Arthroplasty/Joint Replacement

As the largest sesamoid bone in the human body, the patella acts as a fulcrum to enhance the biomechanical advantage of the quadriceps in extension.¹ It is subject to a variety of forces while improving distribution of forces along the extensor mechanism.² With sufficient force, the patella can be dislocated. Acute patellar dislocations are the most common knee injury, encompassing 2% to 3% of all knee injuries³ and occurring in 5.8 per 100,000 individuals.^4-5 These injuries are associated with acute trauma, frequently from sports and physical activities, occurring while in terminal extension with an axial-valgus stress on the knee during rotation.⁶

With acute patellar dislocations, patients are usually in significant discomfort. Often, the patella may spontaneously reduce; if not, closed reduction is usually successful with pressure applied anteromedially on the lateral patellar margin, while simultaneously attempting gentle extension of the leg.⁷ Closed reduction is almost universally successful, and there have only been case reports of irreducible, mainly fixed vertical axis patellar dislocations.^8-11 No reports in the literature have described subacute patellar dislocations because of their rarity. Patients present immediately after dislocation, spontaneously reduce, or have a painless, chronically dislocated patella.

We present a case of an elderly man with dementia and a subacute fixed irreducible patellar dislocation, which was reduced using a technique not described in the literature. The patient and the patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 68-year-old nonambulatory man with a history of dementia and stroke presented to the emergency department with complaints of left knee pain and his knee locked in flexion. The patient’s knee had been in that fixed hyperflexed position for at least 10 days after he sustained a twisting injury to his knee while attempting to get out of bed. At baseline, the patient was mostly bedbound and could walk minimally with maximum support, but, given his dementia, he would often attempt to ambulate by himself. After the injury, the patient did not complain of much pain at rest, but attempts at his group home to straighten his leg had caused severe pain. As a result, the patient was brought to the emergency department to be evaluated for fractures. 

Physical examination in the emergency department revealed atrophy of the lower extremity musculature and a left knee fixed at 120º in flexion. The skin was intact, and there was minimal effusion of the knee joint. The patella was noted to be laterally subluxated and tender to palpation over the lateral and medial facets. He was neurovascularly intact distally and had painless range of motion of his hips. His contralateral right knee had full range of motion with good patellar tracking.

Radiographs of the patient’s knee confirmed a lateral dislocation of the patella (Figures 1A-1C). After oral and intravenous administration of pain medication, a reduction was attempted without success. Next, an intra-articular knee injection of 10 mL of 1% lidocaine was given. After waiting 15 minutes, another reduction was tried. While the pain control was sufficient, the reduction was again unsuccessful. The knee was insufflated with 120 mL of sterile saline and reduction attempted again. By extending the knee and applying a medially directed force to the patella, reduction was successful. The patient was placed into a knee immobilizer and postreduction radiographs were taken (Figures 2A, 2B). Saline was extracted from the knee. The patient was admitted to the hospital where repeat examination of his knees during the next week revealed markedly less pain. The patient was lost to follow-up.

Discussion

Our patient presumably had a low-energy mechanism of injury, resulting in an undiagnosed patellar dislocation with delayed treatment. This subacute patellar dislocation was irreducible using the standard techniques. Alternatively, insufflation of the joint with saline provided the necessary impetus to allow for successful patellar reduction. The history of the patient reveals clues about the mechanism of injury. It is likely that the patient’s nonambulatory status resulted in a weak vastus medialis muscle that placed the patella at risk for dislocation. While the exact mechanism of dislocation is unknown, the patella was unable to be reduced spontaneously because our patient’s knee was maintained in a state of flexion secondary to pain and muscle contraction. The combination of weak quadriceps musculature, increased Q angle, and forced hyperflexion of the knee prevented closed reduction of the patella.

Fixed, irreducible patellar dislocations are rare and discussed infrequently in the literature.^9,11-12 Reported mechanisms are mostly high energy, including blows during athletics and impacts from motor vehicle collisions.^9,13 Vertical axis rotation, as first described by Cooper,¹⁴ is commonly implicated in irreducible patellar dislocations. This occurs when the patella internally rotates 180º on its vertical axis, associated with a large tear of the medial retinaculum but intact quadriceps tendon. The patella is fixed over the lateral femoral condyle with the articular surface pointing anterolaterally. Despite adequate sedation and analgesia, these are notoriously difficult to close-reduce and may necessitate open reduction.³ Our patient, while having a fixed dislocation, did not have a vertical axis component and, therefore, was amenable to our closed reduction attempt.

Our first reduction attempts were unsuccessful, likely because the patient continued to be tense, firing his quadriceps. Even after injecting the knee with lidocaine and eliminating the pain component, the patella was still impinging on the lateral femoral condyle (Figure 3A). By insufflating the knee with saline, we were able to increase the distance from the patella to the trochlea (Figure 3B). This is comparable to a knee arthroscopy, in which joint fluid pressure allows passage of arthroscopic instruments into the patellofemoral joint. We postulate that the farther the patella is anterior to the trochlea, the higher the likelihood that the patella can be reduced to its anatomic position. 

Insufflation of the knee with sterile saline is a novel technique that involves minimal risk compared with the alternatives. Sometimes, for closed reduction to be successful, individuals need to be consciously sedated to relax their muscles and eliminate pain. While conscious sedation is generally considered low risk, complications have been noted, including hypotension, apnea, and retrograde amnesia.¹⁵ Manual closed reduction may also cause additional chondral damage when the medial patellar facet contacts the lateral femoral trochlea. When closed reduction of the patella fails, open reduction is required; this inherently includes all the risks of surgery, such as bleeding, infection, neurovascular injury, and wound complications.  

Our insufflation technique does not require sedation and is minimally invasive. The saline creates space and provides lubrication to allow for easier manipulation of the patella. This theoretically protects the cartilage as the patella passes over the lateral trochlea. In addition to the intended effect of providing more space and lubrication for the reduction of the patella, insufflation of the joint may also relax the vastus musculature.¹⁶ In their study, Torry and colleagues¹⁶ injected 13 knees with 20 mL sterile saline and noted reduction in electromyography readings in the vastus medialis and lateralis muscles. This inhibition of vastus musculature may provide enough relaxation to aid in the successful reduction of the patella.

Our study is limited by our sample size of 1. Because acute patellar dislocations are often easily reduced, our technical trick is not frequently used. Additionally, while we were able to monitor his progress during his inpatient stay, our patient was lost to follow-up after his discharge from the hospital.

 If successful, the insufflation technique eliminates the need for urgent open reduction in the operating room. As a result, we recommend attempting closed reduction using insufflation of the knee with sterile saline for irreducible patellar dislocations before proceeding with open reduction.

Conclusion

Saline insufflation of the knee can be safely and easily performed to aid in the reduction of subacute, difficult patellar dislocations.

As the largest sesamoid bone in the human body, the patella acts as a fulcrum to enhance the biomechanical advantage of the quadriceps in extension.¹ It is subject to a variety of forces while improving distribution of forces along the extensor mechanism.² With sufficient force, the patella can be dislocated. Acute patellar dislocations are the most common knee injury, encompassing 2% to 3% of all knee injuries³ and occurring in 5.8 per 100,000 individuals.^4-5 These injuries are associated with acute trauma, frequently from sports and physical activities, occurring while in terminal extension with an axial-valgus stress on the knee during rotation.⁶

With acute patellar dislocations, patients are usually in significant discomfort. Often, the patella may spontaneously reduce; if not, closed reduction is usually successful with pressure applied anteromedially on the lateral patellar margin, while simultaneously attempting gentle extension of the leg.⁷ Closed reduction is almost universally successful, and there have only been case reports of irreducible, mainly fixed vertical axis patellar dislocations.^8-11 No reports in the literature have described subacute patellar dislocations because of their rarity. Patients present immediately after dislocation, spontaneously reduce, or have a painless, chronically dislocated patella.

We present a case of an elderly man with dementia and a subacute fixed irreducible patellar dislocation, which was reduced using a technique not described in the literature. The patient and the patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 68-year-old nonambulatory man with a history of dementia and stroke presented to the emergency department with complaints of left knee pain and his knee locked in flexion. The patient’s knee had been in that fixed hyperflexed position for at least 10 days after he sustained a twisting injury to his knee while attempting to get out of bed. At baseline, the patient was mostly bedbound and could walk minimally with maximum support, but, given his dementia, he would often attempt to ambulate by himself. After the injury, the patient did not complain of much pain at rest, but attempts at his group home to straighten his leg had caused severe pain. As a result, the patient was brought to the emergency department to be evaluated for fractures. 

Physical examination in the emergency department revealed atrophy of the lower extremity musculature and a left knee fixed at 120º in flexion. The skin was intact, and there was minimal effusion of the knee joint. The patella was noted to be laterally subluxated and tender to palpation over the lateral and medial facets. He was neurovascularly intact distally and had painless range of motion of his hips. His contralateral right knee had full range of motion with good patellar tracking.

Radiographs of the patient’s knee confirmed a lateral dislocation of the patella (Figures 1A-1C). After oral and intravenous administration of pain medication, a reduction was attempted without success. Next, an intra-articular knee injection of 10 mL of 1% lidocaine was given. After waiting 15 minutes, another reduction was tried. While the pain control was sufficient, the reduction was again unsuccessful. The knee was insufflated with 120 mL of sterile saline and reduction attempted again. By extending the knee and applying a medially directed force to the patella, reduction was successful. The patient was placed into a knee immobilizer and postreduction radiographs were taken (Figures 2A, 2B). Saline was extracted from the knee. The patient was admitted to the hospital where repeat examination of his knees during the next week revealed markedly less pain. The patient was lost to follow-up.

Discussion

Our patient presumably had a low-energy mechanism of injury, resulting in an undiagnosed patellar dislocation with delayed treatment. This subacute patellar dislocation was irreducible using the standard techniques. Alternatively, insufflation of the joint with saline provided the necessary impetus to allow for successful patellar reduction. The history of the patient reveals clues about the mechanism of injury. It is likely that the patient’s nonambulatory status resulted in a weak vastus medialis muscle that placed the patella at risk for dislocation. While the exact mechanism of dislocation is unknown, the patella was unable to be reduced spontaneously because our patient’s knee was maintained in a state of flexion secondary to pain and muscle contraction. The combination of weak quadriceps musculature, increased Q angle, and forced hyperflexion of the knee prevented closed reduction of the patella.

Fixed, irreducible patellar dislocations are rare and discussed infrequently in the literature.^9,11-12 Reported mechanisms are mostly high energy, including blows during athletics and impacts from motor vehicle collisions.^9,13 Vertical axis rotation, as first described by Cooper,¹⁴ is commonly implicated in irreducible patellar dislocations. This occurs when the patella internally rotates 180º on its vertical axis, associated with a large tear of the medial retinaculum but intact quadriceps tendon. The patella is fixed over the lateral femoral condyle with the articular surface pointing anterolaterally. Despite adequate sedation and analgesia, these are notoriously difficult to close-reduce and may necessitate open reduction.³ Our patient, while having a fixed dislocation, did not have a vertical axis component and, therefore, was amenable to our closed reduction attempt.

Our first reduction attempts were unsuccessful, likely because the patient continued to be tense, firing his quadriceps. Even after injecting the knee with lidocaine and eliminating the pain component, the patella was still impinging on the lateral femoral condyle (Figure 3A). By insufflating the knee with saline, we were able to increase the distance from the patella to the trochlea (Figure 3B). This is comparable to a knee arthroscopy, in which joint fluid pressure allows passage of arthroscopic instruments into the patellofemoral joint. We postulate that the farther the patella is anterior to the trochlea, the higher the likelihood that the patella can be reduced to its anatomic position. 

Insufflation of the knee with sterile saline is a novel technique that involves minimal risk compared with the alternatives. Sometimes, for closed reduction to be successful, individuals need to be consciously sedated to relax their muscles and eliminate pain. While conscious sedation is generally considered low risk, complications have been noted, including hypotension, apnea, and retrograde amnesia.¹⁵ Manual closed reduction may also cause additional chondral damage when the medial patellar facet contacts the lateral femoral trochlea. When closed reduction of the patella fails, open reduction is required; this inherently includes all the risks of surgery, such as bleeding, infection, neurovascular injury, and wound complications.  

Our insufflation technique does not require sedation and is minimally invasive. The saline creates space and provides lubrication to allow for easier manipulation of the patella. This theoretically protects the cartilage as the patella passes over the lateral trochlea. In addition to the intended effect of providing more space and lubrication for the reduction of the patella, insufflation of the joint may also relax the vastus musculature.¹⁶ In their study, Torry and colleagues¹⁶ injected 13 knees with 20 mL sterile saline and noted reduction in electromyography readings in the vastus medialis and lateralis muscles. This inhibition of vastus musculature may provide enough relaxation to aid in the successful reduction of the patella.

Our study is limited by our sample size of 1. Because acute patellar dislocations are often easily reduced, our technical trick is not frequently used. Additionally, while we were able to monitor his progress during his inpatient stay, our patient was lost to follow-up after his discharge from the hospital.

 If successful, the insufflation technique eliminates the need for urgent open reduction in the operating room. As a result, we recommend attempting closed reduction using insufflation of the knee with sterile saline for irreducible patellar dislocations before proceeding with open reduction.

Conclusion

Saline insufflation of the knee can be safely and easily performed to aid in the reduction of subacute, difficult patellar dislocations.

As the largest sesamoid bone in the human body, the patella acts as a fulcrum to enhance the biomechanical advantage of the quadriceps in extension.¹ It is subject to a variety of forces while improving distribution of forces along the extensor mechanism.² With sufficient force, the patella can be dislocated. Acute patellar dislocations are the most common knee injury, encompassing 2% to 3% of all knee injuries³ and occurring in 5.8 per 100,000 individuals.^4-5 These injuries are associated with acute trauma, frequently from sports and physical activities, occurring while in terminal extension with an axial-valgus stress on the knee during rotation.⁶

With acute patellar dislocations, patients are usually in significant discomfort. Often, the patella may spontaneously reduce; if not, closed reduction is usually successful with pressure applied anteromedially on the lateral patellar margin, while simultaneously attempting gentle extension of the leg.⁷ Closed reduction is almost universally successful, and there have only been case reports of irreducible, mainly fixed vertical axis patellar dislocations.^8-11 No reports in the literature have described subacute patellar dislocations because of their rarity. Patients present immediately after dislocation, spontaneously reduce, or have a painless, chronically dislocated patella.

We present a case of an elderly man with dementia and a subacute fixed irreducible patellar dislocation, which was reduced using a technique not described in the literature. The patient and the patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 68-year-old nonambulatory man with a history of dementia and stroke presented to the emergency department with complaints of left knee pain and his knee locked in flexion. The patient’s knee had been in that fixed hyperflexed position for at least 10 days after he sustained a twisting injury to his knee while attempting to get out of bed. At baseline, the patient was mostly bedbound and could walk minimally with maximum support, but, given his dementia, he would often attempt to ambulate by himself. After the injury, the patient did not complain of much pain at rest, but attempts at his group home to straighten his leg had caused severe pain. As a result, the patient was brought to the emergency department to be evaluated for fractures. 

Physical examination in the emergency department revealed atrophy of the lower extremity musculature and a left knee fixed at 120º in flexion. The skin was intact, and there was minimal effusion of the knee joint. The patella was noted to be laterally subluxated and tender to palpation over the lateral and medial facets. He was neurovascularly intact distally and had painless range of motion of his hips. His contralateral right knee had full range of motion with good patellar tracking.

Radiographs of the patient’s knee confirmed a lateral dislocation of the patella (Figures 1A-1C). After oral and intravenous administration of pain medication, a reduction was attempted without success. Next, an intra-articular knee injection of 10 mL of 1% lidocaine was given. After waiting 15 minutes, another reduction was tried. While the pain control was sufficient, the reduction was again unsuccessful. The knee was insufflated with 120 mL of sterile saline and reduction attempted again. By extending the knee and applying a medially directed force to the patella, reduction was successful. The patient was placed into a knee immobilizer and postreduction radiographs were taken (Figures 2A, 2B). Saline was extracted from the knee. The patient was admitted to the hospital where repeat examination of his knees during the next week revealed markedly less pain. The patient was lost to follow-up.

Discussion

Our patient presumably had a low-energy mechanism of injury, resulting in an undiagnosed patellar dislocation with delayed treatment. This subacute patellar dislocation was irreducible using the standard techniques. Alternatively, insufflation of the joint with saline provided the necessary impetus to allow for successful patellar reduction. The history of the patient reveals clues about the mechanism of injury. It is likely that the patient’s nonambulatory status resulted in a weak vastus medialis muscle that placed the patella at risk for dislocation. While the exact mechanism of dislocation is unknown, the patella was unable to be reduced spontaneously because our patient’s knee was maintained in a state of flexion secondary to pain and muscle contraction. The combination of weak quadriceps musculature, increased Q angle, and forced hyperflexion of the knee prevented closed reduction of the patella.

Fixed, irreducible patellar dislocations are rare and discussed infrequently in the literature.^9,11-12 Reported mechanisms are mostly high energy, including blows during athletics and impacts from motor vehicle collisions.^9,13 Vertical axis rotation, as first described by Cooper,¹⁴ is commonly implicated in irreducible patellar dislocations. This occurs when the patella internally rotates 180º on its vertical axis, associated with a large tear of the medial retinaculum but intact quadriceps tendon. The patella is fixed over the lateral femoral condyle with the articular surface pointing anterolaterally. Despite adequate sedation and analgesia, these are notoriously difficult to close-reduce and may necessitate open reduction.³ Our patient, while having a fixed dislocation, did not have a vertical axis component and, therefore, was amenable to our closed reduction attempt.

Our first reduction attempts were unsuccessful, likely because the patient continued to be tense, firing his quadriceps. Even after injecting the knee with lidocaine and eliminating the pain component, the patella was still impinging on the lateral femoral condyle (Figure 3A). By insufflating the knee with saline, we were able to increase the distance from the patella to the trochlea (Figure 3B). This is comparable to a knee arthroscopy, in which joint fluid pressure allows passage of arthroscopic instruments into the patellofemoral joint. We postulate that the farther the patella is anterior to the trochlea, the higher the likelihood that the patella can be reduced to its anatomic position. 

Insufflation of the knee with sterile saline is a novel technique that involves minimal risk compared with the alternatives. Sometimes, for closed reduction to be successful, individuals need to be consciously sedated to relax their muscles and eliminate pain. While conscious sedation is generally considered low risk, complications have been noted, including hypotension, apnea, and retrograde amnesia.¹⁵ Manual closed reduction may also cause additional chondral damage when the medial patellar facet contacts the lateral femoral trochlea. When closed reduction of the patella fails, open reduction is required; this inherently includes all the risks of surgery, such as bleeding, infection, neurovascular injury, and wound complications.  

Our insufflation technique does not require sedation and is minimally invasive. The saline creates space and provides lubrication to allow for easier manipulation of the patella. This theoretically protects the cartilage as the patella passes over the lateral trochlea. In addition to the intended effect of providing more space and lubrication for the reduction of the patella, insufflation of the joint may also relax the vastus musculature.¹⁶ In their study, Torry and colleagues¹⁶ injected 13 knees with 20 mL sterile saline and noted reduction in electromyography readings in the vastus medialis and lateralis muscles. This inhibition of vastus musculature may provide enough relaxation to aid in the successful reduction of the patella.

Our study is limited by our sample size of 1. Because acute patellar dislocations are often easily reduced, our technical trick is not frequently used. Additionally, while we were able to monitor his progress during his inpatient stay, our patient was lost to follow-up after his discharge from the hospital.

 If successful, the insufflation technique eliminates the need for urgent open reduction in the operating room. As a result, we recommend attempting closed reduction using insufflation of the knee with sterile saline for irreducible patellar dislocations before proceeding with open reduction.

Conclusion

Saline insufflation of the knee can be safely and easily performed to aid in the reduction of subacute, difficult patellar dislocations.

The incidence of hip fractures decreased between 1995 and 2005, but these injuries continue to occur in large numbers. Between 1986 and 2005, the mean annual number of hip fractures was 957.3/100,000, and the majority of these occurred in patients 75 to 84 years old.¹ Investigators have described total hip arthroplasty (THA) performed after initial surgical treatment in patients who developed osteoarthritis (OA) of the hip secondary to a fracture.^2-7 Only 1 of these studies compared these patients with a control group of patients who had THA for primary hip OA.² No study included both previous proximal femur and acetabular fractures.

Postfracture OA may occur when there is residual articular incongruity after fracture or osteonecrosis of the femoral head. THA is commonly used to treat OA when more conservative treatments have failed.⁶ Other indications for conversion to THA include femoral neck nonunion, significant leg-length discrepancy, and femoral head damage caused by previous internal fixation.⁴

Given these conditions and previous study findings, THA performed in patients with previous hip fracture fixation is potentially more complicated than THA for primary OA. We therefore conducted a study to evaluate differences in sociodemographic factors, surgical details, and outcomes between patients who had THA for posttraumatic OA and patients who had THA for primary OA.

Materials and Methods

After obtaining institutional review board approval and patient consent, we used a prospective database to follow 3844 patients who had THA performed for OA by 1 of 17 different surgeons at a single center over an 8-year period. Patients who had THA for secondary causes of hip OA, developmental hip dysplasia, or inflammatory processes were excluded. Of the remaining 1199 patients, 62 (5.2%) had THA for posttraumatic OA after previous acetabular or proximal femur fracture fixation (Figures 1, 2) (no THA was performed at time of initial fracture treatment), and 1137 had THA for primary OA and served as the control group.

We collected data on age, sex, fracture location, reason for THA, time between open reduction and internal fixation (ORIF) and THA, type of components, cement use, leg-length discrepancy, intraoperative complications, blood loss, operating room time, and postoperative complications. All patients were aseptic at time of THA. All posttraumatic OA patients had previous hardware removed; the extent of hardware removal was dictated by the exposure required for prosthesis implantation. These patients were contacted, and clinical follow-up was assessed with modified Harris Hip Score (HHS).⁸ HHS was determined by Dr. Khurana. Statistical analysis was performed with Student t test and Pearson χ² test using PASW Statistics 18 (SPSS, Chicago, Illinois).

The 62 posttraumatic OA patients had 63 fractures, 41 of the proximal femur (femoral neck and intertrochanteric; 65%) and 22 acetabular (35%). This group consisted of 33 females and 29 males. Their mean age at time of THA surgery was 58 years (range, 31-90 years). Mean age of the control patients was 59.4 years (range, 18-95 years). There were 35 right hips and 27 left hips in the posttrauma group. Mean body mass index (BMI) was 28.4 for the posttrauma group and 28.9 for the control group. There were no differences in age (P = .451), sex (P = .674), or BMI (P = .592) between the 2 groups (Table 1).

All 62 posttraumatic OA patients had complete hospital data, and 32 (52%) of the 62 underwent long-term follow-up (mean, 4.3 years; range, 4 months–10.5 years). At time of attempted contact (mean, 6.79 years after THA), 7 patients were deceased; cause of death was an unrelated medical condition (1) or unknown (6). The rest of the patients did not respond to multiple telephone and mail summons. Primary reasons for conversion to THA included OA (34 patients, 54%), development of osteonecrosis (12 patients, 19%), and nonunion (12 patients, 19%). The rest of the patients had fixation failure. The mechanisms of injury were motor vehicle accidents (30 patients), falls (20), and other causes (15).

Results

Thirty-two (52%) of the posttraumatic OA patients had a preoperative leg-length discrepancy. For these patients, mean time between initial fracture fixation and conversion to THA was 74 months (range, 1-480 months). Four patients required grafting with cancellous autogenous bone graft or allograft chips to fill a bony defect. Mean acetabular component diameter was 54 mm. Nineteen patients had acetabular fixation supplemented with screws. (Screw supplementation data were not recorded for control patients.) Three patients (4.7%) with an acetabular fracture had heterotopic bone removed at time of THA. Two patients underwent neurolysis of the sciatic nerve at time of surgery for preexisting nerve palsy.

Mean postoperative hemoglobin was 109 g/L in the posttraumatic OA group and 121 g/L in the control group (P <. 001). Mean postoperative hematocrit was 0.327 and 0.367, respectively (P < .001). Mean amount of Cell Saver (Haemonetics) used by patients was 176.2 and 72.9 mL, respectively (P < .001). Posttrauma patients lost a mean of 360 mL of blood more than control patients did (P < .001) and were transfused a mean of 1.59 units of blood, compared with 0.85 unit in the controls (P < .001). Patients with acetabular fractures required a mean of only 0.65 unit of transfused blood. Mean operating room time was 240.5 minutes for posttrauma patients and 135.6 minutes for control patients (P < .001). In the posttrauma group, mean size of the head of the femoral component was 29 mm (head size was not recorded for the control group). Posttrauma patients had 18 (29%) hybrid cemented hip replacements (femoral component only) and 44 uncemented hip replacements. Data on femoral stem size and type were not reported for either group.

Twenty-four posttrauma patients (39%) had a total of 63 perioperative complications, and 131 control patients (11.5%) had a total of 160 complications (P < .001). Complications in posttrauma patients with proximal femur fractures included excess bleeding (5 patients), in-hospital dislocations (2), and postoperative infections (4: 2 superficial wound infections, 1 implant infection requiring explant, 1 Clostridium difficile infection); in patients with acetabular fractures, there was only 1 dislocation (no infections). The posttraumatic OA group did not develop any symptomatic venous thromboembolic complications. One patient developed a sciatic nerve palsy after surgery. Of the 3 patients who sustained dislocations, 2 were treated with closed reduction and maintenance of implants, and 1 with revision THA. Complications in the control group included 3 infections, 4 dislocations, and 12 cases of extensive blood loss (Table 2).

