Orthopedics

CHICAGO – 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.

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.

CHICAGO – 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.

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.

CHICAGO – 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.

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.

SAN DIEGO – Point-of-care ultrasound should be the go-to approach for the routine assessment of suspected shoulder dislocations in the ED, based on data from a prospective, multicenter study presented at the annual meeting of the American College of Emergency Physicians.

In the observational study, the average time needed to diagnose shoulder dislocation using ultrasound was 18 seconds, far faster than time from triage to x-ray, according to Michael Secko, MD, director of the emergency ultrasound division at Stony Brook University (NY).

The results from this study, called MUDDS (Musculoskeletal Ultrasound to Diagnose Dislocated Shoulders), support point-of-care ultrasound as a faster and more readily performed alternative to x-ray. Of the 46 adult patients enrolled so far in the ongoing study, ultrasound’s sensitivity has been 96% and its specificity 100% when validated by x-ray findings.

In the study, adults presenting to the ED are evaluated with point-of-care ultrasound from a posterior approach using either a curvilinear or linear transducer in the transverse plane. About half of the patients enrolled so far had injuries caused by falls, and many of the others had a shoulder complaint related to being pulled. Slightly more than one-third had a previous shoulder dislocation.

When evaluated with point-of-care ultrasound and x-ray, 23 of the 42 evaluable patients had a dislocation. The time from triage to ultrasound evaluation averaged 60 minutes, 40 minutes faster than the average of 100 minutes from triage to x-ray. Both tests were ordered at the same time.

Ultrasound performed less well for the diagnosis of a fracture, with a sensitivity of only 53%. Dr. Secko said the anterior approach would not be expected to provide a comprehensive assessment for fracture. He noted, for example, that there was no attempt in this study to evaluate patients for the presence of Bankart lesions. However, in those found to have a fracture on point-of-care ultrasound, the specificity of this imaging tool was 96%.

Ultimately, a major goal of this study was to determine whether a posterior point-of-care ultrasound could provide a quick answer to the question, “is it in or out?” Although patients are still being enrolled, Dr. Secko believed there is already good evidence that ultrasound is fast and effective for diagnosing dislocations.

Others have addressed this same question. Citing a meta-analysis published last year, Dr. Secko reported that all but one of four studies evaluating ultrasound for shoulder dislocations found a sensitivity and specificity of 100% (Gottlieb M et al. West J Emerg Med. 2017 Aug;18[5]:937-942).

Many centers have already switched to ultrasound for the evaluation of shoulder dislocations, according to Andrew S. Liteplo, MD, who moderated the ACEP session in which Dr. Secko presented his data. “If you are not already doing this for suspected shoulder dislocation, start right away because it is easy and awesome,” said Dr. Liteplo, who is chief of the division of ultrasound in emergency medicine at Massachusetts General Hospital, Boston. He also advised that ultrasound can also can be performed after reduction to confirm the efficacy of treatment.

Dr. Secko reported no financial relationships relevant to this study.
 

SAN DIEGO – Point-of-care ultrasound should be the go-to approach for the routine assessment of suspected shoulder dislocations in the ED, based on data from a prospective, multicenter study presented at the annual meeting of the American College of Emergency Physicians.

In the observational study, the average time needed to diagnose shoulder dislocation using ultrasound was 18 seconds, far faster than time from triage to x-ray, according to Michael Secko, MD, director of the emergency ultrasound division at Stony Brook University (NY).

The results from this study, called MUDDS (Musculoskeletal Ultrasound to Diagnose Dislocated Shoulders), support point-of-care ultrasound as a faster and more readily performed alternative to x-ray. Of the 46 adult patients enrolled so far in the ongoing study, ultrasound’s sensitivity has been 96% and its specificity 100% when validated by x-ray findings.

In the study, adults presenting to the ED are evaluated with point-of-care ultrasound from a posterior approach using either a curvilinear or linear transducer in the transverse plane. About half of the patients enrolled so far had injuries caused by falls, and many of the others had a shoulder complaint related to being pulled. Slightly more than one-third had a previous shoulder dislocation.

When evaluated with point-of-care ultrasound and x-ray, 23 of the 42 evaluable patients had a dislocation. The time from triage to ultrasound evaluation averaged 60 minutes, 40 minutes faster than the average of 100 minutes from triage to x-ray. Both tests were ordered at the same time.

Ultrasound performed less well for the diagnosis of a fracture, with a sensitivity of only 53%. Dr. Secko said the anterior approach would not be expected to provide a comprehensive assessment for fracture. He noted, for example, that there was no attempt in this study to evaluate patients for the presence of Bankart lesions. However, in those found to have a fracture on point-of-care ultrasound, the specificity of this imaging tool was 96%.

Ultimately, a major goal of this study was to determine whether a posterior point-of-care ultrasound could provide a quick answer to the question, “is it in or out?” Although patients are still being enrolled, Dr. Secko believed there is already good evidence that ultrasound is fast and effective for diagnosing dislocations.

Others have addressed this same question. Citing a meta-analysis published last year, Dr. Secko reported that all but one of four studies evaluating ultrasound for shoulder dislocations found a sensitivity and specificity of 100% (Gottlieb M et al. West J Emerg Med. 2017 Aug;18[5]:937-942).

Many centers have already switched to ultrasound for the evaluation of shoulder dislocations, according to Andrew S. Liteplo, MD, who moderated the ACEP session in which Dr. Secko presented his data. “If you are not already doing this for suspected shoulder dislocation, start right away because it is easy and awesome,” said Dr. Liteplo, who is chief of the division of ultrasound in emergency medicine at Massachusetts General Hospital, Boston. He also advised that ultrasound can also can be performed after reduction to confirm the efficacy of treatment.

Dr. Secko reported no financial relationships relevant to this study.
 

SAN DIEGO – Point-of-care ultrasound should be the go-to approach for the routine assessment of suspected shoulder dislocations in the ED, based on data from a prospective, multicenter study presented at the annual meeting of the American College of Emergency Physicians.

In the observational study, the average time needed to diagnose shoulder dislocation using ultrasound was 18 seconds, far faster than time from triage to x-ray, according to Michael Secko, MD, director of the emergency ultrasound division at Stony Brook University (NY).

The results from this study, called MUDDS (Musculoskeletal Ultrasound to Diagnose Dislocated Shoulders), support point-of-care ultrasound as a faster and more readily performed alternative to x-ray. Of the 46 adult patients enrolled so far in the ongoing study, ultrasound’s sensitivity has been 96% and its specificity 100% when validated by x-ray findings.

In the study, adults presenting to the ED are evaluated with point-of-care ultrasound from a posterior approach using either a curvilinear or linear transducer in the transverse plane. About half of the patients enrolled so far had injuries caused by falls, and many of the others had a shoulder complaint related to being pulled. Slightly more than one-third had a previous shoulder dislocation.

When evaluated with point-of-care ultrasound and x-ray, 23 of the 42 evaluable patients had a dislocation. The time from triage to ultrasound evaluation averaged 60 minutes, 40 minutes faster than the average of 100 minutes from triage to x-ray. Both tests were ordered at the same time.

Ultrasound performed less well for the diagnosis of a fracture, with a sensitivity of only 53%. Dr. Secko said the anterior approach would not be expected to provide a comprehensive assessment for fracture. He noted, for example, that there was no attempt in this study to evaluate patients for the presence of Bankart lesions. However, in those found to have a fracture on point-of-care ultrasound, the specificity of this imaging tool was 96%.

Ultimately, a major goal of this study was to determine whether a posterior point-of-care ultrasound could provide a quick answer to the question, “is it in or out?” Although patients are still being enrolled, Dr. Secko believed there is already good evidence that ultrasound is fast and effective for diagnosing dislocations.

Others have addressed this same question. Citing a meta-analysis published last year, Dr. Secko reported that all but one of four studies evaluating ultrasound for shoulder dislocations found a sensitivity and specificity of 100% (Gottlieb M et al. West J Emerg Med. 2017 Aug;18[5]:937-942).

Many centers have already switched to ultrasound for the evaluation of shoulder dislocations, according to Andrew S. Liteplo, MD, who moderated the ACEP session in which Dr. Secko presented his data. “If you are not already doing this for suspected shoulder dislocation, start right away because it is easy and awesome,” said Dr. Liteplo, who is chief of the division of ultrasound in emergency medicine at Massachusetts General Hospital, Boston. He also advised that ultrasound can also can be performed after reduction to confirm the efficacy of treatment.

Dr. Secko reported no financial relationships relevant to this study.
 

CHICAGO – Encouraging patients with knee osteoarthritis to engage in brisk walking for at least 5 minutes per day pays big dividends in terms of reduced risk of total knee replacement, according to a new analysis of data from the National Institutes of Health-sponsored Osteoarthritis Initiative.
 

Vidyard Video

Whether walking increases or decreases the risk of structural deterioration and total knee replacement (TKR) in patients with knee osteoarthritis has been a controversial topic marked by conflicting data. That’s probably because prior studies haven’t taken into account walking intensity, Hiral Master said at the annual meeting of the American College of Rheumatology.

Ms. Master, a PhD candidate in physical therapy at the University of Delaware, Newark, presented a study of 1,854 patients with knee osteoarthritis who participated in the Osteoarthritis Initiative, all of whom had worn an accelerometer. This permitted calculation of time spent walking at various intensities. Subjects spent an average of 459 minutes per day not walking and 8 minutes walking at moderate to vigorous intensity, defined as a cadence of more than 100 steps per minute.


During 5 years of follow-up, the incidence of TKR was 6%. In this video interview, Ms. Master explains that patients who replaced 5 minutes of not walking with 5 minutes of brisk walking daily had an adjusted 14% reduction in the risk of TKR. A dose-response was evident, with more minutes of moderate to vigorous walking being associated with progressively larger reductions in the risk of this major surgery. Walking at a cadence of less than 100 steps per minute, regardless of duration, was nonprotective.

bjancin@mdedge.com

SOURCE: Master H et al. Arthritis Rheumatol. 2018;70(Suppl 10), Abstract 1166.

CHICAGO – Encouraging patients with knee osteoarthritis to engage in brisk walking for at least 5 minutes per day pays big dividends in terms of reduced risk of total knee replacement, according to a new analysis of data from the National Institutes of Health-sponsored Osteoarthritis Initiative.
 

Vidyard Video

Whether walking increases or decreases the risk of structural deterioration and total knee replacement (TKR) in patients with knee osteoarthritis has been a controversial topic marked by conflicting data. That’s probably because prior studies haven’t taken into account walking intensity, Hiral Master said at the annual meeting of the American College of Rheumatology.

Ms. Master, a PhD candidate in physical therapy at the University of Delaware, Newark, presented a study of 1,854 patients with knee osteoarthritis who participated in the Osteoarthritis Initiative, all of whom had worn an accelerometer. This permitted calculation of time spent walking at various intensities. Subjects spent an average of 459 minutes per day not walking and 8 minutes walking at moderate to vigorous intensity, defined as a cadence of more than 100 steps per minute.


During 5 years of follow-up, the incidence of TKR was 6%. In this video interview, Ms. Master explains that patients who replaced 5 minutes of not walking with 5 minutes of brisk walking daily had an adjusted 14% reduction in the risk of TKR. A dose-response was evident, with more minutes of moderate to vigorous walking being associated with progressively larger reductions in the risk of this major surgery. Walking at a cadence of less than 100 steps per minute, regardless of duration, was nonprotective.

bjancin@mdedge.com

SOURCE: Master H et al. Arthritis Rheumatol. 2018;70(Suppl 10), Abstract 1166.

CHICAGO – Encouraging patients with knee osteoarthritis to engage in brisk walking for at least 5 minutes per day pays big dividends in terms of reduced risk of total knee replacement, according to a new analysis of data from the National Institutes of Health-sponsored Osteoarthritis Initiative.
 

Vidyard Video

Whether walking increases or decreases the risk of structural deterioration and total knee replacement (TKR) in patients with knee osteoarthritis has been a controversial topic marked by conflicting data. That’s probably because prior studies haven’t taken into account walking intensity, Hiral Master said at the annual meeting of the American College of Rheumatology.

Ms. Master, a PhD candidate in physical therapy at the University of Delaware, Newark, presented a study of 1,854 patients with knee osteoarthritis who participated in the Osteoarthritis Initiative, all of whom had worn an accelerometer. This permitted calculation of time spent walking at various intensities. Subjects spent an average of 459 minutes per day not walking and 8 minutes walking at moderate to vigorous intensity, defined as a cadence of more than 100 steps per minute.


During 5 years of follow-up, the incidence of TKR was 6%. In this video interview, Ms. Master explains that patients who replaced 5 minutes of not walking with 5 minutes of brisk walking daily had an adjusted 14% reduction in the risk of TKR. A dose-response was evident, with more minutes of moderate to vigorous walking being associated with progressively larger reductions in the risk of this major surgery. Walking at a cadence of less than 100 steps per minute, regardless of duration, was nonprotective.

bjancin@mdedge.com

SOURCE: Master H et al. Arthritis Rheumatol. 2018;70(Suppl 10), Abstract 1166.

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).

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).

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.

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.

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.

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.

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).

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).

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.

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%.

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).

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).

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.

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.

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.

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.

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).

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).

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.

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%.

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).

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).

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.

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.

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.

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.

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).

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).

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.

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%.

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

The ankle is one of the most commonly injured joints in soccer and represents a significant cost to the healthcare system. The ligaments that stabilize the ankle joint determine its biomechanics—alterations of which result from various soccer-related injuries. Acute sprains are among the most common injury in soccer players and are generally treated conservatively, with emphasis placed on secondary prevention to reduce the risk for future sprains and progression to chronic ankle instability. Repetitive ankle injuries in soccer players may cause chronic ankle instability, which includes both mechanical ligamentous laxity and functional changes. Chronic ankle pathology often requires surgery to repair ligamentous damage and remove soft-tissue or osseous impingement. Proper initial treatment, rehabilitation, and secondary prevention of ankle injuries can limit the amount of time lost from play and avoid negative long-term sequelae (eg, osteochondral lesions, arthritis). On the other hand, high ankle sprains portend a poorer prognosis and a longer recovery. These injuries will typically require surgical stabilization. Impingement-like syndromes of the ankle can undergo an initial trial of conservative treatment; when this fails, however, soccer players respond favorably to arthroscopic debridement of the lesions causing impingement. Finally, other pathologies (eg, stress fractures) are highly encouraged to be treated with surgical stabilization in elite soccer players.

Continue to: EPIDEMIOLOGY

 

 

EPIDEMIOLOGY

With roughly 200,000 professional and around 240 million amateur soccer players, soccer has been recognized as the most popular sport worldwide. Nevertheless, given its rising popularity in society, one must also consider the increasing incidence of injuries as a result. Elite soccer players sustain between 10 and 35 injuries per 1000 competitive playing hours.¹ Approximately 80% are traumatic, and 20% are overuse injuries.² Soccer injuries are more frequent with increasing age of the participants, whereas the incidence of injuries in preadolescent players is low. The incidence of injuries has been found to be higher during competition when compared with practice/training sessions, with some studies showing that 59% of injuries occurred during games.² Amateur or recreational soccer players sustain fewer injuries than professional soccer players, as one would expect, given both the higher intensity of training and match schedule in professionals.

The ankle is one of the most commonly injured joints in soccer, with some studies suggesting it comprises one-fifth of all injuries sustained during soccer, which is only second to those of the knee.² Ankle sprains specifically are quite a common occurrence in soccer.^3-9 A recent study of an English premier league club showed that over a 4-season period, 20% of injuries were of the foot and ankle with a mean return to sport time of 54 days.¹⁰ Of all foot and ankle related injuries, ankle sprains are the most common, followed by bruises/contusions, and tendon lesions. Fractures are very rare (1%) in soccer, but when they do occur they impart a much more extended recovery. During the 2010 Fédération Internationale de Football Association (FIFA) World Cup, ankle sprains were among the most common injuries and approximately half lead to players missing training or competitive matches.⁵

ANATOMY

Knowledge of the biomechanics of both the foot and ankle joints is essential to understand soccer injuries. The ankle joint (talocrural articulation) consists of the distal ends of the tibia and fibula, which form the mortise, and the superior aspect of the talar dome.¹¹ As a hinge joint, the ankle provides 20° of dorsiflexion and 50° of plantar flexion,¹² with stability provided by the lateral, medial, and superior ligamentous complexes. The superior articular surface of the talus is narrower posteriorly, which creates a looser fit within the mortise during plantar flexion.¹¹ This decreased stability could help explain why the most common injury in soccer involves a plantar flexion mechanism.^13,14 Inferiorly, the talus articulates with the calcaneus to form the subtalar joint. It is at this site that the majority of both foot inversion and eversion occurs. The transverse tarsal joints (Chopart’s joints) separate the hindfoot from the midfoot. Movement of this joint depends on the relative alignment of its 2 articulations: the talonavicular and calcaneocuboid joints. During foot eversion, these 2 joints are parallel to each other allowing supple motion and aiding in shock absorption during the heel strike phase of the gait cycle. With foot inversion, the joints become nonparallel and thus lock the transverse tarsal joints providing a rigid lever needed for push-off.^11,12

LATERAL LIGAMENTS

The ankle joint is stabilized laterally by a ligament complex consisting of 3 individual ligaments, all originating from the lateral malleolus: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular ligament (CFL) (Figure 1).^11,12,15 The ATFL is the primary restraint to inversion in plantar flexion, and it helps resist anterolateral translation of the talus in the mortise. However, it is the weakest and therefore the most frequently injured of the lateral ligaments. The PTFL plays only a supplementary role in ankle stability when the lateral ligament complex is intact. It is under the greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the mortise as well as talar external rotation.^13,16 The CFL is the primary restraint to inversion in the neutral or dorsiflexed position. It restrains subtalar inversion, thereby limiting talar tilt within the mortise.

