The Food and Drug Administration has granted priority review of olaratumab, in combination with doxorubicin, for the treatment of patients with advanced soft tissue sarcoma who unsuccessfully underwent prior radiotherapy or surgery for their cancer.

Olaratumab is a human IgG1 monoclonal antibody that directly targets tumor cells by disrupting the platelet-derived growth factor receptor alpha, a receptor that is believed to play a role in tumor growth and progression.

“We are hopeful that, if approved, olaratumab will provide a meaningful addition to the limited treatment options for this rare and difficult-to-treat disease,” Dr. Richard Gaynor, senior vice president of product development and medical affairs for Lilly Oncology, the maker of the drug, said in a written statement issued by company.

The biologics license application submission for olaratumab was based on a phase II clinical trial of 129 patients with metastatic or unresectable soft tissue sarcoma. Sixty-four patients were assigned to the treatment group and received both doxorubicin and olaratumab. Patients in this group continued to receive olaratumab through observed disease progression. Sixty-five patients were assigned to the control group and received only doxorubicin until disease progression was first observed. Patients who received olaratumab in addition to doxorubicin experienced a longer median progression-free survival, compared with patients who only received doxorubicin (6.6 months vs. 4.1 months; stratified hazard ratio, 0.672; 95% confidence interval, 0.442 to 1.021; P = .0615). The results of the phase II clinical trial were reported at the 2015 American Society of Clinical Oncology annual meeting and the 2015 Connective Tissue Oncology Society annual meeting.

The FDA previously granted olaratumab breakthrough therapy, fast track, and orphan drug designation.

[email protected]

On Twitter @jess_craig94

The Food and Drug Administration has granted priority review of olaratumab, in combination with doxorubicin, for the treatment of patients with advanced soft tissue sarcoma who unsuccessfully underwent prior radiotherapy or surgery for their cancer.

Olaratumab is a human IgG1 monoclonal antibody that directly targets tumor cells by disrupting the platelet-derived growth factor receptor alpha, a receptor that is believed to play a role in tumor growth and progression.

“We are hopeful that, if approved, olaratumab will provide a meaningful addition to the limited treatment options for this rare and difficult-to-treat disease,” Dr. Richard Gaynor, senior vice president of product development and medical affairs for Lilly Oncology, the maker of the drug, said in a written statement issued by company.

The biologics license application submission for olaratumab was based on a phase II clinical trial of 129 patients with metastatic or unresectable soft tissue sarcoma. Sixty-four patients were assigned to the treatment group and received both doxorubicin and olaratumab. Patients in this group continued to receive olaratumab through observed disease progression. Sixty-five patients were assigned to the control group and received only doxorubicin until disease progression was first observed. Patients who received olaratumab in addition to doxorubicin experienced a longer median progression-free survival, compared with patients who only received doxorubicin (6.6 months vs. 4.1 months; stratified hazard ratio, 0.672; 95% confidence interval, 0.442 to 1.021; P = .0615). The results of the phase II clinical trial were reported at the 2015 American Society of Clinical Oncology annual meeting and the 2015 Connective Tissue Oncology Society annual meeting.

The FDA previously granted olaratumab breakthrough therapy, fast track, and orphan drug designation.

[email protected]

On Twitter @jess_craig94

The Food and Drug Administration has granted priority review of olaratumab, in combination with doxorubicin, for the treatment of patients with advanced soft tissue sarcoma who unsuccessfully underwent prior radiotherapy or surgery for their cancer.

Olaratumab is a human IgG1 monoclonal antibody that directly targets tumor cells by disrupting the platelet-derived growth factor receptor alpha, a receptor that is believed to play a role in tumor growth and progression.

“We are hopeful that, if approved, olaratumab will provide a meaningful addition to the limited treatment options for this rare and difficult-to-treat disease,” Dr. Richard Gaynor, senior vice president of product development and medical affairs for Lilly Oncology, the maker of the drug, said in a written statement issued by company.

The biologics license application submission for olaratumab was based on a phase II clinical trial of 129 patients with metastatic or unresectable soft tissue sarcoma. Sixty-four patients were assigned to the treatment group and received both doxorubicin and olaratumab. Patients in this group continued to receive olaratumab through observed disease progression. Sixty-five patients were assigned to the control group and received only doxorubicin until disease progression was first observed. Patients who received olaratumab in addition to doxorubicin experienced a longer median progression-free survival, compared with patients who only received doxorubicin (6.6 months vs. 4.1 months; stratified hazard ratio, 0.672; 95% confidence interval, 0.442 to 1.021; P = .0615). The results of the phase II clinical trial were reported at the 2015 American Society of Clinical Oncology annual meeting and the 2015 Connective Tissue Oncology Society annual meeting.

The FDA previously granted olaratumab breakthrough therapy, fast track, and orphan drug designation.

[email protected]

On Twitter @jess_craig94

Hinge knee arthroplasty was introduced in the 1950s.¹ All 4 major ligaments were replaced by the hinge, which provided stabilization while allowing sagittal plane motion. Its goal was stability, not replication of normal kinematics. The addition of methyl methacrylate cement improved fixation and allowed surface design modifications that addressed normal articular motion. Implants such as the Gunston Polycentric,² the Duocondylar,³ and the Geometric⁴ resurfaced the medial and lateral compartments of the knee while preserving the cruciate ligaments. The implants were subject to greater translational forces without the hinge and loosening became a major problem despite the advances in cementing. It became evident in the 1970s that preservation of the cruciates complicated the procedure. Cruciate resection simplified the operation and allowed improved fixation. The ICLH prosthesis resected the cruciates and used the articular surface design to give stability to the knee.^5,6 The total condylar prosthesis had a “tibial” imminence that mimicked the shape of the tibial surface but also sacrificed both of the cruciate ligaments (Figure 1).

Designers recognized that the cruciate ligaments affected knee kinematics; however, they elected to sacrifice the anterior cruciate ligament (ACL) for surgical simplicity and implant longevity.⁶ In the early 1980s, both the cruciate-retaining (CR) total knee arthroplasty (TKA) (Figure 2) and posterior-stabilized (PS) TKA (Figure 3) designs addressed the posterior cruciate ligament (PCL) function. The PCL was preserved in the “cruciate-retaining” TKA, substituted in the “posterior-stabilized” TKA using a cam-post mechanism. The CR TKA designers believed that PCL preservation produced a more balanced knee with a more anatomical result, a more normal joint line, and better function, especially on stair climbing. The PS TKA designers admitted the value of posterior stabilization but argued that it was too difficult to consistently save the PCL in all cases, and that the PS knee was easier for surgeons to implant with more reliable roll back.⁷

The Geometric knee was developed in the 1970s to retain both cruciate ligaments.⁴ Unfortunately, it created a kinematic conflict by using a constrained articular surface design that prevented the motion required by the cruciate ligaments. This conflict resulted in tibial loosening and early failures. The compromised results decreased interest in the bicruciate-retaining (BCR) TKA designs, allowing the CR TKA and PS TKA designs to flourish for the next 20 years with little or no attempts to retain the ACL.

In the 1980s the BCR TKA design was pursued by Townley⁸ and Cartier.⁹ Townley⁸ believed that cruciate resection was a concession to “improper joint synchronization”⁸ and Cartier⁹ thought that cruciate preservation permitted more normal proprioception.⁹ Unlike prior BCR TKA designs, the mid-term clinical results were equal to or better than the standard CR TKA or PS TKA of the time, and 9- to 11-year follow-up demonstrated comparable outcomes.⁸ While these results highlighted the possibility of a BCR TKA, the surgical technique and failures of the Geometric knee discouraged surgeons from pursuing the BCR TKA.

Interest in cruciate-preserving knee arthroplasty returned with partial knee replacements, with patients reporting more normal proprioception and motion.¹⁰ The techniques became more popular with the introduction of the minimally invasive surgeries in the early 2000s and cruciate ligament preservation became a more interesting concept.^11,12 Some surgeons preserved the cruciates by using separate implants for the medial, lateral, and patellofemoral surfaces.¹⁰ These results were acceptable for the time but required considerable surgical talent and did not report 20-year results similar to the CR and PS knees.

Most prosthetic designs attempt to copy the normal knee anatomy. Using fluoroscopic studies and computer analysis, designers began to investigate the motion (or kinematics) of the normal knee and realized that despite the fact the TKA looked like the human knee, the designs were not kinematically correct.¹³

Although TKA successfully treats pain secondary to degenerative joint disease, many patients are unable to return to their prior level of function, with up to 20% reporting dissatisfaction with their level of activity.¹⁴ The observed differences in kinematics between a normal knee and a TKA may explain part of this discrepancy.

Normal Knee Motion

The tibiofemoral articulation in a normal knee follows a reproducible pattern of motion as the knee moves from extension to flexion. The lateral femoral condyle (LFC) translates posteriorly with a combination of rolling and sliding motion, while the medial femoral condyle (MFC) has minimal posterior translation and thus acts as a pivot for knee motion. The MFC is larger, less curved, and has a biphasic shape with 2 distinct radiuses of curvature that correspond to an “extension” and “flexion” facet. The transition between the MFC facets occurs at approximately 30° of flexion, whereby the contact point transfers posteriorly with little condylar translation.^15-17 In contrast, the LFC is smaller, has a single radius of curvature, and gradually translates posteriorly throughout flexion. Static magnetic resonance imaging of the knee from 0° to 120° shows an average of 19 mm posterior translation for the LFC and 2 mm for the MFC.^15-20

In deep flexion, beyond 130°, posterior translation continues for both condyles. The LFC experiences enough excursion to cause loss of joint congruity and partial posterior subluxation.^19,20 The MFC shows little additional posterior translation, yet it too loses joint congruity through condylar lift-off. Contact between the posterior horn of the medial meniscus and the posterior femoral condyle limits further flexion.^16,21

The difference in motion between the condyles leads to internal tibial rotation during flexion. The initial 10° of knee flexion produces 5° of internal rotation, and an additional 15° of internal tibial rotation occurs throughout the remainder of knee flexion.

Fluoroscopic imaging with computed tomography (CT)- or magnetic resonance (MR)-based modeling has shown the dynamic in vivo relationship of the tibiofemoral joint. Studies have confirmed significantly greater LFC posterior translation as compared to the MFC;²² however, in vivo studies have also shown notable variability in articular rotation and translation based on activity. This highlights the role of ligamentous tension and muscle contraction in kinematics.^21-23

The ACL in TKA

The majority of current TKA designs sacrifice the ACL without substituting for its function. The loss of the ACL has significant effects upon the kinematics of the knee.

The ACL is composed of 2 bundles, the anteromedial and posterolateral bundles, which originate on the LFC and insert broadly onto the tibial intercondylar eminence. Its primary role is to resist anterior tibial translation, particularly from 0° to 30° of flexion, which corresponds to the peak quadriceps force that pulls the tibia anteriorly.²⁴ ACL deficiency causes anterior tibial translation during early flexion and abnormal internal tibial rotation.^25-27 ACL deficient knees demonstrate a posterior femoral position in full extension, and increased MFC translation during knee flexion.^28-32

The role of the ACL in knee arthroplasty has been evaluated by comparing unicompartmental knee arthroplasty (UKA) with TKA, as a reflection of ACL preserving vs sacrificing procedures.^33-35 Sagittal plane translation is similar between UKA and normal knees,^33,34 while the CR TKA and PS TKA designs show anterior tibia subluxation in full extension.^33-35 The difference between UKA and TKA is greatest in extension, corresponding to the ACL functional range. These findings highlight kinematic similarities between TKA designs and the ACL deficient knee.

The majority of UKAs demonstrate near-normal kinematics. A small percentage of the study group demonstrated aberrant anterior tibial motion, highlighting a concern over ACL attenuation with time. Additionally, studies that evaluate the ACL in osteoarthritic knees have questioned the baseline integrity of the ACL.36 Yet the long-term outcomes in UKA design have shown preservation of kinematics due to intact cruciates.³⁷

The PCL in TKA

Because the majority of TKA designs sacrifice the ACL, the classic debate has focused on the utility of the native PCL. Both the CR and PS TKA are designed to offer posterior stabilization; however, kinematic studies have demonstrated notable differences.^38,39

The CR TKA design relies on the PCL to resist posterior sag and to prevent the hamstring musculature from pulling the tibia posteriorly during flexion. Studies have shown paradoxical anterior translation of both femoral condyles during flexion, particularly on the medial side of the knee.⁴⁰ There is also increased variability in femoral rollback. It is unclear whether the PCL can function normally in the absence of the ACL, which causes the PCL to adapt a less anatomic vertical position. The PCL may also be unable to function significantly without the ACL because of pre-existing degenerative histological changes.⁴¹

The PS TKA utilizes a cam-post mechanism for posterior stabilization. In contrast to normal knee kinematics, this mechanism creates equal MFC and LFC posterior translation, 8 mm on average at 90° flexion.⁴⁰ The equivalent translation in PS designs contributes to decreased internal tibial rotation and an increased polyethylene wear at the post.

Role of Surface Geometry

The articular geometry of the knee plays an important role in normal knee kinematics. Initial TKA designs used a femoral component with a single radius of curvature for both femoral condyles.⁴²Current TKA designs that match the femoral component to the native femoral anatomy, by differing the medial and lateral condyle geometry, have demonstrated kinematics that better resemble a native knee.⁴³ Additional changes to the radius of curvature along the posterior facet of the femoral condyles may reduce impingement during deep flexion. These “high flex” designs have demonstrated equivalent range of motion in some studies⁴⁴ and improved weight-bearing motion in others.⁴⁵ Surface geometry is important but is not the entire answer to kinematics.

Advances in TKA Design

Knee motion is guided by multiple factors, including the tibiofemoral articular geometry, the surrounding soft tissue tension, and muscle tone. Bicruciate-substituting (BCS) TKA and BCR TKA are forms of evolution from the CR and PS TKA and attempt to respect the function of both cruciate ligaments and provide better kinematics.

The BCS TKA utilizes a modified cam-post articulation to provide both anterior and posterior stabilization (Figure 4).⁴⁶ The surgical approach remains the same and the implant geometry affects the motion. The BCS TKA design demonstrates femoral rollback at 90° with an average of 14 mm for the MFC and 23 mm for the LFC, and 10° internal tibial rotation.^46,47 Additionally, it provides increased sagittal stability during early flexion and an improved pivot shift (indicating improved anterior stabilization).

The BCR designs preserve both cruciates and provide anterior and posterior stabilization. Fluoroscopic imaging has demonstrated contact points in full extension, and posterior rollback at 90° flexion that more closely replicates the normal knee.⁴⁸

Design and Surgical Techniques for Bicruciate Knee Replacements

If all of the ligaments are preserved, the TKA surfaces must allow motion to be driven by the ligaments in combination with the surfaces alone. The femur can be designed anatomically with asymmetric condyles. The femoral box must allow for preservation of the tibial bone island without impinging upon the cruciate ligaments. The tibial surface must be minimally constrained with concavity medially and convexity laterally.

The bone island preservation does not permit a single-piece tibial polyethylene insert. Therefore, the inserts will replicate the UKA designs (Figure 5). The knee should allow greater range of motion with the possibility of heel to buttocks contact. This increased motion will lead to greater roll back of the femur on the tibia and can lead to subluxation of the femoral runner off of the tibial surface on the lateral side, mimicking the normal knee. This subluxation is desirable but may lead to increased wear of the polyethylene on the lateral side of the knee.

The instruments should be specific for the design but must also be user-friendly. The 2 major issues with the surgery are balancing the knee in full extension and flexion, and preservation of the tibial bone island. The preexisting knee deformity should be <10° in all planes to limit the amount of collateral ligament releases. The collaterals must be balanced in a similar fashion to the standard TKA. Flexion contracture can be treated with posterior capsular release around the cruciates or with an increased distal femoral resection (2 mm at the maximum).

It is important to size the femur correctly because it will be difficult to adjust the flexion gap on the tibial side. A 9-mm posterior medial femoral condyle resection is a reasonable guide if the condyle is not atrophic. However, the exact resection thickness will be implant-specific and should be correlated with the dimensions of the prosthesis being implanted. The tibial bone island must be properly rotated with respect to the center line (Akagi’s line)⁴⁹ and must not be undercut. The tibial instrument should include pins or blocks to prevent the sawblades from undercutting the island (Figure 6), as undermining leads to fracture in full extension. If undermining occurs, it may be possible to place a cancellous screw through the island and still preserve the ligaments. The integrity of the island is best tested by bringing the knee to full extension and checking for liftoff of the bone. If there is significant compromise of the island, the bone should be resected and either a CR or PS TKA can be implanted. Della Valle and colleagues⁵⁰ reported a 9.2% incidence (11 of 119 cases) of bone island fracture in their early experience with a BCR TKA and improved this to 1.9% (5/258 cases) after reassessing their technique.

