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Total knee replacement risk soars after arthroscopic surgery for meniscal tear

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Wed, 06/19/2019 - 14:15

– A 5-year follow-up of a major randomized trial comparing methods of meniscal tear management in patients with osteoarthritis showed the risk of total knee replacement was 400% greater in patients who underwent arthroscopic partial meniscectomy than in those who received physical therapy alone, Jeffrey N. Katz, MD, reported at the annual meeting of the American College of Rheumatology.

At 5 years, however, the two divergent initial treatment strategies – arthroscopic surgical repair versus physical therapy – resulted in similar degrees of long-term pain improvement, noted Dr. Katz, a rheumatologist who is professor of medicine and orthopedic surgery at Harvard Medical School, Boston.

“Because that’s the case, a reasonable recommendation – and one that most folks around the world who are thinking about this problem would make – is to have the first choice initially be nonoperative; that is, physical therapy, with surgery reserved for those who don’t improve and who have an interest in undertaking the risks of surgery,” he said.

Dr. Katz presented 5-year follow-up data on 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy. A lot rides on the outcomes of this study, as there is a longstanding debate over the balance of risks and benefits of arthroscopic surgery in this common clinical scenario.

Of the 351 participants, 164 were randomized to and received arthroscopic partial meniscectomy, 109 were randomized to and received a standardized program of physical therapy, and 68 were initially randomized to physical therapy but crossed over to arthroscopic surgery within the first few months because of lack of improvement.

At 5 years of follow-up, all three groups showed similar degrees of improvement in Knee Osteoarthritis and Injury Outcome Score Pain Scale scores, from 40-50 out of a possible 100 at baseline to 20-25 at 6 months, with little change thereafter through 5 years.

The eye-catching finding was the difference in the incidence of total knee replacement (TKR) through 5 years: 10% in those who underwent arthroscopic partial meniscectomy, either as initial therapy or after crossing over from the physical therapy group, compared with 2% in patients who underwent physical therapy alone. Given that more than 400,000 arthroscopic partial meniscectomies are done annually in the United States in patients with knee osteoarthritis, extrapolation from the MeTeOR results suggests an excess of 40,000 total knee replacements in surgically treated patients.

“The higher TKR rates that we observed in surgically treated patients are unexplained, concerning, and require further study. The finding is consistent with the observation in the Osteoarthritis Initiative that TKR rates were higher in patients with arthroscopy as opposed to those treated nonsurgically,” the rheumatologist said.

He proposed two possible explanations for the finding. “It does appear that people who have arthroscopic surgery are then, over the next 5 years, more likely to have total knee replacement. We don’t know whether that is because performing arthroscopic surgery is actually damaging the knee further, leading it to deteriorate more quickly and therefore go on to total knee replacement, or whether when patients develop a relationship with a surgeon and have arthroscopic surgery, they get over some of their apprehension about surgery and may become more likely to accept subsequent surgery for total knee replacement. We hope to find the answer. I think this story is still unfolding because 5 years is a relatively brief period of time in the course of osteoarthritis.

“Arthroscopic surgery certainly offers greater shorter-term improvement, and for some patients that’s worth trading off some downstream risk of joint damage, and for others, they would not want to make that trade-off. So I see it ultimately as a matter of patient choice,” Dr. Katz said.

Knee osteoarthritis affects an estimated 15 million Americans. More than one-half of them have a meniscal tear, the majority of which don’t cause symptoms.

Dr. Katz reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.

SOURCE: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.

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– A 5-year follow-up of a major randomized trial comparing methods of meniscal tear management in patients with osteoarthritis showed the risk of total knee replacement was 400% greater in patients who underwent arthroscopic partial meniscectomy than in those who received physical therapy alone, Jeffrey N. Katz, MD, reported at the annual meeting of the American College of Rheumatology.

At 5 years, however, the two divergent initial treatment strategies – arthroscopic surgical repair versus physical therapy – resulted in similar degrees of long-term pain improvement, noted Dr. Katz, a rheumatologist who is professor of medicine and orthopedic surgery at Harvard Medical School, Boston.

“Because that’s the case, a reasonable recommendation – and one that most folks around the world who are thinking about this problem would make – is to have the first choice initially be nonoperative; that is, physical therapy, with surgery reserved for those who don’t improve and who have an interest in undertaking the risks of surgery,” he said.

Dr. Katz presented 5-year follow-up data on 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy. A lot rides on the outcomes of this study, as there is a longstanding debate over the balance of risks and benefits of arthroscopic surgery in this common clinical scenario.

Of the 351 participants, 164 were randomized to and received arthroscopic partial meniscectomy, 109 were randomized to and received a standardized program of physical therapy, and 68 were initially randomized to physical therapy but crossed over to arthroscopic surgery within the first few months because of lack of improvement.

At 5 years of follow-up, all three groups showed similar degrees of improvement in Knee Osteoarthritis and Injury Outcome Score Pain Scale scores, from 40-50 out of a possible 100 at baseline to 20-25 at 6 months, with little change thereafter through 5 years.

The eye-catching finding was the difference in the incidence of total knee replacement (TKR) through 5 years: 10% in those who underwent arthroscopic partial meniscectomy, either as initial therapy or after crossing over from the physical therapy group, compared with 2% in patients who underwent physical therapy alone. Given that more than 400,000 arthroscopic partial meniscectomies are done annually in the United States in patients with knee osteoarthritis, extrapolation from the MeTeOR results suggests an excess of 40,000 total knee replacements in surgically treated patients.

“The higher TKR rates that we observed in surgically treated patients are unexplained, concerning, and require further study. The finding is consistent with the observation in the Osteoarthritis Initiative that TKR rates were higher in patients with arthroscopy as opposed to those treated nonsurgically,” the rheumatologist said.

He proposed two possible explanations for the finding. “It does appear that people who have arthroscopic surgery are then, over the next 5 years, more likely to have total knee replacement. We don’t know whether that is because performing arthroscopic surgery is actually damaging the knee further, leading it to deteriorate more quickly and therefore go on to total knee replacement, or whether when patients develop a relationship with a surgeon and have arthroscopic surgery, they get over some of their apprehension about surgery and may become more likely to accept subsequent surgery for total knee replacement. We hope to find the answer. I think this story is still unfolding because 5 years is a relatively brief period of time in the course of osteoarthritis.

“Arthroscopic surgery certainly offers greater shorter-term improvement, and for some patients that’s worth trading off some downstream risk of joint damage, and for others, they would not want to make that trade-off. So I see it ultimately as a matter of patient choice,” Dr. Katz said.

Knee osteoarthritis affects an estimated 15 million Americans. More than one-half of them have a meniscal tear, the majority of which don’t cause symptoms.

Dr. Katz reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.

SOURCE: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.

– A 5-year follow-up of a major randomized trial comparing methods of meniscal tear management in patients with osteoarthritis showed the risk of total knee replacement was 400% greater in patients who underwent arthroscopic partial meniscectomy than in those who received physical therapy alone, Jeffrey N. Katz, MD, reported at the annual meeting of the American College of Rheumatology.

At 5 years, however, the two divergent initial treatment strategies – arthroscopic surgical repair versus physical therapy – resulted in similar degrees of long-term pain improvement, noted Dr. Katz, a rheumatologist who is professor of medicine and orthopedic surgery at Harvard Medical School, Boston.

“Because that’s the case, a reasonable recommendation – and one that most folks around the world who are thinking about this problem would make – is to have the first choice initially be nonoperative; that is, physical therapy, with surgery reserved for those who don’t improve and who have an interest in undertaking the risks of surgery,” he said.

Dr. Katz presented 5-year follow-up data on 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy. A lot rides on the outcomes of this study, as there is a longstanding debate over the balance of risks and benefits of arthroscopic surgery in this common clinical scenario.

Of the 351 participants, 164 were randomized to and received arthroscopic partial meniscectomy, 109 were randomized to and received a standardized program of physical therapy, and 68 were initially randomized to physical therapy but crossed over to arthroscopic surgery within the first few months because of lack of improvement.

At 5 years of follow-up, all three groups showed similar degrees of improvement in Knee Osteoarthritis and Injury Outcome Score Pain Scale scores, from 40-50 out of a possible 100 at baseline to 20-25 at 6 months, with little change thereafter through 5 years.

The eye-catching finding was the difference in the incidence of total knee replacement (TKR) through 5 years: 10% in those who underwent arthroscopic partial meniscectomy, either as initial therapy or after crossing over from the physical therapy group, compared with 2% in patients who underwent physical therapy alone. Given that more than 400,000 arthroscopic partial meniscectomies are done annually in the United States in patients with knee osteoarthritis, extrapolation from the MeTeOR results suggests an excess of 40,000 total knee replacements in surgically treated patients.

“The higher TKR rates that we observed in surgically treated patients are unexplained, concerning, and require further study. The finding is consistent with the observation in the Osteoarthritis Initiative that TKR rates were higher in patients with arthroscopy as opposed to those treated nonsurgically,” the rheumatologist said.

He proposed two possible explanations for the finding. “It does appear that people who have arthroscopic surgery are then, over the next 5 years, more likely to have total knee replacement. We don’t know whether that is because performing arthroscopic surgery is actually damaging the knee further, leading it to deteriorate more quickly and therefore go on to total knee replacement, or whether when patients develop a relationship with a surgeon and have arthroscopic surgery, they get over some of their apprehension about surgery and may become more likely to accept subsequent surgery for total knee replacement. We hope to find the answer. I think this story is still unfolding because 5 years is a relatively brief period of time in the course of osteoarthritis.

“Arthroscopic surgery certainly offers greater shorter-term improvement, and for some patients that’s worth trading off some downstream risk of joint damage, and for others, they would not want to make that trade-off. So I see it ultimately as a matter of patient choice,” Dr. Katz said.

Knee osteoarthritis affects an estimated 15 million Americans. More than one-half of them have a meniscal tear, the majority of which don’t cause symptoms.

Dr. Katz reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.

SOURCE: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.

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Key clinical point: Risk of total knee replacement is five times higher after arthroscopic partial meniscectomy.

Major finding: Patients randomized to arthroscopic partial meniscectomy were 400% more likely to subsequently undergo total knee replacement than were those randomized to physical therapy alone.

Study details: This was a presentation of the 5-year follow-up results in 341 participants in the MeTeOR trial, a seven-center study in which middle-age or older subjects with knee pain, a meniscal tear, and osteoarthritic changes on x-ray were randomized to arthroscopic repair or physical therapy.

Disclosures: The presenter reported having no financial conflicts regarding MeTeOR, which was funded by the National Institutes of Health.

Source: Katz JN et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1816.

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Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees

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Thu, 09/19/2019 - 13:16
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Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees

ABSTRACT

The aim of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with refractory knee osteoarthritis (OA). A total of 17 subjects (26 knees) with a median age of 72 years (range: 54-78 years) and a history of knee OA (Kellgren–Lawrence, grade of 3 or 4) underwent treatment with ultrasound-guided injection of micro-fractured adipose tissue. Micro-fractured fat was obtained using a minimal manipulation technique in a closed system (Lipogems), without the addition of enzymes or any other additives. The study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months following this procedure.

When compared with baseline, significant improvements were noted in the mean values of NPRS, FXN, and LEAS at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved at 6 weeks and 12 months. In particular, the average KSS score improved from 74 to 82, the FXN score improved from 65 to 76, and the LEAS score improved from 36 to 47. These values were significantly greater than the previously published minimal clinically important difference described for KSS and FXN in patients who underwent total knee arthroplasty for primary OA. No serious adverse events were reported. The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option for patients with refractory, severe (grade 3 or 4) knee OA.

This study demonstrated significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.

Continue to: Knee OA is...

 

 

Knee OA is a chronic disease that affects all races, genders, and ages, but it is most prevalent in obese and elderly people. Worldwide, arthritis is considered to be the fourth leading cause of disability.1 In developing and developed countries, knee OA may cause a significant decline in the quality of life for individuals >65 years due to joint pain and disability.1 Nonoperative treatment can be successful in patients with mild to moderate arthritis with pain.

Current treatment options for knee OA, including physical therapy and anti-inflammatory drugs, aim to remedy the symptoms, but they do little to treat the underlying causes of knee OA pain. When a patient presents with advanced arthritis of the knee as confirmed by radiographic findings (classified as Kellgren–Lawrence grade of 3 or 4), the standard approach has been a total knee arthroplasty (TKA) after the patient has failed conservative treatment. The annual rate of total knee replacement in the United States has doubled since 2000, especially in those 45 – 65 years.2 The total number of procedures performed each year now exceeds 640,000, at a total annual cost of about $10.2 billion.Multiple studies show that TKA has favorable outcomes in pain relief and functional improvement in patients >60 years when evaluated at a follow-up of 10 years after surgery.2

However, some patients are hesitant to proceed with surgery due to fear of surgical pain and procedural complications. The known complications include deep vein thrombosis, pulmonary embolism, nerve injury, and infection. In addition, up to 20% of patients continue to complain of pain following a total knee replacement.3 Finally, in the young population (<50 years), there are concerns related to the potential need of revision knee surgery in the future.3

Alternative treatments for knee OA have recently emerged, including the use of platelet-rich plasma (PRP). A recent meta-analysis that included 10 randomized controlled trials with a total of 1069 patients demonstrated that, compared with hyaluronic acid and saline, intra-articular PRP injection may have more benefits in pain relief and functional improvement in patients with symptomatic knee OA at 1-year post-injection.4 Another smaller study examined patients who had experienced mild knee OA (Kellgren–Lawrence grade <3) for an average of 14 months. Each patient underwent magnetic resonance imaging for the evaluation of joint damage and then received a single PRP injection. The patients were assessed at regular intervals, with improvement in pain lasting up to 12 months.5

Additional orthobiologic options include the use of bone marrow and adipose-derived stem cell (ASC) injections for a variety of knee conditions, including knee OA. Mesenchymal stem cells (MSCs) are multipotent cells that have been used for the treatment of OA in clinical trials because of their regeneration potential and anti-inflammatory effects.6 Bone marrow stem cells (BMSCs) were first used to repair cartilage damage in humans in 1998. However, BMSCs had particular challenges, including low stem cell yield, pain, and possible morbidities during bone marrow aspiration. An alternative is ASCs, which may be more suitable clinically because of the high stem cell yield from lipoaspirates, faster cell proliferation, and less discomfort and morbidities during the harvesting procedure.7 In addition, these adult stem cells can contribute to the chondrogenic, osteogenic, adipogenic, myogenic, and neurogenic lineages.8 One study demonstrated that the contents of cartilage glycosaminoglycans significantly increased in specific areas of a knee joint treated with ASCs.9,10  This increased glycosaminoglycan content in hyaline cartilage may explain the observed visual analog score (VAS) improvement and clinical results. Other studies suggest that the chondrogenic action of ASCs may depend more on regenerative signaling by activated perivascular cells and signaling of trophic and paracrine mediators, such as vascular endothelial growth factor.9,10 Finally, the mechanism of action may include providing volume, support, cushioning, and filling of soft tissue defects.11

The Lipogems method and device, approved by the U.S. Food and Drug Administration, is used to harvest ASCs, cleanse, and micro-fracture adipose tissue while maintaining the perivascular niche that contains pericytes. The purpose of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with severe refractory knee OA.

Continue to: This report details...

 

 

STUDY PRESENTATION

This report details the outcome of an IRB-approved study of 17 subjects with 26 symptomatic knees with a history of knee OA (Kellgren–Lawrence grade of 3 or 4) diagnosed by a radiograph. Patient demographics are described in the Table.

TABLE. Patient Demographics

Male n (%)

10 (58.8)

Age, mean ± SD (range)

68.27 ± 7.43
(54–78)

BMI, mean ± SD (range)

28.98 ± 4.50
(21.41–34.9)

Kellgren–Lawrence grade 3 (n)

7

Kellgren–Lawrence grade 4 (n)

19

Abbreviation: BMI, body mass index.

The study patients were evaluated by an orthopedic surgeon, Mitchell Sheinkop, who commonly performs total joint replacement in his practice and considers potential patients as candidates for TKA. These patients presented with a Kellgren-Lawrence grade of 3 or 4 knee OA, and all had significant pain that was refractory to conservative treatment, which included medications, physical therapy, and injections. The study patients were offered the Lipogems procedure as an alternative to TKA. Following this procedure, the study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months. The 1989 KSS12 was used for this study. Adverse reactions were also monitored throughout the study period.

METHODS

After obtaining informed consent, the subjects were taken into the operating room, moved to the procedure table, and placed in the prone position for aspiration. After scrubbing with Betadine and draping, 1 mL of lidocaine was used to anesthetize the skin, and a pre-prepared preparation of lidocaine, epinephrine, and sterile saline was infused into the subcutaneous tissue. The micro-fragmented adipose tissue was obtained with minimal manipulation using Lipogems, a closed system using mild mechanical forces and reduction filters. The system processes the lipoaspirate without the addition of enzymes or any other additives. The final product consists of adipose tissue clusters with preserved vascular stromal niche of approximately 500 microns. The lipoaspirate was processed in the same room via a closed system. During the processing, the subject’s puncture wounds were dressed. The knee injection site was prepped with a Betadine swab and DuraPrep. Then, Lipogems was injected intra-articularly under ultrasound guidance.

After the completion of the injection, manual range of motion was administered to the treated joint. The subject was then transferred to the recovery room where vital signs were monitored. Post-procedure instructions were reviewed with the patient by the study staff. The subject was instructed to use an assistive device and avoid weight-bearing for 48 hours and maintain the activities of daily living to a minimum on the day of the procedure. Non-weight-bearing for 48 hours was recommended for reducing discomfort to avoid the use of opioids. Nonsteroidal anti-inflammatory drugs, alcohol, and marijuana must be avoided for 4 weeks after the procedure. Pretreatment and post-treatment outcomes were collected using the NPRS, the 100-point KSS with its FXN, and the LEAS at 6 weeks, 6 months, and 12 months after this procedure. The 1989 KSS12 was used for this study since the same scale was used for previous TKA procedures by our authors, allowing for future comparisons of results.

STATISTICAL ANALYSIS

Mean and standard deviation were used to estimate central tendency and variability. Outcome measures were analyzed using the t test, with the pairwise t test was used for paired and subsequent measurements of the same patient or a knee. All analyses were performed with significance set at P <.05. The minimal clinically important difference (MCID) in patients who underwent TKA for primary OA was between 5.3 and 5.9 for KSS, while the MCID for FXN was between 6.1 and 6.4.13 These values were referenced for our analysis.

Continue to: No significant adverse...

 

 

RESULTS

No significant adverse events were reported in the subjects of this study. Common minor adverse events included pain and swelling, which generally resolved in 48 to 72 hours after the procedure.

NPRS improved from an average of 5.7 at baseline to 3.0 at 6 months and 4.35 at 12 months

Compared with baseline, significant improvements were noted in the mean values of NPRS (Figure 1) at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved from baseline at 6 weeks and 12 months (Figure 2). Significant improvements were also noted in the mean values of FXN (Figure 3) and the mean LEAS significantly improved from baseline at 6 weeks and 6 months (Figure 4).

KSS improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months

DISCUSSION

Knee OA is a disabling condition that affects a substantial proportion of the aging population. The current treatment methods do little to address the degenerative environment of the joint, which includes cytokines such as IL-1 and IL-2. Orthobiologic agents have been used recently to address these issues, which include PRP and MSCs from various sources, including bone marrow and adipose tissue.

FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months

A recent meta-analysis conducted by Cui and colleagues14 evaluated 18 studies of MSC treatment for knee OA with a total of 565 participants (226 males and 339 females). The duration from the onset of knee pain to registration in each study ranged from 3 months to ≥7 years. The follow-up period was 3 months -24 months. The majority of studies recruited patients with knee OA with a severity grade of 1-4 on the K-L scale; K-L grades 1 and 2 and grades 3 and 4 were defined as early OA and advanced OA, respectively. The results suggested that MSC treatment significantly improved pain and functional status, relative to the baseline evaluations in knee OA, and the beneficial effect was maintained for 2 years after treatment. Furthermore, the treatment effectiveness was not reduced over time.14

LEAS improved from an average of 36.6 at baseline to 47.1 at 6 months and 42.0 at 12 months

Included in the abovementioned meta-analysis were 2 papers by Koh and colleagues in 2012 and 2013 on the use of AMSCs for the treatment of OA. 15,16 The first study included 18 patients whose adipose tissue was harvested from the inner side of the infrapatellar fat pad via a skin incision after arthroscopic debridement. The cells were centrifuged and injected into the patient’s knee the same day. The results showed a significant reduction of pain and an increased quality of life for all patients, and a positive correlation was found between the number of cells injected and pain improvements. The authors concluded that AMSCs were a valid cell source for treating cartilage damage.15

In their second study, Koh and colleagues reported their results of treating 30 elderly patients with OA (≥65 years), who had failed conventional treatment, using intra-articular injections of AMSCs.16 This patient population is important since OA most commonly occurs in the elderly population. Patients underwent arthroscopic lavage and cartilage evaluation before receiving an injection of AMSCs delivered in PRP. The authors demonstrated that AMSC therapy for elderly patients with mild to moderate OA was an effective treatment resulting in reduction of pain and regeneration of cartilage.16

In another study, Adriani and colleagues17 performed autologous percutaneous fat injection from January 2012 to March 2015 for the treatment of knee OA. Their 30 patients (12 males and 18 females; mean age of 63.3 years; mean body mass index of 25.1) had stable or progressive knee OA for at least 12 months, no other injection treatments during the previous 12 months, and no prior knee surgeries. The patients were evaluated at baseline and 1 week and at 1, 3, 6, and 12 months after treatment using the NPRS and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) as outcome measures. The average VAS was 7.7 at baseline and improved to 4.3 at 3-month follow-up; however, a slight deterioration (VAS 5.0) was noted at 1 year. Total WOMAC score was 89.9 at baseline, 68.6 at 3 months, and 73.2 at 12-month follow-up.17

Continue to: The results of...

 

 

The results of this study demonstrated significant improvements in pain, quality of life, and function at 12 months after ultrasound-guided injection of ASCs in patients with severe knee OA. Significant improvement that was noted at 6 weeks was maintained through 12 months after the treatment. Improvement was noted in all scales, including the NPRS, the KSS, and the FXN beginning at 3 months and continuing through 12 months. The LEAS was statistically significant through 6 months after the treatment but not significant at 12 months. No serious adverse events were recorded.

In a study by Lee and colleagues,13 the MCID was described for KSS and FXN in patients who underwent TKA for primary OA. This is the minimal change in a scoring measure that is perceived by the patient to be beneficial or harmful. The MCID for KSS was noted to be between 5.3 and 5.9, while the MCID for FXN was between 6.1 and 6.4.13 In our study, the KSS score improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months (a difference of 5.6 and 7.6; P = .18 and.014, respectively). The FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months (a difference of 9.9 and 11; P = .041 and.014, respectively). Therefore, a clinically important difference of KSS and FXN scores was noted at both 6 and 12 months.

The technique used in this study provides autologous, minimally manipulated, fat graft performed in a short time (60-90 minutes), without expansion and/or enzymatic treatment. In addition, the harvesting and the injection of stem cells on the same day is a simple, office-based procedure, and compliant with the U. S. Food and Drug Administration regulations.18 The cost of the procedure averages $3500.

A study limitation is that it is a case series with relatively small numbers and not a randomized controlled study. Therefore, a placebo effect may play a role in our results. Further study with a larger number of patients and randomized controlled studies would be beneficial to support the findings of this study.

CONCLUSION

The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option in patients with refractory severe (grade 3 or 4) knee OA. This study showed significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.

References
  1. Yubo M, Yanyan L, Li L, Tao S, Bo L, Lin C. Clinical efficacy and safety of mesenchymal stem cell transplantation for osteoarthritis treatment: A meta-analysis. PLoS One. 2017;12(4):e0175449.
  2. Jauregui JJ, Cherian JJ, Pierce TP, Beaver WB, Issa K, Mont MA. Long-Term Survivorship and Clinical Outcomes Following Total Knee Arthroplasty. J Arthroplasty. 2015;30(12):2164-2166.
  3. Bourne RB, Chesworth BM, Davis AM, Mahomed NN, Charron KD. Patient satisfaction after total knee arthroplasty: who is satisfied and who is not? Clin Orthop Relat Res. 2010;468(1):57-63.
  4. Dai W-L, Zhou A-G, Zhang H, Zhang J. Efficacy of Platelet-Rich Plasma in the Treatment of Knee Osteoarthritis: A Meta-analysis of Randomized Controlled Trials. Arthroscopy.33(3):659-670.e651.
  5. Halpern B CS, Rodeo SA, Hayter C, Bogner E, Potter HG, Nguyen J. Clinical and MRI outcomes after platelet-rich plasma treatment for knee osteoarthritis. Clin J Sport Med. 2013 May;23.
  6. Mamidi MK, Das AK, Zakaria Z, Bhonde R. Mesenchymal stromal cells for cartilage repair in osteoarthritis. Osteoarthritis Cartilage. 2016;24(8):1307-1316.
  7. Tang Y, Pan ZY, Zou Y, et al. A comparative assessment of adipose-derived stem cells from subcutaneous and visceral fat as a potential cell source for knee osteoarthritis treatment. J Cell Mol Med. 2017.
  8. Izadpanah R, Trygg C, Patel B, et al. Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue. Journal of cellular biochemistry. 2006;99(5):1285-1297.
  9. Ankrum J, Karp JM. Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med. 2010;16(5):203-209.
  10. Togel F, Weiss K, Yang Y, Hu Z, Zhang P, Westenfelder C. Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. A J Physiol Renal Physiol. 2007;292(5):F1626-1635.
  11. Mestak O, Sukop A, Hsueh YS, et al. Centrifugation versus PureGraft for fatgrafting to the breast after breast-conserving therapy. World J Surg Oncol. 2014;12:178.
  12. Insall JN DL, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989 Nov;(248):13-4.
  13. Lee WC, Kwan YH, Chong HC, Yeo SJ. The minimal clinically important difference for Knee Society Clinical Rating System after total knee arthroplasty for primary osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy. 2016.
  14. Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016;12(5):3390-3400.
  15. Koh Y-GC, Yun-Jin. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee osteoarthritis. Knee. 2012;19(6):902-907.
  16. Koh Y-GC, Yun-Jin. Mesenchymal stem cell injections improve symptoms of knee osteoarthritis. Arthroscopy. 2013;29(4):748-755.
  17. Adriani E. MM, et al. Percutaneous Fat Transfer to Treat Knee Osteoarthritis Symptoms: Preliminary Results. Joints. 2017.
  18. Bianchi F, Maioli M, Leonardi E, et al. A New Nonenzymatic Method and Device to Obtain a Fat Tissue Derivative Highly Enriched in Pericyte-Like Elements by Mild Mechanical Forces From Human Lipoaspirates. Cell Transplantation. 2013;22(11):2063-2077
Author and Disclosure Information

Dr. Malanga has been a paid teaching consultant and lecturer for Lipogems, LLC. The other authors report no actual or potential conflict of interest in relation to this article.

Gerard Malanga is a Clinical Professor, Rutgers New Jersey Medical School, Department of Physical Medicine and Rehabilitation, Newark, New Jersey, and Director, New Jersey Regenerative Institute, Cedar Knolls, New Jersey. Jay Panchal is a PGY-3 Resident, Rutgers New Jersey Medical School, Department of Physical Medicine and Rehabilitation, Newark, New Jersey. Mitchell B. Sheinkop is a Director, Orthopedic and Cellular Orthopedic-Regenerative Medicine Program at Weil Foot-Ankle & Orthopedics, Chicago, Illinois.

Address correspondence to: Gerard Malanga, MD, Director, New Jersey Regenerative Institute, 197 Ridgedale Ave #210, Cedar Knolls, NJ 07927 (tel, 973-998-8301; email, gmalangamd@hotmail.com).

Am J Orthop. 2018;47(11). Copyright Frontline Medical Communications Inc. 2018. All rights reserved.

Jay Panchal, MD Gerard Malanga, MD Mitchell Sheinkop, MD . Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees. Am J Orthop. November 19, 2018

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Author and Disclosure Information

Dr. Malanga has been a paid teaching consultant and lecturer for Lipogems, LLC. The other authors report no actual or potential conflict of interest in relation to this article.

Gerard Malanga is a Clinical Professor, Rutgers New Jersey Medical School, Department of Physical Medicine and Rehabilitation, Newark, New Jersey, and Director, New Jersey Regenerative Institute, Cedar Knolls, New Jersey. Jay Panchal is a PGY-3 Resident, Rutgers New Jersey Medical School, Department of Physical Medicine and Rehabilitation, Newark, New Jersey. Mitchell B. Sheinkop is a Director, Orthopedic and Cellular Orthopedic-Regenerative Medicine Program at Weil Foot-Ankle & Orthopedics, Chicago, Illinois.

Address correspondence to: Gerard Malanga, MD, Director, New Jersey Regenerative Institute, 197 Ridgedale Ave #210, Cedar Knolls, NJ 07927 (tel, 973-998-8301; email, gmalangamd@hotmail.com).

Am J Orthop. 2018;47(11). Copyright Frontline Medical Communications Inc. 2018. All rights reserved.

Jay Panchal, MD Gerard Malanga, MD Mitchell Sheinkop, MD . Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees. Am J Orthop. November 19, 2018

Author and Disclosure Information

Dr. Malanga has been a paid teaching consultant and lecturer for Lipogems, LLC. The other authors report no actual or potential conflict of interest in relation to this article.

Gerard Malanga is a Clinical Professor, Rutgers New Jersey Medical School, Department of Physical Medicine and Rehabilitation, Newark, New Jersey, and Director, New Jersey Regenerative Institute, Cedar Knolls, New Jersey. Jay Panchal is a PGY-3 Resident, Rutgers New Jersey Medical School, Department of Physical Medicine and Rehabilitation, Newark, New Jersey. Mitchell B. Sheinkop is a Director, Orthopedic and Cellular Orthopedic-Regenerative Medicine Program at Weil Foot-Ankle & Orthopedics, Chicago, Illinois.

Address correspondence to: Gerard Malanga, MD, Director, New Jersey Regenerative Institute, 197 Ridgedale Ave #210, Cedar Knolls, NJ 07927 (tel, 973-998-8301; email, gmalangamd@hotmail.com).

Am J Orthop. 2018;47(11). Copyright Frontline Medical Communications Inc. 2018. All rights reserved.

Jay Panchal, MD Gerard Malanga, MD Mitchell Sheinkop, MD . Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees. Am J Orthop. November 19, 2018

ABSTRACT

The aim of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with refractory knee osteoarthritis (OA). A total of 17 subjects (26 knees) with a median age of 72 years (range: 54-78 years) and a history of knee OA (Kellgren–Lawrence, grade of 3 or 4) underwent treatment with ultrasound-guided injection of micro-fractured adipose tissue. Micro-fractured fat was obtained using a minimal manipulation technique in a closed system (Lipogems), without the addition of enzymes or any other additives. The study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months following this procedure.

When compared with baseline, significant improvements were noted in the mean values of NPRS, FXN, and LEAS at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved at 6 weeks and 12 months. In particular, the average KSS score improved from 74 to 82, the FXN score improved from 65 to 76, and the LEAS score improved from 36 to 47. These values were significantly greater than the previously published minimal clinically important difference described for KSS and FXN in patients who underwent total knee arthroplasty for primary OA. No serious adverse events were reported. The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option for patients with refractory, severe (grade 3 or 4) knee OA.

This study demonstrated significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.

Continue to: Knee OA is...

 

 

Knee OA is a chronic disease that affects all races, genders, and ages, but it is most prevalent in obese and elderly people. Worldwide, arthritis is considered to be the fourth leading cause of disability.1 In developing and developed countries, knee OA may cause a significant decline in the quality of life for individuals >65 years due to joint pain and disability.1 Nonoperative treatment can be successful in patients with mild to moderate arthritis with pain.

Current treatment options for knee OA, including physical therapy and anti-inflammatory drugs, aim to remedy the symptoms, but they do little to treat the underlying causes of knee OA pain. When a patient presents with advanced arthritis of the knee as confirmed by radiographic findings (classified as Kellgren–Lawrence grade of 3 or 4), the standard approach has been a total knee arthroplasty (TKA) after the patient has failed conservative treatment. The annual rate of total knee replacement in the United States has doubled since 2000, especially in those 45 – 65 years.2 The total number of procedures performed each year now exceeds 640,000, at a total annual cost of about $10.2 billion.Multiple studies show that TKA has favorable outcomes in pain relief and functional improvement in patients >60 years when evaluated at a follow-up of 10 years after surgery.2

However, some patients are hesitant to proceed with surgery due to fear of surgical pain and procedural complications. The known complications include deep vein thrombosis, pulmonary embolism, nerve injury, and infection. In addition, up to 20% of patients continue to complain of pain following a total knee replacement.3 Finally, in the young population (<50 years), there are concerns related to the potential need of revision knee surgery in the future.3

Alternative treatments for knee OA have recently emerged, including the use of platelet-rich plasma (PRP). A recent meta-analysis that included 10 randomized controlled trials with a total of 1069 patients demonstrated that, compared with hyaluronic acid and saline, intra-articular PRP injection may have more benefits in pain relief and functional improvement in patients with symptomatic knee OA at 1-year post-injection.4 Another smaller study examined patients who had experienced mild knee OA (Kellgren–Lawrence grade <3) for an average of 14 months. Each patient underwent magnetic resonance imaging for the evaluation of joint damage and then received a single PRP injection. The patients were assessed at regular intervals, with improvement in pain lasting up to 12 months.5

Additional orthobiologic options include the use of bone marrow and adipose-derived stem cell (ASC) injections for a variety of knee conditions, including knee OA. Mesenchymal stem cells (MSCs) are multipotent cells that have been used for the treatment of OA in clinical trials because of their regeneration potential and anti-inflammatory effects.6 Bone marrow stem cells (BMSCs) were first used to repair cartilage damage in humans in 1998. However, BMSCs had particular challenges, including low stem cell yield, pain, and possible morbidities during bone marrow aspiration. An alternative is ASCs, which may be more suitable clinically because of the high stem cell yield from lipoaspirates, faster cell proliferation, and less discomfort and morbidities during the harvesting procedure.7 In addition, these adult stem cells can contribute to the chondrogenic, osteogenic, adipogenic, myogenic, and neurogenic lineages.8 One study demonstrated that the contents of cartilage glycosaminoglycans significantly increased in specific areas of a knee joint treated with ASCs.9,10  This increased glycosaminoglycan content in hyaline cartilage may explain the observed visual analog score (VAS) improvement and clinical results. Other studies suggest that the chondrogenic action of ASCs may depend more on regenerative signaling by activated perivascular cells and signaling of trophic and paracrine mediators, such as vascular endothelial growth factor.9,10 Finally, the mechanism of action may include providing volume, support, cushioning, and filling of soft tissue defects.11

The Lipogems method and device, approved by the U.S. Food and Drug Administration, is used to harvest ASCs, cleanse, and micro-fracture adipose tissue while maintaining the perivascular niche that contains pericytes. The purpose of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with severe refractory knee OA.

Continue to: This report details...

 

 

STUDY PRESENTATION

This report details the outcome of an IRB-approved study of 17 subjects with 26 symptomatic knees with a history of knee OA (Kellgren–Lawrence grade of 3 or 4) diagnosed by a radiograph. Patient demographics are described in the Table.

TABLE. Patient Demographics

Male n (%)

10 (58.8)

Age, mean ± SD (range)

68.27 ± 7.43
(54–78)

BMI, mean ± SD (range)

28.98 ± 4.50
(21.41–34.9)

Kellgren–Lawrence grade 3 (n)

7

Kellgren–Lawrence grade 4 (n)

19

Abbreviation: BMI, body mass index.

The study patients were evaluated by an orthopedic surgeon, Mitchell Sheinkop, who commonly performs total joint replacement in his practice and considers potential patients as candidates for TKA. These patients presented with a Kellgren-Lawrence grade of 3 or 4 knee OA, and all had significant pain that was refractory to conservative treatment, which included medications, physical therapy, and injections. The study patients were offered the Lipogems procedure as an alternative to TKA. Following this procedure, the study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months. The 1989 KSS12 was used for this study. Adverse reactions were also monitored throughout the study period.

METHODS

After obtaining informed consent, the subjects were taken into the operating room, moved to the procedure table, and placed in the prone position for aspiration. After scrubbing with Betadine and draping, 1 mL of lidocaine was used to anesthetize the skin, and a pre-prepared preparation of lidocaine, epinephrine, and sterile saline was infused into the subcutaneous tissue. The micro-fragmented adipose tissue was obtained with minimal manipulation using Lipogems, a closed system using mild mechanical forces and reduction filters. The system processes the lipoaspirate without the addition of enzymes or any other additives. The final product consists of adipose tissue clusters with preserved vascular stromal niche of approximately 500 microns. The lipoaspirate was processed in the same room via a closed system. During the processing, the subject’s puncture wounds were dressed. The knee injection site was prepped with a Betadine swab and DuraPrep. Then, Lipogems was injected intra-articularly under ultrasound guidance.

After the completion of the injection, manual range of motion was administered to the treated joint. The subject was then transferred to the recovery room where vital signs were monitored. Post-procedure instructions were reviewed with the patient by the study staff. The subject was instructed to use an assistive device and avoid weight-bearing for 48 hours and maintain the activities of daily living to a minimum on the day of the procedure. Non-weight-bearing for 48 hours was recommended for reducing discomfort to avoid the use of opioids. Nonsteroidal anti-inflammatory drugs, alcohol, and marijuana must be avoided for 4 weeks after the procedure. Pretreatment and post-treatment outcomes were collected using the NPRS, the 100-point KSS with its FXN, and the LEAS at 6 weeks, 6 months, and 12 months after this procedure. The 1989 KSS12 was used for this study since the same scale was used for previous TKA procedures by our authors, allowing for future comparisons of results.

STATISTICAL ANALYSIS

Mean and standard deviation were used to estimate central tendency and variability. Outcome measures were analyzed using the t test, with the pairwise t test was used for paired and subsequent measurements of the same patient or a knee. All analyses were performed with significance set at P <.05. The minimal clinically important difference (MCID) in patients who underwent TKA for primary OA was between 5.3 and 5.9 for KSS, while the MCID for FXN was between 6.1 and 6.4.13 These values were referenced for our analysis.

Continue to: No significant adverse...

 

 

RESULTS

No significant adverse events were reported in the subjects of this study. Common minor adverse events included pain and swelling, which generally resolved in 48 to 72 hours after the procedure.

NPRS improved from an average of 5.7 at baseline to 3.0 at 6 months and 4.35 at 12 months

Compared with baseline, significant improvements were noted in the mean values of NPRS (Figure 1) at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved from baseline at 6 weeks and 12 months (Figure 2). Significant improvements were also noted in the mean values of FXN (Figure 3) and the mean LEAS significantly improved from baseline at 6 weeks and 6 months (Figure 4).

KSS improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months

DISCUSSION

Knee OA is a disabling condition that affects a substantial proportion of the aging population. The current treatment methods do little to address the degenerative environment of the joint, which includes cytokines such as IL-1 and IL-2. Orthobiologic agents have been used recently to address these issues, which include PRP and MSCs from various sources, including bone marrow and adipose tissue.

FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months

A recent meta-analysis conducted by Cui and colleagues14 evaluated 18 studies of MSC treatment for knee OA with a total of 565 participants (226 males and 339 females). The duration from the onset of knee pain to registration in each study ranged from 3 months to ≥7 years. The follow-up period was 3 months -24 months. The majority of studies recruited patients with knee OA with a severity grade of 1-4 on the K-L scale; K-L grades 1 and 2 and grades 3 and 4 were defined as early OA and advanced OA, respectively. The results suggested that MSC treatment significantly improved pain and functional status, relative to the baseline evaluations in knee OA, and the beneficial effect was maintained for 2 years after treatment. Furthermore, the treatment effectiveness was not reduced over time.14

LEAS improved from an average of 36.6 at baseline to 47.1 at 6 months and 42.0 at 12 months

Included in the abovementioned meta-analysis were 2 papers by Koh and colleagues in 2012 and 2013 on the use of AMSCs for the treatment of OA. 15,16 The first study included 18 patients whose adipose tissue was harvested from the inner side of the infrapatellar fat pad via a skin incision after arthroscopic debridement. The cells were centrifuged and injected into the patient’s knee the same day. The results showed a significant reduction of pain and an increased quality of life for all patients, and a positive correlation was found between the number of cells injected and pain improvements. The authors concluded that AMSCs were a valid cell source for treating cartilage damage.15

In their second study, Koh and colleagues reported their results of treating 30 elderly patients with OA (≥65 years), who had failed conventional treatment, using intra-articular injections of AMSCs.16 This patient population is important since OA most commonly occurs in the elderly population. Patients underwent arthroscopic lavage and cartilage evaluation before receiving an injection of AMSCs delivered in PRP. The authors demonstrated that AMSC therapy for elderly patients with mild to moderate OA was an effective treatment resulting in reduction of pain and regeneration of cartilage.16

In another study, Adriani and colleagues17 performed autologous percutaneous fat injection from January 2012 to March 2015 for the treatment of knee OA. Their 30 patients (12 males and 18 females; mean age of 63.3 years; mean body mass index of 25.1) had stable or progressive knee OA for at least 12 months, no other injection treatments during the previous 12 months, and no prior knee surgeries. The patients were evaluated at baseline and 1 week and at 1, 3, 6, and 12 months after treatment using the NPRS and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) as outcome measures. The average VAS was 7.7 at baseline and improved to 4.3 at 3-month follow-up; however, a slight deterioration (VAS 5.0) was noted at 1 year. Total WOMAC score was 89.9 at baseline, 68.6 at 3 months, and 73.2 at 12-month follow-up.17

Continue to: The results of...

 

 

The results of this study demonstrated significant improvements in pain, quality of life, and function at 12 months after ultrasound-guided injection of ASCs in patients with severe knee OA. Significant improvement that was noted at 6 weeks was maintained through 12 months after the treatment. Improvement was noted in all scales, including the NPRS, the KSS, and the FXN beginning at 3 months and continuing through 12 months. The LEAS was statistically significant through 6 months after the treatment but not significant at 12 months. No serious adverse events were recorded.

In a study by Lee and colleagues,13 the MCID was described for KSS and FXN in patients who underwent TKA for primary OA. This is the minimal change in a scoring measure that is perceived by the patient to be beneficial or harmful. The MCID for KSS was noted to be between 5.3 and 5.9, while the MCID for FXN was between 6.1 and 6.4.13 In our study, the KSS score improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months (a difference of 5.6 and 7.6; P = .18 and.014, respectively). The FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months (a difference of 9.9 and 11; P = .041 and.014, respectively). Therefore, a clinically important difference of KSS and FXN scores was noted at both 6 and 12 months.

The technique used in this study provides autologous, minimally manipulated, fat graft performed in a short time (60-90 minutes), without expansion and/or enzymatic treatment. In addition, the harvesting and the injection of stem cells on the same day is a simple, office-based procedure, and compliant with the U. S. Food and Drug Administration regulations.18 The cost of the procedure averages $3500.

A study limitation is that it is a case series with relatively small numbers and not a randomized controlled study. Therefore, a placebo effect may play a role in our results. Further study with a larger number of patients and randomized controlled studies would be beneficial to support the findings of this study.

CONCLUSION

The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option in patients with refractory severe (grade 3 or 4) knee OA. This study showed significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.

ABSTRACT

The aim of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with refractory knee osteoarthritis (OA). A total of 17 subjects (26 knees) with a median age of 72 years (range: 54-78 years) and a history of knee OA (Kellgren–Lawrence, grade of 3 or 4) underwent treatment with ultrasound-guided injection of micro-fractured adipose tissue. Micro-fractured fat was obtained using a minimal manipulation technique in a closed system (Lipogems), without the addition of enzymes or any other additives. The study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months following this procedure.

When compared with baseline, significant improvements were noted in the mean values of NPRS, FXN, and LEAS at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved at 6 weeks and 12 months. In particular, the average KSS score improved from 74 to 82, the FXN score improved from 65 to 76, and the LEAS score improved from 36 to 47. These values were significantly greater than the previously published minimal clinically important difference described for KSS and FXN in patients who underwent total knee arthroplasty for primary OA. No serious adverse events were reported. The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option for patients with refractory, severe (grade 3 or 4) knee OA.

This study demonstrated significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.

Continue to: Knee OA is...

 

 

Knee OA is a chronic disease that affects all races, genders, and ages, but it is most prevalent in obese and elderly people. Worldwide, arthritis is considered to be the fourth leading cause of disability.1 In developing and developed countries, knee OA may cause a significant decline in the quality of life for individuals >65 years due to joint pain and disability.1 Nonoperative treatment can be successful in patients with mild to moderate arthritis with pain.

Current treatment options for knee OA, including physical therapy and anti-inflammatory drugs, aim to remedy the symptoms, but they do little to treat the underlying causes of knee OA pain. When a patient presents with advanced arthritis of the knee as confirmed by radiographic findings (classified as Kellgren–Lawrence grade of 3 or 4), the standard approach has been a total knee arthroplasty (TKA) after the patient has failed conservative treatment. The annual rate of total knee replacement in the United States has doubled since 2000, especially in those 45 – 65 years.2 The total number of procedures performed each year now exceeds 640,000, at a total annual cost of about $10.2 billion.Multiple studies show that TKA has favorable outcomes in pain relief and functional improvement in patients >60 years when evaluated at a follow-up of 10 years after surgery.2

However, some patients are hesitant to proceed with surgery due to fear of surgical pain and procedural complications. The known complications include deep vein thrombosis, pulmonary embolism, nerve injury, and infection. In addition, up to 20% of patients continue to complain of pain following a total knee replacement.3 Finally, in the young population (<50 years), there are concerns related to the potential need of revision knee surgery in the future.3

Alternative treatments for knee OA have recently emerged, including the use of platelet-rich plasma (PRP). A recent meta-analysis that included 10 randomized controlled trials with a total of 1069 patients demonstrated that, compared with hyaluronic acid and saline, intra-articular PRP injection may have more benefits in pain relief and functional improvement in patients with symptomatic knee OA at 1-year post-injection.4 Another smaller study examined patients who had experienced mild knee OA (Kellgren–Lawrence grade <3) for an average of 14 months. Each patient underwent magnetic resonance imaging for the evaluation of joint damage and then received a single PRP injection. The patients were assessed at regular intervals, with improvement in pain lasting up to 12 months.5

Additional orthobiologic options include the use of bone marrow and adipose-derived stem cell (ASC) injections for a variety of knee conditions, including knee OA. Mesenchymal stem cells (MSCs) are multipotent cells that have been used for the treatment of OA in clinical trials because of their regeneration potential and anti-inflammatory effects.6 Bone marrow stem cells (BMSCs) were first used to repair cartilage damage in humans in 1998. However, BMSCs had particular challenges, including low stem cell yield, pain, and possible morbidities during bone marrow aspiration. An alternative is ASCs, which may be more suitable clinically because of the high stem cell yield from lipoaspirates, faster cell proliferation, and less discomfort and morbidities during the harvesting procedure.7 In addition, these adult stem cells can contribute to the chondrogenic, osteogenic, adipogenic, myogenic, and neurogenic lineages.8 One study demonstrated that the contents of cartilage glycosaminoglycans significantly increased in specific areas of a knee joint treated with ASCs.9,10  This increased glycosaminoglycan content in hyaline cartilage may explain the observed visual analog score (VAS) improvement and clinical results. Other studies suggest that the chondrogenic action of ASCs may depend more on regenerative signaling by activated perivascular cells and signaling of trophic and paracrine mediators, such as vascular endothelial growth factor.9,10 Finally, the mechanism of action may include providing volume, support, cushioning, and filling of soft tissue defects.11

The Lipogems method and device, approved by the U.S. Food and Drug Administration, is used to harvest ASCs, cleanse, and micro-fracture adipose tissue while maintaining the perivascular niche that contains pericytes. The purpose of this study was to evaluate the safety and efficacy of using autologous, micro-fractured, minimally manipulated adipose tissue in patients with severe refractory knee OA.

Continue to: This report details...

 

 

STUDY PRESENTATION

This report details the outcome of an IRB-approved study of 17 subjects with 26 symptomatic knees with a history of knee OA (Kellgren–Lawrence grade of 3 or 4) diagnosed by a radiograph. Patient demographics are described in the Table.

TABLE. Patient Demographics

Male n (%)

10 (58.8)

Age, mean ± SD (range)

68.27 ± 7.43
(54–78)

BMI, mean ± SD (range)

28.98 ± 4.50
(21.41–34.9)

Kellgren–Lawrence grade 3 (n)

7

Kellgren–Lawrence grade 4 (n)

19

Abbreviation: BMI, body mass index.

The study patients were evaluated by an orthopedic surgeon, Mitchell Sheinkop, who commonly performs total joint replacement in his practice and considers potential patients as candidates for TKA. These patients presented with a Kellgren-Lawrence grade of 3 or 4 knee OA, and all had significant pain that was refractory to conservative treatment, which included medications, physical therapy, and injections. The study patients were offered the Lipogems procedure as an alternative to TKA. Following this procedure, the study subjects were clinically evaluated using the numerical pain rating scale (NPRS), the 100-point Knee Society Score (KSS) with its functional component (FXN), and the lower extremity activity scale (LEAS) at 6 weeks, 6 months, and 12 months. The 1989 KSS12 was used for this study. Adverse reactions were also monitored throughout the study period.

METHODS

After obtaining informed consent, the subjects were taken into the operating room, moved to the procedure table, and placed in the prone position for aspiration. After scrubbing with Betadine and draping, 1 mL of lidocaine was used to anesthetize the skin, and a pre-prepared preparation of lidocaine, epinephrine, and sterile saline was infused into the subcutaneous tissue. The micro-fragmented adipose tissue was obtained with minimal manipulation using Lipogems, a closed system using mild mechanical forces and reduction filters. The system processes the lipoaspirate without the addition of enzymes or any other additives. The final product consists of adipose tissue clusters with preserved vascular stromal niche of approximately 500 microns. The lipoaspirate was processed in the same room via a closed system. During the processing, the subject’s puncture wounds were dressed. The knee injection site was prepped with a Betadine swab and DuraPrep. Then, Lipogems was injected intra-articularly under ultrasound guidance.

After the completion of the injection, manual range of motion was administered to the treated joint. The subject was then transferred to the recovery room where vital signs were monitored. Post-procedure instructions were reviewed with the patient by the study staff. The subject was instructed to use an assistive device and avoid weight-bearing for 48 hours and maintain the activities of daily living to a minimum on the day of the procedure. Non-weight-bearing for 48 hours was recommended for reducing discomfort to avoid the use of opioids. Nonsteroidal anti-inflammatory drugs, alcohol, and marijuana must be avoided for 4 weeks after the procedure. Pretreatment and post-treatment outcomes were collected using the NPRS, the 100-point KSS with its FXN, and the LEAS at 6 weeks, 6 months, and 12 months after this procedure. The 1989 KSS12 was used for this study since the same scale was used for previous TKA procedures by our authors, allowing for future comparisons of results.

STATISTICAL ANALYSIS

Mean and standard deviation were used to estimate central tendency and variability. Outcome measures were analyzed using the t test, with the pairwise t test was used for paired and subsequent measurements of the same patient or a knee. All analyses were performed with significance set at P <.05. The minimal clinically important difference (MCID) in patients who underwent TKA for primary OA was between 5.3 and 5.9 for KSS, while the MCID for FXN was between 6.1 and 6.4.13 These values were referenced for our analysis.

Continue to: No significant adverse...

 

 

RESULTS

No significant adverse events were reported in the subjects of this study. Common minor adverse events included pain and swelling, which generally resolved in 48 to 72 hours after the procedure.

NPRS improved from an average of 5.7 at baseline to 3.0 at 6 months and 4.35 at 12 months

Compared with baseline, significant improvements were noted in the mean values of NPRS (Figure 1) at 6 weeks, 6 months, and 12 months. The mean KSS significantly improved from baseline at 6 weeks and 12 months (Figure 2). Significant improvements were also noted in the mean values of FXN (Figure 3) and the mean LEAS significantly improved from baseline at 6 weeks and 6 months (Figure 4).

KSS improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months

DISCUSSION

Knee OA is a disabling condition that affects a substantial proportion of the aging population. The current treatment methods do little to address the degenerative environment of the joint, which includes cytokines such as IL-1 and IL-2. Orthobiologic agents have been used recently to address these issues, which include PRP and MSCs from various sources, including bone marrow and adipose tissue.

FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months

A recent meta-analysis conducted by Cui and colleagues14 evaluated 18 studies of MSC treatment for knee OA with a total of 565 participants (226 males and 339 females). The duration from the onset of knee pain to registration in each study ranged from 3 months to ≥7 years. The follow-up period was 3 months -24 months. The majority of studies recruited patients with knee OA with a severity grade of 1-4 on the K-L scale; K-L grades 1 and 2 and grades 3 and 4 were defined as early OA and advanced OA, respectively. The results suggested that MSC treatment significantly improved pain and functional status, relative to the baseline evaluations in knee OA, and the beneficial effect was maintained for 2 years after treatment. Furthermore, the treatment effectiveness was not reduced over time.14

LEAS improved from an average of 36.6 at baseline to 47.1 at 6 months and 42.0 at 12 months

Included in the abovementioned meta-analysis were 2 papers by Koh and colleagues in 2012 and 2013 on the use of AMSCs for the treatment of OA. 15,16 The first study included 18 patients whose adipose tissue was harvested from the inner side of the infrapatellar fat pad via a skin incision after arthroscopic debridement. The cells were centrifuged and injected into the patient’s knee the same day. The results showed a significant reduction of pain and an increased quality of life for all patients, and a positive correlation was found between the number of cells injected and pain improvements. The authors concluded that AMSCs were a valid cell source for treating cartilage damage.15

In their second study, Koh and colleagues reported their results of treating 30 elderly patients with OA (≥65 years), who had failed conventional treatment, using intra-articular injections of AMSCs.16 This patient population is important since OA most commonly occurs in the elderly population. Patients underwent arthroscopic lavage and cartilage evaluation before receiving an injection of AMSCs delivered in PRP. The authors demonstrated that AMSC therapy for elderly patients with mild to moderate OA was an effective treatment resulting in reduction of pain and regeneration of cartilage.16

In another study, Adriani and colleagues17 performed autologous percutaneous fat injection from January 2012 to March 2015 for the treatment of knee OA. Their 30 patients (12 males and 18 females; mean age of 63.3 years; mean body mass index of 25.1) had stable or progressive knee OA for at least 12 months, no other injection treatments during the previous 12 months, and no prior knee surgeries. The patients were evaluated at baseline and 1 week and at 1, 3, 6, and 12 months after treatment using the NPRS and the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) as outcome measures. The average VAS was 7.7 at baseline and improved to 4.3 at 3-month follow-up; however, a slight deterioration (VAS 5.0) was noted at 1 year. Total WOMAC score was 89.9 at baseline, 68.6 at 3 months, and 73.2 at 12-month follow-up.17

Continue to: The results of...

 

 

The results of this study demonstrated significant improvements in pain, quality of life, and function at 12 months after ultrasound-guided injection of ASCs in patients with severe knee OA. Significant improvement that was noted at 6 weeks was maintained through 12 months after the treatment. Improvement was noted in all scales, including the NPRS, the KSS, and the FXN beginning at 3 months and continuing through 12 months. The LEAS was statistically significant through 6 months after the treatment but not significant at 12 months. No serious adverse events were recorded.

In a study by Lee and colleagues,13 the MCID was described for KSS and FXN in patients who underwent TKA for primary OA. This is the minimal change in a scoring measure that is perceived by the patient to be beneficial or harmful. The MCID for KSS was noted to be between 5.3 and 5.9, while the MCID for FXN was between 6.1 and 6.4.13 In our study, the KSS score improved from an average of 74.0 at baseline to 79.6 at 6 months and 81.6 at 12 months (a difference of 5.6 and 7.6; P = .18 and.014, respectively). The FXN improved from an average of 65.4 at baseline to 75.2 at 6 months and 76.4 at 12 months (a difference of 9.9 and 11; P = .041 and.014, respectively). Therefore, a clinically important difference of KSS and FXN scores was noted at both 6 and 12 months.

The technique used in this study provides autologous, minimally manipulated, fat graft performed in a short time (60-90 minutes), without expansion and/or enzymatic treatment. In addition, the harvesting and the injection of stem cells on the same day is a simple, office-based procedure, and compliant with the U. S. Food and Drug Administration regulations.18 The cost of the procedure averages $3500.

A study limitation is that it is a case series with relatively small numbers and not a randomized controlled study. Therefore, a placebo effect may play a role in our results. Further study with a larger number of patients and randomized controlled studies would be beneficial to support the findings of this study.

CONCLUSION

The injection of autologous, micro-fractured, minimally manipulated adipose tissue appears to be a safe and effective treatment option in patients with refractory severe (grade 3 or 4) knee OA. This study showed significant improvements in pain, quality of life, and function for at least 12 months in this study population. This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population; however, further investigation is needed.