In patients with long-term follow-up, mean postoperative modified HHS was 81.33 (range, 34.1-100.1). Twelve patients had an excellent score (>90), 10 a good score (80-89), 4 a fair score (70-79), and 6 a poor score (<70). Mean HHS was 84.2 for the 16 patients with a femoral head or neck fracture, 77.7 for the 6 patients with an intertrochanteric fracture, and 84.3 for the 9 patients with an acetabular fracture. Nine patients reported using a cane, 3 required walkers, 2 required wheelchairs, and 18 did not require any walking support. Four (12.5%) of the 32 patients required THA revision a mean of 3.5 years (range, 2 months–8 years) after initial arthroplasty. Reasons for revision were infections (2 patients), multiple dislocations (1), and dissociation of acetabular lining (1) (Table 3). Two of the patients who underwent THA revision had a cemented femoral stem, and 2 did not have any cemented implants. Additional details of the femoral stem components were not available for either group.

Discussion

Patients who develop posttraumatic OA of the hip have limited options. THA has emerged as an excellent option in cases of failed repair of fractures about the hip joint. The results of the present study are consistent with earlier findings of the effectiveness of THA in salvaging posttraumatic hips.^2-7 THA for patients with posttraumatic arthritis of the hip after acetabular or proximal femur fracture is longer and more complicated than THA for primary OA, and there is significantly more blood loss. In addition, the rate of early failure appears to be higher.⁹

In this study, mean amount of blood transfused for patients with previous acetabular fracture was 0.65 unit, much less than the mean of 3.5 units noted by Weber and colleagues.⁶ In their study, complications associated with THA were increased in patients with posttraumatic OA from acetabular fractures. The authors attributed these complications to scarring from previous surgery, retained hardware, heterotopic bone, and residual osseous deformity and deficiency. Our results support their conclusion. Operating times were longer, as well as blood loss and the need for blood transfusions and other blood products were increased in the patients with posttraumatic OA, as compared with patients with primary OA. Fifteen percent of patients with an acetabular fracture had undergone removal of heterotopic bone at time of surgery—similar to the rate of 18% noted in the Weber study.⁶

Our results showed that the rate of revision THA was also higher than in patients with primary THA within the general population—reported to be about 4%.⁹ The higher rate may be the result of the additional surgeries performed on patients with fractures, or hardware retention increasing the infection risk over the years. Our revision rate of 12.5% was similar to the 19% found by Ranawat and colleagues⁷ in their study.

A majority of the patients in our study had favorable long-term HHS. Mean overall HHS was 83, slightly better than the 79 reported by Srivastav and colleagues.⁴ We found that patients with intertrochanteric fractures ultimately had worse outcome scores than patients with acetabular or femoral neck fractures. These results are consistent with findings reported by Mehlhoff and colleagues⁵ in a study comparing patients with femoral neck and intertrochanteric fractures. Mean HHS for the intertrochanteric fracture patients in our study was 77.7, comparable to the mean of 78 reported by Mehlhoff and colleagues.⁵ Mean HHS for the femoral neck or head fractures in our study was 84.2, similar to the mean of 81 they noted. Patients with a previous acetabular fracture in our study had a mean HHS of 84.3, consistent with the 84 reported by Ranawat and colleagues⁷ for patients who had initially undergone ORIF for acetabular fracture. Mean HHS in our study (83) was slightly less than the 88.5 reported by Shi and colleagues¹⁰ in their study of primary THAs.

Few studies have been conducted exclusively on one type of hip fracture (acetabular) or another (proximal femur), and all except 1 did not perform a comparison. Tabsh and colleagues² compared similar cohorts but focused solely on patients with previous proximal femur fractures. The present study included a control group and both acetabular and proximal femur fractures, which allowed us to compare patients with and without previous fracture fixation and to consider the 2 different fracture types and see if they affected outcomes.

The strengths of this study include the large control group and the relatively short data-collection period. The shorter period decreased the influence of improvements in implants on patient outcomes. In addition, the control group was our own population, as we did not compare our cohort of patients with previous internal fixation and patients who had primary THAs in other studies, aside from comparisons for revision rates and HHS.

Although the ultimate long-term follow-up rate for patients with previous internal fixation was 50%, our sample size was still larger than that in most reported studies. Another weakness of our study was the large number of surgeons (17), representing an array of techniques, approaches, and surgical experience. All these factors could have influenced patient outcomes and operative data. In addition, data on revision rates and HHS were not available for our control group, so we could not directly compare these outcomes with those of the posttraumatic group. However, we used previously reported data on revision rates and HHS in primary THAs for comparison with the posttraumatic group.^9,10

Conclusion

In this study, THA was a viable option for patients with posttraumatic arthritis from a previous acetabular or proximal femur fracture. The outcomes, however, were less reliable than the outcomes of primary THA for degenerative arthritis, and the complication rates were higher. Surgeons should counsel patients about the complexity of the procedure as well as its ultimately favorable outcomes. Surgeons should expect additional technical difficulties in the operating room when treating this patient population.

The incidence of hip fractures decreased between 1995 and 2005, but these injuries continue to occur in large numbers. Between 1986 and 2005, the mean annual number of hip fractures was 957.3/100,000, and the majority of these occurred in patients 75 to 84 years old.¹ Investigators have described total hip arthroplasty (THA) performed after initial surgical treatment in patients who developed osteoarthritis (OA) of the hip secondary to a fracture.^2-7 Only 1 of these studies compared these patients with a control group of patients who had THA for primary hip OA.² No study included both previous proximal femur and acetabular fractures.

Postfracture OA may occur when there is residual articular incongruity after fracture or osteonecrosis of the femoral head. THA is commonly used to treat OA when more conservative treatments have failed.⁶ Other indications for conversion to THA include femoral neck nonunion, significant leg-length discrepancy, and femoral head damage caused by previous internal fixation.⁴

Given these conditions and previous study findings, THA performed in patients with previous hip fracture fixation is potentially more complicated than THA for primary OA. We therefore conducted a study to evaluate differences in sociodemographic factors, surgical details, and outcomes between patients who had THA for posttraumatic OA and patients who had THA for primary OA.

Materials and Methods

After obtaining institutional review board approval and patient consent, we used a prospective database to follow 3844 patients who had THA performed for OA by 1 of 17 different surgeons at a single center over an 8-year period. Patients who had THA for secondary causes of hip OA, developmental hip dysplasia, or inflammatory processes were excluded. Of the remaining 1199 patients, 62 (5.2%) had THA for posttraumatic OA after previous acetabular or proximal femur fracture fixation (Figures 1, 2) (no THA was performed at time of initial fracture treatment), and 1137 had THA for primary OA and served as the control group.

We collected data on age, sex, fracture location, reason for THA, time between open reduction and internal fixation (ORIF) and THA, type of components, cement use, leg-length discrepancy, intraoperative complications, blood loss, operating room time, and postoperative complications. All patients were aseptic at time of THA. All posttraumatic OA patients had previous hardware removed; the extent of hardware removal was dictated by the exposure required for prosthesis implantation. These patients were contacted, and clinical follow-up was assessed with modified Harris Hip Score (HHS).⁸ HHS was determined by Dr. Khurana. Statistical analysis was performed with Student t test and Pearson χ² test using PASW Statistics 18 (SPSS, Chicago, Illinois).

The 62 posttraumatic OA patients had 63 fractures, 41 of the proximal femur (femoral neck and intertrochanteric; 65%) and 22 acetabular (35%). This group consisted of 33 females and 29 males. Their mean age at time of THA surgery was 58 years (range, 31-90 years). Mean age of the control patients was 59.4 years (range, 18-95 years). There were 35 right hips and 27 left hips in the posttrauma group. Mean body mass index (BMI) was 28.4 for the posttrauma group and 28.9 for the control group. There were no differences in age (P = .451), sex (P = .674), or BMI (P = .592) between the 2 groups (Table 1).

All 62 posttraumatic OA patients had complete hospital data, and 32 (52%) of the 62 underwent long-term follow-up (mean, 4.3 years; range, 4 months–10.5 years). At time of attempted contact (mean, 6.79 years after THA), 7 patients were deceased; cause of death was an unrelated medical condition (1) or unknown (6). The rest of the patients did not respond to multiple telephone and mail summons. Primary reasons for conversion to THA included OA (34 patients, 54%), development of osteonecrosis (12 patients, 19%), and nonunion (12 patients, 19%). The rest of the patients had fixation failure. The mechanisms of injury were motor vehicle accidents (30 patients), falls (20), and other causes (15).

Results

Thirty-two (52%) of the posttraumatic OA patients had a preoperative leg-length discrepancy. For these patients, mean time between initial fracture fixation and conversion to THA was 74 months (range, 1-480 months). Four patients required grafting with cancellous autogenous bone graft or allograft chips to fill a bony defect. Mean acetabular component diameter was 54 mm. Nineteen patients had acetabular fixation supplemented with screws. (Screw supplementation data were not recorded for control patients.) Three patients (4.7%) with an acetabular fracture had heterotopic bone removed at time of THA. Two patients underwent neurolysis of the sciatic nerve at time of surgery for preexisting nerve palsy.

Mean postoperative hemoglobin was 109 g/L in the posttraumatic OA group and 121 g/L in the control group (P <. 001). Mean postoperative hematocrit was 0.327 and 0.367, respectively (P < .001). Mean amount of Cell Saver (Haemonetics) used by patients was 176.2 and 72.9 mL, respectively (P < .001). Posttrauma patients lost a mean of 360 mL of blood more than control patients did (P < .001) and were transfused a mean of 1.59 units of blood, compared with 0.85 unit in the controls (P < .001). Patients with acetabular fractures required a mean of only 0.65 unit of transfused blood. Mean operating room time was 240.5 minutes for posttrauma patients and 135.6 minutes for control patients (P < .001). In the posttrauma group, mean size of the head of the femoral component was 29 mm (head size was not recorded for the control group). Posttrauma patients had 18 (29%) hybrid cemented hip replacements (femoral component only) and 44 uncemented hip replacements. Data on femoral stem size and type were not reported for either group.

Twenty-four posttrauma patients (39%) had a total of 63 perioperative complications, and 131 control patients (11.5%) had a total of 160 complications (P < .001). Complications in posttrauma patients with proximal femur fractures included excess bleeding (5 patients), in-hospital dislocations (2), and postoperative infections (4: 2 superficial wound infections, 1 implant infection requiring explant, 1 Clostridium difficile infection); in patients with acetabular fractures, there was only 1 dislocation (no infections). The posttraumatic OA group did not develop any symptomatic venous thromboembolic complications. One patient developed a sciatic nerve palsy after surgery. Of the 3 patients who sustained dislocations, 2 were treated with closed reduction and maintenance of implants, and 1 with revision THA. Complications in the control group included 3 infections, 4 dislocations, and 12 cases of extensive blood loss (Table 2).

In patients with long-term follow-up, mean postoperative modified HHS was 81.33 (range, 34.1-100.1). Twelve patients had an excellent score (>90), 10 a good score (80-89), 4 a fair score (70-79), and 6 a poor score (<70). Mean HHS was 84.2 for the 16 patients with a femoral head or neck fracture, 77.7 for the 6 patients with an intertrochanteric fracture, and 84.3 for the 9 patients with an acetabular fracture. Nine patients reported using a cane, 3 required walkers, 2 required wheelchairs, and 18 did not require any walking support. Four (12.5%) of the 32 patients required THA revision a mean of 3.5 years (range, 2 months–8 years) after initial arthroplasty. Reasons for revision were infections (2 patients), multiple dislocations (1), and dissociation of acetabular lining (1) (Table 3). Two of the patients who underwent THA revision had a cemented femoral stem, and 2 did not have any cemented implants. Additional details of the femoral stem components were not available for either group.

Discussion

Patients who develop posttraumatic OA of the hip have limited options. THA has emerged as an excellent option in cases of failed repair of fractures about the hip joint. The results of the present study are consistent with earlier findings of the effectiveness of THA in salvaging posttraumatic hips.^2-7 THA for patients with posttraumatic arthritis of the hip after acetabular or proximal femur fracture is longer and more complicated than THA for primary OA, and there is significantly more blood loss. In addition, the rate of early failure appears to be higher.⁹

In this study, mean amount of blood transfused for patients with previous acetabular fracture was 0.65 unit, much less than the mean of 3.5 units noted by Weber and colleagues.⁶ In their study, complications associated with THA were increased in patients with posttraumatic OA from acetabular fractures. The authors attributed these complications to scarring from previous surgery, retained hardware, heterotopic bone, and residual osseous deformity and deficiency. Our results support their conclusion. Operating times were longer, as well as blood loss and the need for blood transfusions and other blood products were increased in the patients with posttraumatic OA, as compared with patients with primary OA. Fifteen percent of patients with an acetabular fracture had undergone removal of heterotopic bone at time of surgery—similar to the rate of 18% noted in the Weber study.⁶

Our results showed that the rate of revision THA was also higher than in patients with primary THA within the general population—reported to be about 4%.⁹ The higher rate may be the result of the additional surgeries performed on patients with fractures, or hardware retention increasing the infection risk over the years. Our revision rate of 12.5% was similar to the 19% found by Ranawat and colleagues⁷ in their study.

A majority of the patients in our study had favorable long-term HHS. Mean overall HHS was 83, slightly better than the 79 reported by Srivastav and colleagues.⁴ We found that patients with intertrochanteric fractures ultimately had worse outcome scores than patients with acetabular or femoral neck fractures. These results are consistent with findings reported by Mehlhoff and colleagues⁵ in a study comparing patients with femoral neck and intertrochanteric fractures. Mean HHS for the intertrochanteric fracture patients in our study was 77.7, comparable to the mean of 78 reported by Mehlhoff and colleagues.⁵ Mean HHS for the femoral neck or head fractures in our study was 84.2, similar to the mean of 81 they noted. Patients with a previous acetabular fracture in our study had a mean HHS of 84.3, consistent with the 84 reported by Ranawat and colleagues⁷ for patients who had initially undergone ORIF for acetabular fracture. Mean HHS in our study (83) was slightly less than the 88.5 reported by Shi and colleagues¹⁰ in their study of primary THAs.

Few studies have been conducted exclusively on one type of hip fracture (acetabular) or another (proximal femur), and all except 1 did not perform a comparison. Tabsh and colleagues² compared similar cohorts but focused solely on patients with previous proximal femur fractures. The present study included a control group and both acetabular and proximal femur fractures, which allowed us to compare patients with and without previous fracture fixation and to consider the 2 different fracture types and see if they affected outcomes.

The strengths of this study include the large control group and the relatively short data-collection period. The shorter period decreased the influence of improvements in implants on patient outcomes. In addition, the control group was our own population, as we did not compare our cohort of patients with previous internal fixation and patients who had primary THAs in other studies, aside from comparisons for revision rates and HHS.

Although the ultimate long-term follow-up rate for patients with previous internal fixation was 50%, our sample size was still larger than that in most reported studies. Another weakness of our study was the large number of surgeons (17), representing an array of techniques, approaches, and surgical experience. All these factors could have influenced patient outcomes and operative data. In addition, data on revision rates and HHS were not available for our control group, so we could not directly compare these outcomes with those of the posttraumatic group. However, we used previously reported data on revision rates and HHS in primary THAs for comparison with the posttraumatic group.^9,10

Conclusion

In this study, THA was a viable option for patients with posttraumatic arthritis from a previous acetabular or proximal femur fracture. The outcomes, however, were less reliable than the outcomes of primary THA for degenerative arthritis, and the complication rates were higher. Surgeons should counsel patients about the complexity of the procedure as well as its ultimately favorable outcomes. Surgeons should expect additional technical difficulties in the operating room when treating this patient population.

The incidence of hip fractures decreased between 1995 and 2005, but these injuries continue to occur in large numbers. Between 1986 and 2005, the mean annual number of hip fractures was 957.3/100,000, and the majority of these occurred in patients 75 to 84 years old.¹ Investigators have described total hip arthroplasty (THA) performed after initial surgical treatment in patients who developed osteoarthritis (OA) of the hip secondary to a fracture.^2-7 Only 1 of these studies compared these patients with a control group of patients who had THA for primary hip OA.² No study included both previous proximal femur and acetabular fractures.

Postfracture OA may occur when there is residual articular incongruity after fracture or osteonecrosis of the femoral head. THA is commonly used to treat OA when more conservative treatments have failed.⁶ Other indications for conversion to THA include femoral neck nonunion, significant leg-length discrepancy, and femoral head damage caused by previous internal fixation.⁴

Given these conditions and previous study findings, THA performed in patients with previous hip fracture fixation is potentially more complicated than THA for primary OA. We therefore conducted a study to evaluate differences in sociodemographic factors, surgical details, and outcomes between patients who had THA for posttraumatic OA and patients who had THA for primary OA.

Materials and Methods

After obtaining institutional review board approval and patient consent, we used a prospective database to follow 3844 patients who had THA performed for OA by 1 of 17 different surgeons at a single center over an 8-year period. Patients who had THA for secondary causes of hip OA, developmental hip dysplasia, or inflammatory processes were excluded. Of the remaining 1199 patients, 62 (5.2%) had THA for posttraumatic OA after previous acetabular or proximal femur fracture fixation (Figures 1, 2) (no THA was performed at time of initial fracture treatment), and 1137 had THA for primary OA and served as the control group.

We collected data on age, sex, fracture location, reason for THA, time between open reduction and internal fixation (ORIF) and THA, type of components, cement use, leg-length discrepancy, intraoperative complications, blood loss, operating room time, and postoperative complications. All patients were aseptic at time of THA. All posttraumatic OA patients had previous hardware removed; the extent of hardware removal was dictated by the exposure required for prosthesis implantation. These patients were contacted, and clinical follow-up was assessed with modified Harris Hip Score (HHS).⁸ HHS was determined by Dr. Khurana. Statistical analysis was performed with Student t test and Pearson χ² test using PASW Statistics 18 (SPSS, Chicago, Illinois).

The 62 posttraumatic OA patients had 63 fractures, 41 of the proximal femur (femoral neck and intertrochanteric; 65%) and 22 acetabular (35%). This group consisted of 33 females and 29 males. Their mean age at time of THA surgery was 58 years (range, 31-90 years). Mean age of the control patients was 59.4 years (range, 18-95 years). There were 35 right hips and 27 left hips in the posttrauma group. Mean body mass index (BMI) was 28.4 for the posttrauma group and 28.9 for the control group. There were no differences in age (P = .451), sex (P = .674), or BMI (P = .592) between the 2 groups (Table 1).

All 62 posttraumatic OA patients had complete hospital data, and 32 (52%) of the 62 underwent long-term follow-up (mean, 4.3 years; range, 4 months–10.5 years). At time of attempted contact (mean, 6.79 years after THA), 7 patients were deceased; cause of death was an unrelated medical condition (1) or unknown (6). The rest of the patients did not respond to multiple telephone and mail summons. Primary reasons for conversion to THA included OA (34 patients, 54%), development of osteonecrosis (12 patients, 19%), and nonunion (12 patients, 19%). The rest of the patients had fixation failure. The mechanisms of injury were motor vehicle accidents (30 patients), falls (20), and other causes (15).

Results

Thirty-two (52%) of the posttraumatic OA patients had a preoperative leg-length discrepancy. For these patients, mean time between initial fracture fixation and conversion to THA was 74 months (range, 1-480 months). Four patients required grafting with cancellous autogenous bone graft or allograft chips to fill a bony defect. Mean acetabular component diameter was 54 mm. Nineteen patients had acetabular fixation supplemented with screws. (Screw supplementation data were not recorded for control patients.) Three patients (4.7%) with an acetabular fracture had heterotopic bone removed at time of THA. Two patients underwent neurolysis of the sciatic nerve at time of surgery for preexisting nerve palsy.

Mean postoperative hemoglobin was 109 g/L in the posttraumatic OA group and 121 g/L in the control group (P <. 001). Mean postoperative hematocrit was 0.327 and 0.367, respectively (P < .001). Mean amount of Cell Saver (Haemonetics) used by patients was 176.2 and 72.9 mL, respectively (P < .001). Posttrauma patients lost a mean of 360 mL of blood more than control patients did (P < .001) and were transfused a mean of 1.59 units of blood, compared with 0.85 unit in the controls (P < .001). Patients with acetabular fractures required a mean of only 0.65 unit of transfused blood. Mean operating room time was 240.5 minutes for posttrauma patients and 135.6 minutes for control patients (P < .001). In the posttrauma group, mean size of the head of the femoral component was 29 mm (head size was not recorded for the control group). Posttrauma patients had 18 (29%) hybrid cemented hip replacements (femoral component only) and 44 uncemented hip replacements. Data on femoral stem size and type were not reported for either group.

Twenty-four posttrauma patients (39%) had a total of 63 perioperative complications, and 131 control patients (11.5%) had a total of 160 complications (P < .001). Complications in posttrauma patients with proximal femur fractures included excess bleeding (5 patients), in-hospital dislocations (2), and postoperative infections (4: 2 superficial wound infections, 1 implant infection requiring explant, 1 Clostridium difficile infection); in patients with acetabular fractures, there was only 1 dislocation (no infections). The posttraumatic OA group did not develop any symptomatic venous thromboembolic complications. One patient developed a sciatic nerve palsy after surgery. Of the 3 patients who sustained dislocations, 2 were treated with closed reduction and maintenance of implants, and 1 with revision THA. Complications in the control group included 3 infections, 4 dislocations, and 12 cases of extensive blood loss (Table 2).

In patients with long-term follow-up, mean postoperative modified HHS was 81.33 (range, 34.1-100.1). Twelve patients had an excellent score (>90), 10 a good score (80-89), 4 a fair score (70-79), and 6 a poor score (<70). Mean HHS was 84.2 for the 16 patients with a femoral head or neck fracture, 77.7 for the 6 patients with an intertrochanteric fracture, and 84.3 for the 9 patients with an acetabular fracture. Nine patients reported using a cane, 3 required walkers, 2 required wheelchairs, and 18 did not require any walking support. Four (12.5%) of the 32 patients required THA revision a mean of 3.5 years (range, 2 months–8 years) after initial arthroplasty. Reasons for revision were infections (2 patients), multiple dislocations (1), and dissociation of acetabular lining (1) (Table 3). Two of the patients who underwent THA revision had a cemented femoral stem, and 2 did not have any cemented implants. Additional details of the femoral stem components were not available for either group.

Discussion

Patients who develop posttraumatic OA of the hip have limited options. THA has emerged as an excellent option in cases of failed repair of fractures about the hip joint. The results of the present study are consistent with earlier findings of the effectiveness of THA in salvaging posttraumatic hips.^2-7 THA for patients with posttraumatic arthritis of the hip after acetabular or proximal femur fracture is longer and more complicated than THA for primary OA, and there is significantly more blood loss. In addition, the rate of early failure appears to be higher.⁹

In this study, mean amount of blood transfused for patients with previous acetabular fracture was 0.65 unit, much less than the mean of 3.5 units noted by Weber and colleagues.⁶ In their study, complications associated with THA were increased in patients with posttraumatic OA from acetabular fractures. The authors attributed these complications to scarring from previous surgery, retained hardware, heterotopic bone, and residual osseous deformity and deficiency. Our results support their conclusion. Operating times were longer, as well as blood loss and the need for blood transfusions and other blood products were increased in the patients with posttraumatic OA, as compared with patients with primary OA. Fifteen percent of patients with an acetabular fracture had undergone removal of heterotopic bone at time of surgery—similar to the rate of 18% noted in the Weber study.⁶

Our results showed that the rate of revision THA was also higher than in patients with primary THA within the general population—reported to be about 4%.⁹ The higher rate may be the result of the additional surgeries performed on patients with fractures, or hardware retention increasing the infection risk over the years. Our revision rate of 12.5% was similar to the 19% found by Ranawat and colleagues⁷ in their study.

A majority of the patients in our study had favorable long-term HHS. Mean overall HHS was 83, slightly better than the 79 reported by Srivastav and colleagues.⁴ We found that patients with intertrochanteric fractures ultimately had worse outcome scores than patients with acetabular or femoral neck fractures. These results are consistent with findings reported by Mehlhoff and colleagues⁵ in a study comparing patients with femoral neck and intertrochanteric fractures. Mean HHS for the intertrochanteric fracture patients in our study was 77.7, comparable to the mean of 78 reported by Mehlhoff and colleagues.⁵ Mean HHS for the femoral neck or head fractures in our study was 84.2, similar to the mean of 81 they noted. Patients with a previous acetabular fracture in our study had a mean HHS of 84.3, consistent with the 84 reported by Ranawat and colleagues⁷ for patients who had initially undergone ORIF for acetabular fracture. Mean HHS in our study (83) was slightly less than the 88.5 reported by Shi and colleagues¹⁰ in their study of primary THAs.

Few studies have been conducted exclusively on one type of hip fracture (acetabular) or another (proximal femur), and all except 1 did not perform a comparison. Tabsh and colleagues² compared similar cohorts but focused solely on patients with previous proximal femur fractures. The present study included a control group and both acetabular and proximal femur fractures, which allowed us to compare patients with and without previous fracture fixation and to consider the 2 different fracture types and see if they affected outcomes.

The strengths of this study include the large control group and the relatively short data-collection period. The shorter period decreased the influence of improvements in implants on patient outcomes. In addition, the control group was our own population, as we did not compare our cohort of patients with previous internal fixation and patients who had primary THAs in other studies, aside from comparisons for revision rates and HHS.

Although the ultimate long-term follow-up rate for patients with previous internal fixation was 50%, our sample size was still larger than that in most reported studies. Another weakness of our study was the large number of surgeons (17), representing an array of techniques, approaches, and surgical experience. All these factors could have influenced patient outcomes and operative data. In addition, data on revision rates and HHS were not available for our control group, so we could not directly compare these outcomes with those of the posttraumatic group. However, we used previously reported data on revision rates and HHS in primary THAs for comparison with the posttraumatic group.^9,10

Conclusion

In this study, THA was a viable option for patients with posttraumatic arthritis from a previous acetabular or proximal femur fracture. The outcomes, however, were less reliable than the outcomes of primary THA for degenerative arthritis, and the complication rates were higher. Surgeons should counsel patients about the complexity of the procedure as well as its ultimately favorable outcomes. Surgeons should expect additional technical difficulties in the operating room when treating this patient population.