DELTOID LIGAMENT

The deltoid ligament complex consists of 6 continuous adjacent superficial and deep ligaments that function synergistically to resist valgus and pronation forces, as well as external rotation of the talus in the mortise.^11-13,17 The superficial layer crosses both ankle and subtalar joints. It originates from the anterior colliculus and fans out to insert into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle. The tibiocalcaneal (sustentaculum tali) portion is the strongest component in the superficial layer and resists calcaneal eversion. The deep layer crosses the ankle joint only. It functions as the primary stabilizer of the medial ankle and prevents both lateral displacement and external rotation of the talus. It originates from the inferior and posterior aspects of the medial malleolus and inserts on the medial and posteromedial aspects of the talus.^12,17,18

Continue to: SYNDESMOSIS

 

 

SYNDESMOSIS

The ankle syndesmosis, or inferior tibiofibular joint, is the distal articulation between the tibia and fibula. The syndesmosis contributes to ankle mortise integrity through its firm fixation of the lateral malleolus against the lateral surface of the talus. Ligaments comprising the ankle syndesmosis include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the inferior transverse ligament, and the interosseous ligament (IOL).¹²

ANKLE SPRAINS

Ankle sprains are the most common pathology encountered amongst soccer players, representing from one-half to two-thirds of all ankle related injuries. Most sprains occur outside of player contact.

LATERAL ANKLE SPRAINS AND INSTABILITY

Injury to the lateral ligaments of the ankle represents 77% to 91% of all ankle sprains in soccer.^6,19 The greatest risk factor for an ankle sprain in a soccer player is a history of prior sprain.²⁰ Other risk factors include increasing age, player-to-player contact, condition of the pitch, weight-bearing status of the injured limb at the time of injury, and joint instability or laxity.^21,22

The evaluation of an ankle sprain to determine its severity is best done after the acute phase, approximately 4 to 7 days after the initial injury when both pain and swelling have subsided.²³ The anterior drawer (ATFL instability) and talar tilt (CFL instability) tests are useful in evaluating ankle instability in the delayed or chronic setting; however, both have been shown to have limited sensitivity and significant variability amongst different examiners.²⁴

Clinical examination will direct further diagnostic tests including X-rays, magnetic resonance imaging (MRI), and computed tomography (CT). The Ottawa ankle rules are generally helpful in determining whether plain X-rays are indicated in the acute setting.^25,26 (Figure 2) According to these rules, ankle radiographs should be obtained if ankle pain is reported near the malleoli and 1 or more of the following is seen during examination: inability to bear weight immediately after injury and for 4 steps in the emergency department, and bony tenderness at the posterior edge or tip of the malleolus. Stress X-rays are generally not indicated in acute injuries but may be useful in chronic ankle instability cases.²³

Continue to: Ankle sprains cover...

Ankle sprains cover a broad spectrum of injuries; therefore, a grading system was devised to aid in guiding treatment. Grade I (mild) sprains are those with minimal swelling and tenderness but have the ligaments still intact. Grade II (moderate) sprains occur when there are partial ligament tears associated with moderate pain, swelling, and tenderness. Finally, Grade III (severe) sprains are complete ligament tears with marked swelling, hemorrhage, tenderness, loss of function, and abnormal joint motion and instability.^{23, 24}

Initial treatment for all ankle sprains is nonoperative and involves the RICE (rest, ice, compression, elevation) protocol with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute phase (first 4-5 days) with a short period (no >2 weeks) of immobilization.²⁷ Most authors agree that early mobilization followed by phased rehabilitation is warranted to minimize time away from sports.^28-31 Prolonged immobilization (>2 weeks) has detrimental effects and may lead to a longer return to play.^28-31 The rehabilitation protocol is divided into stages: (1) pain and edema control, (2) range of motion (ROM) and strengthening exercises, (3) soccer specific functional training, and (4) prophylactic intervention with balance and proprioception exercises. Surgical intervention is rarely indicated for acute ankle sprains. There are exceptions, however, such as when ankle sprains are associated with other injuries that require acute intervention (eg, fracture, osteochondral lesion). Surgery is indicated in the setting of chronic, recurrent mechanical instability. Anatomical repairs (modified Brostrom) seem to produce better outcomes than non-anatomical reconstructions (eg, Chrisman-Snook). Surgical outcomes are good, and most athletes are able to return to their pre-injury level of function.³²

In athletes, prevention of recurrent sprains is key. Braces may help prevent ankle sprains and bracing has been shown to be superior to taping, as tape loses its restrictive properties within 20 to 30 minutes of initiating activity.^33,34 Application of an orthosis (lace-up ankle orthosis) has been shown to reduce the incidence of ankle re-injury in soccer players with previous ankle sprains. Several studies have found minimal, if any, effect of orthoses on athletic performance.^20,35,36 Low-profile braces for soccer have been developed which allow for minimal disruption of the player’s boot and space proximally to insert the shin guard. Another essential component of prevention is prophylactic intervention with balance and proprioceptive exercises. A study looking at first division men’s league football (soccer) players in Iran showed a significant decrease in re-injury rates with proprioceptive training.³⁷ In 2003, FIFA introduced a comprehensive warm-up program (FIFA 11+), which has since been shown in several studies to decrease the risk of injury in amateur soccer players.^38-40

MEDIAL ANKLE SPRAINS AND INSTABILITY

Soccer places an unusually high demand on both the medial foot and ankle structures when compared with other sports. For instance, striking the ball requires the player to abduct and externally rotate the foot, which preloads medial structures.⁹ Hintermann¹⁸ looked at 54 cases of medial ankle instability and found that injury commonly occurred during landing on an uneven surface, which applies to soccer players when landing after heading the ball or jumping over a tackle. Pronation with eversion and extreme rotational injuries are well known to cause deltoid ligament injury. However, complete rupture of the deltoid ligament is rare and is more often associated with ankle fractures.⁴¹ Due to its close proximity and similarly shared function in medial plantar arch stabilization with the tibiospring and spring ligaments, posterior tibialis tendon dysfunction is also frequently seen in medial ankle instability.¹⁷ After an acute injury, patients can present with a medial ankle hematoma and pain along the deltoid ligament. Although chronic insufficiency is diagnosed based on the feeling of “giving way,” pain in the medial gutter of the ankle and a valgus and pronation deformity of the foot can be corrected by activating the peroneus tertius muscle. Arthroscopy is the most specific way to confirm clinically suspected instability of the medial ankle; however, MRI can demonstrate loss of organized medial fibers (Figures 3A, 3B).¹⁸ Primary surgical repair of deltoid ligament tears yield good to excellent results and should be considered in the soccer player to prevent problems associated with chronic non-repaired tears such as instability, osteoarthritis, and impingement syndromes.¹⁸ After surgical repair, players will undergo extensive physical therapy that progresses to sport-specific exercises with the ultimate goal of returning to competitive play around 4-6 months post-operatively.

HIGH ANKLE SPRAINS (SYNDESMOSIS)

High ankle sprains are much less common than low ankle sprains; however, when they do occur they portend a lengthier rehabilitation and a poorer prognosis, especially if undiagnosed. Lubberts and colleagues⁴² studied the epidemiology of isolated syndesmotic injuries in professional football players. They pooled data from 15 consecutive seasons of European professional football between 2001 and 2016. They examined a total of 3677 players from 61 teams across 17 countries. There were 1320 ankle ligament injuries registered during 15 seasons, of which 94 (7%) were isolated syndesmotic injuries. The incidence of these injuries increased annually between 2001 and 2016. Injuries were 74% contact-related, and isolated syndesmotic injuries were followed by a mean of a 39-day absence.⁴² Moreover, football players may have an increased risk of syndesmotic sprains due to foot planting and cutting action.⁴¹

Continue to: These injuriesa are typically...

These injuries are typically identified with pain over the AITFL and interosseous membrane. Physical examination tests that help identify syndesmotic injuries include the squeeze test, external rotation test, and crossed-leg test.⁴¹ The diagnosis can be made on plain X-ray when there is clear diastasis between the distal tibia and fibula. Two critical measurements on plain films are made 1 cm above the tibial plafond and are used to evaluate the integrity of the syndesmosis: tibiofibular clear space >6 mm, and tibiofibular overlap <1 mm, which indicate disruption of the syndesmosis.⁴³ More subtle injuries can be diagnosed with better sensitivity and specificity using MRI, which can also reveal secondary findings such as bone bruises, ATFL injury, osteochondral lesions, and tibiofibular incongruity.^44,45 Arthroscopy is an invaluable diagnostic tool for syndesmotic injuries with a characteristic triad finding of PITFL scarring, disrupted interosseous ligament, and posterolateral tibial plafond chondral damage.⁴⁶

Classification of the ligaments involved can aid in the selection of appropriate treatment. Grade I injuries involve AITFL tears. Grade IIa injuries involve AITFL and IOL tears. Grade IIb injuries include AITFL, PITFL, and IOL tears. Grade III injuries involve injury to all 3 ligaments, as well as a fibular fracture. Conservative treatment is recommended for Grades I and IIa, while surgical intervention is necessary for Grades IIb and III (Figures 4A, 4B). Compared with other ankle sprains, syndesmotic injuries typically require a more prolonged recovery/rehabilitation. Some studies suggest that these injuries require twice as long to heal.⁴⁷ Hopkinson and colleagues⁴⁸ reported a mean recovery time of 55 days following syndesmotic injuries in cadets at the United States Military Academy at West Point. Some surgeons advocate surgical intervention in professional athletes with mild sprains to expedite return to play.⁴⁹

Surgery has been well established as necessary in more severe injuries where there is clear diastasis or instability of the syndesmosis. Traditionally, screws were used for surgical fixation; however, they often required a second surgery for subsequent removal. There is no general consensus on the optimal screw size, level of placement, or timing of removal.^50,51 More recently, non-absorbable suture button fixation (eg, TightRope; Arthrex) has become more popular and provides certain advantages over screw fixation, such as avoiding the need for hardware removal. TightRope has been shown to provide more accurate stabilization of the syndesmosis as compared with screw fixation.⁵² Since malreduction is the most important indicator of poor long-term functional outcome, suture button fixation should be considered in the treatment of the football player.⁵³ Finally, Colcuc and colleagues⁵⁴ reported a lower complication rate and earlier return to sports in patients treated with knotless suture button devices compared with screw fixation.

OSTEOCHONDRAL LESIONS

Osteochondral lesions (OCLs) are cartilage-bone defects that are usually located in the talus. They can be caused by an acute traumatic event or repetitive microtrauma with no apparent history of trauma (eg, ankle instability). Acute OCLs can occur in soccer secondary to an ankle sprain or ankle fracture. Symptoms of OCLs include pain, swelling, and mechanical symptoms such as catching or locking, and on physical examination, one might see an effusion. The initial imaging modality of choice is radiographing; however, in ankle sprains with continued pain and swelling MRI may be indicated to rule out an underlying OCL. Missed acute lesions have a tendency not to heal and become chronic lesions, which can cause pain and playing disability. It is well established that chronic ankle instability is an important etiologic factor for OCLs. With the normal hydrostatic pressure within the ankle joint, synovial fluid gets pushed into cartilage/bone fissures, which can then lead to cystic degeneration of the subchondral bone.^55-57

Surgical repair of an OCL is dependent on both the size and location of the lesion. Acute lesions can be managed by arthroscopic débridement, microfracture, or fixation of the lesion if enough bone remains attached to the chondral lesion. Return to play is based on development and maturation of fibrocartilage over the lesion (debridement/microfracture) or healing and incorporation of the new graft (chondral repair procedures). Meanwhile, chronic lesions can be managed in 1-stage (microfracture, osteochondral autograft transfer or 2-stage (autologous chondrocyte implantation [ACI]) procedures.^56-57 Additional biologic healing augmentation with platelet-rich plasma has been described as well.⁵⁸ Newer techniques in treating chronic talus OCLs, including ones that have failed to respond to bone marrow stimulation techniques, have been developed more recently such as the use of particulated juvenile articular cartilage allograft (DeNovo NT Natural Tissue Graft^®; Zimmer Biomet).⁵⁹ These newer techniques avoid the need for a 2-stage procedure, as is the case with ACI.

Continue to: Further studies are needed...

Further studies are needed to both investigate long-term outcomes and determine the superiority of the arthroscopic juvenile cartilage procedure compared with microfracture and other cartilage resurfacing procedures. When surgically treating OCLs, one must also restore normal ankle joint biomechanics for the lesion to heal. For instance, in the presence of ankle instability, ligament reconstruction must be performed. Also, one should also consider addressing any hindfoot malalignment with an osteotomy (calcaneus, supramalleolar). In a recent retrospective study, van Eekeren and colleagues⁶⁰ showed that approximately 76% of patients were able to return to sports at long-term follow-up after arthroscopic débridement and bone marrow stimulation of talar OCLs. However, the activity level decreased at long-term follow-up and never attained the pre-injury level.⁶⁰

ANKLE IMPINGEMENT

ANTERIOR ANKLE IMPINGEMENT (FOOTBALLER'S ANKLE)

Anterior ankle impingement is caused by anterior osteophytes on both the distal tibia and talar neck. It is thought to be related to repetitive microtrauma to the anteromedial aspect of the ankle from recurrent ball impact.⁶¹ It is very common amongst soccer players with some studies suggesting that 60% of soccer players have this syndrome. Ankle impingement is characterized by anterior pain with ankle dorsiflexion, decreased dorsiflexion, and swelling. It is primarily diagnosed with lateral ankle X-rays, which will show the osteophytes. An oblique anteromedial X-ray may increase detection of osteophytes (Figure 5). The early stages of anterior impingement can be treated successfully with injections and heel lifts. Treatment of lesions that fail to respond to conservative management involves arthroscopic or open excision of osteophytes. Most patients with no preexisting osteoarthritis treated arthroscopically will experience pain relief and return to full activity, though recurrent osteophyte formation has been noted at long-term follow-up.⁶²

Anterior ankle impingement is most often caused by acute ankle sprains with an inversion type of mechanism.⁶² The subsequent reactive inflammation can cause fibrosis leading to distal fascicle enlargement of the AITFL. Impingement in the anterolateral gutter of this enlarged fascicle can also cause both chronic reactive synovitis and chondromalacia of the lateral talar dome.⁶³ MRI can identify abnormal areas of pathology; however, 50% of cases are diagnosed based on clinical examination alone.⁶³ Patients generally present with a history of anterolateral ankle pain and swelling with an occasional popping or snapping sensation.

Soccer players commonly develop anterior bony impingement due to repetitive loading of the anterior ankle from striking the ball. This repetition can lead to osteophyte formation of the anterior distal tibia and talar neck. After the osteophytes form, decreased dorsiflexion can occur due to a mechanical stop and inflammation of the interposed capsule.

The patient will exhibit tenderness to palpation along the anterolateral aspect of the ankle, with pain elicited at extreme passive dorsiflexion.⁶² Initially, an injection with local anesthetic and corticosteroid can serve both a diagnostic and therapeutic purpose; however, patients who fail conservative treatment can be treated with arthroscopy and resection of the involved scar tissue and osteophytes. The best results are seen in those patients with no concurrent intra-articular lesions or ankle osteoarthritis (Figure 5).⁶² When treated non-operatively, a player may return to play when pain resolves; however, if treated surgically with arthroscopic debridement/resection, a player must wait until his surgical scars have healed prior to attempting return to play.

Continue to: ANTEROMEDIAL ANKLE IMPINGEMENT

 

 

ANTEROMEDIAL ANKLE IMPINGEMENT

Anteromedial ankle impingement is a less common ankle impingement syndrome. It is associated with eversion injuries or following medial malleolar or talar fractures.^64,65 Previous injury to the anterior tibiotalar fascicle of the deltoid complex leads to ligament thickening and subsequent impingement in the anteromedial corner of the talus. Adjacent fibrosis and synovitis are common consequences of impingement; however, osteophyte formation and chondral stripping along the anteromedial talus can also be seen. Patients typically complain of pain along the anteromedial joint line that is worse with activity, clicking or popping sensations, and painful, limited dorsiflexion. On examination, impingement can be detected through palpation over the anterior tibiotalar fascicle of the deltoid ligament and eversion or extreme passive dorsiflexion of the foot, all of which will elicit medial ankle tenderness.^17,62 Initial treatment consists of rest, physical therapy, and NSAIDs. Refractory cases may be amenable to arthroscopic or open resection of the anterior tibiotalar fascicle with débridement of any adjacent synovitis and scar tissue.⁶²

POSTERIOR ANKLE IMPINGEMENT

Posterior ankle impingement is often referred to as “os trigonum syndrome” since the posterior impingement is frequently associated with a prominent os trigonum. An os trigonum is an accessory ossicle representing the separated posterolateral tubercle of the talus. It is usually asymptomatic. However, in soccer players, pain can occur from impaction between the posterior tibial plafond and the os trigonum, or because of soft tissue compression between the 2 opposing osseous structures. The pain is due to repetitive microtrauma (ankle plantarflexion) or acute forced plantarflexion, which can present as an acute fracture of the os trigonum. Because soccer is a sport requiring both repetitive and extreme plantarflexion, it may predispose players to posterior ankle impingement (Figures 6A, 6B).^62,66

Clinically, it can be very difficult to detect and diagnose because the affected structures lie deep and it can coexist with other disease processes (eg, peroneal tendinopathy, Achilles tendinopathy).^62,66 Patients will complain of chronic deep posterior ankle pain that is worse with push-off activities (eg, jumping). On examination, patients will exhibit pain with palpation over the posterolateral process and with the crunch test. Lateral radiograph with the foot in plantar flexion will show the os trigonum impinged between the posterior tibial malleolus and the calcaneal tuberosity. An MRI will demonstrate the os trigonum as well as any associated inflammation and edema, while it can also demonstrate coexisting pathologies.