References
  1. Yubo M, Yanyan L, Li L, Tao S, Bo L, Lin C. Clinical efficacy and safety of mesenchymal stem cell transplantation for osteoarthritis treatment: A meta-analysis. PLoS One. 2017;12(4):e0175449.
  2. Jauregui JJ, Cherian JJ, Pierce TP, Beaver WB, Issa K, Mont MA. Long-Term Survivorship and Clinical Outcomes Following Total Knee Arthroplasty. J Arthroplasty. 2015;30(12):2164-2166.
  3. Bourne RB, Chesworth BM, Davis AM, Mahomed NN, Charron KD. Patient satisfaction after total knee arthroplasty: who is satisfied and who is not? Clin Orthop Relat Res. 2010;468(1):57-63.
  4. Dai W-L, Zhou A-G, Zhang H, Zhang J. Efficacy of Platelet-Rich Plasma in the Treatment of Knee Osteoarthritis: A Meta-analysis of Randomized Controlled Trials. Arthroscopy.33(3):659-670.e651.
  5. Halpern B CS, Rodeo SA, Hayter C, Bogner E, Potter HG, Nguyen J. Clinical and MRI outcomes after platelet-rich plasma treatment for knee osteoarthritis. Clin J Sport Med. 2013 May;23.
  6. Mamidi MK, Das AK, Zakaria Z, Bhonde R. Mesenchymal stromal cells for cartilage repair in osteoarthritis. Osteoarthritis Cartilage. 2016;24(8):1307-1316.
  7. Tang Y, Pan ZY, Zou Y, et al. A comparative assessment of adipose-derived stem cells from subcutaneous and visceral fat as a potential cell source for knee osteoarthritis treatment. J Cell Mol Med. 2017.
  8. Izadpanah R, Trygg C, Patel B, et al. Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue. Journal of cellular biochemistry. 2006;99(5):1285-1297.
  9. Ankrum J, Karp JM. Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med. 2010;16(5):203-209.
  10. Togel F, Weiss K, Yang Y, Hu Z, Zhang P, Westenfelder C. Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. A J Physiol Renal Physiol. 2007;292(5):F1626-1635.
  11. Mestak O, Sukop A, Hsueh YS, et al. Centrifugation versus PureGraft for fatgrafting to the breast after breast-conserving therapy. World J Surg Oncol. 2014;12:178.
  12. Insall JN DL, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989 Nov;(248):13-4.
  13. Lee WC, Kwan YH, Chong HC, Yeo SJ. The minimal clinically important difference for Knee Society Clinical Rating System after total knee arthroplasty for primary osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy. 2016.
  14. Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016;12(5):3390-3400.
  15. Koh Y-GC, Yun-Jin. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee osteoarthritis. Knee. 2012;19(6):902-907.
  16. Koh Y-GC, Yun-Jin. Mesenchymal stem cell injections improve symptoms of knee osteoarthritis. Arthroscopy. 2013;29(4):748-755.
  17. Adriani E. MM, et al. Percutaneous Fat Transfer to Treat Knee Osteoarthritis Symptoms: Preliminary Results. Joints. 2017.
  18. Bianchi F, Maioli M, Leonardi E, et al. A New Nonenzymatic Method and Device to Obtain a Fat Tissue Derivative Highly Enriched in Pericyte-Like Elements by Mild Mechanical Forces From Human Lipoaspirates. Cell Transplantation. 2013;22(11):2063-2077
References
  1. Yubo M, Yanyan L, Li L, Tao S, Bo L, Lin C. Clinical efficacy and safety of mesenchymal stem cell transplantation for osteoarthritis treatment: A meta-analysis. PLoS One. 2017;12(4):e0175449.
  2. Jauregui JJ, Cherian JJ, Pierce TP, Beaver WB, Issa K, Mont MA. Long-Term Survivorship and Clinical Outcomes Following Total Knee Arthroplasty. J Arthroplasty. 2015;30(12):2164-2166.
  3. Bourne RB, Chesworth BM, Davis AM, Mahomed NN, Charron KD. Patient satisfaction after total knee arthroplasty: who is satisfied and who is not? Clin Orthop Relat Res. 2010;468(1):57-63.
  4. Dai W-L, Zhou A-G, Zhang H, Zhang J. Efficacy of Platelet-Rich Plasma in the Treatment of Knee Osteoarthritis: A Meta-analysis of Randomized Controlled Trials. Arthroscopy.33(3):659-670.e651.
  5. Halpern B CS, Rodeo SA, Hayter C, Bogner E, Potter HG, Nguyen J. Clinical and MRI outcomes after platelet-rich plasma treatment for knee osteoarthritis. Clin J Sport Med. 2013 May;23.
  6. Mamidi MK, Das AK, Zakaria Z, Bhonde R. Mesenchymal stromal cells for cartilage repair in osteoarthritis. Osteoarthritis Cartilage. 2016;24(8):1307-1316.
  7. Tang Y, Pan ZY, Zou Y, et al. A comparative assessment of adipose-derived stem cells from subcutaneous and visceral fat as a potential cell source for knee osteoarthritis treatment. J Cell Mol Med. 2017.
  8. Izadpanah R, Trygg C, Patel B, et al. Biologic properties of mesenchymal stem cells derived from bone marrow and adipose tissue. Journal of cellular biochemistry. 2006;99(5):1285-1297.
  9. Ankrum J, Karp JM. Mesenchymal stem cell therapy: Two steps forward, one step back. Trends Mol Med. 2010;16(5):203-209.
  10. Togel F, Weiss K, Yang Y, Hu Z, Zhang P, Westenfelder C. Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. A J Physiol Renal Physiol. 2007;292(5):F1626-1635.
  11. Mestak O, Sukop A, Hsueh YS, et al. Centrifugation versus PureGraft for fatgrafting to the breast after breast-conserving therapy. World J Surg Oncol. 2014;12:178.
  12. Insall JN DL, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989 Nov;(248):13-4.
  13. Lee WC, Kwan YH, Chong HC, Yeo SJ. The minimal clinically important difference for Knee Society Clinical Rating System after total knee arthroplasty for primary osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy. 2016.
  14. Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016;12(5):3390-3400.
  15. Koh Y-GC, Yun-Jin. Infrapatellar fat pad-derived mesenchymal stem cell therapy for knee osteoarthritis. Knee. 2012;19(6):902-907.
  16. Koh Y-GC, Yun-Jin. Mesenchymal stem cell injections improve symptoms of knee osteoarthritis. Arthroscopy. 2013;29(4):748-755.
  17. Adriani E. MM, et al. Percutaneous Fat Transfer to Treat Knee Osteoarthritis Symptoms: Preliminary Results. Joints. 2017.
  18. Bianchi F, Maioli M, Leonardi E, et al. A New Nonenzymatic Method and Device to Obtain a Fat Tissue Derivative Highly Enriched in Pericyte-Like Elements by Mild Mechanical Forces From Human Lipoaspirates. Cell Transplantation. 2013;22(11):2063-2077
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Safety and Efficacy of Percutaneous Injection of Lipogems Micro-Fractured Adipose Tissue for Osteoarthritic Knees
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TAKE-HOME POINTS

  • Severe knee osteoarthritis causes pain and limits functions in a substantial proportion of the aging population.
  • Total knee arthroplasty is often recommended in this group of patients when conservative management has failed.
  • Many patients in this group continue to seek a nonsurgical option for this process.
  • Autologous, micro-fractured, minimally manipulated adipose tissue is easy to harvest, and injection into a knee joint resulted in significant improvement in pain and function for at least 12 months in this study population.
  • This intervention may represent a nonsurgical treatment option to avoid knee joint replacement in this population.
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Complications cluster in inflammatory arthritis patients after total knee replacement

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– Patients with an inflammatory arthritis had significantly higher rates of infections, transfusions, and readmissions following total knee replacement than did patients without inflammatory arthritis in a study of more than 137,000 Americans who underwent this surgery.

Dr. Susan M. Goodman

A sampling of U.S. patients who underwent total knee arthroplasty (TKA) during 2007-2016 showed that among the small percentage of these patients who had an inflammatory arthritis (IA), the rate of periprosthetic joint or wound infection while hospitalized or out to 30 days after surgery was a statistically significant 64% higher relative to patients without inflammatory arthritis, after adjustment for several demographic and clinical confounders, including recent glucocorticoid treatment, Susan M. Goodman, MD, said at the annual meeting of the American College of Rheumatology. The analysis also showed a statistically significant 46% higher relative rate of hospital readmission for any cause during the 90 days after surgery, and a significant 39% relative increase in blood transfusions during the 30 days after TKA in the IA patients.

“These results have important implications for evolving bundled payment models” for TKA, said Dr. Goodman, a rheumatologist at the Hospital for Special Surgery in New York. “Hospitals should receive commensurate resources to maintain access to total TKA for patients with IA.”

For this analysis, Dr. Goodman and her associates classified IA as a patient with a recorded diagnosis of rheumatoid arthritis, spondyloarthritis, or systemic lupus erythematosus if the patient had also received treatment during the year before surgery with a disease-modifying antirheumatic drug, a biologic agent, or a drug that treats systemic lupus erythematosus.



Complications following TKA became a particular concern to hospitals starting in 2013 when the Centers for Medicare & Medicaid Services began a program that penalized hospitals for outcomes such as excessive readmissions following selected types of hospitalizations and also with recent steps to bundle TKA reimbursement with related 90-day outcomes.

“My concern is to ensure that patients with IA aren’t penalized and can maintain access” to TKA despite recent policy moves by the CMS. Faced with potential disincentives to treat patients with an IA, “hospitals might cherry pick patients,” Dr. Goodman said in an interview. The new findings “are a reason for administrators to argue for patients with IA to come out of the cost bundle.”

Dr. Goodman expressed hope that future policies will better reflect the higher levels of risk faced by patients with an IA undergoing TKA. CMS “is pretty responsive,” she said.

The study used data collected by Humana for about 25 million American health insurance beneficiaries during 2007-2016, which included 137,550 people who underwent a TKA. Of these, 3,067 (2%) met the study’s definition for IA, and 134,483 did not. Most of those who did not meet the definition likely had osteoarthritis, Dr. Goodman said. This low percentage of U.S. TKA patients with IA was consistent with numbers in prior reports.

The researchers calculated the relative risk of the IA patients, compared with all the others, for nine potential complications, including acute MI, pneumonia, sepsis, pulmonary embolism, and death. The complications with significantly higher rates among the IA patients after confounder adjustment were 30-day infections, 30-day transfusions, and 90-day readmissions.

Dr. Goodman had no relevant disclosures.

mzoler@mdedge.com

SOURCE: Richardson S et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1932.

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– Patients with an inflammatory arthritis had significantly higher rates of infections, transfusions, and readmissions following total knee replacement than did patients without inflammatory arthritis in a study of more than 137,000 Americans who underwent this surgery.

Dr. Susan M. Goodman

A sampling of U.S. patients who underwent total knee arthroplasty (TKA) during 2007-2016 showed that among the small percentage of these patients who had an inflammatory arthritis (IA), the rate of periprosthetic joint or wound infection while hospitalized or out to 30 days after surgery was a statistically significant 64% higher relative to patients without inflammatory arthritis, after adjustment for several demographic and clinical confounders, including recent glucocorticoid treatment, Susan M. Goodman, MD, said at the annual meeting of the American College of Rheumatology. The analysis also showed a statistically significant 46% higher relative rate of hospital readmission for any cause during the 90 days after surgery, and a significant 39% relative increase in blood transfusions during the 30 days after TKA in the IA patients.

“These results have important implications for evolving bundled payment models” for TKA, said Dr. Goodman, a rheumatologist at the Hospital for Special Surgery in New York. “Hospitals should receive commensurate resources to maintain access to total TKA for patients with IA.”

For this analysis, Dr. Goodman and her associates classified IA as a patient with a recorded diagnosis of rheumatoid arthritis, spondyloarthritis, or systemic lupus erythematosus if the patient had also received treatment during the year before surgery with a disease-modifying antirheumatic drug, a biologic agent, or a drug that treats systemic lupus erythematosus.



Complications following TKA became a particular concern to hospitals starting in 2013 when the Centers for Medicare & Medicaid Services began a program that penalized hospitals for outcomes such as excessive readmissions following selected types of hospitalizations and also with recent steps to bundle TKA reimbursement with related 90-day outcomes.

“My concern is to ensure that patients with IA aren’t penalized and can maintain access” to TKA despite recent policy moves by the CMS. Faced with potential disincentives to treat patients with an IA, “hospitals might cherry pick patients,” Dr. Goodman said in an interview. The new findings “are a reason for administrators to argue for patients with IA to come out of the cost bundle.”

Dr. Goodman expressed hope that future policies will better reflect the higher levels of risk faced by patients with an IA undergoing TKA. CMS “is pretty responsive,” she said.

The study used data collected by Humana for about 25 million American health insurance beneficiaries during 2007-2016, which included 137,550 people who underwent a TKA. Of these, 3,067 (2%) met the study’s definition for IA, and 134,483 did not. Most of those who did not meet the definition likely had osteoarthritis, Dr. Goodman said. This low percentage of U.S. TKA patients with IA was consistent with numbers in prior reports.

The researchers calculated the relative risk of the IA patients, compared with all the others, for nine potential complications, including acute MI, pneumonia, sepsis, pulmonary embolism, and death. The complications with significantly higher rates among the IA patients after confounder adjustment were 30-day infections, 30-day transfusions, and 90-day readmissions.

Dr. Goodman had no relevant disclosures.

mzoler@mdedge.com

SOURCE: Richardson S et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1932.

– Patients with an inflammatory arthritis had significantly higher rates of infections, transfusions, and readmissions following total knee replacement than did patients without inflammatory arthritis in a study of more than 137,000 Americans who underwent this surgery.

Dr. Susan M. Goodman

A sampling of U.S. patients who underwent total knee arthroplasty (TKA) during 2007-2016 showed that among the small percentage of these patients who had an inflammatory arthritis (IA), the rate of periprosthetic joint or wound infection while hospitalized or out to 30 days after surgery was a statistically significant 64% higher relative to patients without inflammatory arthritis, after adjustment for several demographic and clinical confounders, including recent glucocorticoid treatment, Susan M. Goodman, MD, said at the annual meeting of the American College of Rheumatology. The analysis also showed a statistically significant 46% higher relative rate of hospital readmission for any cause during the 90 days after surgery, and a significant 39% relative increase in blood transfusions during the 30 days after TKA in the IA patients.

“These results have important implications for evolving bundled payment models” for TKA, said Dr. Goodman, a rheumatologist at the Hospital for Special Surgery in New York. “Hospitals should receive commensurate resources to maintain access to total TKA for patients with IA.”

For this analysis, Dr. Goodman and her associates classified IA as a patient with a recorded diagnosis of rheumatoid arthritis, spondyloarthritis, or systemic lupus erythematosus if the patient had also received treatment during the year before surgery with a disease-modifying antirheumatic drug, a biologic agent, or a drug that treats systemic lupus erythematosus.



Complications following TKA became a particular concern to hospitals starting in 2013 when the Centers for Medicare & Medicaid Services began a program that penalized hospitals for outcomes such as excessive readmissions following selected types of hospitalizations and also with recent steps to bundle TKA reimbursement with related 90-day outcomes.

“My concern is to ensure that patients with IA aren’t penalized and can maintain access” to TKA despite recent policy moves by the CMS. Faced with potential disincentives to treat patients with an IA, “hospitals might cherry pick patients,” Dr. Goodman said in an interview. The new findings “are a reason for administrators to argue for patients with IA to come out of the cost bundle.”

Dr. Goodman expressed hope that future policies will better reflect the higher levels of risk faced by patients with an IA undergoing TKA. CMS “is pretty responsive,” she said.

The study used data collected by Humana for about 25 million American health insurance beneficiaries during 2007-2016, which included 137,550 people who underwent a TKA. Of these, 3,067 (2%) met the study’s definition for IA, and 134,483 did not. Most of those who did not meet the definition likely had osteoarthritis, Dr. Goodman said. This low percentage of U.S. TKA patients with IA was consistent with numbers in prior reports.

The researchers calculated the relative risk of the IA patients, compared with all the others, for nine potential complications, including acute MI, pneumonia, sepsis, pulmonary embolism, and death. The complications with significantly higher rates among the IA patients after confounder adjustment were 30-day infections, 30-day transfusions, and 90-day readmissions.

Dr. Goodman had no relevant disclosures.

mzoler@mdedge.com

SOURCE: Richardson S et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1932.

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REPORTING FROM THE ACR ANNUAL MEETING

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Key clinical point: Complications were more common after total knee arthroplasty in patients with an inflammatory arthritis.

Major finding: Inflammatory arthritis patients had a 64% higher rate of infections after total knee arthroplasty, compared with patients without inflammatory arthritis.

Study details: Data analysis for 137,550 Americans who underwent total knee arthroplasty during 2007-2016.

Disclosures: Dr. Goodman had no relevant disclosures.

Source: Richardson S et al. Arthritis Rheumatol. 2018;70(Suppl 10): Abstract 1932.

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Geniculate Artery Injury During Primary Total Knee Arthroplasty

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Geniculate Artery Injury During Primary Total Knee Arthroplasty

ABSTRACT

Major arterial injury associated with total knee arthroplasty (TKA) is a rare and potentially devastating complication. However, the rate of injury to smaller periarticular vessels and the clinical significance of such an injury have not been well investigated. The purpose of this study is to describe the rate and outcomes of geniculate artery (GA) injury, the time at which injury occurs, and any associations with tourniquet use.

From November 2015 to February 2016, 3 surgeons at a single institution performed 100 consecutive primary TKAs and documented the presence or absence and the timing of GA injury. The data were then retrospectively reviewed. All TKAs had no prior surgery on the operative extremity. Other variables collected included tourniquet use, tranexamic acid (TXA) administration, intraoperative blood loss, postoperative drain output, and blood transfusion.

The overall rate of GA injury was 38%, with lateral inferior and middle GA injury in 31% and 15% of TKAs, respectively. Most of the injuries were visualized during bone cuts or meniscectomy. The rate of overall or isolated GA injury was not significantly different (P > .05) with either use of intravenous (84 patients) or topical (14 patients) TXA administration. Comparing selective tourniquet use (only during cementation) vs routine use showed no differences in GA injury rate (P = .37), blood loss (P = .07), or drain output (P = .46).

There is a relatively high rate of GA injury, with injury to the lateral GA occurring more often than the middle GA. Routine or selective tourniquet use does not affect the rate of injury.

Continue to: Major arterial injury...

 

 

Major arterial injury associated with total knee arthroplasty (TKA) is a rare and potentially devastating complication. The majority of literature in this context consists of case reports, small case series, and large retrospective studies that have examined the type, location, and mechanism of injury present in these cases.1-13 Reported arterial injuries include occlusion, laceration, aneurysm, pseudoaneurysm, and arteriovenous fistula formation in the femoral (believed to be due to the tourniquet around the proximal thigh) and popliteal arteries causing combinations of ischemia and hemorrhage necessitating treatment ranging from endovascular arterial intervention to amputation.4,5,9-11,13-17 In addition, several studies have asserted that the risk of major arterial injury may be increased with tourniquet use, suggesting that tourniquet use should be minimized for routine primary TKAs.3,6

There are very few cases in the literature specifically addressing injury to the more commonly encountered geniculate arteries (GAs). The medial GAs are typically visualized and coagulated during the standard medial parapatellar approach. In addition, if performed, a lateral release can damage the lateral superior and inferior GAs and the middle GA can be cut with posterior cruciate ligament resection. However, the middle and lateral inferior GAs are anecdotally the most difficult to detect and treat intraoperatively, especially after implantation of TKA and deflation of the tourniquet. The potential lack of recognition of such GA injury can result in harmful sequelae, including ischemia of the patella, hemorrhage, and painful pseudoaneurysms.2,18-29 Currently, there are only 2 case reports of lateral inferior GA injury, 2 cases of medial inferior GA injury, and no reports of middle GA injury.2,23,24,29

The rate, the timing within surgery, the risk factors, including tourniquet use, and the clinical effects of GA injury are largely unknown. If these factors were better understood, prophylactic measures and/or awareness could be better applied to prevent adverse outcomes, especially in cases of the middle and lateral inferior GAs. The aims of this study are to elucidate the rate and timing of middle and lateral inferior GA injury during primary TKA; determine the factors related to injury, including intraoperative blood loss, postoperative drain output, and tranexamic (TXA) acid use; and investigate any differences in the rate of injury with and without the use of a tourniquet.

MATERIALS AND METHODS

PATIENT DEMOGRAPHICS AND SURGICAL TECHNIQUE

From November 2015 to February 2016, 3 surgeons (MJT, TMM, and RTT) at a single institution performed 100 consecutive unilateral primary TKAs and documented the presence or absence and the timing of GA injury. After obtaining approval from our Institutional Review Board, a retrospective study was performed to investigate the prospectively recorded rate of middle and lateral inferior GA injuries occurring during primary TKAs. Patients with a diagnosis of isolated osteoarthritis were included, and those with any previous surgery on the operative knee were excluded. The average age of patients at the time of surgery was 67 years (range, 25-91 years), the average body mass index was 33 kg/m2 (range, 18-54 kg/m2), and there were 63 (63%) female patients.

All TKAs were performed through a medial parapatellar approach with a posterior-stabilized, cemented design, and each patient received a postoperative surgical drain. One of the 3 lead surgeons (TMM) in this study used a tourniquet from the time of incision until the completion of cementation, and the other 2 (MJT and RTT) predominantly used the tourniquet only during cementation. To elucidate any differences in GA injury between these 2 methods of tourniquet use, the patients were categorized into 2 groups base d on tourniquet use. Group 1 included patients in whom a tourniquet was used to maintain a bloodless surgical field from the time of incision until the completion of cementation, and Group 2 included patients in whom tourniquet use was more selective (ie, applied only during cementation). Group 1 comprised 31% (31/100) of patients, while Group 2 comprised 67% (67/100) of patients; no tourniquet was used in 2% (2/100) of cases. In addition, TXA was used in 98% (98/100) of patients: 84 patients received intravenous (IV) and 14 received topical TXA administration.

Continue to: ANALYSIS OF GENICULATE ARTERY INJURY

 

 

ANALYSIS OF GENICULATE ARTERY INJURY

The senior authors critically evaluated the GA during the primary TKAs and documented the presence or absence of injury in the operative reports. GA injury was reported if there was intraoperative visualization of pulsatile bleeding or visualization of arterial lumen in the anatomic areas of the middle and lateral inferior GAs. At 3 separate occasions during the operation, the surgeon looked specifically for pulsatile bleeding or arterial lumen in the areas of the middle and lateral inferior GAs, including after all the femoral and tibial bone cuts were completed, immediately before preparing to cement (before the tourniquet was inflated if there was not one inflated from the start of the procedure), and immediately after the tourniquet was deflated (Figure 1). All bleeding GAs that were visualized were effectively coagulated by cautery. Details regarding the use of TXA (topical or IV), intraoperative blood loss, postsurgical drain output for 24 hours after surgery, and blood transfusion were collected from the patients’ medical records (Table 1).

Surgical documentation template completed by operative surgeon

 

Table 1. Operative Variables

Variable

Value

Total number

100 (100%)

Intraoperative blood loss (mL)

160 (25-500)

Drain output 1st 24 hours (mL)

488 (75-1980)

Total output (mL)

618 (75-2130)

Use of TXA

98 (98%)

Topical TXA

84 (84%)

IV TXA

14 (14%)

Tourniquet entire procedure

31 (31%)

Operative variables other than geniculate artery injury. Data presented as mean (range) or n (%). TXA = tranexamic acid.

STATISTICAL METHODS

Statistical analysis was performed using the JMP software version 10.0.0 (SAS Institute, Inc). The overall rate of GA injury was determined, including the rates of GA injury based on location, time point, and method of diagnosis (pulsatile bleeding or arterial lumen visualization). If >1 GA injury occurred in the same knee, only 1 GA injury was calculated for the overall rate; however, each injury was specified separately when calculating the injury rate for the specific GA. Intraoperative blood loss, postoperative drain output, and the use of TXA were compared between cases in which a GA injury was detected and those in which it was not detected. Before conducting the retrospective review, a power analysis determined that we would require 100 patients to detect a difference in GA injury between Groups 1 and 2 (33 in Group 1 and 67 in Group 2), assuming a 30% rate in Group 1 and a 5% rate of GA injury in Group 2 using Fisher’s exact test. The Fisher’s exact test was used to compare categorical variables, and the Wilcoxon rank sum test was used to compare continuous variables. An alpha value of .05 was considered as statistically significant.

RESULTS

RATE OF GENICULATE ARTERY INJURY

The overall rate of any GA injury was 38% (38/100). Lateral inferior GA injury was more frequently detected than middle GA injury (31% vs 15% of TKAs, respectively; Table 2). Among the 31 lateral inferior GA injuries, 14 were identified as pulsatile bleeding, 7 as lumen visualizations, and 6 as both pulsatile bleeding and lumen visualization; 4 were detected by methods not recorded in the operative report. Of the lateral inferior GA injuries, 11 were identified after the bone cuts, 7 during meniscus removal, 3 during exposure, 1 after tourniquet deflation, and 9 at a time not recorded in the operative report. Of the 15 middle GA injuries, 9 were identified as pulsatile bleeding, 2 as lumen visualizations, and 4 as both pulsatile bleeding and lumen visualization. In addition, 7 of these GA injuries were identified after the bone cuts, 3 during cruciate removal, 1 after meniscus removal, 1 during exposure, and 3 at a time not recorded in the operative report (Table 3).

 

Table 2. Rates of Geniculate Artery Injury Based on Location and Method

Location

Pulsatile Bleeding

Arterial Lumen

Both

Overall Rate

Lateral inferior GA

14 (14%)

7 (7%)

6 (6%)

31 (31%)

Middle GA

9 (9%)

2 (2%)

4 (4%)

15 (15%)

Rates of geniculate artery injury based on location and method of diagnosis. Data presented as n (%). There were 4 additional lateral inferior and 9 middle GA injuries identified by a method not specified in the operative report. GA = geniculate artery.

Table 3. Rates of Geniculate Artery Injury Based on Time Point

Time

Lateral Inferior GA

Middle GA

After bone cuts

11 (11%)

7 (7%)

During meniscus removal

7 (7%)

1 (1%)

During exposure

3 (3%)

1 (1%)

After tourniquet deflation

1 (1%)

0 (0%)

During cruciate removal

0 (0%)

3 (3%)

Not reported

9 (9%)

3 (3%)

Rates of geniculate artery injury based on time point and method of diagnosis. GA = geniculate artery. Data presented as n (%).

FACTORS ASSOCIATED WITH GENICULATE ARTERY INJURY

Mean intraoperative estimated blood loss was 186 mL (standard deviation [SD], 111; range 50–500 mL) in those with a GA injury versus 147 mL (range, 82.25–400 mL) in those without injury (P = .14). Postoperative drain output in the 24 hours after surgery was 467 mL (SD 253, range 100–1105 mL) versus 502 mL (SD 378, range 75–1980 mL) in TKAs with and without GA injury, respectively (P = .82). Total estimated blood loss (combined intraoperative blood loss and 24-hour postoperative drain output) was 613 mL (SD 252, range 150–1105 mL) in TKAs with GA injury versus 620 mL (SD 393, range 75–2130 mL) without injury (P = .44) (Table 4). Overall, there was no statistical difference in blood loss, drain output, or combined output when analyzed according to lateral inferior or middle GA injury (P = .24–.82) (Table 5 and Table 6). No patients required blood transfusion postoperatively after TKA.

 

Table 4. Factors Associated with GA Injury

Outcome

GA Injury

No GA Injury

P Value

Blood loss (mL)

186 (50-500)

147 (25-400)

.1366

24-Hour drain output (mL)

467 (100-1105)

502 (75-1980)

.8240

Total output (mL)

613 (150-1105)

620 (75-2130)

.4368

Differences in outcomes based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery.

 

Table 5. Factors Associated with LIGA Injury

Outcome

LIGA Injury

No LIGA Injury

P Value

Blood loss (mL)

178 (50-400)

153 (25-500)

.2401

24-Hour drain output (mL)

461 (100-890)

501 (75-1980)

.8187

Total output (mL)

610 (150-1080)

621 (75-2130)

.4165

Differences in outcomes based on presence or absence of LIGA injury. Note that there were no significant differences. Values are reported as average (range). LIGA = lateral inferior geniculate artery.

 

Table 6. Factors Associated with MGA Injury

Outcome

MGA Injury

No MGA Injury

P Value

Blood loss (mL)

190 (75-500)

156 (25-400)

.6225

24-Hour drain output (mL)

455 (125-1105)

494 (75-1980)

.6428

Total output (mL)

582 (200-1105)

624 (75-2130)

.6535

Differences in outcomes based on presence or absence of MGA injury. Note that there were no significant differences. Values are reported as average (range). MGA = middle geniculate artery.

IV administration of TXA was associated with a 37% (31/84) rate of GA injury, whereas topical TXA administration was associated with a 43% (6/14) rate of GA injury (P = .77). The rate of overall or isolated GA injury was not significantly different (P = .35–1.0) between IV and topical TXA administration (Table 7). In addition, total combined output was not significantly different (P = .1032) when comparing GA injury and noninjury in the subgroup analysis based on TXA use (IV or topical); however, topical administration was associated with lower intraoperative blood loss than IV administration (P = .0489), whereas IV administration was associated with lower 24-hour postoperative drain output than topical administration (P = .0169). There was no difference in blood loss, 24-hour drain output, or total output between those who did and did not sustain a GA injury in the group of patients who received IV TXA administration (Table 8, P = .2118–.7091). The same was true for those receiving topical TXA administration (Table 9, P = .0912–.9485).

Table 7. Factors Associated with TXA Injury

Outcome

IV TXA (n = 84)

Topical TXA (n = 14)

P Value

Any GA injury

31 (37%)

6 (43%)

.7683

LIGA injury

24 (29%)

6 (43%)

.3498

MGA injury

13 (15%)

2 (14%)

1.0

Blood loss (mL)

170 (25-500)

113 (40-240)

.0489*

24-Hour drain output (mL)

454 (75-1980)

662 (75-1800)

.0169*

Total output (mL)

592 (75-2130)

751 (75-2130)

.1032

Differences in outcomes based on presence or absence of MGA injury. Note that there were no significant differences. Values are reported as n (%) or average (range). TXA = tranexamic acid, GA = geniculate artery, LIGA = lateral inferior geniculate artery, MGA = middle geniculate artery. *denotes statistical significance (P < .05).

 

Table 8. Factors Associated with GA Injury Given IV TXA Use

Outcome

GA Injury

No GA Injury

Difference

P Value

Blood loss (mL)

195 (50-500)

157 (25-400)

38

.2118

24-Hour drain output (mL)

436 (100-1105)

464 (75-1980)

28

.7091

Total output (mL)

594 (150-1105)

592 (75-2130)

2

.6982

Differences in outcomes of those patients who received IV TXA based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery, TXA = tranexamic acid.

 

Table 9. Factors Associated with GA Injury Given Topical TXA Use

Outcome

GA Injury

No GA Injury

Difference

P Value

Blood loss (mL)

163 (100-250)

84 (40-150)

79

.0912

24-Hour drain output (mL)

610 (205-890)

701 (415-1800)

91

.9485

Total output (mL)

719 (405-960)

775 (455-1900)

56

.6982

Differences in outcomes based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery.

Continue to: TOURNIQUET USE

 

 

TOURNIQUET USE

Comparison between Groups 1 (tourniquet use) and 2 (selective tourniquet use) revealed similar rates of overall and specific GA injury, intraoperative blood loss, and 24-hour postoperative drain output (Table 10). Group 1 demonstrated a 29% (9/31) rate of any GA injury versus 40% (27/67) in Group 2 (P = .37). For the specific lateral inferior GA injury, there was an equivalent rate of injury at 29% (9/31 in Group 1, 20/67 in Group 2; P = 1.0). Similarly, Group 1 patients had a 10% (3/31) rate of middle GA injury compared to 16% (11/67) in Group 2 patients (P = .53). Intraoperative estimated blood loss was lower in Group 1 (140 mL; range 25–400 mL) than in Group 2 (171 mL; range 40–500 mL) (P = .07), whereas the average 24-hour postoperative drain output was similar for Groups 1 (484 mL; range 75–1800 mL) and 2 (488 mL; range 100–1980 mL) (P = .46). Total estimated output was slightly less for Group 1 (593 mL; range 75–1900 mL) than for Group 2 (626 mL; range 125–2130 mL) (P = .38). A post hoc power analysis showed that with these rates of GA injury in Groups 1 and 2 and given a 2:1 ratio of the number of patients in Group 2 versus Group 1, a total of 185 patients in Group 1 and 370 patients in Group 2 would be needed to detect a statistically significant difference (P < .05) with a power of 80%.

 

Table 10. Factors Associated with Tourniquet Use

Injury

Group 1 (n = 31)

Group 2 (n = 67)

Difference

P Value

Overall GA injury

9 (29%)

27 (40%)

11%

.3687

Lateral inferior GA

9 (29%)

20 (29%)

0%

1.0

Middle GA

3 (10%)

11 (16%)

6%

.5382

Blood loss (mL)

140 (25-400)

171 (40-500)

31

.0661

24-Hour drain output (mL)

484 (75-1800)

488 (100-1980)

4

.4580

Total output (mL)

593 (75-1900)

626 (125-2130)

33

.3776

Differences in outcomes separated based on use of a tourniquet for the entire case (Group 1) vs use of a tourniquet only during cementation (Group 2). Note that there were no significant differences. Values are reported as n (%) or average (range). GA = geniculate artery.

DISCUSSION

Major arterial injury associated with TKA is a well-known, rare, and potentially devastating complication.1-13 However, the rate of injury to smaller periarticular vessels and the clinical significance of such injury have not been studied. The present study found a high rate of GA injury but no clinically significant difference in intraoperative blood loss or postoperative drain output between patients with GA injury (which was identified and managed with cautery) and those without GA injury. In addition, tourniquet use did not affect the rate of injury or the associated blood loss. To our knowledge, this is the first study that has critically evaluated the rate of GA injury occurring during TKA.

The overall rate of GA injury occurring during primary TKA was 38% with a higher predominance of lateral inferior than middle GA injury (31% vs 15%). Anatomically, it would follow that the lateral GA could be injured at a higher rate as it courses on top of the lateral meniscus, thus being susceptible to injury during cutting of the tibial plateau and meniscectomy. In addition, because the meniscectomy is performed longitudinally along the course of the artery, it may also be potentially lacerated in multiple locations and lengthwise. In theory, there should be a 100% rate of middle GA injury during posterior-stabilized TKA as this artery runs through the cruciate ligaments, which are resected during these cases. However, vessel injury was defined in this study as the visualization of pulsatile bleeding or vessel lumen. It is probable that in the cases in which injury to the middle GA was not visualized, it was cut but simultaneously cauterized. Thus, a lower rate (15%) of injury was detected. Nonetheless, these results still suggest that these periarticular arteries are injured at a higher rate; therefore, it is important for surgeons to specifically identify these injuries intraoperatively and adequately cauterize these vessels. As long as these arteries are cauterized, additional blood loss and potential vascular pseudoaneurysms should be prevented.

The effect of GA injury on intraoperative blood loss, 24-hour postoperative drain output, and total estimated blood loss showed no significant clinical findings in the present study cohort. In addition, examining the injury rate and blood loss based on TXA use also revealed no detrimental clinical associations. Although GA injury could inherently be associated with higher levels of blood loss and drain output, it is important to note that all GA injuries were also effectively coagulated, thus explaining the indifferent results. Accordingly, it should be recommended to surgeons performing primary TKAs to carefully evaluate for GA injury to prevent excessive blood loss or painful pseudoaneurysms. However, there is also a potential for beta error in this study in which a true difference did exist but no statistical difference was found due to the study being underpowered.

Full or selective tourniquet use during TKA did not appear to have any effect on the rate of GA injury, intraoperative blood loss, or 24-hour postoperative drain output. The similarity between GA injury rates perhaps further indicates an equivalent ability to detect these injuries between these two methods because of operative inspection for such injuries. With regard to intraoperative blood loss and drain output, the present findings are similar to previous studies demonstrating equivocal results despite variable tourniquet utilization in TKA.15,30 However, these results differ from those of Harvey and colleagues31, who demonstrated that blood loss inversely correlated with intraoperative tourniquet time. There are risks and benefits related to the use of both full and selective tourniquet methods, but either method does not appear to be advantageous in decreasing the rate of GA injury.

Continue to: Although this is the first study...

 

 

Although this is the first study to investigate the rates of GA injury and the potential clinical effects, there are limitations to this research. First, the study was retrospective in nature despite the fact that the data were collected prospectively. Only acute perioperative follow-up was performed, and thus, we were unable to evaluate longer term effects of GA injury on TKA outcomes. Furthermore, this study is potentially prone to beta error. As discussed above, 185 patients in Group 1 and 370 patients in Group 2 would be needed to detect a statistical difference in the rate of GA injury based on the rates found in this study. This study could also have been underpowered to identify differences in other aspects, such as differences in blood loss and drain. Furthermore, the data collected regarding intraoperative blood loss are estimated data and can be variable. Finally, visualization of vessel lumen and pulsatile bleeding is not a validated method to diagnose GA injuries, and potential injuries may have been missed. Despite such disadvantages, the strengths of this study include the concise results in consecutive patients, the generalizability of the data as multiple surgeons participated, and its first report of nonmajor periarticular artery injury.

CONCLUSIONS

There is a relatively high rate of GA injury, with injury to the lateral GA being visualized more often than injury to the middle GA. The majority of GA injuries occur around the time of bone cuts and meniscectomy, and tourniquet use does not affect the rate of injury. To reduce intraoperative blood loss and postoperative drain output, surgeons should identify and coagulate GA injuries routinely during primary TKA.

References

1. Calligaro KD, Dougherty MJ, Ryan S, Booth RE. Acute arterial complications associated with total hip and knee arthroplasty. J Vasc Surg. 2003;38(6):1170-1177. doi: 10.1016/S0741-5214(03)00918-2.

2. Dennis DA, Neumann RD, Toma P, Rosenberg G, Mallory TH. Arteriovenous fistula with false aneurysm of the inferior medial geniculate artery. A complication of total knee arthroplasty. Clin Orthop Relat Res. 1987(222):255-260.

3. Hagan PF, Kaufman EE. Vascular complication of knee arthroplasty under tourniquet. A case report. Clin Orthop Relat Res. 1990(257):159-161.

4. Holmberg A, Milbrink J, Bergqvist D. Arterial complications after knee arthroplasty: 4 cases and a review of the literature. Acta Orthop Scand. 1996;67(1):75-78. doi: 10.3109/17453679608995616.

5. Hozack WJ, Cole PA, Gardner R, Corces A. Popliteal aneurysm after total knee arthroplasty. Case reports and review of the literature. J Arthroplasty. 1990;5(4):301-305. doi: 10.1016/S0883-5403(08)80087-3.

6. Jeyaseelan S, Stevenson TM, Pfitzner J. Tourniquet failure and arterial calcification. Case report and theoretical dangers. Anaesthesia. 1981;36(1):48-50. doi: 10.1111/j.1365-2044.1981.tb08599.x

7. Mureebe L, Gahtan V, Kahn MB, Kerstein MD, Roberts AB. Popliteal artery injury after total knee arthroplasty. Am Surg. 1996;62(5):366-368.

8. O'Connor JV, Stocks G, Crabtree JD, Jr., Galasso P, Wallsh E. Popliteal pseudoaneurysm following total knee arthroplasty. J Arthroplasty. 1998;13(7):830-832. doi: 10.1016/S0883-5403(98)90039-0.

9. Ohira T, Fujimoto T, Taniwaki K. Acute popliteal artery occlusion after total knee arthroplasty. Arch Orthop Trauma Surg. 1997;116(6-7):429-430. doi: 10.1007/BF00434007.

10. Parfenchuck TA, Young TR. Intraoperative arterial occlusion in total joint arthroplasty. J Arthroplasty. 1994;9(2):217-220. doi: 10.1016/0883-5403(94)90071-X.

11. Rush JH, Vidovich JD, Johnson MA. Arterial complications of total knee replacement. The Australian experience. J Bone Joint Surg Br. 1987;69(3):400-402. doi: 10.1302/0301-620X.69B3.3584193.

12. Smith DE, McGraw RW, Taylor DC, Masri BA. Arterial complications and total knee arthroplasty. J Am Acad Orthop Surg. 2001;9(4):253-257.

13. Zahrani HA, Cuschieri RJ. Vascular complications after total knee replacement. J Cardiovasc Surg (Torino). 1989;30(6):951-952.

14. Isiklar ZU, Landon GC, Tullos HS. Amputation after failed total knee arthroplasty. Clin Orthop Relat Res. 1994(299):173-178.

15. Wakankar HM, Nicholl JE, Koka R, D'Arcy JC. The tourniquet in total knee arthroplasty. A prospective, randomised study. J Bone Joint Surg Br. 1999;81(1):30-33. doi: 10.1302/0301-620X.81B1.0810030.

16. Kumar SN, Chapman JA, Rawlins I. Vascular injuries in total knee arthroplasty. A review of the problem with special reference to the possible effects of the tourniquet. J Arthroplasty. 1998;13(2):211-216. doi: 10.1016/S0883-5403(98)90102-4.

17. DeLaurentis DA, Levitsky KA, Booth RE, et al. Arterial and ischemic aspects of total knee arthroplasty. Am J Surg. 1992;164(3):237-240. doi: 10.1016/S0002-9610(05)81078-5.

18. Langkamer VG. Local vascular complications after knee replacement: a review with illustrative case reports. Knee. 2001;8(4):259-264. doi: 10.1016/S0968-0160(01)00103-X.

19. Moran M, Hodgkinson J, Tait W. False aneurysm of the superior lateral geniculate artery following Total Knee Replacement. Knee. 2002;9(4):349-351. doi: 10.1016/S0968-0160(02)00061-3.

20. Pritsch T, Parnes N, Menachem A. A bleeding pseudoaneurysm of the lateral genicular artery after total knee arthroplasty--a case report. Acta Orthop. 2005;76(1):138-140. doi: 10.1080/00016470510030463.

21. Gaheer RS, Chirputkar K, Sarungi M. Spontaneous resolution of superior medial geniculate artery pseudoaneurysm following total knee arthroplasty. Knee. 2014;21(2):586-588. doi: 10.1016/j.knee.2012.10.021.

22. Law KY, Cheung KW, Chiu KH, Antonio GE. Pseudoaneurysm of the geniculate artery following total knee arthroplasty: a report of two cases. J Orthop Surg (Hong Kong). 2007;15(3):386-389. /doi: 10.1177/230949900701500331.

23. Noorpuri BS, Maxwell-Armstrong CA, Lamerton AJ. Pseudo-aneurysm of a geniculate collateral artery complicating total knee replacement. Eur J Vasc Endovasc Surg. 1999;18(6):534-535.

24. Pai VS. Traumatic aneurysm of the inferior lateral geniculate artery after total knee replacement. J Arthroplasty. 1999;14(5):633-634. doi: 10.1016/S0883-5403(99)90089-X.

25. Julien TP, Gravereaux E, Martin S. Superior medial geniculate artery pseudoaneurysm after primary total knee arthroplasty. J Arthroplasty. 2012;27(2):323 e313-326. doi: 10.1016/j.arth.2011.02.009.

26. Kalsi PS, Carrington RJ, Skinner JS. Therapeutic embolization for the treatment of recurrent hemarthrosis after total knee arthroplasty due to an arteriovenous fistula. J Arthroplasty. 2007;22(8):1223-1225. /doi: 10.1016/j.arth.2006.11.012.

27. Ritter MA, Herbst SA, Keating EM, Faris PM, Meding JB. Patellofemoral complications following total knee arthroplasty. Effect of a lateral release and sacrifice of the superior lateral geniculate artery. J Arthroplasty. 1996;11(4):368-372. doi: 10.1016/S0883-5403(96)80024-6.

28. Aldrich D, Anschuetz R, LoPresti C, Fumich M, Pitluk H, O'Brien W. Pseudoaneurysm complicating knee arthroscopy. Arthroscopy. 1995;11(2):229-230. doi: 10.1016/0749-8063(95)90073-X.

29. Sharma H, Singh GK, Cavanagh SP, Kay D. Pseudoaneurysm of the inferior medial geniculate artery following primary total knee arthroplasty: delayed presentation with recurrent haemorrhagic episodes. Knee Surg Sports Traumatol Arthrosc. 2006;14(2):153-155. doi: 10.1007/s00167-005-0639-4.

30. Abdel-Salam A, Eyres KS. Effects of tourniquet during total knee arthroplasty. A prospective randomised study. J Bone Joint Surg Br. 1995;77(2):250-253. doi: 10.1302/0301-620X.77B2.7706340.

31. Harvey EJ, Leclerc J, Brooks CE, Burke DL. Effect of tourniquet use on blood loss and incidence of deep vein thrombosis in total knee arthroplasty. J Arthroplasty. 1997;12(3):291-296. doi: 10.1016/S0883-5403(97)90025-5.

Author and Disclosure Information

The authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Robert T. Trousdale, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905(tel, 507-284-3663; fax, 507-284-8935; email, trousdale.robert@mayo.edu).

Joseph M. Statz, MD Cameron K. Ledford, MD Brian P. Chalmers, MD Michael J. Taunton, MD Tad. M. Mabry, MD and Robert T. Trousdale, MD . Geniculate Artery Injury During Primary Total Knee Arthroplasty. Am J Orthop. October 29, 2018

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Author and Disclosure Information

The authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Robert T. Trousdale, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905(tel, 507-284-3663; fax, 507-284-8935; email, trousdale.robert@mayo.edu).

Joseph M. Statz, MD Cameron K. Ledford, MD Brian P. Chalmers, MD Michael J. Taunton, MD Tad. M. Mabry, MD and Robert T. Trousdale, MD . Geniculate Artery Injury During Primary Total Knee Arthroplasty. Am J Orthop. October 29, 2018

Author and Disclosure Information

The authors report no actual or potential conflict of interest in relation to this article.

Address correspondence to: Robert T. Trousdale, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905(tel, 507-284-3663; fax, 507-284-8935; email, trousdale.robert@mayo.edu).

Joseph M. Statz, MD Cameron K. Ledford, MD Brian P. Chalmers, MD Michael J. Taunton, MD Tad. M. Mabry, MD and Robert T. Trousdale, MD . Geniculate Artery Injury During Primary Total Knee Arthroplasty. Am J Orthop. October 29, 2018

ABSTRACT

Major arterial injury associated with total knee arthroplasty (TKA) is a rare and potentially devastating complication. However, the rate of injury to smaller periarticular vessels and the clinical significance of such an injury have not been well investigated. The purpose of this study is to describe the rate and outcomes of geniculate artery (GA) injury, the time at which injury occurs, and any associations with tourniquet use.

From November 2015 to February 2016, 3 surgeons at a single institution performed 100 consecutive primary TKAs and documented the presence or absence and the timing of GA injury. The data were then retrospectively reviewed. All TKAs had no prior surgery on the operative extremity. Other variables collected included tourniquet use, tranexamic acid (TXA) administration, intraoperative blood loss, postoperative drain output, and blood transfusion.

The overall rate of GA injury was 38%, with lateral inferior and middle GA injury in 31% and 15% of TKAs, respectively. Most of the injuries were visualized during bone cuts or meniscectomy. The rate of overall or isolated GA injury was not significantly different (P > .05) with either use of intravenous (84 patients) or topical (14 patients) TXA administration. Comparing selective tourniquet use (only during cementation) vs routine use showed no differences in GA injury rate (P = .37), blood loss (P = .07), or drain output (P = .46).

There is a relatively high rate of GA injury, with injury to the lateral GA occurring more often than the middle GA. Routine or selective tourniquet use does not affect the rate of injury.

Continue to: Major arterial injury...

 

 

Major arterial injury associated with total knee arthroplasty (TKA) is a rare and potentially devastating complication. The majority of literature in this context consists of case reports, small case series, and large retrospective studies that have examined the type, location, and mechanism of injury present in these cases.1-13 Reported arterial injuries include occlusion, laceration, aneurysm, pseudoaneurysm, and arteriovenous fistula formation in the femoral (believed to be due to the tourniquet around the proximal thigh) and popliteal arteries causing combinations of ischemia and hemorrhage necessitating treatment ranging from endovascular arterial intervention to amputation.4,5,9-11,13-17 In addition, several studies have asserted that the risk of major arterial injury may be increased with tourniquet use, suggesting that tourniquet use should be minimized for routine primary TKAs.3,6

There are very few cases in the literature specifically addressing injury to the more commonly encountered geniculate arteries (GAs). The medial GAs are typically visualized and coagulated during the standard medial parapatellar approach. In addition, if performed, a lateral release can damage the lateral superior and inferior GAs and the middle GA can be cut with posterior cruciate ligament resection. However, the middle and lateral inferior GAs are anecdotally the most difficult to detect and treat intraoperatively, especially after implantation of TKA and deflation of the tourniquet. The potential lack of recognition of such GA injury can result in harmful sequelae, including ischemia of the patella, hemorrhage, and painful pseudoaneurysms.2,18-29 Currently, there are only 2 case reports of lateral inferior GA injury, 2 cases of medial inferior GA injury, and no reports of middle GA injury.2,23,24,29

The rate, the timing within surgery, the risk factors, including tourniquet use, and the clinical effects of GA injury are largely unknown. If these factors were better understood, prophylactic measures and/or awareness could be better applied to prevent adverse outcomes, especially in cases of the middle and lateral inferior GAs. The aims of this study are to elucidate the rate and timing of middle and lateral inferior GA injury during primary TKA; determine the factors related to injury, including intraoperative blood loss, postoperative drain output, and tranexamic (TXA) acid use; and investigate any differences in the rate of injury with and without the use of a tourniquet.

MATERIALS AND METHODS

PATIENT DEMOGRAPHICS AND SURGICAL TECHNIQUE

From November 2015 to February 2016, 3 surgeons (MJT, TMM, and RTT) at a single institution performed 100 consecutive unilateral primary TKAs and documented the presence or absence and the timing of GA injury. After obtaining approval from our Institutional Review Board, a retrospective study was performed to investigate the prospectively recorded rate of middle and lateral inferior GA injuries occurring during primary TKAs. Patients with a diagnosis of isolated osteoarthritis were included, and those with any previous surgery on the operative knee were excluded. The average age of patients at the time of surgery was 67 years (range, 25-91 years), the average body mass index was 33 kg/m2 (range, 18-54 kg/m2), and there were 63 (63%) female patients.

All TKAs were performed through a medial parapatellar approach with a posterior-stabilized, cemented design, and each patient received a postoperative surgical drain. One of the 3 lead surgeons (TMM) in this study used a tourniquet from the time of incision until the completion of cementation, and the other 2 (MJT and RTT) predominantly used the tourniquet only during cementation. To elucidate any differences in GA injury between these 2 methods of tourniquet use, the patients were categorized into 2 groups base d on tourniquet use. Group 1 included patients in whom a tourniquet was used to maintain a bloodless surgical field from the time of incision until the completion of cementation, and Group 2 included patients in whom tourniquet use was more selective (ie, applied only during cementation). Group 1 comprised 31% (31/100) of patients, while Group 2 comprised 67% (67/100) of patients; no tourniquet was used in 2% (2/100) of cases. In addition, TXA was used in 98% (98/100) of patients: 84 patients received intravenous (IV) and 14 received topical TXA administration.

Continue to: ANALYSIS OF GENICULATE ARTERY INJURY

 

 

ANALYSIS OF GENICULATE ARTERY INJURY

The senior authors critically evaluated the GA during the primary TKAs and documented the presence or absence of injury in the operative reports. GA injury was reported if there was intraoperative visualization of pulsatile bleeding or visualization of arterial lumen in the anatomic areas of the middle and lateral inferior GAs. At 3 separate occasions during the operation, the surgeon looked specifically for pulsatile bleeding or arterial lumen in the areas of the middle and lateral inferior GAs, including after all the femoral and tibial bone cuts were completed, immediately before preparing to cement (before the tourniquet was inflated if there was not one inflated from the start of the procedure), and immediately after the tourniquet was deflated (Figure 1). All bleeding GAs that were visualized were effectively coagulated by cautery. Details regarding the use of TXA (topical or IV), intraoperative blood loss, postsurgical drain output for 24 hours after surgery, and blood transfusion were collected from the patients’ medical records (Table 1).

Surgical documentation template completed by operative surgeon

 

Table 1. Operative Variables

Variable

Value

Total number

100 (100%)

Intraoperative blood loss (mL)

160 (25-500)

Drain output 1st 24 hours (mL)

488 (75-1980)

Total output (mL)

618 (75-2130)

Use of TXA

98 (98%)

Topical TXA

84 (84%)

IV TXA

14 (14%)

Tourniquet entire procedure

31 (31%)

Operative variables other than geniculate artery injury. Data presented as mean (range) or n (%). TXA = tranexamic acid.

STATISTICAL METHODS

Statistical analysis was performed using the JMP software version 10.0.0 (SAS Institute, Inc). The overall rate of GA injury was determined, including the rates of GA injury based on location, time point, and method of diagnosis (pulsatile bleeding or arterial lumen visualization). If >1 GA injury occurred in the same knee, only 1 GA injury was calculated for the overall rate; however, each injury was specified separately when calculating the injury rate for the specific GA. Intraoperative blood loss, postoperative drain output, and the use of TXA were compared between cases in which a GA injury was detected and those in which it was not detected. Before conducting the retrospective review, a power analysis determined that we would require 100 patients to detect a difference in GA injury between Groups 1 and 2 (33 in Group 1 and 67 in Group 2), assuming a 30% rate in Group 1 and a 5% rate of GA injury in Group 2 using Fisher’s exact test. The Fisher’s exact test was used to compare categorical variables, and the Wilcoxon rank sum test was used to compare continuous variables. An alpha value of .05 was considered as statistically significant.

RESULTS

RATE OF GENICULATE ARTERY INJURY

The overall rate of any GA injury was 38% (38/100). Lateral inferior GA injury was more frequently detected than middle GA injury (31% vs 15% of TKAs, respectively; Table 2). Among the 31 lateral inferior GA injuries, 14 were identified as pulsatile bleeding, 7 as lumen visualizations, and 6 as both pulsatile bleeding and lumen visualization; 4 were detected by methods not recorded in the operative report. Of the lateral inferior GA injuries, 11 were identified after the bone cuts, 7 during meniscus removal, 3 during exposure, 1 after tourniquet deflation, and 9 at a time not recorded in the operative report. Of the 15 middle GA injuries, 9 were identified as pulsatile bleeding, 2 as lumen visualizations, and 4 as both pulsatile bleeding and lumen visualization. In addition, 7 of these GA injuries were identified after the bone cuts, 3 during cruciate removal, 1 after meniscus removal, 1 during exposure, and 3 at a time not recorded in the operative report (Table 3).

 

Table 2. Rates of Geniculate Artery Injury Based on Location and Method

Location

Pulsatile Bleeding

Arterial Lumen

Both

Overall Rate

Lateral inferior GA

14 (14%)

7 (7%)

6 (6%)

31 (31%)

Middle GA

9 (9%)

2 (2%)

4 (4%)

15 (15%)

Rates of geniculate artery injury based on location and method of diagnosis. Data presented as n (%). There were 4 additional lateral inferior and 9 middle GA injuries identified by a method not specified in the operative report. GA = geniculate artery.

Table 3. Rates of Geniculate Artery Injury Based on Time Point

Time

Lateral Inferior GA

Middle GA

After bone cuts

11 (11%)

7 (7%)

During meniscus removal

7 (7%)

1 (1%)

During exposure

3 (3%)

1 (1%)

After tourniquet deflation

1 (1%)

0 (0%)

During cruciate removal

0 (0%)

3 (3%)

Not reported

9 (9%)

3 (3%)

Rates of geniculate artery injury based on time point and method of diagnosis. GA = geniculate artery. Data presented as n (%).

FACTORS ASSOCIATED WITH GENICULATE ARTERY INJURY

Mean intraoperative estimated blood loss was 186 mL (standard deviation [SD], 111; range 50–500 mL) in those with a GA injury versus 147 mL (range, 82.25–400 mL) in those without injury (P = .14). Postoperative drain output in the 24 hours after surgery was 467 mL (SD 253, range 100–1105 mL) versus 502 mL (SD 378, range 75–1980 mL) in TKAs with and without GA injury, respectively (P = .82). Total estimated blood loss (combined intraoperative blood loss and 24-hour postoperative drain output) was 613 mL (SD 252, range 150–1105 mL) in TKAs with GA injury versus 620 mL (SD 393, range 75–2130 mL) without injury (P = .44) (Table 4). Overall, there was no statistical difference in blood loss, drain output, or combined output when analyzed according to lateral inferior or middle GA injury (P = .24–.82) (Table 5 and Table 6). No patients required blood transfusion postoperatively after TKA.

 

Table 4. Factors Associated with GA Injury

Outcome

GA Injury

No GA Injury

P Value

Blood loss (mL)

186 (50-500)

147 (25-400)

.1366

24-Hour drain output (mL)

467 (100-1105)

502 (75-1980)

.8240

Total output (mL)

613 (150-1105)

620 (75-2130)

.4368

Differences in outcomes based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery.

 

Table 5. Factors Associated with LIGA Injury

Outcome

LIGA Injury

No LIGA Injury

P Value

Blood loss (mL)

178 (50-400)

153 (25-500)

.2401

24-Hour drain output (mL)

461 (100-890)

501 (75-1980)

.8187

Total output (mL)

610 (150-1080)

621 (75-2130)

.4165

Differences in outcomes based on presence or absence of LIGA injury. Note that there were no significant differences. Values are reported as average (range). LIGA = lateral inferior geniculate artery.

 

Table 6. Factors Associated with MGA Injury

Outcome

MGA Injury

No MGA Injury

P Value

Blood loss (mL)

190 (75-500)

156 (25-400)

.6225

24-Hour drain output (mL)

455 (125-1105)

494 (75-1980)

.6428

Total output (mL)

582 (200-1105)

624 (75-2130)

.6535

Differences in outcomes based on presence or absence of MGA injury. Note that there were no significant differences. Values are reported as average (range). MGA = middle geniculate artery.

IV administration of TXA was associated with a 37% (31/84) rate of GA injury, whereas topical TXA administration was associated with a 43% (6/14) rate of GA injury (P = .77). The rate of overall or isolated GA injury was not significantly different (P = .35–1.0) between IV and topical TXA administration (Table 7). In addition, total combined output was not significantly different (P = .1032) when comparing GA injury and noninjury in the subgroup analysis based on TXA use (IV or topical); however, topical administration was associated with lower intraoperative blood loss than IV administration (P = .0489), whereas IV administration was associated with lower 24-hour postoperative drain output than topical administration (P = .0169). There was no difference in blood loss, 24-hour drain output, or total output between those who did and did not sustain a GA injury in the group of patients who received IV TXA administration (Table 8, P = .2118–.7091). The same was true for those receiving topical TXA administration (Table 9, P = .0912–.9485).

Table 7. Factors Associated with TXA Injury

Outcome

IV TXA (n = 84)

Topical TXA (n = 14)

P Value

Any GA injury

31 (37%)

6 (43%)

.7683

LIGA injury

24 (29%)

6 (43%)

.3498

MGA injury

13 (15%)

2 (14%)

1.0

Blood loss (mL)

170 (25-500)

113 (40-240)

.0489*

24-Hour drain output (mL)

454 (75-1980)

662 (75-1800)

.0169*

Total output (mL)

592 (75-2130)

751 (75-2130)

.1032

Differences in outcomes based on presence or absence of MGA injury. Note that there were no significant differences. Values are reported as n (%) or average (range). TXA = tranexamic acid, GA = geniculate artery, LIGA = lateral inferior geniculate artery, MGA = middle geniculate artery. *denotes statistical significance (P < .05).

 

Table 8. Factors Associated with GA Injury Given IV TXA Use

Outcome

GA Injury

No GA Injury

Difference

P Value

Blood loss (mL)

195 (50-500)

157 (25-400)

38

.2118

24-Hour drain output (mL)

436 (100-1105)

464 (75-1980)

28

.7091

Total output (mL)

594 (150-1105)

592 (75-2130)

2

.6982

Differences in outcomes of those patients who received IV TXA based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery, TXA = tranexamic acid.

 

Table 9. Factors Associated with GA Injury Given Topical TXA Use

Outcome

GA Injury

No GA Injury

Difference

P Value

Blood loss (mL)

163 (100-250)

84 (40-150)

79

.0912

24-Hour drain output (mL)

610 (205-890)

701 (415-1800)

91

.9485

Total output (mL)

719 (405-960)

775 (455-1900)

56

.6982

Differences in outcomes based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery.

Continue to: TOURNIQUET USE

 

 

TOURNIQUET USE

Comparison between Groups 1 (tourniquet use) and 2 (selective tourniquet use) revealed similar rates of overall and specific GA injury, intraoperative blood loss, and 24-hour postoperative drain output (Table 10). Group 1 demonstrated a 29% (9/31) rate of any GA injury versus 40% (27/67) in Group 2 (P = .37). For the specific lateral inferior GA injury, there was an equivalent rate of injury at 29% (9/31 in Group 1, 20/67 in Group 2; P = 1.0). Similarly, Group 1 patients had a 10% (3/31) rate of middle GA injury compared to 16% (11/67) in Group 2 patients (P = .53). Intraoperative estimated blood loss was lower in Group 1 (140 mL; range 25–400 mL) than in Group 2 (171 mL; range 40–500 mL) (P = .07), whereas the average 24-hour postoperative drain output was similar for Groups 1 (484 mL; range 75–1800 mL) and 2 (488 mL; range 100–1980 mL) (P = .46). Total estimated output was slightly less for Group 1 (593 mL; range 75–1900 mL) than for Group 2 (626 mL; range 125–2130 mL) (P = .38). A post hoc power analysis showed that with these rates of GA injury in Groups 1 and 2 and given a 2:1 ratio of the number of patients in Group 2 versus Group 1, a total of 185 patients in Group 1 and 370 patients in Group 2 would be needed to detect a statistically significant difference (P < .05) with a power of 80%.

 

Table 10. Factors Associated with Tourniquet Use

Injury

Group 1 (n = 31)

Group 2 (n = 67)

Difference

P Value

Overall GA injury

9 (29%)

27 (40%)

11%

.3687

Lateral inferior GA

9 (29%)

20 (29%)

0%

1.0

Middle GA

3 (10%)

11 (16%)

6%

.5382

Blood loss (mL)

140 (25-400)

171 (40-500)

31

.0661

24-Hour drain output (mL)

484 (75-1800)

488 (100-1980)

4

.4580

Total output (mL)

593 (75-1900)

626 (125-2130)

33

.3776

Differences in outcomes separated based on use of a tourniquet for the entire case (Group 1) vs use of a tourniquet only during cementation (Group 2). Note that there were no significant differences. Values are reported as n (%) or average (range). GA = geniculate artery.

DISCUSSION

Major arterial injury associated with TKA is a well-known, rare, and potentially devastating complication.1-13 However, the rate of injury to smaller periarticular vessels and the clinical significance of such injury have not been studied. The present study found a high rate of GA injury but no clinically significant difference in intraoperative blood loss or postoperative drain output between patients with GA injury (which was identified and managed with cautery) and those without GA injury. In addition, tourniquet use did not affect the rate of injury or the associated blood loss. To our knowledge, this is the first study that has critically evaluated the rate of GA injury occurring during TKA.