L-ascorbic acid, more commonly know as vitamin C, is an essential micronutrient used in numerous metabolic pathways. It functions physiologically as a water-soluble antioxidant by virtue of its high reducing power, playing a key role in the function of leukocytes, protein metabolism, and production of neurotransmitters.^1-3 Vitamin C also contributes to musculoskeletal health through biosynthesis of carnitine and collagen⁴ and enhancement of intestinal absorption of dietary iron⁵ from plants and vegetables. Unlike most animals, humans are unable to synthesize this essential vitamin and therefore require intake from natural dietary sources or supplements.⁶ The ability of vitamin C to prevent or treat disease has been an area of research interest since the vitamin was identified and isolated by Szent-Györgyi in the 1930s.^7-16 Research in orthopedic surgery has focused on the effects of vitamin C on fracture healing, its potential use in preventing complex regional pain syndrome (CRPS), and its role in the pathophysiology of osteoarthritis. In this article, we review the basics of vitamin C metabolism and summarize the evidence surrounding the role of vitamin C supplementation in orthopedics.

Sources and Metabolism

Vitamin C is found naturally in many fruits and vegetables (Table 1) and is a common fortification in cereals, juices, and multivitamins. Daily recommended intake (Table 2) depends on age and smoking status. Absorption occurs in the distal small intestine, with blood plasma vitamin C concentrations reflecting dietary intake. Pharmacokinetic studies have shown that vitamin C concentrations are tightly regulated through absorption, tissue accumulation, and renal resorption, with plasma concentrations rarely exceeding 100 μmol/L without additional supplementation.¹⁷ Although the usual dietary doses of 100 mg/d (adult) are almost completely absorbed, producing a plasma concentration of 60 μmol/L, higher intake results in an increasingly smaller fraction absorbed.^1,18 Intake of more than 1000 mg/d results in less than 50% absorption¹⁹ (unmetabolized vitamin C is excreted in stool and urine¹). Even at higher doses, vitamin C has low toxicity³; the most common complaints are diarrhea, nausea, and abdominal cramps caused by the osmotic effect of unabsorbed vitamin C in the gastrointestinal tract.¹

Vitamin C Deficiency

The relationship between vitamin C deficiency and the development of scurvy has been documented for centuries. Symptoms are described in the ancient Egyptian, Greek, and Roman literature.²⁰ Ascorbic acid is essential for normal collagen function, as it is a required cofactor for enzymatic transfer of hydroxyl groups to select proline and lysine residues during procollagen formation. Hydroxylysine contributes to the intermolecular cross-links in collagen, and hydroxyproline stabilizes the triple-helix structure of collagen.²¹ Insufficient vitamin C during this process results in collagen that is non-cross-linked, nonhelical, structurally unstable, and weak.²¹ Clinical manifestations of scurvy stem from an underlying impairment of collagen production causing a systemic decrease in connective tissue integrity, capillary fragility, poor wound healing, fatigue, myalgias, arthritis, and even death.²² Vitamin C deficiency has also been implicated as a cause of diffuse bleeding in surgical patients with normal coagulation parameters secondary to capillary fragility.²³ In the United States, the 2003–2004 National Health and Nutrition Examination Survey (NHANES) measured serum vitamin C concentrations in 7277 noninstitutionalized patients 6 years old or older.²⁴ Age-adjusted incidence of subnormal serum vitamin C levels (<28 μmol/L) was 19.6%, and incidence of frank vitamin C deficiency (<11.4 μmol/L) was 7.1%. Reported rates of vitamin C deficiency in hospitalized patients are much higher, with 47% to 60% having subnormal values (<28 μmol/L) and 17% to 19% being vitamin C–deficient (<11.4 μmol/L).^22,25 Identified risk factors for hypovitaminosis C include advanced age, obesity, low socioeconomic status, unemployment, male sex, and concomitant alcohol and tobacco consumption.^22,24,25

Fracture Healing and Prevention

The effects of vitamin C deficiency on bone healing have been studied with animal models as early as the 1940s.^26,27 Early experiments using guinea pigs demonstrated failure of bone graft incorporation, delayed collagen maturation, and decreased collagen and callus formation in scorbutic animals compared with controls that received vitamin C supplementation.^26,27 Based on his work with guinea pigs, Bourne²⁶ reported in 1942 that vitamin C deficiency significantly inhibited the reparative process in damaged bone and that patients with fractures should receive vitamin C supplementation. Building on this early research, Yilmaz and colleagues²⁸ found faster histologic healing for tibia fractures in a rat model for animals that received a single injection of vitamin C 0.5 mg/kg compared with a nonscorbutic control group, and Sarisözen and colleagues²⁹ showed significantly accelerated histologic bone formation and mineralization at the fracture site for rats that received vitamin C supplementation. Moreover, Kipp and colleagues³⁰ found that scorbutic guinea pigs had lower bone mineral density (BMD), decreased bone mineral content, and impaired collagen synthesis of articular cartilage and tendons compared with nondeficient controls.

Besides promoting bone formation, vitamin C improves the mechanical strength of callus formation. Alcantara-Martos and colleagues³¹ used an osteogenic disorder Shionogi (ODS) rat model to examine the effects of vitamin C intake on femoral fracture healing. This particular animal model is unable to produce its own vitamin C. The groups with lower serum vitamin C levels demonstrated lower mechanical resistance of the fracture callus to torsional loads 5 weeks after fracture. Moreover, the group that received vitamin C supplementation showed higher histologic grade of callus formation and demonstrated faster healing rates. The authors suggested that subclinical vitamin C deficiency can delay fracture healing and that vitamin C supplementation in nondeficient patients would improve bone healing.

Other research has demonstrated a link between vitamin C and mesenchymal cell differentiation. Mohan and colleagues³² used an sfx mouse model to show that vitamin C deficiency results in decreased bone formation secondary to impaired osteoblast differentiation, diminished bone density, and development of spontaneous fractures. The authors indicated that not only is vitamin C essential for maintenance of differentiated functions of osteoblasts, but deficiency during early active growth may affect peak BMD levels in humans. Additional studies have demonstrated the role of vitamin C in endochondral bone formation through both induction of osteoblast differentiation and modulation of gene expression in hypertrophic chondrocytes.^33-36 Chronic vitamin C deficiency has been found to depress osteoblast function and differentiation of chondrocytes.³⁷ More recently, Kim and colleagues³⁸ examined the effect of vitamin C insufficiency in Gulo-deficient mice, which are unable to synthesize ascorbic acid. Ascorbic acid insufficiency over 4 weeks led to decreased plasma levels of osteocalcin and bone formation in vivo as well as significantly diminished metaphyseal trabecular bone. Despite all the evidence demonstrating the importance of vitamin C in bone formation and maintenance, many of the underlying processes in this relationship have yet to be determined.

Bone Mineral Density

Several observational studies have found a positive association between vitamin C intake and BMD in postmenopausal women. In a retrospective, cross-sectional study by Hall and Greendale,³⁹ a positive association was found between vitamin C intake and BMD of the femoral neck in 775 participants in the Postmenopausal Estrogen/Progestin Interventions trial. After calcium intake, physical activity level, smoking, estrogen use, age, and body mass index were adjusted for, each 100-mg increase in dietary vitamin C was associated with a 0.017 g/cm² increase in BMD. Wang and colleagues⁴⁰ found a positive association between dietary vitamin C intake and femoral neck BMD in a retrospective analysis of 125 postmenopausal Mexican American women. Other observational studies have reported that decreased intake of vitamin C is associated with osteoporosis⁴¹ and increased rates of BMD loss⁴² and that supplementation with vitamin C may suppress bone resorption in postmenopausal women.⁴³

The results of these studies contrast with the findings of Leveille and colleagues,⁴⁴ who examined the relationship between dietary vitamin C and hip BMD in 1892 postmenopausal women. Although the authors found that women (age, 55-64 years) using vitamin C supplements for more than 10 years had an average BMD 6.7% higher than that of nonusers, they did not find any association between dietary vitamin C intake and BMD. Moreover, NHANES III also found inconsistent associations between vitamin C and BMD among 13,080 adults surveyed in the United States.⁴⁵ Although for premenopausal women dietary ascorbic acid was associated with increased BMD, for postmenopausal women with a history of smoking and estrogen replacement, it was actually associated with lower BMD values. For other subgroups in the study, the relationship was also inconsistent or nonlinear.

The exact mechanism by which ascorbic acid contributes to BMD is not fully delineated. However, it likely is related to the known role of vitamin C in collagen formation, bone matrix development, osteoblast differentiation, and its antioxidant effects limiting bone resorption.^44,46

Hip Fractures

Besides demonstrating positive effects of vitamin C on bone healing and BMD, epidemiologic studies have found evidence of a protective effect of vitamin C on hip fracture risk. In a study of the Swedish Mammography cohort, 66,651 women (age, 40-76 years) were prospectively followed.⁴⁷ The authors found that the odds ratio (OR) for hip fractures among smokers with a low intake of vitamin E (median intake, ≤6.2 mg/d) was 3.0 (95% CI, 1.6-5.4) and for vitamin C (median intake, ≤67 mg/d) was 3.0 (95% CI, 1.6-5.6). Moreover, in smokers with a low intake of both vitamins E and C, OR increased to 4.9 (95% CI, 2.2-11.0). In addition, the Utah Study of Nutrition and Bone Health matched 1215 cases of hip fractures in patients who had ever smoked (age, >50 years) with 1349 controls and found that vitamin C intake above 159 mg/d had a significant protective effect on the incidence of hip fracture; however, a graded relationship was not observed.⁴⁸ Despite the inconsistencies in the NHANES III study regarding the relationship between vitamin C and BMD, Simon and Hudes⁴⁵ found that serum vitamin C was associated with lower risk for self-reported fracture in postmenopausal women who had ever smoked and had a history of estrogen therapy (OR, 0.51; 95% CI, 0.36-0.70). Finally, Sahni and colleagues⁴⁹ followed 958 Framingham cohort men and women (mean age, 75 years) over 17 years and found that those in the highest tertile of total vitamin C intake (median, 313 mg/d) had significantly fewer hip fractures and nonvertebral fractures compared with those in the lowest tertile of intake (median, 94 mg/d). Dietary vitamin C intake was not associated with fracture risk in this study.

Complex Regional Pain Syndrome

Type 1 CRPS is a debilitating condition characterized by severe pain, swelling, and vasomotor instability. It is commonly precipitated by an injury or surgery to an extremity and is a dreaded sequelae in orthopedics,⁵⁰ with incidence rates of 10% to 22% in wrist fractures^51-53 and 10% after foot and ankle surgery.⁵⁴ Although the pathophysiology of CRPS remains unknown, dysregulation and increased permeability of the vasculature caused by free radicals are thought to play an important role.⁵⁵ In dermal burns, high doses of vitamin C therapy slowed progression of vascular permeability and therefore reduced extravascular leakage of fluids and protein.^56,57 The ability of vitamin C to prevent CRPS has been studied in only a handful of trials.

In a double-blind trial, Zollinger and colleagues⁵¹ randomized 127 conservatively treated distal radius fractures to receive either vitamin C 500 mg or placebo daily for 50 days starting on day of injury. Incidence of CRPS (using the diagnostic criteria proposed by Veldman and colleagues⁵⁸) at 1-year follow-up was 22% in the placebo group and 7% in the vitamin C group (95% CI for difference, 2%-26%). Complaints while wearing the cast and fracture type increased the risk for developing CRPS. This initial study was followed up by a prospective, randomized, double-blind multicenter trial by the same authors,⁵² who had 416 patients with 427 wrist fractures receive either placebo or vitamin C 200 mg/d, 500 mg/d, or 1500 mg/d for 50 days. This follow-up study included both operative (11%) and nonoperative (89%) distal radius fractures. Incidence of CRPS was 10.1% in the placebo group and 2.4% in the vitamin C group (P < .002). Although there was an appreciable drop in the relative risk (RR) of developing CRPS between the vitamin C 200-mg/d and 500-mg/d groups (0.41-0.17), there was no additional benefit in the 1500-mg/d group. Pooling the data for these 2 randomized trials showed that the overall RR for developing CRPS was lower with vitamin C supplementation (RR, 0.28; 95% CI, 0.14-0.56; P = .0003).⁵⁹

Results of the 2 trials by Zollinger and colleagues^51,52 have been met with several concerns.^60-62 As a corollary to the unclear etiology of CRPS, several different sets of diagnostic criteria exist, and the criteria are somewhat subjective and imprecise. Although both trials used the Veldman criteria,⁵⁸ the incidence of CRPS in the placebo group dropped unexpectedly between trials, from 22% to 10.1%, and the results may have been different had other criteria been used. Moreover, the idea that toxic oxygen radicals have a role in CRPS and that vitamin C can scavenge these radicals is based on limited data.⁶¹ In the absence of a clear pathophysiologic explanation, some surgeons have been reluctant to treat patients with vitamin C supplementation.

Cazeneuve and colleagues⁵³ also studied the effect of vitamin C supplementation on CRPS in patients with distal radius fractures treated with reduction and intrafocal pinning. Group 1 consisted of 100 patients (treated from 1995 to 1998) who did not receive vitamin C supplementation, and group 2 consisted of 95 patients (treated from 1998 to 2002) who received vitamin C 1000 mg/d for 45 days starting on day of fracture. Patients were followed for up to 90 days after surgery. Incidence of CRPS type 1 was 10% in the untreated group and 2.1% in the group that received vitamin C supplementation.

Vitamin C prophylaxis for CRPS has also been studied in foot and ankle surgery. Besse and colleagues⁵⁴ prospectively compared 2 chronologically successive groups that received (235 feet) or did not receive (185 feet) vitamin C 1000-mg/d supplementation for 45 days. Incidence of CRPS type 1 as diagnosed with International Association for the Study of Pain (IASP) criteria dropped from 9.6% to 1.7% with vitamin C supplementation. In a case series, Zollinger and colleagues⁶³ examined CRPS type 1 rates after performing cementless total trapeziometacarpal semiconstrained joint prosthesis implantations for trapeziometacarpal arthritis. Forty implantations were performed in 34 patients. All patients received vitamin C 500 mg/d for CRPS prevention starting 2 days before surgery for 50 days. There were no cases of CRPS in the postoperative period, according to Veldman or IASP criteria. Although the results of the studies by Cazeneuve and colleagues⁵³ and Besse and colleagues⁵⁴ agree with those of the distal radius fracture trials by Zollinger and colleagues,^51,52 the quasi-experimental design and the lack of blinding and randomization temper the conclusions that can be drawn because of the risk for significant bias.

In a recent systematic review examining the effectiveness of vitamin C supplementation in preventing CRPS in trauma and surgery in the extremities, Shibuya and colleagues⁶⁴ concluded that taking at least 500 mg of vitamin C daily for 45 to 50 days after injury or surgery may help decrease the incidence of CRPS after a traumatic event.

Osteoarthritis

Damage caused by free radicals has long been thought to play an important role in osteoarthritis (OA).^65-67 A cross-sectional study in knee OA found that amounts of joint fluid antioxidants were lower in patients with severe arthritis than in those with intact cartilage, further implicating free radicals in the pathophysiology of OA.⁶⁸ Use of vitamin C for prophylaxis against development or progression of OA is therefore a hot research topic. Thus far, animal studies have had mixed results—several showing a chondroprotective effect of vitamin C^69,70 and others finding either no effect or even a positive association with the development of arthritis.⁷¹

The literature on human subjects, chiefly observational studies, is just as controversial. Wang and colleagues⁴⁰ found vitamin C intake associated with both a 50% risk reduction of bone marrow lesions on magnetic resonance imaging over a 10-year interval (OR, 0.5; 95% CI, 0.29-0.87) and inversely associated with the tibial plateau bone area. Similarly, the Clearwater Osteoarthritis Study, which followed 1023 patients (age, >40 years), showed that participants who took vitamin C supplements were 11% less likely to develop radiographic evidence of OA (RR, 0.89; 95% CI, 0.85-0.93).⁷² Nonetheless, other studies have failed to show such associations⁷³ or have demonstrated the opposite effect. Chaganti and colleagues⁷⁴ analyzed levels of vitamins C and E in the Multicenter Osteoarthritis Study (MOST) cohort of 3026 men and women (age, 50-79 years) and found higher vitamin levels were not protective against incidence of radiographic whole-knee OA and may even have been associated with increased risk.

Conclusion

Vitamin C is an essential micronutrient and a powerful water-soluble antioxidant in numerous biochemical pathways that influence bone health. It has been implicated in the biology of fracture healing, and vitamin C supplementation has been proposed as prophylaxis against hip fractures based on observational data. Results of 2 high-quality double-blind randomized trials support use of vitamin C as prophylaxis against CRPS in wrist fractures treated conservatively and operatively; the evidence for foot and ankle surgery is weaker. Use of vitamin C in OA prevention has tremendous potential, though animal and human study results are controversial. Heterogeneous results and lack of prospective trials preclude any recommendation at this time.

L-ascorbic acid, more commonly know as vitamin C, is an essential micronutrient used in numerous metabolic pathways. It functions physiologically as a water-soluble antioxidant by virtue of its high reducing power, playing a key role in the function of leukocytes, protein metabolism, and production of neurotransmitters.^1-3 Vitamin C also contributes to musculoskeletal health through biosynthesis of carnitine and collagen⁴ and enhancement of intestinal absorption of dietary iron⁵ from plants and vegetables. Unlike most animals, humans are unable to synthesize this essential vitamin and therefore require intake from natural dietary sources or supplements.⁶ The ability of vitamin C to prevent or treat disease has been an area of research interest since the vitamin was identified and isolated by Szent-Györgyi in the 1930s.^7-16 Research in orthopedic surgery has focused on the effects of vitamin C on fracture healing, its potential use in preventing complex regional pain syndrome (CRPS), and its role in the pathophysiology of osteoarthritis. In this article, we review the basics of vitamin C metabolism and summarize the evidence surrounding the role of vitamin C supplementation in orthopedics.

Sources and Metabolism

Vitamin C is found naturally in many fruits and vegetables (Table 1) and is a common fortification in cereals, juices, and multivitamins. Daily recommended intake (Table 2) depends on age and smoking status. Absorption occurs in the distal small intestine, with blood plasma vitamin C concentrations reflecting dietary intake. Pharmacokinetic studies have shown that vitamin C concentrations are tightly regulated through absorption, tissue accumulation, and renal resorption, with plasma concentrations rarely exceeding 100 μmol/L without additional supplementation.¹⁷ Although the usual dietary doses of 100 mg/d (adult) are almost completely absorbed, producing a plasma concentration of 60 μmol/L, higher intake results in an increasingly smaller fraction absorbed.^1,18 Intake of more than 1000 mg/d results in less than 50% absorption¹⁹ (unmetabolized vitamin C is excreted in stool and urine¹). Even at higher doses, vitamin C has low toxicity³; the most common complaints are diarrhea, nausea, and abdominal cramps caused by the osmotic effect of unabsorbed vitamin C in the gastrointestinal tract.¹

Vitamin C Deficiency

The relationship between vitamin C deficiency and the development of scurvy has been documented for centuries. Symptoms are described in the ancient Egyptian, Greek, and Roman literature.²⁰ Ascorbic acid is essential for normal collagen function, as it is a required cofactor for enzymatic transfer of hydroxyl groups to select proline and lysine residues during procollagen formation. Hydroxylysine contributes to the intermolecular cross-links in collagen, and hydroxyproline stabilizes the triple-helix structure of collagen.²¹ Insufficient vitamin C during this process results in collagen that is non-cross-linked, nonhelical, structurally unstable, and weak.²¹ Clinical manifestations of scurvy stem from an underlying impairment of collagen production causing a systemic decrease in connective tissue integrity, capillary fragility, poor wound healing, fatigue, myalgias, arthritis, and even death.²² Vitamin C deficiency has also been implicated as a cause of diffuse bleeding in surgical patients with normal coagulation parameters secondary to capillary fragility.²³ In the United States, the 2003–2004 National Health and Nutrition Examination Survey (NHANES) measured serum vitamin C concentrations in 7277 noninstitutionalized patients 6 years old or older.²⁴ Age-adjusted incidence of subnormal serum vitamin C levels (<28 μmol/L) was 19.6%, and incidence of frank vitamin C deficiency (<11.4 μmol/L) was 7.1%. Reported rates of vitamin C deficiency in hospitalized patients are much higher, with 47% to 60% having subnormal values (<28 μmol/L) and 17% to 19% being vitamin C–deficient (<11.4 μmol/L).^22,25 Identified risk factors for hypovitaminosis C include advanced age, obesity, low socioeconomic status, unemployment, male sex, and concomitant alcohol and tobacco consumption.^22,24,25

Fracture Healing and Prevention

The effects of vitamin C deficiency on bone healing have been studied with animal models as early as the 1940s.^26,27 Early experiments using guinea pigs demonstrated failure of bone graft incorporation, delayed collagen maturation, and decreased collagen and callus formation in scorbutic animals compared with controls that received vitamin C supplementation.^26,27 Based on his work with guinea pigs, Bourne²⁶ reported in 1942 that vitamin C deficiency significantly inhibited the reparative process in damaged bone and that patients with fractures should receive vitamin C supplementation. Building on this early research, Yilmaz and colleagues²⁸ found faster histologic healing for tibia fractures in a rat model for animals that received a single injection of vitamin C 0.5 mg/kg compared with a nonscorbutic control group, and Sarisözen and colleagues²⁹ showed significantly accelerated histologic bone formation and mineralization at the fracture site for rats that received vitamin C supplementation. Moreover, Kipp and colleagues³⁰ found that scorbutic guinea pigs had lower bone mineral density (BMD), decreased bone mineral content, and impaired collagen synthesis of articular cartilage and tendons compared with nondeficient controls.

Besides promoting bone formation, vitamin C improves the mechanical strength of callus formation. Alcantara-Martos and colleagues³¹ used an osteogenic disorder Shionogi (ODS) rat model to examine the effects of vitamin C intake on femoral fracture healing. This particular animal model is unable to produce its own vitamin C. The groups with lower serum vitamin C levels demonstrated lower mechanical resistance of the fracture callus to torsional loads 5 weeks after fracture. Moreover, the group that received vitamin C supplementation showed higher histologic grade of callus formation and demonstrated faster healing rates. The authors suggested that subclinical vitamin C deficiency can delay fracture healing and that vitamin C supplementation in nondeficient patients would improve bone healing.

Other research has demonstrated a link between vitamin C and mesenchymal cell differentiation. Mohan and colleagues³² used an sfx mouse model to show that vitamin C deficiency results in decreased bone formation secondary to impaired osteoblast differentiation, diminished bone density, and development of spontaneous fractures. The authors indicated that not only is vitamin C essential for maintenance of differentiated functions of osteoblasts, but deficiency during early active growth may affect peak BMD levels in humans. Additional studies have demonstrated the role of vitamin C in endochondral bone formation through both induction of osteoblast differentiation and modulation of gene expression in hypertrophic chondrocytes.^33-36 Chronic vitamin C deficiency has been found to depress osteoblast function and differentiation of chondrocytes.³⁷ More recently, Kim and colleagues³⁸ examined the effect of vitamin C insufficiency in Gulo-deficient mice, which are unable to synthesize ascorbic acid. Ascorbic acid insufficiency over 4 weeks led to decreased plasma levels of osteocalcin and bone formation in vivo as well as significantly diminished metaphyseal trabecular bone. Despite all the evidence demonstrating the importance of vitamin C in bone formation and maintenance, many of the underlying processes in this relationship have yet to be determined.

Bone Mineral Density

Several observational studies have found a positive association between vitamin C intake and BMD in postmenopausal women. In a retrospective, cross-sectional study by Hall and Greendale,³⁹ a positive association was found between vitamin C intake and BMD of the femoral neck in 775 participants in the Postmenopausal Estrogen/Progestin Interventions trial. After calcium intake, physical activity level, smoking, estrogen use, age, and body mass index were adjusted for, each 100-mg increase in dietary vitamin C was associated with a 0.017 g/cm² increase in BMD. Wang and colleagues⁴⁰ found a positive association between dietary vitamin C intake and femoral neck BMD in a retrospective analysis of 125 postmenopausal Mexican American women. Other observational studies have reported that decreased intake of vitamin C is associated with osteoporosis⁴¹ and increased rates of BMD loss⁴² and that supplementation with vitamin C may suppress bone resorption in postmenopausal women.⁴³

The results of these studies contrast with the findings of Leveille and colleagues,⁴⁴ who examined the relationship between dietary vitamin C and hip BMD in 1892 postmenopausal women. Although the authors found that women (age, 55-64 years) using vitamin C supplements for more than 10 years had an average BMD 6.7% higher than that of nonusers, they did not find any association between dietary vitamin C intake and BMD. Moreover, NHANES III also found inconsistent associations between vitamin C and BMD among 13,080 adults surveyed in the United States.⁴⁵ Although for premenopausal women dietary ascorbic acid was associated with increased BMD, for postmenopausal women with a history of smoking and estrogen replacement, it was actually associated with lower BMD values. For other subgroups in the study, the relationship was also inconsistent or nonlinear.

