anesthesia with regard to reducing the frequency of deep-vein thrombosis remains to be identified.

Continuous-passive-motion machines offer the theoretical advantage of reducing stasis in the veins of the calf^108,179. However, we are not aware of any documented evidence that the use of such a device reduces the prevalence of deep-vein thrombosis following total knee arthroplasty.

In general, the effect of anticoagulant prophylaxis on the prevalence of deep-vein thrombosis after total knee replacement has been considerably less profound than that after total hip replacement. The reasons for this difference remain to be elucidated. Warfarin is currently the most commonly used agent for prophylaxis against deep-vein thrombosis among orthopaedic surgeons who routinely use prophylaxis. It has, however, lacked popularity in the past because of the historical recommendation to maintain the prothrombin time at two times the control value (international normalized ratio, 3.0 to 4.0), which has resulted in prothrombin times in excess of twenty seconds and rates of bleeding complications of 8 to 10 per cent after joint replacement^119-121 and as high as 22 per cent (eleven of forty-nine patients) after treatment of proximal deep-vein thrombosis¹²⁹. More recently, authors have recognized that anticoagulation with warfarin, either as prophylaxis or as specific treatment for identifiable venous thrombosis, is quite effective when the prothrombin time is maintained between 1.3 and 1.5 times the control value (international normalized ratio, 2.0 to 2.5), resulting in prothrombin times of fifteen to eighteen seconds and considerably lower rates of bleeding complications (in the range of less than 2 per cent)^{82,84,119-121}. Routine use of warfarin for prophylaxis after total knee replacement has decreased the over-all prevalence of deep-vein thrombosis to 30 to 40 per cent but has not changed the distribution of thrombi from proximal to distal^84,178,282. Although the prevalence of deep-vein thrombosis has been reduced considerably, these rates still are unacceptably high and the search for better methods of prevention continues.

Low-molecular-weight dextran was popular for a period of time but, more recently, it was shown to be no more effective than a placebo^83,86. Moreover, dextran is associated with a considerable risk of volume overload and congestive heart failure in elderly patients and occasionally leads to an allergic reaction. Aspirin, in contrast, has relatively few adverse effects and decreases platelet adhesiveness. Numerous studies have compared aspirin with other agents and placebos, but none has definitively demonstrated that aspirin is more effective than a placebo for prophylaxis against deep-vein thrombosis after total knee replacement^108,181,282. Meta-analyses have suggested a possible beneficial effect, but the National Institutes of Health Consensus Conference on thromboembolic disease in 1986 considered aspirin to be ineffective for this purpose²⁰⁵. Even so, aspirin continues to be used frequently after total knee arthroplasty, largely because it is associated with few complications^108,178,282.

Pneumatic compression devices have become popular recently and indeed are intuitively attractive for use with total knee replacement as the calf is the prevalent location for thrombi, which are likely to form secondary to stasis^85,108,128. Thigh-high sleeves are awkward to use after knee arthroplasty as they cover the operative incision. Calf-high sleeves are more practical and have been shown to reduce the prevalence of thrombosis in the veins of the calf after knee arthroplasty¹⁰⁸. More recently, plantar impulse pads have become popular. These devices are more convenient to use, and they work by means of a slightly different mechanism; specifically, they deliver high-impact compression to the sole of the foot, resulting in a high-velocity pulsatile flow in the femoral vein. Early results from a single study suggested that plantar impulse pads were more effective than aspirin for prophylaxis against deep-vein thrombosis after total knee replacement³⁰². Because these devices do not increase the risk of bleeding complications, it is hoped that they will be definitively proved to be effective for the prevention of deep-vein thrombosis.

Fractionated heparin also has been popular recently. This smaller, more homogeneous heparin molecule is characterized by a more favorable binding affinity profile to activated factors X and II, resulting in an antithrombotic effect that is exerted earlier in the clotting cascade and theoretically decreasing the risk of concurrent bleeding complications as compared with the risk with unfractionated heparin. Coagulation times do not need to be monitored, but parenteral subcutaneous administration is required. Fractionated heparin has been shown to be extremely effective for reducing the over-all prevalence of deep-vein thrombosis following total hip replacement^39,290; in the study by Colwell et al.³⁹, for example, deep-vein thrombosis was noted in only eight (6 per cent) of 136 patients who had received fractionated heparin. Like warfarin, however, fractionated heparin has been considerably less effective for prophylaxis against deep-vein thrombosis following total knee arthroplasty^170,235. The over-all rate of deep-vein thrombosis following total knee replacement among patients managed with fractionated heparin reportedly has ranged from 20 to 30 per cent, but the over-all rate of bleeding complications has ranged from 8 to 10 per cent, which is significantly greater than that associated with low-dose warfarin as reported in a number of prospective, controlled studies^{39,170,235,290}. Bleeding complications are more common with use of fractionated heparin, both at the operative wound and at the injection site, but bleeding from the wound may be reduced by beginning the medication no sooner than twelve hours postoperatively.

In summary, the best approach to the prevention of deep-vein thrombosis and fatal pulmonary embolism following total knee arthroplasty has yet to be defined. Augmentation of blood flow by any one of a number of means is an intuitively appealing method for the reduction of stasis. Compression devices, such as calf-high sleeves and plantar impulse pads, are promising but remain to be proved effective. Regional anesthesia also is associated with a decrease in the prevalence of thrombosis in the veins of the calf, but the specifics regarding the type and duration of such anesthesia have yet to be delineated. Finally, a plan of early mobilization, frequently the byproduct of a shorter length of stay in the hospital, probably also contributes to a reduction in the prevalence of thrombosis in the veins of the calf in a way that is difficult to define and quantitate precisely.

The ideal pharmacological agent has not been identified. Clearly, this agent should be associated with a low frequency of bleeding complications, particularly after knee replacement, because the wound tolerates a hematoma quite poorly. Warfarin, aspirin, and fractionated heparin all are somewhat popular at the present time, and each has advantages and disadvantages. While the use of fractionated heparin must be investigated further, warfarin has been shown to be reasonably effective and to be associated with a very low risk of concomitant bleeding complications.

Perhaps the most provocative question concerns the duration of chemoprophylaxis in the setting of a mean hospital stay of four or five days after knee replacement. Two strategies have been proposed. The first, treatment of all patients with extended prophylaxis consisting of administration of warfarin or fractionated heparin for six to twelve weeks after the operation, has the advantage of not requiring routine surveillance for identification of deep-vein thrombosis. Unfortunately, given the 30 to 40 per cent prevalence of deep-vein thrombosis after knee replacement, such extended exposure to anticoagulants is unnecessary for 60 to 70 per cent of patients. Furthermore, exposure of the entire postoperative population to outpatient use of anticoagulants increases the likelihood of bleeding complications. The second strategy involves routine surveillance for deep-vein thrombosis followed by treatment of identified venous disease. Unfortunately, non-invasive screening, such as color flow Doppler and duplex ultrasound, are relatively ineffective for identifying disease in the calf, which is the most common location for deep-vein thrombosis after total knee arthroplasty^101,300. Contrast venography remains quite sensitive for the identification of thrombi in the calf^84,219,300, but it is invasive and is accompanied by some morbidity. Although these screening studies add to hospital costs, the reduced outpatient exposure to anticoagulant agents considerably decreases the risk of bleeding and associated rehospitalization and suggests that routine surveillance may be more cost-effective than extended prophylaxis for all patients^211,212. We believe that, with the advent of better non-invasive studies for identification of deep-vein thrombosis, the most promising of which is magnetic resonance venography¹⁶⁶, the strategy of routine surveillance and selective treatment will be the favored approach in the future.

Problems Related to the Extensor Mechanism

Long-term evaluations have demonstrated that total knee arthroplasty provides excellent relief of pain, improved function, and superior durability^{52,92,142,247}. Improvements in prosthetic design have resulted in increased function and a better range of motion, but there have been persistent problems involving the patellofemoral joint^{8,30,41,49,52,56,75,87,105-107,109,123,141,143,162,200,263,265,277,287}. Many early total knee prostheses failed to provide for resurfacing of the patellofemoral joint. Anterior knee pain has been reported in as many as one-half of patients for whom a patellar resurfacing procedure was not done^{37,66,69-71,88,138,139,156,169,192,197,200,204,215,221,222,264,277,278,292}. Design modifications that allow for resurfacing of the patella have produced superior functional results as well as a reduction in patellofemoral pain^{88,138-140,169,171,221,222,224,225,268,276}, but an additional set of complications has emerged: patellofemoral instability, patellar fracture, loosening or failure of the patellar component, patellar clunk syndrome, and tendon rupture^{37,56,88,125,131,141,194,196,234,274,293,297}. The rate of complications resulting from patellofemoral resurfacing has ranged from seventeen (5 per cent) of 350 knees⁵⁶ to seven of fourteen knees^{33,37,88,109,112,131,169,196,197,200,222,265,274,277,285}, and such complications have accounted for as many as one-half of the total knee revisions performed^10,28,285. Patellofemoral complications have been attributed to errors in operative technique, inferior prosthetic design, and excessive patellofemoral loads. Numerous studies of patellofemoral joint-reaction forces have demonstrated compressive loads of one-half to one times body weight during walking on a level surface, increasing to three to four times body weight with stair-climbing and to as much as seven to eight times body weight during squatting^{130,201,237,264}.

Patellofemoral Instability

The prevalence of patellar subluxation following total kne arthroplasty was as high as four of fourteen knees in one series³³. Failure to obtain satisfactory patellofemoral tracking may result in patellofemoral pain and crepitus as well as wear, failure, loosening, or fracture of the component (or a combination of these problems), which may jeopardize an otherwise successful functional result of a total knee-replacement procedure^{28,37,52,56,176,192,196,197,200,222,231,249,264,283}.

Patellofemoral instability most commonly results from imbalance in the extensor mechanism characterized by excessive tightness of the lateral retinaculum and associated weakness of the vastus medialis muscle^56,200,222. Placement of prosthetic components in an excessively valgus position increases the Q angle and results in an increased lateral force-vector on the patella^{59,173,200,238}. Disruption of the capsular repair, by hemarthrosis, overly intensive physiotherapy, or injury, also may result in patellofemoral instability.

Asymmetrical patellar resection can lead to patellofemoral instability as well. The normal patella is asymmetrical in contour as the thickness of the medial facet is greater than that of the lateral facet; therefore, resection of equal amounts of bone from the medial and lateral facets retains the asymmetry of the patella. Asymmetrical patellar resection (typically, resection of too much bone from the lateral facet) can lead to problems with patellar tracking^96,176,231. Minimum resection of the lateral facet, usually to the level of the subchondral bone, is recommended for optimum function (Fig. 1).

Malpositioning of the femoral, tibial, or patellar component also can predispose to patellofemoral instability^{56,78,134,169,196,222,231}. Internal rotation or medial shift of the femoral component places the trochlear groove more distant from the patella, leaving the patella laterally positioned relative to the femoral component (Fig. 2). If the tibial component is placed in a position of internal rotation relative to the cut surface of the tibial plateau, the tibia will be externally rotated relative to the femur. Such rotation results in lateralization of the tibial tubercle and an increase in the Q angle, which predisposes to lateral patellar subluxation (Fig. 3). Medial shift of the tibial component on the cut surface of the tibial plateau similarly results in lateralization of the tibial tubercle. Lateral placement of the patellar component on the patella also creates problems with the patella being captured in the trochlear groove of the femoral component.

Certain prosthetic designs predispose to problems with patellar tracking. In the presence of an imbalance in the extensor mechanism, a rotationally unconstrained implant may allow excessive external rotation of the tibia and lateralization of the tibial tubercle^31,231. Rand et al.²³³ reported patellofemoral instability in eleven (22 per cent) of fifty knees that had been treated with a kinematic rotating-hinge prosthesis. A similar situation may exist when the arthroplasty is associated with instability of the posterior cruciate and collateral ligaments^266,267. However, prostheses that allow no axial rotation, such as rigid-hinge designs, also have been associated with high rates of patellofemoral instability^{151,197,226,272}. Jones et al.¹⁵¹, for example, noted such instability in fifty-three (49 per cent) of 108 knees that had been treated with a Guepar prosthesis. In a normal knee, as much as 20 degrees of internal rotation of the tibia occurs during early flexion. With a rigid-hinge prosthesis, such internal tibial rotation does not occur; this forces the tibial tubercle to assume a lateral position during flexion and increases the laterally directed forces on the patella.

An intraoperative assessment of patellar tracking is critical in order to minimize patellofemoral instability. True patellofemoral alignment can be assessed only after tourniquet release, which eliminates the tourniquet's binding effect on the extensor mechanism⁵². Should the patella subluxate laterally when the knee is flexed (before closure of the capsule) without additional, medially directed stabilization by the surgeon's thumb (the no-thumb technique), a lateral retinacular release should be performed^134,264.

Patellofemoral instability is treated on the basis of its etiology. Non-operative measures include intensive quadriceps rehabilitation; external patellofemoral bracing; and avoidance of activities, such as squatting or stair-climbing, that involve heavy loading of the patellofemoral joint. When an extensor mechanism imbalance does not respond to these non-operative measures, a lateral retinacular release, often combined with advancement of the vastus medialis muscle (proximal realignment), is indicated¹³⁴. Capsular repair is necessary when initial central patellar tracking reverts to immediate lateral subluxation following a traumatic event. In some patients, a capsular defect is palpable and helps to confirm the diagnosis. Medial transfer of the tibial tubercle, in conjunction with osteotomy of the tibial tubercle, should be considered in instances of severe malalignment that cannot be corrected with soft-tissue procedures alone because of the inherent risk of non-union at the osteotomy site with osteotomy alone. Should non-union at the site of a tibial tubercle osteotomy occur with disruption of the extensor mechanism, salvage options often are complex and include repeat attempts at fixation of the osteotomy site with bone-grafting as opposed to extensor-mechanism allografting¹⁶⁰. Prosthetic revision is performed for patients who have substantial malpositioning of the components that is not amenable to simpler realignment procedures.

Patellar Fracture

Although patellar fracture is a rare complication of total knee arthroplasty^93,126,289, a prevalence of as high as three of fourteen knees was reported in one study³³. Various causes of patellar fracture have been proposed, including trauma, patellar subluxation, improper patellar resection, vascular compromise, component design, component malpositioning, increased flexion, thermal necrosis, and revision arthroplasty^{4,33,37,56,61,93,126,169,176,222,227,244,265,285}. Biomechanical studies have demonstrated that contact forces substantially increase with patellofemoral malalignment, which perhaps explains why there is an increased prevalence of patellar fractures in patients who have such malalignment¹⁵⁵. Both the eccentricity and the magnitude of patellofemoral loads increase with patellar subluxation¹²⁷, and this increases the risk of patellar fracture.

Excessive patellar resection predisposes to patellar fracture, especially if subchondral bone is removed¹⁵³. Reuben et al.²³⁹ demonstrated that patellar resection that results in an osseous thickness of less than fifteen millimeters substantially increases anterior patellar strain. Conversely, too little patellar resection creates a thick patella-patellar component composite and increases patellofemoral joint-reaction forces as well as tension within the quadriceps tendon. Use of a femoral component with an excessive anteroposterior diameter or implantation of the femoral component in a flexed position increases patellofemoral joint-reaction forces and the probability of fracture^222,283. Asymmetrical resection also can result in impaired mechanical strength of the patella, particularly if too much bone is resected from the lateral facet. Finally, it has been shown that, when the patella is prepared for component fixation, the creation of a large central peg-hole increases anterior patellar strain more than the creation of smaller peripheral peg-holes; the former technique, therefore, is associated with an increased risk of fracture^94,231.

Operative disruption of the patellar blood supply resulting in avascular necrosis also has been associated with patellar fracture^{28,126,169,231,265}. Analyses of the patellar blood supply have demonstrated both extraosseous and intraosseous vascular systems^{23,158,257,258}. The extraosseous system comprises a peripatellar anastomotic ring that is supplied by six main arteries (Fig. 4-A). The superior portion of the vascular ring passes anterior to the quadriceps tendon, while the inferior portion passes posterior to the patellar ligament through the fat pad. The intraosseous system comprises the mid-patellar, polar, and quadriceps-tendon blood supplies (Fig. 4-B). The mid-patellar vessels penetrate anteriorly through the middle one-third of the patella and branch into both the proximal and the distal pole. The polar vasculature passes through the proximal fat pad, posterior to the patellar ligament, and then enters and supplies the inferior pole of the patella. Scapinelli^257,258 observed minimum vascular penetration into the superior pole and periphery of the patella, while Bjorkstrom and Goldie²³ demonstrated a superior vascular supply through the quadriceps tendon.