The overall rate of GA injury occurring during primary TKA was 38% with a higher predominance of lateral inferior than middle GA injury (31% vs 15%). Anatomically, it would follow that the lateral GA could be injured at a higher rate as it courses on top of the lateral meniscus, thus being susceptible to injury during cutting of the tibial plateau and meniscectomy. In addition, because the meniscectomy is performed longitudinally along the course of the artery, it may also be potentially lacerated in multiple locations and lengthwise. In theory, there should be a 100% rate of middle GA injury during posterior-stabilized TKA as this artery runs through the cruciate ligaments, which are resected during these cases. However, vessel injury was defined in this study as the visualization of pulsatile bleeding or vessel lumen. It is probable that in the cases in which injury to the middle GA was not visualized, it was cut but simultaneously cauterized. Thus, a lower rate (15%) of injury was detected. Nonetheless, these results still suggest that these periarticular arteries are injured at a higher rate; therefore, it is important for surgeons to specifically identify these injuries intraoperatively and adequately cauterize these vessels. As long as these arteries are cauterized, additional blood loss and potential vascular pseudoaneurysms should be prevented.

The effect of GA injury on intraoperative blood loss, 24-hour postoperative drain output, and total estimated blood loss showed no significant clinical findings in the present study cohort. In addition, examining the injury rate and blood loss based on TXA use also revealed no detrimental clinical associations. Although GA injury could inherently be associated with higher levels of blood loss and drain output, it is important to note that all GA injuries were also effectively coagulated, thus explaining the indifferent results. Accordingly, it should be recommended to surgeons performing primary TKAs to carefully evaluate for GA injury to prevent excessive blood loss or painful pseudoaneurysms. However, there is also a potential for beta error in this study in which a true difference did exist but no statistical difference was found due to the study being underpowered.

Full or selective tourniquet use during TKA did not appear to have any effect on the rate of GA injury, intraoperative blood loss, or 24-hour postoperative drain output. The similarity between GA injury rates perhaps further indicates an equivalent ability to detect these injuries between these two methods because of operative inspection for such injuries. With regard to intraoperative blood loss and drain output, the present findings are similar to previous studies demonstrating equivocal results despite variable tourniquet utilization in TKA.15,30 However, these results differ from those of Harvey and colleagues31, who demonstrated that blood loss inversely correlated with intraoperative tourniquet time. There are risks and benefits related to the use of both full and selective tourniquet methods, but either method does not appear to be advantageous in decreasing the rate of GA injury.

Continue to: Although this is the first study...

 

 

Although this is the first study to investigate the rates of GA injury and the potential clinical effects, there are limitations to this research. First, the study was retrospective in nature despite the fact that the data were collected prospectively. Only acute perioperative follow-up was performed, and thus, we were unable to evaluate longer term effects of GA injury on TKA outcomes. Furthermore, this study is potentially prone to beta error. As discussed above, 185 patients in Group 1 and 370 patients in Group 2 would be needed to detect a statistical difference in the rate of GA injury based on the rates found in this study. This study could also have been underpowered to identify differences in other aspects, such as differences in blood loss and drain. Furthermore, the data collected regarding intraoperative blood loss are estimated data and can be variable. Finally, visualization of vessel lumen and pulsatile bleeding is not a validated method to diagnose GA injuries, and potential injuries may have been missed. Despite such disadvantages, the strengths of this study include the concise results in consecutive patients, the generalizability of the data as multiple surgeons participated, and its first report of nonmajor periarticular artery injury.

CONCLUSIONS

There is a relatively high rate of GA injury, with injury to the lateral GA being visualized more often than injury to the middle GA. The majority of GA injuries occur around the time of bone cuts and meniscectomy, and tourniquet use does not affect the rate of injury. To reduce intraoperative blood loss and postoperative drain output, surgeons should identify and coagulate GA injuries routinely during primary TKA.

ABSTRACT

Major arterial injury associated with total knee arthroplasty (TKA) is a rare and potentially devastating complication. However, the rate of injury to smaller periarticular vessels and the clinical significance of such an injury have not been well investigated. The purpose of this study is to describe the rate and outcomes of geniculate artery (GA) injury, the time at which injury occurs, and any associations with tourniquet use.

From November 2015 to February 2016, 3 surgeons at a single institution performed 100 consecutive primary TKAs and documented the presence or absence and the timing of GA injury. The data were then retrospectively reviewed. All TKAs had no prior surgery on the operative extremity. Other variables collected included tourniquet use, tranexamic acid (TXA) administration, intraoperative blood loss, postoperative drain output, and blood transfusion.

The overall rate of GA injury was 38%, with lateral inferior and middle GA injury in 31% and 15% of TKAs, respectively. Most of the injuries were visualized during bone cuts or meniscectomy. The rate of overall or isolated GA injury was not significantly different (P > .05) with either use of intravenous (84 patients) or topical (14 patients) TXA administration. Comparing selective tourniquet use (only during cementation) vs routine use showed no differences in GA injury rate (P = .37), blood loss (P = .07), or drain output (P = .46).

There is a relatively high rate of GA injury, with injury to the lateral GA occurring more often than the middle GA. Routine or selective tourniquet use does not affect the rate of injury.

Continue to: Major arterial injury...

 

 

Major arterial injury associated with total knee arthroplasty (TKA) is a rare and potentially devastating complication. The majority of literature in this context consists of case reports, small case series, and large retrospective studies that have examined the type, location, and mechanism of injury present in these cases.1-13 Reported arterial injuries include occlusion, laceration, aneurysm, pseudoaneurysm, and arteriovenous fistula formation in the femoral (believed to be due to the tourniquet around the proximal thigh) and popliteal arteries causing combinations of ischemia and hemorrhage necessitating treatment ranging from endovascular arterial intervention to amputation.4,5,9-11,13-17 In addition, several studies have asserted that the risk of major arterial injury may be increased with tourniquet use, suggesting that tourniquet use should be minimized for routine primary TKAs.3,6

There are very few cases in the literature specifically addressing injury to the more commonly encountered geniculate arteries (GAs). The medial GAs are typically visualized and coagulated during the standard medial parapatellar approach. In addition, if performed, a lateral release can damage the lateral superior and inferior GAs and the middle GA can be cut with posterior cruciate ligament resection. However, the middle and lateral inferior GAs are anecdotally the most difficult to detect and treat intraoperatively, especially after implantation of TKA and deflation of the tourniquet. The potential lack of recognition of such GA injury can result in harmful sequelae, including ischemia of the patella, hemorrhage, and painful pseudoaneurysms.2,18-29 Currently, there are only 2 case reports of lateral inferior GA injury, 2 cases of medial inferior GA injury, and no reports of middle GA injury.2,23,24,29

The rate, the timing within surgery, the risk factors, including tourniquet use, and the clinical effects of GA injury are largely unknown. If these factors were better understood, prophylactic measures and/or awareness could be better applied to prevent adverse outcomes, especially in cases of the middle and lateral inferior GAs. The aims of this study are to elucidate the rate and timing of middle and lateral inferior GA injury during primary TKA; determine the factors related to injury, including intraoperative blood loss, postoperative drain output, and tranexamic (TXA) acid use; and investigate any differences in the rate of injury with and without the use of a tourniquet.

MATERIALS AND METHODS

PATIENT DEMOGRAPHICS AND SURGICAL TECHNIQUE

From November 2015 to February 2016, 3 surgeons (MJT, TMM, and RTT) at a single institution performed 100 consecutive unilateral primary TKAs and documented the presence or absence and the timing of GA injury. After obtaining approval from our Institutional Review Board, a retrospective study was performed to investigate the prospectively recorded rate of middle and lateral inferior GA injuries occurring during primary TKAs. Patients with a diagnosis of isolated osteoarthritis were included, and those with any previous surgery on the operative knee were excluded. The average age of patients at the time of surgery was 67 years (range, 25-91 years), the average body mass index was 33 kg/m2 (range, 18-54 kg/m2), and there were 63 (63%) female patients.

All TKAs were performed through a medial parapatellar approach with a posterior-stabilized, cemented design, and each patient received a postoperative surgical drain. One of the 3 lead surgeons (TMM) in this study used a tourniquet from the time of incision until the completion of cementation, and the other 2 (MJT and RTT) predominantly used the tourniquet only during cementation. To elucidate any differences in GA injury between these 2 methods of tourniquet use, the patients were categorized into 2 groups base d on tourniquet use. Group 1 included patients in whom a tourniquet was used to maintain a bloodless surgical field from the time of incision until the completion of cementation, and Group 2 included patients in whom tourniquet use was more selective (ie, applied only during cementation). Group 1 comprised 31% (31/100) of patients, while Group 2 comprised 67% (67/100) of patients; no tourniquet was used in 2% (2/100) of cases. In addition, TXA was used in 98% (98/100) of patients: 84 patients received intravenous (IV) and 14 received topical TXA administration.

Continue to: ANALYSIS OF GENICULATE ARTERY INJURY

 

 

ANALYSIS OF GENICULATE ARTERY INJURY

The senior authors critically evaluated the GA during the primary TKAs and documented the presence or absence of injury in the operative reports. GA injury was reported if there was intraoperative visualization of pulsatile bleeding or visualization of arterial lumen in the anatomic areas of the middle and lateral inferior GAs. At 3 separate occasions during the operation, the surgeon looked specifically for pulsatile bleeding or arterial lumen in the areas of the middle and lateral inferior GAs, including after all the femoral and tibial bone cuts were completed, immediately before preparing to cement (before the tourniquet was inflated if there was not one inflated from the start of the procedure), and immediately after the tourniquet was deflated (Figure 1). All bleeding GAs that were visualized were effectively coagulated by cautery. Details regarding the use of TXA (topical or IV), intraoperative blood loss, postsurgical drain output for 24 hours after surgery, and blood transfusion were collected from the patients’ medical records (Table 1).

Surgical documentation template completed by operative surgeon

 

Table 1. Operative Variables

Variable

Value

Total number

100 (100%)

Intraoperative blood loss (mL)

160 (25-500)

Drain output 1st 24 hours (mL)

488 (75-1980)

Total output (mL)

618 (75-2130)

Use of TXA

98 (98%)

Topical TXA

84 (84%)

IV TXA

14 (14%)

Tourniquet entire procedure

31 (31%)

Operative variables other than geniculate artery injury. Data presented as mean (range) or n (%). TXA = tranexamic acid.

STATISTICAL METHODS

Statistical analysis was performed using the JMP software version 10.0.0 (SAS Institute, Inc). The overall rate of GA injury was determined, including the rates of GA injury based on location, time point, and method of diagnosis (pulsatile bleeding or arterial lumen visualization). If >1 GA injury occurred in the same knee, only 1 GA injury was calculated for the overall rate; however, each injury was specified separately when calculating the injury rate for the specific GA. Intraoperative blood loss, postoperative drain output, and the use of TXA were compared between cases in which a GA injury was detected and those in which it was not detected. Before conducting the retrospective review, a power analysis determined that we would require 100 patients to detect a difference in GA injury between Groups 1 and 2 (33 in Group 1 and 67 in Group 2), assuming a 30% rate in Group 1 and a 5% rate of GA injury in Group 2 using Fisher’s exact test. The Fisher’s exact test was used to compare categorical variables, and the Wilcoxon rank sum test was used to compare continuous variables. An alpha value of .05 was considered as statistically significant.

RESULTS

RATE OF GENICULATE ARTERY INJURY

The overall rate of any GA injury was 38% (38/100). Lateral inferior GA injury was more frequently detected than middle GA injury (31% vs 15% of TKAs, respectively; Table 2). Among the 31 lateral inferior GA injuries, 14 were identified as pulsatile bleeding, 7 as lumen visualizations, and 6 as both pulsatile bleeding and lumen visualization; 4 were detected by methods not recorded in the operative report. Of the lateral inferior GA injuries, 11 were identified after the bone cuts, 7 during meniscus removal, 3 during exposure, 1 after tourniquet deflation, and 9 at a time not recorded in the operative report. Of the 15 middle GA injuries, 9 were identified as pulsatile bleeding, 2 as lumen visualizations, and 4 as both pulsatile bleeding and lumen visualization. In addition, 7 of these GA injuries were identified after the bone cuts, 3 during cruciate removal, 1 after meniscus removal, 1 during exposure, and 3 at a time not recorded in the operative report (Table 3).

 

Table 2. Rates of Geniculate Artery Injury Based on Location and Method

Location

Pulsatile Bleeding

Arterial Lumen

Both

Overall Rate

Lateral inferior GA

14 (14%)

7 (7%)

6 (6%)

31 (31%)

Middle GA

9 (9%)

2 (2%)

4 (4%)

15 (15%)

Rates of geniculate artery injury based on location and method of diagnosis. Data presented as n (%). There were 4 additional lateral inferior and 9 middle GA injuries identified by a method not specified in the operative report. GA = geniculate artery.

Table 3. Rates of Geniculate Artery Injury Based on Time Point

Time

Lateral Inferior GA

Middle GA

After bone cuts

11 (11%)

7 (7%)

During meniscus removal

7 (7%)

1 (1%)

During exposure

3 (3%)

1 (1%)

After tourniquet deflation

1 (1%)

0 (0%)

During cruciate removal

0 (0%)

3 (3%)

Not reported

9 (9%)

3 (3%)

Rates of geniculate artery injury based on time point and method of diagnosis. GA = geniculate artery. Data presented as n (%).

FACTORS ASSOCIATED WITH GENICULATE ARTERY INJURY

Mean intraoperative estimated blood loss was 186 mL (standard deviation [SD], 111; range 50–500 mL) in those with a GA injury versus 147 mL (range, 82.25–400 mL) in those without injury (P = .14). Postoperative drain output in the 24 hours after surgery was 467 mL (SD 253, range 100–1105 mL) versus 502 mL (SD 378, range 75–1980 mL) in TKAs with and without GA injury, respectively (P = .82). Total estimated blood loss (combined intraoperative blood loss and 24-hour postoperative drain output) was 613 mL (SD 252, range 150–1105 mL) in TKAs with GA injury versus 620 mL (SD 393, range 75–2130 mL) without injury (P = .44) (Table 4). Overall, there was no statistical difference in blood loss, drain output, or combined output when analyzed according to lateral inferior or middle GA injury (P = .24–.82) (Table 5 and Table 6). No patients required blood transfusion postoperatively after TKA.

 

Table 4. Factors Associated with GA Injury

Outcome

GA Injury

No GA Injury

P Value

Blood loss (mL)

186 (50-500)

147 (25-400)

.1366

24-Hour drain output (mL)

467 (100-1105)

502 (75-1980)

.8240

Total output (mL)

613 (150-1105)

620 (75-2130)

.4368

Differences in outcomes based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery.

 

Table 5. Factors Associated with LIGA Injury

Outcome

LIGA Injury

No LIGA Injury

P Value

Blood loss (mL)

178 (50-400)

153 (25-500)

.2401

24-Hour drain output (mL)

461 (100-890)

501 (75-1980)

.8187

Total output (mL)

610 (150-1080)

621 (75-2130)

.4165

Differences in outcomes based on presence or absence of LIGA injury. Note that there were no significant differences. Values are reported as average (range). LIGA = lateral inferior geniculate artery.

 

Table 6. Factors Associated with MGA Injury

Outcome

MGA Injury

No MGA Injury

P Value

Blood loss (mL)

190 (75-500)

156 (25-400)

.6225

24-Hour drain output (mL)

455 (125-1105)

494 (75-1980)

.6428

Total output (mL)

582 (200-1105)

624 (75-2130)

.6535

Differences in outcomes based on presence or absence of MGA injury. Note that there were no significant differences. Values are reported as average (range). MGA = middle geniculate artery.

IV administration of TXA was associated with a 37% (31/84) rate of GA injury, whereas topical TXA administration was associated with a 43% (6/14) rate of GA injury (P = .77). The rate of overall or isolated GA injury was not significantly different (P = .35–1.0) between IV and topical TXA administration (Table 7). In addition, total combined output was not significantly different (P = .1032) when comparing GA injury and noninjury in the subgroup analysis based on TXA use (IV or topical); however, topical administration was associated with lower intraoperative blood loss than IV administration (P = .0489), whereas IV administration was associated with lower 24-hour postoperative drain output than topical administration (P = .0169). There was no difference in blood loss, 24-hour drain output, or total output between those who did and did not sustain a GA injury in the group of patients who received IV TXA administration (Table 8, P = .2118–.7091). The same was true for those receiving topical TXA administration (Table 9, P = .0912–.9485).

Table 7. Factors Associated with TXA Injury

Outcome

IV TXA (n = 84)

Topical TXA (n = 14)

P Value

Any GA injury

31 (37%)

6 (43%)

.7683

LIGA injury

24 (29%)

6 (43%)

.3498

MGA injury

13 (15%)

2 (14%)

1.0

Blood loss (mL)

170 (25-500)

113 (40-240)

.0489*

24-Hour drain output (mL)

454 (75-1980)

662 (75-1800)

.0169*

Total output (mL)

592 (75-2130)

751 (75-2130)

.1032

Differences in outcomes based on presence or absence of MGA injury. Note that there were no significant differences. Values are reported as n (%) or average (range). TXA = tranexamic acid, GA = geniculate artery, LIGA = lateral inferior geniculate artery, MGA = middle geniculate artery. *denotes statistical significance (P < .05).

 

Table 8. Factors Associated with GA Injury Given IV TXA Use

Outcome

GA Injury

No GA Injury

Difference

P Value

Blood loss (mL)

195 (50-500)

157 (25-400)

38

.2118

24-Hour drain output (mL)

436 (100-1105)

464 (75-1980)

28

.7091

Total output (mL)

594 (150-1105)

592 (75-2130)

2

.6982

Differences in outcomes of those patients who received IV TXA based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery, TXA = tranexamic acid.

 

Table 9. Factors Associated with GA Injury Given Topical TXA Use

Outcome

GA Injury

No GA Injury

Difference

P Value

Blood loss (mL)

163 (100-250)

84 (40-150)

79

.0912

24-Hour drain output (mL)

610 (205-890)

701 (415-1800)

91

.9485

Total output (mL)

719 (405-960)

775 (455-1900)

56

.6982

Differences in outcomes based on presence or absence of GA injury. Note that there were no significant differences. Values are reported as average (range). GA = geniculate artery.

Continue to: TOURNIQUET USE

 

 

TOURNIQUET USE

Comparison between Groups 1 (tourniquet use) and 2 (selective tourniquet use) revealed similar rates of overall and specific GA injury, intraoperative blood loss, and 24-hour postoperative drain output (Table 10). Group 1 demonstrated a 29% (9/31) rate of any GA injury versus 40% (27/67) in Group 2 (P = .37). For the specific lateral inferior GA injury, there was an equivalent rate of injury at 29% (9/31 in Group 1, 20/67 in Group 2; P = 1.0). Similarly, Group 1 patients had a 10% (3/31) rate of middle GA injury compared to 16% (11/67) in Group 2 patients (P = .53). Intraoperative estimated blood loss was lower in Group 1 (140 mL; range 25–400 mL) than in Group 2 (171 mL; range 40–500 mL) (P = .07), whereas the average 24-hour postoperative drain output was similar for Groups 1 (484 mL; range 75–1800 mL) and 2 (488 mL; range 100–1980 mL) (P = .46). Total estimated output was slightly less for Group 1 (593 mL; range 75–1900 mL) than for Group 2 (626 mL; range 125–2130 mL) (P = .38). A post hoc power analysis showed that with these rates of GA injury in Groups 1 and 2 and given a 2:1 ratio of the number of patients in Group 2 versus Group 1, a total of 185 patients in Group 1 and 370 patients in Group 2 would be needed to detect a statistically significant difference (P < .05) with a power of 80%.

 

Table 10. Factors Associated with Tourniquet Use

Injury

Group 1 (n = 31)

Group 2 (n = 67)

Difference

P Value

Overall GA injury

9 (29%)

27 (40%)

11%

.3687

Lateral inferior GA

9 (29%)

20 (29%)

0%

1.0

Middle GA

3 (10%)

11 (16%)

6%

.5382

Blood loss (mL)

140 (25-400)

171 (40-500)

31

.0661

24-Hour drain output (mL)

484 (75-1800)

488 (100-1980)

4

.4580

Total output (mL)

593 (75-1900)

626 (125-2130)

33

.3776

Differences in outcomes separated based on use of a tourniquet for the entire case (Group 1) vs use of a tourniquet only during cementation (Group 2). Note that there were no significant differences. Values are reported as n (%) or average (range). GA = geniculate artery.

DISCUSSION

Major arterial injury associated with TKA is a well-known, rare, and potentially devastating complication.1-13 However, the rate of injury to smaller periarticular vessels and the clinical significance of such injury have not been studied. The present study found a high rate of GA injury but no clinically significant difference in intraoperative blood loss or postoperative drain output between patients with GA injury (which was identified and managed with cautery) and those without GA injury. In addition, tourniquet use did not affect the rate of injury or the associated blood loss. To our knowledge, this is the first study that has critically evaluated the rate of GA injury occurring during TKA.

The overall rate of GA injury occurring during primary TKA was 38% with a higher predominance of lateral inferior than middle GA injury (31% vs 15%). Anatomically, it would follow that the lateral GA could be injured at a higher rate as it courses on top of the lateral meniscus, thus being susceptible to injury during cutting of the tibial plateau and meniscectomy. In addition, because the meniscectomy is performed longitudinally along the course of the artery, it may also be potentially lacerated in multiple locations and lengthwise. In theory, there should be a 100% rate of middle GA injury during posterior-stabilized TKA as this artery runs through the cruciate ligaments, which are resected during these cases. However, vessel injury was defined in this study as the visualization of pulsatile bleeding or vessel lumen. It is probable that in the cases in which injury to the middle GA was not visualized, it was cut but simultaneously cauterized. Thus, a lower rate (15%) of injury was detected. Nonetheless, these results still suggest that these periarticular arteries are injured at a higher rate; therefore, it is important for surgeons to specifically identify these injuries intraoperatively and adequately cauterize these vessels. As long as these arteries are cauterized, additional blood loss and potential vascular pseudoaneurysms should be prevented.

The effect of GA injury on intraoperative blood loss, 24-hour postoperative drain output, and total estimated blood loss showed no significant clinical findings in the present study cohort. In addition, examining the injury rate and blood loss based on TXA use also revealed no detrimental clinical associations. Although GA injury could inherently be associated with higher levels of blood loss and drain output, it is important to note that all GA injuries were also effectively coagulated, thus explaining the indifferent results. Accordingly, it should be recommended to surgeons performing primary TKAs to carefully evaluate for GA injury to prevent excessive blood loss or painful pseudoaneurysms. However, there is also a potential for beta error in this study in which a true difference did exist but no statistical difference was found due to the study being underpowered.

Full or selective tourniquet use during TKA did not appear to have any effect on the rate of GA injury, intraoperative blood loss, or 24-hour postoperative drain output. The similarity between GA injury rates perhaps further indicates an equivalent ability to detect these injuries between these two methods because of operative inspection for such injuries. With regard to intraoperative blood loss and drain output, the present findings are similar to previous studies demonstrating equivocal results despite variable tourniquet utilization in TKA.15,30 However, these results differ from those of Harvey and colleagues31, who demonstrated that blood loss inversely correlated with intraoperative tourniquet time. There are risks and benefits related to the use of both full and selective tourniquet methods, but either method does not appear to be advantageous in decreasing the rate of GA injury.

Continue to: Although this is the first study...

 

 

Although this is the first study to investigate the rates of GA injury and the potential clinical effects, there are limitations to this research. First, the study was retrospective in nature despite the fact that the data were collected prospectively. Only acute perioperative follow-up was performed, and thus, we were unable to evaluate longer term effects of GA injury on TKA outcomes. Furthermore, this study is potentially prone to beta error. As discussed above, 185 patients in Group 1 and 370 patients in Group 2 would be needed to detect a statistical difference in the rate of GA injury based on the rates found in this study. This study could also have been underpowered to identify differences in other aspects, such as differences in blood loss and drain. Furthermore, the data collected regarding intraoperative blood loss are estimated data and can be variable. Finally, visualization of vessel lumen and pulsatile bleeding is not a validated method to diagnose GA injuries, and potential injuries may have been missed. Despite such disadvantages, the strengths of this study include the concise results in consecutive patients, the generalizability of the data as multiple surgeons participated, and its first report of nonmajor periarticular artery injury.

CONCLUSIONS

There is a relatively high rate of GA injury, with injury to the lateral GA being visualized more often than injury to the middle GA. The majority of GA injuries occur around the time of bone cuts and meniscectomy, and tourniquet use does not affect the rate of injury. To reduce intraoperative blood loss and postoperative drain output, surgeons should identify and coagulate GA injuries routinely during primary TKA.

References

1. Calligaro KD, Dougherty MJ, Ryan S, Booth RE. Acute arterial complications associated with total hip and knee arthroplasty. J Vasc Surg. 2003;38(6):1170-1177. doi: 10.1016/S0741-5214(03)00918-2.

2. Dennis DA, Neumann RD, Toma P, Rosenberg G, Mallory TH. Arteriovenous fistula with false aneurysm of the inferior medial geniculate artery. A complication of total knee arthroplasty. Clin Orthop Relat Res. 1987(222):255-260.

3. Hagan PF, Kaufman EE. Vascular complication of knee arthroplasty under tourniquet. A case report. Clin Orthop Relat Res. 1990(257):159-161.

4. Holmberg A, Milbrink J, Bergqvist D. Arterial complications after knee arthroplasty: 4 cases and a review of the literature. Acta Orthop Scand. 1996;67(1):75-78. doi: 10.3109/17453679608995616.

5. Hozack WJ, Cole PA, Gardner R, Corces A. Popliteal aneurysm after total knee arthroplasty. Case reports and review of the literature. J Arthroplasty. 1990;5(4):301-305. doi: 10.1016/S0883-5403(08)80087-3.

6. Jeyaseelan S, Stevenson TM, Pfitzner J. Tourniquet failure and arterial calcification. Case report and theoretical dangers. Anaesthesia. 1981;36(1):48-50. doi: 10.1111/j.1365-2044.1981.tb08599.x

7. Mureebe L, Gahtan V, Kahn MB, Kerstein MD, Roberts AB. Popliteal artery injury after total knee arthroplasty. Am Surg. 1996;62(5):366-368.

8. O'Connor JV, Stocks G, Crabtree JD, Jr., Galasso P, Wallsh E. Popliteal pseudoaneurysm following total knee arthroplasty. J Arthroplasty. 1998;13(7):830-832. doi: 10.1016/S0883-5403(98)90039-0.

9. Ohira T, Fujimoto T, Taniwaki K. Acute popliteal artery occlusion after total knee arthroplasty. Arch Orthop Trauma Surg. 1997;116(6-7):429-430. doi: 10.1007/BF00434007.

10. Parfenchuck TA, Young TR. Intraoperative arterial occlusion in total joint arthroplasty. J Arthroplasty. 1994;9(2):217-220. doi: 10.1016/0883-5403(94)90071-X.

11. Rush JH, Vidovich JD, Johnson MA. Arterial complications of total knee replacement. The Australian experience. J Bone Joint Surg Br. 1987;69(3):400-402. doi: 10.1302/0301-620X.69B3.3584193.

12. Smith DE, McGraw RW, Taylor DC, Masri BA. Arterial complications and total knee arthroplasty. J Am Acad Orthop Surg. 2001;9(4):253-257.

13. Zahrani HA, Cuschieri RJ. Vascular complications after total knee replacement. J Cardiovasc Surg (Torino). 1989;30(6):951-952.

14. Isiklar ZU, Landon GC, Tullos HS. Amputation after failed total knee arthroplasty. Clin Orthop Relat Res. 1994(299):173-178.

15. Wakankar HM, Nicholl JE, Koka R, D'Arcy JC. The tourniquet in total knee arthroplasty. A prospective, randomised study. J Bone Joint Surg Br. 1999;81(1):30-33. doi: 10.1302/0301-620X.81B1.0810030.

16. Kumar SN, Chapman JA, Rawlins I. Vascular injuries in total knee arthroplasty. A review of the problem with special reference to the possible effects of the tourniquet. J Arthroplasty. 1998;13(2):211-216. doi: 10.1016/S0883-5403(98)90102-4.

17. DeLaurentis DA, Levitsky KA, Booth RE, et al. Arterial and ischemic aspects of total knee arthroplasty. Am J Surg. 1992;164(3):237-240. doi: 10.1016/S0002-9610(05)81078-5.

18. Langkamer VG. Local vascular complications after knee replacement: a review with illustrative case reports. Knee. 2001;8(4):259-264. doi: 10.1016/S0968-0160(01)00103-X.

19. Moran M, Hodgkinson J, Tait W. False aneurysm of the superior lateral geniculate artery following Total Knee Replacement. Knee. 2002;9(4):349-351. doi: 10.1016/S0968-0160(02)00061-3.

20. Pritsch T, Parnes N, Menachem A. A bleeding pseudoaneurysm of the lateral genicular artery after total knee arthroplasty--a case report. Acta Orthop. 2005;76(1):138-140. doi: 10.1080/00016470510030463.

21. Gaheer RS, Chirputkar K, Sarungi M. Spontaneous resolution of superior medial geniculate artery pseudoaneurysm following total knee arthroplasty. Knee. 2014;21(2):586-588. doi: 10.1016/j.knee.2012.10.021.

22. Law KY, Cheung KW, Chiu KH, Antonio GE. Pseudoaneurysm of the geniculate artery following total knee arthroplasty: a report of two cases. J Orthop Surg (Hong Kong). 2007;15(3):386-389. /doi: 10.1177/230949900701500331.

23. Noorpuri BS, Maxwell-Armstrong CA, Lamerton AJ. Pseudo-aneurysm of a geniculate collateral artery complicating total knee replacement. Eur J Vasc Endovasc Surg. 1999;18(6):534-535.

24. Pai VS. Traumatic aneurysm of the inferior lateral geniculate artery after total knee replacement. J Arthroplasty. 1999;14(5):633-634. doi: 10.1016/S0883-5403(99)90089-X.

25. Julien TP, Gravereaux E, Martin S. Superior medial geniculate artery pseudoaneurysm after primary total knee arthroplasty. J Arthroplasty. 2012;27(2):323 e313-326. doi: 10.1016/j.arth.2011.02.009.

26. Kalsi PS, Carrington RJ, Skinner JS. Therapeutic embolization for the treatment of recurrent hemarthrosis after total knee arthroplasty due to an arteriovenous fistula. J Arthroplasty. 2007;22(8):1223-1225. /doi: 10.1016/j.arth.2006.11.012.

27. Ritter MA, Herbst SA, Keating EM, Faris PM, Meding JB. Patellofemoral complications following total knee arthroplasty. Effect of a lateral release and sacrifice of the superior lateral geniculate artery. J Arthroplasty. 1996;11(4):368-372. doi: 10.1016/S0883-5403(96)80024-6.

28. Aldrich D, Anschuetz R, LoPresti C, Fumich M, Pitluk H, O'Brien W. Pseudoaneurysm complicating knee arthroscopy. Arthroscopy. 1995;11(2):229-230. doi: 10.1016/0749-8063(95)90073-X.

29. Sharma H, Singh GK, Cavanagh SP, Kay D. Pseudoaneurysm of the inferior medial geniculate artery following primary total knee arthroplasty: delayed presentation with recurrent haemorrhagic episodes. Knee Surg Sports Traumatol Arthrosc. 2006;14(2):153-155. doi: 10.1007/s00167-005-0639-4.

30. Abdel-Salam A, Eyres KS. Effects of tourniquet during total knee arthroplasty. A prospective randomised study. J Bone Joint Surg Br. 1995;77(2):250-253. doi: 10.1302/0301-620X.77B2.7706340.

31. Harvey EJ, Leclerc J, Brooks CE, Burke DL. Effect of tourniquet use on blood loss and incidence of deep vein thrombosis in total knee arthroplasty. J Arthroplasty. 1997;12(3):291-296. doi: 10.1016/S0883-5403(97)90025-5.

References

1. Calligaro KD, Dougherty MJ, Ryan S, Booth RE. Acute arterial complications associated with total hip and knee arthroplasty. J Vasc Surg. 2003;38(6):1170-1177. doi: 10.1016/S0741-5214(03)00918-2.

2. Dennis DA, Neumann RD, Toma P, Rosenberg G, Mallory TH. Arteriovenous fistula with false aneurysm of the inferior medial geniculate artery. A complication of total knee arthroplasty. Clin Orthop Relat Res. 1987(222):255-260.

3. Hagan PF, Kaufman EE. Vascular complication of knee arthroplasty under tourniquet. A case report. Clin Orthop Relat Res. 1990(257):159-161.

4. Holmberg A, Milbrink J, Bergqvist D. Arterial complications after knee arthroplasty: 4 cases and a review of the literature. Acta Orthop Scand. 1996;67(1):75-78. doi: 10.3109/17453679608995616.

5. Hozack WJ, Cole PA, Gardner R, Corces A. Popliteal aneurysm after total knee arthroplasty. Case reports and review of the literature. J Arthroplasty. 1990;5(4):301-305. doi: 10.1016/S0883-5403(08)80087-3.

6. Jeyaseelan S, Stevenson TM, Pfitzner J. Tourniquet failure and arterial calcification. Case report and theoretical dangers. Anaesthesia. 1981;36(1):48-50. doi: 10.1111/j.1365-2044.1981.tb08599.x

7. Mureebe L, Gahtan V, Kahn MB, Kerstein MD, Roberts AB. Popliteal artery injury after total knee arthroplasty. Am Surg. 1996;62(5):366-368.

8. O'Connor JV, Stocks G, Crabtree JD, Jr., Galasso P, Wallsh E. Popliteal pseudoaneurysm following total knee arthroplasty. J Arthroplasty. 1998;13(7):830-832. doi: 10.1016/S0883-5403(98)90039-0.

9. Ohira T, Fujimoto T, Taniwaki K. Acute popliteal artery occlusion after total knee arthroplasty. Arch Orthop Trauma Surg. 1997;116(6-7):429-430. doi: 10.1007/BF00434007.

10. Parfenchuck TA, Young TR. Intraoperative arterial occlusion in total joint arthroplasty. J Arthroplasty. 1994;9(2):217-220. doi: 10.1016/0883-5403(94)90071-X.

11. Rush JH, Vidovich JD, Johnson MA. Arterial complications of total knee replacement. The Australian experience. J Bone Joint Surg Br. 1987;69(3):400-402. doi: 10.1302/0301-620X.69B3.3584193.

12. Smith DE, McGraw RW, Taylor DC, Masri BA. Arterial complications and total knee arthroplasty. J Am Acad Orthop Surg. 2001;9(4):253-257.

13. Zahrani HA, Cuschieri RJ. Vascular complications after total knee replacement. J Cardiovasc Surg (Torino). 1989;30(6):951-952.

14. Isiklar ZU, Landon GC, Tullos HS. Amputation after failed total knee arthroplasty. Clin Orthop Relat Res. 1994(299):173-178.

15. Wakankar HM, Nicholl JE, Koka R, D'Arcy JC. The tourniquet in total knee arthroplasty. A prospective, randomised study. J Bone Joint Surg Br. 1999;81(1):30-33. doi: 10.1302/0301-620X.81B1.0810030.

16. Kumar SN, Chapman JA, Rawlins I. Vascular injuries in total knee arthroplasty. A review of the problem with special reference to the possible effects of the tourniquet. J Arthroplasty. 1998;13(2):211-216. doi: 10.1016/S0883-5403(98)90102-4.

17. DeLaurentis DA, Levitsky KA, Booth RE, et al. Arterial and ischemic aspects of total knee arthroplasty. Am J Surg. 1992;164(3):237-240. doi: 10.1016/S0002-9610(05)81078-5.

18. Langkamer VG. Local vascular complications after knee replacement: a review with illustrative case reports. Knee. 2001;8(4):259-264. doi: 10.1016/S0968-0160(01)00103-X.

19. Moran M, Hodgkinson J, Tait W. False aneurysm of the superior lateral geniculate artery following Total Knee Replacement. Knee. 2002;9(4):349-351. doi: 10.1016/S0968-0160(02)00061-3.

20. Pritsch T, Parnes N, Menachem A. A bleeding pseudoaneurysm of the lateral genicular artery after total knee arthroplasty--a case report. Acta Orthop. 2005;76(1):138-140. doi: 10.1080/00016470510030463.

21. Gaheer RS, Chirputkar K, Sarungi M. Spontaneous resolution of superior medial geniculate artery pseudoaneurysm following total knee arthroplasty. Knee. 2014;21(2):586-588. doi: 10.1016/j.knee.2012.10.021.

22. Law KY, Cheung KW, Chiu KH, Antonio GE. Pseudoaneurysm of the geniculate artery following total knee arthroplasty: a report of two cases. J Orthop Surg (Hong Kong). 2007;15(3):386-389. /doi: 10.1177/230949900701500331.

23. Noorpuri BS, Maxwell-Armstrong CA, Lamerton AJ. Pseudo-aneurysm of a geniculate collateral artery complicating total knee replacement. Eur J Vasc Endovasc Surg. 1999;18(6):534-535.

24. Pai VS. Traumatic aneurysm of the inferior lateral geniculate artery after total knee replacement. J Arthroplasty. 1999;14(5):633-634. doi: 10.1016/S0883-5403(99)90089-X.

25. Julien TP, Gravereaux E, Martin S. Superior medial geniculate artery pseudoaneurysm after primary total knee arthroplasty. J Arthroplasty. 2012;27(2):323 e313-326. doi: 10.1016/j.arth.2011.02.009.

26. Kalsi PS, Carrington RJ, Skinner JS. Therapeutic embolization for the treatment of recurrent hemarthrosis after total knee arthroplasty due to an arteriovenous fistula. J Arthroplasty. 2007;22(8):1223-1225. /doi: 10.1016/j.arth.2006.11.012.

27. Ritter MA, Herbst SA, Keating EM, Faris PM, Meding JB. Patellofemoral complications following total knee arthroplasty. Effect of a lateral release and sacrifice of the superior lateral geniculate artery. J Arthroplasty. 1996;11(4):368-372. doi: 10.1016/S0883-5403(96)80024-6.

28. Aldrich D, Anschuetz R, LoPresti C, Fumich M, Pitluk H, O'Brien W. Pseudoaneurysm complicating knee arthroscopy. Arthroscopy. 1995;11(2):229-230. doi: 10.1016/0749-8063(95)90073-X.

29. Sharma H, Singh GK, Cavanagh SP, Kay D. Pseudoaneurysm of the inferior medial geniculate artery following primary total knee arthroplasty: delayed presentation with recurrent haemorrhagic episodes. Knee Surg Sports Traumatol Arthrosc. 2006;14(2):153-155. doi: 10.1007/s00167-005-0639-4.

30. Abdel-Salam A, Eyres KS. Effects of tourniquet during total knee arthroplasty. A prospective randomised study. J Bone Joint Surg Br. 1995;77(2):250-253. doi: 10.1302/0301-620X.77B2.7706340.

31. Harvey EJ, Leclerc J, Brooks CE, Burke DL. Effect of tourniquet use on blood loss and incidence of deep vein thrombosis in total knee arthroplasty. J Arthroplasty. 1997;12(3):291-296. doi: 10.1016/S0883-5403(97)90025-5.

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  • During total knee arthroscopy (TKA), 38% of patients will have an injury of a geniculate artery.
  • The lateral inferior geniculate artery is most commonly injured, with a rate of injury of 31%.
  • The middle geniculate artery is injured 15% of the time.
  • The most common time of geniculate artery injury is during bone cutting or removal of the meniscus.
  • There is no difference in rate of geniculate artery injury identification with or without the use of a tourniquet.
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Knee Injuries in Elite Level Soccer Players

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ABSTRACT

As one of the most popular sports in the world, soccer injury rates involving the knee continue to rise. An alarming trend of knee injuries, including increased anterior cruciate ligament ruptures, underscores the need to review our current understanding of these injuries in soccer players. This article includes a critical review of the epidemiology of knee injuries in soccer, anterior cruciate ligament and other ligamentous injuries, cartilage and meniscal injury, post-traumatic osteoarthritis, as well as current prevention initiatives.

Continue to: EPIDEMIOLOGY...

 

 

EPIDEMIOLOGY

There are currently 28 players on each of the Major League Soccer (MLS) teams, and during the 2013 to 2014 academic year, the National Federation of State High School Associations (NFHS) reported that 417,419 boys and 374,564 girls played high school soccer and the National Collegiate Athletic Association (NCAA) reported that 23,602 males and 26,358 females played collegiate soccer.5 As such, knee injuries in this population are a major concern for those involved in sports medicine. Several injuries occurring during soccer involve the lower extremity, particularly the knee.1 In fact, multiple reports estimate that up to 17.6% of soccer-related injuries presenting to the emergency room involved the knee.1,6-9 The majority of these injuries are noncontact injuries, although contact injuries do still occur.10,11

Risk factors for injuries in soccer may be non-modifiable (such as age and gender) and modifiable (such as level of conditioning, force, balance, and flexibility). Inadequate lower motor coordination may result in injury in the adolescent population, and advanced age >28 years in males and >25 years in females is considered as a high-risk factor for injury.12,13 Importantly, gender and age have been reported to play a significant role as risk factors for ACL injury.6 In fact, female players have a 3 to 5 times higher risk of significant knee injury, including ACL injuries, than male players.4,14-16 Preventative programs such as the FIFA 11+ program have been set forth to augment conditioning as part of managing the modifiable risk factors.

Like American football, playing on artificial turf has been questioned as a contributor to injury compared to playing on natural grass.17,18 In recent years, newer generations of artificial turf have been developed to more closely replicate the characteristics of natural grass. Meyers19 compared the incidence, mechanisms, and severity of match-related collegiate men’s soccer injuries on artificial turf and those on natural grass and demonstrated no significant difference in knee injuries between the 2 surfaces. This finding was consistent with previous studies that reported no difference in the incidence of knee injuries on either surface in women’s collegiate and elite-level soccer.15,20,21

Continue to: ACL INJURIES...

 

 

ACL INJURIES

ACL injuries are life-changing events that can significantly affect the career of a soccer athlete. As a major stabilizer of the knee, the ACL primarily prevents anterior tibial translation with the anteromedial bundle and secondarily resists tibial rotation with the posterolateral bundle. The ligament takes origin from the posteromedial aspect of the lateral femoral condyle and inserts anterior to the tibial intercondylar eminence. Grading of ACL injuries is based on the Lachman test, which is performed between 20°and 30° of knee flexion and measures the amount of anterior tibial translation relative to the femur (A = firm endpoint, B = no endpoint; grade I: 3-5 mm, grade II (A/B): 5-10 mm, grade III (A/B): >10 mm).

ACL injury may occur via contact or noncontact mechanisms. Noncontact mechanisms of ACL injury in soccer athletes contribute to about 85% of injuries.6,22-25 Typical noncontact mechanism of injury involves a forceful valgus collapse with the knee near full extension and combined external or internal rotation of the tibia23,26 (Figure 1). This on-field scenario generally involves cutting and torsional movement, as well as landing after a jump, particularly in 1-legged stance. Similarly, a disturbance in balance caused by the opponent may incite a noncontact mechanism resulting in ACL rupture.6,27 Video analyses of professional soccer players have also demonstrated a higher risk of noncontact ACL injury within the first 9 minutes of the match, with the most common playing situation resulting in injury being pressing, followed by kicking and heading.24,25,28 Contact mechanisms resulting in ACL injury, however, are not an uncommon occurrence in soccer players with higher risk for certain positions. Brophy and colleagues29 reviewed ACL injuries in professional and collegiate soccer players and reported a higher risk of ACL injury during defending and tackling. Similarly, Faude and colleagues30 found the risk of injury to be higher in defenders and strikers than in goalkeepers and midfielders.

roth_soccer_f1_0

Female athletes participating in elite-level athletics, especially soccer, represent a high-risk group for ACL injury. In fact, these soccer athletes experience ACL injury at an incidence 3 times higher than that in male athletes.31-35 Female soccer athletes may also be at risk for reinjury to the ACL and contralateral ACL injury. Female gender, in combination with participation in soccer, thus represents a high-risk group for ACL tear in athletics. Allen and colleagues36 retrospectively reviewed 180 female patients who had undergone ACL reconstruction (ACLR) (90 soccer players and 90 non-soccer players) over a mean period of 68.8 months. In their series, soccer players sustained significantly more ACL injuries than non-soccer players, including graft failures (11% vs 1%) and contralateral ACL tears (17% vs 4%).

ACLR is the gold standard treatment for elite soccer athletes. A recent survey of MLS team orthopedic surgeons revealed several important details regarding decision-making in ACLR in this population. From a technical standpoint, the vast majority of surgeons used a single incision, arthroscopically assisted, single-bundle reconstruction (91%). Femoral tunnel drilling was almost equally split between transtibial (51%) and use of an accessory medial portal (46%). Bone-patella-tendon-bone (BPTB) autograft was the most preferred graft choice (68%), and quadriceps tendon autograft was the least preferred. The majority of surgeons preformed ACLR within 4 weeks and permitted return to sport (RTS) without restrictions at 6 to 8 months.37

Continue to: There is a scarcity of literature regarding...

 

 

There is a scarcity of literature regarding the use of soft tissue and BPTB allografts in soccer athletes. However, one study reported no difference in patient-reported outcomes and return to preinjury level of activity (including soccer) with the use of either autograft or allograft BPTB in ACLR.38 The authors’ preference was to avoid the use of allograft in elite-level soccer athletes as the reported rate of ACL re-tear was 4 to 8 times higher than that with autograft reconstruction, as shown in athletes and military personnel.39,40 BPTB autograft and hamstring autograft (semitendinosus and/or gracilis) are common graft choices for soccer athletes. Gifstad and colleagues41 compared BPTB autograft and hamstring autograft in 45,998 primary ACLRs performed in Scandinavia. Although the cohort included, but was not limited to, soccer players, the authors reported an overall risk of revision that was significantly lower in the BPTB autograft group than in the hamstring autograft group (hazard ratio, 0.63; 95% confidence interval, 0.53-0.74).41 Mohammadi and colleagues42 prospectively compared the functional outcomes of 42 competitive soccer players who underwent ACLR with BPTB autograft vs those who underwent ACLR with hamstring autograft at the time of RTS. Players who had undergone ACLR with hamstring autograft demonstrated greater quadriceps torque, as well as better performance with triple-hop, crossover-hop, and jump-landing tests; however, both groups demonstrated similar hamstring torque and performance in 2 other hop tests.42 In the authors’ opinion, there may be a concern regarding the use of hamstring autograft in elite soccer players considering that hamstring strains are extremely common in this athletic population; however, further research would be necessary to elucidate whether this is an actual or a theoretical risk. Although not yet studied in elite-level athletes, early clinical results of ACL repair with suture augmentation show promise for certain injury patterns. These include proximal femoral ACL avulsion injuries (Sherman type 1) of excellent tissue quality that have the ability to be reapproximated to the femoral origin43 (Figures 2A, 2B). In a recent series,43-45 early clinical outcomes were found to be excellent and maintained at midterm follow-up.

roth_soccer_f2

In the NCAA soccer athletes, an overall RTS rate of 85% has been reported in those undergoing ACLR, with a significantly higher rate observed in scholarship versus non-scholarship athletes.46 Howard and colleagues46 reported median time to unrestricted game play of 6.1 months, with 75% returning to the same or higher level position on the depth chart. Among their studied collegiate soccer athletes, 32% reported continued participation in soccer on some level after college (recreational, semiprofessional, or professional).46 RTS rates for MLS soccer players have also been reported to be high, ranging from 74% to 77%, most of them returning within the following season at 10 ± 2.8 months.47,48 These findings were consistent with the RTS rate of 72% reported by the Multicenter Orthopaedic Outcomes Network (MOON) group, which analyzed 100 female and male soccer players undergoing ACLR at a minimum 7-year follow-up. In this series, Brophy and colleagues29,49 reported an RTS at 12 ± 14.3 months, with 85% returning to the same or a higher level of play prior to their injury. Erickson and colleagues47 analyzed a series of 57 ACLRs performed in MLS athletes and reported no significant difference in preinjury or postoperative performance, or between cases and uninjured controls. Arundale and colleagues48 demonstrated no significantly increased risk of lower extremity injury in MLS athletes after ACLR, but the athletes had significantly shorter careers than their uninjured counterparts. Curiously, RTS rates for European professional soccer athletes have been reported to be substantially higher at 95% to 97%.50,51 Although we can only speculate the reasons for such a discrepancy, the difference in RTS rates for similar athletes highlights a need for objective criteria to determine and report RTS rates, while also providing guidelines to prevent reinjury. Such a consensus among orthopedists is not yet present in the literature.

Soccer players and adolescent age in combination have been shown to portend a 3-fold increased risk of revision surgery for ACL failure in a cohort of 16,930 patients from the Swedish National Knee Ligament Register.52 Published data regarding ACL failure and management of revision ACLR in elite-level soccer athletes are currently lacking. However, low failure rates of 3% to 10% requiring revision reconstruction have been reported.47,49 Arundale and colleagues48 reported 2 incidences of players with ACL graft failures, 1 BPTB autograft and 1 BPTB allograft, both of whom were able to return to MLS after revision ACLR. It is the authors’ preference to use ipsilateral hamstring autograft or contralateral BPTB autograft when an ACL revision reconstruction is required.

Continue to: OTHER LIGAMENTOUS INJURIES...

 

 

OTHER LIGAMENTOUS INJURIES

The majority of research efforts regarding knee injuries in this population are focused on the ACL. Correspondingly, literature regarding injury to the collateral ligaments and the posterior cruciate ligament (PCL) in soccer players is sparse. The lateral collateral ligament (LCL) and the medial collateral ligament (MCL) play important roles as primary stabilizers to varus and valgus forces, respectively. The PCL is the primary posterior stabilizer of the knee, preventing posterior translation of the tibia. Injury to these structures may result in significant time lost from soccer and risk of reinjury.53,54

The MCL is the one of the most commonly injured ligaments in sports, including soccer.53,55 The injury mechanism generally involves contact with a resulting valgus force applied to the knee.55 Grading of MCL injuries is based on the amount of medial joint gapping with applied valgus force during examination (grade I: <5 mm, grade II: 5-10 mm, grade III: >10 mm). Kramer and colleagues53 reviewed collateral ligament injuries in the adolescent population and found that MCL injuries occurred 4 times more often than LCL injuries and about 25% were grade III injuries, most commonly occurring in American football and soccer players. Soccer also touts the highest sport-specific MCL injury rate for high school and collegiate athletics, particularly for female NCAA soccer players.56 At the professional level, Lundblad and colleagues55 reported 346 MCL injuries in 27 European teams over an 11-year period, of which 70% were contact-related, and the average time-off from soccer was 28 days.

Most surgeons treat isolated MCL injuries nonoperatively, regardless of grade.57,58 This includes activity modification, use of a hinged knee brace, quadriceps strengthening, and progressive return to play. The literature currently lacks substantial data to guide MCL injury management, specifically in elite soccer athletes. In our experience, grade I injuries are managed nonoperatively and RTS is allowed at 4 to 6 weeks. Grade II injuries are also managed nonoperatively and RTS is allowed at 6 to 8 weeks. Grade III injuries are generally allowed RTS at 8 to 12 weeks and may be considered for surgery in the context of concomitant injuries (eg, posteromedial capsular injury, multiligamentous knee injuries, and meniscal injuries). In some athletes, we consider using a varus unloader brace to help maximize decreased stress on the MCL while still allowing the athlete to be fully weight-bearing. We have found it less ideal to limit weight-bearing in elite athletes, which may negatively affect overall lower extremity neuromuscular proprioception and potentially prolong a safe return to play. Some athletes may experience prolonged soreness at the MCL femoral or tibial attachment despite being able to return to play. It is important to counsel athletes about these prolonged symptoms to set expectations, as this may even occur with grade I MCL injuries. Other rare instances where surgical management may be indicated include persistent pain and instability following nonoperative treatment of grade III injuries and highly displaced tibial avulsions of the ligament resulting in poor healing.59,60

Data regarding LCL injuries in soccer are extremely sparse. In our experience, treatment and RTS rates for isolated LCL injuries are similar to those for MCL injuries. However, it is worth noting that one-quarter of LCL injuries may occur in combination with injury to other posterolateral corner structures.53

PCL injuries are more commonly associated with vehicular trauma but have also been reported to occur in sports at a rate of 33% to 40%.61,62 The mechanism of injury in athletes generally involves a fall onto the hyperflexed knee with the foot in plantarflexion or a direct blow to the anterior tibia in a flexed knee.62,63 Classification of PCL injuries is based on posterior translation of the tibia relative to the femur with the knee flexed to 90°(grade I: 1-5 mm, grade II: 6-10 mm, grade III: >10 mm). In one cohort of 62 patients with isolated PCL injuries, soccer was found to be among the top 5 causes of injury.64 A Scandinavian review of 1287 patients who underwent PCL reconstruction found soccer to be the sport with the highest number of injuries (13.1%).65 The goalkeeper was most commonly subjected to this injury.62 Krutsch and colleagues54 compared PCL injuries in new, professional soccer players to those in players at the closest amateur level of play. In their series, 90% of PCL injuries occurred during preseason in players who were at a lower level of play in the previous season. This finding suggested that a rapid increase in training and playing intensity may have been a significant risk factor for PCL injury. Substantial literature supporting nonoperative or operative management of PCL injuries in soccer athletes is currently lacking. Historically, nonoperative treatment has been the initial management for isolated PCL injuries; however, surgical intervention has become increasingly used for both isolated and combined PCL injuries.66

Continue to: CARTILAGE AND MENISCAL INJURIES...

 

 

CARTILAGE AND MENISCAL INJURIES

The prevalence of osteoarthritis (OA) in retired soccer players is high.67,68 Articular cartilage degeneration with subsequent OA occurs in up to 32% of soccer players and ultimately leads to significant disability and retirement from the sport. High physical demands and concomitant knee injuries probably predispose to the development of posttraumatic OA.69-71

Several techniques addressing cartilage débridement or restoration have been reported, with successful RTS but with variable durability.72-75 Recently, Andrade and colleagues76 performed a systematic review of 217 articular cartilage defects in soccer players that were treated using restoration techniques, including chondroplasty, microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft. Although no superior technique could be ascertained, microfracture and osteochondral autograft procedures led to the quickest return to play, and ACI techniques enhanced long-standing clinical and functional results.76 More recently, osteochondral allograft transplantation has also been described with an 84% return to some level of activity (including soccer) and 60% of athletes returning to high-level sports participation at a mean follow-up of 4.5 years77 (Figures 3A-3C). Although chondroplasty may be successful and allow for a quicker return to play in some soccer players (return to play from 6-12 weeks), the authors believe that a strong cartilage scaffold repair strategy with early weight-bearing, including osteochondral autograft and allograft procedures (return to play from 6-9 months), must also be considered in focal chondral defects to optimize both short-term and potential long-term success.

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Meniscal injuries are also prevalent in the soccer population, and consistent with ACL injuries, female players are at least twice as likely to sustain a meniscal tear.78,79 Meniscal damage can occur in isolation or in association with ACL rupture. Repair techniques should be strongly considered as chondral changes in the setting of meniscal deficiency are a significant short- and long-term concern for elite athletes. However, due to intrinsically poor healing potential, partial meniscectomy is unfortunately more often performed.79,80 In either case, meniscal deficiency is recognized as a precursor to the development of OA as meniscal functionality is lost and the articular cartilage is subjected to increased biomechanical loading.81,82 Nawabi and colleagues83 analyzed RTS in 90 professional soccer players following partial meniscectomy. Median RTS was at 7 weeks for lateral meniscectomies and at 5 weeks for medial meniscectomies. RTS probability was 5.99 times greater after medial meniscectomy at all time points. Lateral meniscectomies were associated with an increased risk of postoperative adverse events, reoperation, and a significantly lower rate of return to play.83 In the case of severe meniscal deficiency, particularly post-meniscectomy, meniscal allograft transplantation (MAT) may be considered. In a series of MATs in lower division Spanish players, 12/14 (85.7%) returned to play at an average of 7.6 months.84 A more recent series of professional players reported 9/12 (75%) RTS as professionals and 2/12 (17%) as semiprofessionals at an average of 10.5 months.85 The authors’ strong preference is to perform meniscus-saving procedures whenever possible. Due to the longer recovery and return to play associated with meniscus repair than partial meniscectomy, most of the soccer players will often prefer to proceed with partial meniscectomy. Despite the ultimate treatment, it is critical that the surgeon and the soccer player have an in-depth conversation concerning the risks and benefits for each procedure and individualize treatment to the individual soccer player accordingly.

Continue to: INJURY PREVENTION...

 

 

INJURY PREVENTION

Given the breadth and the prevalence of soccer-related injuries, the FIFA11+ program was developed in 2006 as an injury prevention measure (Figure 4). The warm-up program includes 15 structured exercises emphasizing core stabilization, thigh muscle training, proprioception, dynamic stabilization, and plyometric exercises. The routine is believed to be easily executed and effective at preventing the incidence of noncontact injuries.86,87 Recently, Sadigursky and colleagues1 performed a systematic review of randomized clinical trials examining the efficacy of FIFA11+. The authors reported a reduction in injuries by 30% and a relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of the program.1 Post-training programs may also be beneficial as it has been shown that performing FIFA11+ both before and after training reduced overall injury rates in male, amateur soccer players.88 Regardless of the prevention program, it is critical that every league, team, medical team, and athlete have a thorough injury prevention strategy to help keep players healthy and not wait until they have instead sustained a significant injury.

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CONCLUSION

Knee injuries are common in soccer, with an alarming number of ACL injuries, as well as other significant pathology. Understanding the unique epidemiology, risk factors, treatment, and injury prevention strategies is critically important in helping medical professionals provide care for all levels of elite soccer players.

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65. Owesen C, Sandven-Thrane S, Lind M, Forssblad M, Granan LP, Årøen A. Epidemiology of surgically treated posterior cruciate ligament injuries in Scandinavia. Knee Surg Sports Traumatol Arthrosc. 2017;25(8):2384-2391. doi:10.1007/s00167-015-3786-2.

66. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092. doi:10.1177/0363546515572770.

67. Anderson CL. High rate of osteoarthritis of the knee in former soccer players. Med Sci Sports Exerc. 1986;18(1):141.

68. Arliani GG, Astur DC, Yamada RK, et al. Early osteoarthritis and reduced quality of life after retirement in former professional soccer players. Clinics (Sao Paulo). 2014;69(9):589-594. doi:10.6061/clinics/2014(09)03.

69. Wong P, Hong Y. Soccer injury in the lower extremities. Br J Sports Med. 2005;39(8):473-482. doi:10.1136/bjsm.2004.015511.

70. Thelin N, Holmberg S, Thelin A. Knee injuries account for the sports-related increased risk of knee osteoarthritis. Scand J Med Sci Sports. 2006;16(5):329-333. doi:10.1111/j.1600-0838.2005.00497.x.

71. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cruciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007;35(10):1756-1769. doi:10.1177/0363546507307396.

72. Mithöfer K, Peterson L, Mandelbaum BR, Minas T. Articular cartilage repair in soccer players with autologous chondrocyte transplantation: functional outcome and return to competition. Am J Sports Med. 2005;33(11):1639-1646. doi:10.1177/0363546505275647

73. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477-484. doi:10.1053/jars.2003.50112.

74. Hangody L, Ráthonyi GK, Duska Z, Vásárhelyi G, Füles P, Módis L. Autologous osteochondral mosaicplasty. Surgical technique. J Bone Joint Surg Am. 2004;86-A Suppl 1:65-72.

75. Sherman SL, Garrity J, Bauer K, Cook J, Stannard J, Bugbee W. Fresh osteochondral allograft transplantation for the knee: current concepts. J Am Acad Orthop Surg. 2014;22(2):121-133. doi:10.5435/JAAOS-22-02-121.

76. Andrade R, Vasta S, Papalia R, et al. Prevalence of articular cartilage lesions and surgical clinical outcomes in football (soccer) players' knees: a systematic review. Arthroscopy. 2016;32(7):1466-1477. doi:10.1016/j.arthro.2016.01.055.

77. Görtz S, Williams RJ, Gersoff WK, Bugbee WD. Osteochondral and meniscal allograft transplantation in the football (soccer) player. Cartilage. 2012;3(1 Suppl):37S-42S. doi:10.1177/1947603511416974.

78. Junge A, Grimm K, Feddermann N, Dvorak J. Precompetition orthopedic assessment of international elite football players. Clin J Sport Med. 2009;19(4):326-328. doi:10.1097/JSM.0b013e3181b21b56.

79. Salzmann GM, Preiss S, Zenobi-Wong M, Harder LP, Maier D, Dvorák J. Osteoarthritis in Football. Cartilage. 2017;8(2):162-172. doi:10.1177/1947603516648186.