The exact mechanism by which ascorbic acid contributes to BMD is not fully delineated. However, it likely is related to the known role of vitamin C in collagen formation, bone matrix development, osteoblast differentiation, and its antioxidant effects limiting bone resorption.^44,46

Hip Fractures

Besides demonstrating positive effects of vitamin C on bone healing and BMD, epidemiologic studies have found evidence of a protective effect of vitamin C on hip fracture risk. In a study of the Swedish Mammography cohort, 66,651 women (age, 40-76 years) were prospectively followed.⁴⁷ The authors found that the odds ratio (OR) for hip fractures among smokers with a low intake of vitamin E (median intake, ≤6.2 mg/d) was 3.0 (95% CI, 1.6-5.4) and for vitamin C (median intake, ≤67 mg/d) was 3.0 (95% CI, 1.6-5.6). Moreover, in smokers with a low intake of both vitamins E and C, OR increased to 4.9 (95% CI, 2.2-11.0). In addition, the Utah Study of Nutrition and Bone Health matched 1215 cases of hip fractures in patients who had ever smoked (age, >50 years) with 1349 controls and found that vitamin C intake above 159 mg/d had a significant protective effect on the incidence of hip fracture; however, a graded relationship was not observed.⁴⁸ Despite the inconsistencies in the NHANES III study regarding the relationship between vitamin C and BMD, Simon and Hudes⁴⁵ found that serum vitamin C was associated with lower risk for self-reported fracture in postmenopausal women who had ever smoked and had a history of estrogen therapy (OR, 0.51; 95% CI, 0.36-0.70). Finally, Sahni and colleagues⁴⁹ followed 958 Framingham cohort men and women (mean age, 75 years) over 17 years and found that those in the highest tertile of total vitamin C intake (median, 313 mg/d) had significantly fewer hip fractures and nonvertebral fractures compared with those in the lowest tertile of intake (median, 94 mg/d). Dietary vitamin C intake was not associated with fracture risk in this study.

Complex Regional Pain Syndrome

Type 1 CRPS is a debilitating condition characterized by severe pain, swelling, and vasomotor instability. It is commonly precipitated by an injury or surgery to an extremity and is a dreaded sequelae in orthopedics,⁵⁰ with incidence rates of 10% to 22% in wrist fractures^51-53 and 10% after foot and ankle surgery.⁵⁴ Although the pathophysiology of CRPS remains unknown, dysregulation and increased permeability of the vasculature caused by free radicals are thought to play an important role.⁵⁵ In dermal burns, high doses of vitamin C therapy slowed progression of vascular permeability and therefore reduced extravascular leakage of fluids and protein.^56,57 The ability of vitamin C to prevent CRPS has been studied in only a handful of trials.

In a double-blind trial, Zollinger and colleagues⁵¹ randomized 127 conservatively treated distal radius fractures to receive either vitamin C 500 mg or placebo daily for 50 days starting on day of injury. Incidence of CRPS (using the diagnostic criteria proposed by Veldman and colleagues⁵⁸) at 1-year follow-up was 22% in the placebo group and 7% in the vitamin C group (95% CI for difference, 2%-26%). Complaints while wearing the cast and fracture type increased the risk for developing CRPS. This initial study was followed up by a prospective, randomized, double-blind multicenter trial by the same authors,⁵² who had 416 patients with 427 wrist fractures receive either placebo or vitamin C 200 mg/d, 500 mg/d, or 1500 mg/d for 50 days. This follow-up study included both operative (11%) and nonoperative (89%) distal radius fractures. Incidence of CRPS was 10.1% in the placebo group and 2.4% in the vitamin C group (P < .002). Although there was an appreciable drop in the relative risk (RR) of developing CRPS between the vitamin C 200-mg/d and 500-mg/d groups (0.41-0.17), there was no additional benefit in the 1500-mg/d group. Pooling the data for these 2 randomized trials showed that the overall RR for developing CRPS was lower with vitamin C supplementation (RR, 0.28; 95% CI, 0.14-0.56; P = .0003).⁵⁹

Results of the 2 trials by Zollinger and colleagues^51,52 have been met with several concerns.^60-62 As a corollary to the unclear etiology of CRPS, several different sets of diagnostic criteria exist, and the criteria are somewhat subjective and imprecise. Although both trials used the Veldman criteria,⁵⁸ the incidence of CRPS in the placebo group dropped unexpectedly between trials, from 22% to 10.1%, and the results may have been different had other criteria been used. Moreover, the idea that toxic oxygen radicals have a role in CRPS and that vitamin C can scavenge these radicals is based on limited data.⁶¹ In the absence of a clear pathophysiologic explanation, some surgeons have been reluctant to treat patients with vitamin C supplementation.

Cazeneuve and colleagues⁵³ also studied the effect of vitamin C supplementation on CRPS in patients with distal radius fractures treated with reduction and intrafocal pinning. Group 1 consisted of 100 patients (treated from 1995 to 1998) who did not receive vitamin C supplementation, and group 2 consisted of 95 patients (treated from 1998 to 2002) who received vitamin C 1000 mg/d for 45 days starting on day of fracture. Patients were followed for up to 90 days after surgery. Incidence of CRPS type 1 was 10% in the untreated group and 2.1% in the group that received vitamin C supplementation.

Vitamin C prophylaxis for CRPS has also been studied in foot and ankle surgery. Besse and colleagues⁵⁴ prospectively compared 2 chronologically successive groups that received (235 feet) or did not receive (185 feet) vitamin C 1000-mg/d supplementation for 45 days. Incidence of CRPS type 1 as diagnosed with International Association for the Study of Pain (IASP) criteria dropped from 9.6% to 1.7% with vitamin C supplementation. In a case series, Zollinger and colleagues⁶³ examined CRPS type 1 rates after performing cementless total trapeziometacarpal semiconstrained joint prosthesis implantations for trapeziometacarpal arthritis. Forty implantations were performed in 34 patients. All patients received vitamin C 500 mg/d for CRPS prevention starting 2 days before surgery for 50 days. There were no cases of CRPS in the postoperative period, according to Veldman or IASP criteria. Although the results of the studies by Cazeneuve and colleagues⁵³ and Besse and colleagues⁵⁴ agree with those of the distal radius fracture trials by Zollinger and colleagues,^51,52 the quasi-experimental design and the lack of blinding and randomization temper the conclusions that can be drawn because of the risk for significant bias.

In a recent systematic review examining the effectiveness of vitamin C supplementation in preventing CRPS in trauma and surgery in the extremities, Shibuya and colleagues⁶⁴ concluded that taking at least 500 mg of vitamin C daily for 45 to 50 days after injury or surgery may help decrease the incidence of CRPS after a traumatic event.

Osteoarthritis

Damage caused by free radicals has long been thought to play an important role in osteoarthritis (OA).^65-67 A cross-sectional study in knee OA found that amounts of joint fluid antioxidants were lower in patients with severe arthritis than in those with intact cartilage, further implicating free radicals in the pathophysiology of OA.⁶⁸ Use of vitamin C for prophylaxis against development or progression of OA is therefore a hot research topic. Thus far, animal studies have had mixed results—several showing a chondroprotective effect of vitamin C^69,70 and others finding either no effect or even a positive association with the development of arthritis.⁷¹

The literature on human subjects, chiefly observational studies, is just as controversial. Wang and colleagues⁴⁰ found vitamin C intake associated with both a 50% risk reduction of bone marrow lesions on magnetic resonance imaging over a 10-year interval (OR, 0.5; 95% CI, 0.29-0.87) and inversely associated with the tibial plateau bone area. Similarly, the Clearwater Osteoarthritis Study, which followed 1023 patients (age, >40 years), showed that participants who took vitamin C supplements were 11% less likely to develop radiographic evidence of OA (RR, 0.89; 95% CI, 0.85-0.93).⁷² Nonetheless, other studies have failed to show such associations⁷³ or have demonstrated the opposite effect. Chaganti and colleagues⁷⁴ analyzed levels of vitamins C and E in the Multicenter Osteoarthritis Study (MOST) cohort of 3026 men and women (age, 50-79 years) and found higher vitamin levels were not protective against incidence of radiographic whole-knee OA and may even have been associated with increased risk.

Conclusion

Vitamin C is an essential micronutrient and a powerful water-soluble antioxidant in numerous biochemical pathways that influence bone health. It has been implicated in the biology of fracture healing, and vitamin C supplementation has been proposed as prophylaxis against hip fractures based on observational data. Results of 2 high-quality double-blind randomized trials support use of vitamin C as prophylaxis against CRPS in wrist fractures treated conservatively and operatively; the evidence for foot and ankle surgery is weaker. Use of vitamin C in OA prevention has tremendous potential, though animal and human study results are controversial. Heterogeneous results and lack of prospective trials preclude any recommendation at this time.

L-ascorbic acid, more commonly know as vitamin C, is an essential micronutrient used in numerous metabolic pathways. It functions physiologically as a water-soluble antioxidant by virtue of its high reducing power, playing a key role in the function of leukocytes, protein metabolism, and production of neurotransmitters.^1-3 Vitamin C also contributes to musculoskeletal health through biosynthesis of carnitine and collagen⁴ and enhancement of intestinal absorption of dietary iron⁵ from plants and vegetables. Unlike most animals, humans are unable to synthesize this essential vitamin and therefore require intake from natural dietary sources or supplements.⁶ The ability of vitamin C to prevent or treat disease has been an area of research interest since the vitamin was identified and isolated by Szent-Györgyi in the 1930s.^7-16 Research in orthopedic surgery has focused on the effects of vitamin C on fracture healing, its potential use in preventing complex regional pain syndrome (CRPS), and its role in the pathophysiology of osteoarthritis. In this article, we review the basics of vitamin C metabolism and summarize the evidence surrounding the role of vitamin C supplementation in orthopedics.

Sources and Metabolism

Vitamin C is found naturally in many fruits and vegetables (Table 1) and is a common fortification in cereals, juices, and multivitamins. Daily recommended intake (Table 2) depends on age and smoking status. Absorption occurs in the distal small intestine, with blood plasma vitamin C concentrations reflecting dietary intake. Pharmacokinetic studies have shown that vitamin C concentrations are tightly regulated through absorption, tissue accumulation, and renal resorption, with plasma concentrations rarely exceeding 100 μmol/L without additional supplementation.¹⁷ Although the usual dietary doses of 100 mg/d (adult) are almost completely absorbed, producing a plasma concentration of 60 μmol/L, higher intake results in an increasingly smaller fraction absorbed.^1,18 Intake of more than 1000 mg/d results in less than 50% absorption¹⁹ (unmetabolized vitamin C is excreted in stool and urine¹). Even at higher doses, vitamin C has low toxicity³; the most common complaints are diarrhea, nausea, and abdominal cramps caused by the osmotic effect of unabsorbed vitamin C in the gastrointestinal tract.¹

Vitamin C Deficiency

The relationship between vitamin C deficiency and the development of scurvy has been documented for centuries. Symptoms are described in the ancient Egyptian, Greek, and Roman literature.²⁰ Ascorbic acid is essential for normal collagen function, as it is a required cofactor for enzymatic transfer of hydroxyl groups to select proline and lysine residues during procollagen formation. Hydroxylysine contributes to the intermolecular cross-links in collagen, and hydroxyproline stabilizes the triple-helix structure of collagen.²¹ Insufficient vitamin C during this process results in collagen that is non-cross-linked, nonhelical, structurally unstable, and weak.²¹ Clinical manifestations of scurvy stem from an underlying impairment of collagen production causing a systemic decrease in connective tissue integrity, capillary fragility, poor wound healing, fatigue, myalgias, arthritis, and even death.²² Vitamin C deficiency has also been implicated as a cause of diffuse bleeding in surgical patients with normal coagulation parameters secondary to capillary fragility.²³ In the United States, the 2003–2004 National Health and Nutrition Examination Survey (NHANES) measured serum vitamin C concentrations in 7277 noninstitutionalized patients 6 years old or older.²⁴ Age-adjusted incidence of subnormal serum vitamin C levels (<28 μmol/L) was 19.6%, and incidence of frank vitamin C deficiency (<11.4 μmol/L) was 7.1%. Reported rates of vitamin C deficiency in hospitalized patients are much higher, with 47% to 60% having subnormal values (<28 μmol/L) and 17% to 19% being vitamin C–deficient (<11.4 μmol/L).^22,25 Identified risk factors for hypovitaminosis C include advanced age, obesity, low socioeconomic status, unemployment, male sex, and concomitant alcohol and tobacco consumption.^22,24,25

Fracture Healing and Prevention

The effects of vitamin C deficiency on bone healing have been studied with animal models as early as the 1940s.^26,27 Early experiments using guinea pigs demonstrated failure of bone graft incorporation, delayed collagen maturation, and decreased collagen and callus formation in scorbutic animals compared with controls that received vitamin C supplementation.^26,27 Based on his work with guinea pigs, Bourne²⁶ reported in 1942 that vitamin C deficiency significantly inhibited the reparative process in damaged bone and that patients with fractures should receive vitamin C supplementation. Building on this early research, Yilmaz and colleagues²⁸ found faster histologic healing for tibia fractures in a rat model for animals that received a single injection of vitamin C 0.5 mg/kg compared with a nonscorbutic control group, and Sarisözen and colleagues²⁹ showed significantly accelerated histologic bone formation and mineralization at the fracture site for rats that received vitamin C supplementation. Moreover, Kipp and colleagues³⁰ found that scorbutic guinea pigs had lower bone mineral density (BMD), decreased bone mineral content, and impaired collagen synthesis of articular cartilage and tendons compared with nondeficient controls.

Besides promoting bone formation, vitamin C improves the mechanical strength of callus formation. Alcantara-Martos and colleagues³¹ used an osteogenic disorder Shionogi (ODS) rat model to examine the effects of vitamin C intake on femoral fracture healing. This particular animal model is unable to produce its own vitamin C. The groups with lower serum vitamin C levels demonstrated lower mechanical resistance of the fracture callus to torsional loads 5 weeks after fracture. Moreover, the group that received vitamin C supplementation showed higher histologic grade of callus formation and demonstrated faster healing rates. The authors suggested that subclinical vitamin C deficiency can delay fracture healing and that vitamin C supplementation in nondeficient patients would improve bone healing.

Other research has demonstrated a link between vitamin C and mesenchymal cell differentiation. Mohan and colleagues³² used an sfx mouse model to show that vitamin C deficiency results in decreased bone formation secondary to impaired osteoblast differentiation, diminished bone density, and development of spontaneous fractures. The authors indicated that not only is vitamin C essential for maintenance of differentiated functions of osteoblasts, but deficiency during early active growth may affect peak BMD levels in humans. Additional studies have demonstrated the role of vitamin C in endochondral bone formation through both induction of osteoblast differentiation and modulation of gene expression in hypertrophic chondrocytes.^33-36 Chronic vitamin C deficiency has been found to depress osteoblast function and differentiation of chondrocytes.³⁷ More recently, Kim and colleagues³⁸ examined the effect of vitamin C insufficiency in Gulo-deficient mice, which are unable to synthesize ascorbic acid. Ascorbic acid insufficiency over 4 weeks led to decreased plasma levels of osteocalcin and bone formation in vivo as well as significantly diminished metaphyseal trabecular bone. Despite all the evidence demonstrating the importance of vitamin C in bone formation and maintenance, many of the underlying processes in this relationship have yet to be determined.

Bone Mineral Density

Several observational studies have found a positive association between vitamin C intake and BMD in postmenopausal women. In a retrospective, cross-sectional study by Hall and Greendale,³⁹ a positive association was found between vitamin C intake and BMD of the femoral neck in 775 participants in the Postmenopausal Estrogen/Progestin Interventions trial. After calcium intake, physical activity level, smoking, estrogen use, age, and body mass index were adjusted for, each 100-mg increase in dietary vitamin C was associated with a 0.017 g/cm² increase in BMD. Wang and colleagues⁴⁰ found a positive association between dietary vitamin C intake and femoral neck BMD in a retrospective analysis of 125 postmenopausal Mexican American women. Other observational studies have reported that decreased intake of vitamin C is associated with osteoporosis⁴¹ and increased rates of BMD loss⁴² and that supplementation with vitamin C may suppress bone resorption in postmenopausal women.⁴³

The results of these studies contrast with the findings of Leveille and colleagues,⁴⁴ who examined the relationship between dietary vitamin C and hip BMD in 1892 postmenopausal women. Although the authors found that women (age, 55-64 years) using vitamin C supplements for more than 10 years had an average BMD 6.7% higher than that of nonusers, they did not find any association between dietary vitamin C intake and BMD. Moreover, NHANES III also found inconsistent associations between vitamin C and BMD among 13,080 adults surveyed in the United States.⁴⁵ Although for premenopausal women dietary ascorbic acid was associated with increased BMD, for postmenopausal women with a history of smoking and estrogen replacement, it was actually associated with lower BMD values. For other subgroups in the study, the relationship was also inconsistent or nonlinear.

The exact mechanism by which ascorbic acid contributes to BMD is not fully delineated. However, it likely is related to the known role of vitamin C in collagen formation, bone matrix development, osteoblast differentiation, and its antioxidant effects limiting bone resorption.^44,46

Hip Fractures

Besides demonstrating positive effects of vitamin C on bone healing and BMD, epidemiologic studies have found evidence of a protective effect of vitamin C on hip fracture risk. In a study of the Swedish Mammography cohort, 66,651 women (age, 40-76 years) were prospectively followed.⁴⁷ The authors found that the odds ratio (OR) for hip fractures among smokers with a low intake of vitamin E (median intake, ≤6.2 mg/d) was 3.0 (95% CI, 1.6-5.4) and for vitamin C (median intake, ≤67 mg/d) was 3.0 (95% CI, 1.6-5.6). Moreover, in smokers with a low intake of both vitamins E and C, OR increased to 4.9 (95% CI, 2.2-11.0). In addition, the Utah Study of Nutrition and Bone Health matched 1215 cases of hip fractures in patients who had ever smoked (age, >50 years) with 1349 controls and found that vitamin C intake above 159 mg/d had a significant protective effect on the incidence of hip fracture; however, a graded relationship was not observed.⁴⁸ Despite the inconsistencies in the NHANES III study regarding the relationship between vitamin C and BMD, Simon and Hudes⁴⁵ found that serum vitamin C was associated with lower risk for self-reported fracture in postmenopausal women who had ever smoked and had a history of estrogen therapy (OR, 0.51; 95% CI, 0.36-0.70). Finally, Sahni and colleagues⁴⁹ followed 958 Framingham cohort men and women (mean age, 75 years) over 17 years and found that those in the highest tertile of total vitamin C intake (median, 313 mg/d) had significantly fewer hip fractures and nonvertebral fractures compared with those in the lowest tertile of intake (median, 94 mg/d). Dietary vitamin C intake was not associated with fracture risk in this study.

Complex Regional Pain Syndrome

Type 1 CRPS is a debilitating condition characterized by severe pain, swelling, and vasomotor instability. It is commonly precipitated by an injury or surgery to an extremity and is a dreaded sequelae in orthopedics,⁵⁰ with incidence rates of 10% to 22% in wrist fractures^51-53 and 10% after foot and ankle surgery.⁵⁴ Although the pathophysiology of CRPS remains unknown, dysregulation and increased permeability of the vasculature caused by free radicals are thought to play an important role.⁵⁵ In dermal burns, high doses of vitamin C therapy slowed progression of vascular permeability and therefore reduced extravascular leakage of fluids and protein.^56,57 The ability of vitamin C to prevent CRPS has been studied in only a handful of trials.

In a double-blind trial, Zollinger and colleagues⁵¹ randomized 127 conservatively treated distal radius fractures to receive either vitamin C 500 mg or placebo daily for 50 days starting on day of injury. Incidence of CRPS (using the diagnostic criteria proposed by Veldman and colleagues⁵⁸) at 1-year follow-up was 22% in the placebo group and 7% in the vitamin C group (95% CI for difference, 2%-26%). Complaints while wearing the cast and fracture type increased the risk for developing CRPS. This initial study was followed up by a prospective, randomized, double-blind multicenter trial by the same authors,⁵² who had 416 patients with 427 wrist fractures receive either placebo or vitamin C 200 mg/d, 500 mg/d, or 1500 mg/d for 50 days. This follow-up study included both operative (11%) and nonoperative (89%) distal radius fractures. Incidence of CRPS was 10.1% in the placebo group and 2.4% in the vitamin C group (P < .002). Although there was an appreciable drop in the relative risk (RR) of developing CRPS between the vitamin C 200-mg/d and 500-mg/d groups (0.41-0.17), there was no additional benefit in the 1500-mg/d group. Pooling the data for these 2 randomized trials showed that the overall RR for developing CRPS was lower with vitamin C supplementation (RR, 0.28; 95% CI, 0.14-0.56; P = .0003).⁵⁹

Results of the 2 trials by Zollinger and colleagues^51,52 have been met with several concerns.^60-62 As a corollary to the unclear etiology of CRPS, several different sets of diagnostic criteria exist, and the criteria are somewhat subjective and imprecise. Although both trials used the Veldman criteria,⁵⁸ the incidence of CRPS in the placebo group dropped unexpectedly between trials, from 22% to 10.1%, and the results may have been different had other criteria been used. Moreover, the idea that toxic oxygen radicals have a role in CRPS and that vitamin C can scavenge these radicals is based on limited data.⁶¹ In the absence of a clear pathophysiologic explanation, some surgeons have been reluctant to treat patients with vitamin C supplementation.

Cazeneuve and colleagues⁵³ also studied the effect of vitamin C supplementation on CRPS in patients with distal radius fractures treated with reduction and intrafocal pinning. Group 1 consisted of 100 patients (treated from 1995 to 1998) who did not receive vitamin C supplementation, and group 2 consisted of 95 patients (treated from 1998 to 2002) who received vitamin C 1000 mg/d for 45 days starting on day of fracture. Patients were followed for up to 90 days after surgery. Incidence of CRPS type 1 was 10% in the untreated group and 2.1% in the group that received vitamin C supplementation.

Vitamin C prophylaxis for CRPS has also been studied in foot and ankle surgery. Besse and colleagues⁵⁴ prospectively compared 2 chronologically successive groups that received (235 feet) or did not receive (185 feet) vitamin C 1000-mg/d supplementation for 45 days. Incidence of CRPS type 1 as diagnosed with International Association for the Study of Pain (IASP) criteria dropped from 9.6% to 1.7% with vitamin C supplementation. In a case series, Zollinger and colleagues⁶³ examined CRPS type 1 rates after performing cementless total trapeziometacarpal semiconstrained joint prosthesis implantations for trapeziometacarpal arthritis. Forty implantations were performed in 34 patients. All patients received vitamin C 500 mg/d for CRPS prevention starting 2 days before surgery for 50 days. There were no cases of CRPS in the postoperative period, according to Veldman or IASP criteria. Although the results of the studies by Cazeneuve and colleagues⁵³ and Besse and colleagues⁵⁴ agree with those of the distal radius fracture trials by Zollinger and colleagues,^51,52 the quasi-experimental design and the lack of blinding and randomization temper the conclusions that can be drawn because of the risk for significant bias.

In a recent systematic review examining the effectiveness of vitamin C supplementation in preventing CRPS in trauma and surgery in the extremities, Shibuya and colleagues⁶⁴ concluded that taking at least 500 mg of vitamin C daily for 45 to 50 days after injury or surgery may help decrease the incidence of CRPS after a traumatic event.

Osteoarthritis

Damage caused by free radicals has long been thought to play an important role in osteoarthritis (OA).^65-67 A cross-sectional study in knee OA found that amounts of joint fluid antioxidants were lower in patients with severe arthritis than in those with intact cartilage, further implicating free radicals in the pathophysiology of OA.⁶⁸ Use of vitamin C for prophylaxis against development or progression of OA is therefore a hot research topic. Thus far, animal studies have had mixed results—several showing a chondroprotective effect of vitamin C^69,70 and others finding either no effect or even a positive association with the development of arthritis.⁷¹

The literature on human subjects, chiefly observational studies, is just as controversial. Wang and colleagues⁴⁰ found vitamin C intake associated with both a 50% risk reduction of bone marrow lesions on magnetic resonance imaging over a 10-year interval (OR, 0.5; 95% CI, 0.29-0.87) and inversely associated with the tibial plateau bone area. Similarly, the Clearwater Osteoarthritis Study, which followed 1023 patients (age, >40 years), showed that participants who took vitamin C supplements were 11% less likely to develop radiographic evidence of OA (RR, 0.89; 95% CI, 0.85-0.93).⁷² Nonetheless, other studies have failed to show such associations⁷³ or have demonstrated the opposite effect. Chaganti and colleagues⁷⁴ analyzed levels of vitamins C and E in the Multicenter Osteoarthritis Study (MOST) cohort of 3026 men and women (age, 50-79 years) and found higher vitamin levels were not protective against incidence of radiographic whole-knee OA and may even have been associated with increased risk.

Conclusion

Vitamin C is an essential micronutrient and a powerful water-soluble antioxidant in numerous biochemical pathways that influence bone health. It has been implicated in the biology of fracture healing, and vitamin C supplementation has been proposed as prophylaxis against hip fractures based on observational data. Results of 2 high-quality double-blind randomized trials support use of vitamin C as prophylaxis against CRPS in wrist fractures treated conservatively and operatively; the evidence for foot and ankle surgery is weaker. Use of vitamin C in OA prevention has tremendous potential, though animal and human study results are controversial. Heterogeneous results and lack of prospective trials preclude any recommendation at this time.

The extensor mechanism of the knee comprises the quadriceps tendon, the patella, and the patellar tendon. The extensor mechanism may be damaged by injury to these structures, with consequences such as the inability to actively extend the knee and hemarthrosis.^1,2 Disruption of this mechanism is rare, and the most common injury pattern is an eccentric contraction of the quadriceps tendon on a flexed knee causing a tendon (quadriceps or patellar) rupture or a patella fracture.^1,2

Patellar tendon ruptures are more common in persons younger than 40 years.¹ Treatment is surgical, regardless of age and physical activity. In the acute setting, repair can be end-to-end suture or transosseous tunnel insertion. End-to-end suturing is difficult in chronic patellar tendon ruptures because of patella alta secondary to quadriceps contraction.³ Treatment options for chronic ruptures may involve transpatellar traction⁴ or tendon reinforcement with fascia lata, a semitendinosus band, or synthetic materials.^3-5 Alternatively, tendon autograft and allografts have also been recommended, especially in extreme situations.^1,6 Furthermore, animal experiments have shown that a compact platelet-rich fibrin scaffold (CPFS) has the potential to accelerate healing of patellar tendon defects and to act as a bioscaffold for graft augmentation.⁷

We describe the case of a 30-year-old man who underwent extensor mechanism reconstruction with cadaveric tendon–patellar tendon–bone allograft for failure of an infected primary end-to-end repair. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 30-year-old healthy man landed on an empty glass fish tank, resulting in a traumatic right-knee arthrotomy. On initial evaluation, the patient had a negative straight-leg-raise test and impaired knee extension. The patient was taken urgently to the operating room for irrigation and débridement and concurrent repair of the patellar tendon laceration. Antibiotic prophylaxis with 2 g of intravenous (IV) cefazolin was given in the emergency room.