Initial treatment consists of rest, NSAIDs, and taping to prevent plantar flexion. Ultrasound-guided cortisone injection of the capsule and posterior bursa can be both therapeutic and diagnostic. A posterior injection can be used to temporize the symptoms so that the soccer player can make it through the season.

Surgical excision is saved for refractory cases, and this can be done either through an open posterolateral approach or arthroscopic techniques. Recently, Georgiannos and Bisbinas⁶⁷ showed in an athletic population that endoscopic excision had both a lower complication rate and a quicker return to sports compared with the traditional open approach. Carreira and colleagues⁶⁸ conducted a retrospective case series of 20 patients (mostly competitive athletes). They found that posterior ankle arthroscopy to address posterior impingement allowed for the maintenance or restoration of anatomic ROM of the ankle and hindfoot, ability to return to at least the previous level of activity, and improvement in objective assessment of pain relief and a higher level of function parameters.⁶⁸

Continue to: TENDON PATHOLOGY

 

 

TENDON PATHOLOGY

SUPERIOR PERONEAL RETINACULUM INJURY

The superior peroneal retinaculum (SPR) forms the roof of the superior peroneal tunnel. The tunnel contains the peroneus brevis and longus tendons and is bordered by the retromalleolar groove of the fibula and the lower aspect of the posterior intramuscular septum of the leg.^69,70 The SPR originates from the posterolateral ridge of the fibula and inserts onto the lateral calcaneus, and it is the primary restraint of the peroneal tendons within the retromalleolar sulcus.

Injury to the retinaculum results from both ankle dorsiflexion and inversion, and forceful reflex contraction of the peroneal muscles, which causes subluxation or dislocation of the contained tendons.⁶⁹ A high level of suspicion is required regarding these injuries since the mechanism of injury is similar to that of a simple lateral ankle sprain. In the setting of retrofibular pain, snapping or popping sensations around the lateral malleolus, or chronic ankle instability that worsens on uneven surfaces, one must consider an injury to the SPR.⁶⁹ Radiographs are not always diagnostic; however, occasionally on an internal rotation view, one may see a cortical avulsion off the distal tip of the lateral malleolus (“fleck sign”) indicating a rim fracture from an SPR injury (Figure 7). MRI is the best imaging modality to assess the peroneal tendons, as well as an SPR injury. Recently, ultrasound has grown in popularity and may be more useful, since it allows for dynamic evaluation of subluxating/dislocating tendons.⁶⁹

Conservative management is often associated with poor outcomes, and surgery is indicated for all acute and chronic dislocations in athletes.⁷¹ Anatomic reconstruction of the SPR is the preferred surgical method.⁷² Peroneus brevis debulking and fibular groove deepening may also augment the retinaculum repair.⁷³ van Dijk and colleagues in their systematic review showed that patients treated with both groove deepening and SPR repair have higher rates of return to the sport than patients treated with SPR repair alone.⁷⁴

STRESS FRACTURES

FIFTH METATARSAL

Fifth metatarsal stress fractures usually occur secondary to lateral overload or avulsion of the peroneus brevis. The fifth metatarsal base can be susceptible to injury in a cavovarus foot. Non-operative treatment typically requires a longer period of immobilization (boot or cast) and necessitates a longer period of non–weight-bearing (anywhere between 6-12 weeks). Therefore, surgery is typically recommended in athletes or in the setting of a recurrent base of the fifth metatarsal fracture to expedite healing and return to play. Return to play is still not recommended until there is evidence of radiographic healing of the fracture. There are certain distinctions with fifth metatarsal stress fractures regarding location and healing rates that need to be taken into account.^75,76 In particular, zone 2 injuries (Jones fractures) represent a vascular watershed area, making these fractures prone to nonunion with nonunion rates as high as 15% to 30%. Occasionally, the cavovarus deformity will require correction as well as a reduction in the risk of recurrence or nonunion. Surgical fixation most commonly consists of a single screw placed in an antegrade fashion.⁷⁷ One must pay attention to screw size since smaller diameter screws (<4.5 mm) are associated with delayed union or nonunion. Moreover, screws that are too long will straighten the curved metatarsal shaft and can lead to fracture distraction or malreduction (Figures 8A, 8B).⁷⁷

Patients have returned to competitive sports within 6 weeks; however, it should be noted that causes of failure were linked to early return and return to sports before a radiographic union can lead to failure of fixation. Ekstrand and van Dijk⁷⁸ studied a large group of professional soccer players and found that out of 13,754 injuries, 0.5% (67) were fifth metatarsal fractures. Of note, they found that 45% of players had prodromal symptoms. Furthermore, after surgical treatment the fractures healed faster, compared with conservative treatment (75% vs 33%); however, there was no significant difference in lay-off days between both groups (80 vs 74 days).⁷⁸ Matsuda and colleagues⁷⁹ looked at 335 male collegiate soccer players, 29 of whom had a history of a fifth metatarsal stress fracture. They found that playing the midfield position and having an everted rearfoot and inverted forefoot alignment were associated with fifth metatarsal stress fractures.⁷⁹ Saita and colleagues⁸⁰ found that restricted hip internal rotation was associated with an increased risk of developing a Jones fracture in 162 professional football players. Finally, Fujitaka and colleagues⁸¹ looked at 273 male soccer players between 2005 and 2013. They found an association between weak toe-grip strength and fifth metatarsal fractures, suggesting that weak toe-grip may lead to an increase in the load applied onto the lateral side of the foot, resulting in a stress fracture.⁸¹

Continue to: NAVICULAR

 

 

NAVICULAR

Another common tarsal bone that sustains stress fractures is the navicular. It is not as common as calcaneal stress fractures in military recruits but can occur in the same type of population, as well as explosive athletics such as sprinters and soccer players. It commonly presents with an indistinct vague achy pain with activity that improves with rest, and pain at the dorsum of the midfoot or along the medial longitudinal arch with activity. It can easily go undiagnosed for quite some time given the difficulty in visualizing the navicular with plain radiographs. Clinically, it is difficult to make the diagnosis, and therefore advanced imaging is necessary when the injury is suspected. Both MRI and CT scans can be used to understand the extent of the injury (Figures 9A-9C). In non-displaced stress fractures, conservative non-operative treatment is the appropriate treatment modality with a brief period of immobilization and non–weight-bearing;⁸² however, operative treatment is also considered in elite athletes. In either case, return to play is discouraged until there is evidence of radiographic healing. When a displacement is noted, or there is a delay in diagnosis, then operative treatment is recommended.

CONCLUSION

Ankle injuries are very common in soccer and can result in decreased performance or significant loss of playing time. Treatment of acute injury generally follows a conservative route, with surgical intervention reserved for severe ruptures or osteochondral fracture of the ankle joint. Chronic ankle pathology resulting in mechanical or functional instability generally requires surgery to repair ligamentous damage and restore normal ankle kinematics. It is critical for the soccer player to receive appropriate rehabilitation prior to returning to play in order to reduce the risk for reinjury and further chronic instability. Prevention and early intervention of ankle injuries is key in preventing the long-term sequelae of ankle injuries, such as arthritis, in former soccer players.

ABSTRACT

The ankle is one of the most commonly injured joints in soccer and represents a significant cost to the healthcare system. The ligaments that stabilize the ankle joint determine its biomechanics—alterations of which result from various soccer-related injuries. Acute sprains are among the most common injury in soccer players and are generally treated conservatively, with emphasis placed on secondary prevention to reduce the risk for future sprains and progression to chronic ankle instability. Repetitive ankle injuries in soccer players may cause chronic ankle instability, which includes both mechanical ligamentous laxity and functional changes. Chronic ankle pathology often requires surgery to repair ligamentous damage and remove soft-tissue or osseous impingement. Proper initial treatment, rehabilitation, and secondary prevention of ankle injuries can limit the amount of time lost from play and avoid negative long-term sequelae (eg, osteochondral lesions, arthritis). On the other hand, high ankle sprains portend a poorer prognosis and a longer recovery. These injuries will typically require surgical stabilization. Impingement-like syndromes of the ankle can undergo an initial trial of conservative treatment; when this fails, however, soccer players respond favorably to arthroscopic debridement of the lesions causing impingement. Finally, other pathologies (eg, stress fractures) are highly encouraged to be treated with surgical stabilization in elite soccer players.

Continue to: EPIDEMIOLOGY

 

 

EPIDEMIOLOGY

With roughly 200,000 professional and around 240 million amateur soccer players, soccer has been recognized as the most popular sport worldwide. Nevertheless, given its rising popularity in society, one must also consider the increasing incidence of injuries as a result. Elite soccer players sustain between 10 and 35 injuries per 1000 competitive playing hours.¹ Approximately 80% are traumatic, and 20% are overuse injuries.² Soccer injuries are more frequent with increasing age of the participants, whereas the incidence of injuries in preadolescent players is low. The incidence of injuries has been found to be higher during competition when compared with practice/training sessions, with some studies showing that 59% of injuries occurred during games.² Amateur or recreational soccer players sustain fewer injuries than professional soccer players, as one would expect, given both the higher intensity of training and match schedule in professionals.

The ankle is one of the most commonly injured joints in soccer, with some studies suggesting it comprises one-fifth of all injuries sustained during soccer, which is only second to those of the knee.² Ankle sprains specifically are quite a common occurrence in soccer.^3-9 A recent study of an English premier league club showed that over a 4-season period, 20% of injuries were of the foot and ankle with a mean return to sport time of 54 days.¹⁰ Of all foot and ankle related injuries, ankle sprains are the most common, followed by bruises/contusions, and tendon lesions. Fractures are very rare (1%) in soccer, but when they do occur they impart a much more extended recovery. During the 2010 Fédération Internationale de Football Association (FIFA) World Cup, ankle sprains were among the most common injuries and approximately half lead to players missing training or competitive matches.⁵

ANATOMY

Knowledge of the biomechanics of both the foot and ankle joints is essential to understand soccer injuries. The ankle joint (talocrural articulation) consists of the distal ends of the tibia and fibula, which form the mortise, and the superior aspect of the talar dome.¹¹ As a hinge joint, the ankle provides 20° of dorsiflexion and 50° of plantar flexion,¹² with stability provided by the lateral, medial, and superior ligamentous complexes. The superior articular surface of the talus is narrower posteriorly, which creates a looser fit within the mortise during plantar flexion.¹¹ This decreased stability could help explain why the most common injury in soccer involves a plantar flexion mechanism.^13,14 Inferiorly, the talus articulates with the calcaneus to form the subtalar joint. It is at this site that the majority of both foot inversion and eversion occurs. The transverse tarsal joints (Chopart’s joints) separate the hindfoot from the midfoot. Movement of this joint depends on the relative alignment of its 2 articulations: the talonavicular and calcaneocuboid joints. During foot eversion, these 2 joints are parallel to each other allowing supple motion and aiding in shock absorption during the heel strike phase of the gait cycle. With foot inversion, the joints become nonparallel and thus lock the transverse tarsal joints providing a rigid lever needed for push-off.^11,12

LATERAL LIGAMENTS

The ankle joint is stabilized laterally by a ligament complex consisting of 3 individual ligaments, all originating from the lateral malleolus: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular ligament (CFL) (Figure 1).^11,12,15 The ATFL is the primary restraint to inversion in plantar flexion, and it helps resist anterolateral translation of the talus in the mortise. However, it is the weakest and therefore the most frequently injured of the lateral ligaments. The PTFL plays only a supplementary role in ankle stability when the lateral ligament complex is intact. It is under the greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the mortise as well as talar external rotation.^13,16 The CFL is the primary restraint to inversion in the neutral or dorsiflexed position. It restrains subtalar inversion, thereby limiting talar tilt within the mortise.

DELTOID LIGAMENT

The deltoid ligament complex consists of 6 continuous adjacent superficial and deep ligaments that function synergistically to resist valgus and pronation forces, as well as external rotation of the talus in the mortise.^11-13,17 The superficial layer crosses both ankle and subtalar joints. It originates from the anterior colliculus and fans out to insert into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle. The tibiocalcaneal (sustentaculum tali) portion is the strongest component in the superficial layer and resists calcaneal eversion. The deep layer crosses the ankle joint only. It functions as the primary stabilizer of the medial ankle and prevents both lateral displacement and external rotation of the talus. It originates from the inferior and posterior aspects of the medial malleolus and inserts on the medial and posteromedial aspects of the talus.^12,17,18

Continue to: SYNDESMOSIS

 

 

SYNDESMOSIS

The ankle syndesmosis, or inferior tibiofibular joint, is the distal articulation between the tibia and fibula. The syndesmosis contributes to ankle mortise integrity through its firm fixation of the lateral malleolus against the lateral surface of the talus. Ligaments comprising the ankle syndesmosis include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the inferior transverse ligament, and the interosseous ligament (IOL).¹²

ANKLE SPRAINS

Ankle sprains are the most common pathology encountered amongst soccer players, representing from one-half to two-thirds of all ankle related injuries. Most sprains occur outside of player contact.

LATERAL ANKLE SPRAINS AND INSTABILITY

Injury to the lateral ligaments of the ankle represents 77% to 91% of all ankle sprains in soccer.^6,19 The greatest risk factor for an ankle sprain in a soccer player is a history of prior sprain.²⁰ Other risk factors include increasing age, player-to-player contact, condition of the pitch, weight-bearing status of the injured limb at the time of injury, and joint instability or laxity.^21,22

The evaluation of an ankle sprain to determine its severity is best done after the acute phase, approximately 4 to 7 days after the initial injury when both pain and swelling have subsided.²³ The anterior drawer (ATFL instability) and talar tilt (CFL instability) tests are useful in evaluating ankle instability in the delayed or chronic setting; however, both have been shown to have limited sensitivity and significant variability amongst different examiners.²⁴

Clinical examination will direct further diagnostic tests including X-rays, magnetic resonance imaging (MRI), and computed tomography (CT). The Ottawa ankle rules are generally helpful in determining whether plain X-rays are indicated in the acute setting.^25,26 (Figure 2) According to these rules, ankle radiographs should be obtained if ankle pain is reported near the malleoli and 1 or more of the following is seen during examination: inability to bear weight immediately after injury and for 4 steps in the emergency department, and bony tenderness at the posterior edge or tip of the malleolus. Stress X-rays are generally not indicated in acute injuries but may be useful in chronic ankle instability cases.²³

Continue to: Ankle sprains cover...

Ankle sprains cover a broad spectrum of injuries; therefore, a grading system was devised to aid in guiding treatment. Grade I (mild) sprains are those with minimal swelling and tenderness but have the ligaments still intact. Grade II (moderate) sprains occur when there are partial ligament tears associated with moderate pain, swelling, and tenderness. Finally, Grade III (severe) sprains are complete ligament tears with marked swelling, hemorrhage, tenderness, loss of function, and abnormal joint motion and instability.^{23, 24}

Initial treatment for all ankle sprains is nonoperative and involves the RICE (rest, ice, compression, elevation) protocol with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute phase (first 4-5 days) with a short period (no >2 weeks) of immobilization.²⁷ Most authors agree that early mobilization followed by phased rehabilitation is warranted to minimize time away from sports.^28-31 Prolonged immobilization (>2 weeks) has detrimental effects and may lead to a longer return to play.^28-31 The rehabilitation protocol is divided into stages: (1) pain and edema control, (2) range of motion (ROM) and strengthening exercises, (3) soccer specific functional training, and (4) prophylactic intervention with balance and proprioception exercises. Surgical intervention is rarely indicated for acute ankle sprains. There are exceptions, however, such as when ankle sprains are associated with other injuries that require acute intervention (eg, fracture, osteochondral lesion). Surgery is indicated in the setting of chronic, recurrent mechanical instability. Anatomical repairs (modified Brostrom) seem to produce better outcomes than non-anatomical reconstructions (eg, Chrisman-Snook). Surgical outcomes are good, and most athletes are able to return to their pre-injury level of function.³²

In athletes, prevention of recurrent sprains is key. Braces may help prevent ankle sprains and bracing has been shown to be superior to taping, as tape loses its restrictive properties within 20 to 30 minutes of initiating activity.^33,34 Application of an orthosis (lace-up ankle orthosis) has been shown to reduce the incidence of ankle re-injury in soccer players with previous ankle sprains. Several studies have found minimal, if any, effect of orthoses on athletic performance.^20,35,36 Low-profile braces for soccer have been developed which allow for minimal disruption of the player’s boot and space proximally to insert the shin guard. Another essential component of prevention is prophylactic intervention with balance and proprioceptive exercises. A study looking at first division men’s league football (soccer) players in Iran showed a significant decrease in re-injury rates with proprioceptive training.³⁷ In 2003, FIFA introduced a comprehensive warm-up program (FIFA 11+), which has since been shown in several studies to decrease the risk of injury in amateur soccer players.^38-40

MEDIAL ANKLE SPRAINS AND INSTABILITY

Soccer places an unusually high demand on both the medial foot and ankle structures when compared with other sports. For instance, striking the ball requires the player to abduct and externally rotate the foot, which preloads medial structures.⁹ Hintermann¹⁸ looked at 54 cases of medial ankle instability and found that injury commonly occurred during landing on an uneven surface, which applies to soccer players when landing after heading the ball or jumping over a tackle. Pronation with eversion and extreme rotational injuries are well known to cause deltoid ligament injury. However, complete rupture of the deltoid ligament is rare and is more often associated with ankle fractures.⁴¹ Due to its close proximity and similarly shared function in medial plantar arch stabilization with the tibiospring and spring ligaments, posterior tibialis tendon dysfunction is also frequently seen in medial ankle instability.¹⁷ After an acute injury, patients can present with a medial ankle hematoma and pain along the deltoid ligament. Although chronic insufficiency is diagnosed based on the feeling of “giving way,” pain in the medial gutter of the ankle and a valgus and pronation deformity of the foot can be corrected by activating the peroneus tertius muscle. Arthroscopy is the most specific way to confirm clinically suspected instability of the medial ankle; however, MRI can demonstrate loss of organized medial fibers (Figures 3A, 3B).¹⁸ Primary surgical repair of deltoid ligament tears yield good to excellent results and should be considered in the soccer player to prevent problems associated with chronic non-repaired tears such as instability, osteoarthritis, and impingement syndromes.¹⁸ After surgical repair, players will undergo extensive physical therapy that progresses to sport-specific exercises with the ultimate goal of returning to competitive play around 4-6 months post-operatively.