The patellar vascular system is disrupted substantially during the performance of a routine total knee arthroplasty^{28,33,37,93,126,139,158,169,183,265,267,270,303}. The medial superior, medial inferior, and supreme genicular arteries are divided during a medial peripatellar arthrotomy. The lateral inferior genicular artery commonly is damaged during lateral meniscectomy or excision of the fat pad. The lateral superior genicular artery is at risk when a lateral retinacular release is performed. The intraosseous vascular network can be disrupted during the creation of fixation holes, particularly large central ones. Technetium bone scans made after arthroplasty have demonstrated reduced patellar vascularity in knees in which a lateral retinacular release was performed^270,303. McMahon et al.¹⁸³ also found reduced patellar vascularity following lateral retinacular release but noted no detrimental effects related to excision of the fat pad. Histological evaluations of patellar specimens obtained after patellar fractures have demonstrated avascular necrosis^139,265.

Malpositioning of components can affect the prevalence, type, severity, and prognosis of patellar fractures^76,93. Errors in joint-line position, the alignment of the lower extremity, or patellar coverage by the prosthesis may increase the risk of fracture. Severe malalignment has been associated with more complex fracture patterns and a worse prognosis^76,93.

Additional risk factors for patellar fracture include increased flexion following total knee arthroplasty, thermal necrosis, and revision total knee arthroplasty. Windsor et al.³⁰⁹ reported that patients who have knee flexion greater than 95 degrees generate increased patellofemoral compression forces and frequently have higher activity levels. The heat of polymerization of the polymethylmethacrylate (reported to be as high as 80 to 90 degrees Celsius in total hip arthroplasty) may exceed the coagulation temperature of tissue proteins, resulting in thermal necrosis of bone^{20,53,100,124,183,305}. Grace and Sim¹⁰⁰ reported that the prevalence of patellar fracture following primary total knee arthroplasty (0.12 per cent; nine of 7754 procedures) was lower than that following revision total knee arthroplasty (0.61 per cent; three of 495 procedures).

Loosening of the Patellar Component

Loosening of a patellar component that was inserted with cement during a total knee arthroplasty has been uncommon, with a reported prevalence of less than 2 per cent in most studies^{37,56,176,221,222}. Rae et al.²²¹, for example, reported such loosening after only two of 132 procedures. The prevalence of loosening following patellar resurfacing without cement has been higher yet variable^{37,56,79,176,221,222}. Firestone et al.⁷⁹, in a study of several different components that were designed to be inserted without cement, reported loosening rates of 0.6 per cent (one of 165 procedures) to 11.1 per cent (thirty-seven of 334 procedures). Factors associated with loosening of the patellar component include insertion of the prosthesis with cement into worn, sclerotic bone; malpositioning of the patellar component; subluxation, fracture, or avascular necrosis of the patella; osteoporosis; asymmetrical resection; loosening of other prosthetic components; and a lack of osseous growth into the porous coating^28,231. A reduction in the rate of loosening of the patellar component requires improved bone preparation and cementing techniques²²¹, proper patellar resection, avoidance of asymmetrical or excessive bone removal, and central patellar tracking.

Options for the treatment of loosening of the patellar component include revision of the component, removal of the component and patellar arthroplasty (smoothing of the remaining patella without resurfacing) if the remaining bone stock is unsatisfactory, and patellectomy. Some patients are asymptomatic and need no treatment, although Brick and Scott²⁸ noted that twelve of sixteen knees eventually were symptomatic enough to need a revision arthroplasty. It should be noted that total dislodgment of the component, most commonly inferiorly, may lead to erosion of the posterior surface of the overlying patellar ligament and an increased risk of disruption of that ligament.

Failure of the Patellar Component

Although failure of polyethylene patellar components has been reported^40,296, this complication primarily has been associated with metal-backed designs^9,10,249,283. The proposed advantages of metal-backed designs were that they would decrease patellar surface strain⁹⁴, support the overlying polyethylene to decrease deformation, and allow for fixation of the patellar component without cement. These designs have failed because of wear and fracture of the polyethylene, dissociation of the polyethylene from the metal plate, dissociation of the pegs from the metal plate, and fracture of the metal plate^9,10,249.

Wear of the polyethylene of a patellar component is not unexpected. Cepulo et al.³⁵ observed that peak patellofemoral contact pressures far exceed the yield strength of polyethylene. Wright and Bartel³¹² reported increased degradation of the polyethylene of retrieved tibial components that had less polyethylene thickness. The addition of a metal backing to a patellar component reduces the polyethylene thickness, which may predispose to increased wear. Also, with metal-backed designs, less wear is required before catastrophic failure occurs because of wear-through of the polyethylene to the underlying metal plate. In most designs, the metal backing does not extend to the edge of the polyethylene. Therefore, as the peripheral polyethylene is loaded, it deforms over the rim of the metal plate and may be severed by the sharp, non-deforming edge of the plate²⁸³.

Dissociation of the polyethylene from the metal plate may result from excessive polyethylene wear or fracture. In most designs, the polyethylene is attached to the metal backing by means of a mechanical gripping of the periphery of the plate by the polyethylene without a chemical bond between the two materials. With advanced wear of the peripheral polyethylene, the integrity of this polyethylene-plate attachment may be disrupted, allowing the polyethylene to dissociate²⁸³.

The fixation pegs of the patellar component may fracture at the site of attachment to the metal plate because of high shear stresses. Substantial shear stresses can occur at the peg-plate junction because of the eccentric loads normally placed on the patella²⁴⁹. These shear stresses are increased when there is patellofemoral malalignment¹⁹². Retrieval analyses of patellar components that had been inserted without cement have shown that osseous growth into the anchoring pegs does occur⁵¹. If the growth into the fixation pegs occurs without accompanying growth into the metal plate itself, a high shear load occurs at the peg-plate junction and increases the risk of peg fracture (Figs. 5-A and 5-B). Rosenberg et al.²⁴⁹ reviewed the results of 122 total knee arthroplasties that had been performed with metal-backed patellar components inserted without cement and noted twelve fatigue fractures at the peg-plate junction. In all twelve knees, there was good osseous growth into the fixation pegs without growth into the porous plate.

Risk factors for failure of the patellar component include excessive body weight, increased postoperative knee flexion (more than 115 degrees), a high level of activity, and male gender^9,10,249,283. Additional factors associated with increased patellofemoral loading and subsequent failure of the component include patellar malalignment, increased thickness of the patella-patellar component composite, an oversized femoral component, malpositioning of the femoral component in flexion, and failure to restore the prosthetic joint line to an anatomical level. Failure of metal-backed patellar components often occurs early, usually within two years after the arthroplasty^9,10,249,283.

Clinical signs of failure of the patellar component include effusion as well as crepitus, which occasionally is audible. Clinical symptoms often appear suddenly following activities associated with increased patellofemoral loading, such as climbing stairs, squatting, or rising from a seated position. Intraoperative findings frequently include black staining of the synovial membrane with metal debris and wear or fragmentation of the polyethylene. The femoral component also may be worn, as it was in eleven of twenty-five patients who had failure of a metal-backed patellar component in the study by Bayley et al.¹⁰. Loose porous-coated beads or titanium-fiber-mesh fragments may be found embedded in the polyethylene of the patellar and tibial components. Therefore, if revision is necessary because of failure of a metal-backed patellar component, the surgeon always must be prepared to revise all three components⁵⁰.

Patellar Clunk Syndrome

Patellar clunk syndrome results from the development of a fibrous nodule at the junction of the posterior aspect of the quadriceps tendon and the proximal pole of the patella. With flexion of the knee, this nodule enters the intercondylar notch of the femoral prosthesis. As the knee is extended, the nodule becomes entrapped within the notch as the quadriceps tendon and the patella migrate proximally. At 30 to 45 degrees from full extension, enough tension is placed on the fibrous nodule to cause it to clunk out of the intercondylar notch (Figs. 6-A, 6-B, and 6-C)^13,125.

Possible causes of this condition include a femoral component with a sharp anterior edge at the superior aspect of the intercondylar notch, malpositioning of the patellar component beyond the proximal border of the patella, postoperative scarring, and alteration of the joint line or the patellar height or thickness.

The recommended treatment includes open or arthroscopic²⁹³ débridement of the fibrous nodule, with or without revision of the patellar component if it is malpositioned superiorly.

Rupture of the Extensor Mechanism

Rupture of the quadriceps tendon or the patellar ligament is an infrequent complication of total knee arthroplasty, with a reported prevalence of 0.17 per cent (fourteen of 8288 procedures)²³⁴ to 2.5 per cent (seven of 281 procedures)¹⁷⁶. The quadriceps tendon ruptures more frequently in patients who have had a lateral retinacular release, perhaps because of devascularization of the tendon or extension of the release too far anteriorly and disruption of the tendinous fibers of the quadriceps²²⁷. The results of operative repair are often suboptimum because of an extensor lag, weakness, or a limited range of motion.

The risk of a rupture of the patellar ligament is increased in patients who have had a previous operation involving the knee and in those who have had a partial release of the patellar ligament to enhance exposure at the time of an arthroplasty. Additional risk factors include closed manipulation of the knee and osteotomy of the tibial tubercle for realignment of the extensor mechanism²³⁴. Numerous methods of treatment have been used, including application of a cast; ligament suture; fixation with wires, staples, or screws; ligament augmentation; and reconstruction of the ligament with use of an extensor mechanism allograft⁶⁸. No single reconstructive procedure has provided consistently satisfactory results. Persistent rupture of the ligament after treatment is common and was noted in eleven of eighteen knees in the study by Rand et al.²³⁴. Ligament rupture remains one of the most dreaded complications of total knee arthroplasty, with difficult and often unsatisfactory options for salvage. Prevention with meticulous operative technique is imperative⁵⁰.

Principles of Operative Technique

If the accuracy of techniques of preparation for insertion of femoral and tibial components is compared with that for insertion of patellar components, it is logical to attribute current patellar problems, in some part, to operative technique. Appropriate operative goals should include accurate patellar resection, maintenance of patellar vascularity, proper positioning of prosthetic components, avoidance of soft-tissue impingement, and central patellar tracking.

The amount of patellar bone excised should ideally be equal to the thickness of the patellar component to be inserted (usually about ten millimeters), thereby restoring the preoperative patellar thickness^{57,96,222,231}. Patellar resection must result in a symmetrical patellar remnant with medial and lateral facets of equal thickness.

Efforts to preserve the vascularity of the patella have included maintenance of the fat pad^{37,52,158,280}, preservation of the lateral superior genicular artery during lateral retinacular release^{37,52,231,280}, and performance of the lateral release two centimeters posterior to the patella in order to maintain penetration of the patella by peripheral vessels^227,231. Avoiding the use of a patellar component with a large central fixation peg helps to preserve the intraosseous blood supply³⁷.

Accurate positioning of all three total knee components is critical. Medial shift and internal rotation of both the femoral and the tibial component and lateral positioning of the patellar component must be avoided to prevent patellar maltracking^78,197. After release of the tourniquet, central patellar tracking must be obtained with use of the no-thumb technique^134,196,264. If patellar subluxation is present, realignment procedures should be done to obtain a balanced extensor mechanism.

Isolated revision of the patellar component has been associated with a higher-than-expected rate of complications, which have included patellar fracture, instability, polyethylene wear-through, infection, peroneal nerve palsy, and extensor lag²². Removal of a well fixed metal-backed patellar component with osseous growth into the anchoring pegs can be difficult but is facilitated by disruption of the peg-plate junction with a diamond-edge saw to gain direct access to the bone-peg interface⁵¹.

Because of the numerous complications that have been associated with patellar resurfacing, many surgeons currently avoid the procedure. Although most surgeons agree that, in order to minimize the antigenic response of retained articular cartilage, it is necessary to resurface the patella in a patient who has rheumatoid arthritis^265,280, controversy remains with regard to the need to resurface a healthy-looking patella in a patient who has osteoarthrosis. Some authors²⁷⁶ have reported similar results with and without patellar resurfacing. Others have reported an increased prevalence of patellofemoral problems, particularly anterior knee pain, after total knee arthroplasty performed without patellofemoral resurfacing^{27,138,222,224,225,247}. Boyd et al.²⁷, in a review of the results of 891 arthroplasties performed with and without patellar resurfacing, reported complication rates of 4 per cent (sixteen of 396 procedures) and 12 per cent (fifty-eight of 495 procedures), respectively. Better results were achieved when patellar resurfacing was performed at the time of the primary arthroplasty than when it was performed as a secondary procedure. If the surgeon chooses not to resurface the patella, the ideal patient is one who has osteoarthrosis and excellent remaining articular cartilage and in whom central patellar tracking can be ensured at the time of the arthroplasty.

In our opinion, the best results of total knee arthroplasty are obtained when maximum attention is paid to accurate patellar resection, patellar vascularity is maintained, central patellar tracking is ensured, and metal-backed patellar components are avoided.

Stiffness

The term stiffness as it relates to total knee replacement has several different meanings that are essentially observer-dependent. From the perspective of the surgeon, stiffness means an inadequate or smaller-than-expected range of motion as measured in a standardized fashion with the patient on an examination table. Active or active-assisted ranges of motion routinely are measured under optimum conditions during the recovery period, and the norms for motion following total knee replacement have been generated on the basis of these data^{81,210,242,262}. Functional capacity also is evaluated to confirm that the clinically derived value for range of motion corresponds with an appropriate level of function (walking, sitting, climbing stairs, and so on)^199,242. A patient who has a range of motion of 90 degrees of flexion to within 10 degrees of full extension on clinical examination and has no pain or functional difficulties is not said to have a stiff knee. However, a patient who, at one year after the arthroplasty, has clinically acceptable motion but also has knee stiffness, difficulty getting out of a chair, pain when climbing stairs, and an observable stiff-knee gait should be evaluated further for underlying problems involving the knee.

From the perspective of the patient, the problem of stiffness has different dimensions that should be integrated into the over-all clinical picture. Although stiffness is closely related to pain, it has a wider application to the patient's experience in attempting to move the knee, particularly during the early postoperative period. Stiffness therefore is closely related to the patient's motivation to achieve a functional range of motion and his or her willingness to endure pain to achieve that goal. For example, a patient who has minimum supportive care at home and must get out of bed for every need probably complains of more stiffness in the knee than one who is receiving total support from family members or nursing-facility staff even though the reported levels of pain may be similar. This little-studied phenomenon may have strong implications for the patient's ultimate assessment of range of motion and functional capacity.

As stiffness is nearly always present during the early postoperative period and gradually decreases over time, it is a valuable marker of improvement throughout the recovery period. Postoperative pain is the most important early cause of knee stiffness. It results in both quadriceps and hamstring guarding and makes passive flexion and extension difficult to perform. This factor was the theoretical basis for the implementation of in-hospital continuous passive motion^38,246. The continuous-passive-motion device cradles the leg and slowly moves it through a prescribed range in order to minimize the guarding response. Regardless of whether it actually minimizes the guarding response, continuous passive motion has not been conclusively shown either to shorten the hospital stay or to increase the range of motion substantially after total knee replacement; therefore, its value in the early postoperative period is questionable when the added cost of this modality is considered. Nevertheless, continuous passive motion within the hospital environment has been generally well accepted, even to the point of its being expected as standard treatment by many patients. It should not be viewed as a substitute for the persistence and encouragement of an experienced physical therapist^199,262. In addition to their role in helping the patient to obtain the desired motion and functional capacity, physical therapists serve in an educational capacity and are well positioned to note early problems with motivation and compliance. This latter contribution is particularly important as the lengths of hospital stays continuously decrease. The lack of direct supervision and the unpredictable quality of home or outpatient physical therapy within the managed-care environment demand that patients who are at high risk for the development of knee stiffness be identified before they leave the hospital.

Postoperative stiffness of the knee usually subsides within six to eight weeks. Range of motion generally improves steadily during the first three months, after which less rapid progress may be seen for an additional nine months or more^242,262. A limited or decreasing range of motion may be indicative of a number of complications, including infection, mechanical complications related to the implant or the soft tissue, impending arthrofibrosis, and reflex sympathetic dystrophy (if the symptoms include severe pain and vasomotor skin changes)¹⁹⁹.

The late onset of knee stiffness after a relatively symptom-free period also may suggest one of several conditions, including infection; overuse synovitis or tendinitis (particularly in a younger, more active patient); synovitis secondary to rheumatoid arthritis, particulate wear debris, or recurrent hemarthrosis; or loosening or breakage of the implant⁷⁴.

Infection

Early infection (within the first six weeks after the operation) is characterized by increasing swelling, erythema, and generalized pain, with or without wound drainage. All of these findings also may be present in a non-infected knee during the immediate postoperative period. The progressive nature of the signs and symptoms, especially after two to three days of rest and immobilization, should lead to early recognition of infection. Late infection is recognized more easily because it develops after a relatively asymptomatic period, although aspiration and culture may be necessary to distinguish an indolent infection from the other causes of synovitis listed previously.