Intraoperatively, after visualizing the patellar tendon laceration and excluding any associated chondral lesions, we proceeded with extensive débridement and irrigation using 9 L of normal saline pulse lavage. After we achieved a clean site, we proceeded to repair the patellar tendon using No. 2 FiberWire sutures (Arthrex, Naples, Florida) with a classic Krackow repair⁸ consisting of 2 sutures run in a 4-row fashion through the patella and the patellar tendon. The suture was securely tightened and then tested for stability to at least 90° of knee flexion. The retinaculum was repaired using No. 0 Vicryl sutures (Ethicon, Somerville, New Jersey). After wound closure and dressing, the patient was placed in a hinged knee brace locked in extension at all times after surgery. Antibiotic treatment with IV cefazolin was administered for 48 hours.

Postoperative management consisted of weight-bearing as tolerated on the operative limb and appropriate deep venous thrombosis prophylaxis. The patient followed up in clinic 2 weeks and 4 weeks after surgery. At 4 weeks, the patient was noted to have a secondary wound infection with superficial dehiscence and serosanguineous drainage. No wound opening was noticed, and local wound care was performed with a 1-week course of oral cephalexin. The patient was scheduled to follow up a few weeks later but did not follow up for a year.

At 1-year follow-up, the patient reported that he had had a steady progression of his knee range of motion (ROM) with decreased pain. However, over time, the patient noted subjective instability of the knee, with frequent falls occurring close to his 1-year follow-up. Examination of his knee showed that his active ROM ranged from 20° in extension to 120° in flexion, with a weak extensor mechanism. Passively, his knee could be brought to full extension. His incision was well healed, but it had an area of bogginess in the middle. Radiographs showed patella alta on the affected knee, with a lengthening of the patellar tendon of 7.70 cm on the right compared with 5.18 cm on the left. Magnetic resonance imaging (MRI) showed moderate-to-severe patellar tendinosis with small fluid pockets around the surgical material and evidence of acute patellar enthesopathy. The laboratory values showed a white blood cell count of 7580/μL (normal, 4500-11,000/μL), an erythrocyte sedimentation rate of 2 mm/h (normal, 1-15 mm/h), and a C-reactive protein level of 1.93 mg/dL (normal, 0.00-0.29 mg/dL). Based on the clinical examination and imaging findings, there was a concern for a possible chronic deep-tissue infection, in addition to failure of the primary patellar tendon repair. Operative versus nonoperative management options were discussed with the patient, and he elected to undergo surgery.

During surgery, the patellar laxity was confirmed, and the patellar tendon was noticed to be chronically thickened and surrounded by unhealthy tissue. Initially, an extensive soft-tissue débridement was performed, and all patellar tendon loculations visualized on the preoperative MRI were drained; a solid purulent-like fluid was expressed. Unfortunately, the extensive and required débridement did not allow the preservation of the patellar tendon. Appropriate cultures were taken and sent for immediate Gram-stain analysis, which returned negative. Tissue samples from the patellar tendon were also sent to the pathology department for analysis. Intraoperatively, the infrapatellar defect was filled temporarily with a tobramycin cement spacer mixed with 2 g of vancomycin in a manner similar to that of the Masquelet technique used for infected long-bone nonunions with bone loss.^9,10 This technique is a 2-stage procedure that promotes the formation of a biologic membrane that allows bone healing in the reconstruction of long-bone defects. The first stage consists of a radical débridement with soft-tissue repair by flaps when needed, with the insertion of a polymethylmethacrylate cement spacer into the bone defect. The second stage is usually performed 6 to 8 weeks later, with removal of the spacer and preservation of the induced membrane, which is filled with iliac crest bone autograft augmented (if necessary) with demineralized allograft.

The incision was closed primarily, and after surgery, the patient was allowed to bear weight as tolerated in a hinged knee brace locked in extension. Final laboratory analysis from cultures and tissue samples revealed acute and chronic inflammation with more than 20 neutrophils per high-powered field. No organisms grew from aerobic, anaerobic, fungal, or mycobacterial cultures. The infectious disease service was consulted and recommended oral cephalexin.

Because all cultures were negative, all laboratory examinations did not indicate any residual infections, and no bony involvement was noticed intraoperatively or in the preoperative knee MRI, we decided to proceed with the second stage of the Masquelet technique after 2 weeks. The patient returned to the operating room for final reconstruction of his patellar tendon using a custom-ordered cadaveric tendon–patellar tendon–bone allograft, the length of which was determined by measuring the contralateral patellar tendon, ie, 5.18 cm (Figure 1A). The previous anterior knee incision was reopened and extended distally past the tibial tuberosity and proximally toward the quadriceps tendon. The antibiotic spacer was removed. We proceeded with a repeat irrigation and débridement and the allograft transfer. The selected allograft was customized by reducing the tibial bone component to an approximately 1×2-cm bone block and by reducing the allograft patellar thickness with an oscillating saw, leaving an approximately 2-mm thick patellar bone graft attached to the patellar tendon. In a similar technique using an oscillating saw, we shaved off the anterior cortex of the patient’s patella to accommodate, in a sandwich fashion, the patellar allograft. Proximally, the quadriceps tendon insertion was split longitudinally and partially separated from the superior pole of the patellar tendon to allow seating and fixation of the modified quadriceps allograft tendon component.

We proceeded with the fixation of the allograft first distally on the patella. The anterior cortex of the tibial tuberosity was resected to allow the perfect seating of the bone block allograft. The graft was secured with a 4.0-mm fully threaded cancellous lag screw and reinforced with a 2.4-mm, 3-hole T-volar buttress plate (Synthes, Paoli, Pennsylvania). The plate was contoured to better fit the patient’s tibia. We sutured the patellar allograft tendon to the patella using two No. 2-0 FiberWire sutures in Krackow suture technique⁸ (Figures 1B, 1C). We obtained good fixation of the patellar tendon, and the distance between the patellar insertion and the inferior patellar pole was the same as before surgery: 5.57 cm and comparable to the contralateral side (Figures 2A-2C). The patellar allograft and autograft sandwich were secured with additional No. 2-0 FiberWire sutures, and the quadriceps allograft and autograft were secured with the cross-stitch technique with the same material. Fine suturing of the quadriceps tendon was done with No. 0 Vicryl sutures. After the fixation was completed, we tested the stability of the reconstruction and found good flexion up to 120°.

The postoperative protocol consisted of weight-bearing as tolerated in full extension and passive knee ROM, using a continuous passive ROM machine from 0° to 45° for the first 4 weeks, followed by active ROM, increased as tolerated, during the next 8 weeks.

The patient was seen in clinic 3 and 9 months after surgery. At the 3-month follow-up appointment, the patient’s examination showed knee ROM from 0° extension to 130° of flexion, no secondary infection signs, and radiographic evidence of a well-healing patellar allograft with symmetric patellar tendon length to the contralateral side. At 9-month follow-up, the patient’s active ROM was from 0° extension to 140° flexion (Figures 3A, 3B), and he had returned to his preinjury level of functioning.

Discussion

This case report describes the successful reconstruction of a patellar tendon defect with cadaveric tendon–patellar tendon–bone allograft. Extensor mechanism injuries are uncommon in general, and the incidence of patellar tendon injury is higher in men than in women.² Patellar tendon tears occur frequently in active patients younger than 40 years, usually as a result of sudden quadriceps contraction with the knee slightly flexed.¹ Treatment of patellar tendon injury is surgical, and functional outcomes for patients with this injury are equivalent to those of patients with quadriceps tendon injuries or patellar fractures.² Acute patellar tendon tears can be repaired by end-to-end suturing or transosseous tunnel insertion in the tibia or patella.¹ Reinforcement is often added between the patella and tibial tuberosity, using a semitendinosus band or wire.¹ End-to-end suture is performed using a thick resorbable suture. It is important to avoid patella alta during suturing, comparing the position of the patella with the contralateral patella with the knee in 45° of flexion. In proximal avulsion, the tendon is anchored to the bone by 2 thick nonresorbable sutures through 2 parallel bone tunnels to the proximal pole of the patella. Distal avulsion is rare in adults, but it can be managed by using staples or suture anchors.¹

End-to-end suturing of chronic patellar tendon defects is difficult more than 45 days after injury primarily because of difficulties in correcting patella alta secondary to the upward force exerted by the quadriceps tendon.^1,3 Extreme situations similar to the case we present warrant Achilles or patellar tendon allograft for reconstruction of the extensor mechanism.^1,3,6,9

Extensor mechanism allograft also provides an effective remedy for severe quadriceps deficiency caused by loss of the patella, patellar tendon, and quadriceps tendon in total knee arthroplasty.¹⁰ However, in such cases, late failure is common, and major quadriceps deficiency occurs after removal of the allograft material.¹⁰ To improve outcome, a novel technique using the medial gastrocnemius muscle transferred to the muscular portion of the vastus medialis and lateralis flaps provides a secure and strong closure of the anterior knee, thereby restoring the extensor mechanism of the knee.¹⁰

Patellar tendon reconstruction with allograft tissue has been successfully used, especially in cases related to chronic patellar tendon ruptures¹¹ and total knee arthroplasty.^6,12-14 Crossett and colleagues¹² showed that, at 2-year follow-up, the average knee score for pain, ROM, and stability had improved from 26 points (range, 6-39 points) before surgery to 81 points (range, 40-92 points). The average knee score for function had also improved: 14 points (range, 0-35 points) before surgery to 53 points (range, 30-90 points).¹² Primary repair may succeed in early intervention, but in an established rupture, allograft reconstruction is often necessary. Achilles tendon is the preferred allograft, with the calcaneus fragment embedded into the proximal tibia as a new tubercle and the tendon sutured into the remaining extensor mechanism.^1,11 The repair is further protected using a cable loop from the superior pole of the patella to a drill hole in the upper tibia.⁹ Techniques have also been described involving passage of the proximal aspect of the allograft tendon through patellar bone tunnels and suture fixation to the native quadriceps tendon.^11,15 However, in our technique, we shaved off the anterior cortex of the patient’s patella to allow a sandwich-type over-position of the allograft to secure fixation to the patella.

Another alternative to allograft reconstruction involves biocompatible scaffolds. Such scaffolds incorporate the use of platelets in a fibrin framework. A CPFS, produced from blood and calcium gluconate to improve healing of patellar tendon defects, has been described in animal studies.⁷ In the rabbit model, CPFS acts as a provisional bioscaffold that can accelerate healing of an injured patellar tendon repair, potentially secondary to several growth factors derived from platelets.⁷ Platelets are biocompatible sources of growth factors, and CPFS can act as a scaffold to restore the mechanical integrity of injured soft tissue.^7,16 In addition, CPFS can act to lower donor-site morbidity associated with harvesting tissue autograft.⁷ However, to our knowledge, such scaffolds have not been used in human trials. The LARS biocompatible ligament (Corin Group PLC, Cirencester, United Kingdom), currently not approved by the US Food and Drug Administration, is used for reconstructions of isolated or multiple knee ligament injuries.¹⁷ This graft requires the presence of healthy tissue with good blood supply from which new tendon or ligament can grow in. Sometimes it is also used for extensor mechanism reconstruction after radical tumor resection around the knee; however, good results are achieved in only 59% of cases,¹⁸ and to our knowledge, only 1 case of primary repair of a patellar tendon rupture has been published.¹⁹

Techniques involving the use of tendon–patellar tendon–bone graft with fixation via the sandwich-type over-position of the allograft for chronic patellar tendon rupture have not been described in the literature. In our patient, given the extensive patellar tendon lesion and inflammation with chronic tissue degeneration, there was no option but to use allograft. To improve the patient’s outcome, we chose the strongest possible allograft, tendon–patellar tendon–bone graft.

Conclusion

Revision patellar tendon reconstruction is a challenging, but necessary, procedure to restore the extensor mechanism of the knee, especially in young, active individuals. Various options to reconstruct the tissue defects are available. Our patient was successfully treated with a tendon–patellar tendon–bone allograft reconstruction.

The extensor mechanism of the knee comprises the quadriceps tendon, the patella, and the patellar tendon. The extensor mechanism may be damaged by injury to these structures, with consequences such as the inability to actively extend the knee and hemarthrosis.^1,2 Disruption of this mechanism is rare, and the most common injury pattern is an eccentric contraction of the quadriceps tendon on a flexed knee causing a tendon (quadriceps or patellar) rupture or a patella fracture.^1,2

Patellar tendon ruptures are more common in persons younger than 40 years.¹ Treatment is surgical, regardless of age and physical activity. In the acute setting, repair can be end-to-end suture or transosseous tunnel insertion. End-to-end suturing is difficult in chronic patellar tendon ruptures because of patella alta secondary to quadriceps contraction.³ Treatment options for chronic ruptures may involve transpatellar traction⁴ or tendon reinforcement with fascia lata, a semitendinosus band, or synthetic materials.^3-5 Alternatively, tendon autograft and allografts have also been recommended, especially in extreme situations.^1,6 Furthermore, animal experiments have shown that a compact platelet-rich fibrin scaffold (CPFS) has the potential to accelerate healing of patellar tendon defects and to act as a bioscaffold for graft augmentation.⁷

We describe the case of a 30-year-old man who underwent extensor mechanism reconstruction with cadaveric tendon–patellar tendon–bone allograft for failure of an infected primary end-to-end repair. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 30-year-old healthy man landed on an empty glass fish tank, resulting in a traumatic right-knee arthrotomy. On initial evaluation, the patient had a negative straight-leg-raise test and impaired knee extension. The patient was taken urgently to the operating room for irrigation and débridement and concurrent repair of the patellar tendon laceration. Antibiotic prophylaxis with 2 g of intravenous (IV) cefazolin was given in the emergency room.

Intraoperatively, after visualizing the patellar tendon laceration and excluding any associated chondral lesions, we proceeded with extensive débridement and irrigation using 9 L of normal saline pulse lavage. After we achieved a clean site, we proceeded to repair the patellar tendon using No. 2 FiberWire sutures (Arthrex, Naples, Florida) with a classic Krackow repair⁸ consisting of 2 sutures run in a 4-row fashion through the patella and the patellar tendon. The suture was securely tightened and then tested for stability to at least 90° of knee flexion. The retinaculum was repaired using No. 0 Vicryl sutures (Ethicon, Somerville, New Jersey). After wound closure and dressing, the patient was placed in a hinged knee brace locked in extension at all times after surgery. Antibiotic treatment with IV cefazolin was administered for 48 hours.

Postoperative management consisted of weight-bearing as tolerated on the operative limb and appropriate deep venous thrombosis prophylaxis. The patient followed up in clinic 2 weeks and 4 weeks after surgery. At 4 weeks, the patient was noted to have a secondary wound infection with superficial dehiscence and serosanguineous drainage. No wound opening was noticed, and local wound care was performed with a 1-week course of oral cephalexin. The patient was scheduled to follow up a few weeks later but did not follow up for a year.

At 1-year follow-up, the patient reported that he had had a steady progression of his knee range of motion (ROM) with decreased pain. However, over time, the patient noted subjective instability of the knee, with frequent falls occurring close to his 1-year follow-up. Examination of his knee showed that his active ROM ranged from 20° in extension to 120° in flexion, with a weak extensor mechanism. Passively, his knee could be brought to full extension. His incision was well healed, but it had an area of bogginess in the middle. Radiographs showed patella alta on the affected knee, with a lengthening of the patellar tendon of 7.70 cm on the right compared with 5.18 cm on the left. Magnetic resonance imaging (MRI) showed moderate-to-severe patellar tendinosis with small fluid pockets around the surgical material and evidence of acute patellar enthesopathy. The laboratory values showed a white blood cell count of 7580/μL (normal, 4500-11,000/μL), an erythrocyte sedimentation rate of 2 mm/h (normal, 1-15 mm/h), and a C-reactive protein level of 1.93 mg/dL (normal, 0.00-0.29 mg/dL). Based on the clinical examination and imaging findings, there was a concern for a possible chronic deep-tissue infection, in addition to failure of the primary patellar tendon repair. Operative versus nonoperative management options were discussed with the patient, and he elected to undergo surgery.

During surgery, the patellar laxity was confirmed, and the patellar tendon was noticed to be chronically thickened and surrounded by unhealthy tissue. Initially, an extensive soft-tissue débridement was performed, and all patellar tendon loculations visualized on the preoperative MRI were drained; a solid purulent-like fluid was expressed. Unfortunately, the extensive and required débridement did not allow the preservation of the patellar tendon. Appropriate cultures were taken and sent for immediate Gram-stain analysis, which returned negative. Tissue samples from the patellar tendon were also sent to the pathology department for analysis. Intraoperatively, the infrapatellar defect was filled temporarily with a tobramycin cement spacer mixed with 2 g of vancomycin in a manner similar to that of the Masquelet technique used for infected long-bone nonunions with bone loss.^9,10 This technique is a 2-stage procedure that promotes the formation of a biologic membrane that allows bone healing in the reconstruction of long-bone defects. The first stage consists of a radical débridement with soft-tissue repair by flaps when needed, with the insertion of a polymethylmethacrylate cement spacer into the bone defect. The second stage is usually performed 6 to 8 weeks later, with removal of the spacer and preservation of the induced membrane, which is filled with iliac crest bone autograft augmented (if necessary) with demineralized allograft.

The incision was closed primarily, and after surgery, the patient was allowed to bear weight as tolerated in a hinged knee brace locked in extension. Final laboratory analysis from cultures and tissue samples revealed acute and chronic inflammation with more than 20 neutrophils per high-powered field. No organisms grew from aerobic, anaerobic, fungal, or mycobacterial cultures. The infectious disease service was consulted and recommended oral cephalexin.

Because all cultures were negative, all laboratory examinations did not indicate any residual infections, and no bony involvement was noticed intraoperatively or in the preoperative knee MRI, we decided to proceed with the second stage of the Masquelet technique after 2 weeks. The patient returned to the operating room for final reconstruction of his patellar tendon using a custom-ordered cadaveric tendon–patellar tendon–bone allograft, the length of which was determined by measuring the contralateral patellar tendon, ie, 5.18 cm (Figure 1A). The previous anterior knee incision was reopened and extended distally past the tibial tuberosity and proximally toward the quadriceps tendon. The antibiotic spacer was removed. We proceeded with a repeat irrigation and débridement and the allograft transfer. The selected allograft was customized by reducing the tibial bone component to an approximately 1×2-cm bone block and by reducing the allograft patellar thickness with an oscillating saw, leaving an approximately 2-mm thick patellar bone graft attached to the patellar tendon. In a similar technique using an oscillating saw, we shaved off the anterior cortex of the patient’s patella to accommodate, in a sandwich fashion, the patellar allograft. Proximally, the quadriceps tendon insertion was split longitudinally and partially separated from the superior pole of the patellar tendon to allow seating and fixation of the modified quadriceps allograft tendon component.

We proceeded with the fixation of the allograft first distally on the patella. The anterior cortex of the tibial tuberosity was resected to allow the perfect seating of the bone block allograft. The graft was secured with a 4.0-mm fully threaded cancellous lag screw and reinforced with a 2.4-mm, 3-hole T-volar buttress plate (Synthes, Paoli, Pennsylvania). The plate was contoured to better fit the patient’s tibia. We sutured the patellar allograft tendon to the patella using two No. 2-0 FiberWire sutures in Krackow suture technique⁸ (Figures 1B, 1C). We obtained good fixation of the patellar tendon, and the distance between the patellar insertion and the inferior patellar pole was the same as before surgery: 5.57 cm and comparable to the contralateral side (Figures 2A-2C). The patellar allograft and autograft sandwich were secured with additional No. 2-0 FiberWire sutures, and the quadriceps allograft and autograft were secured with the cross-stitch technique with the same material. Fine suturing of the quadriceps tendon was done with No. 0 Vicryl sutures. After the fixation was completed, we tested the stability of the reconstruction and found good flexion up to 120°.

The postoperative protocol consisted of weight-bearing as tolerated in full extension and passive knee ROM, using a continuous passive ROM machine from 0° to 45° for the first 4 weeks, followed by active ROM, increased as tolerated, during the next 8 weeks.

The patient was seen in clinic 3 and 9 months after surgery. At the 3-month follow-up appointment, the patient’s examination showed knee ROM from 0° extension to 130° of flexion, no secondary infection signs, and radiographic evidence of a well-healing patellar allograft with symmetric patellar tendon length to the contralateral side. At 9-month follow-up, the patient’s active ROM was from 0° extension to 140° flexion (Figures 3A, 3B), and he had returned to his preinjury level of functioning.

Discussion

This case report describes the successful reconstruction of a patellar tendon defect with cadaveric tendon–patellar tendon–bone allograft. Extensor mechanism injuries are uncommon in general, and the incidence of patellar tendon injury is higher in men than in women.² Patellar tendon tears occur frequently in active patients younger than 40 years, usually as a result of sudden quadriceps contraction with the knee slightly flexed.¹ Treatment of patellar tendon injury is surgical, and functional outcomes for patients with this injury are equivalent to those of patients with quadriceps tendon injuries or patellar fractures.² Acute patellar tendon tears can be repaired by end-to-end suturing or transosseous tunnel insertion in the tibia or patella.¹ Reinforcement is often added between the patella and tibial tuberosity, using a semitendinosus band or wire.¹ End-to-end suture is performed using a thick resorbable suture. It is important to avoid patella alta during suturing, comparing the position of the patella with the contralateral patella with the knee in 45° of flexion. In proximal avulsion, the tendon is anchored to the bone by 2 thick nonresorbable sutures through 2 parallel bone tunnels to the proximal pole of the patella. Distal avulsion is rare in adults, but it can be managed by using staples or suture anchors.¹

End-to-end suturing of chronic patellar tendon defects is difficult more than 45 days after injury primarily because of difficulties in correcting patella alta secondary to the upward force exerted by the quadriceps tendon.^1,3 Extreme situations similar to the case we present warrant Achilles or patellar tendon allograft for reconstruction of the extensor mechanism.^1,3,6,9

Extensor mechanism allograft also provides an effective remedy for severe quadriceps deficiency caused by loss of the patella, patellar tendon, and quadriceps tendon in total knee arthroplasty.¹⁰ However, in such cases, late failure is common, and major quadriceps deficiency occurs after removal of the allograft material.¹⁰ To improve outcome, a novel technique using the medial gastrocnemius muscle transferred to the muscular portion of the vastus medialis and lateralis flaps provides a secure and strong closure of the anterior knee, thereby restoring the extensor mechanism of the knee.¹⁰

Patellar tendon reconstruction with allograft tissue has been successfully used, especially in cases related to chronic patellar tendon ruptures¹¹ and total knee arthroplasty.^6,12-14 Crossett and colleagues¹² showed that, at 2-year follow-up, the average knee score for pain, ROM, and stability had improved from 26 points (range, 6-39 points) before surgery to 81 points (range, 40-92 points). The average knee score for function had also improved: 14 points (range, 0-35 points) before surgery to 53 points (range, 30-90 points).¹² Primary repair may succeed in early intervention, but in an established rupture, allograft reconstruction is often necessary. Achilles tendon is the preferred allograft, with the calcaneus fragment embedded into the proximal tibia as a new tubercle and the tendon sutured into the remaining extensor mechanism.^1,11 The repair is further protected using a cable loop from the superior pole of the patella to a drill hole in the upper tibia.⁹ Techniques have also been described involving passage of the proximal aspect of the allograft tendon through patellar bone tunnels and suture fixation to the native quadriceps tendon.^11,15 However, in our technique, we shaved off the anterior cortex of the patient’s patella to allow a sandwich-type over-position of the allograft to secure fixation to the patella.

Another alternative to allograft reconstruction involves biocompatible scaffolds. Such scaffolds incorporate the use of platelets in a fibrin framework. A CPFS, produced from blood and calcium gluconate to improve healing of patellar tendon defects, has been described in animal studies.⁷ In the rabbit model, CPFS acts as a provisional bioscaffold that can accelerate healing of an injured patellar tendon repair, potentially secondary to several growth factors derived from platelets.⁷ Platelets are biocompatible sources of growth factors, and CPFS can act as a scaffold to restore the mechanical integrity of injured soft tissue.^7,16 In addition, CPFS can act to lower donor-site morbidity associated with harvesting tissue autograft.⁷ However, to our knowledge, such scaffolds have not been used in human trials. The LARS biocompatible ligament (Corin Group PLC, Cirencester, United Kingdom), currently not approved by the US Food and Drug Administration, is used for reconstructions of isolated or multiple knee ligament injuries.¹⁷ This graft requires the presence of healthy tissue with good blood supply from which new tendon or ligament can grow in. Sometimes it is also used for extensor mechanism reconstruction after radical tumor resection around the knee; however, good results are achieved in only 59% of cases,¹⁸ and to our knowledge, only 1 case of primary repair of a patellar tendon rupture has been published.¹⁹

Techniques involving the use of tendon–patellar tendon–bone graft with fixation via the sandwich-type over-position of the allograft for chronic patellar tendon rupture have not been described in the literature. In our patient, given the extensive patellar tendon lesion and inflammation with chronic tissue degeneration, there was no option but to use allograft. To improve the patient’s outcome, we chose the strongest possible allograft, tendon–patellar tendon–bone graft.

Conclusion

Revision patellar tendon reconstruction is a challenging, but necessary, procedure to restore the extensor mechanism of the knee, especially in young, active individuals. Various options to reconstruct the tissue defects are available. Our patient was successfully treated with a tendon–patellar tendon–bone allograft reconstruction.