HIGH ANKLE SPRAINS (SYNDESMOSIS)

High ankle sprains are much less common than low ankle sprains; however, when they do occur they portend a lengthier rehabilitation and a poorer prognosis, especially if undiagnosed. Lubberts and colleagues⁴² studied the epidemiology of isolated syndesmotic injuries in professional football players. They pooled data from 15 consecutive seasons of European professional football between 2001 and 2016. They examined a total of 3677 players from 61 teams across 17 countries. There were 1320 ankle ligament injuries registered during 15 seasons, of which 94 (7%) were isolated syndesmotic injuries. The incidence of these injuries increased annually between 2001 and 2016. Injuries were 74% contact-related, and isolated syndesmotic injuries were followed by a mean of a 39-day absence.⁴² Moreover, football players may have an increased risk of syndesmotic sprains due to foot planting and cutting action.⁴¹

Continue to: These injuriesa are typically...

These injuries are typically identified with pain over the AITFL and interosseous membrane. Physical examination tests that help identify syndesmotic injuries include the squeeze test, external rotation test, and crossed-leg test.⁴¹ The diagnosis can be made on plain X-ray when there is clear diastasis between the distal tibia and fibula. Two critical measurements on plain films are made 1 cm above the tibial plafond and are used to evaluate the integrity of the syndesmosis: tibiofibular clear space >6 mm, and tibiofibular overlap <1 mm, which indicate disruption of the syndesmosis.⁴³ More subtle injuries can be diagnosed with better sensitivity and specificity using MRI, which can also reveal secondary findings such as bone bruises, ATFL injury, osteochondral lesions, and tibiofibular incongruity.^44,45 Arthroscopy is an invaluable diagnostic tool for syndesmotic injuries with a characteristic triad finding of PITFL scarring, disrupted interosseous ligament, and posterolateral tibial plafond chondral damage.⁴⁶

Classification of the ligaments involved can aid in the selection of appropriate treatment. Grade I injuries involve AITFL tears. Grade IIa injuries involve AITFL and IOL tears. Grade IIb injuries include AITFL, PITFL, and IOL tears. Grade III injuries involve injury to all 3 ligaments, as well as a fibular fracture. Conservative treatment is recommended for Grades I and IIa, while surgical intervention is necessary for Grades IIb and III (Figures 4A, 4B). Compared with other ankle sprains, syndesmotic injuries typically require a more prolonged recovery/rehabilitation. Some studies suggest that these injuries require twice as long to heal.⁴⁷ Hopkinson and colleagues⁴⁸ reported a mean recovery time of 55 days following syndesmotic injuries in cadets at the United States Military Academy at West Point. Some surgeons advocate surgical intervention in professional athletes with mild sprains to expedite return to play.⁴⁹

Surgery has been well established as necessary in more severe injuries where there is clear diastasis or instability of the syndesmosis. Traditionally, screws were used for surgical fixation; however, they often required a second surgery for subsequent removal. There is no general consensus on the optimal screw size, level of placement, or timing of removal.^50,51 More recently, non-absorbable suture button fixation (eg, TightRope; Arthrex) has become more popular and provides certain advantages over screw fixation, such as avoiding the need for hardware removal. TightRope has been shown to provide more accurate stabilization of the syndesmosis as compared with screw fixation.⁵² Since malreduction is the most important indicator of poor long-term functional outcome, suture button fixation should be considered in the treatment of the football player.⁵³ Finally, Colcuc and colleagues⁵⁴ reported a lower complication rate and earlier return to sports in patients treated with knotless suture button devices compared with screw fixation.

OSTEOCHONDRAL LESIONS

Osteochondral lesions (OCLs) are cartilage-bone defects that are usually located in the talus. They can be caused by an acute traumatic event or repetitive microtrauma with no apparent history of trauma (eg, ankle instability). Acute OCLs can occur in soccer secondary to an ankle sprain or ankle fracture. Symptoms of OCLs include pain, swelling, and mechanical symptoms such as catching or locking, and on physical examination, one might see an effusion. The initial imaging modality of choice is radiographing; however, in ankle sprains with continued pain and swelling MRI may be indicated to rule out an underlying OCL. Missed acute lesions have a tendency not to heal and become chronic lesions, which can cause pain and playing disability. It is well established that chronic ankle instability is an important etiologic factor for OCLs. With the normal hydrostatic pressure within the ankle joint, synovial fluid gets pushed into cartilage/bone fissures, which can then lead to cystic degeneration of the subchondral bone.^55-57

Surgical repair of an OCL is dependent on both the size and location of the lesion. Acute lesions can be managed by arthroscopic débridement, microfracture, or fixation of the lesion if enough bone remains attached to the chondral lesion. Return to play is based on development and maturation of fibrocartilage over the lesion (debridement/microfracture) or healing and incorporation of the new graft (chondral repair procedures). Meanwhile, chronic lesions can be managed in 1-stage (microfracture, osteochondral autograft transfer or 2-stage (autologous chondrocyte implantation [ACI]) procedures.^56-57 Additional biologic healing augmentation with platelet-rich plasma has been described as well.⁵⁸ Newer techniques in treating chronic talus OCLs, including ones that have failed to respond to bone marrow stimulation techniques, have been developed more recently such as the use of particulated juvenile articular cartilage allograft (DeNovo NT Natural Tissue Graft^®; Zimmer Biomet).⁵⁹ These newer techniques avoid the need for a 2-stage procedure, as is the case with ACI.

Continue to: Further studies are needed...

Further studies are needed to both investigate long-term outcomes and determine the superiority of the arthroscopic juvenile cartilage procedure compared with microfracture and other cartilage resurfacing procedures. When surgically treating OCLs, one must also restore normal ankle joint biomechanics for the lesion to heal. For instance, in the presence of ankle instability, ligament reconstruction must be performed. Also, one should also consider addressing any hindfoot malalignment with an osteotomy (calcaneus, supramalleolar). In a recent retrospective study, van Eekeren and colleagues⁶⁰ showed that approximately 76% of patients were able to return to sports at long-term follow-up after arthroscopic débridement and bone marrow stimulation of talar OCLs. However, the activity level decreased at long-term follow-up and never attained the pre-injury level.⁶⁰

ANKLE IMPINGEMENT

ANTERIOR ANKLE IMPINGEMENT (FOOTBALLER'S ANKLE)

Anterior ankle impingement is caused by anterior osteophytes on both the distal tibia and talar neck. It is thought to be related to repetitive microtrauma to the anteromedial aspect of the ankle from recurrent ball impact.⁶¹ It is very common amongst soccer players with some studies suggesting that 60% of soccer players have this syndrome. Ankle impingement is characterized by anterior pain with ankle dorsiflexion, decreased dorsiflexion, and swelling. It is primarily diagnosed with lateral ankle X-rays, which will show the osteophytes. An oblique anteromedial X-ray may increase detection of osteophytes (Figure 5). The early stages of anterior impingement can be treated successfully with injections and heel lifts. Treatment of lesions that fail to respond to conservative management involves arthroscopic or open excision of osteophytes. Most patients with no preexisting osteoarthritis treated arthroscopically will experience pain relief and return to full activity, though recurrent osteophyte formation has been noted at long-term follow-up.⁶²

Anterior ankle impingement is most often caused by acute ankle sprains with an inversion type of mechanism.⁶² The subsequent reactive inflammation can cause fibrosis leading to distal fascicle enlargement of the AITFL. Impingement in the anterolateral gutter of this enlarged fascicle can also cause both chronic reactive synovitis and chondromalacia of the lateral talar dome.⁶³ MRI can identify abnormal areas of pathology; however, 50% of cases are diagnosed based on clinical examination alone.⁶³ Patients generally present with a history of anterolateral ankle pain and swelling with an occasional popping or snapping sensation.

Soccer players commonly develop anterior bony impingement due to repetitive loading of the anterior ankle from striking the ball. This repetition can lead to osteophyte formation of the anterior distal tibia and talar neck. After the osteophytes form, decreased dorsiflexion can occur due to a mechanical stop and inflammation of the interposed capsule.

The patient will exhibit tenderness to palpation along the anterolateral aspect of the ankle, with pain elicited at extreme passive dorsiflexion.⁶² Initially, an injection with local anesthetic and corticosteroid can serve both a diagnostic and therapeutic purpose; however, patients who fail conservative treatment can be treated with arthroscopy and resection of the involved scar tissue and osteophytes. The best results are seen in those patients with no concurrent intra-articular lesions or ankle osteoarthritis (Figure 5).⁶² When treated non-operatively, a player may return to play when pain resolves; however, if treated surgically with arthroscopic debridement/resection, a player must wait until his surgical scars have healed prior to attempting return to play.

Continue to: ANTEROMEDIAL ANKLE IMPINGEMENT

 

 

ANTEROMEDIAL ANKLE IMPINGEMENT

Anteromedial ankle impingement is a less common ankle impingement syndrome. It is associated with eversion injuries or following medial malleolar or talar fractures.^64,65 Previous injury to the anterior tibiotalar fascicle of the deltoid complex leads to ligament thickening and subsequent impingement in the anteromedial corner of the talus. Adjacent fibrosis and synovitis are common consequences of impingement; however, osteophyte formation and chondral stripping along the anteromedial talus can also be seen. Patients typically complain of pain along the anteromedial joint line that is worse with activity, clicking or popping sensations, and painful, limited dorsiflexion. On examination, impingement can be detected through palpation over the anterior tibiotalar fascicle of the deltoid ligament and eversion or extreme passive dorsiflexion of the foot, all of which will elicit medial ankle tenderness.^17,62 Initial treatment consists of rest, physical therapy, and NSAIDs. Refractory cases may be amenable to arthroscopic or open resection of the anterior tibiotalar fascicle with débridement of any adjacent synovitis and scar tissue.⁶²

POSTERIOR ANKLE IMPINGEMENT

Posterior ankle impingement is often referred to as “os trigonum syndrome” since the posterior impingement is frequently associated with a prominent os trigonum. An os trigonum is an accessory ossicle representing the separated posterolateral tubercle of the talus. It is usually asymptomatic. However, in soccer players, pain can occur from impaction between the posterior tibial plafond and the os trigonum, or because of soft tissue compression between the 2 opposing osseous structures. The pain is due to repetitive microtrauma (ankle plantarflexion) or acute forced plantarflexion, which can present as an acute fracture of the os trigonum. Because soccer is a sport requiring both repetitive and extreme plantarflexion, it may predispose players to posterior ankle impingement (Figures 6A, 6B).^62,66

Clinically, it can be very difficult to detect and diagnose because the affected structures lie deep and it can coexist with other disease processes (eg, peroneal tendinopathy, Achilles tendinopathy).^62,66 Patients will complain of chronic deep posterior ankle pain that is worse with push-off activities (eg, jumping). On examination, patients will exhibit pain with palpation over the posterolateral process and with the crunch test. Lateral radiograph with the foot in plantar flexion will show the os trigonum impinged between the posterior tibial malleolus and the calcaneal tuberosity. An MRI will demonstrate the os trigonum as well as any associated inflammation and edema, while it can also demonstrate coexisting pathologies.

Initial treatment consists of rest, NSAIDs, and taping to prevent plantar flexion. Ultrasound-guided cortisone injection of the capsule and posterior bursa can be both therapeutic and diagnostic. A posterior injection can be used to temporize the symptoms so that the soccer player can make it through the season.

Surgical excision is saved for refractory cases, and this can be done either through an open posterolateral approach or arthroscopic techniques. Recently, Georgiannos and Bisbinas⁶⁷ showed in an athletic population that endoscopic excision had both a lower complication rate and a quicker return to sports compared with the traditional open approach. Carreira and colleagues⁶⁸ conducted a retrospective case series of 20 patients (mostly competitive athletes). They found that posterior ankle arthroscopy to address posterior impingement allowed for the maintenance or restoration of anatomic ROM of the ankle and hindfoot, ability to return to at least the previous level of activity, and improvement in objective assessment of pain relief and a higher level of function parameters.⁶⁸

Continue to: TENDON PATHOLOGY

 

 

TENDON PATHOLOGY

SUPERIOR PERONEAL RETINACULUM INJURY

The superior peroneal retinaculum (SPR) forms the roof of the superior peroneal tunnel. The tunnel contains the peroneus brevis and longus tendons and is bordered by the retromalleolar groove of the fibula and the lower aspect of the posterior intramuscular septum of the leg.^69,70 The SPR originates from the posterolateral ridge of the fibula and inserts onto the lateral calcaneus, and it is the primary restraint of the peroneal tendons within the retromalleolar sulcus.

Injury to the retinaculum results from both ankle dorsiflexion and inversion, and forceful reflex contraction of the peroneal muscles, which causes subluxation or dislocation of the contained tendons.⁶⁹ A high level of suspicion is required regarding these injuries since the mechanism of injury is similar to that of a simple lateral ankle sprain. In the setting of retrofibular pain, snapping or popping sensations around the lateral malleolus, or chronic ankle instability that worsens on uneven surfaces, one must consider an injury to the SPR.⁶⁹ Radiographs are not always diagnostic; however, occasionally on an internal rotation view, one may see a cortical avulsion off the distal tip of the lateral malleolus (“fleck sign”) indicating a rim fracture from an SPR injury (Figure 7). MRI is the best imaging modality to assess the peroneal tendons, as well as an SPR injury. Recently, ultrasound has grown in popularity and may be more useful, since it allows for dynamic evaluation of subluxating/dislocating tendons.⁶⁹

Conservative management is often associated with poor outcomes, and surgery is indicated for all acute and chronic dislocations in athletes.⁷¹ Anatomic reconstruction of the SPR is the preferred surgical method.⁷² Peroneus brevis debulking and fibular groove deepening may also augment the retinaculum repair.⁷³ van Dijk and colleagues in their systematic review showed that patients treated with both groove deepening and SPR repair have higher rates of return to the sport than patients treated with SPR repair alone.⁷⁴

STRESS FRACTURES

FIFTH METATARSAL

Fifth metatarsal stress fractures usually occur secondary to lateral overload or avulsion of the peroneus brevis. The fifth metatarsal base can be susceptible to injury in a cavovarus foot. Non-operative treatment typically requires a longer period of immobilization (boot or cast) and necessitates a longer period of non–weight-bearing (anywhere between 6-12 weeks). Therefore, surgery is typically recommended in athletes or in the setting of a recurrent base of the fifth metatarsal fracture to expedite healing and return to play. Return to play is still not recommended until there is evidence of radiographic healing of the fracture. There are certain distinctions with fifth metatarsal stress fractures regarding location and healing rates that need to be taken into account.^75,76 In particular, zone 2 injuries (Jones fractures) represent a vascular watershed area, making these fractures prone to nonunion with nonunion rates as high as 15% to 30%. Occasionally, the cavovarus deformity will require correction as well as a reduction in the risk of recurrence or nonunion. Surgical fixation most commonly consists of a single screw placed in an antegrade fashion.⁷⁷ One must pay attention to screw size since smaller diameter screws (<4.5 mm) are associated with delayed union or nonunion. Moreover, screws that are too long will straighten the curved metatarsal shaft and can lead to fracture distraction or malreduction (Figures 8A, 8B).⁷⁷

Patients have returned to competitive sports within 6 weeks; however, it should be noted that causes of failure were linked to early return and return to sports before a radiographic union can lead to failure of fixation. Ekstrand and van Dijk⁷⁸ studied a large group of professional soccer players and found that out of 13,754 injuries, 0.5% (67) were fifth metatarsal fractures. Of note, they found that 45% of players had prodromal symptoms. Furthermore, after surgical treatment the fractures healed faster, compared with conservative treatment (75% vs 33%); however, there was no significant difference in lay-off days between both groups (80 vs 74 days).⁷⁸ Matsuda and colleagues⁷⁹ looked at 335 male collegiate soccer players, 29 of whom had a history of a fifth metatarsal stress fracture. They found that playing the midfield position and having an everted rearfoot and inverted forefoot alignment were associated with fifth metatarsal stress fractures.⁷⁹ Saita and colleagues⁸⁰ found that restricted hip internal rotation was associated with an increased risk of developing a Jones fracture in 162 professional football players. Finally, Fujitaka and colleagues⁸¹ looked at 273 male soccer players between 2005 and 2013. They found an association between weak toe-grip strength and fifth metatarsal fractures, suggesting that weak toe-grip may lead to an increase in the load applied onto the lateral side of the foot, resulting in a stress fracture.⁸¹

Continue to: NAVICULAR

 

 

NAVICULAR

Another common tarsal bone that sustains stress fractures is the navicular. It is not as common as calcaneal stress fractures in military recruits but can occur in the same type of population, as well as explosive athletics such as sprinters and soccer players. It commonly presents with an indistinct vague achy pain with activity that improves with rest, and pain at the dorsum of the midfoot or along the medial longitudinal arch with activity. It can easily go undiagnosed for quite some time given the difficulty in visualizing the navicular with plain radiographs. Clinically, it is difficult to make the diagnosis, and therefore advanced imaging is necessary when the injury is suspected. Both MRI and CT scans can be used to understand the extent of the injury (Figures 9A-9C). In non-displaced stress fractures, conservative non-operative treatment is the appropriate treatment modality with a brief period of immobilization and non–weight-bearing;⁸² however, operative treatment is also considered in elite athletes. In either case, return to play is discouraged until there is evidence of radiographic healing. When a displacement is noted, or there is a delay in diagnosis, then operative treatment is recommended.