Mechanical Problems Related to the Implant or the Soft Tissue

Dorr et al.⁵⁸ found that patients who had an excellent clinical result after total knee replacement with either a posterior-cruciate-retaining or a posterior-cruciate-sacrificing design continued to walk with a stiff-knee gait two years postoperatively. These findings suggest that total knee replacement rarely produces a completely normal gait and that some degree of stiffness is associated with even an excellent result. The proper balance of motion, strength, and stability is the goal for a good functional result. Inadequate bone resection combined with persistent ligamentous imbalance or tightness may result in knee stiffness⁶⁵. If symmetrical or asymmetrical tightness is recognized during trial reduction, it can be corrected by revision of the bone cuts or release of the ligaments, or both. If a flexion contracture is present, additional resection of bone from the distal part of the femur or a posterior capsular release, or both, should be performed. If the residual contracture is severe (more than 15 degrees), some additional bone may be removed from the proximal part of the tibia, provided that doing so does not make the flexion gap too wide.

The approach to bone resection in total knee arthroplasty is highly dependent on whether the posterior cruciate ligament is to be preserved or sacrificed^118,135,199. When the ligament is to be preserved, the femur usually is cut first in order to preserve the level of the joint line and to approximate more closely the normal kinematics of the knee. Variable amounts of tibial bone must be resected to provide the proper alignment and stability while preserving and balancing the tension of the posterior cruciate ligament in both flexion and extension. A potential pitfall during this procedure is reversal of the tilt of the tibia in the sagittal plane, which causes tightening of the posterior cruciate ligament in flexion if the rollback mechanism functions according to design. Alternatively, the tibia actually may drop back, thereby altering the patellofemoral mechanics¹³⁵. The problem of tightness in flexion is most important from the standpoint of postoperative stiffness of the knee. If tightness is recognized intraoperatively, recession of the posterior cruciate ligament can be considered or the tibia can be cut again in neutral or with a 5-degree posterior slope. If there is excessive posterior instability due to laxity of the posterior cruciate ligament, a cruciate-substituting design may be selected. Hirsch et al.¹¹⁸ reported that the clinical results achieved with use of a posterior-cruciate-sacrificing device were no different than those achieved with use of a posterior-cruciate-retaining device.

Use of an oversized femoral component or posterior placement of the femoral component may lead to a disproportionately narrow flexion gap. It is difficult to treat this problem by resecting more tibial bone, especially if the extension gap is adequate, because doing so may lead to an unacceptable amount of laxity in extension. Use of a smaller femoral component and resection of more bone from the posterior aspect of the femur expands the flexion gap without affecting stability in extension.

Inadequate release of tight capsular and ligamentous structures is an important cause of stiffness after total knee arthroplasty but is difficult to measure. Poor flexion and extension may result from inadequate release or recession of a tight posterior cruciate ligament. Flexion contractures most commonly result from inadequate posterior capsular release in conjunction with insufficient bone resection. In varus deformities, the medial collateral ligament and, in valgus deformities, the lateral collateral ligament and the iliotibial band often must be released in order to prevent asymmetrical wear of the implant and to promote an optimum range of motion of the knee. External rotation of the femoral component has been found to enhance ligament-balancing in flexion and to facilitate optimum patellar tracking^{5,168,240,269}.

Patellofemoral dysfunction may cause pain that promotes stiffness because of disuse^74,176,269. Conversely, patellofemoral pain may result from knee stiffness, particularly with flexion contractures. A number of possibilities related to the patella should be considered during the evaluation of stiffness after a total knee arthroplasty: a patella that was not resurfaced, inadequate lateral release, asymmetrical cutting of the patella, excessive elevation of the joint line, internal rotation of the femoral component, formation of intra-articular adhesions that tether the patella to surrounding structures (thereby altering the normal tracking mechanism)^175,288, patellar fracture, and loosening of the patellar component.

Finally, the generation of an excessive volume of wear debris over time may cause synovitis, with pain, stiffness, and swelling being the usual clinical result.

Patient-Related Factors

The patient's preferences, expectations, and satisfaction with elective procedures such as total knee replacement recently have received attention as being important indicators of the likelihood of obtaining a good outcome. Preoperative education is important to provide the patient with an understanding of his or her own goals in light of the actual risks and benefits of an operation. The educational process gives the surgeon an opportunity to recognize patients who have unrealistic expectations or inadequate motivation to comply with the postoperative regimen. Patients who have potential problems that may require additional services should be identified as soon as possible so that hospital utilization-review panels and insurers can be notified of the additional needs that may arise.

Host factors that promote arthrofibrosis around the replaced knee joint are not well understood. They should be studied further because it is apparent that certain patients are predisposed to early knee stiffness and unusual amounts of pain and swelling in the absence of infection, bleeding, or mechanical complications²⁷⁹.

Diagnostic Considerations

Physical Examination

The physical examination is the most important diagnostic tool in the evaluation of a patient who has stiffness after a total knee replacement. At least two examinations should be done within the first six weeks to ensure acceptable progress with regard to range of motion and function. Patients who are having problems in these areas should be seen more frequently. Unexpected restriction of the range of motion should be assessed in light of other findings such as swelling, effusion, erythema, skin viability, and drainage.

Radiographic Evaluation

Plain anteroposterior, lateral, and tangential patellar radiographs should be made within the first six weeks and repeated if stiffness and pain increase. Findings associated with stiffness of the knee may include inadequate bone resection, an oversized femoral implant, gross maltracking or subluxation of the patella, or a combination of these.

Bone-scanning is indicated when late stiffness develops after an asymptomatic period. This technique is less useful during the early recovery period and throughout the first postoperative year, when it normally can be expected to demonstrate increased uptake around the implants. Implants inserted without cement tend to be associated with increased bone-scan activity for an even longer period of time²¹.

Aspiration and Culture

When a patient has early progressive stiffness, pain, and swelling, aspiration and culture of the joint fluid should be performed in order to rule out infection. A negative culture, however, does not absolutely rule out infection. If an infection is highly suspected, an arthrotomy may be necessary to obtain tissue for a positive culture. If symptoms develop after a relatively asymptomatic period of one year or more, the joint aspirate also should be examined with polarized light microscopy for evidence of polyethylene wear debris²¹.

Treatment Alternatives

Physical Therapy

The most important initial treatment of a stiff, non-infected knee that appears radiographically satisfactory after a total knee arthroplasty is an adequately supervised course of sustained, intensive physical therapy. This therapy may last from three to six months, depending on the initial results. If some progress is being made and the patient can tolerate the discomfort, the treatment program should be continued.

Manipulation

If range of motion reaches a plateau during the first three months, manipulation of the knee with the patient under regional or general anesthesia should be considered. Manipulation is not necessary within the first postoperative month. In an assessment of the range of motion one year after a total knee replacement, Fox and Poss⁸¹ found that knees that had been manipulated two weeks postoperatively could not be distinguished from those that had not. Moreover, there was a substantial loss of motion during the week after the manipulation. The preoperative range of motion is an important predictor of the range after total knee arthroplasty^210,262. Parsley et al.²¹⁰ reported that seventeen knees that had less than 75 degrees of preoperative flexion gained a mean of 16 degrees (from 61 to 77 degrees), while 257 knees that had more than 95 degrees of preoperative flexion lost a mean of 6 degrees (from 115 to 109 degrees). Knowledge of the preoperative flexion helps the surgeon and the patient to formulate goals for motion and to identify a reasonable threshold for postoperative manipulation.

Débridement

If manipulation of the knee does not lead to a sustained, acceptable improvement in the range of motion, exploration and débridement of the knee may be performed with either open or arthroscopic technique. Good results have been achieved when arthroscopic débridement has been performed for localized tethering of the patella or for fibrous nodules that cause clunking of the patella over the anterior flange of the femoral component^175,288. These conditions, however, usually are not associated with substantial loss of motion. The results of arthroscopic treatment of generalized arthrofibrosis after total knee replacement have not been as good^24,279; in one report²⁴, two of seven patients subsequently had an arthrodesis of the knee and two others were scheduled to have this salvage operation. The results of either open or arthroscopic débridement of a stiff knee after a total knee replacement probably are related most closely to the extent of the intra-articular fibrosis.

Revision

Revision with a modular tibial polyethylene spacer in conjunction with a capsular or ligamentous release may improve the range of motion of the knee, particularly when the procedure is performed to correct a flexion contracture. Intraoperatively, the deformity should be corrected completely with a new, trial spacer in place. If complete correction cannot be achieved, the tibial or the femoral component, or both, should be revised after new cuts are made in the bone to provide optimum flexion and extension gaps. A posterior-cruciate-substituting design should be used whenever both components are revised. This design more readily accommodates alterations in the joint line caused by the new cuts in the bone, and it has the inherent stability to allow generous flexion and extension gaps as well as ligamentous release^11,199,281.

During the revision, it is very important to release fully all structures that may have contributed to stiffness of the knee, including the quadriceps tendon and the vastus intermedius adhesion to the femur and the suprapatellar pouch, the medial and lateral gutters, the collateral ligaments, and the lateral patellar retinaculum²²³. In severe cases, the integrity of the extensor mechanism must be guarded carefully. Avulsion of the patellar ligament from the tibial tubercle is a potentially devastating complication. It can be prevented with use of a systematic approach in which the releases noted previously are utilized and the tendon insertion is sutured and reinforced when appropriate^145,176.

Prevention of Stiffness following Total Knee Replacement

The most fundamental consideration in the prevention of complications of total knee replacement in general and of stiffness in particular is the selection of an implant and an instrumentation system that are complex enough to allow flexibility yet simple enough to minimize the chances of technical error. The selection should be based on a published track record of satisfactory performance over a period of five to ten years, and the technical difficulty should be compatible with the proficiency and experience of the surgeon. Like a normal knee, a total knee prosthesis tolerates tightness (stability) and laxity (flexibility) throughout a given range of motion. In general, a design with less inherent stability or constraint requires more exacting bone cuts and ligament-balancing to deliver an acceptable result. This applies to many posterior-cruciate-sparing designs, particularly those intended to be inserted without cement. Cruciate-substituting designs that are inserted with cement have more inherent stability and better tolerate the extensive ligamentous releases that are necessary for correction of severe varus or valgus deformities. Elevation of the joint line is also better tolerated by posterior-cruciate-substituting implants^11,269. Therefore, posterior-cruciate-substituting designs offer at least a theoretically wider margin of safety. The definitive answer to the problem of selection of implants can be provided only through the implementation of a broad-based outcome database for total knee replacement.

Knowledge of a patient's expectations, goals, and motivation is essential for early detection of potential problems associated with stiffness following total knee replacement. Poor motivation on the part of the patient, little or no preoperative education regarding the procedure, a short hospital stay, and a marginally delivered program of home or outpatient physical therapy constitute a dangerous mix that may result in a less-than-optimum result. A strategy of early identification of problems should be formulated, and appropriate treatment pathways for these outliers should be constructed and tested with the goal of ultimately preventing the harmful and costly long-term effects of stiffness following total knee replacement.

Supracondylar Fracture of the Distal Part of the Femur

A fracture of the distal part of the femur proximal to a total knee-replacement presents a challenging problem, as indicated by the reported results of treatment^{1,25,46,77,122,137,177,195,207,243,256,275}. In thirteen studies that appeared in the orthopaedic literature from 1981 to 1989, a good or excellent result was achieved for fifty-four (69 per cent) of seventy-eight patients in whom such a fracture had been treated operatively compared with sixty-five (68 per cent) of ninety-five patients who had been managed non-operatively. Complications of treatment included malalignment, loss of motion, non-union, infection, and a number of problems associated with prolonged immobilization. Proponents of internal fixation believe that operative treatment best restores mechanical alignment to the limb, permits early mobilization to avoid the complications of prolonged bed rest, and may maximize the healing potential through stable fixation in a region in which the blood supply is already compromised^259,313. Current recommendations include both operative and non-operative treatment of appropriately selected supracondylar fractures proximal to a total knee replacement.

The prevalence of supracondylar fractures after total knee arthroplasty is approximately 1 per cent, with reported rates ranging from 0.5 per cent (twenty-eight of 5233 patients) to 2 per cent (five of 250 patients)^{1,25,46,195,275}. These fractures have been associated with rheumatoid arthritis, chronic steroid therapy, and other conditions that result in osteopenia of the distal part of the femur (Fig. 7). Other, less common contributing factors have included medication-induced osteopenia or an unsteady gait in patients who have a neurological disorder^46,275. Also, arthrofibrosis after a total knee replacement may predispose to fracture by increasing stress in the distal femoral metaphysis, particularly at the time of manipulation^46,111. The association between notching of the anterior aspect of the distal part of the femur during total knee replacement and subsequent supracondylar fracture has been debated. Aaron and Scott¹, in a retrospective review of the results of 250 total knee arthroplasties, reported that five of twelve patients in whom notching of the anterior cortex of the distal part of the femur had occurred at the time of the operation subsequently sustained a supracondylar fracture. They concluded that notching of the distal part of the femur predisposes the patient to subsequent supracondylar fracture. In contrast, Ritter et al.²⁴³ reviewed the records of 180 patients who had anterior femoral notching in association with total knee arthroplasty and found that only one patient subsequently had a supracondylar fracture. Most authors have agreed, however, that notching of the anterior part of the femur during total knee replacement is to be avoided and probably is of more clinical importance in osteopenic bone^1,46,77,243.

The goals of treatment of a supracondylar fracture proximal to a total knee arthroplasty are union of the fracture and a return to the pre-fracture level of function while maintaining the range of motion of the knee.

Non-operative treatment is recommended for non-displaced fractures as well as for minimally displaced fractures when alignment of the fracture and the mechanical axis of the limb are easily achieved and maintained with closed reduction (Figs. 8-A, 8-B, 8-C through 8-D)^113,245. The patient wears an above-the-knee cast for three weeks and is allowed to bear weight on the affected limb as tolerated during this period. Three weeks after the fracture, a cast-brace is applied and range-of-motion exercises are begun. The cast-brace is worn until there is radiographic evidence of callus and the fracture has healed clinically.

Operative treatment is indicated for a displaced fracture if satisfactory alignment cannot be achieved or maintained with closed reduction (Fig. 9-A, 9-B, 9-C through 9-D) or if there is radiographic evidence of prosthetic loosening. Operative treatment should be considered an elective procedure, and the timing of the operation should allow for a thorough medical evaluation and stabilization preoperatively. High-quality anteroposterior and lateral radiographs must be made preoperatively. It is advisable that instruments and implants be available for both internal fixation of the fracture and revision with a long-stem total knee replacement because revision may be necessary if stable internal fixation cannot be obtained or if previously unrecognized loosening of the implant is discovered intraoperatively.

Multiple options are available to provide secure internal fixation of supracondylar fractures of the distal part of the femur. The supracondylar blade-plate and the condylar compression screw and side-plate have been used successfully for many years to treat these fractures^259,313. These devices are most useful when there is little comminution of the distal fragment and for fixation of more proximal fractures. The condylar buttress-plate is preferable when the distal fragment is comminuted because it allows multiple screws to be used for fixation of that fragment. This feature makes the condylar buttress-plate more versatile than the condylar blade-plate and condylar compression-screw systems, which provide a single point of fixation of the distal fragment. Such versatility also makes the condylar buttress-plate preferable for fixation of more distal fractures as well as fractures that extend into the intercondylar region and are not amenable to internal fixation with use of the blade-plate or the condylar compression screw alone.

The intramedullary nail inserted in a retrograde manner through the knee joint is a new device that has been used successfully to treat supracondylar fractures proximal to knee replacements^{115,116,144,182,245}. Intramedullary fixation provides an attractive alternative to lateral plate fixation because of the simplicity of both the instrumentation system and the technique used for insertion of the nail. In addition, intramedullary fixation is biomechanically stronger and less prone to failure than lateral plate fixation^115,116,245. Intramedullary nails are load-sharing devices that may have some inherent advantages, particularly when used to manage patients who have a supracondylar fracture proximal to a knee replacement as they typically have osteopenia of the distal femoral metaphysis.

The operative technique for successful internal fixation of a supracondylar fracture with use of a lateral plate and screws is exacting. High-quality anteroposterior and lateral radiographs must be available preoperatively. The surgeon should carefully assess the level of the fracture, the degree of comminution, and the quality of the cortical bone before choosing the type of lateral plate-and-screw system to be used. The patient is placed in the supine position on a radiolucent operating table to allow for use of the c-arm image-intensifier intraoperatively. A hip roll is placed beneath the ipsilateral hip to rotate the lower extremity internally, and a sterile tourniquet can be used. The fracture should be approached through the previous anterior midline incision, which can be extended laterally and proximally and continued in the midline off the tibial crest distally to provide exposure. The creation of a separate lateral incision, as is typically done for patients who have not had a previous knee replacement, places the soft tissue at risk. This is especially true in the region of the tibial tubercle, where the lateral incision comes close to the anterior scar from the previous knee replacement.