80. Makris EA, Hadidi P, Athanasiou KA. The knee meniscus: structure-function, pathophysiology, current repair techniques, and prospects for regeneration. Biomaterials. 2011;32(30):7411-7431. doi:10.1016/j.biomaterials.2011.06.037

81. Freutel M, Seitz AM, Ignatius A, Dürselen L. Influence of partial meniscectomy on attachment forces, superficial strain and contact mechanics in porcine knee joints. Knee Surg Sports Traumatol Arthrosc. 2015;23(1):74-82. doi:10.1007/s00167-014-2951-3.

82. Papalia R, Del Buono A, Osti L, Denaro V, Maffulli N. Meniscectomy as a risk factor for knee osteoarthritis: a systematic review. Br Med Bull. 2011;99:89-106. doi:10.1093/bmb/ldq043.

83. Nawabi DH, Cro S, Hamid IP, Williams A. Return to play after lateral meniscectomy compared with medial meniscectomy in elite professional soccer players. Am J Sports Med. 2014;42(9):2193-2198. doi:10.1177/0363546514540271.

84. Alentorn-Geli E, Vázquez RS, Díaz PA, Cuscó X, Cugat R. Arthroscopic meniscal transplants in soccer players: outcomes at 2- to 5-year follow-up. Clin J Sport Med. 2010;20(5):340-343. doi:10.1097/JSM.0b013e3181f207dc.

85. Marcacci M, Marcheggiani Muccioli GM, Grassi A, et al. Arthroscopic meniscus allograft transplantation in male professional soccer players: a 36-month follow-up study. Am J Sports Med. 2014;42(2):382-388. doi:10.1177/0363546513508763.

86. Bizzini M, Dvorak J. FIFA 11+: an effective programme to prevent football injuries in various player groups worldwide-a narrative review. Br J Sports Med. 2015;49(9):577-579. doi:10.1136/bjsports-2015-094765.

87. Junge A, Lamprecht M, Stamm H, et al. Countrywide campaign to prevent soccer injuries in Swiss amateur players. Am J Sports Med. 2011;39(1):57-63. doi:10.1177/0363546510377424.

88. Al Attar WSA, Soomro N, Pappas E, Sinclair PJ, Sanders RH. Adding a post-training FIFA 11+ exercise program to the pre-training FIFA 11+ injury prevention program reduces injury rates among male amateur soccer players: a cluster-randomised trial. J Physiother. 2017;63(4):235-242. doi:10.1016/j.jphys.2017.08.004.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Roth is an Orthopedic Surgery Resident, Orlando Health Orthopedic Institute, Orlando, Florida. Dr. Osbahr is Chief of Sports Medicine and Orthopedic Sports Medicine Fellowship Director, Orlando Health Orthopedic Institute and Arnold Palmer Hospital for Children, Orlando, Florida.

Address correspondence to: Travis S. Roth, MD, MS, Orlando Health Orthopedic Institute, 1222 S. Orange Ave, 5th Floor, Orlando, FL 32806 (tel, 407-649-6878; email, travis.roth@orlandohealth.com).

Travis S. Roth, MD, MS Daryl C. Osbahr, MD . Knee Injuries in Elite Level Soccer Players. Am J Orthop.

October 4, 2018

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Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Roth is an Orthopedic Surgery Resident, Orlando Health Orthopedic Institute, Orlando, Florida. Dr. Osbahr is Chief of Sports Medicine and Orthopedic Sports Medicine Fellowship Director, Orlando Health Orthopedic Institute and Arnold Palmer Hospital for Children, Orlando, Florida.

Address correspondence to: Travis S. Roth, MD, MS, Orlando Health Orthopedic Institute, 1222 S. Orange Ave, 5th Floor, Orlando, FL 32806 (tel, 407-649-6878; email, travis.roth@orlandohealth.com).

Travis S. Roth, MD, MS Daryl C. Osbahr, MD . Knee Injuries in Elite Level Soccer Players. Am J Orthop.

October 4, 2018

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Roth is an Orthopedic Surgery Resident, Orlando Health Orthopedic Institute, Orlando, Florida. Dr. Osbahr is Chief of Sports Medicine and Orthopedic Sports Medicine Fellowship Director, Orlando Health Orthopedic Institute and Arnold Palmer Hospital for Children, Orlando, Florida.

Address correspondence to: Travis S. Roth, MD, MS, Orlando Health Orthopedic Institute, 1222 S. Orange Ave, 5th Floor, Orlando, FL 32806 (tel, 407-649-6878; email, travis.roth@orlandohealth.com).

Travis S. Roth, MD, MS Daryl C. Osbahr, MD . Knee Injuries in Elite Level Soccer Players. Am J Orthop.

October 4, 2018

ABSTRACT

As one of the most popular sports in the world, soccer injury rates involving the knee continue to rise. An alarming trend of knee injuries, including increased anterior cruciate ligament ruptures, underscores the need to review our current understanding of these injuries in soccer players. This article includes a critical review of the epidemiology of knee injuries in soccer, anterior cruciate ligament and other ligamentous injuries, cartilage and meniscal injury, post-traumatic osteoarthritis, as well as current prevention initiatives.

Continue to: EPIDEMIOLOGY...

 

 

EPIDEMIOLOGY

There are currently 28 players on each of the Major League Soccer (MLS) teams, and during the 2013 to 2014 academic year, the National Federation of State High School Associations (NFHS) reported that 417,419 boys and 374,564 girls played high school soccer and the National Collegiate Athletic Association (NCAA) reported that 23,602 males and 26,358 females played collegiate soccer.5 As such, knee injuries in this population are a major concern for those involved in sports medicine. Several injuries occurring during soccer involve the lower extremity, particularly the knee.1 In fact, multiple reports estimate that up to 17.6% of soccer-related injuries presenting to the emergency room involved the knee.1,6-9 The majority of these injuries are noncontact injuries, although contact injuries do still occur.10,11

Risk factors for injuries in soccer may be non-modifiable (such as age and gender) and modifiable (such as level of conditioning, force, balance, and flexibility). Inadequate lower motor coordination may result in injury in the adolescent population, and advanced age >28 years in males and >25 years in females is considered as a high-risk factor for injury.12,13 Importantly, gender and age have been reported to play a significant role as risk factors for ACL injury.6 In fact, female players have a 3 to 5 times higher risk of significant knee injury, including ACL injuries, than male players.4,14-16 Preventative programs such as the FIFA 11+ program have been set forth to augment conditioning as part of managing the modifiable risk factors.

Like American football, playing on artificial turf has been questioned as a contributor to injury compared to playing on natural grass.17,18 In recent years, newer generations of artificial turf have been developed to more closely replicate the characteristics of natural grass. Meyers19 compared the incidence, mechanisms, and severity of match-related collegiate men’s soccer injuries on artificial turf and those on natural grass and demonstrated no significant difference in knee injuries between the 2 surfaces. This finding was consistent with previous studies that reported no difference in the incidence of knee injuries on either surface in women’s collegiate and elite-level soccer.15,20,21

Continue to: ACL INJURIES...

 

 

ACL INJURIES

ACL injuries are life-changing events that can significantly affect the career of a soccer athlete. As a major stabilizer of the knee, the ACL primarily prevents anterior tibial translation with the anteromedial bundle and secondarily resists tibial rotation with the posterolateral bundle. The ligament takes origin from the posteromedial aspect of the lateral femoral condyle and inserts anterior to the tibial intercondylar eminence. Grading of ACL injuries is based on the Lachman test, which is performed between 20°and 30° of knee flexion and measures the amount of anterior tibial translation relative to the femur (A = firm endpoint, B = no endpoint; grade I: 3-5 mm, grade II (A/B): 5-10 mm, grade III (A/B): >10 mm).

ACL injury may occur via contact or noncontact mechanisms. Noncontact mechanisms of ACL injury in soccer athletes contribute to about 85% of injuries.6,22-25 Typical noncontact mechanism of injury involves a forceful valgus collapse with the knee near full extension and combined external or internal rotation of the tibia23,26 (Figure 1). This on-field scenario generally involves cutting and torsional movement, as well as landing after a jump, particularly in 1-legged stance. Similarly, a disturbance in balance caused by the opponent may incite a noncontact mechanism resulting in ACL rupture.6,27 Video analyses of professional soccer players have also demonstrated a higher risk of noncontact ACL injury within the first 9 minutes of the match, with the most common playing situation resulting in injury being pressing, followed by kicking and heading.24,25,28 Contact mechanisms resulting in ACL injury, however, are not an uncommon occurrence in soccer players with higher risk for certain positions. Brophy and colleagues29 reviewed ACL injuries in professional and collegiate soccer players and reported a higher risk of ACL injury during defending and tackling. Similarly, Faude and colleagues30 found the risk of injury to be higher in defenders and strikers than in goalkeepers and midfielders.

roth_soccer_f1_0

Female athletes participating in elite-level athletics, especially soccer, represent a high-risk group for ACL injury. In fact, these soccer athletes experience ACL injury at an incidence 3 times higher than that in male athletes.31-35 Female soccer athletes may also be at risk for reinjury to the ACL and contralateral ACL injury. Female gender, in combination with participation in soccer, thus represents a high-risk group for ACL tear in athletics. Allen and colleagues36 retrospectively reviewed 180 female patients who had undergone ACL reconstruction (ACLR) (90 soccer players and 90 non-soccer players) over a mean period of 68.8 months. In their series, soccer players sustained significantly more ACL injuries than non-soccer players, including graft failures (11% vs 1%) and contralateral ACL tears (17% vs 4%).

ACLR is the gold standard treatment for elite soccer athletes. A recent survey of MLS team orthopedic surgeons revealed several important details regarding decision-making in ACLR in this population. From a technical standpoint, the vast majority of surgeons used a single incision, arthroscopically assisted, single-bundle reconstruction (91%). Femoral tunnel drilling was almost equally split between transtibial (51%) and use of an accessory medial portal (46%). Bone-patella-tendon-bone (BPTB) autograft was the most preferred graft choice (68%), and quadriceps tendon autograft was the least preferred. The majority of surgeons preformed ACLR within 4 weeks and permitted return to sport (RTS) without restrictions at 6 to 8 months.37

Continue to: There is a scarcity of literature regarding...

 

 

There is a scarcity of literature regarding the use of soft tissue and BPTB allografts in soccer athletes. However, one study reported no difference in patient-reported outcomes and return to preinjury level of activity (including soccer) with the use of either autograft or allograft BPTB in ACLR.38 The authors’ preference was to avoid the use of allograft in elite-level soccer athletes as the reported rate of ACL re-tear was 4 to 8 times higher than that with autograft reconstruction, as shown in athletes and military personnel.39,40 BPTB autograft and hamstring autograft (semitendinosus and/or gracilis) are common graft choices for soccer athletes. Gifstad and colleagues41 compared BPTB autograft and hamstring autograft in 45,998 primary ACLRs performed in Scandinavia. Although the cohort included, but was not limited to, soccer players, the authors reported an overall risk of revision that was significantly lower in the BPTB autograft group than in the hamstring autograft group (hazard ratio, 0.63; 95% confidence interval, 0.53-0.74).41 Mohammadi and colleagues42 prospectively compared the functional outcomes of 42 competitive soccer players who underwent ACLR with BPTB autograft vs those who underwent ACLR with hamstring autograft at the time of RTS. Players who had undergone ACLR with hamstring autograft demonstrated greater quadriceps torque, as well as better performance with triple-hop, crossover-hop, and jump-landing tests; however, both groups demonstrated similar hamstring torque and performance in 2 other hop tests.42 In the authors’ opinion, there may be a concern regarding the use of hamstring autograft in elite soccer players considering that hamstring strains are extremely common in this athletic population; however, further research would be necessary to elucidate whether this is an actual or a theoretical risk. Although not yet studied in elite-level athletes, early clinical results of ACL repair with suture augmentation show promise for certain injury patterns. These include proximal femoral ACL avulsion injuries (Sherman type 1) of excellent tissue quality that have the ability to be reapproximated to the femoral origin43 (Figures 2A, 2B). In a recent series,43-45 early clinical outcomes were found to be excellent and maintained at midterm follow-up.

roth_soccer_f2

In the NCAA soccer athletes, an overall RTS rate of 85% has been reported in those undergoing ACLR, with a significantly higher rate observed in scholarship versus non-scholarship athletes.46 Howard and colleagues46 reported median time to unrestricted game play of 6.1 months, with 75% returning to the same or higher level position on the depth chart. Among their studied collegiate soccer athletes, 32% reported continued participation in soccer on some level after college (recreational, semiprofessional, or professional).46 RTS rates for MLS soccer players have also been reported to be high, ranging from 74% to 77%, most of them returning within the following season at 10 ± 2.8 months.47,48 These findings were consistent with the RTS rate of 72% reported by the Multicenter Orthopaedic Outcomes Network (MOON) group, which analyzed 100 female and male soccer players undergoing ACLR at a minimum 7-year follow-up. In this series, Brophy and colleagues29,49 reported an RTS at 12 ± 14.3 months, with 85% returning to the same or a higher level of play prior to their injury. Erickson and colleagues47 analyzed a series of 57 ACLRs performed in MLS athletes and reported no significant difference in preinjury or postoperative performance, or between cases and uninjured controls. Arundale and colleagues48 demonstrated no significantly increased risk of lower extremity injury in MLS athletes after ACLR, but the athletes had significantly shorter careers than their uninjured counterparts. Curiously, RTS rates for European professional soccer athletes have been reported to be substantially higher at 95% to 97%.50,51 Although we can only speculate the reasons for such a discrepancy, the difference in RTS rates for similar athletes highlights a need for objective criteria to determine and report RTS rates, while also providing guidelines to prevent reinjury. Such a consensus among orthopedists is not yet present in the literature.

Soccer players and adolescent age in combination have been shown to portend a 3-fold increased risk of revision surgery for ACL failure in a cohort of 16,930 patients from the Swedish National Knee Ligament Register.52 Published data regarding ACL failure and management of revision ACLR in elite-level soccer athletes are currently lacking. However, low failure rates of 3% to 10% requiring revision reconstruction have been reported.47,49 Arundale and colleagues48 reported 2 incidences of players with ACL graft failures, 1 BPTB autograft and 1 BPTB allograft, both of whom were able to return to MLS after revision ACLR. It is the authors’ preference to use ipsilateral hamstring autograft or contralateral BPTB autograft when an ACL revision reconstruction is required.

Continue to: OTHER LIGAMENTOUS INJURIES...

 

 

OTHER LIGAMENTOUS INJURIES

The majority of research efforts regarding knee injuries in this population are focused on the ACL. Correspondingly, literature regarding injury to the collateral ligaments and the posterior cruciate ligament (PCL) in soccer players is sparse. The lateral collateral ligament (LCL) and the medial collateral ligament (MCL) play important roles as primary stabilizers to varus and valgus forces, respectively. The PCL is the primary posterior stabilizer of the knee, preventing posterior translation of the tibia. Injury to these structures may result in significant time lost from soccer and risk of reinjury.53,54

The MCL is the one of the most commonly injured ligaments in sports, including soccer.53,55 The injury mechanism generally involves contact with a resulting valgus force applied to the knee.55 Grading of MCL injuries is based on the amount of medial joint gapping with applied valgus force during examination (grade I: <5 mm, grade II: 5-10 mm, grade III: >10 mm). Kramer and colleagues53 reviewed collateral ligament injuries in the adolescent population and found that MCL injuries occurred 4 times more often than LCL injuries and about 25% were grade III injuries, most commonly occurring in American football and soccer players. Soccer also touts the highest sport-specific MCL injury rate for high school and collegiate athletics, particularly for female NCAA soccer players.56 At the professional level, Lundblad and colleagues55 reported 346 MCL injuries in 27 European teams over an 11-year period, of which 70% were contact-related, and the average time-off from soccer was 28 days.

Most surgeons treat isolated MCL injuries nonoperatively, regardless of grade.57,58 This includes activity modification, use of a hinged knee brace, quadriceps strengthening, and progressive return to play. The literature currently lacks substantial data to guide MCL injury management, specifically in elite soccer athletes. In our experience, grade I injuries are managed nonoperatively and RTS is allowed at 4 to 6 weeks. Grade II injuries are also managed nonoperatively and RTS is allowed at 6 to 8 weeks. Grade III injuries are generally allowed RTS at 8 to 12 weeks and may be considered for surgery in the context of concomitant injuries (eg, posteromedial capsular injury, multiligamentous knee injuries, and meniscal injuries). In some athletes, we consider using a varus unloader brace to help maximize decreased stress on the MCL while still allowing the athlete to be fully weight-bearing. We have found it less ideal to limit weight-bearing in elite athletes, which may negatively affect overall lower extremity neuromuscular proprioception and potentially prolong a safe return to play. Some athletes may experience prolonged soreness at the MCL femoral or tibial attachment despite being able to return to play. It is important to counsel athletes about these prolonged symptoms to set expectations, as this may even occur with grade I MCL injuries. Other rare instances where surgical management may be indicated include persistent pain and instability following nonoperative treatment of grade III injuries and highly displaced tibial avulsions of the ligament resulting in poor healing.59,60

Data regarding LCL injuries in soccer are extremely sparse. In our experience, treatment and RTS rates for isolated LCL injuries are similar to those for MCL injuries. However, it is worth noting that one-quarter of LCL injuries may occur in combination with injury to other posterolateral corner structures.53

PCL injuries are more commonly associated with vehicular trauma but have also been reported to occur in sports at a rate of 33% to 40%.61,62 The mechanism of injury in athletes generally involves a fall onto the hyperflexed knee with the foot in plantarflexion or a direct blow to the anterior tibia in a flexed knee.62,63 Classification of PCL injuries is based on posterior translation of the tibia relative to the femur with the knee flexed to 90°(grade I: 1-5 mm, grade II: 6-10 mm, grade III: >10 mm). In one cohort of 62 patients with isolated PCL injuries, soccer was found to be among the top 5 causes of injury.64 A Scandinavian review of 1287 patients who underwent PCL reconstruction found soccer to be the sport with the highest number of injuries (13.1%).65 The goalkeeper was most commonly subjected to this injury.62 Krutsch and colleagues54 compared PCL injuries in new, professional soccer players to those in players at the closest amateur level of play. In their series, 90% of PCL injuries occurred during preseason in players who were at a lower level of play in the previous season. This finding suggested that a rapid increase in training and playing intensity may have been a significant risk factor for PCL injury. Substantial literature supporting nonoperative or operative management of PCL injuries in soccer athletes is currently lacking. Historically, nonoperative treatment has been the initial management for isolated PCL injuries; however, surgical intervention has become increasingly used for both isolated and combined PCL injuries.66

Continue to: CARTILAGE AND MENISCAL INJURIES...

 

 

CARTILAGE AND MENISCAL INJURIES

The prevalence of osteoarthritis (OA) in retired soccer players is high.67,68 Articular cartilage degeneration with subsequent OA occurs in up to 32% of soccer players and ultimately leads to significant disability and retirement from the sport. High physical demands and concomitant knee injuries probably predispose to the development of posttraumatic OA.69-71

Several techniques addressing cartilage débridement or restoration have been reported, with successful RTS but with variable durability.72-75 Recently, Andrade and colleagues76 performed a systematic review of 217 articular cartilage defects in soccer players that were treated using restoration techniques, including chondroplasty, microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft. Although no superior technique could be ascertained, microfracture and osteochondral autograft procedures led to the quickest return to play, and ACI techniques enhanced long-standing clinical and functional results.76 More recently, osteochondral allograft transplantation has also been described with an 84% return to some level of activity (including soccer) and 60% of athletes returning to high-level sports participation at a mean follow-up of 4.5 years77 (Figures 3A-3C). Although chondroplasty may be successful and allow for a quicker return to play in some soccer players (return to play from 6-12 weeks), the authors believe that a strong cartilage scaffold repair strategy with early weight-bearing, including osteochondral autograft and allograft procedures (return to play from 6-9 months), must also be considered in focal chondral defects to optimize both short-term and potential long-term success.

roth_soccer_f3

Meniscal injuries are also prevalent in the soccer population, and consistent with ACL injuries, female players are at least twice as likely to sustain a meniscal tear.78,79 Meniscal damage can occur in isolation or in association with ACL rupture. Repair techniques should be strongly considered as chondral changes in the setting of meniscal deficiency are a significant short- and long-term concern for elite athletes. However, due to intrinsically poor healing potential, partial meniscectomy is unfortunately more often performed.79,80 In either case, meniscal deficiency is recognized as a precursor to the development of OA as meniscal functionality is lost and the articular cartilage is subjected to increased biomechanical loading.81,82 Nawabi and colleagues83 analyzed RTS in 90 professional soccer players following partial meniscectomy. Median RTS was at 7 weeks for lateral meniscectomies and at 5 weeks for medial meniscectomies. RTS probability was 5.99 times greater after medial meniscectomy at all time points. Lateral meniscectomies were associated with an increased risk of postoperative adverse events, reoperation, and a significantly lower rate of return to play.83 In the case of severe meniscal deficiency, particularly post-meniscectomy, meniscal allograft transplantation (MAT) may be considered. In a series of MATs in lower division Spanish players, 12/14 (85.7%) returned to play at an average of 7.6 months.84 A more recent series of professional players reported 9/12 (75%) RTS as professionals and 2/12 (17%) as semiprofessionals at an average of 10.5 months.85 The authors’ strong preference is to perform meniscus-saving procedures whenever possible. Due to the longer recovery and return to play associated with meniscus repair than partial meniscectomy, most of the soccer players will often prefer to proceed with partial meniscectomy. Despite the ultimate treatment, it is critical that the surgeon and the soccer player have an in-depth conversation concerning the risks and benefits for each procedure and individualize treatment to the individual soccer player accordingly.

Continue to: INJURY PREVENTION...

 

 

INJURY PREVENTION

Given the breadth and the prevalence of soccer-related injuries, the FIFA11+ program was developed in 2006 as an injury prevention measure (Figure 4). The warm-up program includes 15 structured exercises emphasizing core stabilization, thigh muscle training, proprioception, dynamic stabilization, and plyometric exercises. The routine is believed to be easily executed and effective at preventing the incidence of noncontact injuries.86,87 Recently, Sadigursky and colleagues1 performed a systematic review of randomized clinical trials examining the efficacy of FIFA11+. The authors reported a reduction in injuries by 30% and a relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of the program.1 Post-training programs may also be beneficial as it has been shown that performing FIFA11+ both before and after training reduced overall injury rates in male, amateur soccer players.88 Regardless of the prevention program, it is critical that every league, team, medical team, and athlete have a thorough injury prevention strategy to help keep players healthy and not wait until they have instead sustained a significant injury.

roth_soccer_f4

CONCLUSION

Knee injuries are common in soccer, with an alarming number of ACL injuries, as well as other significant pathology. Understanding the unique epidemiology, risk factors, treatment, and injury prevention strategies is critically important in helping medical professionals provide care for all levels of elite soccer players.

ABSTRACT

As one of the most popular sports in the world, soccer injury rates involving the knee continue to rise. An alarming trend of knee injuries, including increased anterior cruciate ligament ruptures, underscores the need to review our current understanding of these injuries in soccer players. This article includes a critical review of the epidemiology of knee injuries in soccer, anterior cruciate ligament and other ligamentous injuries, cartilage and meniscal injury, post-traumatic osteoarthritis, as well as current prevention initiatives.

Continue to: EPIDEMIOLOGY...

 

 

EPIDEMIOLOGY

There are currently 28 players on each of the Major League Soccer (MLS) teams, and during the 2013 to 2014 academic year, the National Federation of State High School Associations (NFHS) reported that 417,419 boys and 374,564 girls played high school soccer and the National Collegiate Athletic Association (NCAA) reported that 23,602 males and 26,358 females played collegiate soccer.5 As such, knee injuries in this population are a major concern for those involved in sports medicine. Several injuries occurring during soccer involve the lower extremity, particularly the knee.1 In fact, multiple reports estimate that up to 17.6% of soccer-related injuries presenting to the emergency room involved the knee.1,6-9 The majority of these injuries are noncontact injuries, although contact injuries do still occur.10,11

Risk factors for injuries in soccer may be non-modifiable (such as age and gender) and modifiable (such as level of conditioning, force, balance, and flexibility). Inadequate lower motor coordination may result in injury in the adolescent population, and advanced age >28 years in males and >25 years in females is considered as a high-risk factor for injury.12,13 Importantly, gender and age have been reported to play a significant role as risk factors for ACL injury.6 In fact, female players have a 3 to 5 times higher risk of significant knee injury, including ACL injuries, than male players.4,14-16 Preventative programs such as the FIFA 11+ program have been set forth to augment conditioning as part of managing the modifiable risk factors.

Like American football, playing on artificial turf has been questioned as a contributor to injury compared to playing on natural grass.17,18 In recent years, newer generations of artificial turf have been developed to more closely replicate the characteristics of natural grass. Meyers19 compared the incidence, mechanisms, and severity of match-related collegiate men’s soccer injuries on artificial turf and those on natural grass and demonstrated no significant difference in knee injuries between the 2 surfaces. This finding was consistent with previous studies that reported no difference in the incidence of knee injuries on either surface in women’s collegiate and elite-level soccer.15,20,21

Continue to: ACL INJURIES...

 

 

ACL INJURIES

ACL injuries are life-changing events that can significantly affect the career of a soccer athlete. As a major stabilizer of the knee, the ACL primarily prevents anterior tibial translation with the anteromedial bundle and secondarily resists tibial rotation with the posterolateral bundle. The ligament takes origin from the posteromedial aspect of the lateral femoral condyle and inserts anterior to the tibial intercondylar eminence. Grading of ACL injuries is based on the Lachman test, which is performed between 20°and 30° of knee flexion and measures the amount of anterior tibial translation relative to the femur (A = firm endpoint, B = no endpoint; grade I: 3-5 mm, grade II (A/B): 5-10 mm, grade III (A/B): >10 mm).

ACL injury may occur via contact or noncontact mechanisms. Noncontact mechanisms of ACL injury in soccer athletes contribute to about 85% of injuries.6,22-25 Typical noncontact mechanism of injury involves a forceful valgus collapse with the knee near full extension and combined external or internal rotation of the tibia23,26 (Figure 1). This on-field scenario generally involves cutting and torsional movement, as well as landing after a jump, particularly in 1-legged stance. Similarly, a disturbance in balance caused by the opponent may incite a noncontact mechanism resulting in ACL rupture.6,27 Video analyses of professional soccer players have also demonstrated a higher risk of noncontact ACL injury within the first 9 minutes of the match, with the most common playing situation resulting in injury being pressing, followed by kicking and heading.24,25,28 Contact mechanisms resulting in ACL injury, however, are not an uncommon occurrence in soccer players with higher risk for certain positions. Brophy and colleagues29 reviewed ACL injuries in professional and collegiate soccer players and reported a higher risk of ACL injury during defending and tackling. Similarly, Faude and colleagues30 found the risk of injury to be higher in defenders and strikers than in goalkeepers and midfielders.

roth_soccer_f1_0

Female athletes participating in elite-level athletics, especially soccer, represent a high-risk group for ACL injury. In fact, these soccer athletes experience ACL injury at an incidence 3 times higher than that in male athletes.31-35 Female soccer athletes may also be at risk for reinjury to the ACL and contralateral ACL injury. Female gender, in combination with participation in soccer, thus represents a high-risk group for ACL tear in athletics. Allen and colleagues36 retrospectively reviewed 180 female patients who had undergone ACL reconstruction (ACLR) (90 soccer players and 90 non-soccer players) over a mean period of 68.8 months. In their series, soccer players sustained significantly more ACL injuries than non-soccer players, including graft failures (11% vs 1%) and contralateral ACL tears (17% vs 4%).

ACLR is the gold standard treatment for elite soccer athletes. A recent survey of MLS team orthopedic surgeons revealed several important details regarding decision-making in ACLR in this population. From a technical standpoint, the vast majority of surgeons used a single incision, arthroscopically assisted, single-bundle reconstruction (91%). Femoral tunnel drilling was almost equally split between transtibial (51%) and use of an accessory medial portal (46%). Bone-patella-tendon-bone (BPTB) autograft was the most preferred graft choice (68%), and quadriceps tendon autograft was the least preferred. The majority of surgeons preformed ACLR within 4 weeks and permitted return to sport (RTS) without restrictions at 6 to 8 months.37

Continue to: There is a scarcity of literature regarding...

 

 

There is a scarcity of literature regarding the use of soft tissue and BPTB allografts in soccer athletes. However, one study reported no difference in patient-reported outcomes and return to preinjury level of activity (including soccer) with the use of either autograft or allograft BPTB in ACLR.38 The authors’ preference was to avoid the use of allograft in elite-level soccer athletes as the reported rate of ACL re-tear was 4 to 8 times higher than that with autograft reconstruction, as shown in athletes and military personnel.39,40 BPTB autograft and hamstring autograft (semitendinosus and/or gracilis) are common graft choices for soccer athletes. Gifstad and colleagues41 compared BPTB autograft and hamstring autograft in 45,998 primary ACLRs performed in Scandinavia. Although the cohort included, but was not limited to, soccer players, the authors reported an overall risk of revision that was significantly lower in the BPTB autograft group than in the hamstring autograft group (hazard ratio, 0.63; 95% confidence interval, 0.53-0.74).41 Mohammadi and colleagues42 prospectively compared the functional outcomes of 42 competitive soccer players who underwent ACLR with BPTB autograft vs those who underwent ACLR with hamstring autograft at the time of RTS. Players who had undergone ACLR with hamstring autograft demonstrated greater quadriceps torque, as well as better performance with triple-hop, crossover-hop, and jump-landing tests; however, both groups demonstrated similar hamstring torque and performance in 2 other hop tests.42 In the authors’ opinion, there may be a concern regarding the use of hamstring autograft in elite soccer players considering that hamstring strains are extremely common in this athletic population; however, further research would be necessary to elucidate whether this is an actual or a theoretical risk. Although not yet studied in elite-level athletes, early clinical results of ACL repair with suture augmentation show promise for certain injury patterns. These include proximal femoral ACL avulsion injuries (Sherman type 1) of excellent tissue quality that have the ability to be reapproximated to the femoral origin43 (Figures 2A, 2B). In a recent series,43-45 early clinical outcomes were found to be excellent and maintained at midterm follow-up.

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In the NCAA soccer athletes, an overall RTS rate of 85% has been reported in those undergoing ACLR, with a significantly higher rate observed in scholarship versus non-scholarship athletes.46 Howard and colleagues46 reported median time to unrestricted game play of 6.1 months, with 75% returning to the same or higher level position on the depth chart. Among their studied collegiate soccer athletes, 32% reported continued participation in soccer on some level after college (recreational, semiprofessional, or professional).46 RTS rates for MLS soccer players have also been reported to be high, ranging from 74% to 77%, most of them returning within the following season at 10 ± 2.8 months.47,48 These findings were consistent with the RTS rate of 72% reported by the Multicenter Orthopaedic Outcomes Network (MOON) group, which analyzed 100 female and male soccer players undergoing ACLR at a minimum 7-year follow-up. In this series, Brophy and colleagues29,49 reported an RTS at 12 ± 14.3 months, with 85% returning to the same or a higher level of play prior to their injury. Erickson and colleagues47 analyzed a series of 57 ACLRs performed in MLS athletes and reported no significant difference in preinjury or postoperative performance, or between cases and uninjured controls. Arundale and colleagues48 demonstrated no significantly increased risk of lower extremity injury in MLS athletes after ACLR, but the athletes had significantly shorter careers than their uninjured counterparts. Curiously, RTS rates for European professional soccer athletes have been reported to be substantially higher at 95% to 97%.50,51 Although we can only speculate the reasons for such a discrepancy, the difference in RTS rates for similar athletes highlights a need for objective criteria to determine and report RTS rates, while also providing guidelines to prevent reinjury. Such a consensus among orthopedists is not yet present in the literature.

Soccer players and adolescent age in combination have been shown to portend a 3-fold increased risk of revision surgery for ACL failure in a cohort of 16,930 patients from the Swedish National Knee Ligament Register.52 Published data regarding ACL failure and management of revision ACLR in elite-level soccer athletes are currently lacking. However, low failure rates of 3% to 10% requiring revision reconstruction have been reported.47,49 Arundale and colleagues48 reported 2 incidences of players with ACL graft failures, 1 BPTB autograft and 1 BPTB allograft, both of whom were able to return to MLS after revision ACLR. It is the authors’ preference to use ipsilateral hamstring autograft or contralateral BPTB autograft when an ACL revision reconstruction is required.

Continue to: OTHER LIGAMENTOUS INJURIES...

 

 

OTHER LIGAMENTOUS INJURIES

The majority of research efforts regarding knee injuries in this population are focused on the ACL. Correspondingly, literature regarding injury to the collateral ligaments and the posterior cruciate ligament (PCL) in soccer players is sparse. The lateral collateral ligament (LCL) and the medial collateral ligament (MCL) play important roles as primary stabilizers to varus and valgus forces, respectively. The PCL is the primary posterior stabilizer of the knee, preventing posterior translation of the tibia. Injury to these structures may result in significant time lost from soccer and risk of reinjury.53,54

The MCL is the one of the most commonly injured ligaments in sports, including soccer.53,55 The injury mechanism generally involves contact with a resulting valgus force applied to the knee.55 Grading of MCL injuries is based on the amount of medial joint gapping with applied valgus force during examination (grade I: <5 mm, grade II: 5-10 mm, grade III: >10 mm). Kramer and colleagues53 reviewed collateral ligament injuries in the adolescent population and found that MCL injuries occurred 4 times more often than LCL injuries and about 25% were grade III injuries, most commonly occurring in American football and soccer players. Soccer also touts the highest sport-specific MCL injury rate for high school and collegiate athletics, particularly for female NCAA soccer players.56 At the professional level, Lundblad and colleagues55 reported 346 MCL injuries in 27 European teams over an 11-year period, of which 70% were contact-related, and the average time-off from soccer was 28 days.

Most surgeons treat isolated MCL injuries nonoperatively, regardless of grade.57,58 This includes activity modification, use of a hinged knee brace, quadriceps strengthening, and progressive return to play. The literature currently lacks substantial data to guide MCL injury management, specifically in elite soccer athletes. In our experience, grade I injuries are managed nonoperatively and RTS is allowed at 4 to 6 weeks. Grade II injuries are also managed nonoperatively and RTS is allowed at 6 to 8 weeks. Grade III injuries are generally allowed RTS at 8 to 12 weeks and may be considered for surgery in the context of concomitant injuries (eg, posteromedial capsular injury, multiligamentous knee injuries, and meniscal injuries). In some athletes, we consider using a varus unloader brace to help maximize decreased stress on the MCL while still allowing the athlete to be fully weight-bearing. We have found it less ideal to limit weight-bearing in elite athletes, which may negatively affect overall lower extremity neuromuscular proprioception and potentially prolong a safe return to play. Some athletes may experience prolonged soreness at the MCL femoral or tibial attachment despite being able to return to play. It is important to counsel athletes about these prolonged symptoms to set expectations, as this may even occur with grade I MCL injuries. Other rare instances where surgical management may be indicated include persistent pain and instability following nonoperative treatment of grade III injuries and highly displaced tibial avulsions of the ligament resulting in poor healing.59,60

Data regarding LCL injuries in soccer are extremely sparse. In our experience, treatment and RTS rates for isolated LCL injuries are similar to those for MCL injuries. However, it is worth noting that one-quarter of LCL injuries may occur in combination with injury to other posterolateral corner structures.53

PCL injuries are more commonly associated with vehicular trauma but have also been reported to occur in sports at a rate of 33% to 40%.61,62 The mechanism of injury in athletes generally involves a fall onto the hyperflexed knee with the foot in plantarflexion or a direct blow to the anterior tibia in a flexed knee.62,63 Classification of PCL injuries is based on posterior translation of the tibia relative to the femur with the knee flexed to 90°(grade I: 1-5 mm, grade II: 6-10 mm, grade III: >10 mm). In one cohort of 62 patients with isolated PCL injuries, soccer was found to be among the top 5 causes of injury.64 A Scandinavian review of 1287 patients who underwent PCL reconstruction found soccer to be the sport with the highest number of injuries (13.1%).65 The goalkeeper was most commonly subjected to this injury.62 Krutsch and colleagues54 compared PCL injuries in new, professional soccer players to those in players at the closest amateur level of play. In their series, 90% of PCL injuries occurred during preseason in players who were at a lower level of play in the previous season. This finding suggested that a rapid increase in training and playing intensity may have been a significant risk factor for PCL injury. Substantial literature supporting nonoperative or operative management of PCL injuries in soccer athletes is currently lacking. Historically, nonoperative treatment has been the initial management for isolated PCL injuries; however, surgical intervention has become increasingly used for both isolated and combined PCL injuries.66

Continue to: CARTILAGE AND MENISCAL INJURIES...

 

 

CARTILAGE AND MENISCAL INJURIES

The prevalence of osteoarthritis (OA) in retired soccer players is high.67,68 Articular cartilage degeneration with subsequent OA occurs in up to 32% of soccer players and ultimately leads to significant disability and retirement from the sport. High physical demands and concomitant knee injuries probably predispose to the development of posttraumatic OA.69-71

Several techniques addressing cartilage débridement or restoration have been reported, with successful RTS but with variable durability.72-75 Recently, Andrade and colleagues76 performed a systematic review of 217 articular cartilage defects in soccer players that were treated using restoration techniques, including chondroplasty, microfracture, autologous chondrocyte implantation (ACI), and osteochondral autograft. Although no superior technique could be ascertained, microfracture and osteochondral autograft procedures led to the quickest return to play, and ACI techniques enhanced long-standing clinical and functional results.76 More recently, osteochondral allograft transplantation has also been described with an 84% return to some level of activity (including soccer) and 60% of athletes returning to high-level sports participation at a mean follow-up of 4.5 years77 (Figures 3A-3C). Although chondroplasty may be successful and allow for a quicker return to play in some soccer players (return to play from 6-12 weeks), the authors believe that a strong cartilage scaffold repair strategy with early weight-bearing, including osteochondral autograft and allograft procedures (return to play from 6-9 months), must also be considered in focal chondral defects to optimize both short-term and potential long-term success.

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Meniscal injuries are also prevalent in the soccer population, and consistent with ACL injuries, female players are at least twice as likely to sustain a meniscal tear.78,79 Meniscal damage can occur in isolation or in association with ACL rupture. Repair techniques should be strongly considered as chondral changes in the setting of meniscal deficiency are a significant short- and long-term concern for elite athletes. However, due to intrinsically poor healing potential, partial meniscectomy is unfortunately more often performed.79,80 In either case, meniscal deficiency is recognized as a precursor to the development of OA as meniscal functionality is lost and the articular cartilage is subjected to increased biomechanical loading.81,82 Nawabi and colleagues83 analyzed RTS in 90 professional soccer players following partial meniscectomy. Median RTS was at 7 weeks for lateral meniscectomies and at 5 weeks for medial meniscectomies. RTS probability was 5.99 times greater after medial meniscectomy at all time points. Lateral meniscectomies were associated with an increased risk of postoperative adverse events, reoperation, and a significantly lower rate of return to play.83 In the case of severe meniscal deficiency, particularly post-meniscectomy, meniscal allograft transplantation (MAT) may be considered. In a series of MATs in lower division Spanish players, 12/14 (85.7%) returned to play at an average of 7.6 months.84 A more recent series of professional players reported 9/12 (75%) RTS as professionals and 2/12 (17%) as semiprofessionals at an average of 10.5 months.85 The authors’ strong preference is to perform meniscus-saving procedures whenever possible. Due to the longer recovery and return to play associated with meniscus repair than partial meniscectomy, most of the soccer players will often prefer to proceed with partial meniscectomy. Despite the ultimate treatment, it is critical that the surgeon and the soccer player have an in-depth conversation concerning the risks and benefits for each procedure and individualize treatment to the individual soccer player accordingly.

Continue to: INJURY PREVENTION...

 

 

INJURY PREVENTION

Given the breadth and the prevalence of soccer-related injuries, the FIFA11+ program was developed in 2006 as an injury prevention measure (Figure 4). The warm-up program includes 15 structured exercises emphasizing core stabilization, thigh muscle training, proprioception, dynamic stabilization, and plyometric exercises. The routine is believed to be easily executed and effective at preventing the incidence of noncontact injuries.86,87 Recently, Sadigursky and colleagues1 performed a systematic review of randomized clinical trials examining the efficacy of FIFA11+. The authors reported a reduction in injuries by 30% and a relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of the program.1 Post-training programs may also be beneficial as it has been shown that performing FIFA11+ both before and after training reduced overall injury rates in male, amateur soccer players.88 Regardless of the prevention program, it is critical that every league, team, medical team, and athlete have a thorough injury prevention strategy to help keep players healthy and not wait until they have instead sustained a significant injury.

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CONCLUSION

Knee injuries are common in soccer, with an alarming number of ACL injuries, as well as other significant pathology. Understanding the unique epidemiology, risk factors, treatment, and injury prevention strategies is critically important in helping medical professionals provide care for all levels of elite soccer players.

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22. Dragoo JL, Braun HJ, Harris AH. The effect of playing surface on the incidence of ACL injuries in National Collegiate Athletic Association American Football. Knee. 2013;20(3):191-195. doi:10.1016/j.knee.2012.07.006.

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25. Waldén M, Krosshaug T, Bjørneboe J, Andersen TE, Faul O, Hägglund M. Three distinct mechanisms predominate in non-contact anterior cruciate ligament injuries in male professional football players: a systematic video analysis of 39 cases. Br J Sports Med. 2015;49(22):1452-1460. doi:10.1136/bjsports-2014-094573.

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27. Giza E, Mithöfer K, Farrell L, Zarins B, Gill T. Injuries in women's professional soccer. Br J Sports Med. 2005;39(4):212-216; discussion 212-216. doi:10.1136/bjsm.2004.011973.

28. Grassi A, Smiley SP, Roberti di Sarsina T, et al. Mechanisms and situations of anterior cruciate ligament injuries in professional male soccer players: a YouTube-based video analysis. Eur J Orthop Surg Traumatol. 2017;27(7):967-981. doi:10.1007/s00590-017-1905-0.

29. Brophy RH, Stepan JG, Silvers HJ, Mandelbaum BR. Defending puts the anterior cruciate ligament at risk during soccer: a gender-based analysis. Sports Health. 2015;7(3):244-249. doi:10.1177/1941738114535184.

30. Faude O, Junge A, Kindermann W, Dvorak J. Risk factors for injuries in elite female soccer players. Br J Sports Med. 2006;40(9):785-790. doi:10.1136/bjsm.2006.027540.

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34. Mihata LC, Beutler AI, Boden BP. Comparing the incidence of anterior cruciate ligament injury in collegiate lacrosse, soccer, and basketball players: implications for anterior cruciate ligament mechanism and prevention. Am J Sports Med. 2006;34(6):899-904. doi:10.1177/0363546505285582.

35. Prodromos CC, Han Y, Rogowski J, Joyce B, Shi K. A meta-analysis of the incidence of anterior cruciate ligament tears as a function of gender, sport, and a knee injury-reduction regimen. Arthroscopy. 2007;23(12):1320-1325.e1326. doi:10.1016/j.arthro.2007.07.003.

36. Allen MM, Pareek A, Krych AJ, et al. Are female soccer players at an increased risk of second anterior cruciate ligament injury compared with their athletic peers? Am J Sports Med. 2016;44(10):2492-2498. doi:10.1177/0363546516648439.

37. Farber J, Harris JD, Kolstad K, McCulloch PC. Treatment of anterior cruciate ligament injuries by major league soccer team physicians. Orthop J Sports Med. 2014;2(11):2325967114559892. doi:10.1177/2325967114559892.

38. Mascarenhas R, Tranovich M, Karpie JC, Irrgang JJ, Fu FH, Harner CD. Patellar tendon anterior cruciate ligament reconstruction in the high-demand patient: evaluation of autograft versus allograft reconstruction. Arthroscopy. 2010;26(9 Suppl):S58-66. doi:10.1016/j.arthro.2010.01.004.

39. Kaeding CC, Aros B, Pedroza A, et al. Allograft versus autograft anterior cruciate ligament reconstruction: predictors of failure from a MOON prospective longitudinal cohort. Sports Health. 2011;3(1):73-81. doi:10.1177/1941738110386185.

40. Pallis M, Svoboda SJ, Cameron KL, Owens BD. Survival comparison of allograft and autograft anterior cruciate ligament reconstruction at the United States Military Academy. Am J Sports Med. 2012;40(6):1242-1246. doi:10.1177/0363546512443945.

41. Gifstad T, Foss OA, Engebretsen L, et al. Lower risk of revision with patellar tendon autografts compared with hamstring autografts: a registry study based on 45,998 primary ACL reconstructions in Scandinavia. Am J Sports Med. 2014;42(10):2319-2328. doi:10.1177/0363546514548164.

42. Mohammadi F, Salavati M, Akhbari B, Mazaheri M, Mohsen Mir S, Etemadi Y. Comparison of functional outcome measures after ACL reconstruction in competitive soccer players: a randomized trial. J Bone Joint Surg Am. 2013;95(14):1271-1277. doi:10.2106/JBJS.L.00724.

43. van der List JP, DiFelice GS. Arthroscopic primary anterior cruciate ligament repair with suture augmentation. Arthrosc Tech. 2017;6(5):e1529-e1534. doi:10.1016/j.eats.2017.06.009.

44. Murray MM, Flutie BM, Kalish LA, et al. The bridge-enhanced anterior cruciate ligament repair (BEAR) procedure: an early feasibility cohort study. Orthop J Sports Med. 2016;4(11):2325967116672176. doi:10.1177/2325967116672176.

45. DiFelice GS, van der List JP. Clinical outcomes of arthroscopic primary repair of proximal anterior cruciate ligament tears are maintained at mid-term follow-up. Arthroscopy. 2018;34(4):1085-1093. doi:10.1016/j.arthro.2017.10.028.

46. Howard JS, Lembach ML, Metzler AV, Johnson DL. Rates and determinants of return to play after anterior cruciate ligament reconstruction in national collegiate athletic association division I soccer athletes: a study of the southeastern conference. Am J Sports Med. 2016;44(2):433-439. doi:10.1177/0363546515614315.

47. Erickson BJ, Harris JD, Cvetanovich GL, et al. Performance and return to sport after anterior cruciate ligament reconstruction in male major league soccer players. Orthop J Sports Med. 2013;1(2):2325967113497189. doi:10.1177/2325967113497189.

48. Arundale AJH, Silvers-Granelli HJ, Snyder-Mackler L. Career length and injury incidence after anterior cruciate ligament reconstruction in major league soccer players. Orthop J Sports Med. 2018;6(1):2325967117750825. doi:10.1177/2325967117750825.

49. Brophy RH, Schmitz L, Wright RW, et al. Return to play and future ACL injury risk after ACL reconstruction in soccer athletes from the Multicenter Orthopaedic Outcomes Network (MOON) group. Am J Sports Med. 2012;40(11):2517-2522. doi:10.1177/0363546512459476.

50. Zaffagnini S, Grassi A, Marcheggiani Muccioli GM, et al. Return to sport after anterior cruciate ligament reconstruction in professional soccer players. Knee. 2014;21(3):731-735. doi:10.1016/j.knee.2014.02.005.

51. Waldén M, Hägglund M, Magnusson H, Ekstrand J. ACL injuries in men's professional football: a 15-year prospective study on time trends and return-to-play rates reveals only 65% of players still play at the top level 3 years after ACL rupture. Br J Sports Med. 2016;50(12):744-750. doi:10.1136/bjsports-2015-095952.

52. Andernord D, Desai N, Björnsson H, Ylander M, Karlsson J, Samuelsson K. Patient predictors of early revision surgery after anterior cruciate ligament reconstruction: a cohort study of 16,930 patients with 2-year follow-up. Am J Sports Med. 2015;43(1):121-127. doi:10.1177/0363546514552788.

53. Kramer DE, Miller PE, Berrahou IK, Yen YM, Heyworth BE. Collateral ligament knee injuries in pediatric and adolescent athletes. J Pediatr Orthop. 2017. doi:10.1097/BPO.0000000000001112.

54. Krutsch W, Zeman F, Zellner J, Pfeifer C, Nerlich M, Angele P. Increase in ACL and PCL injuries after implementation of a new professional football league. Knee Surg Sports Traumatol Arthrosc. 2016;24(7):2271-2279. doi:10.1007/s00167-014-3357-y.

55. Lundblad M, Waldén M, Magnusson H, Karlsson J, Ekstrand J. The UEFA injury study: 11-year data concerning 346 MCL injuries and time to return to play. Br J Sports Med. 2013;47(12):759-762. doi:10.1136/bjsports-2013-092305.

56. Stanley LE, Kerr ZY, Dompier TP, Padua DA. Sex differences in the incidence of anterior cruciate ligament, medial collateral ligament, and meniscal injuries in collegiate and high school sports: 2009-2010 Through 2013-2014. Am J Sports Med. 2016;44(6):1565-1572. doi:10.1177/0363546516630927.

57. Lind M, Jakobsen BW, Lund B, Hansen MS, Abdallah O, Christiansen SE. Anatomical reconstruction of the medial collateral ligament and posteromedial corner of the knee in patients with chronic medial collateral ligament instability. Am J Sports Med. 2009;37(6):1116-1122. doi:10.1177/0363546509332498.

58. Wijdicks CA, Griffith CJ, Johansen S, Engebretsen L, LaPrade RF. Injuries to the medial collateral ligament and associated medial structures of the knee. J Bone Joint Surg Am. 2010;92(5):1266-1280. doi:10.2106/JBJS.I.01229.

59. Marchant MH, Tibor LM, Sekiya JK, Hardaker WT, Garrett WE, Taylor DC. Management of medial-sided knee injuries, part 1: medial collateral ligament. Am J Sports Med. 2011;39(5):1102-1113. doi:10.1177/0363546510385999.

60. Corten K, Hoser C, Fink C, Bellemans J. Case reports: a Stener-like lesion of the medial collateral ligament of the knee. Clin Orthop Relat Res. 2010;468(1):289-293. doi:10.1007/s11999-009-0992-6

61. Fanelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529. doi:10.1016/0749-8063(95)90127-2.

62. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191. doi:10.1007/s00402-002-0471-y.

63. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557. doi:10.1177/036354658701500606.

64. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146. doi:10.1007/s11420-007-9058-z.

65. Owesen C, Sandven-Thrane S, Lind M, Forssblad M, Granan LP, Årøen A. Epidemiology of surgically treated posterior cruciate ligament injuries in Scandinavia. Knee Surg Sports Traumatol Arthrosc. 2017;25(8):2384-2391. doi:10.1007/s00167-015-3786-2.

66. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092. doi:10.1177/0363546515572770.

67. Anderson CL. High rate of osteoarthritis of the knee in former soccer players. Med Sci Sports Exerc. 1986;18(1):141.

68. Arliani GG, Astur DC, Yamada RK, et al. Early osteoarthritis and reduced quality of life after retirement in former professional soccer players. Clinics (Sao Paulo). 2014;69(9):589-594. doi:10.6061/clinics/2014(09)03.

69. Wong P, Hong Y. Soccer injury in the lower extremities. Br J Sports Med. 2005;39(8):473-482. doi:10.1136/bjsm.2004.015511.

70. Thelin N, Holmberg S, Thelin A. Knee injuries account for the sports-related increased risk of knee osteoarthritis. Scand J Med Sci Sports. 2006;16(5):329-333. doi:10.1111/j.1600-0838.2005.00497.x.

71. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cruciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007;35(10):1756-1769. doi:10.1177/0363546507307396.

72. Mithöfer K, Peterson L, Mandelbaum BR, Minas T. Articular cartilage repair in soccer players with autologous chondrocyte transplantation: functional outcome and return to competition. Am J Sports Med. 2005;33(11):1639-1646. doi:10.1177/0363546505275647

73. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477-484. doi:10.1053/jars.2003.50112.

74. Hangody L, Ráthonyi GK, Duska Z, Vásárhelyi G, Füles P, Módis L. Autologous osteochondral mosaicplasty. Surgical technique. J Bone Joint Surg Am. 2004;86-A Suppl 1:65-72.

75. Sherman SL, Garrity J, Bauer K, Cook J, Stannard J, Bugbee W. Fresh osteochondral allograft transplantation for the knee: current concepts. J Am Acad Orthop Surg. 2014;22(2):121-133. doi:10.5435/JAAOS-22-02-121.

76. Andrade R, Vasta S, Papalia R, et al. Prevalence of articular cartilage lesions and surgical clinical outcomes in football (soccer) players' knees: a systematic review. Arthroscopy. 2016;32(7):1466-1477. doi:10.1016/j.arthro.2016.01.055.

77. Görtz S, Williams RJ, Gersoff WK, Bugbee WD. Osteochondral and meniscal allograft transplantation in the football (soccer) player. Cartilage. 2012;3(1 Suppl):37S-42S. doi:10.1177/1947603511416974.

78. Junge A, Grimm K, Feddermann N, Dvorak J. Precompetition orthopedic assessment of international elite football players. Clin J Sport Med. 2009;19(4):326-328. doi:10.1097/JSM.0b013e3181b21b56.

79. Salzmann GM, Preiss S, Zenobi-Wong M, Harder LP, Maier D, Dvorák J. Osteoarthritis in Football. Cartilage. 2017;8(2):162-172. doi:10.1177/1947603516648186.

80. Makris EA, Hadidi P, Athanasiou KA. The knee meniscus: structure-function, pathophysiology, current repair techniques, and prospects for regeneration. Biomaterials. 2011;32(30):7411-7431. doi:10.1016/j.biomaterials.2011.06.037

81. Freutel M, Seitz AM, Ignatius A, Dürselen L. Influence of partial meniscectomy on attachment forces, superficial strain and contact mechanics in porcine knee joints. Knee Surg Sports Traumatol Arthrosc. 2015;23(1):74-82. doi:10.1007/s00167-014-2951-3.

82. Papalia R, Del Buono A, Osti L, Denaro V, Maffulli N. Meniscectomy as a risk factor for knee osteoarthritis: a systematic review. Br Med Bull. 2011;99:89-106. doi:10.1093/bmb/ldq043.

83. Nawabi DH, Cro S, Hamid IP, Williams A. Return to play after lateral meniscectomy compared with medial meniscectomy in elite professional soccer players. Am J Sports Med. 2014;42(9):2193-2198. doi:10.1177/0363546514540271.

84. Alentorn-Geli E, Vázquez RS, Díaz PA, Cuscó X, Cugat R. Arthroscopic meniscal transplants in soccer players: outcomes at 2- to 5-year follow-up. Clin J Sport Med. 2010;20(5):340-343. doi:10.1097/JSM.0b013e3181f207dc.

85. Marcacci M, Marcheggiani Muccioli GM, Grassi A, et al. Arthroscopic meniscus allograft transplantation in male professional soccer players: a 36-month follow-up study. Am J Sports Med. 2014;42(2):382-388. doi:10.1177/0363546513508763.

86. Bizzini M, Dvorak J. FIFA 11+: an effective programme to prevent football injuries in various player groups worldwide-a narrative review. Br J Sports Med. 2015;49(9):577-579. doi:10.1136/bjsports-2015-094765.

87. Junge A, Lamprecht M, Stamm H, et al. Countrywide campaign to prevent soccer injuries in Swiss amateur players. Am J Sports Med. 2011;39(1):57-63. doi:10.1177/0363546510377424.

88. Al Attar WSA, Soomro N, Pappas E, Sinclair PJ, Sanders RH. Adding a post-training FIFA 11+ exercise program to the pre-training FIFA 11+ injury prevention program reduces injury rates among male amateur soccer players: a cluster-randomised trial. J Physiother. 2017;63(4):235-242. doi:10.1016/j.jphys.2017.08.004.

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61. Fanelli GC, Edson CJ. Posterior cruciate ligament injuries in trauma patients: Part II. Arthroscopy. 1995;11(5):526-529. doi:10.1016/0749-8063(95)90127-2.

62. Schulz MS, Russe K, Weiler A, Eichhorn HJ, Strobel MJ. Epidemiology of posterior cruciate ligament injuries. Arch Orthop Trauma Surg. 2003;123(4):186-191. doi:10.1007/s00402-002-0471-y.

63. Fowler PJ, Messieh SS. Isolated posterior cruciate ligament injuries in athletes. Am J Sports Med. 1987;15(6):553-557. doi:10.1177/036354658701500606.

64. Patel DV, Allen AA, Warren RF, Wickiewicz TL, Simonian PT. The nonoperative treatment of acute, isolated (partial or complete) posterior cruciate ligament-deficient knees: an intermediate-term follow-up study. HSS J. 2007;3(2):137-146. doi:10.1007/s11420-007-9058-z.

65. Owesen C, Sandven-Thrane S, Lind M, Forssblad M, Granan LP, Årøen A. Epidemiology of surgically treated posterior cruciate ligament injuries in Scandinavia. Knee Surg Sports Traumatol Arthrosc. 2017;25(8):2384-2391. doi:10.1007/s00167-015-3786-2.

66. LaPrade CM, Civitarese DM, Rasmussen MT, LaPrade RF. Emerging updates on the posterior cruciate ligament: a review of the current literature. Am J Sports Med. 2015;43(12):3077-3092. doi:10.1177/0363546515572770.

67. Anderson CL. High rate of osteoarthritis of the knee in former soccer players. Med Sci Sports Exerc. 1986;18(1):141.

68. Arliani GG, Astur DC, Yamada RK, et al. Early osteoarthritis and reduced quality of life after retirement in former professional soccer players. Clinics (Sao Paulo). 2014;69(9):589-594. doi:10.6061/clinics/2014(09)03.

69. Wong P, Hong Y. Soccer injury in the lower extremities. Br J Sports Med. 2005;39(8):473-482. doi:10.1136/bjsm.2004.015511.

70. Thelin N, Holmberg S, Thelin A. Knee injuries account for the sports-related increased risk of knee osteoarthritis. Scand J Med Sci Sports. 2006;16(5):329-333. doi:10.1111/j.1600-0838.2005.00497.x.

71. Lohmander LS, Englund PM, Dahl LL, Roos EM. The long-term consequence of anterior cruciate ligament and meniscus injuries: osteoarthritis. Am J Sports Med. 2007;35(10):1756-1769. doi:10.1177/0363546507307396.

72. Mithöfer K, Peterson L, Mandelbaum BR, Minas T. Articular cartilage repair in soccer players with autologous chondrocyte transplantation: functional outcome and return to competition. Am J Sports Med. 2005;33(11):1639-1646. doi:10.1177/0363546505275647

73. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, Gill TJ, Rodkey WG. Outcomes of microfracture for traumatic chondral defects of the knee: average 11-year follow-up. Arthroscopy. 2003;19(5):477-484. doi:10.1053/jars.2003.50112.

74. Hangody L, Ráthonyi GK, Duska Z, Vásárhelyi G, Füles P, Módis L. Autologous osteochondral mosaicplasty. Surgical technique. J Bone Joint Surg Am. 2004;86-A Suppl 1:65-72.

75. Sherman SL, Garrity J, Bauer K, Cook J, Stannard J, Bugbee W. Fresh osteochondral allograft transplantation for the knee: current concepts. J Am Acad Orthop Surg. 2014;22(2):121-133. doi:10.5435/JAAOS-22-02-121.

76. Andrade R, Vasta S, Papalia R, et al. Prevalence of articular cartilage lesions and surgical clinical outcomes in football (soccer) players' knees: a systematic review. Arthroscopy. 2016;32(7):1466-1477. doi:10.1016/j.arthro.2016.01.055.

77. Görtz S, Williams RJ, Gersoff WK, Bugbee WD. Osteochondral and meniscal allograft transplantation in the football (soccer) player. Cartilage. 2012;3(1 Suppl):37S-42S. doi:10.1177/1947603511416974.

78. Junge A, Grimm K, Feddermann N, Dvorak J. Precompetition orthopedic assessment of international elite football players. Clin J Sport Med. 2009;19(4):326-328. doi:10.1097/JSM.0b013e3181b21b56.

79. Salzmann GM, Preiss S, Zenobi-Wong M, Harder LP, Maier D, Dvorák J. Osteoarthritis in Football. Cartilage. 2017;8(2):162-172. doi:10.1177/1947603516648186.

80. Makris EA, Hadidi P, Athanasiou KA. The knee meniscus: structure-function, pathophysiology, current repair techniques, and prospects for regeneration. Biomaterials. 2011;32(30):7411-7431. doi:10.1016/j.biomaterials.2011.06.037

81. Freutel M, Seitz AM, Ignatius A, Dürselen L. Influence of partial meniscectomy on attachment forces, superficial strain and contact mechanics in porcine knee joints. Knee Surg Sports Traumatol Arthrosc. 2015;23(1):74-82. doi:10.1007/s00167-014-2951-3.