CONCLUSION

Ankle injuries are very common in soccer and can result in decreased performance or significant loss of playing time. Treatment of acute injury generally follows a conservative route, with surgical intervention reserved for severe ruptures or osteochondral fracture of the ankle joint. Chronic ankle pathology resulting in mechanical or functional instability generally requires surgery to repair ligamentous damage and restore normal ankle kinematics. It is critical for the soccer player to receive appropriate rehabilitation prior to returning to play in order to reduce the risk for reinjury and further chronic instability. Prevention and early intervention of ankle injuries is key in preventing the long-term sequelae of ankle injuries, such as arthritis, in former soccer players.

ABSTRACT

The ankle is one of the most commonly injured joints in soccer and represents a significant cost to the healthcare system. The ligaments that stabilize the ankle joint determine its biomechanics—alterations of which result from various soccer-related injuries. Acute sprains are among the most common injury in soccer players and are generally treated conservatively, with emphasis placed on secondary prevention to reduce the risk for future sprains and progression to chronic ankle instability. Repetitive ankle injuries in soccer players may cause chronic ankle instability, which includes both mechanical ligamentous laxity and functional changes. Chronic ankle pathology often requires surgery to repair ligamentous damage and remove soft-tissue or osseous impingement. Proper initial treatment, rehabilitation, and secondary prevention of ankle injuries can limit the amount of time lost from play and avoid negative long-term sequelae (eg, osteochondral lesions, arthritis). On the other hand, high ankle sprains portend a poorer prognosis and a longer recovery. These injuries will typically require surgical stabilization. Impingement-like syndromes of the ankle can undergo an initial trial of conservative treatment; when this fails, however, soccer players respond favorably to arthroscopic debridement of the lesions causing impingement. Finally, other pathologies (eg, stress fractures) are highly encouraged to be treated with surgical stabilization in elite soccer players.

Continue to: EPIDEMIOLOGY

 

 

EPIDEMIOLOGY

With roughly 200,000 professional and around 240 million amateur soccer players, soccer has been recognized as the most popular sport worldwide. Nevertheless, given its rising popularity in society, one must also consider the increasing incidence of injuries as a result. Elite soccer players sustain between 10 and 35 injuries per 1000 competitive playing hours.¹ Approximately 80% are traumatic, and 20% are overuse injuries.² Soccer injuries are more frequent with increasing age of the participants, whereas the incidence of injuries in preadolescent players is low. The incidence of injuries has been found to be higher during competition when compared with practice/training sessions, with some studies showing that 59% of injuries occurred during games.² Amateur or recreational soccer players sustain fewer injuries than professional soccer players, as one would expect, given both the higher intensity of training and match schedule in professionals.

The ankle is one of the most commonly injured joints in soccer, with some studies suggesting it comprises one-fifth of all injuries sustained during soccer, which is only second to those of the knee.² Ankle sprains specifically are quite a common occurrence in soccer.^3-9 A recent study of an English premier league club showed that over a 4-season period, 20% of injuries were of the foot and ankle with a mean return to sport time of 54 days.¹⁰ Of all foot and ankle related injuries, ankle sprains are the most common, followed by bruises/contusions, and tendon lesions. Fractures are very rare (1%) in soccer, but when they do occur they impart a much more extended recovery. During the 2010 Fédération Internationale de Football Association (FIFA) World Cup, ankle sprains were among the most common injuries and approximately half lead to players missing training or competitive matches.⁵

ANATOMY

Knowledge of the biomechanics of both the foot and ankle joints is essential to understand soccer injuries. The ankle joint (talocrural articulation) consists of the distal ends of the tibia and fibula, which form the mortise, and the superior aspect of the talar dome.¹¹ As a hinge joint, the ankle provides 20° of dorsiflexion and 50° of plantar flexion,¹² with stability provided by the lateral, medial, and superior ligamentous complexes. The superior articular surface of the talus is narrower posteriorly, which creates a looser fit within the mortise during plantar flexion.¹¹ This decreased stability could help explain why the most common injury in soccer involves a plantar flexion mechanism.^13,14 Inferiorly, the talus articulates with the calcaneus to form the subtalar joint. It is at this site that the majority of both foot inversion and eversion occurs. The transverse tarsal joints (Chopart’s joints) separate the hindfoot from the midfoot. Movement of this joint depends on the relative alignment of its 2 articulations: the talonavicular and calcaneocuboid joints. During foot eversion, these 2 joints are parallel to each other allowing supple motion and aiding in shock absorption during the heel strike phase of the gait cycle. With foot inversion, the joints become nonparallel and thus lock the transverse tarsal joints providing a rigid lever needed for push-off.^11,12

LATERAL LIGAMENTS

The ankle joint is stabilized laterally by a ligament complex consisting of 3 individual ligaments, all originating from the lateral malleolus: the anterior talofibular ligament (ATFL), the posterior talofibular ligament (PTFL), and the calcaneofibular ligament (CFL) (Figure 1).^11,12,15 The ATFL is the primary restraint to inversion in plantar flexion, and it helps resist anterolateral translation of the talus in the mortise. However, it is the weakest and therefore the most frequently injured of the lateral ligaments. The PTFL plays only a supplementary role in ankle stability when the lateral ligament complex is intact. It is under the greatest strain in ankle dorsiflexion and acts to limit posterior talar displacement within the mortise as well as talar external rotation.^13,16 The CFL is the primary restraint to inversion in the neutral or dorsiflexed position. It restrains subtalar inversion, thereby limiting talar tilt within the mortise.

DELTOID LIGAMENT

The deltoid ligament complex consists of 6 continuous adjacent superficial and deep ligaments that function synergistically to resist valgus and pronation forces, as well as external rotation of the talus in the mortise.^11-13,17 The superficial layer crosses both ankle and subtalar joints. It originates from the anterior colliculus and fans out to insert into the navicular, neck of the talus, sustentaculum tali, and posteromedial talar tubercle. The tibiocalcaneal (sustentaculum tali) portion is the strongest component in the superficial layer and resists calcaneal eversion. The deep layer crosses the ankle joint only. It functions as the primary stabilizer of the medial ankle and prevents both lateral displacement and external rotation of the talus. It originates from the inferior and posterior aspects of the medial malleolus and inserts on the medial and posteromedial aspects of the talus.^12,17,18

Continue to: SYNDESMOSIS

 

 

SYNDESMOSIS

The ankle syndesmosis, or inferior tibiofibular joint, is the distal articulation between the tibia and fibula. The syndesmosis contributes to ankle mortise integrity through its firm fixation of the lateral malleolus against the lateral surface of the talus. Ligaments comprising the ankle syndesmosis include the anterior inferior tibiofibular ligament (AITFL), the posterior inferior tibiofibular ligament (PITFL), the inferior transverse ligament, and the interosseous ligament (IOL).¹²

ANKLE SPRAINS

Ankle sprains are the most common pathology encountered amongst soccer players, representing from one-half to two-thirds of all ankle related injuries. Most sprains occur outside of player contact.

LATERAL ANKLE SPRAINS AND INSTABILITY

Injury to the lateral ligaments of the ankle represents 77% to 91% of all ankle sprains in soccer.^6,19 The greatest risk factor for an ankle sprain in a soccer player is a history of prior sprain.²⁰ Other risk factors include increasing age, player-to-player contact, condition of the pitch, weight-bearing status of the injured limb at the time of injury, and joint instability or laxity.^21,22

The evaluation of an ankle sprain to determine its severity is best done after the acute phase, approximately 4 to 7 days after the initial injury when both pain and swelling have subsided.²³ The anterior drawer (ATFL instability) and talar tilt (CFL instability) tests are useful in evaluating ankle instability in the delayed or chronic setting; however, both have been shown to have limited sensitivity and significant variability amongst different examiners.²⁴

Clinical examination will direct further diagnostic tests including X-rays, magnetic resonance imaging (MRI), and computed tomography (CT). The Ottawa ankle rules are generally helpful in determining whether plain X-rays are indicated in the acute setting.^25,26 (Figure 2) According to these rules, ankle radiographs should be obtained if ankle pain is reported near the malleoli and 1 or more of the following is seen during examination: inability to bear weight immediately after injury and for 4 steps in the emergency department, and bony tenderness at the posterior edge or tip of the malleolus. Stress X-rays are generally not indicated in acute injuries but may be useful in chronic ankle instability cases.²³

Continue to: Ankle sprains cover...

Ankle sprains cover a broad spectrum of injuries; therefore, a grading system was devised to aid in guiding treatment. Grade I (mild) sprains are those with minimal swelling and tenderness but have the ligaments still intact. Grade II (moderate) sprains occur when there are partial ligament tears associated with moderate pain, swelling, and tenderness. Finally, Grade III (severe) sprains are complete ligament tears with marked swelling, hemorrhage, tenderness, loss of function, and abnormal joint motion and instability.^{23, 24}

Initial treatment for all ankle sprains is nonoperative and involves the RICE (rest, ice, compression, elevation) protocol with the use of nonsteroidal anti-inflammatory drugs (NSAIDs) during the acute phase (first 4-5 days) with a short period (no >2 weeks) of immobilization.²⁷ Most authors agree that early mobilization followed by phased rehabilitation is warranted to minimize time away from sports.^28-31 Prolonged immobilization (>2 weeks) has detrimental effects and may lead to a longer return to play.^28-31 The rehabilitation protocol is divided into stages: (1) pain and edema control, (2) range of motion (ROM) and strengthening exercises, (3) soccer specific functional training, and (4) prophylactic intervention with balance and proprioception exercises. Surgical intervention is rarely indicated for acute ankle sprains. There are exceptions, however, such as when ankle sprains are associated with other injuries that require acute intervention (eg, fracture, osteochondral lesion). Surgery is indicated in the setting of chronic, recurrent mechanical instability. Anatomical repairs (modified Brostrom) seem to produce better outcomes than non-anatomical reconstructions (eg, Chrisman-Snook). Surgical outcomes are good, and most athletes are able to return to their pre-injury level of function.³²

In athletes, prevention of recurrent sprains is key. Braces may help prevent ankle sprains and bracing has been shown to be superior to taping, as tape loses its restrictive properties within 20 to 30 minutes of initiating activity.^33,34 Application of an orthosis (lace-up ankle orthosis) has been shown to reduce the incidence of ankle re-injury in soccer players with previous ankle sprains. Several studies have found minimal, if any, effect of orthoses on athletic performance.^20,35,36 Low-profile braces for soccer have been developed which allow for minimal disruption of the player’s boot and space proximally to insert the shin guard. Another essential component of prevention is prophylactic intervention with balance and proprioceptive exercises. A study looking at first division men’s league football (soccer) players in Iran showed a significant decrease in re-injury rates with proprioceptive training.³⁷ In 2003, FIFA introduced a comprehensive warm-up program (FIFA 11+), which has since been shown in several studies to decrease the risk of injury in amateur soccer players.^38-40

MEDIAL ANKLE SPRAINS AND INSTABILITY

Soccer places an unusually high demand on both the medial foot and ankle structures when compared with other sports. For instance, striking the ball requires the player to abduct and externally rotate the foot, which preloads medial structures.⁹ Hintermann¹⁸ looked at 54 cases of medial ankle instability and found that injury commonly occurred during landing on an uneven surface, which applies to soccer players when landing after heading the ball or jumping over a tackle. Pronation with eversion and extreme rotational injuries are well known to cause deltoid ligament injury. However, complete rupture of the deltoid ligament is rare and is more often associated with ankle fractures.⁴¹ Due to its close proximity and similarly shared function in medial plantar arch stabilization with the tibiospring and spring ligaments, posterior tibialis tendon dysfunction is also frequently seen in medial ankle instability.¹⁷ After an acute injury, patients can present with a medial ankle hematoma and pain along the deltoid ligament. Although chronic insufficiency is diagnosed based on the feeling of “giving way,” pain in the medial gutter of the ankle and a valgus and pronation deformity of the foot can be corrected by activating the peroneus tertius muscle. Arthroscopy is the most specific way to confirm clinically suspected instability of the medial ankle; however, MRI can demonstrate loss of organized medial fibers (Figures 3A, 3B).¹⁸ Primary surgical repair of deltoid ligament tears yield good to excellent results and should be considered in the soccer player to prevent problems associated with chronic non-repaired tears such as instability, osteoarthritis, and impingement syndromes.¹⁸ After surgical repair, players will undergo extensive physical therapy that progresses to sport-specific exercises with the ultimate goal of returning to competitive play around 4-6 months post-operatively.

HIGH ANKLE SPRAINS (SYNDESMOSIS)

High ankle sprains are much less common than low ankle sprains; however, when they do occur they portend a lengthier rehabilitation and a poorer prognosis, especially if undiagnosed. Lubberts and colleagues⁴² studied the epidemiology of isolated syndesmotic injuries in professional football players. They pooled data from 15 consecutive seasons of European professional football between 2001 and 2016. They examined a total of 3677 players from 61 teams across 17 countries. There were 1320 ankle ligament injuries registered during 15 seasons, of which 94 (7%) were isolated syndesmotic injuries. The incidence of these injuries increased annually between 2001 and 2016. Injuries were 74% contact-related, and isolated syndesmotic injuries were followed by a mean of a 39-day absence.⁴² Moreover, football players may have an increased risk of syndesmotic sprains due to foot planting and cutting action.⁴¹

Continue to: These injuriesa are typically...

These injuries are typically identified with pain over the AITFL and interosseous membrane. Physical examination tests that help identify syndesmotic injuries include the squeeze test, external rotation test, and crossed-leg test.⁴¹ The diagnosis can be made on plain X-ray when there is clear diastasis between the distal tibia and fibula. Two critical measurements on plain films are made 1 cm above the tibial plafond and are used to evaluate the integrity of the syndesmosis: tibiofibular clear space >6 mm, and tibiofibular overlap <1 mm, which indicate disruption of the syndesmosis.⁴³ More subtle injuries can be diagnosed with better sensitivity and specificity using MRI, which can also reveal secondary findings such as bone bruises, ATFL injury, osteochondral lesions, and tibiofibular incongruity.^44,45 Arthroscopy is an invaluable diagnostic tool for syndesmotic injuries with a characteristic triad finding of PITFL scarring, disrupted interosseous ligament, and posterolateral tibial plafond chondral damage.⁴⁶

Classification of the ligaments involved can aid in the selection of appropriate treatment. Grade I injuries involve AITFL tears. Grade IIa injuries involve AITFL and IOL tears. Grade IIb injuries include AITFL, PITFL, and IOL tears. Grade III injuries involve injury to all 3 ligaments, as well as a fibular fracture. Conservative treatment is recommended for Grades I and IIa, while surgical intervention is necessary for Grades IIb and III (Figures 4A, 4B). Compared with other ankle sprains, syndesmotic injuries typically require a more prolonged recovery/rehabilitation. Some studies suggest that these injuries require twice as long to heal.⁴⁷ Hopkinson and colleagues⁴⁸ reported a mean recovery time of 55 days following syndesmotic injuries in cadets at the United States Military Academy at West Point. Some surgeons advocate surgical intervention in professional athletes with mild sprains to expedite return to play.⁴⁹

Surgery has been well established as necessary in more severe injuries where there is clear diastasis or instability of the syndesmosis. Traditionally, screws were used for surgical fixation; however, they often required a second surgery for subsequent removal. There is no general consensus on the optimal screw size, level of placement, or timing of removal.^50,51 More recently, non-absorbable suture button fixation (eg, TightRope; Arthrex) has become more popular and provides certain advantages over screw fixation, such as avoiding the need for hardware removal. TightRope has been shown to provide more accurate stabilization of the syndesmosis as compared with screw fixation.⁵² Since malreduction is the most important indicator of poor long-term functional outcome, suture button fixation should be considered in the treatment of the football player.⁵³ Finally, Colcuc and colleagues⁵⁴ reported a lower complication rate and earlier return to sports in patients treated with knotless suture button devices compared with screw fixation.