An indirect reduction technique should be used to reduce these fractures intraoperatively¹⁹¹. Dissection of the soft tissues medially should be avoided to prevent disruption of the important blood supply from this area^191,260. The use of a femoral distractor or a simple external fixation frame helps the surgeon to achieve a satisfactory preliminary indirect reduction¹⁶³. A Steinmann pin can be inserted and used as a joystick to manipulate the distal fragment. Once reduction is achieved, the Steinmann pin can be driven across the fracture to provide preliminary fixation until the plate and screws are applied (Figs. 10-A and 10-B). Autogenous iliac-crest cancellous-bone graft should be added if there is marked comminution of the fracture.

When a locking intramedullary device is to be used, the patient is positioned in the same manner as described previously for insertion of a lateral plate (that is, supine on a radiolucent table with a hip roll beneath the ipsilateral hip). High-quality radiographs must be available preoperatively, and the surgeon must know the distance between the condyles of the femoral prosthesis. A minimum intercondylar distance of twelve millimeters is required in order for an intramedullary nail to be used (Table I). When treating a supracondylar fracture proximal to a posterior stabilized knee replacement, the surgeon must take particular care to ascertain if the intercondylar box is closed or open. If it is closed, use of a retrograde nail is contraindicated as there is no access to the medullary canal.

A routine exposure is performed through the anterior midline scar. Care should be taken not to dissect the medial or lateral soft tissues that are attached to the fracture fragment; it is necessary to remain directly anterior. The knee is flexed 45 to 55 degrees over a sterile bolster. An open reduction is achieved through the fracture, with use of a bone hook to correct the typically occurring recurvatum deformity and reduction forceps to achieve alignment in the coronal plane. The surgeon then performs a provisional reduction by placing one hand behind the proximal border of the tibia and pulling forward, a maneuver similar to that performed in an anterior drawer test. The reduction is verified with use of the c-arm image-intensifier. The medullary canal then is entered at a point midway between the condyles. This starting point is the same as that used for intramedullary instrumentation during a total knee replacement. The medullary canal is reamed progressively, in 0.5-millimeter increments, over a guide-wire to a diameter of 1.0 to 1.5 millimeters greater than that of the supracondylar nail. Nails typically range from eleven to thirteen millimeters in diameter and are available in a variety of lengths. The preoperative use of templates aids in the selection of a nail of the appropriate diameter and length. A larger-diameter nail is preferred, and a nail that is at least twenty-five centimeters long is easier to centralize within the femoral diaphysis and helps to minimize varus or valgus malalignment of the fracture. The intramedullary nail, assembled to the guide-bar, then is inserted over the guide-wire while the surgeon performs the anterior drawer reduction maneuver. The nail is advanced by hand pressure until it lies two millimeters beneath the articular surface. Multiple locking screws then are placed percutaneously with use of the guide system; typically, two screws are placed in the distal fragment and two, in the proximal fragment. Bolts with nuts also are available for use in patients who have marked osteopenia of the distal fragment.

Revision total knee replacement with use of a long-stem femoral component is recommended for all patients who have loosening of the femoral component in association with the supracondylar fracture. As stability of the femoral component may be difficult to determine on the basis of preoperative radiographs, it is recommended that instruments and prosthetic components necessary for revision total knee replacement be available at the time that internal fixation is undertaken. During the revision, the collateral ligaments must be retained and extrusion of cement into the fracture must be avoided. Whenever there is comminution in the region of the origin of the collateral ligaments, a modular metaphyseal femoral replacement (the type of prosthesis used after the resection of tumors) or a combination of a distal femoral allograft and a revision femoral component with an intramedullary stem may be used¹⁶³.

The results obtained with the operative techniques and devices described here that were developed during the 1990's have been markedly better than those of methods described earlier in this section^{113,115,116,182}. Healy et al.¹¹³ reported the results for twenty patients who had been managed with open reduction and internal fixation with use of a condylar blade-plate (seven patients), a condylar compression plate (seven patients), or a condylar buttress-plate (six patients); in addition, fifteen of the twenty patients had been managed with bone-grafting. Union was achieved, without the need for an additional operation, in eighteen of the twenty patients by a mean of sixteen weeks (range, six to twenty-six weeks). In the remaining two patients, union was achieved after a second procedure involving autologous bone-grafting. Ten of the twenty patients had a delayed union (radiographic signs of union were not evident until more than four months after the operation). McLaren et al.¹⁸² reported on seven patients in whom a supracondylar fracture proximal to a total knee replacement had been treated with a supracondylar nail. Radiographic evidence of union was noted in six patients by six weeks, and complete union was achieved in all seven patients by twelve weeks. In a large, multicenter study¹¹⁶ of forty-one such fractures that were treated with internal fixation with a locked intramedullary nail, delayed union occurred in three patients and a non-union, in one. The mean time to union for the remaining thirty-seven patients was thirteen weeks.

References

Aaron, R. K., and |and |Scott, R.: Supracondylar fracture of the femur after total knee arthroplasty. Clin. Orthop.,219: 136-139, 1987.219136 1987 [PubMed]

Abbott, L. C., and |and |Carpenter, W. K.: Surgical approaches to the knee joint. J. Bone and Joint Surg.,27: 277-310, April 1945.27277 1945

Achauer, B. M.; Black, K. S.; and |and |Litke, D. K.: Transcutaneous PO2 in flaps: a new method of survival prediction. Plast. and Reconstr. Surg.,65: 738-745, 1980.65738 1980

Ahmed, A. M.; Burke, D. L.; and |and |Hyder, A.: Force analysis of the patellar mechanism. J. Orthop. Res.,5: 69-85, 1987.569 1987 [PubMed]

Anouchi, Y. S.; Whiteside, L. A.; Kaiser, A. D.; and |and |Milliano, M. T.: The effects of axial rotational alignment of the femoral component on knee stability and patellar tracking in total knee arthroplasty demonstrated on autopsy specimens. Clin. Orthop.,287: 170-177, 1993.287170 1993 [PubMed]

Argenta, L. C.: Controlled tissue expansion in reconstructive surgery. British J. Plast. Surg.,37: 520-529, 1984.37520 1984

Argenta, L. C.; Marks, M. W.; and |and |Pasyk, K. A.: Advances in tissue expansion. Clin. Plast. Surg.,12: 159-171, 1985.12159 1985 [PubMed]

Bandi, W.: Chondromalacia patellae und femoro-patellare Arthrose. Åtiologie, Klinik und Therapie. Helvetica Chir. Acta,Supplementum 11: 1972.Supplementum 11 1972

Bayley, J. C., and |and |Scott, R. D.: Further observations on metal-backed patellar component failure. Clin. Orthop.,236: 82-87, 1988.23682 1988 [PubMed]

Bayley, J. C.; Scott, R. D.; Ewald, F. C.; and |and |Holmes, G. B., Jr.: Failure of the metal-backed patellar component after total knee replacement. J. Bone and Joint Surg.,70-A: 668-674, June 1988.70-A668 1988

Becker, M. W.; Insall, J. N.; and |and |Faris, P. M.: Bilateral total knee arthroplasty. One cruciate retaining and one cruciate substituting. Clin. Orthop.,271: 122-124, 1991.271122 1991 [PubMed]

Beer, K. J.; Lombardi, A. V., Jr.; Mallory, T. H.; and |and |Vaughn, B. K.: The efficacy of suction drains after routine total joint arthroplasty. J. Bone and Joint Surg.,73-A: 584-587, April 1991.73-A584 1991

Beight, J. L.; Yao, B.; Hozack, W. J.; Hearn, S. L.; and |and |Booth, R. E., Jr.: The patellar "clunk" syndrome after posterior stabilized total knee arthroplasty. Clin. Orthop.,299: 139-142, 1994.299139 1994 [PubMed]

Bengtson, S., and |and |Knutson, K.: The infected knee arthroplasty. A 6-year follow-up of 357 cases. Acta Orthop. Scandinavica,62: 301-311, 1991.62301 1991

Bengtson, S.; Knutson, K.; and |and |Lidgren, L.: Treatment of infected knee arthroplasty. Clin. Orthop.,245: 173-178, 1989.245173 1989 [PubMed]

Bengtson, S.; Carlsson, A.; Relander, M.; Knutson, K.; and |and |Lidgren, L.: Treatment of the exposed knee prosthesis. Acta Orthop. Scandinavica,58: 662-665, 1987.58662 1987

Benowitz, N. L.; Kuyt, F.; and |and |Jacob, P., III: Influence of nicotine on cardiovascular and hormonal effects of cigarette smoking. Clin. Pharmacol. and Ther.,36: 74-81, 1984.3674 1984

Berg, M.; Bergman, B. R.; and |and |Hoborn, J.: Ultraviolet radiation compared to an ultra-clean air enclosure. Comparison of air bacteria counts in operating rooms. J. Bone and Joint Surg.,73-B(5): 811-815, 1991.73-B(5)811 1991

Berg-Perier, M.; Cederblad, A.; and |and |Persson, U.: Ultraviolet radiation and ultra-clean air enclosures in operating rooms. UV-protection, economy, and comfort. J. Arthroplasty,7: 457-463, 1992.7457 1992 [PubMed]

Berman, A. T.; Reid, J. S.; Yanicko, D. R., Jr.; Sih, G. C.; and |and |Zimmerman, M. R.: Thermally induced bone necrosis in rabbits. Relation to implant failure in humans. Clin. Orthop.,186: 284-292, 1984.186284 1984 [PubMed]

Berman, A. T.; Coutts, R. D.; Engh, G. A.; Mayor, M. B.; Whiteside, L. A.; and |and |Wilde, A. H.: Symposium: the painful total knee replacement and the influence of component design. Contemp. Orthop.,28: 523-530, 533-536, 541-545, 1994.28523 1994 [PubMed]

Berry, D. J., and |and |Rand, J. A.: Isolated patellar component revision of total knee arthroplasty. Clin. Orthop.,286: 110-115, 1993.286110 1993 [PubMed]

Bjorkstrom, S., and |and |Goldie, I. F.: A study of the arterial supply of the patella in the normal state, in chondromalacia patellae and in osteoarthrosis. Acta Orthop. Scandinavica,51: 63-70, 1980.5163 1980

Bocell, J. R.; Thorpe, C. D.; and |and |Tullos, H. S.: Arthroscopic treatment of symptomatic total knee arthroplasty. Clin. Orthop.,271: 125-134, 1991.271125 1991 [PubMed]

Bogoch, E.; Hastings, D.; Gross, A.; and |and |Gschwend, N.: Supracondylar fractures of the femur adjacent to resurfacing and MacIntosh arthroplasties of the knee in patients with rheumatoid arthritis. Clin. Orthop.,229: 213-220, 1988.229213 1988 [PubMed]

Booth, R. E., Jr., and |and |Lotke, P. A.: The results of spacer block technique in revision of infected total knee arthroplasty. Clin. Orthop.,248: 57-60, 1989.24857 1989 [PubMed]

Boyd, A. D., Jr.; Ewald, F. C.; Thomas, W. H.; Poss, R.; and |and |Sledge, C. B.: Long-term complications after total knee arthroplasty with or without resurfacing of the patella. J. Bone and Joint Surg.,75-A: 674-681, May 1993.75-A674 1993

Brick, G. W., and |and |Scott, R. D.: The patellofemoral component of total knee arthroplasty. Clin. Orthop.,231: 163-178, 1988.231163 1988 [PubMed]

Bridges, S. L., Jr.; Lopez-Mendez, A.; Han, K. H.; Tracy, I. C.; and |and |Alarcon, G. S.: Should methotrexate be discontinued before elective orthopedic surgery in patients with rheumatoid arthritis?. Arthrit. and Rheumat.,32 (Supplement 4): 543, 1989.32 (Supplement 4)543 1989

Bryan, R. S., and |and |Peterson, L. F.: Polycentric total knee arthroplasty: a prognostic assessment. Clin. Orthop.,145: 23-28, 1979.14523 1979 [PubMed]

Buchanan, J. R.; Greer, R. B., III; Bowman, L. S.; Shearer, A.; and |and |Gallaher, K.: Clinical experience with the variable axis total knee replacement. Orthop. Trans.,6: 367, 1982.6367 1982

Burger, R. R.; Basch, T.; and |and |Hopson, C. N.: Implant salvage in infected total knee arthroplasty. Clin. Orthop.,273: 105-112, 1991.273105 1991 [PubMed]

Cameron, H. U., and |and |Fedorkow, D. M.: The patella in total knee arthroplasty. Clin. Orthop.,165: 197-199, 1982.165197 1982 [PubMed]

Cawson, R. A.: Antibiotic prophylaxis for dental treatment. For hearts but not for prosthetic joints. British Med. J.,304: 933-934, 1992.304933 1992

Cepulo, A. J.; Stahurski, T. M.; Moran, J. M.; Matejczyk, M.; and |and |Greenwald, A. S.: Mechanical characteristics of patello-femoral replacements. Trans. Orthop. Res. Soc.,8: 41, 1983.841 1983

Charnley, J., and |and |Eftekhar, N.: Postoperative infection in total prosthetic replacement arthroplasty of the hip-joint. With special reference to the bacterial content of the air of the operating room. British J. Surg.,56: 641-649, 1969.56641 1969

Clayton, M. L., and |and |Thirupathi, R.: Patellar complications after total condylar arthroplasty. Clin. Orthop.,170: 152-155, 1982.170152 1982 [PubMed]

Colwell, C. W., Jr., and |and |Morris, B. A.: The influence of continuous passive motion on the results of total knee arthroplasty. Clin. Orthop.,276: 225-228, 1992.276225 1992 [PubMed]

Colwell, C. W., Jr.; Spiro, T. E.; Trowbridge, A. A.; Morris, B. A.; Kwaan, H. C.; Blaha, J. D.; Comerota, A. J.; |and |Skoutakis, V. A.; and |and |the Enoxaparin Clinical Trial Group: Use of enoxaparin, a low-molecular-weight heparin, and unfractionated heparin for the prevention of deep venous thrombosis after elective hip replacement. A clinical trial comparing efficacy and safety. J. Bone and Joint Surg.,76-A: 3-14, Jan. 1994.76-A3 1994

Conway, W. F.; Gilula, L. A.; and |and |Serot, D. I.: Breakage of the patellar component of a kinematic total knee arthroplasty. A case report. Orthopedics,9: 532-534, 1986.9532 1986 [PubMed]

Cracchiolo, A. III; Benson, M.; Finerman, G. A.; Horacek, K.; and |and |Amstutz, H. C.: A prospective comparative clinical analysis of the first-generation knee replacements: polycentric vs. geometric knee arthroplasty. Clin. Orthop.,145: 37-46, 1979.14537 1979 [PubMed]

Craig, S.: Soft tissue considerations. In Total Knee Revision Arthroplasty, pp. 99-112. Edited by W. N. Scott. Orlando, Florida, Grune and Stratton, 1987.

Craig, S. M.: Soft tissue considerations in the failed total knee arthroplasty. In The Knee, pp. 1279-1295. Edited by W. N. Scott. St. Louis, C. V. Mosby, 1994.