82. Papalia R, Del Buono A, Osti L, Denaro V, Maffulli N. Meniscectomy as a risk factor for knee osteoarthritis: a systematic review. Br Med Bull. 2011;99:89-106. doi:10.1093/bmb/ldq043.

83. Nawabi DH, Cro S, Hamid IP, Williams A. Return to play after lateral meniscectomy compared with medial meniscectomy in elite professional soccer players. Am J Sports Med. 2014;42(9):2193-2198. doi:10.1177/0363546514540271.

84. Alentorn-Geli E, Vázquez RS, Díaz PA, Cuscó X, Cugat R. Arthroscopic meniscal transplants in soccer players: outcomes at 2- to 5-year follow-up. Clin J Sport Med. 2010;20(5):340-343. doi:10.1097/JSM.0b013e3181f207dc.

85. Marcacci M, Marcheggiani Muccioli GM, Grassi A, et al. Arthroscopic meniscus allograft transplantation in male professional soccer players: a 36-month follow-up study. Am J Sports Med. 2014;42(2):382-388. doi:10.1177/0363546513508763.

86. Bizzini M, Dvorak J. FIFA 11+: an effective programme to prevent football injuries in various player groups worldwide-a narrative review. Br J Sports Med. 2015;49(9):577-579. doi:10.1136/bjsports-2015-094765.

87. Junge A, Lamprecht M, Stamm H, et al. Countrywide campaign to prevent soccer injuries in Swiss amateur players. Am J Sports Med. 2011;39(1):57-63. doi:10.1177/0363546510377424.

88. Al Attar WSA, Soomro N, Pappas E, Sinclair PJ, Sanders RH. Adding a post-training FIFA 11+ exercise program to the pre-training FIFA 11+ injury prevention program reduces injury rates among male amateur soccer players: a cluster-randomised trial. J Physiother. 2017;63(4):235-242. doi:10.1016/j.jphys.2017.08.004.

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TAKE-HOME POINTS

  • Soccer is one of the most popular sports in the world and has a high incidence of resultant knee injuries.
  • Significant, identifiable risk factors put soccer players at risk for serious knee injuries, such as ACL ruptures; age, female sex, and position played influence injury susceptibility.
  • ACL injury most commonly occurs via non-contact mechanisms, and female players are at a significantly higher risk of ACL injury than male counterparts.
  • The prevalence of osteoarthritis in retired soccer players is high, underscoring the need to be familiar with meniscal and cartilage repair/restoration techniques and associated outcomes.
  • The FIFA11+ program reduces injury by 30%, with reported relative risk of 0.70 for lower limb injuries, highlighting the significant preventative importance of this warm-up program.
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Composite Fixation of Proximal Tibial Nonunions: A Technical Trick

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Changed
Thu, 09/19/2019 - 13:17

ABSTRACT

Nonunion after a proximal tibia fracture is often associated with poor bone stock, (previous) infection, and compromised soft tissues. These conditions make revision internal fixation with double plating difficult. Combining a plate and contralateral 2-pin external fixator, coined composite fixation, can provide an alternative means of obtaining stability without further compromising soft tissues.

Three patients with a proximal tibia nonunion precluding standard internal fixation with double plating were treated with composite fixation. All 3 patients achieved union with deformity correction at a mean of 5.2 months (range, 5-5.5 months). The average range of motion (ROM) arc was 100° (range, 100°-115°) and postoperative ROM returned to pre-injury levels.

Composite fixation can be a helpful adjunct in the treatment of this challenging problem.

Continue to: Operative management of a proximal tibial nonunion...

 

 

Operative management of a proximal tibial nonunion is challenging, compromised by limited bone stock, pre-existing hardware, stiffness, poor soft tissue conditions, and infection. The goals of treatment include bone union, re-establishment of both joint stability and lower extremity alignment, restoration of an anatomic articular surface, and recovery of function.1 Currently, various treatment options such as plate fixation, bone grafting, intramedullary nailing, external fixation, functional bracing, or a combination of these are available.1-8 Rigid internal fixation is the gold standard for most nonunions. However, sometimes local soft tissues or bone quality preclude standard internal fixation. Bolhofner9 described the combination of a single plate and an external fixator on the contralateral side for the management of extra-articular proximal tibial fractures with compromised soft tissues, and the technique known as composite fixation was coined. The external fixator on 1 side and the plate on the other, generate a balanced, stable environment while limiting the use of foreign hardware, thereby avoiding both additional soft-tissue damage and periosteal stripping.9-11 In this technical article, we describe the indication, technique, and outcomes of 3 patients with proximal tibial nonunions, who were successfully treated with composite fixation.

MATERIALS AND METHODS 

PATIENTS

Between January 2014 and July 2016, 3 patients each with a proximal tibial nonunion that developed after a bicondylar tibial plateau fracture (Schatzker type VI) were treated with composite fixation (Table). The 3 patients were female with an average age of 61 years (range, 60-62 years), and a body mass index of 23.7 kg/m2 (range, 19.0-31.9 kg/m2). All 3 patients had sustained a tibial plateau fracture that was primarily treated with open reduction and internal fixation. Two of them had a diagnosis of rheumatoid arthritis and were being treated with methotrexate and Humira (adalimumab) (case 1), and with methotrexate, prednisolone, and etanercept (case 3). The etanercept was discontinued after discussion with the treating rheumatologist when a deep infection developed. Two patients (cases 1 and 2) were referred to us because of their nonunions. All 3 patients developed extra-articular nonunions with compromised bone stock. Two patients had developed deep infections during treatment of their plateau fractures; 1 of these patients underwent a medial gastrocnemius flap for wound coverage (case 1). The second patient (case 3) with a deep infection underwent partial hardware removal, a Masquelet salvage procedure, and revision plate fixation. However, the infection recurred. The hardware was removed, and 2 débridements with conversion to a hybrid external fixator with thin wire fixation were done. Due to her longstanding rheumatoid arthritis, the patient had bilateral valgus knee malalignment causing the ring fixator to strike her contralateral knee when she walked. The period from the initial tibial plateau fracture to our composite fixation averaged 11.3 months (range, 11-12 months). Indications for the use of the composite fixation comprised previously infected soft tissue on the lateral side and inability to walk with a hybrid thin wire fixator because of valgus knees (case 3), a medial gastrocnemius flap (case 2), and poor bone quality (case 1). Follow-up consisted of clinical examination, Timed Up and Go (TUG) test that is a standardized test for mobility, and radiographic evaluation at routine appointments up to 1 year or until healed.12 At the last follow-up visit, patients filled out the International Knee Documentation Committee (IKDC) subjective knee form.13

donders0918_t1

SURGICAL TECHNIQUE

A fellowship-trained orthopedic trauma surgeon treated all patients. Patients were placed on a radiolucent operating table after general or regional anesthesia. Previous incisions were used. Two patients had a midline incision; the third had both a posteromedial and an anterolateral incision. Five deep tissue cultures were taken after which antibiotics were given intravenously. All unstable or failed hardware was removed. Aggressive débridement of the nonunion was performed. After débridement, multiple holes were drilled with a 2.0 mm drill bit until blood was seen to egress from both sides of the medullary canal. Malalignment of the proximal tibia was corrected and checked fluoroscopically. Fixation was done with an anatomic locking plate (LCP Proximal Tibia Plate 3.5; DePuy Synthes) with a mixture of locking and non-locking screws. In 2 patients, a tricortical graft from the posterior iliac crest was positioned in the defect. Additional autologous bone graft and demineralized bone matrix was added around the nonunion. Although locking screws were used, the fixation did not appear to be strong enough to resist the varus (cases 1 and 2), or the valgus (case 3) deforming forces. Additional fixation was thus needed. However, the contralateral soft tissues were compromised in case 2 (medial gastrocnemius flap), and case 3 (a previously infected area with very tenuous skin laterally), whereas the bone was considered to be of insufficient quality in case 1. The opposite side of the nonunion was stabilized using composite fixation with a 2-pin external fixator to circumvent the need for additional plate fixation. In 2 patients, the plate was placed laterally, and the external fixator medially. In the third patient, the plate was positioned medially, and the external fixator laterally. The plate was always placed first. The external fixator was placed last. Using fluoroscopy, we ensured that the fixator pins would not interfere with the screws. The pins were predrilled and positioned perpendicular to the tibia through small stab incisions. We prefer hydroxyapatite-coated pins (6-mm diameter, XCaliber Bone Screws; Pro-Motion Medical) to increase their holding power in the often osteopenic bone. Postoperative management consisted of toe-touch weight-bearing for 6 weeks and progressed to full weight-bearing at 3 months. Radiographs were taken on postoperative day 1, at 6 weeks, and at 12 weeks until healed. No continuous passive motion was used postoperatively. Antibiotics were continued until cultures were negative. No specific pin care was used. We advised patients to shower daily with the external fixator in place, once the wounds have healed.

Continue to: RESULTS... 

 

 

RESULTS

On average, patients were hospitalized for 5 days (range, 3-7 days). There were no postoperative complications. None of the patients developed a clinically significant pin site infection. There were no re-operations during follow-up. All patients achieved union at a mean of 5.2 months (range, 5-5.5 months) (Figure 1).

donders0918_f1

Deformity correction was achieved in all 3 patients. The average range of motion (ROM) arc was 100° (range, 100°-115°). None of the patients had an extension deficit. TUG test was <8 seconds in all patients. The IKDC knee score averaged 52 (range, 41-66). Of note is that 2 patients already had compromised knee function before the fracture because of rheumatoid arthritis. The Ahlbäck classification of osteoarthritis showed grade 1 in cases 1 and 3, and grade 2 in case 2.14 Postoperative ROM of the knee returned to pre-injury levels in all patients (Figure 2). The 2-pin external fixator was removed at 9 weeks on average (range, 6-12 weeks) postoperatively in the outpatient clinic. At the last follow-up appointment at an average of 10.3 months (range, 9-12 months), all wounds had healed without infection. All patients had a normal neurovascular examination.

donders0918_f2

DISCUSSION

Nonunion after a proximal tibial fracture is rare.4 In cases when nonunions do develop, they most often pertain to the extra-articular component with the plateau component healed. Surgical exposure for débridements, hardware removal, bone grafting, and revision of fixation carries the risk of wound breakdown, necrosis, and infection. The alternative strategy of composite fixation (a plate combined with a contralateral 2-pin external fixator) to limit additional soft tissue compromise was already described in proximal tibial fractures by Bolhofner.9 He treated 41 extra-articular proximal tibial fractures using this composite fixation technique and attained successful results with an average time to union of 12.1 weeks. There was only 1 malunion, 2 wound infections, and 3 delayed unions.

In our practice, we have extrapolated this idea to an extra-articular nonunion that developed after a tibial plateau fracture. With the use of an external fixator, we provided sufficient mechanical stability of the nonunion without unnecessarily compromising previously infected or tenuous soft tissues, a muscle flap, or further devascularizing poor bone. Limitations of this study include the retrospective data and small sample size prone to bias. However, all patients received the same treatment protocol from 1 orthopedic trauma surgeon, follow-up intervals were similar, and data were acquired consistently.

Meanwhile, we have used this technique in a fourth patient with a septic nonunion of a tibial plateau fracture. All 4 patients in whom we have used this method so far have healed successfully.

CONCLUSION

This technique respects both the demand for minimal soft tissue damage and a maximal stable environment without notable perioperative and postoperative complications. It also offers an alternative option for the treatment of a proximal tibial nonunion that is not amenable to invasive revision dual plate fixation. As such, it can be a useful addition to the existing armamentarium of the treating surgeon.

References

1. Wu CC. Salvage of proximal tibial malunion or nonunion with the use of angled blade plate. Arch Orthop Trauma Surg. 2006;126(2):82-87. doi:10.1007/s00402-006-0106-9.

2. Carpenter CA, Jupiter JB. Blade plate reconstruction of metaphyseal nonunion of the tibia. Clin Orthop Relat Res. 1996;332:23-28.

3. Gardner MJ, Toro-Arbelaez JB, Hansen M, Boraiah S, Lorich DG, Helfet DL. Surgical treatment and outcomes of extraarticular proximal tibial nonunions. Arch Orthop Trauma Surg. 2008;128(8):833-839. doi:10.1007/s00402-007-0383-y.

4. Toro-Arbelaez JB, Gardner MJ, Shindle MK, Cabas JM, Lorich DG, Helfet DL. Open reduction and internal fixation of intraarticular tibial plateau nonunions. Injury. 2007;38(3):378-383. doi:10.1016/j.injury.2006.11.003.

5. Mechrefe AP, Koh EY, Trafton PG, DiGiovanni CW. Tibial nonunion. Foot Ankle Clin. 2006;11(1):1-18, vii. doi:10.1016/j.fcl.2005.12.003.

6. Chin KR, Nagarkatti DG, Miranda MA, Santoro VM, Baumgaertner MR, Jupiter JB. Salvage of distal tibia metaphyseal nonunions with the 90 degrees cannulated blade plate. Clin Orthop Relat Res. 2003;(409):241-249.

7. Devgan A, Kamboj P, Gupta V, Magu NK, Rohilla R. Pseudoarthrosis of medial tibial plateau fracture-role of alignment procedure. Chin J Traumatol. 2013;16(2):118-121. doi:10.3760/cma.j.issn.1008-1275.2013.02.011.

8. Helfet DL, Jupiter JB, Gasser S. Indirect reduction and tension-band plating of tibial non-union with deformity. J Bone Joint Surg Am. 1992;74(9):1286-1297.

9. Bolhofner BR. Indirect reduction and composite fixation of extraarticular proximal tibial fractures. Clin Orthop Relat Res. 1995;(315):75-83. doi:10.1097/00003086-199506000-00009.

10. Ries MD, Meinhard BP. Medial external fixation with lateral plate internal fixation in metaphyseal tibia fractures. A report of eight cases associated with severe soft-tissue injury. Clin Orthop Relat Res. 1988;(256):215-223. 

11. Weiner LS, Kelley M, Yang E, et al. The use of combination internal fixation and hybrid external fixation in severe proximal tibia fractures. J Orthop Trauma. 1995;9(3):244-250.

12. Alghadir A, Anwer S, Brismee JM. The reliability and minimal detectable change of Timed Up and Go test in individuals with grade 1-3 knee osteoarthritis. BMC Musculoskelet Disord. 2015;16:174. doi:10.1186/s12891-015-0637-8.

13. Haverkamp D, Sierevelt IN, Breugem SJ, Lohuis K, Blankevoort L, van Dijk CN. Translation and validation of the Dutch version of the International Knee Documentation Committee Subjective Knee Form. Am J Sports Med. 2006;34(10):1680-1684. doi:10.1177/0363546506288854.

14. Ahlbäck S. Osteoartrosis of the knee. A radiographic investigation. Acta Radiol Diagn (Stockh). 1968;Suppl 277:7-72.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Prins is PhD candidate, Department of Surgery, Erasmus Medical Center, Rotterdam, The Netherlands. Dr. Kloen is an Orthopedic Surgeon, and Dr. Donders is PhD candidate, Department of Orthopedic Surgery, Academic Medical Center, Amsterdam, The Netherlands.

Address correspondence to: Peter Kloen, MD, PhD, Department of Orthopedic Surgery, Academic Medical Center, Meibergdreef 9, 1100 DD, Amsterdam, The Netherlands. (tel, 31-205669111; fax, 31-205669117; email, p.kloen@amc.uva.nl).

Jonne Prins, MD Johanna C.E. Donders, MD and Peter Kloen, MD, PhD . Composite Fixation of Proximal Tibial Nonunions: A Technical Trick. Am J Orthop.

September 27, 2018

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Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Prins is PhD candidate, Department of Surgery, Erasmus Medical Center, Rotterdam, The Netherlands. Dr. Kloen is an Orthopedic Surgeon, and Dr. Donders is PhD candidate, Department of Orthopedic Surgery, Academic Medical Center, Amsterdam, The Netherlands.

Address correspondence to: Peter Kloen, MD, PhD, Department of Orthopedic Surgery, Academic Medical Center, Meibergdreef 9, 1100 DD, Amsterdam, The Netherlands. (tel, 31-205669111; fax, 31-205669117; email, p.kloen@amc.uva.nl).

Jonne Prins, MD Johanna C.E. Donders, MD and Peter Kloen, MD, PhD . Composite Fixation of Proximal Tibial Nonunions: A Technical Trick. Am J Orthop.

September 27, 2018

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Prins is PhD candidate, Department of Surgery, Erasmus Medical Center, Rotterdam, The Netherlands. Dr. Kloen is an Orthopedic Surgeon, and Dr. Donders is PhD candidate, Department of Orthopedic Surgery, Academic Medical Center, Amsterdam, The Netherlands.

Address correspondence to: Peter Kloen, MD, PhD, Department of Orthopedic Surgery, Academic Medical Center, Meibergdreef 9, 1100 DD, Amsterdam, The Netherlands. (tel, 31-205669111; fax, 31-205669117; email, p.kloen@amc.uva.nl).

Jonne Prins, MD Johanna C.E. Donders, MD and Peter Kloen, MD, PhD . Composite Fixation of Proximal Tibial Nonunions: A Technical Trick. Am J Orthop.

September 27, 2018

ABSTRACT

Nonunion after a proximal tibia fracture is often associated with poor bone stock, (previous) infection, and compromised soft tissues. These conditions make revision internal fixation with double plating difficult. Combining a plate and contralateral 2-pin external fixator, coined composite fixation, can provide an alternative means of obtaining stability without further compromising soft tissues.

Three patients with a proximal tibia nonunion precluding standard internal fixation with double plating were treated with composite fixation. All 3 patients achieved union with deformity correction at a mean of 5.2 months (range, 5-5.5 months). The average range of motion (ROM) arc was 100° (range, 100°-115°) and postoperative ROM returned to pre-injury levels.

Composite fixation can be a helpful adjunct in the treatment of this challenging problem.

Continue to: Operative management of a proximal tibial nonunion...

 

 

Operative management of a proximal tibial nonunion is challenging, compromised by limited bone stock, pre-existing hardware, stiffness, poor soft tissue conditions, and infection. The goals of treatment include bone union, re-establishment of both joint stability and lower extremity alignment, restoration of an anatomic articular surface, and recovery of function.1 Currently, various treatment options such as plate fixation, bone grafting, intramedullary nailing, external fixation, functional bracing, or a combination of these are available.1-8 Rigid internal fixation is the gold standard for most nonunions. However, sometimes local soft tissues or bone quality preclude standard internal fixation. Bolhofner9 described the combination of a single plate and an external fixator on the contralateral side for the management of extra-articular proximal tibial fractures with compromised soft tissues, and the technique known as composite fixation was coined. The external fixator on 1 side and the plate on the other, generate a balanced, stable environment while limiting the use of foreign hardware, thereby avoiding both additional soft-tissue damage and periosteal stripping.9-11 In this technical article, we describe the indication, technique, and outcomes of 3 patients with proximal tibial nonunions, who were successfully treated with composite fixation.

MATERIALS AND METHODS 

PATIENTS

Between January 2014 and July 2016, 3 patients each with a proximal tibial nonunion that developed after a bicondylar tibial plateau fracture (Schatzker type VI) were treated with composite fixation (Table). The 3 patients were female with an average age of 61 years (range, 60-62 years), and a body mass index of 23.7 kg/m2 (range, 19.0-31.9 kg/m2). All 3 patients had sustained a tibial plateau fracture that was primarily treated with open reduction and internal fixation. Two of them had a diagnosis of rheumatoid arthritis and were being treated with methotrexate and Humira (adalimumab) (case 1), and with methotrexate, prednisolone, and etanercept (case 3). The etanercept was discontinued after discussion with the treating rheumatologist when a deep infection developed. Two patients (cases 1 and 2) were referred to us because of their nonunions. All 3 patients developed extra-articular nonunions with compromised bone stock. Two patients had developed deep infections during treatment of their plateau fractures; 1 of these patients underwent a medial gastrocnemius flap for wound coverage (case 1). The second patient (case 3) with a deep infection underwent partial hardware removal, a Masquelet salvage procedure, and revision plate fixation. However, the infection recurred. The hardware was removed, and 2 débridements with conversion to a hybrid external fixator with thin wire fixation were done. Due to her longstanding rheumatoid arthritis, the patient had bilateral valgus knee malalignment causing the ring fixator to strike her contralateral knee when she walked. The period from the initial tibial plateau fracture to our composite fixation averaged 11.3 months (range, 11-12 months). Indications for the use of the composite fixation comprised previously infected soft tissue on the lateral side and inability to walk with a hybrid thin wire fixator because of valgus knees (case 3), a medial gastrocnemius flap (case 2), and poor bone quality (case 1). Follow-up consisted of clinical examination, Timed Up and Go (TUG) test that is a standardized test for mobility, and radiographic evaluation at routine appointments up to 1 year or until healed.12 At the last follow-up visit, patients filled out the International Knee Documentation Committee (IKDC) subjective knee form.13

donders0918_t1

SURGICAL TECHNIQUE

A fellowship-trained orthopedic trauma surgeon treated all patients. Patients were placed on a radiolucent operating table after general or regional anesthesia. Previous incisions were used. Two patients had a midline incision; the third had both a posteromedial and an anterolateral incision. Five deep tissue cultures were taken after which antibiotics were given intravenously. All unstable or failed hardware was removed. Aggressive débridement of the nonunion was performed. After débridement, multiple holes were drilled with a 2.0 mm drill bit until blood was seen to egress from both sides of the medullary canal. Malalignment of the proximal tibia was corrected and checked fluoroscopically. Fixation was done with an anatomic locking plate (LCP Proximal Tibia Plate 3.5; DePuy Synthes) with a mixture of locking and non-locking screws. In 2 patients, a tricortical graft from the posterior iliac crest was positioned in the defect. Additional autologous bone graft and demineralized bone matrix was added around the nonunion. Although locking screws were used, the fixation did not appear to be strong enough to resist the varus (cases 1 and 2), or the valgus (case 3) deforming forces. Additional fixation was thus needed. However, the contralateral soft tissues were compromised in case 2 (medial gastrocnemius flap), and case 3 (a previously infected area with very tenuous skin laterally), whereas the bone was considered to be of insufficient quality in case 1. The opposite side of the nonunion was stabilized using composite fixation with a 2-pin external fixator to circumvent the need for additional plate fixation. In 2 patients, the plate was placed laterally, and the external fixator medially. In the third patient, the plate was positioned medially, and the external fixator laterally. The plate was always placed first. The external fixator was placed last. Using fluoroscopy, we ensured that the fixator pins would not interfere with the screws. The pins were predrilled and positioned perpendicular to the tibia through small stab incisions. We prefer hydroxyapatite-coated pins (6-mm diameter, XCaliber Bone Screws; Pro-Motion Medical) to increase their holding power in the often osteopenic bone. Postoperative management consisted of toe-touch weight-bearing for 6 weeks and progressed to full weight-bearing at 3 months. Radiographs were taken on postoperative day 1, at 6 weeks, and at 12 weeks until healed. No continuous passive motion was used postoperatively. Antibiotics were continued until cultures were negative. No specific pin care was used. We advised patients to shower daily with the external fixator in place, once the wounds have healed.

Continue to: RESULTS... 

 

 

RESULTS

On average, patients were hospitalized for 5 days (range, 3-7 days). There were no postoperative complications. None of the patients developed a clinically significant pin site infection. There were no re-operations during follow-up. All patients achieved union at a mean of 5.2 months (range, 5-5.5 months) (Figure 1).

donders0918_f1

Deformity correction was achieved in all 3 patients. The average range of motion (ROM) arc was 100° (range, 100°-115°). None of the patients had an extension deficit. TUG test was <8 seconds in all patients. The IKDC knee score averaged 52 (range, 41-66). Of note is that 2 patients already had compromised knee function before the fracture because of rheumatoid arthritis. The Ahlbäck classification of osteoarthritis showed grade 1 in cases 1 and 3, and grade 2 in case 2.14 Postoperative ROM of the knee returned to pre-injury levels in all patients (Figure 2). The 2-pin external fixator was removed at 9 weeks on average (range, 6-12 weeks) postoperatively in the outpatient clinic. At the last follow-up appointment at an average of 10.3 months (range, 9-12 months), all wounds had healed without infection. All patients had a normal neurovascular examination.

donders0918_f2

DISCUSSION

Nonunion after a proximal tibial fracture is rare.4 In cases when nonunions do develop, they most often pertain to the extra-articular component with the plateau component healed. Surgical exposure for débridements, hardware removal, bone grafting, and revision of fixation carries the risk of wound breakdown, necrosis, and infection. The alternative strategy of composite fixation (a plate combined with a contralateral 2-pin external fixator) to limit additional soft tissue compromise was already described in proximal tibial fractures by Bolhofner.9 He treated 41 extra-articular proximal tibial fractures using this composite fixation technique and attained successful results with an average time to union of 12.1 weeks. There was only 1 malunion, 2 wound infections, and 3 delayed unions.

In our practice, we have extrapolated this idea to an extra-articular nonunion that developed after a tibial plateau fracture. With the use of an external fixator, we provided sufficient mechanical stability of the nonunion without unnecessarily compromising previously infected or tenuous soft tissues, a muscle flap, or further devascularizing poor bone. Limitations of this study include the retrospective data and small sample size prone to bias. However, all patients received the same treatment protocol from 1 orthopedic trauma surgeon, follow-up intervals were similar, and data were acquired consistently.

Meanwhile, we have used this technique in a fourth patient with a septic nonunion of a tibial plateau fracture. All 4 patients in whom we have used this method so far have healed successfully.

CONCLUSION

This technique respects both the demand for minimal soft tissue damage and a maximal stable environment without notable perioperative and postoperative complications. It also offers an alternative option for the treatment of a proximal tibial nonunion that is not amenable to invasive revision dual plate fixation. As such, it can be a useful addition to the existing armamentarium of the treating surgeon.

ABSTRACT

Nonunion after a proximal tibia fracture is often associated with poor bone stock, (previous) infection, and compromised soft tissues. These conditions make revision internal fixation with double plating difficult. Combining a plate and contralateral 2-pin external fixator, coined composite fixation, can provide an alternative means of obtaining stability without further compromising soft tissues.

Three patients with a proximal tibia nonunion precluding standard internal fixation with double plating were treated with composite fixation. All 3 patients achieved union with deformity correction at a mean of 5.2 months (range, 5-5.5 months). The average range of motion (ROM) arc was 100° (range, 100°-115°) and postoperative ROM returned to pre-injury levels.

Composite fixation can be a helpful adjunct in the treatment of this challenging problem.

Continue to: Operative management of a proximal tibial nonunion...

 

 

Operative management of a proximal tibial nonunion is challenging, compromised by limited bone stock, pre-existing hardware, stiffness, poor soft tissue conditions, and infection. The goals of treatment include bone union, re-establishment of both joint stability and lower extremity alignment, restoration of an anatomic articular surface, and recovery of function.1 Currently, various treatment options such as plate fixation, bone grafting, intramedullary nailing, external fixation, functional bracing, or a combination of these are available.1-8 Rigid internal fixation is the gold standard for most nonunions. However, sometimes local soft tissues or bone quality preclude standard internal fixation. Bolhofner9 described the combination of a single plate and an external fixator on the contralateral side for the management of extra-articular proximal tibial fractures with compromised soft tissues, and the technique known as composite fixation was coined. The external fixator on 1 side and the plate on the other, generate a balanced, stable environment while limiting the use of foreign hardware, thereby avoiding both additional soft-tissue damage and periosteal stripping.9-11 In this technical article, we describe the indication, technique, and outcomes of 3 patients with proximal tibial nonunions, who were successfully treated with composite fixation.

MATERIALS AND METHODS 

PATIENTS

Between January 2014 and July 2016, 3 patients each with a proximal tibial nonunion that developed after a bicondylar tibial plateau fracture (Schatzker type VI) were treated with composite fixation (Table). The 3 patients were female with an average age of 61 years (range, 60-62 years), and a body mass index of 23.7 kg/m2 (range, 19.0-31.9 kg/m2). All 3 patients had sustained a tibial plateau fracture that was primarily treated with open reduction and internal fixation. Two of them had a diagnosis of rheumatoid arthritis and were being treated with methotrexate and Humira (adalimumab) (case 1), and with methotrexate, prednisolone, and etanercept (case 3). The etanercept was discontinued after discussion with the treating rheumatologist when a deep infection developed. Two patients (cases 1 and 2) were referred to us because of their nonunions. All 3 patients developed extra-articular nonunions with compromised bone stock. Two patients had developed deep infections during treatment of their plateau fractures; 1 of these patients underwent a medial gastrocnemius flap for wound coverage (case 1). The second patient (case 3) with a deep infection underwent partial hardware removal, a Masquelet salvage procedure, and revision plate fixation. However, the infection recurred. The hardware was removed, and 2 débridements with conversion to a hybrid external fixator with thin wire fixation were done. Due to her longstanding rheumatoid arthritis, the patient had bilateral valgus knee malalignment causing the ring fixator to strike her contralateral knee when she walked. The period from the initial tibial plateau fracture to our composite fixation averaged 11.3 months (range, 11-12 months). Indications for the use of the composite fixation comprised previously infected soft tissue on the lateral side and inability to walk with a hybrid thin wire fixator because of valgus knees (case 3), a medial gastrocnemius flap (case 2), and poor bone quality (case 1). Follow-up consisted of clinical examination, Timed Up and Go (TUG) test that is a standardized test for mobility, and radiographic evaluation at routine appointments up to 1 year or until healed.12 At the last follow-up visit, patients filled out the International Knee Documentation Committee (IKDC) subjective knee form.13

donders0918_t1

SURGICAL TECHNIQUE

A fellowship-trained orthopedic trauma surgeon treated all patients. Patients were placed on a radiolucent operating table after general or regional anesthesia. Previous incisions were used. Two patients had a midline incision; the third had both a posteromedial and an anterolateral incision. Five deep tissue cultures were taken after which antibiotics were given intravenously. All unstable or failed hardware was removed. Aggressive débridement of the nonunion was performed. After débridement, multiple holes were drilled with a 2.0 mm drill bit until blood was seen to egress from both sides of the medullary canal. Malalignment of the proximal tibia was corrected and checked fluoroscopically. Fixation was done with an anatomic locking plate (LCP Proximal Tibia Plate 3.5; DePuy Synthes) with a mixture of locking and non-locking screws. In 2 patients, a tricortical graft from the posterior iliac crest was positioned in the defect. Additional autologous bone graft and demineralized bone matrix was added around the nonunion. Although locking screws were used, the fixation did not appear to be strong enough to resist the varus (cases 1 and 2), or the valgus (case 3) deforming forces. Additional fixation was thus needed. However, the contralateral soft tissues were compromised in case 2 (medial gastrocnemius flap), and case 3 (a previously infected area with very tenuous skin laterally), whereas the bone was considered to be of insufficient quality in case 1. The opposite side of the nonunion was stabilized using composite fixation with a 2-pin external fixator to circumvent the need for additional plate fixation. In 2 patients, the plate was placed laterally, and the external fixator medially. In the third patient, the plate was positioned medially, and the external fixator laterally. The plate was always placed first. The external fixator was placed last. Using fluoroscopy, we ensured that the fixator pins would not interfere with the screws. The pins were predrilled and positioned perpendicular to the tibia through small stab incisions. We prefer hydroxyapatite-coated pins (6-mm diameter, XCaliber Bone Screws; Pro-Motion Medical) to increase their holding power in the often osteopenic bone. Postoperative management consisted of toe-touch weight-bearing for 6 weeks and progressed to full weight-bearing at 3 months. Radiographs were taken on postoperative day 1, at 6 weeks, and at 12 weeks until healed. No continuous passive motion was used postoperatively. Antibiotics were continued until cultures were negative. No specific pin care was used. We advised patients to shower daily with the external fixator in place, once the wounds have healed.

Continue to: RESULTS... 

 

 

RESULTS

On average, patients were hospitalized for 5 days (range, 3-7 days). There were no postoperative complications. None of the patients developed a clinically significant pin site infection. There were no re-operations during follow-up. All patients achieved union at a mean of 5.2 months (range, 5-5.5 months) (Figure 1).

donders0918_f1

Deformity correction was achieved in all 3 patients. The average range of motion (ROM) arc was 100° (range, 100°-115°). None of the patients had an extension deficit. TUG test was <8 seconds in all patients. The IKDC knee score averaged 52 (range, 41-66). Of note is that 2 patients already had compromised knee function before the fracture because of rheumatoid arthritis. The Ahlbäck classification of osteoarthritis showed grade 1 in cases 1 and 3, and grade 2 in case 2.14 Postoperative ROM of the knee returned to pre-injury levels in all patients (Figure 2). The 2-pin external fixator was removed at 9 weeks on average (range, 6-12 weeks) postoperatively in the outpatient clinic. At the last follow-up appointment at an average of 10.3 months (range, 9-12 months), all wounds had healed without infection. All patients had a normal neurovascular examination.

donders0918_f2

DISCUSSION

Nonunion after a proximal tibial fracture is rare.4 In cases when nonunions do develop, they most often pertain to the extra-articular component with the plateau component healed. Surgical exposure for débridements, hardware removal, bone grafting, and revision of fixation carries the risk of wound breakdown, necrosis, and infection. The alternative strategy of composite fixation (a plate combined with a contralateral 2-pin external fixator) to limit additional soft tissue compromise was already described in proximal tibial fractures by Bolhofner.9 He treated 41 extra-articular proximal tibial fractures using this composite fixation technique and attained successful results with an average time to union of 12.1 weeks. There was only 1 malunion, 2 wound infections, and 3 delayed unions.

In our practice, we have extrapolated this idea to an extra-articular nonunion that developed after a tibial plateau fracture. With the use of an external fixator, we provided sufficient mechanical stability of the nonunion without unnecessarily compromising previously infected or tenuous soft tissues, a muscle flap, or further devascularizing poor bone. Limitations of this study include the retrospective data and small sample size prone to bias. However, all patients received the same treatment protocol from 1 orthopedic trauma surgeon, follow-up intervals were similar, and data were acquired consistently.

Meanwhile, we have used this technique in a fourth patient with a septic nonunion of a tibial plateau fracture. All 4 patients in whom we have used this method so far have healed successfully.

CONCLUSION

This technique respects both the demand for minimal soft tissue damage and a maximal stable environment without notable perioperative and postoperative complications. It also offers an alternative option for the treatment of a proximal tibial nonunion that is not amenable to invasive revision dual plate fixation. As such, it can be a useful addition to the existing armamentarium of the treating surgeon.

References

1. Wu CC. Salvage of proximal tibial malunion or nonunion with the use of angled blade plate. Arch Orthop Trauma Surg. 2006;126(2):82-87. doi:10.1007/s00402-006-0106-9.

2. Carpenter CA, Jupiter JB. Blade plate reconstruction of metaphyseal nonunion of the tibia. Clin Orthop Relat Res. 1996;332:23-28.

3. Gardner MJ, Toro-Arbelaez JB, Hansen M, Boraiah S, Lorich DG, Helfet DL. Surgical treatment and outcomes of extraarticular proximal tibial nonunions. Arch Orthop Trauma Surg. 2008;128(8):833-839. doi:10.1007/s00402-007-0383-y.

4. Toro-Arbelaez JB, Gardner MJ, Shindle MK, Cabas JM, Lorich DG, Helfet DL. Open reduction and internal fixation of intraarticular tibial plateau nonunions. Injury. 2007;38(3):378-383. doi:10.1016/j.injury.2006.11.003.

5. Mechrefe AP, Koh EY, Trafton PG, DiGiovanni CW. Tibial nonunion. Foot Ankle Clin. 2006;11(1):1-18, vii. doi:10.1016/j.fcl.2005.12.003.

6. Chin KR, Nagarkatti DG, Miranda MA, Santoro VM, Baumgaertner MR, Jupiter JB. Salvage of distal tibia metaphyseal nonunions with the 90 degrees cannulated blade plate. Clin Orthop Relat Res. 2003;(409):241-249.

7. Devgan A, Kamboj P, Gupta V, Magu NK, Rohilla R. Pseudoarthrosis of medial tibial plateau fracture-role of alignment procedure. Chin J Traumatol. 2013;16(2):118-121. doi:10.3760/cma.j.issn.1008-1275.2013.02.011.

8. Helfet DL, Jupiter JB, Gasser S. Indirect reduction and tension-band plating of tibial non-union with deformity. J Bone Joint Surg Am. 1992;74(9):1286-1297.

9. Bolhofner BR. Indirect reduction and composite fixation of extraarticular proximal tibial fractures. Clin Orthop Relat Res. 1995;(315):75-83. doi:10.1097/00003086-199506000-00009.

10. Ries MD, Meinhard BP. Medial external fixation with lateral plate internal fixation in metaphyseal tibia fractures. A report of eight cases associated with severe soft-tissue injury. Clin Orthop Relat Res. 1988;(256):215-223. 

11. Weiner LS, Kelley M, Yang E, et al. The use of combination internal fixation and hybrid external fixation in severe proximal tibia fractures. J Orthop Trauma. 1995;9(3):244-250.

12. Alghadir A, Anwer S, Brismee JM. The reliability and minimal detectable change of Timed Up and Go test in individuals with grade 1-3 knee osteoarthritis. BMC Musculoskelet Disord. 2015;16:174. doi:10.1186/s12891-015-0637-8.

13. Haverkamp D, Sierevelt IN, Breugem SJ, Lohuis K, Blankevoort L, van Dijk CN. Translation and validation of the Dutch version of the International Knee Documentation Committee Subjective Knee Form. Am J Sports Med. 2006;34(10):1680-1684. doi:10.1177/0363546506288854.

14. Ahlbäck S. Osteoartrosis of the knee. A radiographic investigation. Acta Radiol Diagn (Stockh). 1968;Suppl 277:7-72.

References

1. Wu CC. Salvage of proximal tibial malunion or nonunion with the use of angled blade plate. Arch Orthop Trauma Surg. 2006;126(2):82-87. doi:10.1007/s00402-006-0106-9.

2. Carpenter CA, Jupiter JB. Blade plate reconstruction of metaphyseal nonunion of the tibia. Clin Orthop Relat Res. 1996;332:23-28.

3. Gardner MJ, Toro-Arbelaez JB, Hansen M, Boraiah S, Lorich DG, Helfet DL. Surgical treatment and outcomes of extraarticular proximal tibial nonunions. Arch Orthop Trauma Surg. 2008;128(8):833-839. doi:10.1007/s00402-007-0383-y.

4. Toro-Arbelaez JB, Gardner MJ, Shindle MK, Cabas JM, Lorich DG, Helfet DL. Open reduction and internal fixation of intraarticular tibial plateau nonunions. Injury. 2007;38(3):378-383. doi:10.1016/j.injury.2006.11.003.

5. Mechrefe AP, Koh EY, Trafton PG, DiGiovanni CW. Tibial nonunion. Foot Ankle Clin. 2006;11(1):1-18, vii. doi:10.1016/j.fcl.2005.12.003.

6. Chin KR, Nagarkatti DG, Miranda MA, Santoro VM, Baumgaertner MR, Jupiter JB. Salvage of distal tibia metaphyseal nonunions with the 90 degrees cannulated blade plate. Clin Orthop Relat Res. 2003;(409):241-249.

7. Devgan A, Kamboj P, Gupta V, Magu NK, Rohilla R. Pseudoarthrosis of medial tibial plateau fracture-role of alignment procedure. Chin J Traumatol. 2013;16(2):118-121. doi:10.3760/cma.j.issn.1008-1275.2013.02.011.

8. Helfet DL, Jupiter JB, Gasser S. Indirect reduction and tension-band plating of tibial non-union with deformity. J Bone Joint Surg Am. 1992;74(9):1286-1297.

9. Bolhofner BR. Indirect reduction and composite fixation of extraarticular proximal tibial fractures. Clin Orthop Relat Res. 1995;(315):75-83. doi:10.1097/00003086-199506000-00009.

10. Ries MD, Meinhard BP. Medial external fixation with lateral plate internal fixation in metaphyseal tibia fractures. A report of eight cases associated with severe soft-tissue injury. Clin Orthop Relat Res. 1988;(256):215-223. 

11. Weiner LS, Kelley M, Yang E, et al. The use of combination internal fixation and hybrid external fixation in severe proximal tibia fractures. J Orthop Trauma. 1995;9(3):244-250.

12. Alghadir A, Anwer S, Brismee JM. The reliability and minimal detectable change of Timed Up and Go test in individuals with grade 1-3 knee osteoarthritis. BMC Musculoskelet Disord. 2015;16:174. doi:10.1186/s12891-015-0637-8.

13. Haverkamp D, Sierevelt IN, Breugem SJ, Lohuis K, Blankevoort L, van Dijk CN. Translation and validation of the Dutch version of the International Knee Documentation Committee Subjective Knee Form. Am J Sports Med. 2006;34(10):1680-1684. doi:10.1177/0363546506288854.

14. Ahlbäck S. Osteoartrosis of the knee. A radiographic investigation. Acta Radiol Diagn (Stockh). 1968;Suppl 277:7-72.

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  • Treatment goals for a nonunion are bone union, re-establishment of (joint) stability, extremity alignment, and recovery of function.
  • A nonunion of a tibia plateau fracture is often associated with poor soft tissues from previous surgeries and/or infections.
  • Ideally a combination of minimal soft tissue damage and maximal stable fixation is used for salvage.
  • There is a high risk of complications when using dual plating in these cases.
  • A combination of an external fixator with limited internal fixation can be a good alternative.
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Mycobacterium abscessus: A Rare Cause of Periprosthetic Knee Joint Infection

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Mycobacterium abscessus: A Rare Cause of Periprosthetic Knee Joint Infection

ABSTRACT

A 61-year-old woman with a periprosthetic knee joint infection caused by Mycobacterium abscessus was successfully treated with surgical débridement, multidrug antimicrobial therapy, and staged reimplantation. To the authors’ knowledge, this represents the first report of successfully treating this organism after knee arthroplasty.

M. abscessus knee infections are rare, and there are no specific guidelines to inform treatment or successful treatment regimens for periprosthetic knee infections. Medical management alone was not successful in this case and hence cannot be recommended. Using a collaborative multidisciplinary approach, including surgical débridement, staged reimplantation, and multidrug antimicrobials, successful eradication of the periprosthetic joint infection caused by M. abscessus was achieved.  

Continue to: Total knee arthroplasty...

 

 

Total knee arthroplasty (TKA) procedures are projected to increase by more than 6-fold by 2030, with concurrent increases in revision TKA for infection projected.1 Infection after TKA remains one of the most serious complications of the procedure, occurring in <2% of primary TKAs.2 The majority of prosthetic joint infections (PJIs) are caused by staphylococci and streptococci.3 Although infection and treatment of PJIs by mycobacterial species have been described, there are presently no established treatment guidelines for mycobacterial PJIs.4,5

Given the scarcity of clinical experience in dealing with these organisms, and the predicted increasing incidence of revision knee arthroplasty due to infection, we describe an unusual case of a PJI caused by Mycobacterium abscessus (M. abscessus), which was successfully treated using a combination of antimicrobial therapy and staged reconstruction. The patient provided written informed consent for print and electronic publication of this case report.

BACKGROUND

Mycobacteria are common environmental organisms that can survive harsh conditions, including low pH and extreme temperatures. They form biofilms and may be difficult to eradicate in cases of infection.6M. abscessus has proven to be difficult to eradicate due to limited antimicrobial susceptibility, lack of bactericidal options, and the variable presence of the erm gene, which yields inducible resistance to macrolides.7 Post-procedural outbreaks due to mycobacteria have been reported, often attributed to contaminated multiuse instruments, inadequate sterilization of tap water, multiuse vials, or improper skin preparation.6,8-13

CASE REPORT 

A 61-year-old woman was referred with a 3-year history of progressive left knee pain and swelling. Before 8 months, she had undergone knee arthroscopy and had been treated with multiple steroid and hyaluronic acid injections, as well as ultrasound-guided aspiration of a Baker’s cyst (Figures 1A, 1B).

thum0918_f1_0

She elected to proceed with TKA 1 month after her last steroid injection. There was no preoperative concern for native joint infection. At the time of arthroplasty, clear joint fluid was encountered, and a deep tissue culture was taken (Figures 2A-2C).

thum0918_f2

Routine screening cultures for acid-fast bacilli (AFB) returned positive 9 days after the index arthroplasty, with subsequent identification of a nontuberculous mycobacterium (NTM), M. abscessus, subspecies massiliense. Sensitivity tests revealed susceptibility to amikacin, cefoxitin, and tigecycline (Table 1). The isolate was found to have inducible macrolide resistance by erm gene testing.

Table 1. Initial Mycobacterium abscessus massiliense Susceptibilities

Medication

Minimum Inhibitory Concentration

Amikacin

16 (S)

Cefoxitin

16 (S)

Imipenem

8 (I)

Linezolid

16 (I)

Clarithromycin

2 (S)a

Tigecycline

1 (S)

aAt 3 days; erm gene detected at 7 days.

Given no prior surgical suspicion for infection and the uncertain significance of the culture result, treatment options were debated. Medical management was selected based on the presumption that if infection was present, it was a native joint infection in which surgical débridement had already been undertaken at the time of primary arthroplasty. Similar reports for the treatment of M. tuberculosis infection in the knee have been reported with some success.14,15 Short-interval reassessment was planned. Antimicrobial therapy was selected based on susceptibility data and clinical experience and consisted of intravenous (IV) cefoxitin, oral clarithromycin, and thrice-weekly intravenous amikacin. Over the ensuing weeks, she developed fevers, knee swelling, and persistent elevation of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). With known potential of this organism for biofilm formation in other areas of the body and positive repeat cultures of the knee joint fluid, confirming the offending organism, a deep and resistant infection of the implant could not be excluded. Therefore, in an attempt to give the patient the best opportunity for clinical cure, the patient subsequently underwent a 2-stage antibiotic spacer explantation and exchange (Figures 3A, 3B). Moderate caseous material was present throughout the knee joint and the subcutaneous tissues. All bone was débrided, and complete synovectomy was undertaken, along with the removal of all implants. The antibiotic concentrations within the spacer were selected by guidance from the Infectious Disease and Pharmacy based on minimal inhibitory concentrations, with 3 packages of cement (40 g each) utilized and a total of 10 g of amikacin and 24 g of cefoxitin contained within the spacer. The patient continued systemic administration of amikacin, cefoxitin, and clarithromycin.

thum0918_f3

Continue to: One month postoperatively...

 

 

One month postoperatively, her constitutional symptoms, including fevers and night sweats, abated and inflammatory markers (ESR and CRP) had normalized. There were no clinical signs of infection. Amikacin was discontinued due to a 10-dB change on audiologic screening (4-6 kHz range), and tigecycline was substituted. Ultimately, she underwent 15 weeks of antimycobacterial therapy, 10 of which were after the explantation.

Eight weeks after cessation of her antibiotics, she underwent open biopsy. Multiple operative tissue samples showed negative results in pathology and culture tests.

Replantation was performed 14 weeks after stopping antimicrobials and 24 weeks after her explantation. The bone appeared healthy without evidence of osteomyelitis. A constrained reconstruction was secured with tobramycin-impregnated cement. One small island of necrotizing granuloma was observed within the bony cortex on histologic review; the granulomata appeared active with scattered neutrophils along with histiocytes and lymphocytes. AFB stains were negative. Intraoperative cultures, including mycobacterial cultures, were negative.

Based on the histologic evidence that infection may have persisted, and given the high stakes, antimicrobial treatment was reinitiated. Amikacin was again stopped after 3 weeks due to the development of tinnitus; tigecycline was substituted to complete the fourth and final week, at which point all antibiotics were discontinued. The patient was followed up uneventfully for 4 years (Figures 4A-4D and 5A-5C) with normal ESR and CRP. She continues to be ambulatory without assistive devices and walks an average of 30 miles per week without pain or constitutional symptoms.

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Continue to: DISCUSSION...

 

 

DISCUSSION

Diagnosis of acute infection after TKA remains challenging, as some degree of pain, swelling, and even postoperative fevers may be common in noninfected TKA patients. Synovial white blood cell count and differential as well as alpha-defensin levels have been cited as predictive factors of infection.16,17 Deep tissue and synovial fluid cultures offer the advantage of both identification and antimicrobial sensitivity testing of the offending organism. In this case, culture of the knee joint fluid at the time of TKA led to the unexpected finding of M. abscessus infection.

Preventable outbreaks due to M. abscessus have been reported and attributed to contaminated multiuse instruments, inadequate sterilization of tap water, multiuse vials, and improper skin preparation.11-13 Rarely, M. abscessus has been reported as the cause of PJI. When an unusual organism is encountered after native joint instrumentation, an investigation should be undertaken to identify the source of contamination, with the assistance of infection control practitioners and/or the US Food and Drug Administration reporting. Reporting and investigation was undertaken in this case, though no suspect source could be identified.

Although there were no signs of infection prior to the TKA, there is an ongoing debate as to whether intra-articular corticosteroid injections increase the risk of PJIs, and if so, what the optimal amount of time to wait between procedures is. Although several earlier studies have been underpowered to answer these questions,18 this patient underwent TKA 1 month following the corticosteroid injection. Recent meta-analyses have shown no definitive evidence to indicate that this increased her risk of PJI.19,20

Continue to: Treatments for mycobacterial infections...

 

 

Treatments for mycobacterial infections have been described with variable efficacy,21,22 and only 2 cases of successfully treated PJIs have been reported after infection with M. abscessus. Both these cases were described in total hip arthroplasties,23,24 and to the authors’ knowledge, this report represents the first described successfully treated case after TKA. Staged reconstruction remains a standard treatment for invasive organisms chronically infecting prosthetic joint implants, with reimplantation pending joint sterility and improvement in inflammatory markers.3 Previous successful reports of treating M. abscessus describe either resection arthroplasty21 or staged reconstruction.23,24 The authors reported variable multidrug antimicrobial regimens, as summarized in Table 2, as guidelines for the treatment of mycobacterial PJI are currently not available.

thum0918_t2

CONCLUSION

This case report represents an episode of iatrogenic septic arthritis caused by Mycobacteria of the native knee after previous history of instrumentation, corticosteroid, and hyaluronic acid injections, with an overall indolent clinical course until subsequent arthroplasty. There were several important lessons learned, which are as follows: 1) Multidrug combination with antimicrobial therapy combined with aggressive surgical débridement and staged reimplantation permitted successful eradication of TKA PJI caused by M. abscessus in this patient. 2) Initial medical management alone was not successful and cannot be recommended for the treatment of M. abscessus in the setting of PJI. 3) Delaying the surgical débridement and the reconstructive course for a trial of medical management contributed to the ultimate requirement of a tibial tubercle osteotomy for an ankylosed knee at replantation. In this case, we initially had a low index of suspicion for deep infection, contributing to delayed surgical débridement. Ideally, a high degree of clinical suspicion should be maintained for joint infection in the presence of positive culture isolates of M. abscessus, as it may have a delayed clinical presentation of the typical features of PJI (fevers, swelling, erythema, etc). In such cases, the authors recommend consideration of early surgical débridement. 4) Medical management of TKA PJI is not without risks. Careful monitoring of patient side effects during antimicrobial administration remains paramount, as this patient did sustain a degree of hearing loss associated with prolonged medical therapy. 5) In complicated PJIs involving rare and intrinsically resistant organisms, a collaborative multidisciplinary approach, including specialists in orthopedic surgery, infectious disease, microbiology, pharmacy, and pathology, may be the preferred path to clinical cure.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785. doi:10.2106/JBJS.F.00222.

2. Cobo J, Del Pozo JL. Prosthetic joint infection: diagnosis and management. Expert Rev Anti Infect Ther. 2011;9(9):787-802. doi:10.1586/eri.11.95.

3. Toms AD, Davidson D, Masri BA, Duncan CP. The management of peri-prosthetic infection in total joint arthroplasty. J Bone Joint Surg Br. 2006;88(2):149-155. doi:10.1302/0301-620X.88B2.17058.

4. Osmon DR, Berbari EF, Berendt AR, et al. Diagnosis and management of prosthetic joint infection: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2013;56(1):e1-e25. doi:10.1093/cid/cis803.

5. Restrepo C, Schmitt S, Backstein D, et al. Antibiotic treatment and timing of reimplantation. J Orthop Res. 2014;32 Suppl 1:S136-S140. doi:10.1002/jor.22557.

6. De Groote MA, Huitt G. Infections due to rapidly growing mycobacteria. Clin Infect Dis. 2006;42(12):1756-1763. doi:10.1086/504381.

7. Nash KA, Brown-Elliott BA, Wallace RJ Jr. A novel gene, erm(41), Confers inducible macrolide resistance to clinical isolates of Mycobacterium abscessus but is absent from Mycobacterium chelonae. Antimicrob Agents Chemother. 2009;53(4):1367-1376. doi:10.1128/AAC.01275-08.

8. Furuya EY, Paez A, Srinivasan A, et al. Outbreak of Mycobacterium abscessus wound infections among "lipotourists" from the United States who underwent abdominoplasty in the Dominican Republic. Clin Infect Dis. 2008;46(8):1181-1188. doi:10.1086/529191.

9. Jarand J, Levin A, Zhang L, Huitt G, Mitchell JD, Daley CL. Clinical and microbiologic outcomes in patients receiving treatment for Mycobacterium abscessus pulmonary disease. Clin Infect Dis. 2011;52(5):565-571. doi:10.1093/cid/ciq237.

10. Mueller PS, Edson RS. Disseminated Mycobacterium abscessus infection manifesting as fever of unknown origin and intra-abdominal lymphadenitis: case report and literature review. Diagn Microbiol Infect Dis. 2001;39(1):33-37. doi:10.1016/S0732-8893(00)00211-X.

11. Mushatt DM, Witzig RS. Successful treatment of Mycobacterium abscessus infections with multidrug regimens containing clarithromycin. Clin Infect Dis. 1995;20(5):1441-1442. doi:10.1093/clinids/20.5.1441.

12. Tiwari TS, Ray B, Jost KC Jr, et al. Forty years of disinfectant failure: outbreak of postinjection Mycobacterium abscessus infection caused by contamination of benzalkonium chloride. Clin Infect Dis. 2003;36(8):954-962. doi:10.1086/368192.

13. Villanueva A, Calderon RV, Vargas BA, et al. Report on an outbreak of postinjection abscesses due to Mycobacterium abscessus, including management with surgery and clarithromycin therapy and comparison of strains by random amplified polymorphic DNA polymerase chain reaction. Clin Infect Dis. 1997;24(6):1147-1153. doi:10.1086/513656.

14. Gale DW, Harding ML. Total knee arthroplasty in the presence of active tuberculosis. J Bone Joint Surg Br. 1991;73(6):1006-1007. doi:10.1302/0301-620X.73B6.1955424.

15. Kim YH. Total knee arthroplasty for tuberculous arthritis. J Bone Joint Surg Am. 1988;70(9):1322-1330. doi:10.2106/00004623-198870090-00008.

16. Bedair H, Ting N, Jacovides C, et al. The Mark Coventry Award: diagnosis of early postoperative TKA infection using synovial fluid analysis. Clin Orthop Relat Res. 2011;469(1):34-40. doi:10.1007/s11999-010-1433-2.

17. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009. doi:10.1007/s11999-014-3900-7.

18. Marsland D, Mumith A, Barlow IW. Systematic review: the safety of intra-articular corticosteroid injection prior to total knee arthroplasty. Knee. 2014;21(1):6-11. doi:10.1016/j.knee.2013.07.003.

19. Charalambous CP, Prodromidis AD, Kwaees TA. Do intra-articular steroid injections increase infection rates in subsequent arthroplasty? A systematic review and meta-analysis of comparative studies. J Arthroplast. 2014;29(11):2175-2180. doi:10.1016/j.arth.2014.07.013.

20. Xing D, Yang Y, Ma X, Ma J, Ma B, Chen Y. Dose intraarticular steroid injection increase the rate of infection in subsequent arthroplasty: grading the evidence through a meta-analysis. J Orthop Surg Res. 2014;9:107. doi:10.1186/s13018-014-0107-2.

21. Eid AJ, Berbari EF, Sia IG, Wengenack NL, Osmon DR, Razonable RR. Prosthetic joint infection due to rapidly growing mycobacteria: report of 8 cases and review of the literature. Clin Infect Dis. 2007;45(6):687-694. doi:10.1086/520982.

22. Herold RC, Lotke PA, MacGregor RR. Prosthetic joint infections secondary to rapidly growing Mycobacterium fortuitum. Clin Orthop Relat Res. 1987;216(216):183-186. doi:10.1097/00003086-198703000-00029.

23. Petrosoniak A, Kim P, Desjardins M, Lee BC. Successful treatment of a prosthetic joint infection due to Mycobacterium abscessus. Can J Infect Dis Med Microbiol. 2009;20(3):e94-e96.

24. Yinkey LM, Halsey ES, Lloyd BA. Successful tigecycline combination therapy for Mycobacterium abscessus infection of a total hip arthroplasty. Infect Dis Clin Practice. 2010;18(4):269-270. doi:10.1097/IPC.0b013e3181d04a09.

25. AAOS Guidelines: the diagnosis of periprosthetic joint infections of the hip and knee guideline and evidence report. Adopted by the American Academy of Orthopaedic Surgeons Board of Directors; June 18th, 2010. AAOS Publication: 2010.

26. Griffith DE, Aksamit T, Brown-Elliott BA, et al; ATS Mycobacterial Diseases Subcomittee; American Thoracic Society; Infectious Disease Society of America. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175(4):367-416.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Spanyer is an Orthopaedic Surgeon, OrthoCincy Orthopaedics and Sports Medicine, Cincinnati, Ohio. Dr. Kwon is an Orthopaedic Surgeon, Department of Orthopaedic Surgery; and Dr. Nelson is an Infectious Disease Specialist, Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Dr. Foster is an Orthopaedic Surgeon, Avita Orthopaedics, Ontario, Ohio. Dr. Thum-DiCesare is a Neurosurgery Resident, Department of Neurosurgery, University of California Los Angeles (UCLA), Los Angeles, California. Dr. Burke is an Orthopaedic Surgeon, Department of Orthopaedics, Beth Israel Deaconess Hospital, Milton, Massachusetts.

Address correspondence to: Jonathon Spanyer, MD, OrthoCincy Orthopaedics and Sports Medicine, 560 South Loop Road, Edgewood, KY 45017 (tel, 859-301-2663; email, jspanyer@orthocincy.com).

Jonathon M. Spanyer, MD Scott Foster, MD Jasmine A. Thum-DiCesare, MD Young-Min M. Kwon, MD, PhD Dennis W. Burke, MDSandra B. Nelson, MD . Mycobacterium abscessus: A Rare Cause of Periprosthetic Knee Joint Infection. Am J Orthop.

September 26, 2018

 
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Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Spanyer is an Orthopaedic Surgeon, OrthoCincy Orthopaedics and Sports Medicine, Cincinnati, Ohio. Dr. Kwon is an Orthopaedic Surgeon, Department of Orthopaedic Surgery; and Dr. Nelson is an Infectious Disease Specialist, Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Dr. Foster is an Orthopaedic Surgeon, Avita Orthopaedics, Ontario, Ohio. Dr. Thum-DiCesare is a Neurosurgery Resident, Department of Neurosurgery, University of California Los Angeles (UCLA), Los Angeles, California. Dr. Burke is an Orthopaedic Surgeon, Department of Orthopaedics, Beth Israel Deaconess Hospital, Milton, Massachusetts.

Address correspondence to: Jonathon Spanyer, MD, OrthoCincy Orthopaedics and Sports Medicine, 560 South Loop Road, Edgewood, KY 45017 (tel, 859-301-2663; email, jspanyer@orthocincy.com).

Jonathon M. Spanyer, MD Scott Foster, MD Jasmine A. Thum-DiCesare, MD Young-Min M. Kwon, MD, PhD Dennis W. Burke, MDSandra B. Nelson, MD . Mycobacterium abscessus: A Rare Cause of Periprosthetic Knee Joint Infection. Am J Orthop.

September 26, 2018

 
Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Spanyer is an Orthopaedic Surgeon, OrthoCincy Orthopaedics and Sports Medicine, Cincinnati, Ohio. Dr. Kwon is an Orthopaedic Surgeon, Department of Orthopaedic Surgery; and Dr. Nelson is an Infectious Disease Specialist, Division of Infectious Diseases, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. Dr. Foster is an Orthopaedic Surgeon, Avita Orthopaedics, Ontario, Ohio. Dr. Thum-DiCesare is a Neurosurgery Resident, Department of Neurosurgery, University of California Los Angeles (UCLA), Los Angeles, California. Dr. Burke is an Orthopaedic Surgeon, Department of Orthopaedics, Beth Israel Deaconess Hospital, Milton, Massachusetts.