The gap tension should be evaluated either with traditional spacer blocks or with tensioning devices on the medial and lateral side of the knee after the tibial resections are completed. The polyethylene inserts are anatomically different. It may be possible to vary the thickness from medial to lateral, but not in excess of 2 mm.

As the BCR surgical techniques evolve, the balancing and tibial resection may be refined through specialized instrumentation. Such “smart instruments” that incorporate gyros may expedite tibial alignment, and sensor devices may assist with gap balancing. Haptic surgical robotic guides may assist in the tibial resection, facilitating bone island preservation by avoiding any possibility of undermining. At present these assistive aides are not necessary for the operation but may play a future role.

Clinical Results of Knee Arthroplasties

The results of knee replacements improved steadily from the 1970s through the 1990s. The scoring systems were somewhat limited and there was little data on the perception of the patients. The prosthetic designs stabilized at the end of the 1990s with only minor modifications since the year 2000. The 20-year results show similar findings for both the CR and the PS designs. There is little evidence to suggest a clinical correlation with the observed kinematic differences between CR and PS TKA designs.^40,51-58 Multiple studies have demonstrated equivalent range of motion^38,39,59 and subjective outcome measures (Table 1).⁶⁰ A randomized prospective trial that compared kinematics and functional scores between the 2 designs failed to observe significant differences in function despite differences in kinematics.⁴⁶ Equivalence in clinical outcome was further supported by a Cochrane Review meta-analysis that evaluated 1810 patients in 17 selected studies.⁶¹ The Knee Society scores have all been in the 92% to 95% ratings with survivals between 90% and 95%.

However, only 80% to 90% of patients are fully satisfied with their implants. The reasons for the dissatisfaction include unexplained anterior knee pain, stiffness, unexplained swelling, loss of range of motion, changes in proprioception, and loss of preoperative functions.¹⁴

The mid-term results of the BCR knees that were performed in the 1980s showed similar results to the CR and PS knees. Townley⁸ reported excellent clinical results with only 2% loosening at 2 to 11 years after surgery. Cloutier and colleagues9 reported 95% survival with improved proprioception at 9 to 11 years after surgery(Table 2).^62,63

Studies comparing traditional TKA designs with cruciate preserving designs, both UKA and BCR, have found differences in subjective outcomes.^62,64 Comparison of UKA and TKA in the same patient demonstrated significant preference for UKA, particularly with stair-climbing.⁶⁵ Similarly, comparison between BCR and PS TKA or CR TKA demonstrated preference for BCR in 85% of patients.⁶²

The new BCR knee designs have just started to come to the market.⁵⁰ The surgical techniques are much improved over the 1980s and cruciate preservation is certainly much easier now. The new designs can produce full range of motion with kinematics that are almost identical to the normal knee in the cadaver laboratory and in computer analyses. These designs certainly should have a similar 20-year survival to the original BCR knees. However, the critical evaluation will be the patient satisfaction scores. With greater motion, better kinematics, and more precise balancing the scores would improve with these designs.

Conclusion

The cruciate ligaments of the knee are central to control of the motion of the normal knee. TKA is a successful operation with at least a 40- to 50-year history. The techniques have continued to develop but 15% to 20% of patients are dissatisfied with the results.¹⁴ Evaluations of the prostheses are more sophisticated and kinematics appears to have a central position in the evaluation. If the knee is to move more anatomically correctly, all of the ligaments must be preserved. Proprioception certainly plays a role in the patient’s judgment of the result. History has shown that a BCR knee can be implanted with good mid-term results and it should certainly be possible to build on these results and design a knee that will incorporate all of the ligaments with full range of motion and increased levels of activity.

Hinge knee arthroplasty was introduced in the 1950s.¹ All 4 major ligaments were replaced by the hinge, which provided stabilization while allowing sagittal plane motion. Its goal was stability, not replication of normal kinematics. The addition of methyl methacrylate cement improved fixation and allowed surface design modifications that addressed normal articular motion. Implants such as the Gunston Polycentric,² the Duocondylar,³ and the Geometric⁴ resurfaced the medial and lateral compartments of the knee while preserving the cruciate ligaments. The implants were subject to greater translational forces without the hinge and loosening became a major problem despite the advances in cementing. It became evident in the 1970s that preservation of the cruciates complicated the procedure. Cruciate resection simplified the operation and allowed improved fixation. The ICLH prosthesis resected the cruciates and used the articular surface design to give stability to the knee.^5,6 The total condylar prosthesis had a “tibial” imminence that mimicked the shape of the tibial surface but also sacrificed both of the cruciate ligaments (Figure 1).

Designers recognized that the cruciate ligaments affected knee kinematics; however, they elected to sacrifice the anterior cruciate ligament (ACL) for surgical simplicity and implant longevity.⁶ In the early 1980s, both the cruciate-retaining (CR) total knee arthroplasty (TKA) (Figure 2) and posterior-stabilized (PS) TKA (Figure 3) designs addressed the posterior cruciate ligament (PCL) function. The PCL was preserved in the “cruciate-retaining” TKA, substituted in the “posterior-stabilized” TKA using a cam-post mechanism. The CR TKA designers believed that PCL preservation produced a more balanced knee with a more anatomical result, a more normal joint line, and better function, especially on stair climbing. The PS TKA designers admitted the value of posterior stabilization but argued that it was too difficult to consistently save the PCL in all cases, and that the PS knee was easier for surgeons to implant with more reliable roll back.⁷

The Geometric knee was developed in the 1970s to retain both cruciate ligaments.⁴ Unfortunately, it created a kinematic conflict by using a constrained articular surface design that prevented the motion required by the cruciate ligaments. This conflict resulted in tibial loosening and early failures. The compromised results decreased interest in the bicruciate-retaining (BCR) TKA designs, allowing the CR TKA and PS TKA designs to flourish for the next 20 years with little or no attempts to retain the ACL.

In the 1980s the BCR TKA design was pursued by Townley⁸ and Cartier.⁹ Townley⁸ believed that cruciate resection was a concession to “improper joint synchronization”⁸ and Cartier⁹ thought that cruciate preservation permitted more normal proprioception.⁹ Unlike prior BCR TKA designs, the mid-term clinical results were equal to or better than the standard CR TKA or PS TKA of the time, and 9- to 11-year follow-up demonstrated comparable outcomes.⁸ While these results highlighted the possibility of a BCR TKA, the surgical technique and failures of the Geometric knee discouraged surgeons from pursuing the BCR TKA.

Interest in cruciate-preserving knee arthroplasty returned with partial knee replacements, with patients reporting more normal proprioception and motion.¹⁰ The techniques became more popular with the introduction of the minimally invasive surgeries in the early 2000s and cruciate ligament preservation became a more interesting concept.^11,12 Some surgeons preserved the cruciates by using separate implants for the medial, lateral, and patellofemoral surfaces.¹⁰ These results were acceptable for the time but required considerable surgical talent and did not report 20-year results similar to the CR and PS knees.

Most prosthetic designs attempt to copy the normal knee anatomy. Using fluoroscopic studies and computer analysis, designers began to investigate the motion (or kinematics) of the normal knee and realized that despite the fact the TKA looked like the human knee, the designs were not kinematically correct.¹³

Although TKA successfully treats pain secondary to degenerative joint disease, many patients are unable to return to their prior level of function, with up to 20% reporting dissatisfaction with their level of activity.¹⁴ The observed differences in kinematics between a normal knee and a TKA may explain part of this discrepancy.

Normal Knee Motion

The tibiofemoral articulation in a normal knee follows a reproducible pattern of motion as the knee moves from extension to flexion. The lateral femoral condyle (LFC) translates posteriorly with a combination of rolling and sliding motion, while the medial femoral condyle (MFC) has minimal posterior translation and thus acts as a pivot for knee motion. The MFC is larger, less curved, and has a biphasic shape with 2 distinct radiuses of curvature that correspond to an “extension” and “flexion” facet. The transition between the MFC facets occurs at approximately 30° of flexion, whereby the contact point transfers posteriorly with little condylar translation.^15-17 In contrast, the LFC is smaller, has a single radius of curvature, and gradually translates posteriorly throughout flexion. Static magnetic resonance imaging of the knee from 0° to 120° shows an average of 19 mm posterior translation for the LFC and 2 mm for the MFC.^15-20

In deep flexion, beyond 130°, posterior translation continues for both condyles. The LFC experiences enough excursion to cause loss of joint congruity and partial posterior subluxation.^19,20 The MFC shows little additional posterior translation, yet it too loses joint congruity through condylar lift-off. Contact between the posterior horn of the medial meniscus and the posterior femoral condyle limits further flexion.^16,21

The difference in motion between the condyles leads to internal tibial rotation during flexion. The initial 10° of knee flexion produces 5° of internal rotation, and an additional 15° of internal tibial rotation occurs throughout the remainder of knee flexion.

Fluoroscopic imaging with computed tomography (CT)- or magnetic resonance (MR)-based modeling has shown the dynamic in vivo relationship of the tibiofemoral joint. Studies have confirmed significantly greater LFC posterior translation as compared to the MFC;²² however, in vivo studies have also shown notable variability in articular rotation and translation based on activity. This highlights the role of ligamentous tension and muscle contraction in kinematics.^21-23

The ACL in TKA

The majority of current TKA designs sacrifice the ACL without substituting for its function. The loss of the ACL has significant effects upon the kinematics of the knee.

The ACL is composed of 2 bundles, the anteromedial and posterolateral bundles, which originate on the LFC and insert broadly onto the tibial intercondylar eminence. Its primary role is to resist anterior tibial translation, particularly from 0° to 30° of flexion, which corresponds to the peak quadriceps force that pulls the tibia anteriorly.²⁴ ACL deficiency causes anterior tibial translation during early flexion and abnormal internal tibial rotation.^25-27 ACL deficient knees demonstrate a posterior femoral position in full extension, and increased MFC translation during knee flexion.^28-32

The role of the ACL in knee arthroplasty has been evaluated by comparing unicompartmental knee arthroplasty (UKA) with TKA, as a reflection of ACL preserving vs sacrificing procedures.^33-35 Sagittal plane translation is similar between UKA and normal knees,^33,34 while the CR TKA and PS TKA designs show anterior tibia subluxation in full extension.^33-35 The difference between UKA and TKA is greatest in extension, corresponding to the ACL functional range. These findings highlight kinematic similarities between TKA designs and the ACL deficient knee.

The majority of UKAs demonstrate near-normal kinematics. A small percentage of the study group demonstrated aberrant anterior tibial motion, highlighting a concern over ACL attenuation with time. Additionally, studies that evaluate the ACL in osteoarthritic knees have questioned the baseline integrity of the ACL.36 Yet the long-term outcomes in UKA design have shown preservation of kinematics due to intact cruciates.³⁷

The PCL in TKA

Because the majority of TKA designs sacrifice the ACL, the classic debate has focused on the utility of the native PCL. Both the CR and PS TKA are designed to offer posterior stabilization; however, kinematic studies have demonstrated notable differences.^38,39

The CR TKA design relies on the PCL to resist posterior sag and to prevent the hamstring musculature from pulling the tibia posteriorly during flexion. Studies have shown paradoxical anterior translation of both femoral condyles during flexion, particularly on the medial side of the knee.⁴⁰ There is also increased variability in femoral rollback. It is unclear whether the PCL can function normally in the absence of the ACL, which causes the PCL to adapt a less anatomic vertical position. The PCL may also be unable to function significantly without the ACL because of pre-existing degenerative histological changes.⁴¹

The PS TKA utilizes a cam-post mechanism for posterior stabilization. In contrast to normal knee kinematics, this mechanism creates equal MFC and LFC posterior translation, 8 mm on average at 90° flexion.⁴⁰ The equivalent translation in PS designs contributes to decreased internal tibial rotation and an increased polyethylene wear at the post.

Role of Surface Geometry

The articular geometry of the knee plays an important role in normal knee kinematics. Initial TKA designs used a femoral component with a single radius of curvature for both femoral condyles.⁴²Current TKA designs that match the femoral component to the native femoral anatomy, by differing the medial and lateral condyle geometry, have demonstrated kinematics that better resemble a native knee.⁴³ Additional changes to the radius of curvature along the posterior facet of the femoral condyles may reduce impingement during deep flexion. These “high flex” designs have demonstrated equivalent range of motion in some studies⁴⁴ and improved weight-bearing motion in others.⁴⁵ Surface geometry is important but is not the entire answer to kinematics.

Advances in TKA Design

Knee motion is guided by multiple factors, including the tibiofemoral articular geometry, the surrounding soft tissue tension, and muscle tone. Bicruciate-substituting (BCS) TKA and BCR TKA are forms of evolution from the CR and PS TKA and attempt to respect the function of both cruciate ligaments and provide better kinematics.

The BCS TKA utilizes a modified cam-post articulation to provide both anterior and posterior stabilization (Figure 4).⁴⁶ The surgical approach remains the same and the implant geometry affects the motion. The BCS TKA design demonstrates femoral rollback at 90° with an average of 14 mm for the MFC and 23 mm for the LFC, and 10° internal tibial rotation.^46,47 Additionally, it provides increased sagittal stability during early flexion and an improved pivot shift (indicating improved anterior stabilization).

The BCR designs preserve both cruciates and provide anterior and posterior stabilization. Fluoroscopic imaging has demonstrated contact points in full extension, and posterior rollback at 90° flexion that more closely replicates the normal knee.⁴⁸

Design and Surgical Techniques for Bicruciate Knee Replacements

If all of the ligaments are preserved, the TKA surfaces must allow motion to be driven by the ligaments in combination with the surfaces alone. The femur can be designed anatomically with asymmetric condyles. The femoral box must allow for preservation of the tibial bone island without impinging upon the cruciate ligaments. The tibial surface must be minimally constrained with concavity medially and convexity laterally.

The bone island preservation does not permit a single-piece tibial polyethylene insert. Therefore, the inserts will replicate the UKA designs (Figure 5). The knee should allow greater range of motion with the possibility of heel to buttocks contact. This increased motion will lead to greater roll back of the femur on the tibia and can lead to subluxation of the femoral runner off of the tibial surface on the lateral side, mimicking the normal knee. This subluxation is desirable but may lead to increased wear of the polyethylene on the lateral side of the knee.

The instruments should be specific for the design but must also be user-friendly. The 2 major issues with the surgery are balancing the knee in full extension and flexion, and preservation of the tibial bone island. The preexisting knee deformity should be <10° in all planes to limit the amount of collateral ligament releases. The collaterals must be balanced in a similar fashion to the standard TKA. Flexion contracture can be treated with posterior capsular release around the cruciates or with an increased distal femoral resection (2 mm at the maximum).

It is important to size the femur correctly because it will be difficult to adjust the flexion gap on the tibial side. A 9-mm posterior medial femoral condyle resection is a reasonable guide if the condyle is not atrophic. However, the exact resection thickness will be implant-specific and should be correlated with the dimensions of the prosthesis being implanted. The tibial bone island must be properly rotated with respect to the center line (Akagi’s line)⁴⁹ and must not be undercut. The tibial instrument should include pins or blocks to prevent the sawblades from undercutting the island (Figure 6), as undermining leads to fracture in full extension. If undermining occurs, it may be possible to place a cancellous screw through the island and still preserve the ligaments. The integrity of the island is best tested by bringing the knee to full extension and checking for liftoff of the bone. If there is significant compromise of the island, the bone should be resected and either a CR or PS TKA can be implanted. Della Valle and colleagues⁵⁰ reported a 9.2% incidence (11 of 119 cases) of bone island fracture in their early experience with a BCR TKA and improved this to 1.9% (5/258 cases) after reassessing their technique.

The gap tension should be evaluated either with traditional spacer blocks or with tensioning devices on the medial and lateral side of the knee after the tibial resections are completed. The polyethylene inserts are anatomically different. It may be possible to vary the thickness from medial to lateral, but not in excess of 2 mm.

As the BCR surgical techniques evolve, the balancing and tibial resection may be refined through specialized instrumentation. Such “smart instruments” that incorporate gyros may expedite tibial alignment, and sensor devices may assist with gap balancing. Haptic surgical robotic guides may assist in the tibial resection, facilitating bone island preservation by avoiding any possibility of undermining. At present these assistive aides are not necessary for the operation but may play a future role.