Craig, S., and |and |Rees, T. D.: The effects of smoking on experimental skin flaps in hamsters. Plast. and Reconstr. Surg.,75: 842-846, 1985.75842 1985

Cruse, P. J., and |and |Foord, R.: A five-year prospective study of 23,649 surgical wounds. Arch. Surg.,107: 206-210, 1973.107206 1973 [PubMed]

Culp, R. W.; Schmidt, R. G.; Hanks, G.; Mak, A.; Esterhai, J. L., Jr.; and |and |Heppenstall, R. B.: Supracondylar fracture of the femur following prosthetic knee arthroplasty. Clin. Orthop.,222: 212-222, 1987.222212 1987 [PubMed]

Dalldorf, P. G.; Perkins, F. M.; Totterman, S.; and |and |Pellegrini, V. D., Jr.: Deep venous thrombosis following total hip arthroplasty. Effects of prolonged postoperative epidural anesthesia. J. Arthroplasty,9: 611-616, 1994.9611 1994 [PubMed]

D'Ambrosia, R. D.; Shoji, H.; and |and |Heater R.: Secondarily infected total joint replacements by hematogenous spread. J. Bone and Joint Surg.,58-A: 450-453, June 1976.58-A450 1976

Deburge, A., and |and |GUEPAR: Guepar hinge prosthesis. Complications and results with two years' follow-up. Clin. Orthop.,120: 47-53, 1976.12047 1976 [PubMed]

Dennis, D. A.: Patellofemoral complications in total knee arthroplasty: a literature review. Am. J. Knee Surg.,5: 156-166, 1992.5156 1992

Dennis, D. A.: Removal of well-fixed cementless metal-backed patellar components. J. Arthroplasty,7: 217-220, 1992.7217 1992 [PubMed]

Dennis, D. A.; Clayton, M. L.; O'Donnell, S.; Mack, R. P.; and |and |Stringer, E. A.: Posterior cruciate condylar total knee arthroplasty. Average 11-year follow-up evaluation. Clin. Orthop.,281: 168-176, 1992.281168 1992 [PubMed]

d'Hollander, A.; Burny, F.; Monteny, E.; and |and |Donkerwolcke, M.: Extraosseous variations of temperature during polymerization of acrylic cement in hip arthroplasties. Acta Orthop. Scandinavica,47: 186-188, 1976.47186 1976

Dickhaut, S. C.; DeLee, J. C.; and |and |Page, C. P.: Nutritional status: importance in predicting wound-healing after amputation. J. Bone and Joint Surg.,66-A: 71-75, Jan. 1984.66-A71 1984

Donley, B. G.; Matthews, L. S.; and |and |Kaufer, H.: Arthrodesis of the knee with an intramedullary nail. J. Bone and Joint Surg.,73-A: 907-913, July 1991.73-A907 1991

Doolittle, K. H., II, and |and |Turner, R. H.: Patellofemoral problems following total knee arthroplasty. Orthop. Rev.,17: 696-702, 1988.17696 1988 [PubMed]

Dorr, L. D/, and |and |Boiardo, R. A.: Technical considerations in total knee arthroplasty. Clin. Orthop.,205: 5-11, 1986.2055 1986 [PubMed]

Dorr, L. D.; Ochsner, J. L.; Gronley, J.; and |and |Perry, J.: Functional comparison of posterior cruciate-retained versus cruciate-sacrificed total knee arthroplasty. Clin. Orthop.,236: 36-43, 1988.23636 1988 [PubMed]

Dowd, G. S. E.; Linge, K.; Ross, R.; and |and |Bentley, G.: The transcutaneous measurement of oxygen in normal and abnormal skin. In Proceedings of the British Orthopaedic Association. J. Bone and Joint Surg.,64-B(2): 248-249, 1982.64-B(2)248 1982

Drancourt, M.; Stein, A.; Argenson, J. N.; Zannier, A.; Curvale, G.; and |and |Raoult, D.: Oral rifampin plus ofloxacin for treatment of Staphylococcus-infected orthopedic implants. Antimicrob. Agents and Chemother.,37: 1214-1218, 1993.371214 1993

Dupont, J. A., and |and |Baker, S. A.: Complications of patellofemoral resurfacing in total knee arthroplasty. Orthop. Trans.,6: 369, 1982.6369 1982

Eckardt, J. J.; Lesavoy, M. A.; Dubrow, T. J.; and |and |Wackym, P. A.: Exposed endoprosthesis. Management protocol using muscle and myocutaneous flap coverage. Clin. Orthop.,251: 220-229, 1990.251220 1990 [PubMed]

Ecker, M. L., and |and |Lotke, P. A.: Postoperative care of the total knee patient. Orthop. Clin. North America,20: 55-62, 1989.2055 1989

Ecker, M. L., and Lotke, P. A. Wound healing complications. In Total Knee Arthroplasty, pp. 403-407. Edited by J. A. Rand. New York, Raven Press, 1993.

Edwards, E.; Miller, J.; and Chan, K.-H.: The effect of postoperative collateral ligament laxity in total knee arthroplasty. Clin. Orthop.,236: 44-51, 1988.23644 1988 [PubMed]

Eftekhar, N. S.: Total-knee replacement arthroplasty. Results with the intramedullary adjustable total knee prosthesis. J. Bone and Joint Surg.,65-A: 293-309, March 1983.65-A293 1983

Ellingsen, D. E., and |and |Rand, J. A.: Intramedullary arthrodesis of the knee after failed total knee arthroplasty. J. Bone and Joint Surg.,76-A: 870-877, Jan. 1994.76-A870 1994

Emerson, R. H., Jr.; Head, W. C.; and |and |Malinin, T. I.: Reconstruction of patellar tendon rupture after total knee arthroplasty with an extensor mechanism allograft. Clin. Orthop.,260: 154-161, 1990.260154 1990 [PubMed]

Enis, J. E.; Gardner, R.; Robledo, M. A.; Latta, L.; and |and |Smith, R.: Comparison of patellar resurfacing versus nonresurfacing in bilateral total knee arthroplasty. Clin. Orthop.,260: 38-42, 1990.26038 1990 [PubMed]

Evanski, P. M.; Waugh, T. R.; Orofino, C. F.; and |and |Anzel, S. H.: UCI knee replacement. Clin. Orthop.,120: 33-38, 1976.12033 1976 [PubMed]

Ewald, F. C.; Thomas, W. H.; Poss, R.; Scott, R. D.; and |and |Sledge, C. B.: Duo-patella total knee arthroplasty in rheumatoid arthritis. Orthop. Trans.,2: 202, 1978.2202 1978

Fahmy, N. R., and |and |Patel, D. G.: Hemostatic changes and postoperative deep-vein thrombosis associated with use of a pneumatic tourniquet. J. Bone and Joint Surg.,63-A: 461-465, March 1981.63-A461 1981

Falahee, M. H.; Matthews, L. S.; and |and |Kaufer, H.: Resection arthroplasty as a salvage procedure for a knee with infection after a total arthroplasty. J. Bone and Joint Surg.,69-A: 1013-1021, Sept. 1987.69-A1013 1987

Fern, E. D.; Winson, I. G.; and |and |Getty, C. J.: Anterior knee pain in rheumatoid patients after total knee replacement. Possible selection criteria for patellar resurfacing. J. Bone and Joint Surg.,74-B(5): 745-748, 1992.74-B(5)745 1992

Ficat, R. P., and Hungerford, D. S.: Disorders of the Patello-Femoral Joint, pp. 29-32. Baltimore, Williams and Wilkins, 1977.

Figgie, H. E., III; Goldberg, V. M.; Figgie, M. P.; Inglis, A. E.; Kelly, M.; and |and |Sobel, M.: The effect of alignment of the implant on fractures of the patella after condylar total knee arthroplasty. J. Bone and Joint Surg.,71-A: 1031-1039, Aug. 1989.71-A1031 1989

Figgie, M. P.; Goldberg, V. M.; Figgie, H. E., III; and |and |Sobel, M.: The results of treatment of supracondylar fracture above total knee arthroplasty. J. Arthroplasty,5: 267-276, 1990.5267 1990 [PubMed]

Figgie, M. P.; Figgie, H. E., III; Goldberg, V. M.; Heiple, K. G.; and |and |Inglis, A. E.: The salvage of the symptomatic patello-femoral joint following cruciate substituting total knee arthroplasty. Am. J. Knee Surg.,1: 48-55, 1988.148 1988

Firestone, T. P.; Teeny, S. M.; Krackow, K. A.; and |and |Hungerford, D. S.: The clinical and roentgenographic results of cementless porous-coated patellar fixation. Clin. Orthop.,273: 184-189, 1991.273184 1991 [PubMed]

Fitzgerald, R. H., Jr.: Total hip arthroplasty sepsis. Prevention and diagnosis. Orthop. Clin. North America,23: 259-264, 1992.23259 1992

Fox, J. L., and |and |Poss, R.: The role of manipulation following total knee replacement. J. Bone and Joint Surg.,63-A: 357-362, March 1981.63-A357 1981

Francis, C. W.; Marder, V. J.; Evarts, C. M.; and |and |Yaukoolbodi, S.: Two-step warfarin therapy. Prevention of postoperative venous thrombosis without excessive bleeding. J. Am. Med. Assn.,249: 374-378, 1983.249374 1983

Francis, C. W.; Pellegrini, V. D., Jr.; Harris, C. M.; and |and |Marder, V. J.: Antithrombin III prophylaxis of venous thromboembolic disease after total hip or knee replacement. Am. J. Med.,87 (Supplement 3B): 61S-66S, 1989.87 (Supplement 3B)61 1989

Francis, C. W.; Pellegrini, V. D., Jr.; Leibert, K. M.; Totterman, S.; Azodo, M. V.; Harris, C. M.; Cox, C.; and |and |Marder, V. J.: Comparison of two warfarin regimens in the prevention of venous thrombosis following total knee replacement. Thromb. and Haemost.,75: 706-711, 1996.75706 1996

Francis, C. W.; Pellegrini, V. D., Jr.; Marder, V. J.; Totterman, S.; Harris, C. M.; Gabriel, K. R.; Azodo, M. V.; and |and |Leibert, K. M.: Comparison of warfarin and external pneumatic compression in prevention of venous thrombosis after total hip replacement. J. Am. Med. Assn.,267: 2911-2915, 1992.2672911 1992

Francis, C. W.; Pellegrini, V. D., Jr.; Marder, V. J.; Harris, C. M.; Totterman, S.; Gabriel, K. R.; Baughman, D. J.; Roemer, S.; Burke, J.; Goodman, T. L.; and |and |Evarts, C. McC.: Prevention of venous thrombosis after total hip arthroplasty. Antithrombin III and low-dose heparin compared with dextran 40. J. Bone and Joint Surg.,71-A: 327-335, March 1989.71-A327 1989

Freeman, M. A.; Samuelson, K. M.; and |and |Bertin, K. C.: Freeman-Samuelson total arthroplasty of the knee. Clin. Orthop.,192: 46-58, 1985.19246 1985 [PubMed]

Freeman, M. A.; Todd, R. C.; Bamert, P.; and |and |Day, W. H.: ICLH arthroplasty of the knee: 1968-1977. J. Bone and Joint Surg.,60-B(3): 339-344, 1978.60-B(3)339 1978

Friedman, R. J.; Friedrich, L. V.; White, R. L.; Kays, M. B.; Brundage, D. M.; and |and |Graham, J.: Antibiotic prophylaxis and tourniquet inflation in total knee arthroplasty. Clin. Orthop.,260: 17-23, 1990.26017 1990 [PubMed]

Garner, R. W.; Mowat, A. G.; and |and |Hazleman, B. L: Wound healing after operations of patients with rheumatoid arthritis. J. Bone and Joint Surg.,55-B(1): 134-144, 1973.55-B(1)134 1973

Gerwin, M.; Rothaus, K. O.; Windsor, R. E.; Brause, B. D.; and |and |Insall, J. N.: Gastrocnemius muscle flap coverage of exposed or infected knee prostheses. Clin. Orthop.,286: 64-70, 1993.28664 1993 [PubMed]

Goldberg, V. M.; Figgie, H. E., III; and |and |Figgie, M. P.: Technical considerations in total knee surgery. Management of patella problems. Orthop. Clin. North America,20: 189-199, 1989.20189 1989

Goldberg, V. M.; Figgie, H. E., III; Inglis, A. E.; Figgie, M. P.; Sobel, M.; Kelly, M.; and |and |Kraay, M.: Patellar fracture type and prognosis in condylar total knee arthroplasty. Clin. Orthop.,236: 115-122, 1988.236115 1988 [PubMed]

Goldstein, S. A.; Coale, E.; Weiss, A. P.; Grossnickle, M.; Meller, B.; and |and |Matthews, L. S.: Patellar surface strain. J. Orthop. Res.,4: 372-377, 1986.4372 1986 [PubMed]

Goletz, T. H., and |and |Henry, J. H.: Continuous passive motion after total knee arthroplasty. Southern Med. J.,79: 1116-1120, 1986.791116 1986 [PubMed]

Gomes, L. S. M.; Bechtold, J. E.; and |and |Gustilo, R. B.: Patellar prosthesis positioning in total knee arthroplasty. A roentgenographic study. Clin. Orthop.,236: 72-81, 1988.23672 1988 [PubMed]

Goodson, W. H., III, and |and |Hunt, T. K.: Studies of wound healing in experimental diabetes mellitus. J. Surg. Res.,22: 221-227, 1977.22221 1977 [PubMed]

Goodson, W. H., III, and |and |Hunt, T. K.: Wound healing and the diabetic patient. Surg., Gynec. and Obstet.,149: 600-608, 1979.149600 1979

Gordon, L., and |and |Levinsohn, D. G.: Versatility of the latissimus and serratus anterior muscle transplants in providing cover for exposed hardware and endoprostheses. Orthop. Trans.,16: 68, 1992.1668 1992

100

Grace, J. N., and |and |Sim, F. H.: Fracture of the patella after total knee arthroplasty. Clin. Orthop.,230: 168-175, 1988.230168 1988 [PubMed]

101

Grady-Benson, J. C.; Oishi, C. S.; Hanson, P. B.; Colwell, C. W., Jr.; Otis, S. M.; and |and |Walker, R. H.: Postoperative surveillance for deep venous thrombosis with duplex ultrasonography after total knee arthroplasty. J. Bone and Joint Surg.,76-A: 1649-1657, Nov. 1994.76-A1649 1994

102

Green, J. P.: Steroid therapy and wound healing in surgical patients. British J. Surg.,52: 523-525, 1965.52523 1965

103

Greenberg, B.; LaRossa, D.; Lotke, P. A.; Murphy, J. B.; and |and |Noone, R. B.: Salvage of jeopardized total-knee prosthesis: the role of the gastrocnemius muscle flap. Plast. and Reconstr. Surg.,83: 85-89, 97-99, 1989.8385 1989

104

Grogan, T. J.; Dorey, F.; Rollins, J.; and |and |Amstutz, H. C.: Deep sepsis following total knee arthroplasty. Ten-year experience at the University of California at Los Angeles Medical Center. J. Bone and Joint Surg.,68-A: 226-234, Feb. 1986.68-A226 1986

105

Gschwend, N.: Die GSB-Knieprothese. Prinzipielle Uberlegungen und Ergebnisse. Aktuel. Probl. Chir. Orthop.,15: 24-31, 1981.1524 1981 [PubMed]

106

Gschwend, N., and |and |Loehr, J.: The Gschwend-Scheier-Bahler (GSB) replacement of the rheumatoid knee joint. Reconstr. Surg. and Traumatol.,18: 174-194, 1981.18174 1981

107

Gschwend, N.; Scheier, H. J.; Bahler, A.; and |and |Meyer, R. P.: The GSB knee arthroplasty. Internat. Orthop.,3: 281-284, 1980.3281 1980

108

Haas, S. B.; Insall, J. N.; Scuderi, G. R.; Windsor, R. E.; and |and |Ghelman, B.: Pneumatic sequential-compression boots compared with aspirin prophylaxis of deep-vein thrombosis after total knee arthroplasty. J. Bone and Joint Surg.,72-A: 27-31, Jan. 1990.72-A27 1990

109

Habermann, E., and Hungerford, D. Total Knee Arthroplasty: a Comprehensive Approach, p. 241. Edited by D. S. Hungerford, K. A. Krackow, and R. V. Kenna. Baltimore, Williams and Wilkins, 1984.

110

Hallock, G. G.: Salvage of total knee arthroplasty with local fasciocutaneous flaps. J. Bone and Joint Surg.,72-A: 1236-1239, Sept. 1990.72-A1236 1990

111

Hanks, G. A.; Mathews, H. H.; Routson, G. W.; and |and |Loughran, T. P.: Supracondylar fracture of the femur following total knee arthroplasty. J. Arthroplasty,4: 289-292, 1989.4289 1989 [PubMed]

112

Hassenpflug, J.; Holland, C.; Heupel, R.; and |and |Koebke, J.: Patellaveränderungen bei Langzeitbeobachtungen der Kniegelenksendoprothese nach Blauth. Zeitschr. Orthop.,122: 185-197, 1984.122185 1984

113

Healy, W. L.; Siliski, J. M.; and |and |Incavo, S. J.: Operative treatment of distal femoral fractures proximal to total knee replacements. J. Bone and Joint Surg.,75-A: 27-34, Jan. 1993.75-A27 1993

114

Hemphill, E. S.; Ebert, F. R.; and |and |Muench, A. G.: The medial gastrocnemius muscle flap in the treatment of wound complications following total knee arthroplasty. Orthopedics,15: 477-480, 1992.15477 1992 [PubMed]

115

Henry, S. L., and |and |Booth, R. E.: Management of supracondylar fractures above total knee prostheses. Tech. Orthop.,9: 243-252, 1995.9243 1995

116

Henry, S. L.; Busconi, B.; Gold, S.; Watson, T.; Smith, W.; Licht, N.; and Chapman, J.: Management of supracondylar femur fractures proximal to total knee prostheses with the GSH supracondylar intramedullary nail. Read at the Annual Meeting of the Orthopaedic Trauma Association, Sept. 23, 1994.