Address correspondence to: Jonathon Spanyer, MD, OrthoCincy Orthopaedics and Sports Medicine, 560 South Loop Road, Edgewood, KY 45017 (tel, 859-301-2663; email, jspanyer@orthocincy.com).

Jonathon M. Spanyer, MD Scott Foster, MD Jasmine A. Thum-DiCesare, MD Young-Min M. Kwon, MD, PhD Dennis W. Burke, MDSandra B. Nelson, MD . Mycobacterium abscessus: A Rare Cause of Periprosthetic Knee Joint Infection. Am J Orthop.

September 26, 2018

 

ABSTRACT

A 61-year-old woman with a periprosthetic knee joint infection caused by Mycobacterium abscessus was successfully treated with surgical débridement, multidrug antimicrobial therapy, and staged reimplantation. To the authors’ knowledge, this represents the first report of successfully treating this organism after knee arthroplasty.

M. abscessus knee infections are rare, and there are no specific guidelines to inform treatment or successful treatment regimens for periprosthetic knee infections. Medical management alone was not successful in this case and hence cannot be recommended. Using a collaborative multidisciplinary approach, including surgical débridement, staged reimplantation, and multidrug antimicrobials, successful eradication of the periprosthetic joint infection caused by M. abscessus was achieved.  

Continue to: Total knee arthroplasty...

 

 

Total knee arthroplasty (TKA) procedures are projected to increase by more than 6-fold by 2030, with concurrent increases in revision TKA for infection projected.1 Infection after TKA remains one of the most serious complications of the procedure, occurring in <2% of primary TKAs.2 The majority of prosthetic joint infections (PJIs) are caused by staphylococci and streptococci.3 Although infection and treatment of PJIs by mycobacterial species have been described, there are presently no established treatment guidelines for mycobacterial PJIs.4,5

Given the scarcity of clinical experience in dealing with these organisms, and the predicted increasing incidence of revision knee arthroplasty due to infection, we describe an unusual case of a PJI caused by Mycobacterium abscessus (M. abscessus), which was successfully treated using a combination of antimicrobial therapy and staged reconstruction. The patient provided written informed consent for print and electronic publication of this case report.

BACKGROUND

Mycobacteria are common environmental organisms that can survive harsh conditions, including low pH and extreme temperatures. They form biofilms and may be difficult to eradicate in cases of infection.6M. abscessus has proven to be difficult to eradicate due to limited antimicrobial susceptibility, lack of bactericidal options, and the variable presence of the erm gene, which yields inducible resistance to macrolides.7 Post-procedural outbreaks due to mycobacteria have been reported, often attributed to contaminated multiuse instruments, inadequate sterilization of tap water, multiuse vials, or improper skin preparation.6,8-13

CASE REPORT 

A 61-year-old woman was referred with a 3-year history of progressive left knee pain and swelling. Before 8 months, she had undergone knee arthroscopy and had been treated with multiple steroid and hyaluronic acid injections, as well as ultrasound-guided aspiration of a Baker’s cyst (Figures 1A, 1B).

thum0918_f1_0

She elected to proceed with TKA 1 month after her last steroid injection. There was no preoperative concern for native joint infection. At the time of arthroplasty, clear joint fluid was encountered, and a deep tissue culture was taken (Figures 2A-2C).

thum0918_f2

Routine screening cultures for acid-fast bacilli (AFB) returned positive 9 days after the index arthroplasty, with subsequent identification of a nontuberculous mycobacterium (NTM), M. abscessus, subspecies massiliense. Sensitivity tests revealed susceptibility to amikacin, cefoxitin, and tigecycline (Table 1). The isolate was found to have inducible macrolide resistance by erm gene testing.

Table 1. Initial Mycobacterium abscessus massiliense Susceptibilities

Medication

Minimum Inhibitory Concentration

Amikacin

16 (S)

Cefoxitin

16 (S)

Imipenem

8 (I)

Linezolid

16 (I)

Clarithromycin

2 (S)a

Tigecycline

1 (S)

aAt 3 days; erm gene detected at 7 days.

Given no prior surgical suspicion for infection and the uncertain significance of the culture result, treatment options were debated. Medical management was selected based on the presumption that if infection was present, it was a native joint infection in which surgical débridement had already been undertaken at the time of primary arthroplasty. Similar reports for the treatment of M. tuberculosis infection in the knee have been reported with some success.14,15 Short-interval reassessment was planned. Antimicrobial therapy was selected based on susceptibility data and clinical experience and consisted of intravenous (IV) cefoxitin, oral clarithromycin, and thrice-weekly intravenous amikacin. Over the ensuing weeks, she developed fevers, knee swelling, and persistent elevation of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). With known potential of this organism for biofilm formation in other areas of the body and positive repeat cultures of the knee joint fluid, confirming the offending organism, a deep and resistant infection of the implant could not be excluded. Therefore, in an attempt to give the patient the best opportunity for clinical cure, the patient subsequently underwent a 2-stage antibiotic spacer explantation and exchange (Figures 3A, 3B). Moderate caseous material was present throughout the knee joint and the subcutaneous tissues. All bone was débrided, and complete synovectomy was undertaken, along with the removal of all implants. The antibiotic concentrations within the spacer were selected by guidance from the Infectious Disease and Pharmacy based on minimal inhibitory concentrations, with 3 packages of cement (40 g each) utilized and a total of 10 g of amikacin and 24 g of cefoxitin contained within the spacer. The patient continued systemic administration of amikacin, cefoxitin, and clarithromycin.

thum0918_f3

Continue to: One month postoperatively...

 

 

One month postoperatively, her constitutional symptoms, including fevers and night sweats, abated and inflammatory markers (ESR and CRP) had normalized. There were no clinical signs of infection. Amikacin was discontinued due to a 10-dB change on audiologic screening (4-6 kHz range), and tigecycline was substituted. Ultimately, she underwent 15 weeks of antimycobacterial therapy, 10 of which were after the explantation.

Eight weeks after cessation of her antibiotics, she underwent open biopsy. Multiple operative tissue samples showed negative results in pathology and culture tests.

Replantation was performed 14 weeks after stopping antimicrobials and 24 weeks after her explantation. The bone appeared healthy without evidence of osteomyelitis. A constrained reconstruction was secured with tobramycin-impregnated cement. One small island of necrotizing granuloma was observed within the bony cortex on histologic review; the granulomata appeared active with scattered neutrophils along with histiocytes and lymphocytes. AFB stains were negative. Intraoperative cultures, including mycobacterial cultures, were negative.

Based on the histologic evidence that infection may have persisted, and given the high stakes, antimicrobial treatment was reinitiated. Amikacin was again stopped after 3 weeks due to the development of tinnitus; tigecycline was substituted to complete the fourth and final week, at which point all antibiotics were discontinued. The patient was followed up uneventfully for 4 years (Figures 4A-4D and 5A-5C) with normal ESR and CRP. She continues to be ambulatory without assistive devices and walks an average of 30 miles per week without pain or constitutional symptoms.

thum0918_f4

thum0918_f5

Continue to: DISCUSSION...

 

 

DISCUSSION

Diagnosis of acute infection after TKA remains challenging, as some degree of pain, swelling, and even postoperative fevers may be common in noninfected TKA patients. Synovial white blood cell count and differential as well as alpha-defensin levels have been cited as predictive factors of infection.16,17 Deep tissue and synovial fluid cultures offer the advantage of both identification and antimicrobial sensitivity testing of the offending organism. In this case, culture of the knee joint fluid at the time of TKA led to the unexpected finding of M. abscessus infection.

Preventable outbreaks due to M. abscessus have been reported and attributed to contaminated multiuse instruments, inadequate sterilization of tap water, multiuse vials, and improper skin preparation.11-13 Rarely, M. abscessus has been reported as the cause of PJI. When an unusual organism is encountered after native joint instrumentation, an investigation should be undertaken to identify the source of contamination, with the assistance of infection control practitioners and/or the US Food and Drug Administration reporting. Reporting and investigation was undertaken in this case, though no suspect source could be identified.

Although there were no signs of infection prior to the TKA, there is an ongoing debate as to whether intra-articular corticosteroid injections increase the risk of PJIs, and if so, what the optimal amount of time to wait between procedures is. Although several earlier studies have been underpowered to answer these questions,18 this patient underwent TKA 1 month following the corticosteroid injection. Recent meta-analyses have shown no definitive evidence to indicate that this increased her risk of PJI.19,20

Continue to: Treatments for mycobacterial infections...

 

 

Treatments for mycobacterial infections have been described with variable efficacy,21,22 and only 2 cases of successfully treated PJIs have been reported after infection with M. abscessus. Both these cases were described in total hip arthroplasties,23,24 and to the authors’ knowledge, this report represents the first described successfully treated case after TKA. Staged reconstruction remains a standard treatment for invasive organisms chronically infecting prosthetic joint implants, with reimplantation pending joint sterility and improvement in inflammatory markers.3 Previous successful reports of treating M. abscessus describe either resection arthroplasty21 or staged reconstruction.23,24 The authors reported variable multidrug antimicrobial regimens, as summarized in Table 2, as guidelines for the treatment of mycobacterial PJI are currently not available.

thum0918_t2

CONCLUSION

This case report represents an episode of iatrogenic septic arthritis caused by Mycobacteria of the native knee after previous history of instrumentation, corticosteroid, and hyaluronic acid injections, with an overall indolent clinical course until subsequent arthroplasty. There were several important lessons learned, which are as follows: 1) Multidrug combination with antimicrobial therapy combined with aggressive surgical débridement and staged reimplantation permitted successful eradication of TKA PJI caused by M. abscessus in this patient. 2) Initial medical management alone was not successful and cannot be recommended for the treatment of M. abscessus in the setting of PJI. 3) Delaying the surgical débridement and the reconstructive course for a trial of medical management contributed to the ultimate requirement of a tibial tubercle osteotomy for an ankylosed knee at replantation. In this case, we initially had a low index of suspicion for deep infection, contributing to delayed surgical débridement. Ideally, a high degree of clinical suspicion should be maintained for joint infection in the presence of positive culture isolates of M. abscessus, as it may have a delayed clinical presentation of the typical features of PJI (fevers, swelling, erythema, etc). In such cases, the authors recommend consideration of early surgical débridement. 4) Medical management of TKA PJI is not without risks. Careful monitoring of patient side effects during antimicrobial administration remains paramount, as this patient did sustain a degree of hearing loss associated with prolonged medical therapy. 5) In complicated PJIs involving rare and intrinsically resistant organisms, a collaborative multidisciplinary approach, including specialists in orthopedic surgery, infectious disease, microbiology, pharmacy, and pathology, may be the preferred path to clinical cure.

ABSTRACT

A 61-year-old woman with a periprosthetic knee joint infection caused by Mycobacterium abscessus was successfully treated with surgical débridement, multidrug antimicrobial therapy, and staged reimplantation. To the authors’ knowledge, this represents the first report of successfully treating this organism after knee arthroplasty.

M. abscessus knee infections are rare, and there are no specific guidelines to inform treatment or successful treatment regimens for periprosthetic knee infections. Medical management alone was not successful in this case and hence cannot be recommended. Using a collaborative multidisciplinary approach, including surgical débridement, staged reimplantation, and multidrug antimicrobials, successful eradication of the periprosthetic joint infection caused by M. abscessus was achieved.  

Continue to: Total knee arthroplasty...

 

 

Total knee arthroplasty (TKA) procedures are projected to increase by more than 6-fold by 2030, with concurrent increases in revision TKA for infection projected.1 Infection after TKA remains one of the most serious complications of the procedure, occurring in <2% of primary TKAs.2 The majority of prosthetic joint infections (PJIs) are caused by staphylococci and streptococci.3 Although infection and treatment of PJIs by mycobacterial species have been described, there are presently no established treatment guidelines for mycobacterial PJIs.4,5

Given the scarcity of clinical experience in dealing with these organisms, and the predicted increasing incidence of revision knee arthroplasty due to infection, we describe an unusual case of a PJI caused by Mycobacterium abscessus (M. abscessus), which was successfully treated using a combination of antimicrobial therapy and staged reconstruction. The patient provided written informed consent for print and electronic publication of this case report.

BACKGROUND

Mycobacteria are common environmental organisms that can survive harsh conditions, including low pH and extreme temperatures. They form biofilms and may be difficult to eradicate in cases of infection.6M. abscessus has proven to be difficult to eradicate due to limited antimicrobial susceptibility, lack of bactericidal options, and the variable presence of the erm gene, which yields inducible resistance to macrolides.7 Post-procedural outbreaks due to mycobacteria have been reported, often attributed to contaminated multiuse instruments, inadequate sterilization of tap water, multiuse vials, or improper skin preparation.6,8-13

CASE REPORT 

A 61-year-old woman was referred with a 3-year history of progressive left knee pain and swelling. Before 8 months, she had undergone knee arthroscopy and had been treated with multiple steroid and hyaluronic acid injections, as well as ultrasound-guided aspiration of a Baker’s cyst (Figures 1A, 1B).

thum0918_f1_0

She elected to proceed with TKA 1 month after her last steroid injection. There was no preoperative concern for native joint infection. At the time of arthroplasty, clear joint fluid was encountered, and a deep tissue culture was taken (Figures 2A-2C).

thum0918_f2

Routine screening cultures for acid-fast bacilli (AFB) returned positive 9 days after the index arthroplasty, with subsequent identification of a nontuberculous mycobacterium (NTM), M. abscessus, subspecies massiliense. Sensitivity tests revealed susceptibility to amikacin, cefoxitin, and tigecycline (Table 1). The isolate was found to have inducible macrolide resistance by erm gene testing.

Table 1. Initial Mycobacterium abscessus massiliense Susceptibilities

Medication

Minimum Inhibitory Concentration

Amikacin

16 (S)

Cefoxitin

16 (S)

Imipenem

8 (I)

Linezolid

16 (I)

Clarithromycin

2 (S)a

Tigecycline

1 (S)

aAt 3 days; erm gene detected at 7 days.

Given no prior surgical suspicion for infection and the uncertain significance of the culture result, treatment options were debated. Medical management was selected based on the presumption that if infection was present, it was a native joint infection in which surgical débridement had already been undertaken at the time of primary arthroplasty. Similar reports for the treatment of M. tuberculosis infection in the knee have been reported with some success.14,15 Short-interval reassessment was planned. Antimicrobial therapy was selected based on susceptibility data and clinical experience and consisted of intravenous (IV) cefoxitin, oral clarithromycin, and thrice-weekly intravenous amikacin. Over the ensuing weeks, she developed fevers, knee swelling, and persistent elevation of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). With known potential of this organism for biofilm formation in other areas of the body and positive repeat cultures of the knee joint fluid, confirming the offending organism, a deep and resistant infection of the implant could not be excluded. Therefore, in an attempt to give the patient the best opportunity for clinical cure, the patient subsequently underwent a 2-stage antibiotic spacer explantation and exchange (Figures 3A, 3B). Moderate caseous material was present throughout the knee joint and the subcutaneous tissues. All bone was débrided, and complete synovectomy was undertaken, along with the removal of all implants. The antibiotic concentrations within the spacer were selected by guidance from the Infectious Disease and Pharmacy based on minimal inhibitory concentrations, with 3 packages of cement (40 g each) utilized and a total of 10 g of amikacin and 24 g of cefoxitin contained within the spacer. The patient continued systemic administration of amikacin, cefoxitin, and clarithromycin.

thum0918_f3

Continue to: One month postoperatively...

 

 

One month postoperatively, her constitutional symptoms, including fevers and night sweats, abated and inflammatory markers (ESR and CRP) had normalized. There were no clinical signs of infection. Amikacin was discontinued due to a 10-dB change on audiologic screening (4-6 kHz range), and tigecycline was substituted. Ultimately, she underwent 15 weeks of antimycobacterial therapy, 10 of which were after the explantation.

Eight weeks after cessation of her antibiotics, she underwent open biopsy. Multiple operative tissue samples showed negative results in pathology and culture tests.

Replantation was performed 14 weeks after stopping antimicrobials and 24 weeks after her explantation. The bone appeared healthy without evidence of osteomyelitis. A constrained reconstruction was secured with tobramycin-impregnated cement. One small island of necrotizing granuloma was observed within the bony cortex on histologic review; the granulomata appeared active with scattered neutrophils along with histiocytes and lymphocytes. AFB stains were negative. Intraoperative cultures, including mycobacterial cultures, were negative.

Based on the histologic evidence that infection may have persisted, and given the high stakes, antimicrobial treatment was reinitiated. Amikacin was again stopped after 3 weeks due to the development of tinnitus; tigecycline was substituted to complete the fourth and final week, at which point all antibiotics were discontinued. The patient was followed up uneventfully for 4 years (Figures 4A-4D and 5A-5C) with normal ESR and CRP. She continues to be ambulatory without assistive devices and walks an average of 30 miles per week without pain or constitutional symptoms.

thum0918_f4

thum0918_f5

Continue to: DISCUSSION...

 

 

DISCUSSION

Diagnosis of acute infection after TKA remains challenging, as some degree of pain, swelling, and even postoperative fevers may be common in noninfected TKA patients. Synovial white blood cell count and differential as well as alpha-defensin levels have been cited as predictive factors of infection.16,17 Deep tissue and synovial fluid cultures offer the advantage of both identification and antimicrobial sensitivity testing of the offending organism. In this case, culture of the knee joint fluid at the time of TKA led to the unexpected finding of M. abscessus infection.

Preventable outbreaks due to M. abscessus have been reported and attributed to contaminated multiuse instruments, inadequate sterilization of tap water, multiuse vials, and improper skin preparation.11-13 Rarely, M. abscessus has been reported as the cause of PJI. When an unusual organism is encountered after native joint instrumentation, an investigation should be undertaken to identify the source of contamination, with the assistance of infection control practitioners and/or the US Food and Drug Administration reporting. Reporting and investigation was undertaken in this case, though no suspect source could be identified.

Although there were no signs of infection prior to the TKA, there is an ongoing debate as to whether intra-articular corticosteroid injections increase the risk of PJIs, and if so, what the optimal amount of time to wait between procedures is. Although several earlier studies have been underpowered to answer these questions,18 this patient underwent TKA 1 month following the corticosteroid injection. Recent meta-analyses have shown no definitive evidence to indicate that this increased her risk of PJI.19,20

Continue to: Treatments for mycobacterial infections...

 

 

Treatments for mycobacterial infections have been described with variable efficacy,21,22 and only 2 cases of successfully treated PJIs have been reported after infection with M. abscessus. Both these cases were described in total hip arthroplasties,23,24 and to the authors’ knowledge, this report represents the first described successfully treated case after TKA. Staged reconstruction remains a standard treatment for invasive organisms chronically infecting prosthetic joint implants, with reimplantation pending joint sterility and improvement in inflammatory markers.3 Previous successful reports of treating M. abscessus describe either resection arthroplasty21 or staged reconstruction.23,24 The authors reported variable multidrug antimicrobial regimens, as summarized in Table 2, as guidelines for the treatment of mycobacterial PJI are currently not available.

thum0918_t2

CONCLUSION

This case report represents an episode of iatrogenic septic arthritis caused by Mycobacteria of the native knee after previous history of instrumentation, corticosteroid, and hyaluronic acid injections, with an overall indolent clinical course until subsequent arthroplasty. There were several important lessons learned, which are as follows: 1) Multidrug combination with antimicrobial therapy combined with aggressive surgical débridement and staged reimplantation permitted successful eradication of TKA PJI caused by M. abscessus in this patient. 2) Initial medical management alone was not successful and cannot be recommended for the treatment of M. abscessus in the setting of PJI. 3) Delaying the surgical débridement and the reconstructive course for a trial of medical management contributed to the ultimate requirement of a tibial tubercle osteotomy for an ankylosed knee at replantation. In this case, we initially had a low index of suspicion for deep infection, contributing to delayed surgical débridement. Ideally, a high degree of clinical suspicion should be maintained for joint infection in the presence of positive culture isolates of M. abscessus, as it may have a delayed clinical presentation of the typical features of PJI (fevers, swelling, erythema, etc). In such cases, the authors recommend consideration of early surgical débridement. 4) Medical management of TKA PJI is not without risks. Careful monitoring of patient side effects during antimicrobial administration remains paramount, as this patient did sustain a degree of hearing loss associated with prolonged medical therapy. 5) In complicated PJIs involving rare and intrinsically resistant organisms, a collaborative multidisciplinary approach, including specialists in orthopedic surgery, infectious disease, microbiology, pharmacy, and pathology, may be the preferred path to clinical cure.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785. doi:10.2106/JBJS.F.00222.

2. Cobo J, Del Pozo JL. Prosthetic joint infection: diagnosis and management. Expert Rev Anti Infect Ther. 2011;9(9):787-802. doi:10.1586/eri.11.95.

3. Toms AD, Davidson D, Masri BA, Duncan CP. The management of peri-prosthetic infection in total joint arthroplasty. J Bone Joint Surg Br. 2006;88(2):149-155. doi:10.1302/0301-620X.88B2.17058.

4. Osmon DR, Berbari EF, Berendt AR, et al. Diagnosis and management of prosthetic joint infection: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2013;56(1):e1-e25. doi:10.1093/cid/cis803.

5. Restrepo C, Schmitt S, Backstein D, et al. Antibiotic treatment and timing of reimplantation. J Orthop Res. 2014;32 Suppl 1:S136-S140. doi:10.1002/jor.22557.

6. De Groote MA, Huitt G. Infections due to rapidly growing mycobacteria. Clin Infect Dis. 2006;42(12):1756-1763. doi:10.1086/504381.

7. Nash KA, Brown-Elliott BA, Wallace RJ Jr. A novel gene, erm(41), Confers inducible macrolide resistance to clinical isolates of Mycobacterium abscessus but is absent from Mycobacterium chelonae. Antimicrob Agents Chemother. 2009;53(4):1367-1376. doi:10.1128/AAC.01275-08.

8. Furuya EY, Paez A, Srinivasan A, et al. Outbreak of Mycobacterium abscessus wound infections among "lipotourists" from the United States who underwent abdominoplasty in the Dominican Republic. Clin Infect Dis. 2008;46(8):1181-1188. doi:10.1086/529191.

9. Jarand J, Levin A, Zhang L, Huitt G, Mitchell JD, Daley CL. Clinical and microbiologic outcomes in patients receiving treatment for Mycobacterium abscessus pulmonary disease. Clin Infect Dis. 2011;52(5):565-571. doi:10.1093/cid/ciq237.

10. Mueller PS, Edson RS. Disseminated Mycobacterium abscessus infection manifesting as fever of unknown origin and intra-abdominal lymphadenitis: case report and literature review. Diagn Microbiol Infect Dis. 2001;39(1):33-37. doi:10.1016/S0732-8893(00)00211-X.

11. Mushatt DM, Witzig RS. Successful treatment of Mycobacterium abscessus infections with multidrug regimens containing clarithromycin. Clin Infect Dis. 1995;20(5):1441-1442. doi:10.1093/clinids/20.5.1441.

12. Tiwari TS, Ray B, Jost KC Jr, et al. Forty years of disinfectant failure: outbreak of postinjection Mycobacterium abscessus infection caused by contamination of benzalkonium chloride. Clin Infect Dis. 2003;36(8):954-962. doi:10.1086/368192.

13. Villanueva A, Calderon RV, Vargas BA, et al. Report on an outbreak of postinjection abscesses due to Mycobacterium abscessus, including management with surgery and clarithromycin therapy and comparison of strains by random amplified polymorphic DNA polymerase chain reaction. Clin Infect Dis. 1997;24(6):1147-1153. doi:10.1086/513656.

14. Gale DW, Harding ML. Total knee arthroplasty in the presence of active tuberculosis. J Bone Joint Surg Br. 1991;73(6):1006-1007. doi:10.1302/0301-620X.73B6.1955424.

15. Kim YH. Total knee arthroplasty for tuberculous arthritis. J Bone Joint Surg Am. 1988;70(9):1322-1330. doi:10.2106/00004623-198870090-00008.

16. Bedair H, Ting N, Jacovides C, et al. The Mark Coventry Award: diagnosis of early postoperative TKA infection using synovial fluid analysis. Clin Orthop Relat Res. 2011;469(1):34-40. doi:10.1007/s11999-010-1433-2.

17. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009. doi:10.1007/s11999-014-3900-7.

18. Marsland D, Mumith A, Barlow IW. Systematic review: the safety of intra-articular corticosteroid injection prior to total knee arthroplasty. Knee. 2014;21(1):6-11. doi:10.1016/j.knee.2013.07.003.

19. Charalambous CP, Prodromidis AD, Kwaees TA. Do intra-articular steroid injections increase infection rates in subsequent arthroplasty? A systematic review and meta-analysis of comparative studies. J Arthroplast. 2014;29(11):2175-2180. doi:10.1016/j.arth.2014.07.013.

20. Xing D, Yang Y, Ma X, Ma J, Ma B, Chen Y. Dose intraarticular steroid injection increase the rate of infection in subsequent arthroplasty: grading the evidence through a meta-analysis. J Orthop Surg Res. 2014;9:107. doi:10.1186/s13018-014-0107-2.

21. Eid AJ, Berbari EF, Sia IG, Wengenack NL, Osmon DR, Razonable RR. Prosthetic joint infection due to rapidly growing mycobacteria: report of 8 cases and review of the literature. Clin Infect Dis. 2007;45(6):687-694. doi:10.1086/520982.

22. Herold RC, Lotke PA, MacGregor RR. Prosthetic joint infections secondary to rapidly growing Mycobacterium fortuitum. Clin Orthop Relat Res. 1987;216(216):183-186. doi:10.1097/00003086-198703000-00029.

23. Petrosoniak A, Kim P, Desjardins M, Lee BC. Successful treatment of a prosthetic joint infection due to Mycobacterium abscessus. Can J Infect Dis Med Microbiol. 2009;20(3):e94-e96.

24. Yinkey LM, Halsey ES, Lloyd BA. Successful tigecycline combination therapy for Mycobacterium abscessus infection of a total hip arthroplasty. Infect Dis Clin Practice. 2010;18(4):269-270. doi:10.1097/IPC.0b013e3181d04a09.

25. AAOS Guidelines: the diagnosis of periprosthetic joint infections of the hip and knee guideline and evidence report. Adopted by the American Academy of Orthopaedic Surgeons Board of Directors; June 18th, 2010. AAOS Publication: 2010.

26. Griffith DE, Aksamit T, Brown-Elliott BA, et al; ATS Mycobacterial Diseases Subcomittee; American Thoracic Society; Infectious Disease Society of America. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175(4):367-416.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785. doi:10.2106/JBJS.F.00222.

2. Cobo J, Del Pozo JL. Prosthetic joint infection: diagnosis and management. Expert Rev Anti Infect Ther. 2011;9(9):787-802. doi:10.1586/eri.11.95.

3. Toms AD, Davidson D, Masri BA, Duncan CP. The management of peri-prosthetic infection in total joint arthroplasty. J Bone Joint Surg Br. 2006;88(2):149-155. doi:10.1302/0301-620X.88B2.17058.

4. Osmon DR, Berbari EF, Berendt AR, et al. Diagnosis and management of prosthetic joint infection: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2013;56(1):e1-e25. doi:10.1093/cid/cis803.

5. Restrepo C, Schmitt S, Backstein D, et al. Antibiotic treatment and timing of reimplantation. J Orthop Res. 2014;32 Suppl 1:S136-S140. doi:10.1002/jor.22557.

6. De Groote MA, Huitt G. Infections due to rapidly growing mycobacteria. Clin Infect Dis. 2006;42(12):1756-1763. doi:10.1086/504381.

7. Nash KA, Brown-Elliott BA, Wallace RJ Jr. A novel gene, erm(41), Confers inducible macrolide resistance to clinical isolates of Mycobacterium abscessus but is absent from Mycobacterium chelonae. Antimicrob Agents Chemother. 2009;53(4):1367-1376. doi:10.1128/AAC.01275-08.

8. Furuya EY, Paez A, Srinivasan A, et al. Outbreak of Mycobacterium abscessus wound infections among "lipotourists" from the United States who underwent abdominoplasty in the Dominican Republic. Clin Infect Dis. 2008;46(8):1181-1188. doi:10.1086/529191.

9. Jarand J, Levin A, Zhang L, Huitt G, Mitchell JD, Daley CL. Clinical and microbiologic outcomes in patients receiving treatment for Mycobacterium abscessus pulmonary disease. Clin Infect Dis. 2011;52(5):565-571. doi:10.1093/cid/ciq237.

10. Mueller PS, Edson RS. Disseminated Mycobacterium abscessus infection manifesting as fever of unknown origin and intra-abdominal lymphadenitis: case report and literature review. Diagn Microbiol Infect Dis. 2001;39(1):33-37. doi:10.1016/S0732-8893(00)00211-X.

11. Mushatt DM, Witzig RS. Successful treatment of Mycobacterium abscessus infections with multidrug regimens containing clarithromycin. Clin Infect Dis. 1995;20(5):1441-1442. doi:10.1093/clinids/20.5.1441.

12. Tiwari TS, Ray B, Jost KC Jr, et al. Forty years of disinfectant failure: outbreak of postinjection Mycobacterium abscessus infection caused by contamination of benzalkonium chloride. Clin Infect Dis. 2003;36(8):954-962. doi:10.1086/368192.

13. Villanueva A, Calderon RV, Vargas BA, et al. Report on an outbreak of postinjection abscesses due to Mycobacterium abscessus, including management with surgery and clarithromycin therapy and comparison of strains by random amplified polymorphic DNA polymerase chain reaction. Clin Infect Dis. 1997;24(6):1147-1153. doi:10.1086/513656.

14. Gale DW, Harding ML. Total knee arthroplasty in the presence of active tuberculosis. J Bone Joint Surg Br. 1991;73(6):1006-1007. doi:10.1302/0301-620X.73B6.1955424.

15. Kim YH. Total knee arthroplasty for tuberculous arthritis. J Bone Joint Surg Am. 1988;70(9):1322-1330. doi:10.2106/00004623-198870090-00008.

16. Bedair H, Ting N, Jacovides C, et al. The Mark Coventry Award: diagnosis of early postoperative TKA infection using synovial fluid analysis. Clin Orthop Relat Res. 2011;469(1):34-40. doi:10.1007/s11999-010-1433-2.

17. Bingham J, Clarke H, Spangehl M, Schwartz A, Beauchamp C, Goldberg B. The alpha defensin-1 biomarker assay can be used to evaluate the potentially infected total joint arthroplasty. Clin Orthop Relat Res. 2014;472(12):4006-4009. doi:10.1007/s11999-014-3900-7.

18. Marsland D, Mumith A, Barlow IW. Systematic review: the safety of intra-articular corticosteroid injection prior to total knee arthroplasty. Knee. 2014;21(1):6-11. doi:10.1016/j.knee.2013.07.003.

19. Charalambous CP, Prodromidis AD, Kwaees TA. Do intra-articular steroid injections increase infection rates in subsequent arthroplasty? A systematic review and meta-analysis of comparative studies. J Arthroplast. 2014;29(11):2175-2180. doi:10.1016/j.arth.2014.07.013.

20. Xing D, Yang Y, Ma X, Ma J, Ma B, Chen Y. Dose intraarticular steroid injection increase the rate of infection in subsequent arthroplasty: grading the evidence through a meta-analysis. J Orthop Surg Res. 2014;9:107. doi:10.1186/s13018-014-0107-2.

21. Eid AJ, Berbari EF, Sia IG, Wengenack NL, Osmon DR, Razonable RR. Prosthetic joint infection due to rapidly growing mycobacteria: report of 8 cases and review of the literature. Clin Infect Dis. 2007;45(6):687-694. doi:10.1086/520982.

22. Herold RC, Lotke PA, MacGregor RR. Prosthetic joint infections secondary to rapidly growing Mycobacterium fortuitum. Clin Orthop Relat Res. 1987;216(216):183-186. doi:10.1097/00003086-198703000-00029.

23. Petrosoniak A, Kim P, Desjardins M, Lee BC. Successful treatment of a prosthetic joint infection due to Mycobacterium abscessus. Can J Infect Dis Med Microbiol. 2009;20(3):e94-e96.

24. Yinkey LM, Halsey ES, Lloyd BA. Successful tigecycline combination therapy for Mycobacterium abscessus infection of a total hip arthroplasty. Infect Dis Clin Practice. 2010;18(4):269-270. doi:10.1097/IPC.0b013e3181d04a09.

25. AAOS Guidelines: the diagnosis of periprosthetic joint infections of the hip and knee guideline and evidence report. Adopted by the American Academy of Orthopaedic Surgeons Board of Directors; June 18th, 2010. AAOS Publication: 2010.

26. Griffith DE, Aksamit T, Brown-Elliott BA, et al; ATS Mycobacterial Diseases Subcomittee; American Thoracic Society; Infectious Disease Society of America. An official ATS/IDSA statement: diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med. 2007;175(4):367-416.

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TAKE-HOME POINTS:

  • Periprosthetic joint infections due to Mycobacterium abscess have been rarely reported, and no specific guidlines exist to inform treatment.
  • Medical management alone was not successful in our clinical case and cannot be recommended.
  • Combination medical and surgical management may provide the best opportunity for clincal cure of periprosthetic infections.
  • In complicated periprosthetic joint infections involving rare and intrinsically resistant organisms, a collaborative multidisciplinary approach likley represents the preferred path to clinical cure.
  • Successful erradiation of periprosthetic infection with M. abscessus may not preclude acceptable outcomes after revision TKA.
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The Flint Lock: A Novel Technique in Total Knee Arthroplasty Closure

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ABSTRACT

Conventional interrupted sutures are traditionally used in extensor mechanism closure during total knee arthroplasty (TKA). In recent years, barbed suture has been introduced with the proposed benefits of decreased closure time and a watertight seal that is superior to interrupted sutures. Complication rates using barbed sutures and conventional interrupted sutures are similar. We propose a novel closure technique known as the Flint Lock, which is a double continuous interlocking stitch. The Flint Lock provides a quick and efficient closure to the extensor mechanism in TKA. In addition, similar to barbed suture, the Flint Lock should provide a superior watertight seal. It utilizes relatively inexpensive and readily available materials.

Continue to: In 2003, more than 400,000 total knee replacements...

 

 

In 2003, more than 400,000 total knee replacements were performed in the United States. This number is expected to increase in the coming decades to 3 million by the year 2030.1 The surgical approach to knee arthroplasty always involves a capsular incision that needs to be repaired after implantation of the components. The capsular incision repair should be strong enough to allow for immediate range of motion.

Traditionally, repair of the arthrotomy is performed using interrupted sutures. Recently, a running technique using barbed suture has been demonstrated to enable faster closure times.2-6 In addition, a running suture technique using barbed suture provides a superior watertight closure compared with an interrupted suture.7 It has been reported that the barbed suture has the same safety profile as that of interrupted sutures,2,3,4 although extensor mechanism repair failure8 and wound complications9,10 have been reported.

This study proposes a novel technique for arthrotomy closure in total knee arthroplasty (TKA). It is a double continuous interlocking stitch, termed the “Flint Lock.” Based on our clinical experience using this method, this technique has been found to be safe and effective.

TECHNIQUE

The Flint Lock was developed for closure in TKA, which was performed through a standard medial parapatellar approach. Before creating the arthrotomy, a horizontal line is drawn along the medial side of the patella to ensure anatomic alignment of the extensor mechanism during closure of the capsule.

peck0918_f1

The Flint Lock is performed by 2 people working simultaneously. Closure begins at the proximal end of the arthrotomy using 2 No. 1 Vicryl (Ethicon) sutures. Each suture is thrown a single time at the most proximal extent of the arthrotomy with the knee in 30° to 40° of flexion. These sutures are tied off independently from each other (Figure 1). At this point, the knee is flexed to 90° and the sutures are thrown alternately, with the first operator passing medial to lateral through the capsule and the second operator passing lateral to medial. While 1 operator is passing a suture, the other operator holds the other suture tight to maintain tension on the closure. The alternating throws create an interlocking weave as the pattern is repeated and progressively moves distally (Figure 2). This technique results in 2 continuous sutures running in opposing directions. Each No. 1 Vicryl suture is specific to each operator. Therefore, each operator uses the same suture for the entirety of the closure.

peck0918_f2

When the superior pole of the patella is reached, the 2 sutures are tied together, thus creating a segmental closure (Figure 3). Following this tie off, the closure is continued in a similar manner until the inferior pole of the patella is reached. The sutures are then tied off to each other again, creating another segmental closure (Figure 4). The remainder of the arthrotomy is closed continuing the Flint Lock technique, and the 2 sutures are tied off to each other at the distal end of the arthrotomy and cut (Figure 5).

peck0918_f3

peck0918_f4

peck0918_f5

Continue to: The superficial layers are closed at the surgeon’s discretion...

 

 

The superficial layers are closed at the surgeon’s discretion. The authors prefer interrupted 2-0 Vicryl sutures followed by a running 3-0 Monocryl (Ethicon) suture in the subcutaneous layer. Dermabond (Ethicon) skin glue and an Aquacel Ag (ConvaTec) dressing are applied, followed by a compressive bandage.

DISCUSSION

The importance of a strong, tight closure of the arthrotomy in TKA is critical to the success of the procedure. Nevertheless, there are multiple methods to achieve closure. The Flint Lock technique is a novel method that employs basic concepts of surgical technique in an original manner. The continuous nature of the closure should provide a tighter seal, leading to less wound drainage. Persistent wound drainage has been associated with deep wound infections following total joint arthroplasty.11,12 In addition, the double suture provides a safeguard to a single suture rupture, while the segmental quality protects against complete arthrotomy failure.

A potential downside of this technique is that it requires 2 individuals operating 2 needles simultaneously. This presents a potential for a sharp injury to the operators; however, this has not occurred in our experience. A comparable risk with interrupted sutures is probably present because there are often multiple sutures utilized during closure via the interrupted technique.

In 2015, the cost of a single No. 1 barbed suture was $13.14 at our institution, whereas the cost of 2 No. 1 Vicryl sutures was $3.66. Although pricing differs across hospitals, the Vicryl sutures are probably less costly compared with the barbed sutures.

Our experience with the Flint Lock technique has been favorable thus far, with no incidences of postoperative drainage, infection, or extensor mechanism failure. Our current use has been in closure of the knee, but it could be considered in closure of long incisions about the hip as well. A more in-depth analysis of relevant factors, such as time for closure, mechanical strength, cost savings, and clinical outcomes, is needed to further evaluate this method of closure. In addition, biomechanical analysis of the technique would aid in its evaluation. Future studies are needed to analyze these factors to verify the benefits and viability of the Flint Lock technique.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785. doi:10.2106/JBJS.F.00222.

2. Eickmann T, Quane E. Total knee arthroplasty closure with barbed sutures. J Knee Surg. 2010;23(3):163-167. doi:10.1055/s-0030-1268692.

3. Gililland JM, Anderson LA, Sun G, Erickson JA, Peters CL. Perioperative closure-related complication rates and cost analysis of barbed suture for closure in TKA. Clin Orthop Relat Res. 2012;470(1):125-129. doi:10.1007/s11999-011-2104-7.

4. Ting NT, Moric MM, Della Valle CJ, Levine BR. Use of knotless suture for closure of total hip and knee arthroplasties: a prospective, randomized clinical trial. J Arthroplasty. 2012;27(10):1783-1788. doi:10.1016/j.arth.2012.05.022.

5. Stephens S, Politi J, Taylor BC. Evaluation of primary total knee arthroplasty incision closure with use of continuous bidirectional barbed suture. Surg Technol Int. 2011;21:199-203.

6. Levine BR, Ting N, Della Valle CJ. Use of a barbed suture in the closure of hip and knee arthroplasty wounds. Orthopedics. 2011;34(9):e473-e475. doi:10.3928/01477447-20110714-35.

7. Nett M, Avelar R, Sheehan M, Cushner F. Water-tight knee arthrotomy closure: comparison of a novel single bidirectional barbed self-retaining running suture versus conventional interrupted sutures. J Knee Surg. 2011;24(1):55-59. doi:10.1055/s-0031-1275400.

8. Wright RC, Gillis CT, Yacoubian SV, Raven RB 3rd, Falkinstein Y, Yacoubian SV. Extensor mechanism repair failure with use of birectional barbed suture in total knee arthroplasty. J Arthroplasty. 2012;27(7):1413.e1-e4. doi:10.1016/j.arth.2011.08.013.

9. Campbell AL, Patrick DA Jr, Liabaud B, Geller JA. Superficial wound closure complications with barbed sutures following knee arthroplasty. J Arthroplasty. 2014;29(5):966-969. doi:10.1016/j.arth.2013.09.045.

10. Smith EL, DiSegna ST, Shukla PY, Matzkin EG. Barbed versus traditional sutures: closure time, cost, and wound related outcomes in total joint arthroplasty. J Arthroplasty. 2014;29(2):283-287. doi:10.1016/j.arth.2013.05.031.

11. Saleh K, Olson M, Resig S, et al. Predictors of wound infection in hip and knee joint replacement: results from a 20 year surveillance program. J Orthop Res. 2002;20(3):506-515. doi:10.1016/S0736-0266(01)00153-X.

12. Weiss AP, Krackow KA. Persistent wound drainage after primary total knee arthroplasty. J Arthroplasty. 1993;8(3):285-289. doi:10.1016/S0883-5403(06)80091-4.

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Peck is an Orthopedic Surgery Fellow, Hospital for Special Surgery, New York, New York. Dr. Charpentier is an Orthopedic Surgeon, Howard Memorial Hospital, Willits, California. Dr. Srivastava is Associate Professor, Department of Orthopedic Surgery, McLaren-Flint/Michigan State University, Flint, Michigan. Ms. Bowman is a Nurse Practitioner, Department of Orthopedic Surgery, Hurley Medical Center, Flint, Michigan.

Address correspondence to: Jeffrey B. Peck, MD, Center of Hip Preservation, Hospital for Special Surgery, 535 E. 70th St, New York, NY 10021 (tel, 847-702-1589; fax, 810-342-2150; email, JeffreyPeck2007@u.northwestern.edu).

Jeffrey B. Peck, MD Paul M. Charpentier, MD Sherry K. Bowman, ANP-BC Ajay K. Srivastava, MD . The Flint Lock: A Novel Technique in Total Knee Arthroplasty Closure. Am J Orthop.

September 13, 2018

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Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Peck is an Orthopedic Surgery Fellow, Hospital for Special Surgery, New York, New York. Dr. Charpentier is an Orthopedic Surgeon, Howard Memorial Hospital, Willits, California. Dr. Srivastava is Associate Professor, Department of Orthopedic Surgery, McLaren-Flint/Michigan State University, Flint, Michigan. Ms. Bowman is a Nurse Practitioner, Department of Orthopedic Surgery, Hurley Medical Center, Flint, Michigan.

Address correspondence to: Jeffrey B. Peck, MD, Center of Hip Preservation, Hospital for Special Surgery, 535 E. 70th St, New York, NY 10021 (tel, 847-702-1589; fax, 810-342-2150; email, JeffreyPeck2007@u.northwestern.edu).

Jeffrey B. Peck, MD Paul M. Charpentier, MD Sherry K. Bowman, ANP-BC Ajay K. Srivastava, MD . The Flint Lock: A Novel Technique in Total Knee Arthroplasty Closure. Am J Orthop.

September 13, 2018

Author and Disclosure Information

Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

Dr. Peck is an Orthopedic Surgery Fellow, Hospital for Special Surgery, New York, New York. Dr. Charpentier is an Orthopedic Surgeon, Howard Memorial Hospital, Willits, California. Dr. Srivastava is Associate Professor, Department of Orthopedic Surgery, McLaren-Flint/Michigan State University, Flint, Michigan. Ms. Bowman is a Nurse Practitioner, Department of Orthopedic Surgery, Hurley Medical Center, Flint, Michigan.

Address correspondence to: Jeffrey B. Peck, MD, Center of Hip Preservation, Hospital for Special Surgery, 535 E. 70th St, New York, NY 10021 (tel, 847-702-1589; fax, 810-342-2150; email, JeffreyPeck2007@u.northwestern.edu).

Jeffrey B. Peck, MD Paul M. Charpentier, MD Sherry K. Bowman, ANP-BC Ajay K. Srivastava, MD . The Flint Lock: A Novel Technique in Total Knee Arthroplasty Closure. Am J Orthop.

September 13, 2018

ABSTRACT

Conventional interrupted sutures are traditionally used in extensor mechanism closure during total knee arthroplasty (TKA). In recent years, barbed suture has been introduced with the proposed benefits of decreased closure time and a watertight seal that is superior to interrupted sutures. Complication rates using barbed sutures and conventional interrupted sutures are similar. We propose a novel closure technique known as the Flint Lock, which is a double continuous interlocking stitch. The Flint Lock provides a quick and efficient closure to the extensor mechanism in TKA. In addition, similar to barbed suture, the Flint Lock should provide a superior watertight seal. It utilizes relatively inexpensive and readily available materials.

Continue to: In 2003, more than 400,000 total knee replacements...

 

 

In 2003, more than 400,000 total knee replacements were performed in the United States. This number is expected to increase in the coming decades to 3 million by the year 2030.1 The surgical approach to knee arthroplasty always involves a capsular incision that needs to be repaired after implantation of the components. The capsular incision repair should be strong enough to allow for immediate range of motion.

Traditionally, repair of the arthrotomy is performed using interrupted sutures. Recently, a running technique using barbed suture has been demonstrated to enable faster closure times.2-6 In addition, a running suture technique using barbed suture provides a superior watertight closure compared with an interrupted suture.7 It has been reported that the barbed suture has the same safety profile as that of interrupted sutures,2,3,4 although extensor mechanism repair failure8 and wound complications9,10 have been reported.

This study proposes a novel technique for arthrotomy closure in total knee arthroplasty (TKA). It is a double continuous interlocking stitch, termed the “Flint Lock.” Based on our clinical experience using this method, this technique has been found to be safe and effective.

TECHNIQUE

The Flint Lock was developed for closure in TKA, which was performed through a standard medial parapatellar approach. Before creating the arthrotomy, a horizontal line is drawn along the medial side of the patella to ensure anatomic alignment of the extensor mechanism during closure of the capsule.

peck0918_f1

The Flint Lock is performed by 2 people working simultaneously. Closure begins at the proximal end of the arthrotomy using 2 No. 1 Vicryl (Ethicon) sutures. Each suture is thrown a single time at the most proximal extent of the arthrotomy with the knee in 30° to 40° of flexion. These sutures are tied off independently from each other (Figure 1). At this point, the knee is flexed to 90° and the sutures are thrown alternately, with the first operator passing medial to lateral through the capsule and the second operator passing lateral to medial. While 1 operator is passing a suture, the other operator holds the other suture tight to maintain tension on the closure. The alternating throws create an interlocking weave as the pattern is repeated and progressively moves distally (Figure 2). This technique results in 2 continuous sutures running in opposing directions. Each No. 1 Vicryl suture is specific to each operator. Therefore, each operator uses the same suture for the entirety of the closure.

peck0918_f2

When the superior pole of the patella is reached, the 2 sutures are tied together, thus creating a segmental closure (Figure 3). Following this tie off, the closure is continued in a similar manner until the inferior pole of the patella is reached. The sutures are then tied off to each other again, creating another segmental closure (Figure 4). The remainder of the arthrotomy is closed continuing the Flint Lock technique, and the 2 sutures are tied off to each other at the distal end of the arthrotomy and cut (Figure 5).

peck0918_f3

peck0918_f4

peck0918_f5

Continue to: The superficial layers are closed at the surgeon’s discretion...

 

 

The superficial layers are closed at the surgeon’s discretion. The authors prefer interrupted 2-0 Vicryl sutures followed by a running 3-0 Monocryl (Ethicon) suture in the subcutaneous layer. Dermabond (Ethicon) skin glue and an Aquacel Ag (ConvaTec) dressing are applied, followed by a compressive bandage.

DISCUSSION

The importance of a strong, tight closure of the arthrotomy in TKA is critical to the success of the procedure. Nevertheless, there are multiple methods to achieve closure. The Flint Lock technique is a novel method that employs basic concepts of surgical technique in an original manner. The continuous nature of the closure should provide a tighter seal, leading to less wound drainage. Persistent wound drainage has been associated with deep wound infections following total joint arthroplasty.11,12 In addition, the double suture provides a safeguard to a single suture rupture, while the segmental quality protects against complete arthrotomy failure.

A potential downside of this technique is that it requires 2 individuals operating 2 needles simultaneously. This presents a potential for a sharp injury to the operators; however, this has not occurred in our experience. A comparable risk with interrupted sutures is probably present because there are often multiple sutures utilized during closure via the interrupted technique.

In 2015, the cost of a single No. 1 barbed suture was $13.14 at our institution, whereas the cost of 2 No. 1 Vicryl sutures was $3.66. Although pricing differs across hospitals, the Vicryl sutures are probably less costly compared with the barbed sutures.

Our experience with the Flint Lock technique has been favorable thus far, with no incidences of postoperative drainage, infection, or extensor mechanism failure. Our current use has been in closure of the knee, but it could be considered in closure of long incisions about the hip as well. A more in-depth analysis of relevant factors, such as time for closure, mechanical strength, cost savings, and clinical outcomes, is needed to further evaluate this method of closure. In addition, biomechanical analysis of the technique would aid in its evaluation. Future studies are needed to analyze these factors to verify the benefits and viability of the Flint Lock technique.

ABSTRACT

Conventional interrupted sutures are traditionally used in extensor mechanism closure during total knee arthroplasty (TKA). In recent years, barbed suture has been introduced with the proposed benefits of decreased closure time and a watertight seal that is superior to interrupted sutures. Complication rates using barbed sutures and conventional interrupted sutures are similar. We propose a novel closure technique known as the Flint Lock, which is a double continuous interlocking stitch. The Flint Lock provides a quick and efficient closure to the extensor mechanism in TKA. In addition, similar to barbed suture, the Flint Lock should provide a superior watertight seal. It utilizes relatively inexpensive and readily available materials.

Continue to: In 2003, more than 400,000 total knee replacements...

 

 

In 2003, more than 400,000 total knee replacements were performed in the United States. This number is expected to increase in the coming decades to 3 million by the year 2030.1 The surgical approach to knee arthroplasty always involves a capsular incision that needs to be repaired after implantation of the components. The capsular incision repair should be strong enough to allow for immediate range of motion.

Traditionally, repair of the arthrotomy is performed using interrupted sutures. Recently, a running technique using barbed suture has been demonstrated to enable faster closure times.2-6 In addition, a running suture technique using barbed suture provides a superior watertight closure compared with an interrupted suture.7 It has been reported that the barbed suture has the same safety profile as that of interrupted sutures,2,3,4 although extensor mechanism repair failure8 and wound complications9,10 have been reported.

This study proposes a novel technique for arthrotomy closure in total knee arthroplasty (TKA). It is a double continuous interlocking stitch, termed the “Flint Lock.” Based on our clinical experience using this method, this technique has been found to be safe and effective.

TECHNIQUE

The Flint Lock was developed for closure in TKA, which was performed through a standard medial parapatellar approach. Before creating the arthrotomy, a horizontal line is drawn along the medial side of the patella to ensure anatomic alignment of the extensor mechanism during closure of the capsule.

peck0918_f1

The Flint Lock is performed by 2 people working simultaneously. Closure begins at the proximal end of the arthrotomy using 2 No. 1 Vicryl (Ethicon) sutures. Each suture is thrown a single time at the most proximal extent of the arthrotomy with the knee in 30° to 40° of flexion. These sutures are tied off independently from each other (Figure 1). At this point, the knee is flexed to 90° and the sutures are thrown alternately, with the first operator passing medial to lateral through the capsule and the second operator passing lateral to medial. While 1 operator is passing a suture, the other operator holds the other suture tight to maintain tension on the closure. The alternating throws create an interlocking weave as the pattern is repeated and progressively moves distally (Figure 2). This technique results in 2 continuous sutures running in opposing directions. Each No. 1 Vicryl suture is specific to each operator. Therefore, each operator uses the same suture for the entirety of the closure.

peck0918_f2

When the superior pole of the patella is reached, the 2 sutures are tied together, thus creating a segmental closure (Figure 3). Following this tie off, the closure is continued in a similar manner until the inferior pole of the patella is reached. The sutures are then tied off to each other again, creating another segmental closure (Figure 4). The remainder of the arthrotomy is closed continuing the Flint Lock technique, and the 2 sutures are tied off to each other at the distal end of the arthrotomy and cut (Figure 5).

peck0918_f3

peck0918_f4

peck0918_f5

Continue to: The superficial layers are closed at the surgeon’s discretion...

 

 

The superficial layers are closed at the surgeon’s discretion. The authors prefer interrupted 2-0 Vicryl sutures followed by a running 3-0 Monocryl (Ethicon) suture in the subcutaneous layer. Dermabond (Ethicon) skin glue and an Aquacel Ag (ConvaTec) dressing are applied, followed by a compressive bandage.

DISCUSSION

The importance of a strong, tight closure of the arthrotomy in TKA is critical to the success of the procedure. Nevertheless, there are multiple methods to achieve closure. The Flint Lock technique is a novel method that employs basic concepts of surgical technique in an original manner. The continuous nature of the closure should provide a tighter seal, leading to less wound drainage. Persistent wound drainage has been associated with deep wound infections following total joint arthroplasty.11,12 In addition, the double suture provides a safeguard to a single suture rupture, while the segmental quality protects against complete arthrotomy failure.

A potential downside of this technique is that it requires 2 individuals operating 2 needles simultaneously. This presents a potential for a sharp injury to the operators; however, this has not occurred in our experience. A comparable risk with interrupted sutures is probably present because there are often multiple sutures utilized during closure via the interrupted technique.

In 2015, the cost of a single No. 1 barbed suture was $13.14 at our institution, whereas the cost of 2 No. 1 Vicryl sutures was $3.66. Although pricing differs across hospitals, the Vicryl sutures are probably less costly compared with the barbed sutures.

Our experience with the Flint Lock technique has been favorable thus far, with no incidences of postoperative drainage, infection, or extensor mechanism failure. Our current use has been in closure of the knee, but it could be considered in closure of long incisions about the hip as well. A more in-depth analysis of relevant factors, such as time for closure, mechanical strength, cost savings, and clinical outcomes, is needed to further evaluate this method of closure. In addition, biomechanical analysis of the technique would aid in its evaluation. Future studies are needed to analyze these factors to verify the benefits and viability of the Flint Lock technique.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785. doi:10.2106/JBJS.F.00222.

2. Eickmann T, Quane E. Total knee arthroplasty closure with barbed sutures. J Knee Surg. 2010;23(3):163-167. doi:10.1055/s-0030-1268692.

3. Gililland JM, Anderson LA, Sun G, Erickson JA, Peters CL. Perioperative closure-related complication rates and cost analysis of barbed suture for closure in TKA. Clin Orthop Relat Res. 2012;470(1):125-129. doi:10.1007/s11999-011-2104-7.

4. Ting NT, Moric MM, Della Valle CJ, Levine BR. Use of knotless suture for closure of total hip and knee arthroplasties: a prospective, randomized clinical trial. J Arthroplasty. 2012;27(10):1783-1788. doi:10.1016/j.arth.2012.05.022.

5. Stephens S, Politi J, Taylor BC. Evaluation of primary total knee arthroplasty incision closure with use of continuous bidirectional barbed suture. Surg Technol Int. 2011;21:199-203.

6. Levine BR, Ting N, Della Valle CJ. Use of a barbed suture in the closure of hip and knee arthroplasty wounds. Orthopedics. 2011;34(9):e473-e475. doi:10.3928/01477447-20110714-35.

7. Nett M, Avelar R, Sheehan M, Cushner F. Water-tight knee arthrotomy closure: comparison of a novel single bidirectional barbed self-retaining running suture versus conventional interrupted sutures. J Knee Surg. 2011;24(1):55-59. doi:10.1055/s-0031-1275400.

8. Wright RC, Gillis CT, Yacoubian SV, Raven RB 3rd, Falkinstein Y, Yacoubian SV. Extensor mechanism repair failure with use of birectional barbed suture in total knee arthroplasty. J Arthroplasty. 2012;27(7):1413.e1-e4. doi:10.1016/j.arth.2011.08.013.

9. Campbell AL, Patrick DA Jr, Liabaud B, Geller JA. Superficial wound closure complications with barbed sutures following knee arthroplasty. J Arthroplasty. 2014;29(5):966-969. doi:10.1016/j.arth.2013.09.045.

10. Smith EL, DiSegna ST, Shukla PY, Matzkin EG. Barbed versus traditional sutures: closure time, cost, and wound related outcomes in total joint arthroplasty. J Arthroplasty. 2014;29(2):283-287. doi:10.1016/j.arth.2013.05.031.

11. Saleh K, Olson M, Resig S, et al. Predictors of wound infection in hip and knee joint replacement: results from a 20 year surveillance program. J Orthop Res. 2002;20(3):506-515. doi:10.1016/S0736-0266(01)00153-X.

12. Weiss AP, Krackow KA. Persistent wound drainage after primary total knee arthroplasty. J Arthroplasty. 1993;8(3):285-289. doi:10.1016/S0883-5403(06)80091-4.

References

1. Kurtz S, Ong K, Lau E, Mowat F, Halpern M. Projections of primary and revision hip and knee arthroplasty in the United States from 2005 to 2030. J Bone Joint Surg Am. 2007;89(4):780-785. doi:10.2106/JBJS.F.00222.

2. Eickmann T, Quane E. Total knee arthroplasty closure with barbed sutures. J Knee Surg. 2010;23(3):163-167. doi:10.1055/s-0030-1268692.

3. Gililland JM, Anderson LA, Sun G, Erickson JA, Peters CL. Perioperative closure-related complication rates and cost analysis of barbed suture for closure in TKA. Clin Orthop Relat Res. 2012;470(1):125-129. doi:10.1007/s11999-011-2104-7.

4. Ting NT, Moric MM, Della Valle CJ, Levine BR. Use of knotless suture for closure of total hip and knee arthroplasties: a prospective, randomized clinical trial. J Arthroplasty. 2012;27(10):1783-1788. doi:10.1016/j.arth.2012.05.022.

5. Stephens S, Politi J, Taylor BC. Evaluation of primary total knee arthroplasty incision closure with use of continuous bidirectional barbed suture. Surg Technol Int. 2011;21:199-203.

6. Levine BR, Ting N, Della Valle CJ. Use of a barbed suture in the closure of hip and knee arthroplasty wounds. Orthopedics. 2011;34(9):e473-e475. doi:10.3928/01477447-20110714-35.

7. Nett M, Avelar R, Sheehan M, Cushner F. Water-tight knee arthrotomy closure: comparison of a novel single bidirectional barbed self-retaining running suture versus conventional interrupted sutures. J Knee Surg. 2011;24(1):55-59. doi:10.1055/s-0031-1275400.

8. Wright RC, Gillis CT, Yacoubian SV, Raven RB 3rd, Falkinstein Y, Yacoubian SV. Extensor mechanism repair failure with use of birectional barbed suture in total knee arthroplasty. J Arthroplasty. 2012;27(7):1413.e1-e4. doi:10.1016/j.arth.2011.08.013.

9. Campbell AL, Patrick DA Jr, Liabaud B, Geller JA. Superficial wound closure complications with barbed sutures following knee arthroplasty. J Arthroplasty. 2014;29(5):966-969. doi:10.1016/j.arth.2013.09.045.

10. Smith EL, DiSegna ST, Shukla PY, Matzkin EG. Barbed versus traditional sutures: closure time, cost, and wound related outcomes in total joint arthroplasty. J Arthroplasty. 2014;29(2):283-287. doi:10.1016/j.arth.2013.05.031.

11. Saleh K, Olson M, Resig S, et al. Predictors of wound infection in hip and knee joint replacement: results from a 20 year surveillance program. J Orthop Res. 2002;20(3):506-515. doi:10.1016/S0736-0266(01)00153-X.

12. Weiss AP, Krackow KA. Persistent wound drainage after primary total knee arthroplasty. J Arthroplasty. 1993;8(3):285-289. doi:10.1016/S0883-5403(06)80091-4.