Clinical Results of Knee Arthroplasties

The results of knee replacements improved steadily from the 1970s through the 1990s. The scoring systems were somewhat limited and there was little data on the perception of the patients. The prosthetic designs stabilized at the end of the 1990s with only minor modifications since the year 2000. The 20-year results show similar findings for both the CR and the PS designs. There is little evidence to suggest a clinical correlation with the observed kinematic differences between CR and PS TKA designs.^40,51-58 Multiple studies have demonstrated equivalent range of motion^38,39,59 and subjective outcome measures (Table 1).⁶⁰ A randomized prospective trial that compared kinematics and functional scores between the 2 designs failed to observe significant differences in function despite differences in kinematics.⁴⁶ Equivalence in clinical outcome was further supported by a Cochrane Review meta-analysis that evaluated 1810 patients in 17 selected studies.⁶¹ The Knee Society scores have all been in the 92% to 95% ratings with survivals between 90% and 95%.

However, only 80% to 90% of patients are fully satisfied with their implants. The reasons for the dissatisfaction include unexplained anterior knee pain, stiffness, unexplained swelling, loss of range of motion, changes in proprioception, and loss of preoperative functions.¹⁴

The mid-term results of the BCR knees that were performed in the 1980s showed similar results to the CR and PS knees. Townley⁸ reported excellent clinical results with only 2% loosening at 2 to 11 years after surgery. Cloutier and colleagues9 reported 95% survival with improved proprioception at 9 to 11 years after surgery(Table 2).^62,63

Studies comparing traditional TKA designs with cruciate preserving designs, both UKA and BCR, have found differences in subjective outcomes.^62,64 Comparison of UKA and TKA in the same patient demonstrated significant preference for UKA, particularly with stair-climbing.⁶⁵ Similarly, comparison between BCR and PS TKA or CR TKA demonstrated preference for BCR in 85% of patients.⁶²

The new BCR knee designs have just started to come to the market.⁵⁰ The surgical techniques are much improved over the 1980s and cruciate preservation is certainly much easier now. The new designs can produce full range of motion with kinematics that are almost identical to the normal knee in the cadaver laboratory and in computer analyses. These designs certainly should have a similar 20-year survival to the original BCR knees. However, the critical evaluation will be the patient satisfaction scores. With greater motion, better kinematics, and more precise balancing the scores would improve with these designs.

Conclusion

The cruciate ligaments of the knee are central to control of the motion of the normal knee. TKA is a successful operation with at least a 40- to 50-year history. The techniques have continued to develop but 15% to 20% of patients are dissatisfied with the results.¹⁴ Evaluations of the prostheses are more sophisticated and kinematics appears to have a central position in the evaluation. If the knee is to move more anatomically correctly, all of the ligaments must be preserved. Proprioception certainly plays a role in the patient’s judgment of the result. History has shown that a BCR knee can be implanted with good mid-term results and it should certainly be possible to build on these results and design a knee that will incorporate all of the ligaments with full range of motion and increased levels of activity.

Hinge knee arthroplasty was introduced in the 1950s.¹ All 4 major ligaments were replaced by the hinge, which provided stabilization while allowing sagittal plane motion. Its goal was stability, not replication of normal kinematics. The addition of methyl methacrylate cement improved fixation and allowed surface design modifications that addressed normal articular motion. Implants such as the Gunston Polycentric,² the Duocondylar,³ and the Geometric⁴ resurfaced the medial and lateral compartments of the knee while preserving the cruciate ligaments. The implants were subject to greater translational forces without the hinge and loosening became a major problem despite the advances in cementing. It became evident in the 1970s that preservation of the cruciates complicated the procedure. Cruciate resection simplified the operation and allowed improved fixation. The ICLH prosthesis resected the cruciates and used the articular surface design to give stability to the knee.^5,6 The total condylar prosthesis had a “tibial” imminence that mimicked the shape of the tibial surface but also sacrificed both of the cruciate ligaments (Figure 1).

Designers recognized that the cruciate ligaments affected knee kinematics; however, they elected to sacrifice the anterior cruciate ligament (ACL) for surgical simplicity and implant longevity.⁶ In the early 1980s, both the cruciate-retaining (CR) total knee arthroplasty (TKA) (Figure 2) and posterior-stabilized (PS) TKA (Figure 3) designs addressed the posterior cruciate ligament (PCL) function. The PCL was preserved in the “cruciate-retaining” TKA, substituted in the “posterior-stabilized” TKA using a cam-post mechanism. The CR TKA designers believed that PCL preservation produced a more balanced knee with a more anatomical result, a more normal joint line, and better function, especially on stair climbing. The PS TKA designers admitted the value of posterior stabilization but argued that it was too difficult to consistently save the PCL in all cases, and that the PS knee was easier for surgeons to implant with more reliable roll back.⁷

The Geometric knee was developed in the 1970s to retain both cruciate ligaments.⁴ Unfortunately, it created a kinematic conflict by using a constrained articular surface design that prevented the motion required by the cruciate ligaments. This conflict resulted in tibial loosening and early failures. The compromised results decreased interest in the bicruciate-retaining (BCR) TKA designs, allowing the CR TKA and PS TKA designs to flourish for the next 20 years with little or no attempts to retain the ACL.

In the 1980s the BCR TKA design was pursued by Townley⁸ and Cartier.⁹ Townley⁸ believed that cruciate resection was a concession to “improper joint synchronization”⁸ and Cartier⁹ thought that cruciate preservation permitted more normal proprioception.⁹ Unlike prior BCR TKA designs, the mid-term clinical results were equal to or better than the standard CR TKA or PS TKA of the time, and 9- to 11-year follow-up demonstrated comparable outcomes.⁸ While these results highlighted the possibility of a BCR TKA, the surgical technique and failures of the Geometric knee discouraged surgeons from pursuing the BCR TKA.

Interest in cruciate-preserving knee arthroplasty returned with partial knee replacements, with patients reporting more normal proprioception and motion.¹⁰ The techniques became more popular with the introduction of the minimally invasive surgeries in the early 2000s and cruciate ligament preservation became a more interesting concept.^11,12 Some surgeons preserved the cruciates by using separate implants for the medial, lateral, and patellofemoral surfaces.¹⁰ These results were acceptable for the time but required considerable surgical talent and did not report 20-year results similar to the CR and PS knees.

Most prosthetic designs attempt to copy the normal knee anatomy. Using fluoroscopic studies and computer analysis, designers began to investigate the motion (or kinematics) of the normal knee and realized that despite the fact the TKA looked like the human knee, the designs were not kinematically correct.¹³

Although TKA successfully treats pain secondary to degenerative joint disease, many patients are unable to return to their prior level of function, with up to 20% reporting dissatisfaction with their level of activity.¹⁴ The observed differences in kinematics between a normal knee and a TKA may explain part of this discrepancy.

Normal Knee Motion

The tibiofemoral articulation in a normal knee follows a reproducible pattern of motion as the knee moves from extension to flexion. The lateral femoral condyle (LFC) translates posteriorly with a combination of rolling and sliding motion, while the medial femoral condyle (MFC) has minimal posterior translation and thus acts as a pivot for knee motion. The MFC is larger, less curved, and has a biphasic shape with 2 distinct radiuses of curvature that correspond to an “extension” and “flexion” facet. The transition between the MFC facets occurs at approximately 30° of flexion, whereby the contact point transfers posteriorly with little condylar translation.^15-17 In contrast, the LFC is smaller, has a single radius of curvature, and gradually translates posteriorly throughout flexion. Static magnetic resonance imaging of the knee from 0° to 120° shows an average of 19 mm posterior translation for the LFC and 2 mm for the MFC.^15-20

In deep flexion, beyond 130°, posterior translation continues for both condyles. The LFC experiences enough excursion to cause loss of joint congruity and partial posterior subluxation.^19,20 The MFC shows little additional posterior translation, yet it too loses joint congruity through condylar lift-off. Contact between the posterior horn of the medial meniscus and the posterior femoral condyle limits further flexion.^16,21

The difference in motion between the condyles leads to internal tibial rotation during flexion. The initial 10° of knee flexion produces 5° of internal rotation, and an additional 15° of internal tibial rotation occurs throughout the remainder of knee flexion.

Fluoroscopic imaging with computed tomography (CT)- or magnetic resonance (MR)-based modeling has shown the dynamic in vivo relationship of the tibiofemoral joint. Studies have confirmed significantly greater LFC posterior translation as compared to the MFC;²² however, in vivo studies have also shown notable variability in articular rotation and translation based on activity. This highlights the role of ligamentous tension and muscle contraction in kinematics.^21-23

The ACL in TKA

The majority of current TKA designs sacrifice the ACL without substituting for its function. The loss of the ACL has significant effects upon the kinematics of the knee.

The ACL is composed of 2 bundles, the anteromedial and posterolateral bundles, which originate on the LFC and insert broadly onto the tibial intercondylar eminence. Its primary role is to resist anterior tibial translation, particularly from 0° to 30° of flexion, which corresponds to the peak quadriceps force that pulls the tibia anteriorly.²⁴ ACL deficiency causes anterior tibial translation during early flexion and abnormal internal tibial rotation.^25-27 ACL deficient knees demonstrate a posterior femoral position in full extension, and increased MFC translation during knee flexion.^28-32

The role of the ACL in knee arthroplasty has been evaluated by comparing unicompartmental knee arthroplasty (UKA) with TKA, as a reflection of ACL preserving vs sacrificing procedures.^33-35 Sagittal plane translation is similar between UKA and normal knees,^33,34 while the CR TKA and PS TKA designs show anterior tibia subluxation in full extension.^33-35 The difference between UKA and TKA is greatest in extension, corresponding to the ACL functional range. These findings highlight kinematic similarities between TKA designs and the ACL deficient knee.

The majority of UKAs demonstrate near-normal kinematics. A small percentage of the study group demonstrated aberrant anterior tibial motion, highlighting a concern over ACL attenuation with time. Additionally, studies that evaluate the ACL in osteoarthritic knees have questioned the baseline integrity of the ACL.36 Yet the long-term outcomes in UKA design have shown preservation of kinematics due to intact cruciates.³⁷

The PCL in TKA

Because the majority of TKA designs sacrifice the ACL, the classic debate has focused on the utility of the native PCL. Both the CR and PS TKA are designed to offer posterior stabilization; however, kinematic studies have demonstrated notable differences.^38,39

The CR TKA design relies on the PCL to resist posterior sag and to prevent the hamstring musculature from pulling the tibia posteriorly during flexion. Studies have shown paradoxical anterior translation of both femoral condyles during flexion, particularly on the medial side of the knee.⁴⁰ There is also increased variability in femoral rollback. It is unclear whether the PCL can function normally in the absence of the ACL, which causes the PCL to adapt a less anatomic vertical position. The PCL may also be unable to function significantly without the ACL because of pre-existing degenerative histological changes.⁴¹

The PS TKA utilizes a cam-post mechanism for posterior stabilization. In contrast to normal knee kinematics, this mechanism creates equal MFC and LFC posterior translation, 8 mm on average at 90° flexion.⁴⁰ The equivalent translation in PS designs contributes to decreased internal tibial rotation and an increased polyethylene wear at the post.

Role of Surface Geometry

The articular geometry of the knee plays an important role in normal knee kinematics. Initial TKA designs used a femoral component with a single radius of curvature for both femoral condyles.⁴²Current TKA designs that match the femoral component to the native femoral anatomy, by differing the medial and lateral condyle geometry, have demonstrated kinematics that better resemble a native knee.⁴³ Additional changes to the radius of curvature along the posterior facet of the femoral condyles may reduce impingement during deep flexion. These “high flex” designs have demonstrated equivalent range of motion in some studies⁴⁴ and improved weight-bearing motion in others.⁴⁵ Surface geometry is important but is not the entire answer to kinematics.

Advances in TKA Design

Knee motion is guided by multiple factors, including the tibiofemoral articular geometry, the surrounding soft tissue tension, and muscle tone. Bicruciate-substituting (BCS) TKA and BCR TKA are forms of evolution from the CR and PS TKA and attempt to respect the function of both cruciate ligaments and provide better kinematics.

The BCS TKA utilizes a modified cam-post articulation to provide both anterior and posterior stabilization (Figure 4).⁴⁶ The surgical approach remains the same and the implant geometry affects the motion. The BCS TKA design demonstrates femoral rollback at 90° with an average of 14 mm for the MFC and 23 mm for the LFC, and 10° internal tibial rotation.^46,47 Additionally, it provides increased sagittal stability during early flexion and an improved pivot shift (indicating improved anterior stabilization).

The BCR designs preserve both cruciates and provide anterior and posterior stabilization. Fluoroscopic imaging has demonstrated contact points in full extension, and posterior rollback at 90° flexion that more closely replicates the normal knee.⁴⁸

Design and Surgical Techniques for Bicruciate Knee Replacements

If all of the ligaments are preserved, the TKA surfaces must allow motion to be driven by the ligaments in combination with the surfaces alone. The femur can be designed anatomically with asymmetric condyles. The femoral box must allow for preservation of the tibial bone island without impinging upon the cruciate ligaments. The tibial surface must be minimally constrained with concavity medially and convexity laterally.

The bone island preservation does not permit a single-piece tibial polyethylene insert. Therefore, the inserts will replicate the UKA designs (Figure 5). The knee should allow greater range of motion with the possibility of heel to buttocks contact. This increased motion will lead to greater roll back of the femur on the tibia and can lead to subluxation of the femoral runner off of the tibial surface on the lateral side, mimicking the normal knee. This subluxation is desirable but may lead to increased wear of the polyethylene on the lateral side of the knee.

The instruments should be specific for the design but must also be user-friendly. The 2 major issues with the surgery are balancing the knee in full extension and flexion, and preservation of the tibial bone island. The preexisting knee deformity should be <10° in all planes to limit the amount of collateral ligament releases. The collaterals must be balanced in a similar fashion to the standard TKA. Flexion contracture can be treated with posterior capsular release around the cruciates or with an increased distal femoral resection (2 mm at the maximum).

It is important to size the femur correctly because it will be difficult to adjust the flexion gap on the tibial side. A 9-mm posterior medial femoral condyle resection is a reasonable guide if the condyle is not atrophic. However, the exact resection thickness will be implant-specific and should be correlated with the dimensions of the prosthesis being implanted. The tibial bone island must be properly rotated with respect to the center line (Akagi’s line)⁴⁹ and must not be undercut. The tibial instrument should include pins or blocks to prevent the sawblades from undercutting the island (Figure 6), as undermining leads to fracture in full extension. If undermining occurs, it may be possible to place a cancellous screw through the island and still preserve the ligaments. The integrity of the island is best tested by bringing the knee to full extension and checking for liftoff of the bone. If there is significant compromise of the island, the bone should be resected and either a CR or PS TKA can be implanted. Della Valle and colleagues⁵⁰ reported a 9.2% incidence (11 of 119 cases) of bone island fracture in their early experience with a BCR TKA and improved this to 1.9% (5/258 cases) after reassessing their technique.

The gap tension should be evaluated either with traditional spacer blocks or with tensioning devices on the medial and lateral side of the knee after the tibial resections are completed. The polyethylene inserts are anatomically different. It may be possible to vary the thickness from medial to lateral, but not in excess of 2 mm.

As the BCR surgical techniques evolve, the balancing and tibial resection may be refined through specialized instrumentation. Such “smart instruments” that incorporate gyros may expedite tibial alignment, and sensor devices may assist with gap balancing. Haptic surgical robotic guides may assist in the tibial resection, facilitating bone island preservation by avoiding any possibility of undermining. At present these assistive aides are not necessary for the operation but may play a future role.

Clinical Results of Knee Arthroplasties

The results of knee replacements improved steadily from the 1970s through the 1990s. The scoring systems were somewhat limited and there was little data on the perception of the patients. The prosthetic designs stabilized at the end of the 1990s with only minor modifications since the year 2000. The 20-year results show similar findings for both the CR and the PS designs. There is little evidence to suggest a clinical correlation with the observed kinematic differences between CR and PS TKA designs.^40,51-58 Multiple studies have demonstrated equivalent range of motion^38,39,59 and subjective outcome measures (Table 1).⁶⁰ A randomized prospective trial that compared kinematics and functional scores between the 2 designs failed to observe significant differences in function despite differences in kinematics.⁴⁶ Equivalence in clinical outcome was further supported by a Cochrane Review meta-analysis that evaluated 1810 patients in 17 selected studies.⁶¹ The Knee Society scores have all been in the 92% to 95% ratings with survivals between 90% and 95%.