OSTEOCHONDRAL LESIONS

Osteochondral lesions (OCLs) are cartilage-bone defects that are usually located in the talus. They can be caused by an acute traumatic event or repetitive microtrauma with no apparent history of trauma (eg, ankle instability). Acute OCLs can occur in soccer secondary to an ankle sprain or ankle fracture. Symptoms of OCLs include pain, swelling, and mechanical symptoms such as catching or locking, and on physical examination, one might see an effusion. The initial imaging modality of choice is radiographing; however, in ankle sprains with continued pain and swelling MRI may be indicated to rule out an underlying OCL. Missed acute lesions have a tendency not to heal and become chronic lesions, which can cause pain and playing disability. It is well established that chronic ankle instability is an important etiologic factor for OCLs. With the normal hydrostatic pressure within the ankle joint, synovial fluid gets pushed into cartilage/bone fissures, which can then lead to cystic degeneration of the subchondral bone.^55-57

Surgical repair of an OCL is dependent on both the size and location of the lesion. Acute lesions can be managed by arthroscopic débridement, microfracture, or fixation of the lesion if enough bone remains attached to the chondral lesion. Return to play is based on development and maturation of fibrocartilage over the lesion (debridement/microfracture) or healing and incorporation of the new graft (chondral repair procedures). Meanwhile, chronic lesions can be managed in 1-stage (microfracture, osteochondral autograft transfer or 2-stage (autologous chondrocyte implantation [ACI]) procedures.^56-57 Additional biologic healing augmentation with platelet-rich plasma has been described as well.⁵⁸ Newer techniques in treating chronic talus OCLs, including ones that have failed to respond to bone marrow stimulation techniques, have been developed more recently such as the use of particulated juvenile articular cartilage allograft (DeNovo NT Natural Tissue Graft^®; Zimmer Biomet).⁵⁹ These newer techniques avoid the need for a 2-stage procedure, as is the case with ACI.

Continue to: Further studies are needed...

Further studies are needed to both investigate long-term outcomes and determine the superiority of the arthroscopic juvenile cartilage procedure compared with microfracture and other cartilage resurfacing procedures. When surgically treating OCLs, one must also restore normal ankle joint biomechanics for the lesion to heal. For instance, in the presence of ankle instability, ligament reconstruction must be performed. Also, one should also consider addressing any hindfoot malalignment with an osteotomy (calcaneus, supramalleolar). In a recent retrospective study, van Eekeren and colleagues⁶⁰ showed that approximately 76% of patients were able to return to sports at long-term follow-up after arthroscopic débridement and bone marrow stimulation of talar OCLs. However, the activity level decreased at long-term follow-up and never attained the pre-injury level.⁶⁰

ANKLE IMPINGEMENT

ANTERIOR ANKLE IMPINGEMENT (FOOTBALLER'S ANKLE)

Anterior ankle impingement is caused by anterior osteophytes on both the distal tibia and talar neck. It is thought to be related to repetitive microtrauma to the anteromedial aspect of the ankle from recurrent ball impact.⁶¹ It is very common amongst soccer players with some studies suggesting that 60% of soccer players have this syndrome. Ankle impingement is characterized by anterior pain with ankle dorsiflexion, decreased dorsiflexion, and swelling. It is primarily diagnosed with lateral ankle X-rays, which will show the osteophytes. An oblique anteromedial X-ray may increase detection of osteophytes (Figure 5). The early stages of anterior impingement can be treated successfully with injections and heel lifts. Treatment of lesions that fail to respond to conservative management involves arthroscopic or open excision of osteophytes. Most patients with no preexisting osteoarthritis treated arthroscopically will experience pain relief and return to full activity, though recurrent osteophyte formation has been noted at long-term follow-up.⁶²

Anterior ankle impingement is most often caused by acute ankle sprains with an inversion type of mechanism.⁶² The subsequent reactive inflammation can cause fibrosis leading to distal fascicle enlargement of the AITFL. Impingement in the anterolateral gutter of this enlarged fascicle can also cause both chronic reactive synovitis and chondromalacia of the lateral talar dome.⁶³ MRI can identify abnormal areas of pathology; however, 50% of cases are diagnosed based on clinical examination alone.⁶³ Patients generally present with a history of anterolateral ankle pain and swelling with an occasional popping or snapping sensation.

Soccer players commonly develop anterior bony impingement due to repetitive loading of the anterior ankle from striking the ball. This repetition can lead to osteophyte formation of the anterior distal tibia and talar neck. After the osteophytes form, decreased dorsiflexion can occur due to a mechanical stop and inflammation of the interposed capsule.

The patient will exhibit tenderness to palpation along the anterolateral aspect of the ankle, with pain elicited at extreme passive dorsiflexion.⁶² Initially, an injection with local anesthetic and corticosteroid can serve both a diagnostic and therapeutic purpose; however, patients who fail conservative treatment can be treated with arthroscopy and resection of the involved scar tissue and osteophytes. The best results are seen in those patients with no concurrent intra-articular lesions or ankle osteoarthritis (Figure 5).⁶² When treated non-operatively, a player may return to play when pain resolves; however, if treated surgically with arthroscopic debridement/resection, a player must wait until his surgical scars have healed prior to attempting return to play.

Continue to: ANTEROMEDIAL ANKLE IMPINGEMENT

 

 

ANTEROMEDIAL ANKLE IMPINGEMENT

Anteromedial ankle impingement is a less common ankle impingement syndrome. It is associated with eversion injuries or following medial malleolar or talar fractures.^64,65 Previous injury to the anterior tibiotalar fascicle of the deltoid complex leads to ligament thickening and subsequent impingement in the anteromedial corner of the talus. Adjacent fibrosis and synovitis are common consequences of impingement; however, osteophyte formation and chondral stripping along the anteromedial talus can also be seen. Patients typically complain of pain along the anteromedial joint line that is worse with activity, clicking or popping sensations, and painful, limited dorsiflexion. On examination, impingement can be detected through palpation over the anterior tibiotalar fascicle of the deltoid ligament and eversion or extreme passive dorsiflexion of the foot, all of which will elicit medial ankle tenderness.^17,62 Initial treatment consists of rest, physical therapy, and NSAIDs. Refractory cases may be amenable to arthroscopic or open resection of the anterior tibiotalar fascicle with débridement of any adjacent synovitis and scar tissue.⁶²

POSTERIOR ANKLE IMPINGEMENT

Posterior ankle impingement is often referred to as “os trigonum syndrome” since the posterior impingement is frequently associated with a prominent os trigonum. An os trigonum is an accessory ossicle representing the separated posterolateral tubercle of the talus. It is usually asymptomatic. However, in soccer players, pain can occur from impaction between the posterior tibial plafond and the os trigonum, or because of soft tissue compression between the 2 opposing osseous structures. The pain is due to repetitive microtrauma (ankle plantarflexion) or acute forced plantarflexion, which can present as an acute fracture of the os trigonum. Because soccer is a sport requiring both repetitive and extreme plantarflexion, it may predispose players to posterior ankle impingement (Figures 6A, 6B).^62,66

Clinically, it can be very difficult to detect and diagnose because the affected structures lie deep and it can coexist with other disease processes (eg, peroneal tendinopathy, Achilles tendinopathy).^62,66 Patients will complain of chronic deep posterior ankle pain that is worse with push-off activities (eg, jumping). On examination, patients will exhibit pain with palpation over the posterolateral process and with the crunch test. Lateral radiograph with the foot in plantar flexion will show the os trigonum impinged between the posterior tibial malleolus and the calcaneal tuberosity. An MRI will demonstrate the os trigonum as well as any associated inflammation and edema, while it can also demonstrate coexisting pathologies.

Initial treatment consists of rest, NSAIDs, and taping to prevent plantar flexion. Ultrasound-guided cortisone injection of the capsule and posterior bursa can be both therapeutic and diagnostic. A posterior injection can be used to temporize the symptoms so that the soccer player can make it through the season.

Surgical excision is saved for refractory cases, and this can be done either through an open posterolateral approach or arthroscopic techniques. Recently, Georgiannos and Bisbinas⁶⁷ showed in an athletic population that endoscopic excision had both a lower complication rate and a quicker return to sports compared with the traditional open approach. Carreira and colleagues⁶⁸ conducted a retrospective case series of 20 patients (mostly competitive athletes). They found that posterior ankle arthroscopy to address posterior impingement allowed for the maintenance or restoration of anatomic ROM of the ankle and hindfoot, ability to return to at least the previous level of activity, and improvement in objective assessment of pain relief and a higher level of function parameters.⁶⁸

Continue to: TENDON PATHOLOGY

 

 

TENDON PATHOLOGY

SUPERIOR PERONEAL RETINACULUM INJURY

The superior peroneal retinaculum (SPR) forms the roof of the superior peroneal tunnel. The tunnel contains the peroneus brevis and longus tendons and is bordered by the retromalleolar groove of the fibula and the lower aspect of the posterior intramuscular septum of the leg.^69,70 The SPR originates from the posterolateral ridge of the fibula and inserts onto the lateral calcaneus, and it is the primary restraint of the peroneal tendons within the retromalleolar sulcus.

Injury to the retinaculum results from both ankle dorsiflexion and inversion, and forceful reflex contraction of the peroneal muscles, which causes subluxation or dislocation of the contained tendons.⁶⁹ A high level of suspicion is required regarding these injuries since the mechanism of injury is similar to that of a simple lateral ankle sprain. In the setting of retrofibular pain, snapping or popping sensations around the lateral malleolus, or chronic ankle instability that worsens on uneven surfaces, one must consider an injury to the SPR.⁶⁹ Radiographs are not always diagnostic; however, occasionally on an internal rotation view, one may see a cortical avulsion off the distal tip of the lateral malleolus (“fleck sign”) indicating a rim fracture from an SPR injury (Figure 7). MRI is the best imaging modality to assess the peroneal tendons, as well as an SPR injury. Recently, ultrasound has grown in popularity and may be more useful, since it allows for dynamic evaluation of subluxating/dislocating tendons.⁶⁹

Conservative management is often associated with poor outcomes, and surgery is indicated for all acute and chronic dislocations in athletes.⁷¹ Anatomic reconstruction of the SPR is the preferred surgical method.⁷² Peroneus brevis debulking and fibular groove deepening may also augment the retinaculum repair.⁷³ van Dijk and colleagues in their systematic review showed that patients treated with both groove deepening and SPR repair have higher rates of return to the sport than patients treated with SPR repair alone.⁷⁴

STRESS FRACTURES

FIFTH METATARSAL

Fifth metatarsal stress fractures usually occur secondary to lateral overload or avulsion of the peroneus brevis. The fifth metatarsal base can be susceptible to injury in a cavovarus foot. Non-operative treatment typically requires a longer period of immobilization (boot or cast) and necessitates a longer period of non–weight-bearing (anywhere between 6-12 weeks). Therefore, surgery is typically recommended in athletes or in the setting of a recurrent base of the fifth metatarsal fracture to expedite healing and return to play. Return to play is still not recommended until there is evidence of radiographic healing of the fracture. There are certain distinctions with fifth metatarsal stress fractures regarding location and healing rates that need to be taken into account.^75,76 In particular, zone 2 injuries (Jones fractures) represent a vascular watershed area, making these fractures prone to nonunion with nonunion rates as high as 15% to 30%. Occasionally, the cavovarus deformity will require correction as well as a reduction in the risk of recurrence or nonunion. Surgical fixation most commonly consists of a single screw placed in an antegrade fashion.⁷⁷ One must pay attention to screw size since smaller diameter screws (<4.5 mm) are associated with delayed union or nonunion. Moreover, screws that are too long will straighten the curved metatarsal shaft and can lead to fracture distraction or malreduction (Figures 8A, 8B).⁷⁷

Patients have returned to competitive sports within 6 weeks; however, it should be noted that causes of failure were linked to early return and return to sports before a radiographic union can lead to failure of fixation. Ekstrand and van Dijk⁷⁸ studied a large group of professional soccer players and found that out of 13,754 injuries, 0.5% (67) were fifth metatarsal fractures. Of note, they found that 45% of players had prodromal symptoms. Furthermore, after surgical treatment the fractures healed faster, compared with conservative treatment (75% vs 33%); however, there was no significant difference in lay-off days between both groups (80 vs 74 days).⁷⁸ Matsuda and colleagues⁷⁹ looked at 335 male collegiate soccer players, 29 of whom had a history of a fifth metatarsal stress fracture. They found that playing the midfield position and having an everted rearfoot and inverted forefoot alignment were associated with fifth metatarsal stress fractures.⁷⁹ Saita and colleagues⁸⁰ found that restricted hip internal rotation was associated with an increased risk of developing a Jones fracture in 162 professional football players. Finally, Fujitaka and colleagues⁸¹ looked at 273 male soccer players between 2005 and 2013. They found an association between weak toe-grip strength and fifth metatarsal fractures, suggesting that weak toe-grip may lead to an increase in the load applied onto the lateral side of the foot, resulting in a stress fracture.⁸¹

Continue to: NAVICULAR

 

 

NAVICULAR

Another common tarsal bone that sustains stress fractures is the navicular. It is not as common as calcaneal stress fractures in military recruits but can occur in the same type of population, as well as explosive athletics such as sprinters and soccer players. It commonly presents with an indistinct vague achy pain with activity that improves with rest, and pain at the dorsum of the midfoot or along the medial longitudinal arch with activity. It can easily go undiagnosed for quite some time given the difficulty in visualizing the navicular with plain radiographs. Clinically, it is difficult to make the diagnosis, and therefore advanced imaging is necessary when the injury is suspected. Both MRI and CT scans can be used to understand the extent of the injury (Figures 9A-9C). In non-displaced stress fractures, conservative non-operative treatment is the appropriate treatment modality with a brief period of immobilization and non–weight-bearing;⁸² however, operative treatment is also considered in elite athletes. In either case, return to play is discouraged until there is evidence of radiographic healing. When a displacement is noted, or there is a delay in diagnosis, then operative treatment is recommended.

CONCLUSION

Ankle injuries are very common in soccer and can result in decreased performance or significant loss of playing time. Treatment of acute injury generally follows a conservative route, with surgical intervention reserved for severe ruptures or osteochondral fracture of the ankle joint. Chronic ankle pathology resulting in mechanical or functional instability generally requires surgery to repair ligamentous damage and restore normal ankle kinematics. It is critical for the soccer player to receive appropriate rehabilitation prior to returning to play in order to reduce the risk for reinjury and further chronic instability. Prevention and early intervention of ankle injuries is key in preventing the long-term sequelae of ankle injuries, such as arthritis, in former soccer players.

A 65-year-old man with moderately severe osteoarthritis (OA) of the knee presents to your office for his annual exam. During the medication review, the patient mentions he is using glucosamine and chondroitin for his knee pain, which was recommended by a family member. Should you tell the patient to continue taking the medication?

Knee OA is a common condition in the United States, affecting an estimated 12% of adults ages 60 and older and 16% of those ages 70 and older.² The primary goals of OA therapy are to minimize pain and improve function. The American Academy of Orthopedic Surgeons (AAOS) and the American College of Rheumatology (ACR) agree that firstline treatment recommendations include aerobic exercise, resistance training, and weight loss.

Initial pharmacologic therapies include full-strength acetaminophen or oral/topical NSAIDs; the latter are also used if pain is unresponsive to acetaminophen.^3,4 If initial therapy is inadequate to control pain, tramadol, other opioids, duloxetine, or intra-articular injections with corticosteroids or hyaluronate are alternatives.^3,4 Total knee replacement may be indicated in moderate or severe knee OA with radiographic evidence.⁵ Vitamin D, lateral wedge insoles, and antioxidants are not currently recommended.⁶

Prior studies evaluating glucosamine and/or chondroitin have provided conflicting results regarding evidence on pain reduction, function, and quality of life. Therefore, guidelines on OA management do not recommend their use (AAOS, strong; ACR, conditional).^3,4 However, consumption remains high, with 6.5 million US adults reporting use of glucosamine and/or chondroitin in the prior 30 days.⁷

A 2015 systematic review of 43 randomized trials evaluating oral chondroitin sulfate for OA of varying severity suggested there may be a significant decrease in short-term and long-term pain with doses ≥ 800 mg/d compared with placebo (level of evidence, low; risk for bias, high).⁸ However, no significant difference was noted in short- or long-term function, and the trials were highly heterogeneous.

Studies included in the 2015 systematic review found that glucosamine plus chondroitin did not have a significant effect on short- or long-term pain or physical function compared with placebo. Although glucosamine plus chondroitin led to significantly decreased pain compared with other medication, sensitivity analyses conducted for larger studies (N > 200) with adequate methods of blinding and allocation concealment found no difference in pain.⁸ There was no statistically significant difference in adverse events for glucosamine plus chondroitin vs placebo, based on data from three studies included in the review.⁸

This RCT from Roman-Blas et al evaluated chondroitin and glucosamine vs placebo in patients with more severe OA. The study was supported by Tedec-Meiji Farma (Madrid), maker of the combination of chondroitin plus glucosamine used in the study.¹

Continue to: STUDY SUMMARY

 

 

STUDY SUMMARY

Chondroitin + glucosamine not better than placebo

This multicenter, randomized, double-blind, placebo-controlled trial was conducted in nine rheumatology referral centers and one orthopedic center in Spain. The trial evaluated the efficacy of chondroitin sulfate (1,200 mg) plus glucosamine sulfate (1,500 mg) (CS/GS) compared with placebo in 164 patients with Grade 2 or 3 knee OA and moderate-to-severe knee pain. OA grade was ascertained using the Kellgren-Lawrence scale, corresponding to osteophytes and either possible (Grade 2) or definite (Grade 3) joint space narrowing. Knee pain severity was defined by a self-reported global pain score of 40 to 80 mm on a 100-mm visual analog scale (VAS).