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    5 Points on Meniscal Allograft Transplantation

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    ABSTRACT

    Meniscus allograft transplantation (MAT) has yielded excellent long-term functional outcomes when performed in properly indicated patients. When evaluating a patient for potential MAT, it is imperative to evaluate past medical history and past surgical procedures. The ideal MAT candidate is a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency. Existing pathology in the knee needs to be carefully considered and issues such as malalignment, cartilage defects, and/or ligamentous instability may require a staged or concomitant procedure. Once an ideal candidate is identified, graft selection and preparation are critical steps to ensure a proper fit and long-term viability of the meniscus. When selecting the graft, accurate measurements must be taken, and this is most commonly performed using plain radiographs for this. Graft fixation can be accomplished by placing vertical mattress sutures and tying those down with the knee in full extension.

    Continue to: Meniscus tears are common in the young, athletic patient population...

     

     

    Meniscus tears are common in the young, athletic patient population. In the United States alone, approximately 700,000 meniscectomies are performed annually.1 Given discouraging long-term clinical results following subtotal meniscectomy in young patients, meniscal repair is preferred whenever possible.2 Despite short-term symptom relief if subtotal meniscectomy is required, some patients often go on to develop localized pain in the affected compartment, effusions, and eventual development of osteoarthritis. In such patients with symptomatic meniscal deficiency, meniscal allograft transplantation (MAT) has yielded excellent long-term functional outcomes.3-5 Three recently published systematic reviews describe the outcomes of MAT in thousands of patients, noting positive outcomes in regard to pain and function for the majority of patients.6-8 Specifically, in a review conducted by Elattar and colleagues7 consisting of 44 studies comprising 1136 grafts in 1068 patients, the authors reported clinical improvement in Lysholm Knee Scoring Scale score (44 to 77), visual analog scale (48 mm to 17 mm), and International Knee Documentation Committee (84% normal/nearly normal, 89% satisfaction), among other outcomes measures. Additionally, the complication (21.3%) and failure rates (10.6%) were considered acceptable by all authors. The purpose of this article is to review indications, operative preparation, critical aspects of surgical technique, and additional concomitant procedures commonly performed alongside MAT.

    1. PATIENT SELECTION

    When used with the proper indications, MAT offers improved functional outcomes and reduced pain for patients with symptomatic meniscal deficiency. When evaluating a patient for potential MAT, it is imperative to evaluate past medical history and past surgical procedures. The ideal MAT candidate is a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency who does not have (1) evidence of diffuse osteoarthritis (Outerbridge grade <2), including the absence of significant bony flattening or osteophytes in the involved compartment; (2) inflammatory arthritis; (3) active or previous joint infection; (4) mechanical axis malalignment; or (5) morbid obesity (Table). Long-leg weight-bearing anterior-posterior alignment radiographs are important in the work-up of any patient being considered for MAT, and consideration for concomitant or staged realignment high tibial osteotomy (HTO) or distal femoral osteotomy (DFO) should be given for patients in excessive varus or valgus, respectively. Although the decision to perform a realignment osteotomy is made on a patient-specific basis, if the weight-bearing line passes medial to the medial tibial spine or lateral to the lateral tibial spine, HTO or DFO, respectively, should be considered. Importantly, MAT is not typically recommended in the asymptomatic patient.9 Although some recent evidence suggests MAT may have chondroprotective effects on articular cartilage following meniscectomy, there is insufficient long-term outcome data to support the use of MAT as a prophylactic measure, especially given the fact that graft deterioration inevitably occurs at 7 to 10 years, with patients having to consider avoiding meniscus-dependent activities following transplant to protect their graft from traumatic failure.10,11

    Table. Summary of Indications and Contraindications for Meniscal Allograft Transplant (MAT)

    Indications

    Contraindicationsa

    Patients younger than 50 years old with a chief complaint of pain limiting their desired activities

    Diffuse femoral and/or tibial articular cartilage wear

    Body mass index <35 kg/m2

    Radiographic evidence of

    arthritis

    Previous meniscectomy (or non-viable meniscus state) with pain localized to the affected compartment

    Inflammatory arthritis conditions

    Normal or correctable coronal and sagittal alignment

    MAT performed as a prophylactic measure in the absence of appropriate symptoms is highly controversial

    Normal or correctable ligamentous stability

     

    Normal or correctable articular cartilage

     

    Willingness to comply with rehabilitation protocol

     

    Realistic post-surgical activity expectations

     

    aContraindications for MAT are controversial, as the available literature discussing contraindications is very limited. This list is based on the experience of the senior author.

    Long-term prospective studies have shown high graft survival and predominantly positive functional results after MAT. Age indications have expanded, with 1 recent study reporting 6% reoperation rate and zero failures in a cohort of 37 adolescent MAT patients.12 High survival rates hold even among an athletic population, where rates of return to play after MAT have been reported to be >75% for those competing at a high school level or higher.13 In an active military population, <2% of patients progressed to revision MAT or total knee arthroplasty at minimum 2-year follow-up, but 22% of patients were unable to return to military duty owing to residual knee limitations.14 In this series, tobacco use correlated with failure, whereas MAT by high-volume, fellowship-trained orthopedic surgeons decreased rates of failure.

    2. GRAFT SELECTION

    In preparation for MAT, accurate measurements must be taken for appropriate size matching. Several measurement techniques have been described, including using plain radiographs, 3D computed tomography (CT), and magnetic resonance imaging (MRI).15-18 There is limited data regarding the consequences of an improperly sized donor meniscus; however, an oversized lateral meniscus has been shown to increase the contact forces across the articular cartilage.19 Additionally, an undersized allograft may result in normal forces across the articular cartilage but greater forces across the meniscus.19

    When sizing the recipient knee for MAT, accurate width and length measurements are critical. The most common technique used today includes measurements using anteroposterior and lateral radiographic images as described by Pollard and colleagues.15 The width of the meniscus is determined by the distance between 2 vertical lines perpendicular to the joint line, 1 of them tangential to the margin of the tibia metaphysis and the other between the medial and lateral tibial eminence in both knees (Figures 1A,1B). The length of the meniscus is measured on a lateral radiograph. A line is drawn at the level of the articular line between the anterior surface of the tibia above the tuberosity and a parallel line that is tangential to the posterior margin of the tibial plateau. Percent corrections are performed for these dimensions as described in previous publications.

    frank0918_f1_0

    Other techniques have been described to obtain accurate measurements of the recipient knee. For example, obtaining an MRI of the contralateral knee may provide a reproducible method of measuring both the width and length of the medial and lateral menisci.20 CT has been used to measure the lateral meniscus independently, and it has been shown to exhibit less error in the measure of the tibial plateau when compared with X-rays.18 Both CT and MRI are more expensive than simple radiographs, and CT exposes the patient to an increased amount of radiation. Current evidence does not support standard use of these advanced imaging modalities for meniscal sizing.

    Continue to: GRAFT PREPARATION AND PLACEMENT...

     

     

    3. GRAFT PREPARATION AND PLACEMENT

    At the time of surgery, the meniscus allograft is thawed in sterile saline and prepared on the back table. This can be done before or after the diagnostic arthroscopy and bone-slot preparation. Excess soft tissue surrounding the meniscal rim and/or anterior and posterior horns should be removed. Several techniques for MAT have been described, but we generally prefer a bridge-in-slot technique for both medial and lateral MAT.21 To prepare the meniscus allograft for a bridge-in-slot technique, the graft is cut with an oscillating saw to a width of 7 mm, with care taken to ensure that the bony insertions of both meniscal horns are preserved. Next, a transverse cut is made 10 mm below the meniscal horns to set the depth of the bone bridge. To assist with the sizing of the bone bridge, a rectangular sizing block and cutting jig is used (Figures 2A-2C). After marking the middle and posterior thirds of the meniscus, a No. 2 non-absorbable suture is placed at the junction of the posterior and middle thirds of the meniscus. This completes preparation of the allograft prior to implantation.

    frank0918_f2

    Attention is then turned to back the arthroscopy. A standard posteromedial (medial meniscus) or posterolateral (lateral meniscus) accessory incision is made, and a Henning retractor is carefully placed in order to receive the sutures that will be placed through the meniscus allograft via a standard inside-out repair technique. First, a zone-specific cannula is used to place a nitinol wire out the accessory incision. The looped end of the wire is pulled out of the anterior arthrotomy incision that will be used to shuttle the meniscus allograft into the joint. In order to pass the meniscal allograft into the joint, the passing suture previously placed through the meniscus is shuttled through the nitinol wire, and the wire is then pulled out the accessory incision, advancing the meniscus through the anteiror arthrotomy. As the meniscus is introduced, the traction suture is then gently tensioned to get the allograft completely into the joint. Next, the bone bridge is seated into the previously created bone slot, as the soft tissue component is manually pushed beneath the ipsilateral femoral condyle. Under direct visualization, the soft tissue component is reduced with a probe using firm, constant traction. To aid in reduction, it may be useful to apply compartment-specific varus or valgus stress and to cycle the knee once the meniscal complex is reduced.

    4. GRAFT FIXATION

    Once the graft has been passed completely into the joint, with the bone bridge seated into the bone slot, the long end of an Army-Navy retractor is placed firmly through the arthrotomy on the meniscal bone bridge, maintaining a downward force to allow the bridge to remain slotted. To lever down on the posterior aspect of the graft, a freer elevator is used from anterosuperior to posteroinferior. The bone bridge is then secured using a bioabsorbable interference screw, placed central to the bone bridge opposing the block to the ipsilateral compartment. The remainder of the meniscus is secured with an inside-out repair technique, working from posterior to anterior through a standard medial or lateral meniscal repair approach. In total, approximately 6 to 10 vertical mattress sutures are placed, and these can be placed both superiorly and inferiorly on the meniscus. Posteriorly, an all-inside suture repair device may be helpful. Finally, the anterior aspect of the meniscus is repaired to the capsule in an open fashion prior to closing the arthrotomy. Sutures are tied with the leg in extension. The meniscal repair incision is closed in a standard fashion using layers.

    5. CONCOMITANT PATHOLOGY AND MAT

    The presence of concomitant knee pathology in the context of meniscus deficiency is a challenging problem that requires careful attention to all aspects of the underlying condition of the knee. In cases where MAT is indicated, issues of malalignment, cartilage defects, and/or ligamentous instability may also need to be addressed either concomitantly or in staged fashion. For example, medial meniscal deficiency in the setting of varus alignment can be addressed with a concomitant HTO, whereas lateral meniscal deficiency in the setting of valgus malalignment can be addressed with a concomitant DFO. In both cases, the osteotomy corrects an abnormal mechanical axis, offloading the diseased compartment. This accomplishes 2 goals, namely to preserve the new MAT graft and to protect underlying articular cartilage.22-24 The osteotomy is an important contributor to additional pain relief by offloading the compartment, and clinical studies have demonstrated that failure to address malalignment in the setting of surgical intervention for cartilage and meniscal insufficiency leads to inferior clinical outcomes and poor survival of transplanted tissue.25-28

    Continue to: In a meniscus-deficient patient with chondral lesions...

     

     

    In a meniscus-deficient patient with chondral lesions (Outerbridge grade 3 or 4), concomitant MAT and cartilage restoration should be considered. Depending on the size and location of the chondral lesion, options include marrow stimulation, autologous chondrocyte implantation, osteochondral autograft transfer, as well as chondral and/or osteochondral allograft transplantation. In a systematic review of concomitant MAT and cartilage restoration procedures, Harris and colleagues25 found that failure rates of the combined surgery were similar to those of either surgery in isolation.

    Young athletes sustaining anterior cruciate ligament (ACL) tears commonly also have meniscal pathology that must be addressed. Most cases are treated with meniscal repair or partial meniscectomy, but occasionally patients present with ACL tear and symptomatic meniscal deficiency. Specifically, MAT survival relies largely on a knee with ligamentous stability, whereas outcomes of ACL reconstruction are improved with intact and functional menisci.29 The surgical technique for MAT is modified slightly in the setting of performing a concomitant ACL reconstruction, with the ACL tibial tunnel drilled to avoid the meniscal bone slot if possible, followed by femoral tunnel creation. Femoral fixation of the ACL graft is accomplished after preparation of the meniscal slot. The meniscal graft is set into place (sutures are not yet tied), and tibial fixation of the ACL graft is performed next. We typically use an Achilles allograft for the ACL reconstruction, with the bone block used for femoral fixation to avoid bony impingement between the MAT bone bridge/block and the ACL graft. With the knee in full extension, the MAT sutures are tied at the conclusion of the surgical procedure. Concomitant MAT and ACL reconstruction has yielded positive long-term clinical outcomes, improved joint stability, and findings similar to historical results of ACL reconstruction or MAT performed in isolation.30,31

    CONCLUSION

    When used with the proper indications, MAT has demonstrated the ability to restore function and reduce pain. Successful meniscal transplant requires attention to the patient’s past medical and surgical history. Similarly, care must be taken to address any concomitant knee pathology, such as coronal realignment, ligament reconstruction, or cartilage restoration.

    References

    1. Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Rep. 2009;11(11):1-25.

    2. Abrams GD, Frank RM, Gupta AK, Harris JD, McCormick FM, Cole BJ. Trends in meniscus repair and meniscectomy in the United States, 2005-2011. Am J Sports Med. 2013;41(10):2333-2339. doi:10.1177/0363546513495641.

    3. Saltzman BM, Bajaj S, Salata M, et al. Prospective long-term evaluation of meniscal allograft transplantation procedure: a minimum of 7-year follow-up. J Knee Surg. 2012;25(2):165-175. doi:10.1055/s-0032-1313738.

    4. van der Wal RJ, Thomassen BJ, van Arkel ER. Long-term clinical outcome of open meniscal allograft transplantation. Am J Sports Med. 2009;37(11):2134-2139. doi:10.1177/0363546509336725.

    5. Vundelinckx B, Vanlauwe J, Bellemans J. Long-term subjective, clinical, and radiographic outcome evaluation of meniscal allograft transplantation in the knee. Am J Sports Med. 2014;42(7):1592-1599. doi:10.1177/0363546514530092.

    6. Hergan D, Thut D, Sherman O, Day MS. Meniscal allograft transplantation. Arthroscopy. 2011;27(1):101-112. doi:10.1016/j.arthro.2010.05.019.

    7. Elattar M, Dhollander A, Verdonk R, Almqvist KF, Verdonk P. Twenty-six years of meniscal allograft transplantation: is it still experimental? A meta-analysis of 44 trials. Knee Surg Sports Traumatol Arthrosc. 2011;19(2):147-157. doi:10.1007/s00167-010-1351-6.

    8. Verdonk R, Volpi P, Verdonk P, et al. Indications and limits of meniscal allografts. Injury. 2013;44(Suppl 1):S21-S27. doi:10.1016/S0020-1383(13)70006-8.

    9. Frank RM, Yanke A, Verma NN, Cole BJ. Immediate versus delayed meniscus allograft transplantation: letter to the editor. Am J Sports Med. 2015;43(5):NP8-NP9. doi:10.1177/0363546515571065.

    10. Aagaard H, Jørgensen U, Bojsen-Møller F. Immediate versus delayed meniscal allograft transplantation in sheep. Clin Orthop Relat Res. 2003;406(406):218-227. doi:10.1097/01.blo.0000030066.92399.7f.

    11. Jiang D, Ao YF, Gong X, Wang YJ, Zheng ZZ, Yu JK. Comparative study on immediate versus delayed meniscus allograft transplantation: 4- to 6-year follow-up. Am J Sports Med. 2014;42(10):2329-2337. doi:10.1177/0363546514541653.

    12. Riboh JC, Tilton AK, Cvetanovich GL, Campbell KA, Cole BJ. Meniscal allograft transplantation in the adolescent population. Arthroscopy. 2016;32(6):1133-1140.e1. doi:10.1016/j.arthro.2015.11.041.

    13. Chalmers PN, Karas V, Sherman SL, Cole BJ. Return to high-level sport after meniscal allograft transplantation. Arthroscopy. 2013;29(3):539-544. doi:10.1016/j.arthro.2012.10.027.

    14. Waterman BR, Rensing N, Cameron KL, Owens BD, Pallis M. Survivorship of meniscal allograft transplantation in an athletic patient population. Am J Sports Med. 2016;44(5):1237-1242. doi:10.1177/0363546515626184.

    15. Pollard ME, Kang Q, Berg EE. Radiographic sizing for meniscal transplantation. Arthroscopy. 1995;11(6):684-687. doi:10.1016/0749-8063(95)90110-8.

    16. Haut TL, Hull ML, Howell SM. Use of roentgenography and magnetic resonance imaging to predict meniscal geometry determined with a three-dimensional coordinate digitizing system. J Orthop Res. 2000;18(2):228-237. doi:10.1002/jor.1100180210.

    17. Van Thiel GS, Verma N, Yanke A, Basu S, Farr J, Cole B. Meniscal allograft size can be predicted by height, weight, and gender. Arthroscopy. 2009;25(7):722-727. doi:10.1016/j.arthro.2009.01.004.

    18. McConkey M, Lyon C, Bennett DL, et al. Radiographic sizing for meniscal transplantation using 3-D CT reconstruction. J Knee Surg. 2012;25(3):221-225. doi:10.1055/s-0031-1292651.

    19. Dienst M, Greis PE, Ellis BJ, Bachus KN, Burks RT. Effect of lateral meniscal allograft sizing on contact mechanics of the lateral tibial plateau: an experimental study in human cadaveric knee joints. Am J Sports Med. 2007;35(1):34-42. doi:10.1177/0363546506291404.

    20. Yoon JR, Jeong HI, Seo MJ, et al. The use of contralateral knee magnetic resonance imaging to predict meniscal size during meniscal allograft transplantation. Arthroscopy. 2014;30(10):1287-1293. doi:10.1016/j.arthro.2014.05.009.

    21. Lee AS, Kang RW, Kroin E, Verma NN, Cole BJ. Allograft meniscus transplantation. Sports Med Arthrosc. 2012;20(2):106-114. doi:10.1097/JSA.0b013e318246f005.

    22. Agneskirchner JD, Hurschler C, Wrann CD, Lobenhoffer P. The effects of valgus medial opening wedge high tibial osteotomy on articular cartilage pressure of the knee: a biomechanical study. Arthroscopy. 2007;23(8):852-861. doi:10.1016/j.arthro.2007.05.018.

    23. Loening AM, James IE, Levenston ME, et al. Injurious mechanical compression of bovine articular cartilage induces chondrocyte apoptosis. Arch Biochem Biophys. 2000;381(2):205-212. doi:10.1006/abbi.2000.1988.

    24. Mina C, Garrett WE Jr, Pietrobon R, Glisson R, Higgins L. High tibial osteotomy for unloading osteochondral defects in the medial compartment of the knee. Am J Sports Med. 2008;36(5):949-955. doi:10.1177/0363546508315471.

    25. Harris JD, Cavo M, Brophy R, Siston R, Flanigan D. Biological knee reconstruction: a systematic review of combined meniscal allograft transplantation and cartilage repair or restoration. Arthroscopy: 2011;27(3):409-418. doi:10.1016/j.arthro.2010.08.007.

    26. Rue JP, Yanke AB, Busam ML, McNickle AG, Cole BJ. Prospective evaluation of concurrent meniscus transplantation and articular cartilage repair: minimum 2-year follow-up. Am J Sports Med. 2008;36(9):1770-1778. doi:10.1177/0363546508317122.

    27. Kazi HA, Abdel-Rahman W, Brady PA, Cameron JC. Meniscal allograft with or without osteotomy: a 15-year follow-up study. Knee Surg Sports Traumatol Arthrosc. 2015;23(1):303-309. doi:10.1007/s00167-014-3291-z.

    28. Verdonk PC, Verstraete KL, Almqvist KF, et al. Meniscal allograft transplantation: long-term clinical results with radiological and magnetic resonance imaging correlations. Knee Surg Sports Traumatol Arthrosc. 2006;14(8):694-706. doi:10.1007/s00167-005-0033-2.

    29. Shelbourne KD, Gray T. Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the time of surgery. Five- to fifteen-year evaluations. Am J Sports Med. 2000;28(4):446-452. doi:10.1177/03635465000280040201.

    30. Graf KW Jr, Sekiya JK, Wojtys EM; Department of Orthopaedic Surgery, University of Michigan Medical Center, Ann Arbor, Michigan, USA. Long-term results after combined medial meniscal allograft transplantation and anterior cruciate ligament reconstruction: minimum 8.5-year follow-up study. Arthroscopy. 2004;20(2):129-140. doi:10.1016/j.arthro.2003.11.032.

    31. Binnet MS, Akan B, Kaya A. Lyophilised medial meniscus transplantations in ACL-deficient knees: a 19-year follow-up. Knee Surg Sports Traumatol Arthrosc. 2012;20(1):109-113. doi:10.1007/s00167-011-1556-3.

    Author and Disclosure Information

    Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

    Mr. Gitelis and Mr. Meyer are Medical Students, Dr. Frank and Dr. Cvetanovich are Orthopaedic Surgeons, and Dr. Cole is a Professor and Orthopedic Surgeon, Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois.

    Address correspondence to: Brian J. Cole, MD, Department of Orthopaedic Surgery, Rush University Medical, 1611 West Harrison Street, Suite 300, Chicago, IL 60612 (email, brian.cole@rushortho.com).

    Matthew E. Gitelis, BS Rachel M. Frank, MD Maximillian A. Meyer, BSGregory Cvetanovich, MD Brian J. Cole, MD, MBA . 5 Points on Meniscal Allograft Transplantation. Am J Orthop.

    September 4, 2018

     

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    Author and Disclosure Information

    Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

    Mr. Gitelis and Mr. Meyer are Medical Students, Dr. Frank and Dr. Cvetanovich are Orthopaedic Surgeons, and Dr. Cole is a Professor and Orthopedic Surgeon, Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois.

    Address correspondence to: Brian J. Cole, MD, Department of Orthopaedic Surgery, Rush University Medical, 1611 West Harrison Street, Suite 300, Chicago, IL 60612 (email, brian.cole@rushortho.com).

    Matthew E. Gitelis, BS Rachel M. Frank, MD Maximillian A. Meyer, BSGregory Cvetanovich, MD Brian J. Cole, MD, MBA . 5 Points on Meniscal Allograft Transplantation. Am J Orthop.

    September 4, 2018

     

    Author and Disclosure Information

    Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

    Mr. Gitelis and Mr. Meyer are Medical Students, Dr. Frank and Dr. Cvetanovich are Orthopaedic Surgeons, and Dr. Cole is a Professor and Orthopedic Surgeon, Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois.

    Address correspondence to: Brian J. Cole, MD, Department of Orthopaedic Surgery, Rush University Medical, 1611 West Harrison Street, Suite 300, Chicago, IL 60612 (email, brian.cole@rushortho.com).

    Matthew E. Gitelis, BS Rachel M. Frank, MD Maximillian A. Meyer, BSGregory Cvetanovich, MD Brian J. Cole, MD, MBA . 5 Points on Meniscal Allograft Transplantation. Am J Orthop.

    September 4, 2018

     

    ABSTRACT

    Meniscus allograft transplantation (MAT) has yielded excellent long-term functional outcomes when performed in properly indicated patients. When evaluating a patient for potential MAT, it is imperative to evaluate past medical history and past surgical procedures. The ideal MAT candidate is a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency. Existing pathology in the knee needs to be carefully considered and issues such as malalignment, cartilage defects, and/or ligamentous instability may require a staged or concomitant procedure. Once an ideal candidate is identified, graft selection and preparation are critical steps to ensure a proper fit and long-term viability of the meniscus. When selecting the graft, accurate measurements must be taken, and this is most commonly performed using plain radiographs for this. Graft fixation can be accomplished by placing vertical mattress sutures and tying those down with the knee in full extension.

    Continue to: Meniscus tears are common in the young, athletic patient population...

     

     

    Meniscus tears are common in the young, athletic patient population. In the United States alone, approximately 700,000 meniscectomies are performed annually.1 Given discouraging long-term clinical results following subtotal meniscectomy in young patients, meniscal repair is preferred whenever possible.2 Despite short-term symptom relief if subtotal meniscectomy is required, some patients often go on to develop localized pain in the affected compartment, effusions, and eventual development of osteoarthritis. In such patients with symptomatic meniscal deficiency, meniscal allograft transplantation (MAT) has yielded excellent long-term functional outcomes.3-5 Three recently published systematic reviews describe the outcomes of MAT in thousands of patients, noting positive outcomes in regard to pain and function for the majority of patients.6-8 Specifically, in a review conducted by Elattar and colleagues7 consisting of 44 studies comprising 1136 grafts in 1068 patients, the authors reported clinical improvement in Lysholm Knee Scoring Scale score (44 to 77), visual analog scale (48 mm to 17 mm), and International Knee Documentation Committee (84% normal/nearly normal, 89% satisfaction), among other outcomes measures. Additionally, the complication (21.3%) and failure rates (10.6%) were considered acceptable by all authors. The purpose of this article is to review indications, operative preparation, critical aspects of surgical technique, and additional concomitant procedures commonly performed alongside MAT.

    1. PATIENT SELECTION

    When used with the proper indications, MAT offers improved functional outcomes and reduced pain for patients with symptomatic meniscal deficiency. When evaluating a patient for potential MAT, it is imperative to evaluate past medical history and past surgical procedures. The ideal MAT candidate is a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency who does not have (1) evidence of diffuse osteoarthritis (Outerbridge grade <2), including the absence of significant bony flattening or osteophytes in the involved compartment; (2) inflammatory arthritis; (3) active or previous joint infection; (4) mechanical axis malalignment; or (5) morbid obesity (Table). Long-leg weight-bearing anterior-posterior alignment radiographs are important in the work-up of any patient being considered for MAT, and consideration for concomitant or staged realignment high tibial osteotomy (HTO) or distal femoral osteotomy (DFO) should be given for patients in excessive varus or valgus, respectively. Although the decision to perform a realignment osteotomy is made on a patient-specific basis, if the weight-bearing line passes medial to the medial tibial spine or lateral to the lateral tibial spine, HTO or DFO, respectively, should be considered. Importantly, MAT is not typically recommended in the asymptomatic patient.9 Although some recent evidence suggests MAT may have chondroprotective effects on articular cartilage following meniscectomy, there is insufficient long-term outcome data to support the use of MAT as a prophylactic measure, especially given the fact that graft deterioration inevitably occurs at 7 to 10 years, with patients having to consider avoiding meniscus-dependent activities following transplant to protect their graft from traumatic failure.10,11

    Table. Summary of Indications and Contraindications for Meniscal Allograft Transplant (MAT)

    Indications

    Contraindicationsa

    Patients younger than 50 years old with a chief complaint of pain limiting their desired activities

    Diffuse femoral and/or tibial articular cartilage wear

    Body mass index <35 kg/m2

    Radiographic evidence of

    arthritis

    Previous meniscectomy (or non-viable meniscus state) with pain localized to the affected compartment

    Inflammatory arthritis conditions

    Normal or correctable coronal and sagittal alignment

    MAT performed as a prophylactic measure in the absence of appropriate symptoms is highly controversial

    Normal or correctable ligamentous stability

     

    Normal or correctable articular cartilage

     

    Willingness to comply with rehabilitation protocol

     

    Realistic post-surgical activity expectations

     

    aContraindications for MAT are controversial, as the available literature discussing contraindications is very limited. This list is based on the experience of the senior author.

    Long-term prospective studies have shown high graft survival and predominantly positive functional results after MAT. Age indications have expanded, with 1 recent study reporting 6% reoperation rate and zero failures in a cohort of 37 adolescent MAT patients.12 High survival rates hold even among an athletic population, where rates of return to play after MAT have been reported to be >75% for those competing at a high school level or higher.13 In an active military population, <2% of patients progressed to revision MAT or total knee arthroplasty at minimum 2-year follow-up, but 22% of patients were unable to return to military duty owing to residual knee limitations.14 In this series, tobacco use correlated with failure, whereas MAT by high-volume, fellowship-trained orthopedic surgeons decreased rates of failure.

    2. GRAFT SELECTION

    In preparation for MAT, accurate measurements must be taken for appropriate size matching. Several measurement techniques have been described, including using plain radiographs, 3D computed tomography (CT), and magnetic resonance imaging (MRI).15-18 There is limited data regarding the consequences of an improperly sized donor meniscus; however, an oversized lateral meniscus has been shown to increase the contact forces across the articular cartilage.19 Additionally, an undersized allograft may result in normal forces across the articular cartilage but greater forces across the meniscus.19

    When sizing the recipient knee for MAT, accurate width and length measurements are critical. The most common technique used today includes measurements using anteroposterior and lateral radiographic images as described by Pollard and colleagues.15 The width of the meniscus is determined by the distance between 2 vertical lines perpendicular to the joint line, 1 of them tangential to the margin of the tibia metaphysis and the other between the medial and lateral tibial eminence in both knees (Figures 1A,1B). The length of the meniscus is measured on a lateral radiograph. A line is drawn at the level of the articular line between the anterior surface of the tibia above the tuberosity and a parallel line that is tangential to the posterior margin of the tibial plateau. Percent corrections are performed for these dimensions as described in previous publications.

    frank0918_f1_0

    Other techniques have been described to obtain accurate measurements of the recipient knee. For example, obtaining an MRI of the contralateral knee may provide a reproducible method of measuring both the width and length of the medial and lateral menisci.20 CT has been used to measure the lateral meniscus independently, and it has been shown to exhibit less error in the measure of the tibial plateau when compared with X-rays.18 Both CT and MRI are more expensive than simple radiographs, and CT exposes the patient to an increased amount of radiation. Current evidence does not support standard use of these advanced imaging modalities for meniscal sizing.

    Continue to: GRAFT PREPARATION AND PLACEMENT...

     

     

    3. GRAFT PREPARATION AND PLACEMENT

    At the time of surgery, the meniscus allograft is thawed in sterile saline and prepared on the back table. This can be done before or after the diagnostic arthroscopy and bone-slot preparation. Excess soft tissue surrounding the meniscal rim and/or anterior and posterior horns should be removed. Several techniques for MAT have been described, but we generally prefer a bridge-in-slot technique for both medial and lateral MAT.21 To prepare the meniscus allograft for a bridge-in-slot technique, the graft is cut with an oscillating saw to a width of 7 mm, with care taken to ensure that the bony insertions of both meniscal horns are preserved. Next, a transverse cut is made 10 mm below the meniscal horns to set the depth of the bone bridge. To assist with the sizing of the bone bridge, a rectangular sizing block and cutting jig is used (Figures 2A-2C). After marking the middle and posterior thirds of the meniscus, a No. 2 non-absorbable suture is placed at the junction of the posterior and middle thirds of the meniscus. This completes preparation of the allograft prior to implantation.

    frank0918_f2

    Attention is then turned to back the arthroscopy. A standard posteromedial (medial meniscus) or posterolateral (lateral meniscus) accessory incision is made, and a Henning retractor is carefully placed in order to receive the sutures that will be placed through the meniscus allograft via a standard inside-out repair technique. First, a zone-specific cannula is used to place a nitinol wire out the accessory incision. The looped end of the wire is pulled out of the anterior arthrotomy incision that will be used to shuttle the meniscus allograft into the joint. In order to pass the meniscal allograft into the joint, the passing suture previously placed through the meniscus is shuttled through the nitinol wire, and the wire is then pulled out the accessory incision, advancing the meniscus through the anteiror arthrotomy. As the meniscus is introduced, the traction suture is then gently tensioned to get the allograft completely into the joint. Next, the bone bridge is seated into the previously created bone slot, as the soft tissue component is manually pushed beneath the ipsilateral femoral condyle. Under direct visualization, the soft tissue component is reduced with a probe using firm, constant traction. To aid in reduction, it may be useful to apply compartment-specific varus or valgus stress and to cycle the knee once the meniscal complex is reduced.

    4. GRAFT FIXATION

    Once the graft has been passed completely into the joint, with the bone bridge seated into the bone slot, the long end of an Army-Navy retractor is placed firmly through the arthrotomy on the meniscal bone bridge, maintaining a downward force to allow the bridge to remain slotted. To lever down on the posterior aspect of the graft, a freer elevator is used from anterosuperior to posteroinferior. The bone bridge is then secured using a bioabsorbable interference screw, placed central to the bone bridge opposing the block to the ipsilateral compartment. The remainder of the meniscus is secured with an inside-out repair technique, working from posterior to anterior through a standard medial or lateral meniscal repair approach. In total, approximately 6 to 10 vertical mattress sutures are placed, and these can be placed both superiorly and inferiorly on the meniscus. Posteriorly, an all-inside suture repair device may be helpful. Finally, the anterior aspect of the meniscus is repaired to the capsule in an open fashion prior to closing the arthrotomy. Sutures are tied with the leg in extension. The meniscal repair incision is closed in a standard fashion using layers.

    5. CONCOMITANT PATHOLOGY AND MAT

    The presence of concomitant knee pathology in the context of meniscus deficiency is a challenging problem that requires careful attention to all aspects of the underlying condition of the knee. In cases where MAT is indicated, issues of malalignment, cartilage defects, and/or ligamentous instability may also need to be addressed either concomitantly or in staged fashion. For example, medial meniscal deficiency in the setting of varus alignment can be addressed with a concomitant HTO, whereas lateral meniscal deficiency in the setting of valgus malalignment can be addressed with a concomitant DFO. In both cases, the osteotomy corrects an abnormal mechanical axis, offloading the diseased compartment. This accomplishes 2 goals, namely to preserve the new MAT graft and to protect underlying articular cartilage.22-24 The osteotomy is an important contributor to additional pain relief by offloading the compartment, and clinical studies have demonstrated that failure to address malalignment in the setting of surgical intervention for cartilage and meniscal insufficiency leads to inferior clinical outcomes and poor survival of transplanted tissue.25-28

    Continue to: In a meniscus-deficient patient with chondral lesions...

     

     

    In a meniscus-deficient patient with chondral lesions (Outerbridge grade 3 or 4), concomitant MAT and cartilage restoration should be considered. Depending on the size and location of the chondral lesion, options include marrow stimulation, autologous chondrocyte implantation, osteochondral autograft transfer, as well as chondral and/or osteochondral allograft transplantation. In a systematic review of concomitant MAT and cartilage restoration procedures, Harris and colleagues25 found that failure rates of the combined surgery were similar to those of either surgery in isolation.

    Young athletes sustaining anterior cruciate ligament (ACL) tears commonly also have meniscal pathology that must be addressed. Most cases are treated with meniscal repair or partial meniscectomy, but occasionally patients present with ACL tear and symptomatic meniscal deficiency. Specifically, MAT survival relies largely on a knee with ligamentous stability, whereas outcomes of ACL reconstruction are improved with intact and functional menisci.29 The surgical technique for MAT is modified slightly in the setting of performing a concomitant ACL reconstruction, with the ACL tibial tunnel drilled to avoid the meniscal bone slot if possible, followed by femoral tunnel creation. Femoral fixation of the ACL graft is accomplished after preparation of the meniscal slot. The meniscal graft is set into place (sutures are not yet tied), and tibial fixation of the ACL graft is performed next. We typically use an Achilles allograft for the ACL reconstruction, with the bone block used for femoral fixation to avoid bony impingement between the MAT bone bridge/block and the ACL graft. With the knee in full extension, the MAT sutures are tied at the conclusion of the surgical procedure. Concomitant MAT and ACL reconstruction has yielded positive long-term clinical outcomes, improved joint stability, and findings similar to historical results of ACL reconstruction or MAT performed in isolation.30,31

    CONCLUSION

    When used with the proper indications, MAT has demonstrated the ability to restore function and reduce pain. Successful meniscal transplant requires attention to the patient’s past medical and surgical history. Similarly, care must be taken to address any concomitant knee pathology, such as coronal realignment, ligament reconstruction, or cartilage restoration.

    ABSTRACT

    Meniscus allograft transplantation (MAT) has yielded excellent long-term functional outcomes when performed in properly indicated patients. When evaluating a patient for potential MAT, it is imperative to evaluate past medical history and past surgical procedures. The ideal MAT candidate is a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency. Existing pathology in the knee needs to be carefully considered and issues such as malalignment, cartilage defects, and/or ligamentous instability may require a staged or concomitant procedure. Once an ideal candidate is identified, graft selection and preparation are critical steps to ensure a proper fit and long-term viability of the meniscus. When selecting the graft, accurate measurements must be taken, and this is most commonly performed using plain radiographs for this. Graft fixation can be accomplished by placing vertical mattress sutures and tying those down with the knee in full extension.

    Continue to: Meniscus tears are common in the young, athletic patient population...

     

     

    Meniscus tears are common in the young, athletic patient population. In the United States alone, approximately 700,000 meniscectomies are performed annually.1 Given discouraging long-term clinical results following subtotal meniscectomy in young patients, meniscal repair is preferred whenever possible.2 Despite short-term symptom relief if subtotal meniscectomy is required, some patients often go on to develop localized pain in the affected compartment, effusions, and eventual development of osteoarthritis. In such patients with symptomatic meniscal deficiency, meniscal allograft transplantation (MAT) has yielded excellent long-term functional outcomes.3-5 Three recently published systematic reviews describe the outcomes of MAT in thousands of patients, noting positive outcomes in regard to pain and function for the majority of patients.6-8 Specifically, in a review conducted by Elattar and colleagues7 consisting of 44 studies comprising 1136 grafts in 1068 patients, the authors reported clinical improvement in Lysholm Knee Scoring Scale score (44 to 77), visual analog scale (48 mm to 17 mm), and International Knee Documentation Committee (84% normal/nearly normal, 89% satisfaction), among other outcomes measures. Additionally, the complication (21.3%) and failure rates (10.6%) were considered acceptable by all authors. The purpose of this article is to review indications, operative preparation, critical aspects of surgical technique, and additional concomitant procedures commonly performed alongside MAT.

    1. PATIENT SELECTION

    When used with the proper indications, MAT offers improved functional outcomes and reduced pain for patients with symptomatic meniscal deficiency. When evaluating a patient for potential MAT, it is imperative to evaluate past medical history and past surgical procedures. The ideal MAT candidate is a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency who does not have (1) evidence of diffuse osteoarthritis (Outerbridge grade <2), including the absence of significant bony flattening or osteophytes in the involved compartment; (2) inflammatory arthritis; (3) active or previous joint infection; (4) mechanical axis malalignment; or (5) morbid obesity (Table). Long-leg weight-bearing anterior-posterior alignment radiographs are important in the work-up of any patient being considered for MAT, and consideration for concomitant or staged realignment high tibial osteotomy (HTO) or distal femoral osteotomy (DFO) should be given for patients in excessive varus or valgus, respectively. Although the decision to perform a realignment osteotomy is made on a patient-specific basis, if the weight-bearing line passes medial to the medial tibial spine or lateral to the lateral tibial spine, HTO or DFO, respectively, should be considered. Importantly, MAT is not typically recommended in the asymptomatic patient.9 Although some recent evidence suggests MAT may have chondroprotective effects on articular cartilage following meniscectomy, there is insufficient long-term outcome data to support the use of MAT as a prophylactic measure, especially given the fact that graft deterioration inevitably occurs at 7 to 10 years, with patients having to consider avoiding meniscus-dependent activities following transplant to protect their graft from traumatic failure.10,11

    Table. Summary of Indications and Contraindications for Meniscal Allograft Transplant (MAT)

    Indications

    Contraindicationsa

    Patients younger than 50 years old with a chief complaint of pain limiting their desired activities

    Diffuse femoral and/or tibial articular cartilage wear

    Body mass index <35 kg/m2

    Radiographic evidence of

    arthritis

    Previous meniscectomy (or non-viable meniscus state) with pain localized to the affected compartment

    Inflammatory arthritis conditions

    Normal or correctable coronal and sagittal alignment

    MAT performed as a prophylactic measure in the absence of appropriate symptoms is highly controversial

    Normal or correctable ligamentous stability

     

    Normal or correctable articular cartilage

     

    Willingness to comply with rehabilitation protocol

     

    Realistic post-surgical activity expectations

     

    aContraindications for MAT are controversial, as the available literature discussing contraindications is very limited. This list is based on the experience of the senior author.

    Long-term prospective studies have shown high graft survival and predominantly positive functional results after MAT. Age indications have expanded, with 1 recent study reporting 6% reoperation rate and zero failures in a cohort of 37 adolescent MAT patients.12 High survival rates hold even among an athletic population, where rates of return to play after MAT have been reported to be >75% for those competing at a high school level or higher.13 In an active military population, <2% of patients progressed to revision MAT or total knee arthroplasty at minimum 2-year follow-up, but 22% of patients were unable to return to military duty owing to residual knee limitations.14 In this series, tobacco use correlated with failure, whereas MAT by high-volume, fellowship-trained orthopedic surgeons decreased rates of failure.

    2. GRAFT SELECTION

    In preparation for MAT, accurate measurements must be taken for appropriate size matching. Several measurement techniques have been described, including using plain radiographs, 3D computed tomography (CT), and magnetic resonance imaging (MRI).15-18 There is limited data regarding the consequences of an improperly sized donor meniscus; however, an oversized lateral meniscus has been shown to increase the contact forces across the articular cartilage.19 Additionally, an undersized allograft may result in normal forces across the articular cartilage but greater forces across the meniscus.19

    When sizing the recipient knee for MAT, accurate width and length measurements are critical. The most common technique used today includes measurements using anteroposterior and lateral radiographic images as described by Pollard and colleagues.15 The width of the meniscus is determined by the distance between 2 vertical lines perpendicular to the joint line, 1 of them tangential to the margin of the tibia metaphysis and the other between the medial and lateral tibial eminence in both knees (Figures 1A,1B). The length of the meniscus is measured on a lateral radiograph. A line is drawn at the level of the articular line between the anterior surface of the tibia above the tuberosity and a parallel line that is tangential to the posterior margin of the tibial plateau. Percent corrections are performed for these dimensions as described in previous publications.

    frank0918_f1_0

    Other techniques have been described to obtain accurate measurements of the recipient knee. For example, obtaining an MRI of the contralateral knee may provide a reproducible method of measuring both the width and length of the medial and lateral menisci.20 CT has been used to measure the lateral meniscus independently, and it has been shown to exhibit less error in the measure of the tibial plateau when compared with X-rays.18 Both CT and MRI are more expensive than simple radiographs, and CT exposes the patient to an increased amount of radiation. Current evidence does not support standard use of these advanced imaging modalities for meniscal sizing.

    Continue to: GRAFT PREPARATION AND PLACEMENT...

     

     

    3. GRAFT PREPARATION AND PLACEMENT

    At the time of surgery, the meniscus allograft is thawed in sterile saline and prepared on the back table. This can be done before or after the diagnostic arthroscopy and bone-slot preparation. Excess soft tissue surrounding the meniscal rim and/or anterior and posterior horns should be removed. Several techniques for MAT have been described, but we generally prefer a bridge-in-slot technique for both medial and lateral MAT.21 To prepare the meniscus allograft for a bridge-in-slot technique, the graft is cut with an oscillating saw to a width of 7 mm, with care taken to ensure that the bony insertions of both meniscal horns are preserved. Next, a transverse cut is made 10 mm below the meniscal horns to set the depth of the bone bridge. To assist with the sizing of the bone bridge, a rectangular sizing block and cutting jig is used (Figures 2A-2C). After marking the middle and posterior thirds of the meniscus, a No. 2 non-absorbable suture is placed at the junction of the posterior and middle thirds of the meniscus. This completes preparation of the allograft prior to implantation.

    frank0918_f2

    Attention is then turned to back the arthroscopy. A standard posteromedial (medial meniscus) or posterolateral (lateral meniscus) accessory incision is made, and a Henning retractor is carefully placed in order to receive the sutures that will be placed through the meniscus allograft via a standard inside-out repair technique. First, a zone-specific cannula is used to place a nitinol wire out the accessory incision. The looped end of the wire is pulled out of the anterior arthrotomy incision that will be used to shuttle the meniscus allograft into the joint. In order to pass the meniscal allograft into the joint, the passing suture previously placed through the meniscus is shuttled through the nitinol wire, and the wire is then pulled out the accessory incision, advancing the meniscus through the anteiror arthrotomy. As the meniscus is introduced, the traction suture is then gently tensioned to get the allograft completely into the joint. Next, the bone bridge is seated into the previously created bone slot, as the soft tissue component is manually pushed beneath the ipsilateral femoral condyle. Under direct visualization, the soft tissue component is reduced with a probe using firm, constant traction. To aid in reduction, it may be useful to apply compartment-specific varus or valgus stress and to cycle the knee once the meniscal complex is reduced.

    4. GRAFT FIXATION

    Once the graft has been passed completely into the joint, with the bone bridge seated into the bone slot, the long end of an Army-Navy retractor is placed firmly through the arthrotomy on the meniscal bone bridge, maintaining a downward force to allow the bridge to remain slotted. To lever down on the posterior aspect of the graft, a freer elevator is used from anterosuperior to posteroinferior. The bone bridge is then secured using a bioabsorbable interference screw, placed central to the bone bridge opposing the block to the ipsilateral compartment. The remainder of the meniscus is secured with an inside-out repair technique, working from posterior to anterior through a standard medial or lateral meniscal repair approach. In total, approximately 6 to 10 vertical mattress sutures are placed, and these can be placed both superiorly and inferiorly on the meniscus. Posteriorly, an all-inside suture repair device may be helpful. Finally, the anterior aspect of the meniscus is repaired to the capsule in an open fashion prior to closing the arthrotomy. Sutures are tied with the leg in extension. The meniscal repair incision is closed in a standard fashion using layers.

    5. CONCOMITANT PATHOLOGY AND MAT

    The presence of concomitant knee pathology in the context of meniscus deficiency is a challenging problem that requires careful attention to all aspects of the underlying condition of the knee. In cases where MAT is indicated, issues of malalignment, cartilage defects, and/or ligamentous instability may also need to be addressed either concomitantly or in staged fashion. For example, medial meniscal deficiency in the setting of varus alignment can be addressed with a concomitant HTO, whereas lateral meniscal deficiency in the setting of valgus malalignment can be addressed with a concomitant DFO. In both cases, the osteotomy corrects an abnormal mechanical axis, offloading the diseased compartment. This accomplishes 2 goals, namely to preserve the new MAT graft and to protect underlying articular cartilage.22-24 The osteotomy is an important contributor to additional pain relief by offloading the compartment, and clinical studies have demonstrated that failure to address malalignment in the setting of surgical intervention for cartilage and meniscal insufficiency leads to inferior clinical outcomes and poor survival of transplanted tissue.25-28

    Continue to: In a meniscus-deficient patient with chondral lesions...

     

     

    In a meniscus-deficient patient with chondral lesions (Outerbridge grade 3 or 4), concomitant MAT and cartilage restoration should be considered. Depending on the size and location of the chondral lesion, options include marrow stimulation, autologous chondrocyte implantation, osteochondral autograft transfer, as well as chondral and/or osteochondral allograft transplantation. In a systematic review of concomitant MAT and cartilage restoration procedures, Harris and colleagues25 found that failure rates of the combined surgery were similar to those of either surgery in isolation.

    Young athletes sustaining anterior cruciate ligament (ACL) tears commonly also have meniscal pathology that must be addressed. Most cases are treated with meniscal repair or partial meniscectomy, but occasionally patients present with ACL tear and symptomatic meniscal deficiency. Specifically, MAT survival relies largely on a knee with ligamentous stability, whereas outcomes of ACL reconstruction are improved with intact and functional menisci.29 The surgical technique for MAT is modified slightly in the setting of performing a concomitant ACL reconstruction, with the ACL tibial tunnel drilled to avoid the meniscal bone slot if possible, followed by femoral tunnel creation. Femoral fixation of the ACL graft is accomplished after preparation of the meniscal slot. The meniscal graft is set into place (sutures are not yet tied), and tibial fixation of the ACL graft is performed next. We typically use an Achilles allograft for the ACL reconstruction, with the bone block used for femoral fixation to avoid bony impingement between the MAT bone bridge/block and the ACL graft. With the knee in full extension, the MAT sutures are tied at the conclusion of the surgical procedure. Concomitant MAT and ACL reconstruction has yielded positive long-term clinical outcomes, improved joint stability, and findings similar to historical results of ACL reconstruction or MAT performed in isolation.30,31

    CONCLUSION

    When used with the proper indications, MAT has demonstrated the ability to restore function and reduce pain. Successful meniscal transplant requires attention to the patient’s past medical and surgical history. Similarly, care must be taken to address any concomitant knee pathology, such as coronal realignment, ligament reconstruction, or cartilage restoration.

    References

    1. Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Rep. 2009;11(11):1-25.

    2. Abrams GD, Frank RM, Gupta AK, Harris JD, McCormick FM, Cole BJ. Trends in meniscus repair and meniscectomy in the United States, 2005-2011. Am J Sports Med. 2013;41(10):2333-2339. doi:10.1177/0363546513495641.

    3. Saltzman BM, Bajaj S, Salata M, et al. Prospective long-term evaluation of meniscal allograft transplantation procedure: a minimum of 7-year follow-up. J Knee Surg. 2012;25(2):165-175. doi:10.1055/s-0032-1313738.

    4. van der Wal RJ, Thomassen BJ, van Arkel ER. Long-term clinical outcome of open meniscal allograft transplantation. Am J Sports Med. 2009;37(11):2134-2139. doi:10.1177/0363546509336725.

    5. Vundelinckx B, Vanlauwe J, Bellemans J. Long-term subjective, clinical, and radiographic outcome evaluation of meniscal allograft transplantation in the knee. Am J Sports Med. 2014;42(7):1592-1599. doi:10.1177/0363546514530092.

    6. Hergan D, Thut D, Sherman O, Day MS. Meniscal allograft transplantation. Arthroscopy. 2011;27(1):101-112. doi:10.1016/j.arthro.2010.05.019.

    7. Elattar M, Dhollander A, Verdonk R, Almqvist KF, Verdonk P. Twenty-six years of meniscal allograft transplantation: is it still experimental? A meta-analysis of 44 trials. Knee Surg Sports Traumatol Arthrosc. 2011;19(2):147-157. doi:10.1007/s00167-010-1351-6.

    8. Verdonk R, Volpi P, Verdonk P, et al. Indications and limits of meniscal allografts. Injury. 2013;44(Suppl 1):S21-S27. doi:10.1016/S0020-1383(13)70006-8.

    9. Frank RM, Yanke A, Verma NN, Cole BJ. Immediate versus delayed meniscus allograft transplantation: letter to the editor. Am J Sports Med. 2015;43(5):NP8-NP9. doi:10.1177/0363546515571065.

    10. Aagaard H, Jørgensen U, Bojsen-Møller F. Immediate versus delayed meniscal allograft transplantation in sheep. Clin Orthop Relat Res. 2003;406(406):218-227. doi:10.1097/01.blo.0000030066.92399.7f.

    11. Jiang D, Ao YF, Gong X, Wang YJ, Zheng ZZ, Yu JK. Comparative study on immediate versus delayed meniscus allograft transplantation: 4- to 6-year follow-up. Am J Sports Med. 2014;42(10):2329-2337. doi:10.1177/0363546514541653.

    12. Riboh JC, Tilton AK, Cvetanovich GL, Campbell KA, Cole BJ. Meniscal allograft transplantation in the adolescent population. Arthroscopy. 2016;32(6):1133-1140.e1. doi:10.1016/j.arthro.2015.11.041.

    13. Chalmers PN, Karas V, Sherman SL, Cole BJ. Return to high-level sport after meniscal allograft transplantation. Arthroscopy. 2013;29(3):539-544. doi:10.1016/j.arthro.2012.10.027.

    14. Waterman BR, Rensing N, Cameron KL, Owens BD, Pallis M. Survivorship of meniscal allograft transplantation in an athletic patient population. Am J Sports Med. 2016;44(5):1237-1242. doi:10.1177/0363546515626184.

    15. Pollard ME, Kang Q, Berg EE. Radiographic sizing for meniscal transplantation. Arthroscopy. 1995;11(6):684-687. doi:10.1016/0749-8063(95)90110-8.

    16. Haut TL, Hull ML, Howell SM. Use of roentgenography and magnetic resonance imaging to predict meniscal geometry determined with a three-dimensional coordinate digitizing system. J Orthop Res. 2000;18(2):228-237. doi:10.1002/jor.1100180210.

    17. Van Thiel GS, Verma N, Yanke A, Basu S, Farr J, Cole B. Meniscal allograft size can be predicted by height, weight, and gender. Arthroscopy. 2009;25(7):722-727. doi:10.1016/j.arthro.2009.01.004.

    18. McConkey M, Lyon C, Bennett DL, et al. Radiographic sizing for meniscal transplantation using 3-D CT reconstruction. J Knee Surg. 2012;25(3):221-225. doi:10.1055/s-0031-1292651.

    19. Dienst M, Greis PE, Ellis BJ, Bachus KN, Burks RT. Effect of lateral meniscal allograft sizing on contact mechanics of the lateral tibial plateau: an experimental study in human cadaveric knee joints. Am J Sports Med. 2007;35(1):34-42. doi:10.1177/0363546506291404.

    20. Yoon JR, Jeong HI, Seo MJ, et al. The use of contralateral knee magnetic resonance imaging to predict meniscal size during meniscal allograft transplantation. Arthroscopy. 2014;30(10):1287-1293. doi:10.1016/j.arthro.2014.05.009.

    21. Lee AS, Kang RW, Kroin E, Verma NN, Cole BJ. Allograft meniscus transplantation. Sports Med Arthrosc. 2012;20(2):106-114. doi:10.1097/JSA.0b013e318246f005.

    22. Agneskirchner JD, Hurschler C, Wrann CD, Lobenhoffer P. The effects of valgus medial opening wedge high tibial osteotomy on articular cartilage pressure of the knee: a biomechanical study. Arthroscopy. 2007;23(8):852-861. doi:10.1016/j.arthro.2007.05.018.

    23. Loening AM, James IE, Levenston ME, et al. Injurious mechanical compression of bovine articular cartilage induces chondrocyte apoptosis. Arch Biochem Biophys. 2000;381(2):205-212. doi:10.1006/abbi.2000.1988.

    24. Mina C, Garrett WE Jr, Pietrobon R, Glisson R, Higgins L. High tibial osteotomy for unloading osteochondral defects in the medial compartment of the knee. Am J Sports Med. 2008;36(5):949-955. doi:10.1177/0363546508315471.

    25. Harris JD, Cavo M, Brophy R, Siston R, Flanigan D. Biological knee reconstruction: a systematic review of combined meniscal allograft transplantation and cartilage repair or restoration. Arthroscopy: 2011;27(3):409-418. doi:10.1016/j.arthro.2010.08.007.

    26. Rue JP, Yanke AB, Busam ML, McNickle AG, Cole BJ. Prospective evaluation of concurrent meniscus transplantation and articular cartilage repair: minimum 2-year follow-up. Am J Sports Med. 2008;36(9):1770-1778. doi:10.1177/0363546508317122.

    27. Kazi HA, Abdel-Rahman W, Brady PA, Cameron JC. Meniscal allograft with or without osteotomy: a 15-year follow-up study. Knee Surg Sports Traumatol Arthrosc. 2015;23(1):303-309. doi:10.1007/s00167-014-3291-z.

    28. Verdonk PC, Verstraete KL, Almqvist KF, et al. Meniscal allograft transplantation: long-term clinical results with radiological and magnetic resonance imaging correlations. Knee Surg Sports Traumatol Arthrosc. 2006;14(8):694-706. doi:10.1007/s00167-005-0033-2.

    29. Shelbourne KD, Gray T. Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the time of surgery. Five- to fifteen-year evaluations. Am J Sports Med. 2000;28(4):446-452. doi:10.1177/03635465000280040201.

    30. Graf KW Jr, Sekiya JK, Wojtys EM; Department of Orthopaedic Surgery, University of Michigan Medical Center, Ann Arbor, Michigan, USA. Long-term results after combined medial meniscal allograft transplantation and anterior cruciate ligament reconstruction: minimum 8.5-year follow-up study. Arthroscopy. 2004;20(2):129-140. doi:10.1016/j.arthro.2003.11.032.

    31. Binnet MS, Akan B, Kaya A. Lyophilised medial meniscus transplantations in ACL-deficient knees: a 19-year follow-up. Knee Surg Sports Traumatol Arthrosc. 2012;20(1):109-113. doi:10.1007/s00167-011-1556-3.

    References

    1. Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Rep. 2009;11(11):1-25.

    2. Abrams GD, Frank RM, Gupta AK, Harris JD, McCormick FM, Cole BJ. Trends in meniscus repair and meniscectomy in the United States, 2005-2011. Am J Sports Med. 2013;41(10):2333-2339. doi:10.1177/0363546513495641.

    3. Saltzman BM, Bajaj S, Salata M, et al. Prospective long-term evaluation of meniscal allograft transplantation procedure: a minimum of 7-year follow-up. J Knee Surg. 2012;25(2):165-175. doi:10.1055/s-0032-1313738.

    4. van der Wal RJ, Thomassen BJ, van Arkel ER. Long-term clinical outcome of open meniscal allograft transplantation. Am J Sports Med. 2009;37(11):2134-2139. doi:10.1177/0363546509336725.

    5. Vundelinckx B, Vanlauwe J, Bellemans J. Long-term subjective, clinical, and radiographic outcome evaluation of meniscal allograft transplantation in the knee. Am J Sports Med. 2014;42(7):1592-1599. doi:10.1177/0363546514530092.

    6. Hergan D, Thut D, Sherman O, Day MS. Meniscal allograft transplantation. Arthroscopy. 2011;27(1):101-112. doi:10.1016/j.arthro.2010.05.019.

    7. Elattar M, Dhollander A, Verdonk R, Almqvist KF, Verdonk P. Twenty-six years of meniscal allograft transplantation: is it still experimental? A meta-analysis of 44 trials. Knee Surg Sports Traumatol Arthrosc. 2011;19(2):147-157. doi:10.1007/s00167-010-1351-6.

    8. Verdonk R, Volpi P, Verdonk P, et al. Indications and limits of meniscal allografts. Injury. 2013;44(Suppl 1):S21-S27. doi:10.1016/S0020-1383(13)70006-8.

    9. Frank RM, Yanke A, Verma NN, Cole BJ. Immediate versus delayed meniscus allograft transplantation: letter to the editor. Am J Sports Med. 2015;43(5):NP8-NP9. doi:10.1177/0363546515571065.

    10. Aagaard H, Jørgensen U, Bojsen-Møller F. Immediate versus delayed meniscal allograft transplantation in sheep. Clin Orthop Relat Res. 2003;406(406):218-227. doi:10.1097/01.blo.0000030066.92399.7f.

    11. Jiang D, Ao YF, Gong X, Wang YJ, Zheng ZZ, Yu JK. Comparative study on immediate versus delayed meniscus allograft transplantation: 4- to 6-year follow-up. Am J Sports Med. 2014;42(10):2329-2337. doi:10.1177/0363546514541653.

    12. Riboh JC, Tilton AK, Cvetanovich GL, Campbell KA, Cole BJ. Meniscal allograft transplantation in the adolescent population. Arthroscopy. 2016;32(6):1133-1140.e1. doi:10.1016/j.arthro.2015.11.041.

    13. Chalmers PN, Karas V, Sherman SL, Cole BJ. Return to high-level sport after meniscal allograft transplantation. Arthroscopy. 2013;29(3):539-544. doi:10.1016/j.arthro.2012.10.027.

    14. Waterman BR, Rensing N, Cameron KL, Owens BD, Pallis M. Survivorship of meniscal allograft transplantation in an athletic patient population. Am J Sports Med. 2016;44(5):1237-1242. doi:10.1177/0363546515626184.

    15. Pollard ME, Kang Q, Berg EE. Radiographic sizing for meniscal transplantation. Arthroscopy. 1995;11(6):684-687. doi:10.1016/0749-8063(95)90110-8.

    16. Haut TL, Hull ML, Howell SM. Use of roentgenography and magnetic resonance imaging to predict meniscal geometry determined with a three-dimensional coordinate digitizing system. J Orthop Res. 2000;18(2):228-237. doi:10.1002/jor.1100180210.

    17. Van Thiel GS, Verma N, Yanke A, Basu S, Farr J, Cole B. Meniscal allograft size can be predicted by height, weight, and gender. Arthroscopy. 2009;25(7):722-727. doi:10.1016/j.arthro.2009.01.004.

    18. McConkey M, Lyon C, Bennett DL, et al. Radiographic sizing for meniscal transplantation using 3-D CT reconstruction. J Knee Surg. 2012;25(3):221-225. doi:10.1055/s-0031-1292651.

    19. Dienst M, Greis PE, Ellis BJ, Bachus KN, Burks RT. Effect of lateral meniscal allograft sizing on contact mechanics of the lateral tibial plateau: an experimental study in human cadaveric knee joints. Am J Sports Med. 2007;35(1):34-42. doi:10.1177/0363546506291404.