However, only 80% to 90% of patients are fully satisfied with their implants. The reasons for the dissatisfaction include unexplained anterior knee pain, stiffness, unexplained swelling, loss of range of motion, changes in proprioception, and loss of preoperative functions.¹⁴

The mid-term results of the BCR knees that were performed in the 1980s showed similar results to the CR and PS knees. Townley⁸ reported excellent clinical results with only 2% loosening at 2 to 11 years after surgery. Cloutier and colleagues9 reported 95% survival with improved proprioception at 9 to 11 years after surgery(Table 2).^62,63

Studies comparing traditional TKA designs with cruciate preserving designs, both UKA and BCR, have found differences in subjective outcomes.^62,64 Comparison of UKA and TKA in the same patient demonstrated significant preference for UKA, particularly with stair-climbing.⁶⁵ Similarly, comparison between BCR and PS TKA or CR TKA demonstrated preference for BCR in 85% of patients.⁶²

The new BCR knee designs have just started to come to the market.⁵⁰ The surgical techniques are much improved over the 1980s and cruciate preservation is certainly much easier now. The new designs can produce full range of motion with kinematics that are almost identical to the normal knee in the cadaver laboratory and in computer analyses. These designs certainly should have a similar 20-year survival to the original BCR knees. However, the critical evaluation will be the patient satisfaction scores. With greater motion, better kinematics, and more precise balancing the scores would improve with these designs.

Conclusion

The cruciate ligaments of the knee are central to control of the motion of the normal knee. TKA is a successful operation with at least a 40- to 50-year history. The techniques have continued to develop but 15% to 20% of patients are dissatisfied with the results.¹⁴ Evaluations of the prostheses are more sophisticated and kinematics appears to have a central position in the evaluation. If the knee is to move more anatomically correctly, all of the ligaments must be preserved. Proprioception certainly plays a role in the patient’s judgment of the result. History has shown that a BCR knee can be implanted with good mid-term results and it should certainly be possible to build on these results and design a knee that will incorporate all of the ligaments with full range of motion and increased levels of activity.

Nuchal-Type Fibroma

Nuchal-type fibroma (NTF) is a rare benign proliferation of the dermis and subcutis associated with diabetes mellitus and Gardner syndrome.^1,2 Forty-four percent of patients with NTF have diabetes mellitus.² The posterior aspect of the neck is the most frequently affected site, but lesions also may present on the upper back, lumbosacral area, buttocks, and face. Physical examination generally reveals an indurated, asymptomatic, ill-defined, 3-cm or smaller nodule that is hard and white, unencapsulated, and poorly circumscribed.

Histopathologic examination of NTF typically reveals a nodular paucicellular proliferation of thick collagen bundles with inconspicuous fibroblasts, radiation of collagenous septa into the subcutaneous fat, and entrapment of mature adipose tissue and small nerves (quiz image A). Collagen bundles are thickened with entrapment of adipose tissue without increased cellularity (quiz image B). S-100 staining can show the entrapped nerves.

Similar to NTF, sclerotic fibroma is a firm dermal nodule with histologic examination usually demonstrating a paucicellular collagenous tumor. In sclerotic fibromas, the collagen pattern resembles Vincent van Gogh’s painting “The Starry Night” and may be a marker for Cowden disease (Figure 1).³ Solitary fibrous tumors are distinguished by more hypercellular areas, patternless pattern, and staghorn-shaped blood vessels (Figure 2).⁴ Spindle cell lipoma classically demonstrates a mixture of mature adipocytes and bland spindle cells in a mucinous or fibrous background with thick collagen bundles with no storiform pattern (Figure 3). Some variants of spindle cell lipoma have minimal or no fat.⁵ All of these conditions have positive immunohistochemical staining for CD34.

However, dermatofibroma is CD34‒. Dermatofibroma is characterized by an interstitial spindle cell proliferation with a loose storiform pattern, collagen trapping at the outer edges of the tumor, overlying platelike acanthosis, and sometimes follicular induction (Figure 4).

Nuchal-type fibroma also can resemble scleredema. Both lesions can show increased and thickened collagen bundles without notable fibroblast proliferation; the difference is the occurrence of mucin in scleredema. However, incases of late-stage scleredema, mucin is not always demonstrated. Therefore, one can conclude that histologically NTF is closely associated with late-stage scleredema.⁶

Nuchal-Type Fibroma

Nuchal-type fibroma (NTF) is a rare benign proliferation of the dermis and subcutis associated with diabetes mellitus and Gardner syndrome.^1,2 Forty-four percent of patients with NTF have diabetes mellitus.² The posterior aspect of the neck is the most frequently affected site, but lesions also may present on the upper back, lumbosacral area, buttocks, and face. Physical examination generally reveals an indurated, asymptomatic, ill-defined, 3-cm or smaller nodule that is hard and white, unencapsulated, and poorly circumscribed.

Histopathologic examination of NTF typically reveals a nodular paucicellular proliferation of thick collagen bundles with inconspicuous fibroblasts, radiation of collagenous septa into the subcutaneous fat, and entrapment of mature adipose tissue and small nerves (quiz image A). Collagen bundles are thickened with entrapment of adipose tissue without increased cellularity (quiz image B). S-100 staining can show the entrapped nerves.

Similar to NTF, sclerotic fibroma is a firm dermal nodule with histologic examination usually demonstrating a paucicellular collagenous tumor. In sclerotic fibromas, the collagen pattern resembles Vincent van Gogh’s painting “The Starry Night” and may be a marker for Cowden disease (Figure 1).³ Solitary fibrous tumors are distinguished by more hypercellular areas, patternless pattern, and staghorn-shaped blood vessels (Figure 2).⁴ Spindle cell lipoma classically demonstrates a mixture of mature adipocytes and bland spindle cells in a mucinous or fibrous background with thick collagen bundles with no storiform pattern (Figure 3). Some variants of spindle cell lipoma have minimal or no fat.⁵ All of these conditions have positive immunohistochemical staining for CD34.

However, dermatofibroma is CD34‒. Dermatofibroma is characterized by an interstitial spindle cell proliferation with a loose storiform pattern, collagen trapping at the outer edges of the tumor, overlying platelike acanthosis, and sometimes follicular induction (Figure 4).

Nuchal-type fibroma also can resemble scleredema. Both lesions can show increased and thickened collagen bundles without notable fibroblast proliferation; the difference is the occurrence of mucin in scleredema. However, incases of late-stage scleredema, mucin is not always demonstrated. Therefore, one can conclude that histologically NTF is closely associated with late-stage scleredema.⁶

Nuchal-Type Fibroma

Nuchal-type fibroma (NTF) is a rare benign proliferation of the dermis and subcutis associated with diabetes mellitus and Gardner syndrome.^1,2 Forty-four percent of patients with NTF have diabetes mellitus.² The posterior aspect of the neck is the most frequently affected site, but lesions also may present on the upper back, lumbosacral area, buttocks, and face. Physical examination generally reveals an indurated, asymptomatic, ill-defined, 3-cm or smaller nodule that is hard and white, unencapsulated, and poorly circumscribed.

Histopathologic examination of NTF typically reveals a nodular paucicellular proliferation of thick collagen bundles with inconspicuous fibroblasts, radiation of collagenous septa into the subcutaneous fat, and entrapment of mature adipose tissue and small nerves (quiz image A). Collagen bundles are thickened with entrapment of adipose tissue without increased cellularity (quiz image B). S-100 staining can show the entrapped nerves.

Similar to NTF, sclerotic fibroma is a firm dermal nodule with histologic examination usually demonstrating a paucicellular collagenous tumor. In sclerotic fibromas, the collagen pattern resembles Vincent van Gogh’s painting “The Starry Night” and may be a marker for Cowden disease (Figure 1).³ Solitary fibrous tumors are distinguished by more hypercellular areas, patternless pattern, and staghorn-shaped blood vessels (Figure 2).⁴ Spindle cell lipoma classically demonstrates a mixture of mature adipocytes and bland spindle cells in a mucinous or fibrous background with thick collagen bundles with no storiform pattern (Figure 3). Some variants of spindle cell lipoma have minimal or no fat.⁵ All of these conditions have positive immunohistochemical staining for CD34.

However, dermatofibroma is CD34‒. Dermatofibroma is characterized by an interstitial spindle cell proliferation with a loose storiform pattern, collagen trapping at the outer edges of the tumor, overlying platelike acanthosis, and sometimes follicular induction (Figure 4).

Nuchal-type fibroma also can resemble scleredema. Both lesions can show increased and thickened collagen bundles without notable fibroblast proliferation; the difference is the occurrence of mucin in scleredema. However, incases of late-stage scleredema, mucin is not always demonstrated. Therefore, one can conclude that histologically NTF is closely associated with late-stage scleredema.⁶

[Editor's Note: Dr. Sales presents us with both points of view]

POINT: Fistula First for everyone? Sounds good to me

While “do no harm” may be a motto, the truth is, we strive to deliver the best care possible at every moment we interact with patients. There is no argument that an autogenous Arteriovenous Fisutla (AVF) is the best access available for patients—in terms of patency, freedom from intervention and resistance to infection. Thus, providing any other type of access—excluding the bridge catheter—is clearly a “second best” operation.

Other countries boast AVF rates in the upper 80% range and ESRD Network 16 (Alaska, Idaho, Montana, Oregon and Washington) in the U. S. has rates approaching 70%.

If that is the case, why then, does the U. S. still have an overall AVF rate of 63%? It is unlikely that the technical ability of surgeons outside the U. S. or in the upper left corner of our country differs from that of the remainder of the country. Fistula First embarked on a journey to bring this issue to the forefront. Following Drs. Larry Spergel and Tip Jennings advice, many surgeons took to the operating room in an effort to improve the AVF rates in the U. S. In fact, the numbers improved dramatically—but not to the 80+% mark.

Dr. Larry Scher assures us that every arm can have a fistula created and if you are a good interventionalist (or have a good one with whom to work) you can get all of these to mature.

Therefore, all of those 2-2.5mm veins that might not seem “usable,” should be anastomosed carefully to the radial or brachial artery—much as one would perform a distal anastomosis—and coax them into maturing to functional AVFs. If balloon assistance is needed for maturation, make certain the “balloon operator” has a good working knowledge of AV access, lest a nice, big hematoma will greet you, destroying your nicely created AVF. Those of us who cannot achieve the near 100% AVF rate must be technically challenged!

COUNTERPOINT: Fistula First is a bit overdone

Great idea, good execution, too much!

As an early ideologue in the Fistula First movement, I am proud of what we accomplished—education. We got the word out that AVFs were a better option than Arteriovenous Grafts! At the introductory meeting, I did have a rather animated “discussion” with a social worker who was convinced that the reason AVGs outnumbered AVFs was because AVGs reimbursed higher and therefore the surgeons were choosing the AVG for financial reasons (Sometimes it is really hard to maintain your composure!) While it may be true in some quarters, I would venture that was not the real reason affecting the inability of us, as a profession, to deliver the AVF rate that we should.

My alter ego above mentions Drs. Larry Spergel and Tip Jennings—both of whom should be given great credit for opening our eyes to the need for reform. They lead us and we improved. However, the number of AVFs that are being done that are NOT maturing has increased. Just as in any “cult phenomena,” when adherence to a concept supersedes rational thought, the endpoint is blurred. This is what has occurred in the Fistula First.

There are some patients who will never mature an AVF—irrespective of the competence of the vascular surgeon! Many of the veins are simply phlebitic from years of intravenous or venipuncture attacks—now that the PICC teams have learned where the basillic vein is, that vein is often problematic. Additionally, one factor that has never been adequately measured or characterized is skin turgor. Many of our older patients have awful skin turgor and any access (AVF or AVG) will be accompanied by ongoing post-dialysis hematomas with problems.

Our experience has been that octogenarians tend to do better with AVGs than AVFs—heresy to the Fistula First pundits. The number of catheter days is markedly reduced and the long-term outcomes do not vary much in this age group. And guess what, there are some patients who actually do well with a catheter!

Perhaps, two topics are worth mentioning in closing this self-debating article! Fistula First has, appropriately, been renamed Fistula First, Catheter Last! This recognizes the fact that maybe not everyone is a candidate for an AVF—but at the least we should avoid the catheter! The second, much larger issue is whether everyone that is dialyzed should, indeed, be dialyzed! I suspect all readers have been pressured into placing a catheter (or worse) in a patient who has no real chance for a meaningful survival. Additionally, maybe some patients would benefit from nutritional therapy that could delay the onset of dialysis by 6-18 months—imagine how much that would save to an already overburdened system!

Dr. Sales is President, The Cardiovascular Care Group, Westfield , N.J., chief, division of vascular surgery, Overlook Medical Center, Summit, N.J., and clinical assistant professor of Surgery, Mount Sinai School of Medicine, New York, N.Y. Both versions of Dr. Sales are an associate medical editor for Vascular Specialist.

[Editor's Note: Dr. Sales presents us with both points of view]

POINT: Fistula First for everyone? Sounds good to me

While “do no harm” may be a motto, the truth is, we strive to deliver the best care possible at every moment we interact with patients. There is no argument that an autogenous Arteriovenous Fisutla (AVF) is the best access available for patients—in terms of patency, freedom from intervention and resistance to infection. Thus, providing any other type of access—excluding the bridge catheter—is clearly a “second best” operation.

Other countries boast AVF rates in the upper 80% range and ESRD Network 16 (Alaska, Idaho, Montana, Oregon and Washington) in the U. S. has rates approaching 70%.

If that is the case, why then, does the U. S. still have an overall AVF rate of 63%? It is unlikely that the technical ability of surgeons outside the U. S. or in the upper left corner of our country differs from that of the remainder of the country. Fistula First embarked on a journey to bring this issue to the forefront. Following Drs. Larry Spergel and Tip Jennings advice, many surgeons took to the operating room in an effort to improve the AVF rates in the U. S. In fact, the numbers improved dramatically—but not to the 80+% mark.

Dr. Larry Scher assures us that every arm can have a fistula created and if you are a good interventionalist (or have a good one with whom to work) you can get all of these to mature.

Therefore, all of those 2-2.5mm veins that might not seem “usable,” should be anastomosed carefully to the radial or brachial artery—much as one would perform a distal anastomosis—and coax them into maturing to functional AVFs. If balloon assistance is needed for maturation, make certain the “balloon operator” has a good working knowledge of AV access, lest a nice, big hematoma will greet you, destroying your nicely created AVF. Those of us who cannot achieve the near 100% AVF rate must be technically challenged!

COUNTERPOINT: Fistula First is a bit overdone

Great idea, good execution, too much!

As an early ideologue in the Fistula First movement, I am proud of what we accomplished—education. We got the word out that AVFs were a better option than Arteriovenous Grafts! At the introductory meeting, I did have a rather animated “discussion” with a social worker who was convinced that the reason AVGs outnumbered AVFs was because AVGs reimbursed higher and therefore the surgeons were choosing the AVG for financial reasons (Sometimes it is really hard to maintain your composure!) While it may be true in some quarters, I would venture that was not the real reason affecting the inability of us, as a profession, to deliver the AVF rate that we should.

My alter ego above mentions Drs. Larry Spergel and Tip Jennings—both of whom should be given great credit for opening our eyes to the need for reform. They lead us and we improved. However, the number of AVFs that are being done that are NOT maturing has increased. Just as in any “cult phenomena,” when adherence to a concept supersedes rational thought, the endpoint is blurred. This is what has occurred in the Fistula First.

There are some patients who will never mature an AVF—irrespective of the competence of the vascular surgeon! Many of the veins are simply phlebitic from years of intravenous or venipuncture attacks—now that the PICC teams have learned where the basillic vein is, that vein is often problematic. Additionally, one factor that has never been adequately measured or characterized is skin turgor. Many of our older patients have awful skin turgor and any access (AVF or AVG) will be accompanied by ongoing post-dialysis hematomas with problems.

Our experience has been that octogenarians tend to do better with AVGs than AVFs—heresy to the Fistula First pundits. The number of catheter days is markedly reduced and the long-term outcomes do not vary much in this age group. And guess what, there are some patients who actually do well with a catheter!

Perhaps, two topics are worth mentioning in closing this self-debating article! Fistula First has, appropriately, been renamed Fistula First, Catheter Last! This recognizes the fact that maybe not everyone is a candidate for an AVF—but at the least we should avoid the catheter! The second, much larger issue is whether everyone that is dialyzed should, indeed, be dialyzed! I suspect all readers have been pressured into placing a catheter (or worse) in a patient who has no real chance for a meaningful survival. Additionally, maybe some patients would benefit from nutritional therapy that could delay the onset of dialysis by 6-18 months—imagine how much that would save to an already overburdened system!