No significant difference was noted in group characteristics; average age in the CS/GS group was 67 and in the placebo group, 65. Exclusion criteria included BMI ≥ 35, concurrent arthritic conditions, and any coexisting chronic disease that would prevent successful completion of the trial.¹

The primary endpoint was mean reduction in global pain score on a 0- to 100-mm VAS at six months. Secondary outcomes included mean reduction in total and subscale scores in pain and function on the Western Ontario and McMaster Universities Osteoarthritis (WOMAC) index (0–100-mm VAS for each) and the use of rescue medication.

Baseline global pain scores were 62 mm in both groups. Acetaminophen, up to 3 g/d, was the only allowed rescue medication. Clinic visits occurred at 4, 12, and 24 weeks. A statistically significant difference between groups was defined as P < .03.¹

Results. In the intention-to-treat analysis at six months, patients in the placebo group had a greater reduction in pain than the CS/GC group (–20 mm vs –12 mm; P = .029). No other difference was noted between the placebo and CS/GS groups in the total or subscales of the WOMAC index, and no difference was noted in use of acetaminophen. More patients in the placebo group had at least a 50% improvement in pain or function compared with the CS/GS group (47.4% vs 27.5%; P = .01).

Continue to: In the CS/GS group...

In the CS/GS group, 31% did not complete the six-month treatment period, compared with 18% in the placebo group. More patients dropped out because of adverse effects (diarrhea, upper abdominal pain, and constipation) in the CS/GS group than the placebo group (33 vs 19; P = .018).¹

WHAT’S NEW

Pharma-sponsored study finds treatment ineffective

The effectiveness of CS/GS for the treatment of knee OA has been in question for years, but this RCT is the first trial sponsored by a pharmaceutical company to evaluate CS/GS efficacy. This trial found evidence of a lack of efficacy. In patients with more severe OA of the knee, placebo was more effective than CS/GS, and CS/GS had significantly more adverse events. Therefore, it may be time to advise patients to stop taking their CS/GS supplement.

CAVEATS

Cannot generalize findings

The study compared only one medication dosing regimen using a combination of CS and GS. Whether either agent alone, or different dosing, would lead to the same outcome is unknown.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Copyright © 2018. The Family Physicians Inquiries Network. All rights reserved.

Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice (2018; 67[9]:566-568).

A 65-year-old man with moderately severe osteoarthritis (OA) of the knee presents to your office for his annual exam. During the medication review, the patient mentions he is using glucosamine and chondroitin for his knee pain, which was recommended by a family member. Should you tell the patient to continue taking the medication?

Knee OA is a common condition in the United States, affecting an estimated 12% of adults ages 60 and older and 16% of those ages 70 and older.² The primary goals of OA therapy are to minimize pain and improve function. The American Academy of Orthopedic Surgeons (AAOS) and the American College of Rheumatology (ACR) agree that firstline treatment recommendations include aerobic exercise, resistance training, and weight loss.

Initial pharmacologic therapies include full-strength acetaminophen or oral/topical NSAIDs; the latter are also used if pain is unresponsive to acetaminophen.^3,4 If initial therapy is inadequate to control pain, tramadol, other opioids, duloxetine, or intra-articular injections with corticosteroids or hyaluronate are alternatives.^3,4 Total knee replacement may be indicated in moderate or severe knee OA with radiographic evidence.⁵ Vitamin D, lateral wedge insoles, and antioxidants are not currently recommended.⁶

Prior studies evaluating glucosamine and/or chondroitin have provided conflicting results regarding evidence on pain reduction, function, and quality of life. Therefore, guidelines on OA management do not recommend their use (AAOS, strong; ACR, conditional).^3,4 However, consumption remains high, with 6.5 million US adults reporting use of glucosamine and/or chondroitin in the prior 30 days.⁷

A 2015 systematic review of 43 randomized trials evaluating oral chondroitin sulfate for OA of varying severity suggested there may be a significant decrease in short-term and long-term pain with doses ≥ 800 mg/d compared with placebo (level of evidence, low; risk for bias, high).⁸ However, no significant difference was noted in short- or long-term function, and the trials were highly heterogeneous.

Studies included in the 2015 systematic review found that glucosamine plus chondroitin did not have a significant effect on short- or long-term pain or physical function compared with placebo. Although glucosamine plus chondroitin led to significantly decreased pain compared with other medication, sensitivity analyses conducted for larger studies (N > 200) with adequate methods of blinding and allocation concealment found no difference in pain.⁸ There was no statistically significant difference in adverse events for glucosamine plus chondroitin vs placebo, based on data from three studies included in the review.⁸

This RCT from Roman-Blas et al evaluated chondroitin and glucosamine vs placebo in patients with more severe OA. The study was supported by Tedec-Meiji Farma (Madrid), maker of the combination of chondroitin plus glucosamine used in the study.¹

Continue to: STUDY SUMMARY

 

 

STUDY SUMMARY

Chondroitin + glucosamine not better than placebo

This multicenter, randomized, double-blind, placebo-controlled trial was conducted in nine rheumatology referral centers and one orthopedic center in Spain. The trial evaluated the efficacy of chondroitin sulfate (1,200 mg) plus glucosamine sulfate (1,500 mg) (CS/GS) compared with placebo in 164 patients with Grade 2 or 3 knee OA and moderate-to-severe knee pain. OA grade was ascertained using the Kellgren-Lawrence scale, corresponding to osteophytes and either possible (Grade 2) or definite (Grade 3) joint space narrowing. Knee pain severity was defined by a self-reported global pain score of 40 to 80 mm on a 100-mm visual analog scale (VAS).

No significant difference was noted in group characteristics; average age in the CS/GS group was 67 and in the placebo group, 65. Exclusion criteria included BMI ≥ 35, concurrent arthritic conditions, and any coexisting chronic disease that would prevent successful completion of the trial.¹

The primary endpoint was mean reduction in global pain score on a 0- to 100-mm VAS at six months. Secondary outcomes included mean reduction in total and subscale scores in pain and function on the Western Ontario and McMaster Universities Osteoarthritis (WOMAC) index (0–100-mm VAS for each) and the use of rescue medication.

Baseline global pain scores were 62 mm in both groups. Acetaminophen, up to 3 g/d, was the only allowed rescue medication. Clinic visits occurred at 4, 12, and 24 weeks. A statistically significant difference between groups was defined as P < .03.¹

Results. In the intention-to-treat analysis at six months, patients in the placebo group had a greater reduction in pain than the CS/GC group (–20 mm vs –12 mm; P = .029). No other difference was noted between the placebo and CS/GS groups in the total or subscales of the WOMAC index, and no difference was noted in use of acetaminophen. More patients in the placebo group had at least a 50% improvement in pain or function compared with the CS/GS group (47.4% vs 27.5%; P = .01).

Continue to: In the CS/GS group...

In the CS/GS group, 31% did not complete the six-month treatment period, compared with 18% in the placebo group. More patients dropped out because of adverse effects (diarrhea, upper abdominal pain, and constipation) in the CS/GS group than the placebo group (33 vs 19; P = .018).¹

WHAT’S NEW

Pharma-sponsored study finds treatment ineffective

The effectiveness of CS/GS for the treatment of knee OA has been in question for years, but this RCT is the first trial sponsored by a pharmaceutical company to evaluate CS/GS efficacy. This trial found evidence of a lack of efficacy. In patients with more severe OA of the knee, placebo was more effective than CS/GS, and CS/GS had significantly more adverse events. Therefore, it may be time to advise patients to stop taking their CS/GS supplement.

CAVEATS

Cannot generalize findings

The study compared only one medication dosing regimen using a combination of CS and GS. Whether either agent alone, or different dosing, would lead to the same outcome is unknown.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Copyright © 2018. The Family Physicians Inquiries Network. All rights reserved.

Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice (2018; 67[9]:566-568).

A 65-year-old man with moderately severe osteoarthritis (OA) of the knee presents to your office for his annual exam. During the medication review, the patient mentions he is using glucosamine and chondroitin for his knee pain, which was recommended by a family member. Should you tell the patient to continue taking the medication?

Knee OA is a common condition in the United States, affecting an estimated 12% of adults ages 60 and older and 16% of those ages 70 and older.² The primary goals of OA therapy are to minimize pain and improve function. The American Academy of Orthopedic Surgeons (AAOS) and the American College of Rheumatology (ACR) agree that firstline treatment recommendations include aerobic exercise, resistance training, and weight loss.

Initial pharmacologic therapies include full-strength acetaminophen or oral/topical NSAIDs; the latter are also used if pain is unresponsive to acetaminophen.^3,4 If initial therapy is inadequate to control pain, tramadol, other opioids, duloxetine, or intra-articular injections with corticosteroids or hyaluronate are alternatives.^3,4 Total knee replacement may be indicated in moderate or severe knee OA with radiographic evidence.⁵ Vitamin D, lateral wedge insoles, and antioxidants are not currently recommended.⁶

Prior studies evaluating glucosamine and/or chondroitin have provided conflicting results regarding evidence on pain reduction, function, and quality of life. Therefore, guidelines on OA management do not recommend their use (AAOS, strong; ACR, conditional).^3,4 However, consumption remains high, with 6.5 million US adults reporting use of glucosamine and/or chondroitin in the prior 30 days.⁷

A 2015 systematic review of 43 randomized trials evaluating oral chondroitin sulfate for OA of varying severity suggested there may be a significant decrease in short-term and long-term pain with doses ≥ 800 mg/d compared with placebo (level of evidence, low; risk for bias, high).⁸ However, no significant difference was noted in short- or long-term function, and the trials were highly heterogeneous.

Studies included in the 2015 systematic review found that glucosamine plus chondroitin did not have a significant effect on short- or long-term pain or physical function compared with placebo. Although glucosamine plus chondroitin led to significantly decreased pain compared with other medication, sensitivity analyses conducted for larger studies (N > 200) with adequate methods of blinding and allocation concealment found no difference in pain.⁸ There was no statistically significant difference in adverse events for glucosamine plus chondroitin vs placebo, based on data from three studies included in the review.⁸

This RCT from Roman-Blas et al evaluated chondroitin and glucosamine vs placebo in patients with more severe OA. The study was supported by Tedec-Meiji Farma (Madrid), maker of the combination of chondroitin plus glucosamine used in the study.¹

Continue to: STUDY SUMMARY

 

 

STUDY SUMMARY

Chondroitin + glucosamine not better than placebo

This multicenter, randomized, double-blind, placebo-controlled trial was conducted in nine rheumatology referral centers and one orthopedic center in Spain. The trial evaluated the efficacy of chondroitin sulfate (1,200 mg) plus glucosamine sulfate (1,500 mg) (CS/GS) compared with placebo in 164 patients with Grade 2 or 3 knee OA and moderate-to-severe knee pain. OA grade was ascertained using the Kellgren-Lawrence scale, corresponding to osteophytes and either possible (Grade 2) or definite (Grade 3) joint space narrowing. Knee pain severity was defined by a self-reported global pain score of 40 to 80 mm on a 100-mm visual analog scale (VAS).

No significant difference was noted in group characteristics; average age in the CS/GS group was 67 and in the placebo group, 65. Exclusion criteria included BMI ≥ 35, concurrent arthritic conditions, and any coexisting chronic disease that would prevent successful completion of the trial.¹

The primary endpoint was mean reduction in global pain score on a 0- to 100-mm VAS at six months. Secondary outcomes included mean reduction in total and subscale scores in pain and function on the Western Ontario and McMaster Universities Osteoarthritis (WOMAC) index (0–100-mm VAS for each) and the use of rescue medication.

Baseline global pain scores were 62 mm in both groups. Acetaminophen, up to 3 g/d, was the only allowed rescue medication. Clinic visits occurred at 4, 12, and 24 weeks. A statistically significant difference between groups was defined as P < .03.¹

Results. In the intention-to-treat analysis at six months, patients in the placebo group had a greater reduction in pain than the CS/GC group (–20 mm vs –12 mm; P = .029). No other difference was noted between the placebo and CS/GS groups in the total or subscales of the WOMAC index, and no difference was noted in use of acetaminophen. More patients in the placebo group had at least a 50% improvement in pain or function compared with the CS/GS group (47.4% vs 27.5%; P = .01).

Continue to: In the CS/GS group...

In the CS/GS group, 31% did not complete the six-month treatment period, compared with 18% in the placebo group. More patients dropped out because of adverse effects (diarrhea, upper abdominal pain, and constipation) in the CS/GS group than the placebo group (33 vs 19; P = .018).¹

WHAT’S NEW

Pharma-sponsored study finds treatment ineffective

The effectiveness of CS/GS for the treatment of knee OA has been in question for years, but this RCT is the first trial sponsored by a pharmaceutical company to evaluate CS/GS efficacy. This trial found evidence of a lack of efficacy. In patients with more severe OA of the knee, placebo was more effective than CS/GS, and CS/GS had significantly more adverse events. Therefore, it may be time to advise patients to stop taking their CS/GS supplement.

CAVEATS

Cannot generalize findings

The study compared only one medication dosing regimen using a combination of CS and GS. Whether either agent alone, or different dosing, would lead to the same outcome is unknown.

ACKNOWLEDGEMENT

The PURLs Surveillance System was supported in part by Grant Number UL1RR024999 from the National Center For Research Resources, a Clinical Translational Science Award to the University of Chicago. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Center For Research Resources or the National Institutes of Health.

Copyright © 2018. The Family Physicians Inquiries Network. All rights reserved.

Reprinted with permission from the Family Physicians Inquiries Network and The Journal of Family Practice (2018; 67[9]:566-568).

ABSTRACT

Improvements in ultrasound technology have increased the popularity and use of ultrasound as a diagnostic and therapeutic modality for many soccer-related musculoskeletal (MSK) injuries. As a dynamic imaging modality, ultrasound offers increased accuracy and efficacy with minimally invasive procedures, such as guided injections, percutaneous tenotomy, and regenerative therapies, in the clinical setting. Emerging evidence indicates that regenerative therapies, such as platelet-rich-plasma (PRP), mesenchymal stem cells, and amniotic products, are a promising treatment for many MSK injuries and are gaining popularity among professional athletes. PRP is a safe treatment for a number of MSK conditions and has been included in the standard of care. However, conflicting evidence on return-to-play timeframes and efficacy in certain MSK conditions have led to inconsistent recommendations on indications for use, dose, and timing of treatment. Mesenchymal stem cell therapy, while promising, lacks high-level evidence of efficacy despite its increasing use among athletes. Currently, no data are available regarding the outcome of the use of amniotic products for the treatment of injuries in athletes. Furthermore, preparation of many regenerative therapies eclipses the concept of minimal manipulation and is subject to US Food and Drug Administration phase I to III trials. High-level research on regenerative medicine therapies should be continuously conducted to establish their clinical efficacy and safety data.

ABSTRACT

Improvements in ultrasound technology have increased the popularity and use of ultrasound as a diagnostic and therapeutic modality for many soccer-related musculoskeletal (MSK) injuries. As a dynamic imaging modality, ultrasound offers increased accuracy and efficacy with minimally invasive procedures, such as guided injections, percutaneous tenotomy, and regenerative therapies, in the clinical setting. Emerging evidence indicates that regenerative therapies, such as platelet-rich-plasma (PRP), mesenchymal stem cells, and amniotic products, are a promising treatment for many MSK injuries and are gaining popularity among professional athletes. PRP is a safe treatment for a number of MSK conditions and has been included in the standard of care. However, conflicting evidence on return-to-play timeframes and efficacy in certain MSK conditions have led to inconsistent recommendations on indications for use, dose, and timing of treatment. Mesenchymal stem cell therapy, while promising, lacks high-level evidence of efficacy despite its increasing use among athletes. Currently, no data are available regarding the outcome of the use of amniotic products for the treatment of injuries in athletes. Furthermore, preparation of many regenerative therapies eclipses the concept of minimal manipulation and is subject to US Food and Drug Administration phase I to III trials. High-level research on regenerative medicine therapies should be continuously conducted to establish their clinical efficacy and safety data.

ABSTRACT

Improvements in ultrasound technology have increased the popularity and use of ultrasound as a diagnostic and therapeutic modality for many soccer-related musculoskeletal (MSK) injuries. As a dynamic imaging modality, ultrasound offers increased accuracy and efficacy with minimally invasive procedures, such as guided injections, percutaneous tenotomy, and regenerative therapies, in the clinical setting. Emerging evidence indicates that regenerative therapies, such as platelet-rich-plasma (PRP), mesenchymal stem cells, and amniotic products, are a promising treatment for many MSK injuries and are gaining popularity among professional athletes. PRP is a safe treatment for a number of MSK conditions and has been included in the standard of care. However, conflicting evidence on return-to-play timeframes and efficacy in certain MSK conditions have led to inconsistent recommendations on indications for use, dose, and timing of treatment. Mesenchymal stem cell therapy, while promising, lacks high-level evidence of efficacy despite its increasing use among athletes. Currently, no data are available regarding the outcome of the use of amniotic products for the treatment of injuries in athletes. Furthermore, preparation of many regenerative therapies eclipses the concept of minimal manipulation and is subject to US Food and Drug Administration phase I to III trials. High-level research on regenerative medicine therapies should be continuously conducted to establish their clinical efficacy and safety data.