    20. Yoon JR, Jeong HI, Seo MJ, et al. The use of contralateral knee magnetic resonance imaging to predict meniscal size during meniscal allograft transplantation. Arthroscopy. 2014;30(10):1287-1293. doi:10.1016/j.arthro.2014.05.009.

    21. Lee AS, Kang RW, Kroin E, Verma NN, Cole BJ. Allograft meniscus transplantation. Sports Med Arthrosc. 2012;20(2):106-114. doi:10.1097/JSA.0b013e318246f005.

    22. Agneskirchner JD, Hurschler C, Wrann CD, Lobenhoffer P. The effects of valgus medial opening wedge high tibial osteotomy on articular cartilage pressure of the knee: a biomechanical study. Arthroscopy. 2007;23(8):852-861. doi:10.1016/j.arthro.2007.05.018.

    23. Loening AM, James IE, Levenston ME, et al. Injurious mechanical compression of bovine articular cartilage induces chondrocyte apoptosis. Arch Biochem Biophys. 2000;381(2):205-212. doi:10.1006/abbi.2000.1988.

    24. Mina C, Garrett WE Jr, Pietrobon R, Glisson R, Higgins L. High tibial osteotomy for unloading osteochondral defects in the medial compartment of the knee. Am J Sports Med. 2008;36(5):949-955. doi:10.1177/0363546508315471.

    25. Harris JD, Cavo M, Brophy R, Siston R, Flanigan D. Biological knee reconstruction: a systematic review of combined meniscal allograft transplantation and cartilage repair or restoration. Arthroscopy: 2011;27(3):409-418. doi:10.1016/j.arthro.2010.08.007.

    26. Rue JP, Yanke AB, Busam ML, McNickle AG, Cole BJ. Prospective evaluation of concurrent meniscus transplantation and articular cartilage repair: minimum 2-year follow-up. Am J Sports Med. 2008;36(9):1770-1778. doi:10.1177/0363546508317122.

    27. Kazi HA, Abdel-Rahman W, Brady PA, Cameron JC. Meniscal allograft with or without osteotomy: a 15-year follow-up study. Knee Surg Sports Traumatol Arthrosc. 2015;23(1):303-309. doi:10.1007/s00167-014-3291-z.

    28. Verdonk PC, Verstraete KL, Almqvist KF, et al. Meniscal allograft transplantation: long-term clinical results with radiological and magnetic resonance imaging correlations. Knee Surg Sports Traumatol Arthrosc. 2006;14(8):694-706. doi:10.1007/s00167-005-0033-2.

    29. Shelbourne KD, Gray T. Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the time of surgery. Five- to fifteen-year evaluations. Am J Sports Med. 2000;28(4):446-452. doi:10.1177/03635465000280040201.

    30. Graf KW Jr, Sekiya JK, Wojtys EM; Department of Orthopaedic Surgery, University of Michigan Medical Center, Ann Arbor, Michigan, USA. Long-term results after combined medial meniscal allograft transplantation and anterior cruciate ligament reconstruction: minimum 8.5-year follow-up study. Arthroscopy. 2004;20(2):129-140. doi:10.1016/j.arthro.2003.11.032.

    31. Binnet MS, Akan B, Kaya A. Lyophilised medial meniscus transplantations in ACL-deficient knees: a 19-year follow-up. Knee Surg Sports Traumatol Arthrosc. 2012;20(1):109-113. doi:10.1007/s00167-011-1556-3.

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    TAKE-HOME POINTS

    • Patient selection is critical for obtaining long-term functional outcome improvements and reduced pain, with the ideal MAT candidate being a chronologically and physiologically young patient (<50 years) with symptomatic meniscal deficiency.
    • Existing pathology in the knee needs to be carefully considered and issues such as malalignment, cartilage defects, and/or ligamentous instability may require a staged or concomitant procedure.
    • Accurate graft width and length measurements are vital, and the most common technique used today includes measuring the meniscus on anteroposterior and lateral radiographic images.
    • When preparing the graft for the bone-bridge technique, the bone is fashioned to create a bone bridge 10 mm in depth by approximately 7 mm in width, incorporating the anterior and posterior horns of the meniscus.
    • Graft fixation can be accomplished by placing vertical mattress sutures and tying those down with the knee in full extension.
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    Epidemiology of Existing Extensor Mechanism Pathology in Primary Anterior Cruciate Ligament Ruptures in an Active-Duty Population

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    ABSTRACT

    The purpose of this study is to determine the prevalence of potential graft-influencing pathologies of the extensor mechanism of the knee in patients presenting with a primary anterior cruciate ligament (ACL) rupture.

    We performed a retrospective review of the plain radiographs and magnetic resonance imaging (MRI) of all active-duty patients presenting with a primary ACL rupture at our institution between July 2006 and February 2009. Imaging was reviewed to determine the presence of a multipartite patella, unresolved Osgood-Schlatter’s disease, and/or radiographic evidence suggestive of patella tendinopathy.

    A total of 197 patients were reviewed, including 27 females and 170 males. One patient (0.5%) had a bipartite patella and 4 patients (2%) had free-floating ossicles about the tibial tuberosity consistent with unresolved Osgood-Schlatter’s disease. A total of 15 patients (7.6%) showed MRI evidence suggestive of patella tendinopathy.

    This study revealed 20 patients out of 197 (10.1%) who presented with existing extensor mechanism pathologies in radiologic studies. While preoperative imaging is routinely used to confirm clinical suspicion of ACL rupture or identify associated injuries, this study shows that it can also identify existing extensor mechanism pathologies that could ultimately influence the use of an extensor mechanism graft.

    Continue to: Anterior cruciate ligament (ACL) reconstruction...

     

     

    Anterior cruciate ligament (ACL) reconstruction is an extremely common procedure; in fact, an estimated 60,000 to 175,000 ACL reconstructions are performed annually in the United States.1,2 One of the most widely debated aspects of ACL reconstruction is the choice of graft. Grafts are broadly categorized into allografts and autografts. The autograft selections for ACL reconstruction include patellar bone-tendon-bone (pBTB), combined semitendinosus and gracilis hamstrings (HS), free quadriceps tendon (QT)without accompanying bone block, and quadriceps tendon-bone (qTB). Allograft choices predominantly include pBTB and HS, as well as the tibialis anterior and Achilles tendons. The pBTB autograft is traditionally considered the reference standard for ACL reconstruction.3 Recent advances in allograft processing, along with improved fixation techniques and devices, have improved results following the use of soft-tissue autografts and both bony and soft tissue allografts.4 Thus, the optimal graft choice for ACL reconstruction has become controversial in light of several studies demonstrating no significant, long-term difference in clinical and/or functional outcomes based on graft selection.5-7

    Given the lack of a clear gold standard in graft selection, multiple patient factors, such as age, activity demands, and patient preference, should be taken into account when considering the choice of graft. In addition, intrinsic factors that could potentially weaken an autograft should be considered. Several extensor mechanism pathological findings that are easily visualized on either plain radiographs or magnetic resonance imaging (MRI) could potentially affect graft selection. Findings such as a multipartite patella, free ossicles about the tibial tuberosity consistent with Osgood-Schlatter’s disease, and proximal patella tendon thickening suggestive of patellar tendinopathy are easily identifiable on preoperative imaging and could exert adverse effects on pBTB, QT, and qTB autografts. The purpose of this study is to identify the prevalence of these pre-existing conditions in active-duty military patients presenting with acute ACL tears.

    METHODS

    A retrospective review was conducted on all active-duty patients who underwent primary ACL reconstruction at our institution from July 2006 to February 2009. A systematic review of all plain radiographs and MRIs was performed on a calibrated picture archiving and communication system workstation. Imaging review was conducted by 2 of the authors. Pertinent findings included a multipartite patella, free ossicles within the patella tendon, and hypertrophy of the proximal aspect of the patella tendon. Assessment for multipartite patella and unresolved Osgood-Schlatter's disease was made using plain radiographs with MRI for confirmation. Measurements of the patella tendon were performed on the short tau inversion recovery and T2-weighted sagittal MRI images at the point of maximal tendon width. A width of ≥7 mm was considered suggestive of patella tendinopathy based on prior studies.8-10 The prevalence of each finding was then determined based on the total number of patients.

    Continue to: RESULTS...

     

     

    RESULTS

    A total of 197 active-duty patients, including 27 females (13.7%) and 170 males (86.3%), underwent primary ACL reconstruction during the study time period. A total of 93 right knees and 104 left knees were evaluated. The average age at presentation was 29 years (range, 19-45 years).

    Of the 197 patients, only 1 was found to have a multipartite patella (prevalence, 0.5%). This 37-year-old male patient showed a right bipartite patella located in the superior-lateral aspect (Figure 1).

    balog0818_f1

    Four patients had free ossicles within the inferior patellar tendon consistent with unresolved Osgood-Schlatter’s disease (prevalence, 2.0%) (Figure 2). All 4 patients were male, which is consistent with the higher incidence of Osgood-Schlatter’s disease in males than in females. The average age of these patients was 27.5 years (range, 22-33 years).

    balog0818_f2_0

    The most common extensor mechanism pathology present on preoperative imaging was proximal patella tendon thickening suggestive of patella tendinopathy. Thickening of the proximal portion of the patellar tendon was present in 15 of the 197 MRIs (prevalence, 7.6%) (Figure 3). The average width of this thickening was 8.49 mm (7.17-10.17 mm), and the average age of patients with radiographic evidence of patellar tendinopathy was 29.9 years (range, 20-43 years). Gender distribution was predominantly male (14 males, 1 female). Details of all extensor mechanism pathologies found are provided in the Table.

     

    balog0818_f3_1

     

    Table. Identified Extensor Mechanism Pathology

     

     

    Male

    Female

    Total

    Patients

    170

    27

    197

    Multipartite Patella

    1

    0

    1

    Osgood-Schlatter’s Disease

    4

    0

    4

    Patella Tendinopathy

    14

    1

    15

     

     

    20/97 (10.10%)

     

     

     

     

    DISCUSSION

    When considering ACL reconstruction, determination of the graft type is one of the most important decisions to be made, perhaps second only to the decision to perform the surgery itself. Recent multiple, well-designed studies comparing differences among grafts have shown equivalent long-term results, leading to the lack of a universally accepted gold standard.5-7 Thus, both autograft and allograft ACL surgeries are routinely performed in the United States. Surgeons typically take into account factors such as patient age and physical demands, along with their own preferences and/or experience, when considering graft selection. A paucity of research concerning existing pathological conditions that could also influence preoperative decision-making has been observed; most reports consist only of expert opinion.11-13 Our goal is to determine the prevalence of several conditions that could potentially affect an autograft harvested from the extensor mechanism.

    This study revealed an overall prevalence of 10.1% of existing extensor mechanism pathology in patients sustaining an acute ACL tear and presenting for ACL reconstruction. Only 1 (0.5%) showed evidence of a multipartite patella, which is below the reported prevalence of 0.2% to 6%.14 The presence of a multipartite patella could potentially have the most deleterious effect on a qTB autograft. Although not as commonly used as HS, QT, or pBTB autografts, some surgeons prefer a qTB autograft because of its increased surface area, bony fixation, and reported decreased donor site pain.15 A multipartite patella could complicate harvesting, disrupt the bone block, or lead to an unstable segment of the patella. These effects are of great concern since the most common location of a bipartite patella is superior-lateral and the quadriceps tendon has been shown to asymmetrically insert laterally.16 While these potential adverse effects have not been specifically studied, the availability of comparable options makes the use of a qTB autograft in the setting of a bipartite patella questionable.

    Four patients (2%) revealed evidence of ossicles within the inferior patellar tendon consistent with unresolved Osgood-Schlatter’s disease. Osgood-Schlatter’s disease has been reported to occur in up to 21% of active adolescents and is historically considered a self-resolving process.17 Recent papers have reported persistent symptoms in up to 10% of patients, with a small percentage experiencing persistent free ossicles within their patella tendon on MRI.18,19 The presence of such ossicles raises concern about the integrity of the patellar tendon and questions its use as an autograft when present. This concern was published in a report with the surgeon opting to utilize an alternate graft due to the presence of unresolved Osgood-Schlatter’s disease.13

    Fifteen patients (7.6%) demonstrated radiographic evidence suggestive of patella tendinopathy based on the thickness of the proximal patella tendon. Patella tendinopathy is the most common tendinopathy in skeletally mature athletes and one of the most common athletic injuries of the knee, with a reported career prevalence of 22%.20 It is described as an overuse injury due to the cumulative effect of micro trauma without an adequate healing interval. While it remains a clinical diagnosis, patellar tendinopathy often shows radiographic findings best assessed on sagittal MRIs. In general, the normal patella tendon appears as a homogenous low-intensity structure and is of uniform thickness. A tendon affected with tendinopathy typically demonstrates a focal increase in signal on T2-weighted sequences just distal to the tendon origin on the inferior pole of the patella. In addition, the patella tendon will usually demonstrate thickening, primarily in the proximal medial and posterior fibers. Patella marrow changes and indistinct tendon margins can also be present. The sensitivity and specificity of diagnosing patellar tendinopathy on MRI are 78% and 86%, respectively.20 We derived our criteria for MRI evidence suggestive of patella tendinopathy from studies by El-Khoury and colleagues,8 Johnson and colleagues,9 and Popp and colleagues.10 In a 1992 study, El-Khoury and colleagues8 compared MRI findings between a group of patients with a clinical diagnosis of patella tendonitis and a control group without knee complaints. The authors found that the average proximal patella tendon diameter in the control group was 3.7 mm while the average proximal patella tendon diameter in the patella tendinopathy group was 10.9 mm; no patella tendons in the control group were >7 mm.8 In a 1996 study, Johnson and colleagues9 determined that the most reliable MRI finding for patients with patellar tendonitis is significant thickening of the proximal patella tendon seen on the sagittal view. The average thickness in symptomatic patients was 8.5 mm (range, 5-15 mm). The average thickness in the control group was 5.5 mm. None of the control patients had a proximal tendon thickness >7 mm.9 Finally, Popp and colleagues10 reviewed the MRI of 11 knees of patients who underwent surgical débridement of chronic patellar tendonitis and reported an average proximal patella tendon thickness of 12 mm (range, 9-16 mm). We therefore used a proximal patella tendon thickness of >7 mm on the sagittal view as a radiographic finding suggestive of patella tendinopathy. No data regarding symptoms of anterior knee pain were available among our patients. Histological studies of patients with patella tendonitis have shown evidence of chronic inflammation, fibrinoid necrosis, mucoid degeneration, and synovial proliferation within the patella tendon insertion.21 Although no controlled data showing that patella tendons with a history of tendonitis are more prone to failure than those without such history when used as an autograft for ACL reconstruction, the idea of utilizing a diseased tendon for a graft is not ideal. Some surgeons question their patients regarding a history of anterior knee pain and will not use a pBTB autograft in a patient with a positive history.22

    Continue to: The goal of this study is to obtain epidemiological evidence...

     

     

    The goal of this study is to obtain epidemiological evidence of the prevalence of existing extensor mechanism pathologies in patients with acute ACL ruptures and determine how these pathologies may relate to the choice of graft. Out of 197 patients studied, over 10% presented with radiographic evidence of pathologies that could influence the choice of graft. This prevalence is certainly significant enough for surgeons to consider including a radiographic evaluation of the extensor mechanism in their standard ACL rupture work-up.

    This study presents obvious limitations. While we report the prevalence of some extensor mechanism pathologies, no definitive evidence that recommends against the use of these autografts from these affected individuals has yet been published. In addition, our diagnosis of patella tendinopathy is based solely on MRI findings with no information regarding clinical symptoms. This limitation is a weakness as several additional studies have questioned the validity of a 7 mm proximal patella tendon thickness.23,24 Furthermore, no studies demonstrating the inferior strength of autografts with the co-existing findings described in our work have yet been performed.

    CONCLUSION

    We found that 10% of active-duty patients presenting for ACL reconstruction demonstrated radiographic evidence of an extensor mechanism pathology that could affect the harvesting of or integrity of select autografts. Given the recent trend of functionally equivocal results in ACL reconstructions utilizing a variety of grafts, this information could and should influence surgical recommendations for graft utilization to obtain optimal surgical results.

    References

    1. Lyman S, Koulouvaris P, Sherman S, Do H, Mandl LA, Marx RG. Epidemiology of anterior cruciate ligament reconstruction: trends, readmissions, and subsequent knee surgery. J Bone Joint Surg Am. 2009;91(10):2321-2328. doi:10.2106/JBJS.H.00539.

    2. Spindler KP, Wright RW. Clinical practice. Anterior cruciate ligament tear. N Engl J Med. 2008;359(20):2135-2142. doi:10.1056/NEJMcp0804745.

    3. Fu FH, Bennett CH, Lattermann CL, Ma CB. Current trends in anterior cruciate ligament reconstruction. Part 1: Biology and biomechanics of reconstruction. Am J Sports Med. 1999;27(6):821-830. doi:10.1177/03635465990270062501.

    4. Mariscalco MW, Magnussen RA, Mehta D, Hewett TE, Flanigan DC, Kaeding CC. Autograft Versus nonirradiated allograft tissue for anterior cruciate ligament reconstruction: A systematic review. Am J Sports Med. 2014;42(2):492-499. doi:10.1177/0363546513497566.

    5. Shaieb MD, Kan DM, Chang SK, Marumoto JM, Richardson AB. A prospective randomized comparison of patellar tendon versus semitendinosus and gracilis tendon autografts for anterior cruciate ligament reconstruction. Am J Sports Med. 2002;30(2):214-220. doi:10.1177/03635465020300021201.

    6. Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: Allograft versus allograft. Arthroscopy. 2005;21(7):774-785. doi:10.1016/j.arthro.2005.04.112.

    7. Krych AJ, Jackson JD, Hoskin TL, Dahm DL. A meta-analysis of patellar tendon autograft versus patellar tendon allograft in anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(3):292-298. doi:10.1016/j.arthro.2007.08.029.

    8. El-Khoury GY, Wira RL, Berbaum KS, Pope TL, Monu JUV. MR imaging of patellar tendinitis. Radiology. 1992;184(3):849-854. doi:10.1148/radiology.184.3.1509078.

    9. Johnson DP, Wakeley CJ, Watt I. Magnetic resonance imaging of patellar tendonitis. J Bone Joint Surg Br. 1996;78(3):452-457. doi:10.1302/0301-620X.78B3.0780452.

    10. Popp JE, Yu JS, Kaeding CC. Recalcitrant patellar tendinitis. Magnetic resonance imaging, histologic evaluation, and surgical treatment. Am J Sports Med. 1997;25(2):218-222. doi:10.1177/036354659702500214.

    11. Provencher MT, Ryu JH, Gaston T, Dewing CB. Technique: bone-patellar tendon-bone autograft ACL reconstruction in the young, active patient. J Knee Surg. 2011;24(2):83-92. doi:10.1055/s-0031-1280875.

    12. Fu F, Cohen S. Current Concepts in ACL Reconstruction. Thorofare: SLACK Incorporated; 2008.

    13. Cosgarea AJ, Weng MS, Andrews M. Osgood Schlatter’s disease complicating anterior cruciate ligament reconstruction. Arthroscopy. 1993;9(6):700-703. doi:10.1016/S0749-8063(05)80511-0.

    14. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855. doi:10.1007/s11999-008-0367-4.

    15. Fulkerson JP, Langeland R. An alternative cruciate reconstruction graft: the central quadriceps tendon. Arthroscopy. 1995;11(2):252-254. doi:10.1016/0749-8063(95)90078-0.

    16. Scully WF, Wilson DJ, Arrington ED. “Central” quadriceps tendon harvest with patellar bone plug: surgical technique revisited. Arthrosc Tech. 2013;2(4):e427-e432.

    17. Kujala UM, Kvist M, Heinonen O. Osgood-Schlatter’s disease in adolescent athletes. Retrospective study of incidence and duration. Am J Sports Med. 1985;13(4):236-241. doi:10.1177/036354658501300404.

    18. Pihlajamäki HK, Visuri TI. Long-term outcome after surgical treatment of unresolved Osgood-Schlatter disease in young men: surgical technique. J Bone Joint Surg Am. 2010;92(suppl 1 Pt 2):258-264. doi:10.2106/JBJS.J.00450.

    19. Weiss JM, Jordan SS, Andersen JS, Lee BM, Kocher M. Surgical treatment of unresolved Osgood-Schlatter disease: ossicle resection with tibial tubercleplasty. J Pediatr Orthop. 2007;27(7):844-847. doi:10.1097/BPO.0b013e318155849b.

    20. Lian OB, Engebretsen L, Bahr R. Prevalence of jumper’s knee Among elite athletes from different sports: a cross-sectional study. Am J Sports Med. 2005;33(4):561-567. doi:10.1177/0363546504270454.

    21. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC. Overuse injuries of the knee. Magn Reson Imaging Clin N Am. 2009;17(4):725-739, vii. doi:10.1016/j.mric.2009.06.010.

    22. Martens M, Wouters P, Burssens A, Mulier JC. Patellar tendinitis: pathology and results of treatment. Acta Orthop Scand. 1982;53(3):445-450. doi:10.3109/17453678208992239.

    23. Shalaby M, Almekinders LC. Patellar tendinitis: the significance of magnetic resonance imaging findings. Am J Sports Med. 1999;27(3):345-349. doi:10.1177/03635465990270031301.

    24. Reiff DB, Heenan SD, Heron CW. MRI appearances of the asymptomatic patellar tendon on gradient echo imaging. Skeletal Radiol. 1995;24(2):123-126. doi:10.1007/BF00198074.
     

    Author and Disclosure Information

    Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

    Dr. Balog is a Staff Orthopedic Surgeon, Tripler Army Medical Center, Honolulu, Hawaii. Mr. Blanks is a Staff Physician Assistant, OrthoGeorgia, Macon, Georgia. Dr. Dykstra is a Staff Orthopedic Surgeon, Black Hills Orthopedic and Spine Center, Rapid City, South Dakota. Dr. Parada is Staff Orthopedic Surgeon, Eisenhower Army Medical Center, Fort Gordon, Georgia. Dr. Arrington is a Staff Orthopedic Surgeon and Director, Orthopedic Surgery Residency Program, Madigan Army Medical Center, Tacoma, Washington.

    Address correspondence to: LTC Todd P. Balog, MD, 1 Jarrett White Rd, Honolulu, HI 96859 (tel, 832-326-5583; email, tbalog99@gmail.com).

    MAJ Todd P. Balog, MD MAJ Benjamin P. Blanks, PA MAJ Aaron D. Dykstra, MD MAJ Stephen A. Parada, MD COL (ret) Edward D. Arrington, MD . Epidemiology of Existing Extensor Mechanism Pathology in Primary Anterior Cruciate Ligament Ruptures in an Active-Duty Population. Am J Orthop.

    August 31, 2018

    Publications
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    Author and Disclosure Information

    Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

    Dr. Balog is a Staff Orthopedic Surgeon, Tripler Army Medical Center, Honolulu, Hawaii. Mr. Blanks is a Staff Physician Assistant, OrthoGeorgia, Macon, Georgia. Dr. Dykstra is a Staff Orthopedic Surgeon, Black Hills Orthopedic and Spine Center, Rapid City, South Dakota. Dr. Parada is Staff Orthopedic Surgeon, Eisenhower Army Medical Center, Fort Gordon, Georgia. Dr. Arrington is a Staff Orthopedic Surgeon and Director, Orthopedic Surgery Residency Program, Madigan Army Medical Center, Tacoma, Washington.

    Address correspondence to: LTC Todd P. Balog, MD, 1 Jarrett White Rd, Honolulu, HI 96859 (tel, 832-326-5583; email, tbalog99@gmail.com).

    MAJ Todd P. Balog, MD MAJ Benjamin P. Blanks, PA MAJ Aaron D. Dykstra, MD MAJ Stephen A. Parada, MD COL (ret) Edward D. Arrington, MD . Epidemiology of Existing Extensor Mechanism Pathology in Primary Anterior Cruciate Ligament Ruptures in an Active-Duty Population. Am J Orthop.

    August 31, 2018

    Author and Disclosure Information

    Authors’ Disclosure Statement: The authors report no actual or potential conflict of interest in relation to this article.

    Dr. Balog is a Staff Orthopedic Surgeon, Tripler Army Medical Center, Honolulu, Hawaii. Mr. Blanks is a Staff Physician Assistant, OrthoGeorgia, Macon, Georgia. Dr. Dykstra is a Staff Orthopedic Surgeon, Black Hills Orthopedic and Spine Center, Rapid City, South Dakota. Dr. Parada is Staff Orthopedic Surgeon, Eisenhower Army Medical Center, Fort Gordon, Georgia. Dr. Arrington is a Staff Orthopedic Surgeon and Director, Orthopedic Surgery Residency Program, Madigan Army Medical Center, Tacoma, Washington.

    Address correspondence to: LTC Todd P. Balog, MD, 1 Jarrett White Rd, Honolulu, HI 96859 (tel, 832-326-5583; email, tbalog99@gmail.com).

    MAJ Todd P. Balog, MD MAJ Benjamin P. Blanks, PA MAJ Aaron D. Dykstra, MD MAJ Stephen A. Parada, MD COL (ret) Edward D. Arrington, MD . Epidemiology of Existing Extensor Mechanism Pathology in Primary Anterior Cruciate Ligament Ruptures in an Active-Duty Population. Am J Orthop.

    August 31, 2018

    ABSTRACT

    The purpose of this study is to determine the prevalence of potential graft-influencing pathologies of the extensor mechanism of the knee in patients presenting with a primary anterior cruciate ligament (ACL) rupture.

    We performed a retrospective review of the plain radiographs and magnetic resonance imaging (MRI) of all active-duty patients presenting with a primary ACL rupture at our institution between July 2006 and February 2009. Imaging was reviewed to determine the presence of a multipartite patella, unresolved Osgood-Schlatter’s disease, and/or radiographic evidence suggestive of patella tendinopathy.

    A total of 197 patients were reviewed, including 27 females and 170 males. One patient (0.5%) had a bipartite patella and 4 patients (2%) had free-floating ossicles about the tibial tuberosity consistent with unresolved Osgood-Schlatter’s disease. A total of 15 patients (7.6%) showed MRI evidence suggestive of patella tendinopathy.

    This study revealed 20 patients out of 197 (10.1%) who presented with existing extensor mechanism pathologies in radiologic studies. While preoperative imaging is routinely used to confirm clinical suspicion of ACL rupture or identify associated injuries, this study shows that it can also identify existing extensor mechanism pathologies that could ultimately influence the use of an extensor mechanism graft.

    Continue to: Anterior cruciate ligament (ACL) reconstruction...

     

     

    Anterior cruciate ligament (ACL) reconstruction is an extremely common procedure; in fact, an estimated 60,000 to 175,000 ACL reconstructions are performed annually in the United States.1,2 One of the most widely debated aspects of ACL reconstruction is the choice of graft. Grafts are broadly categorized into allografts and autografts. The autograft selections for ACL reconstruction include patellar bone-tendon-bone (pBTB), combined semitendinosus and gracilis hamstrings (HS), free quadriceps tendon (QT)without accompanying bone block, and quadriceps tendon-bone (qTB). Allograft choices predominantly include pBTB and HS, as well as the tibialis anterior and Achilles tendons. The pBTB autograft is traditionally considered the reference standard for ACL reconstruction.3 Recent advances in allograft processing, along with improved fixation techniques and devices, have improved results following the use of soft-tissue autografts and both bony and soft tissue allografts.4 Thus, the optimal graft choice for ACL reconstruction has become controversial in light of several studies demonstrating no significant, long-term difference in clinical and/or functional outcomes based on graft selection.5-7

    Given the lack of a clear gold standard in graft selection, multiple patient factors, such as age, activity demands, and patient preference, should be taken into account when considering the choice of graft. In addition, intrinsic factors that could potentially weaken an autograft should be considered. Several extensor mechanism pathological findings that are easily visualized on either plain radiographs or magnetic resonance imaging (MRI) could potentially affect graft selection. Findings such as a multipartite patella, free ossicles about the tibial tuberosity consistent with Osgood-Schlatter’s disease, and proximal patella tendon thickening suggestive of patellar tendinopathy are easily identifiable on preoperative imaging and could exert adverse effects on pBTB, QT, and qTB autografts. The purpose of this study is to identify the prevalence of these pre-existing conditions in active-duty military patients presenting with acute ACL tears.

    METHODS

    A retrospective review was conducted on all active-duty patients who underwent primary ACL reconstruction at our institution from July 2006 to February 2009. A systematic review of all plain radiographs and MRIs was performed on a calibrated picture archiving and communication system workstation. Imaging review was conducted by 2 of the authors. Pertinent findings included a multipartite patella, free ossicles within the patella tendon, and hypertrophy of the proximal aspect of the patella tendon. Assessment for multipartite patella and unresolved Osgood-Schlatter's disease was made using plain radiographs with MRI for confirmation. Measurements of the patella tendon were performed on the short tau inversion recovery and T2-weighted sagittal MRI images at the point of maximal tendon width. A width of ≥7 mm was considered suggestive of patella tendinopathy based on prior studies.8-10 The prevalence of each finding was then determined based on the total number of patients.

    Continue to: RESULTS...

     

     

    RESULTS

    A total of 197 active-duty patients, including 27 females (13.7%) and 170 males (86.3%), underwent primary ACL reconstruction during the study time period. A total of 93 right knees and 104 left knees were evaluated. The average age at presentation was 29 years (range, 19-45 years).

    Of the 197 patients, only 1 was found to have a multipartite patella (prevalence, 0.5%). This 37-year-old male patient showed a right bipartite patella located in the superior-lateral aspect (Figure 1).

    balog0818_f1

    Four patients had free ossicles within the inferior patellar tendon consistent with unresolved Osgood-Schlatter’s disease (prevalence, 2.0%) (Figure 2). All 4 patients were male, which is consistent with the higher incidence of Osgood-Schlatter’s disease in males than in females. The average age of these patients was 27.5 years (range, 22-33 years).

    balog0818_f2_0

    The most common extensor mechanism pathology present on preoperative imaging was proximal patella tendon thickening suggestive of patella tendinopathy. Thickening of the proximal portion of the patellar tendon was present in 15 of the 197 MRIs (prevalence, 7.6%) (Figure 3). The average width of this thickening was 8.49 mm (7.17-10.17 mm), and the average age of patients with radiographic evidence of patellar tendinopathy was 29.9 years (range, 20-43 years). Gender distribution was predominantly male (14 males, 1 female). Details of all extensor mechanism pathologies found are provided in the Table.

     

    balog0818_f3_1

     

    Table. Identified Extensor Mechanism Pathology

     

     

    Male

    Female

    Total

    Patients

    170

    27

    197

    Multipartite Patella

    1

    0

    1

    Osgood-Schlatter’s Disease

    4

    0

    4

    Patella Tendinopathy

    14

    1

    15

     

     

    20/97 (10.10%)

     

     

     

     

    DISCUSSION

    When considering ACL reconstruction, determination of the graft type is one of the most important decisions to be made, perhaps second only to the decision to perform the surgery itself. Recent multiple, well-designed studies comparing differences among grafts have shown equivalent long-term results, leading to the lack of a universally accepted gold standard.5-7 Thus, both autograft and allograft ACL surgeries are routinely performed in the United States. Surgeons typically take into account factors such as patient age and physical demands, along with their own preferences and/or experience, when considering graft selection. A paucity of research concerning existing pathological conditions that could also influence preoperative decision-making has been observed; most reports consist only of expert opinion.11-13 Our goal is to determine the prevalence of several conditions that could potentially affect an autograft harvested from the extensor mechanism.

    This study revealed an overall prevalence of 10.1% of existing extensor mechanism pathology in patients sustaining an acute ACL tear and presenting for ACL reconstruction. Only 1 (0.5%) showed evidence of a multipartite patella, which is below the reported prevalence of 0.2% to 6%.14 The presence of a multipartite patella could potentially have the most deleterious effect on a qTB autograft. Although not as commonly used as HS, QT, or pBTB autografts, some surgeons prefer a qTB autograft because of its increased surface area, bony fixation, and reported decreased donor site pain.15 A multipartite patella could complicate harvesting, disrupt the bone block, or lead to an unstable segment of the patella. These effects are of great concern since the most common location of a bipartite patella is superior-lateral and the quadriceps tendon has been shown to asymmetrically insert laterally.16 While these potential adverse effects have not been specifically studied, the availability of comparable options makes the use of a qTB autograft in the setting of a bipartite patella questionable.

    Four patients (2%) revealed evidence of ossicles within the inferior patellar tendon consistent with unresolved Osgood-Schlatter’s disease. Osgood-Schlatter’s disease has been reported to occur in up to 21% of active adolescents and is historically considered a self-resolving process.17 Recent papers have reported persistent symptoms in up to 10% of patients, with a small percentage experiencing persistent free ossicles within their patella tendon on MRI.18,19 The presence of such ossicles raises concern about the integrity of the patellar tendon and questions its use as an autograft when present. This concern was published in a report with the surgeon opting to utilize an alternate graft due to the presence of unresolved Osgood-Schlatter’s disease.13

    Fifteen patients (7.6%) demonstrated radiographic evidence suggestive of patella tendinopathy based on the thickness of the proximal patella tendon. Patella tendinopathy is the most common tendinopathy in skeletally mature athletes and one of the most common athletic injuries of the knee, with a reported career prevalence of 22%.20 It is described as an overuse injury due to the cumulative effect of micro trauma without an adequate healing interval. While it remains a clinical diagnosis, patellar tendinopathy often shows radiographic findings best assessed on sagittal MRIs. In general, the normal patella tendon appears as a homogenous low-intensity structure and is of uniform thickness. A tendon affected with tendinopathy typically demonstrates a focal increase in signal on T2-weighted sequences just distal to the tendon origin on the inferior pole of the patella. In addition, the patella tendon will usually demonstrate thickening, primarily in the proximal medial and posterior fibers. Patella marrow changes and indistinct tendon margins can also be present. The sensitivity and specificity of diagnosing patellar tendinopathy on MRI are 78% and 86%, respectively.20 We derived our criteria for MRI evidence suggestive of patella tendinopathy from studies by El-Khoury and colleagues,8 Johnson and colleagues,9 and Popp and colleagues.10 In a 1992 study, El-Khoury and colleagues8 compared MRI findings between a group of patients with a clinical diagnosis of patella tendonitis and a control group without knee complaints. The authors found that the average proximal patella tendon diameter in the control group was 3.7 mm while the average proximal patella tendon diameter in the patella tendinopathy group was 10.9 mm; no patella tendons in the control group were >7 mm.8 In a 1996 study, Johnson and colleagues9 determined that the most reliable MRI finding for patients with patellar tendonitis is significant thickening of the proximal patella tendon seen on the sagittal view. The average thickness in symptomatic patients was 8.5 mm (range, 5-15 mm). The average thickness in the control group was 5.5 mm. None of the control patients had a proximal tendon thickness >7 mm.9 Finally, Popp and colleagues10 reviewed the MRI of 11 knees of patients who underwent surgical débridement of chronic patellar tendonitis and reported an average proximal patella tendon thickness of 12 mm (range, 9-16 mm). We therefore used a proximal patella tendon thickness of >7 mm on the sagittal view as a radiographic finding suggestive of patella tendinopathy. No data regarding symptoms of anterior knee pain were available among our patients. Histological studies of patients with patella tendonitis have shown evidence of chronic inflammation, fibrinoid necrosis, mucoid degeneration, and synovial proliferation within the patella tendon insertion.21 Although no controlled data showing that patella tendons with a history of tendonitis are more prone to failure than those without such history when used as an autograft for ACL reconstruction, the idea of utilizing a diseased tendon for a graft is not ideal. Some surgeons question their patients regarding a history of anterior knee pain and will not use a pBTB autograft in a patient with a positive history.22

    Continue to: The goal of this study is to obtain epidemiological evidence...

     

     

    The goal of this study is to obtain epidemiological evidence of the prevalence of existing extensor mechanism pathologies in patients with acute ACL ruptures and determine how these pathologies may relate to the choice of graft. Out of 197 patients studied, over 10% presented with radiographic evidence of pathologies that could influence the choice of graft. This prevalence is certainly significant enough for surgeons to consider including a radiographic evaluation of the extensor mechanism in their standard ACL rupture work-up.

    This study presents obvious limitations. While we report the prevalence of some extensor mechanism pathologies, no definitive evidence that recommends against the use of these autografts from these affected individuals has yet been published. In addition, our diagnosis of patella tendinopathy is based solely on MRI findings with no information regarding clinical symptoms. This limitation is a weakness as several additional studies have questioned the validity of a 7 mm proximal patella tendon thickness.23,24 Furthermore, no studies demonstrating the inferior strength of autografts with the co-existing findings described in our work have yet been performed.

    CONCLUSION

    We found that 10% of active-duty patients presenting for ACL reconstruction demonstrated radiographic evidence of an extensor mechanism pathology that could affect the harvesting of or integrity of select autografts. Given the recent trend of functionally equivocal results in ACL reconstructions utilizing a variety of grafts, this information could and should influence surgical recommendations for graft utilization to obtain optimal surgical results.

    ABSTRACT

    The purpose of this study is to determine the prevalence of potential graft-influencing pathologies of the extensor mechanism of the knee in patients presenting with a primary anterior cruciate ligament (ACL) rupture.

    We performed a retrospective review of the plain radiographs and magnetic resonance imaging (MRI) of all active-duty patients presenting with a primary ACL rupture at our institution between July 2006 and February 2009. Imaging was reviewed to determine the presence of a multipartite patella, unresolved Osgood-Schlatter’s disease, and/or radiographic evidence suggestive of patella tendinopathy.

    A total of 197 patients were reviewed, including 27 females and 170 males. One patient (0.5%) had a bipartite patella and 4 patients (2%) had free-floating ossicles about the tibial tuberosity consistent with unresolved Osgood-Schlatter’s disease. A total of 15 patients (7.6%) showed MRI evidence suggestive of patella tendinopathy.

    This study revealed 20 patients out of 197 (10.1%) who presented with existing extensor mechanism pathologies in radiologic studies. While preoperative imaging is routinely used to confirm clinical suspicion of ACL rupture or identify associated injuries, this study shows that it can also identify existing extensor mechanism pathologies that could ultimately influence the use of an extensor mechanism graft.

    Continue to: Anterior cruciate ligament (ACL) reconstruction...

     

     

    Anterior cruciate ligament (ACL) reconstruction is an extremely common procedure; in fact, an estimated 60,000 to 175,000 ACL reconstructions are performed annually in the United States.1,2 One of the most widely debated aspects of ACL reconstruction is the choice of graft. Grafts are broadly categorized into allografts and autografts. The autograft selections for ACL reconstruction include patellar bone-tendon-bone (pBTB), combined semitendinosus and gracilis hamstrings (HS), free quadriceps tendon (QT)without accompanying bone block, and quadriceps tendon-bone (qTB). Allograft choices predominantly include pBTB and HS, as well as the tibialis anterior and Achilles tendons. The pBTB autograft is traditionally considered the reference standard for ACL reconstruction.3 Recent advances in allograft processing, along with improved fixation techniques and devices, have improved results following the use of soft-tissue autografts and both bony and soft tissue allografts.4 Thus, the optimal graft choice for ACL reconstruction has become controversial in light of several studies demonstrating no significant, long-term difference in clinical and/or functional outcomes based on graft selection.5-7

    Given the lack of a clear gold standard in graft selection, multiple patient factors, such as age, activity demands, and patient preference, should be taken into account when considering the choice of graft. In addition, intrinsic factors that could potentially weaken an autograft should be considered. Several extensor mechanism pathological findings that are easily visualized on either plain radiographs or magnetic resonance imaging (MRI) could potentially affect graft selection. Findings such as a multipartite patella, free ossicles about the tibial tuberosity consistent with Osgood-Schlatter’s disease, and proximal patella tendon thickening suggestive of patellar tendinopathy are easily identifiable on preoperative imaging and could exert adverse effects on pBTB, QT, and qTB autografts. The purpose of this study is to identify the prevalence of these pre-existing conditions in active-duty military patients presenting with acute ACL tears.

    METHODS

    A retrospective review was conducted on all active-duty patients who underwent primary ACL reconstruction at our institution from July 2006 to February 2009. A systematic review of all plain radiographs and MRIs was performed on a calibrated picture archiving and communication system workstation. Imaging review was conducted by 2 of the authors. Pertinent findings included a multipartite patella, free ossicles within the patella tendon, and hypertrophy of the proximal aspect of the patella tendon. Assessment for multipartite patella and unresolved Osgood-Schlatter's disease was made using plain radiographs with MRI for confirmation. Measurements of the patella tendon were performed on the short tau inversion recovery and T2-weighted sagittal MRI images at the point of maximal tendon width. A width of ≥7 mm was considered suggestive of patella tendinopathy based on prior studies.8-10 The prevalence of each finding was then determined based on the total number of patients.

    Continue to: RESULTS...

     

     

    RESULTS

    A total of 197 active-duty patients, including 27 females (13.7%) and 170 males (86.3%), underwent primary ACL reconstruction during the study time period. A total of 93 right knees and 104 left knees were evaluated. The average age at presentation was 29 years (range, 19-45 years).

    Of the 197 patients, only 1 was found to have a multipartite patella (prevalence, 0.5%). This 37-year-old male patient showed a right bipartite patella located in the superior-lateral aspect (Figure 1).

    balog0818_f1

    Four patients had free ossicles within the inferior patellar tendon consistent with unresolved Osgood-Schlatter’s disease (prevalence, 2.0%) (Figure 2). All 4 patients were male, which is consistent with the higher incidence of Osgood-Schlatter’s disease in males than in females. The average age of these patients was 27.5 years (range, 22-33 years).

    balog0818_f2_0

    The most common extensor mechanism pathology present on preoperative imaging was proximal patella tendon thickening suggestive of patella tendinopathy. Thickening of the proximal portion of the patellar tendon was present in 15 of the 197 MRIs (prevalence, 7.6%) (Figure 3). The average width of this thickening was 8.49 mm (7.17-10.17 mm), and the average age of patients with radiographic evidence of patellar tendinopathy was 29.9 years (range, 20-43 years). Gender distribution was predominantly male (14 males, 1 female). Details of all extensor mechanism pathologies found are provided in the Table.

     

    balog0818_f3_1

     

    Table. Identified Extensor Mechanism Pathology

     

     

    Male

    Female

    Total

    Patients

    170

    27

    197

    Multipartite Patella

    1

    0

    1

    Osgood-Schlatter’s Disease

    4

    0

    4

    Patella Tendinopathy

    14

    1

    15

     

     

    20/97 (10.10%)

     

     

     

     

    DISCUSSION

    When considering ACL reconstruction, determination of the graft type is one of the most important decisions to be made, perhaps second only to the decision to perform the surgery itself. Recent multiple, well-designed studies comparing differences among grafts have shown equivalent long-term results, leading to the lack of a universally accepted gold standard.5-7 Thus, both autograft and allograft ACL surgeries are routinely performed in the United States. Surgeons typically take into account factors such as patient age and physical demands, along with their own preferences and/or experience, when considering graft selection. A paucity of research concerning existing pathological conditions that could also influence preoperative decision-making has been observed; most reports consist only of expert opinion.11-13 Our goal is to determine the prevalence of several conditions that could potentially affect an autograft harvested from the extensor mechanism.

    This study revealed an overall prevalence of 10.1% of existing extensor mechanism pathology in patients sustaining an acute ACL tear and presenting for ACL reconstruction. Only 1 (0.5%) showed evidence of a multipartite patella, which is below the reported prevalence of 0.2% to 6%.14 The presence of a multipartite patella could potentially have the most deleterious effect on a qTB autograft. Although not as commonly used as HS, QT, or pBTB autografts, some surgeons prefer a qTB autograft because of its increased surface area, bony fixation, and reported decreased donor site pain.15 A multipartite patella could complicate harvesting, disrupt the bone block, or lead to an unstable segment of the patella. These effects are of great concern since the most common location of a bipartite patella is superior-lateral and the quadriceps tendon has been shown to asymmetrically insert laterally.16 While these potential adverse effects have not been specifically studied, the availability of comparable options makes the use of a qTB autograft in the setting of a bipartite patella questionable.

    Four patients (2%) revealed evidence of ossicles within the inferior patellar tendon consistent with unresolved Osgood-Schlatter’s disease. Osgood-Schlatter’s disease has been reported to occur in up to 21% of active adolescents and is historically considered a self-resolving process.17 Recent papers have reported persistent symptoms in up to 10% of patients, with a small percentage experiencing persistent free ossicles within their patella tendon on MRI.18,19 The presence of such ossicles raises concern about the integrity of the patellar tendon and questions its use as an autograft when present. This concern was published in a report with the surgeon opting to utilize an alternate graft due to the presence of unresolved Osgood-Schlatter’s disease.13

    Fifteen patients (7.6%) demonstrated radiographic evidence suggestive of patella tendinopathy based on the thickness of the proximal patella tendon. Patella tendinopathy is the most common tendinopathy in skeletally mature athletes and one of the most common athletic injuries of the knee, with a reported career prevalence of 22%.20 It is described as an overuse injury due to the cumulative effect of micro trauma without an adequate healing interval. While it remains a clinical diagnosis, patellar tendinopathy often shows radiographic findings best assessed on sagittal MRIs. In general, the normal patella tendon appears as a homogenous low-intensity structure and is of uniform thickness. A tendon affected with tendinopathy typically demonstrates a focal increase in signal on T2-weighted sequences just distal to the tendon origin on the inferior pole of the patella. In addition, the patella tendon will usually demonstrate thickening, primarily in the proximal medial and posterior fibers. Patella marrow changes and indistinct tendon margins can also be present. The sensitivity and specificity of diagnosing patellar tendinopathy on MRI are 78% and 86%, respectively.20 We derived our criteria for MRI evidence suggestive of patella tendinopathy from studies by El-Khoury and colleagues,8 Johnson and colleagues,9 and Popp and colleagues.10 In a 1992 study, El-Khoury and colleagues8 compared MRI findings between a group of patients with a clinical diagnosis of patella tendonitis and a control group without knee complaints. The authors found that the average proximal patella tendon diameter in the control group was 3.7 mm while the average proximal patella tendon diameter in the patella tendinopathy group was 10.9 mm; no patella tendons in the control group were >7 mm.8 In a 1996 study, Johnson and colleagues9 determined that the most reliable MRI finding for patients with patellar tendonitis is significant thickening of the proximal patella tendon seen on the sagittal view. The average thickness in symptomatic patients was 8.5 mm (range, 5-15 mm). The average thickness in the control group was 5.5 mm. None of the control patients had a proximal tendon thickness >7 mm.9 Finally, Popp and colleagues10 reviewed the MRI of 11 knees of patients who underwent surgical débridement of chronic patellar tendonitis and reported an average proximal patella tendon thickness of 12 mm (range, 9-16 mm). We therefore used a proximal patella tendon thickness of >7 mm on the sagittal view as a radiographic finding suggestive of patella tendinopathy. No data regarding symptoms of anterior knee pain were available among our patients. Histological studies of patients with patella tendonitis have shown evidence of chronic inflammation, fibrinoid necrosis, mucoid degeneration, and synovial proliferation within the patella tendon insertion.21 Although no controlled data showing that patella tendons with a history of tendonitis are more prone to failure than those without such history when used as an autograft for ACL reconstruction, the idea of utilizing a diseased tendon for a graft is not ideal. Some surgeons question their patients regarding a history of anterior knee pain and will not use a pBTB autograft in a patient with a positive history.22

    Continue to: The goal of this study is to obtain epidemiological evidence...

     

     

    The goal of this study is to obtain epidemiological evidence of the prevalence of existing extensor mechanism pathologies in patients with acute ACL ruptures and determine how these pathologies may relate to the choice of graft. Out of 197 patients studied, over 10% presented with radiographic evidence of pathologies that could influence the choice of graft. This prevalence is certainly significant enough for surgeons to consider including a radiographic evaluation of the extensor mechanism in their standard ACL rupture work-up.

    This study presents obvious limitations. While we report the prevalence of some extensor mechanism pathologies, no definitive evidence that recommends against the use of these autografts from these affected individuals has yet been published. In addition, our diagnosis of patella tendinopathy is based solely on MRI findings with no information regarding clinical symptoms. This limitation is a weakness as several additional studies have questioned the validity of a 7 mm proximal patella tendon thickness.23,24 Furthermore, no studies demonstrating the inferior strength of autografts with the co-existing findings described in our work have yet been performed.

    CONCLUSION

    We found that 10% of active-duty patients presenting for ACL reconstruction demonstrated radiographic evidence of an extensor mechanism pathology that could affect the harvesting of or integrity of select autografts. Given the recent trend of functionally equivocal results in ACL reconstructions utilizing a variety of grafts, this information could and should influence surgical recommendations for graft utilization to obtain optimal surgical results.

    References

    1. Lyman S, Koulouvaris P, Sherman S, Do H, Mandl LA, Marx RG. Epidemiology of anterior cruciate ligament reconstruction: trends, readmissions, and subsequent knee surgery. J Bone Joint Surg Am. 2009;91(10):2321-2328. doi:10.2106/JBJS.H.00539.

    2. Spindler KP, Wright RW. Clinical practice. Anterior cruciate ligament tear. N Engl J Med. 2008;359(20):2135-2142. doi:10.1056/NEJMcp0804745.

    3. Fu FH, Bennett CH, Lattermann CL, Ma CB. Current trends in anterior cruciate ligament reconstruction. Part 1: Biology and biomechanics of reconstruction. Am J Sports Med. 1999;27(6):821-830. doi:10.1177/03635465990270062501.

    4. Mariscalco MW, Magnussen RA, Mehta D, Hewett TE, Flanigan DC, Kaeding CC. Autograft Versus nonirradiated allograft tissue for anterior cruciate ligament reconstruction: A systematic review. Am J Sports Med. 2014;42(2):492-499. doi:10.1177/0363546513497566.

    5. Shaieb MD, Kan DM, Chang SK, Marumoto JM, Richardson AB. A prospective randomized comparison of patellar tendon versus semitendinosus and gracilis tendon autografts for anterior cruciate ligament reconstruction. Am J Sports Med. 2002;30(2):214-220. doi:10.1177/03635465020300021201.

    6. Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: Allograft versus allograft. Arthroscopy. 2005;21(7):774-785. doi:10.1016/j.arthro.2005.04.112.

    7. Krych AJ, Jackson JD, Hoskin TL, Dahm DL. A meta-analysis of patellar tendon autograft versus patellar tendon allograft in anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(3):292-298. doi:10.1016/j.arthro.2007.08.029.

    8. El-Khoury GY, Wira RL, Berbaum KS, Pope TL, Monu JUV. MR imaging of patellar tendinitis. Radiology. 1992;184(3):849-854. doi:10.1148/radiology.184.3.1509078.

    9. Johnson DP, Wakeley CJ, Watt I. Magnetic resonance imaging of patellar tendonitis. J Bone Joint Surg Br. 1996;78(3):452-457. doi:10.1302/0301-620X.78B3.0780452.

    10. Popp JE, Yu JS, Kaeding CC. Recalcitrant patellar tendinitis. Magnetic resonance imaging, histologic evaluation, and surgical treatment. Am J Sports Med. 1997;25(2):218-222. doi:10.1177/036354659702500214.

    11. Provencher MT, Ryu JH, Gaston T, Dewing CB. Technique: bone-patellar tendon-bone autograft ACL reconstruction in the young, active patient. J Knee Surg. 2011;24(2):83-92. doi:10.1055/s-0031-1280875.

    12. Fu F, Cohen S. Current Concepts in ACL Reconstruction. Thorofare: SLACK Incorporated; 2008.

    13. Cosgarea AJ, Weng MS, Andrews M. Osgood Schlatter’s disease complicating anterior cruciate ligament reconstruction. Arthroscopy. 1993;9(6):700-703. doi:10.1016/S0749-8063(05)80511-0.

    14. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855. doi:10.1007/s11999-008-0367-4.

    15. Fulkerson JP, Langeland R. An alternative cruciate reconstruction graft: the central quadriceps tendon. Arthroscopy. 1995;11(2):252-254. doi:10.1016/0749-8063(95)90078-0.

    16. Scully WF, Wilson DJ, Arrington ED. “Central” quadriceps tendon harvest with patellar bone plug: surgical technique revisited. Arthrosc Tech. 2013;2(4):e427-e432.

    17. Kujala UM, Kvist M, Heinonen O. Osgood-Schlatter’s disease in adolescent athletes. Retrospective study of incidence and duration. Am J Sports Med. 1985;13(4):236-241. doi:10.1177/036354658501300404.

    18. Pihlajamäki HK, Visuri TI. Long-term outcome after surgical treatment of unresolved Osgood-Schlatter disease in young men: surgical technique. J Bone Joint Surg Am. 2010;92(suppl 1 Pt 2):258-264. doi:10.2106/JBJS.J.00450.

    19. Weiss JM, Jordan SS, Andersen JS, Lee BM, Kocher M. Surgical treatment of unresolved Osgood-Schlatter disease: ossicle resection with tibial tubercleplasty. J Pediatr Orthop. 2007;27(7):844-847. doi:10.1097/BPO.0b013e318155849b.

    20. Lian OB, Engebretsen L, Bahr R. Prevalence of jumper’s knee Among elite athletes from different sports: a cross-sectional study. Am J Sports Med. 2005;33(4):561-567. doi:10.1177/0363546504270454.

    21. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC. Overuse injuries of the knee. Magn Reson Imaging Clin N Am. 2009;17(4):725-739, vii. doi:10.1016/j.mric.2009.06.010.

    22. Martens M, Wouters P, Burssens A, Mulier JC. Patellar tendinitis: pathology and results of treatment. Acta Orthop Scand. 1982;53(3):445-450. doi:10.3109/17453678208992239.

    23. Shalaby M, Almekinders LC. Patellar tendinitis: the significance of magnetic resonance imaging findings. Am J Sports Med. 1999;27(3):345-349. doi:10.1177/03635465990270031301.

    24. Reiff DB, Heenan SD, Heron CW. MRI appearances of the asymptomatic patellar tendon on gradient echo imaging. Skeletal Radiol. 1995;24(2):123-126. doi:10.1007/BF00198074.
     

    References

    1. Lyman S, Koulouvaris P, Sherman S, Do H, Mandl LA, Marx RG. Epidemiology of anterior cruciate ligament reconstruction: trends, readmissions, and subsequent knee surgery. J Bone Joint Surg Am. 2009;91(10):2321-2328. doi:10.2106/JBJS.H.00539.

    2. Spindler KP, Wright RW. Clinical practice. Anterior cruciate ligament tear. N Engl J Med. 2008;359(20):2135-2142. doi:10.1056/NEJMcp0804745.

    3. Fu FH, Bennett CH, Lattermann CL, Ma CB. Current trends in anterior cruciate ligament reconstruction. Part 1: Biology and biomechanics of reconstruction. Am J Sports Med. 1999;27(6):821-830. doi:10.1177/03635465990270062501.

    4. Mariscalco MW, Magnussen RA, Mehta D, Hewett TE, Flanigan DC, Kaeding CC. Autograft Versus nonirradiated allograft tissue for anterior cruciate ligament reconstruction: A systematic review. Am J Sports Med. 2014;42(2):492-499. doi:10.1177/0363546513497566.

    5. Shaieb MD, Kan DM, Chang SK, Marumoto JM, Richardson AB. A prospective randomized comparison of patellar tendon versus semitendinosus and gracilis tendon autografts for anterior cruciate ligament reconstruction. Am J Sports Med. 2002;30(2):214-220. doi:10.1177/03635465020300021201.

    6. Poehling GG, Curl WW, Lee CA, et al. Analysis of outcomes of anterior cruciate ligament repair with 5-year follow-up: Allograft versus allograft. Arthroscopy. 2005;21(7):774-785. doi:10.1016/j.arthro.2005.04.112.

    7. Krych AJ, Jackson JD, Hoskin TL, Dahm DL. A meta-analysis of patellar tendon autograft versus patellar tendon allograft in anterior cruciate ligament reconstruction. Arthroscopy. 2008;24(3):292-298. doi:10.1016/j.arthro.2007.08.029.

    8. El-Khoury GY, Wira RL, Berbaum KS, Pope TL, Monu JUV. MR imaging of patellar tendinitis. Radiology. 1992;184(3):849-854. doi:10.1148/radiology.184.3.1509078.

    9. Johnson DP, Wakeley CJ, Watt I. Magnetic resonance imaging of patellar tendonitis. J Bone Joint Surg Br. 1996;78(3):452-457. doi:10.1302/0301-620X.78B3.0780452.

    10. Popp JE, Yu JS, Kaeding CC. Recalcitrant patellar tendinitis. Magnetic resonance imaging, histologic evaluation, and surgical treatment. Am J Sports Med. 1997;25(2):218-222. doi:10.1177/036354659702500214.

    11. Provencher MT, Ryu JH, Gaston T, Dewing CB. Technique: bone-patellar tendon-bone autograft ACL reconstruction in the young, active patient. J Knee Surg. 2011;24(2):83-92. doi:10.1055/s-0031-1280875.

    12. Fu F, Cohen S. Current Concepts in ACL Reconstruction. Thorofare: SLACK Incorporated; 2008.

    13. Cosgarea AJ, Weng MS, Andrews M. Osgood Schlatter’s disease complicating anterior cruciate ligament reconstruction. Arthroscopy. 1993;9(6):700-703. doi:10.1016/S0749-8063(05)80511-0.

    14. Weckström M, Parviainen M, Pihlajamäki HK. Excision of painful bipartite patella: good long-term outcome in young adults. Clin Orthop Relat Res. 2008;466(11):2848-2855. doi:10.1007/s11999-008-0367-4.

    15. Fulkerson JP, Langeland R. An alternative cruciate reconstruction graft: the central quadriceps tendon. Arthroscopy. 1995;11(2):252-254. doi:10.1016/0749-8063(95)90078-0.

    16. Scully WF, Wilson DJ, Arrington ED. “Central” quadriceps tendon harvest with patellar bone plug: surgical technique revisited. Arthrosc Tech. 2013;2(4):e427-e432.

    17. Kujala UM, Kvist M, Heinonen O. Osgood-Schlatter’s disease in adolescent athletes. Retrospective study of incidence and duration. Am J Sports Med. 1985;13(4):236-241. doi:10.1177/036354658501300404.

    18. Pihlajamäki HK, Visuri TI. Long-term outcome after surgical treatment of unresolved Osgood-Schlatter disease in young men: surgical technique. J Bone Joint Surg Am. 2010;92(suppl 1 Pt 2):258-264. doi:10.2106/JBJS.J.00450.

    19. Weiss JM, Jordan SS, Andersen JS, Lee BM, Kocher M. Surgical treatment of unresolved Osgood-Schlatter disease: ossicle resection with tibial tubercleplasty. J Pediatr Orthop. 2007;27(7):844-847. doi:10.1097/BPO.0b013e318155849b.

    20. Lian OB, Engebretsen L, Bahr R. Prevalence of jumper’s knee Among elite athletes from different sports: a cross-sectional study. Am J Sports Med. 2005;33(4):561-567. doi:10.1177/0363546504270454.

    21. O’Keeffe SA, Hogan BA, Eustace SJ, Kavanagh EC. Overuse injuries of the knee. Magn Reson Imaging Clin N Am. 2009;17(4):725-739, vii. doi:10.1016/j.mric.2009.06.010.

    22. Martens M, Wouters P, Burssens A, Mulier JC. Patellar tendinitis: pathology and results of treatment. Acta Orthop Scand. 1982;53(3):445-450. doi:10.3109/17453678208992239.

    23. Shalaby M, Almekinders LC. Patellar tendinitis: the significance of magnetic resonance imaging findings. Am J Sports Med. 1999;27(3):345-349. doi:10.1177/03635465990270031301.

    24. Reiff DB, Heenan SD, Heron CW. MRI appearances of the asymptomatic patellar tendon on gradient echo imaging. Skeletal Radiol. 1995;24(2):123-126. doi:10.1007/BF00198074.
     

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    TAKE-HOME POINTS

    • Extensor mechanism pathology is a common finding in patients with ACL injuries.
    • Extensor mechanism pathology such as a multipartite patella, unresolved Osgood-Schlatter’s disease, and patella tendinopathy are easily identifiable on standard imaging.
    • It is unknown what type of effect, if any, these pathologies may have on graft strength.
    • The bone-patella tendon-bone and quadriceps autograft are the most likely to be affected.
    • Surgeons should take into account existing extensor mechanism pathology when considering individual patient graft selection for ACL reconstruction.
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