The extensor mechanism of the knee comprises the quadriceps tendon, the patella, and the patellar tendon. The extensor mechanism may be damaged by injury to these structures, with consequences such as the inability to actively extend the knee and hemarthrosis.^1,2 Disruption of this mechanism is rare, and the most common injury pattern is an eccentric contraction of the quadriceps tendon on a flexed knee causing a tendon (quadriceps or patellar) rupture or a patella fracture.^1,2

Patellar tendon ruptures are more common in persons younger than 40 years.¹ Treatment is surgical, regardless of age and physical activity. In the acute setting, repair can be end-to-end suture or transosseous tunnel insertion. End-to-end suturing is difficult in chronic patellar tendon ruptures because of patella alta secondary to quadriceps contraction.³ Treatment options for chronic ruptures may involve transpatellar traction⁴ or tendon reinforcement with fascia lata, a semitendinosus band, or synthetic materials.^3-5 Alternatively, tendon autograft and allografts have also been recommended, especially in extreme situations.^1,6 Furthermore, animal experiments have shown that a compact platelet-rich fibrin scaffold (CPFS) has the potential to accelerate healing of patellar tendon defects and to act as a bioscaffold for graft augmentation.⁷

We describe the case of a 30-year-old man who underwent extensor mechanism reconstruction with cadaveric tendon–patellar tendon–bone allograft for failure of an infected primary end-to-end repair. The patient provided written informed consent for print and electronic publication of this case report.

Case Report

A 30-year-old healthy man landed on an empty glass fish tank, resulting in a traumatic right-knee arthrotomy. On initial evaluation, the patient had a negative straight-leg-raise test and impaired knee extension. The patient was taken urgently to the operating room for irrigation and débridement and concurrent repair of the patellar tendon laceration. Antibiotic prophylaxis with 2 g of intravenous (IV) cefazolin was given in the emergency room.

Intraoperatively, after visualizing the patellar tendon laceration and excluding any associated chondral lesions, we proceeded with extensive débridement and irrigation using 9 L of normal saline pulse lavage. After we achieved a clean site, we proceeded to repair the patellar tendon using No. 2 FiberWire sutures (Arthrex, Naples, Florida) with a classic Krackow repair⁸ consisting of 2 sutures run in a 4-row fashion through the patella and the patellar tendon. The suture was securely tightened and then tested for stability to at least 90° of knee flexion. The retinaculum was repaired using No. 0 Vicryl sutures (Ethicon, Somerville, New Jersey). After wound closure and dressing, the patient was placed in a hinged knee brace locked in extension at all times after surgery. Antibiotic treatment with IV cefazolin was administered for 48 hours.

Postoperative management consisted of weight-bearing as tolerated on the operative limb and appropriate deep venous thrombosis prophylaxis. The patient followed up in clinic 2 weeks and 4 weeks after surgery. At 4 weeks, the patient was noted to have a secondary wound infection with superficial dehiscence and serosanguineous drainage. No wound opening was noticed, and local wound care was performed with a 1-week course of oral cephalexin. The patient was scheduled to follow up a few weeks later but did not follow up for a year.

At 1-year follow-up, the patient reported that he had had a steady progression of his knee range of motion (ROM) with decreased pain. However, over time, the patient noted subjective instability of the knee, with frequent falls occurring close to his 1-year follow-up. Examination of his knee showed that his active ROM ranged from 20° in extension to 120° in flexion, with a weak extensor mechanism. Passively, his knee could be brought to full extension. His incision was well healed, but it had an area of bogginess in the middle. Radiographs showed patella alta on the affected knee, with a lengthening of the patellar tendon of 7.70 cm on the right compared with 5.18 cm on the left. Magnetic resonance imaging (MRI) showed moderate-to-severe patellar tendinosis with small fluid pockets around the surgical material and evidence of acute patellar enthesopathy. The laboratory values showed a white blood cell count of 7580/μL (normal, 4500-11,000/μL), an erythrocyte sedimentation rate of 2 mm/h (normal, 1-15 mm/h), and a C-reactive protein level of 1.93 mg/dL (normal, 0.00-0.29 mg/dL). Based on the clinical examination and imaging findings, there was a concern for a possible chronic deep-tissue infection, in addition to failure of the primary patellar tendon repair. Operative versus nonoperative management options were discussed with the patient, and he elected to undergo surgery.

During surgery, the patellar laxity was confirmed, and the patellar tendon was noticed to be chronically thickened and surrounded by unhealthy tissue. Initially, an extensive soft-tissue débridement was performed, and all patellar tendon loculations visualized on the preoperative MRI were drained; a solid purulent-like fluid was expressed. Unfortunately, the extensive and required débridement did not allow the preservation of the patellar tendon. Appropriate cultures were taken and sent for immediate Gram-stain analysis, which returned negative. Tissue samples from the patellar tendon were also sent to the pathology department for analysis. Intraoperatively, the infrapatellar defect was filled temporarily with a tobramycin cement spacer mixed with 2 g of vancomycin in a manner similar to that of the Masquelet technique used for infected long-bone nonunions with bone loss.^9,10 This technique is a 2-stage procedure that promotes the formation of a biologic membrane that allows bone healing in the reconstruction of long-bone defects. The first stage consists of a radical débridement with soft-tissue repair by flaps when needed, with the insertion of a polymethylmethacrylate cement spacer into the bone defect. The second stage is usually performed 6 to 8 weeks later, with removal of the spacer and preservation of the induced membrane, which is filled with iliac crest bone autograft augmented (if necessary) with demineralized allograft.

The incision was closed primarily, and after surgery, the patient was allowed to bear weight as tolerated in a hinged knee brace locked in extension. Final laboratory analysis from cultures and tissue samples revealed acute and chronic inflammation with more than 20 neutrophils per high-powered field. No organisms grew from aerobic, anaerobic, fungal, or mycobacterial cultures. The infectious disease service was consulted and recommended oral cephalexin.

Because all cultures were negative, all laboratory examinations did not indicate any residual infections, and no bony involvement was noticed intraoperatively or in the preoperative knee MRI, we decided to proceed with the second stage of the Masquelet technique after 2 weeks. The patient returned to the operating room for final reconstruction of his patellar tendon using a custom-ordered cadaveric tendon–patellar tendon–bone allograft, the length of which was determined by measuring the contralateral patellar tendon, ie, 5.18 cm (Figure 1A). The previous anterior knee incision was reopened and extended distally past the tibial tuberosity and proximally toward the quadriceps tendon. The antibiotic spacer was removed. We proceeded with a repeat irrigation and débridement and the allograft transfer. The selected allograft was customized by reducing the tibial bone component to an approximately 1×2-cm bone block and by reducing the allograft patellar thickness with an oscillating saw, leaving an approximately 2-mm thick patellar bone graft attached to the patellar tendon. In a similar technique using an oscillating saw, we shaved off the anterior cortex of the patient’s patella to accommodate, in a sandwich fashion, the patellar allograft. Proximally, the quadriceps tendon insertion was split longitudinally and partially separated from the superior pole of the patellar tendon to allow seating and fixation of the modified quadriceps allograft tendon component.

We proceeded with the fixation of the allograft first distally on the patella. The anterior cortex of the tibial tuberosity was resected to allow the perfect seating of the bone block allograft. The graft was secured with a 4.0-mm fully threaded cancellous lag screw and reinforced with a 2.4-mm, 3-hole T-volar buttress plate (Synthes, Paoli, Pennsylvania). The plate was contoured to better fit the patient’s tibia. We sutured the patellar allograft tendon to the patella using two No. 2-0 FiberWire sutures in Krackow suture technique⁸ (Figures 1B, 1C). We obtained good fixation of the patellar tendon, and the distance between the patellar insertion and the inferior patellar pole was the same as before surgery: 5.57 cm and comparable to the contralateral side (Figures 2A-2C). The patellar allograft and autograft sandwich were secured with additional No. 2-0 FiberWire sutures, and the quadriceps allograft and autograft were secured with the cross-stitch technique with the same material. Fine suturing of the quadriceps tendon was done with No. 0 Vicryl sutures. After the fixation was completed, we tested the stability of the reconstruction and found good flexion up to 120°.

The postoperative protocol consisted of weight-bearing as tolerated in full extension and passive knee ROM, using a continuous passive ROM machine from 0° to 45° for the first 4 weeks, followed by active ROM, increased as tolerated, during the next 8 weeks.

The patient was seen in clinic 3 and 9 months after surgery. At the 3-month follow-up appointment, the patient’s examination showed knee ROM from 0° extension to 130° of flexion, no secondary infection signs, and radiographic evidence of a well-healing patellar allograft with symmetric patellar tendon length to the contralateral side. At 9-month follow-up, the patient’s active ROM was from 0° extension to 140° flexion (Figures 3A, 3B), and he had returned to his preinjury level of functioning.

Discussion

This case report describes the successful reconstruction of a patellar tendon defect with cadaveric tendon–patellar tendon–bone allograft. Extensor mechanism injuries are uncommon in general, and the incidence of patellar tendon injury is higher in men than in women.² Patellar tendon tears occur frequently in active patients younger than 40 years, usually as a result of sudden quadriceps contraction with the knee slightly flexed.¹ Treatment of patellar tendon injury is surgical, and functional outcomes for patients with this injury are equivalent to those of patients with quadriceps tendon injuries or patellar fractures.² Acute patellar tendon tears can be repaired by end-to-end suturing or transosseous tunnel insertion in the tibia or patella.¹ Reinforcement is often added between the patella and tibial tuberosity, using a semitendinosus band or wire.¹ End-to-end suture is performed using a thick resorbable suture. It is important to avoid patella alta during suturing, comparing the position of the patella with the contralateral patella with the knee in 45° of flexion. In proximal avulsion, the tendon is anchored to the bone by 2 thick nonresorbable sutures through 2 parallel bone tunnels to the proximal pole of the patella. Distal avulsion is rare in adults, but it can be managed by using staples or suture anchors.¹

End-to-end suturing of chronic patellar tendon defects is difficult more than 45 days after injury primarily because of difficulties in correcting patella alta secondary to the upward force exerted by the quadriceps tendon.^1,3 Extreme situations similar to the case we present warrant Achilles or patellar tendon allograft for reconstruction of the extensor mechanism.^1,3,6,9

Extensor mechanism allograft also provides an effective remedy for severe quadriceps deficiency caused by loss of the patella, patellar tendon, and quadriceps tendon in total knee arthroplasty.¹⁰ However, in such cases, late failure is common, and major quadriceps deficiency occurs after removal of the allograft material.¹⁰ To improve outcome, a novel technique using the medial gastrocnemius muscle transferred to the muscular portion of the vastus medialis and lateralis flaps provides a secure and strong closure of the anterior knee, thereby restoring the extensor mechanism of the knee.¹⁰

Patellar tendon reconstruction with allograft tissue has been successfully used, especially in cases related to chronic patellar tendon ruptures¹¹ and total knee arthroplasty.^6,12-14 Crossett and colleagues¹² showed that, at 2-year follow-up, the average knee score for pain, ROM, and stability had improved from 26 points (range, 6-39 points) before surgery to 81 points (range, 40-92 points). The average knee score for function had also improved: 14 points (range, 0-35 points) before surgery to 53 points (range, 30-90 points).¹² Primary repair may succeed in early intervention, but in an established rupture, allograft reconstruction is often necessary. Achilles tendon is the preferred allograft, with the calcaneus fragment embedded into the proximal tibia as a new tubercle and the tendon sutured into the remaining extensor mechanism.^1,11 The repair is further protected using a cable loop from the superior pole of the patella to a drill hole in the upper tibia.⁹ Techniques have also been described involving passage of the proximal aspect of the allograft tendon through patellar bone tunnels and suture fixation to the native quadriceps tendon.^11,15 However, in our technique, we shaved off the anterior cortex of the patient’s patella to allow a sandwich-type over-position of the allograft to secure fixation to the patella.

Another alternative to allograft reconstruction involves biocompatible scaffolds. Such scaffolds incorporate the use of platelets in a fibrin framework. A CPFS, produced from blood and calcium gluconate to improve healing of patellar tendon defects, has been described in animal studies.⁷ In the rabbit model, CPFS acts as a provisional bioscaffold that can accelerate healing of an injured patellar tendon repair, potentially secondary to several growth factors derived from platelets.⁷ Platelets are biocompatible sources of growth factors, and CPFS can act as a scaffold to restore the mechanical integrity of injured soft tissue.^7,16 In addition, CPFS can act to lower donor-site morbidity associated with harvesting tissue autograft.⁷ However, to our knowledge, such scaffolds have not been used in human trials. The LARS biocompatible ligament (Corin Group PLC, Cirencester, United Kingdom), currently not approved by the US Food and Drug Administration, is used for reconstructions of isolated or multiple knee ligament injuries.¹⁷ This graft requires the presence of healthy tissue with good blood supply from which new tendon or ligament can grow in. Sometimes it is also used for extensor mechanism reconstruction after radical tumor resection around the knee; however, good results are achieved in only 59% of cases,¹⁸ and to our knowledge, only 1 case of primary repair of a patellar tendon rupture has been published.¹⁹

Techniques involving the use of tendon–patellar tendon–bone graft with fixation via the sandwich-type over-position of the allograft for chronic patellar tendon rupture have not been described in the literature. In our patient, given the extensive patellar tendon lesion and inflammation with chronic tissue degeneration, there was no option but to use allograft. To improve the patient’s outcome, we chose the strongest possible allograft, tendon–patellar tendon–bone graft.

Conclusion

Revision patellar tendon reconstruction is a challenging, but necessary, procedure to restore the extensor mechanism of the knee, especially in young, active individuals. Various options to reconstruct the tissue defects are available. Our patient was successfully treated with a tendon–patellar tendon–bone allograft reconstruction.

In 1887, Midelfart¹ first reported on an intra-articular dislocation of the patella, and since then approximately 50 cases have been reported in the worldwide literature.² Also known as an inferior patellar dislocation, these rare traumatic events occur when the patella dislocates intra-articularly. Because the patella commonly rotates about its horizontal axis, the articular surface is facing proximally or distally. The patella becomes lodged within the trochlea and locks the knee joint. Most cases described in the literature involved adolescent boys, with the patella difficult to reduce. Most patients required open reduction, while those who underwent successful closed reduction often needed general anesthesia.³

Similarly, coronal shear fractures of the femoral condyle (ie, Hoffa fractures) are an uncommon fracture pattern typically seen in adults. These fractures are even more infrequent in skeletally immature patients, with fewer than 5 cases documented in the literature.^4-7 In our case report, we present a 14-year-old boy with a coronal shear fracture of the femoral condyle associated with an intra-articular patellar dislocation. To our knowledge, this constellation of injuries has not been reported. Additionally, closed reduction of the patella was successful after intra-articular lidocaine injection, without the need for sedation or general anesthesia. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 14-year-old boy presented to our institution after sustaining a direct blow to his left knee. The injury occurred as he jumped and landed on a flexed knee while playing with friends. The patient was unable to ambulate after the injury, and his left knee was locked in a slightly flexed position. Examination in the emergency department showed the knee to be held in approximately 60º of flexion, with an obvious bony prominence noted anteriorly over the femoral condyles. The patient was unable to perform a straight leg raise or any active range of motion (ROM) at the knee. Radiographs performed with the knee maintained in flexion confirmed that the patella was displaced into the knee joint and was rotated with the articular surface facing distally. Also noted was a coronal shear fracture of the lateral femoral condyle (Figures 1A, 1B).

The patient received pain medication and an intra-articular lidocaine injection prior to a reduction attempt by the orthopedic resident. With the patient supine, the hip was gently flexed to relax the quadriceps muscle. As the knee was flexed up to 110º, the prominent patella was gripped between the thumb and fingers to gently free and elevate the patella out of the intercondylar notch.

After reduction, an immediate return of normal patellar contour and patellofemoral tracking was observed as the knee was gently extended. There was no obvious defect to the patellar or quadriceps tendons, and the patient was able to perform a straight-leg raise, confirming the integrity of the extensor mechanism. Radiographs performed after the reduction confirmed relocation of the patella in correct anatomic position, as well as a lateral femoral condyle fracture (Figures 2A, 2B). Magnetic resonance imaging (MRI) of the knee confirmed no full-thickness quadriceps or patellar tendon tear. A computed tomography (CT) scan of the knee showed a comminuted fracture of the lateral femoral condyle in the coronal plane, as well as multiple bone fragments within the joint (Figures 3A, 3B). The patient was placed in a bulky soft dressing and underwent open reduction and internal fixation of the fracture.

A 10-cm incision was made over the anterior aspect of the knee, and after dissection to the level of the retinaculum, a lateral parapatellar arthrotomy was performed. The patella was retracted medially to identify and free the fracture fragments. The fracture fragments were provisionally reduced and stabilized with three 0.065-in Kirschner wires. An area of osteochondral impaction proximal to the fracture was elevated and allograft bone was incorporated below the articular surface (Figures 4A, 4B). Rigid fixation of the fracture was achieved using 3 screws (2 Bio-Compression Screws [Arthrex Inc., Naples, Florida] and 1 Synthes cannulated screw [Synthes, West Chester, Pennsylvania]). The screws were placed in posteroanterior (PA) direction and inserted into the weight-bearing articular surface of the femoral condyle (Figures 4C, 4D). The screws were countersunk, and stable fixation with compression of the fracture was achieved. Reduction and screw position were verified with fluoroscopic views. The wound was closed in layers, and the patient was discharged home the next day.

Postoperatively, the patient was non-weight-bearing on the affected limb with a hinged-knee brace to allow for knee ROM exercises immediately. He was also given a continuous passive motion device to maintain knee motion. At the 6-week mark, the patient’s fracture alignment appeared to be well-maintained and showed interval healing. Clinically, the patient was noted to have limited knee ROM. The decision was made to take the patient to the operating room primarily for a manipulation under anesthesia and resection of scar tissue from postoperative arthrofibrosis. Arthroscopic screw removal was also planned as a secondary procedure at the same time in order to prevent the possibility of chondral injury from screw migration. During the procedure, the patient was noted to have improved ROM from 5º to 85º premanipulation to 5º to 110º postoperatively. At 3 months after the initial injury, the patient was allowed to begin progressive weight-bearing on the left knee. At most recent follow-up, after 12 months, the patient was able to ambulate and bear weight on the left leg without pain. Plain radiographs show a well-healed fracture with no evidence of collapse of the femoral condyle (Figures 5A, 5B). His active ROM of the left knee was 5º to 110º without pain (Figures 5C, 5D).

Discussion

In the vast majority of patellar dislocations, the patella dislocates laterally over the trochlear groove. Inferior, or intra-articular, dislocations of the patella are rare. The mechanism of injury is usually a blow onto the patella with a flexed knee. The 2 groups commonly involved are adolescent boys and the elderly.^8,9 In young men, it is thought that lax patellar attachments place adolescents at higher risk for this type of injury.^10-12 While patella fractures and frank extensor mechanism ruptures are uncommon in this age group, the same mechanism of injury can lead to stripping of the deep fibers of the patellar tendon from the superior pole of the patella.^3,13 The intact superficial fibers of the tendon allow the patella to hinge and displace into the joint.¹⁴

Inferior dislocations of the patella are classified into 2 types based on the orientation of the articular surface and the presence of osteophytes.¹⁵ Type I inferior dislocations occur after a direct blow to a flexed knee forces the superior pole of the patella into the intercondylar notch. Type II dislocations are caused by osteophytes on the superior pole of the patella that become wedged in the intercondylar notch and dislocate the patella inferiorly. In type I dislocations, the patella is rotated in the horizontal plane and the articular surface often faces inferiorly, but type II dislocations do not involve rotation of the articular surface. Type II injuries are seen more commonly in the elderly.

Our patient was able to tolerate a closed reduction of the patella after an intra-articular lidocaine injection, and a successful reduction was achieved without great difficulty. However, the majority of reports describe the need for an open reduction of inferior patellar dislocations.^3,8 When closed reductions were a success, they were performed under general anesthesia or conscious sedation.³ It is thought that the difficulty of reduction results from the tension of the quadriceps muscle pulling the patella superiorly into intercondylar notch.^11,16 However, successful closed reduction may be more likely in patients with less patellar rotation and entrapment within the intercondylar notch, as well as in patients whose knee is near full extension at presentation.^17-19 Successful closed reduction is also seen in elderly patients, where dislocation is generally caused by less forceful impact and held by osteophytes. In these patients, the knee is commonly held in extension.^12,15,20-22

The fracture pattern seen in this case also shows a rare fracture in skeletally immature patients, with only a few case reports in the literature. Isolated coronal plane femur fractures account for 0.65% of all femur fractures and are usually seen in adults after high-energy trauma.²³ In the skeletally immature, the fracture can occur with lower-energy mechanisms. The typical mechanism is thought to be a shearing force to the femur caused by an axial load to the knee in 90° or more of flexion.^4,24 A CT scan is recommended for better identification of the fracture and to plan treatment.^25,26 Because of their intra-articular nature and tenuous blood supply, Hoffa fractures tend to do poorly with nonoperative treatment and are prone to displacement and nonunion.^27,28 The goal of operative treatment is to obtain anatomic reduction and rigid fixation. While operative fixation techniques are varied, screw fixation with multiple smaller diameter screws has equal pullout strength compared to larger screws and may minimize damage to the articular cartilage.^29-31 By preserving blood supply to the fracture, and allowing for early active mobilization, operative treatment generally provides good long-term functional outcomes in these fracture patterns.²⁴

Conclusion

We describe a case in which the patella of an adolescent boy dislocated inferiorly into the knee joint, with an associated coronal shear fracture of the lateral femoral condyle. To our knowledge, this constellation of injuries has not been reported. For this uncommon injury pattern, we recommend a sequential treatment algorithm to minimize morbidity. We recommend first attempting a closed reduction of the patella with adequate pain control to avoid the morbidity associated with general anesthesia. After a successful reduction, an advanced imaging study (eg, MRI) is advisable to assess for concomitant soft-tissue injuries and preoperative planning, if necessary. The mechanism of injury and force required to cause a patellar dislocation of this nature leaves a high likelihood of other injuries. When a fracture is noted on plain radiographs after reduction, a CT scan can provide important information for planning surgical fixation of the fracture. Even in a skeletally immature patient, the principle of direct reduction and stable interfragmentary fixation of an articular fracture is critical for long-term function, even after a significant trauma to the knee.

In 1887, Midelfart¹ first reported on an intra-articular dislocation of the patella, and since then approximately 50 cases have been reported in the worldwide literature.² Also known as an inferior patellar dislocation, these rare traumatic events occur when the patella dislocates intra-articularly. Because the patella commonly rotates about its horizontal axis, the articular surface is facing proximally or distally. The patella becomes lodged within the trochlea and locks the knee joint. Most cases described in the literature involved adolescent boys, with the patella difficult to reduce. Most patients required open reduction, while those who underwent successful closed reduction often needed general anesthesia.³

Similarly, coronal shear fractures of the femoral condyle (ie, Hoffa fractures) are an uncommon fracture pattern typically seen in adults. These fractures are even more infrequent in skeletally immature patients, with fewer than 5 cases documented in the literature.^4-7 In our case report, we present a 14-year-old boy with a coronal shear fracture of the femoral condyle associated with an intra-articular patellar dislocation. To our knowledge, this constellation of injuries has not been reported. Additionally, closed reduction of the patella was successful after intra-articular lidocaine injection, without the need for sedation or general anesthesia. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 14-year-old boy presented to our institution after sustaining a direct blow to his left knee. The injury occurred as he jumped and landed on a flexed knee while playing with friends. The patient was unable to ambulate after the injury, and his left knee was locked in a slightly flexed position. Examination in the emergency department showed the knee to be held in approximately 60º of flexion, with an obvious bony prominence noted anteriorly over the femoral condyles. The patient was unable to perform a straight leg raise or any active range of motion (ROM) at the knee. Radiographs performed with the knee maintained in flexion confirmed that the patella was displaced into the knee joint and was rotated with the articular surface facing distally. Also noted was a coronal shear fracture of the lateral femoral condyle (Figures 1A, 1B).

The patient received pain medication and an intra-articular lidocaine injection prior to a reduction attempt by the orthopedic resident. With the patient supine, the hip was gently flexed to relax the quadriceps muscle. As the knee was flexed up to 110º, the prominent patella was gripped between the thumb and fingers to gently free and elevate the patella out of the intercondylar notch.

After reduction, an immediate return of normal patellar contour and patellofemoral tracking was observed as the knee was gently extended. There was no obvious defect to the patellar or quadriceps tendons, and the patient was able to perform a straight-leg raise, confirming the integrity of the extensor mechanism. Radiographs performed after the reduction confirmed relocation of the patella in correct anatomic position, as well as a lateral femoral condyle fracture (Figures 2A, 2B). Magnetic resonance imaging (MRI) of the knee confirmed no full-thickness quadriceps or patellar tendon tear. A computed tomography (CT) scan of the knee showed a comminuted fracture of the lateral femoral condyle in the coronal plane, as well as multiple bone fragments within the joint (Figures 3A, 3B). The patient was placed in a bulky soft dressing and underwent open reduction and internal fixation of the fracture.

A 10-cm incision was made over the anterior aspect of the knee, and after dissection to the level of the retinaculum, a lateral parapatellar arthrotomy was performed. The patella was retracted medially to identify and free the fracture fragments. The fracture fragments were provisionally reduced and stabilized with three 0.065-in Kirschner wires. An area of osteochondral impaction proximal to the fracture was elevated and allograft bone was incorporated below the articular surface (Figures 4A, 4B). Rigid fixation of the fracture was achieved using 3 screws (2 Bio-Compression Screws [Arthrex Inc., Naples, Florida] and 1 Synthes cannulated screw [Synthes, West Chester, Pennsylvania]). The screws were placed in posteroanterior (PA) direction and inserted into the weight-bearing articular surface of the femoral condyle (Figures 4C, 4D). The screws were countersunk, and stable fixation with compression of the fracture was achieved. Reduction and screw position were verified with fluoroscopic views. The wound was closed in layers, and the patient was discharged home the next day.