ABSTRACT

Patient satisfaction has become a topic of interest within orthopedics as the landscape of provider reimbursement continues to evolve to reward value of care. Online internet physician rating sites are becoming increasingly popular ways for patients to subjectively express their provider experience. Understanding what patients value during their episode of care is important in the modern healthcare environment. The purpose of this study is to determine what preferences, if any, patients have when selecting their physician and how they experience care in an outpatient orthopedic setting. A prospective survey was electronically administered to 212 patients in an adult reconstruction clinic. One hundred ninety-six patients (92.5%) completed the survey. Demographic questions regarding age, sex, ethnicity, and prior adult reconstruction surgical history were obtained. When patients were asked how much time they would like the doctor to spend with them on a routine visit, the most common answer was 10 to 15 minutes (41.3%), with only 10.2% patients desiring >20 minutes. The majority of patients (83.1%) believe ≥30 minutes is too long to wait to see their surgeon. Less than half of patients (41.8%) stated that they would feel as though they were receiving below average care if seen only by a nurse practitioner or physician’s assistant at a postoperative visit. Patients reported no significant age, gender, or ethnicity preferences for their physician. Recommendations from friends or other physicians was the most common (66.4%) way for patients to find their physicians, while 12.2% utilized online rating sites during their search. Optimizing patient experiences in the office may include keeping wait times to <30 minutes and educating patients on the roles of physician extenders. More work needs to be done to further elucidate variables influencing the subjective patient experience with their orthopedic care.

Continue to: Patient satisfaction...

Patient satisfaction has become an important focus in the rapidly changing healthcare environment due to the significant impact it has on healthcare delivery, healthcare economics, assessment of the quality of care, development of patient-care models, and quality improvement initiatives.^1-4 Historically, the quality of care was measured by objective metrics such as complication rates, range-of-motion, and the provider’s expert opinion on the outcome. While those metrics are still impactful variables when defining a successful outcome, the medical community is now increasingly recognizing the importance of patients’ perspectives when defining successful treatments. Patient satisfaction is now highly regarded by clinicians and the government when considering outcomes and is even being incorporated into determining the value of care. Under the Affordable Care Act, patients assumed a more active role in clinical decision-making as well as in creating quality and efficiency initiatives.^5,6 By 2017, 2% of the United States government’s Medicare payments will be redistributed among hospitals and physicians based on their quality and efficiency metrics, which are largely determined by patients’ evaluations of care.⁷ As a result, there has been significant interest in identifying variables influencing patient satisfaction and subjective outcomes.^8,9

Patient satisfaction is related to both the outcomes of care and the process of care. As first described by Donabedian,¹⁰patients may be satisfied with the successful outcome of their care, but dissatisfied with how they received their care. The process of care is complex and considers many aspects of healthcare delivery, including time, cost, healthcare provider interactions, and burdens faced. While patient satisfaction with outcomes and process of care are heavily related, they should be regarded separately. It is essential that providers understand what variables are important to patients with regards to how they experience healthcare and choose their provider, especially surrounding elective procedures such as hip and knee arthroplasty.^11,12

Within orthopedic surgery, patient satisfaction scores are beginning to be incorporated as part of the standard-of-care quality metrics obtained along with patient-reported outcome measures (PROMs) at defined time points postoperatively. Furthermore, PROMs and patient satisfaction data are becoming an increasingly important component of medical decision-making.^13-16 Several authors have reported that increased patient satisfaction is correlated with increased compliance, improved treatment outcomes across numerous medical settings, including orthopedics, decreased risk of litigation, and higher patient ratings of the quality of care.^17,18 Various factors, including meeting of expectations, staff politeness, the communication skills of the surgeon, and waiting times, have been suggested to influence eventual patient satisfaction within the surgical literature.^19-21 However, within orthopedic surgery there is a paucity of investigations evaluating how patients determine preferences and satisfaction with the process of care.

The purpose of this study is to determine what preferences, if any, patients have when selecting their physician and how they experience care in an outpatient orthopedic setting. The authors hypothesize that the majority of patients find their physicians through online rating sites or recommendations from family and friends. The authors believe that patients expect to be seen in <30 minutes and will be unsatisfied overall with the amount of time that they spend with their physician.

Continue to: METHODS...

 

 

METHODS

The senior author (BRL) and a research team created a 15-question survey to evaluate patient preferences regarding the demographic characteristics (eg, age, gender, ethnicity) of their physician, wait times in a waiting room, time spent with the physician, care received from physician extenders (eg, nurse practitioners, physician assistants), and how they learned of their physician (Appendix). An a priori power analysis was conducted to determine that approximately 200 patients were needed for inclusion.^11,22 Following Institutional Review Board approval (ORA 15051104), the survey was administered to 212 patients in a single-surgeon, adult reconstruction clinic. The survey was digitally administered on a touch-screen tablet using an electronic independent third party survey center (SurveyMonkey Inc) devoid of any identifying data. The survey was offered to all patients >21 years of age who were English-speaking and in the common area as patients waiting to be seen, from June 2015 to March 2016. A research assistant approached patients in the waiting room and asked if they would like to participate in a short survey regarding what factors influence the patient-physician relationship from the patient’s perspective.

Appendix 1

1. Do you wish to partake in this 3-minute survey?
   1.  
   2.  

 

1. Have you had a prior knee or hip replacement?
   1.  
   2.  

 

1. What is your age?
   1. 30-40 years
   2. 40-50 years
   3. 50-60 years
   4. 60-70 years
   5. 70-80 years
   6. 80+ years

 

1. What is your gender?
   1.  
   2.  

 

1. Which of the following best represents your racial or ethnic heritage?
   1. African American
   2.  
   3.  
   4.  
   5.  

 

1. How much time would you like the doctor to spend talking to you on a routine visit?
   1. 0-5 minutes
   2. 5-10 minutes
   3. 10-15 minutes
   4. 15-20 minutes
   5. 20-30 minutes
   6. >30 minutes

 

1. How long is too long to wait to see the doctor?
   1. 10 minutes
   2. 20 minutes
   3. 30 minutes
   4. 40 minutes
   5. 50 minutes
   6. An hour or more

 

1. If you were to only see a physician’s assistant or nurse practitioner at your follow-up visit and not the doctor, would you feel like you were getting below average care?
   1.  
   2.  

 

1. Overall I am satisfied with the time the doctor spends with me.
   1.  
   2.  

 

1. If you were to need a major surgery, would you want the physician to tell you what he or she would do if they were in your shoes?
   1.  
   2.  

 

1. Would you prefer your doctor to be the same race/ethnicity as you?
   1. No
   2.  
   3. No Preference

 

1. Would you feel more comfortable with a male as opposed to a female orthopedic surgeon?
   1.  
   2.  

 

1. Would you feel more comfortable with a female as opposed to a male orthopedic surgeon?
   1.  
   2.  

 

1. What age would you like your physician to be?
   1. 25-35 years old
   2. 35-45 years old
   3. 45-55 years old
   4. 55-65 years old
   5. 65 years and older
   6. No preference

 

1. How do you usually find your physician?
   1.  
   2. Friends’ recommendations
   3. Healthcare provider’s recommendations
   4. Insurance plans
   5. Online research/ratings
   6. Other

 

Descriptive statistics were used to analyze subject demographics and survey responses. Chi-square analyses and multinomial logistic regressions were utilized to compare responses. All statistical analyses were conducted using SPSS version 24.0 software (SPSS Inc). Statistical significance was set at P < 0.05.

RESULTS

Of the 212 patients who were invited to participate, 196 patients (92.4%) agreed and completed the survey. Demographic and surgical history information can be found in Table 1. The majority of patients were female (62%) and above the age of 50 years (92.4%). Almost half (48.5%) of patients had a prior hip or knee replacement.

Table 1. Survey Respondent Demographics

	Number	Percent
Age Range
30-40 years	4	2.0%
40-50 years	11	5.6%
50-60 years	47	24.0%
60-70 years	84	42.9%
70-80 years	41	20.9%
>80 years	9	4.6%
Gender
Male	74	37.8%
Female	122	62.2%
Ethnicity
African American	39	19.9%
Asian	3	1.5%
Caucasian	140	71.4%
Hispanic	10	5.1%
Other	4	2.0%
Prior knee or hip replacement
Yes	95	48.5%
No	55	28.1%
No Response	46	23.5%

 

When asked how long is too long to wait to see the doctor, 30 minutes (39.8%) was most commonly selected, followed by 40 minutes (24.5%) (Figure 1). When asked how much time patients would like the doctor to spend with them during an office visit, the majority (68.9%) selected either 10 to 15 minutes (41.3%) or 15 to 20 minutes (27.6%) (Figure 2). The majority of patients (92.3%) were satisfied with the amount of time the doctor spent with them. In addition, 94.9% of respondents would want their doctor to tell them what they would do if they were in the patient’s shoes when making decisions regarding their medical care (Table 2). Less than half of respondents (41.8%) believe that seeing a physician extender (eg, nurse practitioner or physician assistant) at a postoperative visit would result in a lower quality of care (Table 2).

Table 2. Responses to Survey Questions

If you were to only see a physician's assistant or nurse practitioner at your follow-up visit and not the doctor, would you feel like you were getting below average care?
Answer choices	Number	Percent
No	114	58.2%
Yes	82	41.8%
If you were to need a major surgery would you want the physician to tell you what he or she would do if they were in your shoes?
Answer choices	Number	Percent
No	10	5.1%
Yes	186	94.9%
Would you prefer your doctor to be the same race/ethnicity as you?
Answer choices	Number	Percent
No	29	14.8%
Yes	3	1.5%
No Preference	164	83.7%

 

When asked if patients preferred a doctor of the same race/ethnicity, the vast majority (83.7%) had no preference (Table 2). There was no significant difference found between male and female respondents when asked if they would feel more comfortable with a male as opposed to a female orthopedic surgeon (P = .118) and vice versa (P = .604) (Table 3). Most patients preferred a physician between the ages of 45 and 55 years (39.3%), followed by 35 and 45 years (23.0%); however, this preference was not statistically significant (Table 4). Older patients were more likely to prefer younger physicians (odds ratio, 4.612 for 25-35 years of age; odds ratio, 1.328 for 35-45 years of age). Only 12.2% of patients reported online research/rating sites as the main resource utilized when selecting their physician (Figure 3). The majority (68.4%) reported that recommendations from either friends (35.2%) or healthcare providers (33.2%) were the main avenues through which they found their physicians.

Table 3. Overall Responses to Questions Regarding Male and Female Orthopedic Surgeons^a

Would you feel more comfortable with a male as opposed to a female orthopedic surgeon?
Answer choices	Number	Percent	Female responses	Male responses	P value
No	164	83.7%	106 (86.9%)	58 (78.4%)	0.118
Yes	32	16.3%	16 (13.1%)	16 (21.6%)
Would you feel more comfortable with a female as opposed to a male orthopedic surgeon?
Answer choices	Number	Percent	Female responses	Male responses	P value
No	186	94.9%	115 (94.3%)	71 (95.9%)	0.604
Yes	10	5.1%	7 (5.7%)	3 (4.1%)

^aResponses were broken down by gender and compared utilizing a 2 x 2 chi-square analysis to test for significant differences in respondents’ gender preferences for their orthopedic surgeon.

 

Table 4. Patient Preferences Regarding Physician Age

What age would you like your physician to be?					95% Confidence Interval
Answer Choices	Number or Responses	Percent	P value	Exp(β)	Lower Bound	Upper Bound
25-35 years	1	0.5%	0.217	4.612	0.407	52.283
35-45 years	45	23.0%	0.161	1.328	0.893	1.975
45-55 years	77	39.3%	0.159	1.276	0.909	1.791
55-65 years	9	4.6%	0.483	1.302	0.624	2.717
≥65 years	2	1.0%	0.272	0.491	0.138	1.748
No preferencea	62	31.6%	Reference

^aNo preference was used as the reference category for the answer choices, while the age bracket “>80 years” was used as the reference for the age of respondent variable.

 

 

Continue to: DISCUSSION... 

 

 

DISCUSSION

The results of this study demonstrate that patients have several expectations and preferences with regards to the care they receive from physicians in the office. Patients prefer to wait <30 minutes before seeing their provider and desire only 10 to 20 minutes with their doctor. Patients do not have specific preferences with regards to the gender or ethnicity of their physician but would prefer a physician in the middle of their career, aged 45 to 55 years. Ultimately, patients do believe that seeing a physician at a postoperative visit is important, as just under half of patients thought that seeing a physician extender alone at a postoperative visit resulted in a lower quality of care.

While these results were obtained in a population specifically seeking the care of an orthopedic adult reconstruction surgeon, the results demonstrate that patients do not necessarily desire an unreasonable amount of time with their doctor. Patients simply want to be seen in a timely fashion and receive the full undivided attention of their doctor for approximately 20 minutes. Similarly, Patterson and colleagues²² found, in their series of 182 patients who presented to an orthopedic surgeon, that there was a significant correlation between time spent with the surgeon and overall patient satisfaction. Interestingly, the authors reported that patient satisfaction was not correlated with education level, sex, marital status, whether the patients were evaluated by a resident physician before seeing the attending surgeon, self-reported mental status, tobacco usage, the type of clinic visit, or the waiting time to see the surgeon (average, about 40 minutes for this cohort).²² Similarly, Teunis and colleagues²³ reported an average 32-minute wait time in 81 patients presenting for care at an orthopedic hand clinic and demonstrated that a longer wait time was associated with decreased patient satisfaction. These results corroborate the findings of this study that a short wait time is important to patients when evaluating the process of care. Additionally, patients do not have unreasonable expectations with regards to the amount of time they would like to spend with the physician. A physician who has a clinic for 9 hours a day would thus be able to see 54 patients and still spend at least 10 minutes with each patient. The quality of the physician-patient interaction is likely more important than the actual amount of time spent; however, based on this study, patients do have certain expectations about how much time physicians should spend with them.

There were no significant sex, age, or ethnicity preferences in our specific patient cohort. However, a sizable percentage of respondents, 41.8%, believed that they were receiving inferior care if they only saw a physician extender at a routine follow-up visit. Many orthopedic surgeons rely on the care provided by physician extenders to enable them to see additional patients. Physician extenders are well trained to provide high-quality care, including at routine postoperative visits. The results of this study, that many patients believe physician extenders provide lower-quality care, may be a result of inadequate patient education regarding the extensive training and education physician extenders undergo. Physician extenders are qualified, licensed healthcare professionals who are playing increasingly important roles within orthopedics and medicine as a whole. As the demand for orthopedic surgeons to see more patients increases, so does the role of physician extenders. Future research is warranted into educating the public regarding the importance of these healthcare providers and the adequacy of their training.

While many practices now routinely obtain patient satisfaction scores, another modality through which patients can express their satisfaction and experiences with healthcare providers is through online internet physician rating sites (IPRS). These sites have exploded in number and popularity in recent years and, according to some studies, have a very real effect on provider selection.²⁴ Interestingly, a low percentage of patients in this study utilized IPRS reviews to find their doctors. In a recent prospective survey study of 1000 consecutive patients presenting for care at the Mayo Clinic, Burkle and Keegan²⁴ reported that 27% of patients would choose not to see a physician based on a negative IPRS review. Interestingly, only 1.0% of patients reported finding their doctor through advertising. Numerous authors have recently addressed advertising in orthopedic surgery, specifically direct-to-consumer marking, including the influence of physician self-promotion on patients.^25,26 Specifically, Halawi and Barsoum²⁶ discussed how direct-to-consumer marketing is commonly disseminated to the public through television and print advertisements, which are modalities more commonly utilized by older generations. However, many advertising agencies are moving toward internet-based advertising, especially through orthopedic group and individual surgeon websites for self-promoting advertisement, as approximately 75% of Americans use the internet for health-related information.^25,27 The fact that many patients in this study did not utilize IPRS reviews or advertising (much of which is electronic) may be a result of the older, less internet-centric demographic that is often seen in an adult reconstruction clinic. Future research is warranted to determine what demographic of patients value IPRS reviews and how those reviews influence physician selection and the patient experience. 

There are several limitations to this study. First, the majority of the surveyed population was Caucasian, and our results may not be equally reflective of diverse ethnic backgrounds. Second, the cohort size, while based on previous studies conducted in a similar fashion, may be underpowered to detect significant differences for 1 or more of these questions. In addition, having a question regarding the patient’s medical background or experiences may have provided further insight as to why patients selected the answers that they did. Furthermore, questions regarding the patient’s education level, religious background, and income brackets may have provided further context in which to evaluate their responses. These questions were omitted in an effort to keep the questionnaire at a length that would maximize enrollment and prevent survey fatigue. Future research is warranted to determine what patient-specific, injury/symptom-specific, and treatment-specific variables influence the subjective patient experience.

CONCLUSION

The vast majority of patients desire only 10 to 20 minutes with their doctor and are highly satisfied with the amount of time their surgeon spends with them. Patients reported no significant gender- or ethnicity-based preferences for their doctor. The majority of patients believe that a wait time exceeding 30 minutes is too long. A greater effort needs to be made to educate patients and the public about the significant and effective roles nurse practitioners and physician assistants can play within the healthcare system. While this cohort did not report notable utilization of IPRS reviews, it remains essential to understand what factors influence patients’ subjective experiences with their providers to ensure that patients achieve their desired outcomes, and report as such on these websites as they continue to gain popularity. Diminishing clinic wait times and understanding patient preferences may lead to a greater percentage of “satisfied” patients. While the majority of focus has been and will likely continue to be on improving patients’ satisfaction with their outcomes, more work needs to be done focusing specifically on the process through which outcomes are achieved.