Dr. Sales is President, The Cardiovascular Care Group, Westfield , N.J., chief, division of vascular surgery, Overlook Medical Center, Summit, N.J., and clinical assistant professor of Surgery, Mount Sinai School of Medicine, New York, N.Y. Both versions of Dr. Sales are an associate medical editor for Vascular Specialist.

[Editor's Note: Dr. Sales presents us with both points of view]

POINT: Fistula First for everyone? Sounds good to me

While “do no harm” may be a motto, the truth is, we strive to deliver the best care possible at every moment we interact with patients. There is no argument that an autogenous Arteriovenous Fisutla (AVF) is the best access available for patients—in terms of patency, freedom from intervention and resistance to infection. Thus, providing any other type of access—excluding the bridge catheter—is clearly a “second best” operation.

Other countries boast AVF rates in the upper 80% range and ESRD Network 16 (Alaska, Idaho, Montana, Oregon and Washington) in the U. S. has rates approaching 70%.

If that is the case, why then, does the U. S. still have an overall AVF rate of 63%? It is unlikely that the technical ability of surgeons outside the U. S. or in the upper left corner of our country differs from that of the remainder of the country. Fistula First embarked on a journey to bring this issue to the forefront. Following Drs. Larry Spergel and Tip Jennings advice, many surgeons took to the operating room in an effort to improve the AVF rates in the U. S. In fact, the numbers improved dramatically—but not to the 80+% mark.

Dr. Larry Scher assures us that every arm can have a fistula created and if you are a good interventionalist (or have a good one with whom to work) you can get all of these to mature.

Therefore, all of those 2-2.5mm veins that might not seem “usable,” should be anastomosed carefully to the radial or brachial artery—much as one would perform a distal anastomosis—and coax them into maturing to functional AVFs. If balloon assistance is needed for maturation, make certain the “balloon operator” has a good working knowledge of AV access, lest a nice, big hematoma will greet you, destroying your nicely created AVF. Those of us who cannot achieve the near 100% AVF rate must be technically challenged!

COUNTERPOINT: Fistula First is a bit overdone

Great idea, good execution, too much!

As an early ideologue in the Fistula First movement, I am proud of what we accomplished—education. We got the word out that AVFs were a better option than Arteriovenous Grafts! At the introductory meeting, I did have a rather animated “discussion” with a social worker who was convinced that the reason AVGs outnumbered AVFs was because AVGs reimbursed higher and therefore the surgeons were choosing the AVG for financial reasons (Sometimes it is really hard to maintain your composure!) While it may be true in some quarters, I would venture that was not the real reason affecting the inability of us, as a profession, to deliver the AVF rate that we should.

My alter ego above mentions Drs. Larry Spergel and Tip Jennings—both of whom should be given great credit for opening our eyes to the need for reform. They lead us and we improved. However, the number of AVFs that are being done that are NOT maturing has increased. Just as in any “cult phenomena,” when adherence to a concept supersedes rational thought, the endpoint is blurred. This is what has occurred in the Fistula First.

There are some patients who will never mature an AVF—irrespective of the competence of the vascular surgeon! Many of the veins are simply phlebitic from years of intravenous or venipuncture attacks—now that the PICC teams have learned where the basillic vein is, that vein is often problematic. Additionally, one factor that has never been adequately measured or characterized is skin turgor. Many of our older patients have awful skin turgor and any access (AVF or AVG) will be accompanied by ongoing post-dialysis hematomas with problems.

Our experience has been that octogenarians tend to do better with AVGs than AVFs—heresy to the Fistula First pundits. The number of catheter days is markedly reduced and the long-term outcomes do not vary much in this age group. And guess what, there are some patients who actually do well with a catheter!

Perhaps, two topics are worth mentioning in closing this self-debating article! Fistula First has, appropriately, been renamed Fistula First, Catheter Last! This recognizes the fact that maybe not everyone is a candidate for an AVF—but at the least we should avoid the catheter! The second, much larger issue is whether everyone that is dialyzed should, indeed, be dialyzed! I suspect all readers have been pressured into placing a catheter (or worse) in a patient who has no real chance for a meaningful survival. Additionally, maybe some patients would benefit from nutritional therapy that could delay the onset of dialysis by 6-18 months—imagine how much that would save to an already overburdened system!

Dr. Sales is President, The Cardiovascular Care Group, Westfield , N.J., chief, division of vascular surgery, Overlook Medical Center, Summit, N.J., and clinical assistant professor of Surgery, Mount Sinai School of Medicine, New York, N.Y. Both versions of Dr. Sales are an associate medical editor for Vascular Specialist.

Case Report

A 70-year-old man with history of coronary artery disease presented with a growing lesion on the right leg of 1 year’s duration. The lesion developed at a vein graft donor site for a coronary artery bypass that had been performed 18 years prior to presentation. The patient reported that the lesion was sensitive to touch. Physical examination revealed a 27-mm, firm, violaceous plaque on the medial aspect of the right upper shin (Figure 1). Mild pitting edema also was noted on both lower legs but was more prominent on the right leg. A 6-mm punch biopsy was performed.

Histology showed diffuse infiltration of the dermis and subcutaneous fat by intermediate-sized atypical blue cells with scant cytoplasm (Figure 2). The tumor exhibited moderate cytologic atypia with occasional mitotic figures, and lymphovascular invasion was present. Staining for CD3 was negative within the tumor, but a few reactive lymphocytes were highlighted at the periphery. Staining for CD20 and CD30 was negative. Strong and diffuse staining for cyto-keratin 20 and pan-cytokeratin was noted within the tumor with the distinctive perinuclear pattern characteristic of Merkel cell carcinoma (MCC). Staining for cytokeratin 7 was negative. Synaptophysin and chromogranin were strongly and diffusely positive within the tumor, consistent with a diagnosis of MCC.

The patient was found to have stage IIA (T2N0M0) MCC. Computed tomography completed for staging showed no evidence of metastasis. Wide local excision of the lesion was performed. Margins were negative, as was a right inguinal sentinel lymph node dissection. Because of the size of the tumor and the presence of lymphovascular invasion, radiation therapy at the primary tumor site was recommended. Local radiation treatment (200 cGy daily) was administered for a total dose of 5000 cGy over 5 weeks. The patient currently is free of recurrence or metastases and is being followed by the oncology, surgery, and dermatology departments.

Comment

Merkel cell carcinoma is a rare aggressive cutaneous malignancy. The exact pathogenesis is unknown, but immunosuppression and UV radiation, possibly through its immunosuppressive effects, appear to be contributing factors. More recently, the Merkel cell polyomavirus has been linked to MCC in approximately 80% of cases.^1,2

Merkel cell carcinoma is more common in individuals with fair skin, and the average age at diagnosis is 69 years.¹ Patients typically present with an asymptomatic, firm, erythematous or violaceous, dome-shaped nodule or a small indurated plaque, most commonly on sun-exposed areas of the head and neck followed by the upper and lower extremities including the hands, feet, ankles, and wrists. Fifteen percent to 20% of MCCs develop on the legs and feet.¹ Our patient presented with an MCC that developed on the right shin at a vein graft donor site.

The development of a cutaneous malignancy in a chronic wound (also known as a Marjolin ulcer) is a rare but well-recognized process. These malignancies occur in previously traumatized or chronically inflamed wounds and have been found to occur most commonly in chronic burn wounds, especially in ungrafted full-thickness burns. Squamous cell carcinomas (SCCs) are the most common malignancies to arise in chronic wounds, but basal cell carcinomas, adenocarcinomas, melanomas, malignant fibrous histiocytomas, adenoacanthomas, liposarcomas, and osteosarcomas also have been reported.³ There also have been a few reports of MCC associated with Bowen disease that developed in burn wounds.⁴ These malignancies generally occur years after injury (average, 35.5 years), but there have been reports of keratoacanthomas developing as early as 3 weeks after injury.^5,6

In some reports, malignancies in skin graft donor sites are differentiated from Marjolin ulcers, as the former appear in healed surgical wounds rather than in chronic unstable wounds and tend to occur sooner (ie, in weeks to months after graft harvesting).^7,8 The development of these malignancies in graft donor sites is not as well recognized and has been reported in donor sites for split-thickness skin grafts (STSGs), full-thickness skin grafts, tendon grafts, and bone grafts. In addition to malignancies that arise de novo, some develop due to metastatic and iatrogenic spread. The majority of reported malignancies in tendon and bone graft donor sites have been due to metastasis or iatrogenic spread.^9-14

Iatrogenic implantation of tumor cells is a well-recognized phenomenon. Hussain et al¹⁰ reported a case of implantation of SCC in an STSG donor site, most likely due to direct seeding from a hollow needle used to infiltrate local anesthetic in the tumor area and the STSG. In this case, metastasis could not be completely ruled out.¹⁰ There also have been reports of osteosarcoma, ameloblastoma, scirrhous carcinoma of the breast, and malignant fibrous histiocytoma thought to be implanted at bone graft donor sites.^14-17 Iatrogenic spread of malignancies can occur through seeding from contaminated gloves or instruments such as hollow bore needles or trocar placement in laparoscopic surgery.¹¹ Airborne spread also may be possible, as viable melanoma cells have been detected in electrocautery plume in mice.¹³

Metastatic malignancies including metastases from SCC, adenocarcinoma, melanoma, malignant fibrous histiocytoma, angiosarcoma, and osteosarcoma also have been reported to develop in graft donor sites.^11,13,18,19 Many malignancies thought to have developed from iatrogenic seeding may actually be from metastasis either by hematogenous or lymphatic spread. A possible contributing factor may be surgery-induced immunosuppression, which has been linked to increased tumor metastasis formation.²⁰ Surgery or trauma have been shown to have an effect on cellular components of the immune system, causing changes such as a shift in T lymphocytes toward immune-suppressive T lymphocytes and impaired function of natural killer cells, neutrophils, and macrophages.²⁰ The suppression of cell-mediated immunity has been shown to decrease over days to weeks in the postoperative period.²¹ In addition to surgery- or trauma-induced immunosuppression, the risk for metastasis may increase due to increased vascular, including lymphatic, flow toward a skin graft donor site.^13,16 Furthermore, trauma predisposes areas to a hypercoagulable state with increased sludging as well as increased platelet counts and fibrinogen levels, which may lead to localization of metastatic lesions.²² All of these factors could potentially work simultaneously to induce the development of metastasis in graft donor sites.

We found that SCCs and keratoacanthomas, which may be a variant of SCC, are among the only primary malignancies that have been reported to develop in skin graft donor sites.^6-8 Malignancies in these donor sites appear to develop sooner than those found in chronic wounds and are reported to develop within weeks to several months postoperatively, even in as few as 2 weeks.^6,8 Tamir et al⁶ reported 2 keratoacanthomas that developed simultaneously in a burn scar and STSG donor site. The investigators believed it could be a sign of reduced immune surveillance in the 2 affected areas.⁶ It has been hypothesized that one cause of local immune suppression in Marjolin ulcers could be due to poor lymphatic regeneration in scar tissue, which would prevent delivery of antigens and stimulated lymphocytes.²³ Haik et al⁷ considered this possibility when discussing a case of SCC that developed at the site of an STSG. The authors did not feel it applied, however, as the donor site had only undergone a single skin harvesting procedure.⁷ Ponnuvelu et al⁸ felt that inflammation was the underlying etiology behind the 2 cases they reported of SCCs that developed in STSG donor sites. The inflammation associated with tumors has many of the same processes involved in wound healing (eg, cellular proliferation, angiogenesis). Ponnuvelu et al⁸ hypothesized that the local inflammation caused by graft harvesting produced an ideal environment for early carcinogenesis. Although in chronic wounds it is believed that continual repair and regeneration in recurrent ulceration contributes to neoplastic initiation, it is thought that even a single injury may lead to malignant change, which may be because prior actinic damage or another cause has made the area more susceptible to these changes.^24,25 Surgery-induced immunosuppression also may play a role in development of primary malignancies in graft donor sites.

There have been a few reports of SCCs and basal cell carcinomas occurring in other surgical scars that healed without complications.^24,26-28 Similar to the malignancies in graft donor sites, some authors differentiate malignancies that occur in surgical scars that heal without complications from Marjolin ulcers, as they do not occur in chronically irritated wounds. These malignancies have been reported in scars from sternotomies, an infertility procedure, hair transplantation, thyroidectomy, colostomy, cleft lip repair, inguinal hernia repair, and paraumbilical laparoscopic port site. The time between surgery and diagnosis of malignancy ranged from 9 months to 67 years.^24,26-28 The development of malignancies in these surgical scars may be due to local immunosuppression, possibly from decreased lymphatic flow; additionally, the inflammation in wound healing may provide the ideal environment for carcinogenesis. Trauma in areas already susceptible to malignant change could be a contributing factor.

Conclusion

Our patient developed an MCC in a vein graft donor site 18 years after vein harvesting. It was likely a primary tumor, as vein harvesting was done for coronary artery bypass graft. There was no evidence of any other lesions on physical examination or computed tomography, making it doubtful that an MCC serving as a primary lesion for seeding or metastasis was present. If such a lesion had been present at that time, it would likely have spread well before the time of presentation to our clinic due to the fast doubling time and high rate of metastasis characteristic of MCCs, further lessening the possibility of metastasis or implantation.

The extended length of time from procedure to lesion development in our patient is much longer than for other reported malignancies in graft donor sites, but the reported time for malignancies in other postsurgical scars is more varied. Regardless of whether the MCC in our patient is classified as a Marjolin ulcer, the pathogenesis is unclear. It is thought that a single injury could lead to malignant change in predisposed skin. Our patient’s legs did not have any evidence of prior actinic damage; however, it is likely that he had local immune suppression, which may have made him more susceptible to these changes. It is unlikely that surgery-induced immunosuppression played a role in our patient, as specific cellular components of the immune system only appear to be affected over days to weeks in the postoperative period. Although poor lymphatic regeneration in scar tissue leading to decreased immune surveillance is not generally thought to contribute to malignancies in most surgical scars, our patient underwent vein harvesting. Chronic edema commonly occurs after vein harvesting and is believed to be due to trauma to the lymphatics. Local immune suppression also may have led to increased susceptibility to infection by the MCC polyomavirus, which has been found to be associated with many MCCs. In addition, the area may have been more susceptible to carcinogenesis due to changes from inflammation from wound healing. We suspect together these factors contributed to the development of our patient’s MCC. Although rare, graft donor sites should be examined periodically for the development of malignancy.

Case Report

A 70-year-old man with history of coronary artery disease presented with a growing lesion on the right leg of 1 year’s duration. The lesion developed at a vein graft donor site for a coronary artery bypass that had been performed 18 years prior to presentation. The patient reported that the lesion was sensitive to touch. Physical examination revealed a 27-mm, firm, violaceous plaque on the medial aspect of the right upper shin (Figure 1). Mild pitting edema also was noted on both lower legs but was more prominent on the right leg. A 6-mm punch biopsy was performed.

Histology showed diffuse infiltration of the dermis and subcutaneous fat by intermediate-sized atypical blue cells with scant cytoplasm (Figure 2). The tumor exhibited moderate cytologic atypia with occasional mitotic figures, and lymphovascular invasion was present. Staining for CD3 was negative within the tumor, but a few reactive lymphocytes were highlighted at the periphery. Staining for CD20 and CD30 was negative. Strong and diffuse staining for cyto-keratin 20 and pan-cytokeratin was noted within the tumor with the distinctive perinuclear pattern characteristic of Merkel cell carcinoma (MCC). Staining for cytokeratin 7 was negative. Synaptophysin and chromogranin were strongly and diffusely positive within the tumor, consistent with a diagnosis of MCC.

The patient was found to have stage IIA (T2N0M0) MCC. Computed tomography completed for staging showed no evidence of metastasis. Wide local excision of the lesion was performed. Margins were negative, as was a right inguinal sentinel lymph node dissection. Because of the size of the tumor and the presence of lymphovascular invasion, radiation therapy at the primary tumor site was recommended. Local radiation treatment (200 cGy daily) was administered for a total dose of 5000 cGy over 5 weeks. The patient currently is free of recurrence or metastases and is being followed by the oncology, surgery, and dermatology departments.

Comment

Merkel cell carcinoma is a rare aggressive cutaneous malignancy. The exact pathogenesis is unknown, but immunosuppression and UV radiation, possibly through its immunosuppressive effects, appear to be contributing factors. More recently, the Merkel cell polyomavirus has been linked to MCC in approximately 80% of cases.^1,2

Merkel cell carcinoma is more common in individuals with fair skin, and the average age at diagnosis is 69 years.¹ Patients typically present with an asymptomatic, firm, erythematous or violaceous, dome-shaped nodule or a small indurated plaque, most commonly on sun-exposed areas of the head and neck followed by the upper and lower extremities including the hands, feet, ankles, and wrists. Fifteen percent to 20% of MCCs develop on the legs and feet.¹ Our patient presented with an MCC that developed on the right shin at a vein graft donor site.