117

Hill, C.; Flamant, R.; Mazas, F.; and |and |Evrard, J.: Prophylactic cefazolin versus placebo in total hip replacement. Report of a multicentre double-blind randomised trial. Lancet,1: 795-797, 1981.1795 1981 [PubMed]

118

Hirsch, H. S.; Lotke, P. A.; and |and |Morrison, L. D.: The posterior cruciate ligament in total knee surgery. Save, sacrifice, or substitute?. Clin. Orthop.,309: 64-68, 1994.30964 1994 [PubMed]

119

Hirsch, J.: Therapeutic range for the control of oral anticoagulant therapy. Arch. Intern. Med.,145: 1187-1188, 1985.1451187 1985 [PubMed]

120

Hirsch, J.: Oral anticoagulant drugs. New England J. Med.,324: 1865-1875, 1991.3241865 1991

121

Hirsch, J., and |and |Levine, M. N.: The optimal intensity of oral anticoagulant therapy. J. Am. Med. Assn.,258: 2723-2726, 1987.2582723 1987

122

Hirsh, D. M.; Bhalla, S.; and |and |Roffman, M.: Supracondylar fracture of the femur following total knee replacement. Report of four cases. J. Bone and Joint Surg.,63-A: 162-163, Jan. 1981.63-A162 1981

123

Hofmann, G. O., and |and |Hagena, F. W.: Pathomechanics of the femoropatellar joint following total knee arthroplasty. Clin. Orthop.,224: 251-259, 1987.224251 1987 [PubMed]

124

Homsy, C. A.: Some Mechanical Aspects of Methyl-Methacrylate Prosthesis Sealing Compound. St. Louis, C. V. Mosby, 1973.

125

Hozack, W. J.; Rothman, R. H.; Booth, R. E., Jr.; and |and |Balderston, R. A.: The patellar clunk syndrome. A complication of posterior stabilized total knee arthroplasty. Clin. Orthop.,241: 203-208, 1989.241203 1989 [PubMed]

126

Hozack, W. J.; Goll, S. R.; Lotke, P. A.; Rothman, R. H.; and |and |Booth, R. E., Jr.: The treatment of patellar fractures after total knee arthroplasty. Clin. Orthop.,236: 123-127, 1988.236123 1988 [PubMed]

127

Huberti, H. H., and |and |Hayes, W. C.: Patellofemoral contact pressures. The influence of Q-angle and tendofemoral contact. J. Bone and Joint Surg.,66-A: 715-724, June 1984.66-A715 1984

128

Hull, R. D.; Raskob, G. E.; Gent, M.; McLoughlin, D.; Julian, D.; Smith, F. C.; Dale, N. I.; Reed-Davis, R.; Lofthouse, R. N.; and |and |Anderson, C.: Effectiveness of intermittent pneumatic leg compression for preventing deep vein thrombosis after total hip replacement. J. Am. Med. Assn.,263: 2313-2317, 1990.2632313 1990

129

Hull, R.; Hirsch, J.; Jay, R.; Carter, C.; England, C.; Gent, M.; Turpie, A. G.; McLoughlin, D.; Dodd, P.; Thomas, M.; Raskob, G.; and |and |Ockelford, P.: Different intensities of oral anticoagulant therapy in the treatment of proximal-vein thrombosis. New England J. Med.,307: 1676-1681, 1982.3071676 1982

130

Hungerford, D. S., and |and |Barry, M.: Biomechanics of the patellofemoral joint. Clin. Orthop.,144: 9-15, 1979.1449 1979 [PubMed]

131

Hungerford, D. S., and |and |Krackow, K. A.: Total joint arthroplasty of the knee. Clin. Orthop.,192: 23-33, 1985.19223 1985 [PubMed]

132

Huo, M. H., and |and |Sculco, T. P.: Complications in primary total knee arthroplasty. Orthop. Rev.,19: 781-788, 1990.19781 1990 [PubMed]

133

Imperiale, T. F., and |and |Horwitz, R. I.: Does prophylaxis prevent postdental infective endocarditis? A controlled evaluation of protective efficacy. Am. J. Med.,88: 131-136, 1990.88131 1990 [PubMed]

134

Insall, J. N.: Disorders of the patella. In Surgery of the Knee, pp. 191-260. Edited by J. N. Insall. New York, Churchill Livingstone, 1984.

135

Insall, J. N.: Presidential address to the Knee Society. Choices and compromises in total knee arthroplasty. Clin. Orthop.,226: 43-48, 1988.22643 1988 [PubMed]

136

Insall, J., and |and |Aglietti, P.: A five to seven-year follow-up of unicondylar arthroplasty. J. Bone and Joint Surg.,62-A: 1329-1337, Dec. 1980.62-A1329 1980

137

Insall, J. N., and Haas, S. B.:Complications of total knee arthroplasty. In Surgery of the Knee, edited by J. N. Insall. Ed. 2, vol. 2, pp. 891-934. New York, Churchill Livingstone, 1994.

138

Insall, J. N.; Lachiewicz, P. F.; and |and |Burstein, A. H.: The posterior stabilized condylar prosthesis: a modification of the total condylar design. Two to four-year clinical experience. J. Bone and Joint Surg.,64-A: 1317-1323, Dec. 1982.64-A1317 1982

139

Insall, J. N.; Scott, W. N.; and |and |Ranawat, C. S.: The total condylar knee prosthesis. A report of two hundred and twenty cases. J. Bone and Joint Surg.,61-A: 173-180, March 1979.61-A173 1979

140

Insall, J.; Tria, A. J.; and |and |Aglietti, P.: Resurfacing of the patella. J. Bone and Joint Surg.,62-A: 933-936, Sept. 1980.62-A933 1980

141

Insall, J.; Tria, A. J.; and |and |Scott, W. N.: The total condylar knee prosthesis: the first 5 years. Clin. Orthop.,145: 68-77, 1979.14568 1979 [PubMed]

142

Insall, J. N.; Binazzi, R.; Soudry, M.; and |and |Mestriner, L. A.: Total knee arthroplasty. Clin. Orthop.,192: 13-22, 1985.19213 1985 [PubMed]

143

Insall, J. N.; Ranawat, C. S.; Aglietti, P.; and |and |Shine, J.: A comparison of four models of total knee replacement prostheses. J. Bone and Joint Surg.,58-A: 754-765, Sept. 1976.58-A754 1976

144

Jabczenski, F. F., and |and |Crawford, M.: Retrograde intramedullary nailing of supracondylar femur fractures above total knee arthroplasty. A preliminary report of four cases. J. Arthroplasty,10: 95-101, 1995.1095 1995 [PubMed]

145

Johanson, N. A.: Extensor mechanism failure. In Knee Arthroplasty, pp. 219-240. Edited by P. A. Lotke. New York, Raven Press, 1995.

146

Johnson, D. P.: Midline or parapatellar incision for knee arthroplasty. A comparative study of wound viability. J. Bone and Joint Surg.,70-B(4): 656-658, 1988.70-B(4)656 1988

147

Johnson, D. P.: The effect of continuous passive motion on wound-healing and joint mobility after knee arthroplasty. J. Bone and Joint Surg.,72-A: 421-426, March 1990.72-A421 1990

148

Johnson, D. P., and |and |Bannister, G. C.: The outcome of infected arthroplasty of the knee. J. Bone and Joint Surg.,68-B(2): 289-291, 1986.68-B(2)289 1986

149

Johnson, D. P., and |and |Eastwood, D. M.: Lateral patellar release in knee arthroplasty. Effect on wound healing. J. Arthroplasty,7 (Supplement): 427-431, 1992.7 (Supplement)427 1992

150

Johnson, D. P.; Houghton, T. A.; and |and |Radford, P.: Anterior midline or medial parapatellar incision for arthroplasty of the knee. A comparative study. J. Bone and Joint Surg.,68-B(5): 812-814, 1986.68-B(5)812 1986

151

Jones, E. C.; Insall, J. N.; Inglis, A. E.; and |and |Ranawat, C. S.: GUEPAR knee arthroplasty results and late complications. Clin. Orthop.,140: 145-152, 1979.140145 1979 [PubMed]

152

Jorgensen, L. N.; Rasmussen, L. S.; Nielsen, P. T.; Leffers, A.; and |and |Albrecht-Beste, E.: Antithrombic efficacy of continuous extradural analgesia after knee replacement. British J. Anaesth.,66: 8-12, 1991.668 1991

153

Josechak, R. G.; Finlay, J. B.; Bourne, R. B.; and |and |Rorabeck, C. H.: Cancellous bone support for patellar resurfacing. Clin. Orthop.,220: 192-199, 1987.220192 1987 [PubMed]

154

Kasdan, M. L., and |and |June, L.: Postoperative results of rheumatoid arthritis patients on methotrexate at the time of reconstructive surgery of the hand. Orthopedics,16: 1233-1235, 1993.161233 1993 [PubMed]

155

Kaufer, H.: Mechanical function of the patella. J. Bone and Joint Surg.,53-A: 1551-1560, Dec. 1971.53-A1551 1971

156

Kaufer, H., and |and |Matthews, L. S.: Spherocentric arthroplasty of the knee. Clinical experience with an average four-year follow-up. J. Bone and Joint Surg.,63-A: 545-549, April 1981.63-A545 1981

157

Kaufman, T.; Eichenlaub, E. H.; Levin, M.; Hurwitz, D. J.; and |and |Klain, M.: Tobacco smoking: impairment of experimental flap survival. Ann. Plast. Surg.,13: 468-472, 1984.13468 1984 [PubMed]

158

Kayler, D. E., and |and |Lyttle, D.: Surgical interruption of patellar blood supply by total knee arthroplasty. Clin. Orthop.,229: 221-227, 1988.229221 1988 [PubMed]

159

Kettlekamp, D. B.; Pryor P.; and |and |Brady, T. A.: Selective use of the variable axis knee. Orthop. Trans.,3: 301-302, 1979.3301 1979

160

Kirk, P.; Rorabeck, C. H.; Bourne, R. B.; Burkart, B.; and |and |Nott, L.: Management of recurrent dislocation of the patella following total knee arthroplasty. J. Arthroplasty,7: 229-233, 1992.7229 1992 [PubMed]

161

Klein, N. E., and Cox, C. V.: Wound problems in total knee arthroplasty. In Knee Surgery, edited by F. H. Fu, C. D. Harner, and K. G. Vince. Vol. 2, pp. 1539-1552. Baltimore, Williams and Wilkins, 1994.

162

Köhler, G.; Mohing, W.; and |and |Richter, R.: Erfahrungen mit Re-Operationen nach teil- und vollprothetischer Versorgung des Kniegelenkes. Aktuel. Probl. Chir. Orthop.,15: 84-90, 1981.1584 1981 [PubMed]

163

Kraay, M. J.; Goldberg, V. M.; Figgie, M.; and |and |Figgie, H. E., III: Distal femoral replacement with allograft/prosthetic reconstruction for treatment of supracondylar fractures in patients with total knee arthroplasty. J. Arthroplasty,7: 7-16, 1992.77 1992 [PubMed]

164

Krackow, K. A.; Maar, D. C.; Mont, M.A.; and |and |Carroll, C., IV: Surgical decompression for peroneal nerve palsy after total knee arthroplasty. Clin. Orthop.,292: 223-228, 1993.292223 1993 [PubMed]

165

Kroese, A. J., and |and |Stiris, G.: The risk of deep-vein thrombosis after operations on a bloodless lower limb. A venographic study. Injury,7: 271-273, 1976.7271 1976 [PubMed]

166

Larcom, P. G.; Lotke, P. A.; Holland, G.; Foster, S.; and |and |Steinberg, M. E.: Comparison of magnetic resonance venography to standard contrast venography in the diagnosis of deep venous thrombosis after total hip and knee surgery. Orthop. Trans.,20: 149, 1996.20149 1996

167

Larsson, J., and |and |Risberg, B.: Fibrinolytic activity in human legs in tourniquet ischemia. Thromb. Res.,11: 817-825, 1977.11817 1977 [PubMed]

168

Laskin, R. S.: Flexion space configuration in total knee arthroplasty. J. Arthroplasty,10: 657-660, 1995.10657 1995 [PubMed]

169

Leblanc, J. M.: Patellar complications in total knee arthroplasty. A literature review. Orthop. Rev.,18: 296-304, 1989.18296 1989 [PubMed]

170

Leclerc, J. R.; Geerts, W. H.; Desjardins, L.; Jobin, F.; Laroche, F.; Delorme, F.; Haviernick, S.; Atkinson, S.; and |and |Bourgouin, J.: Prevention of deep vein thrombosis after major knee surgery—a randomized double-blind trial comparing a low molecular weight heparin fragment (enoxaparin) to placebo. Thromb. and Haemost.,67: 417-423, 1992.67417 1992

171

Levai, J. P.; McLeod, H. C.; and |and |Freeman, M. A.: Why not resurface the patella?. J. Bone and Joint Surg.,65-B(4): 448-451, 1983.65-B(4)448 1983

172

Lewis, V. L., Jr.; Mossie, R. D.; Stulberg, D. S.; Bailey, M. H.; and |and |Griffith, B. H.: The fasciocutaneous flap: a conservative approach to the exposed knee joint. Plast. and Reconstr. Surg.,85: 252-257, 1990.85252 1990

173

Lian, G.; Cracchiolo, A., III; and |and |Lesavoy, M.: Treatment of major wound necrosis following total knee arthroplasty. J. Arthroplasty,4 (Supplement): 23-S32, 1989.4 (Supplement)23 1989

174

Lidwell, O.; Lowbury, E.; Whyte, W.; Blowers, R.; Stanley, S. J.; and |and |Lowe, D.: Effect of ultraclean air in operating rooms on deep sepsis in the joint after total hip or knee replacement: a randomised study. British Med. J.,285: 10-14, 1982.28510 1982

175

Lintner, D. M.; Bocell, J. R.; and |and |Tullos, H. S.: Arthroscopic treatment of intraarticular fibrous bands after total knee arthroplasty. A followup note. Clin. Orthop.,309: 230-233, 1994.309230 1994 [PubMed]

176

Lotke, P. A., and |and |Ecker, M. L.: Influence of positioning of prosthesis in total knee replacement. J. Bone and Joint Surg.,59-A: 77-79, Jan. 1977.59-A77 1977

177

Lotke, P. A.; Ecker, M. L.; Alavi, A.; and |and |Berkowitz, H.: Indications for the treatment of deep venous thrombosis following total knee replacement. J. Bone and Joint Surg.,66-A: 202-208, Feb. 1984.66-A202 1984

178

Lynch, A. F.; Rorabeck, C. H.; and |and |Bourne, R. B.: Extensor mechanism complications following total knee arthroplasty. J. Arthroplasty,2: 135-140, 1987.2135 1987 [PubMed]

179

Lynch, A. F.; Bourne, R. B.; Rorabeck, C. H.; Rankin, R. N.; and |and |Donald, A.: Deep-vein thrombosis and continuous passive motion after total knee arthroplasty. J. Bone and Joint Surg.,70-A: 11-14, Jan. 1988.70-A11 1988

180

McGrath, M. H.: The effect of prostaglandin inhibitors on wound contraction and the myofibroblast. Plast. and Reconstr. Surg.,69: 74-85, 1982.6974 1982

181

McKenna, R.; Galante, J.; Bachmann, F.; Wallace, D. L.; Kaushal, P. S.; and |and |Meredith, P.: Prevention of venous thromboembolism after total knee replacement by high-dose aspirin or intermittent calf and thigh compression. British Med. J.,280: 514-517, 1980.280514 1980

182

McLaren, A. C.; Dupont, J. A.; and |and |Schroeber, D. C.: Open reduction internal fixation of supracondylar fractures above total knee arthroplasties using the intramedullary supracondylar rod. Clin. Orthop.,302: 194-198, 1994.302194 1994 [PubMed]

183

McMahon, M. S.; Scuderi, G. R.; Glashow, J. L.; Scharf, S. C.; Meltzer, L. P.; and |and |Scott, W. N.: Scintigraphic determination of patellar viability after excision of infrapatellar fat pad and/or lateral retinacular release in total knee arthroplasty. Clin. Orthop.,260: 10-16, 1990.26010 1990 [PubMed]

184

McMurray, J. F., Jr.: Wound healing with diabetes mellitus. Better glucose control for better wound healing in diabetes. Surg. Clin. North America,64: 769-778, 1984.64769 1984

185

McNamara, J. J.; Lamborn, P. J.; Mills, D.; and |and |Aaby, G. V.: Effect of short-term pharmacologic doses of adrenocorticosteroid therapy on wound healing. Ann. Surg.,170: 199-202, 1969.170199 1969 [PubMed]

186

Mahomed, N.; McKee, N.; Solomon, P.; Lahoda, L.; and |and |Gross, A. E.: Soft-tissue expansion before total knee arthroplasty in arthrodesed joints. A report of two cases. J. Bone and Joint Surg.,76-B(1): 88-90, 1994.76-B(1)88 1994

187

Mancuso, C. A; Ranawat, C. S.; Esdaile, J. M.; Johanson, N. A.; and |and |Charlson, M. E.: Indications for total hip and total knee arthroplasties. Results of orthopaedic surveys. J. Arthroplasty,11: 34-46, 1996.1134 1996 [PubMed]

188

Manders, E. K.; Schenden, M. J.; Furrey, J. A.; Hetzler, P. T.; Davis, T. S.; and |and |Graham, W. P., III: Soft-tissue expansion: concepts and complications. Plast. and Reconstr. Surg.,74: 493-507, 1984.74493 1984

189

Manders, E. K.; Oaks, T. E.; Au, V. K.; Wong, R. K.; Furrey, J. A.; Davis, T. S.; and |and |Graham, W. P., III: Soft-tissue expansion in the lower extremities. Plast. and Reconstr. Surg.,81: 208-219, 1988.81208 1988

190

Martin, L. C.; McKenney, M. G.; Sosa, J. L.; Ginzburg, E.; Puente, I.; Sleeman, D.; and |and |Zeppa, R.: Management of lower extremity arterial trauma. J. Trauma,37: 591-599, 1994.37591 1994 [PubMed]

191

Mast, J.; Jakob, R.; and Ganz, R.: Reduction with plates. In Planning and Reduction Techniques in Fracture Surgery, pp. 48-129. New York, Springer, 1994.