Postoperatively, the patient was non-weight-bearing on the affected limb with a hinged-knee brace to allow for knee ROM exercises immediately. He was also given a continuous passive motion device to maintain knee motion. At the 6-week mark, the patient’s fracture alignment appeared to be well-maintained and showed interval healing. Clinically, the patient was noted to have limited knee ROM. The decision was made to take the patient to the operating room primarily for a manipulation under anesthesia and resection of scar tissue from postoperative arthrofibrosis. Arthroscopic screw removal was also planned as a secondary procedure at the same time in order to prevent the possibility of chondral injury from screw migration. During the procedure, the patient was noted to have improved ROM from 5º to 85º premanipulation to 5º to 110º postoperatively. At 3 months after the initial injury, the patient was allowed to begin progressive weight-bearing on the left knee. At most recent follow-up, after 12 months, the patient was able to ambulate and bear weight on the left leg without pain. Plain radiographs show a well-healed fracture with no evidence of collapse of the femoral condyle (Figures 5A, 5B). His active ROM of the left knee was 5º to 110º without pain (Figures 5C, 5D).

Discussion

In the vast majority of patellar dislocations, the patella dislocates laterally over the trochlear groove. Inferior, or intra-articular, dislocations of the patella are rare. The mechanism of injury is usually a blow onto the patella with a flexed knee. The 2 groups commonly involved are adolescent boys and the elderly.^8,9 In young men, it is thought that lax patellar attachments place adolescents at higher risk for this type of injury.^10-12 While patella fractures and frank extensor mechanism ruptures are uncommon in this age group, the same mechanism of injury can lead to stripping of the deep fibers of the patellar tendon from the superior pole of the patella.^3,13 The intact superficial fibers of the tendon allow the patella to hinge and displace into the joint.¹⁴

Inferior dislocations of the patella are classified into 2 types based on the orientation of the articular surface and the presence of osteophytes.¹⁵ Type I inferior dislocations occur after a direct blow to a flexed knee forces the superior pole of the patella into the intercondylar notch. Type II dislocations are caused by osteophytes on the superior pole of the patella that become wedged in the intercondylar notch and dislocate the patella inferiorly. In type I dislocations, the patella is rotated in the horizontal plane and the articular surface often faces inferiorly, but type II dislocations do not involve rotation of the articular surface. Type II injuries are seen more commonly in the elderly.

Our patient was able to tolerate a closed reduction of the patella after an intra-articular lidocaine injection, and a successful reduction was achieved without great difficulty. However, the majority of reports describe the need for an open reduction of inferior patellar dislocations.^3,8 When closed reductions were a success, they were performed under general anesthesia or conscious sedation.³ It is thought that the difficulty of reduction results from the tension of the quadriceps muscle pulling the patella superiorly into intercondylar notch.^11,16 However, successful closed reduction may be more likely in patients with less patellar rotation and entrapment within the intercondylar notch, as well as in patients whose knee is near full extension at presentation.^17-19 Successful closed reduction is also seen in elderly patients, where dislocation is generally caused by less forceful impact and held by osteophytes. In these patients, the knee is commonly held in extension.^12,15,20-22

The fracture pattern seen in this case also shows a rare fracture in skeletally immature patients, with only a few case reports in the literature. Isolated coronal plane femur fractures account for 0.65% of all femur fractures and are usually seen in adults after high-energy trauma.²³ In the skeletally immature, the fracture can occur with lower-energy mechanisms. The typical mechanism is thought to be a shearing force to the femur caused by an axial load to the knee in 90° or more of flexion.^4,24 A CT scan is recommended for better identification of the fracture and to plan treatment.^25,26 Because of their intra-articular nature and tenuous blood supply, Hoffa fractures tend to do poorly with nonoperative treatment and are prone to displacement and nonunion.^27,28 The goal of operative treatment is to obtain anatomic reduction and rigid fixation. While operative fixation techniques are varied, screw fixation with multiple smaller diameter screws has equal pullout strength compared to larger screws and may minimize damage to the articular cartilage.^29-31 By preserving blood supply to the fracture, and allowing for early active mobilization, operative treatment generally provides good long-term functional outcomes in these fracture patterns.²⁴

Conclusion

We describe a case in which the patella of an adolescent boy dislocated inferiorly into the knee joint, with an associated coronal shear fracture of the lateral femoral condyle. To our knowledge, this constellation of injuries has not been reported. For this uncommon injury pattern, we recommend a sequential treatment algorithm to minimize morbidity. We recommend first attempting a closed reduction of the patella with adequate pain control to avoid the morbidity associated with general anesthesia. After a successful reduction, an advanced imaging study (eg, MRI) is advisable to assess for concomitant soft-tissue injuries and preoperative planning, if necessary. The mechanism of injury and force required to cause a patellar dislocation of this nature leaves a high likelihood of other injuries. When a fracture is noted on plain radiographs after reduction, a CT scan can provide important information for planning surgical fixation of the fracture. Even in a skeletally immature patient, the principle of direct reduction and stable interfragmentary fixation of an articular fracture is critical for long-term function, even after a significant trauma to the knee.

In 1887, Midelfart¹ first reported on an intra-articular dislocation of the patella, and since then approximately 50 cases have been reported in the worldwide literature.² Also known as an inferior patellar dislocation, these rare traumatic events occur when the patella dislocates intra-articularly. Because the patella commonly rotates about its horizontal axis, the articular surface is facing proximally or distally. The patella becomes lodged within the trochlea and locks the knee joint. Most cases described in the literature involved adolescent boys, with the patella difficult to reduce. Most patients required open reduction, while those who underwent successful closed reduction often needed general anesthesia.³

Similarly, coronal shear fractures of the femoral condyle (ie, Hoffa fractures) are an uncommon fracture pattern typically seen in adults. These fractures are even more infrequent in skeletally immature patients, with fewer than 5 cases documented in the literature.^4-7 In our case report, we present a 14-year-old boy with a coronal shear fracture of the femoral condyle associated with an intra-articular patellar dislocation. To our knowledge, this constellation of injuries has not been reported. Additionally, closed reduction of the patella was successful after intra-articular lidocaine injection, without the need for sedation or general anesthesia. The patient’s guardian provided written informed consent for print and electronic publication of this case report.

Case Report

A 14-year-old boy presented to our institution after sustaining a direct blow to his left knee. The injury occurred as he jumped and landed on a flexed knee while playing with friends. The patient was unable to ambulate after the injury, and his left knee was locked in a slightly flexed position. Examination in the emergency department showed the knee to be held in approximately 60º of flexion, with an obvious bony prominence noted anteriorly over the femoral condyles. The patient was unable to perform a straight leg raise or any active range of motion (ROM) at the knee. Radiographs performed with the knee maintained in flexion confirmed that the patella was displaced into the knee joint and was rotated with the articular surface facing distally. Also noted was a coronal shear fracture of the lateral femoral condyle (Figures 1A, 1B).

The patient received pain medication and an intra-articular lidocaine injection prior to a reduction attempt by the orthopedic resident. With the patient supine, the hip was gently flexed to relax the quadriceps muscle. As the knee was flexed up to 110º, the prominent patella was gripped between the thumb and fingers to gently free and elevate the patella out of the intercondylar notch.

After reduction, an immediate return of normal patellar contour and patellofemoral tracking was observed as the knee was gently extended. There was no obvious defect to the patellar or quadriceps tendons, and the patient was able to perform a straight-leg raise, confirming the integrity of the extensor mechanism. Radiographs performed after the reduction confirmed relocation of the patella in correct anatomic position, as well as a lateral femoral condyle fracture (Figures 2A, 2B). Magnetic resonance imaging (MRI) of the knee confirmed no full-thickness quadriceps or patellar tendon tear. A computed tomography (CT) scan of the knee showed a comminuted fracture of the lateral femoral condyle in the coronal plane, as well as multiple bone fragments within the joint (Figures 3A, 3B). The patient was placed in a bulky soft dressing and underwent open reduction and internal fixation of the fracture.

A 10-cm incision was made over the anterior aspect of the knee, and after dissection to the level of the retinaculum, a lateral parapatellar arthrotomy was performed. The patella was retracted medially to identify and free the fracture fragments. The fracture fragments were provisionally reduced and stabilized with three 0.065-in Kirschner wires. An area of osteochondral impaction proximal to the fracture was elevated and allograft bone was incorporated below the articular surface (Figures 4A, 4B). Rigid fixation of the fracture was achieved using 3 screws (2 Bio-Compression Screws [Arthrex Inc., Naples, Florida] and 1 Synthes cannulated screw [Synthes, West Chester, Pennsylvania]). The screws were placed in posteroanterior (PA) direction and inserted into the weight-bearing articular surface of the femoral condyle (Figures 4C, 4D). The screws were countersunk, and stable fixation with compression of the fracture was achieved. Reduction and screw position were verified with fluoroscopic views. The wound was closed in layers, and the patient was discharged home the next day.

Postoperatively, the patient was non-weight-bearing on the affected limb with a hinged-knee brace to allow for knee ROM exercises immediately. He was also given a continuous passive motion device to maintain knee motion. At the 6-week mark, the patient’s fracture alignment appeared to be well-maintained and showed interval healing. Clinically, the patient was noted to have limited knee ROM. The decision was made to take the patient to the operating room primarily for a manipulation under anesthesia and resection of scar tissue from postoperative arthrofibrosis. Arthroscopic screw removal was also planned as a secondary procedure at the same time in order to prevent the possibility of chondral injury from screw migration. During the procedure, the patient was noted to have improved ROM from 5º to 85º premanipulation to 5º to 110º postoperatively. At 3 months after the initial injury, the patient was allowed to begin progressive weight-bearing on the left knee. At most recent follow-up, after 12 months, the patient was able to ambulate and bear weight on the left leg without pain. Plain radiographs show a well-healed fracture with no evidence of collapse of the femoral condyle (Figures 5A, 5B). His active ROM of the left knee was 5º to 110º without pain (Figures 5C, 5D).

Discussion

In the vast majority of patellar dislocations, the patella dislocates laterally over the trochlear groove. Inferior, or intra-articular, dislocations of the patella are rare. The mechanism of injury is usually a blow onto the patella with a flexed knee. The 2 groups commonly involved are adolescent boys and the elderly.^8,9 In young men, it is thought that lax patellar attachments place adolescents at higher risk for this type of injury.^10-12 While patella fractures and frank extensor mechanism ruptures are uncommon in this age group, the same mechanism of injury can lead to stripping of the deep fibers of the patellar tendon from the superior pole of the patella.^3,13 The intact superficial fibers of the tendon allow the patella to hinge and displace into the joint.¹⁴

Inferior dislocations of the patella are classified into 2 types based on the orientation of the articular surface and the presence of osteophytes.¹⁵ Type I inferior dislocations occur after a direct blow to a flexed knee forces the superior pole of the patella into the intercondylar notch. Type II dislocations are caused by osteophytes on the superior pole of the patella that become wedged in the intercondylar notch and dislocate the patella inferiorly. In type I dislocations, the patella is rotated in the horizontal plane and the articular surface often faces inferiorly, but type II dislocations do not involve rotation of the articular surface. Type II injuries are seen more commonly in the elderly.

Our patient was able to tolerate a closed reduction of the patella after an intra-articular lidocaine injection, and a successful reduction was achieved without great difficulty. However, the majority of reports describe the need for an open reduction of inferior patellar dislocations.^3,8 When closed reductions were a success, they were performed under general anesthesia or conscious sedation.³ It is thought that the difficulty of reduction results from the tension of the quadriceps muscle pulling the patella superiorly into intercondylar notch.^11,16 However, successful closed reduction may be more likely in patients with less patellar rotation and entrapment within the intercondylar notch, as well as in patients whose knee is near full extension at presentation.^17-19 Successful closed reduction is also seen in elderly patients, where dislocation is generally caused by less forceful impact and held by osteophytes. In these patients, the knee is commonly held in extension.^12,15,20-22

The fracture pattern seen in this case also shows a rare fracture in skeletally immature patients, with only a few case reports in the literature. Isolated coronal plane femur fractures account for 0.65% of all femur fractures and are usually seen in adults after high-energy trauma.²³ In the skeletally immature, the fracture can occur with lower-energy mechanisms. The typical mechanism is thought to be a shearing force to the femur caused by an axial load to the knee in 90° or more of flexion.^4,24 A CT scan is recommended for better identification of the fracture and to plan treatment.^25,26 Because of their intra-articular nature and tenuous blood supply, Hoffa fractures tend to do poorly with nonoperative treatment and are prone to displacement and nonunion.^27,28 The goal of operative treatment is to obtain anatomic reduction and rigid fixation. While operative fixation techniques are varied, screw fixation with multiple smaller diameter screws has equal pullout strength compared to larger screws and may minimize damage to the articular cartilage.^29-31 By preserving blood supply to the fracture, and allowing for early active mobilization, operative treatment generally provides good long-term functional outcomes in these fracture patterns.²⁴

Conclusion

We describe a case in which the patella of an adolescent boy dislocated inferiorly into the knee joint, with an associated coronal shear fracture of the lateral femoral condyle. To our knowledge, this constellation of injuries has not been reported. For this uncommon injury pattern, we recommend a sequential treatment algorithm to minimize morbidity. We recommend first attempting a closed reduction of the patella with adequate pain control to avoid the morbidity associated with general anesthesia. After a successful reduction, an advanced imaging study (eg, MRI) is advisable to assess for concomitant soft-tissue injuries and preoperative planning, if necessary. The mechanism of injury and force required to cause a patellar dislocation of this nature leaves a high likelihood of other injuries. When a fracture is noted on plain radiographs after reduction, a CT scan can provide important information for planning surgical fixation of the fracture. Even in a skeletally immature patient, the principle of direct reduction and stable interfragmentary fixation of an articular fracture is critical for long-term function, even after a significant trauma to the knee.

The term spontaneous osteonecrosis of the knee was first used by Ahlbäck¹ in 1968. This term, and the acronym SONK (sometimes SPONK²), has subsequently been used by other authors to refer to an apparent osteonecrosis of the knee, most commonly occurring within the medial femoral condyle. SONK typically occurs in older women who usually do not have the typical osteonecrosis risk factors, such as steroid use, sickle-cell anemia, and excessive alcohol intake. Furthermore, the radiologic appearance of SONK differs from the typical avascular necrosis findings seen with radiography and magnetic resonance imaging (MRI). In particular, on MRI, the abnormality of SONK does not have the typical serpiginous margin of bone infarction, or the double-line sign indicating both sclerosis and granulation tissue.³ SONK is normally seen as a line of signal intensity on T1- and T2-weighted sequences; this line is adjacent to or parallels the subchondral bone with an adjacent area of extensive edema.

There is dispute over the cause of SONK. Yamamoto and Bullough⁴ proposed the lesion is in part a subchondral insufficiency fracture and staged it into 4 parts. Histologic findings suggest at least some SONK lesions are subchondral insufficiency fractures.⁵ Brahme and colleagues⁶ were the first to describe SONK occurring after arthroscopy, and others have documented this finding. The condition has also been referred to as osteonecrosis in the postoperative knee.^7-13 An association of postoperative SONK with cartilage loss and meniscal tear has been proposed.^7-13

We reviewed the clinical, radiologic, and MRI findings in 11 patients with evidence of postarthroscopy SONK to try to identify any risk factors that might predispose them to poor outcomes. Our study population consisted of 11 patients (12 knees) with SONK; 6 of the knees had the lesion before knee arthroscopy, and the other 6 developed the lesion after arthroscopy. We also considered MRI findings in a group of 11 age- and sex-matched patients who underwent knee arthroscopy and did not have or develop SONK. We reviewed the preoperative MRI findings of both groups for meniscal tear, meniscal extrusion, and cartilage loss. We had 2 hypotheses. First, patients with preoperative MRI findings of SONK would have articular cartilage changes, posterior root degeneration, and meniscal extrusion similar to those of patients who developed SONK after arthroscopy. Second, an age- and sex-matched group of patients who underwent arthroscopy and did not develop SONK would be similar in articular cartilage changes, posterior root degeneration or tear, and meniscal extrusion.

Materials and Methods

With institutional review board approval and waived informed consent, we reviewed all imaging studies, particularly the radiographs and MRI studies, of 11 patients (12 knees) who either had SONK before arthroscopy or developed it after arthroscopy. In all these cases, arthroscopy was performed to alleviate mechanical symptoms associated with meniscal tear.

On subsequent review by a musculoskeletal radiologist, 6 patients with SONK had an identifiable lesion before surgery. All patients’ symptoms had not improved with an earlier trial of conservative management. All preoperative and postoperative radiologic and MRI findings were reviewed. The patient group was assembled by writing to all the orthopedic surgeons who performed arthroscopy at our institution and asking for SONK cases seen in their practices. All but 2 cases were performed by a surgeon who treated a predominantly older, less active population. Clinical notes were reviewed for outcomes, and the musculoskeletal radiologist reviewed all radiologic studies. The 4 men and 7 women in the SONK group (1 woman had bilateral knee lesions) ranged in age from 43 to 74 years (mean, 63.8 years), and the 4 men and 7 women in the control group were age-matched to 43 to 75 years (mean, 63.6 years). The controls were chosen from a pool of patients who underwent knee arthroscopy at our institution.

MRI was performed using General Electric 1-T, 1.5-T, or 3-T magnets (GE Healthcare, Milwaukee, Wisconsin) or using Philips 1.5-T or open 0.7-T magnets (Philips Healthcare, Andover, Massachusetts). Imaging included sagittal and coronal proton density–weighted sequences and coronal and axial fat-suppressed T2-weighted sequences. SONK was diagnosed when a low signal line adjacent to the subchondral bone plate on the femoral or tibial condyles was present with an adjacent area of bone marrow edema in the respective condyle or when there was depression of the subchondral bone plate with adjacent edema. The MRI studies were reviewed for lesion location, and medial meniscus and lateral meniscus were reviewed for tear. Type of meniscal tear (horizontal cleavage, radial, complex degenerative) was documented, as was meniscal extrusion. The meniscus was regarded as extruded if the body extended more than 3 mm from the joint margin. Cartilage in the medial and lateral compartment was reviewed according to a modified Noyes scale listing 0 as normal, 1 as internal changes only, 2A as 1% to 49% cartilage loss, 2B as 50% to 90% loss of articular cartilage, 3A as 100% articular cartilage loss with subchondral bone plate intact, and 3B as 100% articular cartilage loss with ulcerated subchondral bone plate.¹⁴ Osteoarthritic severity was similarly classified using the Kellgren-Lawrence scale,¹⁵ where grade 0 is normal; grade 1 is unlikely to have narrowing of the joint space but potentially has osteophytic lipping; grade 2 has both definite narrowing of the joint space and osteophytes; grade 3 has narrowing of the joint space and multiple osteophytes, some sclerosis, and possible deformity of bone contour; and grade 4 has marked narrowing of the joint space, large osteophytes, severe sclerosis, and definite deformity of bone contour. Follow-up clinical notes and radiologic studies were reviewed in the assessment of patient outcomes.

All statistical analyses were performed with SAS 9.2 software (SAS Institute, Cary, North Carolina). Age data were evaluated with the Shapiro-Wilk test and graphical displays and were found to violate normality assumptions, so they are presented as medians and ranges; other variables are presented as count and column percentages. The Wilcoxon rank sum test was used to compare the 2 groups’ age distributions. Fisher exact tests were used to compare proportions between the 2 groups for the other variables. Statistical significance was set at P < .05.

Results

Table 1 lists the demographics and imaging characteristics of the 11 patients—6 had SONK before arthroscopy and 6 developed it after arthroscopy. Comparison of the 11 patients with SONK and the 11 controls is summarized with P values in Table 2. Representative cases that either presented before surgery or developed after surgery are shown in Figures 1 to 4. There were 6 prearthroscopy lesions and 6 postarthroscopy lesions—all 12 in the medial femoral condyle. Eleven of the 12 knees had a medial meniscal tear, and 1 knee had both medial and lateral meniscal tears. In 8 of the 12 knees, the lateral meniscus was normal; in 2 knees, it had mild degeneration; and, in 1 knee, it had a complex tear. Assessment of hyaline cartilage revealed medial cartilage loss ranging from 2A to 3B (median, 2B) in the patients with SONK, and lateral cartilage loss ranging from 0 to 2A (median, 0). At surgery, all knees had a partial medial meniscectomy, and 6 had a partial lateral meniscectomy. Ten of the 12 knees had chondroplasty, 9 patellar and 5 of the medial femoral condyle. Only 4 of the 11 patients with follow-up of more than 1 year went on to joint replacement. Six of the 12 had follow-up of more than 2 years. Of the 6 patients without an identifiable SONK lesion on MRI before arthroscopy, 4 had mild to moderate knee pain 0.5, 2.4, 3.5, and 4 years after surgery. For the other 2 patients, knee replacement was performed 1.5 and 1.8 years after surgery. Of the 6 patients with prearthroscopy SONK, 4 had mild to moderate knee pain 1.5, 3.7, 6.5, and 6.8 years after surgery; the other 2 had knee replacement 0.5 and 1.8 years after surgery. Articular cartilage degeneration and meniscal extrusion were similar (Table 1). In the control group, there was only 1 knee replacement, at 3 years, and the other 11 were functioning 2.6 to 5 years later. The longer follow-up resulted from selection of appropriate controls from the same year. Of the 6 SONK lesions found on preoperative MRI, 3 were read by the interpreting radiologist before surgery as possible SONK lesions, 2 were read as insufficiency fractures, and 1 was read as a possible insufficiency fracture.

Discussion

SONK is well described as a complication of arthroscopic knee surgery. However, this condition more commonly appears spontaneously in a population that has not had surgery. It has become clear that the term SONK may be misleading.¹⁶ In a recent series of postoperative subchondral fractures reported by MacDessi and colleagues,⁵ the average age of patients included in their study was 64 years. Pathologic analysis revealed subchondral fracture with callus formation in all cases. Only 2 knees had evidence of osteonecrosis, which appeared to be secondary to the fracture. Based on these findings, the authors concluded that “further investigation into the etiology of this condition is warranted.” A prominent association with medial meniscal tear has been noted, with the medial femoral condyle predominantly affected. As already mentioned, SONK differs from classical avascular necrosis on several points, including lack of the typical avascular osteonecrosis risk factors and absence of the serpiginous margin and double-line sign seen with typical bone infarction. In addition, the SONK lesions seen on radiographs and MRIs of the knee typically are in the medial femoral condyle and are very different from the typical area of infarction seen in patients with known risk factors for secondary osteonecrosis.

The cause of SONK is not known. Of more importance from a medicolegal standpoint is that these lesions are not necessarily related to arthroscopy.¹⁷ Interestingly, Pape and colleagues¹⁷ noted that some of the lesions they studied may have been present before surgery, which is what we found in 6 (50%) of the SONK knees in our study. Our data thus support the proposition that some SONK lesions are present before arthroscopy, and some cases of so-called postarthroscopy SONK may in fact have been progressing before surgery.

Our data also reinforce the importance of radiologist–orthopedic surgeon communication regarding the presence of SONK. We emphasize the importance of communicating the MRI findings clearly, whether the lesion is called SONK, SPONK, or insufficiency fracture. The orthopedic surgeons in our series may have been unaware of the presence of these lesions before arthroscopic meniscectomy, given the wide variety of terms being used in radiologic reports.

The natural history of spontaneous osteonecrosis of the medial tibial plateau has also been studied.¹⁸ There were 3 outcome patterns—acute extensive collapse of the medial tibial plateau, rapid progression to varying degrees of osteoarthritis, and complete resolution. It has been shown that resolution of SONK can occur in the early stages of the disease, within several months, but often the changes progress to bone destruction and articular cartilage collapse.¹⁹

In our series of patients, there was a female predominance, and mean age was 64 years. We investigated cartilage loss, meniscal tear, and meniscal extrusion to see if we could predict outcomes in patients who had the lesion before arthroscopy and if we could predict who might be at risk for developing the lesion after arthroscopy. Type of surgical procedure was also reviewed. For the sake of simplicity, we divided the follow-up patients into 2 groups: those managed with conservative treatment, which we deemed a reasonable outcome, and those who subsequently required knee joint replacement, which we deemed a poor outcome. As seen from our representative cases, both groups had patients with cartilage loss, meniscal tear, and meniscal extrusion to varying degrees. There were no risk factors pointing to a reasonable or poor outcome. In the group of patients with prearthroscopy lesions, we found the same problem. We were unable to identify a risk factor that might suggest a poor rather than a reasonable outcome. We must also emphasize that, in our review of patient charts, we could find no other causes for osteonecrosis. In particular, arthroscopic causes of acute chondral loss (eg, thermal wash, laser, bupivacaine pain pumps, epinephrine in irrigant) were not identified.

This study consisted of a series of cases managed at our institution over the past 8 years. Our data and this study had several limitations:

We may have been unable to identify other SONK cases that belonged in the group from our institution. In addition, we had only 11 patients for comparison with patients without SONK. Likewise, there were only 6 knees each in the prearthroscopy and postarthroscopy SONK groups. We also used images obtained from 1-T, 1.5-T, and 3-T closed MRI devices and one 0.7-T open device. These were, however, at the same institution.

Timing of our imaging was not uniform. In particular, in 3 of the patients who developed SONK after arthroscopy, preoperative MRI studies were performed quite some time before surgery. However, in these patients, more recent preoperative radiographs did not show any evidence of lesions. It can also be seen that postarthroscopy follow-up of patients varied. It is possible that, on longer follow-up, some of the cases we classified as having a reasonable outcome may have gone on to require total knee arthroplasty. One could argue that, in the patient who developed SONK within 1 year after surgery (Figure 4), the lesion was not related to the surgery. However, this patient’s radiographs 3 months after surgery did not show the SONK lesion but clearly showed prominent medial joint space narrowing—a new finding.

Only 1 musculoskeletal radiologist evaluated the radiographs, MRIs, and tomosynthesis (similar to computed tomography) studies for this investigation.

This lesion is not common, thus giving us a small group to analyze.