The development of a cutaneous malignancy in a chronic wound (also known as a Marjolin ulcer) is a rare but well-recognized process. These malignancies occur in previously traumatized or chronically inflamed wounds and have been found to occur most commonly in chronic burn wounds, especially in ungrafted full-thickness burns. Squamous cell carcinomas (SCCs) are the most common malignancies to arise in chronic wounds, but basal cell carcinomas, adenocarcinomas, melanomas, malignant fibrous histiocytomas, adenoacanthomas, liposarcomas, and osteosarcomas also have been reported.³ There also have been a few reports of MCC associated with Bowen disease that developed in burn wounds.⁴ These malignancies generally occur years after injury (average, 35.5 years), but there have been reports of keratoacanthomas developing as early as 3 weeks after injury.^5,6

In some reports, malignancies in skin graft donor sites are differentiated from Marjolin ulcers, as the former appear in healed surgical wounds rather than in chronic unstable wounds and tend to occur sooner (ie, in weeks to months after graft harvesting).^7,8 The development of these malignancies in graft donor sites is not as well recognized and has been reported in donor sites for split-thickness skin grafts (STSGs), full-thickness skin grafts, tendon grafts, and bone grafts. In addition to malignancies that arise de novo, some develop due to metastatic and iatrogenic spread. The majority of reported malignancies in tendon and bone graft donor sites have been due to metastasis or iatrogenic spread.^9-14

Iatrogenic implantation of tumor cells is a well-recognized phenomenon. Hussain et al¹⁰ reported a case of implantation of SCC in an STSG donor site, most likely due to direct seeding from a hollow needle used to infiltrate local anesthetic in the tumor area and the STSG. In this case, metastasis could not be completely ruled out.¹⁰ There also have been reports of osteosarcoma, ameloblastoma, scirrhous carcinoma of the breast, and malignant fibrous histiocytoma thought to be implanted at bone graft donor sites.^14-17 Iatrogenic spread of malignancies can occur through seeding from contaminated gloves or instruments such as hollow bore needles or trocar placement in laparoscopic surgery.¹¹ Airborne spread also may be possible, as viable melanoma cells have been detected in electrocautery plume in mice.¹³

Metastatic malignancies including metastases from SCC, adenocarcinoma, melanoma, malignant fibrous histiocytoma, angiosarcoma, and osteosarcoma also have been reported to develop in graft donor sites.^11,13,18,19 Many malignancies thought to have developed from iatrogenic seeding may actually be from metastasis either by hematogenous or lymphatic spread. A possible contributing factor may be surgery-induced immunosuppression, which has been linked to increased tumor metastasis formation.²⁰ Surgery or trauma have been shown to have an effect on cellular components of the immune system, causing changes such as a shift in T lymphocytes toward immune-suppressive T lymphocytes and impaired function of natural killer cells, neutrophils, and macrophages.²⁰ The suppression of cell-mediated immunity has been shown to decrease over days to weeks in the postoperative period.²¹ In addition to surgery- or trauma-induced immunosuppression, the risk for metastasis may increase due to increased vascular, including lymphatic, flow toward a skin graft donor site.^13,16 Furthermore, trauma predisposes areas to a hypercoagulable state with increased sludging as well as increased platelet counts and fibrinogen levels, which may lead to localization of metastatic lesions.²² All of these factors could potentially work simultaneously to induce the development of metastasis in graft donor sites.

We found that SCCs and keratoacanthomas, which may be a variant of SCC, are among the only primary malignancies that have been reported to develop in skin graft donor sites.^6-8 Malignancies in these donor sites appear to develop sooner than those found in chronic wounds and are reported to develop within weeks to several months postoperatively, even in as few as 2 weeks.^6,8 Tamir et al⁶ reported 2 keratoacanthomas that developed simultaneously in a burn scar and STSG donor site. The investigators believed it could be a sign of reduced immune surveillance in the 2 affected areas.⁶ It has been hypothesized that one cause of local immune suppression in Marjolin ulcers could be due to poor lymphatic regeneration in scar tissue, which would prevent delivery of antigens and stimulated lymphocytes.²³ Haik et al⁷ considered this possibility when discussing a case of SCC that developed at the site of an STSG. The authors did not feel it applied, however, as the donor site had only undergone a single skin harvesting procedure.⁷ Ponnuvelu et al⁸ felt that inflammation was the underlying etiology behind the 2 cases they reported of SCCs that developed in STSG donor sites. The inflammation associated with tumors has many of the same processes involved in wound healing (eg, cellular proliferation, angiogenesis). Ponnuvelu et al⁸ hypothesized that the local inflammation caused by graft harvesting produced an ideal environment for early carcinogenesis. Although in chronic wounds it is believed that continual repair and regeneration in recurrent ulceration contributes to neoplastic initiation, it is thought that even a single injury may lead to malignant change, which may be because prior actinic damage or another cause has made the area more susceptible to these changes.^24,25 Surgery-induced immunosuppression also may play a role in development of primary malignancies in graft donor sites.

There have been a few reports of SCCs and basal cell carcinomas occurring in other surgical scars that healed without complications.^24,26-28 Similar to the malignancies in graft donor sites, some authors differentiate malignancies that occur in surgical scars that heal without complications from Marjolin ulcers, as they do not occur in chronically irritated wounds. These malignancies have been reported in scars from sternotomies, an infertility procedure, hair transplantation, thyroidectomy, colostomy, cleft lip repair, inguinal hernia repair, and paraumbilical laparoscopic port site. The time between surgery and diagnosis of malignancy ranged from 9 months to 67 years.^24,26-28 The development of malignancies in these surgical scars may be due to local immunosuppression, possibly from decreased lymphatic flow; additionally, the inflammation in wound healing may provide the ideal environment for carcinogenesis. Trauma in areas already susceptible to malignant change could be a contributing factor.

Conclusion

Our patient developed an MCC in a vein graft donor site 18 years after vein harvesting. It was likely a primary tumor, as vein harvesting was done for coronary artery bypass graft. There was no evidence of any other lesions on physical examination or computed tomography, making it doubtful that an MCC serving as a primary lesion for seeding or metastasis was present. If such a lesion had been present at that time, it would likely have spread well before the time of presentation to our clinic due to the fast doubling time and high rate of metastasis characteristic of MCCs, further lessening the possibility of metastasis or implantation.

The extended length of time from procedure to lesion development in our patient is much longer than for other reported malignancies in graft donor sites, but the reported time for malignancies in other postsurgical scars is more varied. Regardless of whether the MCC in our patient is classified as a Marjolin ulcer, the pathogenesis is unclear. It is thought that a single injury could lead to malignant change in predisposed skin. Our patient’s legs did not have any evidence of prior actinic damage; however, it is likely that he had local immune suppression, which may have made him more susceptible to these changes. It is unlikely that surgery-induced immunosuppression played a role in our patient, as specific cellular components of the immune system only appear to be affected over days to weeks in the postoperative period. Although poor lymphatic regeneration in scar tissue leading to decreased immune surveillance is not generally thought to contribute to malignancies in most surgical scars, our patient underwent vein harvesting. Chronic edema commonly occurs after vein harvesting and is believed to be due to trauma to the lymphatics. Local immune suppression also may have led to increased susceptibility to infection by the MCC polyomavirus, which has been found to be associated with many MCCs. In addition, the area may have been more susceptible to carcinogenesis due to changes from inflammation from wound healing. We suspect together these factors contributed to the development of our patient’s MCC. Although rare, graft donor sites should be examined periodically for the development of malignancy.

Case Report

A 70-year-old man with history of coronary artery disease presented with a growing lesion on the right leg of 1 year’s duration. The lesion developed at a vein graft donor site for a coronary artery bypass that had been performed 18 years prior to presentation. The patient reported that the lesion was sensitive to touch. Physical examination revealed a 27-mm, firm, violaceous plaque on the medial aspect of the right upper shin (Figure 1). Mild pitting edema also was noted on both lower legs but was more prominent on the right leg. A 6-mm punch biopsy was performed.

Histology showed diffuse infiltration of the dermis and subcutaneous fat by intermediate-sized atypical blue cells with scant cytoplasm (Figure 2). The tumor exhibited moderate cytologic atypia with occasional mitotic figures, and lymphovascular invasion was present. Staining for CD3 was negative within the tumor, but a few reactive lymphocytes were highlighted at the periphery. Staining for CD20 and CD30 was negative. Strong and diffuse staining for cyto-keratin 20 and pan-cytokeratin was noted within the tumor with the distinctive perinuclear pattern characteristic of Merkel cell carcinoma (MCC). Staining for cytokeratin 7 was negative. Synaptophysin and chromogranin were strongly and diffusely positive within the tumor, consistent with a diagnosis of MCC.

The patient was found to have stage IIA (T2N0M0) MCC. Computed tomography completed for staging showed no evidence of metastasis. Wide local excision of the lesion was performed. Margins were negative, as was a right inguinal sentinel lymph node dissection. Because of the size of the tumor and the presence of lymphovascular invasion, radiation therapy at the primary tumor site was recommended. Local radiation treatment (200 cGy daily) was administered for a total dose of 5000 cGy over 5 weeks. The patient currently is free of recurrence or metastases and is being followed by the oncology, surgery, and dermatology departments.

Comment

Merkel cell carcinoma is a rare aggressive cutaneous malignancy. The exact pathogenesis is unknown, but immunosuppression and UV radiation, possibly through its immunosuppressive effects, appear to be contributing factors. More recently, the Merkel cell polyomavirus has been linked to MCC in approximately 80% of cases.^1,2

Merkel cell carcinoma is more common in individuals with fair skin, and the average age at diagnosis is 69 years.¹ Patients typically present with an asymptomatic, firm, erythematous or violaceous, dome-shaped nodule or a small indurated plaque, most commonly on sun-exposed areas of the head and neck followed by the upper and lower extremities including the hands, feet, ankles, and wrists. Fifteen percent to 20% of MCCs develop on the legs and feet.¹ Our patient presented with an MCC that developed on the right shin at a vein graft donor site.

The development of a cutaneous malignancy in a chronic wound (also known as a Marjolin ulcer) is a rare but well-recognized process. These malignancies occur in previously traumatized or chronically inflamed wounds and have been found to occur most commonly in chronic burn wounds, especially in ungrafted full-thickness burns. Squamous cell carcinomas (SCCs) are the most common malignancies to arise in chronic wounds, but basal cell carcinomas, adenocarcinomas, melanomas, malignant fibrous histiocytomas, adenoacanthomas, liposarcomas, and osteosarcomas also have been reported.³ There also have been a few reports of MCC associated with Bowen disease that developed in burn wounds.⁴ These malignancies generally occur years after injury (average, 35.5 years), but there have been reports of keratoacanthomas developing as early as 3 weeks after injury.^5,6

In some reports, malignancies in skin graft donor sites are differentiated from Marjolin ulcers, as the former appear in healed surgical wounds rather than in chronic unstable wounds and tend to occur sooner (ie, in weeks to months after graft harvesting).^7,8 The development of these malignancies in graft donor sites is not as well recognized and has been reported in donor sites for split-thickness skin grafts (STSGs), full-thickness skin grafts, tendon grafts, and bone grafts. In addition to malignancies that arise de novo, some develop due to metastatic and iatrogenic spread. The majority of reported malignancies in tendon and bone graft donor sites have been due to metastasis or iatrogenic spread.^9-14

Iatrogenic implantation of tumor cells is a well-recognized phenomenon. Hussain et al¹⁰ reported a case of implantation of SCC in an STSG donor site, most likely due to direct seeding from a hollow needle used to infiltrate local anesthetic in the tumor area and the STSG. In this case, metastasis could not be completely ruled out.¹⁰ There also have been reports of osteosarcoma, ameloblastoma, scirrhous carcinoma of the breast, and malignant fibrous histiocytoma thought to be implanted at bone graft donor sites.^14-17 Iatrogenic spread of malignancies can occur through seeding from contaminated gloves or instruments such as hollow bore needles or trocar placement in laparoscopic surgery.¹¹ Airborne spread also may be possible, as viable melanoma cells have been detected in electrocautery plume in mice.¹³

Metastatic malignancies including metastases from SCC, adenocarcinoma, melanoma, malignant fibrous histiocytoma, angiosarcoma, and osteosarcoma also have been reported to develop in graft donor sites.^11,13,18,19 Many malignancies thought to have developed from iatrogenic seeding may actually be from metastasis either by hematogenous or lymphatic spread. A possible contributing factor may be surgery-induced immunosuppression, which has been linked to increased tumor metastasis formation.²⁰ Surgery or trauma have been shown to have an effect on cellular components of the immune system, causing changes such as a shift in T lymphocytes toward immune-suppressive T lymphocytes and impaired function of natural killer cells, neutrophils, and macrophages.²⁰ The suppression of cell-mediated immunity has been shown to decrease over days to weeks in the postoperative period.²¹ In addition to surgery- or trauma-induced immunosuppression, the risk for metastasis may increase due to increased vascular, including lymphatic, flow toward a skin graft donor site.^13,16 Furthermore, trauma predisposes areas to a hypercoagulable state with increased sludging as well as increased platelet counts and fibrinogen levels, which may lead to localization of metastatic lesions.²² All of these factors could potentially work simultaneously to induce the development of metastasis in graft donor sites.

We found that SCCs and keratoacanthomas, which may be a variant of SCC, are among the only primary malignancies that have been reported to develop in skin graft donor sites.^6-8 Malignancies in these donor sites appear to develop sooner than those found in chronic wounds and are reported to develop within weeks to several months postoperatively, even in as few as 2 weeks.^6,8 Tamir et al⁶ reported 2 keratoacanthomas that developed simultaneously in a burn scar and STSG donor site. The investigators believed it could be a sign of reduced immune surveillance in the 2 affected areas.⁶ It has been hypothesized that one cause of local immune suppression in Marjolin ulcers could be due to poor lymphatic regeneration in scar tissue, which would prevent delivery of antigens and stimulated lymphocytes.²³ Haik et al⁷ considered this possibility when discussing a case of SCC that developed at the site of an STSG. The authors did not feel it applied, however, as the donor site had only undergone a single skin harvesting procedure.⁷ Ponnuvelu et al⁸ felt that inflammation was the underlying etiology behind the 2 cases they reported of SCCs that developed in STSG donor sites. The inflammation associated with tumors has many of the same processes involved in wound healing (eg, cellular proliferation, angiogenesis). Ponnuvelu et al⁸ hypothesized that the local inflammation caused by graft harvesting produced an ideal environment for early carcinogenesis. Although in chronic wounds it is believed that continual repair and regeneration in recurrent ulceration contributes to neoplastic initiation, it is thought that even a single injury may lead to malignant change, which may be because prior actinic damage or another cause has made the area more susceptible to these changes.^24,25 Surgery-induced immunosuppression also may play a role in development of primary malignancies in graft donor sites.

There have been a few reports of SCCs and basal cell carcinomas occurring in other surgical scars that healed without complications.^24,26-28 Similar to the malignancies in graft donor sites, some authors differentiate malignancies that occur in surgical scars that heal without complications from Marjolin ulcers, as they do not occur in chronically irritated wounds. These malignancies have been reported in scars from sternotomies, an infertility procedure, hair transplantation, thyroidectomy, colostomy, cleft lip repair, inguinal hernia repair, and paraumbilical laparoscopic port site. The time between surgery and diagnosis of malignancy ranged from 9 months to 67 years.^24,26-28 The development of malignancies in these surgical scars may be due to local immunosuppression, possibly from decreased lymphatic flow; additionally, the inflammation in wound healing may provide the ideal environment for carcinogenesis. Trauma in areas already susceptible to malignant change could be a contributing factor.

Conclusion

Our patient developed an MCC in a vein graft donor site 18 years after vein harvesting. It was likely a primary tumor, as vein harvesting was done for coronary artery bypass graft. There was no evidence of any other lesions on physical examination or computed tomography, making it doubtful that an MCC serving as a primary lesion for seeding or metastasis was present. If such a lesion had been present at that time, it would likely have spread well before the time of presentation to our clinic due to the fast doubling time and high rate of metastasis characteristic of MCCs, further lessening the possibility of metastasis or implantation.