192

Matthews, L. S.; Sonstegard, D. A.; and |and |Henke, J. A.: Load bearing characteristics of the patello-femoral joint. Acta Orthop. Scandinavica,48: 511-516, 1977.48511 1977

193

Mauerhan, D. R.; Nelson, C. L.; Smith, D. L.; Fitzgerald, R. H., Jr.; Slama, T. G.; Petty, R. W.; Jones, R. E.; and |and |Evans, R. P.: Prophylaxis against infection in total joint arthroplasty. One day of cefuroxime compared with three days of cefazolin. J. Bone and Joint Surg.,76-A: 39-45, Jan. 1994.76-A39 1994

194

Mazas, F. B.: Guepar total knee prosthesis. Clin. Orthop.,94: 211-221, 1973.94211 1973 [PubMed]

195

Merkel, K. D., and |and |Johnson, E. W., Jr.: Supracondylar fracture of the femur after total knee arthroplasty. J. Bone and Joint Surg.,68-A: 29-43, Jan. 1986.68-A29 1986

196

Merkow, R. L.; Soudry, M.; and |and |Insall, J. N.: Patellar dislocation following total knee replacement. J. Bone and Joint Surg.,67-A: 1321-1327, Dec. 1985.67-A1321 1985

197

Mochizuki, R. M., and |and |Schurman, D. J.: Patellar complications following total knee arthroplasty. J. Bone and Joint Surg.,61-A: 879-883, Sept. 1979.61-A879 1979

198

Mont, M. A.; Dellon, A. L.; Chen, F.; Hungerford, M. W.; Krackow, K. A.; and |and |Hungerford, D. S.: The operative treatment of peroneal nerve palsy. J. Bone and Joint Surg.,78-A: 863-869, June 1996.78-A863 1996

199

Moreland, J. R.: Mechanisms of failure in total knee arthroplasty. Clin. Orthop.,226: 49-64, 1988.22649 1988 [PubMed]

200

Moreland, J. R.; Thomas, R. J.; and |and |Freeman, M. A. R.: ICLH replacement of the knee: 1977 and 1978. Clin. Orthop.,145: 47-59, 1979.14547 1979 [PubMed]

201

Morrison, J. B.: The forces transmitted by the human knee joint during activity. Thesis, University of Strathclyde, Strathclyde, Scotland, 1967.

202

Mosely, L. H.; Finseth, F.; and |and |Goody, M.: Nicotine and its effect on wound healing. Plast. and Reconstr. Surg.,61: 570-575, 1978.61570 1978

203

Muller, W.: The Knee—Form, Function, and Ligament Reconstruction, pp. 158-167. New York, Springer, 1982.

204

Murray, D. G., and |and |Webster, D. A.: The variable-axis knee prosthesis. Two-year follow-up study. J. Bone and Joint Surg.,63-A: 687-694, June 1981.63-A687 1981

205

National Institutes of Health Consensus Development Conference Statement: Prevention of venous thrombosis and pulmonary embolism. J. Am. Med. Assn.,256: 744-749, 1986.256744 1986

206

Nelson, C. L.: Prevention of sepsis. Clin. Orthop.,222: 66-72, 1987.22266 1987 [PubMed]

207

Nielsen, B. F.; Petersen, V. S.; and |and |Vanmarken, J. E: Fracture of the femur after knee arthroplasty. Acta Orthop. Scandinavica,59: 155-157, 1989.59155 1989

208

Nielsen, P. T.; Jorgensen, L. N.; Albrecht-Beste, E.; Leffers, A. M.; and |and |Rasmussen, L. S.: Lower thrombosis risk with epidural blockade in knee arthroplasty. Acta Orthop. Scandinavica,61: 29-31, 1990.6129 1990

209

Oishi, C. S.; Grady-Benson, J. C.; Otis, S. M.; Colwell, C. W., Jr.; and |and |Walker, R. H.: The clinical course of distal deep venous thrombosis after total hip and total knee arthroplasty, as determined with duplex ultrasonography. J. Bone and Joint Surg.,76-A: 1658-1663, Nov. 1994.76-A1658 1994

210

Parsley, B. S.; Engh, G. A.; and |and |Dwyer, K. A.: Preoperative flexion. Does it influence postoperative flexion after posterior-cruciate-retaining total knee arthroplasty?. Clin. Orthop.,275: 204-210, 1992.275204 1992 [PubMed]

211

Pellegrini, V. D., Jr.; Clement, D.; Lush-Ehmann, C.; Keller, G. S.; and |and |Evarts, C. M.: The natural history of thromboembolic disease following hospital discharge after total hip arthroplasty. Clin. Orthop.,333: 27-40, 1996.33327 1996 [PubMed]

212

Pellegrini, V. D., Jr.; Langhans, M. J.; Totterman, S.; Marder, V. J.; and |and |Francis, C. W.: Embolic complications of calf thrombosis following total hip arthroplasty. J. Arthroplasty,8: 449-457, 1993.8449 1993 [PubMed]

213

Perhala, R. S.; Wilke, W. S.; Clough, J. D.; and |and |Segal, A. M.: Local infectious complications following large joint replacement in rheumatoid arthritis patients treated with methotrexate versus those not treated with methotrexate. Arthrit. and Rheumat.,34: 146-152, 1991.34146 1991

214

Petty, W.; Bryan, R. S.; Coventry, M. B.; and |and |Peterson, L. F.: Infection after total knee arthroplasty. Orthop. Clin. North America,6: 1005-1014, 1975.61005 1975

215

Picetti, G. D., III; McGann, W. A.; and |and |Welch, R. B.: The patellofemoral joint after total knee arthroplasty without patellar resurfacing. J. Bone and Joint Surg.,72-A: 1379-1382, Oct. 1990.72-A1379 1990

216

Poss, R.; Thornhill, T. S.; Ewald, F. C.; Thomas, W. H.; Batte, N. J.; and |and |Sledge, C. B.: Factors influencing the incidence and outcome of infection following total joint arthroplasty. Clin. Orthop.,182: 117-126, 1984.182117 1984 [PubMed]

217

Pring, D. J.; Marks, L.; and |and |Angel, J. C.: Mobility after amputation for failed knee replacement. J. Bone and Joint Surg.,70-B(5): 770-771, 1988.70-B(5)770 1988

218

Puranen, J.; Kortelainen, P.; and |and |Jalovaara, P.: Arthrodesis of the knee with intramedullary nail fixation. J. Bone and Joint Surg.,72-A: 433-442, March 1990.72-A433 1990

219

Rabinov, K., and |and |Paulin, S.: Roentgen diagnosis of venous thrombosis in the leg. Arch. Surg.,104: 134-144, 1992.104134 1992

220

Radovan, C.: Tissue expansion in soft-tissue reconstruction. Plast. and Reconstr. Surg.,74: 482-492, 1984.74482 1984

221

Rae, P. J.; Noble, J.; and |and |Hodgkinson, J. P.: Patellar resurfacing in total condylar knee arthroplasty. Technique and results. J. Arthroplasty,5: 259-265, 1990.5259 1990 [PubMed]

222

Ranawat, C. S.: The patellofemoral joint in total condylar knee arthroplasty. Pros and cons based on five- to ten-year follow-up observations. Clin. Orthop.,205: 93-99, 1986.20593 1986 [PubMed]

223

Ranawat, C. S., and Flynn, W. F., J.: The stiff knee. In Knee Arthroplasty, pp. 141-159. Edited by P. A. Lotke. New York, Raven Press, 1995.

224

Ranawat, C. S.; Insall, J.; and |and |Shine, J.: Duo-condylar knee arthroplasty. Hospital for Special Surgery design. Clin. Orthop.,120: 76-82, 1976.12076 1976 [PubMed]

225

Ranawat, C. S.; Rose H. A.; and |and |Bryan, W. J.: Technique and results of replacement of the patello-femoral joint with total condylar knee arthroplasty. Orthop. Trans.,6: 88, 1982.688 1982

226

Ranawat, C. S.; Wilde, A. H.; and |and |Rovere, G. D.: A conversation with C. S. Ranawat, A. H. Wilde, and G. D. Rovere. Experience with the GUEPAR total-knee prosthesis. Orthop. Rev,5(11): 47-53, 1976.5(11)47 1976

227

Rand, J. A.: Patellar resurfacing in total knee arthroplasty. Clin. Orthop.,260: 110-117, 1990.260110 1990 [PubMed]

228

Rand, J.: Evaluation and management of infected total knee arthroplasty. Sem. Arthroplasty,5: 178-182, 1994.5178 1994

229

Rand, J. A., and |and |Brown, M. L.: The value of indium 111 leukocyte scanning in the evaluation of painful or infected total knee arthroplasties. Clin. Orthop.,259: 179-182, 1990.259179 1990 [PubMed]

230

Rand, J. A., and |and |Bryan, R. S.: Reimplantation for the salvage of an infected total knee arthroplasty. J. Bone and Joint Surg.,65-A: 1081-1086, Oct. 1983.65-A1081 1983

231

Rand, J. A., and |and |Gustilo, R. B.: Technique of patellar resurfacing in total knee arthroplasty. Tech. Orthop.,3: 57-66, 1988.357 1988

232

Rand, J. A.; Bryan, R. S.; and |and |Chao, E. Y.: Failed total knee arthroplasty treated by arthrodesis of the knee using the Ace-Fisher apparatus. J. Bone and Joint Surg.,69-A: 39-45, Jan. 1987.69-A39 1987

233

Rand, J. A.; Chao, E. Y.; and |and |Stauffer, R. N.: Kinematic rotating-hinge total knee arthroplasty. J. Bone and Joint Surg.,69-A: 489-497, April 1987.69-A489 1987

234

Rand, J. A.; Morrey, B. F.; and |and |Bryan, R. S.: Patellar tendon rupture after total knee arthroplasty. Clin. Orthop.,244: 233-238, 1989.244233 1989 [PubMed]

235

RD Heparin Arthroplasty Group: RD heparin compared with warfarin for prevention of venous thromboembolic disease following total hip or knee arthroplasty. J. Bone and Joint Surg.,76-A: 1174-1185, Aug. 1994.76-A1174 1994

236

Rees, T. D.; Liverett, D. M.; and |and |Guy, C. L.: The effect of cigarette smoking on skin-flap survival in the face lift patient. Plast. and Reconstr. Surg.,73: 911-915, 1984.73911 1984

237

Reilly, D. T., and |and |Martens, M.: Experimental analysis of the quadriceps muscle force and patello-femoral joint reaction force for various activities. Acta Orthop. Scandinavica,43: 126-137, 1972.43126 1972

238

Reilly, T. J.; Gradisar, I. A., Jr.; Pakan, W.; and |and |Reilly, M.: The use of postoperative suction drainage in total knee arthroplasty. Clin. Orthop.,208: 238-242, 1986.208238 1986 [PubMed]

239

Reuben, J. D.; McDonald, C. L.; Woodard, P. L.; and |and |Hennington, L. J.: Effect of patella thickness on patella strain following total knee arthroplasty. J. Arthroplasty,6: 251-258, 1991.6251 1991 [PubMed]

240

Rhoads, D. D.; Noble, P. C.; Reuben, J. D.; and |and |Tullos, H. S.: The effect of femoral component position on the kinematics of total knee arthroplasty. Clin. Orthop.,286: 122-129, 1993.286122 1993 [PubMed]

241

Riederman, R., and |and |Noyes, F. R.: Soft tissue skin expansion of contracted tissues prior to knee surgery. Am. J. Knee Surg.,4: 195-198, 1991.4195 1991

242

Ritter, M. A., and |and |Campbell, E. D.: Effect of range of motion on the success of total knee arthroplasty. J. Arthroplasty,2: 95-97, 1987.295 1987 [PubMed]

243

Ritter, M. A.; Faris, P. M.; and |and |Keating, E. M.: Anterior femoral notching and ipsilateral supracondylar femur fracture in total knee arthroplasty. J. Arthroplasty,3: 185-187, 1988.3185 1988 [PubMed]

244

Roffman, M.; Hirsh, D. M.; and |and |Mendes, D. G.: Fracture of the resurfaced patella in total knee replacement. Clin. Orthop.,148: 112-116, 1980.148112 1980 [PubMed]

245

Rolston, L. R.; Christ, D. J.; Halpern, A.; O'Connor, P. L.; Ryan, T. G.; and |and |Uggen, W. M.: Treatment of supracondylar fractures of the femur proximal to a total knee arthroplasty. A report of four cases. J. Bone and Joint Surg.,77-A: 924-931, June 1995.77-A924 1995

246

Romness, D. W., and |and |Rand, J. A.: The role of continuous passive motion following total knee arthroplasty. Clin. Orthop.,226: 34-37, 1988.22634 1988 [PubMed]

247

Rose, H. A., and Ranawat, C. S.: Total condylar knee arthroplasty—a three to eight year follow-up. Read at the Annual Meeting of The American Academy of Orthopaedic Surgeons, Anaheim, California, March 15, 1983.

248

Rose, H. A.; Hood, R. W.; Otis, J. C.; Ranawat, C. S.; and |and |Insall, J. N.: Peroneal-nerve palsy following total knee arthroplasty. A review of The Hospital for Special Surgery experience. J. Bone and Joint Surg.,64-A: 347-351, March 1982.64-A347 1982

249

Rosenberg, A. G.; Andriacchi, T. P.; Barden, R.; and |and |Galante, J. O.: Patellar component failure in cementless total knee arthroplasty. Clin. Orthop.,236: 106-114, 1988.236106 1988 [PubMed]

250

Rothaus, K. O., and Insall, J. N. The role of the delay procedure in patients with multiple prior knee incisions in decreasing the incidence of post-operative wound complications after total knee arthroplasty. Read at the Open Meeting of the Knee Society, New Orleans, Louisiana, Feb. 27. 1994.

251

Rubash, H. E.; Berger, R. A.; Britton, C. A.; Nettrour, W. S.; and |and |Seel, M. J.: Avoiding neurologic and vascular injuries with screw fixation of the tibial component in total knee arthroplasty. Clin. Orthop.,286: 56-63, 1993.28656 1993 [PubMed]

252

Rush, J. H.; Vidovich, J. D.; and |and |Johnson, M. A.: Arterial complications of total knee replacement. The Australian experience. J. Bone and Joint Surg.,69-B(3): 400-402, 1987.69-B(3)400 1987

253

Salibian, A. H., and |and |Anzel, S. H.: Salvage of an infected total knee prosthesis with medial and lateral gastrocnemius muscle flaps. A case report. J. Bone and Joint Surg.,65-A: 681-684, June 1983.65-A681 1983

254

Salvati, E. A.; Robinson, R. P.; Zeno, S. M.; Koslin, B. L.; Brause, B. D.; and |and |Wilson, P. D., Jr.: Infection rates after 3175 total hip and total knee replacements performed with and without a horizontal unidirectional filtered air-flow system. J. Bone and Joint Surg.,64-A: 525-535, April 1982.64-A525 1982

255

Sanders, R., and |and |O'Neill, T.: The gastrocnemius myocutaneous flap used as a cover for the exposed knee prosthesis. J. Bone and Joint Surg.,63-B(3): 383-386, 1981.63-B(3)383 1981

256

Sanders, R.; Regazzoni, P.; and |and |Ruedi, T. P.: Treatment of supracondylar-intracondylar fractures of the femur using the dynamic condylar screw. J. Orthop. Trauma,3: 214-222, 1989.3214 1989 [PubMed]

257

Scapinelli, R.: Blood supply of the human patella. Its relation to ischaemic necrosis after fracture. J. Bone and Joint Surg.,49-B(3): 563-570, 1967.49-B(3)563 1967

258

Scapinelli, R: Studies on the vasculature of the human knee joint. Acta Anatomica,70: 305-331, 1968.70305 1968 [PubMed]

259

Schatzker, J.: Supracondylar fractures of the femur. In The Rationale of Operative Fracture Care, pp. 255-273. Edited by J. Schatzker and M. Tile. New York, Springer, 1987.