Despite our data limitations and the retrospective nature of this study, we compiled a reasonably representative sample of surgical SONK patients that matches other samples reported in the literature. Unfortunately, we could not identify any risk factors pointing to the likelihood of developing SONK or any risk factors pointing to either a reasonable or a poor prognosis in these patients. The etiology of the lesion remains an enigma. Our finding 6 cases of prearthroscopy lesions that did not necessarily result in a poor outcome, combined with our inability to identify any risk factors for SONK, points to the lack of a causal relationship with arthroscopy.

The term spontaneous osteonecrosis of the knee was first used by Ahlbäck¹ in 1968. This term, and the acronym SONK (sometimes SPONK²), has subsequently been used by other authors to refer to an apparent osteonecrosis of the knee, most commonly occurring within the medial femoral condyle. SONK typically occurs in older women who usually do not have the typical osteonecrosis risk factors, such as steroid use, sickle-cell anemia, and excessive alcohol intake. Furthermore, the radiologic appearance of SONK differs from the typical avascular necrosis findings seen with radiography and magnetic resonance imaging (MRI). In particular, on MRI, the abnormality of SONK does not have the typical serpiginous margin of bone infarction, or the double-line sign indicating both sclerosis and granulation tissue.³ SONK is normally seen as a line of signal intensity on T1- and T2-weighted sequences; this line is adjacent to or parallels the subchondral bone with an adjacent area of extensive edema.

There is dispute over the cause of SONK. Yamamoto and Bullough⁴ proposed the lesion is in part a subchondral insufficiency fracture and staged it into 4 parts. Histologic findings suggest at least some SONK lesions are subchondral insufficiency fractures.⁵ Brahme and colleagues⁶ were the first to describe SONK occurring after arthroscopy, and others have documented this finding. The condition has also been referred to as osteonecrosis in the postoperative knee.^7-13 An association of postoperative SONK with cartilage loss and meniscal tear has been proposed.^7-13

We reviewed the clinical, radiologic, and MRI findings in 11 patients with evidence of postarthroscopy SONK to try to identify any risk factors that might predispose them to poor outcomes. Our study population consisted of 11 patients (12 knees) with SONK; 6 of the knees had the lesion before knee arthroscopy, and the other 6 developed the lesion after arthroscopy. We also considered MRI findings in a group of 11 age- and sex-matched patients who underwent knee arthroscopy and did not have or develop SONK. We reviewed the preoperative MRI findings of both groups for meniscal tear, meniscal extrusion, and cartilage loss. We had 2 hypotheses. First, patients with preoperative MRI findings of SONK would have articular cartilage changes, posterior root degeneration, and meniscal extrusion similar to those of patients who developed SONK after arthroscopy. Second, an age- and sex-matched group of patients who underwent arthroscopy and did not develop SONK would be similar in articular cartilage changes, posterior root degeneration or tear, and meniscal extrusion.

Materials and Methods

With institutional review board approval and waived informed consent, we reviewed all imaging studies, particularly the radiographs and MRI studies, of 11 patients (12 knees) who either had SONK before arthroscopy or developed it after arthroscopy. In all these cases, arthroscopy was performed to alleviate mechanical symptoms associated with meniscal tear.

On subsequent review by a musculoskeletal radiologist, 6 patients with SONK had an identifiable lesion before surgery. All patients’ symptoms had not improved with an earlier trial of conservative management. All preoperative and postoperative radiologic and MRI findings were reviewed. The patient group was assembled by writing to all the orthopedic surgeons who performed arthroscopy at our institution and asking for SONK cases seen in their practices. All but 2 cases were performed by a surgeon who treated a predominantly older, less active population. Clinical notes were reviewed for outcomes, and the musculoskeletal radiologist reviewed all radiologic studies. The 4 men and 7 women in the SONK group (1 woman had bilateral knee lesions) ranged in age from 43 to 74 years (mean, 63.8 years), and the 4 men and 7 women in the control group were age-matched to 43 to 75 years (mean, 63.6 years). The controls were chosen from a pool of patients who underwent knee arthroscopy at our institution.

MRI was performed using General Electric 1-T, 1.5-T, or 3-T magnets (GE Healthcare, Milwaukee, Wisconsin) or using Philips 1.5-T or open 0.7-T magnets (Philips Healthcare, Andover, Massachusetts). Imaging included sagittal and coronal proton density–weighted sequences and coronal and axial fat-suppressed T2-weighted sequences. SONK was diagnosed when a low signal line adjacent to the subchondral bone plate on the femoral or tibial condyles was present with an adjacent area of bone marrow edema in the respective condyle or when there was depression of the subchondral bone plate with adjacent edema. The MRI studies were reviewed for lesion location, and medial meniscus and lateral meniscus were reviewed for tear. Type of meniscal tear (horizontal cleavage, radial, complex degenerative) was documented, as was meniscal extrusion. The meniscus was regarded as extruded if the body extended more than 3 mm from the joint margin. Cartilage in the medial and lateral compartment was reviewed according to a modified Noyes scale listing 0 as normal, 1 as internal changes only, 2A as 1% to 49% cartilage loss, 2B as 50% to 90% loss of articular cartilage, 3A as 100% articular cartilage loss with subchondral bone plate intact, and 3B as 100% articular cartilage loss with ulcerated subchondral bone plate.¹⁴ Osteoarthritic severity was similarly classified using the Kellgren-Lawrence scale,¹⁵ where grade 0 is normal; grade 1 is unlikely to have narrowing of the joint space but potentially has osteophytic lipping; grade 2 has both definite narrowing of the joint space and osteophytes; grade 3 has narrowing of the joint space and multiple osteophytes, some sclerosis, and possible deformity of bone contour; and grade 4 has marked narrowing of the joint space, large osteophytes, severe sclerosis, and definite deformity of bone contour. Follow-up clinical notes and radiologic studies were reviewed in the assessment of patient outcomes.

All statistical analyses were performed with SAS 9.2 software (SAS Institute, Cary, North Carolina). Age data were evaluated with the Shapiro-Wilk test and graphical displays and were found to violate normality assumptions, so they are presented as medians and ranges; other variables are presented as count and column percentages. The Wilcoxon rank sum test was used to compare the 2 groups’ age distributions. Fisher exact tests were used to compare proportions between the 2 groups for the other variables. Statistical significance was set at P < .05.

Results

Table 1 lists the demographics and imaging characteristics of the 11 patients—6 had SONK before arthroscopy and 6 developed it after arthroscopy. Comparison of the 11 patients with SONK and the 11 controls is summarized with P values in Table 2. Representative cases that either presented before surgery or developed after surgery are shown in Figures 1 to 4. There were 6 prearthroscopy lesions and 6 postarthroscopy lesions—all 12 in the medial femoral condyle. Eleven of the 12 knees had a medial meniscal tear, and 1 knee had both medial and lateral meniscal tears. In 8 of the 12 knees, the lateral meniscus was normal; in 2 knees, it had mild degeneration; and, in 1 knee, it had a complex tear. Assessment of hyaline cartilage revealed medial cartilage loss ranging from 2A to 3B (median, 2B) in the patients with SONK, and lateral cartilage loss ranging from 0 to 2A (median, 0). At surgery, all knees had a partial medial meniscectomy, and 6 had a partial lateral meniscectomy. Ten of the 12 knees had chondroplasty, 9 patellar and 5 of the medial femoral condyle. Only 4 of the 11 patients with follow-up of more than 1 year went on to joint replacement. Six of the 12 had follow-up of more than 2 years. Of the 6 patients without an identifiable SONK lesion on MRI before arthroscopy, 4 had mild to moderate knee pain 0.5, 2.4, 3.5, and 4 years after surgery. For the other 2 patients, knee replacement was performed 1.5 and 1.8 years after surgery. Of the 6 patients with prearthroscopy SONK, 4 had mild to moderate knee pain 1.5, 3.7, 6.5, and 6.8 years after surgery; the other 2 had knee replacement 0.5 and 1.8 years after surgery. Articular cartilage degeneration and meniscal extrusion were similar (Table 1). In the control group, there was only 1 knee replacement, at 3 years, and the other 11 were functioning 2.6 to 5 years later. The longer follow-up resulted from selection of appropriate controls from the same year. Of the 6 SONK lesions found on preoperative MRI, 3 were read by the interpreting radiologist before surgery as possible SONK lesions, 2 were read as insufficiency fractures, and 1 was read as a possible insufficiency fracture.

Discussion

SONK is well described as a complication of arthroscopic knee surgery. However, this condition more commonly appears spontaneously in a population that has not had surgery. It has become clear that the term SONK may be misleading.¹⁶ In a recent series of postoperative subchondral fractures reported by MacDessi and colleagues,⁵ the average age of patients included in their study was 64 years. Pathologic analysis revealed subchondral fracture with callus formation in all cases. Only 2 knees had evidence of osteonecrosis, which appeared to be secondary to the fracture. Based on these findings, the authors concluded that “further investigation into the etiology of this condition is warranted.” A prominent association with medial meniscal tear has been noted, with the medial femoral condyle predominantly affected. As already mentioned, SONK differs from classical avascular necrosis on several points, including lack of the typical avascular osteonecrosis risk factors and absence of the serpiginous margin and double-line sign seen with typical bone infarction. In addition, the SONK lesions seen on radiographs and MRIs of the knee typically are in the medial femoral condyle and are very different from the typical area of infarction seen in patients with known risk factors for secondary osteonecrosis.

The cause of SONK is not known. Of more importance from a medicolegal standpoint is that these lesions are not necessarily related to arthroscopy.¹⁷ Interestingly, Pape and colleagues¹⁷ noted that some of the lesions they studied may have been present before surgery, which is what we found in 6 (50%) of the SONK knees in our study. Our data thus support the proposition that some SONK lesions are present before arthroscopy, and some cases of so-called postarthroscopy SONK may in fact have been progressing before surgery.

Our data also reinforce the importance of radiologist–orthopedic surgeon communication regarding the presence of SONK. We emphasize the importance of communicating the MRI findings clearly, whether the lesion is called SONK, SPONK, or insufficiency fracture. The orthopedic surgeons in our series may have been unaware of the presence of these lesions before arthroscopic meniscectomy, given the wide variety of terms being used in radiologic reports.

The natural history of spontaneous osteonecrosis of the medial tibial plateau has also been studied.¹⁸ There were 3 outcome patterns—acute extensive collapse of the medial tibial plateau, rapid progression to varying degrees of osteoarthritis, and complete resolution. It has been shown that resolution of SONK can occur in the early stages of the disease, within several months, but often the changes progress to bone destruction and articular cartilage collapse.¹⁹

In our series of patients, there was a female predominance, and mean age was 64 years. We investigated cartilage loss, meniscal tear, and meniscal extrusion to see if we could predict outcomes in patients who had the lesion before arthroscopy and if we could predict who might be at risk for developing the lesion after arthroscopy. Type of surgical procedure was also reviewed. For the sake of simplicity, we divided the follow-up patients into 2 groups: those managed with conservative treatment, which we deemed a reasonable outcome, and those who subsequently required knee joint replacement, which we deemed a poor outcome. As seen from our representative cases, both groups had patients with cartilage loss, meniscal tear, and meniscal extrusion to varying degrees. There were no risk factors pointing to a reasonable or poor outcome. In the group of patients with prearthroscopy lesions, we found the same problem. We were unable to identify a risk factor that might suggest a poor rather than a reasonable outcome. We must also emphasize that, in our review of patient charts, we could find no other causes for osteonecrosis. In particular, arthroscopic causes of acute chondral loss (eg, thermal wash, laser, bupivacaine pain pumps, epinephrine in irrigant) were not identified.

This study consisted of a series of cases managed at our institution over the past 8 years. Our data and this study had several limitations:

We may have been unable to identify other SONK cases that belonged in the group from our institution. In addition, we had only 11 patients for comparison with patients without SONK. Likewise, there were only 6 knees each in the prearthroscopy and postarthroscopy SONK groups. We also used images obtained from 1-T, 1.5-T, and 3-T closed MRI devices and one 0.7-T open device. These were, however, at the same institution.

Timing of our imaging was not uniform. In particular, in 3 of the patients who developed SONK after arthroscopy, preoperative MRI studies were performed quite some time before surgery. However, in these patients, more recent preoperative radiographs did not show any evidence of lesions. It can also be seen that postarthroscopy follow-up of patients varied. It is possible that, on longer follow-up, some of the cases we classified as having a reasonable outcome may have gone on to require total knee arthroplasty. One could argue that, in the patient who developed SONK within 1 year after surgery (Figure 4), the lesion was not related to the surgery. However, this patient’s radiographs 3 months after surgery did not show the SONK lesion but clearly showed prominent medial joint space narrowing—a new finding.

Only 1 musculoskeletal radiologist evaluated the radiographs, MRIs, and tomosynthesis (similar to computed tomography) studies for this investigation.

This lesion is not common, thus giving us a small group to analyze.

Despite our data limitations and the retrospective nature of this study, we compiled a reasonably representative sample of surgical SONK patients that matches other samples reported in the literature. Unfortunately, we could not identify any risk factors pointing to the likelihood of developing SONK or any risk factors pointing to either a reasonable or a poor prognosis in these patients. The etiology of the lesion remains an enigma. Our finding 6 cases of prearthroscopy lesions that did not necessarily result in a poor outcome, combined with our inability to identify any risk factors for SONK, points to the lack of a causal relationship with arthroscopy.

The term spontaneous osteonecrosis of the knee was first used by Ahlbäck¹ in 1968. This term, and the acronym SONK (sometimes SPONK²), has subsequently been used by other authors to refer to an apparent osteonecrosis of the knee, most commonly occurring within the medial femoral condyle. SONK typically occurs in older women who usually do not have the typical osteonecrosis risk factors, such as steroid use, sickle-cell anemia, and excessive alcohol intake. Furthermore, the radiologic appearance of SONK differs from the typical avascular necrosis findings seen with radiography and magnetic resonance imaging (MRI). In particular, on MRI, the abnormality of SONK does not have the typical serpiginous margin of bone infarction, or the double-line sign indicating both sclerosis and granulation tissue.³ SONK is normally seen as a line of signal intensity on T1- and T2-weighted sequences; this line is adjacent to or parallels the subchondral bone with an adjacent area of extensive edema.

There is dispute over the cause of SONK. Yamamoto and Bullough⁴ proposed the lesion is in part a subchondral insufficiency fracture and staged it into 4 parts. Histologic findings suggest at least some SONK lesions are subchondral insufficiency fractures.⁵ Brahme and colleagues⁶ were the first to describe SONK occurring after arthroscopy, and others have documented this finding. The condition has also been referred to as osteonecrosis in the postoperative knee.^7-13 An association of postoperative SONK with cartilage loss and meniscal tear has been proposed.^7-13

We reviewed the clinical, radiologic, and MRI findings in 11 patients with evidence of postarthroscopy SONK to try to identify any risk factors that might predispose them to poor outcomes. Our study population consisted of 11 patients (12 knees) with SONK; 6 of the knees had the lesion before knee arthroscopy, and the other 6 developed the lesion after arthroscopy. We also considered MRI findings in a group of 11 age- and sex-matched patients who underwent knee arthroscopy and did not have or develop SONK. We reviewed the preoperative MRI findings of both groups for meniscal tear, meniscal extrusion, and cartilage loss. We had 2 hypotheses. First, patients with preoperative MRI findings of SONK would have articular cartilage changes, posterior root degeneration, and meniscal extrusion similar to those of patients who developed SONK after arthroscopy. Second, an age- and sex-matched group of patients who underwent arthroscopy and did not develop SONK would be similar in articular cartilage changes, posterior root degeneration or tear, and meniscal extrusion.

Materials and Methods

With institutional review board approval and waived informed consent, we reviewed all imaging studies, particularly the radiographs and MRI studies, of 11 patients (12 knees) who either had SONK before arthroscopy or developed it after arthroscopy. In all these cases, arthroscopy was performed to alleviate mechanical symptoms associated with meniscal tear.

On subsequent review by a musculoskeletal radiologist, 6 patients with SONK had an identifiable lesion before surgery. All patients’ symptoms had not improved with an earlier trial of conservative management. All preoperative and postoperative radiologic and MRI findings were reviewed. The patient group was assembled by writing to all the orthopedic surgeons who performed arthroscopy at our institution and asking for SONK cases seen in their practices. All but 2 cases were performed by a surgeon who treated a predominantly older, less active population. Clinical notes were reviewed for outcomes, and the musculoskeletal radiologist reviewed all radiologic studies. The 4 men and 7 women in the SONK group (1 woman had bilateral knee lesions) ranged in age from 43 to 74 years (mean, 63.8 years), and the 4 men and 7 women in the control group were age-matched to 43 to 75 years (mean, 63.6 years). The controls were chosen from a pool of patients who underwent knee arthroscopy at our institution.

MRI was performed using General Electric 1-T, 1.5-T, or 3-T magnets (GE Healthcare, Milwaukee, Wisconsin) or using Philips 1.5-T or open 0.7-T magnets (Philips Healthcare, Andover, Massachusetts). Imaging included sagittal and coronal proton density–weighted sequences and coronal and axial fat-suppressed T2-weighted sequences. SONK was diagnosed when a low signal line adjacent to the subchondral bone plate on the femoral or tibial condyles was present with an adjacent area of bone marrow edema in the respective condyle or when there was depression of the subchondral bone plate with adjacent edema. The MRI studies were reviewed for lesion location, and medial meniscus and lateral meniscus were reviewed for tear. Type of meniscal tear (horizontal cleavage, radial, complex degenerative) was documented, as was meniscal extrusion. The meniscus was regarded as extruded if the body extended more than 3 mm from the joint margin. Cartilage in the medial and lateral compartment was reviewed according to a modified Noyes scale listing 0 as normal, 1 as internal changes only, 2A as 1% to 49% cartilage loss, 2B as 50% to 90% loss of articular cartilage, 3A as 100% articular cartilage loss with subchondral bone plate intact, and 3B as 100% articular cartilage loss with ulcerated subchondral bone plate.¹⁴ Osteoarthritic severity was similarly classified using the Kellgren-Lawrence scale,¹⁵ where grade 0 is normal; grade 1 is unlikely to have narrowing of the joint space but potentially has osteophytic lipping; grade 2 has both definite narrowing of the joint space and osteophytes; grade 3 has narrowing of the joint space and multiple osteophytes, some sclerosis, and possible deformity of bone contour; and grade 4 has marked narrowing of the joint space, large osteophytes, severe sclerosis, and definite deformity of bone contour. Follow-up clinical notes and radiologic studies were reviewed in the assessment of patient outcomes.

All statistical analyses were performed with SAS 9.2 software (SAS Institute, Cary, North Carolina). Age data were evaluated with the Shapiro-Wilk test and graphical displays and were found to violate normality assumptions, so they are presented as medians and ranges; other variables are presented as count and column percentages. The Wilcoxon rank sum test was used to compare the 2 groups’ age distributions. Fisher exact tests were used to compare proportions between the 2 groups for the other variables. Statistical significance was set at P < .05.

Results

Table 1 lists the demographics and imaging characteristics of the 11 patients—6 had SONK before arthroscopy and 6 developed it after arthroscopy. Comparison of the 11 patients with SONK and the 11 controls is summarized with P values in Table 2. Representative cases that either presented before surgery or developed after surgery are shown in Figures 1 to 4. There were 6 prearthroscopy lesions and 6 postarthroscopy lesions—all 12 in the medial femoral condyle. Eleven of the 12 knees had a medial meniscal tear, and 1 knee had both medial and lateral meniscal tears. In 8 of the 12 knees, the lateral meniscus was normal; in 2 knees, it had mild degeneration; and, in 1 knee, it had a complex tear. Assessment of hyaline cartilage revealed medial cartilage loss ranging from 2A to 3B (median, 2B) in the patients with SONK, and lateral cartilage loss ranging from 0 to 2A (median, 0). At surgery, all knees had a partial medial meniscectomy, and 6 had a partial lateral meniscectomy. Ten of the 12 knees had chondroplasty, 9 patellar and 5 of the medial femoral condyle. Only 4 of the 11 patients with follow-up of more than 1 year went on to joint replacement. Six of the 12 had follow-up of more than 2 years. Of the 6 patients without an identifiable SONK lesion on MRI before arthroscopy, 4 had mild to moderate knee pain 0.5, 2.4, 3.5, and 4 years after surgery. For the other 2 patients, knee replacement was performed 1.5 and 1.8 years after surgery. Of the 6 patients with prearthroscopy SONK, 4 had mild to moderate knee pain 1.5, 3.7, 6.5, and 6.8 years after surgery; the other 2 had knee replacement 0.5 and 1.8 years after surgery. Articular cartilage degeneration and meniscal extrusion were similar (Table 1). In the control group, there was only 1 knee replacement, at 3 years, and the other 11 were functioning 2.6 to 5 years later. The longer follow-up resulted from selection of appropriate controls from the same year. Of the 6 SONK lesions found on preoperative MRI, 3 were read by the interpreting radiologist before surgery as possible SONK lesions, 2 were read as insufficiency fractures, and 1 was read as a possible insufficiency fracture.

Discussion

SONK is well described as a complication of arthroscopic knee surgery. However, this condition more commonly appears spontaneously in a population that has not had surgery. It has become clear that the term SONK may be misleading.¹⁶ In a recent series of postoperative subchondral fractures reported by MacDessi and colleagues,⁵ the average age of patients included in their study was 64 years. Pathologic analysis revealed subchondral fracture with callus formation in all cases. Only 2 knees had evidence of osteonecrosis, which appeared to be secondary to the fracture. Based on these findings, the authors concluded that “further investigation into the etiology of this condition is warranted.” A prominent association with medial meniscal tear has been noted, with the medial femoral condyle predominantly affected. As already mentioned, SONK differs from classical avascular necrosis on several points, including lack of the typical avascular osteonecrosis risk factors and absence of the serpiginous margin and double-line sign seen with typical bone infarction. In addition, the SONK lesions seen on radiographs and MRIs of the knee typically are in the medial femoral condyle and are very different from the typical area of infarction seen in patients with known risk factors for secondary osteonecrosis.

The cause of SONK is not known. Of more importance from a medicolegal standpoint is that these lesions are not necessarily related to arthroscopy.¹⁷ Interestingly, Pape and colleagues¹⁷ noted that some of the lesions they studied may have been present before surgery, which is what we found in 6 (50%) of the SONK knees in our study. Our data thus support the proposition that some SONK lesions are present before arthroscopy, and some cases of so-called postarthroscopy SONK may in fact have been progressing before surgery.

Our data also reinforce the importance of radiologist–orthopedic surgeon communication regarding the presence of SONK. We emphasize the importance of communicating the MRI findings clearly, whether the lesion is called SONK, SPONK, or insufficiency fracture. The orthopedic surgeons in our series may have been unaware of the presence of these lesions before arthroscopic meniscectomy, given the wide variety of terms being used in radiologic reports.

The natural history of spontaneous osteonecrosis of the medial tibial plateau has also been studied.¹⁸ There were 3 outcome patterns—acute extensive collapse of the medial tibial plateau, rapid progression to varying degrees of osteoarthritis, and complete resolution. It has been shown that resolution of SONK can occur in the early stages of the disease, within several months, but often the changes progress to bone destruction and articular cartilage collapse.¹⁹

In our series of patients, there was a female predominance, and mean age was 64 years. We investigated cartilage loss, meniscal tear, and meniscal extrusion to see if we could predict outcomes in patients who had the lesion before arthroscopy and if we could predict who might be at risk for developing the lesion after arthroscopy. Type of surgical procedure was also reviewed. For the sake of simplicity, we divided the follow-up patients into 2 groups: those managed with conservative treatment, which we deemed a reasonable outcome, and those who subsequently required knee joint replacement, which we deemed a poor outcome. As seen from our representative cases, both groups had patients with cartilage loss, meniscal tear, and meniscal extrusion to varying degrees. There were no risk factors pointing to a reasonable or poor outcome. In the group of patients with prearthroscopy lesions, we found the same problem. We were unable to identify a risk factor that might suggest a poor rather than a reasonable outcome. We must also emphasize that, in our review of patient charts, we could find no other causes for osteonecrosis. In particular, arthroscopic causes of acute chondral loss (eg, thermal wash, laser, bupivacaine pain pumps, epinephrine in irrigant) were not identified.

This study consisted of a series of cases managed at our institution over the past 8 years. Our data and this study had several limitations:

We may have been unable to identify other SONK cases that belonged in the group from our institution. In addition, we had only 11 patients for comparison with patients without SONK. Likewise, there were only 6 knees each in the prearthroscopy and postarthroscopy SONK groups. We also used images obtained from 1-T, 1.5-T, and 3-T closed MRI devices and one 0.7-T open device. These were, however, at the same institution.

Timing of our imaging was not uniform. In particular, in 3 of the patients who developed SONK after arthroscopy, preoperative MRI studies were performed quite some time before surgery. However, in these patients, more recent preoperative radiographs did not show any evidence of lesions. It can also be seen that postarthroscopy follow-up of patients varied. It is possible that, on longer follow-up, some of the cases we classified as having a reasonable outcome may have gone on to require total knee arthroplasty. One could argue that, in the patient who developed SONK within 1 year after surgery (Figure 4), the lesion was not related to the surgery. However, this patient’s radiographs 3 months after surgery did not show the SONK lesion but clearly showed prominent medial joint space narrowing—a new finding.

Only 1 musculoskeletal radiologist evaluated the radiographs, MRIs, and tomosynthesis (similar to computed tomography) studies for this investigation.

This lesion is not common, thus giving us a small group to analyze.

Despite our data limitations and the retrospective nature of this study, we compiled a reasonably representative sample of surgical SONK patients that matches other samples reported in the literature. Unfortunately, we could not identify any risk factors pointing to the likelihood of developing SONK or any risk factors pointing to either a reasonable or a poor prognosis in these patients. The etiology of the lesion remains an enigma. Our finding 6 cases of prearthroscopy lesions that did not necessarily result in a poor outcome, combined with our inability to identify any risk factors for SONK, points to the lack of a causal relationship with arthroscopy.