The extended length of time from procedure to lesion development in our patient is much longer than for other reported malignancies in graft donor sites, but the reported time for malignancies in other postsurgical scars is more varied. Regardless of whether the MCC in our patient is classified as a Marjolin ulcer, the pathogenesis is unclear. It is thought that a single injury could lead to malignant change in predisposed skin. Our patient’s legs did not have any evidence of prior actinic damage; however, it is likely that he had local immune suppression, which may have made him more susceptible to these changes. It is unlikely that surgery-induced immunosuppression played a role in our patient, as specific cellular components of the immune system only appear to be affected over days to weeks in the postoperative period. Although poor lymphatic regeneration in scar tissue leading to decreased immune surveillance is not generally thought to contribute to malignancies in most surgical scars, our patient underwent vein harvesting. Chronic edema commonly occurs after vein harvesting and is believed to be due to trauma to the lymphatics. Local immune suppression also may have led to increased susceptibility to infection by the MCC polyomavirus, which has been found to be associated with many MCCs. In addition, the area may have been more susceptible to carcinogenesis due to changes from inflammation from wound healing. We suspect together these factors contributed to the development of our patient’s MCC. Although rare, graft donor sites should be examined periodically for the development of malignancy.

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The Diagnosis: Fibroepithelioma of Pinkus

Fibroepithelioma of Pinkus (FeP) was first described in 1953¹ and was thought to be premalignant as evidenced by the proposed name premalignant fibroepithelial tumor of the skin. This neoplasm now is largely believed to represent a rare form of basal cell carcinoma (BCC). Typical presentation is a smooth, flesh-colored or pink plaque or nodule.² Fibroepithelioma of Pinkus has a predilection for the lumbosacral back, though the groin also has been reported as a common site of incidence.^1,3 Similar to other BCCs, it is seen in older individuals, typically those older than 50 years.^3,4

Clinical diagnosis of FeP can be difficult. The differential diagnosis of FeP can include acrochordon, amelanotic melanoma, compound nevus, hemangioma, neurofibroma, nevus sebaceous, pyogenic granuloma, and seborrheic keratosis.⁵ Dermoscopic evaluation can aid in the diagnosis. A vascular network composed of fine arborizing vessels with or without dotted vessels and white streaks are characteristic findings of FeP. Patients with pigment also demonstrate structureless gray-brown areas and gray-blue dots.⁶

Biopsy with subsequent histopathologic evaluation confirms the diagnosis of FeP. The characteristic microscopic findings of thin eosinophilic epithelial strands with eccrine ducts anastomosing in an abundant fibromyxoid stroma with collections of basophilic cells located at the ends of the epithelial strands were demonstrated in our patient’s histopathologic specimen (Figure). The histologic appearance is similar to syringofibroadenoma of Mascaro. Recognition of basaloid nests, which often demonstrate retraction, and mitotic activity can differentiate FeP from syringofibroadenoma of Mascaro.⁷

Treatment of FeP is largely the same as other BCCs including destruction by electrodesiccation and curettage or complete removal by surgical excision. Several studies have demonstrated effective treatment of nonaggressive BCCs with curettage alone and subjectively reported improved cosmesis compared to electrodesiccation and curettage.^8-10 Although methyl aminolevulinate photodynamic therapy has demonstrated some therapeutic efficacy for superficial and nodular BCCs,¹¹ a case report utilizing the same modality for FeP did not provide adequate response.¹² However, adequate data are not available to assess potential use of this less invasive therapy.

The Diagnosis: Fibroepithelioma of Pinkus

Fibroepithelioma of Pinkus (FeP) was first described in 1953¹ and was thought to be premalignant as evidenced by the proposed name premalignant fibroepithelial tumor of the skin. This neoplasm now is largely believed to represent a rare form of basal cell carcinoma (BCC). Typical presentation is a smooth, flesh-colored or pink plaque or nodule.² Fibroepithelioma of Pinkus has a predilection for the lumbosacral back, though the groin also has been reported as a common site of incidence.^1,3 Similar to other BCCs, it is seen in older individuals, typically those older than 50 years.^3,4

Clinical diagnosis of FeP can be difficult. The differential diagnosis of FeP can include acrochordon, amelanotic melanoma, compound nevus, hemangioma, neurofibroma, nevus sebaceous, pyogenic granuloma, and seborrheic keratosis.⁵ Dermoscopic evaluation can aid in the diagnosis. A vascular network composed of fine arborizing vessels with or without dotted vessels and white streaks are characteristic findings of FeP. Patients with pigment also demonstrate structureless gray-brown areas and gray-blue dots.⁶

Biopsy with subsequent histopathologic evaluation confirms the diagnosis of FeP. The characteristic microscopic findings of thin eosinophilic epithelial strands with eccrine ducts anastomosing in an abundant fibromyxoid stroma with collections of basophilic cells located at the ends of the epithelial strands were demonstrated in our patient’s histopathologic specimen (Figure). The histologic appearance is similar to syringofibroadenoma of Mascaro. Recognition of basaloid nests, which often demonstrate retraction, and mitotic activity can differentiate FeP from syringofibroadenoma of Mascaro.⁷

Treatment of FeP is largely the same as other BCCs including destruction by electrodesiccation and curettage or complete removal by surgical excision. Several studies have demonstrated effective treatment of nonaggressive BCCs with curettage alone and subjectively reported improved cosmesis compared to electrodesiccation and curettage.^8-10 Although methyl aminolevulinate photodynamic therapy has demonstrated some therapeutic efficacy for superficial and nodular BCCs,¹¹ a case report utilizing the same modality for FeP did not provide adequate response.¹² However, adequate data are not available to assess potential use of this less invasive therapy.

The Diagnosis: Fibroepithelioma of Pinkus

Fibroepithelioma of Pinkus (FeP) was first described in 1953¹ and was thought to be premalignant as evidenced by the proposed name premalignant fibroepithelial tumor of the skin. This neoplasm now is largely believed to represent a rare form of basal cell carcinoma (BCC). Typical presentation is a smooth, flesh-colored or pink plaque or nodule.² Fibroepithelioma of Pinkus has a predilection for the lumbosacral back, though the groin also has been reported as a common site of incidence.^1,3 Similar to other BCCs, it is seen in older individuals, typically those older than 50 years.^3,4

Clinical diagnosis of FeP can be difficult. The differential diagnosis of FeP can include acrochordon, amelanotic melanoma, compound nevus, hemangioma, neurofibroma, nevus sebaceous, pyogenic granuloma, and seborrheic keratosis.⁵ Dermoscopic evaluation can aid in the diagnosis. A vascular network composed of fine arborizing vessels with or without dotted vessels and white streaks are characteristic findings of FeP. Patients with pigment also demonstrate structureless gray-brown areas and gray-blue dots.⁶

Biopsy with subsequent histopathologic evaluation confirms the diagnosis of FeP. The characteristic microscopic findings of thin eosinophilic epithelial strands with eccrine ducts anastomosing in an abundant fibromyxoid stroma with collections of basophilic cells located at the ends of the epithelial strands were demonstrated in our patient’s histopathologic specimen (Figure). The histologic appearance is similar to syringofibroadenoma of Mascaro. Recognition of basaloid nests, which often demonstrate retraction, and mitotic activity can differentiate FeP from syringofibroadenoma of Mascaro.⁷

Treatment of FeP is largely the same as other BCCs including destruction by electrodesiccation and curettage or complete removal by surgical excision. Several studies have demonstrated effective treatment of nonaggressive BCCs with curettage alone and subjectively reported improved cosmesis compared to electrodesiccation and curettage.^8-10 Although methyl aminolevulinate photodynamic therapy has demonstrated some therapeutic efficacy for superficial and nodular BCCs,¹¹ a case report utilizing the same modality for FeP did not provide adequate response.¹² However, adequate data are not available to assess potential use of this less invasive therapy.

To the Editor:

Experience, subjective opinion, and relationships with patients are cornerstones of general practice but also can be pitfalls. It is common for a late-presenting patient to offer a seemingly rational explanation for a long-standing lesion. Unless an objective analysis of the clinical problem is undertaken, it can be easy to embark on an incorrect treatment pathway for the patient’s condition.

One of the luxuries of specialist hospital medicine or surgery is the ability to focus on a narrow range of clinical problems, which makes it easier to spot the anomaly, as long as it is within the purview of the practitioner. We report 2 cases of skin malignancies that were assumed to be chronic wounds of benign etiology.

A 63-year-old builder was referred by his general practitioner with a chronic wound on the right forearm of 4 years’ duration. His medical history included psoriasis, and he did not have a history of diabetes mellitus or use of immunosuppressants. The general practitioner suggested possible incidental origin following a prior trauma or a psoriatic-related lesion. The patient reported that the lesion did not resemble prior psoriatic lesions and it had deteriorated substantially over the last 2 years. Furthermore, a small ulcer was starting to develop on the left forearm. Further advice was requested by the general practitioner regarding wound dressings. On examination a sloughy ulcer measuring 8.5×7.5 cm had eroded to expose necrotic tendons with surrounding induration and cellulitis (Figure 1A). In addition, a psoriatic lesion was found on the left forearm (Figure 1B). There were no palpable axillary lymph nodes. Clinical suspicion, incision biopsies, and subsequent histology confirmed cutaneous CD4⁺ T-cell lymphoma. This case was reviewed at a multidisciplinary team meeting and referred to the hematology-oncology department. The patient subsequently underwent chemotherapy with liposomal doxorubicin and radiotherapy over a period of 5 months. An elective right forearm amputation was planned due to erosion of the ulcer through tendons down to bone (Figure 2).

These 2 cases highlight easy pitfalls for an unsuspecting clinician. Although both cases had alternative plausible explanations, they proved to be cutaneous malignancies. The powerful message these cases send is that long-standing chronic wounds should be biopsied to exclude malignancy. Some of the other common underlying causes of wounds that may prevent healing are highlighted in the Table. Vascular insufficiency usually presents in characteristic patterns with a good clinical history and associated signs and findings on investigation. A foreign body, which can be anything from an orthopedic metal implant to a retained stitch from surgery or nonmedical material, may be the culprit and may be identified from a thorough medical history or appropriate imaging.

Infection is another possible explanation of a nonhealing wound. On the face, an underlying dental abscess with a sinus tracking from the root of the tooth to the skin of the cheek or jaw may be the source. Elsewhere on the body, chronic osteomyelitis may be the cause, which may be from any infective origin from Staphylococcus aureus to tuberculosis, and will most commonly present with a discharging sinus but also may present with a nonspecific ulcer.

Chronic wounds also may not heal because of a multitude of patient factors such as poor nutrition, diabetes mellitus, medication (eg, steroids, nonsteroidal anti-inflammatory drugs), other inflammatory causes, and poor mobility. Chronic wounds represent a substantial burden to patients, health care professionals, and the health care system. In the United States alone, they affect 5.7 million patients and cost an estimated $20 billion.¹ Approximately 1% of the Western population will present with leg ulceration at some point in their lives.²

Physical examination of ulcers in any clinical setting can be difficult. We postulate that it can be made more difficult at times in primary care because the patient may add confounding elements for consideration or seemingly plausible explanations. However, whenever possible, a physician should ask, “Could there possibly be an underlying malignancy here?” If there is any chance of malignancy despite plausible explanations being offered, the lesion should be biopsied.

To the Editor:

Experience, subjective opinion, and relationships with patients are cornerstones of general practice but also can be pitfalls. It is common for a late-presenting patient to offer a seemingly rational explanation for a long-standing lesion. Unless an objective analysis of the clinical problem is undertaken, it can be easy to embark on an incorrect treatment pathway for the patient’s condition.

One of the luxuries of specialist hospital medicine or surgery is the ability to focus on a narrow range of clinical problems, which makes it easier to spot the anomaly, as long as it is within the purview of the practitioner. We report 2 cases of skin malignancies that were assumed to be chronic wounds of benign etiology.

A 63-year-old builder was referred by his general practitioner with a chronic wound on the right forearm of 4 years’ duration. His medical history included psoriasis, and he did not have a history of diabetes mellitus or use of immunosuppressants. The general practitioner suggested possible incidental origin following a prior trauma or a psoriatic-related lesion. The patient reported that the lesion did not resemble prior psoriatic lesions and it had deteriorated substantially over the last 2 years. Furthermore, a small ulcer was starting to develop on the left forearm. Further advice was requested by the general practitioner regarding wound dressings. On examination a sloughy ulcer measuring 8.5×7.5 cm had eroded to expose necrotic tendons with surrounding induration and cellulitis (Figure 1A). In addition, a psoriatic lesion was found on the left forearm (Figure 1B). There were no palpable axillary lymph nodes. Clinical suspicion, incision biopsies, and subsequent histology confirmed cutaneous CD4⁺ T-cell lymphoma. This case was reviewed at a multidisciplinary team meeting and referred to the hematology-oncology department. The patient subsequently underwent chemotherapy with liposomal doxorubicin and radiotherapy over a period of 5 months. An elective right forearm amputation was planned due to erosion of the ulcer through tendons down to bone (Figure 2).

These 2 cases highlight easy pitfalls for an unsuspecting clinician. Although both cases had alternative plausible explanations, they proved to be cutaneous malignancies. The powerful message these cases send is that long-standing chronic wounds should be biopsied to exclude malignancy. Some of the other common underlying causes of wounds that may prevent healing are highlighted in the Table. Vascular insufficiency usually presents in characteristic patterns with a good clinical history and associated signs and findings on investigation. A foreign body, which can be anything from an orthopedic metal implant to a retained stitch from surgery or nonmedical material, may be the culprit and may be identified from a thorough medical history or appropriate imaging.

Infection is another possible explanation of a nonhealing wound. On the face, an underlying dental abscess with a sinus tracking from the root of the tooth to the skin of the cheek or jaw may be the source. Elsewhere on the body, chronic osteomyelitis may be the cause, which may be from any infective origin from Staphylococcus aureus to tuberculosis, and will most commonly present with a discharging sinus but also may present with a nonspecific ulcer.

Chronic wounds also may not heal because of a multitude of patient factors such as poor nutrition, diabetes mellitus, medication (eg, steroids, nonsteroidal anti-inflammatory drugs), other inflammatory causes, and poor mobility. Chronic wounds represent a substantial burden to patients, health care professionals, and the health care system. In the United States alone, they affect 5.7 million patients and cost an estimated $20 billion.¹ Approximately 1% of the Western population will present with leg ulceration at some point in their lives.²

Physical examination of ulcers in any clinical setting can be difficult. We postulate that it can be made more difficult at times in primary care because the patient may add confounding elements for consideration or seemingly plausible explanations. However, whenever possible, a physician should ask, “Could there possibly be an underlying malignancy here?” If there is any chance of malignancy despite plausible explanations being offered, the lesion should be biopsied.

To the Editor:

Experience, subjective opinion, and relationships with patients are cornerstones of general practice but also can be pitfalls. It is common for a late-presenting patient to offer a seemingly rational explanation for a long-standing lesion. Unless an objective analysis of the clinical problem is undertaken, it can be easy to embark on an incorrect treatment pathway for the patient’s condition.

One of the luxuries of specialist hospital medicine or surgery is the ability to focus on a narrow range of clinical problems, which makes it easier to spot the anomaly, as long as it is within the purview of the practitioner. We report 2 cases of skin malignancies that were assumed to be chronic wounds of benign etiology.

A 63-year-old builder was referred by his general practitioner with a chronic wound on the right forearm of 4 years’ duration. His medical history included psoriasis, and he did not have a history of diabetes mellitus or use of immunosuppressants. The general practitioner suggested possible incidental origin following a prior trauma or a psoriatic-related lesion. The patient reported that the lesion did not resemble prior psoriatic lesions and it had deteriorated substantially over the last 2 years. Furthermore, a small ulcer was starting to develop on the left forearm. Further advice was requested by the general practitioner regarding wound dressings. On examination a sloughy ulcer measuring 8.5×7.5 cm had eroded to expose necrotic tendons with surrounding induration and cellulitis (Figure 1A). In addition, a psoriatic lesion was found on the left forearm (Figure 1B). There were no palpable axillary lymph nodes. Clinical suspicion, incision biopsies, and subsequent histology confirmed cutaneous CD4⁺ T-cell lymphoma. This case was reviewed at a multidisciplinary team meeting and referred to the hematology-oncology department. The patient subsequently underwent chemotherapy with liposomal doxorubicin and radiotherapy over a period of 5 months. An elective right forearm amputation was planned due to erosion of the ulcer through tendons down to bone (Figure 2).

These 2 cases highlight easy pitfalls for an unsuspecting clinician. Although both cases had alternative plausible explanations, they proved to be cutaneous malignancies. The powerful message these cases send is that long-standing chronic wounds should be biopsied to exclude malignancy. Some of the other common underlying causes of wounds that may prevent healing are highlighted in the Table. Vascular insufficiency usually presents in characteristic patterns with a good clinical history and associated signs and findings on investigation. A foreign body, which can be anything from an orthopedic metal implant to a retained stitch from surgery or nonmedical material, may be the culprit and may be identified from a thorough medical history or appropriate imaging.