260

Schatzker, J. Screws and plates and their application. In Manual of Internal Fixation: Techniques Recommended by the AO-ASIF Group, edited by M. E. Müller, M. Allgöwer, R. Schneider, and H. Willenegger. Ed. 3, pp. 179-290. New York, Springer, 1991.

261

Schoifet, S. D., and |and |Morrey, B. F.: Treatment of infection after total knee arthroplasty by débridement with retention of the components. J. Bone and Joint Surg.,72-A: 1383-1390, Oct. 1990.72-A1383 1990

262

Schurman, D. J.; Parker, J. N.; and |and |Ornstein, D.: Total condylar knee replacement. A study of factors influencing range of motion as late as two years after arthroplasty. J. Bone and Joint Surg.,67-A: 1006-1014, Sept. 1985.67-A1006 1985

263

Schwagerl, W.: Kraftschlussige Kniegelenksendoprothesen. Verhandl. Deutschen Gesellsch. Rheumatol,7: 160, 1981.7160 1981

264

Scott, R. D.: Prosthetic replacement of the patellofemoral joint. Orthop. Clin. North America,10: 129-137, 1979.10129 1979

265

Scott, R. D.; Turoff, N.; and |and |Ewald, F. C.: Stress fracture of the patella following duopatellar total knee arthroplasty with patellar resurfacing. Clin. Orthop.,170: 147-151, 1982.170147 1982 [PubMed]

266

Scott, W. N., and |and |Rubinstein, M.: Posterior stabilized knee arthroplasty. Six years' experience. Clin. Orthop.,205: 138-145, 1986.205138 1986 [PubMed]

267

Scott, W. N.; Rubinstein, M.; and |and |Scuderi, G.: Results after knee replacement with a posterior cruciate-substituting prosthesis. J. Bone and Joint Surg.,70-A: 1163-1173, Sept. 1988.70-A1163 1988

268

Scott, W. N.; Rozbruch, J. D.; Otis, J. C.; Insall, J.; Ranawat, C. S.; and |and |Burstein, A. H.: Clinical and biomechanical evaluation of patella replacement in total knee arthroplasty. Orthop. Trans.,2: 203, 1978.2203 1978

269

Scuderi, G. R.; Insall, J. N.; and |and |Scott, W. N.: Patellofemoral pain after total knee arthroplasty. J. Am. Acad. Orthop. Surg.,2: 239-246, 1994.2239 1994 [PubMed]

270

Scuderi, G.; Scharf, S. C.; Meltzer, L. P.; and |and |Scott, W. N.: The relationship of lateral releases to patella viability in total knee arthroplasty. J. Arthroplasty,2: 209-214, 1987.2209 1987 [PubMed]

271

Sculco, T. P. Local wound complications after total knee arthroplasty. In Total-Condylar Knee Arthroplasty: Technique, Results, and Complications, pp. 194-196. Edited by C. S. Ranawat. New York, Springer, 1985.

272

Sheehan, J. M.: Arthroplasty of the knee. Clin. Orthop.,145: 101-109, 1979.145101 1979 [PubMed]

273

Sikorski, J. M.; Hampson, W. G.; and |and |Staddon, G. E.: The natural history and aetiology of deep vein thrombosis after total hip replacement. J. Bone and Joint Surg.,63-B(2): 171-177, 1981.63-B(2)171 1981

274

Simison, A. J.; Noble, J.; and |and |Hardinge, K.: Complications of the Attenborough knee replacement. J. Bone and Joint Surg.,68-B(1): 100-105, 1986.68-B(1)100 1986

275

Sisto, D. J.; Lachiewicz, P. F.; and |and |Insall, J. N.: Treatment of supracondylar fractures following prosthetic arthroplasty of the knee. Clin. Orthop.,196: 265-272, 1985.196265 1985 [PubMed]

276

Sledge, C. B., and |and |Ewald, F. C.: Total knee arthroplasty experience at the Robert Breck Brigham Hospital. Clin. Orthop.,145: 78-84, 1979.14578 1979 [PubMed]

277

Sledge, C. B.; Stern, P.; Thomas, W. H.; Ewald, F. C.; Poss, R.; and |and |Scott, R. D.: Two year follow-up of the duocondylar total knee replacement. Orthop. Trans.,2: 193, 1978.2193 1978

278

Soudry, M.; Mestriner, L. A.; Binazzi, R.; and |and |Insall, J. N.: Total knee arthroplasty without patella resurfacing. Clin. Orthop.,205: 166-170, 1986.205166 1986 [PubMed]

279

Sprague, N. F., III; O'Connor, R. L.; and |and |Fox, J. M.: Arthroscopic treatment of postoperative knee fibroarthrosis. Clin. Orthop.,166: 165-172, 1982.166165 1982 [PubMed]

280

Steinberg, J.; Sledge, C. B.; Noble, J.; and |and |Stirrat, C. R.: A tissue-culture model of cartilage breakdown in rheumatoid arthritis. Quantitative aspects of proteoglycan release. Biochem. J,180: 403-412, 1979.180403 1979 [PubMed]

281

Stiehl, J. B.; Anouchi, Y.; Dennis, D. A.; Greenwald, A. S.; Krackow, K. A.; Rosenberg, A. G.; Stulberg, S. D.; and |and |Whiteside, L. A.: Symposium: revision total knee replacement. Contemp. Orthop.,30: 249-276, 1995.30249 1995 [PubMed]

282

Stulberg, B. N.; Insall, J. N.; Williams, G. W.; and |and |Ghelman, B.: Deep-vein thrombosis following total knee replacement. An analysis of six hundred and thirty-eight arthroplasties. J. Bone and Joint Surg.,66-A: 194-201, Feb. 1984.66-A194 1984

283

Stulberg, S. D.; Stulberg, B. N.; Hamati, Y.; and |and |Tsao, A.: Failure mechanisms of metal-backed patellar components. Clin. Orthop.,236: 88-105, 1988.23688 1988 [PubMed]

284

Thomas, B. J.; Moreland, J. R.; and |and |Amstutz, H. C.: Infection after total joint arthroplasty from distal extremity sepsis. Clin. Orthop.,181: 121-125, 1983.181121 1983 [PubMed]

285

Thompson, F. M.; Hood, R. W.; and |and |Insall, J.: Patellar fractures in total knee arthroplasty. Orthop. Trans.,5: 490-491, 1981.5490 1981

286

Thorburn, J.; Louden, J. R.; and |and |Vallance, R.: Spinal and general anaesthesia in total hip replacement: frequency of deep vein thrombosis. British J. Anesth.,52: 1117-1121, 1980.521117 1980

287

Thornhill, T. S.; Dalziel, R. W.; and |and |Sledge, C. B.: Alternatives to arthrodesis for the failed total knee arthroplasty. Clin. Orthop.,170: 131-140, 1982.170131 1982 [PubMed]

288

Thorpe, C. D.; Bocell, J. R.; and |and |Tullos, H. S.: Intra-articular fibrous bands. Patellar complications after total knee replacement. J. Bone and Joint Surg.,72-A: 811-814, July 1990.72-A811 1990

289

Tria, A. J., Jr.; Harwood, D. A.; Alicea, J. A.; and |and |Cody, R. P.: Patellar fractures in posterior stabilized knee arthroplasties. Clin. Orthop.,299: 131-138, 1994.299131 1994 [PubMed]

290

Turpie, A. G.: Enoxaparin prophylaxis in elective hip surgery. Acta Chir. Scandinavica,556: 103-107, 1990.556103 1990

291

Urayama, H.; Watanabe, Y.; and |and |Iwa, T. F.: Evaluation of claudicatory extremities by ankle blood pressure and muscle blood flow in exercise testing before and after operations. Vasc. Surg.,25: 1-7, 1991.251 1991

292

Vanhegan, J. A.; Dabrowski, W.; and |and |Arden, G. P.: A review of 100 Attenborough stabilised gliding knee prostheses. J. Bone and Joint Surg.,61-B(4): 445-450, 1979.61-B(4)445 1979

293

Vernace, J. V.; Rothman, R. H.; Booth, R. E., Jr.; and |and |Balderston, R. A.: Arthroscopic management of the patellar clunk syndrome following posterior stabilized total knee arthroplasty. J. Arthroplasty,4: 179-182, 1989.4179 1989 [PubMed]

294

Wahl, L. M.: Hormonal regulation of macrophage collagenase activity. Biochem. and Biophys. Res. Commun.,74: 838-845, 1977.74838 1977

295

Waisbrod, H., and |and |Treiman, N.: Intraosseous venography in patellofemoral disorders. A preliminary report. J. Bone and Joint Surg.,62-B(4): 454-456, 1980.62-B(4)454 1980

296

Wasilewski, S. A., and |and |Frankl, U.: Fracture of polyethylene of patellar component in total knee arthroplasty, diagnosed by arthroscopy. J. Arthroplasty,4 (Supplement): 19-S22, 1989.4 (Supplement)19 1989

297

Webster, D. A., and |and |Murray, D. G.: Complications of variable axis total knee arthroplasty. Clin. Orthop.,193: 160-167, 1985.193160 1985 [PubMed]

298

Weinzweig, N.; Dowden, R. V.; and |and |Stulberg, B. N.: The use of tissue expansion to allow reconstruction of the knee. A case report. J. Bone and Joint Surg.,69-A: 1238-1240, Oct. 1987.69-A1238 1987

299

Weiss, A. P., and |and |Krackow, K. A.: Persistent wound drainage after primary total knee arthroplasty. J. Arthroplasty,8: 285-289, 1993.8285 1993 [PubMed]

300

Wells, P. S.; Lensing, A. W.; Davidson, B. L.; Prins, M. H.; and |and |Hirsh, J.: Accuracy of ultrasound for the diagnosis of deep venous thrombosis in asymptomatic patients after orthopedic surgery. A meta-analysis. Ann. Intern. Med.,122: 47-53, 1995.12247 1995 [PubMed]

301

Werb, Z.: Biochemical actions of glucocorticoids on macrophages in culture. Specific inhibition of elastase, collagenase, and plasminogen activator secretion and effects on other metabolic functions. J. Exper. Med.,147: 1695-1712, 1978.1471695 1978

302

Westrich, G., and |and |Sculco, T.: Prophylaxis against deep venous thrombosis after total knee arthroplasty. Pneumatic plantar compression and aspirin compared with aspirin alone. J. Bone and Joint Surg.,78-A: 826-834, June 1996.78-A826 1996

303

Wetzner, S. M.; Bezreh, J. S.; Scott, R. D.; Bierbaum, B. E.; and |and |Newberg, A. H.: Bone scanning in the assessment of patellar viability following knee replacement. Clin. Orthop.,199: 215-219, 1985.199215 1985 [PubMed]

304

Wilde, A. H., and |and |Stearns, K. L.: Intramedullary fixation for arthrodesis of the knee after infected total knee arthroplasty. Clin. Orthop.,248: 87-92, 1989.24887 1989 [PubMed]

305

Willert, H.-G.; Ludwig, J.; and |and |Semlitsch, M.: Reaction of bone to methacrylate after hip arthroplasty. A long-term gross, light microscopic, and scanning electron microscopic study. J. Bone and Joint Surg.,56-A: 1368-1382, Oct. 1974.56-A1368 1974

306

Wilson, M. G.; Kelley, K.; and |and |Thornhill, T. S.: Infection as a complication of total knee-replacement arthroplasty. Risk factors and treatment in sixty-seven cases. J. Bone and Joint Surg.,72-A: 878-883, July 1990.72-A878 1990

307

Windsor, R. E., and |and |Bono, J. V.: Infected total knee replacements. J. Am. Acad. Orthop. Surg.,2: 44-53, 1994.244 1994 [PubMed]

308

Windsor, R. E.; Insall, J. N.; and |and |Vince, K. G.: Technical consideration of total knee arthroplasty after proximal tibial osteotomy. J. Bone and Joint Surg.,70-A: 547-555, April 1988.70-A547 1988

309

Windsor, R. E.; Scuderi, G. R.; and |and |Insall, J. N.: Patellar fractures in total knee arthroplasty. J. Arthroplasty,4 (Supplement): 63-S67, 1989.4 (Supplement)63 1989

310

Windsor, R. E.; Insall, J. N.; Urs, W. K.; Miller, D. V.; and |and |Brause, B. D.: Two-stage reimplantation for the salvage of total knee arthroplasty complicated by infection. Further follow-up and refinement of indications. J. Bone and Joint Surg.,72-A: 272-278, Feb. 1990.72-A272 1990

311

Wong, R. Y.; Lotke, P. A.; and |and |Ecker, M. L.: Factors influencing wound healing after total knee arthroplasty. Orthop. Trans.,10: 497, 1986.10497 1986

312

Wright, T. M., and |and |Bartel, D. L.: The problem of surface damage in polyethylene total knee components. Clin. Orthop.,205: 67-74, 1986.20567 1986 [PubMed]

313

Zehntner, M. K., and |and |Ganz, R.: Internal fixation of supracondylar fractures after condylar total knee arthroplasty. Clin. Orthop.,293: 219-224, 1993.293219 1993 [PubMed]

Topics

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 2 Diagram demonstrating internal rotation of the femoral component, which moves the trochlear groove medially in relation to the patella.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 4-B The intraosseous vascular system. QT = quadriceps tendon, MP = mid-patellar, and P = polar.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 5-A and 5-B: Lateral radiographs of a knee that was treated with a metal-backed patellar component. Fig. 5-A: Radiograph demonstrating early angulation of the pegs of the patellar component.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 5-B: Subsequent radiograph demonstrating a peg-plate fracture.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 6-A, 6-B, and 6-C: Patellar clunk syndrome. Fig. 6-A: Diagram demonstrating a suprapatellar fibrous nodule entrapped within the intercondylar notch during flexion of the knee.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 6-B Diagram demonstrating how the fibrous nodule clunks out of the intercondylar notch with extension of the knee.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 6-C Intraoperative photograph demonstrating the suprapatellar fibrous nodule.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 7 Anteroposterior and lateral radiographs of a supracondylar fracture in a patient who had osteopenic bone.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 8-A through 8-D: Anteroposterior and lateral radiographs of an impacted supracondylar fracture proximal to a total knee replacement in a patient who had rheumatoid arthritis.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 8-A and 8-B: Before treatment. The normal alignment of the limb has been maintained.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 8-C After closed treatment, which led to an excellent result.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 8-D After closed treatment, which led to an excellent result.

View Large | Download Slide(.ppt)
Add to My JBJS

Figs. 9-A and 9-B: Before treatment.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 9-C Six months after operative stabilization with a locked supracondylar nail.

View Large | Download Slide(.ppt)
Add to My JBJS

Fig. 9-D Six months after operative stabilization with a locked supracondylar nail.

View Large | Download Slide(.ppt)
Add to My JBJS

View Larger

TABLE I INTERCONDYLAR DISTANCE OF COMMONLY USED FEMORAL PROSTHESES

Manufacturer	Prosthesis	Intercondylar Distance
		(mm)
Biomet, Warsaw, Indiana	AGC	18
DePuy, Warsaw, Indiana	AMK	20
Howmedica, Rutherford, New Jersey	PCA	18
Johnson and Johnson, New Brunswick, New Jersey	PFC	20
Osteonics, Allendale, New Jersey	Omnifit	19
Smith and Nephew Richards, Memphis, Tennessee	Genesis	20
Zimmer, Warsaw, Indiana	IB-II	15

Add to My JBJS

TABLE I INTERCONDYLAR DISTANCE OF COMMONLY USED FEMORAL PROSTHESES

Manufacturer	Prosthesis	Intercondylar Distance
		(mm)
Biomet, Warsaw, Indiana	AGC	18
DePuy, Warsaw, Indiana	AMK	20
Howmedica, Rutherford, New Jersey	PCA	18
Johnson and Johnson, New Brunswick, New Jersey	PFC	20
Osteonics, Allendale, New Jersey	Omnifit	19
Smith and Nephew Richards, Memphis, Tennessee	Genesis	20
Zimmer, Warsaw, Indiana	IB-II	15