Infection is another possible explanation of a nonhealing wound. On the face, an underlying dental abscess with a sinus tracking from the root of the tooth to the skin of the cheek or jaw may be the source. Elsewhere on the body, chronic osteomyelitis may be the cause, which may be from any infective origin from Staphylococcus aureus to tuberculosis, and will most commonly present with a discharging sinus but also may present with a nonspecific ulcer.

Chronic wounds also may not heal because of a multitude of patient factors such as poor nutrition, diabetes mellitus, medication (eg, steroids, nonsteroidal anti-inflammatory drugs), other inflammatory causes, and poor mobility. Chronic wounds represent a substantial burden to patients, health care professionals, and the health care system. In the United States alone, they affect 5.7 million patients and cost an estimated $20 billion.¹ Approximately 1% of the Western population will present with leg ulceration at some point in their lives.²

Physical examination of ulcers in any clinical setting can be difficult. We postulate that it can be made more difficult at times in primary care because the patient may add confounding elements for consideration or seemingly plausible explanations. However, whenever possible, a physician should ask, “Could there possibly be an underlying malignancy here?” If there is any chance of malignancy despite plausible explanations being offered, the lesion should be biopsied.

Most divisions within a hospital will have a morbidity or mortality round where they review deaths that occurred in that department, but doing that on an institution-wide level is unusual and important. “It gives a totally different viewpoint,” he says. “When it’s a couple highly selected patients whose cases you examine, you really don’t have an idea at the end if the problems you identified are systemwide issues in your institution.”

The major issue the study identified was an inadequate discussion of goals of care. “This was often a patient who was dying, and in retrospect, it was clear that they were at high risk for death, but there had been no discussion with the patient about prognosis or about symptom management,” Dr. Kobewka says. “It seemed that care was directed at prolonging life. When we looked back at the case, that wasn’t realistic. That accounted for 25% of the quality issues that we identified: The discussion of prognosis and goals of care was inadequate or even absent all together. I think every hospital needs to think about those discussions and how and where and when we have them.”

Another revelation from the study: Errors in care are common but also underdiscussed. “When a physician is aware that maybe there was an error in care, it’s easy for there to be guilt and secrecy,” Dr. Kobewka says. “This is just a reminder that it’s common, and we need an open discussion about it. We need high-level, institution-wide systems to help us with this, but even at the individual provider level, this discussion needs to happen. Any quality improvement process needs engagement of frontline staff.”

Reference

1. Kobewka DM, van Walraven C, Turnbull J, Worthington J, Calder L, Forster A. Quality gaps identified through mortality review [published online ahead of print February 8, 2016]. BMJ Qual Saf. doi:10.1136/bmjqs-2015-004735.

Most divisions within a hospital will have a morbidity or mortality round where they review deaths that occurred in that department, but doing that on an institution-wide level is unusual and important. “It gives a totally different viewpoint,” he says. “When it’s a couple highly selected patients whose cases you examine, you really don’t have an idea at the end if the problems you identified are systemwide issues in your institution.”

The major issue the study identified was an inadequate discussion of goals of care. “This was often a patient who was dying, and in retrospect, it was clear that they were at high risk for death, but there had been no discussion with the patient about prognosis or about symptom management,” Dr. Kobewka says. “It seemed that care was directed at prolonging life. When we looked back at the case, that wasn’t realistic. That accounted for 25% of the quality issues that we identified: The discussion of prognosis and goals of care was inadequate or even absent all together. I think every hospital needs to think about those discussions and how and where and when we have them.”

Another revelation from the study: Errors in care are common but also underdiscussed. “When a physician is aware that maybe there was an error in care, it’s easy for there to be guilt and secrecy,” Dr. Kobewka says. “This is just a reminder that it’s common, and we need an open discussion about it. We need high-level, institution-wide systems to help us with this, but even at the individual provider level, this discussion needs to happen. Any quality improvement process needs engagement of frontline staff.”

Reference

1. Kobewka DM, van Walraven C, Turnbull J, Worthington J, Calder L, Forster A. Quality gaps identified through mortality review [published online ahead of print February 8, 2016]. BMJ Qual Saf. doi:10.1136/bmjqs-2015-004735.

Most divisions within a hospital will have a morbidity or mortality round where they review deaths that occurred in that department, but doing that on an institution-wide level is unusual and important. “It gives a totally different viewpoint,” he says. “When it’s a couple highly selected patients whose cases you examine, you really don’t have an idea at the end if the problems you identified are systemwide issues in your institution.”

The major issue the study identified was an inadequate discussion of goals of care. “This was often a patient who was dying, and in retrospect, it was clear that they were at high risk for death, but there had been no discussion with the patient about prognosis or about symptom management,” Dr. Kobewka says. “It seemed that care was directed at prolonging life. When we looked back at the case, that wasn’t realistic. That accounted for 25% of the quality issues that we identified: The discussion of prognosis and goals of care was inadequate or even absent all together. I think every hospital needs to think about those discussions and how and where and when we have them.”

Another revelation from the study: Errors in care are common but also underdiscussed. “When a physician is aware that maybe there was an error in care, it’s easy for there to be guilt and secrecy,” Dr. Kobewka says. “This is just a reminder that it’s common, and we need an open discussion about it. We need high-level, institution-wide systems to help us with this, but even at the individual provider level, this discussion needs to happen. Any quality improvement process needs engagement of frontline staff.”

Reference

1. Kobewka DM, van Walraven C, Turnbull J, Worthington J, Calder L, Forster A. Quality gaps identified through mortality review [published online ahead of print February 8, 2016]. BMJ Qual Saf. doi:10.1136/bmjqs-2015-004735.

New Society of Hospital Medicine board member Tracy Cardin, ACNP-BC, SFHM, isn’t on the board because she’s a nurse practitioner (NP). But that doesn’t make her election as the first NP or physician assistant (PA) as a voting member of SHM’s oversight panel any less momentous.

“I can’t describe to you how passionately I believe that [NPs and PAs] have a huge role moving forward,” Cardin says. “I think our representation, our visibility, has sort of been flabby and kind of under the wire for a long time. We can really impact the design of care models at the bedside in a way that’s innovative and more efficient and in a way that’s really huge. I think there’s a transformation that’s going to be coming, and we’re going to be a huge part of it.”

Cardin officially started her new position as a board member in March at HM16 in San Diego. She previously—and fittingly—was chair of SHM’s Nurse Practitioner/Physician Assistant Committee. Last year, she received the society’s Award in Excellence in Hospital Medicine for NPs and PAs. She has worked at the University of Chicago for about 10 years.

SHM Past President Robert Harrington Jr., MD, SFHM, who pushed for her inclusion on the board, says that the value of bringing different perspectives to the society’s board can’t be overstated.

“I’m a family medicine–trained hospitalist, and so from firsthand experience, it was important to me before I ever thought about running for the board that there was some representation of our constituency whether that was at the committee level or at the board level,” Dr. Harrington says. “I think that is part of what drew me to seek a higher voice within SHM. … I thought it was important that somebody represent those growing constituencies.”

Dr. Harrington, who among others refers to SHM as a “big tent organization,” says Cardin’s appointment is evidence of that. He believes that his background in family medicine and her background as an NP show healthcare professionals that SHM is not just a group for doctors.

“It does send a message to the rest of our membership that SHM values those other constituencies and that this is not a physician membership organization but rather a membership organization comprised of people who are interested in improving healthcare for our hospitalized patients,” he says.

In fact, Dr. Harrington says one of the first official actions he took as president was to name Cardin an ex officio member of the board. While that meant she could not vote on issues, her perspective alone helped shape conversations.

“Over the course of the last year, she has proven herself to be exactly what I would have hoped she would be: a voice of an important constituency within our membership,” he says. “And as a result of that, [she] ended up being voted into the board.”

Cardin says the time is perfect for her to bring an added viewpoint to the board. First, the number of NPs and PAs is growing.

“NPs and PAs are such a huge part of all acute-care practices,” says Cardin, a past member of Team Hospitalist, the volunteer editorial advisory group for The Hospitalist. “The State of Hospital Medicine surveys showed that 83% of hospitalist groups are utilizing NPs and PAs. I think that is going to be reflected not only in hospitalist practices but in all acute-care practices—there is going to be more deployment and integration of NPs and PAs into practice.

“[SHM] is ahead of the curve recognizing that value.”

Second, healthcare is undergoing payment reform unseen since the introduction of Medicare and Medicaid. Technology is revamping bedside manner, care delivery, and everything in between. And quality of care is more important than ever as doctors will be increasingly paid for how well patients get, not for services provided to them.

“NP and PA providers can have a great impact on care design and throughput as well as other contributions in the hospital environment,” she adds.

Cardin says there can’t be too many educated viewpoints on complicated issues that will affect care delivery in the United States for decades to come. And the first NP/PA voice might be, gulp, just what the doctors ordered.

“We’re at a pivotal time for this organization and also for healthcare in general with the shifts in how we’re paid and what we’re paid for and the complexity of electronic medical records and fragmented healthcare and billing and quality metrics—there’s just so many challenges right now,” she says. “It’s just hugely humbling to be a part of that and try to anticipate what direction that we as a society should go into.” TH

Richard Quinn is a freelance writer based in New Jersey.

New Society of Hospital Medicine board member Tracy Cardin, ACNP-BC, SFHM, isn’t on the board because she’s a nurse practitioner (NP). But that doesn’t make her election as the first NP or physician assistant (PA) as a voting member of SHM’s oversight panel any less momentous.

“I can’t describe to you how passionately I believe that [NPs and PAs] have a huge role moving forward,” Cardin says. “I think our representation, our visibility, has sort of been flabby and kind of under the wire for a long time. We can really impact the design of care models at the bedside in a way that’s innovative and more efficient and in a way that’s really huge. I think there’s a transformation that’s going to be coming, and we’re going to be a huge part of it.”

Cardin officially started her new position as a board member in March at HM16 in San Diego. She previously—and fittingly—was chair of SHM’s Nurse Practitioner/Physician Assistant Committee. Last year, she received the society’s Award in Excellence in Hospital Medicine for NPs and PAs. She has worked at the University of Chicago for about 10 years.

SHM Past President Robert Harrington Jr., MD, SFHM, who pushed for her inclusion on the board, says that the value of bringing different perspectives to the society’s board can’t be overstated.

“I’m a family medicine–trained hospitalist, and so from firsthand experience, it was important to me before I ever thought about running for the board that there was some representation of our constituency whether that was at the committee level or at the board level,” Dr. Harrington says. “I think that is part of what drew me to seek a higher voice within SHM. … I thought it was important that somebody represent those growing constituencies.”

Dr. Harrington, who among others refers to SHM as a “big tent organization,” says Cardin’s appointment is evidence of that. He believes that his background in family medicine and her background as an NP show healthcare professionals that SHM is not just a group for doctors.

“It does send a message to the rest of our membership that SHM values those other constituencies and that this is not a physician membership organization but rather a membership organization comprised of people who are interested in improving healthcare for our hospitalized patients,” he says.

In fact, Dr. Harrington says one of the first official actions he took as president was to name Cardin an ex officio member of the board. While that meant she could not vote on issues, her perspective alone helped shape conversations.

“Over the course of the last year, she has proven herself to be exactly what I would have hoped she would be: a voice of an important constituency within our membership,” he says. “And as a result of that, [she] ended up being voted into the board.”

Cardin says the time is perfect for her to bring an added viewpoint to the board. First, the number of NPs and PAs is growing.

“NPs and PAs are such a huge part of all acute-care practices,” says Cardin, a past member of Team Hospitalist, the volunteer editorial advisory group for The Hospitalist. “The State of Hospital Medicine surveys showed that 83% of hospitalist groups are utilizing NPs and PAs. I think that is going to be reflected not only in hospitalist practices but in all acute-care practices—there is going to be more deployment and integration of NPs and PAs into practice.

“[SHM] is ahead of the curve recognizing that value.”

Second, healthcare is undergoing payment reform unseen since the introduction of Medicare and Medicaid. Technology is revamping bedside manner, care delivery, and everything in between. And quality of care is more important than ever as doctors will be increasingly paid for how well patients get, not for services provided to them.

“NP and PA providers can have a great impact on care design and throughput as well as other contributions in the hospital environment,” she adds.

Cardin says there can’t be too many educated viewpoints on complicated issues that will affect care delivery in the United States for decades to come. And the first NP/PA voice might be, gulp, just what the doctors ordered.

“We’re at a pivotal time for this organization and also for healthcare in general with the shifts in how we’re paid and what we’re paid for and the complexity of electronic medical records and fragmented healthcare and billing and quality metrics—there’s just so many challenges right now,” she says. “It’s just hugely humbling to be a part of that and try to anticipate what direction that we as a society should go into.” TH

Richard Quinn is a freelance writer based in New Jersey.

New Society of Hospital Medicine board member Tracy Cardin, ACNP-BC, SFHM, isn’t on the board because she’s a nurse practitioner (NP). But that doesn’t make her election as the first NP or physician assistant (PA) as a voting member of SHM’s oversight panel any less momentous.

“I can’t describe to you how passionately I believe that [NPs and PAs] have a huge role moving forward,” Cardin says. “I think our representation, our visibility, has sort of been flabby and kind of under the wire for a long time. We can really impact the design of care models at the bedside in a way that’s innovative and more efficient and in a way that’s really huge. I think there’s a transformation that’s going to be coming, and we’re going to be a huge part of it.”

Cardin officially started her new position as a board member in March at HM16 in San Diego. She previously—and fittingly—was chair of SHM’s Nurse Practitioner/Physician Assistant Committee. Last year, she received the society’s Award in Excellence in Hospital Medicine for NPs and PAs. She has worked at the University of Chicago for about 10 years.

SHM Past President Robert Harrington Jr., MD, SFHM, who pushed for her inclusion on the board, says that the value of bringing different perspectives to the society’s board can’t be overstated.

“I’m a family medicine–trained hospitalist, and so from firsthand experience, it was important to me before I ever thought about running for the board that there was some representation of our constituency whether that was at the committee level or at the board level,” Dr. Harrington says. “I think that is part of what drew me to seek a higher voice within SHM. … I thought it was important that somebody represent those growing constituencies.”

Dr. Harrington, who among others refers to SHM as a “big tent organization,” says Cardin’s appointment is evidence of that. He believes that his background in family medicine and her background as an NP show healthcare professionals that SHM is not just a group for doctors.

“It does send a message to the rest of our membership that SHM values those other constituencies and that this is not a physician membership organization but rather a membership organization comprised of people who are interested in improving healthcare for our hospitalized patients,” he says.

In fact, Dr. Harrington says one of the first official actions he took as president was to name Cardin an ex officio member of the board. While that meant she could not vote on issues, her perspective alone helped shape conversations.

“Over the course of the last year, she has proven herself to be exactly what I would have hoped she would be: a voice of an important constituency within our membership,” he says. “And as a result of that, [she] ended up being voted into the board.”

Cardin says the time is perfect for her to bring an added viewpoint to the board. First, the number of NPs and PAs is growing.

“NPs and PAs are such a huge part of all acute-care practices,” says Cardin, a past member of Team Hospitalist, the volunteer editorial advisory group for The Hospitalist. “The State of Hospital Medicine surveys showed that 83% of hospitalist groups are utilizing NPs and PAs. I think that is going to be reflected not only in hospitalist practices but in all acute-care practices—there is going to be more deployment and integration of NPs and PAs into practice.

“[SHM] is ahead of the curve recognizing that value.”

Second, healthcare is undergoing payment reform unseen since the introduction of Medicare and Medicaid. Technology is revamping bedside manner, care delivery, and everything in between. And quality of care is more important than ever as doctors will be increasingly paid for how well patients get, not for services provided to them.

“NP and PA providers can have a great impact on care design and throughput as well as other contributions in the hospital environment,” she adds.

Cardin says there can’t be too many educated viewpoints on complicated issues that will affect care delivery in the United States for decades to come. And the first NP/PA voice might be, gulp, just what the doctors ordered.

“We’re at a pivotal time for this organization and also for healthcare in general with the shifts in how we’re paid and what we’re paid for and the complexity of electronic medical records and fragmented healthcare and billing and quality metrics—there’s just so many challenges right now,” she says. “It’s just hugely humbling to be a part of that and try to anticipate what direction that we as a society should go into.” TH

Richard Quinn is a freelance writer based in New Jersey.